Congestive heart failure (CHF) is a clinical syndrome commonly encountered in small animal practice. Although there are a multitude of underlying cardiac diseases that can predispose patients to heart failure, the development of CHF represents a final common pathway resulting from insufficient cardiac function.
The primary mechanism for the development of CHF is a cascade of neurohormonal responses involving the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) that promotes sodium and water retention, increases in sympathetic tone, and peripheral vasoconstriction. The short-term benefit associated with these changes involves the preservation of adequate perfusion to tissues, chiefly by improving cardiac output and maintaining blood pressure. However, long-term consequences of neurohormonal activation and other mechanical changes lead to elevation of venous pressures resulting in signs of congestion (pulmonary edema, pleural effusion, and ascites). Additionally, neurohormonal activation increases cardiac workload and damages myocardial cells, contributing to progressive cardiac dysfunction.
As the progression of CHF continues, pulmonary edema (or other fluid retention) can cause intractable clinical signs, leading directly to the death of the patient or indirect death (owner-elected euthanasia). In some cases, the ability to maintain normal cardiac output declines, leading to signs of low output failure. In these patients, adequate blood pressure cannot be maintained, resulting in cardiogenic shock, multiple organ dysfunction, and death.