ICU by Dr. KHM
ICU by Dr. KHM
ICU by Dr. KHM
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Table of contents
Topic Page/reference
1 ICU 559 – 560
17 Mode 574
19 NIV 576
20 PEEP 577
21 CPAP 578
22 BiPAP 579
23 Weaning 580
24 SBT 581
30 Mx type 1 RF 591
31 Mx type 2 RF 592
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42 Why Right IJV cannulation is generally preferred over the left IJV? 603
44 CVP 605
47 JVP/ScvO2/SvO2 608
62 DIC 643
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Dr. K H Mozumder
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ICU
An Intensive Care Unit is a specially staffed & equipped ward dedicated for management of patients with life-threatening
illness, injuries or complications. 1950: concept from post-operative recovery or polio epidemic;
1960: developed from respiratory and cardiac care.
Role of an ICU:
1) Physiological optimization of patients to prevent the onset of organ failure.
2) Facilitation of complex surgery.
3) Support of failing organ system by providing-
Intensive nursing
Invasive and non-invasive monitoring
Therapeutic measures otherwise not possible in ward level.
Opportunity for live organ transplantation.
Types of ICU:
1) Multi-disciplinary; e.g. medical ICU, surgical ICU, Burn ICU, etc.
2) Uni-disciplinary; e.g. Neuro ICU, Cardiac ICU, etc.
OR,
1) Open:
Have access to all doctors/specialists for admission and management of patients.
The patients are managed & coordinated by anaesthetist group day to day & co-managed by referring specialist.
Line of responsibilities are unclear.
2) Closed: Admission, mx, discharge and referral policies under the control of intensivist or critical care specialist.
3) Semi-open/Semi-closed
Consultancy Primary physician may consult with an No need, an intensivist is all in all.
intensivist.
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Design of ICU
1) Site: close proximity to relevant acute areas, i.e. operating rooms, emergency departments, CCU, labour wards and
investigation departments.
2) Size: ranges from 1 – 4 bed per 100 total hospital beds (depends on type, availability of HDU and admission policy)
3) Reception area: reception foyer + waiting room for visitors + distressed or interview room+ overnight relatives’ room.
4) Patient areas:
Open multi-bed wards (Single Bed area 150 – 215 sq. feet)
Single bed isolation room (Cubicle)
Mixed 5 bed in cubicle
Specialized rooms/beds if necessary for procedures/surgeries, hemodialysis, burns, use of IABP machines, etc.
Utilities port for each patient bed:
O2 port :3
Medical air ports :2
Suction port :3
Electrical power outlet : 16
Bed side light :1
5) Technical areas: laboratory & workshop for repairing, maintenance and development.
6) Central station:
Communication, Monitoring, Drugs
Storage of notes, radiographs
Emergency trolley/ Crash cart
Security control
7) Nurse 1:1
8) 24 hours on site dedicated cover by medical staff
9) An identifiable consultant
10) Staff areas: Lounge/rest rooms, changing rooms, conference rooms, etc.
3) Immunocompromization:
a) Poor local organ defenses:
Respiratory
Poor cough reflex
Poor ciliary movement
Poor laryngeal reflex
Alimentary
Organism converted to a part of flora
Increased pH may colonize bacteria.
Eye: loss of blinking drying of sclera infection
Genitourinary: Urinary catheterization
4) Structure of ICU:
Closed environment
Lack of well ventilation
Lack of high efficiency particulate air (HEPA) system
Inadequate humidification
Cubicles/open space
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Level 1
Patients recently discharged from a higher level of care
Patients in need of additional monitoring/clinical interventions
Patients requiring critical care outreach service support, clinical input or advice
Level 2
Patients needing preoperative optimisation.
Patients needing extended postoperative care.
Patients stepping down to from level 3 care.
Patients receiving single organ support including basic cardiovascular, renal or respiratory support
Level 3
Patients receiving advanced respiratory support alone.
Patients requiring a minimum of two organs supported.
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Cardiovascular
1) Cardiac arrest
2) Pulse rate <50 0r >150 bpm
3) SBP <90 mmHg; MAP <60 mmHg
4) Poor peripheral perfusion
5) Evidence of inadequate O2 delivery
6) Metabolic acidosis
7) Hyperlactataemia
8) Poor response to volume resuscitation
9) Urine output <0.5 ml/kg/Hour (check urea, creatinine, K+)
Neurological
1) Threatened or obstructed airway.
2) Repeated or prolonged seizures.
3) Absent gag or cough reflex
4) Failure to maintain normal PaO2 and PaCO2.
5) Failure to obey commands.
6) GCS <12
7) Sudden fall in level of consciousness (GCS by <2 points than previous)
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I HUG FAST is a continuous quality improvement (CQI) checklist to ensure reliable application of evidence-based
measures to reduce complications in the ICU.
Infection control
Hand hygiene and head of bed elevation, Ulcer prophylaxis, Glycemic control
Feeding, Analgesia, Sedation, Thromboprophylaxis
b) Breathing
Assessment : -RR, Pattern of breathing, VT
-Chest auscultation
-Use of accessory muscles or not
-Chest wall movement symmetry
c) Circulation
Assessment: -Pulse, BP, signs & symptoms of shock
Monitoring: -ECG
Considering -large bore intravenous access
-volume resuscitation
-arterial cannulation
-central venous cannulation
-vasopressors may be needed.
d) Disability
Assessment: -GCS
Considering: -exclusion of hypoglycemia and reviewing airway, breathing and circulation.
e) Exposure & Evidence: Should look for targeted clinical examination and evidence, the information provided by any
recent investigations, prescriptions or monitoring sheets.
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Dr. K H Mozumder
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Monitoring in ICU
a) Respiratory:
1. ABG & Pulse oximetry
2. Lung function: PaO2, P/F ratio, etCO2, airway pressure & VT for lung compliance & airway
resistance.
b) Circulatory:
1. Pulse; BP (NIBP, ABP); ECG; CVP
2. PAWP
3. Cardiac output; Urine output
4. Peripheral skin temperature
5. Blood lactate, [H+], Base excess & Base deficit.
4) Laboratory reports
a) Hematological including coagulation & biochemistry.
b) Microbiological including culture and sensitivity.
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In stage-3 & 4, there may be little or no pain due to significant tissue damage.
Usual sites: Ischium, greater trochanter, sacrum, heel, malleolus, occiput, etc.
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NON-ANAESTHETIC:
1) Protection of airway, e.g. in unconscious pts, impaired protective laryngeal reflexes, in airway obstruction.
2) Removal of sputum/secretions.
3) CPR
4) Respiratory arrest or RR <8 breaths/min
5) Tachypnoea >35 breaths/min
6) Inability to tolerate oxygen mask/CPAP/NIV; e.g. agitation, confusion.
7) Hypoxaemia (PaO2 <60 mmHg, SpO2 <90%) despite CPAP with FiO2 >0.6
8) Hypercapnia if conscious level is impaired or risk of raised ICP.
9) Worsening respiratory acidosis.
10) Removing the work of breathing in exhausted pts.
C. Following extubation:
1) Airway trauma : edema and stenosis (glottic, subglottic or tracheal); hoarseness (vocal cord
granuloma or paralysis); laryngeal malfunction and aspiration.
2) Laryngospasm
3) Negative-pressure pulmonary edema.
Complications of laryngoscopy
1) Airway trauma: dental damage; lip, tongue or mucosal laceration; sore throat; dislocated mandible;
retropharyngeal dissection.
2) Physiological reflexes: hypoxia, hypercarbia, HTN, tachycardia, raised ICP & IOP, laryngospasm.
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Non-treatable causes:
1) Polyneuropathy of critical illness
Sepsis
Multi-organ failure
Burns
Trauma
Axonal degeneration of motor & sensory nerves
5) Corticosteroid myopathy
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Advanced ventilation
Aims: To minimize further pulmonary damage due to barotrauma, volutrauma and biotrauma.
Strategies are:
1) Low tidal volume (4 – 6 ml/kg of IBW) and airway pressure as low as possible while achieving adequate
oxygenation.
2) Permissive hypercapnia (PaCO2 upto 60 – 70 mmHg).
3) Higher levels of PEEP to achieve adequate alveolar recruitment and oxygenation.
4) Prone ventilation
5) High-frequency oscillatory ventilation (HFOV)
6) Inhaled nitric oxide (NO)
7) Extracorporeal membrane oxygenation therapy (ECMO)
8) Corticosteroids [risks of secondary infection and muscle weakness]
SBTs involve
Removing all respiratory support, typically on a daily basis.
And observing how long the pt is able to breathe unassisted.
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Mechanical ventilation
MV is any means in which physical devices or machines are used to either assist or replace spontaneous respiration. When it
is continued for >21 consecutive days for >6 hours/day, then it is called prolonged mechanical ventilation.
Types:
1) Negative pressure ventilation (Tank ventilator, Iron lung, Cuirass ventilator)
2) Positive pressure ventilation
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5) Multiple trauma
B. Respiratory parameters:
1) Direct measurements: PaO2 <50 mmHg on room air
PaCO2 >50 mmHg in absence of metabolic alkalosis
(A-a)O2 gradient >350 mmHg [A–a gradient = PAO2–PaO2; normally <15 mmHg
but
progressively increases with age upto 20–30 mmHg]
VD/VT >0.6
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Dr. K H Mozumder
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MODE
The method by which the patient and the ventilator interact to perform a ventilatory cycle is called the
mode.
They include:
1) CMV Continuous/Controlled mandatory/mechanical ventilation (the simplest form)
2) ACV Assist control ventilation
3) IMV Intermittent mandatory ventilation
4) SIMV Synchronized intermittent mandatory ventilation
5) MMV Mandatory minute ventilation
6) PCV Pressure control ventilation
7) PSV Pressure support ventilation
8) IRV Inverse I:E ratio ventilation
9) APRV Airway pressure release ventilation
10) HFV High frequency ventilation
11) DLV Differential lung ventilation
In controlled ventilation, the ventilator initiates the breath and perform all the work of breathing (WOB).
In assisted ventilation, the pt initiates or terminates all or some of breathing with variable amount of support
from ventilator.
Inverse ratio ventilation is the ventilation in which the inspiratory phase time is longer than the expiratory phase time.
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Cycling
Inspiratory to expiratory change over or the mechanism that cycle ventilation from inspiratory to expiratory
phase is called cycling.
3) RR : 12 – 20 breaths/min
8) PEEP : 5 – 20 cmH2O
PIP is the maximum pressure during the inspiratory phase time, and it provides an indication of dynamic
compliance.
