The Frank-Starling mechanism is a relationship characterizing stroke volume with pre-load. Stroke volume is dependent on the following:
In a normal heart, increasing pre-load or venous return will result in increased contractility leading to increased stroke volume and ultimately leading to increased cardiac output (CO= Heart Rate x Stroke Volume).
When heart failure occurs, increases in pre-load do not result in a stroke volume sufficient to meet the demands of the body’s peripheral tissues. As a result of the decreasing effective circulating volume of blood, the body responds with multiple ways in an effort to increase tissue perfusion. These include:
The systemic vasoconstriction that results from the above mentioned mechanisms can sustain cardiac output in a heart failure patient for a limited time. As the disease progresses, the cardiac output does not increase appropriately despite increased pre-load. Eventually, the increased in left ventricle end diastolic volume/pressure transmits pressure back to the pulmonary veins leading to the symptoms of pulmonary congestion (dyspnea, orthopnea, PND, etc).
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