Pathophysiology of Left Ventricular Failure

In this article, we will discuss the Pathophysiology of Left Ventricular Failure. So, let’s get started.


Left ventricular output depends on preload, afterload and myocardial contractility. Left ventricular failure occurs due to interaction of this complex mechanisms. Low cardiac output due to LVF leads to complex neuroendocrine changes in which there is stimulation of renin-angiotensin-aldosterone system as well as stimulation of sympathetic system. At first, these try to optimise the left ventricular function called compensatory mechanism, but when these mechanisms also failed then LVF sets in. The activation of renin-angiotensin-aldosterone system increases afterload due to vasoconstriction and salt and water retention. Stimulation of sympathetic system increases both preload and afterload (peripheral vasoconstriction). This also increases myocardial contractility. By this complex mechanism LVF is produced.

By backward failure mechanism, due to rise in left ventricular end-diastolic pressure / volume due to increased afterload, there is rise in left atrial pressure and subsequently rise in pulmonary venous and capillary pressure (>25 mmHg). The raised pulmonary venous pressure is more than plasma oncotic pressure in the capillaries leading to transudation and development of acute pulmonary edema. In long-standing cases or in chronic heart failure, hypoxia produced by edematous lung is potent vasoconstrictor of pulmonary vessels leading to pulmonary arterial hypertension and ultimately edema is relieved slowly. Development of pulmonary arterial hypertension is protective mechanism for acute pulmonary edema.


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