Plateau Pressure is the resting pressure measured during the inspiratory pause (a time of no gas flow), and it
mirrors static compliance. Airway pressure usually falls when there is an inspiratory pause. This lower pressure
is called the plateau pressure.
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Uses:
First-line therapy in patients with type-2 respiratory failure secondary to acute exacerbation of COPD.
It can also be used to support selected patients with hypercapnia secondary to pulmonary edema or
pneumonia or during weaning from invasive ventilation.
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PEEP
Application of positive pressure (5-20 cmH 2O) during expiration as an adjunct to mechanically delivered breath
is referred as PEEP (Positive End Expiratory Pressure).
Relative contraindications
Unilateral lung disease.
Pneumothorax
Hypovolaemia
Intracardiac shunt
Obstructive lung disease
Raised ICP
Advantages
1) Recruits atelectatic alveoli.
2) Counteracts small airway closure.
3) Redistributes lung water.
4) ↓ Intrapulmonary shunt
5) Maintains FRC
6) Improves lung compliance
7) ↑ Oxygenation
Disadvantages:
1) Haemodynamic instability due to increased intrathoracic pressure at higher PEEP (↓ cardiac output, ↓BP)
[Decreased venous return due to increased Right atrial pressure and Increased Pulmonary Vascular
Resistance causes Right ventricular pressure overall impaired diastolic filling of Left ventricle]
2) Barotrauma
3) ↑ ICP
4) ↓ Hepatic and renal blood flow.
5) If intrinsic PEEP is high, the concentration of additional extrinsic PEEP can become crucial as there is a
potential risk of sustained lung hyperinflation if external PEEP is greater than the concentration of intrinsic
PEEP.
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CPAP
Continuous Positive Airway Pressure (CPAP) is defined as ventilation that maintains the airway pressure
above ambient throughout the patient’s breathing cycle. The term is commonly used in reference to
spontaneous ventilation.
CPAP pressure should be 5 – 10 cmH2O (less than lower esophageal sphincter pressure)
Methods
Tightly fitting full face mask
Nasal mask
High-flow nasal cannula
Nasal pillows (Adam’s circuit)
Nasal prongs (for neonate)
Hoods
Indications
Hypoxaemia due to decreased lung volume secondary to abdominal or thoracic surgery (hypoventilation)
ARDS
Pulmonary edema
Pulmonary atelectasis (post-operative)
Sleep apnoea syndrome
Advantages
1. Increased FRC & VT.
2. Prevent alveolar collapse.
3. Increased oxygenation (helps correct hypoxaemia).
4. Increased muscle strength.
5. Decreased intrapulmonary shunting.
6. May be alternated with SIMV during weaning.
7. Monitoring of Expiratory VT and apnoea alarm prevent hypoxia.
8. Reduce WOB and improve hypercapnia in type-2 respiratory failure.
Disadvantages
1. Increased intrathoracic pressure causes decrease in venous return.
2. Decreased cardiac output.
3. Increased ICP.
4. Barotrauma.
5. Decreased hepatic and renal blood flow.
6. Decreased urinary output & GFR.
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BiPAP
Bi-level Positive Airway Pressure (Turbine ventilator).
iPAP= 15 – 25 cmH2O
ePAP= 4 – 10 cmH2O
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Weaning
The process of withdrawing a patient from ventilator support in a staged manner is called weaning. It is a
dynamic process
2) Muscle fatigue signs are: ↑RR, ↓VT, ↑VE, ↓Vital capacity, paradoxical respiration
4) Decreased supply of energy: e.g. hypoxaemia, anaemia, electrolyte imbalance, ↓cardiac output.
Methods of weaning
1) SIMV
2) PSV
3) SBT (Spontaneous Breathing Trial) BiPAP, CPAP, T-piece
4) SIMV + PSV
4) Respiratory mechanics:
Endurance: Maximum Voluntary Ventilation (MVV): twice VE
VT > 5 ml/kg
B. Stable cardiovascular function with minimal requirements for inotropic or vasopressor drugs.
C. Appropriate mental status: pt is arousable or GCS ≥13
D. OTHERS:
Patient should be awake and co-operative with intact neuromuscular and bulbar function.
Primary pathology should have resolved.
Precipitating illness and complicating factors adequately treated.
Low sputum production.
Minimal sedation with absence of severe pain.
Adequate nutritional status.
No fever.
No significant electrolyte imbalance.
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A successful spontaneous breathing trial usually indicates that tracheal extubation will be successful, and if not,
a repeat trial can be performed daily.
A gradual form of weaning is to allow a short period of spontaneous breathing without ventilatory assistance
(e.g. initially 1–5 min) with close observation and monitoring of the patient. The duration and frequency of
these trials is increased as the patient’s condition improves.
Disadvantages of IRV:
Increased gas trapping
Decreased venous return/cardiac output
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Pneumonia
Pneumonia is an acute respiratory illness associated with recently developed radiological pulmonary shadowing,
which may be segmental, lobar or multilobar.
Or,
Pneumonia is an inflammation of the pulmonary substances of the lungs.
Red hepatisation Fibrin forms on the cut surfaces of the affected lobe and it resembles liver.
Resolution Clearance and repair mechanisms restore the normal architecture of the lung.
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Hospital-acquired or nosocomial pneumonia is a new episode of pneumonia occurring at least 2 days after
admission to hospital. It is the second most common hospital-acquired infection (HAI) and the leading cause of
HAI-associated death. The elderly are particularly at risk, along with patients in intensive care units, especially
when mechanically ventilated (VAP).
Healthcare-associated pneumonia (HCAP) is the development of pneumonia in a person who has spent at least
2 days in hospital within the last 90 days, or has attended a hemodialysis unit, received intravenous antibiotics,
or been resident in a nursing home or other long-term care facility.
4) Bacteraemia
Abdominal sepsis
IV cannula infection
Infected emboli
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This can be attributed partly to the prevalence of infection with MDR pathogens like Enterobacter,
Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa and
Enterobacteriaceae (ESKAPE bugs).
D/Ds of VAP:
Atelectasis
Aspiration
Pulmonary embolism with infarction
Pulmonary hemorrhage
Cardiogenic pulmonary edema
ARDS
Fluid overload
Hypersensitivity pneumonitis
Drug reactions: cyclophosphamide, methotrexate
Cryptogenic organizing pneumonia (H/O recent viral infection)
Radiation pneumonitis
Lung contusion
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Dx of VAP:
There is no gold standard for diagnosis. Clinical scores use focal infiltrates on chest x-ray increased FiO 2
requirements, sputum production, temperature, and inflammatory markers to suggest the presence of VAP.
The modified clinical pulmonary infection score (CPIS) at baseline is calculated from the first five variables.
For positive Gram stain and culture, two points are added to the CPIS baseline score. A score of more than six at
baseline or after incorporating the Gram stain or culture result is considered suggestive of pneumonia. CPIS has
low sensitivity and specificity for diagnosing VAP.
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Mx:
Pertinent history taking, physical examination, sending investigations and resuscitation need to be carried out
simultaneously.
2) Sending paired blood culture and endotracheal aspirate or bronchoalveolar lavage (BAL) for Gram stain
and quantitative aerobic culture.
3) Starting empiric antibiotic therapy for suspected infection following local guidelines and it should cover for
MRSA with linezolid or vancomycin.
4) Sending further investigations
FBC
Serum Procalcitonin
C-reactive protein (CRP)
Urea, creatinine
Serum electrolytes
Prothrombin time
Blood culture—two sets (if not sent earlier)
Endotracheal aspirates or fiberoptic bronchoscopy with protected specimen brush (PSB) or
bronchoalveolar lavage (BAL) (in selected cases like immunosuppressed)
Arterial blood gas, lactate
Urine for microscopy
Chest X-ray
ECG or echocardiogram (optional) if the patient is in septic shock
A paired blood culture setwas defined as two separate sets of blood cultures drawn from different peripheral
venous sites or two separate sets of blood cultures where one was taken from a peripheral site and the other from
a central catheter.
Selective decontamination of the digestive tract (SDD) is a technique designed to eradicate aerobic, potentially
pathogenic bacteria colonising the oropharynx and upper gastrointestinal tract, thus eliminating an important
risk factor for nosocomial pneumonia. It has not been widely adopted because of its inconsistent effects on
mortality and concerns about the potential for selecting antibiotic-resistant pathogens.
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Prevention of VAP:
Pharmacological methods Non-pharmacological methods
1) Scrupulous hand hygiene with alcohol 1) Use of noninvasive mask ventilation
based solution
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Respiratory Failure
It may be defined as impairment of normal gas exchange severe enough to require acute therapeutic
interventions.
The term respiratory failure is used when pulmonary gas exchange fails to maintain normal PaO 2 & PaCO2
levels.
Respiratory failure is defined as inadequate gas exchange by the respiratory system with the result of
hypoxaemia (PaO2 <60 mmHg) with or without hypercapnia (PaCO2 >50 mmHg).
Causes of
Type-I RF Type-II RF
High altitude (low ambient O2) COPD
Pneumonia Reduced respiratory drive, e.g. drug overdose, head
Pulmonary edema injury
Pulmonary embolism Upper airway obstruction e.g. edema, infection, FB
Pulmonary fibrosis Late severe acute asthma
Pulmonary contusion (blunt chest Peripheral neuromuscular diseases, e.g. GBS,
trauma) Myasthenia gravis
Pneumothorax Flail chest injury
Bronchial asthma Exhaustion
ARDS, Aspiration, Lung collapse
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Mx of Type-I RF
C/F:
1) Stimulation of carotid body chemoreceptor leading to dyspnoea, tachypnoea and hyperventilation.
4) Sympathetic nervous system stimulation leading to tachycardia, diaphoresis, systemic vasoconstriction and
hypertension.
INV:
1) ABG (Hypoxaemia)
2) X-ray chest
Rx:
1) Maintenance of airway.
2) High flow oxygen therapy
3) Nebulized bronchodilators; Corticosteroids
4) Leukotriene receptor antagonist: Montelukast
5) Respiratory stimulant
6) Treatment of specific precipitating cause.
7) Frequent physiotherapy.
8) Pharyngeal suction, if needed.
9) Antibiotics (if there is evidence of infection).
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Mx of Type-II RF
C/F:
1) Central cyanosis
2) Depressed consciousness level
3) Warm periphery
4) Full bounding pulse
5) Flapping tremor/asterixis
6) Vasodilation
7) Wheeze, prolonged expiration, Hyperinflation, intercostal drawing, pursed lips.
