PHARMACOLOGY Mac

Vapor pressure=
0.75%
243
B/G – 2.4
BP = 50OC)
HALOTHANE: MW- 197

PHYSICAL PROPERTIES: Halogenated alkane

Carbon – fluoride bonds responsible for its non-inflammable/ non-explosive
Preservative- Thymol 0.01% amber- colored bottles prevent spontaneous oxidative decomposition
Least expensive, safe

CVS EFFECTS: Arterial BP↓, HR ↓, CO↓, SVR unchanged

RESPIRATORY EFFECTS: Rapid shallow breathing RR↑, TV↓, alveolar ventilation ↓, PaCO2↑, apneic
threshold ↑, hypoxic drive ↓, Potent bronchodilator  reverse asthma induced bronchospasm
Attenuates airway reflexes, ↓mucociliary fx ↑

CNS EFFECTS: ↑ CBF, ↑ICP, CMRO2 ↓, EEG slowing (↓seizer)

NEUROMUSCULAR: Relaxes skeletal muscle, Potentiates NMBA’s, Trigger MH

RENAL: ↓PBF, ↓GFR, ↓U/O.

HEPATIC: ↓HBF, Hepatic artery vasospasm, ↓metabolism of drugs

BIOTRANSFORMATION: Oxidized in liver by cytochrome p450 Trifluoroacetic acid

TOXICITY: halothane hepatitis extremely rare. Pts. exposed to multiple-halothane anesthetics at short
intervals, middle age obese women, familial predisposition or personal h/o toxicity are at ↑ risk

SIGNS: ↑serum alanine & aspartate transferase, ↑bilirubin and encephalopathy.

CONTRAINDICATIONS:

1. Unexplained liver dysfx following previous exposure

2. Hypovolemic patients
3. Severe cardiac dx (AS)
4. Pheochromocytoma

CAUTION: Pts. with intracranial mass lesion (IC hypertension)

DRUG INTERACTIONS:

1. Myocardial depression exacerbated by β-blockers and Ca.-channel

2. TCA and MAO inhibitors fluctuation in BP and arrhythmias.
3. Combination with aminophylline cause serious ventricular arrhythmia

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 MAC 1.2%,
Vapour Pressure: 240,
B/G: 1.4,
ISOFLURANE: BP: 49OC

PHYSICAL PROPERTIES: Noninflammable, pungent ethereal odor, chemical isomer of enflurane.

CVS EFFECTS: ↓BP and ↓SVR, ↑HR, CO-N/C, dilates coronary arteries, coronary steal syndrome.
RESPIRATORY EFFECTS: ↓TV, ↑RR, ↑PaCO2, ↓MV
Good bronchodilator but not as potent as halothane
CNS EFFECTS: ↑CBF, ↑ICP, ↓CMRO2, ↓seizures, Silent EEG @ 2MAC
NEUROMUSCULAR: relaxes skeletal muscle, potential NMBA
RENAL: ↓RBF, ↓GFR, ↓UOP
HEPATIC: ↓HBF, LFT’s minimally affected
Biotransformation: metabolized to tri fluoroacetic acid

TOXICITY: 20 MAC hours lead to fluoride levels > 50 µmol/L

CONTRAINDICATIONS: No unique contraindication

Drug interaction: epinephrine can be safety administered in doses up to 4.5 µg/ kg

DESFLURANE: MAC 6.0,

Vapor Pressure: 681,
BG: 0.42,
PHYSICAL PROPERTIES: Structurally very similar to isoflurane BP: 23.5
Boils at room temperature – special vaporizer
Very rapid induction and recovery Wake up time < 50%of isoflurane, ¼th as potent as other volatiles. 17
times > potent then N2O

CVS EFFECTS: ↓BP, ↓SVR, HR↑ or N/C, CO ↓ or N/C

Dose not ↑ coronary artery blood flow like isoflurane
RESPIRATORY: ↓TV, ↑RR, ↓AV, ↑PaCO2
Pungency and airway irritation  not suitable for induction
CNS EFFECTS: ↑CBF, ↑ICP, ↓CMRO2, ↓seizures
NEUROMUSCULAR: Potentiates NMBA’s
RENAL: No change or mildly ↓RBF, GFR and UOP
HEPATIC: LFT’s not affected

BIOTRANSFORMATION: Minimal metabolism. Degraded to CO

CONTRAINDICATIONS: severe hypovolemia, MH, IC hypertension

DRUG INTERACTIONS: epinephrine safe up to 4.5µg/kg

Desflurane emergence associated with delirium in children Fentanyl ↓ 1-2µg/kg

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 MAC: 2.0,
Vapour pressure 160,
B/G: 0.65,
SEVOFLURNE: BP: 58.5)

PHYSICAL PROPERTIES: Solubility slightly >Desflurane, Non pungent, rapid induction and recovery in
paediatric and adults. (Emergence delirium)
CVS EFFECTS: ↓BP, ↓SVR, ↓CO, HR N/C. prolongs QT intervals
RESPIRATORY: ↓TV, ↑RR, ↑PaCO2. Reverses bronchospasm
CNS EFFECTS: ↑CBF, ↑ICP, CMRO2 ↓, no seizures
NEUROMUSCULAR: produces adequate muscle relaxation for intubation of children following inhalation
induction
RENAL: ↓RBF, ↓concentra on ability
HEPATIC: ↑HBF, maintain oxygen delivery
BIO TRANSFORMATION: metabolism by P-450 enzyme system
TOXICITY: Soda lime or Baralyme degrade sevo into nephrotoxic Compound A, accumulation of
compound A ↑ses with ↑respiratory gas temperature, low flow anesthesia, dry Baralyme and high
sevoflurane concentration and anesthetics of long duration
Sevoflurane should not be used in pts with pre-existing renal dysfx
Sevo also degraded into hydrogen fluoride which produces acid burn on contact with respiratory
mucosa (Add water into sevo and plastic bottle)
CONTRAINDICATIONS: Severe hypovolemia, MH, IC hypertension
DRUG INTERACTIONS: Potentiates NMBA’s

Elimination half life ∝

ratio of clearance
PHARMACOLOGICAL PRINCIPLES:
PHARMACOKINETICS: (How the body affects a drug)
Study of relations ship of a drug dose, concentration in tissues and time since administration
DEFINED BY 4 PARAMETERS: absorption, distribution, biotransformation and excretion
ELIMINATION: implies drug removal by both biotransformation and excretion
CLEARANCE: is a measurement of the rate of elimination
BIOAVAILABILITY: Fraction of unchanged drug that reaches the systemic circulation
VOLUME OF DISTRIBUTION: The apparent volume into which the drug has been distributed is called its
volume of distribution

BIOTRANSFORMATION: Alteration of a substance by metabolic processes. Liver is the primary organ

metabolic biotransformation divided into phase I and phase II reactions
 Phase I reaction convert a parent drug into more polar metabolites rough oxidation, reduction or
hydrolysis
 Phase II reactions conjugate a parent drug or phase-I metabolite to form a highly polar end product
that can be eliminated in urine.

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CLEARANCE: Volume of plasma cleared of drug per unit of time and is expressed as mls/min
PHARMACODYNAMICS: (How a drug affects a body)
Study of therapeutic and toxic organ system effects of drugs defined by efficacy, potency, therapeutic
ratio, MOA, interaction and structure activity relation ship

MEDIAN EFFECTIVE DOSE: (ED50)

The dose of drug required to produce a given effect in 50% of the population. ED 50 of volatiles = MAC
MEDIAN LETHAL DOSE: (LD50)
The dose that results in death of 50% of population
Therapeutic index is the ration of LD50: ED50
AGONIST: Endogenous or exogenous substances that directly change cell function by binding to
receptors are called agonist
ANTAGONIST: Also binds to receptor but do not cause a direct effect on the cell.
COMPETITIVE ANTAGONIST: Binds reversibly to receptors and can be displaced by high concentration of
agonist
NONCOMPETITIVE ANTAGONIST: Bind to receptors with such affinity that even high concentration of
agonist cannot revers the receptor blockade.
Thiopental  Induction IV 2.5% to 3-6 mg/kg
BARBITURATES (STP) Pentobarbital  Premedication oral 2-4mg/kg
Methohexital Induction IV 1-2mg/kg

MOA: Depresses reticular activating system by suppressing transmission of excitatory neurotransmitter

(ach) and enhance transmission of inhibitory neurotransmitter GABA
PHYSICAL PROPERTIES: Sulphur analogue of pentobarbital yellowish powder with bitter taste and faint
smell of garlic. Water soluble, unstable in solution, short shelf life, painful on arterial injection

PHARMACOKINETICS: pt. Lose consciousness within 30 sec and awakes within 20 minutes (distribution
half-life)
Elimination half-life 3-12h
BIOTRANSFORMATION: hepatic oxidation to inactive water-soluble metabolites
CVS EFFECTS: ↓BP, ↑HR, ↓CO, ↓Myocardial contractility
RESPIRATORY: ↓ Ventilator drive, upper airway obstruction, apnea Bronchospasm in asthmatics and
laryngospasm in lightly anesthetized pts following air way instrumentation
CNS EFFECTS: ↓ CBF, ↓ICP, ↓CMRO2, progressive CNS depression including spinal cord reflexes, potent
hypnotic affect, poor analgesic, very potent anticonvulsant (50-100mg IV STP)
SKELETAL MUSCLE: ↓ tone, poor muscle relaxant when use alone
UTERUS AND PLACENTA: ↓ contrac ons at high doses cross placenta
RENAL: ↓ RBF, ↓GFR
HEPATIC: ↓ HBF, ↑metabolism
EYE: ↓ IOP, corneal, conjunc val, eye lash and eye-lid reflexes abolished
DOSE: Adult -4 mg/kg, Children – 6 mg/kg, Elderly -3 mg/kg
Administered as 2.5% solution IV, Anticonvulsant dose – 50-100 mg IV

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 Distribution HL: 20 min
Elimination HL: 3-12Hrs
Anticonvulsant dose: 50-100 mg IV
INDICATIONS:
1. Induction of anesthesia
2. Maintenance of anesthesia (Suitable for short procedures cumulation )
3. Rx of status epilepticus
4. ↓ ICP
CONTRAINDICATIONS:
1. Airway obstruction
2. Porphyria
3. Previous hypersensitivity reactions
ADVERSE EFFECTS: Hypotension, Respiratory depression, tissue necrosis, when intra-arterial injection,
laryngospasm, bronchospasm, allergic reactions, thrombophlebitis

TREATMENT OF INADVERTENT INTRA-ARTERIAL STP

1. Leave the catheter in place
2. Inject dilute papaverine, procaine or lidocaine to inhibit vasospasm  if this fails then
3. Brachial plexus block or α-Blockade
4. Administer heparin to prevent thrombus formation

DROPERIDOL: (Butyrophenone, structurally similar to haloperide)

MOA  antagonizes activation of dopamine receptors
Tranquilizer antipsychotic, neuroleptic, antiemetic
Duration of action 3-24h Mild α-adrenergic blocking effects
Antiarrhythmic – associated with prolong QT interval and torsades de point
12lead ECG must before droperidol. Cannot give in pts with pheochromocytoma
Dose: 0.05mg/kg intraoperative  2.5mg max
Parkinson dx - Combination with fentanyl produce neuroleptic any movement disorder
(Analgesia, amnesia, immobility)

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 Muscle relaxation does not
ensure unconsciousness,
amnesia or analgesia
NMBA’s (fad indicative of non-depolarizing block)
MOA: Depolarizing muscle relaxants act as ACh receptor agonists, whereas non-depolarizing muscle
relaxants fx as competitive antagonists

REVERSAL OF NM BLOCKADE:
 Because depolarizing muscle relaxants are not metabolized y acetyl cholinesterase, they diffuse
away from NM junction and are hydrolyzed in the plasma and liver by pseudocholinesterase (Plasma
cholinesterase) this is a fairly rapid process.
 With exception of mivacurium, NDMR are not metabolized by either acetyl-cholinesterase or Psudo-
cholinesterase reversal of their blockade depends on redistribution, gradual metabolism, excretion
by the body or administration of specific reversal agents (cholinesterase inhibitors) that inhibit
acetyl-cholinesterase enzyme activity
 By increasing NMJ ACh concentration and inhibiting pseudocholinesterase, cholinesterase inhibitors
can prolong depolarizing blockade.

MONITORING OF NM FUNCTION: 4 patterns

1. Tetany Sustained stimulus of 50-100 H2 lasting 5seconds –itch  a single pulse 0.2 ms in duration
2. Twitch  A single pulse 0.2ms in duration
3. Train-of-four  A series of 4 twitches in 2 s (2H2 frequency) each lasting 0.2ms long
4. DBS (Double burnet stimulation) 3 short high frequency stimulations separated by 20ms interval
followed 750ms later by 2(DBS3,2) or (DBS3,3) additional impulses

Tetany and DBS are preferred methods.

SUCCINYLCHOLINE Ach receptor agonist

PHYSICAL STRUCTURE: Also called diacetylcholine or Suxamethonium - consists of 2 joined Ach
molecules

METABOLISM AND EXCRETION: Rapid onset of action (30-60s) short duration of action (<10min) Low
lipid solubility, rapid metabolism in plasma by pseudocholinesterase into succinyl monocholine.
Duration of action prolonged by high doses or by abnormal metabolism  low levels of pseudo
cholinesterase or hypothermia
↓Pseudocholinesterase Pregnancy, liver dx, RF and drugs (Neostigmine, metoclopramide, esmolol,
pancuronium, OCP, echothiophete)
↓ Pseudocholinesterasemodest prolongation of action 92-20min)
1 normal and 1 abnormal gene (homozygous atypical)  very long blockade (4-8hrs)
Dibucaine-resistant gene most common abnormal pseudocholinesterase gene
Dibucaine number % of inhibition of pseudocholinesterase activity
It is proportional to pseudo cholinesterase fx and independent of enzyme amounts

Adequacy of enzyme is determined in lab quantitatively in U/L (minor factor) and qualitatively by
dibucaine number (major factor)

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Rx Prolonged paralysis from suxa caused by abnormal enzyme should be treated with continued
mechanical ventilation until muscle fx returns to normal

DRUG INTERACTIONS:
1. Cholinesterase inhibitors  Markedly prolong a depolarizing phase I block by 2 mechanisms :
a. Inhibiting acetylcholine esterase
b. ↓ hydrolysis
2. Non depolarizing relaxants Small dose of non-depolarizing relaxants antagonize a depolarizing
phase 1 block. Except pancuronium which augments suxa block by inhibiting pseudo
cholinesterase.

STORAGE: Stored under refrigeration (2-8OC) should be used within 14 days when exposed to room
temperature

DOSE: Adult intubating dose is 1-1.5mg/kg IV Repeated small boluses (10mg) or a suxa drip (1g in 500 or
1000ml) can be used during surgical procedures that require brief but intense paralysis e.g.
otolaryngological endoscopies.

SIDE EFFECTS:
1. CVS  Stimulation of nicotinic receptors and muscarinic receptors can ↑ or ↓ BP and HR. Low
dose of suxa produce negative chronotropic and inotropic effects but higher dose ↑ HR and
contractility and elevate circulating catecholamine levels
Bradycardia in children and after 2nd dose in adults
IV atropine (0.02mg/kg in children and 0.4mg in adults) is normally given prophylactically to
children prior to 1st dose and always before a 2nd dose in adults.
2. Fasciculation Prevented by prior small dose of non-depolarizing
3. HyperkalemiaSerum potassium ↑ by 0.5 mEq/L
4. Muscle pains  ↑ incidence of postop myalgia
Rocuronium prior to suxa prevents fasciculation and myalgias
5. Intragastric pressure elevation  By abdominal wall muscle fasciculation
6. Intraocular pressure elevation  Could compromise injured eye
7. Masseter muscle rigidity  Marked ↑ in tone preven ng laryngoscopy is abnormal and may be
premonitory sign of MH
8. Malignant hyperthermia  Potent trigger of MH
9. Generalized contractions
10. Prolonged paralysis
11. Intracranial pressure elevation Attenuated by hyperventilation
12. Histamine release

INDICATIONS:
1. RSI 4. ECT (Electrical Current Therapy)
2. Full stomach 5. Short surgical procedures
3. Obstetric pts

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CHOLINESTERASE INHIBITORS (Also called ANTICHOLINESTERASES)
1. Primary clinical use is to reverse nondepolarizing muscle blockade
2. Also used in the diagnosis and treatment of Myasthenia Gravis
3. Organophosphates, a special class of cholinesterase inhibitors used in ophthalmology and more
common as pesticides.

ACETYLCHOLINE:
Synthetized in nerve terminal by enzyme choline acetyl transferase which catalyzes the reaction
b/w Acetyl-coenzyme A and choline, After its release, acetylcholine is rapidly hydrolyzed by acetyl-
cholinesterase (True cholinesterase) into acetate and choline
Acetylcholine is the neurotransmitter for entire parasympathetic nervous system and parts of
SNS, some neurons in central nervous system and somatic nerves innervating skeletal muscle
Cholinergic receptors divided into 2 major groups:
1. Nicotinic receptors  Stimulates autonomic ganglia and SM receptors
2. Muscarinic receptors  Bronchial smooth muscle, salivary glands, SA node
Nicotinic receptors blocked by muscle relaxants
Muscarinic receptors blocked by anticholinergic drugs like atropine
They both respond to acetylcholine

 Methacholine (muscarinic agonist) used as a provocative test in asthma

 Bethanechol (muscarinic agonist) used for bladder atony
 Carbachol ( muscarinic + nicotinic agonist) used topically in wide angle glaucoma
 Primary goal while reversing NM blockade is to maximize nicotinic transmission and minimize
muscarinic side effects
2 Types of Reversal:
 SPONTANEOUS REVERSAL : by gradual diffusion, redistribution
Metabolism and excretion form the body of the non-depolarizing relaxant
 PHARMACOLOGICAL REVERSAL By specific reversal agents

MOA OF ANTICHOLINESTERASES:
(Inactivation of acetylcholinesterase by reversibly binding to the enzyme
In excessive doses, cholinesterase inhibitors potentiates a non-depolarizing MM blockade
In addition, these drugs prolong depolarization block of suxa

MUSCARINIC SE OF CHOLINESTERASE INHIBITORS

CVS  ↓HR, Brady-arrhythmias
Pulmonary Bronchial secretions, Bronchospasms
Cerebral Diffuse excitation (By physostigmine-cross BBB)
GIT ↑peristal c ac vity, ↑glandular secre ons, intes nal spasm
Genitourinary ↑bladder tone
Eye pupillary constriction Neostigmine 0.04 – 0.08mg/kg + Glycopyrrolate 0.2mg
Pyridostigmine0.1 – 0.4 mg/kg + Glycopyrolate 0.05mg
Edrophonium0.5 – 1mg/kg + Atropine 0.014
Physostigmine0.01 – 0.03 mg/kg + mg/kg – no anticholine 319
Dr. Tariq Mahr necessary
DOA: (Duration of action) Similar among all cholinesterase inhibitors
Suggested end points of recovery are sustained tetanus for 5sec in response to a 100 H2 stimulus in
anesthetized pt. OR sustained head lift in awake pt.

PHYSOSTIGMINE: (Antidote)
1. Lipid solubility and CNS penetration limits its usefulness as reversal
2. Effective in Rx of central anticholinergic toxicity caused by over dosage of atropine or scopolamine
3. Reverses some CNS depression and delirium associated with use of benzodiazepines and volatile
anesthetics
4. Effective in preventing postoperative shivering
5. Partially antagonizes morphine induced respiratory depression
 Muscarinic SE excessive salivation, vomiting and convulsions
Physostigmine completely metabolized by plasma esterases

ANTICHOLINERGIC
PHARMACOLOGICAL CHARACTERISTICS:
In clinical doses, only muscarinic receptors are blocked by these drugs
CVS: Tachycardia, shortens P-R interval, ↓heart block causes by vagal ac vity, atrial arrhythmias and
junctional rhythms large doses results in dilation of cutaneous vessels  (atropine flush)
RespiratoryInhibit bronchial secretions, relaxation of bronchial smooth muscle ↓ airway resistance
and ↑ses anatomic dead space
CNS Stimulation: Excitation, restlessness or hallucinations
Depression: Sedation and amnesia. Physostigmine reverses these
EyeMydriasis (pupillary dilation) and cycloplegia (inability to accommodate)
GU ↓ ureter and bladder tone leading to urinary reten on
Thermoregulation inhibition of sweat glands ↑temp (atropine Fever)

SCOPOLAMINE: Premedication dose is same as atropine usually given IM. Available as solution
containing 0.3, 0.4 and 1mg/ml
More potent antisialagogen then atropine and causes greats CNS effects Drowsiness and amnesia in
clinical doses prevents motion sickness. Best avoided in closed angle glaucoma

GLYCOPYRROLATE: Synthetic quaternary ammonium containing mandelic acid

Usual dose is one-half that of atropine
Premedication dose is 0.005-0.01mg/kg upto 0.2-0.3 mg in adults
Package as a solution of 0.2mg/ml
Do not cross BBB and is devoid of CNS and ophthalmic activity, potent inhibition of salivary and
respiratory tract secretions
Glycopyrolate has a longer duration of action (2-4h vs 30min) after IV administration

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ADRENERGIC AGONISTS AND ANTAGONISTS
 Norepinephrine is the neurotransmitter responsible for most of the adrenergic activity of
sympathetic nervous system
 Adrenergic receptors are divided into 2 general categories α and β. These further subdivided into α1
and α2 and β1, β2 and β3 these receptors are linked to G proteins, each using guanosine triphosphate
(GTP) as a cofactor
(Post synaptic receptors)

α1- RECEPTORS: Located in smooth muscle trough out body, in the eye, lung, blood vessels, uterus, gut
and genitourinary system α1-agonist associated with mydriasis, bronchoconstriction, vasoconstriction,
uterine contracture and contraction of sphincters in gestro intestinal and genitourinary tracts.
α1stimulation also inhibits insulin secretion and lipolysis
Most important CVS effect of α1stimulation is vasoconstriction  ↑SVR, ↑LV a erload and ↑BP

α2- RECEPTORS: (presynaptic receptors)

Stimulation of α2 receptors in CNS causes sedation and reduces sympathetic outflow  leads to
peripheral vasodilation and lowers BP

β2- RECEPTORS: Most important β1 receptors located in heart. Positive chronotropic (↑HR), inotropic
(↑contrac lity) and dromotropic (↑conduction)
Receptors: located in smooth muscle and gland cells
Relaxes smooth muscle bronchodilation, vasodilation and relaxation of uterus (tocolysis), bladder and
gut Also glycogenolysis, lipolysis, gluconeogenesis and ↑ insulin release
Also induce hypokalemia and dysrhythmias

Β3- RECEPRORS: Found in gall bladder and brain adipose tissue. Play a role in lipolysis and thermogenesis
in brown fat.

VASOPRESSOR:
CATECHOLAMINES
Adrenergic agonists that have a 3,4-dihydroxy benzene structure are known as catecholamines. Typically
short acting
Naturally occurring Epinephrine, norepinephrine and dopamine
Synthetic catecholamine: Dobutamine and isoproterenol

PHENYLEPHRINE: Non-catecholamine direct α1-agonist primary effect is peripheral vasoconstriction with

concomitant rise in SVR and arterial BP
Reflex bradycardia can reduce cardiac output
Dose  Small IV boluses of 50-100µg (0.5-1µg/kg)
Rapidly reverses ↓BP by peripheral vasodila on e.g. spinal anesthesia
Tachyphylaxis occurs with infusions

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METHYLDOPA: Centrally acting α2 agonist (levodopa analog)
↓SVR  ↓ arterial BP (Peak effect within 4hr)
Recommended for treating high BP in pregnancy

CLONIDINE: α2 agonist commonly used for its anti-hypertension and negative chronotropic effects. Also
sedative properties clonidine appears to decrease anesthetic and analgesic requirement (↓MAC) and to
provide sedation and anxiolysis.
Clonidine prolongs the duration of regional blocks
Decreased postoperative shivering,
Inhibition of opioid induced muscle rigidity, Attenuation of opioid with-drawl symptoms
Rx of some chronic pain syndromes
SEBradycardia, Hypotension, sedation respiratory depression and dry mouth
Both drugs are adrenergic agonists but also sympatholytic (↓Sympathetic Outflow)

EPINEPHRINE: α1 β1 β2
Direct stimulation of β1- receptors by epinephrine raises CO and myocardial oxygen demand by
increasing contractility and HR
α1stimulation ↓splanchnic and renal blood flow but ↑ses coronary and cerebral perfusion pressures.
β2 stimulation  vasodilation in skeletal muscles and relaxes bronchial smooth muscle
 Principal pharmacological Rx for anaphylaxis and VF/croup
 Complications  cerebral hemorrhage, coronary ischemia and ventricular dysrhythmias
 Halothane potentiates dysrhythmic effects of epinephrine
 In emergency situations e.g. shock and allergic reactions it can be administered as an IV bolus of
0.05-1mg
 Continuous infusions @ a rate of 2-20 µg/min to improve myocardial contractility and heart rate
 Some local anesthetic solutions containing epinephrine at a concentration of 1:200000 (5µg/ml) or
1:400000 (2.5µg/ml) characterized by less systemic absorption and longer duration of action
 Epinephrine is available in vials at conc. of 1:1000 (1mg/ml)
a 1:100000 (10µg.ml) 0.01 mg/ml concentration is available for pediatric use

EPHEDRINE:
 CVS effects are similar to epinephrine ↑BP, ↑HR, ↑contrac lity and ↑CO. Bronchodilator
 Used as a vasopressor during anesthesia
 non-catecholamine, longer duration of action
 Much less potent, has direct and indirect actions
 Ephedrine stimulates CNS (↑MAC)
 Vasopressor of choice in obstetric use  Dose not ↓uterine blood flow
 Antiemetic properties in association with hypotension following S/A
 Administered as a bolus of 2.5-10 mg, children (0.1 mg/kg)
 Available in 1 ml ampules containing 25 or 50 mg ephidrin

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NOREPINEPHRINE:
 Direct α1 stimulation induces intense vasoconstriction of arterial and venous vessels. ↑myocardial
contractility from β-effects  ↑BP but ↑afterload and reflex bradycardia prevents elevation in CO
 Used with an α-blocker (e.g. phentolamine) to take advantage of its β activity without profound
vasoconstrictions
 ↓ RBF and ↑ myocardial O2 requirements limit the usefulness of norepinephrine to  Refractory
shock which requires potent vasoconstriction to maintain tissue perfusion pressure
 Extravasation of norepinephrine at site of IV administration can cause tissue necrosis
 Administered as a bolus of 0.1µg/kg
 Continuous infusion at a rate of 2-20 µg/kg/min
 Ampules contain 4mg in 4 ml solution

DOPAMINE: Non selective direct and indirect adrenergic agonist

 Small doses ≤ 2µg/kg/min have minimal adrenergic effects but activate dopaminergic receptors (DA1
receptors) vasodilates the renal vasculature and promotes diuresis (Renal dose dopamine)
 At moderate doses (2-10µg/kg/min), β1-stimulation increases myocardial contractility, HR and CO.
Myocardial oxygen demand typically increase more than supply
 α1-effects become prominent at higher doses (10-20µg/kg/min) causing an ↑in SVR and ↓ in RBF
 Dopamine is commonly used in Rx of shock to improve CO2 support BP & maintain renal function
 Used in combination with a vasodilator (GTN or SNP) which reduces afterload and further improves
CO
 Administered as continuous infusion (400mg in 1000ml, 400µg/ml) at rate of 1-20µg/kg/min
 Available in 5ml ampules containing 200 or 400mg dopamine

DOBUTAMINE: Synthetic catecholamine

 Selective β1 agonist
 Primary CVS effects is ↑CO as a result of ↑ contrac lity
 A light decline in SVR by β2 activation prevents much rise in BP
 ↑ Coronary blood flow
 Favourable effects on myocardial oxygen balance make dobutamine a good choice for pts. with
combination of CHF and CAD particularly if SVR and HR are already elevated
 Administered as an infusion (5mg/ml) (2-20µg/kg/min)
 Supplied in 20ml vials containing 250mg

PHENTOLAMINE: α-Blocker
 α1 Antagonism and direct smooth muscle relaxation are responsible peripheral vasodilation and
↓ in arterial BP
 Reflex tachycardia and postural hypotension limits its use to treat hypertension caused by
excessive α-stimulation e.g. pheochromocytoma and clonidine withdrawal.

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β- BLOCKERS
LABETALOL: Mixed antagonists
 Labetalol blocks α1, β1 and β2 receptors
 Mixed blockade reduces SVR and arterial BP
 HR and CO slightly depressed or unchanged
 Labefalol lowers BP without reflex tachycardia because of its combination of α and β effects
 Onset of action  5min after dose (peak effect)
 Initial recommended dose is 0.1-0.25 mg/kg IV over 2minutes twice this amount can be given at 10
min interval until desired BP response is obtained
 Long elimination half-life (>5h) so prolong infusion avoid
 Labetalol (5mg/ml) is available in 20 and 40 ml multi dose containe

ESMOLOL: Ultra short-acting selective β1 antagonist

 ↓HR and to a lesser extent BP
 Successfully used to prevent tachycardia and HTN in response to perioperative stimuli such as
intubation, surgical stimulus and emergence
 Esmolol is as effective as propranolol in controlling ventricular rate of patients with AF or flutter
 Cardioselective, at higher doses it blocks β2-receptors in bronchial and vascular smooth muscle
 Short duration of action  Rapid redistribution (distribution HL 2min and hydrolysis by RBC esterase
(eliminationHL—9min)
 As with all β1 blockers, esmolol should be avoided in patients with sinus bradycardial, heart block >
1st degree, cardiogenic shock and HF
 Administered as bolus (0.2-0.5mg/kg)  for laryngoscopy and intubation
 Supplied as multi-dose vials containing 10ml (10mg/ml)

PROPRANOLOL: Non-selective β1 and β2 antagonist

 BP ↓ by ↓myocardial contrac lity, ↓HR and diminished renin release
 CO and myocardial oxygen demand are reduced
 Particularly useful during ischemia related to ↑BP and ↑HR
 Effective in slowing SVT and occasionally controls recurrent VT/VF caused by myocardial ischemia
 Blocks β-adrenergic effects of thyrotoxicosis and pheochromocytoma
 Concomitant administration of propranolol and verapamil, synergistically depress HR, contractility
and AV-node conduction
 Discontinuation for 24-48 hrs may trigger withdrawal syndrome characterized by hypertension
(reboud), tachycardia and angina
 SE: Bronchospasm, CHF, bradycardia and AV heart block
 Extensively protein bound, cleared by hepatic metabolism
 Elimination HL-100min
 0.5mg increments every 3-5min
 Supplied in 1ml ampules containing 1mg

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 Dilates pulmonary vasculature  ↑ physiological dead space
HYPOTENSIVE AGENTS’ prevents hypoxic pulmonary vasoconstriction V/Q mismatch
↓preload and a erload, ↓SVR, ↓BP

SNP: Relaxes both arteriolar and venous smooth muscle

MOA: Metabolizd to release nitric oxide, which is naturally occurring potent vasodilator released by
endothelial cells, plays an important role in regulating vascular tone in body
 Inhaled Nitric Oxide is selective pulmonary vasodilator beneficial in Rx of reversible pulmonary HTN
and ARDS and OLV
Clinical sues: Potent and reliable antihypertensive
 Diluted to a concentration of 100µg/ml and administered as a continuous infusion (0.5-
10µg/kg/min)
 Extremely rapid onset of actin (1-2min)
 Needs intra-arterial monitoring and use of infusion pumps
 Must be protected from light because of photo degradation

Metabolism: SNP enters RBC  from unstable nitropurusside redical and methemoglobin
 Acute cyanide toxicity: characterized by metabolic acidosis, cardiac arrhythmias and ↑venous
oxygen content (inability to utilize oxygen)
 Another early sign of cyanide toxicity is acute resistance to hypotensive effects of increasing doses
of SNP (Tachyphylaxis)
 Can be avoided if cumulative dose of SNP is < 0.5mg/kg/h
 Pts with cyanide toxicity should be mechanically ventilated with 100% Oxygen to maximize O2
availability
 Rx  Sodium thiosulphate (150/kg over 15min) or 3% sodium nitrate (5mg/kg over 5min)
 Thiocynate accumulation Thyroid dysfx, muscle weakness, nausea, hypoxia and acute toxic
psychosis
Symptomatic patient (or MetHb level is >20 %) –
 Methemoglobinemia: Rx Methylene blue (1-2mg/kg IV)
methylene blue (MB). MB – 1 to 2 mg/kg IV over 5 min
 Risk of cyanide toxicity is not increased by renal failure (total dose should not exceed 7-8 mg/kg – MB can cause
dyspnea, chest pain, hemolysis)

NITROGLYERINE (GTN): (Venous dilator)

MOA: Relaxes vascular smooth muscle, with venous dilatation predominating over arterial dilation
 Metabolized to nitric oxide activates guanylyl cyclase -↑CGMP  ↓intracellular
Cavascular smooth muscle relaxation
Uses:
1. Relieves myocardial ischemia, HTN and ventricular failure
 Diluted to 100µg/ml and administered as infusion (0.5-10µg/kg/min)
 Glass containers and special IV tubing because adsorption in PVC
 Also administered sublingual (peak effect 4min) or transdermal (sustained release for 24h)
Metabolism: Rapid reductive hydrolysis, metabolic products is nitriteconvert hemoglobin to
methemoglobin

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CVS effects: 1. Nitroglycerin ↓mycoardial oxygen demand and ↑ses myocardial oxygen supply
Preload reduction makes it an excellent choice in cardiogenic pulmonary edema
HR is unchanged or minimally increased
Reboud hypertension is less likely than SNP
CNS effects: Headache form dilation of cerebral vessels is common
Respiratory: Relaxes bronchial smooth muscle
Uterus: Effective but transient uterine relaxant
Blood: Inhibit platelet aggregation
NMBA’s: Potentiates Pancuronium blockade

HYDRALAZINE: (Arteriolar dilator)

MOA: Arteriolar dilator causing dilation of precapillary resistance vessels
Uses: Intra operative hypertension controlled with IV 5-20mg.
 Onset of action within 15min and antihypertensive effects use lasts for 2-4 hrs.
 Frequently used to control pregnancy induced hypertension
Metabolism: Under goes acetylation and hydroxylation in liver
CVS effects: ↓SVR  ↓BP, ↑HR, ↑contrac lity and ↑CO. These compensatory responses can be
detrimental to pts with CAD minimized by concurrent administration of β-Blocker
CNS effects: Potent cerebral vasodilator and inhibits CBF autoregulation
Renal: Excellent in RF as RBF maintained or increased

ADENOSINE: Potent vasodilator

MOA: Opens potassium channels, hyperpolarizing nodal tissue and ↓firing leads to AV-block and
slowing of sinus rate in pts with SVT.
Uses: Reduce arterial BP during anesthesia
 Very short half-life(<10s)
 Continuous infusion (60-120µg/kg/min)required for controlled h--------
 Only indication by FDA Paroxysmal SVT including associated with WPW syndrome by IV bolus of
6mg over 1-
 IV bolus for SVT can induce AF and thus administered only ----- appropriate setting where
cardioversion can be performed
 Slows AV conduction (↑P-R interval) and interrupt reentrant arrhythmia
 Large doses depress sinus node and ventricular automamacity leading to brief periods of sinus pause
that resolves spontaneously
 Avoided in pts. with 2nd or 3rd degree block or sick sinus syndrome

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LOCAL ANESTHESIA:
CLINICAL USES:
LA Techniques Concentrations Max. dose Block duration
Bupivacaine Epidural, Spinal, 0.25%,0.5%, 0.75% 3mg/kg 1.5-8h
Infiltration, Blocks

Lidocaine Epidural, spinal nerve 0.5%, 1%, 1.5%,2% 4-5mg/kg 75-120min

block, IVRA, topical 4%,5% 7mg/kg with
epinephrine
Prilocaine Dental nerve blocks 4% 8mg/kg 30-60min
Benzocaine and cocaine are only topical (Esters)

NERVE FIBER CLASSIFICATION:

AαMotor
AβPropioception (Touch and pressure)
AϒMotor
AδPain, Cold temperature, Touch
BPreganglionic autonomic fibres
CPain, warm & cold temperature, touch

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Dr. Tariq Mahr
 Cemitidinehepatotoxicity, interstitial nephritis,
gynecomastia, impotence
Dimenhydramategravinate

H1-RECEPTOR ANTAGONISTS’

DIPHENHYDRAMINE (BENADRYL)
Dose25-50mg, Duration 3-6hrs, sedative and antiemetic
UsesSuppression of allergic symptoms (Urticaria, rhinitis, conjunctivitis)
Vertigo, N&V (motion sickness, menier’s dx) sedation, suppression of cough and dyskinesia (e.g.
Parkinsonism, drug induced extrapyramidal side effects)
 Used for premedication (antiemetic and mild hypnotic effects)
 Newer 2nd generation antihistamines produce no sedation e.g. Loratidine, fexofenadine and
cefirizine available only in oral preparations, used primarily for allergic rhinitis and urticarial
 Meclizine and dimenhydrinate are used primarily as an antiemetic, particularly in motion
sickness and vertigo.

H2-RECEPTOR ANTAGONISTS:
MOA: Competitively inhibit histamine binding to H2 receptor reducing gastric acid output and raising
gastric pH.
Uses:
1. Peptic duodenal and gastric ulcers
2. Hypersecretory states (Zollinger-Ellison Syndrome)
3. Gastroesophageal reflux dx (GERD)
4. IV preparations to prevent stress ulceration in critically ill
5. Reduce perioperative risk of aspiration pneumonia
6. Combined H1+H2 antagonist protect agonist drug induced allergic reactions (e.g. IV
radiocontrast, protamine).
Ranitidine (zantac) PO/IV 150-300 mg/50mg
Onset 1-2h
Duration 10-12h
↓↓↓ Acidity and ↓volume

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ANTACIDS: ↓ gastric pH but ↑volume
MOA: Neutralizes the acidity of gastric fluid by providing a base (usually hydroxide, carbonate,
bicarbonate, citrate or trisilicate) that reacts with hydrogen ions to form water

USES:
1. Rx of gastric and duodenal ulcers
2. GERD
3. Zollinger-Ellison syndrome
4. Protect form aspiration pneumonitis by ↑ing gastric pH
5. Non-particulate antacids (sodium citrate or bicarnonate)
Are much less damaging to lungs alveoli if aspirated

DOSE: 15-30ml orally, 15-30 minutes prior to induction

METOCLOPRAMIDE:
MOA: Act as a prokinetic agent in upper GI tract is not dependent on vagal innervation but is abolished
by anticholinergic agents. It does not stimulate secretions.

UESE: ↑s mulatory effects of acetylcholine on intes nal smooth muscle  ↑LES stone, speeds gastric
emptying and lowers gastric fluid volume.
 Diabetic gastroparesis and GERD
 Prophylaxis of aspiration pneumonia
 Antiemetic  blocks dopamine receptors in chemoreceptor trigger zone of CNS.
 Antiemetic in cancer chemotherapy
 PONV
 Analgesic Renal or biliary colic, uterine cramping

Pantoprazole is only IV PPI

SIDE EFFECTS:
1. Rapid iv injection  abdominal cramping
2. Induce hypertensive crises in pts with pheochromocytoma
CONTRAINDICATION:
1. Absolute intestinal obstruction
2. ParkinsonsDx
DOSE:
10-20mg IV/IM, injected over 5minutes
High doses 1-2mg/kg to prevent emesis during chemoth

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Dr. Tariq Mahr
CRYSTALLOIDS: initial resuscitation fluid
If 3-4L given  Response inadequate  add colloids

R/L: Slightly hypotonic - ↓ Na to 130 mEq/L 273 mOs/L

mEq/L Na+ 130, Cl 109, K+4, Ca+3, Lactate 28. Most physiological fluid whn large volumes needed
Lactate converted by liver  bicarbonate prior to PRBC transfusion
308mOs/L

N/S: Preferred for hypochloremic metabolic alkalosis. Produces dilutional hyperchloremic acidosis in
high dose
Na 154, CL 154

5%DW: Hypotonic, 253 mOsm/L. 50g/L glucose used for pure water replacement and maintenance fluid
for Na restricted pts

9% Normal Saline: Hypertonic 1026mOsm/L severe hyponatremia

%D 5 in NS Hypertonic 586mOsm/L (5% dextrose (278 mOsm/L) + 0.9% NS (308 mOsm/L) = 586 mOsm/L)
Na 154, CL 154, glucose 50g/L

Intra vascular HL crystalloids 20-30 min

Intravascular HL Colloids  3-6 hrs

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Dr. Tariq Mahr
 +
HaemaccelNa2 145 Cl 145 K 5.1  HL – 5 hrs Ph 7.4
+
Gelofusion Na 154 Cl 125 K 0.4  HL – 4 hrs Ph 7.4

Indications for colloid

1. Fluid resuscitation in pts. with severe intravascular fluid deficit (hemorrhagic shock)
2. Fluid resuscitation in severe hypoalbuminemia or conditions with large protein loss e.g. burns (if
>30%
Colloids prepared in N/S  cause hyperchlorenic metabolic acid
Blood derived colloids  Albumin 5% and 25%, plasma protein fraction 5%
Synthetic colloids Dextrose (Dextran) Antiplatelate, antigenic
Goelatin
Starch – less expensive, highly effective
Non antigenic, coagulation not coefficient

Surgical pts.
PRBC’s: Ideal in anemic pts with CCF HCt 50 – 70%
O
Must warm to 37 C during infusion
Stored @ 26 OC
Shelf life 35 days
Trainsfuse within 30 min of removal from fridge
Transfuse unit over maximum 4hrs
Must be compatible with pts ABO Rh D type

Platelets: stored @ 20 – 24 OC on agitator rack

Shelf life 5 days
Transfuse unit within 30min
Indications: thrombocytopenia or dysfx platelets
Platelets < 50000 associated with ↑ bleeding during surgery
1 unit  ↑Plts 10-20000
ABO compatibility desirable but not necessary
Transfuse platelets survive 1-7 days following transfusion

FFP: 1unit  150 ml

Storage  30 OC Warmed to 37OC prior to transfusion
Shelf life 1year if frozen
Once thewed should be transfused within 4 hrs
Should be ABO compatible but not mandatory
Contains all plasma proteins including clotting factor
Indicated in
1. Factor deficiency Vit K def. in ICU
2. Reversal of warfarin therapy
3. Coagulopathy
4. After massive transfusion
Dose  10-15 ml/kg
1unit FFP  ↑factor by 2-3% in adults

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Dr. Tariq Mahr
Cryoprecipitate: Stored @ 30OC
Shelf life  1yr frozen
Once thawed  give within 4hrs
Rich in factor VIII, von Willbrand, XIII, fibrinogen

Management of hemolytic reaction:

1. Stop transfusion immediately
2. Unit should be rechecked
3. Repeat compatibility test
4. Check urine for Hb
5. Osmotic diuresis with mannitol
6. IV fluids
7. If rapid blood loss  Give plts and FFP

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Dr. Tariq Mahr
CXR

ARDS:Life threatening lung condition that hypoxia prevents enough oxygenation to blood causing
hypoxia

Causes:
1. Sepsis
2. Pneumonia
3. Bleeding
4. Trauma to chest or head
5. Toxic inhalation
6. Aspiration

Management: Supportive mechanical ventilation

Treat the cause
↑FiO2, ↑ PEEP

PLEURAL EFFUSION: Fluid in pleural cavity

Causes:
1. CHF
2. Low proteins in blood (↓ albumin)
3. Inflammation (Pericarditis)
4. Lung injury (Trama)
5. Drug reaction
6. Malignancy

S&S: Chest Pain, Cough, Fever, ↑RR, SOB

Rx:
1. Remove fluid
2. Treat the cause CHF Diuretics
Infection  Antibiotics
3. Thoracocentesis if massive
4. Chest tube

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Dr. Tariq Mahr
ATELECTASIS:
Collapsed lung or pneumothorax
Collection of air in space around lungs

Causes:
1. Trama
2. Rib fracture
3. Surgery related  Pleural tear
4. CVP line
5. Spontaneous  no cause
6. COPD, asthma, TB ↑ risk of collapse

S&S:
Chest pain, SOB, ↑HR, ↓BP, Hypotension

Rx: Small  no Rx
Large chest tube

PULMONARY EDEMA:
Collection of fluid in alveoli

Causes:
1. MI 9. head injury
2. IHD 10. Airway obstruction
3. Fluid overload 11. Lung dx
4. Renal failure 12. HTN
5. Elderly 13. MS
6. Aspiration 14. Malignancy
7. Drugs/ toxin
8. Malnutrition

S&S:Pink frothy sputum, crepts, gallop rhythm, ↑JVP, ↑HR, ↑RR,↓ SpO2, ↑CVP

Rx: 100% O2, sitting position, IPPV with PEEP

Opioids, diuretics, vasodilator, suction of ETT

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Dr. Tariq Mahr
 PHARMACOLOGY
PHASE I AND II BLOCKS
Q.1)
a) What is phase I block?
b) What is phase II block?
c) What are the events that lead to the development of phase II block @ nicotinic cholinergic
receptors?
d) What must be done if phase II block appears?

Ans 1)
a) PHASE I BLOCK
Continuous end-plate depolarization due to the binding of depolarizing muscle relaxant to
acetylcholine (ACh) receptors is called phase I block.

b) Phase II block
The ionic and conformational changes in the acetylcholine receptor due to prolonged end-plate
depolarization is called phase II block, which clinically resembles to that of non-depolarizing
muscle relaxants.

c) Prolong end-plate depolarization can cause ionic and (ion channel opening) conformational
changes in the acetylcholine receptors that results in phase II block @ nicotinic cholinergic
receptors.

d) If phase II block appears, tetanic stimulation must be given to increase the evoked response to a
subsequent twitch called posttetanic potentiation. This will transiently increase the
acetylcholine mobilization following tetanic stimulation. This increase in Ach causes binding of
depolarizing muscle relaxant and end-plate depolarization.

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Dr. Tariq Mahar
 Cisatracurium: is a stereo isomer of
atracurium, 4 times more potent. Atracurium
contains 15% Cisatracurium.
MANNITOL AND ATRACURIUM METABOLISM
Q-2)
a) Metabolism of atracurium and factors which alter it?
b) Onset, duration of action and indications and complications of mannitol?
Stored at 2-8oC – Available as a solution of 10µg/ml

Ans)
a. METABOLISM OF ATRACURIUM: (BENZYL ISOQUINOLON)
Atracurium is so extensively metabolized through its pharmacokinetics are independent of renal
and hepatic function and < 10% excreted unchanged by renal and biliary routes.
Two separate processes are responsible for metabolism.
1. ESTER HYDROLYSIS: Catalyzed by nonspecific esterases, not acetyl cholinesterase or
pseudocholinesterase
2. HOFMANN ELIMINATION: A spontaneous, nonenzymatic, chemical breakdown occurs at
physiological PH and temperature.
Because of these 2 factors, atracurium’s duration of action can be markedly ↑ by
hypothermia and to a lesser extent by acidosis.
Laudanosine which is a breakdown product of atracurium Hofmann elimination has been
associated with CNS excitation resulting in elevation MAC and even precipitation of seizures
at very large dose Laudanosine is metabolized by liver and excreted in urine and bile.

Shorter acting in children and infants than in adults

SIDE EFFECTS:
1. Histamine release
2. Hypotension and tachycardia
3. Bronchospasm (should be avoided in asthmatics)
4. Laudanosine toxicity.
5. Hypothermia ↑ses dura on of ac on, acidosis to lesser extent
6. Chemical incompatibility  precipitate as a free acid if goes into an IV line containing alkaline
solution as STP (thiopental)
7. Allergic reactions.

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Dr. Tariq Mahar
MANNITOL
Asn 2.b) Mannitol is the most commonly used osmotic diuretic. It also ↑ RBF, Do not alter urinary PH.
Major effect is to increase water excretion and electrolytes (sodium and K) excretion.
Mannitol activates the intra renal synthesis of vasodilating prostaglandins.
It is also a free radical scavenger.
ONSET: 1-3 hours
DURATION OF ACTION: 3-8hrs
MOA: Diuresis, metabolically inert excreted unchanged.
INDICATIONS:
1. Prophylaxis of ARF (Renal protection)
2. Evaluation of acute oliguria
3. To ↓ ICP
4. To ↓ IOP
5. To preserve donor kidney in renal transplant.

COMPLICATIONS:
1. Hypertonicity.
2. Hypovolemia
3. Hypokalemia
4. Hypernatremia
5. Pulmonary edema in pts with limited cardiac reserve

DOSE: 0.25-1g/kg. (0.5g/kg average)

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Dr. Tariq Mahar
 Solution with NaCl for isotonicity,
Benzethonium chloride preserve at water
soluble, stable in solution, long shelf life
KETAMINE 1-2mg/kg
Q3) A solder sustained multiple bullet injuries on both leg and brought to hospital. BP 74/40 and HR
124b/m
a. What induction agent will you prefer?
b. What is the MOA of agent of choice?
c. What are its effects on respiratory system?

Ans 3)
a. Ketamine will be the induction agent of choice because it will stimulate the sympathetic nervous
system which will increase the BP of this pt., ketamine will induces analgesia, amnesia and
unconsciousness altogether.
b. MOA (dissociative anesthesia)
Ketamine functionally dissociates the thalamus from the limbic cortex. This state of dissociative
anesthesia causes the pt to appear conscious but unable to process or respond to sensory input.

c. EFFECTS ON RESPIRATORY SYSTEM:

1. Ventilator drive minimally affected
2. Rapid IV bolus administration or pretreatment with opioids can cause apnea
3. Ketamine is a potent bronchodilator making it a good induction agent for asthmatic pts.
4. Even upper airway reflexes remain intact pt. at increased risk of aspiration should be
intubated.
5. ↑ Saliva on  premedication with an anticholinergic agent (Glycopyrrolate).

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Dr. Tariq Mahar
 Distribution HL- 5-20 minutes, Meperidine is structurally similar to atropine
Elimination HL Alfentanil – 1.5 hr
Elimination HL Remifentanil – 10 min

OPIOIDS OVERDOSE MANAGEMENT, RECEPTORS, MOA.

MOA:Opioids bind to specific receptors located throughout CNS and other tissue. 4 types of receptors µ,
κ, δ and σ. Opioids bind to these receptors, activate them and produces effective analgesia and weak
sedation by (inhibiting presynaptic release and postsynaptic response to excitatory neurotransmitter
(eg, acetylcholine, substance P) from nociceptive neurons.

CLASSIFICATION OF OPIOID RECEPTORS

RECEPTOR CLINICAL EFFECT AGONISTS

µ (mu) Supraspinal analgesia (µ-1) Morphine

Respiratory depression (µ-2) Met-enkephalin2
Physical dependence Β-endorphin2
Muscle rigidity Fentanyl
Κ(Kappa) Sedation Morphine
Spinal analgesia Nalbuphine (kinz)
Butorphanol
Dynorphin2
Oxycodone
δ (Delta) Analgesia Leu-enkephalin2
Behavioral Β-endorphin2
Epileptogenic
σ(Sigma) Dysphoria Pentazocine (Sosegon)
Hallucinations Nalorphine
Respiratory stimulation Ketamine?

OPIOID OVERDOSE MANAGEMENT:

Sign and Symptoms  (Respiratory depression and pinpoint pupils)

1. Stop any opiate infusion
2. Special monitoring and close nursing observation
3. Marked respiratory depression  large dose naloxone 0.4 mg
4. Continuous naloxone infusion  shorter half-life than opioids (HL-60 min)
5. Small incremental doses of naloxone (0.04mg), reverses respiratory depression but not
analgesia
6. IV Doxapram 1mg/kg followed by 1-2mg/min used as temporary measures
7. antihistamine for itching caused by naloxone,
8. Metoclopramide for N & V.

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 Meperidine + MAO inhibitor  Respiratory arrest,
hypo/hypertension, coma, hyperreflexia

ADVANTAGES OF ROCURONIUM
Q5) what are the advantages of using Rocuronium over Suxamethonium for endotracheal intubation?

Ans 5) ADVANTAGES OF ROCURONIUM OVER SUXA

1. Rocuronium at a dose of 0.9 – 1.2 mg/kg has onset of action that approaches suxa making it a
suitable alternate for RSI but at a cost of (60 Sec) longer duration of action.
2. Rocuronium do not stimulate muscarinic receptors which causes Brady arrhythmias like sinus
bradycardia, junctional R
3. Rocuronium is not a trigger for MH like suxa
4. Rocuronium is not associated with fasciculations and painful analgesia
5. Rocuronium do not increase ICP and IGP
6. Rocuronium do not increase IOP
7. Rocuronium do not cause hyperkalemia.

KETAMINE INDICATIONS AND COMPLICATIONS:

INDICATIONS: (2mg/kg)
1. Shock/asthmatics
2. Paediatric anesthesia
3. Difficult locations like accident sites and casualties of war
4. Analgesia and sedation
5. To sedate asthmatics in ICU
6. Developing countries where equipment and trained staff is short

COMPLICATIONS:
All phenylpiperidine opioids (meperidine, methadone, tramadol)
1. Emergence delirium are weak serotonin reuptake inhibitors and can lead
2. Night mares to serotonin syndrome (confusion, fever, diaphoresis,
shivering, ataxia, myoclonus, hyperreflexia, and death) caused
3. Hallucinations by excessive serotonergic stimulation of the 5-HT1A receptor
4. HTN and tachycardia
5. Prolong recovery
6. ↑ saliva on
7. ↑ ICP
8. Allergic reactions

ABSOLUTE CONTRAINDICATION
1. ICP
2. Airway obstruction although airway is better maintained with ketamine than with other IV
agents

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COMPARISON OF CVS EFFECTS OF VOLATILE A
Q 6) Compare the cardiovascular effects of:
Halothane, Enflurane, Isoflurane, N2O, Sevoflurane

COMPARISION OF CVS EFFECTS OF VOLATILES:

CVS Effects HALO ENFLO ISO DES Sevo N2O

1. HR ↓ ↑ ↑ ↑ Stable ↑
2. CO ↓ ↓ ↓mild ↓mild mild↓ ↑
3. SVR Stable ↓mild ↓ ↓ ↓ Stable
4. MAP ↓ ↓ ↓ ↓ ↓ Stable
5. Sensitization of Yes Slight No No No Yes
myocardium PVR↑
N2O stimulates sympathetic nervous system Release catecholamines ↑epinephrine arrhythmias

PROPERTIES OF MODERN INHALATION ANESTHETICS:

Agent Mwt. MAC% Boling Point Blood/Gas Vapor Pressure

(mm Hg at
20oC)
N2O 44.0 105 -88oC 0.47 248
Halothane 197 1.75 50 2.4 243
(Fluothane)
Isoflurane 187 1.2 49 1.4 240
(Forane)
Sevoflurane 200 2.0 58.5 0.65 160
(Ultane)
Enflurane 184 1.68 56 1.9
Desflurane 23.5 6.0 23.5 0.42 681
(Suprane)

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SEVOFLURANE
Q7) write short notes no:
1. Sevoflurane
2. Etomidate
3. Tramadol
4. Ketorolac.

Ans 7) SEVOFLURANE
Molecular Wt.  200
Boiling point  58.5oC
Vapour pressure  160
Blood/Gas PC 0.65
MAC 2.0

Nor pungency and rapid increase in alveolar concentration makes sevoflurane an (excellent choice for
smooth and rapid induction in pediatric and adult patients) its low blood solubility (0.65) results in rapid
fall in alveolar anaesthetic concentration and a more (rapid emergence than isoflurane).

EFFECTS ON ORGAN SYSTEM:

1. CVS  ↓ BP, ↓SVR, ↓CO (mild), HR (stable), prolongs QT interval

2. Respiratory  Respiratory depression, reverse bronchospasm
3. CNS  ↑CBF, ↑ICP, ↓CMR requirement, impair Autoregulation of CBF
4. Neuromuscular Adequate relaxation of muscles
5. Renal ↓RBF, nephrotoxic end product (compound A) ↓ concentrating ability
6. Hepatic Maintains hepatic blood flow and oxygen delivery

BIOTRANSFORMATION AND TOXICITY:

Metabolism by P-450 enzyme in liver, Baralyme or soda lime degrade sevo into nephrotoxic end product
(Compound A), sevo also degraded into hydrogen fluoride by metal and environmental impurities

CONTRAINDICATION: Severe hypovolemia, susceptibility to MH, ↑ ICP

DRUG INTERACTION: Potentiates NMBA’s.

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Dr. Tariq Mahar
ETOMIDATE
Etomidate is an imidazole derivative the induction properties of which results from GABA receptor
modulation.
It is noted for its haemodynamic stability.

MOA: It depresses the reticular activating system and mimics the inhibitory effects of GABA.
DOSE: 0.2-0.5 mg/kg.

PHARMACOKINETICS:
Absorption Only for IV administration, used for G.A induction
Distribution Highly protein bound, Rapid onset of action.
Biotransformation Rapid hydrolysis by hepatic enzymes and plasma esterases
Excretion End product of hydrolysis excreted in urine.

EFFECTS OF ORGAN SYSTEM:

CVS  Minimal effects, mild ↓ in SVR, Do not release histamine.
Respiratory  Minimal effects on ventilation unless opioids administered
Cerebral ↓CMR, ↓CBF, ↓ICP, CPP well maintained, Post op N&V, seda ve-hypnotic but lacks
analgesia.
Endocrine ↓ Cortisol and aldosterone synthesis long term infusions  adrenocortical suppression

DRUG INTERACTION:
1. Fentanyl ↑ plasma level and prolongs elimina on half life.
2. Opioids ↓ myoclonus, characteris c of etomidate induc on

DICLOFENAC: (Phenylacetic acid derivative NSAID)

Analgesic, anti-inflammatory and antipyretic activity, Maximum dose by any route is 150mg/day in
adults
Children dose  3mg/kg/day in divided doses.

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TRAMADOL AND KETOROLAC

TRAMADOL (OPIOID) (ULTRAM & TRAMOL)

DOSE: 50mg IV/IM, Oral QID

HALF LIFE: 5 - 7 hours
Tramadol is a codeine analog that acts as a (µ, κ, δ and σ) receptors agonist and a reuptake
inhibitor of norepinephrine and serotonin. It is a moderately effective analgesic with low incidence of
respiratory depression, constipation and dependence than other µ-receptor agonists’ ↑↑ N&V
Rarely Tramadol may induce seizures so it is contra indicated in patients with preexisting seizure
disorder and patients receiving MAOI’s

KETOROLAC (NSAID) (TORADOL)

MOA: Parenteral NSAID acts by inhibiting prostaglandin synthesis

USES:
 Shorter and postoperative management of pain.
 Alternative to opioids  minimum CNS side effects.
 Most beneficial in pts at ↑risk of post op respiratory depression or emesis
 More profound analgesic affects in orthopedic and gynecological surgery
DOSE: 60 mg IM or 30mg IV loading and 15-30 mg 6 Ho maintenance

HALF-LIFE: 6-8hrs.

SIDE EFFECTS:
 Prolongs bleeding time-used with caution if ↑ risk of hemorrhage postop
 Renal toxicity by long term use,
 GI ulceration with bleeding and perforation by long term use.

CONTRAINDICATIONS:
1. Renal failure
2. Allergy to aspirin or NSAID.

DRUG INTERACTIONS: Aspirin ↓protein binding, ketorolac do not affect MAC. It ↓ postopera ve opioid
requirements

Other IV NSAIDS: Diclofenac 1mg/kg, Ketoprofen, Parecoxib 20-40 IV

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EFFECT OF ALTERED RENAL FX ON DRUGS

Q-8) how are the pharmacokinetics and pharmacodynamics of the following drugs affected in pt.’s with
altered renal functions?
a. Intravenous agents
b. Inhalational agents
c. Muscle relaxants

Ans a)

INTRAVENOUS AGENTS:
1. Propofol &Etomidate Not significantly affected.
2. Barbiturates  ↑sensi vity to barbiturates during induc ons
Pharmacokinetics unchanged.
3. Ketamine  Pharmacokinetics minimally affected. Some active hepatic metabolites accumulate
in RF.
4. Benzodiazepines  Highly protein bound - ↑ sensi vity in hypoalbuminemia
Accumulation of active metabolites of diazepam
5. Opioids 
 Remifentanil pharmacokinetics unaffected – hydrolysis in blood
 Pharmacokinetics of opioid agonist – antagonist unaffected.
 Accumulation of morphine and meperidine metabolites causes prolong respiratory
depression
 Meperidine metabolite associated with seizures
6. Anticholinergic agents Premedication doses are safe in renal impairment.
Accumulation occurs following repeated doses.
CNS effects of scopolamine ↑by azotemia
7. Phenothiazines  Central depression effects of promethazine ↑by azotemia
8. H2-receptor blocker  Very dependent on renal excretion
Metoclopramide accumulates in renal failure.

Ans. B)

INHALATIONAL AGENTS:

1. Volatile agents  Ideal for patients with renal dysfunction because they do not depend on
kidneys for elimination minimal direct effects on renal blood flow.
Sevoflurane with < 2L /min gas flows is undesirable for pts with renal Dx undergoing long
procedures, fluoride accumulation
2. N2O  Omit or limit the use of N2O to 50% in patients with renal failure to ↑ arterial O2 content
in the presence of anemia

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Ans. C)

MUSCLE RELAXANTS

1. Succinylcholine  Can safely be used in RF if K+< 5

If K +> 5 use nondepolarizing agent
2. Atracurium  Atracurium and Cisatracurium are the drug of choice for muscle relaxation in pts
with renal failure
3. Vecuronium and Rocuronium Effect of both prolonged in renal insufficiency
4. Pancuronium  Elimination half life primarily dependent on renal excretion (60-80%)
5. Metocurine, Gallamine and Decamethonium avoided in renal dysfx
6. Reversal agents’  renal excretion is the principle route of elimination for edrophonium,
neostigmine and pyridostigmine.
Prolong half-live if renal impairment.

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IDEAL VOLATILE ANESTHETIC AGENT
Q.9)
a. What are the characteristics of an ideal volatile anesthetic?
b. What are the advantages and disadvantages of using halothane, Enflurane and isoflurane?

Ans.a)
IDEAL ANESTHETIC GAS
1. It should have a pleasant odor
2. It must be non-irritant to respiratory tract
3. It must allow rapid induction and rapid emergence from anesthesia
4. It must possess low blood/gas solubility.
5. It must be chemically stable in storage and should not interact with the material of circuits or
with soda lime
6. It should be neither flammable nor explosive
7. It should provide muscle relaxation
8. It should provide cardio stability
9. It should provide bronchodilation
10. It shouldn’t trigger malignant hyperthermia and other SE  N&V
11. It should be sufficiently potent to allow the use of high inspired oxygen concentration when
necessary.
12. It should not be metabolized in the body
13. It should be nontoxic
14. It should be allergy proof
15. It should not interact with other drugs e.g: Pressor agents or catecholamine
16. It should be completely inert and eliminated completely & in an unchanged form via lungs.

