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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Cardiovascular Physiology Concepts textbook cover

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


Cardiovascular Physiology Concepts textbook cover

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



Cardiac Afterload

Afterload can be thought of as the "load" that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure. More precisely, afterload is related to ventricular wall stress (σ), where

ventricular wall stress equation

(P, ventricular pressure; r, ventricular radius; h, wall thickness).

This relationship is similar to the Law of LaPlace, which states that wall tension (T) is proportionate to the pressure (P) times radius (r) for thin-walled spheres or cylinders. Therefore, wall stress is wall tension divided by wall thickness. The exact equation depends on the geometry because of different constants for different shapes, and for this reason, the above relationship is expressed as a proportionality.

The pressure that the ventricle generates during systolic ejection is very close to aortic pressure, unless aortic stenosis is present. At a given pressure, wall stress and therefore afterload are increased by an increase in ventricular inside radius (ventricular dilation). A hypertrophied ventricle (thickened wall) reduces wall stress and afterload. Hypertrophy can be thought of as a mechanism that permits more muscle fibers (actually, sarcomere units) to share in the wall tension that is determined at a give pressure and radius. The thicker the wall, the less tension experienced by each sarcomere unit.

Afterload is increased when aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis, and by ventricular dilation. When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.

afterload effects on cardiac Frank-Starling curves
As shown in Figure 1, an increase in afterload shifts the Frank-Starling curve down and to the right (from A to B). The basis for this is found in the force-velocity relationship for cardiac myocytes. Briefly, an increase in afterload decreases the velocity of fiber shortening. Because the period of time available for ejection is finite (~200 msec), a decrease in fiber shortening velocity reduces the rate of volume ejection so that more blood is left within the ventricle at the end of systole (increase end-systolic volume). A decrease in afterload shifts the Frank-Starling curve up and to the left (A to C).

Afterload per se does not alter preload; however, preload changes secondarily to changes in afterload. As shown in Figure 1, increasing afterload not only reduces stroke volume, but it also increases left ventricular end-diastolic pressure (LVEDP) (i.e., increases preload). This occurs because the increase in end-systolic volume is added to the venous return into the ventricle and this increases end-diastolic volume. This increase in preload activates the Frank-Starling mechanism to partially compensate for the reduction in stroke volume caused by the increase in afterload.

afterload effects on ventricular volume
The interaction between afterload and preload is utilized in the treatment of heart failure, in which vasodilator drugs are used to augment stroke volume by decreasing afterload, and at the same time, reduce ventricular preload. This can be illustrated by seeing how ventricular volume changes in response to a decrease in arterial pressure (afterload) as shown in Figure 2. When arterial pressure is reduced, the ventricle can eject blood more rapidly, which increases the stroke volume and thereby decreases the end-systolic volume. Because less blood remains in the ventricle after systole, the ventricle will not fill to the same end-diastolic volume found before the afterload reduction. Therefore, in a sense, the end-diastolic volume (preload) is "pulled along" and reduced as end-systolic volume decreases. Stroke volume increases overall because the reduction in end-diastolic volume is less than the reduction in end-systolic volume.

afterload effects on ventricular pressure-volume loops
The effects of afterload on ventricular end-systolic and end-diastolic volumes can be illustrated using pressure-volume loops (Figure 2). If afterload is increased by increasing aortic diastolic pressure, the ventricle has to generate increased pressure before the aortic valve opens. The ejection velocity after the valve opens is reduced because increased afterload decreases the velocity of cardiac fibers shortening as described by the force-velocity relationship. Because there is only a finite time period for electrical and mechanical systole, less blood is ejected (decreased stroke volume), which increases the ventricular end-systolic volume as shown in the pressure-volume loop. Because end-systolic volume is increased, this extra blood within the ventricle is added to the venous return, which increases end-diastolic volume. Ordinarily, in the final steady-state (after several beats), the increase in end-systolic volume is greater than the increase in end-diastolic volume so that the difference between the two, the stroke volume, is decreased (i.e., the width of the pressure-volume loop is decreased).

Revised 08/07/07



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