8) Peripheral oedema, raised JVP, Hepatomegaly, ascites
INV:
1) ABG (Hypoxaemia, Hypercapnia and Acidosis)
2) X-ray chest
Rx:
1) Maintenance of airway
2) Treatment of specific precipitating cause
3) Controlled oxygen therapy (low flow) 24 – 28%
Start with 24% controlled-flow venturi mask.
Aim for a PaCO2 >7 kPa (52 mmHg); a PaCO2 <5 kPa (37 mmHg) is dangerous.
4) Nebulized bronchodilators
5) Frequent physiotherapy
6) Pharyngeal suction, if required.
7) Antibiotics (if there is evidence of infection)
8) Diuretics (if there is evidence of fluid overload)
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Dr. K H Mozumder
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ARDS
Sponge lung, shock lung, non-cardiogenic pulmonary edema, capillary leak syndrome, traumatic wet lung, &
adult hyaline membrane disease.
2) Bilateral opacities on chest x-ray, not fully explained by effusions, lobar/lung collapse or nodules.
3) Respiratory failure not fully explained by cardiac failure or fluid overload. Objective assessment (by
Echocardiography) must exclude hydrostatic edema if no risk factor is present.
4) Impaired oxygenation:
Mild PaO2:FiO2 >200 mmHg but ≤300 mmHg with PEEP or CPAP ≤5 cmH2O
Moderate PaO2:FiO2 >100 mmHg but ≤200 mmHg with PEEP ≤5 cmH2O
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Pathophysiology of ARDS
Damage of either lung epithelium or endothelium due to direct insult on lung cells or indirect effect resulting
from systemic inflammation.
↓
Sequestration of neutrophil and macrophages in pulmonary capillaries with the release of oxygen free radicals
(OFRs), proteases and leukotrienes.
↓
Increased capillary permeability (capillary leak syndrome)
↓
Damage of type-II pneumocytes leading to surfactant depletion
↓
Exudation & accumulation of protein rich cellular fluid within alveoli (alveolar flooding) and formation of
‘hyaline membranes’.
↓
Combination of loss of surfactant and fluid accumulation leading to ventilation impairment.
↓
V/Q mismatch
↓
Increased intra-pulmonary shunt
Inflection point is defined as the pressure level on a pressure –
↓ volume curve at which collapsed alveoli are recruited (opened) and
Hypoxaemia.
with small changes in pressure, large changes in volume take place.
The principal M/A for both PEEP and CPAP appears to be expansion
of partially collapsed alveoli & this recruitment (re-expansion) of
collapsed alveoli occurs at PEEP or CPAP levels above the inflection
point.
C/F of ARDS
H/O predisposing factors
Acute onset
Unexplained tachypnoea
Sever breathlessness and labored respirations.
Central cyanosis
Fine crepitation throughout both lung fields.
D/Ds of ARDS
Cardiogenic pulmonary edema
Diffuse pneumonia
Alveolar hemorrhage
Acute interstitial lung diseases
Acute immunologic injury (e.g. hypersensitivity, pneumonia)
Toxin injury e.g. radiation, etc.
Neurogenic pulmonary edema.
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Chest x-ray showing diffuse non-homogenous bilateral infiltrates (cotton wool appearance); dependent
areas tend to be most affected.
Phases of ARDS
Exudative 1 week ↑RR, ↓PaO2, dyspnoea; CXR diffuse infiltrates
Proliferative Early in the 2nd Replacement of fibrin and cell debris by collagen.
week ↑PaCO2, persistent hypoxaemia,
CXR diffuse infiltrates + air bronchogram.
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Rx of ARDS
1) GENERAL mx:
Early recognition and treatment of underlying medical and surgical disorders (e.g. sepsis, aspiration,
trauma, etc.)
Empirical treatment of sepsis when indicated and of secondary nosocomial infection.
Good nutritional support.
Strict glycemic control.
Prophylaxis against DVT, GIT bleeding and central venous catheter infections.
Other general care- stress ulcer prevention, physiotherapy, etc.
Minimizing procedures and their complications.
Use of sedatives and NMBA
Haemodynamic management
2) Oxygen therapy: target SpO2 >90% or PaO2 >60 mmHg and reduce FiO2 ≤0.6 to prevent toxicity.
3) Ventilatory support:
When CPAP fails, IPPV with high PEEP
Lung protective strategies to counteract both pathophysiology of ARDS & ventilator associated lung
injury:
a) Low tidal volume (4 – 6 ml/kg of IBW)
b) Permissive hypercapnia (Low VT ventilation with elevated PaCO 2 upto 70 mmHg with pH
>7.2).
c) Inverse I:E ratio
d) Use of higher PEEP (to improve alveolar recruitment, limit atelectasis and reduce
hypoxaemia)
e) FiO2 < 0.6
8) Free radical scavenger, anti-prostaglandins and anti-proteases may have some role.
Morbidity/mortality from ARDS take place usually from the precipitating cause or complications like sepsis,
renal failure, gastrointestinal hemorrhage, etc.
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Prone positioning
The volume of the lung compressed by the mediastinal structures decreases.
Pleural pressure becomes more uniform.
Ventilation-perfusion mismatch is reduced.
Improve gas exchange
Reduce ventilator induced lung injury (VILI)
Recruitment of collapsed lung field by redistribution of edema.
Increased diaphragmatic motion enhances ventilation.
The evidence base is mixed; it appears to depend on the specific cohort of patients, timing and duration of prone
therapy.
Care bundles
Care bundles consist of a number of evidence-based practices each of which has been found to improve outcome
and are easily achievable. When performed collectively, reliably and continuously these bundles confer a greater
probability of survival.
There is an increasing evidence for the utility of care bundles for specific conditions in the intensive care setting.
The most familiar bundles are the Surviving Sepsis campaign resuscitation (6 h) and management (24 h)
bundles and ventilator care bundles.
The ventilator care bundle comprises the following components to reduce VILI or ALI or ARDS:
Low tidal volumes (4 – 6 ml/kg of ideal body weight)
Plateau airway pressure less than 30 cmH2O
Limiting peak inspiratory pressure to 30 cmH2O
Sedation holds and use of sedation scores
Permissive hypercapnia (acceptance of higher than normal PaCO2 with pH > 7.2)
Acceptance of PaO2 7 – 8 kPa, SaO2 >90%
Semirecumbent positioning (head up by 30 – 45 degrees unless contraindicated) during ventilation to
reduce the incidence of VAP
Lung recruitment using higher PEEP to prevent alveolar collapse
Use of longer inspiratory times as with IRV or airway pressure release ventilation (APRV)
Using ventilation modes that allow and support spontaneous respiratory effort.
Avoidance of NMBAs
Protocol-driven weaning
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Universal precautions refers to the practice of avoiding contact with patients' bodily fluids, by means of the
wearing of nonporous articles such as medical gloves, gowns, goggles, and face shields.
1) Simple hygiene.
2) Frequent hand washing.
3) No recapping and the immediate disposal of contaminated needles.
4) Use of gloves and other protective barriers during contact with open wounds & body fluids.
5) Use of disposable equipments where possible.
6) Minimum equipment in OT.
7) Careful disposal of sharps and other equipment.
8) Use of proper techniques for disinfection or the disposal of contaminated materials.
9) Filters on breathing tubing if not disposable.
10) Non-disposable equipment should be decontaminated with 2% glutaraldehyde; washed with soap &
water and then left in glutaraldehyde for a further 3 hours.
11) Contaminated floors and surfaces should be washed with 1% hypochlorite solution.
Antisepsis is the process of prevention of infection by inhibiting or arresting the growth & multiplication of
microorganisms on the surface of the living objects. Antiseptic agents are as follows:
10% povidone-iodine
2% chlorhexidine gluconate (CHG)
70% alcohol
0.5% CHG in 70% isopropyl alcohol
Disinfection is the process of killing of non-sporing microorganisms on the surface of an inanimate object.
Sterilization is the process of killing of all forms of living microorganisms including bacteria, viruses, prions,
fungi and their spores present in inanimate objects by means of physical, chemical or gaseous procedures.
Methods of sterilization:
1 Heat Low temperature Water bath, Vaccine bath & Inspissator
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Autoclave
An autoclave is a device used to sterilize equipment and other supplies by subjecting them to high pressure
saturated steam (moist heat) at 121 ºC at 1 atmospheric pressure for around 15 – 20 min depending on the size
of the load and contents. It was invented by Charles Chamberland in 1884, although a precursor known as the
steam digester was created by Denis Papin in 1679.
Principles of autoclaving
In autoclave, the temperature is increased by increasing the pressure. Steam is used. The moisture portion of the
steam is removed and replaced by sterile air. Indicator tape or tubes are used to be confirmed that the correct
condition is reached. It is useful for metals and fabrics. But there is deterioration of rubber & plastic. The sharp
instruments become blunt. 121 ºC at 1 atmospheric pressure for around 15 – 20 min is required, depending on
the size of the load and contents.
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Vascular catheters
Vascular catheter or intracatheter is a plastic tube, usually attached to a puncturing needle, inserted into a blood
vessel for infusion, injection, or pressure monitoring. First introduced by Werner Forssmann in 1929 and was
awarded Nobel Prize in medicine in 1956 for performing the first right-heart catheterization in a human subject.
Accessible central veins: Internal jugular, Subclavian & Femoral vein; Basilic, external jugular vein.
Advantages Disadvantages
Bleeding can be recognized and Risk of carotid artery puncture
controlled
Internal
Malposition is rare
Jugular
Less risk of pneumothorax
Techniques of cannulation
1) A catheter over a needle
2) A catheter through a needle
3) A catheter over a guidewire (Seldinger’s technique)
Seldinger’s technique
This is a technique of cannulation where the catheter is inserted over a guidewire. In this technique,
1) Introducer needle is used to locate the vein.
2) Guidewire is threaded through the needle and Needle is removed.
3) Skin & vessel are dilated with the help of a dilator.
4) Catheter is placed over the guidewire and Guidewire is removed.
5) Catheter is secured in place.
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Approaches for
Trendelenburg position (to reduce the risk of air embolism & to distend the vein)
Patient’s head turned slightly away from the side of venepuncture.
Triangle formed by the clavicle and sternal & clavicular heads of the SCM muscle is
Internal
located.
Jugular
Needle direction: along the medial border of the lateral head of the SCM, toward the
ipsilateral nipple, at an angle of 30º to the skin, lateral to the carotid artery pulsation.
Right IJV cannulation is generally preferred over the left due to:
1) The larger diameter of the right-sided vein
2) Its more direct path to the SVC
3) The lower dome of the right pleura
4) Absence of the thoracic duct
5) Lower rate of catheter malposition with right-sided access and
6) The relative ease of access for a right-handed operator
Subclavian vein lies posterior to the medial portion of the clavicle and in between the 1 st rib & the clavicle
(though, invariable anatomic position).
