Determinants of Cardiac Performance

There is an aspect of cardiac function that is not as intuitively obvious and not as well understood as the systolic function of the heart; that is the diastolic function of the heart. If the heart does not squeeze well and does not pump a lot of blood the cardiac output goes down. What happens during the filling phase of the heart is crucially important as well. This determines a lot of the symptomatology of people who have impaired cardiac function.

1. PRELOAD - The same phenomenon we discussed when we talked about the determinants of the change of length in the muscle fiber (lecture 1)applies to the heart as a whole. Fiber length was defined earlier as the preload of a muscle strip. If you integrate fiber length or muscle strip length over the entire three dimensional structure of the heart, you get volume. As you increase the volume of a chamber passively during diastole, the pressure within the chamber increases, (diastolic pressure). Think of a balloon that is being blown up. The more air you force into that balloon, the greater the pressure within that balloon and the greater the tension in the wall of the balloon. As the diastolic volume increases in a cardiac chamber the diastolic pressure increases. Clinically and practically it is pretty easy to measure the pressure within the heart. Pressure correlates with stretch and volume. Therefore end diastolic pressure is used as a stand-in for preload because it is easier to measure and because of its unique correlation between volume and pressure for any given heart at any moment in time.

2. AFTERLOAD - In terms of a muscle strip is the force against which it is shortening. In the case of the intact heart (left ventricle) the force that the individual fibers are generating as they contract converts into blood pressure or aortic pressure. Aortic pressure is often used as a stand-in for afterload. We will see that there are ways of altering that force, (that wall tension), in systole that directly affect the performance of the heart even though the aortic pressure itself may not be altered that much.

3. CONTRACTILITY - The innate property of a muscle is to contract. This can be altered with a variety of inotropic agents, (such as, catecholes, digitalis, phosphodiesterase inhibitors). Why would you do this? Usually this is done because the contractility has been diminished by whatever disease process is going on.

4. HEART RATE - In normal exercise HR is a major determinant of increased CO. This is probably the major compensation that normal individuals use to alter their cardiac output.
   

Category: Physiology Notes