Acute Biologic Crisis

Condition that may result to patientmortality if left unattended in a brief period of

time.
Condition that warrants immediateattention for the reversal of disease process and
prevention of further morbidity and mortality.
Cardiac Failure
Description

Is the inability of the heart to pump sufficient blood to meet the

needs of
the tissues for oxygenation and nutrients
CHF is most commonly used when referring to left-sided and rightsided failure
Formerly called Congestive Heart Failure

Etiologic Factors :
-

Increased metabolic rate (eg. fever, thyrotoxicosis)

Hypoxia

Anemia

Cardiac failure most commonly occurs with disorders of cardiac

muscles that result in decreased contractile properties of the heart.
Common underlying conditions that lead to decreased myocardial
contractility include myocardial dysfunction, arterial hypertension,
and valvular dysfunction. Myocardial dysfunction may be due to
coronary artery disease, dilated cardiomyopathy, or inflammatory
and degenerative diseases of the myocardium. Atherosclerosis of
the coronary arteries is the primary cause of heart failure.
Ischemia causes myocardial dysfunction because of resulting
hypoxia and acidosis (from accumulation of lactic acid).
Myocardial infarction causes focal myocellular necrosis, the death
of myocardial cells, and a loss of contractility; the extent of the
infarction is prognostic of the severity of CHF. Dilated
cardiomyopathy causes diffuse cellular necrosis, leading to
decreased contractility. Inflammatory and degenerative diseases
of the myocardium, such as myocarditis, may also damage
myocardial fibers, with a resultant decrease in contractility.
Systemic or pulmonary HPN increases afterload which increases
the workload of the heart and in turn leads to hypertrophy of
myocardial muscle fibers; this can be considered a compensatory
mechanism because it increases contractility. Valvular heart
disease is also a cause of cardiac failure. The valves ensure that
blood flows in one direction. With valvular dysfunction, valve has
increasing difficulty moving forward. This decreases the amount of
blood being ejected, increases pressure within the heart, and

Pathophysiology:

eventually leads to pulmonary and venous congestion.

Left-Sided Cardiac
Failure

Clinical
Manifestations

Right-Sided
Cardiac Failure

Clinical
Manifestations

Pulmonary congestion occurs when the left ventricle cannot pump

the blood out of the chamber. This increases pressure in the left
ventricle and decreases the blood flow from the left atrium. The
pressure in the left atrium increases, which decreases the blood
flow coming from the pulmonary vessels. The resultant increase in
pressure in the pulmonary circulation forces fluid into the
pulmonary tissues and alveoli; which impairs gas exchange.

Dyspnea on exertion
Cough
Adventitious breath sounds
Restless and anxious
Skin appears pale and ashen and feels cool and clammy
Tachycardia and palpitations
Weak, thready pulse
Easy fatigability and decreased activity tolerance

When the right ventricle fails, congestion of the viscera and the
peripheral tissues predominates. This occurs because the right
side of the heart cannot eject blood and thus cannot accommodate
all the blood that normally returns to it from the venous circulation.

Edema of the lower extremities (dependent edema)

Weight gain
Hepatomegaly (enlargement of the liver)
Distended neck veins
Ascites (accumulation of fluid in the peritoneal cavity)
Anorexia and nausea
Nocturia (need to urinate at night)
Weakness

Diagnostics

Chest Xray (may show cardiomegaly or vascular congestion)

Echocardiogram (shows decreased ventricular function and

decreased ejection fraction)

CVP (elevated in right-sided failure)

*pulmonary artery pressure monitoring may be used as guide

treatment in serious case of pulmonary edema
Nursing Diagnoses

Nursing
Management

Activity intolerance r/t imbalance between oxygen supply and

demand secondary to decreased CO

Excess fluid volume r/t excess fluid/sodium intake or retention

secondary to CHF and its medical therapy

Anxiety r/t breathlessness and restlessness secondary to

inadequate oxygenation

Non-compliance r/t to lack of knowledge

Powerlessness r/t inability to perform role responsibilities

secondary to chronic illness and hospitalization

a. Acute phase
-

monitor and record BP, pulse, respirations, ECG and CVP to

detect changes in cardiac output

maintain client in sitting position to decrease pulmonary

congestion and facilitate improved gas exchange

auscultate heart and lung sounds frequently: increasing crackles,

increasing dyspnea, decreasing lung sounds indicate worsening
failure

administer O2 as ordered to improve gas exchange and increase

oxygenation of blood; monitor arterial blood gases (ABG) as
ordered to assess oxygenation

administer prescribed medications on accurate schedule

Monitor serum electrolytes to detect hypokalemia secondary to

diuretic therapy

monitor accurate input and output ( may require Foley cathether

to allow accurate measurement of urine output) to evaluate fluid

status
-

if fluid restriction is prescribed, spread the fluid throughout the day

to reduce thirst

encourage physical rest and organized activities with frequent

rest periods to reduce the work of the heart

provide a calm reassuring environment to decrease anxiety; this

decreases oxygen consumption and demands on the heart

b. Chronic heart failure

Pharmacologic
Therapy

educate client and family about the rationale for the regimen

establish baseline assessment for fluid status and functional

abilities

monitor daily weights to evaluate changes in fluid status

assess at regular intervals for changes in fluid status or functional

activity level

ACE Inhibitors (promotes vasodilation and diuresis by decreasing

afterload and preload eventually decreasing the workload of the
heart.)

Diuretic Therapy. A diuretic is one of the first medications

prescribed to a patient with CHF. Diuretics promote the excretion
of sodium and water through the kidneys

Digitalis (increases the force of myocardial contraction and slows

conduction through the AV node. It improves contractility thus,
increasing left ventricular output.)

Dobutamine.(Dobutrex) is an intravenous medication given to

patients with significant left ventricular dysfunction. A
catecholamine, it stimulates the beta1-adrenergic receptors. Its
major action is to increase cardiac contractility.