Subclavian artery is located posterior to the vein and anterior scalene muscle lies between them.
Optimal location of the catheter tip: just superior to or at the junction of the SVC and the RA
Trendelenburg position (to reduce the risk of air embolism & to distend the vein)
Patient’s head turned slightly away from the side of venepuncture.
Needle direction:
Subclavian
1 – 2 cm inferior to the junction of medial & middle thirds of the clavicle.
Needle is held 5 – 10º to the coronal plane of the body and is directed towards the
suprasternal notch.
Constantly pull back on the plunger as it needle advances.
Femoral artery lies at the junction of the medial & middle thirds of the inguinal ligament.
Pt lies supine.
Needle direction:
Femoral
2 – 3 cm inferior to the inguinal ligament and 1 – 1.5 cm medial to the femoral artery at
the inguinal ligament. 45º with the skin, parallel to the thigh and directed cephalad.
Take care not to advance the needle past the inguinal ligament.
Right femoral vein offers an ergonomic advantage for Rt-handed clinicians and vice versa.
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Infectious:
Line infection; Blood stream infection
Sepsis, Cellulitis
Osteomyelitis
Septic arthritis
Miscellaneous:
Pneumothorax, Haemothorax, hydrothorax, haemomediastinum
Chylothorax (on left side)
Cardiac perforation, cardiac tamponade
Trauma to nearby nerves & arteries
Dysrhythmias
Catheter knotting or malposition
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P = atrial depolarization
QRS = ventricular depolarization
T = ventricular repolarization
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a wave is the pressure increase secondary to atrial contraction. It is the tallest wave.
c wave represents the increase in atrial pressure caused by the closing & bulging of the tricuspid valve
into the RA during ventricular contraction.
Cannon 'a waves' are seen when the atrium contracts against a closed tricuspid valve.
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Causes of
Raised CVP decreased CVP
RVF Venodilators
Tricuspid stenosis & regurgitation Hypovolaemia
Pericardial effusion (cardiac tamponade) Effective hypovolaemia (vasodilatation)
Constrictive pericarditis Dehydration
SVC obstruction; Fluid overload; vasopressors Artefact: transducer is raised inadvertently.
Hyperdynamic circulation
High PEEP settings, positive pressure ventilation
Pulmonary Embolism (PE)
COPD/cor pulmonale
Increase in intrathoracic pressure
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Continuous fiberoptic venous oximetry is a valuable tool for monitoring the balance between oxygen delivery
and consumption at the bedside. Continuous venous oximetry is a sensitive real-time indicator of this balance,
which can be applied as a global or regional indicator – with mixed venous oxygen saturation (SvO 2) and central
venous oxygen saturation (ScvO2) being the most commonly monitored. SvO 2 is a true reflection of the global
balance between oxygen delivery and consumption since it is measured in the pulmonary artery, where venous
blood returning to the right heart from the superior vena cava (SVC), inferior vena cava (IVC) and the coronary
sinus (CS) have mixed. SvO2 has been extensively studied and used clinically to monitor the global balance
between DO2 and VO2.
ScvO2
It is the oxygen saturation of venous blood coming from the head and upper body. It is measured from the
superior vena cava (SVC), that drains blood from the head and upper body to the heart and thus, it is called as
central venous oxygen saturation.
ScvO2 is usually 2 – 3% lower than SvO2. Because it contains predominantly SVC blood from the upper body
Blood from the upper body has a higher oxygen extraction ratio, and thus a lower SO2 than IVC blood.
Of major organs at rest, the brain has high oxygen extraction ratio and the kidneys have the lowest.
Use of SvO2
As an early indicator of imminent haemodynamic failure.
As an indicator of O2 supply or demand in critically ill patients.
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Arterial catheterization
Phlebostatic axis is the junction of the fourth intercostal space and midpoint between the anterior and posterior
chest walls. It is used as the reference point for the level of pressure transducer while measuring intraarterial
pressure.
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Why should a pressure transducer be positioned at the same level as the patient’s heart?
To avoid introducing error by reading hydrostatic pressure (the pressure exerted by a column of fluid) in
addition to blood pressure. For every 10 cm the transducer is below the heart, the system will overread by
7.4mmHg (and will under-read by the same amount if the transducer is above the heart)
What features of an arterial blood pressure measurement system help to reduce errors from excessive damping?
1) The cannula and tubing should be wide-bore, short (no longer than 48 inch), high-pressure (non-compliant)
and kink free.
2) Avoiding tubing extensions and stopcocks.
3) All connections should be tight.
4) The fluid within the tubing should be non-compressible and of low density.
5) 0.9% saline or heparinised saline is usually used, and it must be free of air bubbles and clots.
6) 3-way taps and extra lengths of tubing should be kept to a minimum.
7) The flush system should be pressurised to 300mmHg to allow an infusion at 2 – 4ml/hr to reduce thrombus
formation and also to allow the ‘fast flush test’ to be performed.
8) The waveform should also be displayed so that the waveform changes associated with excessive damping
may be quickly detected and appropriate alterations made to the system.
9) Keeping the cannulated extremity in neutral or slightly extended position.
Why should an intra-arterial blood pressure measurement system have a high natural frequency?
The arterial waveform consists of a fundamental wave and at least eight harmonic waves of increasing
frequency. Should any of those waves oscillate at a similar frequency to the natural frequency of the measuring
system, resonance will occur, resulting in inappropriate amplification of the waves, distorting any readings. For
this reason a system should have a natural frequency which is greater than eight times the maximal anticipated
heart rate.
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Damping is an influence within or upon an oscillatory system that has the effect of reducing or preventing its
oscillation. In physical systems, damping is produced by processes that dissipate the energy stored in the
oscillation.
It indicates the tendency of an oscillating system to return to its resting state. Anything that takes energy out of
the system results in a progressive diminution of amplitude of oscillations.
Damping can be checked by performing a ‘ square wave test’. This is done by activating the flush device, then
quickly releasing it and observing the waveform on the monitor. The waveform will sharply rise and ‘square
off’ at the top when the flush is activated and then the tracing returns to the baseline after it is released. Then
checking the number of oscillations to get an idea about damping:
The square wave test is usually repeated every 8 – 12 hour, or whenever the waveform looks over- or
underdamped, or when the accuracy of the measurement is doubtful.
Whether the system is underdamped or overdamped, MAP always remains the same.
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Hyperdynamic circulation
In effort to compensate, the heart will increase cardiac output (CO) and heart rate (HR), which accounts for the
increased pulse pressure (PP) and sinus tachycardia. The condition sometimes accompanies septic
shock, preeclampsia, and other physiological and psychiatric conditions.
B. NON-INVASIVE measurements
BP
Ultrasound
Transthoracic echocardiography
Thoracic bioimpedance
C. INVASIVE measurements
Direct arterial pressure
Oesophageal Doppler
Transoesophageal echocardiography (TOE)
LiDCO (Lithium dilution CO)
PiCCO (Pulse index continuous CO)
Pulmonary artery (Swan-Ganz) catheter.
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Principle of echocardiography
Echocardiography employs ultrasound of 2 – 10 MHz. A piezoelectrode in the probe transducer converts
electrical energy delivered to the probe into ultrasound waves. These waves then travel through the tissues,
encountering the blood, the heart, and other structures. Sound waves pass readily through tissues of similar
acoustic impedance; however, when they encounter different tissues, they are scattered, refracted or reflected
back toward the ultrasound probe. The echo waves then interact with the ultrasound probe and generate an
electrical signal. By knowing the time delay between the transmitted and the reflected sound wave, the location
of the source of the reflected wave can be determined and the electrical signal can be reconstructed as an image.
Uses of echocardiography
1) Diagnosis of the source of the haemodynamic instability, including
Systolic & diastolic heart failure
Valvular abnormalities
Hypovolaemia
Pericardial tamponade
3) Diagnosis of structural diseases of the heart, such as valvular heart disease, shunts, aortic diseases, etc.
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2) Impermeability/reduced permeability:
Carbapenem resistance in Pseudomonas species.
Aminoglycosides resistance in Anaerobes
3) Target modification:
Altered penicillin binding protein : ß-lactam resistance in MRSA
RNA polymerase mutation : Rifampicin resistance in M. Tuberculosis
DNA gyrase mutation : Ciprofloxacin resistance in Enterobacteriaceae
2) NON-GENETIC:
a) Metabolic inactivity
b) Loss of specific target structure
c) Infection at sites where antimicrobials are excluded or are not active.
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ANTIFUNGALS
1) Systemic (oral/parenteral) agents for systemic infections
Amphotericin B
Flucytosine
Azoles: Imidazolesketoconazole, miconazole, clotrimazole
Triazoles Itraconazole, Fluconazole.
Echinocandins, e.g. Caspofungin, Micofungin, Anidulafungin.
2) Oral systemic agents for mucocutaneous infections, e.g. Griseofulvin, Terbinafine.
3) Topical: Nystatin
Topical azoles, e.g. clotrimazole, miconazole
Topical allylamines, e.g. Terbinafine, Naftifine.
ANTIVIRALS
1) Anti-herpes agents, e.g. Acyclovir, Ganciclovir, Famciclovir, Foscarnet
2) Anti-HIV nucleoside and nucleotide reverse transcriptase inhibitors,
e.g. Zidovudine, Lamivudine, Stavudine
3) Anti-HBV agents: Adefovir, Entecavir
4) Anti-influenza agents: Oseltamivir, Zanamivir, Amantadine, Rimantadine
5) Others: Interferons, Palivizumab, Ribavirin, Imiquimod.
ANTI-PROTOZOALS
Chloroquine, Quinine, Pyrimethamine, Miltefosine, Primaquine, Mefloquine, Sodium stibogluconate,
Proguanil, Sulfadoxine, Metronidazole, Tinidazole
ß-lactam compounds:
1) Penicillins:
a) Penicillin-G, Penicillin-V.
b) Anti-staphylococcal penicillins; e.g. Naficillin.
c) Extended-spectrum penicillins; e.g. Ampicillin and the antipseudomonal penicillins.
2) Cephalosporins: 1st gen : Cefazolin, Cephalexin, Cefadroxil, Cephradine
2nd : Cefaclor, Cefuroxime, Cefoxitin
3rd : Ceftriaxone, Cefpodoxime, Ceftazidime
4th : Cefepime
3) Monobactams, : Aztreonam
4) Carbapenems : Doripenem, Ertapenem, Imipenem, Meropenem.
5) ß-lactamase inhibitors : Clavulanic acid, Sulbactam, Tazobactam.
