MEDICAL SURGICAL NURSING 1

Man  TOTALITY
 Suprasystem
o Individual, family, community, society ADRENAL CORTEX
 Subsystem Glucocorticoids/Steroids
 Gluconeogenesis (formation of new glucose from fats and
Stress Response/SMR (Sympatho-medullary Response/ SAMR proteins)  increased CHON catabolism (breakdown)  (-)
(Sympatho-adreno-medullary response)/GAS (General Adaptation nitrogen balance (catabolism>anabolism)
Response) o Positive nitrogen balance (more protein
 Diaphoresis anabolism)
 Increased B Mineralocorticoid/Aldosterone
 Increased PR  Fluid and sodium retention
 Increased rate/depth resp. o Oliguria <400 ml /24 hrs.
 Pallor o Anuria <100 ml /24 hrs.
 Cold clammy  Potassium excretion
 Weight loss
 Weakness NEUROHYPOPHYSEAL (Hypophysis Cerebri/Sella Turcica)
 Anorexia Anterior (Adenohypophysis)
 Diarrhea  TSH
 Constipation  ACTH
 Urinary frequency  FSH
 Oiguria  LH
 Anuria  MSH (Melanocyte-Stimulating Hormone)
 Transient hyperglycemia  SH (Somatotrophic Hormone)
 Increased in visual acuity
 GH
Posterior (Neurohypophysis)
 Hypothalamus
 ADH
o Sympatho-adrenal medullary
 Oxytocin
o Adreno-cortical
o Neurohypophyseal
ENDOCRINE
Hypoactivity
Adrenal glands
 Congenital absence of glands
 On top of kidneys
 Surgical removal of gland
 Adrenal medulla
o Inner portion  Idiopathic atrophy of glands
o Secretes catecholamines: Hyperactivity
EPINEPHRINE/ADRENALINE  Tumor within or outside the gland
 Vasodilator (coronary artery, cerebral  Failure of kidneys to secrete hormones
artery, peripheral blood vessels)  Failure of liver to deactivate of hormones
 Vasoconstrictor (peripheral arterioles)
 Glycogenolysis (breakdown of DECREASED APG ACTIVITY
glycogen in liver) Pituitary dwarfism
NOREPINEPHRINE/NORADRENALINE  Dwarf (doubled size of infant)
 Vasoconstrictor Frohlicks Syndrome
 Dwarf, obese, mentally retarded, genital atrophy
ADRENAL MEDULLA Simmonds disease/ Pituitary Cachexia
Epi/Norepi (Sympathetic/Adrenergic)  Wizened old man, mental lethargy, teeth start to fall,
 Dilated coronary arteries  increased myocardial amenorrhea, absence of spermatogenesis
perfusion  increased myocardial contraction 
increased PR INCREASED APG ACTIVITY
 Dilated peripheral blood vessels Gigantism
 Relaxation of smooth muscular bronchioles  Before closure of epiphyseal line
bronchodilation  increased rate/depth respiration  Rapid growth of long bones
 Constricted peripheral arterioles  increased o Prolongation/elongation of long bones
peripheral resistance  increased BP Acromegaly
 Constricted arteries of skin  decreased blood supply  After closure of epiphyseal line
 pallor  Increased in bone thickness and hypertrophy of soft tissues
 Increased glycogenolysis  transient hyperglycemia o Enlargement of cartilages
 Sweat glands  stimulation  Nose
 GIT  decreased gastric secretion  decreased  Ears
gastric motility o Enlargement of larynx
 No urine  Deepened voice
o Urinary bladder muscles relaxes o Progmathism/protrusion of jaw
o Urinary sphincter  close  Separation of teeth
 Pupils  dilation  increased visual acuity o Thickening of lips and oral mucous membrane
o Lengthening of chin
o Broad hands/spade-like fingers
o Enlargement of visceral organs
MEDICAL SURGICAL NURSING 2
o Calcium preparations (after meals)
 Calcium carbonate
 Calcium Lactate
 Management  Calcium Chloride 10%
o Cobalt therapy  Calcium gluconate
 Radiation
o Surgical removal o Given with vit. D (tachysterol)
 Hypophysectomy  Dihydrotachysterol
o Inhibit production of growth hormone  Hytakerol
(subcutaneously)  Calciferol
o Somatostatin  Calcifediol
 Sandostatin  Calcidiol
 Octreotide/actreotide ADRENAL CORTEX
1. Glucocorticoid/steroid – gluconeogenesis
DIABETES INSIPIDUS  Fat  increased lipolysis  abnormal fat distribution
 Disorder in water metabolism  decreased ADH  prevent  CHON  increased CHON catabolism  tissue
renal tubules reabsorption of water  polyuria = 5-29 L/24 starvation & muscle wasting
hrs.  Polydipsia  diluted (decreased specific gravity = 2. Mineralocorticoid/aldosterone
1.010-1.025)  increased Na (135-145 mEq/L) 3. Androgen
 All electrolyte testing do not require NPO
Cushing’s
 ADH  Increased GMA
o Oily preparations (Deep IM)  lipodystrophy (rotate  Increased 3S
route of administration) o Sugar
 Pitressin Tannate  Hyperglycemia
 Vasopressin – vasoconstrictor  HPN  Moon facies
o Nasal sprays (clear nasal passages)  Buffalo hump
 Desmopressin Acetate  Truncal obesity
 Lypressin o Salt
 Anti-lipidemic  Fluid retention  Increased BP
o Clofibrate/Atromid S/Clo 5  Hypernatremia
 Hypokalemia
SIADH o Sex
 Increased ADH  Virilism
 Fluid retention  Masculinization
o Increased IV volume (hypervolemia)  Hirsutism
 Increased BP  Management
 Increased renal perfusion  o Cobalt therapy
enhance/increased GFR/ increased o Adrenalectomy
UO  no leg edema o Cortisol inhibitors
o Electrolyte dilution  Dilutional hyponatremia   Aminogluthetemide
fluid move into the cell  Trilostane
 Cerebral edema  Increased ICP  Metyrapone
 Cellular overhydration  Metotane
 Management Addison’s
o Hypophysectomy  Decreased GMA
o Inhibit production of ADH  Decreased 3S
 Demeclocyline/Declomycin PO o Sugar
 Hypoglycemia
Parathormone  Stimulate anterior pituitary gland 
 Promote reabsorption of Ca in the renal tubules and increased ACTH  MSH  tan
excretion of P, essential for blood coagulation, regulate complexion  bronze-skinned
cardiac rhythmicity o Salt
Hypoparathyroidism  Decreased IV volume  hypotension
 Hypocalcemia = hyperphosphatemia  Hyponatremia
o 4.5-5.5 mEq/L  Hyperkalemia  myocardial irritability
o 8-11 mg/dL  altered electrical conduction 
o High calcium diet dysrhythmias  heart arrest
 Tetany o Sex
o (+) Chvostek – tap the Facial nerve (below the  Management
temporals)  muscle twitching of face o Steroids
o Trousseau – occlude blood flow of an extremity
for 1-2 minutes  carpopedal spasm Conns/Primary aldosteronism
 Management  Adenoma of adrenal cortex (benign)
o Can be given sea foods but not milk, dairy  Hyperactivity
products and egg (rich in phosphorus) so check Pheochromocytoma
levels of phosphorus if among the choices, all is  Adenoma of adrenal medulla (benign)
with calcium  Hyperactivity
MEDICAL SURGICAL NURSING 3
 5H o Evaluate amount of radioactive iodine 131
o Hypertension accumulated by the thyroid gland and excreted
o Headache by the kidneys
o Hyperglycemia o No intake of iodine
o Hypermetabolism o Uptake = 15-40%
o Hyperhidrosis o Urine = 40-80%
 Management o PO RAI 131 cocktail (with brassy taste)  24 hr.
o Cobalt therapy urine  2-4 hr. scanner
o Surgical removal of adrenal medullary o E.g. 11am PO RAI 131 6 millicuries  24 hr.
 Assessment urine  1pm scanner
o VMA (Vanillylmandellic Acid)  N: 0.9%-2.4 millicuries
 Level of catecholamine  Low: 0.67
 Blood 0.2-0.9 mg%  High: 3.6
 Urine 0.2-7 mg/24 hrs. o Directly proportional to uptake
o Inversely proportional to urine
Thyroid glands  Thyroid Scan
 Isthmus – connects the two lobes of the thyroid glands o Evaluate RAI 131 stored by thyroid gland to
 Thyroid hormones determine size, shape, location of thyroid gland
o T3 – tri-iodothyronine
o T4 – Thyroxine HYPOTHYROIDISM
o Thyrocalcitonin  Onset of symptoms
 Plasma iodide + tyrosine (amino acid) = thyroglobulin o Cretinism - childhood
(storage form)  T3, T4 o Myxedema - adulthood
o Level of hormones are related to feedback  Cause
mechanism o Primary – failure of thyroid gland to secrete T3 T4
o Secondary – failure of anterior pituitary gland to
Anterior pituitary gland  trophic hormone  target organ secrete TSH
 TSH  thyroid gland  T3 T4  S/sx
 ACTH  Adrenal cortex  SSS o Stunted growth
o Delayed onset of puberty
Assessments o Low VS
 PBI (Protein Bound Iodine) o Mentally sluggish
o Evaluate amount of iodine attached to the protein o Cold intolerant
molecule of the blood o Hypometabolic = weight gain
o 4-8 ug %  Management
o No intake of iodine for 3-4 days o Supplement thyroid extract
 Sea foods  Proloid
 Iodized salt  Cytomel
 Cough syrup  Synthroid
 Salicylate (ASA)  Euthroid
 Estrogenic preparations  Thyrolar
 Dyes  Thyrax
 T3 T4 Determination  Ectroxine
o T3 70-170 ug %  Thyroxine
 More potent than T4  Levo-thyronine
 Will not bind with iodine  Lio-thyronine
 Can readily/penetrate a cell to
stimulate metabolism HYPERTHYROIDISM
o T4 4.7-11 ug %  Grave’s/Basedoue/Parry’s disease/ Thyroitoxicosis/Toxic
o No special preparations Goiter
 TSH Test  Theories:
o 0.4-6.11 ug/ml o LATS (Long-acting thyroid stimulator)
o Decreased T3 T4  APG  stimulate TSH  Gammaglobulin
o Increased T3 T4  APG  inhibit TSH  Cause iodine accumulation and
o Inversely proportional to thyroid function thyroid hyperplasia
 BMR  Triad Symptoms
o Evaluate O2 consumption when at rest  Goiter
o NPO 12 hrs. and good night sleep  Eye signs
o  Hyperthyroidism
 TBMR o Elevated T3 T4
o Theoretical basal metabolic rate o EPS
o 20-30  Anterior pituitary gland will release an
o Pulse pressure + PR/min – 111 exophthalmos producing substance
o Not definitive  Exophthalmos (protrusion
 RAIU (Radioactive Iodine Uptake) of eyeball)
 Proptosis (downward
displacement of eyeball)
MEDICAL SURGICAL NURSING 4
 Lid lag  Partial/Sub-total thyroidectomy – 5/6 of 2 lobes
 Infrequent blinking  Thyroid lobectomy
 Fixed stare  Isthmusectomy
 Peri-orbital edema
 Von Graefe (failure of Post-thyroidectomy management
eyelids to follow movement  Promote patent airway
of eyes when the patient o Position Semi-Fowler’s
looks down) o Not High-Fowler’s – cause strain on neck muscle
 Dalyrimple sign (infrequent which causes tension on suture line (bleeding)
blinking and fixed stare)  Turn to sides
o S/sx  Promote adequate nutrition and fluid and electrolytes
 Increased T3 T4 o As soon as fully awake and with gag reflex
 Diarrhea (Elevation of palate and contraction of
 Voracious increase T3 T4 (Grave’s) pharyngeal muscle)
 Over-excitability SNS (no  Promote adequate bowel-bladder elimination
management sought) o 6-8 hrs. after surgery
o Diaphoresis o If not within 6-8 hrs., palpate presence of bladder
o Tremors distention
o Nervousness  Encourage early ambulation
o Palpitation o Shorten convalescence period
o Constipation o Boost patient’s moral
o Simple goiter/Endemic goiter/ Iodine-deficiency o Get out of bed as soon as VS are stable
goiter/ Non-toxic goiter  Support the head and neck to prevent
o Goiter – enlargement of thyroid gland flexion and hyperextension
 Hormone levels  Complications
 May be normal, o Tetany
above/below normal  Occurs upon accidental removal of
because goiter is simply parathyroid glands
enlargement o 2 recurrent laryngeal nerves
Treatment Modalities  Hoarseness (edema of glottis)
 Anti-thyroid preparation  Aphonia
 Prevent synthesis T3 T4 by blocking utilization of o Bleeding
iodine  Failure to tie/ligate the bleeders
 Example  Check for dampness at the nape
o Tapazole/methimazole  Check for feeling of choking
o PTU (Propylthiouracil)  Evaluate VS
 Differential count  Rapid, weak, feeble,
o Neomercazole/Carbimazole thready pulse
 Adverse effects (prolonged use)  Rapid but shallow
o Agranulocytosis – infection respiration
 Fever o Respiratory obstruction
 Complaint of sore throat  Secondary to bleeding
 Dyspnea  Accumulation of tracheo-bronchial
 Iodine Preparation secretion
 Lugol’s solution/KISS (Potassium Iodide  Laryngospasm
Saturated Solution)  Laryngeal edema
o Reduce vascularity o Thyroid crises/storm
o Increase firmness of gland  High anxiety level pre-op
o Promote storage of T3 T4  Increased T3 TT4  anti-thyroid
 Adrenergic-blocking preparation for 3 months  euthyroid
 Control symptoms of over-excitability of state, normal T3 T4  operation 
SNS post-op stress, infection  increased
 RAI 131 T3 T4 (over-excitability of SNS)
 Fever with tachycardia
 Surgery
 Anti-thyroid preparation
 Management
o High caloric diet
DIABETES MELLITUS
o No colas/caffeinated beverages
Assessments
o Monitor weight
 FPG, RBS, PPBS, OGTT, Hgt
o Provide physical mental rest
o Provide calm/restful environment
HHNK Coma/HHNS
o Elevate head to promote drainage and reduce
peri-orbital edema  Hyperglycemia  hyperosmolar diuresis  glycosuria &
polyuria  ECF dehydration  cerebral dehydration 
Surgeries CNS depression  HHNK
DKA
 Sistrunk’s – thyroglossal cyst
 Increased lipolysis  increased oxidation of fatty acids 
 Radical/Total thyroidectomy
hyperlipidemia & ketone bodies  DKA
o Collar-line/Curvilinear
MEDICAL SURGICAL NURSING 5
Dawn’s phenomenon Brain:
 Normal blood sugar before night time  shoots up  Parietal – sensation
hyperglycemia at the dawn  Occipital – vision
Somogyi/Rebound Hyperglycemia  Temporal – hearing, balance, memory
 Maybe normal bood sugar before the client sleeps  blood  Frontal – attitudes, personality, behavior, learning
sugar depletes at around 2 am  shoots up at around 3 am SPEECH PROBLEM
due to the counter hormone secreted in the body  Brocha’s center – speech
o More of the frontal lobe
Rapid Short Intermediate Long/Slow o Right-handed = left hemisphere (more dominant)
(10-15 (6-8 hrs.)  Wernicke’s – language
min.) Aphasia
Peak 30 m-1 hr 2-4 hrs. 6-12 hrs. 18-24 hrs.  Motor/expressive – unable to talk, unable to written, frontal
Novolog Regular NPH- Neutral Lantus lobe
Humalog insulin Protamine Ultralente  Sensory/Receptive – unable to understand both written and
Lispro Semilente Hagedorn Humulin Y vocal
Aspart Humulin R Lente Glargine  Global – both motor and sensory aphasia
Crystalline Humulin N PZI-  Visual – occipital affectation
Zinc Globin Protamine  Auditory – temporal affectation
Novolin R Novolin L Zinc Insulin
Monotard Ipsilateral
Management  Symptoms on side of lesion
 Take more complex carbohydrates than simple  Right sided lesion/tumor – focal symptoms  puffiness of
carbohydrates because the rate of absorption is slower, thus right life, drool at right side, sag of the right side
no sudden increase in serum glucose Contralateral
 Hypoglycemia  Symptoms on opposite side of lesion
o When patient has altered LOC, give 1 table  Decreased crossing, dequasation of nerve fibers at the
spoon of sugar because the blood vessels in the pyramidal tract
mouth will absorb the glucose o Pyramidal tract – fine motor movements
o The fat content will delay the absorption of  Right-sided lesion/tumor – focal symptoms  paresis,
glucose phlegia of left
o Extreme hypoglycemia
 Epi/Adre 1:1000 SQ GAIT
 Glucagon 1-2 mg IV
 Ataxic – steady  feet together  fall (cerebellum
 IV of glucose 50% - IV push
affectation)
 Exercise
 Dystonic – irregular non-directive movement  muscle
o Reduce dose of insulin
atony
o Remind to take snacks in between
 Dystrophic (Waddling gait) – feet apart  body weight
move to the sides
NEUROLOGIC DISORDERS
o With muscle dystrophy
LOC (LEVEL OF CONSCIOUSNESS)
o Weakness of pelvic girdle
 Cerebral hemispheres – center for consciousness
o Hip dislocation
 RAS at the brainstem – center for wakefulness
 Hemiphlegic – foot dragging
Altered LOC
 Scissors – short, slow steps, legs alternating and crossing
 Causes
each other
o Lesion
o With spastic paralysis
 Tumor
 Steppage – high exaggerated steps (lower motor neuron
 Hematoma
affectation)
 Abscess
o Metabolic depression
REFLEXES
 Hypoglycemia
 Hypoxia  Knee-Jerk
 Fluid and electrolyte imbalance  Bicep – forearm flexion
 Toxic/chemicals  Tricep – forearm extension
 Assessment  Babinski – extension of big toe, fanning of other toes
o Glasgow Coma Scale  Gordon’s – squeeze calf muscle  dorsiflexion of big toe
 Eye opening, Verbal Response, Motor  Chaddocks – stroke inner aspect of legs  dorsiflexion of
Response big toe
 Ophthalmoscope – checks pupillary  Kernigs – flex and extend in lower extremity  pain and
dilation spasm in hamstring muscle
 Decorticate – spinal lesion  Cremasteric – stroke inner aspect of thigh  rise of testes,
 Decerebrate – diencephalon and brain elevate scrotum, use tongue depressor
stem affectation (medulla – respiratory  Brudzinki – bend head toward chest  flexion of ankle,
paralysis) knee and thigh
Brain herniation  Binda – turn head to one side  opposite shoulder will
 Disease of pons and midbrain  decorticate and move upward and inward
decerebrate at the same time
MEDICAL SURGICAL NURSING 6
Stronger muscles  No colas/caffeinated beverages
 Flexor vs. Extensor  No Phenytoin/Dilantin, Na
 Adductor vs. Abductor Luminal/Phenobarbital,
COORDINATION Carbamazepine/Tegretol,
 Romber’s Test Clonazepam/Klonopin
o Stand with feet together, eyes closed  Advice a regular diet prior to EEG
 Fall/sway to one side – cerebellum because a state of hypoglycemia will
affectation alter LOC
Diagnostic Tests  Shampoo hair to cling the electrodes
 Lumbar Puncture/Spinal Tap on non-oily hair
o Consent  With history of seizure/convulsion –
o Local anesthesia into subarachnoidal space continue anticonvulsant
(Lidocaine/Xylocaine 1-2%, Novocaine,  Prevent Status Epilipticus
Tetracaine HCl, Marcaine)  EMG – measures electrical activities of peripheral muscles
 L3-L4, L4-L5, L6-S1 (end of spinal nerve is to diagnose muscle dystrophy and peripheral nerve injuries
above L1 o Jolly’s (Nerve Conduction Velocity)
 C-position/Shrimp position o Several needles and wires will be attached to
 Void before procedure muscles, observed while performing activities
o Immediately prone 30 min.-1 hr.
