CARDIAC FAILURE

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 include increased metabolic rate (egg. fever,
thyrotoxicosis), Hypoxia, Anemia. Cardiac failure most commonly occurs with disorders of
cardiacmuscles that result in decreased contractile properties of the heart. Causing underlying
conditions that lead to decreased myocardial contractility include myocardial dysfunction, arterial
hypertension, and alular 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 my cellular 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 theheart and in turn leads to hypertrophy of myocardial
muscle fibers; this can be considered a compensatory mechanism because it increases contractility.
Alular heart disease is also a cause of cardiac failure. The valves ensure that blood flows in one direction.
With alular 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 FailurePulmonary 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 pulmonarytissues and alveoli; which impairs gas exchange.

Nursing Diagnosis:

 Activity intolerance r/t imbalance between oxygen supply anddemand secondary to

decreased carbon dioxide
 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 responsibilitiessecondary to chronic illness and
hospitalization
Nursing Management (Acute phase)

 Monitor and record BP, pulse, respirations, ECG and CVP to detect changes in cardiac output.
 Maintain client in sitting position to decrease pulmonarycongestion 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 catheter tallow accurate measurement of
urine output) to evaluate fluid status If fluid restriction is prescribed, spread the fluid
throughout the dayto reduce thirst.
 Encourage physical rest and organized activities with frequentrest periods to reduce the work of
the heart.
 Provide a calm reassuring environment to decrease anxiety (thisdecreases oxygen consumption
and demands on the chronic heart failure.
 Educate client and family about the rationale for the regimen stablish baseline assessment for
fluid status and functionalabilities
 Monitor daily weights to evaluate changes in fluid status, assess at regular intervals for changes
in fluidstatus or functionalactivity level

Pharmacologic Therapy

 ACE Inhibitors (promotes vasodilation and diuresis by decreasingafterload 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.).
 (Dobutrex) is an intravenous medication given to patients with significant left ventricular
dysfunction. Acatecholamine, it stimulates the beta1-adrenergic receptors. Itsmajor action is to
increase cardiac contractility.
 Milrinone (Primacor). A phosphodiesterase inhibitor that prolongsthe release and prevents the
uptake of calcium. Causing a decrease in preload and afterload.
 Nitroglycerine (a vasodilator reduces preload).
 Morphine to sedate and vasodilator, decreasing the work of theheartAnticoagulants may be
prescribed.
 Beta-adrenergic blockersmaybe indicated in patients with mild or moderate failure.

Client Education

 Include family member or others in teaching as appropriate

  Teach client the importance of measuring and recording daily weights and report unexplained
increase of 3-5pounds 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 instruction
 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 Myocardial Infarction.

CORONARY ARTERY DISEASE

Coronary artery blood flow is blocked by atheroscleroticnarrowing, thrombus formation or

persistent vasospasm; myocardium supplied by the arteries is deprived of oxygen; persistent ischemia
may rapidly lead to tissue death.

Clinical Manifestations includes chest pain or discomfort (described as aching or squeezing pain,
most common location is sub sternal, 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.

Nursing Diagnosis

 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 15minutes).
 Monitor continuous ECG to detect dysrhythmias.
 Perform 12-lead ECG immediately with new pain or changes in level of pain.
 Monitor respirations, breath sounds, and input and output to detectearly 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 I 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 painstatus.

PharmacologicTherapy

 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-dysrhythmia

Surgical Interventions

 Percutaneous Trans luminal coronary angioplasty (PTCA) –involves the passage of an inflatable
balloon catheter into thestenonic 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 internalmammaryartery and then usedto 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: usesoft toothbrush,
electric razor, avoid trauma or injury; wear or carry medical alert identification.

