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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

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):

          

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Literature review current through: Nov 2016. | This topic last updated: Tue Aug 11 00:00:00 GMT+00:00 2015.
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