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
 Increased in visual acuity  SH (Somatotrophic Hormone)
 GH
 Hypothalamus Posterior (Neurohypophysis)
o Sympatho-adrenal medullary  ADH
o Adreno-cortical  Oxytocin
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
Hyperactivity
o Secretes catecholamines:
 Tumor within or outside the gland
EPINEPHRINE/ADRENALINE
 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 Can be given sea foods but not milk, dairy
products and egg (rich in phosphorus) so check
levels of phosphorus if among the choices, all is
with calcium
 Management o Calcium preparations (after meals)
o Cobalt therapy  Calcium carbonate
 Radiation  Calcium Lactate
o Surgical removal  Calcium Chloride 10%
 Hypophysectomy  Calcium gluconate
o Inhibit production of growth hormone
(subcutaneously) o Given with vit. D (tachysterol)
o Somatostatin  Dihydrotachysterol
 Sandostatin  Hytakerol
 Octreotide/actreotide  Calciferol
 Calcifediol
DIABETES INSIPIDUS  Calcidiol
 Disorder in water metabolism  decreased ADH  prevent ADRENAL CORTEX
renal tubules reabsorption of water  polyuria = 5-29 L/24 1. Glucocorticoid/steroid – gluconeogenesis
hrs.  Polydipsia  diluted (decreased specific gravity =  Fat  increased lipolysis  abnormal fat distribution
1.010-1.025)  increased Na (135-145 mEq/L)  CHON  increased CHON catabolism  tissue
 All electrolyte testing do not require NPO starvation & muscle wasting
2. Mineralocorticoid/aldosterone
 ADH 3. Androgen
o Oily preparations (Deep IM)  lipodystrophy (rotate
route of administration) Cushing’s
 Pitressin Tannate  Increased GMA
 Vasopressin – vasoconstrictor  HPN  Increased 3S
o Nasal sprays (clear nasal passages) o Sugar
 Desmopressin Acetate  Hyperglycemia
 Lypressin  Moon facies
 Anti-lipidemic  Buffalo hump
o Clofibrate/Atromid S/Clo 5  Truncal obesity
o Salt
SIADH  Fluid retention  Increased BP
 Increased ADH  Hypernatremia
 Fluid retention  Hypokalemia
o Increased IV volume (hypervolemia) o Sex
 Increased BP  Virilism
 Increased renal perfusion   Masculinization
enhance/increased GFR/ increased  Hirsutism
UO  no leg edema  Management
o Electrolyte dilution  Dilutional hyponatremia  o Cobalt therapy
fluid move into the cell o Adrenalectomy
 Cerebral edema  Increased ICP o Cortisol inhibitors
 Cellular overhydration  Aminogluthetemide
 Management  Trilostane
o Hypophysectomy  Metyrapone
o Inhibit production of ADH  Metotane
 Demeclocyline/Declomycin PO Addison’s
 Decreased GMA
Parathormone  Decreased 3S
 Promote reabsorption of Ca in the renal tubules and o Sugar
excretion of P, essential for blood coagulation, regulate  Hypoglycemia
cardiac rhythmicity  Stimulate anterior pituitary gland 
Hypoparathyroidism increased ACTH  MSH  tan
 Hypocalcemia = hyperphosphatemia complexion  bronze-skinned
o 4.5-5.5 mEq/L o Salt
o 8-11 mg/dL  Decreased IV volume  hypotension
o High calcium diet  Hyponatremia
 Tetany  Hyperkalemia  myocardial irritability
o (+) Chvostek – tap the Facial nerve (below the  altered electrical conduction 
dysrhythmias  heart arrest
temporals)  muscle twitching of face
o Sex
o Trousseau – occlude blood flow of an extremity
 Management
for 1-2 minutes  carpopedal spasm
o Steroids
 Management
Conns/Primary aldosteronism
MEDICAL SURGICAL NURSING 3
 Adenoma of adrenal cortex (benign) o Theoretical basal metabolic rate
 Hyperactivity o 20-30
Pheochromocytoma o Pulse pressure + PR/min – 111
 Adenoma of adrenal medulla (benign) o Not definitive
 Hyperactivity  RAIU (Radioactive Iodine Uptake)
 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
o Cretinism - childhood
 Plasma iodide + tyrosine (amino acid) = thyroglobulin
(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
 Triad Symptoms
 BMR
o Evaluate O2 consumption when at rest  Goiter
o NPO 12 hrs. and good night sleep  Eye signs
o  Hyperthyroidism
o Elevated T3 T4
 TBMR
MEDICAL SURGICAL NURSING 4
o EPS o Provide physical mental rest
 Anterior pituitary gland will release an o Provide calm/restful environment
exophthalmos producing substance o Elevate head to promote drainage and reduce
 Exophthalmos (protrusion peri-orbital edema
of eyeball)
 Proptosis (downward Surgeries
displacement of eyeball)  Sistrunk’s – thyroglossal cyst
 Lid lag  Radical/Total thyroidectomy
 Infrequent blinking o Collar-line/Curvilinear
 Fixed stare  Partial/Sub-total thyroidectomy – 5/6 of 2 lobes
 Peri-orbital edema  Thyroid lobectomy
 Von Graefe (failure of  Isthmusectomy
eyelids to follow movement
of eyes when the patient Post-thyroidectomy management
looks down)  Promote patent airway
 Dalyrimple sign (infrequent o Position Semi-Fowler’s
blinking and fixed stare) o Not High-Fowler’s – cause strain on neck muscle
o S/sx which causes tension on suture line (bleeding)
 Increased T3 T4  Turn to sides
 Diarrhea  Promote adequate nutrition and fluid and electrolytes
 Voracious increase T3 T4 (Grave’s) o As soon as fully awake and with gag reflex
 Over-excitability SNS (no (Elevation of palate and contraction of
management sought) pharyngeal muscle)
o Diaphoresis  Promote adequate bowel-bladder elimination
o Tremors o 6-8 hrs. after surgery
o Nervousness o If not within 6-8 hrs., palpate presence of bladder
o Palpitation distention
o Constipation  Encourage early ambulation
o Simple goiter/Endemic goiter/ Iodine-deficiency o Shorten convalescence period
goiter/ Non-toxic goiter o Boost patient’s moral
o Goiter – enlargement of thyroid gland o Get out of bed as soon as VS are stable
 Hormone levels  Support the head and neck to prevent
 May be normal, flexion and hyperextension
above/below normal  Complications
because goiter is simply o Tetany
enlargement  Occurs upon accidental removal of
Treatment Modalities parathyroid glands
 Anti-thyroid preparation o 2 recurrent laryngeal nerves
 Prevent synthesis T3 T4 by blocking utilization of  Hoarseness (edema of glottis)
iodine  Aphonia
 Example o Bleeding
o Tapazole/methimazole  Failure to tie/ligate the bleeders
o PTU (Propylthiouracil)  Check for dampness at the nape
 Differential count  Check for feeling of choking
o Neomercazole/Carbimazole  Evaluate VS
 Adverse effects (prolonged use)  Rapid, weak, feeble,
o Agranulocytosis – infection thready pulse
 Fever  Rapid but shallow
 Complaint of sore throat respiration
 Dyspnea o Respiratory obstruction
 Iodine Preparation  Secondary to bleeding
 Lugol’s solution/KISS (Potassium Iodide  Accumulation of tracheo-bronchial
Saturated Solution) secretion
o Reduce vascularity  Laryngospasm
o Increase firmness of gland  Laryngeal edema
o Promote storage of T3 T4 o Thyroid crises/storm
 Adrenergic-blocking  High anxiety level pre-op
 Control symptoms of over-excitability of  Increased T3 TT4  anti-thyroid
SNS preparation for 3 months  euthyroid
 RAI 131 state, normal T3 T4  operation 
post-op stress, infection  increased
 Surgery
T3 T4 (over-excitability of SNS)
 Management
 Fever with tachycardia
o High caloric diet
 Anti-thyroid preparation
o No colas/caffeinated beverages
o Monitor weight DIABETES MELLITUS
MEDICAL SURGICAL NURSING 5
Assessments  Eye opening, Verbal Response,
 FPG, RBS, PPBS, OGTT, Hgt Motor Response
 Ophthalmoscope – checks pupillary
HHNK Coma/HHNS dilation
 Hyperglycemia  hyperosmolar diuresis  glycosuria &  Decorticate – spinal lesion
polyuria  ECF dehydration  cerebral dehydration   Decerebrate – diencephalon and brain
CNS depression  HHNK stem affectation (medulla – respiratory
DKA paralysis)
 Increased lipolysis  increased oxidation of fatty acids  Brain herniation
hyperlipidemia & ketone bodies  DKA  Disease of pons and midbrain  decorticate and
Dawn’s phenomenon decerebrate at the same time
 Normal blood sugar before night time  shoots up
hyperglycemia at the dawn
Somogyi/Rebound Hyperglycemia Brain:
 Maybe normal bood sugar before the client sleeps  blood  Parietal – sensation
sugar depletes at around 2 am  shoots up at around 3 am  Occipital – vision
due to the counter hormone secreted in the body  Temporal – hearing, balance, memory
 Frontal – attitudes, personality, behavior, learning
Rapid Short Intermediate Long/Slow SPEECH PROBLEM
(10-15 (6-8 hrs.)  Brocha’s center – speech
min.) o More of the frontal lobe
Pea 30 m-1 hr 2-4 hrs. 6-12 hrs. 18-24 hrs. o Right-handed = left hemisphere (more dominant)
k  Wernicke’s – language
Novolog Regular NPH- Neutral Lantus Aphasia
Humalog insulin Protamine Ultralente  Motor/expressive – unable to talk, unable to written, frontal
Lispro Semilente Hagedorn Humulin Y lobe
Aspart Humulin R Lente Glargine  Sensory/Receptive – unable to understand both written and
Crystalline Humulin N PZI- vocal
Zinc Globin Protamine  Global – both motor and sensory aphasia
Novolin R Novolin L Zinc Insulin  Visual – occipital affectation
Monotard  Auditory – temporal affectation
Management
 Take more complex carbohydrates than simple Ipsilateral
carbohydrates because the rate of absorption is slower, thus  Symptoms on side of lesion
no sudden increase in serum glucose  Right sided lesion/tumor – focal symptoms  puffiness of
 Hypoglycemia right life, drool at right side, sag of the right side
o When patient has altered LOC, give 1 table Contralateral
spoon of sugar because the blood vessels in the  Symptoms on opposite side of lesion
mouth will absorb the glucose  Decreased crossing, dequasation of nerve fibers at the
o The fat content will delay the absorption of pyramidal tract
glucose o Pyramidal tract – fine motor movements
o Extreme hypoglycemia  Right-sided lesion/tumor – focal symptoms  paresis,
 Epi/Adre 1:1000 SQ phlegia of left
 Glucagon 1-2 mg IV
 IV of glucose 50% - IV push GAIT
 Exercise  Ataxic – steady  feet together  fall (cerebellum
o Reduce dose of insulin affectation)
o Remind to take snacks in between  Dystonic – irregular non-directive movement  muscle
atony
NEUROLOGIC DISORDERS  Dystrophic (Waddling gait) – feet apart  body weight
LOC (LEVEL OF CONSCIOUSNESS) move to the sides
 Cerebral hemispheres – center for consciousness o With muscle dystrophy
 RAS at the brainstem – center for wakefulness o Weakness of pelvic girdle
Altered LOC o Hip dislocation
 Causes  Hemiphlegic – foot dragging
o Lesion  Scissors – short, slow steps, legs alternating and crossing
 Tumor each other
 Hematoma o With spastic paralysis
 Abscess
 Steppage – high exaggerated steps (lower motor neuron
o Metabolic depression
affectation)
 Hypoglycemia
 Hypoxia REFLEXES
 Fluid and electrolyte imbalance
 Knee-Jerk
 Toxic/chemicals
 Bicep – forearm flexion
 Assessment
 Tricep – forearm extension
o Glasgow Coma Scale
 Babinski – extension of big toe, fanning of other toes
MEDICAL SURGICAL NURSING 6
 Gordon’s – squeeze calf muscle  dorsiflexion of big toe  Not to be alarmed if with metallic
 Chaddocks – stroke inner aspect of legs  dorsiflexion of taste, flushing, warm sensation
big toe o Place an ice cap/ice collar on the neck to prevent
 Kernigs – flex and extend in lower extremity  pain and bleeding (carotid)
spasm in hamstring muscle o Place a sandbag over the inguinal area for
 Cremasteric – stroke inner aspect of thigh  rise of testes, pressure, immobilize, keep leg extended to keep
elevate scrotum, use tongue depressor pressure on the femoral artery
 Brudzinki – bend head toward chest  flexion of ankle, o Check popliteal and dorsalis pedis pulse distal to
knee and thigh the site of puncture
 Binda – turn head to one side  opposite shoulder will o Check color and temperature of leg to check
move upward and inward arterial insufficiency (cold, pale)
 Myelogram – x-ray of subarachnoidal spaces after giving a
dye (Pantopaque/Myodin) instraspinously/intrathecally
Stronger muscles o Prepare like in LP
 Flexor vs. Extensor  EEG – measures electrical activities of brain
 Adductor vs. Abductor o Avoid stimulant/depressant
COORDINATION  No colas/caffeinated beverages
 Romber’s Test  No Phenytoin/Dilantin, Na
o Stand with feet together, eyes closed Luminal/Phenobarbital,
 Fall/sway to one side – cerebellum Carbamazepine/Tegretol,
affectation Clonazepam/Klonopin
Diagnostic Tests  Advice a regular diet prior to EEG
 Lumbar Puncture/Spinal Tap because a state of hypoglycemia will
o Consent alter LOC
o Local anesthesia into subarachnoidal space  Shampoo hair to cling the electrodes
(Lidocaine/Xylocaine 1-2%, Novocaine, on non-oily hair
Tetracaine HCl, Marcaine)  With history of seizure/convulsion –
 L3-L4, L4-L5, L6-S1 (end of spinal nerve is continue anticonvulsant
above L1  Prevent Status Epilipticus
 C-position/Shrimp position  EMG – measures electrical activities of peripheral muscles
 Void before procedure to diagnose muscle dystrophy and peripheral nerve injuries
o Immediately prone 30 min.-1 hr. o Jolly’s (Nerve Conduction Velocity)
o FOB 6-8 hrs. to prevent spinal headache o Several needles and wires will be attached to
 Queckenstedt muscles, observed while performing activities
o CSF Pressure  Jugular vein pressure  6-12
sec.
