The Frank-Starling mechanism is a relationship characterizing stroke volume with pre-load. Stroke volume is dependent on the following:
- Pre-load: changes in pre-load affect the end-diastolic volume/pressure which in turn alter stroke volume
- Contractility: can be influenced by sympathetic/parasympathetic nervous system changes and electrolytes. Increases in contractility cause decreases in end-systolic volume while decreases in contractility result in increased end-systolic volumes.
- Afterload: can be altered by changes in vascular resistance or damage to semi-lunar valves of the heart
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:
- Activation of renin-angiotensin-aldosterone system
- Activation of sympathetic nervous system
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).