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Heart Failure

A. Definition
Heart failure is a physiologic state in which the heart is unable to pump
enough blood to meet the metabolic needs of the body (determined oxygen
consumption) at rest or during exercise even though filling pressures are
adequate. The heart fails when, owing to intrinsic disease or structural
defects, it cannot handle a normal blood volume or, in the absence of disease,
it cannot tolerate a sudden expansion in blood volume (e.g., during exercise).
Heart failure is not a disease itself; instead. The term denotes a group of
manifestations related, to inadequate pump performance from either the
cardiac valves or myocardium. Whatever the cause, pump failure results in
hypoperfused tissue followed by pulmonary and systemic venous congestion.
Because heart failure causes vascular congestion, it is often called congestive
heart failure, although this term is no longer advised by most cardiac
specialists. Other term used to denote heart failure include cardiac
decompensate, cardiac insufficiency, and ventricular failure.
Estimates from the American Heart Association indicate 4,7 million
American have heart failure and are alive. The incidence of new cases is
around 400.000 annually. Annually, about 39,387 clients die from heart
failure. The incidence of heart failure approaches 10 in 1000peopel after age

B. Etiology
The performance of the heart depends on two essential components. Fiber
length (Frank-Starling mechanism) and the inherent contractility (isotropic
state) of the muscle. The normal heart automatically responds to maintain
cardiac output. Several factors automatically adjust the extent of shortening
of myocardial fibers and consequently, the stroke volume and cardiac output.
Five interrelated factors are involved: preload, after load, contractility, the
coordinated pattern of contraction, and the heart rate. Adverse changes in
these determinants of myocardial performance ultimately cause the heart of
fail. The causes of heart failure can be divided into tree subgroup:
1. Abnormal Loading Condition
Recall the analogy that the heart muscle is like a stretched rubber band.
When the rubber band is stretched it contracts with more force. The heart
muscle does the same. Venous return stretches the heart and improves
contractility. Extending the analogy, when the rubber band is
overstretched it becomes limp and cannot contract. Likewise, when the
heart overloaded with blood. Excessive stretch and decreased contraction
occurs. Overload develops because blood dose not leave the ventricle
during contraction. Therefore, cardiac workload increases to try to move
2. Abnormal Muscle Function
There art certain conditions that directly interfere with myocardial
contractility. Intrinsic condition are inherent in the cardiac muscle and
include MI; myocardium, an inflammation of the myocardium associated
with viral, bacterial, fungal, or parasitic diseases or toxic chemical injury;
cardiomyopathy; and ventricular aneurysm. Such disorder impair the
contractile Function of the myocardial fibrils, which reduces ventricular
emptying and stork volume.
3. Conditions That Precipitate or Exacerbate Heart Failure
 Physical or Emotional Stress
Stannous physical exercise and strong emotions (fear, excitement, and
anxiety) increase sympathetic nervous tone and catecholamine
release. This increases myocardial work by increasing heart rate,
myocardial, and blood pressure.
 Dysrhythmias
Cardiac dysrhythmias, most notably tachycardia (rapid heart rate).
Are the most common factors precipitating heart failure. A rapid
heartbeat shorten the time or ventricular filling (diastole), which in
turn reduces cardiac output and decreases myocardial perfusion. In
addition. The workload ad oxygen requirements of the myocardium
 Infection
Any systemic infection increases the oxygen demand of the body
tissues. The heart must keep pace with theses demands. Fever and
hypoxemia, which occur in some pulmonary infection, further tax the
ailing heart and may precipitate failure.
 Anemia
Reduction in the oxygen-curing capacity of the blood. As in anemia,
necessitates increased cardiac output to meet body’s need for oxygen.
Whereas a normal heart my adjust to the increased worked, a
compromises heart cannot, and failure ensues
 Thyroid Disorder
Thyrotoxicosis, associated with hyperthyroidism, augments the
metabolic need of the body, accelerating heart rate and the workload
of the heat. If thyrotoxicosis is untreated, heart failure may occur. In
hypothyroidism, the thyroids produce an inadequate amount of
thyroxin (thyroid hormone). This can indirectly lead to heart failure
by predisposing the client to coronary atherosclerosis.
 Pregnancy
Heart failure rank high among causes of death during pregnancy, like
anemia and hyperthyroidism, pregnancy increases the metabolic need
of the body, thereby increasing he workload of the heart. Pregnant
women with rheumatic vulvular disease are particular prone to heart
 Puget’s Disease
In some cases, Puget’s disease also increases myocardial worked.
This daises causes vascular proliferation in the bones. When the
diseases involves over one third of the skeleton, a high cardiac output
state exists and may tax the compromised heart.
 Nutritional Deficiency
Thiamine (vitamin B1) deficiency causes beriberi. It occurs in culture
in which polished rice constitutes the primary food sources.
 Pulmonary disease
Increased pressure in the pulmonary system due to chronic
obstructive lung disease, severe pulmonary embolization, or primary
pulmonary artery hypertension can produces sizable resistance to
right ventricular.
 Hypervolemia
An excess in circulating blood volume can result from poor renal
function, cardiac disease, medication, or excessive intake of sodium
(promoting water retention).

