Pathophysiology of systolic heart failure

Richard Cubbon and Ajay Shah

in Chronic Heart Failure

Published on behalf of Oxford University Press

Published in print October 2008 | ISBN: 9780199542338
Published online May 2011 | e-ISBN: 9780191740053 | DOI:

Series: Oxford Cardiology Library

Pathophysiology of systolic heart failure

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Chronic heart failure (CHF) is a clinical syndrome in which pathological stress or injury is associated with a failure of cardiac performance to meet the metabolic demands of the body and therefore results in clinical symptoms.

In the normal heart, cardiac output increases up to four fold during exercise; this response is diminished in CHF.

Multiple intrinsic and extrinsic control mechanisms exist to optimise cardiac performance, both acutely and chronically, through modulation of cardiac physiology and structure.

CHF is characterized by activation of a portfolio of compensatory mechanisms including activation of the renin-angiotensin-aldosterone and sympathetic nervous systems.

An index cardiac insult may initiate maladaptive compensatory mechanisms instigating a vicious cycle of progressive myocardial damage, hence resulting in a deteriorating clinical syndrome of CHF.

Systole—the period of the cardiac cycle when ventricular activity occurs and blood is ejected

Diastole—the period of the cardiac cycle when the heart fills with blood

Cardiac cycle—the series of cardiac electromechanical events that comprise each beat

Heart rate—the number of cardiac cycles per minute

Chronotropy—modulation of heart rate

Stroke volume—the volume of blood ejected from the heart during systole

Inotropism—modulation of myocardial contractility

Lusitropism—modulation of cardiac relaxation

Cardiac output—the volume of blood pumped by the heart during 1 min

Preload—the stretching force experienced by the myocardium prior to onset of contraction

Afterload—the stretching force experienced by the myocardium during contraction

Remodelling—cardiac structural and functional adaptation in response to chronic changes in workload

Chapter.  3752 words.  Illustrated.

Subjects: Cardiovascular Medicine

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