o CSF  CT scan
 Volume: 90-150 mL o Without contrast – no prep
 Transparency: clear o With contrast via IV (Thallium, Technetium,
 Color: colorless Neohydrin) – NPO for 6 hours
 Yellowish (Xantochromia) =  MRI
old blood clot  Skull x-ray
 CHON: 15-45 mg%
 Inc. = tumor, MS, GBS PARKINSON’S DISEASE/Paralysis Agitans
 Glucose: 50-80 mg% (glycorrakia)  Degeneration of basal ganglia due to decreased supply of
 Chloride: 118-132 mEq/L dopamine
 WBC: 0-8/mL = Pleocytosis  Risk Factors: History of Encephalitis, Head Trauma,
 Gammaglobulin: 3-9 % Smoking, Hypertension, CO2 Monoxide, Use of
 MS (IgG) Contraceptive Pills
 Pneumo-encephalogram – x-ray of the brain ventricles after  Neuronal Degeneration of the substantia nigra of the
introduction of air/O2 midbrain  decreased inhibitory neurotransmission 
o Prepare for LP decreased dopamine  impairment of the extrapyramidal
o Withdraw 20 mL of CSF, then give 20 mL of O2 tract (basal ganglia)  imbalance in voluntary movement
 Cerebral Angiogram – x-ray of the cerebral vascular system  triad symptoms (non-intention tremors <pill-rolling
with the use of dyes (Conray/Diodrast) into the femoral or movement of thumb against fingers>, rigidity <micrographia
carotid arteries or minute illegible handwriting, cogwheel or jerky motion for
o Same with Carotid/Femoral arteriography every passive movement>, bradykinesia/dyskinesia
o Secure consent <freezing phenomenon or transient inactivity>)
o Prepare a local anesthetic (puncture a major  Impairment of the extrapyramidal tract (basal ganglia) 
weakness of the muscles of expression  “mask-like/blank
blood vessel)
facies”
o Dye administration
 Imbalance in voluntary movement  triad symptoms 
 NPO for at least 6 hrs. – prevent
impairment of the muscles responsible for speech 
dilution of dye
drooling and microphonia or slow, monotonous voice with
 Check for allergies
poor articulation
 Submit to Serum Crea –nephrotoxic
 Shuffling/propulsive/festination gait
MEDICAL SURGICAL NURSING 7
 Stooped posture o Separate antibodies in the blood in exchange
 Walking on toes with accelerated pace with donor blood
Management  Establish artificial airway
 Dopamine – cannot pass through blood-brain barrier o ET/Tracheostomy insertion
 Levodopa – metabolic precursor, absorbed by substantia  Receive anticholinesterase/cholinergic agent – increase
nigra, acted upon by decarboxylase which will be converted uptake of acetylcholine, increase number of functioning
into dopamine acetylcholine receptors
o Dopar – Larodopa o Prostigmine/Neostigmine
o Carbidopa – Sinemet o Mestinon/Pyridostigmine
o Amantadine HCl – Symmetril o CHOLINERGIC CRISIS/ PNS activation
o Trihexyphenidyl – Artane  Give anti-cholinergic Atropine Sulfate,
o Benztropint Mecylate – Cogentin Scopolamine
o Biperidine HCl – Akineton
o Endoginous dopa MULTIPLE SCLEROSIS
 Bromocriptine  Myelin sheath – fat-like covering of nerve fibers
 Partodel  Chronic lingering illness until death
 Risk factor: Autoimmune disease, post-viral disease,
 MAOI Pregnancy, Stress, Use of amphetamines
o Selequitine  Demyelination (damage of myelin sheaths) of nerve fibers of
o Eldepryl brain and spinal cord  replaced by sclerotic patches of
o Carbex necrotic tissue  trigger inflammatory reaction  form
 Surgery inflammatory exudate/edema  scarring/fibrosis  failure
o Stereotactic – uses electrical stimulator, interrupt of transmission of electrical impulses Charcot triad of
symptoms
the nerve fiber pathway
 Thalamotomy – thalamus  Charcot triad of symptoms
 Pallidotomy – deep Globus pallidus o Tremors = spastic-ataxic gait
Nursing Diagnosis o Nystagmus (movement from side to
 Impaired mobility side)/strabismus (movement toward the midline)/
o Do regular exercises to improve muscle tone and dysconjugate (movement away from the midline)
strength and prevent contractures CN 3 (Oculomotor – pupil contraction, eye
o Give something to hold onto – stress ball, hand accumulation), 4 (Trochlear – superior oblique
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 
reduce number of functional acetylcholine receptors  Lumbar Puncture
o Elevated CSF CHON, G-globulin
 Normal: Axons  release excitatory neurotransmitter 
acetylcholine attach to acetylcholine receptor of the muscle  MRI
fibers  muscle contraction  muscle atony and weakness o Evaluate extent of demyelination
 paralysis Management
o Ocular muscle  ptosis, diplopia  Symptomatic
o Facial and lingual muscle  Supportive
 Dysphagia  Steroids – reduce edema around site of demyelination
 Mastication impairment  ABCR – prevent proliferation/activation of T cells
 Snarling smile – clenched teeth and o Avonex
jaw hangs open o Betaseron
o Respiratory paralysis  respiratory distress  o Copaxone
MYASTHENIA CRISIS (no treatment sought) o Rebif
Diagnosis
 Tensilon Test GUILLIAN-BARRE SYNDROME
Management Pathological Changes
 Thymectomy (suprasternal notch)  Polyradiculoneuritis (“Radiculo” – cranial nerves)
o Thymus gland  T cells  antibodies o Ocular
production o Oro-pharyngeal muscles
o Remove antibodies (autoimmune) o Facial
o Thymoma  Peripheral neuritis – demyelination of peripheral nerves
 Plasmapheresis/Plasma exchange
MEDICAL SURGICAL NURSING 8
o Ascending paralysis o Aspilet
 Autonomic dysfunction o Ascription
o Over-excite SNS & PNS o Dipyridamole/Persantin/Pexid
o Under-excite SNS & PNS o Ticlopidine/Ticlid
o Clopidogrel/Plavix/Clovix
Parkinson’s – Male (Freddie Roach)  Anti-coagulant
MS – Female (Alma Moreno) o Coumadin PO
G B S – both sexes (girl, boy) o Heparin SQ, IV
MG – early onset in female, late onset in male  Antidote: Protamine Sulfate
 Check PTT
CVA/ APOPLEXY  Plasminogen activator – plasmin lysis
 Cerebral ischemia  Cerebral infarction/necrosis o Streptokinase
 Cerebral anoxia (4 minutes)  cerebral infarction  Antidote: Aminocaproic acid
Pathology o Urokinase
 Occlusive o Altiplase
o Embolism o Retavase
 MI, endocarditis, dysrhythmia, o t-PA (tissue type)
fracture, CA
 Cerebral decongestant
 Sudden onset
o Mannitol (Hyperosmolar solution)
o Thrombolism  Sol  ITS  IV  increased renal
perfusion  increased UO
 DM, Atherosclerosis, Hypertension,
o Dexamethasone (Decadron)
Smoking
 Gradual onset  Only steroid that crosses blood-brain
 TIA – should appear only for 24 hrs. barrier
 Nuchal pain  Mechanical ventilation/ambubagging
o Decrease PCO2 by hyperventilation (MV) 
 Paresthesia
increased RR  excrete O2  decreased ICP
 Light-headedness
TUMORS
 Transient loss of memory
According to origin
 Transient loss of speech
 Glioma – from brain tissue
 Hemorrhagic
 Meningioma – from brain covering
o Hemorrhage
 Neuroma – from cranial nerves
 Hypertension, aneurysm
According to location
 Stress, physical activity
 Supratentorial – cerebrum, anterior 2/3 of brain
Symptoms
 Infratentorial – cerebellum, brainstem, post. 1/3 of brain
 Depends on area of necrosis
 Increased intracranial pressure
Symptoms
INCREASED INTRACRANIAL PRESSURE
 Earliest sign: papilledema (compression of optic nerve)
Early signs
Management
 Restlessness and hippus (alternate pupillary dilatation and
 Surgery
constriction)
o Craniotomy – coronal/butterfly incision
 Projectile vomiting
o Craniectomy
 Papilledema
 Radiation therapy
 Choked disc
 Headache (cephalalgia) – arising and worsen with change in
Head surgery
head position
 DON’Ts after surgery

o Trendelenburg
Late signs: Cushing triad changes
 Increase ICP
 Increased SBP, normal/decreased DBP = widened pulse
 Compress diaphragm
pressure
o Suction
 Decreased PR
 Increases ICP
 Decreased RR  Insertion of tube – triggers cough
 Increased metabolic rate  Increased temp. reflex  increased ICP
 Progressive altered LOC  decreased temp.  If needed, do it orally because nasal
Causes may cause nasal trauma thereby
 Increased CSF volume causing CSF leak
 Increased brain tissue bulk/size  Halo sign (use gauze)
 Increased cerebral blood flow  Sugar
o PpCO2 (hypercarbia, hypercapnea) dilated o Restrain
cerebral blood vessel  increased cerebral  Increases ICP
blood flow  cerebral congestion  increased o Insert rectal tube/thermometer
ICP  Vagal stimulation  PNS
Management o Constipation
 Anti-thrombotic/ anti-platelet aggregate  Increase cerebral blood flow
o ASA – prolonged prothrombin time, GI upset
MEDICAL SURGICAL NURSING 9
 Supratentorial – 45 HOB (Semi-Fowler’s)  Blood typing
o Promote venous return
 Infratentorial – 10-15 HOB ANEMIA
o Prevent compression of brainstem Causes
o Don’t place client on back  place on  Decreased erythropoiesis (formation and maturation of
unoperated side RBC)
o If on operated side, not more than 20 minutes to  CHON – cell wall, structure, membrane
prevent cerebral  Iron – pigment hemoglobin
 Vit. B12 – synthesis of nucleic acid
HEMATOLOGIC DISORDERS  Folic Acid - mature
BLOOD DYSCRASIA  Vit. C – catalyst for iron absorption
Pathology o Iron Deficiency Anemia
 Pancytopenia – decreased production of blood cell  Microcytic, hypochromic anemia
 Overproduction of defective cells  Vinson-Plummer Syndrome
 Spleen disorders  Dysphagia
 Defect in the coagulation mechanism  Atrophic glossitis (tongue)
Diagnosis  Stomatitis/Mucositis (oral
 CBC, Hgb, Hct (percentage of blood cell in plasma) mucosa)
 BT, PT, CT o Megaloblastic Anemia
 Erythrocyte index  Macrocytic, hyperchromic anemia
o MCV (Mean Corpuscular Volume)  Folate deficiency and Pernicious
anemia
 Evaluates size of RBC
 Beefy red tongue (reddish, sore
 80-94 cu. Microns
tongue due to gastric atrophy)
 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
MEDICAL SURGICAL NURSING 10
remission/absent o Invade/ infiltrate vital organs  splenomegaly,
symptoms hepatomegaly, increased ICP, renal insufficiency
 Blood loss and renal failure
o Normocytic, normochromic anemia According to onset of symptoms
o Hypovolemia  Acute Leukemia
o Hypovolemic shock (loss of 15-25%) o Sudden, short duration (<6 mos.)
 N: 4-6 L o Predominant cell: immature blast cells
o FWB
Signs and symptoms
 Decreased Hgb count  reduction in the O2 carrying  Chronic Leukemia
capacity of the blood  tissue hypoxia o Gradual, long duration
o Brain: restlessness, HA, syncope, irritability o Predominant cell: mature WBC
o Heart: angina pain, increased PR, weakness  o Remission and exacerbation
easy fatigability (earliest complain) WBC
o Respi: increased RR, SOB  Bone Marrow
o GIT: anorexia, angular cheilosis (lesion at angles o Granulocytes  myeloblast  myelocyte (N, E,
of mouth) B)
o Skin and M. Membrane: pallor, brittle hair, o Non-granulocytes  monoblast, monocyte
intolerance to cold, brittle nails  spoon-shaped  Lymphoid Tissue
(Koilonychia) o Non-granulocytes  lymphobast 
lymphocytes
According to predominantly cells
 Acute/Chronic Lymphocytic Leukemia (ALL)
o Most common for children
 Acute/Chronic Myelocytic/Myelogenous Leukemia (CML)
POLYCYTHEMIA VERA o Most common for adults
 Tissue hypoxia  release of humoral substance 
erythropoietin  stimulates BM activity  increased
basophils  increased erythropoiesis  capillary MULTIPLE MYELOMA
congestion, hemoconcentration, compensatory hypertrophy  Plasma cells secrete Ig (CHON)  antibodies
o Increased basophils  increased cellular activity  Proliferation of abnormal plasma cells (uncapable of
(increased cellular metabolism  weight loss producing functional Ig)
and increased temperature) and release of o Infection
histamine (pruritus) o Hemoconcentration  hypertension and
o Capillary congestion thrombus formation
 Ruddiness of the skin “Phletora” o Secrete osteoclast activating factor  increased
 Capillary engorgement bleeding  bone destruction (calcium losses from bone 
anemia brittle, pathologic fracture and hypercalcemia 
o Hemoconcentration hypercalciuria  calcium crystallize  nidus,
 HA, dizzinesss, blurring of vision nucleus  stone) and increased bone resorption
 Hypertension  bone pain (skull, vertebrae, scapula, clavicle,
 Sluggish blood flow  thrombus pelvis, femur)
formation Diagnostics
o Compensatory hypertrophy  BM biopsy
 Hepato-splenomegaly (splenomegaly  Urine: Bence-Jones protein
first)  CBC with differential count
Management  Hct determination
 Increase fluid intake  Serum calcium
 Engage in activities  Calcium urine
 Anti-neoplastic agents (Anti-metabolite) Management
o Methotrexate/Mexate  Chemotherapy
 Blood phlebotomy
o Opening of vein to gradually withdraw blood HODGKIN’S/Malignant Lymphoma/Lymphosarcoma
 Risk factors: familial history, exposure to carcinogen,
LEUKEMIA exposure to environmental pollutant, post-viral illness
Pathology (Epstein-Barr virus)
 Uncontrolled, abnormal proliferation/multiplication of  Incidence is high in males <20, >50
immature blast cells (WBC)  infection Diagnosis
o Increased cellular activity  increased cellular  Biopsy: Reed-Sternberg cells
metabolism  increased temperature Symptom:
o Crowd/congest/accumulation in bone marrow   A (Local) – painless lymphadenopathy (earliest)
joint pain, joint swelling, hinder/prevent  B (Systemic) – fever, weight loss, night sweats
production of blood cells (decreased RBC) zS  Management
anemia, decreased platelet  thrombocytopenia  Surgery
 bleeding  Chemotherapy

GASTROINTESTINAL DISORDERS
MEDICAL SURGICAL NURSING 11
ACHALASIA/Aperistalsis  Maintain IBW
Pathology  Avoid very hot and very cold drinks
 Absence/degeneration of Myenteric Aurbach Plexus (nerve  Render oral hygiene
fiber that innervate/stimulate esophageal activity   Take SFF
Aperistalsis)
 Megaesophagus – dilated esophagus when food PEPTIC ULCER DISEASE
accumulate at lower end of esophagus  Erosion of a circumscribed area in GIT due to digestive
 Cardiospasm – failure of cardiac sphincter to relax to allow action of HCl and Pepsin (protein-digesting enzyme, digests
food to enter stomach living tissues)
Symptoms  Most common areas (bathe with pepsin)
 Sternal pain – compression of food at sternum o Lesser end of esophagus
 Halitosis – decomposed food o Lesser curvature of stomach  gastric ulcer
 Esophagitis o Upper end of duodenum  duodenal ulcer
o Dysphagia  Autodigestion theory
o Odynophagia  Gastric ulcer – no buffering for HCl
 Regurgitation/pyrosis  Duodenal ulcer – increased acid load/acid chyme
Management Barriers against pepsin
 Esophagomyotomy – opening/division of the muscle fibers  GIT  mucin  film/coat
of esophagus  GIT  blood supply  prevent gastric anoxia
 Cardiomyotomy – dividing esophageal and cardiac muscle  Duodenum  bile and pancreatic enzyme (alkaline) 
 Hellers’ neutralize
 Nissen Fundoplication – lower end of esophagus is covered Basic pathologic changes
using the fundus of the stomach  Absence of protective mucin
 TPN (hyperalimentation) – glucose, lipids, amino acids  Gastric anoxia
o Central line – subclavian vein (well supported by  Absence of bile and pancreatic enzyme
shoulder muscle) Risk factors
 Need for hypertonic glucose >10% or  Poor dietary habit (not eating and eating hurriedly)
more than 10 days o Lower economic strata: gastric ulcer
 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
 Outpouching/ballooning  Previous infection of GIT brought about by Helicobacter
 Cause: congenital weakness of supporting wall pylori (from raw pork and beef)
 Risk factor: chronic esophagitis o Enzyme release  destruction of gastric mucosa
According to location  loss of mucin
 Zenker Pulsion – upper 1/3  Smoking
 Traction – middle 1/3 o Nicotine  vasoconstriction  gastric anoxia
 Epiphrenic – lower 1/3 o Nicotine  destroys alkalinity of bile and
Management pancreatic enzymes
 Surgery  Blood Type
o Transthoracic incision (Traction and Epiphrenic) o “O” – Ulcer (high in pepsinogen)
GERD o “A” – Cancer
Pathology Signs and Symptoms
 Inappropriate relaxation of the lower esophageal sphincter  Pain – mid-epigastric, burning, gnawing
causing the backflow of gastric content into the esophagus Gastric ulcer Duodenal ulcer
 Risk factor: pregnancy, caffeine, obesity, High in fat, alcohol, Radiate to left epigastric Radiate to right epigastric
high estrogen levels 30 min. – 2 hrs. p.c. 2-4 hrs. p.c.
 Management Food – aggravates Food – relieve
o Decrease pressure in LES Vomiting – relieve Vomiting - none
 Urecholine Weight loss Weight gain
 Bethanecol Decreased HCl – Increased HCl -
 Domperidone hypochlorhydria hyperchlorhydria
Management of Esophageal disorders Hematemesis Melena
 Assume upright position Management
 Avoid eating and drinking 2 hrs. before retiring  Buffers – food and antacid (an hour after meal, in between
 Avoid coffee, fatty foods, alcohol, smoking, spices/irritants meals, at bedtime)
MEDICAL SURGICAL NURSING 12
 Decrease CHON (potent secretagogue  HCl)  Marginal Ulcer
 Increased CHO o HCl is in contact with the anastomosis
 Encourage fat intake (polyunsaturated)  intestinal mucosa  Pernicious Anemia
 interogastrone  decrease gastric secretion, decrease o Loss of intrinsic factor  B12deficiency
gastric motility  Malnutrition
 Administer H2-receptor antagonist (block release of COLON DISORDERS
histamine by parietal cell) CHRONIC INFLAMMATORY BOWEL DISEASE
 Antacid and H2 blocker – can be both given, give H2 blocker Crohn’s/Regional Enteritis Ulcerative Colitis
ahead of antacid because antacid has a local coating effect Site Transmural (all layers) Entire length of colon:
Complication SI: segment  Terminal Descending colon (recto-
 Perforation – ulcer invaded the serosa, submucosa, Ilium sigmoid)
muscularis of stomach LI: Ascending colon
o Gastric and intestinal content leak to peritoneal Predisposin Hereditary, auto-immune Bacteria, stress, allergen
cavity g
o Abdominal distention Factor
o Boardlike, rigid, hypoactive bowel sound Pathologic Sub-mucosal lymph Diffuse mucosal
 Peritonitis lesion nodes ulceration
o Abdominal distention Payers Patches  Inflammatory infiltrate –
o Boardlike, rigid, hypoactive bowel sound cobblestone Crypt abscess
 Bleeding (fissures/ulcers)
 Pyloric obstruction Constricted  “String
o Result from stenosis coming from fibrosis sign”
 Intractable ulcer Pain RLQ Generalized crampy -
o Ulcer is not responding to medications LLQ
Diarrhea 3-5x/day 15-20x/day
Stool Mucoid, pus Mucoid, pus, blood
Semi-soft to soft Watery stool
Management:
 Symptomatic
Management  NSAIDs
 Billroth I  Intestinal antibacterial – Sulfonamide
o Remove distal third  anastomose to duodenum  Avoid stimulants
o Sub-total gastrectomy with gastro-duodenostomy INTESTINAL OBSTRUCTION
 Billroth II/Polya/Hoffmeister Mechanically
o Remove distal third  anastomose to jejunum o Tumor (Recto-sigmoid, descending colon)
 Billroth III o Risk factors
o Esophago-jejunostomy  History of Crohn’s and Ulcerative Colitis, Chronic
o Cancer of the stomach constipation
 Gastrorrhaphy - Suturing of a perforated stomach  High in saturated fat, high CHON, low fiber, high
 Antrectomy intake of beef
o Remove antrum  Polyposis – Pre-cancer lesion
o Antrum  gastrin  HCl stimulation  2-3 yrs. of change from benign to
o Palliative surgery for intractable ulcer malignant
 Vagotomy o Syptoms
o Remove a portion of vagus nerve  R-sided – melena
o Vagus nerve  increase gastric secretion,  L-sided – hematochezia
increase gastric motility o Volvulous
 Pyloroplasty - enlarge pyloric opening o Intussusception
o Diverticulosis
Complication of Gastric Surgery o Adhesion
 Dumping Syndrome Neurogenic/Functional
o Rapid passage of hyperosmolar solution into  Paralytic Ileus/Adynamic colon
jejunum  jejunum distention Causes
o Local effect  jejunum distention  increased o Anesthesia
intestinal motility o Peritonitis – intestinal decompression
o Systemic effect  hyperosmolar solution  fluid  Miller-Abbott
shift  IV to jejunum  shock-like  Cantor
o Eat foods on recumbent position  Harris
o Dry meal  Baker’s
o No sweets, no CHO-rich foods o Hypokalemia – tone
 CHO – 1-2 hrs. p.c.  Hirschprung’s Disease
 CHON – 2-4 hr. p.c. Vascular
o Management  Mesenteric
 Delay gastric emptying  Thrombosis
Management
 Propantheline Bromide
 Gastric decompression
 Bentyl Buscopan
o Levine
MEDICAL SURGICAL NURSING 13
o Euald  Low protein – ESHD (End-Stage)
o Salem  Anti-coma regimen
o Sump o Enema – cleanse colon of urease-splitting
o Moss microorganism
 Surgery o Neomycin by enema or NGT – non-absorbable
o Hemicolectomy antibiotic that prevents growth urease-splitting
 Lap microorganism
 Open o Duphalac/Lactulose PO – decrease pH to inhibit
o APR (Abdominoperineal Resection)/Miles growth of urease-splitting microorganism
 Surgical removal of descending colon,
sigmoid, rectum, anal sphincter BILIARY TRACT OBSTRUCTION
Symptoms
HEPATO-BILIARY DISORDERS  Pain: Biliary cholic – severe RUQ pain radiating to
LIVER CIRRHOSIS  Hemolytic jaundice – increased unconjugated bilirubin
Types:  Obstructive jaundice – increased conjugated bilirubin
 Biliary (Cholelithiasis)
 Post-necrotic  Hepatocellular jaundice – increased conj. And unconj.
