– A complex clinical syndrome that results when the heart is unable to pump an adequate supply of blood to meet the body’s metabolic needs, leading to inadequate tissue perfusion; vascular, cardiac, and pulmonary congestion; and diminished functional capacity.
Causes and Incidence
Congestive heart failure (CHF) can have a number of causes, which can be classified as either decreasing myocardial motility or increasing myocardial workload. Causes that decrease motility include coronary artery disease, myocarditis, cardiomyopathy, tumors, lupus erythematosus, and scleroderma, as well as drugs such as beta-blockers and calcium antagonists. Workload is increased by hypertension, valvular heart disease, intracardiac shunting, anemia, hyperthyroidism, and arteriovenous fistulas. Pericarditis, tamponade, and cardiac dysrhythmias interfere with ventricular filling. The incidence of CHF is increasing as the population ages. It is estimated that 2.5 to 3 million Americans have CHF, and it is the most common hospital discharge diagnosis for individuals over 65 years of age.
When the heart is unable to pump a sufficient supply of blood to meet the body’s demands, three primary compensatory mechanisms attempt to maintain cardiac function: (1) the sympathetic nervous system response increases, with increased catecholamine discharge, in an effort to increase myocardial contractility, which in turn causes vasoconstriction that increases peripheral resistance and cardiac workload; (2) cardiac fluid volume increases in an effort to stretch the fibers in the ventricles and increase the force of the contraction; and (3) the myocardium hypertrophies in an attempt to increase the amount of contractile tissue available and thus increase contractility.
When these compensatory mechanisms are insufficient or when they are active over extended periods, they become ineffective and eventually contribute to failure of the pump. Pump failure usually begins with the left ventricle and progresses to the right ventricle. It may be either acute or chronic, depending on the cause.
Left ventricle failure
Tachycardia, fatigue and dyspnea on exertion, intolerance to cold, cough, bloodtinged sputum, restlessness, paroxysmal nocturnal dyspnea, insomnia, crackles and wheezes in the lungs, ventricular and atrial gallops
Right ventricle failure
Fatigue, fullness in the neck and abdomen, ankle swelling, distention of neck veins, weakness, anorexia, nausea, liver enlargement, nocturia, ascites, tricuspid murmur
Acute pulmonary edema occurs with acute heart failure and is manifested as extreme dyspnea, cyanosis, hyperpnea, and plunging oxygen saturation. Death occurs if the condition is not treated immediately. Myocardial infarction and renal failure are other complications of CHF.
Elevated blood urea nitrogen, creatinine, glucose; decreased potassium, sodium; elevated aspartate aminotransferase, bilirubin; prolonged partial thromboplastin time
Arterial blood gases
Decreased oxygen saturation
Complete blood count
Decreased hemoglobin and hematocrit with anemia
Cardiomegaly; engorged pulmonary vasculature
To visualize increased or decreased chamber dimensions, decreased wall motion
Definitive diagnosis of cause and extent of damage
Heart transplantation for end-stage failure; intraaortic balloon pump to provide circulatory assistance; left ventricular assistive device for those awaiting transplantation.
Diuretics to reduce edema and ventricular filling volume; vasodilators, antihypertensives, or alpha-adrenergic blocking agents to dilate vessels and reduce venous filling pressure and peripheral resistance; inotropics (digitalis) to increase contractility; angiotensinconverting enzyme inhibitors to reduce angiotensin II in individuals with advanced CHF.
Bed rest with head elevated; oxygenation; low-salt diet; fluid restriction; monitoring and support of vital functions; prevention of thrombosis, pneumonia, and skin breakdown; stress reduction.