Left ventricular failure occurs when the left ventricle in unable to pump blood into systemic circulation. Pressure increases in the left atrium and pulmonary veins; then the lungs become congested with blood, causing elevated pulmonary pressure and pulmonary edema.
To compensate, the cardiac muscle hypertrophies eventually resulting in decreased ventricular compliance. Decreased compliance requires higher filling pressure to produce the same stroke volume. Increased muscle mass impedes oxygenation of the heart muscle, which leads to decreased contraction force and heart failure.
As cardiac output fails, stretch receptors and baroreceptors stimulate the sympathetic nervous system, releasing catecholamines that increase the force and rate of myocardial contraction.
This causes increased systemic resistance, increased venous return, and reduced blood flow to the limbs, viscera and kidneys.
Sweating results from sympathetic cholinergic fibers, there is extra work for the heart muscle, and there is less systemic blood flow.
The renal system responds by releasing renin-angiotensin, which sets off a chain of events – vasoconstriction, leading to increased aldosterone release, causing sodium and water retention and, in turn, increasing preload. Finally, sodium and water retention becomes excessive, resulting in signs of systemic venous congestion and fluid overload.