Ans. B) ADVANTAGES AND DISADVANTAGES OF VOLATILE

Agent Advantages Disadvantages
Halothane 1. Smooth induction 1. Arrhythmias
2. Bronchodilatation 2. Liver toxicity when repeated
3. Minimal stimulation of salivary and bronchial secretions 3. Slow recovery compared with
other newer agents
Enflurane 1. Low risk of hepatic toxicity 1. Epileptogenic
2. Low incidence of arrhythmias 2. Avoid in pt.’s with renal disease
3. No need of preservative 3. Avoid in those taking enzyme
inducing drugs.
Isoflurane 1. Rapid recovery 1. Pungent odor which makes
2. Little risk of hepatic or renal toxicity induction very unpleasant
3. Very low risk of arrhythmias
4. Provides muscle relaxation
5. Not epileptogenic
Desflurane 1. Low blood solubility therefore rapid recovery 1. Irritant to airways so cannot used
2. Minimal biotransformations so nontoxic to liver and kidney for induction
3. No convulsive activity EEG 2. Cause ↑ HR at high concentration
3. Requires special vaporizer
4. It is expensive gas

Sevoflurane 1. Smooth, fast induction 1. Produce toxic metabolites

2. Rapid recovery 2. Instability with CO2 absorber
3. Easy to use-conventional vaporizer. 3. Relative expense

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DRUG EFFECTS ON CVS AND RESPIRATORY SYSTEM
Q 10) what are the effects of following drugs on CVS and respiratory system?
a. Sevoflurane
b. Propofol
c. Pethidine
d. Ketamine.

a) SEVOFLURANE:
CVS effects:  Stable HR, mild ↓ in BP, SVR and CO, prolongs QT interval
Respiratory effects:  Respiratory depression reverses bronchospasm

b) PROPOFOL:
MOA Facilitates inhibitory neurotransmission mediated by GABA
CVS effects:
 ↓SVR, ↓BP, ↓ cardiac contractility, ↓ preload
 Markedly impairs normal arterial baroreceptor response to hypotension
 Changes in HR and CO severe enough leading to asystole particularly at extreme of
age, mediations or surgery related to oculocardiac reflex
 Myocardial O2 supply and demand mismatch.
 ↑Coronary sinus lactate production.

Respiratory effects:
 Profound respiratory depression that usually causes apnea following an induction dose.
 When used for conscious sedation in subanesthetic doses Propofol inhibits hypoxic ventilatory drive
and depresses the normal response to hypercarbia.
 Propofol induced depression of upper airway reflexes proves helpful during intubation or LMA
placement without paralysis
 Propofol release histamine but can used in asthmatics

c) PETHIDINE  (MEPERIDINE)
CVS effects: Direct myocardial depression at high doses
Atropine like action may case tachycardia
Respiratory effects: Bronchodilator, Reduce shivering d/t hypothermia or epidural

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d) KETAMINE (Phencyclidine):
Ketamine + theophylline  seizures
CVS effects:
Stimulation of sympathetic nervous system cause ↑BP, ↑HR, and ↑CO. ↑ Myocardial
work and ↑PA pressure ketamine avoided in CAD, uncontrolled HTN, CHF and aneurysms.
Indirect stimulatory effects on heart are beneficial to patient with acute hypovolemic shock.

Respiratory effects:
Ventilator drive minimally affected, rapid IV bolus or pretreatment with Opioid can
cause apnea potent bronchodilator making it ideal induction agent for asthmatic pts.
Upper airway reflexes remains intact but still pt at increased risk of aspiration should be
intubated ↑salivationpremedication with an anticholinergic (Glycopyrrolate)

CNS effects:
↑ CMRO2, CBF and ICP, potent analgesic, Emergence delirium, EEG-loss of alpha wave
predominant theta wave
_____________________________________________________________________________________

PROPOFOL INFUSION SYNDROME:

Use of Propofol infusions for long term sedation of children who are critically ill or
young adult neurosurgical pt.’s associated with lipemia, metabolic acidosis and death.

INDICATIONS OF PROPOFOL: (Phenol derivative)

1. Inductions of anesthesia when rapid recovery of consciousness is required
2. Sedation during regional anesthesia
3. During endoscopies. Adult: 1.5-2.5mg/kg
4. Total IV anesthesia Children: 3-3.5mg/kg
Elderly: 1.25mg/kg
5. Sedation in ICU

CONTRAINDICATION: Air way obstruction, hypersensitivity.

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 st
Tubocurarine was the 1 muscle relaxant used clinically
Decamethonium was an older depolarizing agent.
MUSCLE RELAXANTS
Q 11) Define the onset of action and duration of action and elimination half-life of muscle relaxants.
What are the major difference between Rocuronium and Atracurium with regard to metabolism and
elimination?

Ans. 11)
Drug Onset of action Duration of action Elimination half life (dose mg/Kg)
Succinylcholine 30-60 Ec 5-10 min 1.0
Rocuronium 1.5 min(90s) 35-75 min 0.8
Mivacurium 2.5-3min 15-20 min 0.2
Atracurium 2.5-3min 30-45 min 0.5
Cisatracurium 2-3 min 40-75 min 0.2
Vecuronium 2-3 min 45-90 min 0.12 (Bisquaternary relaxation)
Pancuronium 2-3 min 60-120 min 0.12 (Bisquaternary relaxation)
Pipecuronium 2-3 min 80-120 min 0.1
Doxacurium 4-5 min 90-150 min 0.07

Difference between Atracurium and norcuron (Vecuronium)

Atracurium (Benzylisoquinoline) Vecuronium (steroid)
Metabolism (two separate processes) Metabolism
1- Ester hydrolysis Little metabolism in liver
2- Hoffmann elimination

Elimination Elimination
10% excreted unchanged by renal and biliary route Primary biliary excretion 75% - 25 % renal
rest chemical breakdown by Hofmann degradation excretion

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Dr. Tariq Mahar
 Prilocaine is the safest LA
LOCAL ANESTHETICS
Q.12) Give biological classification of local anesthetics
Describe their mode of action? How their pharmacological activity is influenced? What factors
determine their systemic toxicity?

Ans. 12)
BIOLOGICAL CLASSIFICATION OF LA
LA are biologically classified into 2 groups
1. Esters  Procaine, chloroprocaine, Tetracaine, Cocaine, benzocaine
2. Amides  Bupivacaine, lidocaine, mepivacaine, Prilocaine, ropivacaine.

MODE OF ACTION:
Most local anesthetics bind the α-subunit and blocks voltage-gate sodium channels from inside the cell,
preventing channel activation and inhibits Na+ influx which is associated with membrane depolarization.

PHARMACOLOGICAL ACTIVITY
Pharmacological activity is influenced by certain factors
1. Potency  The higher the lipid solubility, the greater the potency
2. Degree of ionization the closer the pKa of LA to tissue Ph the more rapid the onset time.
3. Protein binding  the greater the protein binding, the longer the duration of action.
4. Lipid solubility  Higher lipid solubility, longer duration of action

FACTORS DETERMINING SYSTEMIC TOXICITY

Systemic absorption of injected LA depends on blood flow which is determined by following factors:
1. Site of injection
2. Presence of vasoconstrictors
3. LA agent
4. Dose
5. Absorption
6. Distribution, metabolism and protein binding.

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Dr. Tariq Mahar
SYSTEMIC TOXICITY OF LIDOCAINE
Q. 13) Short note on systemic toxicity of lidocaine
The most common cause of LA toxicity is inadvertent intravascular injection but it can also cause by over
dosage and rapid absorption lidocaine is the current standard agent for local anesthesia

Uses:
1. Standard antiarrhythmic
2. Local infiltrations 0.5 – 1%
3. Peripheral nerve blocks
4. IVRA (Bier’s Block)
5. Subarachnoid anesthesia 5%
6. Epidural anesthesia 1-2%
7. Topical use in upper airways before intubation 2-4%
8. Lowers ↑BP

TOXICITY: Toxicity is often directly proportionate to potency.

Neurological:
1. Light headedness, tinnitus, perioral numbness, confusion
2. Muscle twitching, auditory and visual hallucinations
3. Tonic clonic seizure, unconsciousness, respiratory arrest

CVS: less common with lidocaine – mostly bupivacaine

1. Can be fatal
2. HTN, tachycardia
3. ↓contrac lity, ↓CO, Hypotension
4. Sinus bradycardia, ventricular arrhythmias, circulatory arrest

Respiratory:
1. Lidocaine depresses ventilator drive.
2. Apnea result from phrenic and intercostal nerve paralysis or depression of medullary respiratory
center following direct exposure to LA
3. LA relaxes bronchial smooth muscle

Musculoskeletal: LA are myotoxic, Concomitant steroid or epinephrine injection worsens the

myonecrosis

Hematological: Lidocaine ↓coagula on and ↑ fibrinolysis

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Dr. Tariq Mahar
Neostigmine: 0.04 mg/kg

Q. 14)
DOSE: 0.04 mg/kg (maximum 0.08 mg/kg)
ONSET: 5-10min
DURATION OF ACTION: more than 1 hour
MOA: inactivation of acetyl-cholinesterase (anticholinesterase)

CLINICAL CONSIDERATIONS:
1. Cannot bass BBB
2. Pediatric and elderly pts. require less dose
3. Muscarinic side effects minimized by prior or concomitant administration of an anticholinergic
agent.
4. Neostigmine crosses placenta resulting in fetal bradycardia thus atropine is a better choice in
pregnant pts.
5. Used to treat myasthenia gravis, urinary bladder atony and paralytic ileus.
6. (0.05-0.1) 50-100µg as an adjunct to intrathecal anesthesia  prolongs blocks

SIDE EFFECTS:
1. Nausea
2. Vomiting
3. Fecal incontinence
4. Delayed recovery room discharge
5. Atropine-resistant bradycardia @ higher doses (200µg) 0.2 mg

INADVERTENT INTRA-ARTERIAL STP - TREATMENT

1. Leave the catheter in place
2. Inject dilute papaverine, procaine or lidocaine to inhibit vasospasm
3. If this failed brachial plexus block or α-blockade
4. Administer heparin to prevent thrombus formation

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Dr. Tariq Mahar
FENTANYL 50-100 µg
Q-15) DOSE: 50-100 µg (PCA dose  20- 30 µg)
ONSET OF ACTION: 5-10 min
DURATION OF ACTION: 1-3 hours
ELIMINATION HALF-LIFE: 2-4 hours

ADVANTAGES:
1. Available in a variety of preparations for parenteral, transdermal and transmucosal
administration
2. 80-100 times more potent than morphine in acute settings
3. Fentanyl lozenges can be used for break through pain
4. Transdermal fentanyl is an excellent alternative to sustained release morphine particularly when
oral medicine is not possible.
5. Can be used by PCA allowing pt. to treat him for break through pain
6. Epidural and subarachnoid fentanyl relieves pain with low total dose and fewer side effects.
7. Continuous infusions also reduce drug requirements and ↓SE.
8. Transdermal routs avoids hepatic first pass metabolism

DISADVANTAGES:
1. High firs-pass metabolism 70% when given orally.
2. Oral opioids can cause excessive sedation and constipation and nausea
3. Physical dependence occurs when large dose used
4. Major disadvantage of transdermal route is slow onset and inability to rapidly change dose in
response to changing requirement
5. Very lipophilic with short duration of action parent rally
6. IV fentanyl will cause abdominal and chest wall rigidity.
7. Major problem with intraspinal opioid is tolerance
8. Other common side effects are nausea, pruritus, bradycardia, urinary retention and respiratory
depression.

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 Dibucaine, a local anesthetic inhibits PC activity by 80%
But in heterozygous atypical enzyme only 20%
SUCCINYLCHOLINE APNEA 1-1.5 mg/kg

Q 16) how would you diagnose, treat and investigate a suspected case of Suxamethonium apnea?

Ans)

DIAGNOSIS: Tow methods

1. Quantitative by adequacy of pseudocholinesterase in laboratory in units per litter (minor factor).
2. Qualitatively by Dibucaine number (major factor).

TREATMENT:
Prolonged paralysis from Suxamethonium by decreased or abnormal pseudo-cholinesterase should be
treated with continued mechanical ventilation until muscle function returns to normal.

INVESTIGATION:
1. High dose given? or
2. Abnormal metabolism
a. Hypothermia? ↓ rate of hydrolysis OR
b. Low pseudo-cholinesterase level? (pregnancy, liver dx, RF, drugs)
c. Genetically aberrant enzymes? (Homozygous or heterozygous)

Low pseudocholinesterase levels  2-20 min apnea

Heterozygous enzyme  20-30 min apnea
Homozygous atypical enzyme  4-8 hour apnea
Dibucaine resistant gene most common
Determine Dibucaine number (% of inhibition of pseudo-cholinesterase activity)
Acquired causes: Pregnancy, malnutrition, Plasmapheresis, myxedema, newborn, lupus, and drug
induced.

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Dr. Tariq Mahar
FLUMAZENIL (0.1-0.2 mg)

Q 17) write short notes on:

1. Flumazenil
2. Lithium
3. Mivacurium

FLUMAZENIL
Flumazenil is a competitive antagonist of benzodiazepine receptor. It rapidly reverses all CNS effects of
benzodiazepines
It rapidly clears form plasma and metabolized by liver
DOSE: 0.1 – 0.2mg 1mg max DURATION: 45-90 min
ELIMINATION HL: less than 1 hour

INDICATIONS:
1. Reversal of sedation
2. Over dosage in self-poisoning
3. Diagnostic tool for coma (maximum 2mg)
4. ICU for reversal of prolong sedation

CONTRAINDICATIONS:
1. Epileptic patients
2. Severe head injury

PRECAUTIONS:
1. Dependence  withdrawal symptoms
2. Anxiety after rapid reversal of sedation

VECURONIUM: is Pancuronium minus a quaternary methyl group (a monoquaternary relaxant)

Primary biliary excretion 75%
Long term use in ICU  prolonged neuromuscular blockade (up to several days)

Risk factors include:

1. female gender
2. Renal failure
3. Long-term or high dose corticosteroid therapy and
4. Sepsis
Equipotent with Pancuronium but with shorter elimination HL,
Vecuronium and STP (thiopental) can form a precipitate that can obstruct flow through an intravenous
line and lead to particulate pulmonary emboli.
Vecuronium is devoid of significant cardiovascular effects.

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Dr. Tariq Mahar
LITHIUM
Lithium (bipolar disorder)
USES: Lithium is the drug of choice for treating acute manic episodes and preventing their recurrence as
well as suppressing episodes of depression
Lithium has a narrow therapeutic range with a desirable blood concentration between 0.8-1 mEq/L

SIDE EFFECTS:
1. Reversible T-wave changes
2. Mild leukocytosis
3. Hypothyroidism
4. Vasopressin resistant diabetes insipidus-like syndrome
BLOOD TOXICITY:
Blood levels should be checked perioperatively
Fluid restriction and overdiuresis should be avoided

Toxic blood concentration can cause:

1. Confusion 6. Wide QRS complex
2. Sedation 7. AV block
3. Muscle weakness 8. Hypotension
4. Tremor 9. Seizures.
5. Slurred speech

DRUG INTERACTION
1. ↓ MAC
2. Prolong NMBA’s action.

MIVACURIUM

DOSE: 0.2 mg/kg

ONSET: 3 minutes
DURATION: 15-20 minutes
PHYSICAL STRUCTURE: Benzylisoquinoline NDMR
METABOLISM:
Mivacurium like Succinylcholine metabolized by pseudocholinesterase, It is only minimally
metabolized by true cholinesterase.
Prolong action in patients with low pseudocholinesterase
If atypical homozygous  3-4 hrs blockade
Edrophonium more effective reversal of Mivacurium
SIDE EFFECTS:
1. Histamine release
2. CVS effects.

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CLINICAL CONSIDERATION:

Its principle advantage is its brief duration of action (15-20) which is longer than phase I block of
suxa.
Children tend to exhibit faster onset and shorter duration of action than adults.
Short duration of action markedly prolongs by prior administration of Pancuronium.

_____________________________________________________________________________________
Doxacurium long acting devoid of any CVS and histamine releasing effects
Pancuronium SE:
1. Hypertension and tachycardia (vagal blockade + sympathetic stimulation). Cautions use in CAD
and idiopathic, hypertrophic subaortic stenosis
2. Arrhythmias (ventricular dysrhythmias
3. Allergic reactions: Pts hypersensitive to bromides

MAC
Q.18) what is MAC? What are the factors which affects MAC?
Ans.)
MAC: The minimum alveolar concentration of inhaled anesthetic is the alveolar concentration that
prevents movement in 50% of patients in response to a standardized stimulus e.g.: surgical incision.
 MAC is a useful measure because it mirrors brain partial pressure and allows comparison of
potency b/w agents
 MAC ↓6% per decade of age, regardless of vola le agent
 MAC can be altered by several physiological and pharmacological variables.
Factors ↑MAC Factors ↓ MAC
1. Young age 1. Elderly
2. Chronic alcohol abuse 2. Hypo/Hyperthermia
3. Hypernatremia 3. Acute alcohol ingestion
4. Pyrexia/ hyperthermia 4. Anemia
5. Hypercapnia 5. PaO2< 40
6. Thyrotoxicosis/hyperthyroidism 6. Hypotension
7. Cocaine, ephedrine and acute 7. Myxedema
amphetamine toxicity 8. Hyponatremia
o
8. Hyperthermia if > 42 C 9. Pregnancy (↓by 1/3 at 8 weeks)
10. Drugs: eg. LA, opioids, ketamine,
Barbiturates, Benzodiazepines, Verapamil,
Lithium, Methyldopa, Clonidine

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IDEAL IV ANESTHESIA AGENT:
Q. 20) what are the properties of ideal IV anesthetic agent?

Ans) IDEAL IV ANESTHETIC AGENT

1) Rapid onset
2) Rapid recovery
3) Analgesia at sub-anesthetic concentrations
4) Minimal CVS and respiratory depression
5) No emetic effect
6) No excitatory phenomena (eg. Cough, hiccup, myoclonus) on induction
7) No emergency phenomena (e.g. nightmares, hallucinations)
8) No interaction with NMBA’s
9) No pain on injection
10) No venous sequelae
11) Safe in injected inadvertently into artery.
12) No toxic effects on other organs
13) No release of histamine
14) No hypersensitivity reaction
15) Water soluble
16) Long shelf life
17) No stimulation of porphyria’s

BRONCHODILATORS BRONCHOCONSTRICTORS
β2 agonists e.g. salbutamol Atracurium/ Pantoprazole
Ketamine/GTN STP
Sevoflurane (Reverse bronchospasm) Propranolol /β-Blockers
Halothane / Isoflurane Carboprost
Meperidine Epinephrine/Ephedrine Diamorphine /Morphine
Ipratropium Bromide /Aminophylline Diclofenac
NSAIDS

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PHARMACOLOGICAL PROPERTIES OF ANTIARRHYTHMIC DRUGS
LIDOCAINE (class 1b):
Dose:  50-100mg repeated after 5-10 min, followed by continuous infusion
Metabolism and elimination: Extensive 1st pass hepatic metabolism
Elimination HL:< 2h
Side effects: CNS toxicity (Confusion, tremor, paresthesia, dizziness, and convulsions)
Cardiotoxicity (Bradycardia, hypotension, asystole)

ADENOSINE: 0.2 mg/kg.

Dose: 3mg repeated upto 6mg and 12mg after 1-2 minutes
Metabolism and elimination  vascular endothelium
Elimination HL < 10 seconds
Side effects: Dyspnea, flushing, bronchospasm, bradycardia (avoid in asthmatics)

DIGOXIN: 0.25- 0.5 mg IV loading over 10-20 min

Dose: Loading dose 250-500µg I.V over 10-20 min
Metabolism and elimination  mostly excreted unchanged via kidneys
Elimination HL 36 hours
Side effects:  Cardiac arrhythmias (Ventricular arrhythmias, heart block)
+
Toxicity ↑ ↓K CNS toxicity (fatigue, agitation, nightmares, visual disturbances, anorexia,
nausea & abdominal pain)

AMIODARONE (class 3): 300mg IV loading in 30 min in 100 ml saline

Dose:  5mg/kg over 5 - 10 min, followed by infusion of 900mg/24 hours
Metabolism and elimination: Hepatic- active metabolite accumulate in tissues
Elimination HL:  35- 40 days
Side effects:bradycardia, hypotension, DVT, corneal micro-deposits, cutaneous rash, and
hypothyroidism

MAGNESIUM SULPHATE: MgSO4

HL:< 1 hour 2g in 10 min
Dose:  8 mmols over 10 - 15 min, followed by continuous infusion of 4 – 72 mmols over 24 hours
Metabolism and Elimination: Redistributed or excreted unchanged via kidneys
Side effects: Vasodilation, hyporeflexia, NM blockade, electrolyte disturbance, cardiac arrest

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MIDAZOLAM 0.01 – 0.1 mg/kg (2-7mg IV)

Benzodiazepines are classified by their duration of action into

1. Long acting  Diazepam
2. Medium acting Temazepam
3. Short acting  Midazolam

MOA: benzodiazepines excretes these action by binding to benzodiazepine receptor, which is part of
GABA receptor complex Benzodiazepine receptors are found throughout brain and spinal cord
characteristic CNS effects seen with all benzodiazepines are
1. Anxiolysis
2. Sedation
3. Amnesia
4. Antiepileptic activity

MIDAZOLAM:
An imidazobenzodiazepine derivative
Highly lipid soluble  penetrates the brain rapidly, water soluble at low PH
Onset of action:  90 sec
Duration of action: 20-60 min
Metabolism: hepatic
Elimination half life 2 h
1.5 – 2 times more potent than diazepam
Use:  short term IV sedative
Dose:  Premedication -15 mg orally or 5 mg IM, children 70 – 100 µg/kg PR
Sedation: 2 – 7 mg IV (< 4 mg in elderly) or 0.01 -0.1 mg/kg
Induction  0.1 – 0.4 mg/kg incremental boluses of 0.5 – 1 mg
Intensive therapy: IV infusion 0.03-0.1 mg/kg/hr
May cause paradoxical disinhibition especially in the elderly

HALOPERIDOL: Neuroleptic antipsychotic  Blocks dopamine receptors

Long duration of action
Dose: 2 – 5mg IV
Potent antiemetic: 1.25 mg IV effective for postop N & V
Causes neuroleptic malignant syndrome
Used for acutely agitated patient
Extrapyramidal reactions

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ATROPINE: 0.4 – 0.6 mg
DESCRIPTION: (tropic acid + tropine)
Tertiary amine therefore crosses BBB

MOA: Muscarinic acetylcholine antagonist (ANTI CHOLINERGIC)

INDICATIONS:
1. Brady arrhythmias vagal blockade at AV and sinus node increases heart rate.
2. Ipratropium bromide, a derivative of atropine very effective in Rx of acute exacerbation of COPD
when combined with β-agonist
3. Antisialagogue effect.

CONTRAINDICATIONS:
1) Obstructive uropathy
2) CAD
3) Glaucoma
4) Myasthenia gravis

SIDE EFFECTS:
1. ↓ Secre ons
2. ↓ LES tone
3. Relaxes bronchial smooth muscle
4. Confusion in elderly

DOSE: adult dose – 0.4-0.6 mg premedication dose 0.01-0.02 mg/kg

Cardiac arrest -3mg Pediatrics dose: 0.01 – 0.02 mg/kg

CENTRAL ANTICHOLINERGIC SYNDROME

Over dosage of anticholinergic medication
CNS changes that range from unconsciousness to hallucination agitation and delirium in elderly
Other systemic manifestations Dry mouth, tachycardia, atropine flush, atropine fever and impaired
vision
Antidote Physostigmine 0.01 – 0.03 mg/kg

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DOXAPRAM: 0.5-1mg/kg
DESCRIPTION: Respiratory stimulant
MOA: Activation of carotid chemoreceptor and medulla
Indication:
1. Stimulates hypoxic drive (↑TV + ↑R/R) low dose
2. At higher dose stimulates medulla (Respiratory center)

Contraindications:
1. Epilepsy 3. acute asthma
2. Airway obstruction 4. Severe CVS disease (CAD)

Side Effects:
1. Risk of arrhythmia 5. Pulmonary dysfx – wheezing, tachypnea
2. Hypertension 6. Vomiting
3. Tachycardia 7. Laryngospasm
4. CNS effects – confusion, dizziness,
seizures

Dose: 0.5 -1 mg/Kg (maximum dose 4 mg/kg)

Onset of action: 1 min
Duration of action: 5- 12 min

MAGNESIUM
MOA: Intracellular cat-ion – inhibits calcium ion influx into cells through calcium channels owing to high
intracellular Mg levels

INDICATIONS:
1. Hypomagnesaemia 3. Eclamptic seizures
2. Arrhythmias (torsade point) 4. Severe asthma

CONTRAINDICATION:
1. Myasthenia 2. Muscular dystrophy 3. Heart block

SIDE EFFECTS:
1. CNS depression 2. Hypotension 3. Muscle weakness

DOSE: Hypomagnesaemia  10-15 mg/kg in 20 min then 1g/hr.

Arrhythmias/ asthma  2g in 10 min
------------------------------- 10 min then ________________

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NALOXONE: (0.5-1 µg/kg)
DESCRIPTION:
Pure opioid antagonist

MOA:
Competitive antagonist at opioid receptor

INDICATIONS:
1. Opioid overdose
2. Used in low doses to reverse pruritus associated with epidural opioids
3. As depot IM injection in newborn of mother given opioids

CAUTION:
1. Beware re-narcotization if reversing long acting opioids
2. Caution in opioid addicts – may precipitate acute withdrawal

Dose:
Increments of 0.5 -1 µg/kg every 3-5 min (0.4 mg/ml vial diluted to 0.04mg/ml) continuous
infusion of 4-5 µg/kg/hr. is recommended
Opioid /epidural pruritis – 0.1 µg bolus + 0.3 µg in IV fluid

PROPOFOL:
Phenol derivative – Rapid onset / Rapid recovery 1% white aqueous emulsion having soya bean oil and
purified egg phosphate extremely lipid soluble, long shelf life, pain on IV injection Minimal hangover
effects.

Apnea more common than STP

Drug of choice when LMA is used CO2 suppressed laryngeal reflexes
Distribution HL  2-8 min
Pain on injection ↓by mixing lidocaine and castor oil prepara on
Disodium edetate 0.005% or 0.025% sodium Meta bisulfate decreases rate of growth of micro-organism
Antipruritic - Antiemetic – Anticonvulsant
Excitatory phenomena occasionally
Edetate disodium (EDTA) is a chelating (KEE-late-ing)
agent. A chelating agent is capable of removing a heavy
metal, such as lead or mercury, from the blood. EDTAis
used to lower blood levels of calcium when they have
become dangerously high

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ANAESTHESIA TRIAD DIFFICULT LARYNGOSCOPY
Sleep When epiglottis cannot be seen during
Muscle relaxation and laryngoscopy
Analgesia

GENERAL ANAESTHESIA
DIFFICULT INTUBATION Is an altered physiological state characterized
When an experienced anesthetist; of more than by reversible loss of consciousness, analgesia of
3 years did not intubate after 3 attempts within the entire body, amnesia and some degree of
10 minutes. muscle relaxation.

DIFFICULT AIRAY
When patients’ saturation remains < 90% after
giving 100% O2 with tightly fitting mask

CLASSIFICATION OF ANTIARRHYTHMICS

CLASS EXAMPLE MODE OF ACTION INDICATIONS

1a Quinidine, Na+ channel blocker Prevention of SVT
Procainamide Atrial Tachycardia
Disopyramide
1b Lidocaine Na+ channel Blocker Prevention of VT/VF
Mexiletine (Mexitil) during ischemia
Phenytoin
1c Flecainide Na channel blocker Conversion/ Prevention
Propafenone of SVT,VT,VF
2 β-Blockers (propranolol, esmolol, β-receptor blockade Tachyarrhythmia’s, rate
metoprolol) control in AF, MI, AV
node re-entry
tachycardia
3 Amiodarone (Cordarone) Inhibition of inward K+ current. Prevention of SVT, VT,
Bretylium (Prolongs repolarization) VF
Sotalol
4 Diltiazem (Cardizem) Ca+ channel blocker Rate control in AF,
Verapamil prevent of AV node
re-entrant tachycardia
5 Digoxin
Adenosine

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 2
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 PREOPRATIVE ASSESSMENT
AIMS OF PREOPERATIVE ASSESSMENT:
 Confirm that surgery proposed is realistic when comparing the likely benefits to the patient with
possible risks involved.
 Anticipate potential problems.
 Ensure adequate facilities and appropriately trained staff available.
 Ensure patient is prepared correctly for the operation
 Provide appropriate information to patient and obtain consent.
 Prescribe premedication and specific prophylactic measures if needed
 Ensure proper documentation of assessment process.

PREOPERATIVE FEATURES ↑SES PERIOPERATIVE COMPLICATIONS OR MORTALITY

DEMOGRAPHIC/ SURGICAL: PHYSIOLOGIAL:
1. Age >70 years 1- Dyspnea @ rest or on minimal exertion
2. Major thoracic, abdominal, 2- MI < 6 months previously
Cardiovascular surgery
3- Cardiac surgery requiring treatment
3. Perforated viscous
4. Intestinal obstruction 4- Confusion state
5. Palliative surgery 5- Clinical jaundice
6. Smoking 6- Significant wt loss > 10% in 1 month
7. Cytotoxic and corticosteroid treatment 7- Cough with sputum especially if persistent.
8. DM 8- Hemorrhage or anemia requiring transfusion

Laboratory Fasting:
Plasma urea >20 mmoles/L Clear fluids -> 2 hours
Serum Albumin<30 g/l Breast milk ->4 hours
Hb < 10 g/L Light meal, infant formula and other milk -> 6 Ho
Fatty or fried food -> 8 hours
OBJECTIVES OF PREMEDICATION:
1. Allay anxiety and fear
2. Reduce secretions.
3. Enhance the hypnotic effects of general anesthetic agents
4. Reduce postoperative nausea and vomiting
5. Produce amnesia
6. Reduce volume and increase PH of gastric contents.
7. Attenuate vagal reflexes
8. Attenuate sympathomimetic responses

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ASA CLASSIFICATION:
Class I A normal healthy individual.
Class II A patient with mild systemic disease.
Class III A patient with severe systemic disease that is not incapacitating.
Class IV A patient with incapacitating disease that is a constant threat to life
Class V A moribund pt not expected to survive 24 hrs with or without operation
Class E Added as a suffix for emergency surgery.

INDICATIONS FOR INHALATIONAL INDUCTION:

1. Young children
2. Upper airway obstructions e.g. epiglottitis
3. Lower airway obstruction with foreign body
4. Bronchopleural fistula or empyema
5. No accessible veins

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 PRACTICAL CONDUCT OF ANAESTHESIA
STAGES OF ANAESTHESIA:
Stage 1: stage of analgesia
Stage 2: stage of excitementeyelash reflex abolished, eyelid reflex present.
Stage 3 Surgical anesthesia light, medium, deep.
Stage 4: Stage of impending respiratory and circulatory failure
Patient not permitted to reach this stage.
Lacrimation and swallowing present in light plane of stage 3
Laryngeal spasm may occur above light – medium stage 3 due to stimulation.

INADEQUATE DEPTH OF ANAESTHESIA:

1. Tachypnea
2. Tachycardia
3. HTN
4. Sweating

LMA:
Types 4
1. Reusable LMA,
2. Improved Disposable LMA,
3. ProSeal LMA: it has an orifice through which a NG-tube can be inserted and facilitates PPV
4. Fastrach LMA that facilitates intubating patients with difficult airway

INDICATIONS:
1. Alternative to ventilation through facemask or TT during SV (spontaneous ventilation)
2. Short procedures
3. Difficult airways (can’t ventilate, can’t intubate)
4. Used as a conduit for intubating stylet (eg, gum-elastic bougie), ventilating jet stylet, flexible FOB, or
small diameter (6.0-mm) TT.
5. Several LMA are available that have been modified to facilitate placement of large ETT

CONTRAINDICATION:
1. Pharyngeal pathology (abscess)
2. Pharyngeal obstruction
3. Full stomach (pregnancy, hiatus hernia)
4. Low pulmonary compliance (restrictive airway disease) requiring peak inspiratory pressure > 30cmH2O

INDICATIONS OF TT:
1. Provision of clear airway 3. Head and neck operations e.g. ENT, dental
2. Unusual position eg, prone or sitting 4.Protection of respiratory tract from blood and gastric
Contents

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COMPLICATIONS OF TT
1. Trauma to lips or teeth
2. Trauma to larynx or vocal cords
3. Epistaxis after nasal intubation
4. Tracheal stenosis
5. Arrhythmias
6. HTN

COMMON CAUSES OF DIFFICULT INTUBATION:

ANAESTHETIST RELATED:
1. Inadequate preoperative assessment
2. Inadequate equipment preparation
3. Inexperience
4. Poor technique

EQUIPMENT RELATED:
1. Malfunction
2. Unavailability
3. No trained assistant.

PATIENT RELATED:
 Congenital
1. Syndromes (Down, Pierre Robin, Treacher Collins, Marfan’s)
2. Achondroplasia
3. Cystic hygroma
4. Encephalocele

 Acquired
1. Morbid obesity 11. Ankylosing spondylitis
2. Pregnancy 12.Cervical fracture/ instability/ fusion
3. Acromegaly 13. Trismus
4. Airway edema e.g. abscess, infection
5. Airway compression e.g. goiter
6. Airway scarring e.g. radiotherapy
7. Tumors/ polyps
8. FB
9. Nerve palsy
10. RA/OA

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INDICATIONS FOR CONTROLLED HYPOTENSIVE ANESTHESIA:

Expected major blood loss

1. Pelvic surgery for malignancy
2. Head and neck surgery requiring reconstruction.
3. Large vessel vascular surgery
4. Revision of hip prosthesis
5. Reconstructive spinal surgery with scoliosis correction

Complex neurosurgery
1. Excision of intracranial or spinal meningiomas
2. AV malformations
3. Pituitary surgery
4. Craniofacial reconstructions

Microsurgery Intraocular surgery

1. Middle ear surgery 1. Vitrectomy
2. FESS ( Functional endoscopic sinus surgery) 2. Choroid surgery
3. Nerve and micro-vascular surgery
4. Plastic free flap grafting

ANATOMICAL FACTORS ASSOCIATED WITH DIFFICULT LARYNGOSCOPY:

1. Short muscular neck
2. Protruding incisors (Buck teeth)
3. Long, high arched palate
4. Receding lower jaw
5. Poor mobility of mandible
6. Increased anterior depth of mandible
7. Increased posterior depth of mandible
8. Decreased atlanto-occipital distance

MALLAMPATI CLASSIFICATION:(PHARYNGEAL VEIW)

Class I: Pharyngeal pillars, soft palate and uvula visible
Class II: Only soft palate and uvula visible
Class III: Only soft palate visible
Class IV: Soft palate not visible

CORMACK AND LEHANE GRADING (Laryngoscopic view)

Grade I: Vocal cords visible
Grade II Arytenoids cartilages and posterior part of vocal cords visible
Grade III: Epiglottis visible
Grade IV: Epiglottis not visible

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PREOPERATIVE ASSESSMENT OF AIRWAY:
1. General appearance of neck face, maxilla and mandible.
2. Jaw movement
3. Head extension and neck movement
4. Teeth and oropharynx.
5. Soft tissues of neck CT/ MRI neck
6. Chest and cervical spine X-rays
7. Previous anesthetic records
8. Mallampati classification
9. Thyromental distance
10. Mouth opening

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 MONITORING:
STANDARDS
Q-1) what mandatory monitoring is recommended for GA?

Standard I: Qualified anesthesia personnel shall be present in the room throughout the conduct of all
G.A, R.A and MAC
Standard II: during all anesthetics, the patient’s oxygenation, ventilation, circulation and temperature
shall be continually evaluated.
1. Oxygenation FiO2 O2 analyzer
Blood O2 – Pulse oximetry.
2. Ventilation  Chest movements and audible breath sounds
ETCO2 – capnography
3. Circulation  ECG Palpation of a pulse
Arterial BP Pulse oximetry
HR
4. Temperature  Thermistor or thermocouple.

CAPNOGRAPH
Q. 2)
a) What is capnography? Draw, label and explain paralyzed anesthetized normal young healthy pts.
Capnograph?
b) List the causes of ↑ETCO2 during anesthesia?
c) List the causes of ↓ ETCO2 during anesthesia?
d) What are the clinical applications of capnography?
e) What are the clinical effects of hypercarbia?

Ans a) CAPNOGRAPHY: Determination of ETCO2 on a capnograph to confirm adequate ventilation is

called capnography
A: A normal capnograph demonstrating
the three phases of expiration: phase
Idead space; phase IImixture of dead
A normal space and alveolar gas; phase IIIalveolar
capnograph of a gas plateau. B: Capnograph of a patient
young healthy with severe chronic obstructive pulmonary
person disease. No plateau is reached before the
demonstrating next inspiration. The gradient between
three phases of end-tidal CO2 and arterial CO2 is
expiration increased. C: Depression during phase III
indicates spontaneous respiratory
effort. D: Failure of the inspired CO2 to
return to zero may represent an
Phase I  Dead space
incompetent expiratory valve or exhausted
Phase II  Mixture of dead CO2 absorbent. E: The persistence of
space and alveolar gas exhaled gas during part of the inspiratory
Phase III  Alveolar gas cycle signals the presence of an
plateau. incompetent inspiratory valve.

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HYPERCARBIA

Ans.b) CAUSES OF HYPERCARBIA: PaCO2> 50 (6.3 kPa) ↑ETCO2 or PaCO2

1. Pyrexia
2. Sepsis
3. Malignant hyperthermia (sudden doubling or tripling of ETCO2)
4. NMS
5. Serotonin syndrome
6. Thyroid storm
7. Respiratory depression drugs, sedatives, opioids
8. Bronchospasm
9. Inadequate MV during IPPV (MV – minute volume) hypoventilation
10. Faulty breathing system.
11. Airway obstruction
12. Excessive dead space
13. Exhausted soda lime
14. Inadequate FGF
15. Circuit valve fault
16. Ineffective breathing during SV

Rx
 ↑ FiO2
 ↑MV, if SV then start assisted ven la on
 Check ETT cuff pressure and circuit leaks
 Exclude rebreathing of CO2 on capnograph change soda lime.
 Check disconnections within the breathing system ↑ dead space
 Ensure expiratory valves not sticking
 Maintain adequate depth of anesthesia
 If continue to ↑, exclude MH or thyroid storm

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HYPOCARBIA
Ans c) CAUSES OF HYPOCARBIA: PaCO2 < 35 (4.5 kpa)
↓ ETCO2 or PaCO2
1. Hypovolemia
2. Hypothermia
3. ↓ Metabolic rate
4. Disconnected analyzer or faulty.
5. Esophageal intubation
6. Accidental extubation
7. ↓ CO or ↓ CO2 production (CO-Cardiac output)
8. Impaired gas exchange
9. Metabolic acidosis
10. Hyperventilation
11. Deep anesthesia
12. Air/Gas embolism (sudden ↓)

Rx
1. 100% O2
2. Check patient, monitors, connections and ventilator.
3. If cardiac arrest ALS
4. Hand ventilated with 100% O2 and look for chest movements
5. If CO present  check ETT/LMA and confirm its patency.
6. If in doubt remove airway device and replace it
7. If circuit obstruction confirmed  change to self-inflating bag with
Low ETCO2:
1. Check vital signs and look for causes of low CO
2. Look for over ventilation
3. Consider air /gas embolism  compress bleeding points and irrigate wound
4. Check ABG’s  Monitor need replacing or recalibration

Ans d) CLINICAL APPLICATIONS OF CAPNOGRAPH

1. Capnograph is a valuable monitor of pulmonary, cardiovascular and anaesthetic breathing
system useful during all general anesthesia procedures (Mandatory)
To assess adequacy of ventilation
2. Both types of capnograph (no diverting and diverting) relay on the absorption of infrared light
by CO2 (principle)
3. Rapidly and reliably defects esophageal intubation or accidental extubation
4. Sudden cessation of ETCO2 indicates circuit disconnect ion
5. Sudden doubling or tripling of ETCO2 indicates MH
6. Sudden ↓ in ETCO2 indicates embolism
7. Detection of rebreathing, soda lime exhaustion, estimation of PaCO2 and monitoring of IPPV and
hyperventilation

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Ans e)
CLINICAL EFFECTS OF HYPERCARBIA
1. ↑ CO
2. ↑ arterial BP
3. Tachycardia
4. Arrhythmias
5. ↑ CBF
6. CO2 narcosis
7. Respiratory acidosis
8. Shift ODC to Right
9. Respiratory stimulation in awake, G.A and paralysis eliminate this
10. Hypoxia Displace oxygen form alveoli

PULSE OXIMETRY
Q.3)
a) What is the principle of pulse oximetry?
b) What are the various components of pulse oximeter?
c) What are the limitations of pulse oximetry?
d) What are the advantages of pulse oximetry?
e) What are the disadvantages of pulse oximetry?

Ans a)
PRINCIPLE:
Pulse oximeters combine the principles of oximetry and plethysmography to measure the oxygen
saturation in arterial blood (noninvasively) Spectrophotometry.

Ans b)
COMPONENTS:
Pulse oximeter has a sensor containing light sources (2 or 3 light emitting diodes) and a light detector ( a
photodiode) which can be placed across a finger, ear lobe, toe or any other perfused tissue that can be
transilluminated a microprocessor which provides SpO2 of arterial blood

Ans c)
LIMITATIONS:
1. Vasoconstriction cold, hypovolemia, vascular disease
2. Calibration  mostly calibration points are in b/w 80-100%
3. Delay in response  instrumental and circulatory
4. Interference  methylene blue, bilirubin or nail polish, large venous pulsations, ambient light,
infrared heaters and surgical diathermy.

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Ans d)
ADVANTAGES OF PULSE OXIMETRY:
Pulse oximeters are mandatory monitors for any anesthetic procedure requiring sedation
Following are the advantages:
1. Useful when patient oxygenation need to be measured frequently like pulmonary lung disease
2. Helpful in monitoring neonates at risk of retinopathy of prematurity.
3. Pulse oximeters indicates tissue perfusion
4. Also measures heart rate
5. Diagnosis of hypoxia  possible in esophageal intubation
6. Helps identify postoperative pulmonary complications

Ans c)
DISADVANTAGES OF PO:
1. Cannot detect bronchial intubation
2. Cannot detect low FiO2
3. Inaccurate @ low SpO2
4. Other causes of pulse oximetry artifact are:
 Excessive ambient light
 Motion
 Methylene blue dye
 Venous pulsations in a dependent limb
 Low perfusion (↓CO, anemia, hypothermia, ↑SVR)
 Malpositioned sensor
 Optical shunting
5. Inaccurate @ low temperature
6. Inaccurate @ Excessive ambient light

BIS MONITOR
BISPECTRAL INDEX SCALE: is a dimensionless scale from 0 to 100
BIS value of 65-85 recommended for sedation
BIS value of 40-65 recommended for GA
BIS value < 40 near suppression  ↑ Burst suppress cor cal silence

ADVANTAGES OF BIS:
1. ↓ pa ent awareness dressing anesthesia
2. ↓drug use
3. Facilitates faster wake up time
4. Shorter stay in recovery
LIMITATIONS:
1. ↓ anesthe c usage cause lighter anesthesia
2. Ability to generate an inspiratory pressure of 250 mmH2O
3. Forceful hand grip

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PERIPHERAL NERVE STIMULATION
INDICATIONS:
1. PNS is helpful in assessing paralysis during RSI
2. Assess paralysis during continuous infusions of NMBA’s
3. PNS can help locate nerves to be blocked by R.A
Ulnar nerve stimulation of adductor pollicis muscle and facial nerve stimulation of orbicularis oculi are
most commonly monitored

PATTERNS OF STIMULATION:
All stimuli are 200 µs in duration and equal current intensity
Twitch: A twitch is a single pulse that is derived from every 1 to every 10 s (1 - 0.1 Hz)
Train of four: This stimulation denotes 4successive 200µs stimuli in 2s (2Hz). The twitches in train of four
patterns progressively fade as relaxation increase
The ratio of responses to 1st& 4th twitches is a sensitive indicator of non depolarizing muscle paralysis
Observer visually the disappearance of twitches
Disappearance of 4th twitch represents 75% block, 3rd twitch an 80% block, and 2nd twitch a 90% block
Clinical relaxation requires 75-95% block
Tetany: At 50 or 100 Hz is a sensitive test of neuromuscular function. Sustained contraction for 5 sec
indicates adequate but not necessarily complete reversal from neuromuscular blockade.
Double burst stimulation (DBS): Represents two variations of tetany that are less painful to patient
DBS 3,3 and DBS3,2 DBS is more sensitive than train of four stimulation for clinical (ie, visual) evaluation of
fade.
The diaphragm, Rectus abdominis, laryngeal adductors, and orbicularis oculi muscles recover from
neuromuscular blockade sooner than the adductor pollicis.

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MRI
Q4)
a. What are the special problems in MRI suite for pt. and anesthetist
b. How these problems overcome?
c. Which monitors are mandatory in MRI suite?

Ans a)
SPECIAL PROBLEMS IN MRI SUITE
PATIENT:
1. Prolong procedure
2. Claustrophobia
3. Immobility

ANESTHETIST:
1. No ferromagnetic objects use like implanted prosthetic joints, artificial pacemakers, surgical
clips, batteries, ordinary anesthesia machine, watches, pens or credit cards
2. Ordinary metal lead wires for pulse oximeters or ECG may acts as anntenas, may attract enough
radiofrequencey to distort MRI image or even cause patient burns.
3. Poor access to patient’s airway
4. Hypothermia in paediatric pts
5. Dim light in pts tunnel and
6. Loud noise (100dB)

Ans b)
SORTING OF PROBLEMS:
1. Modified monitors compatible with MRI environment
2. Non ferromagnetic ECG electrodes
3. Graphite and copper cables
4. Extra-long BP cuff tubing
5. Fibreoptic technologies
6. MRI compatible ventilators
7. Long circle system or Mapelson D breathing circuits
8. Anesthesia machine with no ferromagnetic component e.g. (aluminum gas cylinder)

Ans c) MANDATORY MONITORS IN MRI SUITE

1. Pulse oximetry
2. Plastic precordial stethoscope
3. ECG
4. BP monitoring
5. ETCO2 not mandatory
6. All emergency equipment to convert sedation to G.A (ETTs , resuscitation bag etc)
7. Continuous presence of anesthesia personnel

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CVP
INDICATIONS OF CVC
1. Monitoring of CVP
2. Fluid resuscitation (shock)
3. Infusion of Caustic drugs
4. TPN
5. Aspiration of air emboli
6. Insertion Transcutaneous pacing leads
7. Venous access in pt. with poor peripheral veins

CONTRAINDICATIONS:
1. Renal cell tumors extension into RA
2. Fungating tricuspid valve vegetations.
3. Anticoagulants
4. ipsilateral carotid endarterectomy

COMPLICATIONS:
1. Pneumothorax
2. Infection
3. Air embolism
4. Carotid puncture
5. Hematoma
6. Arythmias
7. Hemothorax
8. Chylothorex
9. Cardiac perforation
10. Cardiac tamponed
The shape of the central venous waveform
Technique: Seldinger’s technique (catheter over a guide wire) corresponds to the events of cardiac contraction
(Figure) :

Position: Tredelenburg position (head down) a waves from atrial contraction are absent in
atrial fibrillation and are exaggerated in
1. ↓ risk of air embolism
junctional rhythms (cannon waves);
Distended RIJ vein
Information obtained c waves are due to tricuspid valve elevation
during early ventricular contraction;
1. Cardiac function
2. RA pressure v waves reflect venous return against a closed
tricuspid valve; and the
3. Lt ventricular filling
4. AF (absent a wave) x and y descents are probably caused by the
downward displacement of the tricuspid valve
5. JR (Junctional rhythm )exaggerated a-wave (common wave)
during systole and tricuspid valve opening during
6. Volume status diastole.
7. Cardiac tamponed (BP ↓ and CVP↑)

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 ANESTHETIC EQUIPMENT AND PHYSICS
N2O
Q.1 a) what is the MAC value, melting point, boiling point and critical temperature of Nitrous Oxide?
b) What are the conditions in which N2O is best avoided?
c) What are effects of N2O?

Ansa) NITROUS OXIDE (N2O) (Laughing Gas)

Only inorganic gas in clinical use
MAC value  10.5% (inexpensive)
o
Melting point  -91 C (inorganic)
Boiling point  88oC (cardio stable)
o
Critical temperature  36.5 C (↑ catecholamine’s arrhythmias)
Critical pressure  2.6bar (↑RR ↓ TV)
Molecular wt.  44 (↓↓ hypoxic ven lator drive)
Oil/ water solubility coefficient  3.2 (↑ NM blockade)
Blood/gas solubility coefficient 0.47 @ 37 C
N2O is a gas at room temp and ambient pressure
Sweet smelling, nonirritant, colorless, good analgesic, week anesthetic stored in compressed form as a
liquid in blue cylinders at pressure 44bar (4400kPa)
65% N2O ↓MAC of volatile agents to 50%

Ans b)

CONDITIONS HAZARDOUS FOR N2O USE:

1. Air embolism ↑CBF, CBV and ICP
2. Pneumothorax ↑CMRO2 (O2 consumption)
3. Acute intestinal obstruction No muscle relaxation
4. Intracranial air Do not trigger MH
5. Pulmonary air cysts ↓RBF, GFR, U/O
6. Intraocular air bubbles ↓hepa c blood flow
7. Tympanic membrane grafting Causes PONV
8. Pts. With pulmonary HTN Elimination  Exhalation

N2O manufactured by heating ammonium nitrate (thermal decomposing) stored in H-Cylinders

connected by a manifold. Bulk storage is very expensive and only in very large institutes.
N2O E-cylinders attached to anesthesia machine

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 PROCESS: Nitrous Oxide is manufactured by decomposing molten Ammonium Nitrate at a temperature of 250º - 260º C,
to generate Nitrous Oxide and steam. CHEMICAL REATION:-NH4NO3 ---------> N2O | + 2H20 |
N2O manufactured by heating ammonium nitrate (thermal decomposition) Stored in H-Cylinders connected by a manifold.
Bulk storage is very expensive and only in very large institutes N2O E-Cylinders attached to anaesthesia machine

Ans. C) SIDE EFFECTS OF N2O:

1. Diffusion hypoxia
2. Effect on closed gas spaces: ↑ in volume of space or ↑ pressure
3. CVS depression
4. Teratogenic changes  avoided in early pregnancy
5. Toxicity  Affects Vit. B12 synthesis
Interfere with folic acid metabolism
Agranulocytosis and bone marrow aplasia
Megaloblastic anemia
Myeloneuropathy
Sub-acute combined degeneration of spinal cord

CRITICAL TEMPERATURE:
The critical temperature of a substance is the temperature above which that substance cannot
be liquefied by pressure, irrespective of its magnitude.
CT:-
O2 - -118,
N2O 36.5,
Air 141,
Entonox -7oC

GAUGE PRESSURE: Refers to the difference b/w the pressures of the contents of cylinder and the
ambient pressure.

TRIPLE POINT OF WATER: The temperatures at which water exists simultaneously in solid, liquid and
gaseous state. 0.01oC or 273.16oK

DIFFUSION HYPOXIA: At the time of emergence, N2O eliminated so rapidly that alveolar O2 and CO2 are
diluted and causes DH (Denitrogenation)

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MAPLESON CIRCUITS
Describe briefly the Mapleson classification of anesthesia circuits. Indicates to which group, the circuit in
common use belongs?

MAPLESON CLASSIFICATION OF BREATHING SYSTEMS:

SYSTEMS
Mapleson classified anesthetic
sthetic breathing system into 5-subtype
5
(Lack or Magill)

1. MAPLESON A SYSTEM:: Most efficient system for SV least efficient for CV. Most commonly used
version is magill attachment FGF= MV (80ml/kg/min) for SV

FGG

IPPV=2.5xMV
(200ml/kg/min)

2. MAPLESON B SYSTEM:: No clinical role FGF 2xMV

3. MAPLESON C SYSTEM:: Used in some hospitals to ventilate with oxygen during transport. High FGF
rates require to prevent Rebreathing also called water to-and-fro system.. FGF = 2xMV

Disconnection  most common  right angle connector & TT

Leaks  most common  Base plate of CO2 absorber
Bain

4. MAPLESON D SYSTEM: More efficient during controlled ventilation (Bain

( circuit).
). Bain coaxial
modification is the most commonly used version of mapleson D-system.
system. FGF supplied by narrow
inner tube FGF in CMV 1-2xMV (70ml/kg/min). Bain ↓the circuits bulk and retains heat and humidity
better than A system by counter current exchange. A disadvantage
disadvantage is that inner tube may become
disconnected resulting in hypoxemia and hypercapnia (Respiratory acidosis)  (Pethick test)

SV/FGF=2-3xMV
150-150 ml/kg/min

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5. MAPLESON E SYSTEM: (AYRE’S
AYRE’S T-PIECE)
T
Used extensively in paediatrics
Rebreathing is prevented if the FGF rate is 2.5-3xMV.
2.5 3xMV. FGF 4L/min recommended with paediatric
mapleson E system. Scavenging is difficult.

6. MAPLESON F SYSTEM:: Jackson rees modification of ayres T-Piece

T Piece includes an open ended bag to the
end of corrugated tube.
Advantages: Visual,, evidence of breathing during SV, allow CV and Scavenging, pro
provides a CPAP
during SV and PEEP-(IPPV)
(IPPV) possible to confirm FGF is
i entering the system.

FGF
SV CMV
2-3x MV 2xMV

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 235
Dr. Tariq Mahar
 Device through which we can deliver high pressure O2 source (at about 400 kPa
from either anesthesia machine or direct from a pipeline), On/Off trigger and
connection tubing
VENTURI
Q. B a) what is a venture injection device?
b) How does it work?
c) What are the indications for its use?
Bernouli effect: fall of pressure @ constriction

Ans a) The injector is frequently termed a venturi. The principles of venturi were first formulated by
Bernoulli but later venturi laid the new design
It’s a (relationship b/w pressure and velocity at any point in a fluid)
Fluid through constriction  ↑velocity

Ans b) It works by creating an open system with high flow to the nose and mouth with a fixed FiO2
Masks are known as ‘venturi’ or venti masks or high air flow with oxygen-entrainment (HAFOE) system.

The venturi effect is a jet effect. It is the reduction in fluid pressure that results when a fluid flows
through a constricted section of pipe. It is named often Giovanni Battista venturi, an Italian physicist.

c) INDICATIONS IN ANESTHETIC PRACTICE

1. Oxygen therapy by venturi mask
2. Nebulizes
3. Portable suction apparatus
4. Oxygen tents
5. As a driving gas in ventilator
6. Used in Operations on larynx, trachea or lung

Venturi effect is created which entrains atmospheric air and allows intermittent insufflation of lungs
with O2-enriched air at airway pressures of 2.5-3.0 kPa

Complications: Barotrama, gastric distension, awareness

VENTURI PRINCIPLE:  as fluid pass thru construction, there is ↑ in velocity. Beyond the construction
the velocity ↓ to the initial value

VENRURI:  it is a tube with a construction in with the cores section gradually dec. and then inc.

Bernoulli's principle states that an increase in the speed of a fluid occurs simultaneously with a decrease
in pressure or a decrease in the fluid's potential energy

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 APNEIC INSUFFLATION OF O2
Q.4) what is apneic insufflation of oxygen? What is its mechanism, indications and limitations?

Ans )APNEIC INSUFFLATION OF OXYGEN:

Passive insufflation of non-respirating airways with high FiO2 to prolongs the time to critical
desaturation.
MECHANISM:
Basically during apnea oxygen is absorbed form alveolus across the pulmonary vasculature leaving
behind ↓O2 concentration in the alveoli. In order to re-establish equilibrium oxygen with high flow and
high concentration replenish the O2 depleted alveoli thus maintaining oxygenation @ critical situations
Eg: RSI after suxa is given.
Indications:
1. RSI 4. Micro laryngeal surgery
2. Thoracic surgery 5. Bronchoscopy
3. Asphyxia neonatoreum 6. Intubation

Limitations: CO2 is not removed during apnea and it accumulates in blood and tissues resulting in
respiratory acidosis. Under ideal conditions a healthy adult could survive 1 hour easily.
That why is inferior to ECMO or bypass and therefore used only in emergencies and for short
procedures.

GAUGE PRESSURE
Q5 a) define
1. Absolute pressure 3. Gauge pressure
2. Atmospheric pressure 4. Differential pressure

b) Write gauge pressure of full cylinders of following gases in SI units of pressure.

Ans
1. ABSOLUTE PRESSURE: is the sum of gauge pressure and atmospheric pressure.
2. ATMOSPHERIC PRESSURE: is the pressure exerted by the weight of the atmosphere.
1 atmpr. At sea level  101,325 Pascals kPa
3. GAUGE PRESSURE: is equal to the absolute pressure minus atmospheric pressure.
4. DIFFERENTIAL PRESSURE: Is the difference in pressure between two points.

b) GAUGE PRESSURE OF FULL GAS CYLINDERS

I. Oxygen 137 bar
II. Air 137 bar
III. Entonox 137 bar
IV. Helium 137 bar
V. CO2 50 bar
VI. N2O 44bar

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MEDICAL GAS SUPPLY
Q6.
a) How different medical gases are supplied in OT?
b) What are the safety mechanisms involved?
c) What types of cylinders are used?
Ans
a) MEDICAL GAS SUPPLY TO OT
Medical gases are delivered from these central supply sources of hospital to operating rooms
through a pipeline network. Hospital gas delivery system appears in OT rooms as hose drops,
gas columns or elaborate articulating arms. Anesthesia machine connects with these pipelines
by color coded hose, and non interchangeable diameter index safety system fitting that
prevents incorrect hose attachments.
E-cylinder of oxygen, N2O and air attach directly to anesthesia machine. These cylinders have pin
index safety system to prevent incorrect attachment.
b) SAFETY MECHANISMS:
i. Color coded hoses/pips/cylinders
ii. Non interchangeable DISS (Pipelines)
iii. PISS ( on E-cylinders)
iv. Monitoring by central and area alarm system
v. Indicator lights
vi. Audible signals.
vii. Pressure relief valves in anesthesia machine and ventilator and cylinder
c) TYPES OF CYLINDERS USED
1. H-Cylinders (High pressure cylinder) in bank storage.
2. E-Cylinders (Emergency Cylinders) if hospital gas system fails

SURGICAL DIATHERMY
Q. 7) Write note on surgical diathermy and its hazards
 A surgical diathermy machine is used to pass electric current of high frequency (1 MHz) through
the body in order to cause cutting and/or coagulation by burning local tissue where current
density is high
 In the electrical circuit involving diathermy these are two connections with patient. In unipolar
diathermy there are (1) Patient plate and the (2) Active electrode used by surgeon. In bipolar
diathermy these is no pt. plate and current travels from one side of diathermy and out through
other side.
 Use bipolar diathermy when pacemaker present.
 The effect of passing electric current through body varies from slight physical sensation, muscle
contraction or VFib. The severity depends on amount and frequency of current.
 2types 1. Unipolar 2) Bipolar.

HAZARDS: 1. Burn. 2. Pacemaker dysfunction. 3. Ventricular fibrillation.

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OXYGEN CONTENT:
Q. 8)
a) What is Oxygen flux?
b) What is the arterial oxygen content?
c) Draw ODC?

Ans)
a) OXYGEN FLUX:
Amount of Oxygen delivered to the peripheral tissues per minutes i.e T oxygen content delivered/min
O2 flux = O2 bound to Hb + dissolved O2
1000mlsO2/min
TOTAL OXYGEN CONTENT
Sum of that in solution plus
That carried by haemoglobin.

b) ARTERIAL OXYGEN CONTENT: Sum of that in dissolved arterial blood plus

That carried by haemoglobin.
c) ODC see Respiration

ADVERSE EFFECTS OF IPPV

1) Altered V/Q relationships
2) ↓CO due to ↓ in venous return d/t ↑ intra thoracic pressures
3) Pulmonary barotrama – repetitive high peak inflation pressures.
4) Pulmonary volutrama – repetitive collapse and reexpansion of (n) or diseased lungs.
5) ↑ Physiological dead space.

STORAGE OF OXYGEN
Q.9) what are the different methods of storage of Oxygen for medical use give brief description of these
methods?

Ans 9) METHODS OF STORAGE OF OXYGEN

Medical grade oxygen (99% and 99.5% pure) is manufactured by fractional distillation of liquefied air
methods of storage for oxygen are:

1) Bank of high pressure cylinders connected by manifold:

(H-Cylinders)
These are 2 separate banks of H-cylinders connected by manifold. Only one bank is utilized at
one time. The number of cylinders in each bank depends on the anticipated daily usage by hospital.
They all have non-return valves. The supply automatically shifts from one group to other when
one group is exhausted. This changeover also activates an electric signaling system which alerts the staff
to change empty cylinder (vacuum insulated evaporator) -170oC

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Dr. Tariq Mahar
2) Liquid storage tank: this is more economical for large hospitals. Liquid O2 must store well below its
critical temperature of -119oC because gases can be liquefied by pressure only if stored below these
CT. These tanks are placed some distance away from hospital building due to risk of fire.

T=-170 P=10.5 bass

3) Emergency E-cylinders: Available in OT to guard against a hospital-gas system failure. A pressure of

1000psig indicates an E-cylinder is half full and has 330L of Oxygen.
If cylinder exhausted @ rate of 3L/min, it will be empty in 110 min.

HAZARDS OF OXYGEN
Q. 10) Briefly discus the adverse effects of oxygen?

Ans. 10)

HAZARDS OF OXYGEN THERAPY

Oxygen therapy can result in both respiratory and non-respiratory toxicity, depending on patient’s
susceptibility, FiO2 and duration of therapy.

Following are the hazards of oxygen therapy:

1.) FIRE: Oxygen vigorously supports combustion.

2.) HYPOVENTILATION: This complication primarily seen in patients with COPD who have chronic
retention of CO2. These pts have altered respiratory drive that depends on maintenance of relative
hypoxemia. ↑PaO2 in these pts to normal can cause severe hypoventilation.
3.) ABSORPTION ATELECTASIS: High concentrations of oxygen can cause pulmonary atelectasis in areas
of low V/Q ratios.
4.) PULMONARY TOXICITY: Prolonged high concentration of oxygen is known to damage lungs. Oxygen
mediated injury of alveolar capillary membrane produces a syndrome that is pathologically and
clinically indistinguishable from ARDS
5.) HYPERBARIC O2 TOXICITY: May present initially with retrosternal chest tightness and burning and
cough. Continued prolong exposure to hyperbaric O2 will lead to CNS toxicity leading to convulsions
6.) BRONCHOPULMONARY DYSPLASIA: in newborn infants.
7.) RETINOPATHY OF PREMATURITY: Retrolental fibroplasia is a neovascular retinal disorder. Oxygen
promotes disorganized vascular proliferation, fibrosis, retinal detachment and blindness.
8.) CNS TOXICITY: Convulsions due to prolong hyperbaric O2 therapy
9.) CVS DEPRESSION: By hyperbaric oxygen therapy.
10.) DEPRESSED HAEMOPOIESIS: Long term exposure to ↑ FiO2.

