The Cardiovascular System: Preload
Preload is the volume of blood the ventricle is able to hold during diastole. It is often monitored by the mean blood pressure in the corresponding atrium (right atrium for the right ventricle; left atrium for the left ventricle) because the pressure in the corresponding atrium is similar to the ventricle during diastole when the AV valve is open. (The AV valve between the right atrium and right ventricle is the tricuspid valve, and the AV valve between the left atrium and the left ventricle is the bicuspid or mitral valve). It should be noted that part of the filling blood volume (preload) for the ventricle arrives during passive diastole when the AV valve has already opened and blood simply flows directly into the ventricle. During the last third of diastole, atrial contraction adds an additional 15-30% filling volume. Preload is a representation of the circulating blood volume emptying into the ventricle of the heart.
- As circulating blood volume increases, preload increases.
- As circulating blood volume decreases, preload decreases.
As mentioned previously, the preload is clinically monitored by the mean blood pressure in the corresponding atrium. For the right ventricle, the preload is measured by the central venous pressure (CVP). For the left ventricle, preload is measured by the pulmonary artery occlusion pressure (PAOP)—formerly referred to as pulmonary capillary wedge pressure (PCWP) or pulmonary artery wedge pressure (PAWP).
But events other than blood volume may also affect preload. One theory related to preload is Starling's Law. Starling was a physiologist who proposed that the larger the blood volume in the ventricle prior to contraction, the larger the cardiac output due to the elasticity of the myocardium. As the ventricle is filled with blood volume, the ventricular myocardium is stretched like a rubber band or an elastic bag (like a balloon). During diastole, the more blood that fills the ventricle, the more the myocardium stretches. During systole, the myocardium contracts and ejects the increased blood volume with one contraction. Starling’s Law actually corresponds clinically until the myocardium is stretched so far, that it loses elasticity. Then contraction becomes incomplete and results in residual blood volume that does not get ejected out of the semilunar valve but remains in the ventricle.
Another influence on preload is the functional status of the cardiac valves. If the AV valve regurgitates during systole—that is, allows blood to backflow from the ventricle into the atrium (as with a prolapsed mitral valve)—then the blood volume in the atrium rises not from circulating blood volume but from regurgitated ventricular blood.
Also, if thoracic pressure is elevated—as with emphysema or a tension pneumothorax or PEEP—then the increased thoracic pressure may inhibit the return of blood to the heart even though blood pressure readings in the atria may appear elevated.
So there are a variety of factors that may influence preload, but generally the concept is a reflection of returning blood volume to one side of the heart. Generally:
- When preload increases, cardiac output increases.
- When preload decreases, cardiac output decreases.