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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. Independent Effects of Preload To examine the independent effects of preload, assume that aortic 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. The ventricle will eject blood to the same end-systolic volume. 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. 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: Independent Effects of Afterload If afterload is increased by increasing aortic diastolic pressure, and if the preload (end-diastolic volume) and inotropy are held constant, this will result in less stroke volume and an increase in end-systolic volume. 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 diastolic pressure), the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases. These changes are illustrated below:
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 and shifts the end-systolic pressure-volume relationship (ESPVR) to the left, 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:
Interdependent Effects of Preload, Afterload and Inotropy In the intact heart, preload, afterload and inotropy are not held 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. RK Revised 04/05/2007 |
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DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice. © 1999-2008 Richard E. Klabunde, all rights reserved. |