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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)


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Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)



Effects of Preload, Afterload and Inotropy on Ventricular Pressure-Volume Loops

Ventricular pressure-volume (PV) loops an are excellent tool for visualizing changes in ventricular function in response to changes in preload, afterload and inotropy. These ventricular changes can be complex because preload, afterload and inotropy are interdependent variables, meaning that when one variable is changed, the other variables change. Therefore, it is first important to understand the independent effects of each of these variables on ventricular function when the other variables are held constant. The next step is then to see how changing a variable leads to changes in the other variables in a more intact system. Please note that the independent changes depicted below do no illustrate what normally happens in the body in response to a change in preload, afterload or inotropy. It is important, however, to understand the independent effects so that one can understand the more complex interactions that occur in the body, and that are discussed on another page.

Independent Effects of Preload

To examine the independent effects of preload, assume that aortic systolic and diastolic pressure (afterload), and inotropy are held constant. If preload is increased by increasing the end-diastolic volume (this occurs with increased venous pressure), then as the ventricle contracts it will develop greater pressure and eject blood more rapidly because the Frank-Starling mechanism will be activated by the increased preload. With no change in afterload or inotropy, the ventricle will eject blood to the same end-systolic volume despite the increase in preload. The net effect will be an increase in stroke volume, shown by an increase in the width of the PV loop. Ejection fraction (EF) will increase slightly. This ability to contract to the same end-systolic volume is a property of cardiac muscle that can be demonstrated using isolated cardiac muscle and studying isotonic (shortening) contractions under the condition of constant afterload.  When muscle preload length is increased, the contracting muscle shortens to the same minimal length as found before the preload was increased (see Effects of Preload on Cardiac Fiber Shortening). If preload is decreased (e.g., this occurs when central venous pressure decreases), opposite changes occur; namely, stroke volume is decreased, but the end-systolic volume is unchanged. The independent effects of preload on the left ventricular PV loop are shown below:

Preload effects on ventricular pressure-volume loops

Independent Effects of Afterload

If afterload is increased by increasing aortic pressure, and if the preload (end-diastolic volume) and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume as shown below. Stroke volume is reduced because the increased afterload reduces the velocity of muscle fiber shortening and the velocity by which the blood is ejected (see force-velocity relationship). The reduced stroke volume at the same end-diastolic volume reduces the ejection fraction. If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases. These changes are illustrated below:

Afterload effects on ventricular pressure-volume loops

Independent Effects of Inotropy

Increasing inotropy increases the velocity of fiber shortening at any given preload and afterload (see force-velocity relationship). This enables the ventricle to increase the rate of pressure development and ejection velocity, which leads to an increase in stroke volume and ejection fraction, and a decrease in end-systolic volume. In PV loop diagrams, increased inotropy increases the slope of the end-systolic pressure-volume relationship (ESPVR), which permits the ventricle to generate more pressure at a given LV volume. Decreasing inotropy has the opposite effects; namely, increased end-systolic volume and decreased stroke volume and ejection fraction. The effects of inotropy on PV loops are shown below:

Inotropy effects on ventricular pressure-volume loops

Interdependent Effects of Preload, Afterload and Inotropy

In the intact heart, preload, afterload and inotropy do not remain constant. To further complicate matters, changing any one of these variables usually changes the other two variables. Therefore, the above PV loops, although they illustrate the independent effects of these three variables, they do not represent what happens when the heart is in the body. However, if one understands the independent effects of these variables, then it is relatively easy combine the loops to illustrate what occurs when multiple variables change. To learn more about these interactions, CLICK HERE.

Revised 05/23/2011



DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.