 Laennec’s  Obstruction:
 Cardiac o Tea-colored urine
Diagnosis o Clay-colored stool
 Peritoneoscopy with liver biopsy o Absence of bile salt (emulsifier) in duodenum
o AST/SGOT  N/V
o ALT/SGPT **  Steatorrhea (fat indigestion)
o SLDH  Hypoprothrombinemia  bleeding
 Increased 1 & 2 – myocardial insult Gall Stones
 Increased 3 – lung parenchyma  Metabolic – obese  hypercholesterolenemia  increased
 Increased 4 & 5 – liver disorders concentrated bile  nideus/nucleus  gall stones
Symptoms  Inflammation  alteration in constituent of bile 
 Earliest: hepatomegaly decreased solubility of cholesterol  nidus/nucleus  gall
 Late: Small contracted, atrophic/shrinkage liver stones
 Hypoalbuminemia  Stasis  biliary stricture stasis in flow of bile 
 Hyperaldosteronemia increased concentration of bile  gall stone
 Portal hypertension
o Symptom
 Earliest sign: ascites Cholesterol-filled gallstone dissolver
 Hydrothorax  Chenix, Ursodiol
 Esophageal Varices  Chrnodeoxycholic acid
 Sclerotherapy (Na  Ursodeoxycholic acid
Morrhuate, Sotradecol Na) T-tube
– non-bleeding  To bypass/divert the flow of bile until the post-operative
 Avoid activities that edema subsides
increase abdominal  Prevent bile peritonitis
pressure  Drains only when there is increased biliary pressure
 Output bottle: in line with incision
 Vasoconstrictor:
o Increased output – obstruction (not entering
Vasopressin/Pitressin
Tannate, Epi/Adr. duodenum)
o N: 300-500 mL/24 hrs.
 Tamponade
 Hemorrhoids  Use excoriation barrier to prevent skin irritation when bile
o Shunt drains into skin
 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
MEDICAL SURGICAL NURSING 14
o Edematous pancreatic capsule  left flank pain  Ocular pain
radiating to back/epigrastric pain  vomiting  Headache
o Pancreatic cell necrosis  Loss of peripheral vision/ tunnel vision  bumping objects
 Leukocytosis on sides
 Hyperglycemia (destruction of Islets of  Halos/rainbows around lights
Langerhans)  Acute – eye pain
 Hypocalcemia (trapping of Ca in  Chronic – asymptomatic
feces) Management
 Increased serum amylase and serum  Medications
lipase o Miotic/cholinergic drugs
o Interstitial bleeding  blood-retained  Pilocarpine
retroperitoneal fluid  Carbachol
 Peritonitis (+Blumberg’s sign)  Phyrostigmine
 Rebound tenderness o Carbonic Anhydrase
 Cullen’s sign o B-blocker
 Bluish discoloration around  Timoptic/Timolol Maleate
the umbilicus  Betoptic/Betaxolol
 Turner’s sign o Glycerol/Glycerine PO – decrease IOP
 Bluish discoloration in the  Surgery
left flank area o Trabeculoplasty – open angle
Diagnosis: o Iridectomy/Iridotomy – closed angle
 Lipase – elevated for the next 2 weeks
Management ACID- BASE ALTERATIONS
 Rest GIT – prevent pancreatic stimulation HYDROGEN IONS
o NPO
 Circulate in the body in 2 forms:
o Gastric decompression o Volatile H of carbonic acid
o H2-blocker  Excreted by lungs – 13,000-30,000 mEq/day as
o Antacid CO2  deep breathing
o PPI o Non-volatile form of H and organic acids
 3rd generation antimicrobials  Excreted by the kidneys 50 mEq/day
o Cephalosporin ACIDS
 Plasma expanders  End products of metabolism
o Dextran  Contain H ions
o Haes-steril  H ion donors
o Voluven  Strength determined by the amount of H ions present
EYE DISORDERS  Determines pH of body fluids by its content
CATARACT BASES
 Gradual, painless loss of vision  Contain no H ions
Types  H ion receptors
 Degenerative/Senile  Increase in acids  acidity
 Congenital  Increase in bicarbonate  alkalinity
 Metabolic – DM, malnutrition, severe dehydration, prolonged pH (7.4)
use of steroids  pH of 7 – neutral
 Traumatic – prolonged exposure to UV light  <7 – acid
Diagnosis
 >7 – alkaline
 Slit-lamp microscope/biomicroscope
ACID-BASE BALANCE
Management
 There is continuous acid production from metabolic
 Use of antioxidant – Beta-carotine
processes
 Bifocal magnifying lens
 Ways to remove acid
 Surgery: ICCE, ECCE, Facoemulsification (sutureless o Buffers
technique)
o Respiratory
Complication
o Kidneys
 Bleeding – only after ICCE, ECCE
o Stomach (vomit)
o Severe headache, pain
 Acidic
 Panophthalmitis – faulty aseptic technique
o CO2
o Photophobia
o Urine
o Chemosis
o Stomach
o Hypopion
o Dischagres  Alkaline
o Intestines – from bile and pancreatic juice
GLAUCOMA
 Tonometry – diagnose glaucoma, measures IOP o HCO3 (metabolic)
 Gonioscopy – juncture/angle between the iris & cornea, BUFFER SYSTEMS
diagnoses closed angle glaucoma  Absorb or release H ions as needed
 Closed/Acute – iris and cornea – MEDICAL EMERGENCY!  Fastest acitng regulartory system
 Open/Chronic – trabecular meshwork  Act as sponges
Signs and symptoms  3 main systems
MEDICAL SURGICAL NURSING 15
o Bicarbonate-carbonic acid buffer (body’s major
buffer) RESPIRATORY ACIDOSIS
 HCl + NaHCO3  NaCL + H2CO3  Carbonic Acid Excess
(H2O + CO2)  Exhaling of CO2 inhibited
 H2CO3 – 1.2 mEq/L  Increased H2CO3  retained carbonic acid
 HCO3 – 24 mEq/L  pH falls below 7.35
o Phosphate buffer  Cause: hypoventilation
o Protein buffer o Decreased airway
 Some of amino acids contain free o Decreased compliance
radicals (-COOH), which can o Recoil
dissociate into (CO2) and (H+) Signs and symptoms (CNS depression)
 COOH  COO2 + H  Restless, confusion, apprehension, somnolence
 Cells can also act as buffers by shifting H+ in and out of cell  Asterixis
 Acidosis  Coma
o Increased H in the ECF  cells can accept H+ in
 H/A, papilledema, decreased reflexes
exchange for another cation like K+
 Dyspnea and tachypnea
RESPIRATORY REGULATION
 CV: tachycardia, HTN, atrial and vent.
Mechanism of control
Dysrhythmias
 Hyperventilation – blow off CO2
 Increased serum K, Ca
 Hypoventilation – retain CO2
Compensation
Regulation rapid
o Hyperventilation
 Seconds to minutes reaching maximum effectiveness in
o Problem – depressed breathing, build up of CO2
hours
Treatment
 Measured by PaCO2 – normal (35-45 mmHg)
 Correct underlying cause of alveolar
RENAL REGULATION
hyponventilation
Mechanism of Control
 Artificial airway
 Excretion of retention of H+ or HCO3
Regulation…slow  Removal of foreign body of secretions
 Hours to 2-3 days to change pH  Oxygen inhalation at low flow rate
o SaO2 – amount of oxygen carried by
 Ca maintain balance indefinitely in chronic imbalances
ALTERATIONS IN ACID-BASE BALANCE the hemoglobin
 Imbalances occur when compensatory mechanisms fail  Maintain adequate hydration IV (LR)/PO
o LR changes into bicarbonate in liver
 Classification of imbalances
o Respiratory: affect carbonic acid concentration  Medications: bronchodilators, NaHCO3
o Metabolic: affect bicarbonate  Low CHO, Hi-fat diet – reduces CO2 production
Nursing Management
 Assessment of breath sounds and respiratory
rate; monitor K and Ca levels
BLOOD GAS VALUES  Maintain patent airway
 Arterial blood gas (ABG) values provide information about  Positioning/turning every 2 hrs.
o Acid-base status  Pulmonary hygiene (postural drainage, chest
o Underlying cause of imbalance clapping)
o Body’s ability to regulate pH RESPIRATORY ALKALOSIS
o Overall oxygen status  Carbonic acid deficit
 pH 7.35 (7.4) to 7.45  Increased exhaling of CO2
 PaCO2 35 (40) to 45 mmHg  pH rises above 7.45
 HCO3 22(24) to 26 mEq/L (assumed average values for  Cause: hyperventilation
ABG interpretation) o Hysteria
 PaO2 80-100 mmHg o Over ventilation by mech. vent
 Oxygen concentration >94% o Fever
 Base excess/deficit ±2 mEq/L o Pain
 Compensation:
ACID-BASE IMBALANCES o Hypoventilation
Primary cause of origin: o Problem: increased in breathing = loss of CO2 in
 Metabolic blood
o Changes brought about by systemic alterations o Response: kidney secrete HCO3
(cellular level)  Most common A-B disturbance in critical patients
 Respiratory  Causes:
o Lungs o Hyperventiltion
o Anxiety, fever
Compensation  Signs and symptoms (CNS irritability)
 Corrective response of kidneys and/or lungs o Deep rapid breathing
 Compensated o Light-headedness or dizziness due to dec.
o Restoration of pH and 20:1 ratio cerebral blood flow
 Uncompensated o Agitation, hyperactive reflexes
o Inability to adjust pH or 20:1 ratio o Circumoral and peripheral paresthesias
MEDICAL SURGICAL NURSING 16
o Carpopedal spasms o Confusion
o Decreased serum K, Ca o Twitching
 Nursing management o Tremors
o Teach how to relieve/prevent anxiety o Hypokalemia
o Assist with breathing techniques and breathing o Hypocalcemia
acids as Rx  Treatment
o Positioning for comfort o Treat cause
o Assist with relaxation techniques o Administer Na, K, Ammonium Cl,
o Protection fro injury o Diamox – increase excretions of HCO3
o Meds as Rx  Nursing management
o Ca gluconate for tetany o Monitoring LOC and confusion
o Monitor K and Ca levels o Reorientation, protection from harm
Respiratory acidosis Respiratory alkalosis o Monitor serum electrolytes
Increased PCO2 Decreased PCO2
Increased carbonic acid Decreased carbonic acid Metabolic acidosis Metabolic alkalosis
Increased H+ - low pH (<7.35) Decreased H+ - low pH (>7.35) Decreased carbonic acid Increased carbonic acid
Compensation: increased Compensation: decreased Increased H+ - low pH (<7.35) Decreased H+ - low pH (>7.35)
bicarbonate bicarbonate Decreased bicarbonate Increased bicarbonate
METABOLIC ACIDOSIS Compensation: hyperventilation Compensation: hypoventilation
 Base-bicarbonate deficit
 Low pH (<7.35) Mixed Acid-Base Disorders
 Low plasma bicarbonate (base)  Exists when 2 or more disorders are present at the same
 Cause – relative gain in H+ (lactic acidosis, ketoacidosis) or time
actual loss of HCO3 (renal failure, diarrhea) ABG interpretation
 Compensation: 1. Identify the problem
o Problem: low HCO3 or high H+ ion a. Acidosis vs. alkalosis
o Response: lungs hyperventilate  get rid of CO2 b. Compensated vs. uncompensated
 Causes: HCO3 loss; acid retention 2. Identify the source of the problem
o DM/DKA a. CO2 – 35-45
o High-fat diet; malnutrition b. HCO3 – 22-26
o RF
ALTERATIONS IN FLUID AND ELECTROLYTES
o Severe diarrhea
BODY FLUID DISTRIBUTION
 Signs and Symptoms (CNS depression) By weight
o Hyperventilation  Adult women – 50-55%
o Headache  Adult men – 66-72%
o Dizziness  Elderly – 47%
o Kussmaul resp  Infants – 75-80%
o Weakness By compartment
o Twitching  Extracellular 30%
o Hyper-K and Ca  Intracellular 70%
 Treatment  Intravascular 6%
o Treat cause  Interstitial 24%
o NaHCO3 ELECTROLYTES
 Nursing mgt  Active chemicals that carry positive (cations) and negative
o Frequent assessment of vital signs esp (anions)
respiratory rate and rhythm (compensatory
mechanisms) FLUID BALANCE MECHANISMS
o Reorientation  Kidneys
o Safety precautions for confusion  Lungs
o For ketoacidosis, NaHCO3  Skin
o Education about DM
METABOLIC ALKALOSIS HORMONAL CONTROL
 Bicarbonate excess  ADH
 High pH (>7.45)  Aldosterone
 Loss of H+ ion or gain HCO3  RAAS
 Most common causes vomiting, gastric suctioning (NG tube) o Low BP (low BV and CO)  juxtaglomerular
– loss of acid cells  renin  Angio I – ACE – Angio II 
 Others: abuse of antacids increase BV  VC  increase BP
o Retention of base o Angio II  Adrenal cortex  aldosterone  Na
o K wasting diuretics  Hypokalemia ret.  ADH  fluid retention by renal tubules
 Signs and symptoms (CNS irritability) (decreased UO)  BV  increased BP
o Hypoventilation  ANP (Atrial natriuretic peptide)
o Numbness o Cardiac hormone stored in atrial cells
o Bradycardia o Released when atrial pressure increases (CHF,
CRF, Hi-Na intake)
MEDICAL SURGICAL NURSING 17
o Counteracts effects of RAAS  decreased BP Daily weight – most reliable indicator of fluid loss or gain in all ages
and decreased IV volume (1kg = 1000ml)
Accurate weight: same time, same scale, same amount of clothing
REGULATION OF BODY FLUID VOLUME Gerontologic considerations:
 Hypervolemia  inhibits  thirst, ADH release,  Reduced homeostatic mechanisms: cardiac, renal, and
aldosterone release  increased urination of dilute urine  respiratory function
normal fluid volume restored  Decreased body fluid percentage by 6%
 Hypovolemia  stimulates  thirst, ADH release,  Decreased thirst sensation, fails to drink enough
aldosterone release  decreased urination of dilute urine  Medication use
 normal fluid volume restored  Presence of other concomitant conditions
 UO: 1ml/kg/hr.
