How does afterload affect end systolic volume

Click here for information on Cardiovascular Physiology Concepts, 3rd edition, a textbook published by Wolters Kluwer Klabunde What is Afterload? Afterload can be thought of as the "load" that the heart must eject blood against. In simple terms, the afterload of the left ventricle is closely related to the aortic pressure. 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 cardiac chamber shape, which changes during the cardiac cycle; therefore, a single geometric relationship is sometimes assumed. For this reason, the above relationship is expressed as a proportionality to highlight how pressure, radius and wall thickness contribute to afterload. The pressure that the ventricle generates during systolic ejection is very close to aortic pressure unless aortic stenosis is present, in which case the left ventricular pressure during ejection can be much greater than aortic pressure.

At a given intraventricular 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 parallel muscle fibers actually, sarcomere units to share in the wall tension that is determined at a give pressure and radius. If pulmonary venous flow decreases, then the ventricle will fill to a smaller end-diastolic volume decreased preload; green loop in figure.

To summarize, changes in preload alter the stroke volume; however, end-systolic volume is unchanged if afterload and inotropy are held constant. There is, however, a caveat to this discussion. If the concept of ventricular wall stress is used to define afterload instead of simply aortic pressure, then changes preload volume produce a small change in ventricular wall stress and therefore afterload.

Because of this, small changes in end-systolic volume are observed when end-diastolic volume is altered even if aortic pressure and inotropy are controlled. For example, increasing end-diastolic volume leads to a small increase in end-systolic volume because of increased wall stress afterload at end-diastole. If afterload is increased by increasing aortic pressure, the isovolumetric contraction phase is prolonged because the ventricle will need to generate a higher pressure to overcome the elevated aortic diastolic pressure.

Therefore, ejection begins at a higher aortic diastolic pressure. If preload end-diastolic volume and inotropy are held constant, this will result in a smaller stroke volume and an increase in end-systolic volume red loop in figure.

Stroke volume is reduced because increased afterload reduces the velocity of muscle fiber shortening and the velocity at which the blood is ejected see force-velocity relationship. A reduced stroke volume at the same end-diastolic volume results in reduced ejection fraction.

If afterload is reduced by decreasing aortic pressure, the opposite occurs - stroke volume and ejection fraction increase, and end-systolic volume decreases green loop in figure.

Increasing inotropy increases the velocity of muscle fiber shortening at any given preload and afterload see force-velocity relationship. Arnold Sibanda. Quite informative and good for sharpening critical thinking skills! This was very helpful, thank you. Thank you! Krishna gopal. Me a nurse in a conmunity as a community nurse. Plz subscribe me. Shahzad Ahmed Malik. Evonne Smith.