What is 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. To appreciate the afterload on individual muscle fibers, afterload is often expressed as ventricular wall stress (σ), where
(P, ventricular pressure; r, ventricular radius; h, wall thickness).
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, which has a thickened wall, has less wall stress and reduced afterload. Hypertrophy, therefore 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.
How Afterload Affects Stroke Volume and Preload
As shown in the figure, an increase in afterload shifts the Frank-Starling curve down and to the right (from point A to B), which decreases stroke volume (SV) and at the same time increases left ventricular end-diastolic pressure (LVEDP). 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 (increased end-systolic volume). In contrast, a decrease in afterload shifts the Frank-Starling curve up and to the left (A to C), which increases SV and at the same time reduces LVEDP.
Afterload per se does not alter preload; however, preload changes secondarily to changes in afterload. 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.