Effect of heart failure and digoxin on the Frank-Starling relationship.
The normal set point required to maintain adequate tissue perfusion is a cardiac output of 5 L/min.
During heart failure the relationship between cardiac output and venous pressure becomes shifted down and to the right (patient moves from point A to B).
Sympathetic activation and increased fluid retention result in an increased venous pressure (preload) which acts to increase cardiac output by increasing the stretch of cardiac fibers (patient moves from B to C).
If cardiac output remains below 5 L/min, the kidney continues to retain fluid, and venous pressure continues to rise, until either a 5 L/min cardiac output is achieved, or the patient “drowns in their own fluids” (e.g. due to pulmonary congestion).
Digoxin can shift the curve upwards and to the left by a mechanism different from sympathetic stimulation (increased contractility - so that the patient ideally moves from point C to D).
The resulting increase in blood flow to the kidney results in a diuresis (patient moves from D to E) with an associated reduction in venous pressure due to reduced venous volume.