Acute Biologic Crisis
Condition that may result to patientmortality if left unattended
in a briefperiod of time.
Condition that warrantsimmediateattention for the reversal of
diseaseprocess and prevention of furthermorbidity 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 right- sided failure- Formerly called Congestive
Heart Failure
Etiologic Factors :
Increased metabolic rate (eg. fever, thyrotoxicosis) Hypoxia
Anemia
Pathophysiology:
- 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 eventually leads
to pulmonary and venous congestion.
Left-Sided Cardiac Failure
- 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.
Clinical Manifestations
- 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
Right-Sided Cardiac Failure
- 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.
Clinical Manifestations
- 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- 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
Nursing Management
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 heartb. Chronic heart
failure- 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
Pharmacologic Therapy - 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.- 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
Client Education 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 InfarctionDescription - Occurs when the heart
muscle is deprived of oxygen and nutrient-rich 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
Diagnostics
Laboratory Tests
Imaging Studies - Electrocardiogram (12-lead) capable of
diagnosing MI in 80% of patients, making it an indispensable,
noninvasive, and cost-effective tool. Reading shows ST elevation,
accompanied by T-wave 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
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.
Nursing Diagnoses 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
Nursing Management 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 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
Surgical Interventions 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
Client Education 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
Acute Pulmonary failureDescription- 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 Alveolar hypoventilation Diffusion
abnormalities Ventilation-perfusion mismatching Shunting
Pathophysiology 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
Clinical Manifestations 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 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
Nursing Diagnoses Impaired Gas Exchange related to capillary
membrane obstruction from fluid Excess Fluid Volume related to
excess preload
Nursing Management 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. 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
Pharmacologic Therapy 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
Client Education- 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 FailureDescription a sudden loss of kidney function
caused by failure of renal circulation or damage to the tubules or
glomeruli
Etiologic factora. Prerenal - caused by decrease blood flow to
kidneys like severe dehydration,diuretic therapy,circulatory
collapse,hypovolemia or shock;readily reversible when recognized
and treatedb. Intrarenal caused by disease process, ischemia, or
toxic conditions such as acute glomerulonephritis,vascular
disorders,toxic agents, or severe infectionc. Postrenal caused by
any condition that obstructs urine flow such as benign prostatic
hyperplasia,renal or urinary tract calculi, or tumors
Pathophysiology 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.
Clinical Manifestations *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: - uremia - confusion - GI complaints - fluid in the lungs
- infection
Diagnostics 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: - kidney ultrasonography - plain films of
the abdomen - KUB radiography - excretory urography - renal scan -
retrograde pyelography - computed tomography scan and
nephrotomography
Nursing Diagnoses Excess Fluid Volume Imbalanced Nutrition: Less
than Body Requirements Deficient Knowledge Risk for Infection
Nursing Management 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
Pharmacologic Therapy 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 accidentDescription 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 use of hormonal contraceptives
Clinical Manifestations 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 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
Nursing Diagnoses 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
Nursing Management 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 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
Pharmacologic Therapy 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
Surgical Intervention 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
Client Education 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 PressureDescription- 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
Diagnostics skull radiography CT scan MRI* 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 Ineffective Cerebral Tissue Perfusion related
to Increased ICP Risk for Infection Impaired Physical Mobility Risk
for Ineffective Airway Clearance
Nursing Management 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
Pharmacologic therapy 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
METABOLIC EMERGENCIESDKADescription 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
Etiology 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 - muscle wasting - leg cramps - recurrent
infections
Diagnostics 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
Nursing Diagnoses Deficient Fluid Volume Risk for Injury Risk
for Skin Impaired Integrity Ineffective Breathing Pattern Disturbed
Sensory Perception Knowledge Deficit Anxiety
Nursing Management 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 lethargy and fatigue vision changes rapid onset of
lethargy stupor and coma neurologic changes
Diagnostics 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
Nursing Diagnoses Decreased Cardiac Output Deficient Fluid
Volume Hyperthermia Disturbed Sensory Perception Risk for Impaired
Skin Integrity Risk for Aspiration Deficient Knowledge
Nursing Management 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
Massive BleedingDescription 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 28/ min)
restless, anxious, decreased LOC cardiac dysrhtymias (abnormalities
of cardiac rhythm) decreased urinary output
Diagnostics 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
Nursing Diagnoses Impaired Tissue Perfusion Deficient Fluid
volume Decreased cardiac Output
Nursing Management 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
Perform and document continuous serial assessments of hemodynamic
parameters such as VS, capillary refill, CVP, cardiac rhythm, LOC,
urinary output and laboaratory findings
Pharmacotherapy Crystalloids and blood products to maintain
adequate circulating volume status Sodium Bicarbonate to correct
acidosis state Vasopressor such as Dopamine
Client Education Explain procedures to the client Support the
family by explaining emergency measures and interventions
BurnsDescription An alteration in skin integrity resulting in
tissue loss or injury caused by heat, chemicals, electricity or
radiation
EtiologyTypes of burn injurya. 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
affectedb. Chemical burns are caused by direct contact with either
acidic or alkaline agents; they alter tissue perfusion leading to
necrosisc. 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
lightningd. Radiation burns: are usually associated with sunburn or
radiation treatment for cancer; are usually superficial; extensive
exposure to radiation may lead to tissue damage
Pathophysiology 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 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 (third-degree burn)
Silver-colored, raised or charred area, usually at the site of
electrical contact
Diagnostics*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
Nursing Diagnoses 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
Nursing Management 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 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 - 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
Pharmacotherapy Antibiotic prophylaxis will eradicate bacterial
component Pain therapy Tetanus prophylaxis Topical antimicrobial
Enzymatic debriding agents such as collagenase,
fibrinolysin-desoxyribonuclease, 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)
Client Education 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
PoisoningDescription 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
Pathophysiology 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
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.
*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
Clinical Manifestationsa. 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 b.
Food poisonings: nausea, vomiting, diarrhea, abdominal cramps,
fever , chills, dehydration, headachec. 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 arrestd. 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
Diagnostics*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 ABG analysis used to evaluate oxygenation
Nursing Diagnoses 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
Nursing Management 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
Pharmacotherapy*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
Client Education 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 InjuriesDescription 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
Nursing Diagnoses Ineffective Airway Clearance 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
Nursing Management 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 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
Pharmacotherapy Tetanus immunization Antibiotics for infection
control Analgesics for pain
Client Education Provide explanations of all procedures done
Families usually require emotional support and honest discussions
about therapeutic interventions and plans