Cardiovascular Physiology Concepts
                                    Richard E. Klabunde, Ph.D.

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

In the intact organism, changes in preload, afterload and inotropy are interdependent, meaning that when one variable is changed, it usually alters the other two variables. The independent effects of preload, afterload and inotropy are described elsewhere (CLICK HERE). The following discussion illustrates the interdependent changes that can occur as preload, afterload and inotropy are altered. These interdependent effects are illustrated using left ventricular pressure-volume loops.

Interactions between Preload and Afterload at Constant Inotropy

An increase in preload (end-diastolic volume) leads to an increase in stroke volume because of the Frank-Starling mechanism. If afterload and inotropy do not change, then the end-systolic volume will not change. The heart simply ejects all of the extra blood that filled it. However, if the increased stroke volume leads to an increase in cardiac output and arterial pressure, then the afterload on the ventricle increases, which partially offsets the increased stroke volume by increasing the end-systolic volume. The reason for this is that the increased afterload reduces the velocity of fiber shortening and therefore the ejection velocity (see force-velocity relationship).  Conversely, a decrease in preload reduces stroke volume, but this reduction is partially offset by the decreased afterload (reduced aortic pressure) so that the end-systolic volume decreases slightly.  The effects of changes in preload when arterial pressure changes are shown below:

Interdependent Effects of Changes in Afterload

If afterload is increased (e.g., increasing aortic diastolic pressure by increasing systemic vascular resistance), the stroke volume is reduced and the end-systolic volume increased. The increased end-systolic volume, however, leads to a secondary increase in end-diastolic volume because more blood is left inside the ventricle following ejection and this extra blood is added to the venous return, thereby increasing ventricular filling. This secondary increase in preload, through the operation of the Frank-Starling mechanism, partially offsets the reduction in stroke volume caused by the initial increase in afterload. Consequently, in a normal heart, changes in aortic pressure have little effect on stroke volume. However, in heart failure patients in which the end-diastolic volume is already maximal, an increase in aortic pressure can significantly reduce stroke volume. If afterload (aortic pressure) is reduced, the opposite changes occur - stroke volume increases due to the decrease in end-systolic volume, accompanied by a smaller reduction in end-diastolic volume. This is the basis for giving an arterial dilator to enhance cardiac output in heart failure patients. Stroke volume can be significantly enhanced in heart failure patients by reducing afterload. These effects of afterload on stroke volume and preload are shown below:

Interdependent Effects of Changes in Inotropy

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. Increased inotropy also increases the rate of pressure development and ejection velocity, which increases stroke volume and ejection fraction, and decreases end-systolic volume. With less blood remaining in the ventricle after ejection, the ventricle fills to a smaller end-diastolic volume during diastole. A patient in acute heart failure due to a loss of inotropy may be given a positive inotropic drug to increase stroke volume and to reduce ventricular preload, both of with are beneficial (CLICK HERE for more information).  Decreasing inotropy has the opposite effects; namely, it increases end-systolic volume and decreases stroke volume and ejection fraction, accompanied by a small secondary increase in end-diastolic volume. The effects of inotropy on PV loops are shown below:

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.