MECHANISMS CONTROLLING FLUID MOVEMENT Assessment of Fluid balance:
 Diffusion (solute) HL  BP measurement
 Osmosis (fluid) LH o Indirect
Movement of fluid through capillary walls depends on: o Direct: pulmonary artery caths:
 Hydrostatic pressure – pressure exerted on the walls of  PAP – 15-20mmHg
blood vessels, push  PAWP – 6-12mmHg
 Osmotic pressure – pressure exerted by the protein in the o CVP – 0-7 mmHg, 5-10cmH20
plasma, hold/pull (ITIV)  PE
 The direction of fluid movement depends on the differences  UO
of hydrostatic and osmotic pressure  Weight
OSMOLALITY
 Amount of chemicals (Na, CHON, glucose, Cl, HCO3) Types of Solutions:
dissolved in the liquid part (serum) of the blood Hypotonic Isotonic Hypertonic
 Controlled by ADH Stays put Expands volume
 Osmolality = 2 x Na + Glu/18 + BUN/2.8 Hydrates cells
 N: 285-295 mOsm/kg IV dehydration IV dehydration w/ IT
Cellular dehydration
OSMOLARITY & IC overload
 Drawing power of a solution D5%W
Tap Water
 N: 285-195 mOsm/L RL D10%W
0.45% NaCl
ACTIVE TRANSPORT 0.9% NaCl D5%NSS
0.33% NaCl
 Physiologic pump that moves fluid from an are af lower NS Albumin
concentration to one of higher concentration
 Movement against the concentration gradient **D5W is metabolized rapidly, leaving free water to be absorbed. NOT
 Sodium-potassium pump maintains the higher concentration used in the head injured client  increased ICP
of extracellular sodium and intracellular potassium
 Requires adenosine (ATP) for energy IV Infusions:
o From metabolism aided by oxygen Assess:
Fluid Shifts  Urine output
 Plasma to ITF (edema)  Infusion site
o Due to:  Flow rate
 Increased venous HP  IV container
 Decreased plasma OP  IV tubing
 Increased IT OP
 IT to plasma Reactions:
o Due to:  Infiltration
 Increased plasma OP o DC IV; remove catheter
 Increased IT HP o Apply cold compress within first 30 minutes,
Fluid movement between ECF and ICF warm moist heat
 Increased ECF osmolality (water deficit, Na excess)  cell  Phlebitis
shrinks o Apply warm compress
 Decreased ECF osmolality (water excess, Na deficit)  cell
swells CENTRAL VENOUS LINE
Average daily fluid sources  Flushed daily with Saline or Heparin
 1200-1500 – Ingested water  Change dressing 3x/week
 700-1000 ml – Food  Check for infection
 200-400 ml – Metabolic Oxidation  Discard 5-10 ml when drawing blood
 2100-2900 – Total  Use port for designating purpose
 Valsalva’s maneuver when removing or changing tubing
Average Daily Fluid Loses
 1200-1700 ml – Urine DEHYDRATION
 100-250 ml – Feces Causes Symptoms Care
 350-400 – Skin by diffusion Vomiting Thirst, dry, warm skin Hydrate
 100-150 – Perspiration Diarrhea Poor skin turgor Daily weight
 350-400 – Lungs Diuresis Dark, odorous urine Skin care
Decrease IV Weight loss
MEDICAL SURGICAL NURSING 18
replacement  Helps govern normal ECF osmolality
INTRACELLULAR FLUID VOULME DEFICIT (ICFVD) is:  Helps maintain acid-base balance
 Rare in health adults  Activates nerve & muscle cells
 Often in older adults and in acute water loss  Influences water distribution (with chloride)
The desired outcome is restoration of fluid volume through  Sodium in all body fluids
 IV replacement  NV: 135-145 mEq/L
 Correction of the underlying cause  Major source: Table salt
FLUID VOLUME EXCESS: OVERHYDRATION/ FLUID OVERLOAD Sodium imbalances:
Types:  Hyponatremia - <135
 Isotonic: hypervolemia  circulatory overload & interstitial o Due to:
edema  CHF  Absorption f large volume of isotonic,
 Hypertonic: rare  intracellular dehydration Na free irrigating solution
 Hypotonic: water intoxication, intracellular expansion  Inadequate Na intake
Circulatory overload: o Manifestations:
Causes:  Diarrhea, hyperactive bowel sounds,
 Increased IV fluids abdominal cramps
 Kidney failure  Elevated BP
 Heart failure  Adventitious lung sounds
Symptoms:  Lethargy, confusion
 Tachycardia  Weakness & tremor
 Flushed skin  Dry ski, pale, dry mucous membranes
 Neck vein distention o Treatment:
 Hypertension  IV infusions of saline if with
 CVP (>15 mmH20) hypovolemia
 Tachypnea  Diuretics if with hypervolemia
 Oral sodium replacement
 Cough
 If due to SIADH, give Lithium
 Dyspnea
 Hypernatremia - >135
 Pulmonary edema
o Sodium excess
Management:
o Cause: water loss or sodium gain
 Fluid restriction
o Manifestations:
 Na restriction (if w/ hyperNa)
 Thirst
 Diuretics
 Restlessness
 Digoxin (if cardiac related)  Weight changes
o Treatment:
INTRACELLULAR FLUID VOLUME EXCESS (ICFVE)
 Dilute sodium
 Referred to as water intoxication or hypotonic over-hydration  Promote excretion
 Less frequent  D5W
 Results from either:  Diuretics
o Water excess or  Assess for cerebral edema
o Solute deficit (often sodium)
Manifestations: POTASSIUM
 Headache, nausea, vomiting  Neuromuscular activity
 Behavioral changes: progressive apprehension,  Acid-base balance
disorientation, confusion, drowsiness, decreased muscle  Helps control ICF osmolality & ICF osmotic pressure
strength, weight gain  80% excreted renal
 Vital signs: bradycardia with an increased systolic blood  20% excreted GI
pressure (widen pulse pressure), increased RR, muscle  NV: 3.5-5 mEq/L
twitching  Major source: Fruits (melon, honeydew, cantaloupe)
Effect of potassium on ECG:
ELECTROLYTES
 Moderate hypokalemia – flat T wave
Basic principles in treatment:
 Severe hypokalemia – with U wave
 Electrolyte deficits
 Moderate Hyperkalemia – flat T wave, prominent U wave
o Treatment
 Severe hyperkalemia – no P wave, wide QRS
 Drug supplements
Potassium imbalances:
 Food
Hypokalemia
 Assess complications
o Manifestations:
 Remove cause
 Electrolyte excess  Anorexia, vomiting, diarrhea, paralytic ileus, distention
o Treatment  Muscle weakness, paralysis, leg cramps, muscle
 Antagonist flabbiness
 Hydration  Fatigue, lethargy, decreased DTR
 Remove cause  Confusion, depression
 Assess Treatment:
SODIUM  Administer oral or IV K as prescrived
 Main extracellular fluid cation  Oral K can cause nausea
o Should be with food in the stomach
MEDICAL SURGICAL NURSING 19
o Oral liq prep  Dysrhythmia
 IV potassium  Heart block
o NEVER GIVEN PER IV PUSH, IM, or SC  Critical: cardiac arrest
o A dilution of no more than 1mEq/10ml  Polyuria
o When incorporated to IV sol, invert & shake IV  Bone pain, fracture
bag to mix it Management:
o Max: 5-10mEq/hr not to exceed 20mEq/hr  Discontinue all Ca
o If receiving >10 mEq/hr, connect pt. to a cardiac
monitor MAGNESIUM
o Check site for infiltration. Can cause phlebitis  NV: 1.6-2.6 mg/dl
Hyperkalemia  Cofactor in enzymatic reactions:
Manifestations: o Involving ATP
 Hypotension o DNA replication
 Weaker cardiac contraction o mRNS production
 Explosive diarrhea, intestinal colic  Binds to Ca2 receptors
 Hyperactive bowel sounds  Can block Ca2 channels

Treatment: Hypomagnesimia
 Discontinue all K preparations Cause S&S Treatment
 K excreting diuretic Alcoholism Similar to Adm Mag sulfate IV
 Kayexelate prep (H ion in exchange for K in the intestine); Malabsoprtion hypocalcemia Encourage food high
Cleansing enema first DKA in Mg (meat, fish,
 Dialysis – severe Hyper K Prolonged gastric legumes, cocoa,
suction nuts, whole grain
 IV adm of D10% or 20% 100ml with 10-20 U regular insulin
cereal, vegies)
 Use fresh blood if BT is needed by pt
Meds that decreased
 Avoid food high in K Mg: diuretics,
gentamycin, cisplatin
CALCIUM
 NV: 8.5-10.5 mg/dL Hypermagnesimia
 Extracellular: blocks Na gates in nerve and muscle Cause S&S Treatment
cells Renal failure Flushing hypotension Stop any Mg
 Clotting Addisons Dowsiness supplements or
 99% - bones & teeth Excess replacement lethargy medications with Mg
 1% - serum & soft tissue lithium Restrict food with Mg
 Most activity carried out by ionized Ca Medications with
 9nverse relationship with phosphate increase Mg
 Major source: GLV, dairy products Mg supplements
Hypocalcemia Antacids with Mg
 Manifestations:
 Tetany symptoms: twitching around mouth, BURNS
tingling and numbness of fingers,  Occur when injuryto the tissues
carpopedal spasms, facial spasm, Types:
laryngospasm, later convulsions  Thermal
 Dysrhythmia, palpitation o Caused by flame, flash, scalds, or contact with
 Pathological fracture hot objects
 Prolonged bleeding time o Most common type of burn
 Trousseu & Chvostek
 Management:
 Monitor organ functions  Chemical
 Adm oral and IV calcium as Rx o Result from tissue injury and destruction from
 If given per IV: acids, alkalis, and organic compounds
o Warm injection to body temp o Alkali burns – hard to manage coz they can
o Give slowly & monitor EKG cause protein hydrolysis & liquefaction
 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.
 Mild to moderate hypercalemic state: weakness, o Tissue destruction may continue72hrs after injury
fatigue, depression
 Smoke inhalation
 Severe: extreme lethargy, depressed sensorium, o Result from inhalation of hot ir or noxious
confusion, coma
chemicals
MEDICAL SURGICAL NURSING 20
o Cause damage to respiratory tract Classification of burn injury
o Major predictor of mortality in burn victims  Depth of burn
o Treat quickly! o ABA advocates categorizing the burn according
o Types: to depth of skin destruction
 Carbon monoxide poisoning  Partial thickness burns
 Produced by the  Full thickness burns
incomplete combustion of o Defined by degrees – 1st, 2nd, 3rd, and 4th
burning materials  Extent of burn in percent of TBSA – rule of 9s
 Inhaled CO displaces o Lund- Browder
oxygen o Rule of 9s
o Hypoxia  Location of burn – upper is more dangerous
o Carboxy o Face, neck, chest  respiratory obstruction
hemoglobenimia o Hands, feet, joints, eyes  self care
o Death o Ears, nose, buttocks, perineum  infection
 Treat with 100% humidified o Circumferential burns of the extremities can
O2 cause circulatory compromise
 Cherry red appearance o Patients may also develop compartment
 Inhalation injury above glottis syndrome
 Thermally produced  Patient risk factors
 Hot air, steam, smoke o Older adults heal more slowly than younger
 Mucosal burns of adults
oropharynx & larynx o Physical debilitation render patient less able to
 Mechanical obstruction can recover
occur quickly  Alcoholism
o True medical  Drug abuse
emergency  Malnutrition
 Reliable clues: o Concurrent fractures, head injuries
o Presence of PHASES OF BURN MANAGEMENT
facial burns  Prehospital care
o Singed nasal o Remove the person from the source of the burn and
hair stop the burning process
o Hoarseness, o Rescuer must be protected from becoming part of the
painful incident
swallowing o Electrical injuries
o Darkened oral &  Remove patient from contact with source
mucous o Chemical injuries
membranes  Brush solid particles off the skin
o Carbonaceous  Use water lavage
sputum o Small thermal burns
 Inhalation injury below glottis  Cover with clean, cool tap water-dampened
 Related to the length of towel
exposure to smoke or toxic o Large thermal burns
fumes  Airway, breathing, and circulation
 Pulmonary edema = 12-  Do not immerse in cool water or pack with
24hrs after the burn ice
 Manifests as ARDS  Removed burned clothing
 Wrap in clean, dry sheet or blanket
 Inhalation injury
 Observe for signs of respiratory
distress or compromise
 Electrical  Treat quickly
o Result from coagulation necrosis caused by
intense heat generated from and electric current  Emergent
o May result from direct damage to nerves & o Period of time required 2to resolve immediate
vessels, causing tissue anoxia & death problems
o Severity depends upon: o Up to 72 hours
 Amount of voltage o Hypovolemic shock and edema
 Tissue resistance o Burn shock phase
 Current pathways o Begins with fluid loss and edema formation and
 Surface area continues until fluid mobilization and diuresis begin
 Duration of the flow o Pathophysiology
o Iceberg effect – severity of damage is underneath Fluid and Electrolyte shifts
o Patients are at risk for dysrhythmia, severe  Greatest threat is hypovolemic shock,
metabolic acidosis, and myoglobinuria caused by a massive shift of fluids out
 Cold thermal of BV as a result of increased capillary
o Frostbite permeability
MEDICAL SURGICAL NURSING 21
 Colloidal osmotic pressure decreases  Other care measures
 The net result of the fluid shift is IV  Facial care
volume depletion o Performed by the open method
 Normal insensible loss- 30 -50 ml  Eye care for corneal burns
 Severely burned patient- 200 to 400  Hands and arms should be extended and elevated on
ml/hr pillows or slings
 RBCs are hemolyzed by a circulating  Ears should be kept free of pressure
factor released at the time for the burn o No use of pillows
 Thrombosis
 Perineum must be kept as clean and dry as possible
 Elevated hematocrit
 Early ROM exercises – while bathing
 Na shift into interstitial; spaces and
 Drug therapy
remains until edema formation ceases
 K shift develops because injured cells  Analgesics and sedatives
and hemolyzed RBCs release  Tetanus immunization
Inflammation and healing o Given routinely to all burn patients
 Neutrophils and monocytes  Antimicrobial agents
accumulate at the site of the injury o Topical agents
Immunologic changes  Silver sulfadiazine (Silvadene)
 Burn injury causes widespread  Mafenide acetate (Sulfamylon)
impairment of the immune system o Systemic agents are not usuallu used in
 Skin barrier is destroyed controlling burn flora
 Bone marrow is depressed  Nutritional therapy
o Clinical manifestation  Fluid replacement takes priority over nutritional needs
 Shock from pain and hypovolemia  Early and aggressive nutritional support within hours of
 Blisters burn injury
 Adynamic ileus o Optimizes wound healing
o Complication  Hypermetabolic state
 CV o Resting metabolic expenditure may be
 Impaired microcirculation and increased by 50% to 100% above normal
increase viscosity o Core temperature is elevated
 Upper respiratory injury o Caloric needs are about 5000 kcal/day
 Edema formation o Early continuous enteral feeding
 Lower airways
 Direct insult at the alveolar level  Acute
 Intersititial edema o Mobilization of extracellular fluid and subsequent diuresis
 Urinary o Concluded when the burned area is completely covered with skin
 Renal failure grafts, or when the wounds are healed
o Management o Pathophysiology
 Airway management  Diuresis from fluid mobilization occurs, and the patient is less
 Early ET intubation edematous
 Escharotomies of the chest wall  Bowel sound return
 Fiberoptic bronchoscopy  Healing begins when WBCs surround the burn wound and
 Humidified air and 100% O2 phagocytosis occurs
 Necrotic tissue begins to slough
 Fluid therapy  Granulation tissue forms
 Parkland (Baxter) formula  A partial thickness burn wound heals from the edges
 Colloidal solutions – after 48 hours  Full thickness burns must be covered by skin grafts
 Two large bore IV lines for > 15% TBSA o Clinical manifestations
 Type of fluid replacement based on size/depth of burn,  Partial thickness wounds form eschar
age and individual considerations o Laboratory values
 Sodium
 Hyponatremia
o Excessive GI suction
o Diarrhea
 Wound care  Water intoxication
 Should be delayed until a patent airway adequate  Hypernatremia
circulation, and adequate fluid replacement have been o Successful fluid replacement
established o Improper tube feedings
 Cleansing  Potassium
o Can be done in cart shower, shower, or bed  Hypokalemia
 Debridement o Complications
o Need to be done in the OR  Infection
o Loose necrotic skin is removed  May progress to transient bacteremia  sepsis
o Allograft or homograft
 Usually from cadaver  Neurologic system
 Typically used with newer  No problem unless there is severe hypoxia
biosynthetic options
 MEDICAL SURGICAL NURSING 22
 Hallucinations
 Delirium GENITOURINARY DISORDERS
 Transient state Functions of the Kidneys
 Musculoskeletal  Urine formation
 Decrease ROM o Glomerular filtration
 Contractures o Tubular reabsorption
 GI o Tubular secretion
 Paralytic ileus  Excretion of waste products
 Diarrhea o Urea (major)
 Constipation o Creatinine, phosphates
 Curling’s ulcer o Sulfates, uric acid
 Endocrine  Regulation of electrolytes
 Increase blood glucose levels o Sodium
 Increased insulin production o Potassium
 Hyperglycemia  Regulation of acid-base balance
o Nursing and Collaborative Management o Phosphoric, sulfuric acid
 Wound care o Buffers: phosphate ions, ammonia
 Daily observation  Control of water balance
 Enzymatic debridement o ADH (vasopressin)
o Speeds up removal of dead tissue from  Control of BP
health wound bed o RAAS
 Excision and grafting  Regulation of RBC production
 Eschar is removed down to the SC tissue or fascia o Erythropoietin
 Graft is placed on clean, viable tissue  Located at costovertebral angle
 Wound is covered with autograft Diagnostic Tests
 Donor skin is taken with dermatome  Laboratory tests
 Cultured epithelial autographs (CEAs) o Routine urinalysis
o Grown from biopsies obtained from o Creatinine clearance
patient’s own skin o Blood studies: BUN (8-25 mg/dl), serum
o Used in patients with a large body surface creatinine (0.6-1.3 mg/dl), creatinine
burn area or those with limited skin for clearance (85-135 ml/min), serum
harvesting electrolytes
 Artificial skin  Cystoscopy
 Pain management  Abdominal X-ray (KUB)
 Patients experience two kinds of o IV Pyelography
pain Percutaneous Renal Biopsy
o Continuous  Check VS; urine color; bleeding at site
background pain  Bedrest after procedure
o Treatment induced  If there is a suspicion for a kidney mass
pain  Done in the OR
 Nonpharmacologic
o Relaxation A. Acute Renal Failure: sudden, potentially reversible
o Visualization, guided  Causes
imagery o Pre-renal: r/t decreased renal perfusion (shock, trauma,
 Physical and Occupational therapy dehydration, CHF, cardiogenic shock)
 Good time fr exercise during o Renal: r/t structural renal damage (acute tubular necrosis,
wound cleaning BT, AGN, nephrotoxic infection)
 Nutritional therapy o Post-renal: r/t mechanical obstruction within urinary tract