Milrinone (Primacor). A phosphodiesterase inhibitor that prolongs

the release and prevents the uptake of calcium. This in turn,
promotes

vasodilation, causing a decrease in preload and afterload and

decreasing the workload of the heart.

Client Education

Nitroglycerine ( a vasodilator reduces preload)

Morphine to sedate and vasodilate,decreasing the work of the

heart

Anticoagulants may be prescribed. Beta-adrenergic blockers

maybe indicated in patients with mild or moderate failure

Include family member or others in teaching as appropriate

Weight monitoring: teach client the importance of measuring and

recording daily weights and report unexplained increase of 3-5
pounds

Diet: sodium restriction to decrease fluid overload and potassium

rich foods to replenish loss from medications; do not restrict water
intake unless directed

Medication regime: explain the importance of following all

medication instructions

Activity: help client plan paced activity to maximize available

cardiac output

Symptoms: report to MD promptly any of the following: chest pain,

new onset of dyspnea on exertion, paroxysmal and nocturnal
dyspnea

Report even minor changes to MD as they may be an early sign

of decompensation

Acute Myocardial Infarction

Description
- Occurs when the heart muscle is deprived of oxygen and nutrientrich blood. However, in the case of MI, this deprivation occurs over
a sustained period to the point at which irreversible cell death and
necrosis take place. Infarction results from sustained ischemia and
is irreversible causing cellular death and necrosis.

Etiologic factors

Physical exertion

Emotional stress

Weather extremes

Digestion after a heavy meal

Valsalva maneuver

Hot baths or showers

Sexual excitation

Pathophysiologic characteristic (Coronary artery disease)

Pathophysiology

Coronary artery blood flow is blocked by atherosclerotic

narrowing, thrombus formation or persistent vasospasm;
myocardium supplied by the arteries is deprived of oxygen;
persistent ischemia may rapidly lead to tissue death

Clinical
Manifestations

Chest pain or discomfort ( described as aching or squeezing pain,

most common location is substernal, radiating to neck, jaw, back,
shoulders, left arm or occasionally the right arm)

complain of heartburn or indigestion

pallor, diaphoresis, cold skin, shortness of breath, weakness,

dizziness, anxiety, and feelings of impending doom

Electrocardiogram (12-lead) capable of diagnosing MI in 80%

of patients, making it an indispensable, noninvasive, and costeffective tool. Reading shows ST elevation, accompanied by Twave inversion; and later new pathologic Q wave

Cardiac Enzymes elevated CK with MB isoenzymes >5percent

(early diagnosis); elevated Troponin (early to late diagnosis); or
elevated LDH with flipped isoenzymes (late diagnosis)

WBC count leukocytosis (10,000/mm3 to 20,000/mm3) appears

on thesecond day after AMI and dis appears after 1 week

Positron Emission Tomography (PET) is used to evaluate cardiac

metabolism and to assess tissue perfusion

Magnetic Resonance Imaging helps identify the site and extent of

an MI

Diagnostics

Laboratory Tests

Imaging Studies

Nursing Diagnoses

Nursing
Management

Tranesophageal Echocrdiography (TEE) is an imaging technique

in which transducer is placed against the wall of the esophagus;
the image of the myocardium is clearer when the esophageal site
is used.

Acute Pain related to myocardial ischemia resulting from coronary

artery occlusion

Ineffective Tissue Perfusion related to thrombus in coronary artery

Decreased Cardiac Output related to negative inotropic changes

in the heart secondary to myocardial ischemia

Impaired Gas Exchange related to decreased cardiac output

Anxiety and Fear related to hospital admission and fear of death

Assess pain status frequently with pain scale

Assess hemodynamic status including BP, HR, LOC, skin color,

and temperature (every 5 minutes during with pain;every 15
minutes)

Monitor continuous ECG to detect dysrhytmias

Perform 12-lead ECG immediately with new pain or changes in

level of pain

Monitor respirations, breath sounds, and input and output to dtect

early signs of heart failure

Monitor O2 saturation and administer O2 as prescribed

Provide for physiological rest to decrease oxygen demands on

heart

Keep client NPO or progress to liquid diet as ordered; maintain IV

access for medication as needed

Provide a calm environment and reassure client and family to

decrease stress, fear and anxiety

Report significant changes immediately to physician to ensure

rapid treatment of complications

Maintain bed rest for 24 to 36 hours and gradually increase

activity as ordered while closely monitoring CO,ECG and pain

status

Pharmacologic
Therapy

Surgical
Interventions

Client Education

Acute Pulmonary failure

Nitroglycerine (to dilate coronary vessels and increase blood flow)

Morphine Sulfate (to relieve chest pain)

Anticoagulant (heparin) and Antiplatelet (aspirin) - to prevent

additional clot formation

Streptokinase (to dissolve clot)

Beta blockers (to decrease cardiac work)

Anti-dysrhytmic drugs

Percutaneous transluminal coronary angioplasty (PTCA)

involves the passage of an inflatable balloon catheter into the
stenonic coronary vessel, which is then dilated, resulting in
compression of the atherosclerotic plaque and widening of the
vessel

Coronary artery bypass grafting (CABG) done by harvesting

either a saphenous vein from the leg or the left internal
mammaryartery and then used to bypass areas of obstruction in
the heart

Include appropriate family members whenever possible

Explain cardiac rehabilitation program if ordered

Explain modifiable risk factors and develop a plan with client

including supportive resources to change lifestyle to decrease
these factors

Explain medication regime as prescribed; identify side effects to

report (provide written instructions for later reference)

Stress the importance of immediate reporting of chest pain or

signs of decreased CO2

Instruct about bleeding precautions if client is on anticoagulant

therapy: use soft toothbrush, electric razor, avoid trauma or injury;
wear or carry medical alert identification

Description

Defined as a fall in arterial oxygen tension and a rise in arterial

carbon dioxide tension.

- The ventilation and/or perfusion mechanisms in the lung are

impaired.

