Heart failure is defined as the pathophysiologic state in which an abnormality of cardiac

function is responsible for inadequate systemic function (Woods, et. al, 2010). It is not
considered as a disease but a collection of signs and symptoms, the final pathway of a
group of diseases, the end-result of most cardiovascular states.
According to the New York Heart Association (1964), congestive heart failure may be
classified into four functional states. Class I (Mild) are patients with cardiac disease but
without resulting limitation of physical activity. Ordinary physical activity does not cause
undue fatigue, palpitation, dyspnea (shortness of breath), or anginal pain. Class II (Mild)
are patients with cardiac disease resulting in slight limitation of physical activity. They are
comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or
anginal pain. On the other hand, Class III (Moderate) are patients with cardiac disease
resulting in marked limitation of physical activity. They are comfortable at rest, but less
than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain. The last
classification is Class IV (Severe) are patients with cardiac disease where in there is
inability to carry out any physical activity without discomfort.
Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at
rest. If any physical activity is undertaken, discomfort is increased (New York Heart
Association, 1964).3 Case Study: A Post-Prosthetic Valve Replacement Patient with
Congestive Heart Failure Causes. An array of different problems can cause congestive
heart failure. Among them is coronary (ischemic) heart disease resulting from insufficient
blood flow to the myocardium, or heart muscle. This is usually caused by atherosclerosis,
the buildup of fatty substances or plaque on the walls of the arteries that carry blood to
the heart muscle. The hearts ability to perform decreases because ischemia results in
the delivery of less oxygen and fewer nutrients to the heart muscle. A heart attack may
also cause congestive failure. During a heart attack, the heart muscle is deprived of
oxygen, resulting in tissue death and scarring. The development of heart failure depends
on the extent and location of scarring. Long-standing high blood pressure is another
common cause of heart failure. Because there is greater resistance against which the
heart must pump, the heart muscle works harder. This results in an enlargement of the
heart muscle, especially of the left ventricle, the hearts main pumping chamber.
Eventually, this enlarged muscle tissue weakens, setting the stage for heart failure,
especially if the pumping ability of the enlarged chamber greatly decreases. Arrhythmias
(irregular heartbeats) can also lead to heart failure, but they usually have to be severe
and prolonged, with a rapid rate of more than 140 beats per minute, and must often occur
in the presence of an already weakened heart. They change the pattern of filling and
pumping of blood from the heart. This condition may also lower output of blood to the
point of heart failure. Valvular heart diseases are another cause of heart failure, which
results when a narrowed or leaking valve fails to direct blood flow properly through the
heart. The problem may be congenital (inborn) or due to an infection such as endocarditis
or rheumatic fever. This increases the hearts workload, thereby increasing risk of
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Case Study: A Post-Prosthetic Valve Replacement Patient with Congestive Heart Failure
developing heart failure. (6)
Cardiomyopathy
, a disease of the heart muscle itself, can
also lead to heart failure. Causes of cardiomyopathy include infection, alcohol abuse, and
cocaine abuse. When heart failure seems to have no known causes, it is known as
idiopathic heart failure (Soufer, 1992).
Manifestations.
Soufer (1992) further elaborates the manifestations often seen in
patients with heart failure. The particular symptoms that an individual experiences are
determined by which side of the heart is involved in the heart failure. For example, the
left atrium receives oxygenated blood from the lungs and passes it onto the left
ventricle, which pumps it to the rest of the body (Porth, 2007). When the left side isnt
pumping efficiently, blood backs up in the vessels of the lungs, and sometimes fluid is
forced out of the lung vessels and into the breathing spaces themselves. This pulmonary
congestion causes shortness of breath. The other major symptoms of left-sided heart
failure are fatigue, dyspnea, orthopnea, paroxysmal nocturnal dyspnea , and the sputum
production that comes from pulmonary congestion (Soufer, 1992).
