Endocrine Response to Heart Failure

Abstract

Cardiac failure is a clinical entity of various causes and severity characterized by an inability of the heart to deliver a sufficient amount of blood to meet the metabolic demands of the body at rest or during exercise. Thus, as acute or chronic heart failure develops, several compensatory mechanisms are activated to maintain an adequate perfusion to vital organs such as the brain and the heart, at the expense of other non-essential organs such as the kidneys, the gut or the muscles. The neurohumoral systems involved in the maintenance of blood pressure when heart function is failing are the same as those implicated in the regulation of blood pressure when dehydration or severe losses of blood volume occur i.e. the sympathetic nervous system, the renin-angiotensin-aldosterone system and plasma arginine vasopressin. This endocrine response results in various degrees of peripheral vasoconstriction and renal sodium retention depending on the severity of the cardiocirculatory imbalance. In advanced heart failure, however, the increase in peripheral resistance and the enhanced sodium reabsorption with subsequent volume expansion are likely to compromise myocardial function by increasing afterload as well as myocardial oxygen consumption. A vicious circle is established that will lead to further irreversible myocardial damage despite the activation of other systems with vasodilatory and natriuretic properties such as the atrial natriuretic peptide or the protaglandins. An integrated scheme demonstrating the neurohumoral consequences of heart failure is presented in Fig. 1.