Etiologic factors

Pathophysiology

Clinical
Manifestations

Alveolar hypoventilation

Diffusion abnormalities

Ventilation-perfusion mismatching

Shunting

progression of pulmonary edema occurs when capillary

hydrostatic pressure is increased, promoying movement of fluid
into the interstitial space of the alveolar-capillary membrane.
Initially, increased lymphatic flow removes the excess fluids, but
continued leakage eventually overwhelms this mechanism. Gas
exchange becomes impaired by the thick membrane. Increasing
interstitial fluid pressure ultimately causes leaks into the alveolar
sacs, impairing ventilation and gas exchange

Tachypnea

Tachycardia

Cold, clammy skin and frank diaphoresis are apparent especially

around the forehead and face

Percussion reveals hyperresonance in patients with COPD; dull or

flat on patients with atelectasis or pneumonia

Diminished breath sounds; absence of breath sounds of the

affected lung in patients with pneumothorax; wheezes on patients

with asthma; ronchi on patients with bronchitis and crackles may

reveal suspicion of pulmonary edema

Diagnostics

Nursing Diagnoses

Nursing
Management

ABG analysis indicates respiratory failure when PaO2 is low and

PaCO2 is high and the HCO3 level is normal

Chest Xray is used to identify pulmonary diseases such as

emphysema, atelectasis, pneumothorax, infiltrates and effusions

Electrocardiogram (ECG) can demonstrate arrhytmias, commonly

found with cor pulmonale and myocardial hypoxia

Pulse oximetry reveals a decreasing SpO2 level

WBC count aids detection of an underlying infection;abnormally

low hemoglobin and hematocrit levels signal blood loss,indicating
decrease oxygen carrying capacity

PA catheterization is used to distinguish pulmonary causes from

cardiovascular causes of acute respiratory failure

Impaired Gas Exchange related to capillary membrane

obstruction from fluid

Excess Fluid Volume related to excess preload

Assess the patients respiratory status at least every 2 hours or

more as indicated

Position the patient for optimal breathing effort when he isnt

intubated. Put the call bell within easy reach to reassure the
patient and prevent necessary exertion

Maintain the normothermic environment to reduce patients

oxygen demand

Monitor vital signs, heart rhythm, and fluid intake and output,
including daily weights, to identify fluid overload or impending
dehydration

After intubation, auscultate the lungs to check for accidental

intubation of the esophagus or mainstem bronchus.

Dont suction too often without identifying the underlying cause of

an equipment alarm.

Pharmacologic
Therapy

Client Education

Watch oximetry and capnography values because these may

indicate changes in patients condition

Note the amount and quality of lung secretions and look for
changes in the patients status

Check cuff pressure on the ET tube to prevent erosion from an

overinflated cuff

Implement measures to prevent nasal tissue necrosis

Be alert of GI bleeding

Provide a means of communication for patients who are intubated

and alert

Reversal agents such as Naloxone (Narcan) are given if drug

overdose is suspected

Bronchodilators are given to open airways

Antibiotics are given to combat infection

Corticosteroids may be given to reduce inflammation

Continuous IV solutions of positive inotropic agents may be given

to increase cardiac output, and vasopressors may be given to
induce vasoconstrictions to improve or maintain blood pressure

Diuretics may be given to reduce fluid overload and edema

Include family member or others in teaching as appropriate

Weight monitoring: teach client the importance of measuring and

recording daily weights and report unexplained increase of 3-5
pounds

Diet: sodium restriction to decrease fluid overload and potassium

rich foods to replenish loss from medications; do not restrict water
intake unless directed

Medication regime: explain the importance of following all

medication instructions

Instruct client and family to maintain elevation of the head of the

client at least 45 degrees ; position increases chest expansion
and mobilizes fluid from the chest into more dependent areas

Acute Renal Failure

Description
Etiologic factor

Pathophysiology

Clinical
Manifestations

a sudden loss of kidney function caused by failure of renal

circulation or damage to the tubules or glomeruli

Prerenal - caused by decrease blood flow to kidneys like severe

dehydration,diuretic therapy,circulatory collapse,hypovolemia or
shock;readily reversible when recognized and treated

Intrarenal caused by disease process, ischemia, or toxic

conditions such as acute glomerulonephritis,vascular disorders,toxic
agents, or severe infection

Postrenal caused by any condition that obstructs urine flow such

as benign prostatic hyperplasia,renal or urinary tract calculi, or
tumors
-

Acute renal failure is classified as prerenal, intrarenal or

postrenal. All conditions that lead to prerenal failure impair blood
flow to the kidneys (renal perfusion), resulting in a decreased
glomerular filtration rate and increased tubular resorption of
sodium and water. Intrarenal failure results from damage to the
kidneys. Postrenal failure results from obstructed urine flow.

*A change in blood pressure and volume signals pre renal failure, the
patient may have the following:
-

Oliguria

Tachycardia

Hypotension

Dry mucous membranes

Flat jugular veins

Lethargy progressing to coma

Decreased cardiac output and cool, clammy skin in patient with

heart failure

*As renal failure progresses, the patient may manifest the following
signs and symptom:

Diagnostics

uremia

confusion

GI complaints

fluid in the lungs

infection

Blood studies reveal elevated BUN, serum creatinine, and

potassium levels and decreased blood pH, bicarbonate, HCT,
and Hb levels

Urine studies show cats, cellular debris, decreased specific

gravity and, in glomerular diseases, proteinuria and urine
osmolality close to serum osmolality.