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Dr. Tariq Mahar
 Respiratory failure: impairment of normal gas exchange never enough to aquire acute therapeutic
intervention

OXYGEN DELIVERY:
Q. 11) what are the different ways in which oxygen can be administered to a spontaneously breathing
pt.?

Ans. 11) WAYS OF O2 DELIVERY TO PT

1) Nasal cannula
1-6 L/min
2) Nasal mask
3) Simple non-reservoir oxygen masks.5-8 L/min (Hudson masks)simple mask
4) Reservoir bag masks  2types: a) Partial Rebreathing mask b) Non-Rebreathing mask.
7-15 L/min.
5) Bag-Mask-Valve system
6) Air-Entrainment Venturi Masks 20%, 28%, 35%, 40%
7) Air-Entrainment Nebulizers.
8) BiPap or CPap (air oxygen flow meters and blenders)
9) Oxygen concentrator
10) Oxygen hoods- neonates and infants
11) Oxygen tents
12) Helium-oxygen (Heliox) therapy  Industries and deep sea diving.
13) Hyperbaric oxygen  Decompression sickness, gas embolism, gas gangrene, CO poisoning, Rx of
wounds.

SERUM O2 MEASUREMENT:
1) Oxygen tension Clarke’s electrode, transcutaneous electrodes fluorescence-based blood gas
analysis and ion-selective electrodes.
2) Oxygen content  volumetric method, blood hemolysis, galvanic cell and calorimetric method.
3) Oxygen saturationOximetry.

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Dr. Tariq Mahar
 h) Linkage between N2O and O2 flow meters helps ensure a minimum O2 concentration of 21-25%
nd
and does not affect the flow of 2 gas.

FLOWMETERS
PRINCIPLE: Once pressure is ↓ to safe level it will pass through flow
 Gas lines proximal to flow valves are (1 bar) considered to be in high-pressure circuit whereas
those between flow valves and common gas outlet are part of low-pressure circuit of the
machine
 Two types of flow meters on anesthesia machine
a) Constant pressure variable orifice and
b) Electronic flow meter.

PROBLEMS:
a) Vertical tube misalignment
b) Dirt in flow tube.
c) Sticking of a float/Bobbin at top of tube.
d) Static electricity
e) Back pressure
f) Leakage

SAFETY FEATURES OF FLOW METER

a) Full off and full on position prevent flow valve damage.
b) Touch and color coded knobs to prevent wrong gas turn on and off.
c) Oxygen knob is fluted, larger and protrudes further than other knobs and is positioned furthest
to the right.
d) To minimize the effect of friction between gas and tube wall, floats/bobbin are designed to
rotate constantly which keeps them centered in the tube.
e) Coating the tube’s interior with conductive substance (gold or tin) ↓the effect of sta c
electricity.
f) O2 flow meter always positioned downstream (nearest to vaporizer) to ↓ risk of leakage
(hypoxic mixture).
g) 150ml/min O2 is delivered when anesthesia machine turned on and the operator forget to turn
the oxygen flow.

MEDICAL AIR
Medical air is being used more frequently in combination with oxygen during anesthesia because of the
potential hazards of N2O and high concentrations of oxygen.

 Air is compressed to 137 bar and is obtained by bleeding oxygen and nitrogen.
 Medical grade G & H size cylinder with grey body color and white and black shoulder color or
through a pipeline system medical air is supplied.
 Its critical temperature is -140.6oC so it exists as a gas

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Dr. Tariq Mahar
USES:
1. Driving gas for ventilators
2. To operate power tools e.g. orthopedic drills (7bar)
3. Together with oxygen and volatile agent or IV agent for maintenance of anesthesia

ADVANTAGES:
1. Readily available
2. Non-toxic
___________________________________________________________________________________

WASTE GAS SCAVENGERS: dispose of gases that have been vented from breathing circuit by APL valve
and ventilator spill valve.

Safe levels of exposure, the national Institute for

Occupational Safety & Health (NIOSH)
recommends limiting the concentration of
N2O25 ppm (parts per million) & Halogenated
agents 2ppm (0.5 ppm if nitrous oxide also
used)
SCAVENGING SYSTEM
Q12
a) What is the advantage of a scavenging system?
b) What are the methods available for scavenging in OT’s?

Ans.
a) ADVANTAGE:
Scavenging system which is attached to the expiratory port of the ventilator, collects waste gas from
ventilator and anesthesia machine and dispose it outside the operation theater to prevent the
adverse effects of pollution on theater staff in OT’s.

b) METHODS OF SCAVENGING:
There are 3 types of scavenging system:
1. ACTIVE SYSTEM: Works by generating a negative pressure within the system to propel waste
gases to the outside atmosphere. Powered by a vacuum pump or venturi system, there must be
a pressure limiting device to prevent the patient’s lung form negative pressure (Pulmonary
edema)
2. SEMI-ACTIVE SYSTEM: This system has variable performance and efficacy. Waste gases may be
conducted to the extraction side of the air conditioning system which generates a small negative
pressure within the scavenging tubing.
3. PASSIVE SYSTEM: These systems vent the expired gas to outside environment. Gas movement is
generated by the patient. Total length of tubing must be accurate non excessive and not
resistant to expiration. The pressure can be altered by wind conditions at the external terminal

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Dr. Tariq Mahar
CLOSED CIRCUIT ANESTHESIA
Q-13)

a) Describe close circuit anesthesia? Indicate how it is different from other techniques?
b) What are the advantages and disadvantages of CCA?
c) What factors determines the delivery of inhalational anesthetic?
d) Is any special equipment necessary for CCA?

Ans. A) ANESTHESIA SYSTEMS:

Classified as non-Rebreathing, partial rebreathing or total rebreathing

1. NON-REBREATHING (OPEN SYSTEM)
FGF into the breathing circuit exceeds the patient’s minute ventilation. All gases not
absorbed by the patient are exhausted through APL valve and there is no flow through the
CO2 absorber and no gas is rebreathed by the patient.
2. PARTIAL –REBREATHING (SEMI OPEN OR SEMI CLOSED)
FGF < patients MV provided to pt. but > rate of uptake of all gases by the patient. Therefore
exhaled gas can take one of the 3 routes
1) It can be evacuated by APL valve
2) Absorb by CO2 absorber
3) Rebreathed by patient.
3. TOTAL REBREATHING (CLOSED SYSTEM) (CIRCLE SYSTEM)
Does not evacuate any gas through APL valve, all exhaled gases except CO2 are rebreathed &
CO2 must be eliminated by CO2 absorber to prevent hypercapnia, Total amount of FG
delivered to the system must nearly equal the amount of gas taken up by patient’s lungs.

Ans b) ADVANTAGES OF CLOSED CIRCUIT ANESTHESIA

1) Conserves heat and humidity

2) ↓ anesthe c pollu on
3) Allows early detection of circuit leaks and metabolic changes
4) Demonstrates the principles of anesthetic uptake.
5) O2 reservoir if failure of supply
6) Cost saving

DISADVANTAGES OF CLOSED CIRCUIT ANESTHESIA

1) Greater risk of hypoxia and hypercapnia.

2) Greater risk of anesthetic overdose.
3) Requires a high level of vigilance/ monitoring
4) Requires comprehensive understanding of pharmacokinetics

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Dr. Tariq Mahar
Ans c) FACTOR DETERMINING THE DELIVERY OF VOLATILE AGENT

1) FGF rates are the only factor that determines the consumption of anesthetic agent.
2) Other includes potency, blood and tissue solubility and amount of vapor produced.
3) Expense of volatile agent.
4) Discharge form recovery room or hospital. Indirect
5) Incidence of N&V.

Ans d) SPECIAL EQUIPMENT FOR CLOSED CIRCUIT ANESTHESIA

1) Oxygen analyzer
2) Vaporizers and flow meters must be accurate

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Dr. Tariq Mahar
 PHYSICS

1 atm= 1bars= 100 kPa,

TEMPERATURE MEASUREMENT 760 mmHg, 1000 cmH2O=760 torr

Body temperatures can be monitored at following sites: 1. atmospheres (symbol = atm)

2. millimeters of mercury (symbol = mm Hg)
1. Rectal  chance of perforation 3. Pascals (symbol = Pa) or, more commonly,
kiloPascals (symbol = kPa)
2. Nasopharyngeal Reflects brain temperature One atm. equals 760.0 mm Hg,
3. Oesophageal
4. Tympanic membrane risk of perforation
Skin, urinary bladder

 Core temperature is best measured via PAC

METHODS: Temperature is measured using a thermometer which measure To directly or indirectly

1. DIRECT:
Liquid expansion (mercury or alcohol)
Bimetallic strip
Chemical

2. INDIRECT:
Resistance wire
Thermistor
Thermocouple

Thermistors are semiconductors made from fused oxides of heavy metals such as cobalt, manganese
and nickel and can be made to have +ve or –ve temperature coefficients.
Advantage used to detect very small temperature changes

Thermocouple Thermometers works on the principle – Seebeck effect

Advantage  Very inexpensive

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Dr.Tariq Mahar
 Device to deliver precisely knowing variable gas making
of anesthetizing and life sustaining gas VIE

BASIC DEFINITIONS:
Low pressure expressed in SI units of kPa
High pressure expressed in bar (100kpa =1 bar)

MASS: Amount of matter in body. SI unit kg

LENGTH: Distance b/w two points. SI unit metre
VELOCITY: Distance travelled per unit time V=D/T m/s
DENSITY: Mass per unit volume P= m/v kg/m3
ACCELERATION: Rate of change of velocity a=v/T m/s
FORCE: Gives acceleration to a mass F=ma N= 1kg m/s2
WEIGHT: Force exerted by gravity on a mass. W=kg x 9.81 m/s2
MOMENTUM: Mass multiplied by velocity m = m x v
WORK: Undertaken when a force moves an object W= F x L = non =J
PRESSURE: Force per unit area. P=F/a N/m2x Pascal
ENERGY: Capacity for doing work U=J= force x distance
POWER: Rate of performing work P= Watt = J/s
TEMPERATURE: Tendency to gain or lose heat K or oC
OoC = 32oF = 273 oK
ABSOLUTE TEMPERATURE = OoK = -273 oC
STANDARD TEMPERATURE= OoC or 273.15 K
STANDARD PRESSURE = 760 mmHg or 101.325 kPa
1 atmospheric pressure = 760 mmHg
=1 bar
=760 torr
=1 atmospherc absolute (ata)
=14.7 Lb/in2 Psi
=101.325 kPa
=10.33 cmH2O

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Dr.Tariq Mahar
 Oxygen flush- intermediate pressure system
nd
(2 stage regulator) 1 bars

GAS LAWS
BOYLE’S LAW: At constant temperature, the volume of a given mass of gas varies inversely with its
absolute pressure.

V x I/P (at constant temperature)

or PV = K (constant)
or P1V1 = P2V2

Applications:
To find out the content of a gaseous cylinder and how long will that last
P1Absolute pressure = 13800 kPa
V1 Volume of empty cylinder = 10 Litters
P2 Atmospheric pressure = 100 kPa
V2content of the cylinder
P1V1 = P2V2
or V2 = P1V1/ P2 = 13800 x 10 /100 = 1380 Litters
If we use oxygen at a rate of 8L /min, the above content will be exhausted in:
1380/8 = 172 minutes or 2hr and 52 min

Absolute pressure = gauge pressure + atmospheric pressure

=137bar or 13700 kPa + 100 kPa
=13800 kPa

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Dr.Tariq Mahar
 High pressure = 2000 PS1 =138 bars pressure regulating b----
Intermediate = 40-60 = 4 hass up to flow meter
Low pressure = 14.7 psi – 1 bass flow meter and after word

CHARLE’S LAW: (Gay Lussac’s Law)

At constant pressure, the volume of a given mass of gas is directly proportional to its absolute
temperature
V α T (at constant pressure)
Or V= TK2
Or V/T = K2
Or V1/T1 = V2/T2

Application: Temperature compensation in vaporizers

THIRD GAS LAW: (Perfect gas law)

At constant volume, the absolute pressure of a given mass of a gas is directly proportional to its absolute
temperature
PαT
Or P = Tk3
Or P/T = k3
Or P1/T1 = P2/T2

Application:
1. Explosion can occur if cylinders are kept at high temperature
2. Weakening of cylinder metal can be dangerous as cylinder can with stand pressures up to 210 bar
3. Hydrogen thermometer which is used as a standard for scientific temperature measurement

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DALTON’S LAW OF PP

AVOGADRO’S HYPOTHESIS
IDEAL GAS EQUATION:
Combining the three gas laws
PV =KT
Or P1 V1/T1 = P2V2/T2

Application: It helps to determine volume of a gas on simultaneous change in temperature and pressure

DALTON’S LAW OF PARTIAL PRESSURE:

States that “pressure exerted by a mixture of gases is equal to the sum of their individual pressure or
partial pressure
Application:
1. Calculating partial pressures of individual gases in a mixture of gas e.g. Entonox and air
2. Effect of humidity on the partial pressure of gases
3. Filling of cylinders with gas mixtures

AVOGADRO’S HYPOTHESIS: States that:

“Equal volumes of gases at the same temperature and pressure contain equal numbers of molecules”

Avogadro’s number: Is the number of molecules in 1kg molecular weight of a substance and is equal to
6.022 x 1023
 Under standard temperature and pressure 1 Gm molecular weight of any gas occupies a volume of
22.4 Liters One mole of Halothane 197g
Oxygen 32g
N2O 44g
CO2 44g

LAW OF LAPLACE: Pressure inside a bubble is directly proportional to the surface tension and inversely
proportional to radius of curvature
=

Applications:
1. Amount of halothane going to a patient in a particular concentration
2. Quantity of a gas produced by liquid N2O
3. Calibration of vaporizers.

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Dr.Tariq Mahar
CALCULATING AMOUNT OF HALOTHANE GOING TO PATIENT AT PARTICULAR CONCENTRATION:
Vapours of halothane produced by 1ml of liquid halothane

22.4 1000 ℎ ℎ
ℎ ℎ

. .
Or = 210 mls of vapours

Now let flow of oxygen  8L/min and

Concentration of halothane  1%
1% halothane means every 100mls of vapour mixture contain 1ml of halothane vapours.

For a FGF of 8 = 80 ℎ ℎ

If 210ml of vapours are produced by 1ml of liquid halothane then 80ml of vapours are produced by X ml
of liquid halothane

= = 0.38 of liquid halothane

i.e. 0.38ml of liquid halothane will produce 80mls of vapours pre minute when oxygen flows at a rate of
8L/min carrying 1% halothane

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 CRITICAL PRESSURE: Pressure requires to liquefy a gas @ its critical temperature

CRITICAL TEMPERATURE:

QUANTITY OF GAS PRODUCED BY LIQUID N2O:

Full N2O cylinder weighs 3.4kg or 3400g if one mole of N2O (44g) occupies 22.4 litres then
22.4
3400 = 3400 = 1730
44
Wight of an empty cylinder is mentioned on the cylinder.
Now if liquid N2O weighs 1.3 Kg then
3 kg = 3000g

3000
= 68.18
44

68.18 x 22.4 = 1527 litres

So 1527 litres of N2O will be produced by 3kg liquid N2O

CRITICAL TEMPERATURE:
The critical temperature of a substance is the temperature above which that substance cannot be
liquefied by pressure, irrespective of its magnitude

Oxygen 118
Nitrogen 147 Gases at room temperature
Air 141
CO2 31 At higher pressures these are mixtures of gas and liquid @ room
N2O 36.4 temperature

FILLING RATIO: it is the mass of liquid gas divided by the mass of water that cylinder could hold.
Normally a cylinder of N2O is filled to a ratio of 0.67
Incomplete filling of cylinder is necessary because thermally induced expansion of liquid in a full cylinder
cause an explosion.

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ENTONOX (also known as 'gas and air' or Entonox)

ENTONOX: CT  -7OC
 It is compressed gas mixture containing 50% oxygen and 50% N2O
 The mixture is compressed into cylinders containing gas at a pressure of 137 bar (2000Lb/inch2) Psi
 The presence of oxygen reduces the critical temperature of N2O so it does not liquefy. (Poynting
effect)
 Cooling of a cylinder of Entonox to a temperature below -7OC results in separation of liquid N2O

PRECAUTIONS:
1. Entonox cylinder should be stored horizontally for a period of not less than 24 hrs @ a
temperature of 5OC or above
2. The cylinder should be inverted several times before use

PRESSURE RELIEF VALVES:

Modern anesthesia systems contains a variety of pressure relief valves
1. PRV on back bar of anesthesia machine operating @ 35kPa protects flow meters and
vapourizers from excessive pressure
2. PRV in modern ventilators set @ 7 kPa to protect pt from barotrauma
3. PRV in scavenging system operating @ 0.2 – 0.3 kPa to protect patient from negative pressure
applied to lungs

PRESSURE REGULATORS: Two important fx in machine

1. They reduce high pressures of compressed gases to manageable levels (acts as PRV)
2. They minimize fluctuations in the pressure within anesthesia machine, which would necessitate
frequent manipulations of flow meter controls.

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 Blood is non-Newtonian fluid

FLOW OF FLUIDS

VISCOSITY: Is defined as that property of a fluid that causes it to resist flow

η=

 Units of coefficient of viscosity are Pascal seconds.

Fluids that obey this formula are referred as Newtonian fluids
Viscosity of liquids ↓ ↑ in temperature
Viscosity of gases ↑  ↑ in temperature

LAMINAR FLOW: Smooth, orderly flow of fluid such that molecular travel with greatest velocity
in axial stream while the velocity of those in contact with wall of tube may be virtually zero

HAGEN-POISEUILLE FORMULA:
It describes the relationship between various factors which affect flow through a tube provided
the flow is laminar

Q=

Q flow
ΔP  pressure gradient along the tube
rradius of tube
L length of tube
ɳviscosity of fluid

Hagen-Poiseuille’s formula applies only to Newtonian fluids

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TURBULENT FLOW:
The fluid no longer moves in orderly planes but swirls and eddies around in a haphazard
manner viscosity affects laminar flow but turbulent flow is affected by changes in density

CRITICAL POINT OR CRITICAL VELOCITY:

As the velocity of fluid increases, a certain point is reached at which the characteristics
of flow change from laminar to turbulent.
Critical point is dependent upon several factors formulated by Reynolds as Reynolds
number:
Reynolds Number =
V linear velocity
R  radius of tube
P  density
ɳ viscosity
Reynolds number > 2000  Turbulent flow
Reynolds number < 2000  Laminar flow

Applications:
1. In URT Obstruction of any severity, flow is inevitable turbulent thus for the same
respiratory effort a ↓ TV is achieved than when flow is laminar.
2. In anesthetic breathing systems, a sudden change in diameter of tube or irregularity of
wall is responsible for a change from laminar to turbulent
3. Resistance to breathing is much greater when TT of small diameter is used

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VENTURI

VENTURE PRINCIPLE: As fluid passed through a constriction there is an increase in velocity. Beyond the
constriction the velocity decrease to the initial value
At the constriction the kinetic energy ↑ due to ↑ velocity

Applications:
1. Oxygen therapy by venture masks in COPD
2. Nebulizers
3. Portable suction apparatus
4. Oxygen tents
5. As a driving gas in a ventilator
6. Rigid bronchoscope

BERNOULLI’S PRINCIPLE: As fluid passes through a constriction there is an increase in velocity of fluid
(↑kine c energy) and a reduc on in pressure (↓ poten al energy) beyond the constriction the velocity
↓ to ini al value

COANDA EFFECT: When a gas flows through a tube “venture” and enters a Y junction, gas tends to cling
either to one side of the tube or to the other. The gas is not divided equally between two outlets.

Applications:
1. Anesthetic ventilators (Fluidic ventilators)
2. Maldistribution of gas flow to alveoli due to broncho constriction
3. Myocardial infarction in cases where there may be narrowing before the branching of a
coronary artery

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HEAT AND VAPORIZATION

HEAT: is the energy which may be transferred form a body at a hotter temperature to one at a colder
temperature

HEAT CAPACITY: Amount of heat required to raise the temperature of the body by 1OC. SI unit  J/K
SPECIFIC HEAT CAPACITY: of a substance is the energy required to raise the temperature 1kg a
substance by 1OK.
Heat capacity = mass x specific heat capacity
 Heat is lost form patients by process of:
1. Conduction 2.Convection 3.Radiation 4.Evaporation

VAPOUR PRESSURE: Is the pressure exerted by vapours above the liquid

SATURATED VAPOUR PRESSURE: In a closed container and @ STP the vapour pressure is at equilibrium
when the number of molecules escaping form the liquid is equal to the number of molecular re-entering
the liquid phase.
SVP of liquids is independent of ambient pressure but increase with increasing temperature

HEAT OF VAPORIZATION: The amount of heat required to convert a unit mass of liquid in to a vapor
without a change in temperature of liquid is termed heat of vaporization

BOILING PINT: of a liquid is the temperature at which its saturated vapour pressure becomes equal to
the ambient pressure.

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SOLUBILITY
HENRY’S LAW: States that “At a given temperature the amount of a gas which dissolve in a liquid is
directly proportional to the partial pressure of the gas in equilibrium with the liquid
Henry’s law applies only if the temperature is constant
The solubility of a gas depends on the
1. Partial pressure
2. Temperature
3. Gas concerned
4. Liquid concerned

Applications:
1. CO2 has a higher solubility coefficient than oxygen therefore for a given partial pressure gradient
CO2 diffuses 20 times more rapidly than oxygen as PO2 increases
2. Increased concentration of dissolved oxygen as PO2 increases
3. Increased solubility of nitrogen and other gases into tissue fluids during deep sea-diving and
hyperbaric chambers due to the effect of increase partial pressure
4.
BUNSEN SOLUBILITY COEFFICIENT:
Volume of gas which dissolves in a unit volume of liquid at a given temperature when the gas in
equilibrium with the liquid is at a pressure of 1 atmosphere

OSTWALD SOLUBILITY COEFFICIENT:

Volume of gas which dissolves in a unit volume of liquid at a given temperature
Thus Ostwald sol coefficient is independent of pressure

DIFFUSION
PARTITION COEFFICIENT: Ratio of the amount of a substance in one phase being of equal volume and in
equilibrium
Partition coefficient may be applied to two liquids but Ostwald coefficient applies to partition between
gas and liquid
FICK’S LAW OF DIFFUSION: States that the “rate of diffusion of a substance across unit area is
proportional to concentration gradient
Applications: transport of a gas or vapour across physiological membrane or interface e.g. O2, CO2 and
anesthetic vapours

GRAHAM’S LAW: (Applies to gases only)

States that the rate of diffusion of a gas is inversely proportional to the square root of its molecular
weight”
Applications:
1. separation of mixtures
2. Flowmeter calibration

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Dr.Tariq Mahar
Diffusion depends on :
1. Tension gradient
2. Solubility
3. Membrane concerned, its area, thickness and its constituents
4. Molecular size

DALTON’S LAW OF PARTIAL PRESSURE:

States that pressure exerted by a mixture of gas is equal to the sum of their individual pressure or partial
pressure
Application:
1. Calculating partial pressure of individual gases in a mixture of gas e.g.: Entonox and air
2. Effect of humidity on the partial pressure of gases
3. Filling of cylinders with gas mixtures.

OSMOSIS: Net movement of solvent molecules across a semipermeable membrane till concentration on both sides

OSMOLARITY: Refers to osmotic pressure produced by all substances in a fluid (Osmoles per litre of so
lution)
OSMOLALITY: Refers to the number of osmoles per kg of water or other solvent

ONCOTIC PRESSURE: osmotic pressure exerted by plasma proteins alone.

Plasma oncotic pressure is relatively small approximately 1mosm/L equivalent to 25 mmHg
Total plasma oncotic pressure  300mOsmol/L or 6.5 bar

AMPERE: Is defined as the current which if flowing in two parallel wires of infinite length, placed !metre
apart in a vacuum, produces a force of 2 x 10-7 N/m on each of the wire ampere (A) is the SI unit of
electric current
ELECTRIC CHARGE: measuse of the amount of electricity SI unit  coulomb ©
COULOMB: quantity of electric charge that passes some point when a current of 1 ampire flows for a
period of 1s
C= A x s
VOLT: 1 volt is defined as the potential difference which produces a current of 1 ampere in a substance
when the rate of energy dissipation is 1 watt.

( )
=
( )

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Dr.Tariq Mahar
OHM’S LAW

OHM’S LAW: States that the current flowing through a resistance is proportional to the potential
difference across it
Unit for electrical resistance is ohm(Ω)
OHM: Is that resistance which will allow 1 ampere of current to flow under the influence of a potential
difference of 1 volt
Resistance (Ω) = Potential (v)/ current
3 classes of electrical insulation designed to minimize risk of a patient or anesthetist forming part of air
electrical circuit b/w live conductor of a piece of equipment and ground are:
1. Class I equipment fully earthed
2. Class II equipment  Double insulated
3. Class III equipment  low voltage

DEFIBRILLATOR: Is an instrument in which electric charge is stored in a capacitor and then released in
controlled fashion. (Capacitance is the ability to store electric charge)
Direct current (DC) is used and is more effective, causes less myocardial damage and is less myocardial
damage and is less arrhythmogenic than AC

ISOTOPES AND RADIATION

ISOTOPES: Are variations of similar atoms but with different numbers of neurons

RADIOISOTOPES: Isotopes with unstable nuclei are known as radio isotopes and are radioactive
Radioactive decay: the process of change form one unstable isotope to another is known as radioactive
decay. Rate of decay is measured by half-life

HALF-LIFE: of an isotope is the time required for half of the radioactive atoms present to disintegrate
Radioactive decay unit’s gamma rays alpha or beta particles
These all cause damage to or death of cells
USES OF RADIOISOTOPES:
1. Treatment of cancer (cobalt – 60 and caesium 137)
2. Thyrotoxicosis (iodine - 131)
3. Diagnostic purposes (Technietium 99m, xenon-133) are used in imaging techniques such as scanning
4. Chromium-51 measure red cell volume
SI unit for radioactivity is Becquerel
X-RAYS: are electromagnetic radiation produce when a beam of electrons is accelerated from a cathode
to strike an anode. X-rays used for imaging purpose

PRINCIPLE OF MRI: hydrogen ion is the body and has a strong response to an external magnetic field
SI unit for magnetic flux density is tesla (T)

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Dr.Tariq Mahar
 CVS
PACEMAKERS:
Q) 56 years old man scheduled for elective hernia repair. He has an implant PPM.

a) What are the different types of pacemakers?

b) How will you assess pacemaker function in this patient?
c) What are anesthetic concerns in this patent?
d) What is meant by VVI pacemakers?

A) TYPES OF PACEMAKER:

1. Temporary:
a) Single pacing
b) Dual pacing.
2. Permanent:
a) Asynchronies (AOO, VOO, DOO)
b) Single chamber demand pacing (VVI, AAI)
c) Dual chamber AV sequential pacing (DDD)
 VVI and DDD are most commonly used

B) ASSESSMENT OF PACEMAKERS FX:

1. Assess ECG which will show pacing spikes.

Spike rate should be identical to set (TPM) or programmed (PPM)
2. Slower rate may indicate low battery.
3. Every impulse should be followed by palpable arterial pulse
4. A CXR is useful in excluding fracture or displacement of pacing leads.
5. If pacemaker malfunction is suspected cardio logical consultation is necessary.

C) ANESTHETIC CONCERNS /MANAGEMENT:

1. Determine whether EMI (electromagnetic interference) is likely to occur or not  if likely  it will suppress
the pacemaker generator  minimized by limiting its use to short bursts, limiting its power
output, placing its grounding plate as far as from pacemaker generator and using bipolar cautery
2. It is advisable to use bipolar electrocautery system.
3. Determine the need to reprogram use pacemaker or convert it to asynchronous mode, if
needed it should be done preoperatively.
4. Continuous monitoring of arterial pulse wave is mandatory to ensure continuous perfusion
during electrocautery.
5. Suxamethonium induced fasciculation or post-operative shivering can suppress pacemaker
generator.

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Dr. Tariq Mahar
 6. Hypo/ hyperkalemia alters pacing and can result in failure of ventricular depolarization.
7. If PPM malfunctions intra-operatively, it should generally be converted to an asynchronous
mode.
8. Myocardial ischemia, infarction or scarring can also cause failure of ventricular capture.
9. All anesthetic agents can be used safely in pacemaker patients
10. LA with light I/V sedation usually needed for placement of pacemaker

D) VVI pacemakers:

1. Single chamber demand pacing

2. Most commonly used
3. Ventricular inhibition pacer.
4. Suppress by normal activity of QRS complex.

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Dr. Tariq Mahar
IHD (Ischemic heart disease)
Q2- A 55years old male K/C of IHD, scheduled for lapchole.

a) What are the risks factors involved?

b) What measures would you take to minimize the risk?

Ans. a)

RISK FACTORS

Cardiac:

Major
1. Recent MI < 1 month to planned surgery
2. USA (unstable angina)
3. DHF (decompensated heart failure)
4. Significant arrhythmias
5. Severe valvular disease (AS/MS)
6. CABG/ PTCA < 6 weeks

Intermediate:
1. Prior MI > 1month to planned surgery
2. Stable mild angina
3. Compensated heart failure
4. DM
5. Renal insufficiency

Minor:
1. Advance age
2. Abnormal ECG
3. Rhythm other than sinus e.g. AF
4. Low functional capacity
5. H/O stroke.
6. Uncontrolled systemic HTN.

Major risk factors of CAD

1. ↑age 7.) DM
2. Male sex 8.) Obesity
3. +ve family history 9.) H/O CVA
4. Smoking 10.) Menopause
5. HTN 11.) Use of OCP (Oral contraceptive pills).
6. Hyperlipidemia 12.) Sedentary life style Physical inactivity, High stress

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Dr. Tariq Mahar
Surgical:

High risk (cardiac risk >5%)

1. Emergency major operations particularly in the elderly
2. Major vascular surgery e.g. aortic.
3. Peripheral vascular surgery.
4. Anticipated prolonged surgeries associated with large fluid shifts/blood

Intermediate risk (cardiac risk < 5%)

1. Carotid endarterectomy
2. Head and neck surgery.
3. Intra-peritoneal and intra-thoracic surgery
4. Orthopedic surgery.
5. Prostate surgery.

Low risk (cardiac risk< 1%)

1. Endoscopic procedures.
2. Superficial procedures.
3. Cataract surgery.
4. Breast surgery.

FUNCTIONAL CAPACITY:
Exercise tolerance  expressed in METS
(Duke Activity Status Index) (DASI)
1-4 METS Minor exercise (dress change) slow walk
4-10 ETS  Moderate exercise (climb on stares) Play golf
>10 METS  Vigorous exercise (swimming)

MANAGEMENT OF IHD:
OBEJETIVES: To maintain a balanced myocardial oxygen supply-demand relationship

PREOP MANAGEMENT:
History is of prime importance in IHD
Ask about symptoms, treatment, complications and results of previous evaluations provide enough
estimates of disease severity and ventricular function.
Functional class, activity level (walking, climbing stairs)
Medications, allergies, smoking, previous anesthetics
General physical examination:
Airway assessment (MD, TM distance, loose teeth, artificial dentures etc)

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Dr. Tariq Mahar
Investigations:

a) ECG e) ETT (FC, ischemia)

b) Cardiac enzymes f) ECHO (WMA wall motion abnormality, EF)
c) CXR (cardiomegaly) g) MP myocardialc perfusion scans (Thallium, Dobutamine)
d) Holter monitoring, (Ischemic episodes) h) Coronary angiography

Premedication: Benzodiazepine alone or in combination with opioid Is most commonly used, to allay
fear, anxiety, pain and prevents adverse affects of sympathetic activation on myocardial oxygen supply
demand balance.

Prophylactic β-blockers have shown to reduce incidence of intraoperative and postoperative ischemia
complications.

INTRAOP MANAGEMENT:

1) Tachycardia and B.P should be controlled by deep anesthesia or β-blockers.

2) Avoid hypotension, hypoxemia and Hypercarbia.
3) Hb >9-10 g/dl.
4) Standard monitoring + invasive monitoring with arterial line, CVP and pulmonary artery
catheters are advised.
5) TEE in cardiac surgeries.
6) If ICD (implantable cardioverter defibrillator) patient  problems with the use of surgical electrocautery
7) RA is a good choice for procedures involving extremities; perineum and possibly lower abdomen
avoid hypotension by phenyl-ephedrine, ephedrine or epinephrine.
8) Propofol, barbiturates, etomidate, benzodiazepines, opioids and various combinations can be
used (Etomidate+ fentanyl +atracurium).
9) Ketamine is contraindicated in IHD
10) Rocuronium, Vecuronium and atracurium are good relaxants for IHD
11) Reversal of relaxants by glycopyrrolate instead of atropine ↓ tachycardia

POSTOP MANAGEMET:

1. Anticipate/ avoid hypertension and tachycardia @ emergence by giving lidocaine, esmolol etc.
2. Post op ICU care.
3. If major surgery supplemental O2 for 3-4 days.
4. Shivering  meperidine 20-30 mg I/V.
5. Hypothermia  forced air warming blanket.
6. Post op pain  generous analgesia or RA e.g. epidural.
7. If fluid overload  CXR  congestion  furosemide 20-40mg I/V
8. Unexplained hypotensionischemia  12 lead ECG.
9. Altered mental status  Neurophysician consultation.

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Dr. Tariq Mahar
HTN
Long standing uncontrolled hypertension accelerates atherosclerosis and hypertensive organ damage.
HTN is a major risk factor for cardiac, cerebral, renal and vascular diseases.
Complications: MI, CHF, stroke, renal failure, peripheral occlusive disease and aortic dissection
Definition: Consistently elevated diastolic BP > 90-95 mmHg and a systolic pressure > 140-160 mmHg

CLASSIFICATION:
Category of BP Systolic B.P Diastolic BP
Normal _________________ <130 ___________ <85
High normal _____________ 130-139 __________ 85-89
Stage 1 mild _____________ 140-159 __________ 90-99
Stage 2 moderate ________ 160-179 __________ 100-109
Stage3 sever ____________ 180-209 __________ 110-119
Stage4 very sever ________ >210 __________ >120
Malignant HTN ___________ Medical Emergency

Pathophysiology: Essential (Idiopathic) accounts for 80-95% of HTN Associated with abnormal baseline
elevated in Cardiac output and systemic vascular resistance (CO &SVR) or both.
Extracellular fluid volume and plasma rennin activity may be low normal or high.
The chronic ↑in a er load results in LVH & altered diastolic function. HTN also alters cerebral auto-
regulation (limit may be in the range of mean blood pressures of 110-180mmhg)

(ARBs) Angiotensin II receptor blockers

TREATMENT:
(ACE) Angiotensin-converting enzyme
Reverse LVH & altered cerebral auto-regulation. (CKD) Chronic kidney disease
HTN – low dose thiazide diuretic is 1st choice. (SNP) Sodium nitroprusside
(GTN) Nitroglycerin
ACE inhibitor – 1st line choice  pts with LV dysfunction or HF.
ACE inhibitor or ARB – 1st line choice  pts with hyperlipidemia, CKD and DM
β -Blocker 1st line choice  pts with CAD
In black patients’  diuretic or Ca+ channel blocker.
In elderly patients  diuretic with or without β-Blocker or Ca+ channel blocker alone.
Pt’s with moderate to severe HTN –requires 2nd or 3rd drugs Diuretics, β-Blocker, ACE-inhibitors.

MANAGEMENT OF HTN:
OBJECTIVES: To maintain an appropriate stable blood pressure range within 10-20% of baseline level
PREOP MANAGEMENT:
1. Antihypertensive drug therapy should continue till surgery
2. Surgery should be postponed until DBP < 110, particularly those with evidence of end organ
damage.
3. History Ask about severity and duration, drugs, complications functional class, edema,
syncope and claudication.

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Dr. Tariq Mahar
 4. Physical examination: Ophthalmoscopy most useful examination after BP readings. S4 gallop
common in pts with LVH.
5. Measure BP in both supine and standing positions.
6. Preoperative fluid administration prevents severe hypotension @ induction
7. Airway assessment
8. Investigations:
a.) ECG. d.) Cr. & BUN. c.) ECHO (for LVH)
b.) CXR (boot shape). e.) UCE (hypokalemia should be corrected)
9. Premedication: reduces anxiety and is highly desirable in hypertensive’s
 Mild to moderate HTN anxiolytic agent midazolam
 Antihypertensive continue till surgery.

INTRAOP MANAGEMENT:
1. Arterial blood pressures should generally be kept within 10-20 % of preoperative levels. If severe
HTN > 180/120 is present then kept within high normal range 150-140/90-80 mmHg to maintain
CBF in longstanding HTN.
2. Standard monitoring with intra arterial monitoring reserved for major procedures associated
with rapid or marked changes in cardiac preload and after load. Other include ECG, Urine
Output
3. Several techniques may be used before intubation to attenuate the hypertensive response:
a.) Deep anesthesia with a patent volatile agent for 5-10 minutes
b.) The duration of laryngoscopy should be as short as possible.
c.) Administer a bolus of an opioid e.g. fentanyl 5 μg/kg
d.) Administering lidocaine 1.5mg /kg I/v
e.) β -adrenergic blockade with esmolol, propranolol or labetalol.
f.) Using topical airway anesthesia e.g. lidocaine 4mg spray.
Ketamine is contraindicated  sympathetic stimulation –HTN, Parkinsonism and vasopressors used very
cautiously.
Intraoperative hypertension not responding to ↑ anesthetic depth can be treated with parenteral
antihypertensive e.g. GTN, SNP, labetalol, hydralazine etc.
Reversible causes such as inadequate depth of anesthesia, hypoxemia or Hypercapnia should always be
excluded before starting antihypertensives.

POSTOP MANAGEMENT:
 Postoperative HTN is common and anticipated in pts having uncontrolled HTN
 Close BP monitoring in recovery.
 Sustained HTN can cause formation of wound hematomas and disruption of vascular sutures line.
 HTN could be enhanced by respiratory abnormalities, pain, volume overload or bladder distension
 Treat the cause.
 Parenteral antihypertensive like labetalol given if necessary
 When patient resumes oral intake, preoperative medications restarted.

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Dr. Tariq Mahar
MYOCARDIAL OXYGEN SUPPLY-DEMAND BALANCE

Q.45, years old gentleman had major MI 8 weeks ago. He requires an urgent laparotomy
a) Write down factors governing myocardial O2 supply demand?
b) How will you evaluate and prepare this patient?
c) What problems do you anticipate intra/ postop?

Ans a) FACTORS AFFECTING MYOCARDIAL OXYGEN SUPPLY-DEMAND BALANCE

SUPPLY:
1. Heart rate (diastolic time)
2. Coronary perfusion pressure (aortic diastolic BP, Ventricular EDP)
3. Arterial oxygen content (arterial oxygen tension, Hb. concentration)
4. Coronary vessel diameter.

DEMAND:
1. Basal requirement
2. Heart rate
3. Wall tension (Preload, Afterload)
4. Contractility

Ans b) Cardiac risk factors and surgical risk factors for evaluation /assess preoperative management of
IHD for preparation.

Ans c)
INTRAOP PROBLEMS
↑Sympathetic stimulation due to
1. Light anesthesia 5. Blood loss
2. Inadequate analgesia 6. Hypoxia
3. Surgical stimulus 7. Hypercarbia
4. Large fluid shifts 8. Hypovolaemia
These all can provoke ↑HR and hypertension, which then increase demand and decrease supply
deteriorating myocardial oxygen balance.

TOP PROBLEMS
1. Tachycardia due to inadequate analgesia, emergence and Hb < 9 gm. /dl.
2. ↑myocardial ischemia during emergence and extubation.
3. Hypotension  ECG  Ischemia.
4. Respiratory abnormalities like hypoxia and Hypercarbia.
5. Fluid overload.
All these factors can also influence and deteriorate myocardial oxygen supply-demand balance.

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Dr. Tariq Mahar
MITRAL STENOSIS:
Q. A 20 year old female pt. presents with # shaft of femur as a result of RTA; ORIF is planned. She is
diagnosed case of MS for last 5 years.
a) What is pathophysiology of MS?
b) Write down pre anesthetic evaluation?
c) Write down anesthetic technique with special reference to hemodynamic goals?
d) Write down normal MV area?
e) Complications of MS during anesthesia and how will you prevent them?

Ans.a) PATHOPHYSIOLOGY OF MS
1. MS almost always occurs as a delayed complication of acute rheumatic fever.
2. Rheumatic process causes valve leaflets to thicken, calcify and become funnel shaped. Annular
calcification also present.
3. Mitral commissure fuses.
4. Chordae tendineae fuses and shorten
5. Valve cusp become rigid  valve leaflets typically display bowing or doming during diastole on
echo.
6. Significant restrictions of blood flow through mitral valve results in higher trans-valvular
pressure gradients.
7. LA dilates and promotes SVT particularly AF and thrombus in LA appendage
8. ↑LA pressures  pulmonary edema ↑PVR and pulmonary HTN.
9. ↓Lung compliance and ↑WOB (work of breathing) chronic dyspnea.
10. RVH TR & PR (pulmonary valve regurgitation)
11. ↑Incidence of pulmonary emboli, infarction, hemoptysis and recurrent bronchitis
12. ↑LA compression of left recurrent laryngeal nerve  hoarseness.
13. LV function normal, but is small and poorly filled.

Ans b) PER ANESTHETIC EVALUATION:

History: Ask about exercise tolerance, fatigability, SOB, dyspnea, orthopnea, PND.
NYHA functional class is useful for grading severity of HF.
Chest pain, neurological Sx, and prior procedures like valvotomy or valve replacement
Review of medications, especially digoxin for its toxicity.

PHYSICAL EXAMINATION:
 Mitral facies  Malar flush on cheeks.
 Peripheral cyanosis
 Signs of RHF (↑JVP, hepatosplenomegaly, ascites, pedal edema)
 Tapping apex beat (loud S1, opening snap, diastolic murmur)

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Dr. Tariq Mahar
INVESTIGATIONS:
 ECG: P mitral, AF, Notched P wave if SR
 CXR: Calcification, ↑LA, kerley-B line.
 ECHO:↑Pressure gradients/ valvular areas ↓
 LFT’s: assessing hepatic function
 ABG’s: If significant pulmonary Sx
 Coagulation profile: PT, APTT, INR.

ANESTHETIC TECHNIQUE:
Because surgery of lower extremity is planned, the delivered anesthetic technique is Epidural anesthesia
because more gradual onset of sympathetic blockade then spinal.

GOALS (HAEMODYNAMIC)
The principal hemodynamic goals are to maintain a SR sinus rhythm (if present preoperatively) and to avoid
tachycardia, large increase in CO and both hypovolaemia and fluid overload by judicious fluid therapy.
Adequate preload, high normal SVR
Avoid hypoxia, Hypercarbia and acidosis  exacerbation PHTN.

MONITORING: full hemodynamic monitoring of direct intra arterial pressure and PA pressures is
generally indicated for all major surgeries particularly those associated with large fluid shifts.

If GA then avoid ketamine, Pancuronium and N2O

Intra-operative tachycardia can be controlled by deepening anesthesia with an opioid (fentanyl,
morphine) or β-Blocker (esmolol).
In the presence of AF, ventricular rate can be controlled by digoxin
Marked hemodynamic deterioration from sudden SVT necessitates cardioversion.
Phenylephrine is preferred over ephedrine as a vasopressor.
Marked HTN or after load reduction should be treated with vasodilator only with full hemodynamic
monitoring.

Ans d) Normal mitral valve area 4-6cm2

1. Symptom free until 1.5- 2.5 cm2
2. Moderate stenosis 1-1.5cm2
3. Critical / severe stenosis < 1 cm2

Ans e) Complications of MS during anesthesia

1. Pulmonary edema 6. AF
2. PAH 7. CVA
3. RHF 8.MI
4. ↓Lung compliance 9. Renal artery embolism.
5. Pulmonary emboli/ infarction.

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BRADYCARDIA
A patent presents for prostatectomy has a pulse of 38b/m
a) Enumerate the common causes of bradycardia?
b) How will you evaluate this patient preoperatively

Ans) Any cardiac rhythm with a rate < 60 b/m is bradycardia

CAUSES:
PREOPRATIVE:
1. Pre-existing cardiac disease.
2. CHB (complete heart block)
3. Drugs (β-Blocker, CCB Calcium channel blockers, Digoxin)
4. Hypothyroidism
5. ↑ICP
6. ↑IOP
7. Myocardial ischemia
8. Hypothermia

INTRAOPERATIVE:
1. Deep anesthesia
2. Repeated dose of Suxamethonium
3. Rapid acting opioids
4. Halothane
5. Propofol
6. Surgical stimulation (eye ball traction, cervical/ anal dilatation)
7. Hyperkalemia
8. Low dose atropine
9. Sick sinus syndrome
10. ↑ICP

POSTOPERATIVE:
1. Hypoxia
2. Hypothermia
3. Intraoperative use of β-blocker/CCB
4. High spinal
5. Inadvertent intravascular injection of local anesthesia during epidural

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Ans b.) EVALUATION OF PATIENT:
1.History
 Any co-existing cardiac disease (previous MI) (previous CHB)
 Drug history (Ant-arrhythmic, β-Blocker, CCB, Digoxin)
 Malfunctioning implanted PPM (low battery)
 Evaluation of hypothyroidism
2.Examination:
1. B.P.
2. HR (rate, rhythm, volume)
3. Apex beat
4. Auscultation (any additional sound)
5. Carotid bruit.

3. Investigations:
1. ECG (long lead II)
2. Holter monitoring
3. ECHO
4. Electrophysiological study
5. CXR
6. Cardiac enzymes
7. Electrolytes
8. Thyroid fx test
9. Serum digoxin level

TREATMENT:
1. Treat the cause (hypoxemia) (stop surgical shunt)
2. Anticholinergics (atropine, glycopyrrolate)
3. Epinephrine
4. If refractory  TPM/PPM

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 PEA
Q. What is pulseless electrical activity?
Q. What causes it? Algorithm for PEA

Pulseless Electrical Activity:: Rhythm on monitor, without palpable pulse

Cause:
1. Severe hypovolaemia 6. Profound hypoxemia
2. Cardiac tamponade 7. Severe acidosis
3. Ventricular rupture 8. Pulmonary embolism
4. Dissecting aortic aneurysm 9. Drugs related after prolong CPR

5. Tension Pneumothorax atropine induced

Pulseless electrical activity algorithm

algorithm.
VF/VT, ventricular fibrillation and pulseless
ventricular tachycardia

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 ALGORITHM FOR PEA

1-Pulse less electrical activity

(PEA = rhythm on monitor, without detectable pulse)
↓
2-Primary ABCD survey
 Focus: basic CPR and defibrillation.
 Check –responsiveness
 Activate- emergency response system
 Call- for defibrillator
a- Airway – open the airway
b- Breathing – provide positive pressure ventilations
c- Circulation – give chest compression
d- Defibrillation – assess +shock for VF/VT
↓
3-Secondary ABCD survey
Focus: more advanced assessment and treatments
a) Airway – place airway device ASAP
b) Breathing – confirm and secure airway device.
c) Breathing –confirm effective oxygenation and ventilation.
d) Circulation-establish IV access.
e) Circulation –identify rhythm-monitor.
f) Circulation –administer drugs appropriate for rhythm & conduction monitor
g) Circulation – assess for occult blood flow
h) D/D search for and treat identified reversible causes
↓
4-Review For Most Frequent Causes

 Hypovolaemia • Tamponade (cardiac)

 Hypoxia • Tension pneumothorax
 Hydrogen ion-acidosis • Thrombosis, coronary (ACS)
 Hyper/hypokalemia • Thrombosis, pulmonary (embolism)
 Hypothermia
 Tablets (drug OD, accidental)
↓
5-Epinephrine
1mg IV push, repeat every 3 to 5 minutes
↓

6-Atropine 1mg IV
Repeat every 3 to 5 min as needed to a total dose of 0.04mg/kg.

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ASYSTOLE
Q. a) List the causes of cardiac arrest during operation?
b) Write down algorithm for pulse less VT?

Ans. a) CAUSES OF CARDIAC ARREST

1 Procedures associated with excessive vagal activity (eye traction, cervical dilatation)
2 Pre-existing CHB, second degree HB, or trifascicular block.
3 Disconnected ECG leads.
4 Excessively low voltage on ECG.
5 Hypoxia (obstructed airway, bronchial or esophageal, intubation, oxygen failure)
6 Hypovolemia (hemorrhagic shock, anaphylaxis)
7 Hypo/ Hyperkalemia (renal failure, Suxamethonium induced Hyperkalemia after burns).
8 Hypothermia
9 Tension Pneumothorax
10 Cardiac tamponade.
11 Drug over dosage (Propofol, β-blocker, LA toxicity).
12 Thromboembolism
13 Equipment failure
14 High spinal
15 Total spinal

Cardiac arrest can only be diagnosed clinically by palpating carotid artery (absent pulse)

CAUSES OF VT:
1 IHD
2 Ventricular scarring after MI or previous cardiac surgery.
3 Right ventricular failure
4 Electrolyte abnormalities in pts with prolong QT interval
(TCA, antihistamines, phenothiazine’s or Brugada syndrome)
5 SVT e.g. WPW syndrome may cause a broad complex tachycardia

TORSADE DE POINTES: is a specific polymorphic form of VT.

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 59
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PULSELESS VT
Ans b)
ALGORYTHM FOR PULSELESS VT
If not already done, give O2 and establish IV access
↓
Pulse No use VF protocol

↓yes

Adverse signs
 SBP<90
 Chest pain
 Heart failure
 Rate > 150bpm
No yes

If hypokalemia Synchronized DC shock

100-360 J

 Give KCL up to 60mmols

 Give MgSO4 5ml 50% in 30 min

Amiodarone 150 mg IV If hypokalemia

Over 10min

or
Lidocaine 50mg IV over Amiodarone 150mg I in 10min
2 min repeated every 5 min
To a maximum of 200 mg
Further cardio version as necessary
Synchronized DC shock
100-200-360J

If necessary, further Amiodarone For refractory cases consider

150mg IV over 10min, then 300mg additional pharmacological agents
Over 1hour and repeat shock Amiodarone, lidocaine, Sotalol,
Procainamide, or over drive pacing
Note:
1 For torsade pointes, use MgSO4 or overdrive pacing (expert help recommended)
2 DC shock always given under sedation / GA.

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 ADULT BLS ALGORHYTHM

Collapsed/ sick patient

Shout for HELP and assess pt.

Signs
No of life yes

Call resuscitation team Assess ABCDE

Reorganize & treat O2
Monitoring IV access
CPR 30:2
With O2 & airway adjuncts

Apply pads/monitor Call resuscitation team

Attempt defibrillation if appropriate
If appropriate

Advance life support Handover to

When resuscitation team arrive Resuscitation team

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 62
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 ADULS ALS ALGORYTHM

Unresponsive

Open airway
Look for signs of life
Call rescue team

CPR 30:2
Until defib/monitor attached

Assess rhythm

Shock-able Non shock-able

(VF/Pulse less VT) (PEA/asystole)

1 shock During CPR

360J -correct reversible causes
Mono phasic -check electrodes & contact
-IV access, airway, O2
-Uninterrupted, compressions
-When airway secures
-Give epinephrine every 3-5 min
Atropine
-Consider Amiodarone and Mg.

Immediately resume
CPR 30:2
For 2min

Reversible cause:
1. Hypoxia 5. Tension pneumothorax
2. Hypovolaemia 6. Tamponade, cardiac
3. Hypo/hyperkalemia 7. Toxins (drug )
4. Hypothermia 8. Thrombosis coronary and pulmonary.

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SYNCOPE

Q. a) why should anesthesiologist be concerned about H/O syncope?

b) Causes of syncope?

Ans. a)
 A history of syncope in elderly patients should always raise the possibility of arrhythmias and
underlying organic heart disease.
 Cardiac syncope results form an abrupt arrhythmia that suddenly compromises CO and impairs
cerebral perfusion.
 Both Brady and tachyarrhythmia’s can produce syncope.

b). Causes:
Cardiac:
1. Tachyarrhythmia’s >180 b/min 7. Primary pulmonary HTN
2. Brady-arrhythmias < 40 b/min 8. Pulmonary embolism.
3. Aortic stenosis. 9. Cardiac tamponade.
4. Hypertrophic cardiomyopathy.
5. Massive MI
6. TOF

Non cardiac
1. Vasovagal (vasodepressor reflex) 6. Autonomic dysfunction
2. Carotid sinus hypersensitivity 7. Sustained valsalva maneuver
3. Neuralgias 8. Seizures
4. Hypovolaemia 9. Metabolic (-Hypoxia,
5. Sympathectomy -Hypocapnia
-Hypoglycemia)

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CARDIAC CYCLE
7 Phases
1 Atrial systole
2 Isovolumetric ventricular contraction
3 Rapid ventricular ejection
4 Reduced ventricular ejection
5 Isovolumetric ventricular relaxation.
6 Rapid ventricular filling
Reduced ventricular filling.

CHAIN OF SURVIVAL: The 5 links in adult chain of survival are

 Immediate recognition of cardiac arrest and activation of emergency response
 Early CPR with an emphasis on chest compressions
 Rapid defibrillation
 Effective advanced life support.
 Integrated post cardiac arrest care
A strong
trong chain of survival can improve chance of survival and recovery for victims of heart attack, stroke
and other emergencies

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Dr. Tariq Mahar
CARDIOVERSION
Q.) A 55 years old man with new onset AF is scheduled for elective cardioversion
A) What are the indications and complications of cardioversion?
B) How would you evaluate this patient?
C) What minimum monitors and anesthetic equipment required.

a) INDICATIONS FOR DC CARDIOVERSION:

1. To terminate SVT and VT caused by reentry
2. To terminate AF and Flutter, pre-excitation syndromes and VT or VF
3. Emergency cardioversion for any tachyarrhythmia’s associated with significant hypotension, CHF
or angina.
COMPLICATION OF CARDIOVERSION:
1. Myocardial depression.
2. Post shock arrhythmias (VF)
3. Arterial embolism.

b) EVALUATION FOR CARDIOVERSION:

1. Pt. should be evaluated and treated like GA.
2. Should fast for 6-8hrs to ↓aspira on risk.
3. Airway reflexes will be depressed by sedatives and anesthetics.
4. 12 lead ECG for confirmation of arrhythmias just before and after the procedure.
5. Preoperative laboratory investigations should be normal.
6. Antiarrhythmic e.g. quinidine should be started in pt. with AF 1-2days prior to procedure.
Anticoagulation also started.
7. TEE must be performed immediately before to rule out an atrial thrombus.

c) MINIMUM MONITORING
 ECG, BP & pulse oximetry,
 Precordial stethoscope  breath sounds,
 Conscious level  continuous verbal contact

EQUPMENTS
DC fibrillator
Transcutaneous pacing
Reliable IV access
A functional bag-mask device capable of delivering 100% O2
An Oxygen source (from pipeline or cylinder)
Airway trolley (laryngoscopes, ETT, LMA, bougie, Guedel airway
A functioning suction apparatus
Anesthetic drug kit
Crash cart that includes all necessary drugs and equipment for CPR

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PAIN PATHWAY

Primary afferent neurons

(Dorsal root ganglia @ each spinal cord level) 1st order neurons

Gray matter of ipsilateral dorsal horn

(1st six lamina of dorsal horn  modulation of pain)

Contralateral spinothalamic tract 2nd order neuron

Lateral & medial spinothalamic tract

Thalamus
3rd order neuron
Postcentral gyrus of parietal cortex & sylvian fissure

ALLODYNIA: Perception of ordinary non noxious stimulus as pain

ANALGESIA: Absence of pain perception
ANESTHESIA: Absence of all sensations
DYSESTHESIA: unpleasant or abnormal sensation with or without stimulus
HYPERAESTHESIA: ↑ response to mild s mulus
HYPOAESTHESIA: ↓ cutaneous sensa on
PARESTHESIA: Abnormal sensation without stimulus
HYPOALGESIA: ↓response to noxious s mula on
HYPERALGESIA: ↑ response to noxious stimulation
HYPERPATHIA: Hyperaesthesia + allodynia+hyperalgesia

Referred pain: Phenomenon of convergence b/w visceral and somatic sensory input is called referred
pain
Pain measurement: Numerical rating scale, faces rating scale, visual analog scale & McGill Pain
Questionnaire most commonly used
Psychological evaluation:  Minnesota multiphasic Personality Inventory MMPI and Beck depression
inventory

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 68
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 RESPIRATION:
SIGNIFICANCE OF PULMONARY TESTS:
Q1 -60yrs old pt K/C COPD, scheduled for open cholecystectomy
a. What pulmonary tests you recommend?
b. Indicate the significance of each test?

Ans.
a. Pulmonary tests:
1. Peak flow
2. Spirometry
3. Flow volume loops
4. ABG’s
5. CXR
b. Significance of each test
1) Peak Flow:
1. A useful test for COPD.
2. Done by a peak flow meter.
3. Coughing is ineffective if peak flow < 200L/min ↑chances of retention of secretions
↑infec on
2) Spirometry:
1. Useful test to quantify severity of ventilation dysfunction
2. Check FEV1 and FEV1/FVC ratio (n>70%)
3. Reversibility with salbutamol should be tested in COPD
3) Flow volume loops:
1. Used in assessment of airway obstruction form both extrinsic and intrinsic causes.
2. More accurate information of ventilatory function.
3. Provide severity of disease
4. Peak flows @ different lung volumes recorded
4) ABG’s
1. Measure baseline gases in blood useful for any pt. breathless on minimal exertion.
2. Detects CO2 retention. A resting PaCO2> 45 mmHg is predictive of pulmonary
complications and suggestive of ventilatory failure
3. Demonstrate usual level of oxygenation.
4. Useful to set realistic parameters postoperatively.
5) CXR:
1. Essential for major surgery.
2. Preferably erect PA film should be taken.
3. Abnormality predicts risk of complications
4. Reveals lung pathology, cardiac size.

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VOLATILE TRANSFER FACTORS
Q.2 what are the physical, anatomical and physiological factors which determines the volatile anesthetic
transfer form trachea to tissue?

1. Inspiratory gas concentration F1

2. Alveolar gas concentration FA
3. Arterial gas concentration Fa

1. ALVEOLAR GAS CONCENTRATION: (FA)

Determined by
a. Uptake
b. Ventilation
c. Concentration effect and 2nd gas effect

1) Uptake: three factors affect anesthetic uptake

1. Solubility in the blood (B/G coefficient).
2. Alveolar blood flow, which is equal to CO ↑CO↑uptake. Slow alveolar rise in par al
pressures delayed the induction.
3. Difference in partial pressure b/w alveolar gas and venous blood.
 It depends up on tissue uptake.
 If there is no uptake by tissues then venous and alveolar pressure become identical
 Tissue uptake depends on:
1. Tissue solubility of agent.
2. Tissue blood flow
3. Difference b/w arterial blood and tissue partial pressure.

2) Ventilation: lowering of alveolar partial pressure by ↓uptake can be countered by ↑alveolar

ventilation ↑AV ↓ APP  ↓ uptake and vice versa

3) Concentration effect:
 Increasing the inspired concentration not only ↑ the alveolar concentra on but also ↑its
rate of rise
 Augmented blood flow
 2nd gas effect the concentration effect of one gas upon another is called second gas effect

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2. ARTERIAL GAS CONCENTRATION: (Fa)
V/Q mismatch
 It depends upon venous admixture, alveolar dead space and non-uniform alveolar gas
distribution
 Existence of V/Q mismatch will ↑ the A-a difference
 Mismatch acts as a restriction to flow
3. Pulmonary surfactant: ↓ alveolar surface tension
4. Chest wall compliance + lung compliance (N)  100ml/cmH2O
5. FRC : ↓ in obese  airway resistance
6. Intrapulmonary shunting: ↑ shunting  ↑ hypoxemia
7. Airway diameter and resistance
8. Tissue resistance
9. FeV1 /FVC ratio
10. ↑WOB  due to ↓ chest lung compliance + ↑ airway resistance
11. Alveolar dead space
12. V/Q rations  (N) 0.3-3
13. Venous admixture
14. Hypoventilation  due to volatile agent effect

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INTERCOSTALS BLOCK AND PAIN RELIEF
Q.3 65 years old male smoker and K/c of COPD, H/O falls and # 7-9th rib Lt. Side
CXR normal
a. Outline various methods of pain relief?
b. Draw and label intercostals space?
c. How would you prepare intercostals block?

Ans
a. METHODS OF PAIN RELIEF
1. Intercostals nerve block
2. Paravertebral nerve block
3. Thoracic epidural with PCA
4. Low dose opioids
5. NSAID.

b. DIAGRAM

Vein
Artery
Intercostal Nerve

Plera
Lungs

c. INTERCOSTALS BLOCK

Technique:
 Pt in lateral decubitus or supine position
 The level of each rib is palpated and marked in mid and post axillary line
 A skin wheal is raised over inferior border @ selected ribs
 22-25 G needle is inserted down the inferior edge of rib until it passes through
 Advance the needle 0.5cms underneath the rib.
 Follow a negative aspiration (for blood/air), 3-5ml of LA @ each level
Complications:
1. Toxic levels of LA in blood (Highest risk).
2. Intravascular injection.
3. PneumothoraxCXR.

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Q.4 Make a simple drawing with labels to show trachea, main and segmental bronchi?

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COPD
Q.5
a. Describe the post op. pain management after cholecystectomy in a pt. suffering from
COPD?
b. What is the management of narcotic complications in this pt.?

Ans

a) POST OPERATIVE PAIN MANAGEMENT IN COPD PT.

Good analgesia is essential for the maintenance of efficient respiratory function with physiotherapy
and early mobilization.
1. Local anesthetic applied to gall bladder bed may reduce postoperative analgesic
requirement. (0.25% Bupivacaine 20%)
2. Thoracic epidural (T8-T9)
1. Improves GI motility
2. Improves early mobility
3. Improves post respiratory function
4. Improves oxygenation.
3. Paravertebral nerve block @ T8-T9
4. Local infiltration of LA@ incision site.
5. Oral or rectal acetaminophen
6. NSAID if not volume overloaded.
7. Opioids but with extra precaution as they can provoke asthma and respiratory depression
(Best option is Meperidine).

b) MANAGEMENT OF NARCOTIC COMPLICATIONS IN COPD

1. Opioids can provoke bronchospasm by releasing histamine and ↑ central vagal tone which
can be treated by 1. Inhaled β-agonsits e.g. Salbutamol or Solmeterol or Terbutaline
2. IV Aminophylline e.g. Theophylline
2. Opioids can cause reverse respiratory depression which can lead to ↑PCO2, ↓PO2 which can
be corrected by controlled ventilation.
3. Opioid antagonist e.g. Naloxone can be used to reverse effect of opioids (0.04mg
increment).

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COPD
Q. 50 years old male K/C of COPD, scheduled for THR.
a. How will prepare this patient for anesthesia and surgery?
b. Enumerate salient features of post op management?

Ans.

a. PREOP ASSESSMENT AND PREPARATION:

ASSESSMENT:

History:
1. Ask about duration and severity o disease.
2. Ask about hospital admissions.
3. Ask about cough and sputum production (color)
4. Functional class.(grading of dyspnea)
5. Assess for signs of RHF and PAH.
6. Drugs history especially steroid use.
7. Family history
8. Previous anesthetics.
9. Allergy
10. Co-morbidities
11. H/O orthopnea and PND
12. Smoking.