 Psychosocial care
 3 phases
 Rehabilitative
o Oliguric/ anuric phase
 Begins when wounds are healed by primary intention or by
 8-15 days- output <400 ml/day. Toxins
grafting
accumulate- metabolic acidosis – Azotemia
 4-6 weeks – area becomes raised and hyperemic
(increased BUN, creatinine), hyperK
 Mature healing – 6 months to 2 years
 Decreased pH, bicarbonate, Na, and Ca;
 Discoloration of scar fades with time
azotemia (elevated serum levels of urea,
 Pressure can help keep scar flat
creatinine, and uric acid
 Healed areas must be protected from direct sunlight for 1
year
o Early diuretic phase
 Newly healed areas can be hypersensitive or hyposensitive
to cold, heat, and touch  Extends from the time daily output >400
 Complications ml/day- BUN stops increasing, UO >3-5
o Contractures L/day, hyponatremia, hypokalemia, change
in LOC; 2-3 weeks
o Recovery phase
Emotional needs of the family
o A common emotional response is regression  Extends from 1st day BUN falls to the day it
returns to normal; 3-12 months
o Early psychiatric intervention
MEDICAL SURGICAL NURSING 23
B. CRF: Gradual progressive and irreversible loss of renal function o AntiHTN (HTN- because of fluid retention), diuretics
 Causes o Epogen – stimulate bone marrow to produce RBCs
o Pre-renal: gout, DM, subacute bacterial o Antipruritics; good skin care
endocarditis o Dialysis for hyperkalemia and fluid imbalances
o Renal: SLE, CGN, polynephritis o Assess for infection, cardiac arrhythmias
o Post-renal: BPH
 Phases Types of Dialysis
o Decreased renal reserve: BUN normal; polyuria;  Hemodialysis
GFR: 35-50% o Removes wastes and fluids rapidly than PD
o Renal insufficiency: BUN, creatinine- slightly o Removes toxic wastes and impurities
elevated; GFR: 20-35% o Blood removed from surgically created access site 
o Renal failure: BUN, creatinine increased; with dialyzing unit  osmosis, diffusion
physical manifestations; GFR: 20-25% o CRF
o ESRD: atrophy and fibrosis of renal tubules; GFR  Vascular access
<20%, BUN, creatinine – high levels, oliguria  Temporary- subclavian or
ARF Interventions femoral
 Dialysis  Permanent- shunt, in arm
 Monitor F&E, acids and bases; observe for fluid overload o Care post insertion
 Moderate CHON restriction, high in calories, CHO, low K  Can be done rapidly
 I&O, weigh daily, monitor creatinine and BUN  Takes about 4 hours
 Fluid restriction  Done 3x a week
o Renal shutdown program o Access routes:
 Replaces actual losses  Subclavian cath
 Actual urine output and insensible loss  AV shunt
 Diuretic therapy to treat oliguric phase  AV fistula
 Sodium polystyrene sulfonate (Kayexalate)  AV graft
 Monitor for patient’s response to medications o Nursing Responsibilities
 Monitor for infection and anemia  Monitor venous access site for bleeding
CRF  Don’t use arm for BP, IVT, or venipuncture
 Manifestations:  Auscultate for bruits and palpate for thrills
o Azotemia, metabolic acidosis  Weight before (wet weight) and after (dry
o Altered LOC due to accumulation of wastes weight) the procedure
 Monitor for shock and hypovolemia
o Irregular heart rate
(because of too much pressure);
o Yellow bronze skin due to altered metabolic process
disequilibrium syndrome
o Dry, scaly skin and severe itching due to uremic frost
 Occurs after dialysis; rapid
o Proteinuria, glycosuria (because of hyperglycemia – change in the composition of the
delay in release of insulin in uremic patients and ECF during dialysis
decreased sensitivity of cells to insulin)  Solutes removed from blood
o Diminished erythropoietin secretion- anemia faster than from CSF and brain
o Renal phosphate excretion and vitamin D synthesis  fluid pulled into the brain 
are diminished K secretion increases cerebral edema
o Hypocalcemia – bleeding tendencies, osteoporosis  Symptoms: N/V, H/A, HPN,
 Interventions restlessness, agitation, seizures
o Dialysis, monitor I&O, F&E, manage symptoms  Peritoneal
o Kidney transplant o Removes toxins from the blood - uses peritoneal
 Must find donor membranes as a semi-permeable dialyzing membrane
 Waiting period long o Phases
 Good survival rate – 1 year 95-97%  Infusion/inflow time (5-10 minutes)
 Must take immunosuppressant for life  Dwelling phase (20-30 minutes)
 Donor sources: relative/ cadaver  Drainage/ outflow phase (20-30 minutes)
o Nursing care:  Solution is drained taking toxins
 Pre-op: Routine care; psycho-spiritual care; and wastes with it
discuss: verbalize expectations, dialysis, o CRF
immunosuppression  Peritoneal dialysis
 Post-op care: ICU, I/O, BP, weight changes,  Semipermeable membrane
electrolytes, may have fluid volume deficit,  Catheter inserted through
high risk for infection; Assess for acute abdominal wall into peritoneal
rejection (4 days-2 years) - Symptoms: cavity
oliguria, fever, pain and tenderness over
 Cost less
transplant site, increased WBC (unusual
 Fewer restrictions
inflammatory reaction, symptoms of RF
o Low CHON diet- limit accumulation of end products of  Can be done at home
CHON metabolism  Risk of peritonitis
o Fluid restrictions  3 phases – inflow, dwell, and
o Monitor for fluid overload outflow
 Automated peritoneal dialysis
MEDICAL SURGICAL NURSING 24
 Done at home at night o For C&S: catheterized or clean catch
 Maybe 6-7 times/week
 A small portable machine called Classification
a cycler performs the exchanges  Acute/ Chronic
of PD solution automatically  Upper/ Lower
 Connects to cycler at HS and  Ascending/ Descending
cycler performs exchanges
overnight Urinary Tract Infection
 CAPD  Signs
 Continuous ambulatory o Frequency, urgency, dysuria
peritoneal dialysis o Hypogastric pain
 Done as outpatient o Malaise
 Usually 4x/day o Fever, chills
 Doctor orders number of o N/V
exchanges o Low back pain
o Considerations o Urinalysis findings
 Warm the dialysate: 37-38 deg C (dry  Complications
heating: microwave or dialysate warmer o Stenosis
pad) o Obstruction
 Incorporate meds after warming o Ulceration
prior to infusion
o ALL COULD LEAD TO RENAL INSUFFICIENCY 
 Measure I&O
RENAL FAILURE
 Check outflow rate
 Facilitate ouflow: Fowler’s, gentle bladder
Management
pressure
 Maintain strict asepsis: Assess site for  C and S before antibiotic therapy
redness, exudate, tenderness  Increase fluid intake (3 L/day)
 Monitor BUN, creatinine, VS, I&O, signs of  If alkaline urine: acidify, acid ash diet (meat, fish, eggs, foul,
sepsis cheese), vitamin C, aminoglycosides (Streptomycin)
 Avoid increase intra-abdominal pressure  If acidic urine: alkalinize; alkaline ash diet (milk, vegetables,
(coughing, Valsalva straining)  hernia fruits), NaHCO3, Methenamine, Nitrofurantoin
(inguinal, incisional, umbilical), leaks and  Perineal hygiene especially sexual intercourse
GERD  Regular bladder emptying
 Measure weight: before and after draining  Hot sitz bath
dialysate (dry weight)
 Maintain adequate nutrition: adequate OBSTRUCTIVE UROPATHIES
CHON (clean – egg white), vitamins (FA, UROLITHIASIS/ NEPHROLITHIASIS
B6, C)  Formation of stones in the urinary tract secondary to precipitates
o Complications caused by stasis, altered purine metabolism
 Peritonitis  Risk factors
o Diet high in calcium and CHON
Transplant Meds o Urinary stasis
 Corticosteroids o Dehydration – increases urine concentration
 Cytotoxic- inhibit T and B lymphocytes o Obstructive disorders
 T-cell depressors o Metabolic disorders – uric acid accumulation
o UTI  alkaline stones
Urinary Problems o Prolonged immobility
I. Urinary Infections URINARY CALCULI (UROLITHIASIS)
 Pyelonephritis  Types of stones: Staghorn (fixed) and free
 Perinephric abscess/ renal carbuncle o Ca Oxalates phosphates
 TB of the kidney o Uric acid
 Cystitis  Signs
o Colicky pain: colic, severe flank pain radiating to
Predisposing factors
vulva or testes
 Urinary stasis and obstruction o N/V
o Most common
 Management
o Result in:
o Fluids, ambulation
 Poor urinary drainage
o Pain control
 Dilatation
o Alkaline stones  ascorbic acid, lithostat, acid
 Stasis of urine
ash, low Na, Ca, CHON diet, avoid oxalate-rich
 Presence of foreign body
o Acidic stones  alkaline ash, Na HCO3, avoid
 Lowered body resistance
purine, Allopurinol, avoid cysteine-rich (lechon,
 Neurogenic bladder dysfunctions
chicken)
 Bacteriuria: conclusive of UTI o Low purine diet for uric acid stones
o E. Coli- most common
o Surgery
o Clean catch midstream urine
MEDICAL SURGICAL NURSING 25
 Urolithotomy/ nephrolithotomy  Ebola/MERS-CoV
(nephrostomy tube) SIRS (Systemic Inflammatory Response Syndrome)
 ESWL – extracorporeal shockwave  Severe systemic response to a condition (trauma,
lithotripsy infection/sepsis, burn)
BENIGN PROSTATIC HYPERPLASIA  Provokes an acute inflammatory reaction indicated by 2 or
 Increased androgen activity more s/s (CRITERIA)
Manifestations o Abnormally up or low body temp
 Urinary frequency  Less 36C (96.8 F) or more 38C
 Urinary dribbling (100.4F)
 Strain upon urination  hematuria o PR more than 90 bpm
 Increased residual urine (N: 5-10 mL) o RR more than 20 bpm
Interventions o Low CO2 in arterial blood – less 32 mmHg (35-
 Administer Finastride (Proscar) – reduce size of prostate 40)
 Surgical removal of prostate – chronic hematuria, infection, o WBC significant up or down – less 4K or more
hydronephrosis, hydroureter o Immature neutrophils – >10%
o TURP – resectoscope or laser inserted thru urethra to Other Causes
remove adenoma  Pancreatitis
o Suprapubic – incision in abdomen and bladder  Hemorrhage
o Retropubic – abdominal incision  Ischemia
o Perineal – bet scrotum & anus – highest risk for  Complications of surgery
impotence  Adrenal insufficiency
 CBI (Continuous bladder irrigation) after surgery to promote  PE
hemostasis and limit clots that block the catheter  Complicated aortic aneurysm
 Hyperplasia  engage in sex  release of prostatic fluid upon  Cardiac tamponade
ejaculation  Anaphylaxis
PROSTATE CANCER  Drug overdose
 Metastasis to bony pelvis and spine  Polypropylene Mesh Surgical Implant
 Biopsy o Tissue implants for urogyne
 Interventions Management
o Radical prostatectomy  Treat underlying cause
BLADDER CANCER  Antioxidants (improve s/s)
 Risk factors o Selenium
o Male 50-70 years o Glutamine (Gln or Q)
o Smoking  Essential amino acids
o Exposure to aromatic amines o Vitamin E
o Cytoxan exposure o Eicosapentaenoic acid (EPA)
o Chronic bladder infection  EPA or icosapentaenoic acid
 Surgical Management  Omega-3 fatty acid
o Removal fo the bladder with diversions  Fish oil, human breast milk, cod liver
o Ureterosigmoidostomy oil
o Cutaneous Ureterostomy  Salmon, sardines, seaweeds
 Ileal conduit Complications
o Nursing care  Acute lung injury  ARDS  prone (decrease
 Care of the stoma - assess for possible compression, expand alveoli)
obstruction  Acute kidney injury
 Prevent skin breakdown  Shock
 Wash skin around stoma with  Multiple organ dysfunction syndrome (MODS)
mild soap and water
 Measure I&O MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)
 “MOF” Multi-organ failure
ACUTE BIOLOGIC CRISIS  “MSOF” Multi-system Organ Failure
 Conditions that may result to patient mortality if left  Altered organ function in an acutely ill patient requiring
unattended in a brief period of time medical intervention to achieve homeostasis
 Conditions that warrants immediate attention for  Homeostasis cannot be maintained without intervention
o Reversal of disease process  Involves 2 or more organ systems
o Prevention of further morbidity and mortality Causes
 Cardiac failure and dysrhythmias  Infection
 Respiratory failures, S. Asthmaticus and ARDS/PE  Injury (accident, surgery)
 Renal Failure & ESRD  Hypoperfusion
 Burns  Hypermetabolism
 Hepatic Coma  Sepsis (most common)  septic shock
 Diabetic Ketoacidosis/HHNKC  SIRS
 Thyroid crisis & adrenal crisis Pathophysiology
 Multi-organ failure, SIRS and shock  Causes  uncontrolled inflammatory response  final
 Aortic aneurysms/CVA/ACS stage of a continuum SIRS (systemic inflammatory response
MEDICAL SURGICAL NURSING 26
syndrome) + infection  sepsis  severe sepsis  MODS
 death
 Respiratory failure (72 hours post-insult)  Hepatic failure
(5-7 days)  jaundice, icteric sclera  GI bleeding (10-15 EMERGENCY AND DISASTER NURSING
days)  Renal failure (11-17 days)  Death (3 weeks)  Concept of emergency is whatever the patient or family
Pathophysiology Theories considers it to be
 Gut hypothesis (most popular) Emergency Nursing
o Splanchnic hypoperfusion  mucosal ischemia  Specialized education, training and expertise in assessing
 structural and cellular function changes  and identifying patient’s health care problems in crisis
increased gut permeability  changed gut situation
immune function  increased bacteria  Within a time-limited, high-pressured care environment
translocation  hepatic dysfunction  spread of
toxins into system  activates immune response Issues in “E” Nursing Care
 tissue injury + organ dysfunction  Diversity of conditions and situations
 Endotoxin macrophage hypothesis  Legal issues
o Gram-negative infections  cytokines are  Occupational health and safety risks
produced and released  release of endotoxins  Providing holistic care in a fast-paced technology-driven
(tumor necrosis factor-alpha, interleukin-1, environment
interleukin-6, thromboxane A2, prostacyclin,  Disaster nursing
platelet activating actor, nitric oxide) o Weapons of terror and mass destruction
 Tissue hypoxia-microvascular hypothesis o Exposed to biologic and other weapons
o Macro and microvascular changes insufficient o Mass casualty incident
supply of oxygen occurs
o Hypoxemia Consent and Privacy: Documentation
o Cell death and organ dysfunction  Consent to examine and to treat
Diagnosis Exemptions: all 3 must be present
 Sepsis-Related Organ Failure Assessment (SOFA) score o Unconscious/in critical conditions
1994 o Unable to make decisions
o Multiple organ dysfunction score o Without family and friends
o Describe and quantitate the degree of organ  Statement of privacy policy of the institution
dysfunction in six organ system o HIPAA (Health Insurance Portability AND
o Using similar physiologic variables Accountability Act)
Stages o Patients with violent events/high profile cases
 Stage 1  Alias
o Mild respiratory alkalosis + oliguria  Limited access to patient’s profile
o Hyperglycemia  “Extra privacy”
o Increased insulin requirements
 Stage 2 Limiting Health Risk Exposures
o Tachypneic  Strict universal precaution
o Hypocapneic + hypoxemic o Blood borne diseases
o Moderate liver dysfunction  Personal High-Efficiency Particulate Air (HEPA) filter masks
o Possible hematologic abnormalities (N95)
 Stage 3 o MDR TB
o Develops shock + azotemia o SARS
o Acid-base disturbances o Ebola/MersCoV
o Significant coagulation abnormalities  Decontamination Procedures
 Stage 4 o Highly contagious organism
o Vasopressor dependent o Hazardous chemicals/gases
o Oliguric or anuric o Radiation
o Ischemic colitis o Acts of terrorism
o Lactic acidosis follows o Natural/man-made disasters
Management
 No agent that can reverse established organ failure Violence in “E” Department
 Supportive care  Effects of substance abuse, injury/other “E”
o Safeguarding hemodynamics, respiration  Emotionally labile
 Adequate tissue oxygenation (primary target)  Feuding gangs/families
 Enteral nutrition o Separate rooms
o Within 36 hrs. of admission to ICU  Measures
 Human recombinant activated protein C (activated o Security officers
drotrecogin alfa) “Xigris” o Silent alarm systems
o Reduce 28-day mortality o Metal detectors
o Anti-thrombotic  Prisoners/underguard
o Anti-inflammatory o Handcuffed to bed
o Profibrinolytic properties o Ensure safety to staff and other patients
o Improve outcomes in people with severe sepsis o Hand/ankle restraint never released
MEDICAL SURGICAL NURSING 27
o Guard always present o Be aware of hospital policy and state laws for
o Patient face down evidence collection
 To avoid head-butting, biting, spitting  Advanced directives
 Restraints used on violent patients o Durable power of attorney
PRN o If DNR, but a near kin is saying to save the
 Chemical restraints PRN patient, do code
 Gunfire
o Measures: in the following order Certifications for Emergency Nursing
 Self-protection (priority)  BCLS/BLS (Basic Cardiac Life Support)
 Control by security and police officers o Noninvasive assessment and management skills
 Care provided to injured for airway maintenance and CPR
Helping Family Cope with Sudden Death  ACLS (Advanced Cardiac Life Support)
 Private place o Invasive airway management skills,
 Talk with family together pharmacology and electrical treatment, special
 Reassure everything possible was done resuscitation (AED) Automatic External
 Encourage group support Defibrillator
 Avoid giving sedation to family  PALS (Pediatric Advanced Life Support)
 Encourage viewing of body
 Spend time with family Principles of Emergency Nursing
 Encourage verbalizations  Triage
 No volunteering unnecessary information  Primary Survey and resuscitation interventions
Principle of emergency care o Quick assessment
 Triage (French “trier”)  Secondary survey and resuscitation interventions
 (To sort, to choose) o Detailed head to toe assessment
o Sort patient into groups based on severity of  Care of the ER patient
health problems and immediately of treatment  Disposition  morgue
o Management of priorities  Case management
o Levels of acuity o Allocate the resources
o Highest acuity  Patient/family health teaching
 Receive quickest evaluation,
treatment Triage under Mass casualty conditions (Disaster Triage)
 Prioritized resource utilization (x-rays,  Disaster situation
labs, CT scan) o Number of casualties exceed resource
HOSPITAL TRIAGE capabilities
Levels  Emergent (class I/red tag)
 Resuscitation o Airway compromise, hemorrhagic shock
o Prevent death  Urgent (class II/yellow tag)
o Shock, anaphylaxis, severe hypoglycemia o Needs treatment within 30 min.-2 hrs.