Creatinine clearance testing is used to measure the GFR and

estimate the number of remaining functioning nephrons

Electrocardiogram (ECG) shows tall, peaked T waves, a

widening QRS complex, and disappearing P waves if increased
potassium is present

*other studies used to determine the cause of renal failure:

Nursing Diagnoses

kidney ultrasonography

plain films of the abdomen

KUB radiography

excretory urography

renal scan

retrograde pyelography

computed tomography scan and nephrotomography

Excess Fluid Volume

Imbalanced Nutrition: Less than Body Requirements

Deficient Knowledge

Nursing
Management

Pharmacologic
Therapy

Risk for Infection

Monitor intake and output

Observe for oliguria followed by polyuria

Weigh daily and observe for edema

Monitoring of complications of electrolyte imbalances, such as

acidosis and hyperkalemia

Allow client to verbalize concerns regarding disorder

Encourage prescribed diet: moderate protein restriction, high in

carbohydrates, restricted potassium

Once diuresis phase begins, evaluate slow return of BUN,

creatinine, phosphorus, and potassium to normal

use volume expanders are prescribed to restore renal perfusion

in hypotensive clients and Dopamine IV to increase renal blood
flow

Loop diuretics to reduce toxic concentration in nephrons and

establish urine flow

ACE inhibitors to control hypertension

Antacids or H2 receptor antagonists to prevent gastric ulcers

Kayexelate to reduce serum potassium levels and sodium

bicarbonate to treat acidosis

* avoid nephrotoxic drugs

Client Education

Dietary and fluid restrictions, including those that may be

continued after discharge

Signs of complications such as fluid volume excess, CHF, and

hyperkalemia

Monitor weight, blood pressure, pulse, and urine output

Avoid neprotoxic drugs and substances: NSAIDs, some

antibiotics, radiologic contrast media, and heavy metals; consult
care provider prior to taking any OTC drugs

Recovery of renal function requires up to 1 year; during this

period, nephrons are vulnerable to damage from nephrotoxins

Stroke/Cerebrovascular accident
Description

is a condition where neurological deficits occur as a result of

decreased blood flow to a localized area of the brain

thrombosis of the cerebral arteries supplying the brain or of the

intracranial vessels occluding blood flow

embolism from a thrombus outside the brain, such as in the

heart, aorta, or common carotid artery

hemorrhage from an intracranial artery or vein, such as from

hypertension, ruptured aneurysm, AVM, trauma, hemorrhagic
disorder, or septic embolism

Pathophysiology

the underlying event leading to stroke is oxygen and nutrient

deprivation; if the arteries become blocked, auto regulatory
mechanisms maintain cerebral circulation until collateral
circulation develops to deliver blood to the affected area; if the
compensatory mechanisms become overworked or cerebral
blood flow remains impaired for more than a few minutes,
oxygen deprivation leads to infarction of brain tissue

Risk factors

hypertension

family history of stroke

history of TIA

cardiac disease, including arrhythmias, coronary artery disease,

acute myocardial infarction, dilated myopathy, and valvular
disease

diabetes mellitus

familial hyperlipidemia

cigarette smoking

increased alcohol intake

obesity, sedentary lifestyle

Clinical
Manifestations

use of hormonal contraceptives

hemiparesis on the affected side ( may be more severe in the

face and arm than in leg)

unilateral sensory defect (such as numbness, or tingling)

generally on the same side as the hemiparesis

slurred or indistinct speech or the inability to understand speech

blurred or indistinct vision, double vision, or vision loss in one

eye (usually described as a curtain coming down or gray-out of
vision)

mental status changes or loss of consciousness (particularly if

associated with one of the above symptoms)

very severe headache (with hemorrhagic)

*A stroke in the left hemisphere produces symptoms on the right

side of the body; in the right hemisphere, symptoms on the left side
Diagnostics

CT scan discloses structural abnormalities, edema, and lesions,

such as nonhemorrhagic infarction and aneurysms

MRI is used to identify areas of ischemia, infarction and cerebral

swelling

DSA is used to evaluate patency of the cerebral vessels and

shows evidence of occlusion of the cerebral vessels, a lesion or
vascular abnormalities

Cerebral angiography shows details of disruption or

displacement of the cerebral circulation by occlusion or
hemorrhage

Carotid Duplex scan is a high frequency ultrasound that shows

blood flow through the carotid arteries and reveals stenosis due
to atherosclerotic plaque and blood clots

Transcranial Doppler studies are used to evaluate the velocity of

blood flow through major intracranial vessels, which can indicate
vessel diameter

Brain scan shows ischemic areas but may not be conclusive for
up to 2 weeks after stroke

Single photon emission CT scanning and PET scan show areas

of altered metabolism surrounding lesions that arent revealed by

other diagnostic tests

Nursing Diagnoses

Nursing
Management

Lumbar puncture reveals bloody CSF when stroke is

hemorrhagic

EEG is used to identify damaged areas of the brain and to

differentiate seizure activity from stroke

A blood glucose test shows whether the patients symptoms are

related to hypoglycemia

Hemoglobin and hematocrit level may be elevated in severe

occlusion

Baseline CBC, platelet count, PTT, PT, fibrinogen level and

chemistry panel are obtained before thrombolytic therapy

Ineffective Tissue Perfusion related to decreased cerebral blood

flow

Risk for Prolonged Bleeding related to use of thrombolytic

agents

Increased Risk for Aspiration related to depressed gag reflex,

Impaired swallowing

Impaired Physical Mobility related to loss of muscle tone

Encourage active range of motion on unaffected side and

passive range of motion on the affected side

Turn client every 2 hours

Monitor lower extremities for thrombophlebitis

Encourage use of unaffected arm for ADLs

Teach client to put clothing on affected side first

Resume diet orally only after successfully completing a

swallowing evaluation

Collaborate with occupational and physical therapists

Try alternate methods of communication with aphasia patients

Accept clients frustration and anger as normal to loss of function

Pharmacologic
Therapy

Surgical Intervention

Client Education

Teach client with homonymous hemianopsia to overcome the

deficit by turning the head side to side to be able to fully scan the
visual field