Examination:
1. GPE specially clubbing and cyanosis.
2. Chest auscultation/percussion/ breath sounds.
3. Clubbing
4. Peripheral cyanosis.

Investigation:
1. FBC,UCE’s
2. ECG
3. CXR ↑lung marking (hyperinfla on)
4. Peak flow
5. Spirometry PFT FEV1 = <0.7 Obstructive
6. Flow volume loops FVC >0.7 n or restrictive
7. ABG’s
8. ECHO (if RHF/PAH)

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PREPARATION:

1. Ensure any element of reversible flow. Consider a trial of oral prednisolone combined with
review by respiratory physician
2. RHF/PAH (cor pulmonale) Optimize the pt (diuretics and digoxin)+(vasodilation)
3. Add salbutamol to premedication and continue perioperative (bronchospasm)
4. Avoid histamine releasing drugs  to avoid bronchospasm
5. Chest physiotherapy Spirometry  ↓secre ons (chest percussion and postural drainage)
6. If symptoms are worse than IV steroids with bronchodilator started
7. Plan for short acting opioids analgesics intraoperative (fentanyl)
8. Advise smoking cessation 8 weeks before surgery or 1 week before if surgery planned early then
for 12 hours to ↓secretions and ↓ pulmonary complica on
9. Treat infections if any – Antibiotics.

b. POST OP. MANAGEMENT:

1. Deep extubation to prevent bronchospasm
2. Patients with FEV1 below 50% most likely requires a period of postoperatively ventilation
3. Recovery in sitting position
4. Mobilize ASAP
5. Regular chest physiotherapy
6. Supplemental O2 with venturi mask. FiO2 minimum as possible
7. Start antibiotics if sputum becomes purulent or pyrexia
8. Continue nebulization with salbutamol and ipratropium
9. Epidural or PCA for post op pain.

NOTE: Nitrous oxide should be avoided in patients with bullae and pulmonary HTN  Pneumothorax
and ↑PAH can occur. Bullae  Pneumothorax PPVTension Pneumothorax

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ASPIRATION PNEUMONITIS
Q. 7 discuss briefly predisposing factors, diagnosis and treatment of aspiration pneumonitis?

PREDISPOSING FACTORS:
1. General anesthesia
2. Neurogenic dysphagia
3. ↓ lower esophageal sphincter tone
4. Anatomical abnormalities of upper aerodigestive tract.
5. Pharmacological agents altering consciousness (sedative narcotics)
6. Extreme of age (elderly, neonate)
7. Full stomach
8. Pregnancy
9. Delayed gastric empting
10. K/c of reflux disease e.g. GERD
11. Diabetes Mellitus
12. Obesity

DIAGNOSIS:
Clinical: chest auscultation reveals wheeze and craps.
CXR: diffuse infiltration pattern specially (Rt.) lower lobe

MANAGEMENT:
1. Tilt the operating table to 30o head down to facilitate gastric contents to drain out
(Trendelenburg)
2. Maintain cricoids pressure (except while vomiting , esophageal Rupture)
3. RSI with cricoids pressure-ETT- cuff inflated ASAP
4. Quick suctioning before administrating 100% O2 with PPV
5. Give 100% O2 before and after suctioning to prevent hypoxia
6. OG tube should be inserted to empty the stomach
7. PH value of gastric content should be determined
8. Trachea bronchiole aspirate is collected and sent for C/S
9. Use β-agonist if there is any bronchospasm (wheeze)
10. Send ABG’s to determine severity of hypoxia
11. Early application of PEEP is recommended to improve pulmonary function
12. Antibiotics should start soon after organism isolated
13. Surgery should be abandoned if severe morbidity develops
14. Flexible bronchoscopy for liquid removal and rigid bronchoscopy for solid removal.
15. IV steroids and pulmonary lavage via flexible bronchoscope ↓ inflamma on.
16. Transferred to critical care unit for further monitoring and respiratory case.

B/G Coefficient: Ratio of concentration of anesthetic gas in each of 2 phases @ equilibrium

Diffusion Hypoxia: Elimination N2O is so rapid that alveolar O2 and CO2@ are diluted and causes DH

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 Aim: To correct hypoxemia, relieving bronchospasm, mobilizing and reducing secretions to decrease the incidence
of postoperative pulmonary complications.

Q.8) you have been asked to evaluate the following Pt. for admission to ICU

50 years old male, h/o smoking 30cig/d since 20 yrs

H/O chronic productive cough with dyspnea on exertion
B/L rhonchi on auscultation, pt is drowsy.
ABG’s: PH-7.2, PCO2-80, PO2 -45, HCO3-29, SPO2 70% on air.

a) What do these blood gases show?

b) Discuss the management of this pt. regarding inhalation, ventilation and drug therapy?

Ans

a) Respiratory acidosis with compensatory response

b) GOAL/AIM: To reverse the imbalance b/w CO2 production and alveolar ventilation

MANAGEMENT:
As this pt is drowsy (CO2 narcosis) it’s an indication for endotracheal intubation and mechanical
ventilation
 Pre-oxygenation followed by RSI with cricoids pressure
 Controlled ventilation with PCV if PIP >30 on volume control
 FiO2 initially 100% then tapers off down according to ABG’s
 Ventilation should be adjusted to maintain (n) arterial PH, whereas normalization of CO2
retention causes alkalosis
 Peak inspiratory pressure must be 30mmHg.

DRUG THERAPY:
1. Antibiotics according to cultures
2. IV bronchodilators
3. Inhaled bronchodilator
4. IV steroids.
5. Respiratory stimulant e.g. Doxapram for awake pts.
6. IV diuretics.

Avoid morphine and atracurium

↑ I:E ratio 1:3 or more
PEEP > Exp pause value
↓ TV
↑ RR

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ASTHMA:
Q-9) A 20 years old man k/c asthma is on regular medication, consisting of inhaled salbutamol and
theophylline 223mg BD
He reported to emergency department with breathlessness and inability to speak over the preceding 4
hours
O/E: pulse 120/min, B.P160/100, R/R 45/min. mild cyanosis and expiratory wheeze
a. What 2 investigations are vital for assessment of this pt and why?
b. How would you manage this pt?
c. What problems do you anticipate in such pt. undergoing emergency surgery?

Ans.a)
1. ABG’s  As pt is mildly cyanosed, ABG’s will check PaO2, PaCO2, PH (rule out respiratory acidosis).
2. CXR To see hyperinflated lungs, bullae and Pneumothorax.

Ans.b)
MANAGEMENT:
ABG’s  As this pt is in severe respiratory distress immediate action:
1) 100% O2.
2) IV access.
3) Nebulize with salbutamol 5mg. IV salbutamol 250µg slow bolus.
4) Nebulize with ipratropium bromide 0.5 mg.
5) IV hydrocortisone 100mg IV 6 hourly.
6) As this pt. is exhausted, hypoxia worsening and CO2 rising, immediate need of ventilation
required. RSI with cricoids pressure, STP or propofol/Suxamethonium
7) If no response to initial management consider aminophylline 5mg/kg in 20 min
8) If ↓conscious level  adrenaline (IV 10µg up to 100µg)
9) Do ABG’s, CXR and FBC (check K+ which ↓ with β2- agonist therapy)
10) Consider ICU and mechanical ventilation with prolong I: E ratios.

Induction agent Ketamine if hemodynamically unstable

Ans c)
1. ↓pulmonary reserve
2. Full stomach
3. Respiratory acidosis
4. Hyperreactive airways.
5. Bronchospasm  (instrumentation)
6. Drug allergy. (histamine release)
7. FEV1, FEV1/FVC ratio or PFR < 50%  severe asthma.
8. Respiratory failure
9. Airway resistance during expiration (delay rise of ETCO2, on capnograph)
10. Emergence can precipitate bronchospasm (deep extubation)

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 PO2 in air  160 mmHg
PO2 in airway  150 mmHg
PAO2 in alveoli  126 mmHg PvO2-40mmHg
PCO2 in end capillary  126 mmHg PaO2=102-Age/3
PaO2 in artery  62-100
PO2 in cell27mmHg
PO2 mitochondria 1-2 mmHg

PvCO2  46mmHq
PaCO2  40
PA CO2  40
P with CO2  40

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LAPAROSCOPIC SURGERY
Q.10- A 45 years old women is scheduled for a laparoscopic cholecystectomy K/C of obesity and H/O
smoking.
a) What are the advantages of lap choly?
b). How laparoscopic surgery affects intra op pulmonary function?
c) Did pt position affect oxygenation?
d) Does it affect cardiac function?
e) What special monitoring needed?
f) Does the pt require GA with ETT?
g) Complications of laparoscopic surgery?

Ans
a) ADVANTAGES:
1. Much smaller incision (key hole)
2. ↓Post operative pain
3. ↓ Post operative pulmonary complication
4. ↓ Post operative ileus
5. Short hospital stay
6. Early mobilization
7. Small surgical scar

b) AFFECT ON PULMONARY FUNCTIONS INTRAOPERATIVELY:

All these changes should be exaggerated
1. ↓ Lung compliance
in this obese patent with long history of
2. ↓PH
smoking and increase in post operative
3. ↑PCO2 pulmonary complication
4. ↑PIP
5. Atelectasis
6. ↓FRC
7. V/Q mismatch
8. Intrapulmonary shunting
9. ↓ PO2

c) AFFECT OF PATIENT POSITION ON OXYGENATION:

a. Head down, trendelenburg position causes upward shift of abdominal viscera, and diaphragm
due to which FRC, TLV and pulmonary compliance decrease. This obese pt. and assumed
pulmonary disease due to smoking will cause hypoxemia
b. Trachea also shifted upward due to with ETT which is anchored at mouth can migrate into right
mainstem bronchus.
c. After insufflations patient position changed to steep head up position (reverse Trendelenburg),
to facilitate surgical dissection. The respiratory affects reverse by ↑ing FRC and ↓ing WOB

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d) AFFECT ON CARDIAC FX.
High insufflations pressures (>25cmH2O or 18mmHg)
Tends to collapse major abdominal veins specially inferior vena cava which decrease venous return and
leads to a drop in preload and CO followed by hypercarbia which stimulate SNS and thus increase BP, HR
and risk of arrhythmias
Trendelenburg position: ↑Preload, MAP and CO
Reverse Trendelenburg position: ↓ Preload, MAP and CO.

e) SPECIAL MONITORING
1. ETCO2
2. Low TV and ↑R/R causes error in ETCO2
3. Arterial–line in cardiac Pt.
4. Pulse oximetry.
5. ECG
6. NIBP

f) G.A WITH ETT:

Trachea intubation with PPV is preferable for:
1. ↑ Risk of regurgitation.
2. Necessity of controlled ventilation to prevent hypercapnia.
3. High PIP required due to pneumoperitoneum.
4. NM blockade to allow lower insufflations pressures,
5. Better visualization and prevent unexpected pt movements.
6. NG tube and gastric decompression to ↓ risk of visceral perfora on
7. Obese pts to ↓ hypoxemia, hypercarbia and aspira on.

g) COMPLICATIONS OF LAPAROSCOPIC SURGERY:

1. Haemorrhage
2. Peritonitis – If a viscus perforated during trocar introduction.
3. Fulguration has been associated with bowel burns and bowel gas explosions.
4. Subcutaneous emphysema
5. Pneumomediastinum
6. Pneumothorax
7. Venous CO2 embolism.
8. Bradycardia and sinus arrest  vagal stimulation during trocar insertion
9. Intraoperative hypotension
10. Nausea and vomiting

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 PHYSIOLOGICAL EFFECTS OF PNEUMOPERITONEUM
Airway pressure ↑ Venous returns↓
FRC ↓ SVR ↑
Pulmonary compliance ↓ CO↑ 
V/Q mismatch ↑ Risk of arrhythmias ↑
Risk of regurgitation ↑ ICP ↑
CCP ↓

FRC
Q. 11 a. what is FRC? What are the factors that alter FRC?
b. Draw a diagram showing lung volumes and capacities.

Ans a)
FRC: The lung volume at the end of normal exhalation is called functional residual capacity (FRC).
It is the sum of RV and ERV.
Measured by nitrogen washout OR helium wash in technique or by body plethysmography.

FACTORS ALTERING FRC:

1. Body habitus: FRC and height. Obesity ↓↓FRC.
2. Sex: FRC is ↓ in females 10%
3. Posture: FRC ↓ in supine or prone position.
No further ↓ with head down posi on up to 30o
4. Lung disease: FRC ↓ in restric ve lung diseases.
5. Diaphragmatic tone:

Ans b) SPIORGRAM

Showing lung volumes and capacities

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DEAD SPACE

Q12. A) What is anatomic dead space?

What is alveolar dead space?
What is physiological dead space?
b.) what factors affects dead space?

Ans a)
ANATOMIC DEAD SPACE: Dead space that is composed of gases in non respiratory airways.
ALVEOLAR DEAD SPACE: Dead space that is composed of gases in alveoli that are not perfused.
PHYSIOLOGICAL DEAD SPACE: The sum of anatomic and alveolar dead space is referred as physiological
dead space.

Dead space is normally 150ml for most adults in upright position (approx 2ml/Kg) and is nearly all
anatomic

Ans b) FACTORS AFFECTING DEAD SPACE:

1. Posture:
a. Upright ↑
b. Supine ↓
2. Position of airway:
a. Neck extension ↑
b. Neck flexion ↓
3. ↑Age ↑
4. Artificial airway ↓
5. PPV ↑
6. Drugs –anticholinergic ↑
7. Pulmonary perfusion ↑
8. Emphysema ↑

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Pso: O2 tension @ which hemoglobin is 50% saturated. Normal Pso in adult is 26.6mmHg (3.4kPa)

Hb-ODC
Q. 13 a) what are the factors that influence hemoglobin ODC?

b) Draw a diagram of hemoglobin-ODC?

Ans a) Factors influencing Hb–ODC:

1. Hydrogen ion concentration (PH)
2. CO2 Tension.
3. Temperature
4. 2,3 Diphosphoglycerate (2,3-DPG) concentration
5. CO
6. Methemoglobin

Ans b)

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Bicarbonate largest fraction of CO2 in blood
Respiratory quotient: Ratio of total CO2 production to 0.8
RQ= VCO2/VO2, O2 consumption
VCO2 CO2 consumption - 200ml /min
VO2 O2 consumption  250 ml /ml
(Overfeeding)
Lipogenesis  RQ > I
Lypolysis  RQ < 0.7
(Fasting)

Transpulmonary pressure = Palveolar – Pinterpleural

Lung compliance 150-200 ml/cmH2O
Chest wall compliance  200ml/cmH2O
Closing capacity  the volume at which airway begins to close in dependent parts of lung

Vital capacity  Maximum volume of gas that can be exhaled following maximum inspiration
Normal CV = 60-70 ml/kg
FRC Lung volume at the end of normal exhalation is FRC
Normal total airway resistance= 0.5-2 cmH2O/L/s 70-100ml blood is within capillaries undergoing gas
exchange.
Absolute shunt  anatomic shout and lung units where V/Q is O
Relative shunt  area of lung with low but finite V/Q ratio (↓V/Q)

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 GYNAE AND OBS

Q. 1) a 20 year old FTP primigravida, admitted for EMLSCS. Pulse 160, BP 200/110, unconscious, H/O fits
@ home 6hrs ago?

a. What will you include in your initial assessment?

b. How will you propose her for surgery and anesthesia?
c. What anesthetic technique would you choose?

Ans.
a. INITIAL ASSESSMENT:
History:
Patient’s medical history
Patient’s gynecological/ Obstetric history
Drug history
NPO
Family history (epilepsy)
Fits history (duration, tongue bite, incontinence, K/C epilepsy.)

Examination:
General physical examination
GCS
Edema
Clubbing/ cyanosis/ peripheries
Airway (tongue bite, secretions, neck extension)
Vitals/ peripheral pulses
Urine output
Murmur and crepts
NVB Vs HVB

INVESTIGATIONS:
CBC (Hb., PLt, TLC), UCE’s
PT/INR, LFT’s, urine DR
CXR

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FITS (ECLAMPSIA)
Ans
b. AIM: Immediate control of fits and secondary prevention of further fits by loading IV MgSO4.
PREPARATION:
1. This patient requires stabilization prior to administration of any anesthesia.
2. Patent airway (ETT, PPV)
3. Monitoring BP, HR, SPO2 and ECG.
4. 2 wide bore cannula or CVP  fluid management.
5. Control HTN  IV SNP/GTN/Labetalol/MgSO4/Hydralazine/Mannitol/Lasix.
6. Aspiration prophylaxis. (metoclopramide, Ranitidine, or Nonparticulate antacid)
7. Arrange blood products (PRBC, Plt, FFP, if Hb. < 7, Plt < 50,000)
8. Arrange for post operative ICU and ventilator.
9. Catheterize and monitor U/O.
10. Delivery of fetus and placenta ASAP
11. DVT prophylaxis (pregnancy is hypercoagulable states)
12. Fetal monitoring.

Ans
c. General anesthesia is an ideal choice as pt. is unconscious.
 RSI with cricoids pressure
 ETT + CMV
 IV STP/propofol.
 Succinylcholine
 NMBA’s for maintenance (atracurium, Rocuronium) +volatiles
 Postoperative ICU with IPPV

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PIH
Q. 2) 28 years old for elective c/s + moderate PIH

A. Define PIH, preeclampsia, eclampsia & HELLP syndrome

B. What preoperative investigations are mandatory in PIH?
C. What is the place for regional anesthesia?
D. What are the drawback of GA in PIH
E. What are complications of PIH?

Ans. A)
PIH (pregnancy induced hypertension)

Hypertension which develops in pregnancy OR

Systolic BP >140 or diastolic BP>90mmHg OR
A consistent ↑in systolic or diastolic pressure by 30 & 15 mmHg respectively above the pts normal
baseline

PRE-ECLAMPSIA: Trial of HTN, proteinuria> 500mg/day and edema (hand and face) occurring after 20
wks gestation and resolving within 48h after delivery

ECLAMPSIA: when seizures occur in preeclampsia

HELLP SYNDROM: PIH associated with hemolysis, elevated liver enzymes and low platelets count.

SEVERE PIH: BP > 160/110, proteinuria > 5g/day, oliguria < 500ml/d, pulmonary edema, CNS
manifestation (headache, visual disturbance, seizers) hepatic tenderness or HELLP syndrome.

PATHOPHYSIOLOGY:
PIH primarily affects primigravida particularly those with vascular disorders.
Abnormal prostaglandin metabolism and endothelial dysfunction leads to vascular hyper reactivity 
↓placental perfusion  systemic manifestation.

TREATMENT:
1. Bed rest
2. Sedation
3. Antihypertensive (Labetalol, Hydralazine, or methyldopa)
4. MgSO4 to treat hyperreflexia and to prevent convulsions. Therapeutic Mg levels 4-6mg/L.

MONITORS: B.P., Pulse oximetry, ETCO2, ECG, A-Line, CVP and PAC  if pulmonary edema.

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And B)
PREOP INVESTIGATIONS:
1. CBC (specially Plt. count)
2. PT/INR (Coagulation profile)
3. LFT
4. Urea and Creatinine
5. Urine DR
6. CXR.

Ans. C)
In the absence of coagulopathy, continuous epidural anesthesia is the 1st choice for most pts with PIH
during labor, vaginal delivery and cesarean section
Epidural anesthesia avoids ↑.risk of failed intubation due to severe edema of upper airway.

Epidural anesthesia ↓ catecholamine secre on and improve uteroplacental perfusion in these pts,
provided that hypotension is avoided by judicious colloid fluid bolus (250-500cc) before epidural
activation (RA avoided if PH < 100000, 70000 is acceptable)

Ans. D)
DRAWBACKS OF GA IN PIH:
1. ↑Risk of failed intuba on.
2. ↑Laryngoscopic and intuba on response.
3. Effects of anesthetic drugs on patient and fetus (fetal depression)
4. Chance of pulmonary aspiration of gastric contents.

Ans E)
COMPLICATIONS OF PIH:
Neurological Pulmonary Hepatic Hematological
Headache Upper airway edema Elevated Enzymes Coagulopathy
Visual disturbances Pulmonary edema Impaired Function Thrombocytopenia
Hyperexcitability Hematoma Platelets dysfunction
Seizures Rupture Prolong APTT.
Intra cranial hemorrhage
Cerebral edema

CVS Renal
↓Intravascular volume Proteinuria
↑Arteriolar Resistance ↑Na+ retention
HTN ↓GFR
Heart failure Renal Failure.

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APGAR:

Q. ) 35 years old, 36 weeks pregnant, undergoing EMLSCS, under GA due to fetal distress.
How will you assess and manage the newborn?

 Evaluation and treatment are carried out simultaneously:

 If the neonate is obviously depressed, the cord is clamped early resuscitation initiated immediately.
 Respirations are assessed by auscultation of chest where as HR is determined by palpation of pulse
@ the base of umbilical cord or auscultation of pericardium.
 Keep the neonate warm.
 APGAR score @ 1minute and again @ 5minates after delivery remains the most valuable assessment
of neonate.
1minute score correlates with survival and 5min score  neurological out come
 Choanal atresia and esophageal atresia should be ruled out by a catheter.

APGAR SCORE

Points
Sign 0 1 2
Heart Rate Absent < 100 >100
Respiratory effort Absent Slow, irregular Good, Crying
Muscle tone Flaccid Some flexion Active motion
Reflex irritability No response Grimace Crying
Color Blue or pale Body pink, extremities All pink
blue

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NEONATAL MANAGEMENT:

MANAGEMENT: @1minute  facilitates resuscitations

1. APGAR 8-10:- Requires only gentle stimulation.
-Flicking of foot
-Rubbing at the back
-Additional drying
-Suctioning through mouth and nose
2. APGAR 5-7: - Mildly asphyxiated
-Gentle stimulation
-100% O2 blown across the face.
3. APGAR 3-4:- Moderately asphyxiated.
-Requires temporary assisted PPV with mask and bag
4. APGAR 0-2:- Severely depressed
-Immediate intubation
-Chest compressions may be required

 INDICATIONS FOR PPV

1. Apnea
2. Gasping respirations.
3. Persistent central cyanosis with 100% Oxygen
4. HR< 100bpm

 INDICATIONS FOR ENDOTRACHEAL INTUBATION:

1. Ineffective ventilation
2. Prolonged mask ventilation
3. To administer drugs

 INDICATIONS FOR CHEST COMPRESSIONS

1. HR<60 bpm
2. HR 60-80bpm and not rising after 30sec of adequate ventilation with 100 % O2

 VOLUME RESUSCITATION IV 10 ml /kg R/L or N/S or Blood

BP of a neonate > 3kg 70/40 mmHg

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MATERNAL MORTALITY:

Q.4) what are the major causes of maternal mortality?

Discus anesthetic deaths and then treatment and prevention

Ans. CAUSES OF MATERNAL MORTALITY:

1. Severe hemorrhage 6. CVA/ intracranial hemorrhage
2. Pulmonary embolism/ Amniotic fluid 7. Anesthesia
embolism 8. Cardiomyopathy
3. Severe PIH/ Eclampsia 9. Severe sepsis
4. HELLP syndrome 10. Unknown
5. Uterine Rupture

ANESTHETIC DEATHS:
Inadequate assessment
Inadequate preparation and resuscitation
Inappropriate technique
Lack of supervision
Results from hypoxemia
a. Acid aspiration
b. Failure to intubate
c. Difficulty in maintaining airway during G/A

PREVENTION AND TREATMENT:

1. Acid aspiration:
1. Antacid (Na+ citrate)
2. H2 receptor blocker e.g. (ranitidine)
3. Prokinetic drugs e.g. (metoclopramide)
2. Anticipate difficult intubation
1. Mallampati classification 5. Short neck
2. Thyromental distance 6. Airway edema
3. Receding chin 7. Prepare intubation trolley,
4. Enlarge breast bougie and stylet and LMA
3. Difficulty in maintaining airway
1. Chin lift 4. Airway insertion
2. Jaw thrust 5. Suction
3. Head tilt
4. Regional anesthesia
1. Adequate preload 3. Adequate doses
2. Proper positioning

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ECTOPIC PREGNANCY

Q.5 26 years old in shock is thought to have ectopic pregnancy

a) How will you resuscitate her?
b) Outline your anesthetic management?

Ans.)
a. AIM: To restore hemodynamic in order to prevent irreversible organ damage (brain, heart ,kidney)

RESUSCITATION:
1. Resuscitation and operation must be done simultaneously.
2. To maintain airway if required (ETT+IPPV)
3. 2 large bore 14G IV cannula and central line.
4. IV fluids –crystalloids, colloids and blood products after cross matching (according to
hemodynamic and clinical presentation)
5. If refractory to fluid therapy then consider vasopressors or IV inotropes.
6. Correct any hypothermia and acidosis
7. Insert a Foley catheter to monitor urine output (volume status)
8. Send baseline investigations: CBC, Coagulation profiles, ABG’s, Blood for cross-matching

b. ANESTHETIC MANAGEMENT:
1. General anesthesia with rapid sequence induction once abdomen has been surgically prepared.
2. GA may precipitate cardiovascular collapse so consider ketamine as an induction agent.
3. Consider intra-arterial and central venous monitoring.
4. Consider HDU/ICU postoperatively.
5. Correct anemia and coagulopathy.
6. PCA analgesia.
7. HDU/ITU until stable.

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HYPOTENSION AFTER EPIDURAL TOPUP

Q-6 Primigravida, hypotensive in delivery suite following an epidural “top-up” by a midwife 5 minutes
ago, list likely cause and initial management.

CAUSES
1. Decrease sympathetic tone.
2. Hypovolemia
3. Aortocaval compression
4. Over dosage
5. Unintentional intrathecal injection
6. Anemia
7. No preload

INITIAL MANAGEMENT:
1. IV fluid boluses
2. Ephedrine (5-15mg)
3. Phenylephrine (25-50μg)
4. Supplemental O2.
5. Lt. uterine displacement.
6. Avoid head elevation.
7. Re-checking the epidural site.
8. Check the signs of sensory/ motor blockade
9. Monitor BP every 1-2 minutes for next 15 min

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CVS CHANGES IN PREGNANCY:

Q.7) what are the cardiovascular changes during pregnancy?

1. ↑ CO (Cardiac Output)
2. ↑ Blood Volume (1000-1500ml) to meet maternal and fetal metabolic demands.
3. ↑ Plasma Volume > Red cell mass  Dilutional anemia (↓blood viscosity)
4. ↑ Stroke Volume
5. ↑ Heart Rate.
6. ↓ Hb ↑CORight shift of ODC.
7. ↓ SVR↓SBP and ↓DBP
8. Blunted response to vasopressor and inotropes.
9. Cardiac chambers enlarges+ myocardial hypertrophy.
10. PAP, PAWP, CVP—normal.
11. Greatest ↑ in CO during labour and immediate after delivery
CO returns to normal after 2 weeks of delivery.
12. Supine hypotension syndrome  Obstruction of IVC by uterus characterized by:
1. Hypotension
2. Pallor
3. Sweating
4. N&V trendelenburg position exacerbate the compression, Rx  turn the patient on Lt
Lateral side.
13. Aortocaval compression:  Gravid uterus compresses aorta when lie supine  ↓blood flow to
lower extremities and ↓ uteroplacental circula on fetal distress Fetal asphyxia.
Management: Lt uterine displacement by a wedge under hip (R)
14. Chronic partial caval obstruction  3rd trimester  edema legs
15. CXR Enlarge heart due to displacement by diaphragm.
16. ECG  left axis deviation and T-wave changes.
17. GPE Ejection systolic murmur (grade I or II)
Exaggerated splitting of S1
S3 Audible

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RESPIRATORY CHANGES IN PREGNANCY

Q. 8- What are the changes in respiratory system of pregnant patient

who is full term and of concern to anesthesiologist?

Ans.8) RESPIRATORY CHANGES:

1. ↑ O2Consumption.
2. ↑ Minute ventilation.
3. ↑TV and R/R.
4. ↑PaO2
5. ↓PaO2 (compensatory ↓HCO2)
6. ↓ Airway resistance.
7. ↓FRC
8. ↑2.3DPG offsets O2 affinity for Hb.
9. Elevation of diaphragm  compensated by ↑ AP diameter of chest Thoracic breathing
10. ↓ Physiological dead space.
11. ↑ Intra pulmonary shunting.
12. CXR-Prominent vascular markings due to engorged capillaries + ↑ diaphragm

CONCERNS FOR ANAESTHESIOLOGIST:

1. Combination of ↓ FRC and ↑O2 consumptions promotes rapid desaturation during periods of
apnea Pre-Oxygenation is mandatory.
2. Closing Volume exceeds FRC when lie supine Atelectasis and hypoxemia parturient should not
lie completely flat without supplemental O2.
3. ↑uptake of inhalational agents due to ↓FRC and ↑MV↓MAC
4. ↓ Dead Space ↓arterial ETCO2.
5. Capillary engorgement of respiratory mucosa predisposes upper airway to trauma, bleeding and
obstruction. Gentle laryngoscopy and use of small ETT (6.0-6.5).

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PAIN PATHWAYS DURING LABOUR

Q. 9-Write a note on pain pathways during labor

Ans.
PAIN PATHWAY DURING LABOUR
The pain of labor arises from:
1. Contraction of myometrium against the resistance of cervix and perineum.
2. Dilatation of cervix and lower uterine segment.
3. Stretching and compression of pelvic and perineal structures.

1st stage: pain is mostly visceral:

Initially confined to T11-T12 dermatomes but eventually involves T10-L1 dermatomes as labour
enters active phase.
Visceral afferent fibers
↓
Sympathetic nerve fibers
↓
Uterine and cervical plexus
↓
Hypogastric and aortic plexus
↓
Enters spinal cord with T10 - L1 nerve roots

Pain is primarily in lower abdomen but increasingly referred to lumbosacral area, gluteal region and
thighs as labour progress

2nd stage:
Onset of perineal pain at the end of 1st stage signals beginning of fetal descent and 2nd stage of
labour.
Sensory innervations of perineum  Pudendal nerve S2 - S4.
Pain during 2nd stage involves T10-S4 dermatomes.

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PAIN MANAGEMENT IN LABOUR

PAIN MANAGEMENT DURING LABOUR:

PSYCHOLOGICAL
1. Patient education and positive conditioning about birthing.
2. Lamaze technique  most popular
a. Deep breathing @ the beginning of each contraction
b. Concentrates away from pain
3. Hypnosis
4. TENS
5. Biofeedback
6. Acupuncture.

PARENTERAL:
1. Opioids e.g. meperidine and fentanyl (morphine not used)
2. Nalbuphine little or no sedation.
3. Promethazine in combination with meperidine (↓ anxiety, ↓Opioid dose, ↓nausea)
4. Ketamine  Powerful analgesia in low dose

REGIONAL most popular method of pain relief in labor and delivery β2 adrenergic agonists
1. Epidural
2. Spinal
3. Pudendal nerve block.

TOCOLYTICS
1. Ritodrine given IV as 100-350 µg/min
β2 adrenergic agonists
2. Terbutaline given orally 2.5-5 mg 4-6 h
3. Magnesium.6gm IV over 30 min followed by 2-4 g/h
4. Nifedipine.CCB
5. NO (Nitric Oxide)

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DIFFERENCE OF G.A (PREGNANT VS NON PREGNANT)
Q. How does G.A of a FTP differ from G.A. form GA of a non-pregnant lady undergoing laparotomy?

Following anesthetic considerations makes GA of a FTP differ from non-pregnant lady:

1. More risk of aspiration (antacid prophylaxis)
2. Tow lives at stake.
3. Risk of GA drugs increased  fetal depression so ↓ dose of drugs used.
4. ↓ use of opioids a er delivery intraoperative aten placental transfer
5. ↓use of volatile anesthetics (↓ MAC)
6. Difficulty in making position @ table (Lt. tilt)
7. More chances of failed intubation (airway edema)
8. Special monitoring of FHR and uterine activity with Doppler/ Tocodynamometer during
induction/ emergence/ recovery.
9. Special premedication with β-agonist (Ritodrine) to abort preterm labor.
10. Baby resuscitation table/ pediatrician must be present.

BROMAGE SCALE: Most frequently used measure of motor blockade is bromage scale.
Grade Criteria Degree of block
I Free movement of leg and feet. Nil 0%
II Flex knees + free movement of feet Partial 33%
III Free movement of feet Almost Complete 66%
IV Unable to move legs or feet Complete 100%

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SPINAL ANESTHESIA:
Q. 11)
a. Describe the technique of spinal anesthesia?
b. Complication?
c. Structures passing through midline
d. Advantages and disadvantages.
e. Contraindications
f. Drugs used
g. Advantage of spinal anesthesia in LSCS
h. PDPH.

Ans.
A) TECHNIQUE OF SA:
I. Midline approach:
1. Sitting midline/ lying on side.
2. Mark a line joining the iliac crest (L3-L4).
3. Now feel for the spinous process of lumbar vertebrae
4. Raise a wheal S/C with local anesthetic in interspace b/w two vertebra
5. Insert a 23-2.9G spinal needle in midline in interspace
6. 15o cephalad angulation - advance until a click /pop felt-remove the stylet.
7. CSF coming out-inject the drug.

II. Paramedian approach:

1. 1-2cms lateral to upper border of spinous process.
2. Insert a spinal needle perpendicular to skin.
3. Withdraw slightly and reinsert if bone ahead.
4. 15omedially and 30o cephalad to pass over the lamina and then interlaminar space
5. Advance until a click /pope felt.

After free flow of CSF in both approaches, the desired volume of LA injected.

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Ans.
B) COMPLICATIONS OF SPINAL ANESTHESIA
Acute:
1. High spinal 5. Inadvertent intravascular injection
2. Total spinal 6. Hypotension
3. Cardiac arrest 7. Respiratory depression
4. Partial block 8. Apnea

Late:
1. PDPH 9. Neurological damage
2. Backache 10. Spinal artery syndrome
3. Infection 11. Nerve root damage
4. Hematoma 12. Spinal card damage
5. Arachnoiditis 13. Cauda equine syndrome
6. Encephalitis 14. Urinary retention
7. Meningitis 15. Incontinence
8. Abscess

C) STRUCTURES PASSING IN MIDLINE SPINE

1. Skin
2. Subcutaneous fat pad
3. Supraspinous ligament
4. Interspinous ligament
5. Ligamentum flavum
6. Epidural space
7. Dura matter
8. Subdural space
9. Arachnoid membrane
10. Subarachnoid space

D) ADVANTAGES & DISADVANTAGES

Advantages Disadvantages
1. Pt. awake 1. More hypotension then GA
2. Less drug usage 2. Expertise needed
3. No Laryngoscopic response 3. Partial block
4. No regurgitation in full stomach 4. Single shot
5. Early mobilization 5. Limited duration
6. Early return of gut motility 6. Inadequate analgesia is difficult to
7. Pts satisfaction correct
8. Less cognitive impairment 7. Rapid changes in B.P & CO
9. Cost effective
10. ↓ risk of DVT and embolism

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E) CONTRAINDICATION
Absolute
1. Pt. refusal
2. Fixed CO (MS/AS)
3. Infection at the site of injection
4. Coagulopathy
5. Severe Hypovolemia
6. ↑ ICP
7. Allergy to LA

Relative
1. Hypovolemia
2. Spinal cord deformity
3. Sepsis
4. Uncooperative pt.
5. Pre existing neurological deficit (MG)

Controversial
1. Prior back surgery
2. Inability to communicate with pt.
3. Complicated surgery

F) DRUGS USED IN S/A:

Inj. bupivacaine 0.75%, 0.5 (10-15mg) (hyperbaric)
Also lidocaine 50-60 mg
Tetracaine 7-10mg
- extended duration of action (90-120 min)
- More potent, slow onset (5-10 min)
- Dose not cause neurological sequelae
Factor affecting duration:
- Drug dose
- Combined with epinephrine 0.1 mg ↑ quality and dura on
Factor affecting spread:
- Baricity
- Position of Pt.
- Level / site of injection
- Drug volume
- Obesity
- Pregnancy
- Spread of injection
- Barbotage
- Direction of needle bevel

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G) ADVANTAGES OF S/A IN LSCS
1. Awake mother can enjoy birth of a child
2. ↓risk of pulmonary aspira on
3. ↓neonatal exposure to drugs
4. ↓risk of failed intuba on
5. Early return of GI function
6. ↓ periopera ve ischemia ( ↓morbidity & mortality)
7. ↓ incidence of DVT (early mobiliza on)
8. No postoperative delirium or cognitive dysfunction

Spinal Opioid doses:

Drug Intrathecal Epidural
Morphine 0.25-0.5mg 5mg
Meperidine 10-15mg 50-100mg
Fentanyl 125-25mg 50-150mg
Hyperbaric bupivacaine and Tetracaine most commonly used agents of S.A

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PDPH

H) PDPH due to breach in dura mater

PDPH is due to ↓ ICP with compensatory cerebral vasodila on

S/S:
1. Bilateral frontal / retro orbital that extends to neck, occipital headache
2. Extension of neck
3. Constant / throbbing headache
Associated with photophobia and nausea

HALLMARK: Aggravated by sitting /standing

Relieved by lying down flat

ASSOCIATED FACTORS:
1. Needle size (<23G)
2. Needle type cutting point > pencil point
3. Pt population young, female, pregnancy
Onset: 12-72 post procedure

TREATMENT:
1. Conservative for mild headache:
Recumbent position Bed rest (Lay flat)
Oral analgesia (NSAIDs, acetamines) Hydration
Epidural saline injection 50 ml Stool softeners
Caffeine sodium benzoate 500mg/h Soft diet
I/V or Oral fluid administration

2. Moderate to severe headache:

o Epidural blood patch  15-20ml of autologous blood into epidural space @ the level of
dural puncture
o It’s a 2 person technique with 2 I.V line
o Effect is immediate

D/D:
Preeclampsia Pneumocephalus
Caffeine withdrawal Venous sinus thrombosis
Subarachnoid hematoma Migraine
Subdural hematoma Meningitis
Musculoskeletal

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INDICATIONS FOR C/SECTIONS

Major indications for LSCS

1. Previous classic C/Section
2. Previous myomectomy of uterus reconstruction
3. ↑ risk of haemorrhage
4. Placenta previa
5. Abruption placentae
6. Vaginal reconstruction
7. Fetopelvic disproportion (CPD) cephalopelvic disproportion
8. Transvers or oblique lie
9. Breach presentation
10. DUA (dysfunctional uterine activity)
11. Fetal distress
12. Umbilical cord prolapsed
13. APH
14. Amnionitis
15. Genital herpes with ruptured membranes

SIGNS OF FETAL DISTRESS

1. Nonassuring FHR pattern
2. Fetal scalp PH < 7.20
3. Meconium stained amniotic fluid
4. Oligohydramnios
5. Intrauterine growth restriction IGR

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 FAILED INTUBATION ALGORITHM
Q.12) A pt. presents of EM-LSCS, intubation is found to be impossible after induction & laryngoscopy
How will you proceed?

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 NEONATAL RESUSCITATION ALGORITHM

Note:
 ETT may be considered at several steps
 Intrauterine asphyxia during labour is the
most common cause of neonatal
depression

Fetal monitoring:
1. FHR monitoring (Baseline HR, baseline variability, acceleration, decelerations)
2. Fetal PH > 7.2
3. Scalp lactate concentration
4. Fetal SpO2
5. Fetal ST-segment analysis

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Placenta Previa
Presents as painless vaginal bleeding
All parturient with vaginal bleeding are assumed to have PP until proved otherwise

CLASSIFICATION:
Grade1: placenta in lower segment
Grade2: placenta reaches internal cervical OS
Grade3: placenta partially covering internal cervical os (Partial Placenta Previa)
Grade4: placenta completely covering internal cervical os.(central or complete Placenta Previa)
Major: Grade 3&4
Minor: Grade 1&2
Placenta Accretes: Adherent to surface.
Placenta Increta: Invades myometrium
Placenta Percreta: completely penetrates the myometrium

Management:
Immediate:
1. 2 anesthetists.
2. Two 14G IV access
3. Cross matched blood must be available-administer early
4. Senior obstetrician must be present
5. Consider RA if cardiovascularly stable, CSE preferable
6. Consider intra-arterial & CVP monitoring
7. If G.A required, RSI used – consider TIVA, avoid volatile
8. Syntocinon 5 IU slow IV for delivery of placenta followed by infusion of 30-40 IU over 4 hrs.
9. Early recons to ergometrine 500µg/m or Carboprost 250µg IM intramyometrial

Late:
1. If intra operative hemorrhage persist, surgeon should consider B-lynch suture
2. Hysterectomy may be required
3. HDU/ITU monitoring following c-section chance of PPH

Carboprost  prostaglandin F2α short half life

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HYPONATREMIA
Defined as serum Na+ < 135 mmols/L
Mild 125-134
Moderate 120-124 no elective surgery if
Severe <120 Na+ <120 or symptomatic

CLINICAL MANIFESTATIONS
If Na+ 125-130  GI Sx Nausea/Vomiting.
If Na+ < 125 NV, muscular weakness, headache, lethargy, psychosis, ↑ICP, seizures, coma &
respiratory depression.

CAUSES:
1. Diuretics 11.primary polydipsia
2. Salt losing nephropathies 12. SIADH
3. Aldosterone deficiency 13. Hypothyroidism
4. Osmotic dieresis (glucose, mannitol) 14 Drug induced
5. Renal tubular acidosis 15. Nephrotic Syndrome
6. Vomiting 16.TURP syndrome
7. Diarrhea
8. Sweating
9. Burns
10. 3rd spacing

Treatment:
1. Acute symptomatic hyponatremia (develops in <48hrs) e.g. TURP syndromes.
 SIADH aim to raise Na+ by 2mmols/L/hr until symptom resolve
 Infuse hypertonic saline (3% NaCl) @ rate of 1.2-2.4 ml/kg/hr.

2. Chronic symptomatic hyponatremia (present for > 48hrs)

 Aim to correction (Na+ by 5-10mmol/d.
 Rapid correction (Na+ rise of >0.5mmol/L/hr) can lead to central pontine myelinolysis, subdural
hemorrhage and cardiac failure.
 Give furosemide and replace saline losses with 0.9% saline IV.
 Monitor electrolytes and U/O carefully.
3. Consult with endocrinologist
4. Treat the case.
5. SIADH  fluid restriction + Demeclocycline
6. A symptomatic hyponatremia  Restrict fluid to 1L/day

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HYPERNATREMIA
Defined as serum Na+ > 145mmol/L
Mild -145-150
Moderate-151-160 No elective surgery
Severe ->160 Na+>155 or Hypovolemia

CLINICAL MANIFESTATION
CNS symptoms if Na+> 155 Thirst, confusion, seizures
If due to water deficiency hypotension, tachycardia and ↓ skin turgor

CAUSES:
Impaired thirst coma, essential hypernatremia
Solute diuresis  Osmotic diuresis (DKA, nonketotic hyperosmolar, mannitol administration)
Excessive water loss  Neurogenic diabetes. Insipidus
Nephrogenic DI
Sweating
Combined disorder  coma + hypertonic NG feeding

TREATMENT:
Correct over at least 48hrs to prevent  cerebral edema & convulsion.
Oral fluids if possible –Treat the cause
1. Hypovolemic (Na+ deficit) 0.9% saline until corrected then 0.45% saline
2. Water deficit  Estimate TBW deficit and 5% dextrose.
3. Hypervolemic (Na+ excess)Diuretics and 5% dextrose OR HDx.
4. Diabetes insipidus  Replace urinary losses and desmopressin
5. Plasma Na+ should not ↓faster than 0.5mEq/L.

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 112
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 PAEDIATRICS
HARE LIP (CLEFT LIP)
1-2 hours Procedure

Q. 1) Two month old child is brought to OT for hare lip

a) What problems you anticipate in the pt?
b) Write down your anesthetic management of this pt?

Ans a) ANTICIPATED PROBLEMS:

1. Infants may have associated syndromes like Pierre-Robin, Treacher-collin and Goldenhar
syndromes so look for other abnormalities e.g. cleft palate.
Treacher Collins syndrome (TCS) is an autosomal
2. An anticipated difficult airway, careful assessment needed dominant congenital disorder characterized by
craniofacial deformities, involving ears, eyes and
3. Hypothermia so cover the peripheries with warm blanket cheekbones ...

4. Difficult IV cannulation
Goldenhar syndrome (also known as Oculo-Auriculo-
5. Cardiac manifestations due to congenital anomalies Vertebral (OAV) syndrome) is a rare congenital defect
characterized by incomplete development of the ear,
6. Laryngoscopy may be difficult nose, soft palate, lip, and mandible

7. Increased chances of URTI’s

8. Shared airway
9. 1-2 hour procedure blood loss minimized

Ans b) ANESTHETIC MANAGEMENT HARE LIP

History:
1. Moe of delivery with associated problems
2. Gestational age at birth
3. Feeding history obtain consent for suppository
4. Family history.
Examination:
1. GPE 5. IV cannulation
2. Airway assessment specially cleft palate 6. Runny nose
3. Murmur 7. Anemia
4. Wheezing

Premedication: IM atropine 20µg/kg 30 min preoperatively if difficult airway

Investigations: FBC, ECHO
Induction: Inhalational induction + ETT (A preformed RAE may be obstructed or kinked by the gag,
especially the smaller sizes. A reinforced tube will resist compression but needs to be carefully secured
at correct length) +IPPV
Maintenance: Isoflurane + O2 + air
Throat pack, eyes padded
Fentanyl 2–4 µg/kg + suppository (paracetamol 30 mg/kg <1 year or diclofenac 1 mg/kg >1 year) + local
infiltration with adrenaline, Codeine phosphate 1 mg/kg IM prior to reversal
Preformed tubes (such as the oral and Armored or reinforced tubes have the typical left-facing bevel
nasal RAE tubes, named after the tip and Murphy eye. Their distinctive feature is a metal wire
inventors Ring, Adair and Elwyn) coil embedded in the wall of the tube shaft 179
Dr. Tariq Mahar
 30 min procedure,
PYLORIC STENOSIS Blood loss minimal,
st
 Paracetamol suppository 20-40mg/kg + fentanyl for pain Common in 1 born males
 Prevent hypothermia
 Dexamethasone 0.1mg/kg for prevention of post op swelling
 Consider infra-orbital nerve block for post op pain relief

Emergence:
 Extubate awake
 Suction of pharynx gently
 Nasal stent for patent airway
 Post op analgesia with paracetamol, diclofenac, codeine phosphate

_____________________________________________________________________________________

Q2- Write down preoperative and operative management of 4kg infant who requires pyloromyotomy?

Ans PREOP MANAGEMENT

1. History, examination (CVS, chest and airway) labs (FBS, UCE, ABG)
2. Persistent vomiting causes depletion of Na+, K+, Cl and hydrogen ions causing hypochloraemic
metabolic alkalosis.
3. Consider rapid sequence if there is excessive nasogastric loss (>2ml/kg/h).
4. Correction of volume deficit and metabolic alkalosis by N/S with KCl
5. Avoid R/L fluid resuscitation with D/S + 20 meq KCl/L (Total 16 ml)
6. Fluid and electrolytes corrected preoperatively otherwise post pones
7. Risk of pulmonary aspiration  NG or OG suction mandatory
Fentanyl (1 µg/kg) + paracetamol
8. Correct hypothermia
suppository (20–30 mg/kg) + local
9. Chloride must be ≥ 90mmol/L infiltration up to 1 ml/kg of 0.25%
bupivacaine
INTRAOP MANAGEMETN: May be performed laparoscopically
1. RSI, awake intubation or inhalational induction considered
2. Paracetamol suppository 30-40 mg/kg and fentanyl 1µg/Kg +local infiltrate
3. Procedure requires muscle relaxation
4. Local infiltration ↓postop pain
5. Extubate awake in Lt. lateral position
6. Prevent hypothermia
7. Feed within 6 hours but maintain I/V fluids
8. Use an apnea alarm over night
9. Remove NG after procedure

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 Neonate  Firs 44 wks of post conceptual age
Premature <37 wks gestational age
Infants 1-12 months age
Low birth wt  < 2.5 kg
FEATURES OF NEONATES AND INFANTS
Q. 3) Enumerate anatomical, physiological, Pharmacological & metabolic features of neonates & infants

ANATOMICAL FEATURES:
1. Non-compliant left ventricle.
2. Residual fetal circulation
3. Difficult venous and arterial cannulation
4. Large head and tongue
5. Narrow nasal passage
6. Anterior and cephalad larynx
7. Long epiglottis
8. Short trachea and neck
9. Prominent adenoids and tonsils
10. Weak intercostal and diaphragmatic muscles
11. High resistance to air flow

PHYSIOLOGICAL FEATURES:
1. Heart rate dependant CO
2. Faster heart rate
3. Low blood pressure
4. Faster respiratory rate
5. Lower lung compliance
6. ↓FRC
7. High BSA to body wt ratio
8. High TBW content (total body water)

PHARMACOLOGICAL FEATURES:
1. Immature hepatic biotransformation
2. ↓Protein binding
3. Rapid ↑ in FA/F1 ratio
4. Rapid induction and recovery
5. ↑MAC
6. Large volume of distribution for water soluble drugs.
7. Immature NMJ

METABOLIC FEATURES:
1. ↑O2 consumption
2. ↑CO2 production
3. ↑alveolar ven la on
4. Greater heat loss (thin skin, low fat content)
5. Volatile anesthetics inhibit thermogenesis in brown adipocytes.

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PARTIAL LARYNGOSPASM MX
1. 100% Oxygen
2. CPAP
3. Gentile assisted ventilation
4. Propofol 1-2mg/Kg bolus

COMPLETE LARYNGOSPASM MX
1. 100% Oxygen
2. CPAP
3. Early administration of suxa 1-2mg/kg and atropine 10µg/kg
4. Assisted ventilation may exacerbates the condition

Daily fluid maintenance: calculated from calorie requirement for

Infant  100Kcal/Kg 1Kcal,
Older child  75 Kcal/Kg and
Adults 35 kcal/kg, Each kilocalorie requires 1 ml of water for metabolism
If under a radiant heater or undergoing phototherapy, 30 ml/kg is added to the regime If

Blood Volume Weight

Neonate 90ml/kg 3-12 (month) Wt. = M+9/2
Infant 85ml/kg 1-6year Wt. = (years + 4) x 2
Child 80 ml/kg

ETT size = Age/4 + 4 ETT Length = Age/2 + 12

INGUINAL HERNIA:
Q.4) what are the anesthetic considerations of a 2 month old infant undergoing inguinal hernia repair.
Ans.) Anesthetic considerations:
1. Post conceptional age 12. Cautious fluid administration (risk of fluid
2. Prematurity over load)
3. Feeding history 13. Preferable inhalational induction
4. Family history 14. Post induction laryngospasm/
5. NPO status. bronchospasm
6. URTI/ Runny nose 15. Caudal block for postop pain relief
7. Murmurs Specially diastolic (pathological) 16. post op analgesia (PO/Rectal)
8. Regurgitation (aspiration risk) 17. Hypothermia
9. Difficult I/V access. 18. Malignant hyperthermia
10. Difficult intubation 19. Masseter spasm
11. Difficult mask ventilation 20. Restoration of feeding

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AYRE’S T-PIECE WITH JACKSON REES MODIFICALTION
POST-OPERATIVE
OPERATIVE PAIN MANAGEMENT

Q.5) You are asked to anesthetize a 5 year old child, Wt. 15 kg for orchidopexy and (L) inguinal hernia.
a) Which anesthetic breathing system is suitable for this child and why?
b) What options are available for postop pain control?

Ans a) Ayre’s T-Piece

Piece with Jackson Rees modification
Advantages:
1. Most commonly used circuit in pediatrics
p practice
2. Assessment of tidal volume
3. Ability to partially occlude bag for CPAP and PEEP
4. Potential for assisted manual and controlled
co ventilation
5. Qualitative appreciation
ciation of lung compliance
6. Reduction in dead space during SV
7. Suitable for all children < 20 kg
8. Low resistance, Valveless
eless and light weight

Ans b) POSTOPERATIVE PAIN CONTROL

1. Parenteral opioids: FENTANYL 1-2 1 µg/kg,
g/kg, morphine 0.5mg/kg meperidine 0.5 mg/kg
2. Parenteral NSAIDS: ketorolac 0.5mg/kg
3. Rectal acetaminophen (paracetamol) 40mg/kg.
4. PCA for young children 6-7 7 years (morphine
(morp and hydromorphene)
5. Epidural infusions (LA + Opioid)
Opioid e.g. bupivacaine 0.1% with fentanyl
6. Caudal block
7. Local infiltration @ surgical incision site.
8. Rectal diclofenac / IM diclofenac
diclo
9. Ilioinguinal nerve block / Iliohypogastric
Ilioh block

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CAUDAL BLOCK
Q.6) what are the indications, contra indication, complications, and technique of caudal block?
Ans 6) INDICATIONS:
1. Circumcision –also ring block
2. Inguinal herniorrhaphy/ herniotomy/ hydrocele/ Orchidopexy.
3. Hypospadias repair
4. Anal surgery
5. Club foot repair (congenital ) Club foot (talipes equinovarus) is a deformity
6. Subumbilical procedures in G. Surgery and orthopedics of the foot and ankle that a baby can be born
with. It is not clear exactly what causes talipes.
CONTRAINDICATIONS: In most cases, it is diagnosed by the typical
1. Infection around sacral hiatus appearance of a baby's foot after they are born.

2. Coagulopathy
3. Anatomic abnormalities
COMPLICATIONS:
1. Local anesthetic toxicity
2. Intravascular injection
3. Motor block
4. Inadvertent dural puncture
5. Urinary retention
6. Paraesthesiae
7. Hypotension
ADVANTAGES:
Simple, safe, successful wide range of indications

TECHNIQUE OF CAUDAL ANESTHESIA: (pediatric)

A short bevel 22 gauge needle can be used. Loss of resistance should be assessed with
saline, not air because air is associated with hemodynamically significant air embolism. After the
characteristic “Pop” that signals penetration of sacrococcygeal membrane, the needle is lowered and
advanced only a few millimeters to avoid entering the dural sac or the anterior body of sacrum.
Aspiration is used to check blood or CSF
Local anesthetic with epinephrine (1:200000) test dose 2ml, helps exclude intravascular placement.
 Most commonly used anesthetic agents are.
1. 1% Lidocaine 5mg/kg (upto 7mg if combined with epinephrine)
2. 0.125 - 0.25% Bupivacaine 2.5mg/kg.
 Volume of LA required is:
1. Sacral block – 0.5ml/kg of 0.25% Bupivacaine
2. Mid thoracic block – 1.25ml/kg of 0.19% Bupivacaine
3. Lumbar block – 1ml/kg of 0.25% Bupivacaine
 Supplements to extend CEA
Ketamine 0.5mg/kg (preservative free) Clonidine 1µg/kg
Diamorphine 30µg/kg Morphine 50µg/kg (preservative free)

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 Moderate to severe chest infection  Postpone surgery
Post viral, apyrexial and no chest signs  Fit for surgery even if running nose

URTI
Q. 7) A five year old child presents for RIH repair
The mother gives a h/o URTI 1 week ago. The child has a running nose.
a) What are the signs and symptoms you look for before deciding to anesthetize this child?
b) What will be your course of action?
c) What are the risks involved in anesthetizing this child with URTI?

Ans 7)
a. Signe and symptoms: Productive cough, running nose (infective or not), fever, D&V,
Inspiratory rhonchi, ↑R/R, sore throat, intercostal recession

b. My course of action will be postponement of the surgery for at least 2 weeks so that the URTI will be
subsided otherwise there will be more chances of postoperative pulmonary complications.

c. Risks with URTI:

1. Increased risk of postoperative pulmonary complications
 Wheeze crepts on auscultation
 Laryngospasm excess secretions
 Hypoxemia airway obstruction
 Atelectasis laryngospasm and Bronchoconstriction
 Cough
If surgery cannot be deferred then
1. Anticholinergic medications
2. Mask ventilation
3. Humidification of inspired gases
4. Longer than usual stay in recovery room

Postponement:
URTI 2 weeks
LRTI 4 weeks
Broncholitis  6 weeks

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PYLORIC STENOSIS:
Q.8) A 5 weeks old infant has a h/o projectile vomiting following each feed. The infant is severely
dehydrated with rapid pulse and sunken eyes. How will you manage this pt. preoperatively?

Ans. AIM: to correct volume deficit and metabolic alkalosis and electrolytes

PREOPERATIVE MANAGEMENT:
Assessment of dehydration and hypovolemia and electrolytes
As this infant is severely dehydrated, he must be treated as following:
1. Administer 100% Oxygen
2. Normal Saline N/S 0.9% +20 mmol of KCL/L
3. This must be administered @ a rate of 100ml/kg (severe dehydration)
4. Assess after the administration of the above regimen
5. Now maintenance volume  5% D/W + 0.45% N/S +20mmol/L KCL for maintenance according
to body wt.
6. NG or OG should be passed to decompress the GIT and replace the aspirate with same amount
of 0.9% N/S
7. Do urgent UCE’s to confirm the successful hydration
8. Surgery should be delayed or postponed until the correction of electrolytes.

Early signs of hypovolemia:

1. Capillary refill time > 2Sec Maintenance if body wt.is 3kg
2. Cold, blue peripheries 3kg x 10 = 30ml/h
3. ↑core peripheral temp gap
4. Thready pulse

Late sighs of hypovolemia

1. Oliguria
2. ↓level of consciousness

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TEMPERATURE REGULATION
Q.9) A one year old child presents for laparotomy.
a) What are the methods available to reduce perioperative heat loos in this child?
b) How does anesthesia impair temperature homeostasis?
c) What is the role of brown fat?

Ans.
a. METHODS TO ↓ HEAT LOSS PERIOPERATIVELY:
1. Theatre should be heated before surgery to warm the walls and raise ambient temperature
to 26 0C or more
2. Doors to OT should d stay close to avoid cold air currents
3. Avoid exposure of child. Head should be covered with polythene
4. Use active warming devise including warming air blankets and warming mattresses and
warming lights.
5. Humidified and warm anesthetic gases (use HME filter)
6. All perioperative
perative fluids specially blood should be given by blood warmer
7. Cleansing fluids should be kept warm as well
8. At last but not least, temperature monitoring is essential

b. EFFECTS OF ANESTHESIA ON TEMPERATURE REGULATION

1. General anesthesia especially volatile agents depress the thermoregulatory response. Heat
is lost from the core of the cooler peripheral tissues
2. Volatile anesthetics inhibit thermogenesis in brown adipocytes.
adipocyte
3. RA also leads to hypothermia by causing vasodilation and subsequent internal redistribution
of heat. Hypothalamus receives altered perception
perception of temperature in blocked derma
dermatomes

Heat and moisture exchanger (HMEHME) Heat and

exchange moisturizers (HME)) are devices used
in mechanically ventilated patients intended to
help prevent complications due to "drying of the
respiratory mucosa, such as mucus plugging
and endotracheal tube (ETT) occlusion

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 F- Fasting
M- Monitoring Never
R – Rapport forget
A – Airway /Atropine these
D – Drug and dilutions in
I – IV lines Pediatric
BROWN FAT O – Oxygen anesthesia
Ans c) BROWN FAT S –Stethoscope (precordial)

 Brown fat provides nonshivering thermogenesis by its metabolism which is the major mechanism of
heat production in neonates
 Brown fat is severely limited in premature infants and in sick neonates who are deficient in fat
stores.
 Brown fat is found in back, shoulder, leg and around major thoracic vessels.
 Metabolism of brown fat increases O2 consumption and may worsen pre-existing hypoxia
 Volatile anesthetics inhibit thermogenesis in brown adipocytes.
_____________________________________________________________________________________

CONGENITAL DIAPHRAGMATIC HERNIA

Q. 10) write down the anesthetic considerations of congenital diaphragmatic hernia?

Ans ) HALL MARKS OF CDH

1. Hypoxia
2. Scaphoid abdomen
3. Evidence of bowel in thorax by auscultation or radiography

Diagnosis antenatally by ultrasound

Pulmonary hypoplasia and malrotation of intestine almost always present
Marked pulmonary HTN
40-50% mortality
High frequency Oscillatory ventilation (HFOV) improve ventilation and O2
ECMO if patient fails to stabilize

ANAESTHETIC CONSIDERATIONS:
1. Gastric distension minimized by NG tube
2. Avoid high levels of PPV
3. Preoxygenated and intubated awake.
4. Maintenance with low concentration of volatile, opioids, relaxants
5. N2O contraindicated if hypoxia and expansion of air in bowel
6. Peek inspiratory airway pressure < 30 cmH2O
7. A sudden fall in lung compliance, BP, or Oxygenation may signal a contralateral pneumothorax-
chest tube
8. Monitor ABG’s

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 Choking – coughing – cyanosis
TRACHEOESOPHAGEAL FISTULA Type III is most common
Anesthetic considerations
Preoperative:
1. Identify all congenital anomalies
2. Prevent aspiration pneumonia  head up, oral-esophageal tube and avoiding feedings
3. Surgery postponed until any pneumonia cleared by antibiotics
4. Copious pharyngeal secretion  requires frequent suctioning before and during surgery.

Intraoperative:
1. Before intubation, PPV avoided  gastric distension may interfere with lung expansion
2. Awake intubation without muscle relaxants.
3. Key to success is correct ETT position  ideally the tip of the tube lies b/w fistula and carina so
that anesthetic gases pass into the lungs instead of stomach.
4. A precordial stethoscope should be placed in (L) dependent axilla
5. A drop in O2 saturation indicates that retracted lung needs to be re-expended
6. BP monitoring by A-line
7. Blood should be immediately available
8. Requires 100% O2 despite risk of retinopathy of prematurity

Postoperative:
1. Most pts. Requires continue ETT and IPPV in immediate postop patient
2. Neck extension and instrumentation (suctioning) of esophagus should be avoided  disrupt the
surgical repair.
3. Postop complications include GER, aspiration pneumonia, tracheal compression and anesthetic
leakage.

ANESTHETIC MANAGEMENT OF FB ASPIRATION

Minor manipulation of airway can convert partial into complete obstruction
Supraglottic FB:  inhalational induction and gentle upper airway endoscopy to remove object and/or
secure the airway
Subglottic FB: inhalational induction followed by rigid bronchoscopy by surgeon or ETT and flexible
bronchoscopy
Close communication and cooperation b/w surgeon and anesthetist is essential
Pre operative lateral neck radiograph shows FB
Stridor, drooling, hoarseness, tachypnea, chest retractions and a preference for upright position are
predictive of airway obstruction
Total obstruction can occur @ any time  prepare for tracheostomy before induction of GA
Laryngoscopy should not be performed before induction  Laryngospasm
Smaller than usual size ETT should be used
If failed intubation  1.) Rigid bronchoscopy or
2.) Emergency tracheostomy

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MALIGNANT HYPERTHERMIA
Q.
a) What is malignant hyperthermia, its S/S and D/d of trismus?
b) How would you manage an episode of MH?
c) What is the mechanism of action, dose and side effects of dantrolene?

