Neurohumoral compensation

Neurohumoral compensation

Heart failure is accompanied by neurohumoral compensatory responses. These mechanisms help to maintain cardiac output and arterial blood pressure. Although these responses are initially beneficial, they are responsible for aggravation and progression of the disease. Neurohumoral responses include activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system (RAAS), and increased release of endothelin-1.

The fall in cardiac output is registered by the baroreceptors located in the carotid sinus and aortic arch. This stimulates both RAAS and sympathetic activity.

Catecholamines bind to αreceptors, resulting in systemic arterial vasoconstriction, thus increasing systemic vascular resistance and venous pressure. Binding to β1receptors in the myocardium increases the heart rate and makes contractions more forceful, in an attempt to increase cardiac output.

All these events increase the workload of the heart. Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (ADH), which causes fluid retention in the kidneys. This increases the blood volume and blood pressure.

Hypotension and reduced renal perfusion also stimulates the RAAS-activity. Stimulation of the RAAS promotes salt and fluid retention in the kidneys, increasing the blood volume. It also increases the release of angiotensin II, which causes vasoconstriction and stimulates secretion of more norepinephrine and aldosterone. RAAS activation results in increased cardiac contractility, afterload, and preload.

The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodelling of the heart over the long term.


The best way to differentiate systolic from diastolic dysfunction is to measure


A decrease in cardiac output leads to


The effect of noradrenaline on the heart does NOT include: