Disease Process 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.

Symptoms

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

Potential Complications 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.

Diagnostic Tests

Blood chemistry
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

Chest x-ray
Cardiomegaly; engorged pulmonary vasculature

Echocardiography
To visualize increased or decreased chamber dimensions, decreased wall motion

Cardiac catheterization
Definitive diagnosis of cause and extent of damage

Treatments

Surgery
Heart transplantation for end-stage failure; intraaortic balloon pump to provide circulatory assistance; left ventricular assistive device for those awaiting transplantation.

Drugs
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.

General
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.