C. Pathophysiology
The healthy heart can meet the demands of life through the use of cardiac
reserve. Cardiac reserve is the heart’s ability to increase output in response to
stress. The normal heart can increase its output up to five times the resting
level. However, the failing heart, even at rest, is pumping near its capacity
and thus has lost much of its reserve. The compromised heart has a limited
ability to respond to the body’s needs for increased output in situations of

Ventricular dilation
Ventricular dilation refers to lengthening of the muscle fibbers, which
increases the volume of the heart chambers. Dilation causes an increase in
preload and thus cardiac output, because a stretched muscle contracts more
forcefully (starling’s law). However, dilation has limits as a compensatory
mechanism. Muscle fibbers, if stretched be yond a certain point, become
ineffective. Second, a dilated heart requires more oxygen. thus, the dilated
heart with a normal coronary blood flow can suffer from a lack of oxygen.
Hypoxia of the heart further decreases the muscle’s ability to contract.
Ventricular hypertrophy
Ventricular hypertrophy is an increase in the diameter of the muscle
fibbers in order to increase the contractile power of the musclefibers. Like
dilation, hypertrophy has limits as a compensatory mechanism. A
hypertrophied heart does far greater work than a normal-sized heart and, as a
consequence, has a greater demand for oxygen.

Increased Sympathetic Nervous System Stimulation

Increased sympathetic nervous system stimulation is the least effective
compensatory mechanism and often proves to be more of a burden than a
blessing. Sympathetic activity produces venous and arteriolar constriction,
thus increasing peripheral vascular resistance (after load) and myocardial
workload. In addition. Sympathetic stimulation reduces renal blood flow. And
the kidneys respond by retaining water and sodium. The expanded blood
volume increases the load on an already compromised heart. Finally,
tachycardia occurs as a cardiac response to distension of the great veins at
their atrial attachment as well as to an increase in circulating catecholamine.
The myocardium of the lift ventricle may either
1) Be diseased and unable to meet normal circulatory demands or
2) Be intrinsically normal but unable to meeting creased circulatory needs.
When failure first begins, the left ventricle fails to eject a sufficient
amount of blood. At this point, the compensatory mechanisms of sympathetic
nervous system activation (tachycardia, dilation, and hypertrophy) maintain
perfusion. When these mechanisms fail, the amount of blood remaining in the
left ventricle at the end of diastole increases. This increase in residual blood
in turn decreases the ventricle’s capacity to receive blood from the left atrium.
The left atrium.

D. Manifestations and Complications

In addition to the previous manifestations for the various classifications of
heart failure, other sign and symptoms commonly are seen.
A fall in cardiac output activates mechanism that cause increased salt and
water retention. This causes weight gain and further increases pressures in the
capillaries, resulting in edema. Nocturia, voiding more than one time at night,
develops as edema fluid from dependent tissues is reabsorbed when the client
is supine. Paroxysmal nocturnal dyspnea (PND), a frightening condition in
which the client awakens at night acutely short of breath, also may develop.
Paroxysmal nocturnal dyspnea occurs when edema fluid that has accumulate
during the day is reabsorbed into the circulation at night, causing fluid
overload and pulmonary congestion. Severe heart failure may cause dyspnea
at rest as well as with activity, signifying little or no cardiac reserve. Both an
S and an S4 gallop may be heard on auscultation.
The compensatory mechanism initiated in heart failure can lead
complications in other body systems. Congestive hepatomegaly ang
splenomegaly caused by engorgement of the portal venous system results in
increased abdominal pressure, ascites, and gastrointestinal problems. With
prolonged right-sided heart failure, liver function may be impaired.
Myocardial distention can precipitate dysrhythmias, further impairing cardiac
output. Pleural effusions and other pulmonary problems may develop.
F. Nursing Care
Obtain both subjective and objective data when assessing the client with
heart failure.
 Health history, complaints of increasing shortness of breath, dyspnea with
exertion, decreasing activity tolerance, or paroxysmal nocturnal dyspnea;
number of pillows used for sleeping; recent weight gain; presence of a
cough; chest or abdominal pain; anorexia or nausea; history of cardiac
disease, previous episodes of heart failure; other risk factors such as
hypertension or diabetes; current medication; usual diet and activity and
recent changes.
 Physical examination: general appearance; ease of breathing, conversing,
changing positions; apparent anxiety; vital sign including apical pulse;
colors of skin and mucous membranes; neck vein distension, peripheral
pulses, capillary refill, presence and degree of edema; heart and breath
sounds; abdominal contour, bowel sounds, tenderness; right upper
abdominal tenderness, liver enlargement.