o FOB 6-8 hrs. to prevent spinal headache
 Queckenstedt  CT scan
o CSF Pressure  Jugular vein pressure  6-12 o Without contrast – no prep
sec. o With contrast via IV (Thallium, Technetium,
o CSF Neohydrin) – NPO for 6 hours
 Volume: 90-150 mL  MRI
 Transparency: clear  Skull x-ray
 Color: colorless
 Yellowish (Xantochromia) = PARKINSON’S DISEASE/Paralysis Agitans
old blood clot  Degeneration of basal ganglia due to decreased supply of
 CHON: 15-45 mg% dopamine
 Inc. = tumor, MS, GBS  Risk Factors: History of Encephalitis, Head Trauma,
 Glucose: 50-80 mg% (glycorrakia) Smoking, Hypertension, CO2 Monoxide, Use of
 Chloride: 118-132 mEq/L Contraceptive Pills
 WBC: 0-8/mL = Pleocytosis  Neuronal Degeneration of the substantia nigra of the
 Gammaglobulin: 3-9 % midbrain  decreased inhibitory neurotransmission 
 MS (IgG) decreased dopamine  impairment of the extrapyramidal
 Pneumo-encephalogram – x-ray of the brain ventricles after tract (basal ganglia)  imbalance in voluntary movement
introduction of air/O2  triad symptoms (non-intention tremors <pill-rolling
o Prepare for LP movement of thumb against fingers>, rigidity <micrographia
o Withdraw 20 mL of CSF, then give 20 mL of O2 or minute illegible handwriting, cogwheel or jerky motion for
 Cerebral Angiogram – x-ray of the cerebral vascular system every passive movement>, bradykinesia/dyskinesia
with the use of dyes (Conray/Diodrast) into the femoral or <freezing phenomenon or transient inactivity>)
carotid arteries  Impairment of the extrapyramidal tract (basal ganglia) 
o Same with Carotid/Femoral arteriography weakness of the muscles of expression  “mask-like/blank
o Secure consent facies”
o Prepare a local anesthetic (puncture a major  Imbalance in voluntary movement  triad symptoms 
blood vessel) impairment of the muscles responsible for speech 
o Dye administration drooling and microphonia or slow, monotonous voice with
 NPO for at least 6 hrs. – prevent poor articulation
dilution of dye  Shuffling/propulsive/festination gait
 Check for allergies  Stooped posture
 Submit to Serum Crea –nephrotoxic  Walking on toes with accelerated pace
 Not to be alarmed if with metallic Management
taste, flushing, warm sensation  Dopamine – cannot pass through blood-brain barrier
o Place an ice cap/ice collar on the neck to prevent  Levodopa – metabolic precursor, absorbed by substantia
bleeding (carotid) nigra, acted upon by decarboxylase which will be converted
o Place a sandbag over the inguinal area for into dopamine
pressure, immobilize, keep leg extended to keep o Dopar – Larodopa
pressure on the femoral artery o Carbidopa – Sinemet
o Check popliteal and dorsalis pedis pulse distal to o Amantadine HCl – Symmetril
the site of puncture o Trihexyphenidyl – Artane
o Check color and temperature of leg to check o Benztropint Mecylate – Cogentin
arterial insufficiency (cold, pale) o Biperidine HCl – Akineton
 Myelogram – x-ray of subarachnoidal spaces after giving a o Endoginous dopa
dye (Pantopaque/Myodin) instraspinously/intrathecally  Bromocriptine
o Prepare like in LP  Partodel
 EEG – measures electrical activities of brain
o Avoid stimulant/depressant
MEDICAL SURGICAL NURSING 7
 MAOI  Demyelination (damage of myelin sheaths) of nerve fibers
o Selequitine of brain and spinal cord  replaced by sclerotic patches of
o Eldepryl necrotic tissue  trigger inflammatory reaction  form
o Carbex inflammatory exudate/edema  scarring/fibrosis  failure
 Surgery of transmission of electrical impulses Charcot triad of
o Stereotactic – uses electrical stimulator, interrupt symptoms
the nerve fiber pathway  Charcot triad of symptoms
 Thalamotomy – thalamus o Tremors = spastic-ataxic gait
 Pallidotomy – deep Globus pallidus o Nystagmus (movement from side to
Nursing Diagnosis side)/strabismus (movement toward the midline)/
 Impaired mobility dysconjugate (movement away from the midline)
o Do regular exercises to improve muscle tone and CN 3 (Oculomotor – pupil contraction, eye
strength and prevent contractures accumulation), 4 (Trochlear – superior oblique
o Give something to hold onto – stress ball, hand muscle), 6 (Abducens – lateral rectus muscle of
roll eye)
 Loss of self-esteem o Scanning of speech – difficulty of pronouncing
 Risk for aspiration the first syllable of the word, frontal lobe
 Self-care deficit demyelination
 Risk for constipation  Other signs and symptoms
 Safety: risk for physical injury o L-hermittes – electrical stimulation in the
posterior trunk upon bending (demyelination of
MYASTHENIA GRAVIS the spinal cord, mid-clavicular vertebrae)
 Failure in the transmission of electrical impulses at the myo- o Loss of sensation (parietal lobe demyelination)
neural junction due to blockage/destruction in acetylcholine o Euphoria
(excitatory) receptor o Apathy – “deadma”
 Autoimmune disorder  release antibodies  block Diagnosis
acetylcholine receptor  reduce uptake of acetylcholine   Lumbar Puncture
reduce number of functional acetylcholine receptors o Elevated CSF CHON, G-globulin
 Normal: Axons  release excitatory neurotransmitter   MRI
acetylcholine attach to acetylcholine receptor of the muscle o Evaluate extent of demyelination
fibers  muscle contraction  muscle atony and weakness Management
 paralysis  Symptomatic
o Ocular muscle  ptosis, diplopia  Supportive
o Facial and lingual muscle  Steroids – reduce edema around site of demyelination
 Dysphagia  ABCR – prevent proliferation/activation of T cells
 Mastication impairment o Avonex
 Snarling smile – clenched teeth and o Betaseron
jaw hangs open o Copaxone
o Respiratory paralysis  respiratory distress  o Rebif
MYASTHENIA CRISIS (no treatment sought)
Diagnosis GUILLIAN-BARRE SYNDROME
 Tensilon Test Pathological Changes
Management  Polyradiculoneuritis (“Radiculo” – cranial nerves)
 Thymectomy (suprasternal notch) o Ocular
o Thymus gland  T cells  antibodies o Oro-pharyngeal muscles
production o Facial
o Remove antibodies (autoimmune)  Peripheral neuritis – demyelination of peripheral nerves
o Thymoma o Ascending paralysis
 Plasmapheresis/Plasma exchange  Autonomic dysfunction
o Separate antibodies in the blood in exchange o Over-excite SNS & PNS
with donor blood o Under-excite SNS & PNS
 Establish artificial airway
o ET/Tracheostomy insertion Parkinson’s – Male (Freddie Roach)
 Receive anticholinesterase/cholinergic agent – increase MS – Female (Alma Moreno)
uptake of acetylcholine, increase number of functioning G B S – both sexes (girl, boy)
acetylcholine receptors MG – early onset in female, late onset in male
o Prostigmine/Neostigmine
o Mestinon/Pyridostigmine CVA/ APOPLEXY
o CHOLINERGIC CRISIS/ PNS activation  Cerebral ischemia  Cerebral infarction/necrosis
 Give anti-cholinergic Atropine Sulfate,  Cerebral anoxia (4 minutes)  cerebral infarction
Scopolamine Pathology
 Occlusive
MULTIPLE SCLEROSIS o Embolism
 Myelin sheath – fat-like covering of nerve fibers  MI, endocarditis, dysrhythmia,
 Chronic lingering illness until death fracture, CA
 Risk factor: Autoimmune disease, post-viral disease,  Sudden onset
Pregnancy, Stress, Use of amphetamines
MEDICAL SURGICAL NURSING 8
o Thrombolism o Dexamethasone (Decadron)
 DM, Atherosclerosis, Hypertension,  Only steroid that crosses blood-brain
Smoking barrier
 Gradual onset  Mechanical ventilation/ambubagging
 TIA – should appear only for 24 hrs. o Decrease PCO2 by hyperventilation (MV) 
 Nuchal pain increased RR  excrete O2  decreased ICP
 Paresthesia TUMORS
 Light-headedness According to origin
 Transient loss of memory  Glioma – from brain tissue
 Transient loss of speech  Meningioma – from brain covering
 Hemorrhagic  Neuroma – from cranial nerves
o Hemorrhage According to location
 Hypertension, aneurysm  Supratentorial – cerebrum, anterior 2/3 of brain
 Stress, physical activity  Infratentorial – cerebellum, brainstem, post. 1/3 of brain
Symptoms
 Depends on area of necrosis
 Increased intracranial pressure Symptoms
 Earliest sign: papilledema (compression of optic nerve)
INCREASED INTRACRANIAL PRESSURE Management
Early signs  Surgery
 Restlessness and hippus (alternate pupillary dilatation and o Craniotomy – coronal/butterfly incision
constriction) o Craniectomy
 Projectile vomiting  Radiation therapy
 Papilledema
 Choked disc Head surgery
 Headache (cephalalgia) – arising and worsen with change in  DON’Ts after surgery
head position o Trendelenburg
  Increase ICP
Late signs: Cushing triad changes  Compress diaphragm
 Increased SBP, normal/decreased DBP = widened pulse o Suction
pressure  Increases ICP
 Decreased PR  Insertion of tube – triggers cough
 Decreased RR reflex  increased ICP
 If needed, do it orally because nasal
 Increased metabolic rate  Increased temp.
may cause nasal trauma thereby
 Progressive altered LOC  decreased temp.
causing CSF leak
Causes
 Halo sign (use gauze)
 Increased CSF volume
 Sugar
 Increased brain tissue bulk/size
o Restrain
 Increased cerebral blood flow  Increases ICP
o PpCO2 (hypercarbia, hypercapnea) dilated o Insert rectal tube/thermometer
cerebral blood vessel  increased cerebral  Vagal stimulation  PNS
blood flow  cerebral congestion  increased o Constipation
ICP  Increase cerebral blood flow
Management
 Supratentorial – 45 HOB (Semi-Fowler’s)
 Anti-thrombotic/ anti-platelet aggregate o Promote venous return
o ASA – prolonged prothrombin time, GI upset
 Infratentorial – 10-15 HOB
o Aspilet
o Prevent compression of brainstem
o Ascription
o Don’t place client on back  place on
o Dipyridamole/Persantin/Pexid
unoperated side
o Ticlopidine/Ticlid
o If on operated side, not more than 20 minutes to
o Clopidogrel/Plavix/Clovix
prevent cerebral
 Anti-coagulant
o Coumadin PO HEMATOLOGIC DISORDERS
o Heparin SQ, IV BLOOD DYSCRASIA
 Antidote: Protamine Sulfate Pathology
 Check PTT
 Pancytopenia – decreased production of blood cell
 Plasminogen activator – plasmin lysis
 Overproduction of defective cells
o Streptokinase
 Spleen disorders
 Antidote: Aminocaproic acid
o Urokinase  Defect in the coagulation mechanism
o Altiplase Diagnosis
o Retavase  CBC, Hgb, Hct (percentage of blood cell in plasma)
o t-PA (tissue type)  BT, PT, CT
 Cerebral decongestant  Erythrocyte index
o Mannitol (Hyperosmolar solution) o MCV (Mean Corpuscular Volume)
 Sol  ITS  IV  increased renal  Evaluates size of RBC
perfusion  increased UO  80-94 cu. Microns
MEDICAL SURGICAL NURSING 9
 Anisocytosis – abnormal size  Paresthesia due to degeneration of
(microcytic vs. macrocytic) nerves
o MCH (Mean Corpuscular Hemoglobin)  Supplement what is lacking
 Evaluate Hgb content of RBC  Fe intake (hematinic)
 22-28 micromicrograms  Increased hemolysis
(hyperchromic vs. hypochromic) o Hemolytic Anemia
o MCHC (Mean Corpuscular Hemoglobin Causes
Concentration)  Exposure on ionizing agent
 Evaluate Hgb in grams/100 ml Packed  Post-viral
RBC  Drug-induced
 30-36g/100 ml PRBC  Transfusion of improperly cross-
 Coombs matched blood
o Evaluate immune bodies that adhere to RBC Symptoms
causing hemolysis and agglutination of RBC  Hemolytic jaundice (increased RBC
 Schilling hemolysis  increased unconjugated
o Evaluate rate of absorption of Vit. B12 bilirubin  hyperbilirubinemia)
o Assesses presence of Pernicious Anemia: absent Management
B12 in urine  PRBC
o Administer radioactive Vit. B12 per orem, collect  Splenectomy
24 hr. urine to determine presence or absence of  BM depression
B12 o Hypoplastic Anemia
o Normal: parietal cells  g. mucosa  intrinsic  BM depression  decreased WBC
factor  B12 present in urine (leukopenia  infection) and
o Management: lifetime parenteral B12 decreased platelet (thrombocytopenia
 BM tap/Puncture/aspiration  bleeding)
o Evaluate size, shape, characteristic of different  Reverse isolation
blood cells  Avoid sources of bleeding
o Poikilocytosis – abnormal shape  Constipation
o Metarubricyte/nucleated  Use soft-bristled
 Erythroblast (immature) – with nuclei  Use electric shave
 RBC – without nuclei  Avoid parenteral inj. (use
sharpest needle if highly
needed)
 Avoid crowds
o Preparation  FWB
 Consent  Bone marrow transplantation
 Prepare sternum, anterior/posterior  Syngeneic – twin
iliac crest  apply pressure dressing  Allogeneic – rel/non-rel
 Lymph node biopsy o Compatible
o Cervical leukocyte
o Axillary antigen
o Mediastinal  Autologous – harvest
o Inguinal during period of
 Blood typing remission/absent
symptoms
ANEMIA  Blood loss
Causes o Normocytic, normochromic anemia
 Decreased erythropoiesis (formation and maturation of o Hypovolemia
RBC) o Hypovolemic shock (loss of 15-25%)
 CHON – cell wall, structure, membrane  N: 4-6 L
 Iron – pigment hemoglobin o FWB
 Vit. B12 – synthesis of nucleic acid Signs and symptoms
 Folic Acid - mature  Decreased Hgb count  reduction in the O2 carrying
 Vit. C – catalyst for iron absorption capacity of the blood  tissue hypoxia
o Iron Deficiency Anemia o Brain: restlessness, HA, syncope, irritability
 Microcytic, hypochromic anemia o Heart: angina pain, increased PR, weakness 
 Vinson-Plummer Syndrome easy fatigability (earliest complain)
 Dysphagia o Respi: increased RR, SOB
 Atrophic glossitis (tongue) o GIT: anorexia, angular cheilosis (lesion at angles
 Stomatitis/Mucositis (oral of mouth)
mucosa) o Skin and M. Membrane: pallor, brittle hair,
o Megaloblastic Anemia intolerance to cold, brittle nails  spoon-shaped
 Macrocytic, hyperchromic anemia (Koilonychia)
 Folate deficiency and Pernicious
anemia
 Beefy red tongue (reddish, sore
tongue due to gastric atrophy)
MEDICAL SURGICAL NURSING 10
POLYCYTHEMIA VERA MULTIPLE MYELOMA
 Tissue hypoxia  release of humoral substance   Plasma cells secrete Ig (CHON)  antibodies
erythropoietin  stimulates BM activity  increased  Proliferation of abnormal plasma cells (uncapable of
basophils  increased erythropoiesis  capillary producing functional Ig)
congestion, hemoconcentration, compensatory hypertrophy o Infection
o Increased basophils  increased cellular activity o Hemoconcentration  hypertension and
(increased cellular metabolism  weight loss thrombus formation
and increased temperature) and release of o Secrete osteoclast activating factor  increased
histamine (pruritus) bone destruction (calcium losses from bone 
o Capillary congestion brittle, pathologic fracture and hypercalcemia 
 Ruddiness of the skin “Phletora” hypercalciuria  calcium crystallize  nidus,
 Capillary engorgement bleeding  nucleus  stone) and increased bone resorption
anemia  bone pain (skull, vertebrae, scapula, clavicle,
o Hemoconcentration pelvis, femur)
 HA, dizzinesss, blurring of vision Diagnostics
 Hypertension  BM biopsy
 Sluggish blood flow  thrombus  Urine: Bence-Jones protein
formation  CBC with differential count
o Compensatory hypertrophy  Hct determination
 Hepato-splenomegaly (splenomegaly  Serum calcium
first)  Calcium urine
Management Management
 Increase fluid intake  Chemotherapy
 Engage in activities
 Anti-neoplastic agents (Anti-metabolite) HODGKIN’S/Malignant Lymphoma/Lymphosarcoma
o Methotrexate/Mexate  Risk factors: familial history, exposure to carcinogen,
 Blood phlebotomy exposure to environmental pollutant, post-viral illness
o Opening of vein to gradually withdraw blood (Epstein-Barr virus)
 Incidence is high in males <20, >50
LEUKEMIA Diagnosis
Pathology  Biopsy: Reed-Sternberg cells
 Uncontrolled, abnormal proliferation/multiplication of Symptom:
immature blast cells (WBC)  infection  A (Local) – painless lymphadenopathy (earliest)
o Increased cellular activity  increased cellular  B (Systemic) – fever, weight loss, night sweats
metabolism  increased temperature Management
o Crowd/congest/accumulation in bone marrow   Surgery
joint pain, joint swelling, hinder/prevent  Chemotherapy
production of blood cells (decreased RBC) zS 
anemia, decreased platelet  thrombocytopenia GASTROINTESTINAL DISORDERS
 bleeding ACHALASIA/Aperistalsis
o Invade/ infiltrate vital organs  splenomegaly, Pathology
hepatomegaly, increased ICP, renal insufficiency  Absence/degeneration of Myenteric Aurbach Plexus (nerve
and renal failure fiber that innervate/stimulate esophageal activity 
According to onset of symptoms Aperistalsis)
 Acute Leukemia  Megaesophagus – dilated esophagus when food
o Sudden, short duration (<6 mos.) accumulate at lower end of esophagus
o Predominant cell: immature blast cells  Cardiospasm – failure of cardiac sphincter to relax to allow
food to enter stomach
Symptoms
 Chronic Leukemia  Sternal pain – compression of food at sternum
o Gradual, long duration  Halitosis – decomposed food
o Predominant cell: mature WBC  Esophagitis
o Remission and exacerbation o Dysphagia
WBC o Odynophagia
 Bone Marrow  Regurgitation/pyrosis
o Granulocytes  myeloblast  myelocyte (N, E, Management
B)  Esophagomyotomy – opening/division of the muscle fibers
o Non-granulocytes  monoblast, monocyte of esophagus
 Lymphoid Tissue  Cardiomyotomy – dividing esophageal and cardiac muscle
o Non-granulocytes  lymphobast   Hellers’
lymphocytes  Nissen Fundoplication – lower end of esophagus is covered
According to predominantly cells using the fundus of the stomach
 Acute/Chronic Lymphocytic Leukemia (ALL)  TPN (hyperalimentation) – glucose, lipids, amino acids
o Most common for children o Central line – subclavian vein (well supported by
 Acute/Chronic Myelocytic/Myelogenous Leukemia (CML) shoulder muscle)
o Most common for adults  Need for hypertonic glucose >10% or
more than 10 days
MEDICAL SURGICAL NURSING 11
 Increased rate  hyperglycemia   Stress  Parasympathetic/Vagal
hyperosmolar diuresis (glycosuria, o Executives: duodenal ulcer
polyuria) o Increased gastric secretion
 Insulin – only drug compatible with o Increased gastric motility
TPN  Ulcerogenic Agent
 CBG TID to check for hyperosmolar  Gastric stimulant
diuresis brought about by  Personality – Type A (highly competitive, highly aggressive,
hyperglycemia highly ambitious)
 Monitor I/O and serum electrolytes  Age
 Monitor for Venous thrombosis (pain o Gastric ulcer – >40
and swelling at jaw, neck, shoulder o Duodenal ulcer – 30-40
where the TPN is inserted)  Sex
 Effectivity: body weight o Gastric ulcer – both
o Duodenal ulcer – male (poor stress mgt.)