Porth (2007) adds that right-sided failure occurs when there is resistance to the flow of
blood from the right heart structures (right atrium, right ventricle, pulmonary or lung
artery) into the lungs or when the tricuspid valve, which separates the right atrium from
the right ventricle, fails to work properly. This results in a backup of fluid and pressure in
the veins that empty into the right side of the heart. Pressure then builds up in the liver
and the veins in the legs. The liver enlarges and may become painful and swelling of the
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Case Study: A Post-Prosthetic Valve Replacement Patient with Congestive Heart Failure
ankles or legs occurs (Soufer, 1992).
The major symptoms of right-sided heart failure are edema and nocturia (Woods, et. al,
2010). The different types of edema possible are d
ependent edema
, edema that results in
enlargement or swelling of the liver, ascites, and edema of the skin or soft tissues.
Because congestive heart failure causes the body to fill with excess fluids, the kidneys
may not be able to dispose of the extra sodium and water, a condition known as kidney
failure. Sodium that would normally be eliminated through the urine remains in the body,
causing it to retain even more water, thereby aggravating the problem of excess fluid
associated with congestive heart failure (Soufer, 1992).
Diagnosis.
According to the Framingham Study (McKee, et. al, 1971), the
d
iagnosis of congestive heart failure requires the simultaneous presence of at least 2
major criteria or 1 major criterion in conjunction with 2 minor criteria that they have
formulated.
The major criteria includes p
aroxysmal nocturnal dyspnea, neck vein
distention, rales, radiographic cardiomegaly (increasing heart size on chest radiography),
acute pulmonary edema, S3 gallop, increased central venous pressure (greater than 16
centimeters fluid at right atrium), hepatojugular reflux and weight los greater than 4.5
kilograms in 5 days in response to treatment. The minor criteria is composed of bilateral
ankle edema, nocturnal cough, dyspnea on ordinary exertion, hepatomegaly, pleural
effusion, decrease in vital capacity by one third from maximum recorded and tachycardia
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Case Study: A Post-Prosthetic Valve Replacement Patient with Congestive Heart Failure
(heart rate greates than 120 beats per minute).
Minor criteria are acceptable only if they
can not be attributed to another medical condition (such as pulmonary hypertension,
chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome).
The Framingham
Heart Study criteria are 100% sensitive and 78% specific for identifying persons with
definite congestive heart failure (McKee, et. al, 1971).
Complications.
Watson (2000) discovered that t
he common complications of heart
failure include irregular heart rhythms or arrythmias, stroke, thromboembolism and organ
dysfunctions.
(1) One of these are m
alignant
ventricular arrhythmias
which are common
in end stage heart failure. For example, sustained ventricular tachycardia occurs in up to
10% of patients with advanced heart failure who are referred for cardiac transplantation
(Watson, 2000). In patients with ischemic heart disease, these arrhythmias often have
mechanisms in scarred myocardial tissue. An episode of sustained ventricular
tachycardia
indicates a high risk for recurrent ventricular arrhythmias and sudden cardiac death.
Congestive heart failure predisposes to (2)
stroke
and (3)
thromboembolism
, with an
overall estimated annual incidence of approximately 2% (Watson, 2000). Factors
contributing to the increased thromboembolic risk in patients with heart failure include
low cardiac output (with relative stasis of blood in dilated cardiac chambers), regional
wall motion abnormalities (including formation of a left ventricular aneurysm), and
associated atrial fibrillation. Patients with heart failure and chronic venous insufficiency
may also be immobile, and this contributes to their increased risk of thrombosis,
including deep venous thrombosis and pulmonary embolism.
Mild to moderate heart
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Case Study: A Post-Prosthetic Valve Replacement Patient with Congestive Heart Failure
failure is associated with an annual risk of stroke of about 1.5% (compared with a risk of
less than 0.5% in those without heart failure), rising to 4% in patients with severe heart
failure (Watson, 2000). (4)
Organ dysfunction
occurs when there is a decrease in the
oxygen supply to the different organ tissues in the body. Because of the lack of oxygen,
compensatory mechanisms act but eventually decompensate leading to dysfunction of
organs (Porth, 2007).