Thrombolytics for emergency treatment of ischemic stroke

Aspirin or Ticlopidine (Ticlid) as an antiplatelet agent to prevent

recurrent stroke

Benzodiazepines to treat patients with seizure activity

Anticonvulsants to treat seizures or to prevent them after the

patients condition has stabilized

Stool softeners to avoid straining, which increase ICP

Antihypertensives and antiarrhythmics to treat patients with risk

factors for recurrent stroke

Corticosteroids to minimize associated cerebral edema

Hyperosmolar solutions (Mannitol) or diuretics are given to

clients with cerebral edema

Analgesics to relieve the headaches that may follow a

hemorrhagic stroke

Craniotomy to remove hematoma

Carotid endarterectomy to remove atherosclerotic plaques from

the inner arterial wall

Extracranial bypass to circumvent an artery thats blocked by

occlusion or stenosis

Educate client and family about CVA and CVA prevention

Educate client and family about community resources

Educate client and family about physical care and need for
psychosocial support

Educate client and family about medication

Increased Intracranial Pressure

Description

- prolonged pressure greater than 15mmHg or 180mmH2O measured in

the lateral ventricles

Etiology

Cerebral Edema is an increase in volume of brain tissue due to

alterations in capillary permeability, changes in functional or the
structural integrity of the cell membrane or an increase in the
interstitial fluids

Hydrocephalus is an increase in the volume of CSF within the

ventricular system; it may be noncommunicating hydrocephalus
where the drainage from the ventricular system is impaired

Pathophysiology

Blood flow exerts pressure against a weak arterial wall,

stretching it like an overblown balloon and making it to rupture;
rupture is followed by a subarachnoid hemorrhage, in which
blood spills into space normally occupied by CSF. Sometimes,
blood spills into brain tissue, where a clot can cause potentially
fatal increased ICP and brain tissue damage

Clinical
manifestations

blurring of vision, decreased visual acuity and diplopia are the

earliest signs of increased ICP

headache, papilledema or the swelling of optic disk and

vomiting

change of LOC

skull radiography

CT scan

MRI

Diagnostics

* Lumbar puncture is not performed because of brain herniation caused

by sudden release of pressure
*Laboratory tests are performed to augment and monitor treatment
approaches; serum osmolarity monitors hydration status and ABGs
measure pH, oxygen and carbon dioxide
Nursing Diagnoses

Nursing
Management

Ineffective Cerebral Tissue Perfusion related to Increased ICP

Risk for Infection

Impaired Physical Mobility

Risk for Ineffective Airway Clearance

Assess neurological status every 1 to 2 hours and report any

deterioration; include LOC, behavior, motor/sensory function,

pupil size and response, vital signs with temperature

-

Maintain airway; elevate head of 30 degree or keep flat as

prescribed; maintain head and neck in neutral position to
promote venous drainage

Assess for bladder distention and bowel constipation; assist

client when necessary to prevent Valsava maneuver

Plan nursing care so it is not clustered because prolonged

activity may increase ICP; provide quiet environment and limit
noxious stimuli; limit stimulants such as radio, TV and
newspaper; avoid ingesting stimulants such as coffee, tea, cola
drinks and cigarette smoke

Maintain fluid restriction as prescribed

Keep dressings over catheter dry and change dressings as

prescribed; monitor insertion site for CSF leakage or infection;
monitor clients for signs and symptoms of infection; use aseptic
technique when in contact with ICP monitor

Osmotic diuretics such as Mannitol and loop diuretics such as

Furosemide ( Lasix) are mainstays used to decrease ICP

Corticosteroids are effective in decreasing ICP especially with

tumors

Surgical Intervention

A drainage catheter, inserted via ventriculostomy into lateral

ventricle, can be done to monitor ICP and to drain CSF to
maintain normal pressure; if used the system is calibrated with
transducer is leveled 1 inch above the ear; sterile is of utmost
importance

Client Education

Teach the client at risk for increased ICP to avoid coughing,

blowing the nose, straining for bowel movements, pushing
against the bed side rails, or performing isometric exercises

Advice the client to maintain neutral head and neck alignment

Encourage the family to maintain a quiet environment and

minimize stimuli

Educate the family that upsetting the client may increase ICP

Pharmacologic
therapy

METABOLIC EMERGENCIES
DKA
Description

Etiology

Life threatening metabolic acidosis resulting from persistent

hyperglycemia and breakdown of fats into glucose, leading to
presence of ketones in blood; can be triggered by emotional
stress, uncompensated exercise,infection, trauma, or insufficient
or delayed insulin administration
Decreased or missed dose of insulin

Illness or infection

Undiagnosed and untreated diabetes

Pathophysiology

In the absence of endogenous insulin, the body breaks down

fats for energy. In the process, fatty acids develop too rapidly
and are converted to ketones, resulting to severe metabolic
acidosis. As acidosis worsens, blood glucose levels increase
and hyperkalemia worsens. The cycle continues until coma and
death occur

Clinical
manifestations

Acetone breath

Poor appetite or anorexia

Nausea and vomiting

Abdominal pain

Blurred vision

Weakness

Headache

Dehydration

Thirst or polydipsia

Orthostatic hypotension

Hyperventilation (Kussmaul respirations)

Mental status changes in DKA vary from patient to patient

weight loss

Diagnostics

Nursing Diagnoses

Nursing Management

muscle wasting

leg cramps

recurrent infections

Serum glucose is elevated (200 to 800 mg/dl)

Serum Ketone Level is increased

Urine acetone test is positive

Arterial Blood Gas analysis reveals metabolic acidosis

ECG findings shows tall tented T waves and widened QRS

complex changes related to hyperkalemia; later with
hypokalemia, shows flattened T wave and the presence of U
wave

Serum osmolality is elevated

Deficient Fluid Volume

Risk for Injury

Risk for Skin Impaired Integrity

Ineffective Breathing Pattern

Disturbed Sensory Perception

Knowledge Deficit

Anxiety

Restore fluid, electrolyte and glucose balance with IV infusions

and medications, analyze intake and out, blood glucose, urine
ketones, vital signs, oxygenation and breathing pattern

Maintain skin integrity; promote healing of impaired skin; prevent

infection by turning and positioning client every 2 hours; provide
pressure relief as indicated; manage incontinence and
perspiration with skin protective barriers and cleansing; provide
appropriate nutrition and oxygen support