Ans
a. MALIGNANT HYPERTHERMIA:
Def: MH is a myopathy, characterized by an acute hypermetabolic state within muscle tissue following
induction of G.A it can also occur postoperatively without trigger agents
 Trigger agents are volatile agents and suxa.
 Diagnosis by caffeine –halothane contracture test (CHCT)
 Pathophysiology involves abnormal ryanodine (RyRs) receptor
S and S:
1. Masseter muscle rigidity
2. Tachycardia and Early sign during anesthesia
3. Hypercarbia (↑ETCO2) x2 or x3.
Other signs:
Tachypnea, arrhythmias, HTN, mottled cyanosis, hyperthermia, fever, sweating, metabolic
acidosis, hyperkalemia, myoglobinemia, myoglobinuria

D/D OF HYPERTHERMIA PERIOPERATIVELY

1. Malignant hyperthermia
2. Neuroleptic malignant syndrome (NMS)
3. Thyroid storm
4. Pheochromocytoma
5. Drug induced hyperthermia (serotonin syndrome)
6. Iatrogenic hyperthermia
7. Brain stem /Hypothalamic injury
8. Sepsis
9. Transfusion reaction.

b. MANAGEMENT OF AN EPISODE OF MH
GOAL: Terminate the MH episode and treating complications like acidosis and hyperkalemia
1. The triggering agent must be stopped
2. Call for help
3. Hyperventilate with O2 at high flows
4. Dantrolene must be given immediately 2.5mg/kg
5. Administer sodium bicarbonate 1-2meq/kg IV
6. Change anesthetic tubing and soda lime

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 7. Institute cooling measures (lavage, cooling blankets and cold IV fluids, ice packs, ↓OT
temperature)
8. Administer inotropes and antiarrhythmic agents as necessary
9. Administer additional doses of dantrolene if needed
10. Invasive monitoring of arterial BP and CVP
11. Monitor ABG’s , ETCO2, U/O, K+, Ca+, clotting studies
12. Treat severe hyperkalemia with dextrose 25-50g IV and regular insulin 10-20U IV (adult
dose)
13. Mannitol or furosemide to establish diuresis and prevent ARF from myoglobinuria.

DANTROLENE
Ans c) MOA OF DANTROLENE
Dantrolene, a hydantoin derivative directly interferes with muscle contraction by binding the ryanodine
(Ryr1) receptor on calcium channel and inhibiting calcium ion release form sarcoplasmic reticulum

DOSE: 2.5mg/kg IV every 5 minutes until the episode is terminated.

Upper limit is 10mg/kg (max)
Half-life is 6hrs
After initial control 1mg/kg IV every 6 hours
for next 24-48hrs to prevent relapse
Can be used for thyroid storm and NMS

SIDE DFFFECTS:
1. Generalized muscle weakness
2. Respiratory pneumonia
3. Aspiration pneumonia
4. Phlebitis.

Dantorlene is packaged as 20mg of lyophilized powder to dissolved in 60ml sterile water

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 Exomphalos is a weakness of the baby's abdominal wall
where the umbilical cord joins it. This weakness allows the
abdominal contents, mainly the bowel and the liver to protrude
outside the abdominal cavity where they are contained in a
loose sac that surrounds the umbilical

GASTROSCHISIS/EXOMPHALOS

Replacement of abdominal contents into abdominal cavity

ANESTHETIC CONSIDERATIONS:
PREOPERATIVE:
1. Obvious neonatal diagnosis from birth. Now usually diagnosed inutero
2. Gastroschisis is defect in anterior abdominal wall usually on (Right) causing herniation of
abdominal contents without a covering sac.
3. In exomphalos, there is a failure of gut to return to abdominal cavity during fetal development
resulting in persistent herniation through extra embryonic part of umbilical cord, which covers
it.
4. ↑incidence of associated anomalies including cardiac disease in exomphalos. A full cardiac
assessment should be performed
5. Gastroschisis ass. with LBW and thickened bowel wall due to amniotic fluid
6. Exposed abdominal contents  large evaporative heat and water losses and predispose to
infection. It should initially be covered with cling film or an equivalent

INTRAOPERATIVE:
1. Already intubated and ventilated. Otherwise intubate conventionally
2. NG tube and esophageal temperature /stethoscope
3. Two IV cannulas for maintenance and volume
4. Arterial monitoring is useful
5. Heat conservation is important. Warm the theatre and use a warming mattress or hot air
mattress, radiant heater. Keep the patient's head covered. Use warmed fluids
6. Intraoperative analgesia: Fentanyl 5-10µg/kg or epidural if extubation within 48 hr is
contemplated

POSTOPERATIVE:
 Post op ventilation, especially if abdomen is tense, should be in the head up position
 Pay assiduous attention to fluid balance. There may be large losses into the abdomen of crystalloid
and protein.

SPECIAL CONSIDERATIONS:
1. IV line in arms as abdominal distention impair venous return from lower body
2. It is simpler to insert a percutaneous long line at this stage for later parenteral feeding.
Postoperatively, progressive oedema makes cannulation more difficult.
3. Manual ventilation to assess the effect of replacement of abdominal contents on lung
compliance to determine the correct degree of abdominal reduction
4. Complete reduction is not always possible. A silo is then created around the extra-
abdominal contents to be gradually reduced on the intensive care unit. Fluid loss and
infection are major issues.

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 Endocrinology
DM
Q.1 a) Describe briefly the anesthetic consideration of DM patent?
b) How will you prepare a diabetic pt. for anesthesia and surgery?

Ans. a)
ANESTHETIC CONSIDERATIONS:
History:
1. Duration of DM
2. Drug history
3. Previous anesthetic history
4. Problems of indigestion
5. Functional class.
6. Comorbids.
7. Allergies.
8. Smoking and alcohol.

Examination:
 30% person type-I D.M.
 Airway assessment
 TMJ & cervical spine mobility (glycosylation)
 CVS (HTN, IHD, CVA, MI, Ischemia, CMP, arrhythmias)
 Renal (Proteinuria and ↑Cr, renal failure) nephropathy
 Pulmonary (chest infections, cardiomegaly)
 GIT (gastroparesis, prone to reflux)
 Look all over for any infection especially foot
 Retinopathy

GOAL: To rule out end organ damage and optimize the pt. maximally

End organ damage:

Retinopathy, nephropathy, neuropathy, CAD
High normal glucose, metabolic stability

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 Insulin HL 4-8 minutes
Hypoglycemia  Diaphoresis, tachycardia and
Ans b) nervousness
PREPARATION FOR ANESTHESIA AND SURGERY <50 mg/dl

Investigations:
 HbA1c : Identify Pts. @ ↑ risk of periopera ve hyperglycemia
 CXR: Cardiomegaly, pulmonary congestion, Pleural effusion, infection
 ECG: Silent myocardial ischemia and infarction
 FBS
 UCE
 Blood sugar
 Urine DR: Ketones and glucose
 ECHO –if IHD
 Carotid Doppler scan – if H/O CVA

Preparation:
1. Stop long acting OHD 24 hours before surgery. (sulfonylurea’s, metformin)
2. Check blood glucose 4Ho
3. Start (R) insulin on sliding scale
4. Aspiration prophylaxis
5. Place 1st on list if possible
6. Premedicate with midazolam
7. Omit morning dose of insulin on the day of surgery
8. FBS before surgery and after induction
9. Consider RSI if gastroparesis suspected.

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Q2 Discuss intraoperative management of a pt. with IDDM undergoing major surgery
Ans.

AIM:
- To prevent and correct dehydration and ketoacidosis
- To prevent end organ damage and optimize maximally
- To prevent hypoglycemia, hyperglycemia and hypokalemia.
- To maintain euglycemia, acid base and electrolyte balance.

INTRAOP MANAGEMENT:
1. The primary goal of intraoperative blood sugar management is to avoid hypoglycemia (Brain
depends on glucose)
 Anesthetized patient do not show any signs.
 Monitor blood sugar regularly
 If hypoglycemia occurs
 Give 25% dextrose water IV.
 Give 1mg glucagone (IV or IM)
 10-20g of sugar by NG.
2. Poor blood sugar control > 180 mg/dl also carries risk of hyperosmolarity, infection and poor
wound healing. Post operatively.
3. Two common technique for perioperative insulin management in DM are as follows:

Bolus Administration Continuous infusion

Preoperative D5W (1.5 ml/kg/h) NPH-insulin D5W (1ml/Kg/H)
(half morning dose) Regular Insulin:
U/H =Plasma Glucose/150
Intraoperative Regular insulin (as per sliding scale) Same as preoperative
Postoperative Same as intraoperative (RIS/S) Same as preoperative

4. A general target for intraoperative maintenance of blood glucose is 120-150 mg/dl

5. Tight control with continuous infusion technique preferable type-I D.M.
6. 20 mEq of KCL to each liter of fluid as insulin causes an intracellular K+ shift.
7. The key to any management regimen is to monitor plasma glucose levels frequently.
8. Portable spectrophotometers capable of determining glucose concentration in a drop of blood
within a minute.
9. Pts. who take NPH or protamine zinc insulin (PZI) are @ ↑risk of allergic reaction to protamine
anaphylactic shock and death.
10. Ringer lactate is controversial. N/S is the best choice.
11. RSI with cricoid pressure if gastroparesis suspected RA-good option.

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POST OP MANAGEMENT:
1. Close monitoring of blood sugar  stress hyperglycemia
2. If large amounts of R/L are given intra operatively, blood sugar will tend to rise 24-48hrs
postoperatively.
3. Diabetic out patient may require overnight hospital admission if persistent N&V from
gastroparesis prevents oral intake.

DIAGNOSIS OF DM:
Fasting  126mg/dl (7.0 mmol/L)
Glucose tolerance test  200mg/dl (11.1 mmol/L)

GKI:

GKI infusions
A GKI infusion can be considered during the perioperative period for:

 Patients with uncontrolled or poorly controlled diabetes (as determined by HbA1c)

 Patients with type 1 diabetes who are undergoing major surgery
 Patients who might not be able to start eating normally within 4 hours after surgery

The standard GKI regimen:

500mL dextrose 10% with 10mmol potassium chloride and
10units of Actrapid® insulin to run at 100mL/hr
.
The insulin concentration should be varied according to blood glucose levels.
In special circumstances (eg, patients with heart failure or those with renal failure who
require fluid restriction), a 20% dextrose solution with 20units of insulin with or without
potassium chloride, running at
50mL/hr, can be used instead.

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HYPOTHYROIDISM

Q.3.a) What are the clinical features of hypothyroidism?

b.) Anesthetic considerations of such patient?

Ans a)
CLINICAL FEATURES CAUSES
1. Weight gain 1. Autoimmune Dx (hashimotor thyroiditis)
2. Cold intolerance 2. Thyroidectomy
3. Muscle fatigue 3. Radioactive iodine
4. Lethargy 4. Antithyroid medication
5. Constipation 5. Iodine deficiency
6. Hypoactive reflexes 6. Secondary hypothyroidism
7. Dull facial expression and 7. Cretinism (neonatal hypothyroid)
8. Depression. (physical and mental retardation)

Diagnosis: Confirmed by ↓free T4 level.

Rx  Thyroid hormone preparation (Thyroxin)

MYXEDEMA COMA: life threatening dx result from extreme hypothyroidism.

S&S:  Impaired mentation, hypoventilation, hypothermia, hyponatremia and CHF. More common in
elderly Precipitated by infection, surgery or trauma

Rx: IV thyroid hormones (levothyroxine 300-500 mg loading dose followed by 50mg levothyroxine
maintenance/day)

Ans b) ANAESTHETIC CONSIDERATIONS:

A. PREOPERATIVE:
1. Euthyroid state is ideal. Check other autoimmune dx, Co-existing dx.
2. If clinical evidence of hypothyroidism  Delay elective surgery to obtain euthyroid state.
3. If surgery is urgent then IV thyroid hormones slowly with ECG monitoring.
4. If subclinical hypothyroidism can proceed to surgery with no special preparation
5. Assess airway  Tracheal deviation and rule out retrosternal goiter
6. Ask about dyspnea, dysphagia and stridor – anticipate difficult airway.
7. Look for distended neck veins that not change with respiration.
(Superior vena caval syndrome)
8. No sedation required  very prone to drug induced respiratory depression
9. Investigations: 1. FBS, 2. UCE, 3.serum Ca, 4.TFT’s, 5.Mg, 6. CXR & thoracic inlet view to
assess tracheal compression.
10. H2 receptor antagonists and metoclopramide –aspiration prophylaxis.

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 B. INTRAOPERATIVE
1. More susceptible to hypotensive effects of anesthetic agents because of ↓CO, blunted
baroreceptor reflexes and ↓ intravascular volume
2. Ketamine is recommended for induction.
3. Hypothermia due to ↓BMR- warm I/V fluids
4. Hypoglycemia, anemia, hyponatremia – N/S, 25% D/W, PRBC.
5. Anticipate difficult intubation because of large tongue

C. POSTOPERATIVE
1. Delayed recovery due to hypothermia. Forced air warming blankets
2. Respiratory depression  Ketorolac will be a good choice for pain
3. Slow drug biotransformations.
4. Prolong mechanical ventilation.
5. Awake extubation

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HYPERTHYROIDISM
Q 4. 30 year old female present with a diffuse swelling in neck, she has a recent history of wt loss with
frequent palpitations and sweating
O/E she is hyperexcitable with fine tremors of outstretched hands. Her B.P is 160/100 & pulse 120bpm.

a. What is most probable diagnosis?

b. How will you prepare her for surgery?
c. On what grounds you can say pt. is ready for surgery?
d. How will you manage this patent intraoperatively?
e. Following surgery this pt. develops airway obstruction.
Give causes and management?

Ans. A.) Thyrotoxicosis (Graves’ disease)

Ans B.) PREOPERATIVE PREPARATION:
1. Patient must be euthyroid with medical treatment and all elective surgery should be postponed
till euthyroid
2. Airway assessment –anticipated difficult airway
3. Anti-thyroid medications and β-Blockers should be continued till the morning of surgery.
4. Any H/O anticoagulants
5. Listen for stridor (superior venacaval syndrome)
6. Thyroid function test must be normal (euthyroid)
7. HR must be <85bpm
8. Check range of neck movement.
9. If emergency surgery hyperdynamic circulation should be controlled by esmolol infusion.
10. Investigation: TFT’s, FBS, UCE, RBS, CXR, ECG, ECHO, Serum Ca& Mg, Thoracic inlet, IDL, CT scan.

Ans C)
1. Normal TFT’s (Euthyroid)
2. HR< 85 –controlled by esmolo infusion
3. No hand tremors.

Ans D) INTRAOPERATIVE MANAGEMENT

1. Close monitoring of CVS and body temperature (malignant hypertension)
2. Eyes should be padded if exophthalmos  Risk of corneal abrasion
3. Ketamine, pancuronium, adrenergic agonists best avoided
4. Thiopental may be the induction agent of choice (Antithyroid in high doses)
5. Adequate fluids to ↓ hypotensive response at induction.
6. Adequate depth of anesthesia before laryngoscopy and surgical stimulation to avoid
tachycardia, hypertension and ventricular arrhythmias
7. Cautions used of NMBA‘s  ↑incidence of myopathies and MG.
8. Consider superficial cervical plexus block for postop pain.

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Ans E) POSTOPERATIVE COMPLICATIONS
1. Thyroid storm – medical emergency can occur intraoperatively
2. Recurrent laryngeal nerve palsy horsiness (U/L), aphonia and stridor(B/L)
3. Hematoma formation  Reopen the wound and evacuate the clot.
4. Hypoparathyroidism  Cause acute hypocalcaemia.
5. Pneumothorax
6. Trachiomalacia
With regard to this patent as she developed airway obstruction the most common cause will be
hematoma formation.
Immediate treatment Opening the wound and remove the clot and then reassess for
reintubation

THYROIDSTORM:
1. Hyperpyrexia
2. Tachycardia
3. Altered consciousness
4. Hypotension.

Rx
1. Hydration and cooling
2. Esmolol infusion or propranolol I/V (0.5 mg increments until HR is <100/min)
3. Propylthiouracil (250-500 mg 6Ho)
4. Sodium Iodide (1 gm IV 12Ho)
5. Correct precipitating cause e.g. infection.
6. Post op ICU
7. Cortisol (Adrenal gland suppress)100-200 mg 8 Ho

HYPOPARATHYROIDISM:
Q. 5) you are asked to see a pt. in recovery room. She is cyanosed, had a thyroidectomy incision and has
started to twitch?
a) What is the 1st thing you could do?
b) List 4 causes specific to this?
c) Why is she twitching?
d) What 2 signs you would look for to confirm the diagnosis in this pt. and what treatment would
you give?

Ans a) The 1st thing I would do is primary survey (ABCDE)

Airway assessment is the priority.
Secure the airway with ETT.

b) Causes:
1. Tracheomalacia 3. Recurrent laryngeal nerve palsy B/L
2. Hematoma 4. Pneumothorax

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Ans c) Due to the accidental excision of unilateral/bilateral parathyroid gland which causes
hypocalcaemia cause twitching (tetany)

Ans d)

1. Trousseau’s sign(Carpopedal spasm following inflation of a tourniquet above systolic BP for 3min)
Flexed wrist, finger drawn together
2. Chvostek’s sign Tapping over face @ parotid gland will cause painful twitching
3. Prolong QT interval.

Rx: IV Ca-chloride.

Q.6) 78 years old male, scheduled for repair of hip #, sustained 2days ago. H/O DM 30 years controlled
with 30 u NPH daily. He is heavy smoker with chronic cough and wheeze.
BP 140/80, R/R-16, Temp 37oC, Hb-8.9, RBS-380

a. Name and give reasons for the investigations you will request to help in your management?
b. What are the hazards of poor diabetic control inperioperative?
c. How would you achieve adequate blood sugar level in this?
d. Will you ask for pre-operative blood transfusion?

Ans a) Combined investigations for DM and COPD.

HbA1c, FBS, RBS, CP, UCE, CXR
ECG, PFT, ABG, ECHO

Ans b) HAZADES OF POOR DIABETIC CONTROL

1. Hyperosmolar diabetic coma- poor perfusion↓Oxygena on cerebral or coronary
thrombosis
2. Hypoglycemia Intraoperative management.
3. Intraoperative MI/Ischemia
4. CVA
5. Infections
6. Poor wound healing.

Ans c) sec Q 1&2 (By continuous infusion technique)

Ans d) Yes, transfuse 1point PRBC preoperatively.

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PHEOCHROMOCYTOMA
Q.7 Describe the perioperative management of a pt. undergoing excision of pheochromocytoma?

Ans GOALS: Focus on the adequacy of adrenergic blockade and volume replacement.

PREOPERATIVE:
1. Evaluate resting arterial BP
2. Orthostatic BP
3. HR and ventricular ectopy
4. ECG for evidence of ischemia
5. Preoperative α-adrenergic blockade with PHENOXYBENZAMINE will help correct volume deficit
other than hypertension and hyperglycemia.
6. 24hrs ambulatory BP monitoring.
7. Aim BP< 140/90 and HR < 100
8. Co-existing dx
9. Airway assessment.
10. Previous anesthetics
11. Allergy
12. Smoking and alcohol.
13. Investigations  Routine labs + ECHO + blood glucose + ECG
14. Premedication with sedatives and α-adrenergic blockade

INTRAOPERATIVE:
1. Good IV access
2. Direct arterial pressure monitoring
3. Urine output
4. CVP If young and healthy
5. PAC  If evidence of catcholamine cardiomyopathy
6. Intubate when deep anesthesia established.
7. Etomidate/propofol Alfentanyl  Rocuronium/ vecuronium ETT with CMV  IPPV
8. Avoid suxa, ketamine, pancurominum, halothane, atopine, atracurium, morphine and pethidine.
9. Regional anesthesia should not be used
10. Maintain with isoflurane
11. Intraoperative hypertension  phentolamine, SNP or nicardipine
12. After tumour ligation or resection, hypotension form hypovolemia occurs.
13. Fluid resuscitation with crystalloid to maintain CVP @ 10-15 cm H2O
14. Vasopressor or inotropes may be required like phenylephrine noradrenaline

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Dr. Tariq Mahar
POST OPERATIVE:

1. ICU/ HDU.
2. Monitor blood glucose and pressures
3. If bilateral adrenal resection  immediate steroid support.
4. IV hydrocortisone 100mg bolus
5. Epidural with opioid (morphine) for good pain relief
 Clinical manifestations: Paroxysmal headaches, HTN, Sweating and palpitations.
 Diagnosis: 1. Urinary VMA, norepinephrine and epinephrine ↑↑
2. Fractionated plasma metanephrine levels (superior)

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MORBID OBESE
Q8.) A 50 years old female, morbidly obese is scheduled for openchole
a. How will you evaluate and prepare and prepare and premedicate this patent?
b. Give your anesthetic management?
c. What problems you will encounter in this pt postoperatively, give your management?

Ans a)
Obesity is associated with HTN, DM, IHD, Cholelithiasis
The triad of obesity  (HTN, Type II DM and obesity) is known as metabolic syndrome.
Morbid obesity > 35BMI />40 BMI
Obesity >30BMI
Pickwickian syndrome: Complication of
extreme obesity
PREOP ASSESSMENT: 1. Hypercapnia
CVS: ↑blood vlume, ↑CO, ↑SV 2. Cyanosis induced polycythemia
3. RHF
Arterial hypertension and LVH
4. Somnolence
Pulmonary hypertension and corpulmonele
Evaluate for IHD, LVF and PHTN.

Respiration: -↑O2 consumption (demand) - ↓ Chest wall compliance

-↑CO2 production - V/Q mismatch
-↑alveolar ven la on - Hypoxia
-↓FRC
(Pickwickian syndrome) Obesity-hypoventilation syndrome (↓respiratory drive)
(OSAS): Obstructive sleep apnea syndrome (loud snoring)
 (↑ Periopera ve pulmonary complica ons)
 Anticipated difficult airway management
 Prone to desaturate rapidly
 CPAP trial postop

GIT: Hiatus hernia, GERD, gastroparesis, hyperacidic gastric fluid, ↑risk of gastric cancer, ↑risk of
aspiration, Fatty liver.

Endocrine: Insulin resistance may cause glucose intolerance and NIDDM

Airway: Anticipated difficult airway management during induction and upper airway obstruction during
recovery. (Fiberoptic intubation FOI recommended/difficult airway trolley DAT)
↓Atlanto-axila movement, Large tongue, narrow airways

General: Technical problem of IV access and nerve blockade

Calculate BMI
Ask about snoring, somnolence, and periodic breathing, apnea pauses

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Investigations: FBC, UCE, CXR, Urine D/R, PFT’s, PT/INR, ECHO, ECG, ABG’s, RBS/FBS.

PREMEDICATION: Respiratory depressants should be avoided

Aspiration prophylaxis  H2 receptor antagonist and metoclopramide

Ans b)
INTRAOP MANAGEMENT
1. Appropriate table and large BP cuff
2. Full preoxygenation (3-5min)
3. CMV with large TV
4. Awake fiberoptic intubation strongly recommended if difficult airway
5. Confirmation of breathe sounds by ETCO2
6. ↓FRC increased by administering PEEP.
7. Increasing I:E ratio may ↓airway pressure
8. ↑FiO2 needed in lithotomy, prone and trendelenburg positions
9. Large loading dose required to produce same plasma concentration
10. ↓ local anesthetic requirement
11. ↑blood loss is common, due to difficult surgical condi ons

Ans c)
POSTOPERATIVE PROBLEMS
1. Respiratory failure is the major postope problem
2. Extubate awake when NMBA’s effects completely reversed and no doubt that an adequate
airway and ventilation will be maintained
3. Pulmonary atelectasis  head up 30-45ositting position
4. Desaturation O2 supplemental, regular chest physiotherapy and incentive spirometry
5. Thromboembolism DVT prophylaxis, mobilize asap
6. OSA ptspostop CPAP
7. Wound infections  antibiotics
8. DVT and pulmonary embolism  DVT Prophylaxis

Ideal B.W. – wt associated with lower mortality for given ht

IBW (kg) = ht cm/-x (x former-100) (x for female =105)

( )
BMI = ℎ ( )
( [ ])

BMI = Wt in Kg divided by ht. in meters squared (wt/ht2)

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 LIVER
Q. 1) Systemic problems encountered in a patient with long standing cirrhosis
How would you evaluate the risk of surgery in such patients?
Ans a)
1) GIT portal HTN
1. Ascites
2. Esophageal varices
3. Hemorrhoids
4. GI bleed 5) Hematological
1. Anemia
2) Circulatory 2. Coagulopathy
1. Hyper-dynamic state (↑ Cardiac 3. Hypersplenism
output) 4. Thrombocytopenia/ Leucopenia.
2. Systemic arteriovenous shunts
3. Low SVR 6) Infections
4. Cirrhotic cardiomyopathy 1. Spontaneous bacterial peritonitis.

3) Pulmonary: 7) Metabolic:
1. ↑intrapulmonary shun ng 1 Hyponatremia
2. ↓FRC Restrictive ventilator defect 2. Hypokalemia
3. Pleural effusion ↑WOB 3. Hypomagnesaemia
4. Respiratory alkalosis 4. Hypoalbuminemia
5. Hypoglycemia
4) Renal:
1. ↑Na reabsorp on. 8) Neurological:
2. ↓Renal perfusion 1. Encephalopathy.
3. Hepatorenal syndrome

Ans B)
CHILD’S CLASSIFICATION FOR EVALUATION (MODIFIED BY POGH)
Risk Group A B C
Bilirubin (mg/dl) <2.0 2.0-3.0 >3.0
Albumen g/dl >3.5 3.0-3.5 <3.0
Ascites None Controlled poorly
Controlled
Encephalopathy Absent Minimum Coma
Mortality rate (%) 2-5% 10% 50%
PT sec <18 18-20 >20
INR <1.7 1.7-2.3 >2.3
Nutrition Excellent Good Poor

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Dr. Tariq Mahar
CIRRHOSIS
Q.) What are the anesthetic considerations in a patient with cirrhosis scheduled for major abdominal
surgery?

Ans)
PREOP CONSIDERATIONS:
1. History (Duration of Dx, severity, ascites, medications, nutrition)
2. Functional class.
3. Comorbidities
4. Previous anesthetics
5. Drug history
6. Allergy
7. Smoking and alcohol
8. Neurological status
9. General physical examination.
10. Airway assessment.
11. Volume status.
Hepatic dysfx and ↑ periopera ve risk.
So evaluate by child’s classification.
12. Investigations
1. FBC
2. UCE’s
3. Clotting screen
4. Glucose
5. LFT’s
6. ABG’s
7. CXR
8. Urine DR.
9. Serum albumin
10. Serum ammonia
11. Hepatitis screening LRCP, CT, MRI and cholangiogram.
12. ERCP
13. Special preoperative consideration:
1) Arrange FFP, Platelets, cryoprecipitate and PRBC.
2) Correction of anemia PRBC’s
3) If pulmonary function compromise (large ascites) paracentesis of ascetic fluid
4) Correction of coagulopathy  FFP, Platelets and cryoprecipitate
5) Correction of encephalopathy Oral lactulose or neomycin
14. Premedication’s:
Aspiration prophylaxis (ascites)
Lorazepam and thiamin’s alcoholic pts with withdrawal

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INTRAOP CONSIDERATIONS:
GOAL: To preserve existing hepatic function and prevents any further deterioration in liver function.
1. Universal precautions are indicated in preventing contact with blood and body fluid if patients
are carriers of hepatitis B and C virus.
2. Pre-oxygenation and ‘RSI with cricoid pressure, using Propofol or etomidate and low dose suxa
most common
3. For unstable patient and those with active bleeding an awake intubation or RSI with cricoid
pressure using ketamine and suxa are best advised.
4. Requires larger than (n) loading dose and smaller than (n) maintenance dose of NMBA needed
(Pancuronium, Rocuronium, Vecuronium)
5. Cisatracurium-NMBA of choice  unique non-hepatic metabolism
6. Halothane is best avoided (LFT deteriorate postoperatively) Isoflurane 1st choice.
7. Remifentanil and fentanyl are good opioid choice.
8. Na+ restricted patients so use colloid IV fluids (albumin) ↑OP
9. Avoid profound hypotension and renal shutdown  colloid IV fluids as ascitic patient and
prolong procedure  large fluid shift
10. Avoid unnecessary transfusion  significant transfusioncitrate toxicity treated by IV calcium.
11. Monitor persistent ↓UO despite adequate fluid replacement.
12. Special monitoring includes: ECG, Pulse Oximetry, ETCO2 , arterial line, CVP, PAC, temperature,
ABG’s and Urine Output
13. Postop pain  acetaminophen.

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 EYE
IOP
Q).
a) What is normal intraocular pressure?
b) What are the factors affecting IOP during GA?
c) What is oculocardiac reflex? How you manage it?

Ans.)
a. Normal IOP  12-20mmHg.
b. Factor that affect IOP during GA are:
1. ↑Venous pressure ↑ IOP
2. ↑Globe volume ↑IOP
3. Laryngoscopy ↑IOP
4. Intubation ↑IOP
5. Airway obstruction ↑IOP
6. Coughing, vomiting, valsalva ↑IOP
7. Trendelenburg position ↑IOP
8. Tightly fitted face mask ↑IOP
9. Improper prone position ↑IOP
10. Retrobulbar hemorrhage↑IOP
11. Blinking / squinting ↑IOP
12. Anticholinergics ↑IOP
13. Suxamethonium ↑IOP

All anesthetic agents ↓IOP except:

1. Suxamethonium.
2. Atropine.
3. Ketamine.

Effect of cardiac and respiratory variables on IOP

Variable Effect
CVP↑ IOP↑
CVP↓ IOP↓
Arterial BP↑ IOP↑
Arterial BP↓ IOP↓
PaCO2↑ IOP↑
PaCO2↓ IOP↓
PO2↑ No effect
PO2↓ IOP↑

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OCR
Ans c) OCULOCARDIAC REFLEX:
 Traction on extraocular muscles or pressure on eye ball can elicit cardiac dysrhythmia ranging
from bradycardia and ventricular actopy to sinus arrest or ventricular fibrillation.
 OCR is most common in pediatric pts. undergoing strabismus surgery.Also occur in cataract
extraction, enucleation, retinal detachment
 In awake pts associated with somnolence and nausea
 This reflex consists of trigeminal afferent (V1)and vagal efferent path described in 1908

Management:
1. Immediate notification of surgeon and temporary cessation of surgical stimulation until HR ↑
2. Confirmation of adequate ventilation, oxygenation and depth of anesthesia
3. Administration of IV atropine (10μg/kg)
4. In recalcitrant episodes  infiltration of rectus muscles with local anesthetics
The reflex eventually fatigues itself with repeated traction on EOM. (Extra Ocular Muscle)

PERIBULBAR BLOCKADE
The needle does not penetrate the cone formed by the extraocular muscle
Advantage: Less risk of eye penetration, optic nerve and artery, and less pain on injection
Disadvantage: Slow onset and ↑ likelihood of ecchymosis
Technique: Patient supine position looking direct head typical anesthesia conjunctivae one or two
trans-conjunctival rejection eyelid retracted inferotemporal injection b/w lateral limbus.
Needle advanced orbital floor slightly medial to and cephalad to 5ml L/A
Second 5ml through conjunctiva on nasal side

Strabismus
Q. what are the anesthetic concerns in a seven year old child presenting for strabismus surgery?

Ans.)
Anesthetic concerns:
GOALS:
To maintain IOP and to prevent OCR

PREOP. CONCERNS:
1. GA is indicated in children and uncooperative patients as even small head movements could be
disastrous during microsurgery.
2. Pts may be apprehensive  possibility of permanent blindness.
3. Pediatric patients have associated congenital disorders e.g. down’s syndromes.
4. Elderly pts often have co-morbidities like DM, HTN, CAD
5. GPE and airway assessment with relevant history. (General Physical Examination)

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INTRAOP. CONCERNS:
1. Choice of induction technique depends on other medical problems.
2. Laryngoscopy and intubation duration must be as short as possible to control IOP- Also blunted
by prior I.V Lidocaine or opioid
3. Coughing during intubation must be avoided by deep anesthesia and profound paralysis.
4. A NDMR is used instead of Suxamethonium ↑IOP. (non depolarizing muscle relaxants)
5. Most pts with open globe injury have full stomach and require a RSI with cricoids pressure.
6. Pulse oximetry and capnograph monitoring particularly important.
7. Kinking and obstruction of ETT, breathing circuit disconnection and unintentional extubation
minimized by reinforced or preformed RAE tube.
8. More chances of hyperthermia in infants because of head to toe draping
9. ETCO2 differentiate this hyperthermia with MH.
10. Adequate IV hydration to avoid hypotension (deep anesthesia ↓CVS s mula on)
11. Intraoperative IV metoclopramide or 5HT3 antagonist (Ondansetron) ↓PON dexamethasone
4mg in adults  if strong H/O PONV.

POSTOP CONCERNS:
1. PONV  IV metoclopramide, 5HT3 antagonist and dexamethasone
2. Coughing on ETT could be prevented by extubating indeepanesthesia
3. IV Lidocaine 1.5mg/kg to prevent cough reflexes temporarily
4. Severe postop pain is unusually sufficient following ophthalmic procedure.
5. Meperidine 15-25 mg are usually sufficient
6. Sever pain signal  intraocular HTN, corneal abrasion or other surgical complications.

Retrobulbar blockade
LA (lidocaine or bupivacaine) is injection behind the eyeinto the cone formed by EOM. Addition of
epinephrine ↓bleeding and prolongs anesthesia. Hyaluronidase 3-7ut/ml enhances the Retrobulbar
spread of local anesthetic.

Complications:
1. Retrobulbarhemorrhage
2. Globe perforation
3. Optic Nerve atrophy.
4. Frank convulsions Rx
5. OCR Positive (PPV)
6. Trigeminal Nerve block To prevent hypoxia, bra
7. Respiratory arrest. and cardiac arrest

8. Post-Retrobulbar apnea syndrome unconsciousness +apnea

Contraindications:
1. Bleeding disorder.
2. Extreme myopia. 3. Open eye injury

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OPEN EYE INJURY:
Q. 12 years old boy is scheduled for emergency repair of ruptured globe, after being shot in the eye with
pellet gun?
What are the anesthetic concerns?

Ans. )
GOALS:
1. To prevent further damage to eye by avoiding ↑IOP
2. To prevent pulmonary aspiration with a full stomach.

PREOP CONCERNS:
1. Routine history, physical examination and last oral intake.
2. Consider to have a full stomach as gastric emptying is delayed by pain and fear that follow trauma.
3. Despite the aspiration risk these pts require GA.
4. Metoclopramide ↑LES tone, speeds gastric emptying, lowers gastric fluid volume and excretes
antiemetic effect.
5. Ranitidine (H2 receptor blocker) inhibits gastric acid secretions.
6. Non particulate antacid (sodium citrate) should be given prior to induction.

INTRAOP CONCERNS:
7. RSI with cricoid pressure. Avoid direct pressure on globe and ↑CVP
8. STP and Propofol are ideal induction agents as they ↓ IOP
9. Prior administration of fentanyl or lidocaine attenuates the hypertensive response to laryngoscopy
and intubation  ↓ IOP
10. Rapid onset of action that ↓ aspiration risk and profound muscle relaxation that ↓ risk of valsalva
response during intubation
11. Succinylcholine should be given even knowing that it ↑ intragastric and intraocular pressures

POSTOP CONCERN:
1. Pt. again at risk of aspiration during extubation and emergence so it should be delayed until pt.
awake and has intact airway reflexes
2. Intra op antiemetic + NG suction ↓risk of PONV.

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 KIDNEY
CRF
Q.1 what are the specific anesthetic problems in pt with CRF?

Ans ). AIM: To preserve the remaining renal function by maintaining normovolemia

PREOPERATIVE CONSIDERATIONS:

a. History and examination:

1. Determine underlying case, previous surgery and examination drug therapy (most common
 creation or revision AV-fistula in LA or RA)
2. Complete evaluation for optimal medication condition.
3. Reversible manifestations of uremia should be controlled.
4. Check for HTN, DM, IHD and anemia.
5. Type of dialysis
i. Peritoneal
ii. Hemodialysis. and AV-fistula and Fast dialysis.
6. Ask about U/O per day.
7. Examine for fluid overload. (Dependant edema, basal crept) or hypovolemia.
8. Avoid venous access in AV fistula arm-cannulate dorsum of hand.
9. A-Line on radial artery + NIBP
10. Look for fluid and electrolytes disturbances.
11. If major surgery planned, post op ICU/Renal care.

b. Investigations:
1. FBS  aim for 8-10g/dl Hb. (Transfuse if Hb < 6-7)
2. Electrolytes  if K+ > 6mmols/L then dialysis before surgery.
3. Coagulation profile  if R.A is considered
4. ECG Hyperkalemia, ischemia, conduction blocks, LVH
5. CXR and ABG  hypoxemia and acid bass balance in pts with dyspnea
6. BUN and Creatinine assess adequacy of dialysis.
7. Serum albumin
8. Blood glucose.
9. Drug toxicity if any  should be corrected.
10. ECCH Major surgical procedures of assess cardiac function.

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INTRAOPERATIVE CONSIDERATIONS:
a. Premedication:
1. Reduced doses of an opioid or benzodiazepine.
2. Promethazine for additional sedation and as an antiemetic.
3. H2 receptor blocker indicated in Pts with N&V or GI Bleed.
4. Metoclopramide ↑gastric emptying, prevent nausea and ↓ risk of aspira on
5. Preoperative antihypertensive should continue till surgery.

b. Induction:
1. Pts with N&V or GI bleed should undergo RSI with cricoids Pressure
2. Dose of induction agents should be ↓ in cri cally ill pts.
3. STP (2-3mg/kg), Propofol (1-2mg/kg) or Etomidate (0.2-0.4 mg/kg) if hemodynamically
unstable
4. An Opioid, β-Blocker or lidocaine to blunt hypertensive intubation response
5. Suxamethonium can be used if K+ < 5 otherwise Rocuronium or atracurium

c. Maintenance:
1. Volatile agents, N2O , propofol, fentanyl, and morphine are satisfactory maintenance
agents.(Isoflurane is best choice)
2. Controlled ventilation to avoid respiratory acidosis
3. Avoid NSAID’s e.g. ketorolac  use paracetamol as analgesic.
4. Maintain U/O  0.5 ml /kg/hr.
5. Avoid N2O in anemic pts.

d. Monitoring:
1. BP (NIBP) avoid in arm with AV fistula  occlusion
2. Intra-arterial, CVP and PA catheters are indicated major surgery, major fluid shifts.
3. A-line must in poorly controlled HTN.
4. Aggressive invasive monitoring in DM.
5. ECG, ETCO2, A-Line, CVP, PA, temperature, pulse oximetry, U/O and esophageal Doppler
(large fluid shifts).

e. Fluid therapy:
1. Superficial operations 5% Dextrose in water
2. Major fluid losses or shift  crystalloids, colloids or both.
3. Avoid R/L in Hyperkalemia  Use N/S instead
4. Glucose free solutions  if glucose intolerance with uremia
5. Blood loss  PRBC’s

f. Emergence: excretion of neostigmine and anticholinergic is prolonged (50% excreted in urine)

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POSTOPERATIVE CONSIDERATIONS
1. Time and need for postop dialysis
2. Good analgesia (morphine, fentanyl, paracetamol)
3. Fluid balance and U/O monitoring
4. Avoid nephrotoxic drugs
5. Avoid hypotension
6. ICU/HDU for postop renal case.

INDICATIONS FOR DIALYSIS:

1. Fluid overload
2. Hyperkalemia
3. Severe acidosis
4. Metabolic encephalopathy
5. Pericarditis
6. Coagulopathy
7. Refractory GUSx
8. Drug toxicity.

_____________________________________________________________________________________

Acute or sudden illness

Examples of acute conditions where dialysis may be used include:

Metabolic acidosis or a change of the blood pH to acidic. Usually, this condition can be treated by neutralizing the acidic blood
with sodium bicarbonate. However, dialysis may be needed in cases where this is impractical or if there is a risk of fluid overload.

Electrolyte imbalance such as severe hyperkalemia where the blood level of potassium is raised.

Overload of fluid in the body that diuretics cannot relieve.

Acute poisoning where the harmful substance can be removed by dialysis. Lithium, a drug used to treat mood disorders and the
pain reliever aspirin are two examples of drugs that can be removed using dialysis

Uremia - Certain complications of the condition uremia where urea and other waste material builds up in the blood. Such
complications include pericarditis (inflammation of the pericardium in the heart), encephalopathy or a disease affecting brain
function and gastrointestinal tract bleeding.

Chronic or long-term illness

 Renal failure where symptoms are manifesting

 In the case of a lowered glomerular filtration rate (GFR) that has dropped to less than 10-15 mls/min/1.73m2, although in
diabetics dialysis is started before this stage is reached.
 In cases of low GFR where medication is unable to control fluid overload and rising levels of serum potassium or
phosphorus.

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TURP
Q2-a) what are the indications, preoperative assessment, perioperative management of TURP
b) What is TURP syndrome?
e) What are the major complications associated with TURP? How you manage?

Ans a) INDICATIONS FOR TURP:

1. Moderate to severe lower urinary tract symptoms (LUTS) in patients who do not respond to
medical therapy (BPH)
2. Persistent gross hematuria
3. Recurrent UTI’s
4. Renal insufficiency
5. Bladder stone
6. Prostatic carcinoma
 TURP technique always selected for Pts  prostate volume <40-50 of alternative
technique used if  prostate volume >80 ml
 Long standing enlarged prostate  impaired renal function

PREOPERATIVE ASSESSMENT:
1. Assess renal impairment
2. Pts mostly elderly with co-existing diseases, e.g. IHD, HTN, DM, COPD
3. Uncontrolled heart failure pts are at ↑ risk due to intraoperative fluid absorption
4. Assess mental state and communication.GCS
5. Blood should be cross matched and available for anemic pts and pts with large glands.
6. Mortality rate of TURP is 0.2-6%
7. Common causes of death  MI, pulmonary edema and renal failure

TECHNIQUE:
1. Spinal anesthesia OR Epidural anesthesia
2. G.A. (if pt. is very obese or H/O reflux disease)

R.A ↓ incidence of post opera ve venous thrombosis

Also less likely to mask and sign and symptom of TURP syndrome or bladder perforation

OBTURATOR REFLEX: Regional anesthesia does not abolish this reflex

External rotation and adduction of thigh secondary to stimulation of obturator nerve by electrocautery
current through lateral bladder wall.
This reflex (muscle contraction) is only reliably blocked only by muscle paralysis during general
anesthesia.

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INTRAOP MANAGEMENT:
1) Large I.V cannula 14 & 16G and warmed IV fluids
2) Blood loss difficult to assess can be assessed clinically or calculated by measuring Hb of
discarded irrigation fluid.
3) Blood loss and size and wt of gland excised, the duration of resection and expertise of surgeon
4) Antibiotic coverage (Gram –ve coverage)
5) Obturator refluxes need to convert R.A to G.A
6) Start fluid therapy with crystalloids. Due to absorption of irrigation fluid do not give excessive
volume.
7) Use colloid if there is hypotension
8) Never use dextrose.
9) Transfuse blood if required
10) Hypothermia due to large volume of irrigation fluid absorption ↑ ambient temperature of OR
and warm fluids.
11) Risk for complication ↑ with resec on me> 1hr.

POST OP MANAGEMENT:
1. Send FBC, Cr and electrolytes.
2. Discomfort from catheter or bladder spasm.
3. Continue bladder irrigation for 24 hours clot retention can give distended and painful bladder.
4. Good analgesia.
5. Observe for bleeding.

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TURP SYNDROME:
Ans b) TURP syndrome
Definition: systemic absorption of irrigating fluid >2L during TURP due to opening of extensive venous
sinuses in the prostate can cause S & S commonly referred to as TURP syndrome.

Manifestation:
1. Hyponatremia
2. Hypoosmolality
3. Fluid overload. (CHF, pulmonary edema, hypotension)
4. Hemolysis.
5. Solute toxicity (hyperglycemia, hyperammonemia (glycine)
Hyperglycemia (sorbitol), intravascular volume expansion (mannitol)

 Presentation: This syndrome presents intraoperatively or postoperatively as headache, restlessness,

confusion, cyanosis, dyspnea, arrhythmias, hypotension or seizures could be rapidly FATAL.
 Irrigation Fluid:
-Electrolyte solutions avoided  Disperse electrocautery current.
-Water provides excellent visibility  RBC lysis and water intoxication reserved for tumors only (due to
significant absorption)
-For TURP, slightly hypotonic, nonelectrolyte irrigating solutions such as glycine 1.5% (230 mOsm/L) or
as mixture of sorbitol 2.7% and mannitol 0.54% are most commonly used.
-Less common solution are sorbitol 3.3% mannitol 3%, dextrose 2.5-4%, and urea 1%.
-High irrigation pressure ↑solute and fluid absorption.
-Absorption of irrigation fluid dependent on duration of resection as well as height (pressure) of
irrigation fluid 40cm
-Most resections lasts 45-60 min and on average 20ml /min fluid absorbed
-Pulmonary congestion or pulmonary edema  pts with limited cardiac reserves
-Hypotonicity  hyponatremia + Hypoosmolality serious neurological manifestation
-Sx of hyponatremia when < 120 mEq/L. Na < 100  acute intravascular hemolysis
-Solute toxicity  hyperglycemia  glycine (inhibitory neurotransmitter)
In CNS  Transient blindness following TURP

Ideal Irrigation Fluid:

1. Non conductive
2. Non hemolytic
3. Neutral density
4. Clear-view

Treatment:
1. Absorbed water must be eliminated.
2. Hypoxemia and hypoperfusion must be avoided.

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Dr. Tariq Mahar
 3. Managed with fluid restriction and loop diuretics.
4. Symptomatic hyponatremia resulting in seizures or coma should be treated with hypertonic
saline.
5. Seizures  midazolam, diazepam, STP or phenytoin.
6. ETT+IPPV  to prevent aspiration until pts mental status normalizes
7. Hypertonic saline should give @ a rate not faster than 100ml /hr.

Ans. C) MAJOR COMPLICATIONS OF TURP:

1. Hemorrhage
2. TURP syndrome
3. Hypothermia.
4. Bladder perforation
5. DIC
6. Septicemia

MANAGEMENT OF COMPLICATIONS:
1. HYPONATREMIA:
S&S: appears when Na+ < 120mEq/L
If Na+ <100mEq/L acute intravascular hemolysis
Rx: early recognition
Based on severity of Dx
1. Absorbed water must be eliminated.
2. Hypoxemia and hypoperfusion avoided.
3. Fluid restriction
4. Loop diuretics
5. Hypertonic saline 3%, if < 100mEq/L
6. Seizures midazolam, diazepam or phenytoin
7. ETT+IPPVto prevent aspiration (Until GCS normal)
8. Admit to ICU/HDU for Na+ monitoring

2. HYPOTHERMIA:
Heat loss to large irrigation fluid (cold)
Temperature fall 1Co /hr.
Rx- warm irrigation fluid + ↑ ambient temp of OT

3. BLADDER PERFORATION:
S & S: 1. sudden unexplained hypotension. 2. Abdominal pain. 3. Bradycardia (Vagal stimulation)
Rx-Surgical intervention

4. SEPSIS:
Prophylactic antibiotics
1. Gentamicin 2. Cefazolin 3. Levofloxacin

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5. DIC:
Release of thromboplastin form prostate into circulation during surgery, Dilutional thrombocytopenia
due to absorption of irrigation fluid
S/S: Diffuse uncontrollable bleeding, confirm by lab investigation.
Rx fibrinolysis  amino capric acid
FFP, cryoprecipitate,
Tranexamic acid

MONITORING IN TURP
1. ECG lead II, V5
2. NIBP
3. PA catheter (if LVSD/PAH)
4. CVP
5. Temperature
6. ETCO2 (in GA)
7. Pulse Oximetry
8. Mental Status
9. Blood loss.

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OLIGURIA/ARF

DEFINITIONS:
-OLIGURIA: Reduced urine production (<0.5mL/kg/hr)
-ARF: Deterioration of renal function over hours/days that results in failure to excrete nitrogenous waste
products.
PRESENTATION: May present as polyuria, oliguria or anuria
CLASSIFICATION: According to site of lesion: Pre-renal, Renal or Post-renal.

IMMEDIATE MANAGEMENT:
1. Hourly U/O measurement via urinary catheter.
2. Exclude blocked catheter by flushing within 50 ml saline via bladder syringe
3. Maintain normovolemia:
a. Fluid challenge 250-500 ml bolus in 15 min.
b. CVP @ 10-15 cm H2O
4. Maintain BP @ normal levels (MAP > 70)
5. Treat life threatening electrolyte disturbance. (Hyperkalemia > 6.5)
6. Stop nephrotoxic drugs.
7. Consider mannitol or furosemide to promote some diuresis.
8. Refer to nephrologists for further management of ARF
9. Refer to urologist for urinary obstruction.
10. Suprapubic catheter or percutaneous nephrostomy may be needed.

INVESTIGATIONS: FBC, UCE, coagulation screen, creatine kinase, ABG’s, urinary Na+, osmolality.

RISK FACTORS:
1. Pre-existing chronic renal dx (acute on chronic RF)
2. Renal trauma
3. Tumor
4. BPH
5. Hypotension
6. Hypovolemia
7. Dehydration
8. Nephrotoxins (antibiotics, contrast agents, NSAID, ACE inhibitors, myoglobin)
9. Sepsis
10. DM, HTN, PIH, HF, crush injury
11. Prolonged surgery, CABG.
12. Consider pre-loading with saline for pts @ risk of renal failure

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UNCONTROLLED HTN

Q. 4) A 59yr old man with recent onset of HTN is scheduled for reconstruction of stenotic left renal
artery.
His preoperative BP is 180/110
a. What is the cause & pathophysiology of this man’s HTN?
b. How diagnosis is made and which pts benefit from surgery?
c. What anti HTN drugs used to control perioperative BP?
d. What intraop and postop considerations important for anesthetist?

Ans a)
CAUSE: The case of this man’s HTN is renovascular disease which is surgically correctable form (sudden
onset)

PATHOPHYSIOLOGY: Atheromatous plaque in renal artery causes obstruction to kidney perfusion which
release renin increasing circulation angiotensin II and aldosterone resulting in peripheral vascular
constrictions and Na+ retention.
This results in marked systemic arterial hypertension

Ans b)
DIAGNOSIS: The most sensitive diagnostic screening test is MRA (magnetic resonance angiography) of
renal artery others include renal scan or Doppler ultrasound of renal arteries.
Definitive diagnosis  radiocontrast renal arteriography

Treatment:
 Percutaneous balloon angioplasty with stenting done @ the same time OR
Surgery: Patient with renal artery stenosis with a plasma renin activity ratio on the two sides is >1.5: 1
have a greater than 90% cure rate following surgery.

Ans c)
ANTIHYPERTENSIVE AGENTS:
1. Ace inhibitors e.g. enalapril at only IV agent.
2. Angiotensin II antagonists.
3. β-Blockers e.g. metoprolol, esmolol.
4. Centrally acting agents e.g. clonidine, methyldopa.

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Ans d)
INTRAOPERATIVE CONSIDERATIONS:
1. Major procedure with potential of large blood loss, fluid shift and hemodynamic changes.
2. An extensive retroperitoneal dissection necessitates large volume of IV fluid replacements
3. Lager bore IV access is mandatory.
4. Heparinization contributes to ↑ blood loss.
5. Monitoring with A-line, CVP, and PA catheter mandatory
6. U/O should be monitored carefully.
7. Generous hydration with solute diuresis with mannitol recommended
8. Fenoldopam to control hypertension intraoperatively
9. Topical cooling of affected kidney during anesthesia required.

POSTOPERATIVE CONSIDERATIONS:
1. Close hemodynamic monitoring.
2. Mostly pts have CAD & ↑ mortality if MI so monitor ECG.

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 GERIATRICS
Age related physiological changes:
CVS: GI FUNCTIONS:
1. ↓Arterial elas city 1. ↓ Hepatic function
2. ↑A er load 2. ↓ Hepa c blood flow
3. ↑SBP 3. ↓ Biotransformation
4. LVH 4. ↓ Albumin production
5. ↓Adrenergic ac vity 5. ↓ Plasma cholinesterase
6. ↓Res ng HR.
6. ↑ Gastric Ph
7. ↓Baroreceptor reflex
8. ↓Ability to ↑HR in response 7. Prolonged gastric emptying
9. ↓Hypovolaemia, hypotension& hypoxia
NERVOUS SYSTEM:
RENAL: 1. ↓ Brain mass
1. ↓ Renal Blood flow 2. ↓Neurons
2. ↓ GFR 3. CBF ↓
3. ↓ Renal tubular fx 4. ↓ Dopaminergic receptors
4. Impaired Na handling. 5. ↑threshold for all sensory modali es. (Including
5. ↓ concentra ng& diluting capacity. touch, temp., sensation, hearing,
6. ↓ Drug excretion proprioception)
7. ↓ Renin-aldosterone responsiveness 6. ↓dose of LA & GA drugs
+
8. Impaired K excretion. 7. ↓ Cogni ve func ons
8. Short term memory effect
RESPIRATORY: 9. Postoperative cognitive dysfunction (acute
1. ↓ Pulmonary elasticity. confusional state, delirium)
2. ↓ Alveolar surface area
3. ↑ Residual volume MUSCULOSKELETAL:
4. ↑ Closing capacity 1. Skeletal muscle atrophy
5. ↑ V/Q mismatching 2. NMJ thickness
6. ↓ PaO2 3. Skin atrophy
7. ↑ Chest wall rigidity. 4. Frial veins
8. ↓ Cough 5. Arthritic joints
9. ↓ Vital capacity. 6. Limited movements
10. Blunted response to hypoxia/Hypercapnia.

METABOLIC AND ENDOCRINE:

1. ↓Wt
2. ↓Basal and maximal O2 consumption
3. ↓ Heat production
4. ↑ Heat loss
5. ↑ Insulin resistance
6. ↓ Response to β blockers
7. ↑Circulating norepinephrine levels

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 Neuromuscular disease:
MYASTHENIA GRAVIS:

 MG is characterized by weakness and easy fatigability of skeletal muscle and is classified

according to whether pt has only ocular or ocular and non-ocular
ocular muscle weakness
weakness.
 It is caused by autoimmune destruction
d or inactivation of postsynaptic
stsynaptic acetylcholine receptors
at NMJ. (Neuromuscular junction)
 Highest in women during their 3rd decade.
 IgG antibodies found in 85--90% patients with generalized MG and 50-70% 70% with ocular MG
 Associated with thymic hyperplasia and thymoma 65% and other autoimmune disorders
(hypothyroidism,
hypothyroidism, hyperthyroidism and rheumatoid arthritis) are also present in 10% of patients.
 The course of disease is marked by Exacerbations and remissions (partial or complete)
complete).
 Ocular muscles are most commonly affected fluctuating ptosis and diplopia
 If bulbar involvement  laryngeal and pharyngeal muscle weakness, dysarthria, difficulty in
chewing and swallowing and pulmonary aspiration
 Muscle le strength improves with rest but deteriorates with exertion.
 Rx Anti cholinesterase drugs must commonly be used to treat muscle weakness of
pyridostigmine  excessive administration  cholinergic crisis (↑ ↑ weakness, saliv
salivation,
diarrhea, meiosis, bradycardia)
 Edrophonium test is diagnostic.
diagnostic
 Moderate to severe disease
disease combination of anticholinesterase & immunomodulating therapy.
 Plasmapheresis
lasmapheresis is reserved for Patients
Patients with dysphagia or respiratory failure and to normalize
muscle strength preoperatively.
preoperati
 Thymectomy improves the clinical condition.

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MYASTHENIA GRAVIS
ANESTHETIC CONCERNS OF MYASTHENIA GRAVIS:

AIM: To maintain excellent muscle strength preoperatively.

Preoperative consideration:

1. Preoperative evaluation should focus on recent course of disease muscle groups affected,
optimal drug therapy and co-existing illnesses.
2. Optimize the condition aggressively with preoperative IV immunoglobulin and Plasmapheresis.
3. Pts with respiratory muscles or bulbar involvement are @ ↑risk of aspira on
4. Premedication with metoclopramide or H2 receptor blocker ↓risk of aspira on
5. Premedication with opioids, benzodiazepines is usually omitted.

INTRAOP CONCERNS:

1. Avoid NMBA’S if possible  if necessary Cisatracurium or Mivacurium.

2. A volatile agent based anesthetic is most satisfactory.
3. NMBA should be monitored very closely with a nerve stimulator.

POSTOP CONCEERNS:

1. These pts are @greatest risk of post operative respiratory failure so ventilator functions should
be evaluated carefully before extubation.
2. Disease duration of more than 6 years, concomitant pulmonary disease, a peak inspiratory
pressure of < -25 cmH2O (ie, -20 cm H2O), a vital capacity < 4ml /kg, and a pyridostigmine dose
>750 mg/dl are predictive of the need of postoperative ventilation following Thymectomy
3. Anticholinesterase drugs should be restarted when pt resumes oral intake
4. ↑ weakness in last trimester of pregnancy and early postpartum period
5. Epidural anesthesia is preferable. Because it avoids respiratory problems and NMBA use during
GA.

GOALS: Major goal include preventing pulmonary aspiration, avoiding excessive respiratory depression
avoiding NMBA and avoiding agents known to trigger malignant hyperthermia.

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 DAY CASE ANESTHESIA
Q.

a) What are the advantages and disadvantages of ambulatory surgery?

b) What are pt selection criteria for ambulatory surgery?
c) What are the common surgical procedures done as day care?

Ans.
a.)
ADVANTAGES OF DAY CASE SURGERY:
1. Cost effective.
2. Same day discharge
3. Minimal hospital stay
4. Minimum risk of nosocomial infection and DVT
5. Minimum use of drugs
6. Early ambulation.

DISADVANTAGES: (Children)
1. Behavioral problems.
2. Separation from parents or family.
3. Alteration of sleep pattern
4. Bed wetting
5. PONV
6. Delayed bleeding
7. Pain.

Ans.
b.)“PATIENT SELECTION CRITERIA FOR DAYCASE”
1. ASA II and medically stable ASA III.
2. Age >52 weeks post conceptual age > 6 month no upper age limit.
3. BMI <35 if > 35 discuss with anesthetic team.
4. Generally healthy (can climb 2 Heights of stairs).
5. Short procedure <60 min with no risk of pain, bleeding and prolong immobilization.
6. Should be exerted by a responsible adult.
7. Suitable home conditions with adequate toilet and telephone facilities
8. Should live within 1 hour travelling distance from hospital.

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Ans.

c.) SURGICAL PROCEDURES COMMON IN DAY CASE:

1. Gynecology:
D&C, Laparoscopy, Vaginal TOP, Colposcopy, Hysteroscopy

2. Plastic Surgery:
Dupuytren’s Contracture release, Nerve decompression (Carpal tunnel release)

3. Eye:
Strabismus correction, cataract, EUA

4. ENT:
Adenoidectomy, tonsillectomy, myringotomy, insertion of Grommet, FB removal, polyp removal,
SMR

5. Urology:
Cystoscopy, circumcision, vasectomy

6. Orthopedics:
Arthroscopies, carpal tunnel release, ganglion removal, bunion operation, removal of metal
wire.

7. General Surgery:
Breast lump, hernia, varicose veins, endoscopy, laparoscopic cholecystectomy,
hemorrhoidectomy, anal fissurectomy

8. Pediatrics:
Circumcision, orchidopexy, squint, dental extractions

Discharge criteria:
1. Stable vital sign.
2. Fully awake and oriented
3. Able to eat and drink.
4. Passed urine.
5. Ambulant.
6. Pain and nausea well controlled.
7. At least 1 hr wait postoperatively is a sensible condition of discharge
8. minimal bleeding or wound drainage

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Hypothermia, Acidosis and Coagulopathy  Lethal triad of death

TRAUMA
Q.1) 60 yrs old male, RTA, breathless, C/O severe excruciating pain on Rt. Side of chest O/E: Paradoxical
breathing, pulse 140 bpm, B.P. 90/60 mmHg, SpO2 80% on air

a) Likely diagnosis?
b) Investigations?
c) Management?

Ans
a. Diagnosis: Pneumothorax secondary to flail chest (Rib #)

b. Investigations:
1. CXR
2. ABG’s
3. ECG
4. FBC/UCE’s
5. CT/MRI chest
6. ECHO
7. FAST scan (focused assessment with sonography for trauma)

c. Management:
1. Primary survey
2. Resuscitation
3. Secondary survey
4. Tertiary survey.

1) PRIMARY SURVEY: (ABCDE)

A. Airway: Establishing and maintaining an airway is always the first priority with Manual Inline
Stabilization (MILS)
Tracheal intubation if: GCS < 8 failed BLS, respiratory failure and maxillary #.
B. Breathing: Assessment of ventilation by look, listen and feel approach. Rule out immediate
life threatening chest injures e.g.: Tension Pneumothorax, hemothorax, cardiac tamponade
etc
C. Circulation: 1st priority in restoring adequate circulation is to stop bleeding, 2nd priority 
fluid resuscitation.
D. Disability: Rapid neurological assessment by AVPU system. Awake, verbal response, painful
response, unresponsive.
E. Exposure: Pt should be undressed to allow examination for injuries

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2) RESUSCITATION:
-High flow 100% Oxygen.
-Take two large bore IV cannulas.
-Arterial line
-Send blood for FBC and UCE’s and order CXR
-ABG’s
-Start warm IV fluids (crystalloids, colloids or blood)
-Exclude tension pneumothorax  if suspected then perform needle decompression
(2ndintercostals space, mid-clavicular line) followed by chest drain.

RESUSCITATION GOALS:
Parameter Goal
BP SBP >80, MAP 50-60
HR <120
SpO2 >95%
U/O 0.5ml/kg/hr
Mental status Following commands accurately
Lactate level < 1.6 mmlol/L
Base deficit >-5
Hb. > 8.0g/dl

SECONDARY AND TERTIARY SERVEY:

3) Secondary survey:
A more detailed head to toe examination after ABC stabilization, aimed at identifying other non life
threatening injuries.
-Planning for further laboratory and radiographic studies including FAST scan
-Forming a workable differential diagnosis e.g.
For chest injury
1. Simple or tension pneumothorax.
2. Hemothorax
3. Multiple rib # i.e flail chest
4. Pulmonary contusion
5. Non-life threatening blunt myocardial injury.

4) TERTIARY SURVEY: Patient’s evaluation that identifies all injuries after initial resuscitation and
operative interventions.
-It typically occurs within 24 hours of injuries.
-It consists of another head-to-toe examination.
-Review of all laboratory and imaging studies.

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CLINICAL INDICES OF SHOCK
Q. 2) Young male with severe multiple injures is brought to ER
a) How you will assess preoperatively?
b) Give clinical indices for blood loss?
c) What are the hazards of full stomach?

Ans a)
Primary/ Secondary survey

Ans b) CLINICAL INDICES FOR BLOOD LOSS (SHOCK):

Pathophysiology Clinical Manifestation

a. Mild ↓Peripheral perfusion of organs Feeling cold, postural
(<20% of blood lost) able to withstand prolong hypotension, tachycardia, cool,
ischemia (skin, fat, muscle and pale, moist, skin, collapsed neck
bone) Plt-normal veins, concentrated urine.
b. Moderate ↓Central perfusion of organs Thirst, supine hypotension,
(20-40% of blood lost) able to tolerate only brief tachycardia, oliguria, anuria.
ischemia (liver, gut, kidneys)
Metabolic acidosis present.
c. Severe ↓Perfusion of heart and brain, Agitation, confusion or
(>40% of blood lost) severe metabolic acidosis, obtundation, supine
possible respiratory acidosis. hypotension, tachycardia, rapid
deep respiration.