ESOPHAGEAL DIVERTICULUM  Previous infection of GIT brought about by Helicobacter
 Outpouching/ballooning pylori (from raw pork and beef)
 Cause: congenital weakness of supporting wall o Enzyme release  destruction of gastric mucosa
 Risk factor: chronic esophagitis  loss of mucin
According to location  Smoking
 Zenker Pulsion – upper 1/3 o Nicotine  vasoconstriction  gastric anoxia
 Traction – middle 1/3 o Nicotine  destroys alkalinity of bile and
 Epiphrenic – lower 1/3 pancreatic enzymes
Management  Blood Type
 Surgery o “O” – Ulcer (high in pepsinogen)
o Transthoracic incision (Traction and Epiphrenic) o “A” – Cancer
GERD Signs and Symptoms
Pathology  Pain – mid-epigastric, burning, gnawing
 Inappropriate relaxation of the lower esophageal sphincter Gastric ulcer Duodenal ulcer
causing the backflow of gastric content into the esophagus Radiate to left epigastric Radiate to right epigastric
 Risk factor: pregnancy, caffeine, obesity, High in fat, alcohol, 30 min. – 2 hrs. p.c. 2-4 hrs. p.c.
high estrogen levels Food – aggravates Food – relieve
 Management Vomiting – relieve Vomiting - none
o Decrease pressure in LES Weight loss Weight gain
 Urecholine Decreased HCl – Increased HCl -
 Bethanecol hypochlorhydria hyperchlorhydria
 Domperidone Hematemesis Melena
Management of Esophageal disorders Management
 Assume upright position
 Buffers – food and antacid (an hour after meal, in between
 Avoid eating and drinking 2 hrs. before retiring
meals, at bedtime)
 Avoid coffee, fatty foods, alcohol, smoking, spices/irritants
 Decrease CHON (potent secretagogue  HCl)
 Maintain IBW
 Increased CHO
 Avoid very hot and very cold drinks
 Encourage fat intake (polyunsaturated)  intestinal mucosa
 Render oral hygiene
 interogastrone  decrease gastric secretion, decrease
 Take SFF
gastric motility
 Administer H2-receptor antagonist (block release of
PEPTIC ULCER DISEASE
histamine by parietal cell)
 Erosion of a circumscribed area in GIT due to digestive
 Antacid and H2 blocker – can be both given, give H2 blocker
action of HCl and Pepsin (protein-digesting enzyme, digests
ahead of antacid because antacid has a local coating effect
living tissues) Complication
 Most common areas (bathe with pepsin)  Perforation – ulcer invaded the serosa, submucosa,
o Lesser end of esophagus muscularis of stomach
o Lesser curvature of stomach  gastric ulcer o Gastric and intestinal content leak to peritoneal
o Upper end of duodenum  duodenal ulcer
cavity
 Autodigestion theory
o Abdominal distention
 Gastric ulcer – no buffering for HCl
o Boardlike, rigid, hypoactive bowel sound
 Duodenal ulcer – increased acid load/acid chyme
 Peritonitis
Barriers against pepsin
o Abdominal distention
 GIT  mucin  film/coat
o Boardlike, rigid, hypoactive bowel sound
 GIT  blood supply  prevent gastric anoxia
 Bleeding
 Duodenum  bile and pancreatic enzyme (alkaline) 
 Pyloric obstruction
neutralize
o Result from stenosis coming from fibrosis
Basic pathologic changes
 Intractable ulcer
 Absence of protective mucin o Ulcer is not responding to medications
 Gastric anoxia
 Absence of bile and pancreatic enzyme
Risk factors
 Poor dietary habit (not eating and eating hurriedly)
o Lower economic strata: gastric ulcer
MEDICAL SURGICAL NURSING 12
Management INTESTINAL OBSTRUCTION
 Billroth I Mechanically
o Remove distal third  anastomose to duodenum o Tumor (Recto-sigmoid, descending colon)
o Sub-total gastrectomy with gastro-duodenostomy o Risk factors
 Billroth II/Polya/Hoffmeister  History of Crohn’s and Ulcerative Colitis, Chronic
o Remove distal third  anastomose to jejunum constipation
 Billroth III  High in saturated fat, high CHON, low fiber, high
o Esophago-jejunostomy intake of beef
o Cancer of the stomach  Polyposis – Pre-cancer lesion
 Gastrorrhaphy - Suturing of a perforated stomach  2-3 yrs. of change from benign to
 Antrectomy malignant
o Remove antrum o Syptoms
o Antrum  gastrin  HCl stimulation  R-sided – melena
o Palliative surgery for intractable ulcer  L-sided – hematochezia
 Vagotomy o Volvulous
o Remove a portion of vagus nerve o Intussusception
o Vagus nerve  increase gastric secretion, o Diverticulosis
increase gastric motility o Adhesion
 Pyloroplasty - enlarge pyloric opening Neurogenic/Functional
 Paralytic Ileus/Adynamic colon
Complication of Gastric Surgery Causes
 Dumping Syndrome o Anesthesia
o Rapid passage of hyperosmolar solution into o Peritonitis – intestinal decompression
jejunum  jejunum distention  Miller-Abbott
o Local effect  jejunum distention  increased  Cantor
intestinal motility  Harris
o Systemic effect  hyperosmolar solution  fluid  Baker’s
shift  IV to jejunum  shock-like o Hypokalemia – tone
o Eat foods on recumbent position  Hirschprung’s Disease
o Dry meal Vascular
o No sweets, no CHO-rich foods  Mesenteric
 CHO – 1-2 hrs. p.c.  Thrombosis
 CHON – 2-4 hr. p.c. Management
o Management  Gastric decompression
 Delay gastric emptying o Levine
 Propantheline Bromide o Euald
 Bentyl Buscopan o Salem
 Marginal Ulcer o Sump
o HCl is in contact with the anastomosis o Moss
 Pernicious Anemia  Surgery
o Loss of intrinsic factor  B12deficiency o Hemicolectomy
 Malnutrition  Lap
COLON DISORDERS  Open
CHRONIC INFLAMMATORY BOWEL DISEASE o APR (Abdominoperineal Resection)/Miles
Crohn’s/Regional Enteritis Ulcerative Colitis  Surgical removal of descending colon,
Site Transmural (all layers) Entire length of colon: sigmoid, rectum, anal sphincter
SI: segment  Terminal Descending colon (recto-
Ilium sigmoid) HEPATO-BILIARY DISORDERS
LI: Ascending colon LIVER CIRRHOSIS
Predisposing Hereditary, auto-immune Bacteria, stress, allergen Types:
Factor  Biliary
Pathologic Sub-mucosal lymph Diffuse mucosal  Post-necrotic
lesion nodes ulceration  Laennec’s
Payers Patches  Inflammatory infiltrate –  Cardiac
cobblestone Crypt abscess Diagnosis
(fissures/ulcers)  Peritoneoscopy with liver biopsy
Constricted  “String o AST/SGOT
sign” o ALT/SGPT **
Pain RLQ Generalized crampy - o SLDH
LLQ  Increased 1 & 2 – myocardial insult
Diarrhea 3-5x/day 15-20x/day  Increased 3 – lung parenchyma
Stool Mucoid, pus Mucoid, pus, blood  Increased 4 & 5 – liver disorders
Semi-soft to soft Watery stool Symptoms
 Earliest: hepatomegaly
Management:
 Late: Small contracted, atrophic/shrinkage liver
 Symptomatic
 Hypoalbuminemia
 NSAIDs
 Hyperaldosteronemia
 Intestinal antibacterial – Sulfonamide
 Portal hypertension
 Avoid stimulants
MEDICAL SURGICAL NURSING 13
o Symptom Cholesterol-filled gallstone dissolver
 Earliest sign: ascites  Chenix, Ursodiol
 Hydrothorax  Chrnodeoxycholic acid
 Esophageal Varices  Ursodeoxycholic acid
 Sclerotherapy (Na T-tube
Morrhuate, Sotradecol Na)  To bypass/divert the flow of bile until the post-operative
– non-bleeding edema subsides
 Avoid activities that  Prevent bile peritonitis
increase abdominal  Drains only when there is increased biliary pressure
pressure  Output bottle: in line with incision
 Vasoconstrictor: o Increased output – obstruction (not entering
Vasopressin/Pitressin duodenum)
Tannate, Epi/Adr. o N: 300-500 mL/24 hrs.
 Tamponade  Use excoriation barrier to prevent skin irritation when bile
 Hemorrhoids drains into skin
o Shunt  Cholecystokinin – for gall bladder contraction
 Porto-caval (PV-IVC) Surgery
 Spleno-renal (SV-LRV)  Kocher’s incision – biliary surgery
 Meso-caval (SMV-IVC)
 Hassab’s Operation – Gastric ACUTE HEMORRHAGIC PANCREATITIS
devascularization Risk factors
Pathology  Alcoholism
 CHON  NH4  Urea (kidneys)  Penetrating duodenal ulcer
 Failure of liver to detoxify ammonia  NH4 intoxication   Complication of ERCP
hepatic coma/encephalopathy  Abdominal trauma
o Earliest symptom: sleep reversal  Drug-induced (immunosuppressant, anti-hypertensives,
o Earliest sign: (+) asterixis diuretics)
o Fetor hepaticus (ammoniacal odor of breath) Pathology (Autodigestion)
 Sources of ammonia  Trypsinogen (protiolytic enzyme) – enterokinase
o Exogenous: CHON, amine radicals (duodenum)  trypsin  digest pancreatic cells and
o Endogenous: urease-splitting organ  CHON  surrounding cell membrane  pancreatic cell destruction
NH4  release of histamine’s bradykinin  VD & increased
Management capillary permeability
 High protein – regeneration of liver o Edematous pancreatic capsule  left flank pain
 Low protein – ESHD (End-Stage) radiating to back/epigrastric pain  vomiting
 Anti-coma regimen o Pancreatic cell necrosis
o Enema – cleanse colon of urease-splitting  Leukocytosis
microorganism  Hyperglycemia (destruction of Islets of
o Neomycin by enema or NGT – non-absorbable Langerhans)
antibiotic that prevents growth urease-splitting  Hypocalcemia (trapping of Ca in
microorganism feces)
o Duphalac/Lactulose PO – decrease pH to inhibit  Increased serum amylase and serum
growth of urease-splitting microorganism lipase
o Interstitial bleeding  blood-retained
BILIARY TRACT OBSTRUCTION retroperitoneal fluid
Symptoms  Peritonitis (+Blumberg’s sign)
 Pain: Biliary cholic – severe RUQ pain radiating to  Rebound tenderness
 Hemolytic jaundice – increased unconjugated bilirubin  Cullen’s sign
 Obstructive jaundice – increased conjugated bilirubin  Bluish discoloration around
(Cholelithiasis) the umbilicus
 Hepatocellular jaundice – increased conj. And unconj.  Turner’s sign
 Obstruction:  Bluish discoloration in the
o Tea-colored urine left flank area
o Clay-colored stool Diagnosis:
o Absence of bile salt (emulsifier) in duodenum  Lipase – elevated for the next 2 weeks
 N/V Management
 Steatorrhea (fat indigestion)  Rest GIT – prevent pancreatic stimulation
 Hypoprothrombinemia  bleeding o NPO
Gall Stones o Gastric decompression
 Metabolic – obese  hypercholesterolenemia  increased o H2-blocker
concentrated bile  nideus/nucleus  gall stones o Antacid
 Inflammation  alteration in constituent of bile  o PPI
decreased solubility of cholesterol  nidus/nucleus  gall  3rd generation antimicrobials
stones o Cephalosporin
 Stasis  biliary stricture stasis in flow of bile   Plasma expanders
increased concentration of bile  gall stone o Dextran
o Haes-steril
o Voluven
MEDICAL SURGICAL NURSING 14
EYE DISORDERS BASES
CATARACT  Contain no H ions
 Gradual, painless loss of vision  H ion receptors
Types  Increase in acids  acidity
 Degenerative/Senile  Increase in bicarbonate  alkalinity
 Congenital pH (7.4)
 Metabolic – DM, malnutrition, severe dehydration, prolonged  pH of 7 – neutral
use of steroids  <7 – acid
 Traumatic – prolonged exposure to UV light  >7 – alkaline
Diagnosis ACID-BASE BALANCE
 Slit-lamp microscope/biomicroscope  There is continuous acid production from metabolic
Management processes
 Use of antioxidant – Beta-carotine  Ways to remove acid
 Bifocal magnifying lens o Buffers
 Surgery: ICCE, ECCE, Facoemulsification (sutureless o Respiratory
technique) o Kidneys
Complication o Stomach (vomit)
 Bleeding – only after ICCE, ECCE  Acidic
o Severe headache, pain o CO2
 Panophthalmitis – faulty aseptic technique o Urine
o Photophobia o Stomach
o Chemosis  Alkaline
o Hypopion o Intestines – from bile and pancreatic juice
o Dischagres o HCO3 (metabolic)
GLAUCOMA BUFFER SYSTEMS
 Tonometry – diagnose glaucoma, measures IOP  Absorb or release H ions as needed
 Gonioscopy – juncture/angle between the iris & cornea,  Fastest acitng regulartory system
diagnoses closed angle glaucoma  Act as sponges
 Closed/Acute – iris and cornea – MEDICAL EMERGENCY!  3 main systems
 Open/Chronic – trabecular meshwork o Bicarbonate-carbonic acid buffer (body’s major
Signs and symptoms buffer)
 Ocular pain  HCl + NaHCO3  NaCL + H2CO3
 Headache (H2O + CO2)
 Loss of peripheral vision/ tunnel vision  bumping objects  H2CO3 – 1.2 mEq/L
on sides  HCO3 – 24 mEq/L
 Halos/rainbows around lights o Phosphate buffer
 Acute – eye pain o Protein buffer
 Chronic – asymptomatic  Some of amino acids contain free
Management radicals (-COOH), which can
 Medications dissociate into (CO2) and (H+)
o Miotic/cholinergic drugs  COOH  COO2 + H
 Pilocarpine  Cells can also act as buffers by shifting H+ in and out of cell
 Carbachol  Acidosis
 Phyrostigmine o Increased H in the ECF  cells can accept H+ in
o Carbonic Anhydrase exchange for another cation like K+
o B-blocker RESPIRATORY REGULATION
 Timoptic/Timolol Maleate Mechanism of control
 Betoptic/Betaxolol  Hyperventilation – blow off CO2
o Glycerol/Glycerine PO – decrease IOP  Hypoventilation – retain CO2
 Surgery Regulation rapid
o Trabeculoplasty – open angle  Seconds to minutes reaching maximum effectiveness in
o Iridectomy/Iridotomy – closed angle hours
 Measured by PaCO2 – normal (35-45 mmHg)
ACID- BASE ALTERATIONS RENAL REGULATION
HYDROGEN IONS Mechanism of Control
 Circulate in the body in 2 forms:  Excretion of retention of H+ or HCO3
o Volatile H of carbonic acid Regulation…slow
 Excreted by lungs – 13,000-30,000 mEq/day as  Hours to 2-3 days to change pH
CO2  deep breathing  Ca maintain balance indefinitely in chronic imbalances
o Non-volatile form of H and organic acids ALTERATIONS IN ACID-BASE BALANCE
 Excreted by the kidneys 50 mEq/day
 Imbalances occur when compensatory mechanisms fail
ACIDS
 Classification of imbalances
 End products of metabolism
o Respiratory: affect carbonic acid concentration
 Contain H ions o Metabolic: affect bicarbonate
 H ion donors
 Strength determined by the amount of H ions present
 Determines pH of body fluids by its content
MEDICAL SURGICAL NURSING 15
BLOOD GAS VALUES  Positioning/turning every 2 hrs.
 Arterial blood gas (ABG) values provide information about  Pulmonary hygiene (postural drainage, chest
o Acid-base status clapping)
o Underlying cause of imbalance RESPIRATORY ALKALOSIS
o Body’s ability to regulate pH  Carbonic acid deficit
o Overall oxygen status  Increased exhaling of CO2
 pH 7.35 (7.4) to 7.45  pH rises above 7.45
 PaCO2 35 (40) to 45 mmHg  Cause: hyperventilation
 HCO3 22(24) to 26 mEq/L (assumed average values for o Hysteria
ABG interpretation) o Over ventilation by mech. vent
 PaO2 80-100 mmHg o Fever
 Oxygen concentration >94% o Pain
 Base excess/deficit ±2 mEq/L  Compensation:
o Hypoventilation
ACID-BASE IMBALANCES o Problem: increased in breathing = loss of CO2 in
Primary cause of origin: blood
 Metabolic o Response: kidney secrete HCO3
o Changes brought about by systemic alterations  Most common A-B disturbance in critical patients
(cellular level)  Causes:
 Respiratory o Hyperventiltion
o Lungs o Anxiety, fever
 Signs and symptoms (CNS irritability)
Compensation o Deep rapid breathing
 Corrective response of kidneys and/or lungs o Light-headedness or dizziness due to dec.