 Emergent o Open fractures, large wounds
o Prevent major life threatening situation  Non urgent (class III/green tag)
o Profuse bleeding, status epilepticus with no RF, o Treatment delayed >2 hrs.
PE with no RF o Closed fractures, sprains/strains, contusions,
 Urgent abrasions
o Non-life threatening o “Walking wounded”
o Requires 1 or 2 resources  Expectant (class IV/black tag)
 Med by IV or IM, invasive procedures, o Expected and allowed to die; dead
imaging studies, frequent monitoring o Massive head trauma, high cervical SCI,
o Pneumonia, abdominal pain, complex lacerations extensive burns
 Non-urgent Psychological Reactions secondary to disaster
o Need only 1 resource  Panic
o Simple fracture, viral symptoms  Hysteria
 Minor  Despair
o No resources needed  Depression
o Simple rashes Principles of Mass casualty principles
Legal & Ethical Issues in ER  Triage
 Negligence – doing your work improperly  System of notification/activation of “E” preparedness
 Malpractice – going beyond your scope o Group paging systems, instant electronic based
 “Good Samaritan Laws” alert messages, TV flash alerts
o May protect private citizens  Hospital “E” prepared ness: Personnel roles and
o But usually do not apply to emergency personnel responsibilities
on duty o Hospital incident commander, medical command
o “Abandoned or isolated place” (Phils.) physician, triage officer, public info officer
 Informed/implied consent  Event resolution
 Duty to report suspected crimes to the police o Deactivating “E” response plan
 Duty to gather evidence in criminal investigations o Resume normal operations
MEDICAL SURGICAL NURSING 28
 Debriefing  Check expiration date
o Promote effective coping strategies FIRE DRILL
o Every 6-12 months
Phases of Mass Casualty Disaster of “E” Management o Search for fire
 Mitigation o Wet linens, towels
o Reduce damages before disaster o Door, windows
o Public Education o Appliances, plugs, outlets
o Coning, land use management o All things on 1 side (hallway)
o Fire wall door
 Preparedness o Fire hazards
o Enhance ability to respond to disaster
o Develop plans of action in response to disasters
o Practice drills and exercises for “E” personnel HEAT-RELATED ILLNESSES
o Putting warning systems in place o Heat exhaustion
o Developing evacuation plans o Heat stroke
 Response o Risks
o Responding safely to an emergency o Meds (anticholinergics, diuretics, phenothiazines
o Includes actions taken to save lives and prevent (thorazine), anti H2, antidepressants
further property damage in an emergency  Sweat production
situation o Betablockers, ACE inhibitors
o Response is putting your preparedness in action  Restrict blood flow to skin  impair
 Rehabilitation/recovery release heat
o Both short-term and long-term o Amphetamines, cocaine
o Begins after disaster  Increased muscle activity, body heart
o Purpose: o ETOH
 Restore community to a normal state  Excrete more body H2O
o Risks
Mass evacuation (hospital) o Dehydration
 Ambulatory 1st o Lack of sleep
 Wheelchair next o Fatigue
 Bed bound last o Obesity
 Unit manager can authorize patient evacuation o Strenuous activities
 Evacuation plan HEAT EXHAUSTION
Common reasons for going to ER o Syndrome caused by dehydration during heat exposure over
 Chest pain hrs-days
 Abdominal pain o Precursor to heat stroke
 Headache o Not true medical “E”
 Fever o S/S
Common “codes” used in the hospital setting o Flu like s/s + diaphoresis + GI s/s
 Code blue o Temp not significantly increased (normal or
o Members (MD, floor/unit RN, respiratory subnormal)
therapist, pharmacist, ICU RN) o Moist clammy skin
o Dead patient o Management
 Rapid Response Team o Bed rest in cool place; legs and feet up 12-18
o Response team in a nearly dying patient inches
o Same members as in code blue team o Constrictive clothing removed
o Prevent “code blue/death” o ORS/sports drink (Gatorade) if alert
 Code gray – violence o Cold packs (neck, arm pits, chest, abd, groin)
 Code red  Abundant blood supply
o Fire o Soak person in cool water
o Deactivated ONLY by head of security o Fan while spraying person’s skin
 Code black – bioterrorism, bombing o Crushed Na tabs dissolved in adequate H2O
 Code pink  Prevent GI s/s
o Baby is being stolen o Prevent sun exposure (10a-4p); use sunscreen
o Deactivated ONLY by head of security SPF >15
 Crash Cart o If no improvement in 30 min. – seek medical
FIRE EXTINGUISHER attention
 PASS method HEAT STROKE
o P pull the pin o Failure of heat regulatory mechanism
o A aim the spout o Body temp exceeds 40.5 C (105 F)
o S squeeze the handle o Organ dysfunction  death
o S sweep the fire o Risk factors
o Strenuous physical activity/wearing thick clothing
 Do not use to extinguish BIG fire
in hot humid conditions
 Monthly inspection by the fire/security department
o Chronic exposure to hot humid weather
MEDICAL SURGICAL NURSING 29
o s/s  Nitrogen bubbles formation due to rapid changes in
o Dry, hot skin, neuro changes atmospheric pressure
o Presence of sweat does not rule out presence of  In joints (shoulder)/muscle spaces
heat stroke  Air embolism  stroke paralysis, death
o Treatment  Management
o Patent airway o Obtain detailed history
o Rapid cooling measures o ABC – 100% O2
 Ice packs (necks, groins, arm pits) o CXR/VQ scan – Pulmonary embolism
 Cold water immersion o IV Plain NSS/LRS
 Wet body with tepid H2O + rapid o Lower HOB/Left lateral
fanning  If suspect air embolism
 stop cooling till temp drops to 102 f  Trap air in apex ventricle  prevent
o At the hospital going to lung circulation
 O2 via NC or mask o HBO/Recompression chamber
 Large bore IV cannula/needle  Hyperbaric O2
 IVF NSS
 Cooling blankets
 No ASA/antipyretics
 Aggravate coagulopathy NEAR DROWNING
FROSTBITE  Recovery post submersion
o Cold-related injury that may or may not be associated with  Leads to death by suffocation from submersion in the liquid
hypothermia medium (water)
o Cause  Prevention
o Inadequate insulation against cold o No swimming alone
o Skin exposed to cold o Test H2O depth before diving head 1st; never
o Insufficient clothing dive in shallow water
o Risk o No ETOH
o Smokers, ETOH, PVD o Enough H2O rescue equipment readily available
o Early s/s  First aid
o White waxy areas on nose, cheeks, ears o Patent airway; spine stabilization
o Treatment o Ventilator support (CPR)
o First aid  Hospital care
 Body heat (superficial type) o O2 treatment
o Hospital o ET PRN
 Rapid rewarming in H2O bath o GI decompression PRN
 Fresh water drowning
HIGH ALTITUDE ILLNESSES o Water fills lungs + bloodstream
o Elevations > 5K ft.
o Blood cells swell, burst
o O2 decreased  hypoxia
o Fluid in lungs prevent air going in lung  cardiac
o Acclimatization
arrest
o Compensation to high altitude o Hypotonic aspiration
o 3 conditions resulting from high altitude
 Salt water drowning
o Acute mountain sickness o Salt water fills lungs
o High altitude cerebral edema o Salt H2O draw blood from bloodstream into lungs
o High altitude pulmonary edema  liquid build up in alveoli  O2 not reach
o Risk blood  cardiac arrest  drowning in your own
o Rapid ascending (most common) fluids
o Sleeping at 8k elevations o Hypertonic  hemoconcentration
o Treatment  Management
o First aid o ABC
 Descent to lower altitude areas o ET with PEEP ( Positive and Expiratory
 1600-3300 ft. Pressure)
o Rest o O2
o O2  CPR  CAB (min. of 100 bpm)
 ABG
DECOMPRESSION SICKNESS (DCS)  Rewarming
 “the bends”, caisson disease  ECG
 “chokes”, “staggers”  Foley catheter
 Incidence ANAPHYLACTIC REACTION
o Diving  Acute systemic hypersensitivity reaction within few
o Rapid ascent seconds/minutes
o Loss of air in tank  Ex: meds, other agents (insect sting, bees), food
o High latitude flying  S/s
o Flying in commercial aircraft within 24 hrs. post- o Respiratory symptoms
diving o Drop BP (massive vasodilation)
MEDICAL SURGICAL NURSING 30
 Treatment o Weight, serum lytes
o Patent airway o Hydration (IVF) 1L/kg
o Epinephrine SQ/IM injection followed by AntiH2 o Food, gastric content, serum, feces analysis
drug o Antiemetics
o Lactus bacillus
POISONING  Acidophilus (Lactinex, Erceflora
 Swallowed poisons (corrosive)  Yogurt, Yakult
o Alkaline (detergent, bleach, button batteries, SNAKE BITES
oven cleaners)  Pit vipers (Crotalidae)
o Acid (bowel cleaners, rust removers, metal o Most frequent poisonous snake bites (triangular
cleaners, pool cleaners) head)
 Can cause multiple organ failure esp. neuro
 Treatment  Treatment
o Offer 3 glasses of milk/water via NGT to dilute o Immobilize injured part below the heart
poison o Cleanse cover wound
o Bring unused poison to hospital for identification o Do not use ice/tourniquet, heparin,
o Do not induce vomiting just keep on NPO corticosteroids during acute stage (6-8 hrs.)
o If not sure of cause of poisoning – CALL Poison  Ice/tourniquet  decreased
Call Center circulation  necrosis
o (02) 524 1078 (Philippines)  Corticosteroid  depress Ig
OVERDOSE production  hinder antivenin action
 Ipecac (Ipecacuanha plant)
 Treatment o No ETOH, caffeine
o Ipecac to induce vomiting EXCEPT in corrosive  Up venom absorption
substances o Never leave patient; bring snake to hospital
o Gastric lavage  Hospital
 Send contents to lab for toxicology o Antivenom/antivenin/antitoxin PRN
test  Effective within 4 hrs. of bite
o Activated charcoal administration  Less effective within 12 hrs of bite
 Constipation o Tetanus prophylaxis
o O2
CARBON MONOXIDE POISONING o IVF NSS or LRS with large bore needle
 Bind to Hgb o Analgesics
o Low O2 in blood o Antibiotics
o Carboxyhemoglobin o Anaphylaxis treatments
 Easily absorbs by Hgb (200x) than O2 o Safety in snake transport  stunned snake, not
 S/s dead
o Cerebral hypoxia o Bite time: daytime & early evening
o Coma o May apply bandage
 Pulse oxymeter NOT valid indicator o 1-9 y/o
o Hgb saturation NOT O2 sat.  Cardinal s/s
 Prevention o Edema
o First alert o Ecchymosis
 Management o Hemorrhagic bullae
o Serum ABG
o Reverse cerebral and myocardial hypoxia SPIDER BITES
o Eliminate carbon monoxide  Venomous spiders
 If inhaled o Brown recluse
o Expose to fresh air (open windows, doors) o Black widow
o Loosen tight clothing  Dark places
o CPR PRN; 100% O2 o Closets, shoes, attics
o Prevent chill; apply blankets Brown Recluse
FOOD POISONING  S/s
 S/s o Painless
o Diarrhea – absent (botulism, shellfish, fish o Site: red-purple (2-8 hrs)
poisoning)  Necrosis (2-4 days)
o Fever (salmonella, fish poisoning, fava  Wound healing: 2-3 mos.
beans/field beans/bell beans) o 24-72 hrs.
o Respiratory paralysis (botulism, chemical, plant,  Fever, chills
animal poisoning)  N/V, malaise
o Severe vomiting  alkalosis  Joint pain
o Severe diarrhea  acidosis  Treatment
o Hypovolemic shock o Wound cleaning: soap, H2O
 Management o HBO treatment
o ABC o Surgery debridement
MEDICAL SURGICAL NURSING 31
o Antibiotics o Delayed primary closure
Black Widow  Antibiotics
 Bite: pinprick sensation  Tetanus shot/booster
 Systemic affect  Photos (Polaroid camera)
o Rapid: 30 mins.
 S/s INTRA-ABDOMINAL INJURIES
o Abdominal rigidity  Penetrating trauma (Serious  sx)
o N/V o Liver (most frequently injured solid organ)
o HTN  Causes
o Up PR o Gunshot (MGW)
o Paresthesia  Velocity of entry (most important
 Pain severe prognostic factor)
 Pain 1-2 days  Hi-velocity  extensive
 Management tissue damage
o Ice over site  Symptoms
 Decrease systemic toxin delivery  Stab wounds (MSW)
o Cardiopulmo check  Low velocity  less
o Antivenin (horse-based) effective penetration
o Blunt trauma
ANIMAL BITE  Causes: MVA, falls, blows, explosions
Dog bites  Associated with extra-ABD injuries
 Responsible for majority of deaths from animal bites (chest, head, UE, LE)
 Difficult to detect
 Rabies virus in saliva and nerves of rabid animal
 Abdominal assessment

Cat bites
 High risk for infection (Pasteurella in salvia)
o Absent BS
Management
 Early sign of intraperitoneal injury
 Report to public health authorities
 Abd distention, pain, rigid, rebound
o Animal bite center
tenderness
 Follow up screening of offending animal for rabies o S/s of shock
 Rabies prophylaxis o Internal bleeding
 Anti-tetanus toxin  Ultrasound, CT
HUMAN BITE o Left shoulder pain  ruptured spleen
 Associated with rapes, sexual assaults/forms of battery o Right shoulder pain  liver laceration
 Hand/UE
 Management
o Most common site
o ABC +DE
 Contains more bacteria CRUSH INJURIES
 Management  Caught between 2 opposing forces
o Note for pus, erythema, necrosis o MVA, collapsed building
o Photographs
 Monitor for
o Soap & H2O o Hypovolemic shock
o Antibiotic  Extravasation of blood and plasma
o Tetanus toxoid into injured area post release of
o Social worker consult compression
o Police report o Paralysis
o Documentation o Skin erythema and blistering
INSECT STINGS o Damaged body part
 IgE-mediated  anaphylaxis  Swollen, tense, hard
 Management o Renal dysfunction
o Removal of stinger (tweezer)  Muscle damage  rhabdomyolysis
o Soap and water  Myoglobinuria
o Avoid scratching  Tubular necrosis
 H2 response  Management
o Ice application o ABC
 Decrease swelling and venom o Note for acute renal insufficiency (ARI)
absorption o Splinting
o AntiH2, analgesic PO  Major sof tissue injuries
o W/o for systems of anaphylaxis  Control bleeding and pain
WOUNDS o Extremity injury
 Management FRACTURES
o Wound cleansing  Kinds: Open, Comminuted, Simple
o Primary closure  Management
 Sutures, staples o ABC
 Dermabond, steri-strips o Neurovascular checking
MEDICAL SURGICAL NURSING 32
 Pain, pressure complaints o CAB
o Aplly splint o Compression!!!