ACUTE PULMONARY FAILURE

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

Progression of pulmonary edema occurs when capillary hydrostatic pressure is increased,

promoting 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 Manifestation

 Tachypnea –Tachycardia
 Cold, clammy skin and frank diaphoresis are apparent especially around the forehead and face
 Percussion reveals hyper resonance 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; rhonchi on patients with bronchitis and
crackles may reveal suspicion of pulmonary edema

Nursing Diagnosis

 Impaired Gas Exchange related to capillary membrane obstruction from fluid

 Excess Fluid Volume related to excess preload

NursingManagement
 Assess the patient’s respiratory status at least every 2 hours or more as indicated
 Position the patient for optimal breathing effort when he isn’t intubated. Put the call bell within
easy reach to reassure the patient and prevent necessary exertion
 Maintain the norm thermic environment to reduce patient’s 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
main stem bronchus.
 Don’t suction too often without identifying the underlying cause of an equipment alarm.
 Watch oximetry and scenography values because these may indicate changes in patient’s
condition
 Note the amount and quality of lung secretions and look for changes in the patient’s 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 (Narran) 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 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 3-5pounds.
 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

Is a sudden loss of kidney function caused by failure of renal circulation or damage to the
tubules or glomeruli.

Etiologic factor

 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.
 Post renal – caused by any condition that obstructs urine flow such as benignprostatic
hyperplasia, renal or urinary tract calculi, or tumors.

Acute renal failure is classified as perennial, intracranial or post renal. All conditions that lead to
perennial failure impair blood flow to the kidneys (renal perfusion), resulting in a decreased glomerular
filtration rate and increased tubular desorption of sodium and water. Intracranial failure results from
damage to the Kidneys. Post renal failure results from obstructed urine flow.

Clinical Manifestations

A change in blood pressure and volumesignal 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.

Nursing Diagnosis

 Excess Fluid Volume

 Imbalanced Nutrition: Less than Body Requirements
 Deficient Knowledge
 Riskfor 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, keratinize, 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 nephrotoxic 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
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

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 alular 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

Nursing Diagnosis

 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 swallowing evaluation -Collaborate with
occupational and physical therapists
 Try alternate methods of communication with aphasia patients. Accept client’s frustration and
anger as normal to loss of function
 Teach client with homonymous hemianopia to overcome the deficit by turning the head side to
side to be able to fully scan the visual field

Pharmacologic Therapy

 Thrombolytic for emergency treatment of ischemic stroke

 Aspirin or Ticlopidine (Tic lid) 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 patient’s condition has stabilized -
Stool softeners to avoid straining, which increase ICP
 Antihypertensive and antiarrhythmic to treat patients with risk factors for recurrent stroke -
Corticosteroids to minimize associated cerebral edema
 Hyperosmolar solutions (Manito) or diuretics are given to clients with cerebral edema
 Analgesics to relieve the headaches that may follow hemorrhagic stroke.

Surgical Intervention

 Craniotomy to remove hematoma

 Carotid endarterectomy to remove atherosclerotic plaques from the inner arterial wall
 Extra cranial bypass to circumvent an artery that’s 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 PRESSURE
Prolonged pressure greater than 15mm Hg or 180 mm H 2 O 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 no communicating 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.

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

Nursing Diagnosis

 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
Val Sava 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 Manito and loop diuretics such as Furosemide (Lasix) are mainstays
used to decrease ICP
 Corticosteroids are effective in decreasing ICP especially withtumors

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 quiet environment and minimize stimuli
 Educate the family that upsetting the client may increase ICP


METABOLIC EMERGENCIES DKA

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

Nursing Diagnosis

 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 asappropriate
 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

Life threatening metabolic disorder of hyperglycemia usually recurring with DM types 2
medications, infections, acute illness, invasive procedure, or a chronic illness.