 Compensated cerebral blood flow
o Restoration of pH and 20:1 ratio o Agitation, hyperactive reflexes
 Uncompensated o Circumoral and peripheral paresthesias
o Inability to adjust pH or 20:1 ratio o Carpopedal spasms
o Decreased serum K, Ca
RESPIRATORY ACIDOSIS  Nursing management
 Carbonic Acid Excess o Teach how to relieve/prevent anxiety
 Exhaling of CO2 inhibited o Assist with breathing techniques and breathing
 Increased H2CO3  retained carbonic acid acids as Rx
 pH falls below 7.35 o Positioning for comfort
 Cause: hypoventilation o Assist with relaxation techniques
o Decreased airway o Protection fro injury
o Decreased compliance o Meds as Rx
o Recoil o Ca gluconate for tetany
Signs and symptoms (CNS depression) o Monitor K and Ca levels
 Restless, confusion, apprehension, somnolence Respiratory acidosis Respiratory alkalosis
 Asterixis Increased PCO2 Decreased PCO2
Increased carbonic acid Decreased carbonic acid
 Coma
Increased H+ - low pH (<7.35) Decreased H+ - low pH (>7.35)
 H/A, papilledema, decreased reflexes
Compensation: increased Compensation: decreased
 Dyspnea and tachypnea
bicarbonate bicarbonate
 CV: tachycardia, HTN, atrial and vent. METABOLIC ACIDOSIS
Dysrhythmias
 Base-bicarbonate deficit
 Increased serum K, Ca
 Low pH (<7.35)
Compensation
 Low plasma bicarbonate (base)
o Hyperventilation
o Problem – depressed breathing, build up of CO2  Cause – relative gain in H+ (lactic acidosis, ketoacidosis) or
Treatment actual loss of HCO3 (renal failure, diarrhea)
 Correct underlying cause of alveolar  Compensation:
hyponventilation o Problem: low HCO3 or high H+ ion
o Response: lungs hyperventilate  get rid of CO2
 Artificial airway
 Causes: HCO3 loss; acid retention
 Removal of foreign body of secretions
o DM/DKA
 Oxygen inhalation at low flow rate
o High-fat diet; malnutrition
o SaO2 – amount of oxygen carried by
o RF
the hemoglobin
o Severe diarrhea
 Maintain adequate hydration IV (LR)/PO
 Signs and Symptoms (CNS depression)
o LR changes into bicarbonate in liver
o Hyperventilation
 Medications: bronchodilators, NaHCO3 o Headache
 Low CHO, Hi-fat diet – reduces CO2 production o Dizziness
Nursing Management o Kussmaul resp
 Assessment of breath sounds and respiratory o Weakness
rate; monitor K and Ca levels o Twitching
 Maintain patent airway o Hyper-K and Ca
MEDICAL SURGICAL NURSING 16
 Treatment ELECTROLYTES
o Treat cause  Active chemicals that carry positive (cations) and negative
o NaHCO3 (anions)
 Nursing mgt
o Frequent assessment of vital signs esp FLUID BALANCE MECHANISMS
respiratory rate and rhythm (compensatory  Kidneys
mechanisms)  Lungs
o Reorientation  Skin
o Safety precautions for confusion
o For ketoacidosis, NaHCO3 HORMONAL CONTROL
o Education about DM  ADH
METABOLIC ALKALOSIS  Aldosterone
 Bicarbonate excess  RAAS
 High pH (>7.45) o Low BP (low BV and CO)  juxtaglomerular
 Loss of H+ ion or gain HCO3 cells  renin  Angio I – ACE – Angio II 
 Most common causes vomiting, gastric suctioning (NG tube) increase BV  VC  increase BP
– loss of acid o Angio II  Adrenal cortex  aldosterone  Na
 Others: abuse of antacids ret.  ADH  fluid retention by renal tubules
o Retention of base (decreased UO)  BV  increased BP
o K wasting diuretics  Hypokalemia  ANP (Atrial natriuretic peptide)
 Signs and symptoms (CNS irritability) o Cardiac hormone stored in atrial cells
o Hypoventilation o Released when atrial pressure increases (CHF,
o Numbness CRF, Hi-Na intake)
o Bradycardia o Counteracts effects of RAAS  decreased BP
o Confusion and decreased IV volume
o Twitching
o Tremors REGULATION OF BODY FLUID VOLUME
o Hypokalemia  Hypervolemia  inhibits  thirst, ADH release,
o Hypocalcemia aldosterone release  increased urination of dilute urine 
 Treatment normal fluid volume restored
o Treat cause  Hypovolemia  stimulates  thirst, ADH release,
o Administer Na, K, Ammonium Cl, aldosterone release  decreased urination of dilute urine
o Diamox – increase excretions of HCO3  normal fluid volume restored
 Nursing management  UO: 1ml/kg/hr.
o Monitoring LOC and confusion MECHANISMS CONTROLLING FLUID MOVEMENT
o Reorientation, protection from harm  Diffusion (solute) HL
o Monitor serum electrolytes  Osmosis (fluid) LH
Movement of fluid through capillary walls depends on:
Metabolic acidosis Metabolic alkalosis  Hydrostatic pressure – pressure exerted on the walls of
Decreased carbonic acid Increased carbonic acid blood vessels, push
Increased H+ - low pH (<7.35) Decreased H+ - low pH (>7.35)  Osmotic pressure – pressure exerted by the protein in the
Decreased bicarbonate Increased bicarbonate plasma, hold/pull (ITIV)
Compensation: hyperventilation Compensation: hypoventilation  The direction of fluid movement depends on the differences
of hydrostatic and osmotic pressure
Mixed Acid-Base Disorders OSMOLALITY
 Exists when 2 or more disorders are present at the same  Amount of chemicals (Na, CHON, glucose, Cl, HCO3)
time dissolved in the liquid part (serum) of the blood
ABG interpretation  Controlled by ADH
1. Identify the problem  Osmolality = 2 x Na + Glu/18 + BUN/2.8
a. Acidosis vs. alkalosis  N: 285-295 mOsm/kg
b. Compensated vs. uncompensated OSMOLARITY
2. Identify the source of the problem
 Drawing power of a solution
a. CO2 – 35-45
 N: 285-195 mOsm/L
b. HCO3 – 22-26
ACTIVE TRANSPORT
ALTERATIONS IN FLUID AND ELECTROLYTES  Physiologic pump that moves fluid from an are af lower
BODY FLUID DISTRIBUTION concentration to one of higher concentration
By weight  Movement against the concentration gradient
 Adult women – 50-55%  Sodium-potassium pump maintains the higher concentration
 Adult men – 66-72% of extracellular sodium and intracellular potassium
 Elderly – 47%  Requires adenosine (ATP) for energy
o From metabolism aided by oxygen
 Infants – 75-80%
Fluid Shifts
By compartment
 Plasma to ITF (edema)
 Extracellular 30%
o Due to:
 Intracellular 70%
 Increased venous HP
 Intravascular 6%  Decreased plasma OP
 Interstitial 24%  Increased IT OP
MEDICAL SURGICAL NURSING 17
 IT to plasma  Infiltration
o Due to: o DC IV; remove catheter
 Increased plasma OP o Apply cold compress within first 30 minutes,
 Increased IT HP warm moist heat
Fluid movement between ECF and ICF  Phlebitis
 Increased ECF osmolality (water deficit, Na excess)  cell o Apply warm compress
shrinks
 Decreased ECF osmolality (water excess, Na deficit)  cell CENTRAL VENOUS LINE
swells  Flushed daily with Saline or Heparin
Average daily fluid sources  Change dressing 3x/week
 1200-1500 – Ingested water  Check for infection
 700-1000 ml – Food  Discard 5-10 ml when drawing blood
 200-400 ml – Metabolic Oxidation  Use port for designating purpose
 2100-2900 – Total  Valsalva’s maneuver when removing or changing tubing

Average Daily Fluid Loses DEHYDRATION

 1200-1700 ml – Urine Causes Symptoms Care
 100-250 ml – Feces Vomiting
Thirst, dry, warm skin
 350-400 – Skin by diffusion Diarrhea Hydrate
Poor skin turgor
 100-150 – Perspiration Diuresis Daily weight
Dark, odorous urine
 350-400 – Lungs Decrease IV Skin care
Weight loss
replacement
Daily weight – most reliable indicator of fluid loss or gain in all ages INTRACELLULAR FLUID VOULME DEFICIT (ICFVD) is:
(1kg = 1000ml)  Rare in health adults
Accurate weight: same time, same scale, same amount of clothing  Often in older adults and in acute water loss
Gerontologic considerations: The desired outcome is restoration of fluid volume through
 Reduced homeostatic mechanisms: cardiac, renal, and  IV replacement
respiratory function  Correction of the underlying cause
 Decreased body fluid percentage by 6% FLUID VOLUME EXCESS: OVERHYDRATION/ FLUID OVERLOAD
 Decreased thirst sensation, fails to drink enough Types:
 Medication use  Isotonic: hypervolemia  circulatory overload & interstitial
 Presence of other concomitant conditions edema  CHF
 Hypertonic: rare  intracellular dehydration
Assessment of Fluid balance:  Hypotonic: water intoxication, intracellular expansion
 BP measurement Circulatory overload:
o Indirect Causes:
o Direct: pulmonary artery caths:  Increased IV fluids
 PAP – 15-20mmHg  Kidney failure
 PAWP – 6-12mmHg  Heart failure
o CVP – 0-7 mmHg, 5-10cmH20 Symptoms:
 PE  Tachycardia
 UO  Flushed skin
 Weight  Neck vein distention
 Hypertension
Types of Solutions:  CVP (>15 mmH20)
Hypotonic Isotonic Hypertonic  Tachypnea
Stays put Expands volume  Cough
Hydrates cells
 Dyspnea
IV dehydration IV dehydration w/ IT  Pulmonary edema
Cellular dehydration
& IC overload Management:
D5%W
Tap Water  Fluid restriction
RL D10%W
0.45% NaCl  Na restriction (if w/ hyperNa)
0.9% NaCl D5%NSS
0.33% NaCl  Diuretics
NS Albumin
 Digoxin (if cardiac related)
**D5W is metabolized rapidly, leaving free water to be absorbed. NOT
used in the head injured client  increased ICP INTRACELLULAR FLUID VOLUME EXCESS (ICFVE)
 Referred to as water intoxication or hypotonic over-hydration
IV Infusions:  Less frequent
Assess:  Results from either:
 Urine output o Water excess or
 Infusion site o Solute deficit (often sodium)
 Flow rate Manifestations:
 IV container  Headache, nausea, vomiting
 IV tubing  Behavioral changes: progressive apprehension,
disorientation, confusion, drowsiness, decreased muscle
Reactions: strength, weight gain
MEDICAL SURGICAL NURSING 18
 Vital signs: bradycardia with an increased systolic blood  NV: 3.5-5 mEq/L
pressure (widen pulse pressure), increased RR, muscle  Major source: Fruits (melon, honeydew, cantaloupe)
twitching Effect of potassium on ECG:
 Moderate hypokalemia – flat T wave
ELECTROLYTES  Severe hypokalemia – with U wave
Basic principles in treatment:  Moderate Hyperkalemia – flat T wave, prominent U wave
 Electrolyte deficits  Severe hyperkalemia – no P wave, wide QRS
o Treatment Potassium imbalances:
 Drug supplements Hypokalemia
 Food o Manifestations:
 Assess complications  Anorexia, vomiting, diarrhea, paralytic ileus, distention
 Remove cause  Muscle weakness, paralysis, leg cramps, muscle
 Electrolyte excess flabbiness
o Treatment  Fatigue, lethargy, decreased DTR
 Antagonist  Confusion, depression
 Hydration Treatment:
 Remove cause
 Administer oral or IV K as prescrived
 Assess
 Oral K can cause nausea
SODIUM
o Should be with food in the stomach
 Main extracellular fluid cation
o Oral liq prep
 Helps govern normal ECF osmolality
 IV potassium
 Helps maintain acid-base balance o NEVER GIVEN PER IV PUSH, IM, or SC
 Activates nerve & muscle cells o A dilution of no more than 1mEq/10ml
 Influences water distribution (with chloride) o When incorporated to IV sol, invert & shake IV
 Sodium in all body fluids bag to mix it
 NV: 135-145 mEq/L o Max: 5-10mEq/hr not to exceed 20mEq/hr
 Major source: Table salt o If receiving >10 mEq/hr, connect pt. to a cardiac
Sodium imbalances: monitor
 Hyponatremia - <135 o Check site for infiltration. Can cause phlebitis
o Due to: Hyperkalemia
 Absorption f large volume of isotonic, Manifestations:
Na free irrigating solution  Hypotension
 Inadequate Na intake  Weaker cardiac contraction
o Manifestations:  Explosive diarrhea, intestinal colic
 Diarrhea, hyperactive bowel sounds,  Hyperactive bowel sounds
abdominal cramps
 Elevated BP Treatment:
 Adventitious lung sounds  Discontinue all K preparations
 Lethargy, confusion  K excreting diuretic
 Weakness & tremor
 Kayexelate prep (H ion in exchange for K in the intestine);
 Dry ski, pale, dry mucous membranes
Cleansing enema first
o Treatment:
 Dialysis – severe Hyper K
 IV infusions of saline if with
hypovolemia  IV adm of D10% or 20% 100ml with 10-20 U regular insulin
 Diuretics if with hypervolemia  Use fresh blood if BT is needed by pt
 Oral sodium replacement  Avoid food high in K
 If due to SIADH, give Lithium
 Hypernatremia - >135 CALCIUM
o Sodium excess  NV: 8.5-10.5 mg/dL
o Cause: water loss or sodium gain  Extracellular: blocks Na gates in nerve and muscle
o Manifestations: cells
 Thirst  Clotting
 Restlessness  99% - bones & teeth
 Weight changes  1% - serum & soft tissue
o Treatment:  Most activity carried out by ionized Ca
 Dilute sodium  9nverse relationship with phosphate
 Promote excretion  Major source: GLV, dairy products
 D5W Hypocalcemia
 Diuretics  Manifestations:
 Assess for cerebral edema  Tetany symptoms: twitching around mouth,
tingling and numbness of fingers,
POTASSIUM carpopedal spasms, facial spasm,
 Neuromuscular activity laryngospasm, later convulsions
 Acid-base balance  Dysrhythmia, palpitation
 Helps control ICF osmolality & ICF osmotic pressure  Pathological fracture
 80% excreted renal  Prolonged bleeding time
 20% excreted GI  Trousseu & Chvostek
MEDICAL SURGICAL NURSING 19
 Management:  Chemical
 Monitor organ functions o Result from tissue injury and destruction from
 Adm oral and IV calcium as Rx acids, alkalis, and organic compounds
 If given per IV: o Alkali burns – hard to manage coz they can
o Warm injection to body temp cause protein hydrolysis & liquefaction
o Give slowly & monitor EKG  Damage continues after alkali is
 Adm meds that increase Ca absorption neutralized
o AlOH & Vit D o Results in injuries to:
 Take oral Ca 1-2 hrs pc or HS for maximal  Skin
intestinal absorption  Eyes
 Increase oral intake of Ca  Respiratory system
 10% Ca for tx of severe Ca deficit  Liver & kidney
Hypercalcemia o Flush with running water. DO NOT IMMERSE.
Manifestations: o Clothing with chemical should be removed.
o Tissue destruction may continue72hrs after injury
 Mild to moderate hypercalemic state: weakness,
 Smoke inhalation
fatigue, depression
o Result from inhalation of hot ir or noxious
 Severe: extreme lethargy, depressed sensorium,
chemicals
confusion, coma
o Cause damage to respiratory tract
 Dysrhythmia o Major predictor of mortality in burn victims
 Heart block o Treat quickly!