 1 hand placed distal to fx
 Other hand placed under fx BLOOD SPILL/BODY FLUID SPILL
 Splint applied beyond joint near fx o Bleach (sodium hypochlorite) for 10 mins.
o If open fx  apply dressing (moist, sterile) o Hospital disinfectant
o Hospital  x-ray  splint o Hospital policy/control
MULTIPLE TRAUMAS
 Single catastrophic event SUPERBUGS
 Life threatening injuries to at least 2 distinct organs or Contact
systems o VRE (Vancomycin Resistant Enterococcus)
 Management o MRSA (Methicillin Staphylococcus Aureus)
o ABC + DE o ESBL (Extended Spectrum Betalactamases)
o Airway (primary survey) o MDRO (Multiple Drug Resistant Organism)
SEXUAL ASSAULT o Clostridium Difficile
 Rape trauma syndrome Droplet
 Sexual assault nurse examiner (SANE) o Buckholderia Cepacia
Management o Treatment
 PE  Ceftazidime
 Specimen collection  Doxycycline, Piperacillin, Meropenem
 Potential complications o New Delhi Metallo Betalactamase Resistant Organism
o STDs/STIs (NDM-1)
 Ceftriaxone (Rocephin) IM - Precaution:
Gonorrhea o Contact isolation
 Metronidazole (Flagyl) PO x1 o Droplet precaution
 Azithromycin (Zythromax) PO x1 Treatment
o Pregnancy o Zyvox (linezolid)
o HIV/Hepa B
 Follow up care
o Counseling

AIRWAY OBSTRUCTION MERSCoV (Sept. 2012)

Partial o Dr. Ali Mohamed Zaki in Jeddah, Saudi Arabia
o Hypoxia, hypercabnia, respiratory and arrest o S/s
o Breath and cough spontaneously o 7-day history of fever, cough, expectoration,
Complete shortness of breath
o Hypoxia  permanent brain injury/death within 3-5 mins. o 14 days incubation
o Weak ineffective cough o NO CURE
Causes o 2 investigational vaccines as of June 2015
o Aspiration of foreign bodies MERS
o Bolus of meat (adult): most common o Fever, cough, shortness of breath, myalgia
o Anaphylaxis o “Pneumonia”
o Viral/bacterial infection o GI s/s  diarrhea
o Trauma o SIRS  respiratory failure  MODS  death
o Inhalation/chemical burns o Occurrence
Management o Immunocompromised
o Abdominal thrust o Diagnosis
o Travel History
HEMORRHAGE o S/s
Management o CXR  both patchy infiltrates consistent with
o Control external hemorrhage viral pneumonitis lower based
o Direct pressure; CBR o Chest CT  interstitial infiltrates
o Tourniquet (last resort) o CBC  low WBC and lymphocytes
o Control of internal bleeding
o Hemostan (Tranexamic acid) *MERSCoV and EBOLA notes from Ma’am Pe Benito
SHOCK
o S/s: cool moist skin, falling BP NATURAL CALAMITIES
Treatment o Go Bag
o ABC + DE o Non-perishable foods
o Patent airway and maintain breathing  Canned foods, biscuits, snacks,
o Determine cause chocolates
o IVF and blood transfusion using large bore cath o Battery-operated/rewinding-operated gadgets
o Monitoring  Phone, light, radio
o Pressure points for control of bleeding o First aid kits/meds
CPR Guidelines (AHA 2010) o Info kit (contacts)
MEDICAL SURGICAL NURSING 33
o Water  Measures earthquake
o Life vest TSUNAMIS
LIGHT INJURIES o Usually follows after a big earthquake
o Single lightning stroke – >1M volts o Tsunami warning
o High voltage – >1k volt
o Produce injury by VOLCANIC ERRUPTIONS
o Direct striking o Evacuation route
o Splashing nearby strike area
o Travel via ground (step voltage) IONIZING ROUTE
o Prevention o Geiger scale
o Seek shelter o Detects ionizing radiation
o No use phone o Duration of exposure
o Stay away from windows o Distance
o First aid o Radiation level
 ABC
 CPR PRN DECONTAMINATION
 Sterile dressings to wound sites o Remove everything
o Hospital care o Rinse with H2O
 Check Serum Crea o Soap then rinse
TORNADOES
o Twister SETTINGS FOR END-OF-LIFE CARE
o Funnel clouds o Palliative care
o Within few minutes o Comprehensive care to patients (+ families)
o Take-cover whose disease is not responsive to cure
o Basement o Focus: comfort
o Hospice care
FLOODS/TYPHOONS o Interdisciplinary care and services provided
o Within few hours-days primarily in the home to terminally ill patients +
o First aid it families
o Food/drink o Focus: quality of life
o Battery opens o Home, nursing home, assisted living, hospital
o Emergency numbers
o Evacuation centers

HURRICANE
o Most frequently injured in traumatic injuries
o Liver – right quadrant pain ONCOLOGY NURSING
WILD FIRES o Carcinogenesis
o Contain fire o Etiology (multi-causal)
o Extinguish fire  Genetics
o Evacuation route  Lifestyle
o 4 triangles (Fire tetrahedron)  Weak immune system
o O2  Physical
o Fuel  Chemical
o Heat o Process
o Chain reaction  Initiation – exposure
o Primary treatment for burns  Promotion – repeated exposure
o ABC  Progression – increase in size
o Cover wounds with sterile dressings  Proliferation – spread
o Parkland Fluid Resuscitation  Hematogenous
o Do not go inside burning building or area of fire unless  Lymphatics**
cleared o Cancer Prevention
o Primary – risk reduction
EARTHQUAKES  Smoking cessation
o Drop-duck-cover head  Weight reduction
o Go to top of building  Vaccination
o Nearest exit o Secondary – early detection
o Avoid windows/glass o Tertiary – palliative care
o No elevator o Cancer Diagnosis
o Richter scale o Symptomatology – CAUTION US
o Compare earthquakes – measured in at least 3 o Diagnostics
areas  Imaging
 Epicenter  Biopsy
 Magnitude  Incisional
o Seismograph  Excisional
MEDICAL SURGICAL NURSING 34
 Needle aspiration o Tis – carcinoma in situ (Latin: “in its place”
 Staging – clinical, treatment o T1, T2, T3, T4 – increase in tumor size and
 Grading – cellular involvement
o Modes of Analysis o Nodes
 Paraffin method – 24 hrs., Phil – 1 wk. o Nx – cannot be assessed
 RFS – 15-30 mins., not soaked in formalin
o The cell cycle Staging
o G0 (resting cells capable of re-entering growth cycle) o 0 – cancer in situ
 G1 (RNA synthesis)  S (DNA synthesis)  G2 o 1 – tumor limited to disease of origin
(RNA CHON synthesis)  M (cell division/ mitosis) o 2 – lymphatic involvement limited spread
o Rapid: GI, skin, bone marrow o 3 – extensive local and regional spread
o Slow: reproductive, pancreas o 4 – wide spread metastasis
o 5 years CA free – negative – CA survivor
o Categories of neoplasms Diagnostic tests
o Carcinoma o Papanicolau (PAP) smear
 Malignant cells from epithelial cells (lines o Self breast exam (SBE)
cavities, structures on top of connective o Done 1 week post menstruation
tissues) o Clinical breast exam (CBE)
o Sarcoma o Mammography
 Cancer of connective tissues (bones, o Digital rectal exam
cartilage, fat) o Testicular self exam
o Lymphoma
o Fecal occult blood test/ Guaiac Test
 Cancer of lymphocytes (Hodgkin’s)
o No red meat, no dark colored foods
o Leukemia/ Myeloma
o Prostate exam (Digital rectal exam + PSA)
 Ca of blood forming cells of bone marrow
o Sigmoidoscopy/ colonoscopy
o Pathogenesis: Theories of CA causation
o Biopsy
o Cellular transformation and derangement
o Rapid frozen section (RFS)
(arrangement) theory
 Carcinogenesis o Other dx test
o Failure of immune response theory o MRI
o Predisposing factors o CT scan
o Age o Ultrasound
o Gender: males: prostate; female: breast C- change in bladder or bowel habit
o Viruses and bacterias A- a sore that does not heal
U- unusual bleeding or discharge
o HPV (human papilloma virus)  cervix CA
T- thickening or lump
o Hepa B, C virus  Liver CA
I- indigestion or dysphagia
o Helicobacter pylori  Gastric CA O- obvious
o Precancerous lesions N- nagging cough or hoarseness of voice
o Diet: high fat, low fiber A- anorexia
o Obesity L- loss of weight
o Endometrial CA
o Occupation/ Environmental/ Physical agents
o Genetics Most common sites of reported deaths (2010)
o Hormones o Trachea, bronchus, lungs
o Estrogen  breast CA o Breast
o Other forms of risk factors o Leukemia
o Geographic location (SBMA, city) Management of CA
o Sexual practices Modes
o Chemical agents o Primary tx – treatment of choice
 Nitrates o Adjunct
 Nicotine (smoking) o Used together with primary tx
 Pesticides o Assist primary tx
 Polyvinyl o Adjuvant
 Hair dyes o Tx given post primary tx to increase cure
 CFC o Neo-adjuvant
 Aromatic amines o Tx give prior to surgery
 Alcohol Radiation
 Asbestos o Beams of high-energy waves or streams of particles
 Benzene and lead o Localized treatment
o Immunocompromised states o Destroys rapidly dividing cells
o Small tumors respond best
Tumor staging system (TNM) o Types
o Tumor
o Internal radiation – brachytherapy/particulate
o Tx – cannot be assessed
 Radioactive
o T0 – no tumor
o External radiation- teletherapy/ionizing
MEDICAL SURGICAL NURSING 35
 Non radioactive; not threat to others o MRM – pectoralis minor
o 6 feet away; 30 minutes per shift; lead container o Nursing mgt: s/p breast
Nursing Considerations: Chemo Precautions o Fowlers
o Wear (PPE) chemo gloves, long sleeved gowns, mask with o Promote mobility
shield PRN Hodgkin’s lymphoma
o Double flush Risk factors:
o Check for extravasation o male 15-40 years old
o Only in peripheral IV o Immunosuppressed
o Observe chemo precautions until 72 hours post last chemo o Hx of mononucleosis or Epsteinn Barr virus
tx Early manifestations
o Medications o Painless swelling of the neck
o Cell cycle specific – anti-metabolites Late sign
o Non-specific – alkylating agents, more dangerous o Organomegaly
Complications of radiation and chemotherapy
o Nausea and vomiting Cervical CA
o Constipation o Cause: unknown
o Fluids and high fiber foods o Risk factor
o Stool softener o HPV
o Diarrhea o Oral contraceptive
o Offer liquids o Tobacco use
o Stomatitis/ Xerostomia o Early age at first coitus
o Good oral hygiene o Frequent douching
o Avoid spicy or hot foods o Diagnostic
o Offer topical agents for pain relief as ordered o Pap smear
o Apply KY jelly to lips o Colposcopy
o Offer popsicles o Biopsy (“punch”)
o Avoid alcohol, tobacco o Surgical mgt
o Alopecia o Cryosurgery
o Plan for wig, scarf, turban, or hat BEFORE hair o Radiotherapy
loss o Hysterectomy
o Reassure patient that hair will grow back after  TAH
therapy  TAHBSO
o Myelosuppression Prostate CA
o Thrombocytopenia (platelets) o Causes
o Leukopenia (WBC)/ Neutropenia (granulocytes) o Hormones
o Anemia o STD
o Infertility o Multiple sexual partner
o Sperm bank for male and oophorexy (ovary o High fat diet
function reservation) for female o Coude’ or tiemen catheter
Breast CA o Dx
o Risk factors o Biopsy
o Age o PSE- prostate specific antigen
o Sex o Digital exam
o Familial history o Nursing assessment
o Early menarche (before age 11) o Asymptomatic: early stage
o Late menopause (55 years old) o Hematuria
o Nulliparity o Dysuria
o Obesity o Enlargement of prostate
o Assessment o Low back pain
o Asymptomatic o Medical mgt
 Lump on upper outer quadrant o Estrogen hormones
o Late signs (Malignant)  Diethylstillbesterol
 Irregular shaped mass  Estradiol
 Fixed nodules, adheres to chest wall  Chlorotrianisine
o Diagnostic exam o RT
o Biopsy o Surgical mgt
o Breast self examination (SBE/CBE)  TURP
 1 wk post start of menstruation  Orchiectomy
o Medical management o Nursing mgt: s/p TURP
o Administer: anti-estrogen receptor: Tamoxifen  Increase Fluid Intake 2400-
citrate (Nolvadex), Taxol (paclitaxel) 3000ml/day unless CI
o Chemotherapeutic agent:  Monitor for bleeding
 Cyclophosphamide RESPIRATORY SYSTEM
o Simple (Total) Mastectomy Oxygenation
MEDICAL SURGICAL NURSING 36
 Process of acquiring, transporting and utilizing oxygen for  Fever
cellular metabolism (diffusion)  Body malaise (fever  vasodilation  blood pools in
 Components muscles  sore muscles)
o Respiration Complications
o Circulation  Osteomyelitis
Common problems  Meningitis
 Ineffective airway clearance  Encephalitis
 Impaired breathing pattern Nursing care
 Impaired gas exchange – pulse oximeter  Positioning
 Altered tissue perfusion o Proetz vs. Parkinsons
 Decreased cardiac output  Bred rest
 Activity intolerance  Increase OFI
 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
 Chest pain o Nasal decongestants (Adrenergics/PPA)
 Pallor, erythema, cyanosis o Anti-histamines (Chlorphenamine)
 Edema o Analgesic/anti-pyretic (Paracetamol)
 ALOC  Surgery
 Palpitations o FESS/Functional Endoscopic Sinus Surgery –
 Body weakness drain sinuses and build-up of pus (no incision,
use of scopes)
FUNCTIONS  Watch out for DOB
 Gas exchange  Position HOB elevted
 Maintaining fluid status o Cald wel luc procedure/Radical Antrum Operation
 Communication (incision under upper lip)
 Eliminating metabolic wastes  Transphenoidal Hypophysectomy
 Acid-base balance regulation Nursing Care Post-Sinus Surgery
o Acidosis = CNS depression  Positioning – HOB elevated
RESPIRATORY DYSFUNCTION  Soft diet
Results to the following problems o No hard, rough, coarse foods
 Impaired gas exchange  toxemia, acid base imbalance o No vigorous chewing
(acidosis), hyperventilation (alkalosis)  No dentures for 10 days
o Hypoxemia  Avoid brushing teeth
o Hypercapnea  Gargle with non-stinging mouthwash
 Fluid imbalance  Avoid blowing nose/sneezing (2 weeks)
 Build-up of metabolic wastes
TONSILLITIS/Pharyngitis/Adenoiditis
RESPIRATORY DISORDERS Cause: infection (viral or bacterial/GABHS)
EPISTAXIS Types: Acute/Chronic (more than 3x in a year)
Cause Complications: RF, RHD, AGN
 Injury Manifestations
 Irritation  Dysphagia
 Polyps  Odynophagia
 Drug use  Sore throat
 Leukemia  pancytopenia  Cough
Complications: aspiration/obstruction  Halitosis
Nursing care  Fever
 Positioning – HOB elevated and leaning forward  Body malaise
 Bred rest  Peritonsillar abscess (bacterial)
 Apply pressure on the soft tissue of the nose  Coryza (viral)
 Ice compress (15-20 min.) Nursing Care
 Close monitoring  Diet: soft and non-irritating
Medical Management o Avoid milk/dairy – thicken mucus secretions
 Nasal packing (3-5 days)  TGC (tamarind, ginger, calamansi)
 Surgery: electric cautery  watch out for DOB  Hydration
RHINOSINUSITIS  Gargle with warm saline (soothing effects)
Sinus – air-filled cavity, keeps skull light  Bed rest
Cause: infection  Oral hygiene
Types: Acute or Chronic Medical Management
Manifestations  Pharmacotherapy
 Nasal congestion o Oral antiseptis (mouthwash/lozenges)
 Nasal drip (coryza) o Anti-inflammatory agents
 Headache o Anti-microbials
MEDICAL SURGICAL NURSING 37
o Aminopenicillins, macrolides o Race
 Surgery Diagnosis
o Tonsillectomy  Bronchoscopy – monitor extent of metastasis
Nursing Care for Tonsillectomy Management
 Pre-Op  Partial laryngectomy (laryngofissurethyrotomy)
o Check for loose tooth o Portion of the larynx is removed along with one
 Post-Op vocal cord and the tumor
o Immediate post-op: prone head to side to drain o All the other structures remain including the
secretions airway and no difficulty in swallowing is expected
o Semi-fowler’s o Used for smaller cancers of the larynx
o Watch out for frequent swallowing once awake  Total laryngectomy
(8-14 days post op risk for bleeding) o Complete removal of the larynx can provide the
o Diet: progressive desired cure in most advanced laryngeal cancers
 1-3 days clear liquids (no milk and o Laryngeal structures are removed
dairy) Nursing Care
 4-5 days general liquids  HOB elevated (keep upright)
 6-7 days soft diet  Suction secretions PRN
 8 days and beyond DAT  Tracheostomy care
o Hydration o Every 8 hours, PRN
o No throat clearing and avoid coughing o Safest: saline
o Dark-colored stools are normal at first few days o Dry using sterile gauze
because bleeding is normal o Clean stoma using half-strength hydrogen
peroxide, dry using sterile gauze
LARYNGITIS o Cuff – not usual part of tracheostomy tube
 Inflammation of the larynx often occurs as a result of voice  Secures to prevent dislodgement
abuse or exposure to dust, chemicals, smoke and other  Prevents aspiration – not routinely
pollutants as part of URTI deflated
Co-morbidity: GERD  Prevents pneumothorax
Manifestations  15 mmHg (15-25 mmHg)
 Hoarseness or aphonia (less than 2 weeks)  Strict aspiration precaution
 Severe cough o Semi-solid
Management  Alternative means of communication
 Rest
 Antibiotics as needed
o Aminopenicillin ACUTE LUNG INJURY
o Oral antiseptics  Trigger inflow reaction  form inflammatory
 PPI – reflux laryngitis exudates/infiltrates  inflammatory edema  reduced lung
 Continuous positive airway at bedtime compliance  hypoxemia  acute respiratory distress
 Monitor for malignancy  Increased permeability of the alveolar membrane fluid shifts
 Position: High Fowler’s into the alveolar and interstitial spaces  pulmonary edema
 crackles
LARYNGEAL CANCER  Destruction to the alveolar wall  decreased surfactant 
 Uncontrolled cell growth atelectasis
 Accounts for half of all head and neck Cancer
 Most common among people 60-70 y/o CHRONIC AIRFLOW LIMITATION/OAD
 Male, >40 y/o  Refers to group of conditions marked by increased airway
Manifestations resistance resulting to impaired inflow of oxygen to the lungs
 Persistent hoarseness (2 weeks) associated with otalgia and Risk factors: SOAP
dysphagia  Smoking
 Persistent cough or pain and burning throat especially when  Occupation
consuming hot liquids or citrus juices  Allergies
 Lump on the throat  Pollution
