Pathophysiology and Rx Overview

To place our patient's clinical presentation and management options in perspective, we shall now briefly review the basic pathophysiology of heart failure along with the important principles of drug therapy.

Heart failure is a common disorder that accounts for a significant number of hospital admissions. Major causes include coronary artery disease, dilated cardiomyopathy and hypertension. Heart failure is also a very serious problem. Patients with severe congestive failure have a very poor prognosis.

Heart failure is present when the heart is unable to pump sufficient blood to meet the metabolic needs of the body at normal filling pressures. This definition assumes that venous return is normal.

The pathophysiology of failure is initiated by heart damage. The body's response is a characteristic pattern of neurohormonal reflexes that potentiate the problem. Activated neurohormonal systems include neurosympathetic, renin-angiotensin-aldosterone, or RAAS, and vasoactive peptides such as endothelin and vasopressin.

Initially, these responses are adaptive and beneficial but, in the long term, they are maladaptive and deleterious. For example, catecholamines cause vasoconstriction, increased cardiac work and are cytotoxic to myocardial cells. The renin-angiotensin-aldosterone system (RAAS) results in sodium and water retension with volume overload. Angiotensin is also a potent vasoconstrictor. Pathologically, myocytes are lost or become abnormal. This may result in a remodeling, or change, in the shape of the heart, often associated with fibrosis and dilatation.

The first step in patient care is to determine if failure is due to systolic and/or diastolic dysfunction. In addition to observations made at the bedside, this is readily accomplished by echocardiography. Distinguishing systolic and diastolic dysfunction significantlt impacts the choice of therapy, although these abnormalities are often combined.