 Critical: cardiac arrest o Types:
 Polyuria  Carbon monoxide poisoning
 Bone pain, fracture  Produced by the
Management: incomplete combustion of
 Discontinue all Ca burning materials
 Inhaled CO displaces
MAGNESIUM oxygen
 NV: 1.6-2.6 mg/dl o Hypoxia
 Cofactor in enzymatic reactions: o Carboxy
o Involving ATP hemoglobenimia
o DNA replication o Death
o mRNS production  Treat with 100% humidified
 Binds to Ca2 receptors O2
 Can block Ca2 channels  Cherry red appearance
 Inhalation injury above glottis
Hypomagnesimia  Thermally produced
Cause S&S Treatment  Hot air, steam, smoke
Alcoholism Similar to Adm Mag sulfate IV  Mucosal burns of
Malabsoprtion hypocalcemia Encourage food high oropharynx & larynx
DKA in Mg (meat, fish,
 Mechanical obstruction can
Prolonged gastric legumes, cocoa,
occur quickly
suction nuts, whole grain
o True medical
cereal, vegies)
emergency
Meds that decreased
 Reliable clues:
Mg: diuretics,
o Presence of
gentamycin, cisplatin
facial burns
o Singed nasal
Hypermagnesimia
hair
Cause S&S Treatment
o Hoarseness,
Renal failure Flushing hypotension Stop any Mg painful
Addisons Dowsiness supplements or swallowing
Excess replacement lethargy medications with Mg o Darkened oral &
lithium Restrict food with Mg mucous
Medications with membranes
increase Mg o Carbonaceous
Mg supplements sputum
Antacids with Mg  Inhalation injury below glottis
 Related to the length of
BURNS exposure to smoke or toxic
 Occur when injuryto the tissues fumes
Types:
 Pulmonary edema = 12-
 Thermal
24hrs after the burn
o Caused by flame, flash, scalds, or contact with
 Manifests as ARDS
hot objects
o Most common type of burn
MEDICAL SURGICAL NURSING 20
 Electrical  Emergent
o Result from coagulation necrosis caused by o Period of time required 2to resolve immediate
intense heat generated from and electric current problems
o May result from direct damage to nerves & o Up to 72 hours
vessels, causing tissue anoxia & death o Hypovolemic shock and edema
o Severity depends upon: o Burn shock phase
 Amount of voltage o Begins with fluid loss and edema formation and
 Tissue resistance continues until fluid mobilization and diuresis begin
 Current pathways o Pathophysiology
 Surface area Fluid and Electrolyte shifts
 Duration of the flow  Greatest threat is hypovolemic shock,
o Iceberg effect – severity of damage is underneath caused by a massive shift of fluids out
o Patients are at risk for dysrhythmia, severe of BV as a result of increased capillary
metabolic acidosis, and myoglobinuria permeability
 Cold thermal  Colloidal osmotic pressure decreases
o Frostbite  The net result of the fluid shift is IV
Classification of burn injury volume depletion
 Depth of burn  Normal insensible loss- 30 -50 ml
o ABA advocates categorizing the burn according  Severely burned patient- 200 to 400
to depth of skin destruction ml/hr
 Partial thickness burns  RBCs are hemolyzed by a circulating
 Full thickness burns factor released at the time for the burn
o Defined by degrees – 1st, 2nd, 3rd, and 4th  Thrombosis
 Extent of burn in percent of TBSA – rule of 9s  Elevated hematocrit
o Lund- Browder  Na shift into interstitial; spaces and
o Rule of 9s remains until edema formation ceases
 Location of burn – upper is more dangerous  K shift develops because injured cells
o Face, neck, chest  respiratory obstruction and hemolyzed RBCs release
o Hands, feet, joints, eyes  self care Inflammation and healing
o Ears, nose, buttocks, perineum  infection  Neutrophils and monocytes
o Circumferential burns of the extremities can accumulate at the site of the injury
cause circulatory compromise Immunologic changes
o Patients may also develop compartment  Burn injury causes widespread
syndrome impairment of the immune system
 Patient risk factors  Skin barrier is destroyed
o Older adults heal more slowly than younger  Bone marrow is depressed
adults o Clinical manifestation
o Physical debilitation render patient less able to  Shock from pain and hypovolemia
recover  Blisters
 Alcoholism  Adynamic ileus
 Drug abuse o Complication
 Malnutrition  CV
o Concurrent fractures, head injuries  Impaired microcirculation and
PHASES OF BURN MANAGEMENT increase viscosity
 Prehospital care  Upper respiratory injury
o Remove the person from the source of the burn and  Edema formation
stop the burning process  Lower airways
o Rescuer must be protected from becoming part of the  Direct insult at the alveolar level
incident  Intersititial edema
o Electrical injuries  Urinary
 Remove patient from contact with source  Renal failure
o Chemical injuries o Management
 Brush solid particles off the skin  Airway management
 Use water lavage  Early ET intubation
o Small thermal burns  Escharotomies of the chest wall
 Cover with clean, cool tap water-dampened  Fiberoptic bronchoscopy
towel  Humidified air and 100% O2
o Large thermal burns
 Airway, breathing, and circulation  Fluid therapy
 Do not immerse in cool water or pack with  Parkland (Baxter) formula
ice  Colloidal solutions – after 48 hours
 Removed burned clothing
 Two large bore IV lines for > 15% TBSA
 Wrap in clean, dry sheet or blanket
 Type of fluid replacement based on size/depth of burn,
 Inhalation injury
age and individual considerations
 Observe for signs of respiratory
distress or compromise
 Treat quickly
 MEDICAL SURGICAL NURSING 21
 Wound care  Hypernatremia
 Should be delayed until a patent airway adequate o Successful fluid replacement
circulation, and adequate fluid replacement have been o Improper tube feedings
established  Potassium
 Cleansing  Hypokalemia
o Can be done in cart shower, shower, or bed o Complications
 Debridement  Infection
o Need to be done in the OR  May progress to transient bacteremia  sepsis
o Loose necrotic skin is removed
o Allograft or homograft  Neurologic system
 Usually from cadaver  No problem unless there is severe hypoxia
 Typically used with newer  Hallucinations
biosynthetic options  Delirium
 Other care measures  Transient state
 Facial care  Musculoskeletal
o Performed by the open method  Decrease ROM
 Eye care for corneal burns  Contractures
 Hands and arms should be extended and elevated on  GI
pillows or slings  Paralytic ileus
 Ears should be kept free of pressure  Diarrhea
o No use of pillows  Constipation
 Perineum must be kept as clean and dry as possible  Curling’s ulcer
 Early ROM exercises – while bathing  Endocrine
 Drug therapy  Increase blood glucose levels
 Analgesics and sedatives  Increased insulin production
 Tetanus immunization  Hyperglycemia
o Given routinely to all burn patients o Nursing and Collaborative Management
 Antimicrobial agents  Wound care
o Topical agents  Daily observation
 Silver sulfadiazine (Silvadene)  Enzymatic debridement
 Mafenide acetate (Sulfamylon) o Speeds up removal of dead tissue from
o Systemic agents are not usuallu used in health wound bed
controlling burn flora  Excision and grafting
 Nutritional therapy  Eschar is removed down to the SC tissue or fascia
 Fluid replacement takes priority over nutritional needs  Graft is placed on clean, viable tissue
 Early and aggressive nutritional support within hours of  Wound is covered with autograft
burn injury
 Donor skin is taken with dermatome
o Optimizes wound healing
 Cultured epithelial autographs (CEAs)
 Hypermetabolic state
o Grown from biopsies obtained from
o Resting metabolic expenditure may be
patient’s own skin
increased by 50% to 100% above normal
o Used in patients with a large body surface
o Core temperature is elevated
burn area or those with limited skin for
o Caloric needs are about 5000 kcal/day
harvesting
o Early continuous enteral feeding
 Artificial skin
 Pain management
 Acute
o Mobilization of extracellular fluid and subsequent diuresis  Patients experience two kinds of
o Concluded when the burned area is completely covered with skin pain
grafts, or when the wounds are healed o Continuous
o Pathophysiology background pain
 Diuresis from fluid mobilization occurs, and the patient is less o Treatment induced
edematous pain
 Bowel sound return  Nonpharmacologic
 Healing begins when WBCs surround the burn wound and o Relaxation
phagocytosis occurs o Visualization, guided
 Necrotic tissue begins to slough imagery
 Granulation tissue forms  Physical and Occupational therapy
 A partial thickness burn wound heals from the edges  Good time fr exercise during
 Full thickness burns must be covered by skin grafts wound cleaning
o Clinical manifestations  Nutritional therapy
 Partial thickness wounds form eschar  Psychosocial care
o Laboratory values  Rehabilitative
 Sodium  Begins when wounds are healed by primary intention or by
 Hyponatremia grafting
o Excessive GI suction  4-6 weeks – area becomes raised and hyperemic
o Diarrhea  Mature healing – 6 months to 2 years
 Water intoxication  Discoloration of scar fades with time
 Pressure can help keep scar flat
 MEDICAL SURGICAL NURSING 22
 Healed areas must be protected from direct sunlight for 1 o Early diuretic phase
year  Extends from the time daily output >400
 Newly healed areas can be hypersensitive or hyposensitive ml/day- BUN stops increasing, UO >3-5
to cold, heat, and touch L/day, hyponatremia, hypokalemia, change
 Complications in LOC; 2-3 weeks
o Contractures o Recovery phase
 Extends from 1st day BUN falls to the day it
Emotional needs of the family returns to normal; 3-12 months
o A common emotional response is regression B. CRF: Gradual progressive and irreversible loss of renal function
o Early psychiatric intervention  Causes
o Pre-renal: gout, DM, subacute bacterial
GENITOURINARY DISORDERS endocarditis
Functions of the Kidneys o Renal: SLE, CGN, polynephritis
 Urine formation o Post-renal: BPH
o Glomerular filtration  Phases
o Tubular reabsorption o Decreased renal reserve: BUN normal; polyuria;
o Tubular secretion GFR: 35-50%
 Excretion of waste products o Renal insufficiency: BUN, creatinine- slightly
o Urea (major) elevated; GFR: 20-35%
o Creatinine, phosphates o Renal failure: BUN, creatinine increased; with
o Sulfates, uric acid physical manifestations; GFR: 20-25%
 Regulation of electrolytes o ESRD: atrophy and fibrosis of renal tubules; GFR
o Sodium <20%, BUN, creatinine – high levels, oliguria
o Potassium ARF Interventions
 Regulation of acid-base balance  Dialysis
o Phosphoric, sulfuric acid  Monitor F&E, acids and bases; observe for fluid overload
o Buffers: phosphate ions, ammonia  Moderate CHON restriction, high in calories, CHO, low K
 Control of water balance  I&O, weigh daily, monitor creatinine and BUN
o ADH (vasopressin)  Fluid restriction
 Control of BP o Renal shutdown program
o RAAS  Replaces actual losses
 Regulation of RBC production  Actual urine output and insensible loss
o Erythropoietin  Diuretic therapy to treat oliguric phase
 Located at costovertebral angle  Sodium polystyrene sulfonate (Kayexalate)
Diagnostic Tests  Monitor for patient’s response to medications
 Laboratory tests  Monitor for infection and anemia
o Routine urinalysis CRF
o Creatinine clearance  Manifestations:
o Blood studies: BUN (8-25 mg/dl), serum o Azotemia, metabolic acidosis
creatinine (0.6-1.3 mg/dl), creatinine o Altered LOC due to accumulation of wastes
clearance (85-135 ml/min), serum o Irregular heart rate
electrolytes o Yellow bronze skin due to altered metabolic process
 Cystoscopy o Dry, scaly skin and severe itching due to uremic frost
 Abdominal X-ray (KUB) o Proteinuria, glycosuria (because of hyperglycemia –
o IV Pyelography delay in release of insulin in uremic patients and
Percutaneous Renal Biopsy decreased sensitivity of cells to insulin)
 Check VS; urine color; bleeding at site o Diminished erythropoietin secretion- anemia
 Bedrest after procedure o Renal phosphate excretion and vitamin D synthesis
 If there is a suspicion for a kidney mass are diminished K secretion increases
 Done in the OR o Hypocalcemia – bleeding tendencies, osteoporosis
 Interventions
A. Acute Renal Failure: sudden, potentially reversible o Dialysis, monitor I&O, F&E, manage symptoms
 Causes o Kidney transplant
o Pre-renal: r/t decreased renal perfusion (shock, trauma,  Must find donor
dehydration, CHF, cardiogenic shock)  Waiting period long
o Renal: r/t structural renal damage (acute tubular necrosis,  Good survival rate – 1 year 95-97%
BT, AGN, nephrotoxic infection)  Must take immunosuppressant for life
o Post-renal: r/t mechanical obstruction within urinary tract  Donor sources: relative/ cadaver
 3 phases o Nursing care:
o Oliguric/ anuric phase  Pre-op: Routine care; psycho-spiritual care;
 8-15 days- output <400 ml/day. Toxins discuss: verbalize expectations, dialysis,
accumulate- metabolic acidosis – Azotemia immunosuppression
(increased BUN, creatinine), hyperK  Post-op care: ICU, I/O, BP, weight changes,
 Decreased pH, bicarbonate, Na, and Ca; electrolytes, may have fluid volume deficit,
azotemia (elevated serum levels of urea, high risk for infection; Assess for acute
creatinine, and uric acid rejection (4 days-2 years) - Symptoms:
oliguria, fever, pain and tenderness over
MEDICAL SURGICAL NURSING 23
transplant site, increased WBC (unusual  Can be done at home
inflammatory reaction, symptoms of RF  Risk of peritonitis
o Low CHON diet- limit accumulation of end products of  3 phases – inflow, dwell, and
CHON metabolism outflow
o Fluid restrictions  Automated peritoneal dialysis
o Monitor for fluid overload  Done at home at night
o AntiHTN (HTN- because of fluid retention), diuretics  Maybe 6-7 times/week
o Epogen – stimulate bone marrow to produce RBCs  A small portable machine called
o Antipruritics; good skin care a cycler performs the exchanges
o Dialysis for hyperkalemia and fluid imbalances of PD solution automatically
o Assess for infection, cardiac arrhythmias  Connects to cycler at HS and
cycler performs exchanges
Types of Dialysis overnight
 Hemodialysis  CAPD
o Removes wastes and fluids rapidly than PD  Continuous ambulatory
o Removes toxic wastes and impurities peritoneal dialysis
o Blood removed from surgically created access site 
 Done as outpatient
dialyzing unit  osmosis, diffusion
 Usually 4x/day
o CRF
 Vascular access  Doctor orders number of
exchanges
 Temporary- subclavian or
o Considerations
femoral
 Warm the dialysate: 37-38 deg C (dry
 Permanent- shunt, in arm
heating: microwave or dialysate warmer
o Care post insertion
pad)
 Can be done rapidly
 Incorporate meds after warming
 Takes about 4 hours
prior to infusion
 Done 3x a week
 Measure I&O
o Access routes:
 Check outflow rate
 Subclavian cath
 Facilitate ouflow: Fowler’s, gentle bladder
 AV shunt
pressure
 AV fistula
 Maintain strict asepsis: Assess site for
 AV graft
redness, exudate, tenderness
o Nursing Responsibilities
 Monitor BUN, creatinine, VS, I&O, signs of
 Monitor venous access site for bleeding
sepsis
 Don’t use arm for BP, IVT, or venipuncture
 Avoid increase intra-abdominal pressure
 Auscultate for bruits and palpate for thrills
(coughing, Valsalva straining)  hernia
 Weight before (wet weight) and after (dry
(inguinal, incisional, umbilical), leaks and
weight) the procedure
GERD
 Monitor for shock and hypovolemia
 Measure weight: before and after draining
(because of too much pressure);
dialysate (dry weight)
disequilibrium syndrome
 Maintain adequate nutrition: adequate
 Occurs after dialysis; rapid
CHON (clean – egg white), vitamins (FA,
change in the composition of the
B6, C)
ECF during dialysis
o Complications
 Solutes removed from blood  Peritonitis
faster than from CSF and brain
 fluid pulled into the brain  Transplant Meds
cerebral edema
 Corticosteroids
 Symptoms: N/V, H/A, HPN,
 Cytotoxic- inhibit T and B lymphocytes
restlessness, agitation, seizures
 T-cell depressors
 Peritoneal
o Removes toxins from the blood - uses peritoneal
Urinary Problems
membranes as a semi-permeable dialyzing membrane
I. Urinary Infections
o Phases
 Pyelonephritis
 Infusion/inflow time (5-10 minutes)
 Dwelling phase (20-30 minutes)  Perinephric abscess/ renal carbuncle
 Drainage/ outflow phase (20-30 minutes)  TB of the kidney
 Solution is drained taking toxins  Cystitis
and wastes with it
o CRF Predisposing factors
 Peritoneal dialysis  Urinary stasis and obstruction
 Semipermeable membrane o Most common
 Catheter inserted through o Result in:
abdominal wall into peritoneal  Poor urinary drainage
cavity  Dilatation
 Stasis of urine
 Cost less
 Presence of foreign body
 Fewer restrictions
 Lowered body resistance
MEDICAL SURGICAL NURSING 24
 Neurogenic bladder dysfunctions o Surgery
 Bacteriuria: conclusive of UTI  Urolithotomy/ nephrolithotomy
o E. Coli- most common (nephrostomy tube)
o Clean catch midstream urine  ESWL – extracorporeal shockwave
o For C&S: catheterized or clean catch lithotripsy
BENIGN PROSTATIC HYPERPLASIA
Classification  Increased androgen activity
 Acute/ Chronic Manifestations
 Upper/ Lower  Urinary frequency
 Ascending/ Descending  Urinary dribbling
 Strain upon urination  hematuria
Urinary Tract Infection  Increased residual urine (N: 5-10 mL)
 Signs Interventions
o Frequency, urgency, dysuria  Administer Finastride (Proscar) – reduce size of prostate
o Hypogastric pain  Surgical removal of prostate – chronic hematuria, infection,
o Malaise hydronephrosis, hydroureter
o Fever, chills o TURP – resectoscope or laser inserted thru urethra to
o N/V remove adenoma
o Low back pain o Suprapubic – incision in abdomen and bladder
o Urinalysis findings o Retropubic – abdominal incision
 Complications o Perineal – bet scrotum & anus – highest risk for
o Stenosis impotence
o Obstruction  CBI (Continuous bladder irrigation) after surgery to promote
o Ulceration hemostasis and limit clots that block the catheter
o ALL COULD LEAD TO RENAL INSUFFICIENCY   Hyperplasia  engage in sex  release of prostatic fluid upon
RENAL FAILURE ejaculation
PROSTATE CANCER
Management  Metastasis to bony pelvis and spine
 C and S before antibiotic therapy  Biopsy
 Increase fluid intake (3 L/day)  Interventions
 If alkaline urine: acidify, acid ash diet (meat, fish, eggs, foul, o Radical prostatectomy
cheese), vitamin C, aminoglycosides (Streptomycin) BLADDER CANCER
 If acidic urine: alkalinize; alkaline ash diet (milk, vegetables,  Risk factors
fruits), NaHCO3, Methenamine, Nitrofurantoin o Male 50-70 years
 Perineal hygiene especially sexual intercourse o Smoking
 Regular bladder emptying o Exposure to aromatic amines
 Hot sitz bath o Cytoxan exposure
o Chronic bladder infection
OBSTRUCTIVE UROPATHIES  Surgical Management
UROLITHIASIS/ NEPHROLITHIASIS o Removal fo the bladder with diversions
 Formation of stones in the urinary tract secondary to precipitates o Ureterosigmoidostomy
caused by stasis, altered purine metabolism o Cutaneous Ureterostomy
 Risk factors  Ileal conduit
o Diet high in calcium and CHON o Nursing care
o Urinary stasis  Care of the stoma - assess for possible
o Dehydration – increases urine concentration obstruction
o Obstructive disorders  Prevent skin breakdown
o Metabolic disorders – uric acid accumulation  Wash skin around stoma with
o UTI  alkaline stones mild soap and water
o Prolonged immobility  Measure I&O
URINARY CALCULI (UROLITHIASIS)
 Types of stones: Staghorn (fixed) and free ACUTE BIOLOGIC CRISIS
o Ca Oxalates phosphates  Conditions that may result to patient mortality if left
o Uric acid unattended in a brief period of time
 Signs  Conditions that warrants immediate attention for
o Colicky pain: colic, severe flank pain radiating to o Reversal of disease process
vulva or testes o Prevention of further morbidity and mortality
o N/V  Cardiac failure and dysrhythmias
 Management  Respiratory failures, S. Asthmaticus and ARDS/PE
o Fluids, ambulation  Renal Failure & ESRD
o Pain control  Burns
o Alkaline stones  ascorbic acid, lithostat, acid  Hepatic Coma
ash, low Na, Ca, CHON diet, avoid oxalate-rich  Diabetic Ketoacidosis/HHNKC
o Acidic stones  alkaline ash, Na HCO3, avoid  Thyroid crisis & adrenal crisis
purine, Allopurinol, avoid cysteine-rich (lechon,  Multi-organ failure, SIRS and shock
chicken)
 Aortic aneurysms/CVA/ACS
o Low purine diet for uric acid stones
 Ebola/MERS-CoV
MEDICAL SURGICAL NURSING 25
SIRS (Systemic Inflammatory Response Syndrome)  Respiratory failure (72 hours post-insult)  Hepatic
 Severe systemic response to a condition (trauma, failure (5-7 days)  jaundice, icteric sclera  GI bleeding
infection/sepsis, burn) (10-15 days)  Renal failure (11-17 days)  Death (3
 Provokes an acute inflammatory reaction indicated by 2 or weeks)
more s/s (CRITERIA) Pathophysiology Theories
o Abnormally up or low body temp  Gut hypothesis (most popular)
 Less 36C (96.8 F) or more 38C o Splanchnic hypoperfusion  mucosal ischemia
(100.4F)  structural and cellular function changes 
o PR more than 90 bpm increased gut permeability  changed gut
o RR more than 20 bpm immune function  increased bacteria
o Low CO2 in arterial blood – less 32 mmHg (35- translocation  hepatic dysfunction  spread of
40) toxins into system  activates immune response
o WBC significant up or down – less 4K or more  tissue injury + organ dysfunction
o Immature neutrophils – >10%  Endotoxin macrophage hypothesis
Other Causes o Gram-negative infections  cytokines are
 Pancreatitis produced and released  release of endotoxins
 Hemorrhage (tumor necrosis factor-alpha, interleukin-1,
 Ischemia interleukin-6, thromboxane A2, prostacyclin,
 Complications of surgery platelet activating actor, nitric oxide)
 Adrenal insufficiency  Tissue hypoxia-microvascular hypothesis
 PE o Macro and microvascular changes insufficient
 Complicated aortic aneurysm supply of oxygen occurs
 Cardiac tamponade o Hypoxemia
 Anaphylaxis o Cell death and organ dysfunction
Diagnosis
 Drug overdose
 Sepsis-Related Organ Failure Assessment (SOFA) score
 Polypropylene Mesh Surgical Implant
1994
o Tissue implants for urogyne
o Multiple organ dysfunction score
Management
o Describe and quantitate the degree of organ
 Treat underlying cause
dysfunction in six organ system
 Antioxidants (improve s/s) o Using similar physiologic variables
o Selenium Stages
o Glutamine (Gln or Q)
 Stage 1
 Essential amino acids
o Mild respiratory alkalosis + oliguria
o Vitamin E
o Hyperglycemia
o Eicosapentaenoic acid (EPA)
o Increased insulin requirements
 EPA or icosapentaenoic acid
 Stage 2
 Omega-3 fatty acid
o Tachypneic
 Fish oil, human breast milk, cod liver
o Hypocapneic + hypoxemic
oil
o Moderate liver dysfunction
 Salmon, sardines, seaweeds
o Possible hematologic abnormalities
Complications
 Stage 3
 Acute lung injury  ARDS  prone (decrease
o Develops shock + azotemia
compression, expand alveoli)
o Acid-base disturbances
 Acute kidney injury
o Significant coagulation abnormalities
 Shock
 Stage 4
 Multiple organ dysfunction syndrome (MODS) o Vasopressor dependent
o Oliguric or anuric
MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS) o Ischemic colitis
 “MOF” Multi-organ failure o Lactic acidosis follows
 “MSOF” Multi-system Organ Failure Management
 Altered organ function in an acutely ill patient requiring  No agent that can reverse established organ failure
medical intervention to achieve homeostasis  Supportive care
 Homeostasis cannot be maintained without intervention o Safeguarding hemodynamics, respiration
 Involves 2 or more organ systems  Adequate tissue oxygenation (primary target)
Causes  Enteral nutrition
 Infection o Within 36 hrs. of admission to ICU
 Injury (accident, surgery)  Human recombinant activated protein C (activated
 Hypoperfusion drotrecogin alfa) “Xigris”
 Hypermetabolism o Reduce 28-day mortality
 Sepsis (most common)  septic shock o Anti-thrombotic
 SIRS o Anti-inflammatory
Pathophysiology o Profibrinolytic properties
 Causes  uncontrolled inflammatory response  final o Improve outcomes in people with severe sepsis
stage of a continuum SIRS (systemic inflammatory response
syndrome) + infection  sepsis  severe sepsis  MODS
 death
MEDICAL SURGICAL NURSING 26
EMERGENCY AND DISASTER NURSING  Chemical restraints PRN
 Concept of emergency is whatever the patient or family  Gunfire
considers it to be o Measures: in the following order
Emergency Nursing  Self-protection (priority)
 Specialized education, training and expertise in assessing  Control by security and police officers
and identifying patient’s health care problems in crisis  Care provided to injured
situation Helping Family Cope with Sudden Death
 Within a time-limited, high-pressured care environment  Private place
 Talk with family together
Issues in “E” Nursing Care  Reassure everything possible was done
 Diversity of conditions and situations  Encourage group support
 Legal issues  Avoid giving sedation to family
 Occupational health and safety risks  Encourage viewing of body
 Providing holistic care in a fast-paced technology-driven  Spend time with family
environment  Encourage verbalizations
 Disaster nursing  No volunteering unnecessary information
o Weapons of terror and mass destruction Principle of emergency care
o Exposed to biologic and other weapons  Triage (French “trier”)
o Mass casualty incident  (To sort, to choose)
o Sort patient into groups based on severity of
Consent and Privacy: Documentation health problems and immediately of treatment
 Consent to examine and to treat o Management of priorities
Exemptions: all 3 must be present o Levels of acuity
o Unconscious/in critical conditions o Highest acuity
o Unable to make decisions  Receive quickest evaluation,
o Without family and friends treatment
 Statement of privacy policy of the institution  Prioritized resource utilization (x-rays,
o HIPAA (Health Insurance Portability AND labs, CT scan)
Accountability Act) HOSPITAL TRIAGE
o Patients with violent events/high profile cases Levels
 Alias  Resuscitation
 Limited access to patient’s profile o Prevent death
 “Extra privacy” o Shock, anaphylaxis, severe hypoglycemia
 Emergent
Limiting Health Risk Exposures o Prevent major life threatening situation
 Strict universal precaution o Profuse bleeding, status epilepticus with no RF,
o Blood borne diseases PE with no RF
 Personal High-Efficiency Particulate Air (HEPA) filter masks  Urgent
(N95) o Non-life threatening
o MDR TB o Requires 1 or 2 resources
o SARS  Med by IV or IM, invasive procedures,
o Ebola/MersCoV imaging studies, frequent monitoring
 Decontamination Procedures o Pneumonia, abdominal pain, complex lacerations
o Highly contagious organism  Non-urgent
o Hazardous chemicals/gases o Need only 1 resource
o Radiation o Simple fracture, viral symptoms
o Acts of terrorism  Minor
o Natural/man-made disasters o No resources needed
o Simple rashes
Violence in “E” Department Legal & Ethical Issues in ER
 Effects of substance abuse, injury/other “E”  Negligence – doing your work improperly
 Emotionally labile  Malpractice – going beyond your scope
 Feuding gangs/families  “Good Samaritan Laws”
o Separate rooms o May protect private citizens
 Measures o But usually do not apply to emergency personnel
o Security officers on duty
o Silent alarm systems o “Abandoned or isolated place” (Phils.)