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12 mandatory physiological variables including GCS with each variable point from 0 to 4. (12 × 5 = 60)
Temperature (rectal)
MAP, HR, RR
Arterial pH
Oxygenation
Na+, K+, creatinine,
Hct, WBC
GCS
Age= 6 points; Chronic health evaluation= 5 points; Total points= 71; Computed after 24 hours of ICU
care.
2) APACHE-III
3) SAPS= Simplified Acute Physiology Score
6) GCS
7) SOFA, q-SOFA= quick Sepsis-related Organ Failure Assessment Score
10) RIFLE= Risk, Injury, Failure, Loss and End-stage kidney classification.
11) Murry lung injury scoring
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Use of vasoconstrictors
MAP< 50 mmHg
Episodes of VF/VT
HR< 40 bpm
Inadequate DO2 causing base deficit >-10
CI <2 L/min/m2
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Fever is a temperature that exceeds the normal daily variation in temperature for each individual patient. The
current recommendations for the definition of a fever in ICU patients are as follows:
1) A body temperature of 38.3ºC (101ºF) or higher represents a fever, and deserves further evaluation.
2) A lower threshold of 38ºC (100.4ºF) can be used for immunocompromised patients, particularly those with
neutropenia.
Non-INFECTIOUS:
1) SIRS
2) Early postoperative fever
3) Pulmonary embolism
4) Platelet transfusions
5) Drug fever caused by amphotericin, penicillins, cephalosporins, phenytoin, procainamide, quinidine, etc.
6) Thyrotoxicosis
7) Adrenal crisis
8) Acalculous cholecystitis
9) Iatrogenic
Normal saline use into tracheal tube prior to introduction of catheter serves two purposes:
a) Stimulates active expiratory effort and
b) Removal of secretion.
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Sounds production:
Breath Originate mainly from the rapid turbulent airflow in the larynx, trachea and main bronchi.
Bowel Produced by passage of air through small intestine and it requires gastric emptying.
4th Ventricular origin (stiff ventricle and augmented atrial contraction) related to atrial
filling.
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CLINICAL ASSESSMENT
1) Ability to walk upstairs
2) RR
3) Cough test
(Cough following a deep breath):
Inadequate cough, if FVC <20 ml/kg; FEV1 <15 ml/kg; PEFR <200 L/min
A wet productive cough/self-propagated paroxysms of coughing indicates that patient is susceptible to
pulmonary infections.
OTHERS
1) Schneider’s match blowing test: It measures maximum breathing capacity (MBC).
(Blow a match stick from a distance of 6 inches with-
Mouth wide open
Chin rested/supported
No purse lipping
No head movement
No air movement in the room
Mouth and match at the same level)
Interpretation:
Able to blow out the match : MBC > 60 L/min; FEV1 >1.6 L
Cannot blow out : MBC < 60 L/min; FEV1 <1.6 L
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Inflammation is a complex reaction to injurious agents (such as microbes and damaged, usually necrotic,
cells) that consists of vascular responses, migration and activation of leukocytes and systemic reactions.
Cardinal signs of inflammation are: rubor, calor, tumor, dolor & functio laesa.
Cross infection is the transfer of an infectious agent or disease from one pt to other in a hospital.
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Bacteraemia Presence of viable bacteria in the blood without multiplication and specific
symptoms.
Septicaemia Presence of viable bacteria in the blood with multiplication and specific
symptoms and signs.
Causes of SIRS:
Pancreatitis
Trauma
Cardio-pulmonary bypass
Vasculitis, etc.
MODS It is the presence of two or more altered organ functions in acutely ill patients
such that homeostasis can’t be maintained without intervention.
Shock The defining feature of shock is a level of oxygen delivery (DO 2) that fails to
meet the metabolic requirements of the tissues.
Shock is a systemic state of low tissue perfusion that is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.
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Principles of mx of shock:
1) Treatment of the underlying pathological condition;
2) Optimisation of circulating blood volume;
3) Optimisation of cardiac output;
4) Optimisation of blood pressure;
5) Restoration of vascular tone;
6) Optimisation of oxygen delivery; and
7) Support of any organ failure.
Ischaemia–reperfusion syndrome
During the period of systemic hypoperfusion, cellular and organ damage progresses due to the direct effects of
tissue hypoxia and local activation of inflammation. Further injury occurs once normal circulation is restored to
these tissues. The acid and potassium load that has built up can lead to direct myocardial depression, vascular
dilatation and further hypotension.
The cellular and humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi)
are flushed back into the circulation where they cause further endothelial injury to organs such as the lungs and
the kidneys. This leads to acute lung injury, acute renal injury, multiple organ failure and death.
Reperfusion injury can currently only be attenuated by reducing the extent and duration of tissue hypoperfusion.
Endocrine shock
Endocrine shock may present as a combination of hypovolaemic, cardiogenic or distributive shock. Causes of
endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency.
Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac
responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There
may also be an associated cardiomyopathy.
Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous
catecholamines. Adrenal insufficiency may be due to pre-existing Addison’s disease or be a relative
insufficiency due to a pathological disease state, such as systemic sepsis.
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Additional modalities
Central venous pressure
Invasive blood pressure
Cardiac output
Base deficit and serum lactate
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Classification of shock
The causes of circulatory failure or shock may be categorized as either low flow or stroke volume, or low
peripheral arteriolar resistance (vasodilation).
Examples
Low flow or SV Hypovolaemic Internal or external hemorrhage, severe burns, salt & water
depletion, etc.
Neurogenic Major brain or spinal injury, high cervical cord trauma, GBS, etc.
Objective markers of inadequate tissue oxygen delivery which can aid earlier identification of shock:
Increasing base deficit.
Elevated blood lactate level and
Reduced urine output.
In early hemorrhagic shock: narrow In more advanced stage SBP falls and
pulse pressure (↓ SBP, ↑ DBP). peripheries become cool (due to hypovolemia
associated with capillary leak)
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SEPTIC shock
Predisposing factors:
Intrinsic factors Age <10 yr and >70 yr
Co-morbidities: DM, IHD, Malignancy
Immunosuppression
Both Gram (+ ve) and Gram (- ve) bacteria can cause septic shock but traditionally more associated with Gram
(-ve) bacteria.
C/F: INITIALLY:
1) Hyperthermia, chills
2) Nausea, vomiting
3) Tachycardia, Tachypnoea
4) Flushing, warm periphery
5) Vasodilation, hyperdynamic circulation
6) High cardiac output
7) Hypotension
8) Oliguria
9) Acute mental instability
LATER:
1) Hypotension (due to hypovolemia or poor myocardial function)
2) Low cardiac output
3) Feeling cool and cold periphery.
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The endotoxin (a component of LPS) and exotoxin (if present) bind with CD4 receptor on leukocyte’s
(especially monocyte and phagocyte) endothelial cell and other cell types.
Initiation of synthesis, release and activation of cascade of mediators derived from plasma or cell.
But, in the advanced stages of septic shock, cardiac dysfunction is more prominent and the CO is reduced,
resulting in haemodynamic pattern that resembles cardiogenic shock, i.e. High CVP, High SVR and Low CO.
2) Maintenance of adequate perfusion with intravenous fluids and inotropic and vasopressor agents.
3) Supportive treatment of complications such as ARDS, Renal failure, GIT bleeding, DIC, etc.
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2) Antimicrobial therapy:
Blood cultures should be obtained prior to administration of antibiotics.
Broad spectrum antibiotic is appropriate.
Removal of infection source: catheters, abscess, etc.
6) Others:
Prevention of venous thrombosis by LMWH.
GIT care- H2 blocker, PPI.
Renal support- Haemofiltration or hemodialysis (if needed)
Nutritional support- start early and preferably through enteral route.
Maintaining plateau pressure at ≤30 cmH2O in ventilator-dependent patients.
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HYPOVOLAEMIC shock
It is an emergency condition in which excessive blood and fluid loss make the heart unable to pump enough blood to the
body.
Causes
1) Blood loss due to
Bleeding from cut injury
Bleeding from other injuries
Internal bleeding such as in the GIT.
Moderate hypovolaemia Decreased perfusion of organs that can withstand ischemia poorly (pancreas, spleen, kidney,
(20 – 40%) etc.)
Thirst, Tachycardia, Oliguria
Laboratory findings:
1) Hematocrit: may be normal if rapid blood loss occurs and assessed early.
2) Lactate: Increased
3) ABG: ↓pH, ↓HCO3-, ↑Base deficit
4) Urine osmolality increased (>1.010)
5) Urinary Na+ <10 mmol/L
6) Blood urea, S. creatinine, S. electrolytes
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c) Neuroendocrine response:
On venous end:
Angiotensin & vasopressin enhance sympathetic effecttachycardia
Adrenergic discharge causing constriction of large venules & small veins divert to heart
increased diastolic filling increased SV.
On arteriolar end:
Constriction of precapillary sphincter & arterioles lead to redistribution of blood to vital organs
(brain, heart)
Treatment:
1) General principles:
Airway, breathing & circulation
I/V access: two large bore cannula
A quick search should be made for source of blood and fluid loss.
Central venous catheter insertion.
2) Fluid resuscitation: choice of initial fluid therapy is determined by availability & patient’s condition.
a) Crystalloids:
Isotonic fluid: Ringer’s lactate is the best (contains more physiological electrolytes). 0.9% NaCl and 5% DNS
can also be used.
For adult initial bolus of 1- 2 liters.
For paediatrics 20 ml/kg bolus and assess response.
Hypertonic saline (3% NaCl)
b) Colloids:
Natural: 20% albumin, purified protein fraction, FFP
Synthetic: Hydroxyethylstarch 6%, Dextran – 70, Dextran – 40
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CRYSTALLOIDS:
Advantages Disadvantages
Readily available Short lived haemodynamic effect (<30 min)
Less expensive Pulmonary edema and peripheral edema may develop.
Simple to infuse large volume Hartmann’s solution is contraindicated in DM.
Balanced salt solution approximate ECF Large Na+ and H2O load.
composition. No O2 carrying capacity.
COLLOIDS:
Advantages Disadvantages
Small volume is required Expensive and less available
Longer-lived hemodynamic effect (4 Reduced platelet aggregation
hours) RBC sludging
Minimum peripheral edema Allergic reaction
Renal dysfunction
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CARDIOGENIC shock
Systemic hypoperfusion secondary to severe depression of cardiac output and sustained systolic arteriolar
hypotension despite elevated filling pressure.
Etiologies
1) Acute MI or ischemia
2) LVF
3) Ventricular septum rupture
4) Papillary muscle or chordal rupture; in severe MR.