Promote safety by analyzing vital signs, client communication,

LOC and emotional response, and activity tolerance; implement

falls prevention measures

-

Assist client to verbalize concerns and cope effectively with

illness and fears

Assist client to update Medic-Alert bracelet information as

appropriate

Pharmacotherapy

Administer IV Insulin and fluid and electrolyte replacements

based on laboratory test results

Client Education

Instruct client about the nature and causes of DKA (such as

excess glucose intake, insufficient medications or physiological
and/or psychological stressors) any new medications

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC COMA

Description
- Life threatening metabolic disorder of hyperglycemia usually
recurring with DM type 2 medications, infections, acute illness,
invasive procedure, or a chronic illness
Etiology

Medications

Infections

acute illness

invasive procedure

chronic illness

Pathophysiology

glucose production and release into the blood is increased or

glucose uptake by the cells is decreased; when the cells dont
receive glucose, the liver responds by converting glycogen to
glucose for release into the bloodstream; when all excess
glucose molecules remain in the serum, osmosis cause fluid
shifts.; the cycle continues until fluid shifts in the brain cause
coma and death

Clinical
Manifestations

severe dehydration

hypotension and tachycardia

diaphoresis

tachypnea

polyuria, polydipsia and polypahgia

Diagnostics

Nursing Diagnoses

Nursing Management

lethargy and fatigue

vision changes

rapid onset of lethargy

stupor and coma

neurologic changes

Serum glucose is elevated, sometimes 800 to 2,000 mg/dl

Ketones are absent, urine and serum ketones are absent

Urine glucose levels are positive

Serum osmolality is increased

Serum Sodium levels are elevated and the serum potassium

level is usually normal

ABG results are usually normal, without evidence of acidosis

Decreased Cardiac Output

Deficient Fluid Volume

Hyperthermia

Disturbed Sensory Perception

Risk for Impaired Skin Integrity

Risk for Aspiration

Deficient Knowledge

Assess the patients LOC, respiratory status and oxygenation

Monitor the patients VS; changes may reflect the patients

hydration status

Monitor patients blood glucose and serum electrolytes

Administer regular insulin IV as ordered, by continuous infusion

and titrate dosage based on the patients blood glucose levels

Maintain intact skin integrity by turning every 2 hours, use of

pressure relief aids, nutritional support, use of skin moisturizers
and barriers, and management of incontinence

Prevent aspiration by using appropriate feeding precautions,

elevate head of bed 15 to 30 degrees during and after feeding
for 1 hour; if BP is too unstable to elevate head of bed with
feeding, then withhold oral feedings

Pharmacotherapy

IV infusion of NS to replace fluids and sodium, regular insulin IV

to manage the hyperglycemia, and potassium to replace losses
and shifts

Client Education

Instruct client and family about HHNK, symptoms to report, and

administration of new medications

Provide patient and family education to foster prevention of

future episodes

Description

Uncontrolled bleeding

Etiology

Result of blunt or penetrating trauma

Gastrointestinal or genitourinary bleeding

Hemoptysis

Pathophysiology

Due to the lack of adequate circulating blood volume causing

dcreased tissue perfusion and metabolism resulting in hypoxia,
vasoconstriction and shunting of the available circulating blood
volume to the vital organs(heart and brain);Symphathetic
nervous system stimulation, hormonal release of antidiuretic
hormone and the angiotensin-renin mechanisms and neural
responses attempt to compensate for the loss of circulating
volume but eventually metabolic acidosis, multi organ system
failure occurs

Clinical
Manifestations

cool, clammy, pale skin (esp. distal extremities)

delayed capillary refill (>3 seconds)

weak, rapid pulses

decreased blood pressure (systolic pressure <90mmHg)

rapid shallow respirations(>28/ min)

restless, anxious, decreased LOC

Massive Bleeding

Diagnostics

Nursing Diagnoses

Nursing Management

cardiac dysrhtymias (abnormalities of cardiac rhythm)

decreased urinary output

evidence of bleeding from thorocostomy that indicates bleeding

from chest area

abdominal or pelvic CT scan, abdominal ultrasound or

peritoneal lavage indicate intra abdominal bleeding

Endoscopy indicates upper or lower GI bleeding

Angiography procedures diagnose severe vascular damage

Extremity radiographs show long bone fractures

Hemoglobin and hematocrit from the CBC are decreased due to

blood loss

Elevated serum lactate if bleeding continues and client becomes

acidotic

ABGs show metabolic acidosis as blood loss continues

Baseline coagulation studies should be reviewed; initial PT/PTT

and platelet counts will be within normal limits but as
coagulation factors become depleted, clotting times will increase
and platelet counts will decrease

Serum electrolytes to assess renal function

Impaired Tissue Perfusion

Deficient Fluid volume

Decreased cardiac Output

Establish an adequate airway, breathing pattern, and applying

supplemental oxygen

Give priority interventions to control bleeding such as direct

pressure to wound site, or assisting with surgical interventions

Establish IV access and begin with fluid replacement

Draw blood specimens as ordered to assist in evaluation of

hemoglobin, hematocrit, electrolyte, oxygenation andhydration
status

Insert an indwelling catheter and NG tube to assist in accurate

recording of fluid balance status

Pharmacotherapy

Client Education

Perform and document continuous serial assessments of

hemodynamic parameters such as VS, capillary refill, CVP,
cardiac rhythm, LOC, urinary output and laboaratory findings

Crystalloids and blood products to maintain adequate circulating

volume status

Sodium Bicarbonate to correct acidosis state

Vasopressor such as Dopamine

Explain procedures to the client

Support the family by explaining emergency measures and

interventions

An alteration in skin integrity resulting in tissue loss or injury

caused by heat, chemicals, electricity or radiation

Burns
Description
Etiology

Pathophysiology

Types of burn injury

a

Thermal: results from dry heat (flames) or moist heat (steam or

hot liquids); it is the most common type; it causes cellular
destruction that results in vascular, bony, muscle, or nerve
complications; thermal burns can also lead to inhalation injury if
the head and neck area is affected