Etiology

 Medications
 Infections
 Acute illness
  Invasive procedure
 Chronic illness

Glucose production and release into the blood is increased or glucose uptake by the cells is
decreased; when the cells don’t 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 polyphagia
 Lethargy and fatigue
 Vision changes
 Rapid onset of lethargy -Stupor and coma
 Neurologic changes

Nursing Diagnosis

 Decreased Cardiac Output

 Deficient Fluid Volume
 Hyperthermia -Disturbed Sensory Perception
 Risk for Impaired Skin Integrity
 Risk for Aspiration
 Deficient Knowledge

Nursing Management

 Assess the patient’s LOC, respiratory status and oxygenation

 Monitor the patient’s VS; changes may reflect the patient’s hydration status
 Monitor patient’s blood glucose and serum electrolytes
 Administer regular insulin IV as ordered, by continuous infusion and titrate dosage based on the
patient’s 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 Ivo 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 BLEEDING
Uncontrolled bleeding

Etiology

 Result of blunt or penetrating trauma

 Gastrointestinal or genitourinary bleeding
 Hemoptysis

Due to the lack of adequate circulating blood volume causing creased tissue perfusion and
metabolism resulting in hypoxia, vasoconstriction and shunting of the available circulating blood volume
to the vital organs(heart and brain); Sympatheticnervous 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
 Cardiac dysrhythmias (abnormalities of cardiac rhythm)
 Decreased urinary output

Nursing Diagnosis

 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, and 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 laboratory 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

BURNS
An alteration in skin integrity resulting in tissue loss or injury caused by heat, chemicals,
electricity or radiation.

Etiology

Types of Burn Injury

 Thermal: results from dry heat (flames) or moist heat (steam or hot liquids); it is the
most common type; itcauses 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

The pathophysiology 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 first24 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 thrombosis veins), without
blisters (third-degree burn)
 Silver-colored, raised or charred area, usually at the site of electrical contact

Nursing Diagnosis

 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 patient’s 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 or pharyngeal or tracheal suctioning as indicated by the patient’s inability to clear his
airway
 Monitor the patient’s cardiac and respiratory status
 Assess LOC for changes such as confusion, restlessness or decreased responsiveness -solution
for chemical burns
 Place the patient in semi-Fowler’s 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 patient’s intake and output every hour, insert an indwelling catheter
 Assess the patient’s 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 no
pharmacologic 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 patient’s sign and symptoms of infection; may obtain wound culture and administer
antimicrobials 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, parenthesis, 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, pain or
sustains are used with a moisture barrier to protect surrounding tissue
 Recommended dressings include polyurethane films (Op-site, Tegaderm), absorbent
hydrocolloid dressings (Dodder)

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, and avoid smoking
imbed
 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

POISONING
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 that’s inhaled or ingested. The extent
of damage depends on 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 they’re believed to act on the CNS similarly to a
very potent anesthetic. Hydrocarbons sensitize the myocardial tissue and allow it to be sensitize to
catecholamine’s, resulting in arrhythmias.

Clinical Manifestations

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

Nursing Diagnosis

 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
 Flumazenil (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 INJURIES
Is a physical injury or wound that’s 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

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

Nursing Diagnosis

 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 patient’s ABCs and initiate emergency measures

 Administer supplemental oxygen as ordered
 Immobilize the patient’s head and neck with an immobilization device, sandbags, backboard and
tape
 Assist with cervical X-rays

 Monitor VS and note significant changes

 Immobilize fractures -Monitor the patient’s oxygen saturation and cardiac rhythm for
arrhythmias
 Assess the patient’s neurologic status, including LOC and papillary and motor response
 Obtain blood studies, including type and crosshatch -Insert large bore IV catheter and infuse
normal saline or lactated Ringer’s solution
 Assess the patient for multiple injuries
 Assess the patient’s 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
 Catanduanes State University

College of Health Sciences

Virac, Catanduanes

NURSING CARE MANAGEMENT OF PATIENTS IN

ACUTE BIOLOGIC CRISIS

Submitted by:
Arnold Temporosa
BSN-4A

Submitted to:
Professor MARY ELAINE TAPEL

October 2018