Neurohumoral Adapations

Pathophysiology of heart failure: Neurohumoral adaptations

Author

Wilson S Colucci, MD

Section Editor

Stephen S Gottlieb, MD

Deputy Editor

Susan B Yeon, MD, JD, FACC

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: May 2016. &#124 This topic last updated: Aug 11, 2015.

INTRODUCTION — The signs and symptoms of heart failure (HF) are due in part to compensatory mechanisms utilized by the body in an attempt to adjust for a primary deficit in cardiac output. Neurohumoral adaptations, such as activation of the renin-angiotensin-aldosterone and sympathetic nervous systems by the low-output state, can contribute to maintenance of perfusion of vital organs in two ways [1,2]:

●Maintenance of systemic pressure by vasoconstriction, resulting in redistribution of blood flow to vital organs.

●Restoration of cardiac output by increasing myocardial contractility and heart rate and by expansion of the extracellular fluid volume.

In HF, these adaptations tend to overwhelm the vasodilatory and natriuretic effects of compensatory pathways including natriuretic peptides, nitric oxide, prostaglandins, and bradykinin [3-5]. Volume expansion is often effective because the heart can respond to an increase in venous return with an elevation in end–diastolic volume that results in a rise in stroke volume (via the Frank-Starling mechanism). (See "Pathophysiology of heart failure: Left ventricular pressure-volume and other hemodynamic relationships".)

There are, however, a number of maladaptive consequences of neurohumoral activation (algorithm 1):

●The elevation in diastolic pressures is transmitted to the atria and to the pulmonary and systemic venous circulations; the ensuing elevation in capillary pressures promotes the development of pulmonary congestion and peripheral edema.

●The increase in left ventricular afterload induced by the rise in peripheral resistance can both directly...