Ans c.) HAZARDS OF FULL STOMACH:

1. ↑Chances of regurgita on of stomach contents (PPV) aspiration pneumonitis.

2. N&V
3. ↑intragastric pressure
4. ↓LES tone
5. Respiratory Obstruction
6. Hypoxemia
7. V/Q mismatch
8. Shunting.

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BLUNT CHEST INJURY
Q.3)
a) What harmful effects can occur due to blunt chest injury?
b) What will be the clinical and diagnostic features?
c) Enumerate your steps of management for each?

Ans )
a. Trauma to chest may severely compromise function of heart or lung, leading to cardiogenic shock or
hypoxemia.
Following can occur after blunt chest injury:
1. Simple pneumothorax
2. Tension pneumothorax
3. Multiple rib fractures (flail chest)
4. Hemothorax
5. Pulmonary contusion
6. Cardiac tamponade
7. Myocardial contusion
8. Aortic rupture
9. Oesophageal rupture
10. Diaphragmatic rupture
11. Tracheobronchial injury.

Ans b & c)

1-SIMPLE PNEUMOTHORAX:
S&S: ↓ or absent breath sounds, hypoxemia, hypotension and tachycardia, hyperresonant on
percussion, hypercarbia.
Diagnosis:  CXR shows ipsilateral lung collapse or hyperlucent lung.
Management: 
1. Initial assessment with primary, surveys
2. Wound closure with aseptic technique.
3. Chest tube with under water seal in 4th or 5th intercostal space, anterior to mid axillary line.

2.-TENSION PNEUMOTHORAX:
S&S:Ipsilateral absence of breath sounds, hyperresonance to percussion, contralateral tracheal shift,
distended neck veins, hypoxemia, hypotension and tachycardia
Diagnosis:  CXR shows ipsilateral lung completely collapsed, mediastinum and trachea shifted to
contralateral side.
Management:
1. Initial primary survey and resuscitation
2. Immediate insertion of 14 G over the needle catheter into 2nd intercostal space @ midclavicular line.
This will convert a tension pneumothorax to a simple pneumothorax.
3. Chest tube placement is definitive treatment.

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3-PULMONARY CONTUSION:
S&S:  Seat belt bruising, hypoxemia, ↓RSBI PaO2/FiO2 < 300, flail chest
Diagnosis: CXR shows patchy infiltrates
Management: 
1. Primary and secondary survey
2. Depending upon level of oxygenation  ↑FiO2 CPAP TI & PPV (small TV & PIP < 30
cmsH2O)

4-MYOCARDIAL CONTUSION: Associated with sternal #

S&S: Arrhythmias, ST changes, ↑CKMB, ↑ Troponin, ↑ CVP in hypotension is the earliest indica on.
Diagnosis: Echo is diagnostic
Management:
1. Primary and secondary surveys
2. Shift to ICU/mechanical ventilation.
3. Inotropic support with dobutamine.

5-CARDIAC TEMPONADE: life threatening chest injury.

S&S: Neck vein distension, hypotension and muffled heart sound (BECK’S TRIAD)
Pulsus paradoxus ( > 10mmHg ↓ in BP during spontaneous inspira on, and a high index of suspicious
Diagnosis: FAST scan or ECHO  if not available  presence of BECKS TRAIAD
Management:
1. Primary survey
2. Pericardiocentesis for temporary relief
3. Definitive treatment is thoracotomy.

6-BLUNT AORTIC INJURY

S&S: hypotension, multiple injuries, pseudocoarctation
Diagnosis:
1. Spiral CT
2. TEE
3. Supine CXR shows (wide mediastinum, pleural capping,
Lt Hemothorax, tracheal deviated to RP, depression of Lt Mainstem bronchus, loss of aortic knob
and # thoracic spine)

Management:
1. SBP> 80 mmHg to prevent further deterioration
2. Surgical intervention.

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7-OESOPHAGIAL RUPTURE:
S&S: Severe chest and abdominal pain gastric contents in chest drain.
Diagnosis:  Contrast study or endoscopy.
Management: Urgent surgery otherwise mediastinitis (↑↑ mortality)

8-DIAPHRAGMATIC RUPTURE:
S&S:  75% on Lt Side. Stomach and colon herniate into chest  Strangulation further complication.
↓ Breath sounds, respiratory distress, hypoxemia, chest and abdominal pain
Diagnosis: CXR shows elevated hemidiaphragm, gas bubbles above it, mediastinum shifts to opposite
side, NG in chest.
Management:
1. Stabilize
2. Surgical repair.

9-TRACHEOBRONCHIAL INJURY
S&S:  Hoarseness, subcutaneous emphysema and palpable crepitus, Total airway obstruction, severe
respiratory distress Intubation or Tracheostomy
Diagnosis: CT scan shows transection of trachea /bronchus, pneumothorax, bronchopulmonary
fistula, massive mediastinal and cervical emphysema.
Management: Urgent Repair via thoracotomy.

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BLUNT ABDOMINAL TRAUMA
Q.4 25 years male brought to ER  beaten with stick and had multiple blow to abdomen and chest. HR-
135, BP-70/50, R/R35, vomited multiple times and looks pale Hb-7.5g/dl. Surgeon decided for
exploratory laparotomy

a) Name commonly injured organs in blunt abdominal trauma?

b) What procedure is performed in ER to rule out internal abdominal bleed?
c) What premedication you will advise?
d) Describe your induction and maintenance with justification of drugs

Ans.
a. Commonly injured organs in blunt abdominal trauma
are: Liver, Spleen, Kidney and Gut

b. FAST scan OR abdominal CT

Diagnostic peritoneal lavage (DPL)  Presence of >10ml of blood is indication for Exp.
Laparotomy.

c. Premedication:
-Aspiration prophylaxis:
H2 receptor prophylaxis: Ranitidine
Proton Pump inhibitor e.g.: Omeprazole.
Prokinetic drug e.g.: Metoclopramide
Blood transfusion if needed.
-Antibiotic prophylaxis.

d. Induction and maintenance:

1. Two large bore IV cannula and invasive BP monitoring.
CVP will be preferable (to monitor volume status).
2. Adequate IV fluids (crystalloids, colloids) must be warm.
3. Blood should be in hand (cross-matches)
4. RSI with cricoid pressure because of full stomach.
5. STP, propofol or etomidate according to condition.
Use ketamine if marked hypotension and CV instability.
6. Suxa for rapid onset of NM blocked and quick intubation as pt is assumed full stomach.
7. Standard ETT and IPPV anesthesia
8. Avoid N2O gaseous distension and PONV.
9. Maintain with isoflurane and atracurium and opioids
10. NG or OG if basilar skull #
11. Vasopressors like ephedrine if refractory hypotension.
12. Give antibiotics.

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 13. If unresponsive to vasopressors, inotropes should be started if septic then 1st line agent is
norepinephrine otherwise epinephrine
14. Vasopressin is a useful 2nd line agent vasoconstrictor.
15. Steroids could be useful specially if adrenal failure
16. High inflation pressures due to abdominal distension and pulmonary edema/ARDS.
17. Aim for TV 6ml/kg, PEEP 5-10, peak airway pressure < 30, allow some CO2 retention if necessary
18. Postop ICU/HDU.
19. Good analgesia
20. Supplemental O2 for 3 days by nasal/ face mask.

EXTREMITY TRAUMA
Q.5.) 20 years old boy after a motorbike accident # both femurs
There is no injury. Fully conscious, HR-140, BP-110/70
Trauma surgeon wants both limbs to be operated asap.
a. List anesthetic considerations and problems of this pt.
b. How will you manage these problems?
c. Give your choice of anesthesia and justify?

Ans
a. Anesthetic consideration:
1. NPO status
2. Hydration status
3. Chest radiograph
4. Cervical stability.
5. Concealed hemorrhage
6. Coagulation profile
7. Fat embolism syndrome
8. Compartment syndrome
9. Infection
10. Rhabdomyolysis
11. Renal failure
12. Post of hypothermia and shivering
13. Risk of pulmonary aspiration.

b. Management:
1. Aspiration prophylaxis Ranitidine, Metoclopramide, Na citrate.
2. Warm IV fluids to ↓ hypothermia.
3. Exclude any thoracic injury by CXR
4. Manual inline stabilization (MILS) if cervical instability.
5. Blood, platelets and FFP’s should be arranged for occult blood loss
6. Proceed for operation ASAP (D/W surgeon) to ↓ risk of fat emboli.
7. Antibiotics prophylaxis for infections

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 8. Avoid local anesthetics as they mask the cardinal signs of compartmental syndrome.
9. If compartmental syndrome diagnosed by clinical sighs then early fasciotomy to save the
limb is required.

c. Choice of anesthesia:
 Choice will be GA with RSI and cricoid pressure because NPO status is not known so we have to
secure airway form aspiration.
 As femoral # is associated with 2-3 liters of occult blood loss and this pt had bilateral fracture so
there is much greater chance of hemodynamic instability intraoperatively so GA will be the
definite choice.
 There is also ↑ chance of coagulopathy because of large blood loss due to bilateral femur #.
 Risk of fat embolism is also increased.

-Revised Trauma Score:

Coded value GCS SBP (mmHg) R/R(bpm)

0 3 0 0
1 4-5 <50 >5
2 6-8 50-75 5-9
3 9-12 76-90 >30
4 13-15 >90 10-3

If RTS is < 11  transport to trauma center.

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 APACHEE II
Trauma & injury severity score (TRISS)
Sequential organ failure assessment (SOFA)
TRAUMA SCORING
Q.6. a) What is trauma scoring?
b) Briefly outline the major scoring system?

TRAUMA SORE:

Ans. a)
 Trauma score is a simple physiological measure of injury severity.
 Trauma scoring should be simple, quick to perform and appropriate for use in the fields.
 The aim is for triage and prediction of outcome

Ans b) One of the most common trauma scoring system is prehospital index.
PHI is a triage-oriented trauma severity scoring systems, comprising of 4 components.
1. Systolic blood pressure
2. Pulse
3. Respiratory status
4. Level of consciousness.

PREHOSPITAL INDEX
Condition Score
SBP in mmHg
>100 0
86-100 1
75-85 2
<75 5
Pulse b/min
>120 0
51-120 3
<50 5
Respiratory status b/min
Normal 0
Labored /shallow 3
<10 5
Level of consciousness
Normal 0
Confused 3
No intelligible words 5

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BONE CEMENT (BCIS)Polymethylmethacrylate (PMMA)
Def.: CVS collapse in response to insertion of polymethylmethacrylate cement during hip arthroplasty
procedures.

Clinical manifestations:
1. Hypoxia
2. Hypotension
3. Dysrhythmias
4. Pulmonary HTN
5. ↓ CO
6. Cardiac arrest
-Emboli most frequently occur during insertion of femoral prosthesis.
-Emboli could be of air, fat, bone marrow and bone debris.

Management:
1. 100% Oxygen prior to cementing.
2. Maintain normovolemia by monitoring CVP
3. Vasopressors and inotropes if needed
4. Creating a vent hole in distal femur to relieve intramedullary pressure.
5. High pressure lavage of femoral shaft to remove debris.
6. By using un-cemented femoral components.

Disadvantage:
Gradual loosening of the prosthesis
Resulting from breakage of small pieces of cement over the year

Cementless implants: Made of porous material that allows the natural bone to grow into them.
Lasts longer and advantageous for younger and active pts cementless implants requires healthy active
bone formation therefore cemented implants still preferred for elderly > 80 year cementless implants
could be of metal, plastic or ceramic.

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PNEUMATIC TOURNIQUETS:
USE: Pneumatic tourniquets on the upper or lower extremity, creates a bloodless field that greatly
facilitate the surgery.

POTENTIAL PROBLEMS:
1. Hemodynamic changes
2. Pain
3. Metabolic alterations
4. Arterial thromboembolism
5. Pulmonary embolism transient muscle dysfunction.
6. Permanent peripheral nerve injury
7. Rhabdomyolysis
8. ↑body temperature in paediatric pts.

Tourniquet pain:
1. Unmyelinated slow-conduction C fibers resistant to local anesthetic block plays a critical role.
2. Pain gradually becomes so severe over time that patient may require supplemental analgesia, if
not GA, despite a regional block that is adequate for surgical incision
3. During GA pain manifested as marked HTN, ↑HR and diaphoresis
4. Cuff deflation causes ↓CVP, ↓BP, ↑HR, ↓temperature, ↑PCO2, ↑ETCO2, ↑serum lactate and
↑serum K+ levels.
5. These metabolic alterations cause ↑ in minute ven la on in spontaneously breathing pa ent
and rarely dysrhythmias.

Contraindication:
Significant calcific arterial disease
Marked HTN, tachycardia, diaphoresis,
Can be sued safely in sickle cell disease
Inflate 100mmHg above systolic B.P Not > 2 hrs.

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FAT EMBOLISM SYNDROME
FES classically presents within 72 hours following long bone or pelvic fractures
FES is a triad of dyspnea, confusion and petechiae
FES can also be seen after CPR, parenteral feeding, lipid infusion and liposuction.

DIAGNOSIS: Petechiae on chest, upper extremities, axilla and conjunctiva. Fat globules may found in
retina, urin and sputum.
CXR  normal  diffuse patchy pulmonary infiltrates

SIGNS DURING GA: ↓ETCO2, ↓SPO2, ↑PA pressures.

TREATMENT: 2 fold prophylactic and supportive

1. Prophylactic: Rx  Early stabilization of the #.
2. Supportive  O2 with CPAP ventilation.
High dose corticosteroids  presence of cerebral edema

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 MAX 6U/hr or GIK Regimen
Albertie regime:
DM 10% Dextrose/ 10U Insuline/ 10 meq KCL

RISK DURING ANESTHESIA:

CVS:-IHD, MI, atherosclerosis, HTN, CVA, cardiomyopathy, HTN, CVA, cardiomyopathy, HTN,
D.Nephropathy, autonomic neuropathy (interferes with control of breathing e.g. GA off delayed gastric
emptying.

AIMS: Avoid hypoglycemia perioperatively

Maintain euglycemia
Correct acid base and electrolyte abnormalities.
Prevents and correct dehydrations and associated ketoacidosis

DKA: Life threatening complication of DM characterized by tachypnea, acute abdomen, N&V and
changes in sensorium. Kussmaul breathing triggered by infection (glycosuria and ketonuria)

Rx: Correcting hypovolemia, hypokalemia and hyperglycemia several liters of N/S + insulin infusion

HONKC: Life threatening complication of DM, characterized by dehydration, hyperosmolality,

Altered mental status and scizor, Non ketoacidosis
Rx Fluid resuscitation with N/S, insulin and K+

Signs of diabetic auto neuropathy

1. HTN
2. Ischemia (Painless)
3. Orthostatic hypoperfusion
4. Resting tachycardia
5. Early satiety.
6. Lack of swatting
7. Impotence
8. Lack of heart rat variably
9. Reduced heart rate with response to atropine and propranolol
10. Neurogenic bladder

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 Neurosurgery:
FACTORS REGULATING CBF
Q1. A 35 years old man falls from moving truck suffers head injury.
He is in coma, hemodynamically stable. Scheduled for craniotomy
a. Enumerate various factors that regulate CBF?
b. Outline your initial pre-operative management?
c. How will you control ICP during induction?
d. The surgeon complains of ‘tight brain intraoperatively what measures you will take?
e. What will be your choice of intraoperative fluid give reason?

Ans a) FACTORS AFFECTING CBF: (Regulating)

 Cerebral blood flow varies with metabolic activity.
Most commonly measured with isotope e.g. xenon (133Xe) and newer technique, positron emission
tomography (PET).
 Total CBF in adult average 750 ml/min (15-20% of Cardiac output)
Factors
1. Cerebral perfusion pressure (CPP) Xenon is a chemical element with
Is the difference b/w MAP and ICP or CVP symbol Xe and atomic number 54. It is a
colorless, dense, odorless noble gas found in the
CPP= MAP – ICP or CVP Earth's atmosphere in trace

CPP is normally 80-100mmHg

Moderate to severe ↑ in ICP (>30mmHg) significantly compromise CPP and CBF
CPP < 50mmHg shows slowing on EEG.
CPP b/w 25 and 40mmHg  Flat EEG
CPP < 25 irreversible brain damage

2. Autoregulation: Brain tolerates wide swings in blood pressure with little or no change in blood flow
↓ CPP cerebral vasodilation
↑CPP  cerebral vasoconstriction
In healthy individuals CBF remains constant b/w MAP of about 60-160mmHg. Beyond this limit blood
flow becomes pressure dependent.
Pressure above 150-160mmHg disrupts BBB  cerebral edema & hemorrhage CBF 750 ml/min (15-20% CO)
CPP  80-100mmHg
3. Respiratory gas tension: ICP < 10
ICHTN > 15
CBF x Pa CO2 b/w tension of 20-80 mmHg
Sever hypoxemia PaO2< 50 profoundly ↑CBF

4. Temperature: CBF changes 5-7% per 1oC change in temperature

Hypothermia  ↓ CMR & CBF, Hyperthermia  ↑CMR & CBF
CMR ↓ by 50% if temperature of brain falls by 10Co
Above 42oC Oxygen activity begins to ↓ and may reflect cell damage

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5. Viscosity: ↓Hct↓ viscosity  ↑CBF but impairs O2 delivery
↑Hct ↑ viscosity  ↓CBF (polycythemia)
Hematocrit 30% optimal cerebral oxygen delivery

6. Autonomic influences: ↑sympathetic stimulation  vasoconstriction  ↓CBF.

-autonomic innervation play an important role in cerebral vasospasm following brain injury and stroke

MANAGENENT IN HEAD INJURY

Ans b) PREOPERATIVE MANAGEMENT IN HEAD INJURY:

1. Ensure the patency of airway, adequacy of ventilation and oxygenation and correction of
hypotension in ER
2. Simultaneous neurological evaluation by GCS and CNS examination
3. GCS score of 8 or less associated with 35% mortality
4. Airway obstruction and hypoventilation are common
5. Hypoxemia  supplemental oxygen.
6. Assumed cervical spine injury  In line stabilization should be used during airway manipulation
to maintain head in neutral position
7. Pts. with obvious hypoventilation, absent gag reflex, or persistent GCS < 8 requires tracheal
intubation and hyperventilation
8. All pts should be regarded as full stomach so RSI with cricoid pressure
9. Adverse effects of intubation on ICP are blunted by prior administration of STP 2-4 mg/kg or
propofol and rapid onset NMBA.
10. Suxamethonium ↑ ICP so Rocuronium or mivacurium is suitable.
11. If difficult intubation anticipated awake intubation, fiber optictechnique or tracheostomy may
be necessary.
12. Blind nasal intubation is contraindicated in basilar skull # suggested by CSF rhinorrhea or
otorrhea, hemotympanum or ecchymosis into periorbital tissues (Raccoon sign) or behind the
ear (battle’s sign)
13. In pt with head trauma, correction of hypotension and control of bleeding is priority before any
radiographic studies and definitive neurosurgical treatment
14. Fluid resuscitation with colloid and blood prevent brain edema.
15. Vasopressor if severe hypotensive
16. Glucose-containing or hypotonic solution should not be used
17. Hematocrit should be maintained above 30%
18. Invasive monitoring of arterial line, CVP or PA monitoring and ICP are valuable
19. Pt should be stabilized prior to any CT or angiographic studies
20. If neurological deterioration before surgery consider mannitol
21. Ventriculostomy or subdural bolt for ICP monitoring

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 Cushing Phenomenon:
↑BP, ↑ICP, ↓HR

INTRAOPERATIVE MANAGEMENT IN HEAD INJURY:

1. A barbiturate – Opioid – N2O – NMBA technique is commonly used
2. N2O should be avoided when air is entrapped within cranium and during hypotension – Head
elevated to 15-30o
3. Surgical stimulation  ↑ BP  ↑ ICP – tight brain associated with Bradycardia (Cushing
phenomenon)
Ventriculostomy advantage  Removal of CSF to ↓ ICP.
4. Tight brain treated with additional doses of induction agent, ↑concentra on of inhala onal
agents (deep anesthesia)
Antihypertensive e.g. β-blocker if HTN with tachycardia
Hyperventilation but avoid PCO2< 30
Stop any vasodilator until dura is opened
Atropine or glycopyrrolate if excessive vagal tone
5. Extubation depends on severity of injury, Comorbids and preop GCS.
6. Young pts. Conscious preoperatively may be extubated after removal of localized lesion whereas
pts. with diffuse brain injury remain intubated

POSTOP MANAGEMENT:
1. Persistent ICHTN requires continued paralysis, sedation
Hyperventilation and a barbiturate infusion postoperatively
2. Post op ICU/ITU.
3. DIC –Rx platelets, FFP, cryoprecipitate
4. ARDS-mechanical ventilation(Apply PEEP only if ICP monitored)
5. Diabetes insipidus if injury to pituitary stalk, desmopressin
6. GI hemorrhage  due to stress ulceration

PREOP MANAGEMENT IN ELECTIVE CRANIOTOMY

AIM: to maintain ICP within normal limits
1. Presences or absence of intracranial HTN.
2. CT and MRI should be reviewed for cerebral edema
3. Examination includes neurological assessment documenting mental status and any existing
sensory or motor deficits.
4. Medications reviewed specially corticosteroids, diuretics and anticonvulsants.
5. Investigations for electrolytes and hyperglycemia. Anticonvulsant levels. Premedication best
avoided if IC HTN suspected.
Normal ICP  Benzodiazepine (diazepam or midazolam)
Corticosteroids and anticonvulsants continue till surgery

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 Total CSF Volume 150ml
CSF Production 21ml/h (500ml/day)

INTRACRANIAL HYPERTENSION
Q.2. a.) What is intra-cranial hypertension?
b.) What are the different methods used to assess ICP?
c.) How will you treat intracranial hypertension?

Ans a) INTRACRANIAL HYPERTENSION

A sustained increase in ICP above 15mmHg is called intracranial hypertension.

Causes:
1. Expanding tissue or fluid mass.
2. Depressed skull fracture.
3. Interference with normal absorption of CSF
4. Excessive CBF or
5. Systemic disturbances promoting brain edema.

S&S:
1. Headache
2. N&V
3. Papilledema
4. Focal neurological deficits
5. Altered consciousness.

Ans b.) METHODS TO ASSESS ICP:

Definition ICP: Supratentorial CSF pressure measured in the lateral ventricles or over the cerebral cortex
and is normally 10mmHg or less.
These are three methods to assess or monitor ICP:
1. Intraventricular catheter most accurate method
Ventriculostomy is done by NS, a burr hole is drilled in skull @ lateral ventricle. ICP can be
lowered by draining CSF through it.
2. Subdural screw inserted through a hole drilled in the skull. Its sensors record pressure from
inside the subdural space.
3. Epidural sensor less invasive than other methods.
Usually done when there is severe head injury/CNS disease. High ICP can be treated by draining
CSF through catheter.

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Ans c.) TREATMENT OF INTRACRANIAL HYPERTENSION:

Ideal treatment is directed @ underlying cause.

1. Correct metabolic disturbances.

2. Vasogenic edema particularly that associated with tumors respond to corticosteroids
(dexamethasone)  promote BBB repair
3. Fluid restriction
4. Osmotic agents –mannitol
5. Loop diuretics –furosemide
6. Moderate hyperventilation (PaCO2 30-33)  ↓CBF  ↓ ICP
7. Mannitol excellent in rapidly decreasing ICP.
-Principal disadvantage is a transient ↑ in intravascular volume
-Mannitol should not be used in intracranial aneurysm, arteriovenous malformations or
intracranial hemorrhage until cranium is opened

BRAIN HERNIATION: Sustained elevations in ICP can lead to catastrophic herniation of brain.
Herniation may occur at any one of the following four sites:

1. Cingulate gyrus.
2. Uncinate gyrus
3. Cerebellar tonsils
4. Any area beneath a defect in skull (Transcalvarial).

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ECT
Q3.) What will be your anesthetic management of patient with psychiatric illness for ECT?

Ans ) GOAL: The goal of ECT is to produce a therapeutic generalized seizure 30-60 sec in duration and air
way maintenance.

MANAGEMENT:
1. G.A is routinely used for ECT to ensure amnesia and neuromuscular blockade to prevent injuries
2. Anesthesiologist must present for airway management and cardiovascular monitoring.
3. Amnesia is required for only brief period (1-5 min)
4. Only a short acting induction agent with anticonvulsant, properties needed e.g. barbiturates,
benzodiazepine or propofol.
5. Seizure threshold is increased and seizure duration ↓by these agents.
6. Following adequate preoxygenation, methohexital 0.5-1 mg /kg is most commonly used.
Propofol 1-1.5mg/kg is alternative.
7. Alfentanil 10-25mg/kg is a useful adjunct.
8. NM blockade achieved by Suxamethonium 0.25-0.5mg/kg.
9. Controlled mask ventilation using a self-inflating bag device or anesthesia circle system required
until spontaneous respiration resumes.
10. Hyperventilation and caffeine ↑seizure dura on without increasing electrical s mula on.
11. Standard monitoring + ECG
12. Premedication with glycopyrrolate prevent profuse secretion associated with seizure and to
attenuate bradycardia

Physiological effects of ECT:

1. Immediate parasympathetic stimulation Bradycardia and hypotension for 15 sec followed by
prolog 5 min sympathetic stimulation  ↑HR, HTN, Dysrhythmias, ↑ myocardial O2 demand.

Absolute contraindications:
1. Recent MI < 3 month
2. Recurrent stroke < 3 month
3. Intra cranial mass
4. ICP
5. DHF
6. Pheochromocytoma
7. IC aneurysm

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POSTERIOR FOSSA SURGERY
Q4. What is the Rx of venous air embolism?

Craniotomy for a mass in posterior fossa presents potential problems:

1. Obstructive hydrocephalus  CSF obstruction  ↑ICP ventriculostomy.
2. Brainstem injury  vital circulatory and respiratory centers and CN and nuclei
3. Positioning mostly prone or modified lateral. Sitting position (some surgery)
4. Pneumocephalus due to sitting position.
5. Venous air embolism  highest in sitting position

VENOUS AIR EMBOLISM

Definition: Entry of air into pulmonary arterial circulation through open veins or sinuses.

Presentation: Immediate fall in ETCO2 and SpO2 ↑ end dal nitrogen

Air entry noted by surgeon and detection of air bubbles with precordial Doppler ultrasonography or TEE

Treatment:
1. Inform surgeon
2. ABC & 100% O2
3. Stop N2O if in use
4. Flood area with saline /cover wound with wet swabs
5. Raise venous pressure  elevate legs, compress neck veins
6. Attempt to aspirate air from CVP line
7. Head down, left lateral position  limits air flow in pulmonary circulation
8. Standard resuscitation  fluids, vasopressor, inotropes
9. IV dexamethasone 8mg.

Monitors: Capnograph, ET nitrogen, ABG, precordial Doppler ultrasonography or ETT.

Paradoxical air embolism: Air into arterial circulation. Results in stroke or coronary artery occlusion

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CSF
Q. 5
a) What are the cases of BBB disruptions?
b) Where CSF is formed and what are its major functions?
c) Write down CSF flow tract?

Ans )
a. CAUSES OF BBB DISRUPTION:
1. Severe hypertension
2. Tumors
3. Trauma
4. Strokes
5. Infections
6. Marked hypercapnia
7. Hypoxia
8. Sustained seizure activity.

b. CEREBROSPINAL FLUID:
Formation: most of the CSF is formed by choroid plexus of cerebral ventricles (mainly lateral)
(Involves active Na+ secretion) in adults normal total CSF production is 21ml/h (500ml/day) yet
total CSF volume at any time is 150ml.

Function: It major function is to protect the CNS against trauma (safety Cushion)
↓CSF produc on:
1. Acetazolamide
2. Corticosteroids
3. Frusemide
4. Spironolactone
5. Isoflurane
6. Vasoconstrictors.

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 c. CSF FLOW TRACT:
1. Choroid
id plexus of lateral ventricles
2. Foramen of monro
3. Third ventricle
4. Cerebral aqueduct of sylvius
5. 4th ventricle
6. Foramen of magendie and foramen
forame of luschka
7. Cerebellomedullary
medullary cistern (cisterna magna)
8. Subarachnoid space
9. Circulating in brain and spinal cord
10. Arachnoid granulations over cerebral hemispheres
11. Cerebral venous sinuses.

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GB SYNDROME:
Q.6) Write down the signs, symptoms, diagnosis and treatment of acute idiopathic polyneuropathy (G.B.
Syndrome)
Hyporeflexia is the condition of below normal or absent reflexes
Areflexia. It can be tested for by using a reflex hammer. It is the
opposite of a condition called hyperreflexia.

Ans ) Signs And Symptoms:

1. Ascending motor paralysis (sudden onset) Paresthesia: An abnormal sensation, typically tingling or pricking
2. Areflexia (‘pins and needles’), caused chiefly by pressure on or damage to
peripheral nerves.
3. Paresthesia.
4. Respiratory muscle paralysis if bulbar involvement.
5. Initial revival respiratory or GI infections.

Diagnosis:
Sudden onset of ascending motor paralysis, areflexia and paresthesia followed by viral respiratory or GI
infections

Complications: Sepsis, ARDS, Pulmonary Embolism or Cardiac Arrest.

Treatment:
1. Plasmapheresis
2. Immunoglobulin therapy.

Anesthetic considerations:
1. Aspiration is a risk (pharyngeal and intercostal muscle weakness)
2. Exaggerated hypertensive or hypotensive response
3. Intra-arterial monitoring  wide swings in BP
4. Suxamethonium contra indicated  Hyperkalemia
5. Pancuronium avoided  Autonomic effects.
6. Postoperative ventilation  Respiratory muscle weakness.

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 st
Mount Vernon formula  colloid 0.5ml/kg /1%burn given at 4hrs interval for 1 12 hours, then @ 6hr interval for next 12hrs.
Brook formula  colloid 0.5 ml/kg+ crystalloid 1.5 ml/kg

BURNS
Q.) A 40 years old male had 30% thermal burns 3 days ago. He is now scheduled for excision and grafting
under GA, he is fully conscious,
BP 140/85 and HR 110/min, he has a dry cough.
A. How are the burns classified?
B. What are the important points as regard preoperative evaluation of this pt?
C. How will you assess hemodynamic status in this patient?

ANS A) CLASSIFICATION OF BURNS

Burns are classified according to the % of BSA involved and the depth of skin destroyed
1. First-degree burns  limited to epithelium
2. Second-degree burns extends into dermis
3. Third degree burns  destroy the entire skin thickness. (pain less)

Major thermal burns is considered to be a second-degree burns involving at least 25% BSA or a third
degree burn of at least 10% of the BSA (Body Surface Are)
Electrical burns are more serious than superficial inspection would indicate because of underlying tissue
damage.

ANS B) PREOPERATIVE EVALUATION

As this patient has a dry cough, the pulmonary function can be directly and indirectly affected.
1. Direct inhalational injury is usually limited to upper airway edema that can lead to life
threatening airway obstruction
2. Direct inhalational injury to lower airways could be due to smoke and toxic products of
combustions.
3. Deactivation of surfactant can lead to atelectasis and pulmonary shunting.

Fluid Regimens:
1. Measure wt.
2. Estimate % are of burn ‘rule of 9’ for adult and rule of 10 for children
3. Proceed with regimen if > 15% in adults and > 10% in children
4. Parkland formula 1st 24hr =(B. Wt. x %burn x 4) R/L - 5% in first 24 h
5. Muir and Barclay formula 4hourly requirement = (wt x % Burn X 0.5) 4 hourly.

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Dr. Tariq Mahar
 4. Indication of inhalation Injury include stridor, hoarseness, facial burns, singed nasal hair or
eyebrows, soot in sputum or in oropharynx and respiratory distress or history of combustion in a
closed space.
5. Major Burns after pulmonary function even in the absence of direct lung injury, such as
pulmonary edema and ARDS.
6. Circumferential burns of thorax ↓chest wall compliance and further ↑peak inspiratory
pressures.
7. CO inhalation shifts ODC to left ↓ Oxyhaemoglobin saturation treated with 100% oxygen
(hyperbaric O2 can be used).
8. Cyanide toxicity occurs after plastic burns  hyperbaric oxygen
(Normal blood cyanide level is <0.2μg/ml)

ANS C) ASSESSMENT OF HAEMODYNAMIC STATUS:

1. Large fluid shift from plasma to interstitial space causes ↓intravascular volume which is most
pronounced in 1st 24 hours replaced with crystalloids e.g. R/L 2-4 ml/kg / % BSA burned
2. CO decreases  due to ↓plasma volume.
3. Monitoring of urine output indicates perfusion of vital organs
4. If volume replacement does not provide adequate dieresis 1ml/kg/hr than inotropic support
with renal dose dopamine may be beneficial
5. After 24 -48 hrs. BP & HR are typically elevated due to high output failure (due high level of
circulatory catecholamine)

Electrolyte disturbances in burned pt:

1. Hyperkalemia followed by Hypokalemia. Electrical burns myoglobinuria renal failure.
2. Monitor: ECG, A. line, CVP, PAC, temperature, pulse oximetry.
3. Indications for early intubation :
a. Hypoxia
b. Upper airway edema
c. Presence of copious secretions.
4. Succinylcholine is contraindicated in burn patients after 1st 24 hours ↑ K+Cardiac arrest.
Up to 1-2 years

The Parkland formula is mathematically expressed as:

where mass is in kilograms (kg), area as a percentage of total body surface area, and volume is in milliliters
(mL). For example, a person weighing 75 kg with burns to 20% of his or her body surface area would require
4 x 75 x 20 = 6,000 mL of fluid replacement within 24 hours. The first half of this amount is delivered within 8
hours from the burn incident, and the remaining fluid is delivered in the next 16 hours.[4]
The burn percentage in adults can be estimated by applying the Wallace rule of nines (see total body surface
area): 9% for each arm, 18% for each leg, 18% for the front of the torso, 18% for the back of the torso, and
9% for the head and 1% for the perineum

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 REGIONAL ANESTHESIA
LUMBAR VERTEBRA

SOMATIC BLOCKADE:
Sensory blockade interrupts both somatic and visceral painful stimuli, whereas motor blockade produces
skeletal muscle relaxation.
DIFFERENTIAL BLOCKADE: Typically results in sympathetic blockade (judged by temp sensitivity) that
may be two segments higher than sensory block (pain, light touch) which in turn is usually two segment
higher than motor blockade.

AUTONOMIC BLOCKADE: Interruption of efferent autonomic transmission at the spinal nerve roots can
produce sympathetic and some parasympathetic blockade

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SPINAL ANESTHESIA
Q1

a. What are the advantages and disadvantages of spinal anesthesia compared to G.A?
b. What are the indications, absolute and relative contraindications?
c. What drug will you prefer for spinal anesthesia? Give reasons

Ans

a. Advantages of S.A over G.A

1. The metabolic stress response to surgery and anesthesia is reduced by SAB
2. Particularly in hip surgery (elective) there may be up to a 20-30% ↓ blood loss
3. SAB ↓ incidence of venous thromboembolic complications by as much as 50%
4. Pulmonary compromise appears to be less
5. ETT is avoided – no hypertensive response to intubation and laryngoscopy
6. Mental status can be followed
7. No regurgitation in full stomach
8. Early mobilization
9. Early return of gut motility
10. Patient’s satisfaction
11. Cost effective

For disadvantages, contraindications,

drugs see Gynae. and Obs. page

Indications:
1. Lower abdominal surgeries
2. Inguinal
3. Urogenital
4. Pelvic and perineal
5. Lower extremity
6. Lumbar spinal surgery
7. Orthopedics
8. Obstetrics

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Dr. Tariq Mahar
EPIDURAL ANESTHESIA
Produce analgesia by blocking conduction intradural spinal verve roots

INDICATIONS:
1. Operative anesthesia Hip & knee surgery, amputation
2. Obstetric anesthesia Labour & delivery
3. Post-operative pain control
4. Chronic pain management
5. Caudal anesthesia in children for post op pain

ADVANTAGES OF EPIDURAL VS G.A

1. Avoidance of airway manipulations
2. Useful for asthmatic
3. Useful for known difficult airways.
4. Pts with full stomach – no regurgitation
5. ↓stress response  ↓hypertension and tachycardia
6. Less venous thromboembolism  proven benefit in hip surgery
7. Improve bowel motility
8. Awake pt. during procedure – desirable for C-sections and arthroscopic
9. Less postop N&V and sedation
10. Better post op control of pain by continuous epidural analgesia specially in thoracic, upper
abdominal and orthopedic procedures
11. Less pulmonary complications due to pain control and no airway manipulation
12. Early mobilization, less recovery room time.

DISADVANTAGES OF EPIDURAL VS GA
1. Slower in onset (10-20min)
2. High failure rate – less reliable
3. Contraindications like coagulopathy, haemodynamic instability, spinal instrumentation and pt.
refusal

ADVANTAGES OF EPIDURAL OVER SPINAL

1. Epidural anesthesia can produce segmental block focused only on the area of surgery or pain
e.g. during labour
2. Gradual onset of sympathetic block allows time to manage hypotensive
3. Epidural anesthesia duration can be prolonged by re-dosing through an indwelling epidural
catheter
4. More flexibility in the density of block e.g. if less motor blockade is required as in labor analgesia
or postop pain - ↓LA can be used
5. Less chances of dural puncture  ↓PDPH

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Dr. Tariq Mahar
DISADVANTAGES OF EPIDURAL OVER SPINAL
1. Onset is slower
2. ↑ chance of LA toxicity because large amount of LA used and if a vein is entered with needle or
catheter
3. Less reliable, not as dense as spinal and could be patchy or one-sided

CONTRAINDICATIONS TO EPIDURAL
Absolute: Relative:
1. Pt. refusal 1. ↑ ICP
2. Sepsis with hemodynamic instability 2. Prior back injury with neurological
3. Uncorrected hypovolemia deficit
4. Coagulopathy 3. Neurological disease such Multiple
5. Clopidogrel Sclerosis
4. Chronic back pain
5. Localized infection @ injection site

COMPLICATIONS OF EPIDURAL
1. Hypotension fluid preload and pt.’s position
2. Inadvertent intravascular injection of LA aspirate for blood, test dose
3. Subarachnoid injection of large volume of LA  total spinal aspirate CSF
4. PDPH  Positional Headache analgesics, caffeine, blood patch
5. Epidural hematomas almost always coagulopathy  CT or MRI surgical decompression
16-18G tuohy needle 8cms long
TECHNIQUE FOR LUMBAR EPIDURAL:
1. Resuscitation equipment must be immediately available.
2. Good IV access and give appropriate fluid preload to prevent hypotension
3. Give sedation if necessary
4. Sitting or left lateral position
5. Choose the desired interspace e.g. L4-L5 and palpate
6. All aseptic measures should be taken and make a skin wheal
7. Epidural needle inserted in midline through skin wheal until increased resistance of ligaments
felt (Ligamentum Flavum)
8. Now remove the stylet and attach a syringe with 3-4ml of air or saline
9. Advance few millimeters inside with tapping of syringe intermittently, Ligamentum flavum
produce a marked ↑ in resistance and is the last layer before epidural space.
10. After passing Ligamentum flavum a ‘pop’ or ‘give’ is felt and loss of resistance makes syringe
inject easily
11. The syringe is removed &threads the catheter about 5cm into space
12. The epidural needle is withdrawn carefully without dislodgement of the catheter. Attach an
injector port to catheter
13. Aspirate it for blood or CSF, if negative give test dose 2ml
14. Catheter is then tapped in place
SOLUTION FOR DIFFERENT EPIDURAL BLOCKADE
Placebo  Saline
Sympatholytics  0.5 % lidocaine 219
Dr. Tariq Mahar Somatic  1% lidocaine
All fibres  2% lidocaine
COMBINED SPINAL-EPIDURAL CSE
TECHNIQUE:
For a CSE anesthesia, a long spinal needle is inserted through an epidural needle that has been placed in
ES and dura is punctured. When CSF is obtained from spinal needle, dose of LA e.g. Bupivacaine is given.
Remove spinal needle and then epidural catheter is threaded into epidural space. Now remove epidural
needle and attach injector port

ADVANTAGE:
1. Fast onset of an intense spinal block so that the surgery can proceed quickly
2. Epidural catheter do extend the duration of block for prolong surgical procedures.
3. For post operative pain management

COMBINED EPIDURAL-GENERAL (CEG):

ADVANTAGES
1. Useful in intra thoracic or upper abdominal procedure which needed controlled ventilation and
excellent intraoperative postoperative pain relief
2. Early postoperative mobilization to prevent pulmonary and thromboembolic complications
3. By using epidural catheter intraoperatively, ↓GA drugs required which results in fewer
↓hemodynamic effects and faster awakening
4. At the same time airway is protected, ventilation is controlled and hypnosis and amnesia
provided.

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 PERIPHERAL NERVE BLOCKS
INTERSCALENE BLOCK
CONTRAINDICATIONS TO PNB
1. Uncooperative patient / children
2. Bleeding diathesis
3. Infection
4. Local anesthetic toxicity
5. Peripheral neuropathy

Differential diagnosis IB
1. Anxiety
2. Ipsilateral phrenic nerve block
3. Pneumothorax
4. Cervical epidural anesthesia
5. Dural sleeve  S.A

INTERSCALENE BRACHIAL PLEXUS BLOCK

Indication: Most optimal for procedures on shoulder, arm and forearm. Produce a block that is most
intense at C5-C7 dermatomes and last intense in C8 –T1 dermatomes.

Technique: Palpation of interscalene groove when pt. supine and head rotated 30o contralateral side. Ex
JV crosses interscalene groove @ level of cricoid cartilage. After skin wheal with 25G needle @ level of
cricoid cartilage, a 22G needle introduced perpendicularly to skin and advanced slightly medially and
caudally until paresthesia or evoked contraction in arm elicited. Successful when response noted in
deltoid or pectoralis muscle
A total of 30-40ml LA injected
For procedures like total shoulder arthroplasty, catheters may be inserted and kept in place for postop
pain control

Complications:
1. Incidental blockade of stellate ganglion, phrenic nerve or recurrent laryngeal nerve (Respiratory
failure). Display Horner’s syndrome, dyspnea and hoarseness respectively
2. ↑ risk of intra-arterial (vertebral artery) injection produce seizure
3. Inadvertent epidural, subarachnoid or subdural injection
4. Puncture of pleura and pneumothorax

Immediate onset of dyspnea  inadvertent spinal anesthesia

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AXILLARY BLOCK
INDICATION: Most common approach to brachial plexus block provides an excellent block for
procedures distal to elbow.

TECHNIQUE: Most commonly performed by one of the several technique that use axillary arterial pulse
as a starting point

1. Transarterial
2. Paresthesia
3. Nerve stimulators
4. Ultrasound
5. Perivascular infiltration  Performed by injecting local anesthetic in a ring around axillary a.
Patient is positioned supine with arm abducted and the elbow flexed @ 90o and externally
rotated @ shoulder leaving the arm lying across the pt’s head

Transarterial technique: The pulse of axillary artery identified as high in the axilla as possible.
Using “immobile needle “technique a 22G needle is inserted until bright red blood is aspirated.
Needle is then slightly advanced or withdrawn until blood aspiration ceases. LA can be injected
posteriorly, anteriorly or in both locations. Total of 40ml LA injected. Distal pressure on sheath
during injection promote cephalad spread

Complications:
1. Intravascular injection
2. Postoperative neuropathies
3. Hematoma
4. Infection

BIER BLOCK (IVRA)

Q.a) how is anesthesia produced by IVRA technique?
b) What are the complications? How can these be avoided?

Ans.
a. Bier’s Block also called intravenous regional anesthesia most commonly used for wrist and hand
surgery such as carpal tunnel release, trigger finger release and ganglion resection.
Bier’s block works by local anesthetic diffusion form IV space to nerve fibers in the vicinity of veins.
Duration is 90 min. High patient satisfaction and allows rapid discharge of patient.

TECHNIQUE: Secure IV access to the limb that is to be anesthetized. IV access in the opposite limb for
administration of fluids and medications, IV line must be as distal as possible and usually in the back of
hand. A double tourniquet is placed around the upper arm. The arm is exsanguinated by elevating and
wrapping it tightly with wide elastic band (Esmarch)

The distal then proximal tourniquet is then inflated to 250mmHg Esmarch removed, distal tourniquet
cuff is then deflated and 40-50ml of 0.5% lidocaine injected. Anesthesia sets within minutes and
surgical procedure might begin. 222
Dr. Tariq Mahar
Ans.
b. COMPLICATIONS:
1. LOCAL ANESTHETIC TOXICITY: will happen if injected LA rapidly enters the central circulation.
This only happens if tourniquets cuff are purposefully or accidently deflated. Anesthetist should
have immediate access to tourniquet tubing and pressuring device. Tubing should be secured
and situated to avoid any accidental disconnection
2. Perioral numbness
3. Metallic taste
4. Ringing in ears
5. Seizures tourniquet should be slowly and repeatedly deflated and re-inflated.
6. Agitation
7. Tearfulness.

ANKLE BLOCK

Indications: Procedures on distal foot.

5 nerves supply sensation to the foot
1. Saphenous nerve
2. Deep peroneal nerve
3. Superficial peroneal nerve
4. Posterior tibial nerve
5. Sural nerve

Technique: Ring like field distribution around ankle and directed @ 5 nerves innervating the foot
- Deep perineal, superficial peroneal and saphenous nerve can be blocked by infiltrating LA on a
malleolar level line across the anterior aspect of foot in the apex of groove formed by extensor
hallicuslongus tendon and extensor digitorumlongus tendon 5-8 ml LA on both lateral and
medial sides each
- Tibial nerve block is performed by injecting 5-8 ml LA in a fan like manner posterior to medial
malleolus.
- Sural nerve block performed posterior to lateral malleolus by injecting 5-8 ml LA

Complications: hydrostatic damage to nerves by aggressive injection

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INTERCOSTAL BLOCK
INDICATIONS:

1. Used as supplements to GA
2. Postoperative analgesia following thoracic and upper abdominal surgeries
3. Relief of pain associated with rib #, HZ & cancer

TECHNIQUE: Pt. in the lateral decubitus or supine position

Level of each rib is palpated and marked in mid and posterior axillary line. A skin wheal is raised over the
inferior border at the selected ribs and “walked off” until it steps off the rib inferiorly. The needle
advanced 0.5cms underneath the rib and following a negative aspiration for blood or air, 3-5ml LA is
injected at each level.

COMPLICATIONS:

1. Highest blood level of LA per volume injection of any block in the body  careful aspiration
2. Risk of pneumothorax – CXR

PENILE BLOCK
INDICATIONS: Penile surgery or postoperative pain relief
Nerve Supply: Pudendal verve  Dorsal nerve of penis bilaterally
Genitofemoral and ilioinguinal  sensation to base of penis
Technique: a fan-shaped (triangular) field block with 10-15ml of LA injected at base of penis blocks the
sensory nerve without risk of vascular injury
If more profound block is needed-dorsal nerve is blocked just lateral to the base of penis bilaterally with
a 25 G needle just penetrating Bucks’ fascia at 10:30 and 1:30o clock positions
1ml of LA is injected on each side without pressure
Epinephrine or other vasoconstrictors should be avoided to prevent end artery spasm and ischemic
injury.

COMPLICATIONS: Intravascular injection.

NERVE IDENTIFICATION
1. Loss of resistance (epidural, Paravertebral)
2. Measured advancement of needle (intercostal, peribulbar)
3. Relation to arterial pulsation/ transfixion (femoral, brachial plexus)
4. Paraesthesia
5. Percutaneous electrical stimulation (commonest)
6. Ultrasound guided

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BRACHIAL PLEXUS:

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FLUID AND ELECTROLYTES DISTURBANCE
Q. 1) what is the physiological response to rapid loss of 1liter blood in an adult?

Ans.1) PHYSIOLOGICAL RESPONSE:

↓ Blood volume  ↓venous return  ↓ RA pressure  ↓ CO  ↓ systolic BP ↓ pulse pressure
COMPENSATORY MECHANISM:
1. Baroreceptor  ↓firing  ↑HR
Vasoconstriction
↑adrenaline secre ons
2. Atrial receptors: ADH secretion (Water retention)
(Stretch receptors) Aldosterone release (Na retention)
Dilutional anemia  water transfers from
ECF to circulation
3. Carotid receptors: ↑ Respiratory Rate.
OTHER SIGNS:
Cold peripheries, Pallor, Cyanosis and ↑ Capillary refill me > 2 Sec.
_____________________________________________________________________________________
Q.2) How will you assess and calculate daily fluid requirement of 70 kg adult male, vomiting since 2 days
Ans 2) assessment and calculation of daily fluid requirement
[Daily maintenance requirement 2640]
Replace
1. Pre-existing fluid deficit (NPO, sweating, vomit)
2. Normal Losses (maintenance fluid)
3. Surgical losses (blood, insensible loss)
Maintenance fluid:
1st 10Kg  4ml /kg/h
Next 10 Kg  add 2ml/kg/h
Next 1 Kg  add 1ml/kg/h
(Maintenance loss include urine output, GI losses, sweat, insensible losses form skin and lungs)
Maintenance for 70kg man = 110ml/h
Pre-existing losses = Duration of fast X maintenance fluid
Pre-existing abnormal losses
1. Preop bleeding/vomiting /diarrhea
2. Occult losses (trauma, ascites and infected tissues)
3. ↑ sensible losses (↑ R/R, fever swea ng)
Daily fluid requirement = Maintenance X 24 h
=110 X 24
=2640ml+792ml+729ml (vomiting since 2 days)
50% (1320ml) should be given in 1st hour
25% each (660) should be given in subsequent hours
Pyrexia ↑fluid requirement by 15% for every 1oC above (n)
As this pt is vomiting since 2 days  30% increase in volume should be given

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Q 3) Describe briefly the methods of assessment of fluid and blood loss during surgery and criteria for
replacement?

Ans 1)
1. Clinical assessment
2. Assessment of intravascular volume by:
a. Physical examination (most reliable preoperatively)
b. Investigations
c. Maintenance loss  Body wt 4:2:1 formula.
70kg=110ml/hr
d. NPO loss  Maintenance fluid X hours of fasting
(Deficit) 110 X 8 (assume) = 880ml
1st hour – 50% (440ml)
2nd hour – 25% (220ml)
3rd hour – 25% (220ml)
e. Blood loss  Visual assessment
-Suction container/ Irrigation fluid
-Laparotomy pads – 150ml
-Surgical swabs 4 X 4 = 10m
-Weight all the swabs
3rd space loss – site of incision – Small  2 - 4ml/h
Medium 4 - 6ml/h
Large  8 - 10ml/h
3. Urine output /h
4. NG aspirate
5. 3rd space loss (internal redistribution of fluids)
Assess haemodynamics: Pulse, BP, CVP, Capillary refill, peripheries, Hb, HCT.
6. Criteria for replacement  allowable blood loss

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MASSIVE TRANSFUSION AND HAZARDS
Q.4) what is massive blood transfusion and its hazards?

Ans.) MASSIVE TRANSFUSION:

Defined as the need to transfuse one to two times the patient blood volume, for most adults that is
equal to 10-20Units.
HAZARDS
1. Dilutional thrombocytopenia
2. DIC
3. Sepsis
4. ALI (Acute Lung Injury)
5. Citrate toxicity
6. Pulmonary edema /circulatory overload
7. Hypothermia  ventricular arrhythmias – V. fib.
8. Embolism
9. Hyperkalemia (1u PRBC  ↑4 mEq K+)
10. Acid-Base disturbances (metabolic alkalosis) as citrate are converted to HCO3 by liver
11. Infections (hep. B,C,HIV, CMV)
12. Immune suppression.

COMPLICATIONS OF BLOOD TRANSFUSION:

1. Acute hemolytic reaction
Chills, Fever, Nausea Awake
Chest and flank pain patient
Hyperthermia, tachycardia,
Hypotension, hemoglobinuria Anesthetized pt.
Diffuse oozing in surgical field
2. Delayed hemolytic reactions
Mild also called extravascular hemolysis.

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Na+ DEFICIT
Q. 5) An 80 kg woman is lethargic and is found to have a plasma Na+ 118 mEq/L. How much NaCl must
be given to raise her plasma Na+ to 130 mEq/L?
HYPONATREMIA:
+ +
Ans.5) Na deficit = TBW X (130-118) Defined as serum Na < 135 mmlol/L
Mild 125 -134
TBW is approximately 50% of body wt. in females
Moderate 120-124
Now: Severe < 120
Na+ deficit = 80 X 0.5 X (130 – 118)
=480 mEq
Now because the 0.9% N/S contains 154 mEq/L
Pt. should receive 480 mEq/154mEq or 3.12 L of N/S.
Correction rate of 0.5mEq/L/hr should be given over 24 hours = 130 ml/h

 Hypertonic saline 3% NaCl is indicated when Na+< 110 mEq/L and should be given continuously as it
can precipitate pulmonary edema, hypokalemia, metabolic acidosis and transient hypotension
1G Na = 43mEq
1G NaCl = 17 mEq
 Hyponatremia presents postoperatively as agitation, confusion or somnolence.

Na+ Excess
Q. 6) A 70kg man is found to have plasma Na+ of 160mEq/L Mild 145-150
Moderate 151-160
What is his water deficit? Severe > 160

Ans. 6) Normal Na+ - 140 mEq/L

TBW in males – 60% of body wt

Normal TBW X 140 = Present TBW X 160

(70 X 0.6) X 140 = Present TBW X 160
Present TBW = 36.75L
Water deficit = Normal TBW - Present TBW
(70 X 0.6) – 36.7 = 5.3L
To replace this deficit over 48 h
Give 5300ml of 5% Dextrose over 48hr. = 110ml/hr.
NON HEMOLYTIC IMMUNE COMPLICATIONS
1. Febrile reactions 8. Hepatitis 15. Syphilis
2. Urticaria 9. AIDS 16. Brucellosis
3. Anaphylaxis 10. CMV 17-Salmonellosis
4. Pulmonary edema 11. EBV 18-Yersinioses
5. Graft VS host disease 12. Malaria 19-Rickettsiosis
6. Purpura 13. Toxoplasmosis
7. Immune suppression 14. Chaga’s disease

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 +
DEFINITION: Normal K 3.5 - 5.5 mEq/L
HYPERKALEMIA Mild 5.5 - 6.0
CLINICAL MANIFESTATIONS: Moderate 6.1 - 7.0
1. Generalized muscle weakness Severe > 7.0
2. Fatigue
3. Paraesthesia
4. N&V & D
5. Dehydration
6. Incidental laboratory findings.
7. ECG changes: Peaked T-waves, widened QRS, prolonged PR intervals, Loss of P-wave, loss of R-
wave amplitude, sine wave pattern and asystole.

CAUSES:
1. ↑intake: -foods high in K+ e.g. banana or K supplements
-Rapid blood transfusion
2. Intercompartmental shift:
Trauma, Burns, Suxamethonium, acidosis, Exercise, Rhabdomyolisis, hypertonicity, malignant
hyperthermia
3. ↓ Excre on:
Renal failure, adrenocortical insufficiency
4. Drugs: K+ sparing diuretics, NSAID’s, β-blocker, digoxin.

INVESTIGATIONS: U&E, Ca+, ABG’s, ECG.

AVOID:
1) R/L (Hartmann’s) 2) Suxamethonium 3) Hypothermia 4) Acidosis (Respiratory)

TREATMENT:
 Cardiac monitoring, IV access
 If hyperkalemia severe or ECG changes are present
1. IV Calcium chloride 3-5ml of 10% in 2minutes or
2. IV Calcium Chloride 10ml of 10% in 2 minutes
3. Insulin 10Units in 50ml 5% Dextrose IV over 30-60min
4. If acidotic  Sodium bicarbonate 50mEq/L
5. Beta-agonist Salbutamol 5 mg nebulized
 Re-check K+ level frequently
 Ion exchange resin – Calcium resonium 15g PO (30g PR) 8hourly (Kayexalate)
 If initial management fails  dialysis or hemofiltration.
 Postpone any elective surgery.
 For life threatening surgery  1st treat hyperkalemia

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HYPOKALEMIA Mild – 3.0- 3.5
Moderate 2.5 – 3.0
CLINICAL MANIFESTATIONS: Severe- 2.5

1. Mostly asymptomatic until K+ < 3

2. Palpitations
3. Muscular weakness
4. Abdominal cramps
5. N & V
6. Arrhythmias
7. Polyuria
8. Respiratory failure
9. ECG changes: Flattening or inversion of T-wave, Prominent U-waves, prolong PR interval

CAUSES:
1. ↓ Intake: -Iatrogenic-- No K+ added to IV fluids
-Malnutrition
2. Renal losses: Renal tubular acidosis, hyperaldosteronism, leukemia, ↓ Mg
3. GI Losses: Diarrhea, vomiting, laxatives, NG suctions, fistula, and pyloric stenosis.
4. Intercompartmental shift: insulin, alkalosis, hypothermia,
5. Drug side effect: Diuretics, Steroids.
6. Beta agonists  salbutamol

TREATMENT:
1. ABC, cardiac monitoring and IV access
2. If severe hypokalemia with cardiac arrhythmias give KCl 20 mEq/hour via a CVP with cardiac
monitoring in HDU/ICU
3. If moderate hypokalemia  40 mEq KCl in 1Litter infuse peripheral
4. Consider oral K+ supplements K-Oxalate
5. Withhold any diuretics
6. Check K+ level regularly
7. Switch any diuretics to K+-sparing diuretics e.g. Spironolactone or amloride

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SICKLE CELL DISEASE
a. What is sickle cell anemia? Give its pathophysiology and causative factors intraoperatively for crisis?
b. Which procedure (maneuver) is contraindicated during limb surgery of sickled pt?
c. Describe your perioperative management?

Ans a)
SICKLE CELL ANEMIA:
Definition: Hereditary hemolytic anemia resulting by formation of abnormal hemoglobin (HbS)
SSA  Both parents have genetic defect (homozygous) HbSS.
SST only one parent has sickle gene (heterozygous) HbAS
All black pts. Should have sickle test preoperatively

PATHOPHYSIOLOGY:
Conditions which favor the formation of deoxyhemoglobin can precipitate sickling in pts with HbSS these
factors include:
 Hypoxia, hypothermia, hyperthermia, dehydration, acidosis, infection, pain, hypertonicity,
↑2,3DPG
 (3) Types of sickle cell crisis due to these factors:
1. Vaso occlusive crisis
2. Aplastic crisis
3. Splenic sequestration crisis

Diagnosis: Hb. electrophoresis

FBC including reticulocyte count (sickle cell, sideroblast, Howell-jolly bodies)
Ans b)
Bier’s block is contraindicated in sickle cell anemia avoid pneumatic tourniquet because this can cause
the following, which can precipitate sickling
 Hemodynamic changes
 Pain
 ↑ body temperature in children
 Metabolic alterations
 Arterial thromboembolism /DVT
 Pulmonary embolism

Pneumatic tourniquets can safely be used in sickle cell anemia by maintaining O2, normocarbia,
hydration and normocarbia, hydration and normothermia

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Ans c)
PERIOPERATIVE MANAGEMENT:
1. Optimize the patient
2. Should be well hydrated
3. Infections should be controlled
4. Hb should be at an acceptable level Preop transfusion if needed
5. Partial exchange transfusion before major surgery recommended
6. Exchange transfusion ↓ses viscosity, ↑O2 carrying capacity and ↓ sickling
7. Avoid conditions that might promote Hb desaturation or low flow state
8. ↑ CO by compensa on should be maintained
9. Mild alkalosis help avoid sickling
10. Avoid pneumatic tourniquets
11. Hypoxemia and pulmonary complications are the major risk factor
12. Supplemental O2, optimal pain control, chest physiotherapy and early ambulation are
desirable to avoid such complications.
_____________________________________________________________________________________

Howell–Jolly bodies are histopathological findings of basophilic nuclear remnants

(clusters of DNA) in circulating erythrocytes. During maturation in the bone marrow
late erythroblasts normally expel their nuclei, but in some cases a small portion of
DNA remains.

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ACID-BASE
BASE DISTURBANCE
ACID-BASE DISORDER
DISORDER PRIMARY CHANGE COMPENSATORY RESPONSE
Respiratory
Acidosis ↓PH ↑PaCO2 ↑HCO3
Alkalosis ↑PH ↓PaCO2 ↓HCO3
Metabolic
Acidosis ↓PH ↓HCO3 ↓PaCO2
Alkalosis ↑PH ↑HCO3 ↑PaCO2

DIAGNOSIS:

PH

Decreased Increased

PCO2 PaCO2

Decreased Increased
Decreased Increased
Respiratory Metabolic
Metabolic Acidosis Respiratory acidosis Alkalosis Alkalosis

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RESPIRATORY ACIDOSIS
Plasma HCO2 ↑ 1mEq/L for 10mmHg ↑ in
Defined as a “Primary increase in PaCO2 ↑
PaCO2 above 40mmHg
CAUSES: Alveolar hypoventilation
1. CNS depression  Drugs, sleep disorder, OHS(Obesity hypoventilation syndrome), Cerebral ischemia and
cerebral trauma
2. Neuromuscular disorders Myopathies and neuropathies.
3. Chest wall abnormalities  flail chest, kyphoscoliosis.
4. Pleural abnormalities  Pneumothorax, pleural effusion.
5. Airway obstruction  FB, Tumor, laryngospasm, asthma, COPD.
6. Parenchymal lung disease pulmonary edema, emboli, pneumonia, aspiration and interstitial
lung disease.
7. Ventilator malfunction ↓ Minute ven la on

Increased CO2 production Treatment

1. Large caloric loads. ↓caloric intake
2. Malignant hyperthermia Dantrolene
3. Shivering Pethidine
4. Prolonged seizures Diazepam
5. Thyroid storm Antithyroids
6. Extensive thermal injury (Burns)

TREATMENT:
1. Increase alveolar ventilation
2. Improve alveolar ventilation can be temporary achieved by lung, bronchodilation, reversal of
narcosis, doxapram, ↑lung compliance by diuretics
3. Indications for mechanical ventilation are moderate to severe acidosis (PH < 7.20), CO2 narcosis,
and impending respiratory muscle fatigue
4. Chronic respiratory acidosis  return PCO2 to pts normal baseline  normalization of PCO2 or
hyperoxia precipitate sever hypoventilation
5. Increased FiO2
6. I/V NaHCO3 if PH < 7.10 and HCO3 < 15

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METABOLIC ACIDOSIS
Primary decrease in HCO3 (Marked hyperventilation Kussmaul’s respiration)
ANION GAP: The difference b/w the major measured cations and major measured anions
Anion gap = Na+- (CL- + HCO-3)
140 - (104 + 24) = 12 mEq/L
Normal range = 7-14 mEq/L
Differential diagnosis of metabolic acidosis is facilitated by calculation of anion gap

CAUSES:
↑ anion gap
1. Renal failure
2. Ketoacidosis (DM or starvation) – replace fluid deficit
3. Nonketotic hyperosmolar coma
4. Alcoholics
5. Lactic acidosis  MI – adequate oxygenation and tissue perfusion
6. In born errors of metabolism
7. Rhabdomyolysis
8. Toxins  salicylate, methanol, ethylene glycol, paraldehyde, sulphur.