Chemical burns are caused by direct contact with either acidic

or alkaline agents; they alter tissue perfusion leading to necrosis

Electrical burns; severity depends on type and duration of

current and amount of voltage; it follows the path of least
resistance(muscles, bone, blood vessels and nerves); sources
of electrical injury include direct current, alternating current and
lightning

Radiation burns: are usually associated with sunburn or

radiation treatment for cancer; are usually superficial; extensive
exposure to radiation may lead to tissue damage

It depends on the cause and classification of the burn; the

injuring agents denatures cellular proteins; some cells die
because of traumatic or ischemic necrosis; loss of collagen

cross-linking also occurs with denaturation, creating abnormal

osmotic and hydrostatic pressure gradients that cause
intravascular fluid to move into interstitial spaces; Cellular injury
triggers the release of mediators of inflammation, contributing to
local and in the case of major burns , systemic increases in
capillary permeability
Clinical
Manifestations

Diagnostics

Localized pain and erythema, usually without blisters in the first

24 hours (first degree burn)

Chills, headache, localized edema, nausea and vomiting (most

severe first degree burn)

Thin-walled, fluid filled blisters appearing within minutes of the

injury, with mild to moderate edema and pain (second degree
superficial partial thickness burn)

White, waxy appearance to damaged area(second degree

partial-thickness burn)

White, brown or black leathery tissue and visible thrombosed

vessels due to destruction of skin elasticity(dorsum of hand,
most common site of thrombosed veins), without blisters (thirddegree burn)

Silver-colored, raised or charred area, usually at the site of

electrical contact

*Rule of Nines chart determines the percentage of body surface area

(BSA)covered by the burn
-

ABG levels may be normal in the early stages but may reveal
hypoxemia and metabolic acidosis

Carboxyhemoglobin level may reveal the extent of smoke

inhalation due to the presence of carbon monoxide

Complete blood count may reveal a decrease hemoglobin due

to hemolysis, increased hematocrit and leukocytosis

Electrolyte levels show hyponatremia and hyperkalemia,other

laboratory tests reveals elevated BUN,decreased total protein
and albumin

Creatinine kinase (CK) and myoglobin levels may be elevated

Presence of myoglobin in urine may lead to acute tubular

necrosis
Risk for Deficient Fluid Volume

Risk for Infection

Impaired Physical Mobility

Imbalanced Nutrition: Less than Body Requirements

Ineffective Breathing Pattern

Impaired Tissue Perfusion

Risk for Impaired Gas Exchange

Anxiety

Risk for Ineffective Thermoregulation

Pain

Impaired Skin Integrity

Assess patients ABCs; monitor arterial oxygen saturation and

serial ABG values and anticipate the need for ET intubation and
mechanical ventilation

Auscultate breath sounds

Administered supplemental humidified oxygen as ordered

Perform oropharyngeal or tracheal suctioning as indicated by

the patients inability to clear his airway

Nursing Diagnoses

Nursing Management

Monitor the patients cardiac and respiratory status

Assess LOC for changes such as confusion,

restlessness or
decreased responsiveness
-

Irrigate the wound with amounts of water or normal

saline
solution for chemical burns
-

Place the patient in semi-Fowlers position to maximize

chest
expansion; keep patient as quiet and comfortable to minimize
oxygen demand
-

Prepare the patient for an emergency escharotomy of

the chest
and neck for deep burns
-

Administer rapid fluid replacement therapy as ordered

*For burn patient in shock

Pharmacotherapy

Monitor VS and hemodynamic parameters

Assess patients intake and output every hour, insert an

indwelling cathether

Assess the patients level of pain, including nonverbal indicators

and administer analgesics such as Morphine Sulfate IV as
ordered

Keep the patient calm, provide periods of uninterrupted rest

between procedures and use nonpharmacologic pain relief
measures as appropriate

Obtain daily weights and monitor intake, including daily calorie

counts; provide high calorie, high protein diet

Administer histamine 2 receptor antagonists as ordered to

reduce risk of ulcer formation

Assess the patients sign and symptoms of infection; may obtain

wound culture and administer antimicrobials an antipyretics as
ordered

Administer tetanus prophylaxis if indicated

Perform burn wound care as ordered; prepare patient for

grafting as indicated

Assess the neurovascular status of the injured area, including

pulses, reflexes, paresthesia, color and temperature of the
injured area at least 2 to 4 hours or more frequently as indicated

Assist with splinting, positioning, compression therapy and

exercise to the burned area as indicated; maintain the burned
area in a neutral position to prevent contractures and minimize
deformity

Explain all procedures to the patient before performing them

Antibiotic prophylaxis will eradicate bacterial component

Pain therapy

Tetanus prophylaxis

Topical antimicrobial

Enzymatic debriding agents such as collagenase, fibrinolysindesoxyribonuclease, papin or sutilins are used with a moisture
barrier to protect surrounding tissue

Recommended dressings include polyurethane films(Op-site,

Tegaderm), absorbent hydrocolloid dressings (Duoderm)

Environmental safety: use low temperature setting for hot water

heater, ensure access to and adequate number of electrical
cords/outlets, isolate household chemicals, avoid smoking inbed

Use of household smoke detectors with emphasis on

maintenance

Proper storage and use of flammable substances

Evacuation plan for family

Care of burn at home

Signs and symptoms of infection

How to identify risk of skin changes

Use of sunscreen to protect healing tissue and other protective

skin care

Description

Substances that are harmful to humans that are inhaled,

ingested (food, drug overdose) or acquired by contact

Etiology

Carbon monoxide inhalation

Food poisoning

Drug overdose

Insecticide surface absorption

The pathophysiology of poisons depends on the substance

thats inhaled or ingested. The extent of damage depends on
the pH of the substance, the amount ingested, its form and the
length of exposure to it. Substances with an alkaline pH cause

Client Education

Poisoning

Pathophysiology

tissue damage by liquefaction necrosis, which softens the

tissue. Acids produce coagulation necrosis. Coagulation
necrosis denatures proteins when substance contacts tissue.
This limits the extent of the injury by preventing penetration of
the acid into the tissue.

