In reality, contractility would be enhanced by the sympathetic stimulation accompanying the shock state, but replacing volume would further support the patient's compensatory mechanisms by calling on the Starling mechanism to enhance strength of contraction. For the patient in congestive heart failure who is volume overloaded, the ventricle has the opposite problem. Overfilling raises pressure, thereby augmenting myocardial stretch or preload. Initially, this serves as a compensatory mechanism because the patient's cardiac function rises to the peak of the Starling curve and cardiac output is optimized. However, clinicians usually focus on preload of the left ventricle, which is the largest and last chamber to send blood to most of the body.
Pressure is determined by the stretch or the amount of tension placed on the heart muscle.
This measurement is possible since at end diastole, when the mitral valve is open, there is communication between the left ventricle, the left atria, and the pulmonary vascular bed. The venous system can be thought of as a large reservoir that can hold blood in the periphery or send it back to the heart, depending on the state of vasodilation or vasoconstriction. For example, a drug that dilates the venous system, such as nitroglycerin, reduces preload by causing a greater percentage of the blood to remain in peripheral circulation. Conversely, when greater blood pressure is needed, sympathetic stimulation causes vasoconstriction to send blood back centrally to augment cardiac output. Gravity affects this distribution.