o Metal detectors  Informed/implied consent
 Prisoners/underguard  Duty to report suspected crimes to the police
o Handcuffed to bed  Duty to gather evidence in criminal investigations
o Ensure safety to staff and other patients o Be aware of hospital policy and state laws for
o Hand/ankle restraint never released evidence collection
o Guard always present  Advanced directives
o Patient face down o Durable power of attorney
 To avoid head-butting, biting, spitting o If DNR, but a near kin is saying to save the
 Restraints used on violent patients patient, do code
PRN
MEDICAL SURGICAL NURSING 27
Certifications for Emergency Nursing  Preparedness
 BCLS/BLS (Basic Cardiac Life Support) o Enhance ability to respond to disaster
o Noninvasive assessment and management skills o Develop plans of action in response to disasters
for airway maintenance and CPR o Practice drills and exercises for “E” personnel
 ACLS (Advanced Cardiac Life Support) o Putting warning systems in place
o Invasive airway management skills, o Developing evacuation plans
pharmacology and electrical treatment, special  Response
resuscitation (AED) Automatic External o Responding safely to an emergency
Defibrillator o Includes actions taken to save lives and prevent
 PALS (Pediatric Advanced Life Support) further property damage in an emergency
situation
Principles of Emergency Nursing o Response is putting your preparedness in action
 Triage  Rehabilitation/recovery
 Primary Survey and resuscitation interventions o Both short-term and long-term
o Quick assessment o Begins after disaster
 Secondary survey and resuscitation interventions o Purpose:
o Detailed head to toe assessment  Restore community to a normal state
 Care of the ER patient
 Disposition  morgue Mass evacuation (hospital)
 Case management  Ambulatory 1st
o Allocate the resources  Wheelchair next
 Patient/family health teaching  Bed bound last
 Unit manager can authorize patient evacuation
Triage under Mass casualty conditions (Disaster Triage)  Evacuation plan
 Disaster situation Common reasons for going to ER
o Number of casualties exceed resource  Chest pain
capabilities  Abdominal pain
 Emergent (class I/red tag)  Headache
o Airway compromise, hemorrhagic shock  Fever
 Urgent (class II/yellow tag) Common “codes” used in the hospital setting
o Needs treatment within 30 min.-2 hrs.  Code blue
o Open fractures, large wounds o Members (MD, floor/unit RN, respiratory
 Non urgent (class III/green tag) therapist, pharmacist, ICU RN)
o Treatment delayed >2 hrs. o Dead patient
o Closed fractures, sprains/strains, contusions,  Rapid Response Team
abrasions o Response team in a nearly dying patient
o “Walking wounded” o Same members as in code blue team
 Expectant (class IV/black tag) o Prevent “code blue/death”
o Expected and allowed to die; dead  Code gray – violence
o Massive head trauma, high cervical SCI,  Code red
extensive burns o Fire
Psychological Reactions secondary to disaster o Deactivated ONLY by head of security
 Panic  Code black – bioterrorism, bombing
 Hysteria  Code pink
 Despair o Baby is being stolen
 Depression o Deactivated ONLY by head of security
Principles of Mass casualty principles  Crash Cart
 Triage FIRE EXTINGUISHER
 System of notification/activation of “E” preparedness  PASS method
o Group paging systems, instant electronic based o P pull the pin
alert messages, TV flash alerts o A aim the spout
 Hospital “E” prepared ness: Personnel roles and o S squeeze the handle
responsibilities o S sweep the fire
o Hospital incident commander, medical command  Do not use to extinguish BIG fire
physician, triage officer, public info officer  Monthly inspection by the fire/security department
 Event resolution  Check expiration date
o Deactivating “E” response plan FIRE DRILL
o Resume normal operations o Every 6-12 months
 Debriefing o Search for fire
o Promote effective coping strategies o Wet linens, towels
o Door, windows
Phases of Mass Casualty Disaster of “E” Management o Appliances, plugs, outlets
 Mitigation o All things on 1 side (hallway)
o Reduce damages before disaster o Fire wall door
o Public Education o Fire hazards
o Coning, land use management
MEDICAL SURGICAL NURSING 28
HEAT-RELATED ILLNESSES  IVF NSS
o Heat exhaustion  Cooling blankets
o Heat stroke  No ASA/antipyretics
o Risks  Aggravate coagulopathy
o Meds (anticholinergics, diuretics, phenothiazines FROSTBITE
(thorazine), anti H2, antidepressants o Cold-related injury that may or may not be associated with
 Sweat production hypothermia
o Betablockers, ACE inhibitors o Cause
 Restrict blood flow to skin  impair o Inadequate insulation against cold
release heat o Skin exposed to cold
o Amphetamines, cocaine o Insufficient clothing
 Increased muscle activity, body heart o Risk
o ETOH o Smokers, ETOH, PVD
 Excrete more body H2O o Early s/s
o Risks o White waxy areas on nose, cheeks, ears
o Dehydration o Treatment
o Lack of sleep o First aid
o Fatigue  Body heat (superficial type)
o Obesity o Hospital
o Strenuous activities  Rapid rewarming in H2O bath
HEAT EXHAUSTION
o Syndrome caused by dehydration during heat exposure over HIGH ALTITUDE ILLNESSES
hrs-days o Elevations > 5K ft.
o Precursor to heat stroke o O2 decreased  hypoxia
o Not true medical “E” o Acclimatization
o S/S o Compensation to high altitude
o Flu like s/s + diaphoresis + GI s/s o 3 conditions resulting from high altitude
o Temp not significantly increased (normal or o Acute mountain sickness
subnormal) o High altitude cerebral edema
o Moist clammy skin o High altitude pulmonary edema
o Management o Risk
o Bed rest in cool place; legs and feet up 12-18 o Rapid ascending (most common)
inches o Sleeping at 8k elevations
o Constrictive clothing removed o Treatment
o ORS/sports drink (Gatorade) if alert o First aid
o Cold packs (neck, arm pits, chest, abd, groin)  Descent to lower altitude areas
 Abundant blood supply  1600-3300 ft.
o Soak person in cool water o Rest
o Fan while spraying person’s skin o O2
o Crushed Na tabs dissolved in adequate H2O
 Prevent GI s/s DECOMPRESSION SICKNESS (DCS)
o Prevent sun exposure (10a-4p); use sunscreen  “the bends”, caisson disease
SPF >15  “chokes”, “staggers”
o If no improvement in 30 min. – seek medical  Incidence
attention o Diving
HEAT STROKE o Rapid ascent
o Failure of heat regulatory mechanism o Loss of air in tank
o Body temp exceeds 40.5 C (105 F) o High latitude flying
o Organ dysfunction  death o Flying in commercial aircraft within 24 hrs. post-
o Risk factors diving
o Strenuous physical activity/wearing thick clothing  Nitrogen bubbles formation due to rapid changes in
in hot humid conditions atmospheric pressure
o Chronic exposure to hot humid weather  In joints (shoulder)/muscle spaces
o s/s  Air embolism  stroke paralysis, death
o Dry, hot skin, neuro changes  Management
o Presence of sweat does not rule out presence of o Obtain detailed history
heat stroke o ABC – 100% O2
o Treatment o CXR/VQ scan – Pulmonary embolism
o Patent airway o IV Plain NSS/LRS
o Rapid cooling measures o Lower HOB/Left lateral
 Ice packs (necks, groins, arm pits)  If suspect air embolism
 Cold water immersion  Trap air in apex ventricle  prevent
 Wet body with tepid H2O + rapid going to lung circulation
fanning o HBO/Recompression chamber
 stop cooling till temp drops to 102 f  Hyperbaric O2
o At the hospital
 O2 via NC or mask
 Large bore IV cannula/needle
MEDICAL SURGICAL NURSING 29
NEAR DROWNING OVERDOSE
 Recovery post submersion  Ipecac (Ipecacuanha plant)
 Leads to death by suffocation from submersion in the liquid  Treatment
medium (water) o Ipecac to induce vomiting EXCEPT in corrosive
 Prevention substances
o No swimming alone o Gastric lavage
o Test H2O depth before diving head 1st; never  Send contents to lab for toxicology
dive in shallow water test
o No ETOH o Activated charcoal administration
o Enough H2O rescue equipment readily available  Constipation
 First aid
o Patent airway; spine stabilization CARBON MONOXIDE POISONING
o Ventilator support (CPR)  Bind to Hgb
 Hospital care o Low O2 in blood
o O2 treatment o Carboxyhemoglobin
o ET PRN  Easily absorbs by Hgb (200x) than O2
o GI decompression PRN  S/s
 Fresh water drowning o Cerebral hypoxia
o Water fills lungs + bloodstream o Coma
o Blood cells swell, burst  Pulse oxymeter NOT valid indicator
o Fluid in lungs prevent air going in lung  cardiac o Hgb saturation NOT O2 sat.
arrest  Prevention
o Hypotonic aspiration o First alert
 Salt water drowning  Management
o Salt water fills lungs o Serum ABG
o Salt H2O draw blood from bloodstream into lungs o Reverse cerebral and myocardial hypoxia
 liquid build up in alveoli  O2 not reach o Eliminate carbon monoxide
blood  cardiac arrest  drowning in your own  If inhaled
fluids o Expose to fresh air (open windows, doors)
o Hypertonic  hemoconcentration o Loosen tight clothing
 Management o CPR PRN; 100% O2
o ABC o Prevent chill; apply blankets
o ET with PEEP ( Positive and Expiratory FOOD POISONING
Pressure)  S/s
o O2 o Diarrhea – absent (botulism, shellfish, fish
 CPR  CAB (min. of 100 bpm) poisoning)
 ABG o Fever (salmonella, fish poisoning, fava
 Rewarming beans/field beans/bell beans)
 ECG o Respiratory paralysis (botulism, chemical, plant,
 Foley catheter animal poisoning)
ANAPHYLACTIC REACTION o Severe vomiting  alkalosis
 Acute systemic hypersensitivity reaction within few o Severe diarrhea  acidosis
seconds/minutes o Hypovolemic shock
 Ex: meds, other agents (insect sting, bees), food  Management
 S/s o ABC
o Respiratory symptoms o Weight, serum lytes
o Drop BP (massive vasodilation) o Hydration (IVF) 1L/kg
 Treatment o Food, gastric content, serum, feces analysis
o Patent airway o Antiemetics
o Epinephrine SQ/IM injection followed by AntiH2 o Lactus bacillus
drug  Acidophilus (Lactinex, Erceflora
 Yogurt, Yakult
POISONING SNAKE BITES
 Swallowed poisons (corrosive)  Pit vipers (Crotalidae)
o Alkaline (detergent, bleach, button batteries, o Most frequent poisonous snake bites (triangular
oven cleaners) head)
o Acid (bowel cleaners, rust removers, metal  Can cause multiple organ failure esp. neuro
cleaners, pool cleaners)  Treatment
o Immobilize injured part below the heart
 Treatment o Cleanse cover wound
o Offer 3 glasses of milk/water via NGT to dilute o Do not use ice/tourniquet, heparin,
poison corticosteroids during acute stage (6-8 hrs.)
o Bring unused poison to hospital for identification  Ice/tourniquet  decreased
o Do not induce vomiting just keep on NPO circulation  necrosis
o If not sure of cause of poisoning – CALL Poison  Corticosteroid  depress Ig
Call Center production  hinder antivenin action
o (02) 524 1078 (Philippines)
MEDICAL SURGICAL NURSING 30
o No ETOH, caffeine Cat bites
 Up venom absorption  High risk for infection (Pasteurella in salvia)
o Never leave patient; bring snake to hospital Management
 Hospital  Report to public health authorities
o Antivenom/antivenin/antitoxin PRN o Animal bite center
 Effective within 4 hrs. of bite  Follow up screening of offending animal for rabies
 Less effective within 12 hrs of bite  Rabies prophylaxis
o Tetanus prophylaxis  Anti-tetanus toxin
o O2 HUMAN BITE
o IVF NSS or LRS with large bore needle  Associated with rapes, sexual assaults/forms of battery
o Analgesics  Hand/UE
o Antibiotics o Most common site
o Anaphylaxis treatments  Contains more bacteria
o Safety in snake transport  stunned snake, not
 Management
dead
o Note for pus, erythema, necrosis
o Bite time: daytime & early evening
o Photographs
o May apply bandage
o Soap & H2O
o 1-9 y/o
o Antibiotic
 Cardinal s/s o Tetanus toxoid
o Edema o Social worker consult
o Ecchymosis o Police report
o Hemorrhagic bullae o Documentation
INSECT STINGS
SPIDER BITES
 IgE-mediated  anaphylaxis
 Venomous spiders
 Management
o Brown recluse
o Removal of stinger (tweezer)
o Black widow
o Soap and water
 Dark places o Avoid scratching
o Closets, shoes, attics  H2 response
Brown Recluse o Ice application
 S/s  Decrease swelling and venom
o Painless absorption
o Site: red-purple (2-8 hrs) o AntiH2, analgesic PO
 Necrosis (2-4 days) o W/o for systems of anaphylaxis
 Wound healing: 2-3 mos. WOUNDS
o 24-72 hrs.  Management
 Fever, chills o Wound cleansing
 N/V, malaise o Primary closure
 Joint pain  Sutures, staples
 Treatment  Dermabond, steri-strips
o Wound cleaning: soap, H2O o Delayed primary closure
o HBO treatment  Antibiotics
o Surgery debridement  Tetanus shot/booster
o Antibiotics  Photos (Polaroid camera)
Black Widow
 Bite: pinprick sensation INTRA-ABDOMINAL INJURIES
 Systemic affect  Penetrating trauma (Serious  sx)
o Rapid: 30 mins. o Liver (most frequently injured solid organ)
 S/s  Causes
o Abdominal rigidity o Gunshot (MGW)
o N/V  Velocity of entry (most important
o HTN prognostic factor)
o Up PR  Hi-velocity  extensive
o Paresthesia tissue damage
 Pain severe
 Symptoms
 Pain 1-2 days
 Stab wounds (MSW)
 Management
 Low velocity  less
o Ice over site
penetration
 Decrease systemic toxin delivery
o Blunt trauma
o Cardiopulmo check
 Causes: MVA, falls, blows, explosions
o Antivenin (horse-based) effective
 Associated with extra-ABD injuries
(chest, head, UE, LE)
ANIMAL BITE
 Difficult to detect
Dog bites
 Abdominal assessment
 Responsible for majority of deaths from animal bites
 Rabies virus in saliva and nerves of rabid animal
MEDICAL SURGICAL NURSING 31
o Absent BS  Follow up care
 Early sign of intraperitoneal injury o Counseling
 Abd distention, pain, rigid, rebound
tenderness AIRWAY OBSTRUCTION
o S/s of shock Partial
o Internal bleeding o Hypoxia, hypercabnia, respiratory and arrest
 Ultrasound, CT o Breath and cough spontaneously
o Left shoulder pain  ruptured spleen Complete
o Right shoulder pain  liver laceration o Hypoxia  permanent brain injury/death within 3-5 mins.
 Management o Weak ineffective cough
o ABC +DE Causes
CRUSH INJURIES o Aspiration of foreign bodies
 Caught between 2 opposing forces o Bolus of meat (adult): most common
o MVA, collapsed building o Anaphylaxis
 Monitor for o Viral/bacterial infection
o Hypovolemic shock o Trauma
 Extravasation of blood and plasma o Inhalation/chemical burns
into injured area post release of Management
compression o Abdominal thrust
o Paralysis
o Skin erythema and blistering HEMORRHAGE
o Damaged body part Management
 Swollen, tense, hard o Control external hemorrhage
o Renal dysfunction o Direct pressure; CBR
 Muscle damage  rhabdomyolysis o Tourniquet (last resort)
 Myoglobinuria o Control of internal bleeding
 Tubular necrosis o Hemostan (Tranexamic acid)
 Management SHOCK
o ABC o S/s: cool moist skin, falling BP
o Note for acute renal insufficiency (ARI) Treatment
o Splinting o ABC + DE
 Major sof tissue injuries o Patent airway and maintain breathing
 Control bleeding and pain o Determine cause
o Extremity injury o IVF and blood transfusion using large bore cath
FRACTURES o Monitoring
 Kinds: Open, Comminuted, Simple o Pressure points for control of bleeding
 Management CPR Guidelines (AHA 2010)
o ABC o CAB
o Neurovascular checking o Compression!!!