 Pain in the adam’s apple that radiates to the ear Common Types
 Dyspnea, enlarged hot liquids or citrus juices  COPD
Risk Factors  Bronchial Asthma
 Carcinogens
o Asbestos COPD
o Alcohol and tobacco  Group of disorders characterized by progressive
o Paint fumes, wood dust, cement dust deterioration (irreversible) in pulmonary functioning
Forms
 Other factors
1. Pulmonary Emphysema
o Straining of voice
 Air-trapping within the tracheobronchial tree)
o Chronic laryngitis
 Abnormal distention of the airspaces beyond the
o Nutritional deficiency (riboflavin)
 Terminal bronchioles and destruction of the walls of the
o Familial predisposition
alveoli
o Age, males
 Pink, puffer
MEDICAL SURGICAL NURSING 38
 Barrel-chest deformity BRONCHIAL ASTHMA
2. Chronic Bronchitis  Hypersensitive and hyper responsive airway
 Presence of cough and sputum production for at least  Nature: instrinsic in origin due to immunologic factors
3 months in each of 2 consecutive years Mechanism: Allergy
 Blue, bloater Mediators: IgE and Histamine
 Smoker’s cough Problems:
Risk factors: SOP  Inflammation of the airway (leukotrienes, histamines,
Etiology:  Increased mucus production
 Chronic irritation  Bronchoconstriction
Genetic: Alpha 1 Anti-trypsin deficiency – enzyme that prevents Triggers
elastase, which destroys elastin  Environmental factors – change in temperature or humidity
Essential Features (ABC)  Atmospheric pollutants – cigarettes, industrial smoke
 Age >40 y/o  Strong odors – perfume, insecticides
 Breathlessness  Allergens – feathers, dust, foods, pollens, laundry
 Cough (chronic and productive) detergents
 With hypoxic drive for breathing  Exercise
 Carbon Dioxide Narcosis – CNS depression  Stress or emotional quest
Problems  Medications – aspirin, NSAIDs
 Increased mucus production Manifestations
 Bronchoconstriction  Triad of Bronchial Asthma
 Retention of CO2 o Cough
Common Manifestations o Dyspnea
 Dyspnea – exertional dyspnea o Wheezing
 Cough (persistent and productive)  Restlessness/Agitation
 Lethargic behavior  Hyperventilation
 Body weakness  Wheezing
 Weight loss – catabolism  Nursing alert: status asthmaticus
Diagnosis Nursing Care
 PFT (Pulmonary Function Test)  During acute phase
o Spirometry** – measures lung volume and  Position: orthopneic/Fowler’s
capacity  Bed rest
o Oximetry  DBE
 ABG Analysis  Close monitoring
 If stable
o Diet: hypoallergenic (high calories, low CHON,
Complications high CHO)
 Pneumonia  septic schock o Avoid known triggers
o Pleuritic chest pain Medical Management
o DOB  O2 therapy
o Cough  Pharmacotherapy (Acute phase)
o Rusty colored o Analeptic agents
o Fever  Theophylline therapeutic level 10-20
o Chills mcg/mL
 Respiratory Failure o Bronchodilators – adrenergic agents 
o Inability of lungs to clear carbon dioxide Hypokalemia
 Pulmonary Hypertension  Beta selective adrenergic agonist
 Cor Pulmonale  Isoproterenol (Isuprel)
o Right-sided heart failure  Selective – beta2 adrenergic agonist
Nursing Care  Short-acting: Albuterol
 DBE (Pursed-lip technique) (Proventil), Terbutaline
 Position: HOB elevated or orthopneic (Bricanyl), Salbutamol
 Diet: high calories, high CHON, low CHO (Ventolin, Asmalin)
 Hydration  Long-acting: Salmetrol
 CPT (serevent), Formetrol
 Bed rest as needed (Foradil)
 Avoid exertion and stress o Corticosteroids – beclomethasone, budenoside,
Management fluticasone
 Oxygen support (low flow only/2-3 lpm)  Pharmacotherapy (Preventive)
 Pharmacotherapy o Anticholinergics – ipratropium, tiotropium
o Bronchodilators o Mast cell stabilizers – Nedocromil (Tilade),
o Anti-cholinergics (Ipratropium) Cromolyn (Intal)
o Mucolytics o Leukotrine inhibitors – Montekulast (Singulair),
o Steroids Zafirlukast (Accolate), Zileuton (Zyflo)
o MDIs  MDIs – deep breath, hold breath for 3-5 seconds, gargle if
med is with steroids
 Immunization
MEDICAL SURGICAL NURSING 39
BRONCHOGENIC CANCER  Promote lung expansion
Etiology: smoking or exposure to chemicals  Keep chest tube below chest level
Incidence: common among males  Avoid kinks or loops
Prognosis: poor (detected late)  Observe for intermittent fluctuations during respirations
Classification  Avoid clamping the tube
 Small cell lung cancer  Check connection and observe for bubbling or air leaks
 Non small cell lung cancer  Keep a vaselinized gauze at bed side
o Epidermal, adenocarcinoma, large cell cancer  Responsibility: in cases of breakages or pulling of tubes
Warning signs  Reassessment
 Nagging cough Summary of Respiratory Diseases
 Hemoptysis A. Restrictive
 Chest pain  Reduced lung compliance  reduced lung volume 
 Dyspnea hypoxemia  increased RR  respiratory alkalosis
 Weight loss  Reduced VC, TLC, RV
Diagnosis  Earliest signs
 X-ray o Dyspnea upon exertion
 CT scan  Inflammation of lung parenchyma
 Bronchoscopy o Pneumonia
 Thoracoscopy o ARDS
 Biopsy o Space occupying lesion – Cancer
Management o Surgery
 Surgery o GBS
o Turn on unaffected side o Pleural disease – Pleural effusion
 Wedge resection B. Obstructive
 Segmentectomy  Limitation of airflow on expiration
 Lobectomy
 Failure of air to move out of lungs  CO2
o Pneumonectomy
retention  respiratory acidosis
 Turned on back (Semi-Fowler’s)
 Chronic Airway Limitation/COPD
 Nursing alert: watch out for
C. Vascular
mediastinal shift
 Pulmonary embolism
 Palpate trachea regularly
PLEURAL EFFUSION  Obstruction  hypoxia/hypoxemia 
constriction of the pulmonary vasculature 
 Accumulation of air, water, or blood in the pleural space
increased pulmonary vascular resistance 
resulting to an alteration in the normal intrathoracic pressure
pulmonary hypertension  RV Failure (Cor
 Pleura – seal and maintains negative pressure
Pulmonale)
Cause: I-I
 High ventilation-perfusion ratio
 Injury (chest wall trauma/rib fracture) – blunt
Vital Capacity (300-500 ml) – amt of inhaled/exhaled air
 Instrumentation (surgical procedures) Total Lung Capacity (6 L)
Forms Residual (1 – 1.5 L)
 Pneumothorax
 Hydrothorax CHEST TUBE DRAINAGE
 Hemothorax 1 – Way Bottle (H2O sealed chest drainage)
Concept: lung compression  Air vent
Complication: Atelectasis 2 – Way Bottle
Manifestations 1. Output bottle
 Dyspnea 2. Water-sealed bottle
 Agitation 3 – Way Bottle
 Asymmetrical chest expansion 1. Output bottle
 Decreased tactile fremitus 2. Water-sealed bottle
 Decreased breath sounds 3. Vacuum-controlled bottle
Diagnosis: CXR Nursing Care
Management 1. Airtight
 Pleurodesis 2. 18 inches
 Thoracostomy 3. Taped
Approaches: needle vs. tube 4. Oscillation/tidalling/fluctuations
o Thoracentesis (needle thoracostomy) o Absence of oscillation
 <1500cc  Lungs have re-expanded
 Turn client from side to side
o CTT (tube thoracostomy)  Remind client to perform DB exercises
 >1500cc 5. Stripping/Milking/Squeezing
 Consent o With extra caution
 2-3 ICS –air o Prevent tension pneumothorax – avoid applying
 5-6 ICS – fluid heavy pressure
Nursing Care  Reveals blood clot which causes
 Positioning (HOB elevated) and monitoring absence of oscillation
 Secure connection 6. Bubbling
MEDICAL SURGICAL NURSING 40
o Presence – desired negative pressure from the CORONARY ARTERY DISEASE/ASHD/IHD - Chronic
suction apparatus  Occlusion of the coronary arteries that results to impaired
o Intermittently perfusion of the myocardium
o Continuous – leakage  Main risk factor: HTN
7. Measure  Concept: oxygen debt
o One-way – put tape mark  Mechanism: atherosclerosis
8. Change  Outcome: ischemia
o Sterile bottle, sterile glass rod  LAD – anterior (Lead 2 in ECG)
o Clamping – causes tension pneumothorax  Classic manifestation
o Bottle breakage, immerse tube in sterile water o Chest pain “angina pectoris”
o If in 3-way, two bottles are broken, make 1-way  Types
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
 Management: reduce demand and increase supply of o E – exertion related
oxygen o R – relieved by rest or nitrates
 Nursing interventions: bed rest o S – short duration (20 minutes)
CAD Assessment
HYPERTENSION Manifestations
 Persistent elevation of BP; 140 mmHg systolic and 90 o Dyspnea **
mmHg diastolic (WHO) o Diaphoresis
 Most significant risk factor for CVDs o Increased RR, HR or BP
 Regarded as “silent killer” o Diagnostics
 Hypertensive crisis – single sudden severe elevation in BP o ECG – T wave inversion
(S: min. 180, D: min. 120) o Cardiac Biomarkers
o Emergency – with organ damage  CKMB – most accurate, most specific,
 Catapres (Clonidine) lasts for 3 days, appears in blood 4-6
 Calci-block (Nifedipine) hrs. after MI
 Captopril (Capoten)  Troponin – sudden increase because
o Urgency – without organ damage of sensitivity, up to 3 weeks
 Diagnostic Criteria for Hypertension Incision and Focus
o 2 consecutive days of elevated BP within 2 o Head and neck – airway
weeks o Chest and back – breathing
Types o Peripheral – circulation
 Primary/Essential ACUTE CORONARY SYNDROME
o No specific cause/multivariate  Unstable angina/Pre-infarct angina
 Secondary o Holter monitoring
o Due to co-morbidity  Acute myocardial Infarction
Manifestation o ST elevation – zone of injury **
 Throbbing occipital headache, dizziness, visual disturbance,  First seen in patients with cardiac
edema, epistaxis, retinal hemorrhages diseases
 Monitor for enlarged Q wave next
Classification of BP for adults o T wave inversion – zone of ischemia
 Stage I o Enlarged Q wave – zone of infarction
 Stage II Nursing care
 Stage III o Bed rest
 Stage IV o Position: HOB elevated
Complications of HTN o DBE
 Atherosclerosis o Avoid stress
 CAD Medical Management
 CVD/CVA o O2 therapy
 PAOD o Pharmacotherapy
o NTG tablets **
Management (Exercise>diet)  Take sublingually
Step 1 – lifestyle modification  Check expiration date
 Focus: wt. reduction  Max. of 3, 5 min. interval
Step 2 – inadequate response o Anti-HTN agents
 Monotherapy (diuretics/beta blockers/ACEI) o Anti-platelet drugs
Step 3 – inadequate response o PCI (Percutaneous Coronary Intervention)
 Monotherapy (dosage adjustment/shift)  Percutaneous Transluminal
Step 4 – inadequate response Angioplasty (PTA)
 Combitherapy (2 or more)
MEDICAL SURGICAL NURSING 41

Not recommended if Possible Complications of MI
occlusion >70%  Arrythmia – V. Fib – most common complication
 Coronary stent o Caused by sympathetic stimulation triggered by
o Surgical Management the chest pain  treat CHEST PAIN first!!!!
 CABG o PR >200, irregular, chaotic heart beat
Coronary Artery Bypass Graft o ECG no specific QRS complex
o Possible blood vessels  Cardiogenic Shock – most fatal complication
o Radial o Cardiac Index = CO / body surface area (sq. m.)
o Internal mammary/intrathoracic – best  2.8 – 4.2 L/min/sq. m.
o Saphenous o MAP = SBP + 2 DBP / 3
 N: 70-80 mmHg
MYOCARDIAL INFARCTION o Mgt: Counterpulsation technique
 Heart wall damage due to cessation of blood flow in the  Fluoroscope
coronary circulation  IABP (Intraaortic balloon pump)
 Death of myocardial cells from inadequate oxygenation,  Ventricular rupture
often caused by a sudden, complete blockage of a coronary  Pericardial effusion
artery characterized by localized formation of necrosis with  Cardiac Tamponade
subsequent healing by scar formation and fibrosis  Pericarditis/Dressler’s Syndrome
 Mechanism: AA o Develops 1-6 weeks after
o Atherosclerosis o Supine position aggravates position
o Arteriospasm o Pain is relieved by orthopneic position
Assessment o Treated by NSAIDs
 Chest pain  CVA
o Prolonged, substernal pain o Embolism
o Partial occlusion by atheroma/plaque   Ventricular Failure
decreased blood supply  8-10 seconds   Renal Failure
myocardial ischemia  angina o Decreased CO  decreased renal perfusion 
o 15-20 minutes  myocardial infarct  chest
renal ischemia  sub. Cessation RF  ARF
pain Management
o Characteristics o Relief of pain
 S – sudden o Decrease cardiac workload
 A – anterior chest pain – substernal,
o Prevent complications
left jaw, left shoulders, referred
o MONAR
epigastric pain
 V – vague discomfort or vise-grip pain o Morphine
 E – exercise  Morphine > Demerol – Demerol
 R - rest causes sudden hypotension,
 S – short duration Morphine has sustained effect,
o Myocardial ischemia  anaerobic metabolism relieves pain with severe intensity
 metabolite  lactic acid  chest pain  VD o Oxygen
 decreased BP & alteration  weak pulse o Nitrates
 DOB o Anti-coagulants/anti-platelets/clot blusters
 Diaphoresis  Given in the first 3 hours (window hour
 Increased BP then drops for clot formation)
o 10 seconds – oxygen storage in brain o Rehabilitation
 Increased HR, RR, Temp. (low-grade fever) o CBR without BRP
o Metabolite  lactic acid  ensuing o mMeds
inflammatory process  increased neutrophils o ASA
 leukocytosis  low–grade fever  replaced o NTG – must feel burning/tingling sensation, every
fibrostatic tissue  fibrin 5 minutes, max. of 3 doses
 N/V o Isosorbide mono/dinitrates (ISMN/ISDN)
Diagnostics Nursing care
 ECG o CBR without BRP – bedside commode
 Cardiac biomarkers o Position: HOB elevated
o Troponin I – most accurate (early and late o DBE
diagnosis, starts to elevate 2-3 hrs. after o Close monitoring
myocardial injury, stays elevated for 3 weeks o Diet: high in fiber
o CPK-MB – earliest diagnosis of MI o Avoid stress and strain
o SLDH – late diagnosis of MI (elevate 2-3 days
after myocardial injury) CARDIAC TAMPONADE
 1 & 2 – increase if with myocardial o Rapid unchecked rise in intrapericardial pressure impairs
insult diastolic filling of the heart due to blood or fluid accumulating
 3 – increase if lung parenchyma injury in pericardial sac
 4 & 5 – increase if skeletal muscle or o Possible causes
liver damage o Effusion (cancer/bacterial infections),
o SGOT/AST hemorrhage from trauma/non-trauma causes, MI
MEDICAL SURGICAL NURSING 42
o Chronic alcoholism, infection, pregnancy and post-partum
disorders, metabolic and immunologic disorders, chronic
Manifestations HTN
o Dyspnea Diagnosis
o Anxiety o 2D Echocardiogram
o Diaphoresis o Cardiac catheterization
o Reduced arterial BP (pulsus paradoxus) o CXR
o Narrow pulse pressure o ECG
o Neck vein distention Assessment
o Pallor cyanosis o Chest pain, dyspnea, cough, crackles, enlarged heart,
o Water-bottle heart dependent pitting edema, enlarged liver, jugular vein
Diagnostics distention, murmur, S3 S4 sounds, syncope
o CXR shows cardiomegaly and widened mediastinum Collaborative Management
o ECG o Nursing care
Collaborative Management o Semi-Fowler’s to High Fowler’s
o Nursing care o Bed rest
o Position HOB elevated o Diet: Low Na
o Maintain on bed rest o Fluid restriction
o Close monitoring o Close monitoring
o Medical
o Pericardiocentesis
o Medical Management
HEART FAILURE o Diuretics
o A condition characterized by the inability of the heart to o Dual chamber pacing
pump blood in response to metabolic needs of the body o Surgery: heart transplant or cardiomyoplasty
o HF – Chronic vs. CHF – Acute o Cardiac Resynchronization Therapy
o Two types
o R – sided Pacemaker Nursing Instructions
o L – sided o Check HR regularly
Etiology o Avoid exposure to magnetic devices
o Cardiac pathology: CAD, MI, CMP, VHD o Avoid use of mobile phones directly on top of pacemaker
o Pulmonary conditions: COPD placement
Problems o Avoid vigorous movement of the shoulders
o Failure to eject blood - L-sided but develops problem in o Never use microwave ovens, use cellphone on opposite side
backflow of blood of pacemaker
o Backflow of blood - R-sided
Assessment VASCULAR DISEASES
o SOB ANEURYSM
o Easy fatigability o Permanent localized dilation of an artery
o Decreased ejection fraction (N: >55%) o Sac formed by dilation of an artery secondary to weakness
Collaborative management and stretching of artery wall
o 4Ds Types
o Decrease fluid intake o Fusiform – diffuse dilation affecting the entire circumference
o Decrease sodium in diet of the artery
o Saccular
o Digoxin
o Dissecting
 Withhold if 60 bpm
o Diuretics Sites
o Cerebral Aneurysm
o Increase potassium in diet
o Severe headache
o To prevent digitalis toxicity (hypokalemia 
o Thoracic Aortic Aneurysm
digitalis toxicity)
o Diuretics o Maybe asymptomatic
o Left Ventricular Assist Device o Pain, boring and constant, during supine position
o Abdominal Aortic Aneurysm
CARDIOMYOPATHY (CMP) o Asymptomatic
o Myocardium around left ventricle becomes flabby, altering o Feel their heart beating
cardiac > decreased CO Management
o Increased HR and increased muscle mass compensate in o Pharmacotherapy
early stage but later stage > HF o Anti-HTN
Types o Surgery
o Dilated (Congestive) – dilated chambers contract poorly o Clipping or aneurysmectomy
causing blood to pool and reducing CO o Stent/graft insertion
o Hypertrophic (Obstructive) – hypertrophied LV can’t relax
and fill properly PERIPHERAL VASCULAR DISORDERS
Possible causes o Decreased blood flow/insufficiency
Arteries – responsible for tissue perfusion (oxygenated blood)
MEDICAL SURGICAL NURSING 43
o Buerger’s disease
Venous – responsible for venous return (unoxygenated blood)
o Varicose veins, DVT

SMOKING
 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