Normal anion gap (hyperchloremic)

1. Diarrhea –most common cause
2. Cholestyramine –anion exchange resin
3. Ingestion of CaCl2 and MgCl2
4. Fistulas pancreatic , biliary or small bowl
5. Renal tubular acidosis
6. Carbonic anhydrase inhibitor – acetazolamide
7. Dilutional large amount of HCO3 free fluid
8. TPN Total parenteral nutrition.
9. ↑ intake of chloride containing acids
1. Ammonium chloride
2. Lysine hydrochloride
3. Arginine hydrochloride

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TREATMENT:
1. Treat the cause
2. If arterial blood PH < 7.20  NaHCO3 may be necessary
3. NaHCO3 can be given empirically as a fixed dose (1mEu/kg) derived from calculated bicarbonate
space.
4. Severe acidemia  Controlled ventilation
5. Serial ABG’s are mandatory
6. Profound or refractory acidemia requires acute hemodialysis with a bicarbonate dialysate
7. NaHCO3 in cardiac arrest or low flow states not recomended
8. DKA  Replace existing fluid deficit as well as insulin, K, phosphate and Mg.
9. Lactic acidosis  Restoring adequate oxygenation and tissue perfusion
10. Salicylate poisoning Alkalinization of urine with NaHCO3

BICARBONATE SPACE
Defined as “the volume to which HCO3 will distribute when it is given intravenously”

Calculation:
NaHCO3 = Base deficit X 0.3 X Body wt.
In practice only 50% of the calculated dose is usually given after which another ABG measured.

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RESPIRATORY ALKALOSIS
Primary decrease in PaCO2 (↑ alveolar ven la on)

Plasma HCO3 ↓ 2mEq/L for each 10mmHg acute ↓ in PaCO2 below 40

CAUSES:
Central stimulation:
1. Pain
2. Anxiety
3. Ischemia
4. Stroke
5. Tumor
6. Infection
7. Fever
8. Drugs – salicylates, progesterone (pregnancy) and doxapram

Peripheral stimulation
1. Hypoxemia
2. High altitude
3. Pulmonary dx CHF, Pulmonary edema, embolism, asthma
4. Severe anemia
5. Sepsis
6. Metabolic encephalopathies

Iatrogenic:
Ventilator induced

Treatment:
1. Correction of underlying cause is the only treatment
2. For severe alkalemia PH > 7.60  IV HCL or ammonium chloride

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METABOLIC ALKALOSIS:

Primary increase in plasma HCO2

1. Chloride sensitive  ↓NaCl & ECF depletion.
2. Chloride resistant  Associated with enhanced mineralocorticoid activity

CAUSES:
Chloride sensitive:
1. Gastrointestinal Vomiting, gastric drainage, chloride diarrhea villous anemia
2. Renal  Diuretics, Posthypercapnic, Low chloride intake.
3. Sweat  Cystic fibrosis

Chloride resistant:
1. Primary hyperaldosteronism The presence of alkalemia &
2. Secondary hyperaldosteronism hypokalemia precipitate severe atrial
3. Cushing’s syndrome & ventricular arrythmias
4. Licorice ingestion
5. Barther’s syndrome
6. Severe hypokalemia

Miscellaneous:
1. Massive blood transfusion
2. Acetate containing colloids
3. Alkali therapy
4. Hypercalcemia Milk-alkali syndrome, bone metastasis.
5. Sodium penicillins
6. Glucose feeding after starvation.

TREATMENT:
1. Treat the cause
2. Treatment of choice for chloride sensitive MA NaCl and KCl
3. H2 receptor blocker  if loss of gastric fluid is a factor
4. Acetazolamide  for edematous Pts.
5. Spironolactone  if ↑ mineralocor coid ac vity
6. If PH >7.60  IV HCl or IV ammonium chloride or hemodialysis.

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 POSTANESTHETIC CARE

AIRWAY OBSTRUCTION & COMPLICATIONS

CAUSES OF RESPIRATORY OBSTRUCTION DURING ANAESTHESIA

EQUIPMENT RELATED:
1. Valve malfunction or kinking of breathing system
2. Surgical compression of tracheal tube
3. Occlusion of T.T lumen dueto secretions or blood
4. TT’s cuff herniation or over inflation
5. Esophageal or bronchial intubation

PATIENT RELATED:
1. Soft tissue edema in oropharynx 8.Strictures
2. Secretions 9.Pneumothorax
3. Tumour 10. Bronchospasm
4. Laryngospasm 11. Tracheomalacia.
5. Recurrent laryngeal nerve palsy
6. laryngotracheobronchitis
7. Compression of TT by hematoma, thyroid tumours

MANAGEMENT OF AIRWAY OBSTRUCTION: (In Recovery Room)

 The most common airway complication is partial respiratory obstructions,
 Most commonly due to tongue falling back against posterior pharynx.
 Usually presents as sonorous respiration.
 Total obstruction causes, cessation of air flow, absent breath sounds and paradoxic chest
movements

Management:
1. Supplemental oxygen should be given during corrective measures
2. A combined jaw thrust and head tilt maneuver pulls the tongue forward and opens the airway. An
oral or nasal airway alleviates the problem  exclude equipment failure
3. If above maneuver fails, laryngospasm should be considered, Characterized by high pitched
crowning noises but silent with complete glottic closure.
4. The jaw thrust maneuver particularly combined with gentle positive airway pressure via a tight filling
face mask usually breaks the laryngospasm.
5. Any secretions or blood in hypopharynx should be suctioned to prevent recurrence.
6. Refractory laryngospasm should be treated aggressively with small dose of suxa 10-20 mg and
temporary IPPV with 100% O2 to prevent sever hypoxemia or negative pressure pulmonary edema.
7. Endotracheal intubation may occasionally be needed for ventilation
8. If intubation is unsuccessful  cricothyrotomy is indicated
9. Glottic edema is a common cause of airway obstruction in children, I/V corticosteroids
(Dexamethasone 0.5mg/kg) OR aerosolized racemic epinephrine (0.5ml of 2.25 % solution with 3ml
N/S) may be useful.
10. Post-operative wound hematomas following head and neck, thyroid and carotid procedures can
quickly compromise airway, so opening the wound immediately relieves tracheal compression.
11. Throat packings left in hypopharynx unintentionally following oral surgery can cause immediate or
delayed airway obstruction

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Dr. Tariq Mahar
HICCUPS:
Regular and repeated spasmodic diaphragmatic movements may occur after I/V induction associated
with vagal stimulation.

TREATMENT:
1. Anticholinergics premedication ↓ incidence
2. Persistent hiccups abolished by deepening anesthesia, stimulating nasopharynx with suction
catheter or metoclopramide
3. Muscle relaxation if surgical compromise.

LARYNGOSPASM:
Acute glottis closure by vocal cords
Presents as crowing or absent inspiratory sounds and marked tracheal tug

Management:
1. Remove stimulus that precipitate laryngospasm.
2. Apply 100% O2 with tight face mask and closed expiratory valve.
3. Do suction to remove secretions and blood from airway
4. Apply CPAP and attempt manual ventilation.
5. Forcible jaw thrust or anterior pressure on the body of mandible just anterior to mastoid process
(Larson’s Point) may break laryngospasm by a combination of stimulation and airway clearance
6. Deepening anesthesia with small doses of propofol 20-50mg, reduce spasms
7. If laryngospasm fails to improve and O2 is falling consider a small dose of suxa 0.1-0.5mg /kg
8. If it is severe enough a full dose of suxa 1.0mg/kg should be given and tracheal intubation done.
9. If no venous access suxa can be given I/M or S/C 2-4mg /kg
10. Consider a change in airway management e.g. LMA instead of tracheal tube to prevent recurrence.
11. Cricothyroidotomy is life saving
12. Doxapram, a respiratory stimulant has also been used successfully in laryngospasm.

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Dr. Tariq Mahar
BRONCHOSPASM:

Presents as expiratory wheeze, prolong expiratory phase and ↑ven lator infla on pressures and
upwardly sloping ECO2 pleatue.

RISK FACTORS:
1. Asthma,
2. Respiratory infection,
3. Atopy,
4. Smoking

CAUSES:
1. Pungent volatile anesthetic e.g. isoflurane, desflurane
2. Insertion of artificial airway during light anesthesia
3. Stimulation of carina or bronchi by tracheal tube
4. β-Blockers
5. Histamine releasing drugs.
6. Drug hypersensitivity, pulmonary aspiration and FB in lower airway also present as bronchospasm

MANAGEMENT: is aimed at preventing hypoxemia and resolving bronchospasm.

1. 100% O2 should be given.

2. Anesthesia deepened if appropriate.
3. Aggravating factors removed e.g. TT repositioned and surgery stopped.
4. Bronchodilators in increments e.g. aminophylline or salbutamol
5. Volatile anesthetics and ketamine are also effective bronchodilator.
6. Epinephrine is indicated in life threatening situations and may be given via tracheal tube.
7. Steroids and H1 receptor antagonist indicated in later management of sever case.
8. If hypoxemia develops in spontaneously breathing pt, then TT and artificial ventilation should be
considered.
9. Peep and high ventilator rates should be avoided.
10. Hypercapnia may have to be tolerated in order to avoid gas trapping and barotrauma.
11. If pt. receiving IPPV, ventilation should be adjusted to peak airway pressure

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Dr. Tariq Mahar
Mendelson’s syndrome: is a potential fatal complication of anesthesia, perioperative aspiration of gastric contents is called
Mendelson’s syndrome.

ASPIRATION OF GASTRIC CONTENTS:

Common during difficult intubation, emergency cases and obese or pregnant
Bronchospasm may be the first sign, cyanosis, coughing, tachypnea and hypotension. If large quantity of
gastric content is aspirated, respiratory obstruction, ventilation perfusion mismatch and intrapulmonary
shunting produce severe hypoxemia with later development of clinical pneumonitis and or infection.

MANAGEMENT:
1. Preoperative fasting, H2 receptor blocker and prokinetic drug e.g. metoclopramide.
2. If GA is the plan then tracheal intubation is must achieved by RSI with cricoids pressure.
3. Awake intubation is advisable if difficult intubation is predicted.
4. Tracheal tube should not be removed during emergency until protective airway reflexes are
regained and pt. is awake.
5. If aspiration occurs during anesthesia, further regurgitation should be prevented by immediate
application of cricoids pressure.
6. Pt. SHOULD BE PLACED IN A HEAD DOWN POSITION (Trendlenburg Position)
7. Tracheal suction to facilitate removal of aspirate.
8. IPPV instituted must not be delayed if significant hypoxia
9. Bronchodilator therapy
10. ↑FiO2
11. If hypoxemia is refractory, PEEP may be instituted
12. Surgery should be abandoned if significant morbidity develops.
13. Flexible bronchoscope for liquids removal and rigid for solid removal
14. I/V steroids and pulmonary lavage via flexible bronchoscope ↓inflammation
15. Order CXR and ABG’s helps in assessment in severity
16. Transferred to critical care unit for further monitoring and respiratory care.

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Dr. Tariq Mahar
HYPOXEMIA:
CLASSIFICATION OF HYPOXIAS:

Hypoxia Pathophysiologic category Clinical Example

Hypoxic hypoxia: ↓pBarom or ↓FiO2 (<21%)  Altitude, O2 equipment error
alveolar hypoventilation  Drug overdose, COPD exacerbation
Pulmonary diffusion defect  Emphysema, Pulmonary emboli
Pulmonary V/Q mismatch  Asthma, Pulmonary emboli
R-L shunt  Atelectasis, cyanotic congenital heart Dx
Circulatory Hypoxia Reduced cardiac output Congestive heart failure, MI,
dehydration
Hemic hypoxia Reduced hemoglobin content Anemia
Reduced hemoglobin function Carboxyhemoglobinemia,
Methemoglobinemia
Demand hypoxia ↑O2 Consumption Fever, seizures
Histotoxic hypoxia Inability of cell to utilize Oxygen Cyanide toxicity
PBarom , barometric pressure; COPD, chronic obstructive pulmonary disease; V/Q ventilation/perfusion; RL, right to left.

CAUSES OF HYPOXEMIA DURING ANAESTHESIA:

1. Hypoxic inspired gas mixture due to equipment failure e.g. cylinder or pipeline oxygen supply failure
or misconnection.
2. Inaccurate settings or leak in flow meters
3. Obstruction or leak in breathing system.
4. Hypoventilation due to inadequate ventilation (↓MV or TT obstruc on).
5. Respiratory depression
6. V/Q mismatch like bronchial intubation, secretions, atelectasis, pneumothorax, bronchospasm,
aspiration, edema, embolus.
7. Low cardiac output
8. Methemoglobinemia
9. Malignant hyperthermia

Note: pulmonary shunting and atelectasis during anesthesia are much more likely to cause hypoxemia
than is hypoventilation.

MANAGEMENT OF HYPOXEMIA:
If hypoxemia is detected during anesthesia the following drill should be instituted:
1. A.B.C. Ensure an adequate airway, ensure adequate ventilation and check for an adequate CO by
feeling carotid pulse
2. Test the integrity of breathing system by manual ventilation of lungs and confirm bilateral chest
movement and breath sounds Blow down the tracheal tube if necessary.
3. Confirm the position and patency of tracheal tube by assessing capnogram, passing a suction
catheter through tracheal tube and auscultate the chest.
4. Exclude delivery of a hypoxic gas mixture using an oxygen analyzer, Increase FiO2 to 100%.
5. Now search for any clinical evidence of V/Q mismatch with early exclusion of pneumothorax.
If atelectasis or ↓FRC gentle hyperinflation and apply PEEP
6. If diagnosis is difficult, measure core temperature and consider ABG analysis and CXR.

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Dr. Tariq Mahar
PNEUMOTHEORAX:
CAUSES:
1. Trauma
2. Central venous cannulation via subclavian approach
3. Brachial plexus blockade
4. Cervical and thoracic surgery
5. Barotrauma
6. Spontaneously in pts with asthma, COPD or Marfan’s syndrome.
7. High peak inspiratory airway pressures during mechanical ventilation.

Sing and symptoms:

1 Unequal air entry
2 Asymmetrical chest movement
3 Wheeze
4 surgical emphysema
5 ↑CVP
6 Mediastinal shift.
7 Hypoxemia
8 Hypercapnia. 9. Hypotension.
CXR provides definitive diagnosis.

Note: A pneumothorax should be excluded during anesthesia if unexplained tachycardia, hypotension,

hypoxemia, hypoventilation (SV) or high inflation pressures (CMV) occurs intraoperatively.

MANAGEMENT:
1 Nitrous oxide should be discontinued
2 Lungs ventilated with 100% oxygen, using low inflation pressures
3 The presence of air in pleural space confirmed by aspiration through I/V cannula (14G) inserted into
chest wall in 2nd intercostal space in midclavicular line or 5th space in mid axillary line. If
pneumothorax is under tension a hissing sound will be heard as air is released.
4 If pneumothorax is confirmed, I/V cannula should be left in place and a formal chest drain is inserted
to decompress the pneumothorax

Note: In tension pneumothorax air is forced into thorax during inspiration but cannot escape during expiration Ipsilateral
lung collapsed, mediastinum and trachea shifted to contralateral side, simple pneumothorax develop into tension PT by positive
pressure ventilation.

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Dr. Tariq Mahar
HYPERTENSION: 25% > than baseline (preoperatively)
Intraoperative acute HTN ↑risk of ischemia, infarc on and hemorrhage in other organs and in particular
brain

CAUSES OF HTN DURING ANESTHESIA:

PRE-EXISTING
1. Undiagnosed or poorly controlled HTN
2. PIH
3. Withdrawal of antihypertensive medication
4. ↑ ICP

↑ SYMPATHETIC TONE:
5. Inadequate analgesia
6. Inadequate anesthesia
7. Hypoxemia
8. Airway manipulations ( laryngoscopy, extubation)
9. Hypercapnia

Drug overdose:
10. Vasoconstrictors (norepinephrine, phenylephrine)
11. Inotropes (Dobutamine)
12. Mixed inotropes vasoconstrictors (Epinephrine, ephedrine)
13. Ketamine
14. Ergometrine

OTHERS:
15. Hypervolemia/ Fluid overload
16. Aortic cross- clamping.
17. Pheochromocytoma
18. Malignant hyperthermia
19. Thyroid storm
20. Measurement errors.

Post operative causes:

1. Uncontrolled or poorly on
2. Inadequate analgesia
3. Distended bladder
4. Hypercarbia
5. Hypoxemia
6. Acidosis.

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Dr. Tariq Mahar
 RISK OF PERIOPERATIVE HTN:
1. Myocardial ischemia/ infarction 4. Stroke
2. Hypertensive heart failure 5. Renal failure
3. Hemorrhage 6. Aortic dissection

MANAGEMENT OF HTN:

PREOPERATIVE:

1. Continue adequate antihypertensive drugs to chronic hypertensive pt

2. Anxiolytic premedication to make pt. calm and relaxed.
3. Surgery should be postponed until adequate control is achieved <180/100
4. Perioperative β blockade ↓mortality in pts @risk of MI.
5. History, physical examination and investigations e.g.: ECG, Ophthalmoscopy, CXR, renal function
and UCE

PERIOPERATIVELY: (intraop)

1. Stimulating events such as laryngoscopy, surgical incision, extubation and aortic cross-clamping
etc causes surge in sympathetic tone results in significant ↑in arterial pressure.
2. These events usually be anticipated and short acting opioid e.g. fentanyl 10 μg/kg, β-blocker e.g.
esmolol 0.5mg/kg, lidocaine 1mg/kg or temporary deepening of anesthesia may be used to
prevent. Potentially damaging HTN, duration of laryngoscopy as short as possible
3. Exclude potential causes of vasodilation hydralazine, nitroglycerin, nitropruside
4. If no pathological cause is found then use of an antihypertensive agent such as labetalol or
hydralazine may be indicated if HTN persists.

POSTOPERATIVE:

1. Post operative HTN is common and anticipated in pts having poorly controlled HTN
2. Close B.P monitoring in recovery room.
3. Sustained ↑B.P. can cause formation of wound hematomas and disruption of vascular
suture lines.
4. HTN could be enhanced by respiratory abnormalities, pain, volume overload or bladder
distension Treat the cause.
5. I/V antihypertensive like labetalol given if necessary.
6. When pt resumes oral intake, preoperative medications restarted

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Dr. Tariq Mahar
HYPOTENSION:
MAP 25% < baseline value hypotension impairs perfusion and oxygenation of vital organs but during
anesthesia due to ↓ myocardial and cerebral metabolic rates it is less likely.

CAUSES OF HYPOTENSION DURING ANESTHESIA:

1. ↓CO
2. Hypovolaemia
3. Hemorrhage
4. GI fluid losses
5. Pulmonary embolus
6. Aortocaval compression
7. Pericardial effusion/ tamponade
8. ↑Intrathoracic pressure like mechanical ventilation, PEEP
9. Pneumothorax
10. Head up position

MYOCARDIAL CONTRACTILITY
1. Drugs like most anesthetic agents, β-Blockers, Ca+ blockers
2. Acidosis
3. Ischemia / infarction
4. Arrhythmias
5. Pericardial tamponade

↓ AFTERLOAD:
1. Drugs like anesthetic agents, antihypertensive.
2. Hypersensitivity, due to drugs, colloids, blood etc
3. Histamine release due to morphine, atracurium etc.
4. Central regional blockade (local anesthetics)

MANAGEMENT:
1. Preoperative correction of hypovolaemia helps to avoid excessive reduction in BP following
induction of anesthesia
2. For intraoperative hypotension a working diagnosis should be established and treatment should
be commenced aiming to correct cause of hypotension
3. Most commonly I/V fluids or ↓ anesthe c concentra on is effec ve in most pa ents but ensure
sufficient anesthetics to avoid awareness.
4. If hypotension persists after excluding significant pathological cause, vasopressor agent eg
ephedrine 5mg or metaraminol 1mg given
5. Treatment of hypotension should follow sequence of assess  treat  reassess.

ENDOCARDIAL VIABILITY RATIO:

The ration of DPTI/TTI is EVR and represents myocardial oxygen supply-demand balance. Normal EVR >1
value less than 0.7 is associated with subendocardial ischemia DPTI  Diastolic pressure time index
reflects coronary blood supply. TTI  Tension time index reflects oxygen demand.

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Dr. Tariq Mahar
HYPOVOLEMIA:
SIGNS:

1. Thirst 5. ↓Tissue turgor.

2. Dryness of mucous membranes 6. Tachycardia.
3. Cool peripheries 7. Postural hypotension.
4. Oliguria (UO < 0.5 ml/kg/hr)

CAUSES:

Preoperative:
1. Hemorrhage like trauma, obstetric, GI, major vessel rupture. 5. Fistulae.
2. Vomiting 6. Fever.
3. Intestinal obstruction. 7. Diuretics
4. Diarrhea 8. Burns.
9. Fasting

Intraoperative:
1. Hemorrhage
2. Insensible loss e.g. sweating, expired water vapors
3. Third space loss eg prolong and extensive surgeries
4. Drainage of stomach, bowel or ascites.
5. Urine output
6. Deficit – NPO

PERIOPERATIVE FLUID MANAGEMENT:

70 kg male with 8 hours fasting

Maintenance fluid requirement

1st 10kg 4 x 10 = 40
Next 10kg 2 x10 = 20
For each kg above 20 kg 1 x 50 = 50
110 ml/hr is the maintenance fluid requirement

Preexisting deficits (NPO) can be estimated by multiplying normal maintenance rate by length of the fast
i.e.
110 x 8 = 880ml
NPO Mainte. Blood loss Other losses (Urine Output)
(Evaporative &3rd space loss)
1st hour 440 ml 110ml Suction sponges 10 ml Degree of tissue trauma fluid req.
laps 100- 150ml Minimal 2ml/kg
nd
2 hour 220ml 110ml Moderate 4ml/kg
Severe 8ml/kg
rd
3 hour 220ml 110ml

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Dr. Tariq Mahar
 ( )
ABL =EBV

HAEMORRHAGE:
 For most patient transfusion point corresponds to Hb.b/w 7 & 8 g/dl
 A level of 10 g/dl generally used for elderly and those with significant cardiac or pulmonary disease
 Patient with normal hematocrit should be transfused only after losses greater than 10-20% of blood
volume
 Transfusion point can be determined preoperatively form hematocrit and estimating blood volume.

ALLOWABLE BLOOD LOSS:

Example: An 85 kg woman has preoperative hematocrit of 35%. How much blood loss will decrease her
hematocrit to 30 %.

1. Estimated blood volume =65 ml/kg x 85 kg = 5525 ml.

2. RBCV 35 % = 5525 x 35 % =1934 ml
3. RBCV 30 % = 5525 X 30 % = 1658 ml
4. Red cell loss @ 30 % = 1934-1658 = 276 ml
5. Allowable blood loss = 3 x 276 = 828 ml

 Transfusion are not recommended until hematocrit ↓ to 24% (Hb. < 8)

 One unit of PRBC will ↑Hb to 1 g/dl and hematocrit 2-3% (adults)
 10 ml/kg transfusion of PRBC will ↑ Hb 3 g/dl and hematocrit by 10 %

AVERAGE BLOOD VOLUMES:

Premature neonate 95 ml/kg EBV X
Full term neonate 85 ml/kg
Infants 80 ml/kg
Men 75 ml/kg
Woman 65 ml/kg

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Dr. Tariq Mahar
ARRHYTHMIAS:
CAUSES OF ARRHYTHMIAS DURING ANESTHESIA:
CARDIORESPIRATORY:

1 Hypoxemia 4. Hypercapnia
2 Hypotension 5. Myocardial Ischemia
3 Hypocapnia

METABOLIC:

1. Inadequate analgesia
2. Inadequate anesthesia
3. Airway manipulation
4. Sympathomimetic
5. Hyperthyroidism
6. Electrolyte disturbance (hyperkalemia/ hypokalemia, hypo/hypercalcaemia)
7. Malignant hyperthermia

SURGICAL:

1 Increased vagal tone (tractionon eye, anus and peritoneum)

2 Direct cardiac stimulation (chest surgery, CVP cannula)
3 Dental surgery.

DRUGS:

1 Vagolytic (Atropine,Pancuronium)
2 Sympathomimetic (epinephrine, ephedrine)
3 Volatile anesthetics (halothane, enflurane)
4 Digoxin

MANAGEMENT:

1 Preoperative correction of fluid, electrolyte and acid base balance

2 optimization of CAD and HTN
3 ECG monitoring
4 Treat the cause
5 If persists  specific antiarrhythmic or electrical cardio-version is indicated.

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Dr. Tariq Mahar
THROMBOEMBOLUS:
An embolus is the passage of a non-blood mass through vascular system
Thromboembolus occurs usually form deep veins of the leg or pelvis
Uncommon during anesthesia

Risk factors:

1 Immobility 6. Pelvic or limb surgery

2 Prolong hospital stay 7. HRT
3 Major trauma 8. Past H/O venous TE
4 Malignancy
5 Smoking

Sign and symptoms:

During anesthesia, pulmonary thromboembolism

Presents with tachycardia, hypoxemia, arrhythmia, hypotension, bronchospasm, acute, ↓ in ETCO2 or
cardiovascular collapse.

MANAGEMENT:

1. Risk factors should be managed actively to prevent DVT.

2. OCP or HRT should be stopped 6 weeks before elective surgery in risky patients
3. Prophylactic heparin, graduated compression stockings and intermittent calf compression reduce
likelihood of new thrombosis
4. Use of subarachnoid or epidural anesthesia reduces the risk of postoperative DVT in some surgical
groups.
5. If intraoperative pulmonary embolism is suspected, lungs should be ventilated with 100% O2,
bronchodilator therapy, fluid loading and inotropic support should be considered.
6. After initial management anticoagulation and rarely surgical removal of embolus may be indicated.
7. In extreme presentations, cardiac arrest protocols should be used.

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Dr. Tariq Mahar
GAS EMBOLUS:
CAUSES:

1 Surgical wound.
2 Positions that place operative site above Rt. atrium e.g. sitting, park bench, knee-chest, and
head up positions.
3 Vascular catheters. (IV lines)
4 Laporoscopy and thoracoscopy.

CLINICAL PRESENTAION:

An entry rate of 0.5 ml/kg/min (30 ml) produces clinical signs

1 Rapid ↓in ETCO2 5. Arrhythmias

2 Hypoxemia 4. ↑ PA pressures
3 Tachycardia 6. Millwheel murmur.

MANAGEMENT:

1 To prevent intraoperative air embolus adjusts patient’s position and site of operative field with
respect to Rt. atrium.
2 If air embolism is detected, further entry is prevented by flooding the operative site with saline.
3 During head and neck procedures, venous pressure @ surgical site may be increased by
compressing jugular veins.
4 Application of PEEP increases venous pressure and decrease ingress of air
5 During insufflations procedures, surgeon should be instructed to depressurize the insufflated
body cavity.
6 Nitrous oxide should be discontinued to avoid expansion of gas bubbles
7 Lungs should be ventilated with 100% O2
8 Gas may be aspirated from RV or RA via a venous catheter.
9 Expansion of intravascular volume, inotropic support and internal or external cardiac massage
may be necessary.
10 Placing pt in head down left lateral may help allowing gas to escape from RV into RA and vena-
cava.

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Dr. Tariq Mahar
AWARENESS:
 Psychological sequel includes insomnia, depression and post traumatic stress disorder (PTSD)
with distressing flash backs
 Light anesthesia particularly when paralyzed by relaxations is associated with highest risk more
likely in(emergency and obstetric surgery)
 Breathing system malfunctions and disconnections also associated with awareness.

SIGNS:
Paralyzed patient:
From activation of sympathetic nervous system
1. Sweating
2. Tachycardia
3. HTN
4. Tear formation
5. Pupillary dilatations
Un-paralyzed patient: experiencing noxious stimulation may move or grimace

ESPECIALIZED MONITORING:

1. Processed EEG such as bispectral index scale (BIS monitor)

2. Auditory evoked potential monitoring system

MANAGEMENT:

1. Anesthesia should be deepened immediately.

2. If arterial pressure is low despite inadequate anesthetic then ↑arterial pressure by I/V fluids,
ventilator settings or vasopressors.
3. Consider I/V midazolam 5 mg
4. If patient complains postoperatively, the anesthetist should be informed and should visit the
patient.
5. If there is genuine awareness and clear anesthetic error then prompt apology and explanation
should be provided.
6. It is advisable that anesthetist always record the timing (absolute and relative to surgery) and
dose of anesthetics.

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Dr. Tariq Mahar
HYPOTHERMIA:
Body temperature < 36 ⁰C
Protective during times of cerebral or cardiac ischemia ↓ CMRO2
Preoperative hypothermia is associated with ↑ mortality rate
Metabolic rate ↓ by 10% for each 1 ⁰C ↓ in core temperature

CAUSES: hypothalamus controls core body temperature

1. Low ambient temperature 5. Use of wet packs
2. High air flow in OT 6. Operations on open body cavities
3. Exposed body 7. Irrigation and I/V infusion of cold fluid
4. Ventilation with cold and dry gas 8. ↑ Risk in neonates, infants, elderly and burns.

Intra operative monitoring

Thermistor or thermocouple
RX
Postoperative shivering
1. Pethidine 0.33 mg/kg 4. Methylphenidate
2. Doxapram 1.5 mg/kg 5. Physostigmine
3. Clonidine 2µg/kg 6. Ondansetron 0.1 mg/kg Onset

DELETERIOUS EFFECTS OF HYPOTHERMIA:

1. Cardiac arrhythmias and ischemia

2. Increased peripheral vascular resistance (↑SVR)
3. Left shift of hemoglobin-oxygen saturation curve
4. Reversible coagulopathy (platelets dysfx)
5. Post operative protein catabolism and stress response
6. Altered mental status
7. Impaired renal function
8. ↓ drug metabolism
9. Poor wound healing
10. ↑ incidence of infection

MANAGEMENT:

Phase (I) Prewarming with forced air warming blankets

Phase (II)
1. Forced air warming blankets
2. Warm water blankets
3. Heated humidification of inspired gases
4. Warm I/V fluids
5. ↑ ambient OR temperature
6. Keep pt anesthetized until temperature is normalized

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Dr. Tariq Mahar
 HYPERTHERMIA:

Core body temperature > 37.5⁰C

↑metabolic rate  acidosis (no treatment) sweating and vasodilation hypovolaemia and tissue
hypoxia  seizures and CNS damage

CAUSES:
1 Sepsis and infection
2 Drug reactions
3 Anaphylaxis
4 Incompatible blood transfusion
5 Pheochromocytoma
6 Thyroid storm
7 Malignant hyperthermia

MANAGEMENT:
1 General measures include exposure of body surface, application of icepacks, use of fans and
cold I/V fluids and gastric lavage with cold I/V fluid
2 Specific measures depend on the cause.
3 Paracetamol and NSAID may reduce core-temperature if cause is sepsis related
4 Any unexplained ↑in temperature especially if it is increasing rapidly  urgent exclusion of
malignant hyperthermia.

SECONDARY THERAPY:
Antihistamines e.g. chlorpheniramine 20 mg I/V
Corticosteroids e.g. hydrocortisone 100mg I/V
Catecholamine infusions e.g. epinephrine 0.05 -0.1 µg/kg/min
Consider bicarbonate for acidosis 0.5 m-mole/kg
Airway evaluation before extubation
Bronchodilators e.g. salbutamol 2.5mg/kg for persistent bronchospasm

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Dr. Tariq Mahar
 MANAGEMENT AIMS:
1. Correct hypoxemia
2. Restore intravascular fluid volume
3. Inhibit further release of chemical mediators

ANAPHYLAXIS: Ig-E mediated

CAUSES:

1. Muscle relaxant e.g. suxamethonium

2. Antibiotics e.g. penicillin (most common) Any bronchospasm, hypotension,
3. Latex (2nd most common) arrhythmia or urticaria, should be
4. Radiocontrast media
considered to be due to anaphylaxis
5. Blood products
6. Colloids until proved otherwise
7. Protamine
8. SK
9. Bone cement
10. Atropine and opioids etc.

SIGNS:

1. Urticaria
2. Cutaneous flushing
3. Bronchospasm
4. Hypotension
5. Arrhythmias
6. Cardiac arrest

Early signs: Coughing, skin erythema, difficulty with ventilation and loss of palpable pulse.
The conscious PH impending doom, dyspnea, dizziness, palpitation and nausea

MANAGEMENT:
Skin prick test, intradermal test and RAST
AIM To obtund the effect of anaphylaxis mediators and to prevent their further release
INITIAL THERAPY:

1. Stop administration of drugs likely to cause anaphylaxis

2. Maintain airway, give 100% oxygen – Call for help
3. Lay patient supine with feet elevated
4. Give epineph50 mg-feet element
5. Give epinephrine 50 µg-1000µg until improvement occurs
6. Start volume expansion with crystalloids or colloids

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Dr. Tariq Mahar
SAFE MAXIMUM DOSE:
Lidocaine: 4mg/kg with epinephrine 7mg/kg
Bupivacaine: 2mg/kg with epinephrine 3mg/kg
Prilocaine: 6mg/kg with epinephrine 8mg/kg

LOCAL ANAESTHETIC TOXICITY

CAUSE:

1. Accidental intravenous injection

2. Excessively rapid absorption.
3. Absolute over dosage

SIGN AND SYMPTOMS:

1. Dizziness,
2. Drowsiness,
3. Confusion,
4. Tinnitus and
5. Circumoral tingling
6. Metallic taste
7. Tonic-clonic convulsion if severe toxicity cardiovascular symptoms include bradycardia and
hypotension and it usually occurs at 4-6 times the concentrations @which convulsion occur, CV
collapse occurs earlier with bupivacaine than with lidocaine  ↑ myocardial binding

MANAGEMENT:

1. Before block adequate preparation (IV access, resuscitation equipment)

2. Adequate monitoring.
3. Test dose of local anesthetic which contains epinephrine results in tachycardia if intravascular.
4. LA should always be injected slowly with repeated aspirations for blood, constant verbal contact
and observation of patient.
5. Addition of epinephrine ↓ speed of absorp on.
6. If toxicity of occurs  injection must be stopped and patient assessed
7. Airway should be checked and oxygen should be administered.
8. If hypoventilation or apnea  lungs ventilated with umbo or breathing system.
9. If patent unconscious or unable to maintain airway  tracheal intubation
10. I/V fluids and vasopressors for hypotension.
11. Arrhythmias should be treated appropriately.
12. Heart block may require pacing.
13. Anticonvulsants (diazepam 10mg, STP 50mg) for convulsions.

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Dr. Tariq Mahar
NEEDLESTICK INJURY:
Hollow needles >risk than solid (surgical) needles

UNIVERSAL PRECAUTIONS:

1. No recapping and immediate disposal of contaminated needles

2. Use of gloves and other barriers during contact with open wound and body fluid
3. Frequent hand washing.
4. Proper techniques for disinfection or disposal of contaminated material
5. Particular caution by pregnant health care workers , and no contact with patient by workers
who have exudative or weeping dermatitis

MANAGEMENT:

1. Cleaning the wound and notifying the appropriate authority.

2. Serological status should be established.
3. Prophylactic IFN (with or without ribavirin) following a high risk inoculation form hepatitis C
patient.
4. Prophylactic zidovudine reduces risk of HIV following contaminated needlestick.
5. A hepatitis B vaccine is strongly recommended prophylactically for anesthesia personnel
6. The risk of acquiring HIV after single needle stick injury is 0.4-0.5%

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Dr. Tariq Mahar
PATIENT POSITINS:
TRENDELENBURG: (Head down)

CVS  Baroreceptor activation, ↓CO, ↓SVR, ↓HR, ↓BP

Respiratory ↓lung capacities, ↑V/Q mismatch, ↑atelectasis, ↑ risk of regurgitation
Other ↑ ICP, ↓ CBF, ↑ IOP in pts with glaucoma

REVERSE TRENELENBURG: (Head up)

CVS ↓Preload, ↓ CO, ↓BP, Baroreflex ↑sympathe c tone, ↑HR, ↑SVR

Respiratory:  ↓WOB in spontaneous respira on, ↑ FRC
Other  ↓CPP and ↓CBF

LITHOTOMY:

CVS ↑Preload, ↑circulating blood volume, ↑BP, ↑CO

Respiratory↓Vital capacity, ↑ risk of aspiration

PRONE:

CVS Blood pooling in extremities, compression of abdominal muscles ↓preload, ↓CO, ↓BP.
Respiratory  ↓total lung compliance and ↑WOB
Others  Extreme head rotation ↓cerebral venous drainage and ↓CBF

ATERAL DECUBITUS:

CVS  CO unchanged, ↓BP (↓SVR) (Rt. Side >Lt. Side)

Respiratory ↓volume and ↑perfusion of dependent lung, ↑ventilation of dependent lung in awake
(no V/Q mismatch), ↓ventilation of dependent lung in anesthetized V/Q mis

SITTING:

CVS Blood pooling in lower extremities, ↓CO, ↓BP, ↑ HR, ↑ SVR

Respiratory: ↑ lung volumes and ↑FRC, ↑WOB
Others ↓CBF

COMPLICATION:

Air embolism, alopecia, Backache, compartment syndrome, corneal abrasion, digit amputation
Retinal ischemia, skin necrosis and Nerve palsies (Brachial plexus, common peroneal, radial, ulnar)

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Dr. Tariq Mahar
BRADYCARDIA
A patent presents for prostatectomy has a pulse of 38b/m
a) Enumerate the common causes of bradycardia?
b) How will you evaluate this patient preoperatively

Ans) Any cardiac rhythm with a rate < 60 b/m is bradycardia

CAUSES:
PREOPRATIVE:
1. Pre-existing cardiac disease.
2. CHB (complete heart block)
3. Drugs (β-Blocker, Calcium channel blockers, Digoxin)
4. Hypothyroidism
5. ↑ICP
6. ↑IOP
7. Myocardial ischemia
8. Hypothermia

INTRAOPERATIVE:
1. Deep anesthesia
2. Repeated dose of Suxamethonium
3. Rapid acting opioids
4. Halothane
5. Propofol
6. Surgical stimulation (eye ball traction, cervical/ anal dilatation)
7. Hyperkalemia
8. Low dose atropine
9. Sick sinus syndrome
10. ↑ICP

POSTOPERATIVE:
1. Hypoxia
2. Hypothermia
3. Intraoperative use of β-blocker/CCB
4. High spinal
5. Inadvertent intravascular injection of local anesthesia during epidural

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Dr. Tariq Mahar
Ans b.) EVALUATION OF PATIENT:
1.History
 Any co-existing cardiac disease (previous Mi) (previous CHB)
 Drug history (Ant-arrhythmic, β-Blocker, CCB, Digoxin)
 Malfunctioning implanted PPM (low battery)
 Evaluation of hypothyroidism
2.Examination:
1. B.P.
2. HR (rate, rhythm, volume)
3. Apex beat
4. Auscultation (any additional sound)
5. Carotid bruit.

3. Investigations:
1. ECG (long lead II)
2. Holter monitoring
3. ECHO
4. Electrophysiological study
5. CXR
6. Cardiac enzymes
7. Electrolytes
8. Thyroid fx test
9. Serum digoxin level

TREATMENT:
1. Treat the cause (hypoxemia) (stop surgical shunt)
2. Anticholinergics (atropine, glycopyrrolate)
3. Epinephrine
4. If refractory  TPM/PPM

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Dr. Tariq Mahar
 PEA
Q. What is pulseless electrical activity?
Q. What causes it? Algorithm for PEA

Pulseless Electrical Activity: Rhythm on monitor, without palpable pulse

Cause:
1. Severe hypovolaemia 6. Profound hypoxemia
2. Cardiac tamponade 7. Severe acidosis
3. Ventricular rupture 8. Pulmonary embolism
4. Dissecting aortic aneurysm 9. Drugs related after prolong CPR

5. Tension Pneumothorax atropine induced

Pulseless electrical activity algorithm

algorithm.
VF/VT, ventricular fibrillation and pulseless
ventricular tachycardia

3
Dr. Tariq Mahar
 ALGORITHM FOR PEA

1-Pulse less electrical activity

(PEA = rhythm on monitor, without detectable pulse)
↓
2-Primary ABCD survey
 Focus: basic CPR and defibrillation.
 Check –responsiveness
 Activate- emergency response system
 Call- for defibrillator
a- Airway – open the airway
b- Breathing – provide positive pressure ventilations
c- Circulation – give chest compression
d- Defibrillation – assess +shock for VF/VT
↓
3-Secondary ABCD survey
Focus: more advanced assessment and treatments
a) Airway – place airway device ASAP
b) Breathing – confirm and secure airway device.
c) Breathing –confirm effective oxygenation and ventilation.
d) Circulation-establish IV access.
e) Circulation –identify rhythm-monitor.
f) Circulation –administer drugs appropriate for rhythm & conduction monitor
g) Circulation – assess for occult blood flow
h) D/D search for and treat identified reversible causes
↓
4-Review For Most Frequent Causes

 Hypovolaemia • Tamponade (cardiac)

 Hypoxia • Tension pneumothorax
 Hydrogen ion-acidosis • Thrombosis, coronary (ACS)
 Hyper/hypokalemia • Thrombosis, pulmonary (embolism)
 Hypothermia
 Tablets (drug OD, accidental)
↓
5-Epinephrine
1mg IV push, repeat every 3 to 5 minutes
↓

6-Atropine 1mg IV
Repeat every 3 to 5 min as needed to a total dose of 0.04mg/kg.

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Dr. Tariq Mahar
ASYSTOLE
Q. a) List the causes of cardiac arrest during operation?
b) Write down algorithm for pulse less VT?

Ans. a) CAUSES OF CARDIAC ARREST

1 Procedures associated with excessive vagal activity (eye traction, cervical dilatation)
2 Pre-existing CHB, second degree HB, or trifascicular block.
3 Disconnected ECG leads.
4 Excessively low voltage on ECG.
5 Hypoxia (obstructed airway, bronchial or esophageal, intubation, oxygen failure)
6 Hypovolemia (hemorrhagic shock, anaphylaxis)
7 Hypo/ Hyperkalemia (renal failure, Suxamethonium induced Hyperkalemia after burns).
8 Hypothermia
9 Tension Pneumothorax
10 Cardiac tamponade.
11 Drug over dosage (Propofol, β-blocker, LA toxicity).
12 Thromboembolism
13 Equipment failure
14 High spinal
15 Total spinal

Cardiac arrest can only be diagnosed clinically by palpating carotid artery (absent pulse)

CAUSES OF VT:
1 IHD
2 Ventricular scarring after MI or previous cardiac surgery.
3 Right ventricular failure
4 Electrolyte abnormalities in pts with prolong QT interval
(TCA, antihistamines, phenothiazine’s or Brugada syndrome)
5 SVT e.g. WPW syndrome may cause a broad complex tachycardia

TORSADE DE POINTES: is a specific polymorphic form of VT.

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Dr. Tariq Mahar
 6
Dr. Tariq Mahar
PULSELESS VT
Ans b)
ALGORYTHM FOR PULSELESS VT
If not already done, give O2 and establish IV access
↓
Pulse No use VF protocol

↓yes

Adverse signs
 SBP<90
 Chest pain
 Heart failure
 Rate > 150bpm
No yes

If hypokalemia Synchronized DC shock

100-360 J

 Give KCL up to 60mmols

 Give MgSO4 5ml 50% in 30 min

Amiodarone 150 mg IV If hypokalemia

Over 10min

or
Lidocaine 50mg IV over Amiodarone 150mg I in 10min
2 min repeated every 5 min
To a maximum of 200 mg
Further cardio version as necessary
Synchronized DC shock
100-200-360J

If necessary, further Amiodarone For refractory cases consider

150mg IV over 10min, then 300mg additional pharmacological agents
Over 1hour and repeat shock Amiodarone, lidocaine, Sotalol,
Procainamide, or over drive pacing
Note:
1 For torsade pointes, use MgSO4 or overdrive pacing (expert help recommended)
2 DC shock always given under sedation / GA.

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Dr. Tariq Mahar
 ADULT BLS ALGORHYTHM

Collapsed/ sick patient

Shout for HELP and assess pt.

Signs
No of life yes

Call resuscitation team Assess ABCDE

Reorganize & treat O2
Monitoring IV access
CPR 30:2
With O2 & airway adjuncts

Apply pads/monitor Call resuscitation team

Attempt defibrillation if appropriate
If appropriate

Advance life support Handover to

When resuscitation team arrive Resuscitation team

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Dr. Tariq Mahar
 9
Dr. Tariq Mahar
 ADULS ALS ALGORYTHM

Unresponsive

Open airway
Look for signs of life
Call rescue team

CPR 30:2
Until defib/monitor attached

Assess rhythm

Shock-able Non shock-able

(VF/Pulse less VT) (PEA/asystole)

1 shock During CPR

360J -correct reversible causes
Mono phasic -check electrodes & contact
-IV access, airway, O2
-Uninterrupted, compressions
-When airway secures
-Give epinephrine every 3-5 min
Atropine
-Consider Amiodarone and Mg.

Immediately resume
CPR 30:2
For 2min

Reversible cause:
1. Hypoxia 5. Tension pneumothorax
2. Hypovolaemia 6. Tamponade, cardiac
3. Hypo/hyperkalemia 7. Toxins (drug )
4. Hypothermia 8. Thrombosis coronary and pulmonary.

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Dr. Tariq Mahar
SYNCOPE

Q. a) why should anesthesiologist be concerned about H/O syncope?

b) Causes of syncope?

Ans. a)
 A history of syncope in elderly patients should always raise the possibility of arrhythmias and
underlying organic heart disease.
 Cardiac syncope results form an abrupt arrhythmia that suddenly compromises CO and impairs
cerebral perfusion.
 Both Brady and tachyarrhythmia’s can produce syncope.

b). Causes:
Cardiac:
1. Tachyarrhythmia’s >180 b/min 7. Primary pulmonary HTN
2. Brady-arrhythmias < 40 b/min 8. Pulmonary embolism.
3. Aortic stenosis. 9. Cardiac tamponade.
4. Hypertrophic cardiomyopathy.
5. Massive MI
6. TOF

Non cardiac
1. Vasovagal (vasodepressor reflex) 6. Autonomic dysfunction
2. Carotid sinus hypersensitivity 7. Sustained valsalva maneuver
3. Neuralgias 8. Seizures
4. Hypovolaemia 9. Metabolic (-Hypoxia,
5. Sympathectomy -Hypocapnia
-Hypoglycemia)

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Dr. Tariq Mahar
CARDIAC CYCLE
7 Phases
1 Atrial systole
2 Isovolumetric ventricular contraction
3 Rapid ventricular ejection
4 Reduced ventricular ejection
5 Isovolumetric ventricular relaxation.
6 Rapid ventricular filling
7 Reduced ventricular filling.

CHAIN OF SURVIVAL: The 5 links in adult chain of survival are

 Immediate recognition of cardiac arrest and activation of emergency response
 Early CPR with an emphasis on chest compressions
 Rapid defibrillation
 Effective advanced life support.
 Integrated post cardiac arrest care
A strong
trong chain of survival can improve chance of survival and recovery for victims of heart attack, stroke
and other emergencies

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Dr. Tariq Mahar
CARDIOVERSION
Q.) A 55 years old man with new onset AF is scheduled for elective cardioversion
A) What are the indications and complications of cardioversion?
B) How would you evaluate this patient?
C) What minimum monitors and anesthetic equipment required.

a) INDICATIONS FOR DC CARDIOVERSION:

1. To terminate SVT and VT caused by reentry
2. To terminate AF and Flutter, pre-excitation syndromes and VT or VF
3. Emergency cardioversion for any tachyarrhythmia’s associated with significant hypotension, CHF
or angina.
COMPLICATION OF CARDIOVERSION:
1. Myocardial depression.
2. Post shock arrhythmias (VF)
3. Arterial embolism.

b) EVALUATION FOR CARDIOVERSION:

1. Pt. should be evaluated and treated like GA.
2. Should fast for 6-8hrs to ↓aspira on risk.
3. Airway reflexes will be depressed by sedatives and anesthetics.
4. 12 lead ECG for confirmation of arrhythmias just before and after the procedure.
5. Preoperative laboratory investigations should be normal.
6. Antiarrhythmic e.g. quinidine should be started in pt. with AF 1-2days prior to procedure.
Anticoagulation also started.
7. TEE must be performed immediately before to rule out an atrial thrombus.

c) MINIMUM MONITORING
 ECG, BP & pulse oximetry,
 Precordial stethoscope  breath sounds,
 Conscious level  continuous verbal contact

EQUPMENTS
DC fibrillator
Transcutaneous pacing
Reliable IV access
A functional bag-mask device capable of delivering 100% O2
An Oxygen source (from pipeline or cylinder)
Airway trolley (laryngoscopes, ETT, LMA, bougie, Guedel airway
A functioning suction apparatus
Anesthetic drug kit
Crash cart that includes all necessary drugs and equipment for CPR

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Dr. Tariq Mahar
PAIN PATHWAY

Primary afferent neurons

(Dorsal root ganglia @ each spinal cord level) 1st order neurons

Gray matter of ipsilateral dorsal horn

(1st six lamina of dorsal horn  modulation of pain)

Contralateral spinothalamic tract 2nd order neuron

Lateral & medial spinothalamic tract

Thalamus
3rd order neuron
Postcentral gyrus of parietal cortex & sylvian fissure

ALLODYNIA: Perception of ordinary non noxious stimulus as pain

ANALGESIA: Absence of pain perception
ANESTHESIA: Absence of all sensations
DYSESTHESIA: unpleasant or abnormal sensation with or without stimulus
HYPERAESTHESIA: ↑ response to mild s mulus
HYPOAESTHESIA: ↓ cutaneous sensa on
PARESTHESIA: Abnormal sensation without stimulus
HYPOALGESIA: ↓response to noxious s mula on
HYPERALGESIA: ↑ response to noxious stimulation
HYPERPATHIA: Hyperaesthesia + allodynia+hyperalgesia

Referred pain: Phenomenon of convergence b/w visceral and somatic sensory input is called referred
pain
Pain measurement: Numerical rating scale, faces rating scale, visual analog scale & McGill Pain
Questionnaire most commonly used
Psychological evaluation:  Minnesota multiphasic Personality Inventory MMPI and Beck depression
inventory

14
Dr. Tariq Mahar
 15
Dr. Tariq Mahar
 PACU: (Post Anesthesia Care Unit)
Q1. A) What are the causes of delayed recovery from GA?
B) How will you manage such a case?

Ans A) Patient fails to regain consciousness 30-60min after surgery under general anesthesia.

CAUSES:

1. Residual anesthesia effect (sedative, analgesic, NMBA’s)

2. Drug overdose (opioids, NMBA’s, sedatives, inhalation agents)
3. Hypothermia
4. Metabolic disturbances like -Hypercarbia/Hypocapnia (hypocarbia)
5. Perioperative stroke. -Hypoxemia
-Hypercalcemia
-Hyper/hypoglycemia
-↑Mg
-↓Na

Ans B)

MANAGEMENT: Rule out and treat the cause

 Opioid overdose  Naloxone 0.04mg (increments)

 Benzodiazepine overdose  Flumazenil 0.2 mg (increments)
 NMBA’s effect Use nerve stimulator and repeat Neostigmine/ Pyrolate if needed
 Hypothermia Use forced warm blankets
↑ambient temperature of PACU
Warm I/V fluids
Keep patient anesthetized until temp normalizes.
 Perioperative stroke neurophysician consultation for CT
 Metabolic disturbances: Send investigation and ABG‘s
&correct them accordingly

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Dr. Tariq Mahar
Q2) what are the causes and treatment of post operative HTN?

CAUSES:

Pre-existing
1. Undiagnosed HTN or poorly controlled
2. PIH
3. Withdrawal of anti-hypertensive.
4. ↑ICP

↑Sympathe c tone
1. Inadequate analgesia
2. Hypoxia
3. Hypercapnia
4. Airway instrumentation (nasal and Guedel airway, frequent suctioning)
5. Bladder distension (Catheter Obstruction)

Drug over dosage:

1. Epinephrine
2. Ephedrine/ Phenylephrine
3. Ketamine
4. Ergotamine.

Others:
1. Fluid over dosage.
2. Pheochromocytoma
3. Malignant Hyperthermia
4. Thyroid storm
5. Metabolic acidosis
6. Measurement error (small cuff)

TREATMENT:
OBJECTIVE: Control blood pressure to prevent end organ damage (Brain, heart, kidney)
1. Mild HTN do not require any treatment (only observes)
2. BP >25 % form baseline will be consider to teat
3. Along with ↑BP associated adverse effects like myocardial ischemia, heart failure or bleeding
should be treated.
4. Mild to moderate HTN should be treated with I.V. β-Blockers like labetalol, esmolol or
propranolol. If asthmatic then Ca+ blocker
5. Patient with limited cardiac reserves needs invasive monitoring, treat them with I.V. infusion of
GTN, SNP, nicardipine or fenoldopam
6. Control pain via analgesia.
7. Catheterize if bladder is distended or examine the existing catheter
8. O2 via face mask.
9. Send investigation e.g. cardiac enzymes, UCE’s
10. Monitor ECG and pulse oximeter
11. Anxiolytics.

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Dr. Tariq Mahar
MEDICAL ILLNESS PREDISPOSE PTS TO DELAYED RECOVERY OR PROLONG PARALYSIS

1. Chronic hypertension ↓brain tolerance to episodes of hypotension

2. Diabetes  prone to hypoglycemia and hyperosmotic, nonketotic coma
3. Live dx  ↓drug metabolism and biliary excre on
4. Hepatic encephalopathy  alters consciousness
5. Kidney dx  ↓excre on of drugs.
6. Uremia  also affects consciousness
7. Prior CVA or symptomatic carotid bruit  ↑risk of CVA
8. Sever hypothyroidism.

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Dr. Tariq Mahar
POSTOPETATIVE PROBLEMS:
Q 3) Enumerate the problems that can occur in immediate post operative period. Briefly give the
management.

Ans.) Problems in immediate postoperative period:

1. Delayed recovery 8. HTN

2. Post operative pain 9. Thyroid storm
3. PONV 10.Hypotension
4. Hypothermia/ Shivering 11.Hypoxemia
5. Agitation 12.Hypovolaemia
6. Airway obstruction 13.Fever.
7. Hypoventilation /Hypercarbia.

MANAGEMENT:

1-DELAYED EMERGENCE:
1. Rule out any drug overdose and treat accordingly.
2. Correct hypothermia
3. Correct electrolytes
4. Correct acidosis
5. Neuro Physician consultation if stroke is suspected

2-POST OP PAIN:
Pre-operative  NSAIDS/acetaminophen
Intra-operative  local infiltration, nerve blockade or caudal, epidural infusion if catheter left in place

3-PONV:
1. Metoclopramide 0.15 mg/kg.
2. Ondansetron 4mg
3. Dexamethasone 4-10mg
4. Adequate hydration.
5. Intraoperative Propofol infusion

4-AGITATION: Midazolam or Physostigmine /haloperidol

5-HYPOTHERMIA /SHIVERING:
1. Forced warm blankets.
2. ↑ Ambient temperature of PACU
3. Warm I/V fluids
4. Oxygen via face mask and meperidine 10-50mg for shivering

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Dr. Tariq Mahar
6-AIRWAY OBSTRUCTION:
1. Supplemental oxygen
2. Jaw thrust
3. Head tilt
4. Chin lift
5. Oral/ Nasal airway
6. I/V steroids for glottis edema (children)

7-HYPOVENTILATION /HYPERCARBIA: Identify the cause.

1. Good analgesia
2. Reversal of residual NMBA effect.
3. Opioid antidote  Naloxone alternatively dexamethasone
4. Benzodiazepine antidote  flumazenil
5. Control ventilation if circulatory depression or sever acidosis PH <7.15

8-HTN:
1. Good analgesia 4. Direct acting vasodilators e.g. GTH, SNP
2. β-Blockers like labetalol, esmolol 5. α2 agonists.
3. Ca+ Blockers like verapamil if asthmatic methyldopa (Rx)
Aldomet
Classes: Alpha2 Agonists,
9-THYROID STORM: (Medical emergency) Central-Acting

1. Dexamethasone 6. I/V fluids

2. Propylthiouracil 7. Vasopressor
3. Na/K iodide. 8. Digoxin (a fib)
4. β-blockers 9. Post operative ICU
5. Surface cooling 10. Admission

10-HYPOTENSION:
1. Adequate O2
2. Vasopressors 6. Head up position
3. Correct acidosis 7. 12 lead ECG ischemia/infarction
4. If surgical bleeding resuscitate with fluids
5. If resistant  then use inotropes

11-HYPOXEMIA:
1. Assess ECG 4. Rule out airway obstruction
2. Oxygen via face mask. 5. Correct hypothermia

12-HYPOVOLEMIA:
-Resuscitate with fluids, -Monitor urine out put

13 FEVER: Treat the casus

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Dr. Tariq Mahar
POSTOP APNEA:

Q4. What is the D/D of post-operative apnea?

How will you treat it?

D/D OF POST OF APNEA:

1. Succinyl apnea
2. Previous H/O OSA
3. Opioid overdose/ sedatives overdosage
4. Inadequate reversal of NMBA
5. Residual effects of inhalational agents.
6. Hypocarbia or Hypocapnia
7. Hyperoxemia in COPD pts. especially smokers
8. Morbid obesity
9. Airway obstruction.
10. Unsecure airway of semi conscious pts in PACU
11. Retro-bulbar block.

TREATMENT:
1. Jaw thrust, head tilt, chin lift and supplemental oxygen
2. Reversal of opioids/sedatives overdosage.
BiPAP: Bilevel Positive Airway Pressure,
3. Reversal of NMBA’s after checking with nerve stimulator CPAP: Continuous Positive Airway Pressure.
4. BiPAP/ CPAP in morbid obese K/C of OSA pt. (Obstructive Sleep Apnoea) IPPV: Intermittent Positive Pressure
Ventilation
5. Clear the airway (secretions, Blood)
6. Use of oral/nasal airway in semiconscious pts
7. Rebreathing face masks for COPD Pt.
8. Venturi device for COPD patients
9. Support the airway with IPPV if required.
10. Succinylcholine apnea  FFP’s and electively ventilate till diagnosis is established or breathing
regained

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Dr. Tariq Mahar
POSTOPERATIVE PAIN MANAGEMENT:

Q.5) Describe post operative pain management of a young lady?

Ans.)
PREOP:
 Acetaminophen ↓post opera ve opioid requirements
 NSAID’s

INTRAOP:
 Local anesthetic infiltration
 Nerve blockades (ilioinguinal/ caudal/ Epidural)
 I.V. Opioids (fentanyl, nalbuphine, morphine)
 I.M. NSAID’s (Diclofenac)

POSTOP:
Mild to moderate:

 Oral acetaminophen + Codeine, oxycodone, hydrocodone

 Opioids (Nalbuphine 5-10mg) or (Tramadol)
 NSAID (Ketorolac 30mg

Moderate to Severe:

 Parenteral/ Inrtraspinal opioids (fentanyl, morphine)

 Regional anesthesia (epidural)
 Specific nerve blocks e.g. (caudal, femoral, intercostal, interscalene)
 PCA (for inpatients) when fully awake
 Meperidine, hydromorphane, morphine

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Dr. Tariq Mahar
HYPOXEMIA MANAGEMENT:

Q6.) A 29 year old female brought to PACU after an uneventful lap-choley under G/A. In recovery her
SpO2 is 88%

a) Discus the causes of hypoxemia in recovery?

b) How will you manage it?

Ans. a)
CASUES:

Physiological Pathological
1. Low FiO2 1. Airway obstruction (bronchospasm)
2. Hypoventilation (↓PaCO2) 2. Atelectasis
3. V/Q mismatch. 3. Bronchial intubation (Rt.)
4. Intrapulmonary shunting. 4. Aspiration.
5. Pulmonary edema.
6. Pneumothorax/ Pulmonary embolism.

Ans b)
MANAGEMENT:
1. Oxygen therapy with or without positive airway pressure
2. Oxygen concentration must be controlled in COPD Pts to prevent acute respiratory failure.
3. Until the cause is established pt should receive 100% O2 via non-rebreathing mask.
4. Persistent hypoxemia despite 50% O2 is indicative of PEEP or CPAP.
5. Bronchospasm should be treated with aerosolized bronchodilators/ IV aminophylline.
6. Chest tube should be inserted for any symptomatic pneumothorax
7. Diuretics should be given for any fluid overload.
8. Bronchoscopy is useful in re-expanding lobar atelectasis caused by bronchial mucous plugs or
particulate aspiration
9. Semi-upright position helps maintain FRC.

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Dr. Tariq Mahar
PONV (Post Operative Nausea and Vomiting):
Q.7) a) what are the common risk factors for PONV?. b). How would you manage (PONV).

a) RISK FACTORS FOR PONV

Patient factor:
1. Young age.
2. Female gender, particularly if menstruating on day of surgery of in first trimester of pregnancy.
3. Large body habitus (obesity)
4. H/O prior postoperative emesis.
5. H/O motion sickness.

Anesthesia techniques:
1. General anesthesia
2. Drugs (Opioids, Volatile agents, ? Neostigmine).

Surgical procedures:
1. Strabismus (squint) surgery 4. Orchiopexy
2. Ear surgery 5. Tonsillectomy
3. Laparoscopy 6. Ovum retrieval

Postoperative factors:
1. Postoperative pain
2. Hypotension.

b) MANAGEMENT: Aim: Reassure correct vital signs adequate analgesia and hydration
1. Propofol anesthesia ↓PONV incidence.
2. H/O smoking also ↓PONV
3. 5-HT3 antagonist  Ondansetron 4mg (0.1mg/kg children)
Granisetron,(an antiemetic used in conjunction with cancer chemotherapy)
Dolasetron, prevents and treat established PONV
4. ODT (orally disintegrating tablets) preparation of Ondansetron  post discharge PONV
5. Metoclopramide 0.15 mg/kg I/V  Extra-pyramidal SE
6. Dexamethasone 4-10mg (0.1 mg/kg in children) for refractory PONV
7. Adequate hydration 20 ml/kg and stimulation of P6 acupuncture point.
8. Droperidol I.V. Prolong QT interval fatal arrhythmias  not used

VOMITING CENTRE: Lateral reticular formation of medulla, closed to 4th ventricle.