 Pain, pressure complaints
o Aplly splint BLOOD SPILL/BODY FLUID SPILL
 1 hand placed distal to fx o Bleach (sodium hypochlorite) for 10 mins.
 Other hand placed under fx o Hospital disinfectant
 Splint applied beyond joint near fx o Hospital policy/control
o If open fx  apply dressing (moist, sterile)
o Hospital  x-ray  splint SUPERBUGS
MULTIPLE TRAUMAS Contact
 Single catastrophic event o VRE (Vancomycin Resistant Enterococcus)
 Life threatening injuries to at least 2 distinct organs or o MRSA (Methicillin Staphylococcus Aureus)
systems o ESBL (Extended Spectrum Betalactamases)
o MDRO (Multiple Drug Resistant Organism)
 Management
o Clostridium Difficile
o ABC + DE
Droplet
o Airway (primary survey)
o Buckholderia Cepacia
SEXUAL ASSAULT
o Treatment
 Rape trauma syndrome
 Ceftazidime
 Sexual assault nurse examiner (SANE)  Doxycycline, Piperacillin, Meropenem
Management o New Delhi Metallo Betalactamase Resistant Organism
 PE (NDM-1)
 Specimen collection Precaution:
 Potential complications o Contact isolation
o STDs/STIs o Droplet precaution
 Ceftriaxone (Rocephin) IM - Treatment
Gonorrhea o Zyvox (linezolid)
 Metronidazole (Flagyl) PO x1
 Azithromycin (Zythromax) PO x1
o Pregnancy
o HIV/Hepa B
MEDICAL SURGICAL NURSING 32
MERSCoV (Sept. 2012) HURRICANE
o Dr. Ali Mohamed Zaki in Jeddah, Saudi Arabia o Most frequently injured in traumatic injuries
o S/s o Liver – right quadrant pain
o 7-day history of fever, cough, expectoration, WILD FIRES
shortness of breath o Contain fire
o 14 days incubation o Extinguish fire
o NO CURE o Evacuation route
o 2 investigational vaccines as of June 2015 o 4 triangles (Fire tetrahedron)
MERS o O2
o Fever, cough, shortness of breath, myalgia o Fuel
o “Pneumonia” o Heat
o GI s/s  diarrhea o Chain reaction
o SIRS  respiratory failure  MODS  death o Primary treatment for burns
o Occurrence o ABC
o Immunocompromised o Cover wounds with sterile dressings
o Diagnosis o Parkland Fluid Resuscitation
o Travel History o Do not go inside burning building or area of fire unless
o S/s cleared
o CXR  both patchy infiltrates consistent with
viral pneumonitis lower based EARTHQUAKES
o Chest CT  interstitial infiltrates o Drop-duck-cover head
o CBC  low WBC and lymphocytes o Go to top of building
o Nearest exit
*MERSCoV and EBOLA notes from Ma’am Pe Benito o Avoid windows/glass
o No elevator
NATURAL CALAMITIES o Richter scale
o Go Bag o Compare earthquakes – measured in at least 3
o Non-perishable foods areas
 Canned foods, biscuits, snacks,  Epicenter
chocolates  Magnitude
o Battery-operated/rewinding-operated gadgets o Seismograph
 Phone, light, radio  Measures earthquake
o First aid kits/meds TSUNAMIS
o Info kit (contacts) o Usually follows after a big earthquake
o Water o Tsunami warning
o Life vest
LIGHT INJURIES VOLCANIC ERRUPTIONS
o Single lightning stroke – >1M volts o Evacuation route
o High voltage – >1k volt
o Produce injury by IONIZING ROUTE
o Direct striking o Geiger scale
o Splashing nearby strike area o Detects ionizing radiation
o Travel via ground (step voltage) o Duration of exposure
o Prevention o Distance
o Seek shelter o Radiation level
o No use phone
o Stay away from windows DECONTAMINATION
o First aid o Remove everything
 ABC o Rinse with H2O
 CPR PRN o Soap then rinse
 Sterile dressings to wound sites
o Hospital care SETTINGS FOR END-OF-LIFE CARE
 Check Serum Crea o Palliative care
TORNADOES o Comprehensive care to patients (+ families)
o Twister whose disease is not responsive to cure
o Funnel clouds o Focus: comfort
o Within few minutes o Hospice care
o Take-cover o Interdisciplinary care and services provided
o Basement primarily in the home to terminally ill patients +
families
FLOODS/TYPHOONS o Focus: quality of life
o Within few hours-days o Home, nursing home, assisted living, hospital
o First aid it
o Food/drink
o Battery opens
o Emergency numbers
o Evacuation centers
MEDICAL SURGICAL NURSING 33
ONCOLOGY NURSING o Obesity
o Carcinogenesis o Endometrial CA
o Etiology (multi-causal) o Occupation/ Environmental/ Physical agents
 Genetics o Genetics
 Lifestyle o Hormones
 Weak immune system o Estrogen  breast CA
 Physical o Other forms of risk factors
 Chemical o Geographic location (SBMA, city)
o Process o Sexual practices
 Initiation – exposure o Chemical agents
 Promotion – repeated exposure  Nitrates
 Progression – increase in size  Nicotine (smoking)
 Proliferation – spread  Pesticides
 Hematogenous  Polyvinyl
 Lymphatics**  Hair dyes
o Cancer Prevention  CFC
o Primary – risk reduction  Aromatic amines
 Smoking cessation  Alcohol
 Weight reduction  Asbestos
 Vaccination  Benzene and lead
o Secondary – early detection o Immunocompromised states
o Tertiary – palliative care
o Cancer Diagnosis Tumor staging system (TNM)
o Symptomatology – CAUTION US o Tumor
o Diagnostics o Tx – cannot be assessed
 Imaging o T0 – no tumor
 Biopsy o Tis – carcinoma in situ (Latin: “in its place”
 Incisional o T1, T2, T3, T4 – increase in tumor size and
 Excisional involvement
 Needle aspiration o Nodes
 Staging – clinical, treatment o Nx – cannot be assessed
 Grading – cellular
o Modes of Analysis Staging
 Paraffin method – 24 hrs., Phil – 1 wk. o 0 – cancer in situ
 RFS – 15-30 mins., not soaked in formalin o 1 – tumor limited to disease of origin
o The cell cycle o 2 – lymphatic involvement limited spread
o G0 (resting cells capable of re-entering growth cycle) o 3 – extensive local and regional spread
 G1 (RNA synthesis)  S (DNA synthesis)  G2 o 4 – wide spread metastasis
(RNA CHON synthesis)  M (cell division/ mitosis)
o Rapid: GI, skin, bone marrow Diagnostic tests
o Slow: reproductive, pancreas o Papanicolau (PAP) smear
o 5 years CA free – negative – CA survivor o Self breast exam (SBE)
o Categories of neoplasms o Done 1 week post menstruation
o Carcinoma o Clinical breast exam (CBE)
 Malignant cells from epithelial cells (lines o Mammography
cavities, structures on top of connective o Digital rectal exam
tissues) o Testicular self exam
o Sarcoma o Fecal occult blood test/ Guaiac Test
 Cancer of connective tissues (bones, o No red meat, no dark colored foods
cartilage, fat) o Prostate exam (Digital rectal exam + PSA)
o Lymphoma o Sigmoidoscopy/ colonoscopy
 Cancer of lymphocytes (Hodgkin’s) o Biopsy
o Leukemia/ Myeloma o Rapid frozen section (RFS)
 Ca of blood forming cells of bone marrow o Other dx test
o Pathogenesis: Theories of CA causation o MRI
o Cellular transformation and derangement o CT scan
(arrangement) theory o Ultrasound
 Carcinogenesis C- change in bladder or bowel habit
o Failure of immune response theory A- a sore that does not heal
o Predisposing factors U- unusual bleeding or discharge
o Age T- thickening or lump
o Gender: males: prostate; female: breast I- indigestion or dysphagia
o Viruses and bacterias O- obvious
o HPV (human papilloma virus)  cervix CA N- nagging cough or hoarseness of voice
o Hepa B, C virus  Liver CA A- anorexia
o Helicobacter pylori  Gastric CA L- loss of weight
o Precancerous lesions
o Diet: high fat, low fiber
MEDICAL SURGICAL NURSING 34
Most common sites of reported deaths (2010) o Late menopause (55 years old)
o Trachea, bronchus, lungs o Nulliparity
o Breast o Obesity
o Leukemia o Assessment
Management of CA o Asymptomatic
Modes  Lump on upper outer quadrant
o Primary tx – treatment of choice o Late signs (Malignant)
o Adjunct  Irregular shaped mass
o Used together with primary tx  Fixed nodules, adheres to chest wall
o Assist primary tx o Diagnostic exam
o Adjuvant o Biopsy
o Tx given post primary tx to increase cure o Breast self examination (SBE/CBE)
o Neo-adjuvant  1 wk post start of menstruation
o Tx give prior to surgery o Medical management
Radiation o Administer: anti-estrogen receptor: Tamoxifen
o Beams of high-energy waves or streams of particles citrate (Nolvadex), Taxol (paclitaxel)
o Localized treatment o Chemotherapeutic agent:
o Destroys rapidly dividing cells  Cyclophosphamide
o Small tumors respond best o Simple (Total) Mastectomy
o Types o MRM – pectoralis minor
o Internal radiation – brachytherapy/particulate o Nursing mgt: s/p breast
 Radioactive o Fowlers
o External radiation- teletherapy/ionizing o Promote mobility
 Non radioactive; not threat to others Hodgkin’s lymphoma
o 6 feet away; 30 minutes per shift; lead container Risk factors:
Nursing Considerations: Chemo Precautions o male 15-40 years old
o Wear (PPE) chemo gloves, long sleeved gowns, mask with o Immunosuppressed
shield PRN o Hx of mononucleosis or Epsteinn Barr virus
o Double flush Early manifestations
o Check for extravasation o Painless swelling of the neck
o Only in peripheral IV Late sign
o Observe chemo precautions until 72 hours post last chemo o Organomegaly
tx
o Medications Cervical CA
o Cell cycle specific – anti-metabolites o Cause: unknown
o Non-specific – alkylating agents, more dangerous o Risk factor
Complications of radiation and chemotherapy o HPV
o Nausea and vomiting o Oral contraceptive
o Constipation o Tobacco use
o Fluids and high fiber foods o Early age at first coitus
o Stool softener o Frequent douching
o Diarrhea o Diagnostic
o Offer liquids o Pap smear
o Stomatitis/ Xerostomia o Colposcopy
o Good oral hygiene o Biopsy (“punch”)
o Avoid spicy or hot foods o Surgical mgt
o Offer topical agents for pain relief as ordered o Cryosurgery
o Apply KY jelly to lips o Radiotherapy
o Offer popsicles o Hysterectomy
o Avoid alcohol, tobacco  TAH
o Alopecia  TAHBSO
o Plan for wig, scarf, turban, or hat BEFORE hair Prostate CA
loss o Causes
o Reassure patient that hair will grow back after o Hormones
therapy o STD
o Myelosuppression o Multiple sexual partner
o Thrombocytopenia (platelets) o High fat diet
o Leukopenia (WBC)/ Neutropenia (granulocytes) o Coude’ or tiemen catheter
o Anemia o Dx
o Infertility o Biopsy
o Sperm bank for male and oophorexy (ovary o PSE- prostate specific antigen
function reservation) for female o Digital exam
Breast CA o Nursing assessment
o Risk factors o Asymptomatic: early stage
o Age o Hematuria
o Sex o Dysuria
o Familial history o Enlargement of prostate
o Early menarche (before age 11) o Low back pain
MEDICAL SURGICAL NURSING 35
o Medical mgt  Apply pressure on the soft tissue of the nose
o Estrogen hormones  Ice compress (15-20 min.)
 Diethylstillbesterol  Close monitoring
 Estradiol Medical Management
 Chlorotrianisine  Nasal packing (3-5 days)
o RT  Surgery: electric cautery  watch out for DOB
o Surgical mgt RHINOSINUSITIS
 TURP Sinus – air-filled cavity, keeps skull light
 Orchiectomy Cause: infection
o Nursing mgt: s/p TURP Types: Acute or Chronic
 Increase Fluid Intake 2400- Manifestations
3000ml/day unless CI  Nasal congestion
 Monitor for bleeding  Nasal drip (coryza)
RESPIRATORY SYSTEM
 Headache
Oxygenation
 Fever
 Process of acquiring, transporting and utilizing oxygen for
 Body malaise (fever  vasodilation  blood pools in
cellular metabolism (diffusion)
muscles  sore muscles)
 Components
Complications
o Respiration
 Osteomyelitis
o Circulation
Common problems  Meningitis
 Ineffective airway clearance  Encephalitis
Nursing care
 Impaired breathing pattern
 Positioning
 Impaired gas exchange – pulse oximeter
o Proetz vs. Parkinsons
 Altered tissue perfusion
 Bred rest
 Decreased cardiac output
 Increase OFI
 Activity intolerance
 Mist therapy
General Manifestations (increased demand, decreased supply   Close monitoring (watch out for complications)
reduce oxygen demand to complement the low supply of oxygen) Medical Management
 Dyspnea  Pharmacotherapy
o Nasal decongestants (Adrenergics/PPA)
 Chest pain
o Anti-histamines (Chlorphenamine)
 Pallor, erythema, cyanosis
o Analgesic/anti-pyretic (Paracetamol)
 Edema
 Surgery
 ALOC o FESS/Functional Endoscopic Sinus Surgery –
 Palpitations drain sinuses and build-up of pus (no incision,
 Body weakness use of scopes)
 Watch out for DOB
FUNCTIONS  Position HOB elevted
 Gas exchange o Cald wel luc procedure/Radical Antrum Operation
 Maintaining fluid status (incision under upper lip)
 Communication  Transphenoidal Hypophysectomy
 Eliminating metabolic wastes Nursing Care Post-Sinus Surgery
 Acid-base balance regulation  Positioning – HOB elevated
o Acidosis = CNS depression  Soft diet
RESPIRATORY DYSFUNCTION o No hard, rough, coarse foods
Results to the following problems o No vigorous chewing
 Impaired gas exchange  toxemia, acid base imbalance  No dentures for 10 days
(acidosis), hyperventilation (alkalosis)  Avoid brushing teeth
o Hypoxemia  Gargle with non-stinging mouthwash
o Hypercapnea  Avoid blowing nose/sneezing (2 weeks)
 Fluid imbalance
 Build-up of metabolic wastes TONSILLITIS/Pharyngitis/Adenoiditis
Cause: infection (viral or bacterial/GABHS)
RESPIRATORY DISORDERS Types: Acute/Chronic (more than 3x in a year)
EPISTAXIS Complications: RF, RHD, AGN
Cause Manifestations
 Injury  Dysphagia
 Irritation  Odynophagia
 Polyps  Sore throat
 Drug use  Cough
 Leukemia  pancytopenia  Halitosis
Complications: aspiration/obstruction  Fever
Nursing care  Body malaise
 Positioning – HOB elevated and leaning forward  Peritonsillar abscess (bacterial)
 Bred rest  Coryza (viral)
MEDICAL SURGICAL NURSING 36
Nursing Care Risk Factors
 Diet: soft and non-irritating  Carcinogens
o Avoid milk/dairy – thicken mucus secretions o Asbestos
 TGC (tamarind, ginger, calamansi) o Alcohol and tobacco
 Hydration o Paint fumes, wood dust, cement dust
 Gargle with warm saline (soothing effects)  Other factors
 Bed rest o Straining of voice
 Oral hygiene o Chronic laryngitis
Medical Management o Nutritional deficiency (riboflavin)
 Pharmacotherapy o Familial predisposition
o Oral antiseptis (mouthwash/lozenges) o Age, males
o Anti-inflammatory agents o Race
o Anti-microbials Diagnosis
o Aminopenicillins, macrolides  Bronchoscopy – monitor extent of metastasis
 Surgery Management
o Tonsillectomy  Partial laryngectomy (laryngofissurethyrotomy)
Nursing Care for Tonsillectomy o Portion of the larynx is removed along with one
 Pre-Op vocal cord and the tumor
o Check for loose tooth o All the other structures remain including the
 Post-Op airway and no difficulty in swallowing is expected
o Immediate post-op: prone head to side to drain o Used for smaller cancers of the larynx
secretions  Total laryngectomy
o Semi-fowler’s o Complete removal of the larynx can provide the
o Watch out for frequent swallowing once awake desired cure in most advanced laryngeal cancers
(8-14 days post op risk for bleeding) o Laryngeal structures are removed
o Diet: progressive Nursing Care
 1-3 days clear liquids (no milk and  HOB elevated (keep upright)
dairy)  Suction secretions PRN
 4-5 days general liquids  Tracheostomy care
 6-7 days soft diet o Every 8 hours, PRN
 8 days and beyond DAT o Safest: saline
o Hydration o Dry using sterile gauze
o No throat clearing and avoid coughing o Clean stoma using half-strength hydrogen
o Dark-colored stools are normal at first few days peroxide, dry using sterile gauze
because bleeding is normal o Cuff – not usual part of tracheostomy tube
 Secures to prevent dislodgement
LARYNGITIS  Prevents aspiration – not routinely
 Inflammation of the larynx often occurs as a result of voice deflated
abuse or exposure to dust, chemicals, smoke and other  Prevents pneumothorax
pollutants as part of URTI  15 mmHg (15-25 mmHg)
Co-morbidity: GERD  Strict aspiration precaution
Manifestations o Semi-solid
 Hoarseness or aphonia (less than 2 weeks)  Alternative means of communication
 Severe cough
Management
 Rest ACUTE LUNG INJURY
 Antibiotics as needed  Trigger inflow reaction  form inflammatory
o Aminopenicillin exudates/infiltrates  inflammatory edema  reduced lung
o Oral antiseptics compliance  hypoxemia  acute respiratory distress
 PPI – reflux laryngitis  Increased permeability of the alveolar membrane fluid shifts
 Continuous positive airway at bedtime into the alveolar and interstitial spaces  pulmonary edema
 Monitor for malignancy  crackles
 Position: High Fowler’s  Destruction to the alveolar wall  decreased surfactant 
atelectasis
LARYNGEAL CANCER
 Uncontrolled cell growth CHRONIC AIRFLOW LIMITATION/OAD
 Accounts for half of all head and neck Cancer  Refers to group of conditions marked by increased airway
resistance resulting to impaired inflow of oxygen to the lungs
 Most common among people 60-70 y/o
Risk factors: SOAP
 Male, >40 y/o
 Smoking
Manifestations
 Occupation
 Persistent hoarseness (2 weeks) associated with otalgia and
dysphagia  Allergies
 Persistent cough or pain and burning throat especially when  Pollution
consuming hot liquids or citrus juices Common Types
 Lump on the throat  COPD
 Pain in the adam’s apple that radiates to the ear  Bronchial Asthma
 Dyspnea, enlarged hot liquids or citrus juices
MEDICAL SURGICAL NURSING 37
COPD Management
 Group of disorders characterized by progressive  Oxygen support (low flow only/2-3 lpm)
deterioration (irreversible) in pulmonary functioning  Pharmacotherapy
Forms o Bronchodilators
1. Pulmonary Emphysema o Anti-cholinergics (Ipratropium)
 Air-trapping within the tracheobronchial tree) o Mucolytics
 Abnormal distention of the airspaces beyond the o Steroids