5) Ventricular free wall rupture with subacute tamponade.
Pathophysiology:
Myocardial infarction and/or myocardial dysfunction
Hypotension Hypoxia
Ischemia
Death
STAGES of cardiogenic shock:
1) Compensated
2) Decompensated hypotension
3) Irreversible shock: activation of complement cascade and irreversible myocardial & peripheral tissue
damage.
C/F:
of the low cardiac output state Cold, clammy grey skin
Slowed capillary refill time
Oliguria, Sweating, Confusion
Hypotension, Tachycardia
Investigations:
1) 12 lead ECG, Echocardiography, CXR
2) Swan Ganz catheterization: SvO2
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Rx of cardiogenic shock:
1) General measures:
Oxygen supplementation
Propped up position
Opioids: Morphine (Relieve pain & anxiety; Provide sedation; Lessen cardiac stress)
2) Resuscitation:
If PAWP <10 mmHg, provide balanced salt solution.
GTN: Reduce both preload & afterload finally reduce EDPIncrease O2 delivery to ischemic areas.
3) Pharmacological support:
a) Inotropes:
Dobutamine Improves ventricular performance without increasing O2 demand. Dose: upto 40 µg/kg/min
(ß1)
Dopamine D1 & D2 stimulation at low dose; α and ß stimulation at high dose.
Renal dose (D1) : < 5 µg/kg/min (Improves renal function; Inhibit noradrenaline release)
Intermediate/Cardiac dose : 5 – 10 µg/kg/min (Improves cardiac function without increasing O 2
demand)
Vasoconstrictor dose (α) : >10 µg/kg/min (Increased O2 demand; Increase HR; Decrease renal
function)
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NEUROGENIC shock
Produced by peripheral vasodilation due to vasomotor tone loss as a result of spinal cord injury, regional
anaesthesia or administration of autonomic blocking agents.
Effects:
1) Blood pooled in periphery decrease venous returndecrease CO
2) Above the level of injury:
Adrenergic system activated increase HR Increase force of contraction.
Bradycardia, if cardiac sympathetic flow affected.
3) Loss of vasomotor tone causes impaired cellular metabolism.
Causes:
1) Spinal cord injury at spinal cord T3 or above.
2) Regional anaesthesia
3) Administration of autonomic blocking agents.
C/F:
Extremities: warm above & cool below injury.
BP low
HR rapid, thready, may be bradycardia
Sign of spinal shock & spinal cord injury
Absent all voluntary reflexes & neurogenic activity below level of injury.
Loss of sensation
Flaccid paralysis below injury.
Imaging studies:
To find out any trauma: radiograph of cervical, thoracic & lumbosacral spine.
Review after being transferred to ICU.
Rx:
1) Supportive
Secure airway, oxygenation, & ventilation
I/V access
Assess bladder function, if needed.
5) Rehabilitation:
Nursing and support personnel
Prevent pressure sore.
Prevent UTI
Early consultation and counselling by physiatrist.
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SPINAL shock
The term ‘spinal shock’ applies to all phenomena surrounding physiologic or anatomic transection of spinal cord
that result in temporary loss or depression of all or most spinal reflex activity below the level of injury.
Causes:
1) Spinal cord injury following trauma and surgery.
2) Inflammatory lesion of spinal cord.
3) Infective cause
4) Metastatic lesion in spinal cord.
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DIC/Consumption coagulopathy
Pathological activation of coagulation by a disease process leading to fibrin clot formation, consumption of
platelet and clotting factors (I, II, XIII) and secondary fibrinolysis. Consequence is initial thrombosis followed
by increased bleeding tendency due to consumption of clotting factors and fibrinolytic activity.
Pathophysiology of DIC:
DIC
Bleeding
C/F
Bruising
Bleeding from wounds, venipuncture sites, GIT,
lung, uteroplacental bed.
Capillary microthrombosis may lead to
MOF/MODS/TOF (total organ failure)/MSOF
(Multisystem OF).
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Lab. Findings
Thrombocytopenia
Low titre of fibrinogen, coagulation factor and antithrombin-III.
High titre of FDP
Prolonged PT, APTT & TT.
Rx
1) Directed as underlying cause: antibiotic, blood transfusion and other treatments, wound dressing, etc.
2) Supportive: Oxygen therapy and treatment of respiratory failure, if present.
3) Administration of FFP, platelet & possibly cryoprecipitate.
4) Inj. Antithrombin-III
5) Heparin in chronic DIC & major coagulopathy.
6) Administration of activated protein C should be considered in sepsis related DIC.
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Dr. K H Mozumder
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Dr. K H Mozumder
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Cardiac:
Decreased myocardial contractility
Decreased response to inotropes
Ventricular dilatation
Hepatic:
Altered metabolism of CHO, fat & protein.
Decreased protein synthesis
Decreased drug metabolism
Impaired bilirubin excretion
Immune system:
Decreased T-cell function
Impaired chemotaxis & phagocytosis.
Essential nutrients:
Nutrients that cannot be synthesized from other nutrients inside the body and that’s why must be supplied from
outside are called the essential nutrients. They are as follows:
8–10 AAs: PVT TIM HALL: Phenylalanine, Valine, Threonine, Tryptophan, Isoleucine, Methionine, Histidine,
Arginine, Leucine, and Lysine.
13 Vitamins
16 minerals
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Indications:
ABSOLUTE
1) Gut failure or severe gut dysfunction.
2) Inability to tolerate enteral feeding.
RELATIVE
1) Moderate to severe malnutrition.
2) Abdominal sepsis.
3) Prolonged ileus.
4) Severe necrotizing pancreatitis.
5) Severe inflammation of bowel.
6) Massive bowel resection.
Complications:
1) CATHETER related
Catheter sepsis
Pneumothorax
Haemothorax
Chylothorax (left side)
Air embolism
Thromboembolism
Cardiac tamponade
3) METABOLIC
Hyperchloremic acidosis
Hyperglycemia
Rebound hypoglycemia (if stopped suddenly)
Hyperlipidaemia
Excess CO2 production
Fat embolism
Azotaemia
Pancreatitis
4) HEPATIC dysfunction
Steatosis
Intrahepatic cholestasis
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Monitoring:
1) CLINICAL SIGNS
Body weight and fluid balance daily.
Triceps skin fold thickness
Abdominal girth
Mid arm circumference
Handgrip strength
2) INVESTIGATION
Serum urea, creatinine, electrolytes and osmolality daily.
Urine urea and osmolality daily.
Blood glucose should be measured frequently.
Liver function and plasma Ca2+, PO43-, Mg2+ should be done twice a week.
FBC every 1 – 3 days.
Prothrombin Time (PT) once a week.
Iron, folate, vit-B12 should be measured at least weekly.
24 hours nitrogen balance.
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To reduce that, there has been interest to dietary components with immunomodulatory properties:
1) Glutamine:
The most abundant amino acid in the body.
Fuel for electrolytes and some lymphoid cell.
Maintain gut mucosal integrity & cellular function.
Precursor of glutathione.
Can significantly reduce mortality & length of hospital stay.
2) Arginine
Proliferation of T-cell.
Increase NK cell function.
Improves cell mediated immunity & survival.
3) Taurine
An abundant amino acid with role of membrane stabilization & Ca2+ influx regulation.
Has antioxidant properties.
Immunonutrition:
Combination of omega-3 fatty acids, arginine, nucleotides and glutamine in enteral feeding is called
immunonutrition. Study shows reduction of mortality with immunonutrition.
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Causes of thrombocytopenia:
1) Sepsis
2) Dilutional thrombocytopenia
3) Thrombotic thrombocytopenic purpura (TTP)
4) Idiopathic thrombocytopenic purpura (ITP)
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BMR It is the amount of energy expended while at rest in a neutrally temperate environment,
in the post-absorptive state (meaning that the digestive system is inactive, which
requires about 12 hours of fasting).
It is the minimum rate of energy expenditure per unit time at rest. It is usually expressed
as Joules/hour-kg body mass. It is calculated by Harris-Benedict equation and Schofield’s
equation.
Harris-Benedict It is a method used to estimate an individual’s BMR and daily kilocalorie requirements.
equation or The estimated BMR value is multiplied by a number that corresponds to the individual’s
principle activity level. BMR calculation:
For male= 66.5 + (13.75 ×body wt in kg) + (5 ×height in cm) – (6.8 ×age in yr)
For female=655 + (9.6 ×body wt in kg) + (1.8 ×height in cm) – (4.7 ×age in yr)
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Routes of feeding:
1) ENTERAL:
Oral
Naso-gastric (with fine bore catheter or wide bore catheter)
Naso-duodenal
Naso-jejunal
Percutaneous gastrostomy
Percutaneous jejunostomy
Percutaneous endoscopic gastrostomy (PEG)
Radiologically inserted gastrostomy (RIG)
2) PARENTERAL:
Dedicated central venous line
Peripheral polyurethane catheter
Peripherally inserted central catheter.
Enteral feeding
Indication:
1) Swallowing is inadequate or impossible.
2) Presence of normal working gut is essential.
Contraindications:
1) Non-functioning gut: obstruction, anatomical disruption, ischemia, etc.
2) Generalized peritonitis.
3) Severe shock state.
Enteral nutrition
Advantages Disadvantages
1) Cheaper 1) Patients require a functioning and intact
2) Non-invasive gastrointestinal tract.
3) Bowel integrity & function is maintained 2) Diarrhoea (upto 40% patients)
4) Normal intestinal flora are preserved 3) Nausea and vomiting (associated with ileus,
5) Bacterial translocation is minimized or prevented gastric stasis, abdominal distention)
and reduced risk of sepsis 4) Risk of aspiration and pulmonary injury.
6) Normal gastric acidity and gastrointestinal barrier 5) Risk of direct pulmonary instillation of feed.
function is preserved.
7) Enhanced secretion of IgA.
8) Reduced stress ulceration.
9) Nitrogen uptake and incorporation, carbohydrate
and lipid utilization all favour anabolism and
weight retention.
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Parenteral nutrition
Advantages Disadvantages
1) Useful in short bowel syndrome and intestinal 1) Expensive
obstruction 2) Invasive
2) Useful in any cause of failure to establish 3) Catheter infection risk
enteral feeding. 4) Risk of electrolyte imbalance, hepatic steatosis,
3) Helpful in prolonged ileus. azotemia, etc.
5) Hyperglycaemia, which impairs immune
response as well as promote osmotic
dehydration.
6) Fluid and lipid overload.