PONV pathway:
Afferent: CTZ  vestibular apparatus  cerebellum  higher cortical and brainstem centers 
solitary tract nucleus.
Efferent: CN V, VII, IX, X, XII and spinal nerves to GI tract, diaphragm and abdominal muscles

38
Dr. Tariq Mahar
CTZ chemoreceptor trigger zone (area postrema), floor of 4th ventricle (poorly developed BBB)
1st line  hyoscine, cyclizine and metaclopromide
2nd line  5 HT3 antagonist
3rd line combination or refractory Dexamethasone

39
Dr. Tariq Mahar
 40
Dr. Tariq Mahar
ALDRETE RECOVERY SCORE:
Q8- write down discharge criteria form PACU and ambulatory surgery

POSTANESTTHETIC ALDRETE RECOVERY SCORE

Original Criteria Modified criteria Point Value

Color Oxygenation.
Pink SpO2 > 92 % on room air 2
Pale or dusky SpO2 >90 % on Oxygen 1
Cyanotic SpO2< 90% on Oxygen 0

Respiration
Can breathe deeply and cough Breathes deeply and coughs freely 2
Shallow but adequate exchange Dyspnea, shallow or limited breathing 1
Apnea or Obstruction Apnea 0
Circulation
Blood pressure within 20% of normal Blood pressure ± 20 mmHg of normal 2
Blood pressure within 20-50% of normal Blood pressure ±20-50 mmHg of normal 1
Blood pressure deviating > 50% form normal Blood pressure more than ±50mmHg ˶ ˶ 0

Consciousness
Awake, alert, and oriented Fully awake 2
Arousable but readily drifts back to sleep Arousable on calling 1
No movement Not responsive. 0
Activity:
Moves all extremities. Same 2
Moves two extremities. Same 1
No movement. Same 0

Note:
Ideally the patient should be discharged form PACU when the total score is 10 but a minimal of 9 is
required
Majority meats discharge criteria within 60 min in PACU.

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Dr. Tariq Mahar
Post anesthesia discharge scoring system (PADS):

DISCHARGE CRITERIA AFTER AMBULATORY SURGERY

Post anesthesia discharge scoring system (PADS)

Criteria: Points

Vital signs:
Within 20% of preoperative baseline 2
Within 20-40% of preoperative baseline 1
>40% of preoperative baseline 0

Activity level:
Steady gait, no dizziness, at preoperative level 2
Requires assistance 1
Unable to ambulate 0

Nausea and vomiting:

Minimal, treated with oral medication 2
Moderate, treated with parenteral medication 1
Continues after repeated medications 0

PAIN: minimal or none, acceptable to patient,

Controlled with oral medication:

Yes 2
No 1

Surgical bleeding:
Minimal No dressing change required 2
Moderate  up to two dressing changes 1
Severe  three or more dressing changes 0

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Dr. Tariq Mahar
Fever: TACHYCARDIA:
PERIOPERATIVE CAUSES: PREOPERATIVE CAUSES
1. Infections 1) Anxiety
2. Drug reactions 2) Pain
3. Blood reaction. 3) Fever
4. Tissue destruction 4) Hypoxemia
5. Connective tissue disorder. 5) Hypercapnia
6. Granulomatous disorder. 6) Hypotension
7. Trauma 7) Anemia
8. Infarction 8) Hypovolaemia
9. Thrombosis 9) CHF
10. Neoplastic disorders 10) Cardiac Tamponade
11. Thyroid storm 11) Tension pneumothorax
12. Adrenal (Addison crisis) 12) Thromboembolism
13. Pheochromocytoma 13) Anticholinergics
14. Malignant hyperthermia 14) B-agonists e.g. salbutamol (ventolin)
15. Acute gout 15) Vasodilators e.g. GTN
16. Acute porphyria 16) Allergy
17) Drug withdrawal
18) Hypoglycemia
19) Thyrotoxicosis
20) Pheochromocytoma
21) Adrenal crisis
22) Carcinoid syndrome
23) Acute porphyria

43
Dr. Tariq Mahar
 MISCELLANEOUS

ANESTHESIA MACHINE CHECKOUT LIST

1. Verity backup ventilation equipment is available and functioning (high pressure system)
2. Check O2sylinder supply
3. Check central pipeline supply (tug test) (low pressure system)
4. Check initial status of low pressure system
5. Perform leak check of machine low pressure system
6. Turn on machine master switch and all other necessary electrical equipment
7. Test flow meters (scavenging system)
8. Adjust and check scavenging system (Breathing system)
9. Calibrate O2 monitor (analyzer)
10. Check initial status of breathing system
11. Perform leak check of breathing system (Pecthk’s test)
12. Test ventilation system and unidirectional valves i.e.
Manual and automatic ventilation system
13. 13 Check, calibrate and/or set alarm limits of all monitors
14. Check final status of machine
a. Vapourizers off
b. APL valve open
c. Selector switch to bag mode
d. All flow meters to zero
e. Patient suction level adequate
f. Breathing system ready to use

Same machine in successive cases  only check 10-14

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Dr. Tariq Mahar
STATUS EPILEPTICUS

Definition: medical emergency

Defined as continuous seizure activity lasting for 30 minutes, or intermittent acting of same
duration without recovery of consciousness between episodes

Management:
AIM: To terminate seizure activity, prevent recurrence and to manage both the precipitating cause and
complications resulting from seizure
1. Basic life support – ABC – 100% oxygen ( ETT+ IPPV)
2. Check blood sugar and treat hypoglycemia
3. Termination of seizures with IV lorazepam (0.1mg/kg) or diazepam(0.1 mg/kg) as a first line therapy
4. Second line therapy if seizures not terminated within 10 minutes, phenytoin 15-17mg/kg by slow IV
infusion (rage <50 mg/min)
5. Intubation and ventilation to maintain PaO2 and PaCO2 within normal ranger
6. Fluid resuscitation to maintain adequate systemic BP and CPP
7. Inotropes may be required particularly if GA is needed to control seizures
8. Search for causes of seizures and treat the cause
9. Start propofol anesthesia for refractory status epilepticus if seizures not controlled after 30min with
2nd line therapy
10. Ensure therapeutic levels of long-acting anticonvulsants if epileptic
11. Consider 3rd line therapy e.g.: phenobarbitone 20mg/kg by infusion
12. Management of complications – hyperthermia, rhabdomyolysis, cardiac arrhythmias, aspiration and
13. pulmonary edema
14. Investigations  ABG, FBC, UCE’s blood glucose, EEG, CT-scan

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BRAIN DEATH

BRAIN DEATH: defined as irreversible cessation of all brain function.

Spinal cord function below C1 may still be present

BRAIN DEATH CRITERIA:

Brain death criteria can be applied only in the absence of hypothermia, hypotension,
metabolic or endocrine abnormalities, NMBAs or drugs known to depress brain function
Generally acceptable clinical criteria for brain death include the following:
1. Coma
2. Absent motor activity, including decerebrate and decorticate posturing (spinal reflexes may be
present in some)
3. Absent brain stem reflexes including the pupillary, corneal, vestibule ocular (caloric) and gag (and/or
cough) reflexes.
4. Absence of ventilatory effort with arterial CO2 tension 60 mmHg or 20 mmHg above the pretest level
 Repeating the examination is optional <2h
 Apnea test should be reserved for last because of its detrimental effects on ICP.
 Confirmatory test:
Decerebrate posture is an abnormal body posture that involves the arms and
1. Isoelectric EEG
legs being held straight out, the toes being pointed downward, and the head
2. Angiography and neck being arched backwards. The muscles are tightened and held rigidly.
3. Transcranial Doppler This type of posturing usually means there has been severe damage to the
brain
4. Radio isotopic studies

These tests generally not required

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MECHANICAL VENTILATION
INDICATIONS:
Respiratory gas tensions:
1. PaO2< 50 mmHg on room air PaCO2> 50mmHg (in the absence of metabolic acidosis)
2. PaO2/FiO2 ration <300 mmHg
3. PA-a O2 gradient >350 mmHg
4. VD/VT> 0.6

Clinical indices:
5. Respiratory rate >35 b/min

Mechanical indices:
6. Tidal volume <5ml/kg
7. Vital capacity <15ml/Kg
8. Maximum inspiratory force < -25cmH2O (ie – 15 cm H2O)

MECHANICAL CRITERIA FOR WEANING /EXTUBATION

1. Inspiratory pressure < -25 cmH2O
2. Tidal volume > 5ml/kg
3. Vital capacity >10 ml/kg
4. Minute ventilation <10ml/kg Breaths/min
=
5. RSBI < 100 V

_____________________________________________________________________________________
PEEP: Application of positive pressure during expiration as an adjunct to a mechanically delivered breath
is called PEEP

CPAP: Application of positive pressure threshold during both inspiration and expiration with
spontaneous breathing is referred to as CPAP

Risk of gastric distension and regurgitation  Used in alert pts with intact airway reflexes.

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SEPSIS
SEPSIS: Is the systemic inflammatory response to infection
MO
DS: Progressive dysfunction of two or more organs that is associated with sepsis
SEPTIC SHOCK: Sepsis associated with hypotension (SBP<90, MAP <60)
Despite adequate fluid resuscitation

DIAGNOSTIC CRITERIA FOR SEPSIS

INFECTIVE VARIABLES
Fever > 38.3oC, Hypothermia, HR > 90, tachypnea, altered mental status, significant edema,
hyperglycemia

INFLAMMATORY VARIABLES:
Leukocytosis > 12000, Leukopenia, normal TLC with > 10% immature forms
CRP > 2, Procalcitonin (PCT) > 2

HEMODYNAMIC VARIABLES
SBP < 90, MAP < 60, CI >3.5, SVO2>70%

ORGAN DYSFUNCTION VARIABLES

Hypoxemia PaO2/FiO2< 300, Acute oliguria U/O < 0.5 ml/kg/hr, Creatinine ↑> 0.5mg/dl, coagula on
abnormality INR >1.5, APTT >60 sec, ileus, thrombocytopenia <100000, hyperbilirubinemia TB> 4mg/dl

TISSUE PERFUSION VARIABLES

Hyperlactatemia> 1mmlol /L, ↓capillary refill or mo ling

TREATMENT OF SEPTIC SHOCK: Medical Emergency

Treatment is 3fold
1. Control and eradication of infection by IV antibiotics
2. Fluid resuscitation with inotropes to maintain organ perfusion
3. Supportive Rx of complications like ARDS, ARF, GI bleeding and DIC

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SICK LAPAROTOMY (ASA 3 OR MORE)
PRESENTATION:
 Usually perforated viscus or bowel ischemia/ obstruction
 Septic – tachycardia, hypotension, hypovolemia

IMMEDIATE MANAGEMENT
 Review pt. in ward – ABC -100% Oxygen
 Examine Pt. and check FBC, U & E, coagulation, amylase, ECG, cross match
 ABGs if dyspneic base deficit/ raised lactate sign of inadequate resuscitation
 Resuscitate according to goals (HR, BP, CVP, ABG’s, BE, UOP)
 Optimize and discuss with surgical team, condition and timing of surgery
 Consider need for invasive monitoring (CVP, a-Line)

RESUSCITATION GOALS:
 HR < 100 b/m
 MAP > 60 mmHg
 CVP 8-12 cmH2O
 Mixed venous SaO2> 70%
 Hb 7-9g/dl (higher for IHD pt.)
 UOP > 0.5 ml/kg/hr
 PH – normal
 Lactate normal or falling

PREOPERATIVE MANAGEMENT:
 ABC – oxygenation. Intubate and IPPV if required. May need transfer to ICU if signs of organ
dysfunction and surgery not urgent.
 Ensure adequate resuscitation, particularly oxygenation and circulation.
 Replace volume with R/L, N/S or colloid. Hypovolemic pts need CVP.
 Failure to reach resuscitation goals with fluids alone is an indication for vasopressor or inotropes
(if septic -1st line agent – norepinephrine)
 Antibiotics depending on diagnosis
 Morning time for surgery is best when all senior doctors available
 Delaying pts with ischemic bowel or bleeding will cause deterioration
Sodium bicarbonate occasionally needed for acidotic patients in renal failure or with hyperkalemia.
Normally acidosis improves with resuscitation.

INTRAOPERATIVE MANAGEMENT
 Good IV access and invasive BP monitoring prior to induction.
 Consider epidural according to diagnosis for pain if needed.
 RSI with cricoid pressure. STP, Propofol, etomidate or ketamine accordingly.
 Standard ETT anesthesia with air /O2 and avoid N2O (distension, PONV)

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  Vasopressors must be prepared in case severe hypotension following induction. If inotropes
required-start early (vasopressin noradrenaline).
 If pts unresponsive to vasopressor give hydrocortisone 200 mg IV
 CVP monitoring necessary for volume status
 Ventilation could be difficult in theatre with high inflation pressures due to abdominal distention
and pulmonary edema/ ARDS
 Aim for VT 6ml/kg, PEEP 5-10 cmH2O, peak airway pressure < 30
 Allow some CO2 retention if necessary

POST OPERATIVE MANAGEMENT

1. ICU/HDU if physiological compromised /Prolong stay in recovery.
2. Good analgesia. (IV, continuous infusion or epidural)
3. Oxygen for 3days at 3-4 L/m by nasal/facemask delivery

NEUROMUSCULAR JUNCTION
Definition: Region of approximation between a motor neuron and muscle cell is NMJ.
Each ACh receptor in NMJ consists of 5 protein subunits:
2α subunits and single β, δ and ε units Only 2 α units capable of binding Isoform contains a ɣ subunit
instead of ε subunit  fetal or immature receptor
Eaton – Lambert Myasthenic Syndrome  ↓release of ACh
Myasthenia Gravis --------------------------------------------------------- ↓ no: of receptors

ACh rapidly hydrolyzed into acetate and choline by acetylcholinester also called specific cholinesterase
or true cholinesterase embedded into motor end-plate membrane adjacent to ACh receptor
Cations flow through open ACh receptor channels (Sodium and Calcium in, and potassium out)
generating end-plete potential

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SAFETY FEATURES OF ANESTHESIA MACHINE
1. Color coded hoses/ Pipelines/Cylinders
2. Diameter index safety system DISS or NIST (non-interchangeable screw thread)
3. PISS for cylinders
4. Non interchangeable Schrader valve connectors on wall sockets
5. Pressure relief valves- pressure regulators 35kp or 7kpa and 0.2 kpa
6. Flow restrictors – flow-meters
7. Oxygen flow meter on dawn stream side (Rt. Side)
8. Pressure gauges indicator pipeline and cylinder pressures
9. Oxygen flush valves
10. Interlocks b/w vaporizers.
11. Oxygen failure alarm (OFWD) 28 psi electronic sensors in newer machines
12. Oxygen failure protection device (OFPD) < 20psig O2 stops – other gases stops
13. Hypoxic- mixtures alarm (hypoxy gaurds or ration controller prevents mixtures which contains less
than 21- 25% oxygen
a) Link 25
b) ORMC - O2 pressure shut off valves
14 Ventilator alarms –warns about low or high airway pressures.
15 Alarms on all above physiological monitors
16 Battery backup
17 Reservoir bag.
UNK 25—Ensures FiO2 25%

PHYSIOLOGICAL MONITORS: HR, NIBP, SpO2, ETCO2, To, arterial BP, CVP.

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VAPORIZERS
All modern vaporizers are agent specific, capable of deliver a constant concentration of agent regardless
of temperature changes or flow through the vaporizer.
3 Types:
1. Plenum
2. Draw over
3. Electronic

1. PLENUM VAPORIZER: Driven by positive pressure from the anesthetic machine, usually mounted on
machine.
 Accurately calibrated to deliver a precise concentration of volatile anesthetic vapor over a
wide range of FGF
 Accurately splitting the incoming gas into two streams  Variable by pass flow –
High resistance to flow
 Example – TEC type, copper kettle

2. DRAW OVER VAPORIZER:

 Driven by negative pressure developed by patient.
 Performance depends on MV of patient (↑MV ↓Output)
 Accurate calibration is impossible
 Very low resistance to gas flow
 Used for emergency use in the field
 Example – OMV, EMO

3. ELECTRONIC:
 Dual-circuit gas – vapors blender
 Specifics for desflurane
 Heated to 39oC and pressurized to 200 kPa therefore requires electrical powers
 Warm-up period is required after switching on
 Will fail if mains power is lost
 Alarm sound if vaporizer is empty

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Dr. Tariq Mahar
 Agent specific
Efficient
TEC VAPORIZERS Variable bypass

1) TEC Mark-2 obsolete single bypass chamber

2) TEC Mark 3 ↑ by pass capacity
a. Improved vapourization ↑by pass capacity
b. ↑area of wicks – improve ventilation
c. ↓ pumping effect – long tube
d. Improved accuracy @ low FGF
e. Bimetallic strip situated in by pass channel

3) TEC Mark 4 
a. No spillage into by pass if inverted
b. Inability to turn two vaporizers @ same time

(Control knob,
4) TEC Mark 5
Release button,
a. Improved surface area for vaporization Locking lever
b. Improved key-filling action (accurate temp compensation) 15-35 oC very accurate,
Dual current gas vapor blends
c. Easier mechanism for switching on rotary valve and lock with one hand
not variable bypass)
5) TEC 6
a. Heated electrically to 39oC with 2 atm pressure
Large capacity
b. Electronic monitors and alarms (LED display)
Delivers 1% -18%
c. FGF does not enter vaporizing chamber Dial release
d. Desflurance vapors enter into path of FGF LED) light emitting
diode display
e. Percentage control dials (1-18%)
microprocessor based
f. Dial calibration is from 1% to 18 % vapour blander
g. Backup 9 volt battery if mains supply fails Thermostatic control
Pressurized chamber
Dragger D-Vaporizer

VOLATILE AGENT USED BY VAPORIZER PER HOUR:

3 x FGF (L/min) x volume % = mls liquid used/ hours

1ml of liquid volatile agent yields about 200ml vapour

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HAZARDS OF VAPORIZERS

1. Incorrect agent
2. Tipping
3. Simultaneous administration
4. Overfilling
5. Leaks
6. Electronic failure

Factors affecting concentration distal to vapouizer

1. SVP - ↑SVP - ↑con. deliv

2. Temp - ↑T - ↑SVP - ↑conc. deliv
3. Splitting ratio
4. Surface area of vapour chamber
5. Flow charactersistics
6. Amount of liquid in vapor cahmber
7. Intermittent back pressure
8. Gas composition

SAFETY FEATURES:

1. Keyed fillers
2. Low filling points
3. Secured vaporizers
4. Interlocks
5. Concentration dial increases output when rotated counterclockwise

CAPACITIES:

Tipping
Vapour 19.1 200ml Yes
Vapor 2000 300ml No
Tec 4 125ml Yes
Tec 5 225ml Yes
Tec6 375ml No
Tec 7 225ml Yes
Aladin (ADU) 250ml No

Single vapourizer, Novel system, 2 major components – 2 flow sesors, CPO, thermal compensation
angentcanrrette

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Dr. Tariq Mahar
 Poynting effect: effect of 1 gas on another to change CT

ANTIDISCONNECT DEVICE:
Is used to prevent accidental detachment of the gas outlet hose that connects the machine to the
breathing circuit

OXYGEN FLUSH VALVE: provides high flow (35-55 L/min) (600-1200 mls/s) of oxygen directly to common
gas outlet by passing the flow meters and vaporizers
 Used to rapidly refill or flush the breathing circuit
 Real potential for lung barotrauma if patient is connected to the breathing circuit as O2 is
supplied @ line pressure of 3-4bar.

AUXILIARY COMMON GAS OULET:

Used primarily for performing low pressure circuit leak test

FACTOR AFFECTING VOLATILE GAS CONCENTRATION IN THE BREATHING CIRCUITS

1. Anesthetic uptake in patient lungs
2. Minute ventilation
3. Total FGF
4. Volume of breathing circuit
5. Presence of gas leaks

OXYGEN ANALYZERS: (types 3)

1. Polarographic (Clark electrode)

Elector chemical sensors
2. Galvanic (fuel cell)
3. Paramagnetic  Expensive, self-calibrating, faster response

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 A pneumotachegraph is a fixed- orifice flow-meter
that can function as a spirometer

SPIROMETERS: Also called respire meters

Used to measure exhaled tidal volume in breathing circuit on all anesthesia machines, typically near
exhalation valve

WRIGHT RESPIROMETER: Also called vane anemometer

Employs a rotating vane of low mass in expiratory limb in front of the expiratory valve of circle system
The flow of gas across vanes causes their rotation which is measured electronically, photoelectrically or
mechanically

CIRCUIT PRESSURE: Breathing circuit pressure usually reflects airway pressures if it is measured as close
to patient airway as possible most accurate measurement are from Y-connections

↑Airway pressure:
1. Worsening pulmonary compliance
2. ↑ in TV
3. Obstruction in circuit, tt or patient’s airway

↓ Airway pressure:
1. Improved pulmonary compliance
2. ↓ in TV
3. Leak in circuit.

APL VALVE: Also called pressure relief or pop-off valve

 Fully open during spontaneous ventilation

 Partially closed during manual or assisted bag ventilation
 Risk of pulmonary barotrauma or hemodynamic compromise if closed too much or fully closed
 APL valves on modern machines acts as true pressure – limiting devices that can never be
completely closed – upper limit 70-80 cmH2O

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 Minimizes water and heat loss

HUMIDIFIERS:
ABSOLUTE HUMIDITY:
Wight of water vapor in 1L of gas (mg/L)

RELATIVE HUMIDITY:
Ratio of the actual mass of water present in a volume of gas to the maximum amount of water possible
at a particular temperature
 At 37oC and 100% relative humidity, absolute humidity is 44 mg/L
 At room temperature (21oC and 100% humidity) it is 18 mg/L
 Tracheal intubation and high FGF bypass the normal humidification system (upper respiratory tract)
and expose lower airways to dry < 10 mg/L room temperature gases
 Prolong humidification of gases by LRT leads to:
1. Dehydration of mucosa
2. Altered ciliary function
3. If excessively prolonged  Inspiration of secretions,
Atelectasis and even
V/Q mismatch in pts. with lung dx
 Humidification and heating of inspiratory gases is most important for small pediatric patients and
older patients with severe underlying lung pathology eg. Cystic fibrosis

PASSIVE HUMIDIFIERS:
Simplest designs are condenser humidifiers or heat and moisture exchanger (HME)
 These devices do not add heat or vapor but contains a hygroscopic material that traps exhaled
humidification which is then released in subsequent inhalation
 ↑apparatus dead space > 60 ml can cause significant rebreathing in pediatric pts.
 ↑ breathing circuit resistance
 ↑ WOB during spontaneous respira ons
 Excessive saturation of HME with water or secretions causes obstruction
 Acts as effective fillers protect breathing circuit and anesthesia machine from bacterial or viral
contamination

ACTIVE HUMIDIFIERS: Adds water to gas

1. Passover humidifier  passing gas over a water chamber
2. Wick humidifier  passing gas through a saturated wick
3. Bubble through humidifier  Bubbling through water

4. Vapor- phase humidifier  mixing it with vaporized water

Dew point is the temperature form which relative humidity can be obtained

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HEATED HUMIDIFIERS: With thermostatically controlled elements are most effective

Hazards:

1. Thermal lung injury

2. Nosocomial infections
3. ↑ airway resistance
4. Interference with flow meter fx
5. ↑ chance of circuit disconnec on
 Heated humidifiers are particularly valuable with children as they help prevent both hypothermia
and plugging of small tracheal tubes by dried secretions
 Active humidifiers do not filter respiratory gases

MEASUREMENT:

Relative humidity is measured by:

1. Hair hygrometer
2. Wet and dry bulb hygrometer
3. Regrciults hygrometer

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VENTILATORS
Modern ventilators generate positive pressure and gas flow in the upper airway.
These are 4 phases of ventilatory cycle:
1. Inspiratory phase
2. Transition phase form inspiration to expiration
3. Expiratory phase  Passive
4. Transition phase form expiration to inspiration

VENTILATOR CIRCUIT DESIGN:

Double – circuit system ventilators  TV delivered by bellows
Piston ventilators  No bellows, electrically driven pistons, Deliver accurate TV

SPILL VALVE: The ventilator used on anesthesia machine contains its own pressure relief valve called spill
valve, which is pneumatically closed during inspiration so that positive pressure can be generated.

PEAK INSPIRATORY PRESSURE:

Highest circuit pressure generated during an inspiratory cycle
Provides an indication of dynamic compliance

PLATEAU PRESSURE:
Pressure measured during an inspiratory pause (times of no gas flow) and mirrors static compliance
a. In normal person PIP is equal or slightly > than plateau pressure
b. ↑ in both PIP and PP can be due to ↑TV or ↓ pulmonary compliance
c. ↑PIP without any change in PP signals ↑ FGF rate or ↑airway resistance

CAUSES OF ↑PIP WITH ↑ PP:

1. ↑TV
2. ↓ pulmonary compliance  (Pulmonary edema, Trendelenburg position, effusion, Ascites,
peritoneal gas insufflation, tension pneumonia, Endo bronchial
intubation)

CAUSES OF ↑PIP WITH UNCHANGED PP:

1. ↑ inspiratory FGF rate

2. ↑ airway resistance (Kinked ETT, bronchospasm, secretions, FB aspiration, airway
compression, ETT cuff herniation

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VENTILATOR PROBLEMS:

1. Ventilator FGF coupling

2. Excessive positive pressure
3. TV discrepancies  Causes:
1. Breathing circuit compliance
2. Compression losses 3%
3. FGF coupling
4. Leaks in machine, circuit, patents airway

 Compliance for standard adult breathing circuit is 5 ml/cmH2O

If PIP is 20cm H2O 100ml of set TV is lost to expanding circuit

 If TV is 500ml –then 15ml of set TV is lost due to compression of gases

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Dr. Tariq Mahar
 -Arterial BP should be viewed as an indicator
but not a measure of organ perfusion

B.P MONITORING
NONINVASIVE ARTERIAL BP MONITORING TECHNIQUES:

1. PALPATION
2. DOPPLER PROBE: Useful in obese, pediatric and patient in shock
i. Transmits an ultra-sonic signal that is reflected by underlying tissue
ii. Probe movement or electro-cautery interferes with the signal
iii. Only systolic pressures can be reliably determined

AUSCULTATION: Motion artifact and electro cautery limits its use

OSCILLOMETRY: Should not used on patients on CP Bypass

ARTERIAL TONOMETRY: Measure beat-to-beat arterial B.P

CONTRAINDICATIONS: Techniques that rely on BP cuff are best avoided in extremities with vascular
abnormalities e.g.: dialysis should or with IV lines

INDICTIONS: Use of any anesthetic, no matter how trivial is an absolute indication.

INVASIVE ARTERIAL BP MONITORING: (Gold Standard)

INDICATIONS:
1. Induced hypotension
2. Anticipated wide BP swings
3. End organ disease necessitating precise beat to beat BP regulation
4. Need for multiple arterial blood gas analysis

CONTRAINDICATIONS:

1. Avoid in arteries without collateral blood flow

2. Preexisting vascular insufficiency e.g.: Raynaud’s phenomenon

ALLEN’S TEST: Is a simple but not very reliable method for determining the adequacy of ulnar collateral
circulation

SELECTION OF ARTERY FOR CANNULATION:

1. Radial artery: Commonly cannulated, superficial location and collateral flow
2. Ulnar artery: Difficult, deeper and more tortuous course
3. Brachial artery: Large and easily identifiable in antecubital fossa
Risk of kinking, less waveform distortion
4. Femoral artery: Excellent access, prove to pseudoaneurysim and formation of atheroma
↑incidence of infec on and arterial thrombosis
Aseptic necrosis of hof is rare in children

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 5. Dorsalispedis and posterior tibial arteries: Most distorted wave form modified Allen’s test
should be performed
6. Axillary artery: Surrounded by axillary plexus
Nerve damage result from hematoma or traumatic cannulation

COMPLICATIONS:
1. Hematoma
2. Bleeding
3. Vasospasm
4. Arterial thrombosis
5. Embolization of air bubbles or thrombi
6. Skin necrosis
7. Nerve damage
8. Infection
9. Loss of digits
10. Unintentional intra-arterial drug injection

FACTORS ASSOCIATED WITH ↑ RATE OF COMPLICATIONS:

1. Prolong cannulation
2. Hyperlipidemia
3. Repeated insertion attempts
4. Female gender
5. Extracorporeal circulation
6. Use of vasopress

Risk is minimized when:

1. Ratio of catheter to artery size is small
2. Heparinized saline is continuously infused through catheter @ 2-3 ml/
3. Aseptic technique

STRAIN GAUGE PRINCIPLE: Most pressure transducers are resistance types and are based on strain
gauge principle

The sensing elements are arranged as wheatstone bridge circuit

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PULMONARY ARTERY CATHETER (PAC)

INDICATIONS:

Cardiac Dx
1. CAD with LV dysfunction or recent infarction
2. Valvular heart disease
3. Heart failure (Cardiomyopathy, temponade, corpulmonel)

Pulmonary Dx
1. Acute respiratory failure e.g. (ARDS)
2. Severe COPD

Complex fluid Mx

1. Shock
2. ARF
3. Acute Burns
4. Hemorrhagic pancreatietis

Specific surgical procedures:

1. Pericardiectomy
2. Aortic aneurysm repair
3. Sitting craniotomies
4. Portal systemic shunts
5. Liver transplants

High risk obstetrics:

1. Severe toxemia
2. Placental abruption

CONTRAINDICATIONS: (Relative)
1. Complete LBBB (risk of CHB)
2. WPW syndrome and ebstein’s malformation (Risk of tachy-arrhythmias)

COMPLICATIONS:
1. Arterial puncture
2. Bleeding
3. Pneumothorax
4. Airembolism
5. Arrhythmias (V-Tac or AF)
6. RBBB
7. CHB
8. Pulmonary artery rupture
9. Catheter related sepsis

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 10. Thrombophlebitis
11. Venous thrombosis
12. Pulmonary infarction
13. Valvularvegetations or endocarditis
14. Deaths

HEMODYNAMIC DATA DERIVED FROM PAC:

1. CO/CI
2. TPR
3. PVR
4. SV/SI

MEASURED VALUES FORM PAC:

1. Pulmonary artery pressure

2. Pulmonary artery wedge pressure
3. Cardiac output
4. Mixed venous oxygen saturation
5. Right heart pressure (CVP)

DERIVED VALUES FORM PAC:

1. Stroke volume
2. Systemic vascular resistance (SVR)
3. Pulmonary vascular resistance (PVR)
4. Left cardiac work
5. Right cardiac work
6. Cardiac index

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 AIRWAY OBSTRUCTION & COMPLICATIONS

CAUSES OF RESPIRATORY OBSTRUCTION DURING ANAESTHESIA

EQUIPMENT RELATED:
1. Valve malfunction or kinking of breathing system
2. Surgical compression of tracheal tube
3. Occlusion of T.T lumen dueto secretions or blood
4. TT’s cuff herniation or over inflation
5. Esophageal or bronchial intubation

PATIENT RELATED:
1. Soft tissue edema in oropharynx 8. Strictures
2. Secretions 9. Pneumothorax
3. Tumour 10. Bronchospasm
4. Laryngospasm 11. Tracheomalacia.
5. Recurrent laryngeal verve palsy
6. laryngotracheobronchitis
7. Compression of TT by hematoma, thyroid tumours

MANAGEMENT OF AIRWAY OBSTRUCTION: (In Recovery Room)

 The most common airway complication is partial respiratory obstructions,
 Most commonly due t tongue falling back against posterior pharynx.
 Usually presents as sonorous respiration.
 Total obstruction causes, cessation of air flow, absent breath sounds and paradoxic chest
movements

Management:
1. Supplemental oxygen should be given during corrective measures
2. A combined jaw thrust and head tilt maneuver pulls the tongue forward and opens the airway. An
oral or nasal airway alleviates the problem  exclude equipment failure
3. If above maneuver fails, laryngospasm should be considered, Characterized by high pitched
crowning noises but silent with complete glottic closure.
4. The jaw thrust maneuver particularly combined with gentle positive airway pressure via a tight filling
face mask usually breaks the laryngospasm.
5. Any secretions or blood in hypopharynx should be suctioned to prevent recurrence.
6. Refractory laryngospasm should be treated aggressively with small dose of suxa 10-20 mg and
temporary IPPV with 100% O2 to prevent sever hypoxemia or negative pressure pulmonary edema.
7. Endotracheal intubation may occasionally be needed for ventilation
8. If intubation is unsuccessful  cricothyrotomy is indicated
9. Glottic edema is a common cause of airway obstruction in children, I/V corticosteroids
(Dexamethasone 0.5mg/kg) OR aerosolized racemic epinephrine (0.5ml of 2.25 % solution with 3ml
N/S) may be useful.
10. Post-operative wound hematomas following head and neck, thyroid and carotid procedures can
quickly compromise airway, so opening the wound immediately relieves tracheal compression.
11. Throat packings left in hypopharynx unintentionally following oral surgery can cause immediate or
delayed airway obstruction

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Dr. Tariq Mahar
HICCUPS:
Regular and repeated spasmodic diaphragmatic movements may occur after I/V induction associated
with vagal stimulation.

TREATMENT:
1. Anticholinergics premedication ↓ incidence
2. Persistent hiccups abolished by deepening anesthesia, stimulating nasopharynx with suction
catheter or metoclopramide
3. Muscle relaxation if surgical compromise.

LARYNGOSPASM:
Acute glottis closure by vocal cords
Presents as crowing or absent inspiratory sounds and marked tracheal tug

Management:
1. Remove stimulus that precipitate laryngospasm.
2. Apply 100% O2 with tight face mask and closed expiratory valve.
3. Do suction to remove secretions and blood from airway
4. Apply CPAP and attempt manual ventilation.
5. Forcible jaw thrust or anterior pressure on the body of mandible just anterior to mastoid process
(Larson’s Point) may break laryngospasm by a combination of stimulation and airway clearance
6. Deepening anesthesia with small doses of propofol 20-50mg, reduce spasms
7. If laryngospasm fails to improve and O2 is falling consider a small dose of suxa 0.1-0.5mg /kg
8. If it is sever enough a full doseof suxa 1.0mg/kg should be given and tracheal intubation done.
9. If no venous access suxa can be given I/M or S/C 2-4mg /kg
10. Consider a change in airway management e.g. LMA instead of tracheal tube to prevent recurrence.
11. Cricothyroidotomy is life saving
12. Doxapram, a respiratory stimulant has also been used successfully in laryngospasm.

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Dr. Tariq Mahar
BRONCHOSPASM:

Presents as expiratory wheeze, prolong expiratory phase and ↑ven lator infla on pressures and
upwardly sloping ECO2 pleatue.

RISK FACTORS:
1. Asthma,
2. Respiratory infection,
3. Atopy,
4. Smoking

CAUSES:
1. Pungent volatile anesthetic e.g. isoflurane, desflurane
2. Insertion of artificial airway during light anesthesia
3. Stimulation of carina or bronchi by tracheal tube
4. β-Blockers
5. Histamine releasing drugs.
6. Drug hypersensitivity, pulmonary aspiration and FB in lower airway also present as bronchospasm

MANAGEMENT: is aimed at preventing hypoxemia and resolving bronchospasm.

1. 100% O2 should be given.

2. Anesthesia deepened if appropriate.
3. Aggravating factors removed e.g. TT repositioned and surgery stopped.
4. Bronchodilators in increments e.g. aminophylline or salbutamol
5. Volatile anesthetics and ketamine are also effective bronchodilator.
6. Epinephrine is indicated in life threatening situations and may be given via tracheal tube.
7. Steroids and H1 receptor antagonist indicated in later management of sever case.
8. If hypoxemia develops in spontaneously breathing pt, then TT and artificial ventilation should be
considered.
9. Peep and high ventilator rates should be avoided.
10. Hypercapnia may have to be tolerated in order to avoid gas trapping and barotrauma.
11. If pt. receiving IPPV, ventilation should be adjusted to peak airway pressure

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Dr. Tariq Mahar
Mendelson’s syndrome: is a potential fatal complication of anesthesia, perioperative aspiration of gastric contents is called
Mendelson’s syndrome.

ASPIRATION OF GASTRIC CONTENTS:

Common during difficult intubation, emergency cases and obese or pregnant
Bronchospasm may be the first sign, cyanosis, coughing, tachypnea and hypotension. If large quantity of
gastric content is aspirated, respiratory obstruction, ventilation perfusion mismatch and intrapulmonary
shunting produce severe hypoxemia with later development of clinical pneumonitis and or infection.

MANAGEMENT:
1. Preoperative fasting, H2 receptor blocker and prokinetic drug e.g. metoclopramide.
2. If GA is the plan then tracheal intubation is must achieved by RSI with cricoids pressure.
3. Awake intubation is advisable if difficult intubation is predicted.
4. Tracheal tube should not be removed during emergency until protective airway reflexes are
regained and pt. is awake.
5. If aspiration occurs during anesthesia, further regurgitation should be prevented by immediate
application of cricoids pressure.
6. Pt. SHOULD BE PLACED IN A HEAD DOWN POSITION (Trendlenburg Position)
7. Tracheal suction to facilitate removal of aspirate.
8. IPPV instituted must not be delayed if significant hypoxia
9. Bronchodilator therapy
10. ↑FiO2
11. If hypoxemia is refractory, PEEP may be instituted
12. Surgery should be abandoned if significant morbidity develops.
13. Flexible bronchoscope for liquids removal and rigid for solid removal
14. I/V steroids and pulmonary lavage via flexible bronchoscope ↓inflammation
15. Order CXR and ABG’s helps in assessment in severity
16. Transferred to critical care unit for further monitoring and respiratory care.

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Dr. Tariq Mahar
HYPOXEMIA:
CLASSIFICATION OF HYPOXIAS:

Hypoxia Pathophysiologic category Clinical Example

Hypoxic hypoxia: ↓pBarom or ↓FiO2 (<21%)  Altitude, O2 equipment error
alveolar hypoventilation  Drug overdose, COPD exacerbation
Pulmonary diffusion defect  Emphysema, Pulmonary emboli
Pulmonary V/Q mismatch  Asthma, Pulmonary emboli
R-L shunt  Atelectasis, cyanotic congenital heart Dx
Circulatory Hypoxia Reduced cardiac output Congestive heart failure, MI,
dehydration
Hemic hypoxia Reduced hemoglobin content Anemia
Reduced hemoglobin function Carboxyhemoglobinemia,
Methemoglobinemia
Demand hypoxia ↑O2 Consumption Fever, seizures
Histotoxic hypoxia Inability of cell to utilize Oxygen Cyanide toxicity
PBarom , barometric pressure; COPD, chronic obstructive pulmonary disease; V/Q ventilation/perfusion; RL, right to left.

CAUSES OF HYPOXEMIA DURING ANAESTHESIA:

1. Hypoxic inspired gas mixture due to equipment failure e.g. cylinder or pipeline oxygen supply failure
or misconnection.
2. Inaccurate settings or leak in flow meters
3. Obstruction or leak in breathing system.
4. Hypoventilation due to inadequate ventilation (↓MV or TT obstruc on).
5. Respiratory depression
6. V/Q mismatch like bronchial intubation, secretions, atelectasis, pneumothorax, bronchospasm,
aspiration, edema, embolus.
7. Low cardiac output
8. Methemoglobinemia
9. Malignant hyperthermia

Note: pulmonary shunting and atelectasis during anesthesia are much more likely to cause hypoxemia
than is hypoventilation.

MANAGEMENT OF HYPOXEMIA:
If hypoxemia is detected during anesthesia the following drill should be instituted:
1. A.B.C. Ensure an adequate airway, ensure adequate ventilation and check for an adequate CO by
feeling carotid pulse
2. Test the integrity of breathing system by manual ventilation of lungs and confirm bilateral chest
movement and breath sounds Blow down the tracheal tube if necessary.
3. Confirm the position and patency of tracheal tube by assessing capnogram, passing a suction
catheter through tracheal tube and auscultate the chest.
4. Exclude delivery of a hypoxic gas mixture using an oxygen analyzer, Increase FiO2 to 100%.
5. Now search for any clinical evidence of V/Q mismatch with early exclusion of pneumothorax.
If atelectasis or ↓FRC gentle hyperinflation and apply PEEP
6. If diagnosis is difficult, measure core temperature and consider ABG analysis and CXR.

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Dr. Tariq Mahar
PNEUMOTHEORAX:
CAUSES:
1. Trauma
2. Central venous cannulation via subclavian approach
3. Brachial plexus blockade
4. Cervical and thoracic surgery
5. Barotrauma
6. Spontaneously in pts with asthma, COPD or Marfan’s syndrome.
7. High peak inspiratory airway pressures during mechanical ventilation.

Sing and symptoms:

1 Unequal air entry
2 Asymmetrical chest movement
3 Wheeze
4 surgical emphysema
5 ↑CVP
6 Mediastinal shift.
7 Hypoxemia
8 Hypercapnia. 9. Hypotension.
CXR provides definitive diagnosis.

Note: A pneumothorax should be excluded during anesthesia if unexplained tachycardia, hypotension,

hypoxemia, hypoventilation (SV) or high inflation pressures (CMV) occurs intraoperatively.

MANAGEMENT:
1 Nitrous oxide should be discontinued
2 Lungs ventilated with 100% oxygen, using low inflation pressures
3 The presence of air in pleural space confirmed by aspiration through I/V cannula (14G) inserted into
chest wall in 2nd intercostal space in midclavicular line or 5th space in mid axillary line. If
pneumothorax is under tension a hissing sound will be heard as air is released.
4 If pneumothorax is confirmed, I/V cannula should be left in place and a formal chest drain is inserted
to decompress the pneumothorax

Note: In tension pneumothorax air is forced into thorax during inspiration but cannot escape during expiration Ipsilateral
lung collapsed, mediastinum and trachea shifted to contralateral side, simple pneumothorax develop into tension PT by positive
pressure ventilation.

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Dr. Tariq Mahar
HYPERTENSION: 25% > than baseline (preoperatively)
Intraoperative acute HTN ↑risk of ischemia, infarc on and hemorrhage in other organs and in particular
brain

CAUSES OF HTN DURING ANESTHESIA:

PRE-EXISTING
1. Undiagnosed or poorly controlled HTN
2. PIH
3. Withdrawal of antihypertensive medication
4. ↑ ICP

↑ SYMPATHETIC TONE:
5. Inadequate analgesia
6. Inadequate anesthesia
7. Hypoxemia
8. Airway manipulations ( laryngoscopy, extubation)
9. Hypercapnia

Drug overdose:
10. Vasoconstrictors (norepinephrine, phenylephrine)
11. Inotropes (Dobutamine)
12. Mixed inotropes vasoconstrictors (Epinephrine, ephedrine)
13. Ketamine
14. Ergometrine

OTHERS:
15. Hypervolemia/ Fluid overload
16. Aortic cross- clamping.
17. Pheochromocytoma
18. Malignant hyperthermia
19. Thyroid storm
20. Measurementerrors.

Post operative causes:

1. Uncontrolled or poorly on
2. Inadequate analgesia
3. Distended bladder
4. Hypercarbia
5. Hypoxemia
6. Acidosis.

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Dr. Tariq Mahar
 RISK OF PERIOPERATIVE HTN:
1. Myocardial ischemia/ infarction 4. Stroke
2. Hypertensive heart failure 5. Renal failure
3. Hemorrhage 6. Aortic dissection

MANAGEMENT OF HTN:

PREOPERATIVE:

1. Continue adequate antihypertensive drugs to chronic hypertensive pt

2. Anxiolytic premedication to make pt. calm and relaxed.
3. Surgery should be postponed until adequate control is achieved <180/100
4. Perioperative β blockade ↓mortality in pts @risk of MI.
5. History, physical examination and investigations e.g.: ECG, Ophthalmoscopy, CXR, renal function
and UCE

PERIOPERATIVELY: (intraop)

1. Stimulating events such as laryngoscopy, surgical incision, extubation and aortic cross-clamping
etc causes surge in sympathetic tone results in significant ↑in arterial pressure.
2. These events usually be anticipated and short acting opioid e.g. fentanyl 10 μg/kg, β-blocker e.g.
esmolol 0.5mg/kg, lidocaine 1mg/kg or temporary deepening of anesthesia may be used to
prevent. Potentially damaging HTN, duration of laryngoscopy as short as possible
3. Exclude potential causes of vasodilation hydralazine, nitroglycerin, nitropruside
4. If no pathological cause is found then use of an antihypertensive agent such as labetalol or
hydralazine may be indicated if HTN persists.

POSTOPERATIVE:

1. Post operative HTN is common and anticipated in pts having poorly controlled HTN
2. Close B.P monitoring in recovery room.
3. Sustained ↑B.P. can cause formation of wound hematomas and disruption of vascular
suture lines.
4. HTN could be enhanced by respiratory abnormalities, pain, volume overload or bladder
distension Treat the cause.
5. I/V antihypertensive like labetalol given if necessary.
6. When pt resumes oral intake, preoperative medications restarted

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Dr. Tariq Mahar
HYPOTENSION:
MAP 25% < baseline value hypotension impairs perfusion and oxygenation of vital organs but during
anesthesia due to ↓ myocardial and cerebral metabolic rates it is less likely.

CAUSES OF HYPOTENSION DURING ANESTHESIA:

1. ↓CO
2. Hypovolaemia
3. Hemorrhage
4. GI fluid losses
5. Pulmonary embolus
6. Aortocaval compression
7. Pericardial effusion/ tamponade
8. ↑Intrathoracic pressure like mechanical ventilation, PEEP
9. Pneumothorax
10. Head up position

MYOCARDIAL CONTRACTILITY
1. Drugs like most anesthetic agents, β-Blockers, Ca+ blockers
2. Acidosis
3. Ischemia / infarction
4. Arrhythmias
5. Pericardial tamponade

↓ AFTERLOAD:
1. Drugs like anesthetic agents, antihypertensive.
2. Hypersensitivity, dueto drugs, colloids, blood etc
3. Histamine release due to morphine, atracurium etc.
4. Central regional blockade (local anesthetics)

MANAGEMENT:
1. Preoperative correction of hypovolaemia helps to avoid excessive reduction in BP following
induction of anesthesia
2. For intraoperative hypotension a working diagnosis should be established and treatment should
be commenced aiming to correct cause of hypotension
3. Most commonly I/V fluids or ↓ anesthe c concentra on is effec ve in most pa ents but ensure
sufficient anesthetics to avoid awareness.
4. If hypotension persists after excluding significant pathological cause, vasopressor agent eg
ephedrine 5mg or metaraminol 1mg given
5. Treatment of hypotension should follow sequence of assess  treat  reassess.

ENDOCARDIAL VIABILITY RATIO:

The ration of DPTI/TTI is EVR and represents myocardial oxygen supply-demand balance. Normal EVR >1
value less than 0.7 is associated with subendocardial ischemia DPTI  Diastolic pressure time index
reflects coronary blood supply. TTI  Tension time index reflects oxygen demand.

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Dr. Tariq Mahar
HYPOVOLEMIA:
SIGNS:

1. Thirst 5. ↓Tissue turgor.

2. Dryness of mucous membranes 6. Tachycardia.
3. Cool peripheries 7. Postural hypotension.
4. Oliguria (UO < 0.5 ml/kg/hr)

CAUSES:

Preoperative:
1. Hemorrhage like trauma, obstetric, GI, major vessel rupture. 5. Fistulae.
2. Vomiting 6. Fever.
3. Intestinal obstruction. 7. Diuretics
4. Diarrhea 8. Burns.
9. Fasting

Intraoperative:
1. Hemorrhage
2. Insensible loss e.g. sweating, expired water vapors
3. Third space loss eg prolong and extensive surgeries
4. Drainage of stomach, bowel or ascites.
5. Urine output
6. Deficit – NPO

PERIOPERATIVE FLUID MANAGEMENT:

70 kg male with 8 hours fasting

Maintenance fluid requirement

1st 10kg 4 x 10 = 40
Next 10kg 2 x10 = 20
For each kg above 20 kg 1 x 50 = 50
110 ml/hr is the maintenance fluid requirement

Preexisting deficits (NPO) can be estimated by multiplying normal maintenance rate by length of the fast
i.e.
110 x 8 = 880ml
NPO Mainte. Blood loss Other losses (Urine Output)
(Evaporative &3rd space loss)
1st hour 440 ml 110ml Suction sponges 10 ml Degree of tissue trauma fluid req.
laps 100- 150ml Minimal 2ml/kg
nd
2 hour 220ml 110ml Moderate 4ml/kg
Severe 8ml/kg
rd
3 hour 220ml 110ml

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Dr. Tariq Mahar
 ( )
ABL =EBV

HAEMORRHAGE:
 For most patient transfusion point corresponds to Hb.b/w 7 & 8 g/dl
 A level of 10 g/dl generally used for elderly and those with significant cardiac or pulmonary disease
 Patient with normal hematocrit should be transfused only after losses greater than 10-20% of blood
volume
 Transfusion point can be determined preoperatively form hematocrit and estimating blood volume.

ALLOWABLE BLOOD LOSS:

Example: An 85 kg woman has preoperative hematocrit of 35%. How much blood loss will decrease her
hematocrit to 30 %.

1. Estimated blood volume =65 ml/kg x 85 kg = 5525 ml.

2. RBCV 35 % = 5525 x 35 % =1934 ml
3. RBCV 30 % = 5525 X 30 % = 1658 ml
4. Red cell loss @ 30 % = 1934-1658 = 276 ml
5. Allowable blood loss = 3 x 276 = 828 ml

 Transfusion are not recommended until hematocrit ↓ to 24% (Hb. < 8)

 One unit of PRBC will ↑Hb to 1 g/dl and hematocrit 2-3% (adults)
 10 ml/kg transfusion of PRBC will ↑ Hb 3 g/dl and hematocrit by 10 %

AVERAGE BLOOD VOLUMES:

Premature neonate 95 ml/kg EBV X
Full term neonate 85 ml/kg
Infants 80 ml/kg
Men 75 ml/kg
Woman 65 ml/kg

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Dr. Tariq Mahar
ARRHYTHMIAS:
CAUSES OF ARRHYTHMIAS DURING ANESTHESIA:
CARDIORESPIRATORY:

1 Hypoxemia 4. Hypercapnia
2 Hypotension 5. Myocardial Ischemia
3 Hypocapnia

METABOLIC:

1. Inadequate analgesia
2. Inadequate anesthesia
3. Airway manipulation
4. Sympathomimetic
5. Hyperthyroidism
6. Electrolyte disturbance (hyperkalemia/ hypokalemia, hypo/hypercalcaemia)
7. Malignant hyperthermia

SURGICAL:

1 Increased vagal tone (tractionon eye, anus and peritoneum)

2 Direct cardiac stimulation (chest surgery, CVP cannula)
3 Dental surgery.

DRUGS:

1 Vagolytic (Atropine,Pancuronium)
2 Sympathomimetic (epinephrine, ephedrine)
3 Volatile anesthetics (halothane, enflurane)
4 Digoxin

MANAGEMENT:

1 Preoperative correction of fluid, electrolyte and acid base balance

2 optimization of CAD and HTN
3 ECG monitoring
4 Treat the cause
5 If persists  specific antiarrhythmic or electrical cardio-version is indicated.

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Dr. Tariq Mahar
THROMBOEMBOLUS:
An embolus is the passage of a non-blood mass through vascular system
Thromboembolus occurs usually form deep veins of the leg or pelvis
Uncommon during anesthesia

Risk factors:

1 Immobility 6. Pelvic or limb surgery

2 Prolong hospital stay 7. HRT
3 Major trauma 8. Past H/O venous TE
4 Malignancy
5 Smoking

Sign and symptoms:

During anesthesia, pulmonary thromboembolism

Presents with tachycardia, hypoxemia, arrhythmia, hypotension, bronchospasm, acute, ↓ in ETCO2 or
cardiovascular collapse.

MANAGEMENT:

1. Risk factors should be managed actively to prevent DVT.

2. OCP or HRT should be stopped 6 weeks before elective surgery in risky patients
3. Prophylactic heparin, graduated compression stockings and intermittent calf compression reduce
likelihood of new thrombosis
4. Use of subarachnoid or epidural anesthesia reduces the risk of postoperative DVT in some surgical
groups.
5. If intraoperative pulmonary embolism is suspected, lungs should be ventilated with 100% O2,
bronchodilator therapy, fluid loading and inotropic support should be considered.
6. After initial management anticoagulation and rarely surgical removal of embolus may be indicated.
7. In extreme presentations, cardiac arrest protocols should be used.

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Dr. Tariq Mahar
GAS EMBOLUS:
CAUSES:

1 Surgical wound.
2 Positions that place operative site above Rt. atrium e.g. sitting, park bench, knee-chest, and
head up positions.
3 Vascular catheters. (IV lines)
4 Laporoscopy and thoracoscopy.

CLINICAL PRESENTAION:

An entry rate of 0.5 ml/kg/min (30 ml) produces clinical signs

1 Rapid ↓in ETCO2 5. Arrhythmias

2 Hypoxemia 4. ↑ PA pressures
3 Tachycardia 6. Millwheel murmur.

MANAGEMENT:

1 To prevent intraoperative air embolus adjusts patient’s position and site of operative field with
respect to Rt. atrium.
2 If air embolism is detected, further entry is prevented by flooding the operative site with saline.
3 During head and neck procedures, venous pressure @ surgical site may be increased by
compressing jugular veins.
4 Application of PEEP increases venous pressure and decrease ingress of air
5 During insufflations procedures, surgeon should be instructed to depressurize the insufflated
body cavity.
6 Nitrous oxide should be discontinued to avoid expansion of gas bubbles
7 Lungs should be ventilated with 100% O2
8 Gas may be aspirated from RV or RA via a venous catheter.
9 Expansion of intravascular volume, inotropic support and internal or external cardiac massage
may be necessary.
10 Placing pt in head down left lateral may help allowing gas to escape from RV into RA and vena-
cava.

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Dr. Tariq Mahar
AWARENESS:
 Psychological sequel includes insomnia, depression and post traumatic stress disorder (PTSD)
with distressing flash backs
 Light anesthesia particularly when paralyzed by relaxations is associated with highest risk more
likely in(emergency and obstetric surgery)
 Breathing system malfunctions and disconnections also associated with awareness.

SIGNS:
Paralyzed patient:
From activation of sympathetic nervous system
1. Sweating
2. Tachycardia
3. HTN
4. Tear formation
5. Pupillary dilatations
Un-paralyzed patient: experiencing noxious stimulation may move or grimace

ESPECIALIZED MONITORING:

1. Processed EEG such as bispectral index scale (BIS monitor)

2. Auditory evoked potential monitoring system

MANAGEMENT:

1. Anesthesia should be deepened immediately.

2. If arterial pressure is low despite inadequate anesthetic then ↑arterial pressure by I/V fluids,
ventilator settings or vasopressors.
3. Consider I/V midazolam 5 mg
4. If patient complains postoperatively, the anesthetist should be informed and should visit the
patient.
5. If there is genuine awareness and clear anesthetic error then prompt apology and explanation
should be provided.
6. It is advisable that anesthetist always record the timing (absolute and relative to surgery) and
dose of anesthetics.

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Dr. Tariq Mahar
HYPOTHERMIA:
Body temperature < 36 ⁰C
Protective during times of cerebral or cardiac ischemia ↓ CMRO2
Preoperative hypothermia is associated with ↑ mortality rate
Metabolic rate ↓ by 10% for each 1 ⁰C ↓ in core temperature

CAUSES: hypothalamus controls core body temperature

1. Low ambient temperature 5. Use of wet packs
2. High air flow in OT 6. Operations on open body cavities
3. Exposed body 7. Irrigation and I/V infusion of cold fluid
4. Ventilation with cold and dry gas 8. ↑ Risk in neonates, infants, elderly and burns.

Intra operative monitoring

Thermistor or thermocouple
RX
Postoperative shivering
1. Pethidine 0.33 mg/kg 4. Methylphenidate
2. Doxapram 1.5 mg/kg 5. Physostigmine
3. Clonidine 2µg/kg 6. Ondansetron 0.1 mg/kg Onset

DELETERIOUS EFFECTS OF HYPOTHERMIA:

1. Cardiac arrhythmias and ischemia

2. Increased peripheral vascular resistance (↑SVR)
3. Left shift of hemoglobin-oxygen saturation curve
4. Reversible coagulopathy (platelets dysfx)
5. Post operative protein catabolism and stress response
6. Altered mental status
7. Impaired renal function
8. ↓ drug metabolism
9. Poor wound healing
10. ↑ incidence of infection

MANAGEMENT:

Phase (I) Prewarming with forced air warming blankets

Phase (II)
1. Forced air warming blankets
2. Warm water blankets
3. Heated humidification of inspired gases
4. Warm I/V fluids
5. ↑ ambient OR temperature
6. Keep pt anesthetized until temperature is normalized

24
Dr. Tariq Mahar
 HYPERTHERMIA:

Core body temperature > 37.5⁰C

↑metabolic rate  acidosis (no treatment) sweating and vasodilation hypovolaemia and tissue
hypoxia  seizures and CNS damage

CAUSES:
1 Sepsis and infection
2 Drug reactions
3 Anaphylaxis
4 Incompatible blood transfusion
5 Pheochromocytoma
6 Thyroid storm
7 Malignant hyperthermia

MANAGEMENT:
1 General measures include exposure of body surface, application of icepacks, use of fans and
cold I/V fluids and gastric lavage with cold I/V fluid
2 Specific measures depend on the cause.
3 Paracetamol and NSAID may reduce core-temperature if cause is sepsis related
4 Any unexplained ↑in temperature especially if it is increasing rapidly  urgent exclusion of
malignant hyperthermia.

SECONDARY THERAPY:
Antihistamines e.g. chlorpheniramine 20 mg I/V
Corticosteroids e.g. hydrocortisone 100mg I/V
Catecholamine infusions e.g. epinephrine 0.05 -0.1 µg/kg/min
Consider bicarbonate for acidosis 0.5 m-mole/kg
Airway evaluation before extubation
Bronchodilators e.g. salbutamol 2.5mg/kg for persistent bronchospasm

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Dr. Tariq Mahar
 MANAGEMENT AIMS:
1. Correct hypoxemia
2. Restore intravascular fluid volume
3. Inhibit further release of chemical mediators

ANAPHYLAXIS: Ig-E mediated

CAUSES:

1. Muscle relaxant e.g. suxamethonium

2. Antibiotics e.g. penicillin (most common) Any bronchospasm, hypotension,
3. Latex (2nd most common) arrhythmia or urticaria, should be
4. Radiocontrast media
considered to be due to anaphylaxis
5. Blood products
6. Colloids until proved otherwise
7. Protamine
8. SK
9. Bone cement
10. Atropine and opioids etc.

SIGNS:

1. Urticaria
2. Cutaneous flushing
3. Bronchospasm
4. Hypotension
5. Arrhythmias
6. Cardiac arrest

Early signs: Coughing, skin erythema, difficulty with ventilation and loss of palpable pulse.
The conscious PH impending doom, dyspnea, dizziness, palpitation and nausea

MANAGEMENT:
Skin prick test, intradermal test and RAST
AIM To obtund the effect of anaphylaxis mediators and to prevent their further release
INITIAL THERAPY:

1. Stop administration of drugs likely to cause anaphylaxis

2. Maintain airway, give 100% oxygen – Call for help
3. Lay patient supine with feet elevated
4. Give epineph50 mg-feet element
5. Give epinephrine 50 µg-1000µg until improvement occurs
6. Start volume expansion with crystalloids or colloids

26
Dr. Tariq Mahar
SAFE MAXIMUM DOSE:
Lidocaine: 4mg/kg with epinephrine 7mg/kg
Bupivacaine: 2mg/kg with epinephrine 3mg/kg
Prilocaine: 6mg/kg with epinephrine 8mg/kg

LOCAL ANAESTHETIC TOXICITY

CAUSE:

1. Accidental intravenous injection

2. Excessively rapid absorption.
3. Absolute over dosage

SIGN AND SYMPTOMS:

1. Dizziness,
2. Drowsiness,
3. Confusion,
4. Tinnitus and
5. Circumoral tingling
6. Metallic taste
7. Tonic-clonic convulsion if severe toxicity cardiovascular symptoms include bradycardia and
hypotension and it usually occurs at 4-6 times the concentrations @which convulsion occur, CV
collapse occurs earlier with bupivacaine than with lidocaine  ↑ myocardial binding

MANAGEMENT:

1. Before block adequate preparation (IV access, resuscitation equipment)

2. Adequate monitoring.
3. Test dose of local anesthetic which contains epinephrine results in tachycardia if intravascular.
4. LA should always be injected slowly with repeated aspirations for blood, constant verbal contact
and observation of patient.
5. Addition of epinephrine ↓ speed of absorp on.
6. If toxicity of occurs  injection must be stopped and patient assessed
7. Airway should be checked and oxygen should be administered.
8. If hypoventilation or apnea  lungs ventilated with umbo or breathing system.
9. If patent unconscious or unable to maintain airway  tracheal intubation
10. I/V fluids and vasopressors for hypotension.
11. Arrhythmias should be treated appropriately.
12. Heart block may require pacing.
13. Anticonvulsants (diazepam 10mg, STP 50mg) for convulsions.

27
Dr. Tariq Mahar
NEEDLESTICK INJURY:
Hollow needles >risk than solid (surgical) needles

UNIVERSAL PRECAUTIONS:

1. No recapping and immediate disposal of contaminated needles

2. Use of gloves and other barriers during contact with open wound and body fluid
3. Frequent hand washing.
4. Proper techniques for disinfection or disposal of contaminated material
5. Particular caution by pregnant health care workers , and no contact with patient by workers
who have exudative or weeping dermatitis

MANAGEMENT:

1. Cleaning the wound and notifying the appropriate authority.

2. Serological status should be established.
3. Prophylactic IFN (with or without ribavirin) following a high risk inoculation form hepatitis C
patient.
4. Prophylactic zidovudine reduces risk of HIV following contaminated needlestick.
5. A hepatitis B vaccine is strongly recommended prophylactically for anesthesia personnel
6. The risk of acquiring HIV after single needle stick injury is 0.4-0.5%

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Dr. Tariq Mahar
PATIENT POSITINS:
TRENDELENBURG: (Head down)

CVS  Baroreceptor activation, ↓CO, ↓SVR, ↓HR, ↓BP

Respiratory ↓lung capacities, ↑V/Q mismatch, ↑atelectasis, ↑ risk of regurgitation
Other ↑ ICP, ↓ CBF, ↑ IOP in pts with glaucoma

REVERSE TRENELENBURG: (Head up)

CVS ↓Preload, ↓ CO, ↓BP, Baroreflex ↑sympathe c tone, ↑HR, ↑SVR

Respiratory:  ↓WOB in spontaneous respira on, ↑ FRC
Other  ↓CPP and ↓CBF

LITHOTOMY:

CVS ↑Preload, ↑circulating blood volume, ↑BP, ↑CO

Respiratory↓Vital capacity, ↑ risk of aspiration

PRONE:

CVS Blood pooling in extremities, compression of abdominal muscles ↓preload, ↓CO, ↓BP.
Respiratory  ↓total lung compliance and ↑WOB
Others  Extreme head rotation ↓cerebral venous drainage and ↓CBF

ATERAL DECUBITUS:

CVS  CO unchanged, ↓BP (↓SVR) (Rt. Side >Lt. Side)

Respiratory ↓volume and ↑perfusion of dependent lung, ↑ventilation of dependent lung in awake
(no V/Q mismatch), ↓ventilation of dependent lung in anesthetized V/Q mis

SITTING:

CVS Blood pooling in lower extremities, ↓CO, ↓BP, ↑ HR, ↑ SVR

Respiratory: ↑ lung volumes and ↑FRC, ↑WOB
Others ↓CBF

COMPLICATION:

Air embolism, alopecia, Backache, compartment syndrome, corneal abrasion, digit amputation
Retinal ischemia, skin necrosis and Nerve palsies (Brachial plexus, common peroneal, radial, ulnar)

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Dr. Tariq Mahar