Clinical
Manifestations

Diagnostics

*The mechanism of action for inhalants is unknown, but theyre

believed to act on the CNS similarly to a very potent anesthetic.
Hydrocarbons sensitize the myocardial tissue and allow it to be
sensitize to cathecolamines, resulting in arrhythmias

Carbon monoxide inhalation: mild exposure nausea, vomiting,

mild throbbing headache, flu-like symptoms; moderate exposure
dyspnea, dizziness, confusion, increased severity of mild
symptoms; severe/prolonged exposure seizures, coma,
respiraotory arrest, hypotension and dysrhytmias

Food poisonings: nausea, vomiting, diarrhea, abdominal

cramps, fever , chills, dehydration, headache

Drug overdose: depends upon the substance ingested;

symptoms may include nausea, vomiting, CNS depression or
agitation, altered pupil response, respiratory changes such as
tachypnea or bradypnea, alterations in temperature control,
seizures or cardiac arrest

Surface absorption of insecticides( organophosphates or

carbamates): nausea, vomiting, diarrhea, headache, dizziness,
weakness or tremors, mild to severe respiratory distress, slurred
speech, seizures, and cardio-pulmonary arrest

*The diagnosis of many poisonings is based on a thorough client

history and clinical manifestations
-

laboratory toxicology screens (serum,vomitus, stool and urine)

determine the extent of the absorption

baseline blood work such as CBC, electrolytes, renal and

hepatic studies enable future determination of organ and tissue
damage

Chest Xray may show aspiration pneumonia in inhalation

poisoning

Abdominal Xrays may reveal iron pills or other radiopaque

substances

Nursing Diagnoses

Nursing Management

Pharmacotherapy

Client Education

ABG analysis used to evaluate oxygenation

Risk for Ineffective Airway Clearance

Risk For Decreased Cardiac Output

Deficient Fluid Volume

Ineffective Breathing Pattern

Impaired Tissue Perfusion

Risk for Injury

Anxiety

Risk for Self-directed Violence

Hopelessness

Assist with the management of an effective airway, breathing

pattern and circulatory status

Give treatment of life-threatening dysrhythmias and conditions

as ordered; continual monitoring of vital signs, cardiac rhythm
and neurological status and supportive care is essential

Assist in the hastening in the elimination of the medication or

poison, decrease the amount of absorption and administer
antidotes as ordered

for specific treatment contact the poison center

*antidotes will vary with medication ingested

-

Ipecac syrup 30ml PO followed by 240ml water is used for adults

Activated charcoal powder slurry 30 to 100g PO or per NG tube

Magnesium Citrate will be used for GI evacuation

Naloxone (Narcan) for respiratory depression caused by narcotic

overdose
Flumazanil (Romazicon) for benzodiazepine ingestions
Assist the client and family in seeking the appropriate referrals
and provide client education to further complications or
incidence of overdose

Ensure that the client and family understand discharge

instruction for follow up care or reason for admission

Multiple Injuries
Description

Is a physical injury or wound thats inflicted by an external or

violent act; it may be intentional or unintentional; involve injuries
to more than one body area or organ

Etiology

Weapons

Automobile collision

Physical confrontation

Falls

Unnatural occurrence to the body

*Type of trauma which determines the extent of injury

-

Blunt trauma leaves the body intact

Penetrating trauma disrupts the body surface

Perforating trauma leaves entrance and exit

Pathophysiology

A physical injury can create tissue damage caused by stress

and strain on surrounding tissue which results to infection, pain ,
swelling and potential compartment syndrome or it can be life
threatening if it affects a highly vascular or vital organ

Diagnostics

Chest Xray detect rib and sterna fractures, pneumothorax, flail

chest, pulmonary contusion and lacerated or ruptured aorta

Angiography studies performed with suspected aortic

laceration or rupture

Ct scan, cervical spine Xrays, skull Xrays, Angiogram test for

a patient with head trauma

ABG analysis to evaluate respiratory status and determine

acidotic and alkalotic states

CBC to indicate the amount of blood loss

Coagulation studies to evaluate clotting ability

Serum electrolyte levels to indicate the presence of electrolyte

imbalances

Ineffective Airway Clearance

Nursing Diagnoses

Nursing Management

Ineffective Breathing Pattern

Impaired Gas Exchange

Deficient Fluid Volume

Decreased Cardiac Output

Impaired Tissue Perfusion

Impaired Skin Integrity

Risk for infection

Anxiety

Pain

Disturbed Body Image

Assess the patients ABCs and initiate emergency measures

Administer supplemental oxygen as ordered

Immobilize the patients head and neck with an immobilization

device, sandbags, backboard and tape

Assist with cervical Xrays

Monitor VS and note significant changes

Immobilize fractures

Monitor the patients oxygen saturation and cardiac rhythm for

arrhythmias

Assess the patients neurologic status, including LOC and

papillary and motor response

Obtain blood studies, including type and crossmatch

Insert large bore IV catheter and infuse normal saline or lactated

Ringers solution

Assess the patient for multiple injuries

Assess the patients wounds and provide wound care as

appropriate; cover open wounds and control bleeding by

applying pressure and elevating extremities

Pharmacotherapy

Client Education

Assess for increased abdominal distention and increased

diameter of extremities

Administer blood products as appropriate

Monitor the patient for signs of hypovolemic shock

Provide pain medication as appropriate

Provide reassurance to the patient and his family

Tetanus immunization

Antibiotics for infection control

Analgesics for pain

Provide explanations of all procedures done

Families usually require emotional support and honest

discussions about therapeutic interventions and plans