Refeeding syndrome:
Feeding of malnourished patient particularly after a period of starvation may result in severe metabolic
disturbance, most notably hypophosphataemia. Hypophosphataemia developing after initiating parenteral or
enteral nutrition has been termed as the refeeding syndrome.
Mechanism: Total body phosphorus depletion plus influx of phosphorus during refeeding lead to severe
decrease in extracellular phosphorus.
Causes of hypoproteinemia:
1) Lack of protein in diet.
2) Malabsorption (in gastro-enteropathy).
3) Liver diseases: hepatitis, cirrhosis & fibrotic changes in liver.
4) Renal failure: nephrotic syndrome, AGN.
5) Congenital deficiency of one or more plasma proteins.
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Dr. K H Mozumder
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Dr. K H Mozumder
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ACID-BASE DISORDER
Primary change Compensatory change
Respiratory acidosis ↑PaCO2 ↓pH ↑HCO3-
Respiratory alkalosis ↓PaCO2 ↑pH ↓HCO3-
Metabolic acidosis ↓ HCO3- ↓pH ↓PaCO2
Metabolic alkalosis ↑ HCO3- ↑pH ↑PaCO2
Compensatory responses:
Expected changes
Disturbance
pH HCO3-
Acute
↓0.08 ↑ 1 mmol/L per 10 mmHg PaCO2 rise
Respiratory acidosis
Chronic
↓0.08 ↑ 4 mmol/L per 10 mmHg PaCO2 rise
Respiratory acidosis
Acute
↑0.03 ↓ 2 mmol/L per 10 mmHg PaCO2 fall
Respiratory alkalosis
Chronic
↑0.03 ↓ 5 mmol/L per 10 mmHg PaCO2 fall
Respiratory alkalosis
pH PaCO2
Metabolic acidosis ↓0.015 ↓1.2 mmHg per 1 mmol/L HCO3- fall
Metabolic alkalosis ↑0.015 ↑0.7 mmHg per 1 mmol/L HCO3- rise
pH pH (potential of hydrogen) is the negative logarithm (base 10) of hydrogen ion concentration.
Acid A chemical substance that dissociates in the water to produce H+, then can acts as a proton
[H+] donor. e.g. HCl, H2CO3
Strong acid dissociates more completely (100%).
Buffer A weak acid or its conjugate base which acts to minimize any change in [H+]. e.g.
Bicarbonate buffer (H2CO3/HCO3-)
Phosphate buffer (H2PO4-/HPO42-)
Protein buffer (PrH/Pr-)
Haemoglobin buffer (HbH/Hb-)
Ammonia buffer (NH3/NH4+)
Compensation The body’s attempt to return the acid base status to normal, i.e. pH closer to 7.4
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Compensatory mechanisms:
1) Blood and tissue buffers (within seconds)
2) Pulmonary buffers (within minutes) (+)/(-) respiratory centers (↑)/(↓) alveolar ventilation (↓)/(↑)
PaCO2pH becomes normal.
During Respiratory alkalosis: rapid excretion of large amount of HCO3- through kidneys.
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Respiratory acidosis
CAUSES:
1) Alveolar hypoventilation:
CNS depression: drug overdose, sleep disorder, obesity hypoventilation syndrome
Neuromuscular disorder: myopathy, neuropathy (e.g. GBS, MND, Myasthenia, etc.)
Chest wall deformity: flail chest, kyphoscoliosis
Pleural abnormality: pneumothorax, pleural effusion
Airway obstruction: COPD, Br. Asthma, FB, etc.
Parenchymal lung disease: pulmonary edema, pulmonary embolism.
Ventilator malfunction.
Rx:
1) Reverse the imbalance between CO2 production and alveolar ventilation.
2) Increase alveolar ventilation with an aim to reduce PaCO2 (carbon dioxide production).
3) Mechanical ventilation.
4) Tromethamine.
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Metabolic acidosis
Mechanisms:
1) Consumption of HCO3- by strong nonvolatile acids.
2) Renal or gastric wasting of HCO3-.
3) Rapid dilution of ECF compartment with bicarbonate–free fluid.
CAUSES:
A. HIGH Anion Gap Metabolic Acidosis (HAGMA):
1) Failure to excrete endogenous non-volatile acid, e.g. renal failure (GFR <20ml/min).
2) Increased endogenous non-volatile acid production
Ketoacidosis (DM, starvation) & Lactic acidosis
Mixed acidosis (HONK, Alcoholism)
Inborn errors of metabolism.
3) Ingestion of toxins, e.g. salicylates, methanol, ethylene glycol, paraldehyde, toluene, sulfur, etc.
4) Rhabdomyolysis.
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Rx of metabolic acidosis:
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Dr. K H Mozumder
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Anion gap It is the difference between unmeasured anions and unmeasured cations (UA – UC) and calculated
by the difference between primary measured cations (Na +, K+) and the primary measured anions
(Cl-, HCO3-) in serum.
Advantage:
1) Simple to measure and evaluate acid base disorder.
2) Can be done at bedside.
Disadvantage:
1) Reduced anions i.e. hypoalbuminaemia, which is common in critical illness, will reduce AG
and may mask an elevated AG.
2) Unmeasured cations (such as lithium and hyperglobulinaemia), hypercalcaemia and
hypermagnesaemia will reduce AG.
3) Calculations of AG involves measurement of electrolytes, therefore is dependent on the
accuracy of measurement process.
Bicarbonate space The volume of distribution of HCO3- when given intravenously, equals to ECF space.
Standard It is the concentration of HCO3- in plasma, equilibrated for temperature 37ºC, PaO 2 ≥100 mmHg,
Bicarbonate (SBC) PaCO2=40 mmHg.
Aim is to eliminate the respiratory component of the acid-base status. Therefore, Low SBC
true metabolic acidosis & High SBC true metabolic alkalosis.
Base excess/deficit A measure of metabolic alkalosis/acidosis expressed as the amount of acid or base required to
return pH of blood to 7.4 and PaCO2 to 40 mmHg at full oxygen saturation and 37ºC.
Normal = -2 to +2 mmol/L;
Positive value = Metabolic Alkalosis &
Negative value = Metabolic Acidosis.
Osmolal gap The discrepancy between the measured and calculated plasma osmolality is referred to as an
Osmolal gap. Normal Osmolal gap = 10 – 15 mOsm/L.
Glucose(mg/dl)
Effective plasma osmolality= 2[Na+] +
18
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Dr. K H Mozumder
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Hyponatremia
Causes/Classification:
A. Decreased total sodium content: (Hypovolaemic; preservation of circulatory volume takes place at the
expense of plasma osmolarity)
Extra-renal: Vomiting
Diarrhoea
Integumentary loss (sweating, burns)
Third-spacing
C/F:
Mild – moderate (Na+ >125 mEq/L): usually frequently asymptomatic.
Early symptoms (non-specific): anorexia, nausea, weakness.
Progressive cerebral edema
Lethargy, confusion, seizures, coma, death.
Non-cardiogenic pulmonary edema.
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Rx of hyponatremia:
Treatment of the underlying cause. Mild (oral); moderate (oral + 0.9% NaCl IV); Severe (3% NaCl)
0.9% NaCl is generally the treatment of choice for hyponatremic patients with decreased total body sodium
content.
Water restriction is the primary treatment for hyponatremic patients with normal or increased total body
sodium content.
Demeclocycline (antagonizes ADH activity at the renal tubules) is a useful adjunct to water restriction in
the treatment of patients with SIADH.
Correction of plasma Na+ to greater than 125 mEq/L is usually sufficient to alleviate symptoms.
The rapidity at which hyponatremia to be corrected should be tailored to the severity of symptoms.
X
Because 0.9% NaCl contains 154 mEq sodium per Litre of solution, so the pt should receive Litre of
154
0.9% NaCl to correct the deficit. Correction rate for:
Mild symptoms: 0.5 mEq/Hr or less
Moderate: 1 mEq/Hr or less
Severe: 1.5 mEq/Hr or less
Infusion rate =?
Hypertonic saline (3% NaCl) may be indicated in markedly symptomatic patients with plasma Na+ <115
mmol/L.
Any co-existing isotonic fluid deficits should be replaced with an isotonic solution.
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1 gram (1000 mg) sodium contains = 43 mmol Na+ [1 mmol Na+ = 23 mg sodium]
1 gram (1000 mg) NaCl contains = 17 mmol Na+ = 390 mg sodium
Plasma or extracellular Na+ concentration is more indicative of water balance than total body sodium
content.
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Dr. K H Mozumder
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Hypernatremia
Hyperosmolarity is usually, but not always, associated with hypernatremia.
C/F:
Cellular dehydration causing restlessness, lethargy, hyperreflexia, seizures, coma & death.
Focal intracerebral hemorrhage or SAH due to rapid decrease in brain volumes causing rupture of the
cerebral veins.
Acute hypernatremia is the worst.
Chronic hypernatremia is usually better tolerated than the acute form. Because 24 – 48 hours later,
intracellular osmolarity begins to rise as a result of increases in intracellular inositol and amino acid
(glutamine & taurine) concentrations. As intracellular solute concentration increases, neuronal water
content slowly returns to normal.
Rx:
Aim : to restore plasma osmolarity to normal as well as correcting the underlying cause.
Target : to reduce plasma Na+ concentration not at a rate faster than 0.5 mmol/L/Hr
Water deficit should generally be corrected over 48 hr with a hypotonic solution such as 5% DA.
Rapid correction can result in seizures, cerebral edema, permanent neurological damage & death.
Infusion rate =
Any co-existing isotonic fluid deficits should be replaced with an isotonic solution.
Anaesthetic considerations:
Associated fluid deficits in hypernatremia (i.e. hypovolaemia) accentuates any vasodilation or cardiac
depression from anaesthetic agents and predisposes to hypotension and hypoperfusion of tissues.
Elective surgery should be postponed in patients with significant hypernatremia (Na + >150 mmol/L) until
the cause is established and fluid deficits are corrected.
Hypovolaemic patients are particularly sensitive to sympathetic blockade from spinal or epidural
anaesthesia. If an anaesthetic must be administered prior to adequate correction of hypovolaemia, ketamine
may be the choice of induction agent.
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Dr. K H Mozumder
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C/F H/O polydipsia, polyuria (often >6 L/day) and absence of hyperglycemia.
Urinary osmolarity < plasma osmolarity.
Marked polyuria without glycosuria.
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Dr. K H Mozumder
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Potassium balance
Inter-compartmental shifts of potassium occurs due to changes in:
Extracellular pH: (acidosis increases extracellular and plasma [K+] approx. 0.2 – 1.2 mEq/L per 0.1 unit
pH changes).