Nursing Diagnoses and Interventions

Heart failure impacts quality of life, interfering with such daily activities
as self-care and role performance. Reducing the oxygen demand of the heart
is major nursing care goal for the client in acute heart failure. This includes
providing rest and carrying out prescribed treatment measures to reduce
cardiac work, improve contractility, and manage symptoms.

Decreased Cardiac Output

As the heart fails as a pump, stroke volume and tissue perfusion decrease.
 Monitor vital signs and oxygen saturation as indicated.
Decreased cardiac output stimulates the SNS to increase the heart rate in
an attempt to restore CO. Tachycardia at rest is common. Diastolic blood
pressure may initially be elevated because of vasoconstriction; in late
stages compensatory mechanism fail, and BP falls. Oxygen saturation
levels provides a measure of gas exchange and tissue perfusion.
 Auscultate heart and sounds regularly.
S1 and S2 may be diminished if cardiac function is poor. A ventricular
gallop (S3) is an early sign of heart failure; atrial gallop (S4) may also be
present. Crackles are often heard in the lung bases; increasing crackles,
dyspnea, and shortness of breath indicate worsening failure.
 Administer supplemental oxygen as needed. This improves oxygenation of
the blood, decreasing the effects of hypoxia and ischemia.
 Administer prescribed medication as ordered. Drugs are used to decrease
the cardiac workload and increase the effectiveness of contractions.
 Encourage rest, explaining the rationale. Elevate the head of the bed to
reduce the work of breathing. Provide a bed side commode, and assist
with ADLs. Instruct to avoid the Valsava maneuver. These measure
reduce cardiac workload.

Excess Fluid Volume

As cardiac output falls, compensatory mechanisms cause salt and water
retention, increasing blood volume. This increased fluid volume places
additional stress on the already failing ventricles, making them work harder to
move the fluid load.
 Assess respiratory status and auscultate lung sounds at least every 4
hours. Notify the physician of significant changes in condition. Declining
respiratory status indicates worsening left heart failure.
 Monitor intake and output. Notify the physician if urine out-put is less
than 30 mL/h. Weigh daily. Careful monitoring of fluid volume is
important during treatment heart failure. Diuretics may reduce
circulating volume, reducing hypovolemia despite persistent peripheral
edema. A fall in urine output may indicate significantly reduced cardiac
output and renal ischemia. Weight is an objective measure of fluid status:
1 L of fluid is equal to 2.2 lb of weight.
 Record abdominal girth every shift. Note complaints of a loss of appetite,
abdominal discomfort, or nausea. Venous congestion can lead to ascites
and may affect gastrointestinal function and nutritional status.
 Monitor and record hemodynamic measurements. Report significant
change and negative trends. Hemodynamic measurements provide a
means of monitoring conditions and response to treatment.
 Restrict fluid as ordered. Allow choices of fluid type and timing of intake,
scheduling most fluid intake during morning and afternoon hours. Offer
ice chips and frequent mouth care; provide hard candies if allowed.
Providing choices increase the client’s sense of control. Ice chips, hard
candies, and mouth care relieve dry mouth and thirst and promote

Activity Intolerance
Client with heart failure have little or no cardiac reserve to meet increase
oxygen demands. As the disease progresses and cardiac function is further
compromised, activity intolerance increases. The low cardiac output and
inability participate in activities may hinder self-care.
 Organize nursing care to allow rest periods. Grouping activities together
allows adequate to “recharge.”
 Assist with ADLs as needed. Encourage independence within prescribed
limits. Assisting with ADLs help ensure that care needs are met while
reducing cardiac workload. Involving the client promotes a sense of
control and reduces helplessness.
 Plant and implement progressive activities. Use passive and active ROM
exercise and appropriate. Consult with physical therapist on activity plan.
Progressive activity slowly increases exercise capacity by strengthening
and improving cardiac function without strain. Activity also helps prevent
skeletal muscle atrophy. ROM exercise prevent complication of
immobility in severely compromised clients.
 Provide written and verbal information about activity after discharge.
Written information provides a reference for important information.
Verbal information allows clarification and validation of the material.

Deficient Knowledge: Low-Sodium Diet

Diet is an important part of long-term management of heart failure to
manage fluid retention.
 Discuss the rational the sodium restriction. Understanding fosters
compliance with the prescribed diet.
 Consult with dietitian to plan and teach a low-sodium and, if necessary
for weight control, low-kcal diet. Provide a list of high-sodium, high-fat,
high-cholesterol foods to avoid. Dietary planning and teaching increase
the client’s sense of control and participation in disease management.
Food lists are useful memory aids.
 Assist the client to construct a 2-day meal plan choosing food low in
sodium. This allows learning assessment, clarification of
misunderstandings, and reinforcement of teaching.
 Encourage small, frequent meals rather than three heavy meals per day.
Small, frequent meals provide continuing energy resources and decrease
the work required to digest a large meals.