Vol. 7, Issue 9, Part C (2021)

Congestive heart failure is a syndrome that can be caused by a variety of abnormalities, including pressure and volume overload, loss of muscle, primary muscle disease or excessive peripheral demands such as high output failure. In the usual form of heart failure, the heart muscle has reduced contractility. This produces a reduction in cardiac output, which then becomes inadequate to meet the peripheral demands of the body. The 4 primary determinants of left ventricular (LV) performance are generally altered as follows: (1) There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling pressure is increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood pressure is often reduced, there is an increase in systemic vascular resistance (afterload), which can further reduce cardiac output. (4) Heart rate is generally increased as part of a compensatory mechanism associated with an increase in sympathetic tone and circulating catecholamines. In patients with coronary disease, there is often an imbalance between myocardial oxygen supply and demand. An increase in heart size may be particularly deleterious by increasing wall tension because of the Laplace relation and increasing myocardial oxygen consumption.

Intrinsic compensatory mechanisms include an increase in catecholamines, which increase contractility and heart rate in an attempt to maintain cardiac output; cardiac muscle hypertrophy, which helps maintain cardiac function; a rise in LV filling pressure, which can optimize performance according to the Frank-Starling mechanism; and an increase in peripheral arterial-venous oxygen extraction so as to maximize the oxygen delivered for a given cardiac output. Although these compensatory mechanisms are initially helpful, many of them may actually be excessive, such as an increase in catecholamines and systemic vascular resistance.