Circulating insulin and catecholamine: directly affect Na+ - K+ - ATPase activity and decreases plasma
[K+] by increasing cellular uptake of potassium in the liver and skeletal muscle by insulin & activation of ß2
receptors. Alpha-adrenergic activity may impair the intracellular movement of K+.
Plasma osmolarity: increased osmolarity (hypernatremia, hyperglycemia, mannitol, etc.) increases plasma
[K+] 0.6 mEq/L per 10 mOsmol/L increases in plasma osmolarity.
Kidneys can excrete as much as 500 mEq potassium/day when potassium intake is increased slowly.
High renal tubular flow rates (as during osmotic diuresis) increase potassium secretion by keeping the
capillary-to-renal tubular gradient for potassium secretion high and thus excretion of potassium
becomes high.
Main source of K+ elimination is kidney. Main source of K+ intake are fruits and nuts.
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Dr. K H Mozumder
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Hypokalaemia
Causes: C/F:
Mild hypokalaemia
= 3 – 3.5
mmol/L
Moderate
hypokalaemia =
2.5 – 3 mmol/L
Severe hypokalaemia
< 2.5
mmol/L
Rx:
1) Oral
replacement over several days using a potassium
chloride solution, 60 – 80 mmol/day when serum
[K+] is > 3 mmol/L.
(1 TSF syrup KT = 6.7 mmol K+)
Potassium bicarbonate or equivalent (K+ acetate or K+ citrate) is preferred with metabolic acidosis.
Chronic mild hypokalaemia (K+ = 3 – 3.5 mmol/L) without ECG changes does not substantially increase
anaesthetic risk.
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Intraoperative:
Vigilant ECG monitoring.
IV potassium should be administered only if atrial or ventricular arrhythmias develop.
Glucose-free IV solutions should be used.
Hyperventilation should be avoided. (alkalosis will cause further hypokalaemia)
Dosage of NMBAs should be reduced by 25 – 30%.
Peripheral nerve stimulator (PNS) should be used to follow both the degree of NMB and the adequacy of
reversal from neuromuscular blockade.
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Hyperkalaemia
Causes:
C/F:
1) Cardiac manifestations: [K+] > 7 mmol/L;
VFasystoleheart stops at diastole.
Hypocalcaemia, hyponatremia and acidosis accentuate the cardiac effects of hyperkalaemia.
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K+ is mostly intracellular cation. So, normally it has a tendency to move outside the cells due to the
concentration gradient.
As plasma [K+] rises, this concentration gradient gets reversed. So, potassium will move into the cells and
RMP can become more positive, to the point of even causing contraction. When RMP gets so high that it
is above the threshold potential, meaning that once the myocardial cells depolarizes and contracts, it
cannot repolarize to allow another contraction.
That means all myocardial cells are depolarized and this inactivates Na+ channels in the heart.
So, there will be no spontaneous firing by myocardial cells and heart cannot contract anymore and it stops
at diastole.
Ischaemic tissue does not receive oxygen. So, there is lack of ATP and Na + - K+ - ATPase does not work. Once
K+ leaves the cell, it cannot be pumped back into the cell. That’s why potassium rises in the surrounding
interstitium of ischaemic tissues.
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Rx of hyperkalaemia:
1) Reduction of potassium intake and correction of underlying abnormalities.
2) Stabilization of cell membrane potential: Inj. Calcium gluconate 10%, 10 ml IV slowly over 10 min.
(Rapid effect but short lived; calcium can potentiate digoxin toxicity)
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± 8.5 Atrial paralysis (no evidence of atrial activity); broad and slurred QRS
complex; QRS interval approximates to 0.2 sec; T-wave remains tall and
slender.
Further hyperkalaemia may result in VT, VF.
Hypercalcaemia (calcium rigor): heart relaxes less during diastole and eventually stops in
systole.
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ABG analysis
An arterial blood gas is a blood test that is performed using blood from an artery and it measures the arterial
oxygen tension, PaCO2 and pH.
Indications:
1) To evaluate the adequacy of ventilatory support.
2) To evaluate the acid base status and management plan.
3) To evaluate O2 carrying capacity of blood (PaO2, HbO2, Hb %).
4) To quantitate the pt’s response to therapeutic intervention and/or diagnostic evaluation.
5) To monitor severity and progression of a documented disease process.
Contraindications:
1) Bleeding diathesis.
2) Severe PVD; absence of peripheral pulse.
3) Infection over site of needle puncture.
4) AV fistula of same limb
5) Abnormal modified Allen’s test
Parameters of ABG:
Measured Calculated
Normal values Normal values
pH 7.35 – 7.45 Standard Bi Carbonate 22 – 28 mmol/L
PaO2 80 – 100 mmHg Base excess - 2 to +2 mmol/L
PaCO2 35 – 45 mmHg Anion gap 10 – 18 mmHg
SaO2 95 – 100% P50 25 – 27 mmHg
Lactate 0.5 – 2 mmol/L (A – a)O2 < 30 mmHg
Electrolytes: Na+, K+, Cl-, Ca2+ CaO2 15 – 24 ml/dl
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Functional classification:
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
Technical classification:
Uncompensated
Partially compensated
Fully compensated
Characteristic classification:
Single disorder:
Respiratory disorder
Metabolic disorder
Compensating disorder
Mixed disorder:
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Allen’s test
(Designed by Dr. Edgar Van Nuys Allen; professor of cardiovascular medicine, Mayo Clinic, Rochester,
Minnesota)
Allen’s test is a simple, but not reliable, method for assessing the safety of radial artery cannulation. In this
test, the patient exsanguinates his or her hand by making a fist. While the operator occludes the radial &
ulnar arteries with fingertip pressure, the patient relaxes the blanched hand.
Collateral flow through the palmar arterial arch is confirmed by flushing of the thumb within 5 sec after pressure
on the ulnar artery is released. Delayed return of normal color (5–10 s) indicates an equivocal test or insufficient
collateral circulation (>10 s). The Allen’s test is of such questionable utility that many practitioners routinely
avoid it.
a) Sufficient collateral flow: flushing of the thumb within 5 sec after pressure on the ulnar artery is released.
b) Equivocal test: delayed return of normal color (5 – 10 sec) of the thumb after pressure on the ulnar artery is
released.
c) Insufficient collateral circulation: requiring > 10 sec for returning normal color of the thumb after pressure
on the ulnar artery is released.
Alternatively, blood flow distal to the radial artery occlusion can be detected by palpation, Doppler probe,
plethysmography, or pulse oximetry. Unlike Allen’s test, these methods of determining the adequacy of
collateral circulation do not require patient cooperation.
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b) With both arteries compressed the subject is asked to clench and unclench the hand 10 times. The hand is
then held open, ensuring that the wrist and fingers are not hyperextended and splayed out. The palm is
observed to be blanched.
c) The ulnar artery is released and the time taken for the palm and especially the thumb and thenar eminence
to become flush is noted.
The modified Allen's test is performed by simultaneously compressing both the radial and ulnar arteries,
followed by exsanguination of blood from the palm by repeated clenching and unclenching of the fist. The
pressure over the ulnar artery is then released while continuing to maintain pressure over the radial artery. A
delay in flushing of the palm by 5 – 6 seconds is suggestive of abnormal ulnar-artery patency.
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(Ref:http://www.nejm.org/action/showMediaPlayer?
doi=10.1056%2FNEJMicm1001091&aid=NEJMicm1001091_attach_1&area=)
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Pathogenesis:
MEN 1: It results from inactivating mutations in ‘menin’, a tumour suppressor gene on chromosome 11.
MEN 2: Mutations in the RET proto-oncogene on chromosome 10 cause constitutive activation of a membrane-
associated tyrosine kinase.
Dx:
MEN 1:
Annual history & Physical examination
Measurement of S. Calcium, gastrointestinal hormones and prolactin.
MRI of the pituitary gland is performed at less frequent intervals.
MEN 2:
Annual history & Physical examination
Measurement of S. Calcium, S. Calcitonin and urinary catecholamine metabolites.
[Because MEN syndromes are hereditary, family members should be screened for early signs of
Phaeochromocytoma, thyroid cancer, and hyperparathyroidism.]
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Narcotic is the term which refers to a general class of drugs that blunt sensation and depress consciousness.
Advantages of fentanyl over morphine as analgesic in ICU or for long term analgesia:
More rapid onset of action (as lipid solubility of fentanyl is 600 times more than that of morphine).
Less risk of hypotension (no histamine release)
Absence of active metabolites.
Advantages of Remifentanil:
Analgesic effect upto 10 min.
Broken down by non-specific esterases in tissue and RBC.
No dose adjustments necessary for renal or hepatic failure.
Dose of remifentanil:
Bolus = 1.5 mcg/kg
Continuous infusion = 0.5 – 15 mcg/kg/hr
Morphine Fentanyl
Onset of action 5 – 10 min 1 – 2 min
PCA
demand (bolus) 0.5 – 3 mg 15 – 75 mcg
lockout interval 10 – 20 min 3 – 10 min
Since renal dysfunction is more prevalent in ICU patients, there is a high risk for accumulation of the neurotoxic
metabolite.
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This method uses an electronic infusion pump that can be activated by the patient. When pain is sensed, the pt
presses a button connected to the pump to receive a small intravenous bolus of drug. After each bolus, the pump
is disabled for a mandatory time period (lockout interval) to prevent overdosing. The minimum lockout interval
is determined by the time required to achieve peak drug effect.
Anxiety is characterized by exaggerated feelings of fear or apprehension that are sustained by internal
mechanisms more than external events.
Delirium is an acute confusional state that may, or may not, have agitation as a component.
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A continuous infusion of midazolam will result in progressive drug accumulation in tissues. To avoid
excessive sedation from drug accumulation, midazolam infusions should be limited to ≤ 48 hr.
Midazolam
Highly lipid soluble.
Metabolized by CYP450 enzyme system in liver.
Active metabolite (1- hydroxy midazolam) is cleared by kidneys.
Loading dose = 0.01 – 0.05 mg/kg
Continuous infusion = 0.02 – 0.1 mg/kg/hr
Onset of action = 2 – 5 min
Duration (after bolus) = 1 – 2 hr
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5 No rapid eye movement (REM) sleep Sleep deprivation, delirium and psychosis
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c) A 50-year-old male was admitted in medicine ward with fever and cough for
last 10 days. Now he became confused, dyspnoeic and hypotensive.
Evaluate
Criteria for referring to ICU
Criteria for immediate artificial ventilation
How will you monitor in ICU
Mention the parameters to be monitored of a ventilatory patients in ICU
What the haemodynamic supports usually used in ICU.
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Dr. K H Mozumder