 Terminal bronchioles and destruction of the walls of the o MDIs
alveoli  Immunization
 Pink, puffer BRONCHIAL ASTHMA
 Barrel-chest deformity  Hypersensitive and hyper responsive airway
2. Chronic Bronchitis  Nature: instrinsic in origin due to immunologic factors
 Presence of cough and sputum production for at least Mechanism: Allergy
3 months in each of 2 consecutive years Mediators: IgE and Histamine
 Blue, bloater Problems:
 Smoker’s cough  Inflammation of the airway (leukotrienes, histamines,
Risk factors: SOP  Increased mucus production
Etiology:  Bronchoconstriction
 Chronic irritation Triggers
Genetic: Alpha 1 Anti-trypsin deficiency – enzyme that prevents  Environmental factors – change in temperature or humidity
elastase, which destroys elastin  Atmospheric pollutants – cigarettes, industrial smoke
Essential Features (ABC)  Strong odors – perfume, insecticides
 Age >40 y/o  Allergens – feathers, dust, foods, pollens, laundry
 Breathlessness detergents
 Cough (chronic and productive)  Exercise
 With hypoxic drive for breathing  Stress or emotional quest
 Carbon Dioxide Narcosis – CNS depression  Medications – aspirin, NSAIDs
Problems Manifestations
 Increased mucus production  Triad of Bronchial Asthma
 Bronchoconstriction o Cough
 Retention of CO2 o Dyspnea
Common Manifestations o Wheezing
 Dyspnea – exertional dyspnea  Restlessness/Agitation
 Cough (persistent and productive)  Hyperventilation
 Lethargic behavior  Wheezing
 Body weakness  Nursing alert: status asthmaticus
 Weight loss – catabolism Nursing Care
Diagnosis  During acute phase
 PFT (Pulmonary Function Test)  Position: orthopneic/Fowler’s
o Spirometry** – measures lung volume and  Bed rest
capacity  DBE
o Oximetry  Close monitoring
 ABG Analysis  If stable
o Diet: hypoallergenic (high calories, low CHON,
high CHO)
Complications o Avoid known triggers
 Pneumonia  septic schock Medical Management
o Pleuritic chest pain  O2 therapy
o DOB  Pharmacotherapy (Acute phase)
o Cough o Analeptic agents
o Rusty colored  Theophylline therapeutic level 10-20
o Fever mcg/mL
o Chills o Bronchodilators – adrenergic agents 
 Respiratory Failure Hypokalemia
o Inability of lungs to clear carbon dioxide  Beta selective adrenergic agonist
 Pulmonary Hypertension  Isoproterenol (Isuprel)
 Cor Pulmonale  Selective – beta2 adrenergic agonist
o Right-sided heart failure  Short-acting: Albuterol
Nursing Care (Proventil), Terbutaline
 DBE (Pursed-lip technique) (Bricanyl), Salbutamol
 Position: HOB elevated or orthopneic (Ventolin, Asmalin)
 Diet: high calories, high CHON, low CHO  Long-acting: Salmetrol
 Hydration (serevent), Formetrol
 CPT (Foradil)
 Bed rest as needed o Corticosteroids – beclomethasone, budenoside,
 Avoid exertion and stress fluticasone
MEDICAL SURGICAL NURSING 38
 Pharmacotherapy (Preventive)  >1500cc
o Anticholinergics – ipratropium, tiotropium  Consent
o Mast cell stabilizers – Nedocromil (Tilade),  2-3 ICS –air
Cromolyn (Intal)  5-6 ICS – fluid
o Leukotrine inhibitors – Montekulast (Singulair), Nursing Care
Zafirlukast (Accolate), Zileuton (Zyflo)  Positioning (HOB elevated) and monitoring
 MDIs – deep breath, hold breath for 3-5 seconds, gargle if  Secure connection
med is with steroids  Promote lung expansion
BRONCHOGENIC CANCER  Keep chest tube below chest level
Etiology: smoking or exposure to chemicals  Avoid kinks or loops
Incidence: common among males  Observe for intermittent fluctuations during respirations
Prognosis: poor (detected late)  Avoid clamping the tube
Classification  Check connection and observe for bubbling or air leaks
 Small cell lung cancer  Keep a vaselinized gauze at bed side
 Non small cell lung cancer  Responsibility: in cases of breakages or pulling of tubes
o Epidermal, adenocarcinoma, large cell cancer  Reassessment
Warning signs Summary of Respiratory Diseases
 Nagging cough A. Restrictive
 Hemoptysis  Reduced lung compliance  reduced lung volume 
 Chest pain hypoxemia  increased RR  respiratory alkalosis
 Dyspnea  Reduced VC, TLC, RV
 Weight loss  Earliest signs
Diagnosis o Dyspnea upon exertion
 X-ray  Inflammation of lung parenchyma
 CT scan o Pneumonia
 Bronchoscopy o ARDS
 Thoracoscopy o Space occupying lesion – Cancer
 Biopsy o Surgery
Management o GBS
 Surgery o Pleural disease – Pleural effusion
o Turn on unaffected side B. Obstructive
 Wedge resection  Limitation of airflow on expiration
 Segmentectomy  Failure of air to move out of lungs  CO2
 Lobectomy retention  respiratory acidosis
o Pneumonectomy  Chronic Airway Limitation/COPD
 Turned on back (Semi-Fowler’s) C. Vascular
 Nursing alert: watch out for  Pulmonary embolism
mediastinal shift  Obstruction  hypoxia/hypoxemia 
 Palpate trachea regularly constriction of the pulmonary vasculature 
PLEURAL EFFUSION increased pulmonary vascular resistance 
 Accumulation of air, water, or blood in the pleural space pulmonary hypertension  RV Failure (Cor
resulting to an alteration in the normal intrathoracic pressure Pulmonale)
 Pleura – seal and maintains negative pressure  High ventilation-perfusion ratio
Cause: I-I Vital Capacity (300-500 ml) – amt of inhaled/exhaled air
 Injury (chest wall trauma/rib fracture) – blunt Total Lung Capacity (6 L)
 Instrumentation (surgical procedures) Residual (1 – 1.5 L)
Forms
 Pneumothorax CHEST TUBE DRAINAGE
 Hydrothorax 1 – Way Bottle (H2O sealed chest drainage)
 Hemothorax  Air vent
Concept: lung compression 2 – Way Bottle
Complication: Atelectasis 1. Output bottle
Manifestations 2. Water-sealed bottle
 Dyspnea 3 – Way Bottle
 Agitation 1. Output bottle
 Asymmetrical chest expansion 2. Water-sealed bottle
 Decreased tactile fremitus 3. Vacuum-controlled bottle
 Decreased breath sounds Nursing Care
Diagnosis: CXR 1. Airtight
Management 2. 18 inches
 Pleurodesis 3. Taped
 Thoracostomy 4. Oscillation/tidalling/fluctuations
Approaches: needle vs. tube o Absence of oscillation
o Thoracentesis (needle thoracostomy)  Lungs have re-expanded
 <1500cc  Turn client from side to side
 Remind client to perform DB exercises
o CTT (tube thoracostomy) 5. Stripping/Milking/Squeezing
MEDICAL SURGICAL NURSING 39
o With extra caution Step 3 – inadequate response
o Prevent tension pneumothorax – avoid applying  Monotherapy (dosage adjustment/shift)
heavy pressure Step 4 – inadequate response
 Reveals blood clot which causes  Combitherapy (2 or more)
absence of oscillation
6. Bubbling CORONARY ARTERY DISEASE/ASHD/IHD - Chronic
o Presence – desired negative pressure from the  Occlusion of the coronary arteries that results to impaired
suction apparatus perfusion of the myocardium
o Intermittently  Main risk factor: HTN
o Continuous – leakage  Concept: oxygen debt
7. Measure  Mechanism: atherosclerosis
o One-way – put tape mark  Outcome: ischemia
8. Change
 LAD – anterior (Lead 2 in ECG)
o Sterile bottle, sterile glass rod
 Classic manifestation
o Clamping – causes tension pneumothorax
o Chest pain “angina pectoris”
o Bottle breakage, immerse tube in sterile water
 Types
o If in 3-way, two bottles are broken, make 1-way
bottle  Stable
o Place moist, non-porous dressing  Unstable
Angina Pectoris
CARDIOVASCULAR DISORDERS o S – sudden
Concept: Oxygen Debt o A – anterior chest
 Demand exceeds supply o V – vague
o E – exertion related
 Management: reduce demand and increase supply of
o R – relieved by rest or nitrates
oxygen
o S – short duration (20 minutes)
 Nursing interventions: bed rest
CAD Assessment
Manifestations
HYPERTENSION
o Dyspnea **
 Persistent elevation of BP; 140 mmHg systolic and 90 o Diaphoresis
mmHg diastolic (WHO) o Increased RR, HR or BP
 Most significant risk factor for CVDs o Diagnostics
 Regarded as “silent killer” o ECG – T wave inversion
 Hypertensive crisis – single sudden severe elevation in BP o Cardiac Biomarkers
(S: min. 180, D: min. 120)  CKMB – most accurate, most specific,
o Emergency – with organ damage lasts for 3 days, appears in blood 4-6
 Catapres (Clonidine) hrs. after MI
 Calci-block (Nifedipine)  Troponin – sudden increase because
 Captopril (Capoten) of sensitivity, up to 3 weeks
o Urgency – without organ damage Incision and Focus
 Diagnostic Criteria for Hypertension o Head and neck – airway
o 2 consecutive days of elevated BP within 2 o Chest and back – breathing
weeks o Peripheral – circulation
Types ACUTE CORONARY SYNDROME
 Primary/Essential  Unstable angina/Pre-infarct angina
o No specific cause/multivariate o Holter monitoring
 Secondary  Acute myocardial Infarction
o Due to co-morbidity o ST elevation – zone of injury **
Manifestation  First seen in patients with cardiac
 Throbbing occipital headache, dizziness, visual disturbance, diseases
edema, epistaxis, retinal hemorrhages  Monitor for enlarged Q wave next
o T wave inversion – zone of ischemia
Classification of BP for adults o Enlarged Q wave – zone of infarction
 Stage I Nursing care
 Stage II o Bed rest
 Stage III o Position: HOB elevated
 Stage IV o DBE
Complications of HTN o Avoid stress
 Atherosclerosis Medical Management
 CAD o O2 therapy
 CVD/CVA o Pharmacotherapy
 PAOD o NTG tablets **
 Take sublingually
Management (Exercise>diet)  Check expiration date
Step 1 – lifestyle modification  Max. of 3, 5 min. interval
 Focus: wt. reduction o Anti-HTN agents
Step 2 – inadequate response o Anti-platelet drugs
o PCI (Percutaneous Coronary Intervention)
 Monotherapy (diuretics/beta blockers/ACEI)
MEDICAL SURGICAL NURSING 40
 Percutaneous Transluminal Possible Complications of MI
Angioplasty (PTA)  Arrythmia – V. Fib – most common complication
 Not recommended if o Caused by sympathetic stimulation triggered by
occlusion >70% the chest pain  treat CHEST PAIN first!!!!
 Coronary stent o PR >200, irregular, chaotic heart beat
o Surgical Management o ECG no specific QRS complex
 CABG  Cardiogenic Shock – most fatal complication
Coronary Artery Bypass Graft o Cardiac Index = CO / body surface area (sq. m.)
o Possible blood vessels  2.8 – 4.2 L/min/sq. m.
o Radial o MAP = SBP + 2 DBP / 3
o Internal mammary/intrathoracic – best  N: 70-80 mmHg
o Saphenous o Mgt: Counterpulsation technique
 Fluoroscope
MYOCARDIAL INFARCTION  IABP (Intraaortic balloon pump)
 Heart wall damage due to cessation of blood flow in the  Ventricular rupture
coronary circulation  Pericardial effusion
 Death of myocardial cells from inadequate oxygenation,  Cardiac Tamponade
often caused by a sudden, complete blockage of a coronary  Pericarditis/Dressler’s Syndrome
artery characterized by localized formation of necrosis with o Develops 1-6 weeks after
subsequent healing by scar formation and fibrosis o Supine position aggravates position
 Mechanism: AA o Pain is relieved by orthopneic position
o Atherosclerosis o Treated by NSAIDs
o Arteriospasm  CVA
Assessment o Embolism
 Chest pain  Ventricular Failure
o Prolonged, substernal pain  Renal Failure
o Partial occlusion by atheroma/plaque  o Decreased CO  decreased renal perfusion 
decreased blood supply  8-10 seconds  renal ischemia  sub. Cessation RF  ARF
myocardial ischemia  angina Management
o 15-20 minutes  myocardial infarct  chest o Relief of pain
pain o Decrease cardiac workload
o Characteristics o Prevent complications
 S – sudden o MONAR
 A – anterior chest pain – substernal, o Morphine
left jaw, left shoulders, referred  Morphine > Demerol – Demerol
epigastric pain causes sudden hypotension,
 V – vague discomfort or vise-grip pain Morphine has sustained effect,
 E – exercise relieves pain with severe intensity
 R - rest o Oxygen
 S – short duration o Nitrates
o Myocardial ischemia  anaerobic metabolism o Anti-coagulants/anti-platelets/clot blusters
 metabolite  lactic acid  chest pain  VD  Given in the first 3 hours (window hour
 decreased BP & alteration  weak pulse for clot formation)
 DOB o Rehabilitation
 Diaphoresis o CBR without BRP
 Increased BP then drops o mMeds
o 10 seconds – oxygen storage in brain o ASA
 Increased HR, RR, Temp. (low-grade fever) o NTG – must feel burning/tingling sensation, every
o Metabolite  lactic acid  ensuing 5 minutes, max. of 3 doses
inflammatory process  increased neutrophils o Isosorbide mono/dinitrates (ISMN/ISDN)
 leukocytosis  low–grade fever  replaced Nursing care
fibrostatic tissue  fibrin o CBR without BRP – bedside commode
 N/V o Position: HOB elevated
Diagnostics o DBE
 ECG o Close monitoring
 Cardiac biomarkers o Diet: high in fiber
o Troponin I – most accurate (early and late o Avoid stress and strain
diagnosis, starts to elevate 2-3 hrs. after
myocardial injury, stays elevated for 3 weeks CARDIAC TAMPONADE
o CPK-MB – earliest diagnosis of MI o Rapid unchecked rise in intrapericardial pressure impairs
o SLDH – late diagnosis of MI (elevate 2-3 days diastolic filling of the heart due to blood or fluid accumulating
after myocardial injury) in pericardial sac
 1 & 2 – increase if with myocardial o Possible causes
insult o Effusion (cancer/bacterial infections),
 3 – increase if lung parenchyma injury hemorrhage from trauma/non-trauma causes, MI
 4 & 5 – increase if skeletal muscle or
liver damage
o SGOT/AST Manifestations
MEDICAL SURGICAL NURSING 41
o Dyspnea o ECG
o Anxiety Assessment
o Diaphoresis o Chest pain, dyspnea, cough, crackles, enlarged heart,
o Reduced arterial BP (pulsus paradoxus) dependent pitting edema, enlarged liver, jugular vein
o Narrow pulse pressure distention, murmur, S3 S4 sounds, syncope
o Neck vein distention Collaborative Management
o Pallor cyanosis o Nursing care
o Water-bottle heart o Semi-Fowler’s to High Fowler’s
Diagnostics o Bed rest
o CXR shows cardiomegaly and widened mediastinum o Diet: Low Na
o ECG o Fluid restriction
Collaborative Management o Close monitoring
o Nursing care
o Position HOB elevated
o Maintain on bed rest o Medical Management
o Close monitoring o Diuretics
o Medical o Dual chamber pacing
o Pericardiocentesis o Surgery: heart transplant or cardiomyoplasty
o Cardiac Resynchronization Therapy
HEART FAILURE
o A condition characterized by the inability of the heart to Pacemaker Nursing Instructions
pump blood in response to metabolic needs of the body o Check HR regularly
o HF – Chronic vs. CHF – Acute o Avoid exposure to magnetic devices
o Two types o Avoid use of mobile phones directly on top of pacemaker
o R – sided placement
o L – sided o Avoid vigorous movement of the shoulders
Etiology o Never use microwave ovens, use cellphone on opposite side
o Cardiac pathology: CAD, MI, CMP, VHD of pacemaker
o Pulmonary conditions: COPD
Problems VASCULAR DISEASES
o Failure to eject blood - L-sided but develops problem in ANEURYSM
backflow of blood o Permanent localized dilation of an artery
o Backflow of blood - R-sided o Sac formed by dilation of an artery secondary to weakness
Assessment and stretching of artery wall
o SOB Types
o Easy fatigability o Fusiform – diffuse dilation affecting the entire circumference
o Decreased ejection fraction (N: >55%) of the artery
Collaborative management o Saccular
o 4Ds o Dissecting
o Decrease fluid intake Sites
o Decrease sodium in diet o Cerebral Aneurysm
o Digoxin o Severe headache
 Withhold if 60 bpm o Thoracic Aortic Aneurysm
o Diuretics o Maybe asymptomatic
o Increase potassium in diet o Pain, boring and constant, during supine position
o To prevent digitalis toxicity (hypokalemia  o Abdominal Aortic Aneurysm
digitalis toxicity) o Asymptomatic
o Diuretics o Feel their heart beating
o Left Ventricular Assist Device Management
o Pharmacotherapy
CARDIOMYOPATHY (CMP) o Anti-HTN
o Myocardium around left ventricle becomes flabby, altering o Surgery
cardiac > decreased CO o Clipping or aneurysmectomy
o Increased HR and increased muscle mass compensate in o Stent/graft insertion
early stage but later stage > HF
Types PERIPHERAL VASCULAR DISORDERS
o Dilated (Congestive) – dilated chambers contract poorly o Decreased blood flow/insufficiency
causing blood to pool and reducing CO Arteries – responsible for tissue perfusion (oxygenated blood)
o Hypertrophic (Obstructive) – hypertrophied LV can’t relax o Buerger’s disease
and fill properly Venous – responsible for venous return (unoxygenated blood)
Possible causes o Varicose veins, DVT
o Chronic alcoholism, infection, pregnancy and post-partum
disorders, metabolic and immunologic disorders, chronic
HTN
Diagnosis
o 2D Echocardiogram
o Cardiac catheterization
o CXR SMOKING
MEDICAL SURGICAL NURSING 42
 Nicotine
o Catecholamine  epinephrine  VC  HPN
 increased heart workload
o Increased myo oxygen demand
o Platelet aggregation  increased thrombin form
 Carbon monoxide + Hgb = CarboxyHgb  interfere with O2
transport  transient hypoxia
STRESSOR
 SAMR/SMR  VC

ECG
 P-wave – atrial depolarization/contraction
 PR interval – 0.12-0.20
 QRS complex – ventricular depolarization/contraction
 ST segment – depolarization and beginning of repolarization
 T- wave – ventricular repolarizarion
 QT interval – entire duration of depo and repo – 0.36 – 0.42
 PP interval – atrial rate and rhythm
 RR interval – 1 QRS to next QRS; vent. Rate and rhythm
Lead Placement
 V1 – 4th ICS rt. Sternal border
 V2 – 4th ICS left
 V3 – diagonally 4th and 5th
 V4 – 5th ICS
 V5 – 5th ICS, ant. Axillary line
 V6 – 5th ICS, mid axillary line