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Ventricular systole. (Red arrow is path from left ventricle to aorta. Afterload is largely dependent upon aortic pressure.

In cardiac physiology, afterload is used to measure the tension produced by a chamber of the heart in order to contract.[1] If the chamber is not mentioned, it is usually assumed to be the left ventricle. However, the strict definition of the term relates to the properties of a single cardiac myocyte. It is therefore only of direct relevance in the laboratory; in the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent.

Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber, and thus is a consequence of the aortic pressure, since the pressure in the ventricle must be greater than the systemic pressure in order to open the aortic valve. Everything else held equal, as afterload increases, cardiac output decreases.

Mathematical definition of afterload remains elusive to contemporary medical imaging. Cardiac imaging is a somewhat limited modality in defining Afterload because it is greatly incumbent upon interpretation of volumetric data. Prior work defining End Diastolic Volume (EDV) is mathematically close to Afterload but is better matched to Preload.

Preload best describes the maximum viscous blood volume/mass of end Diastole while Afterload better describes the maximum tension/compliance state of the semisolid myocardial muscle mass in end Systole. Precise mathematical labeling of Afterload and Preload is a further challenge since both maximum measurements (volume/tension) occur simultaneously in the late Time phase of Systole. More simply stated, Preload is well addressed by computational interpretation of imaging derived blood volumetric data. Afterload remains beholden to definition of myocardial muscle work and is perhaps still better illustrated on a chalkboard.



Disease processes that increase the left ventricular afterload include increased blood pressure and aortic valve disease.

Systemic Hypertension (HTN) (Increased blood pressure) increases the left ventricular afterload because the left ventricle has to work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure.

Pulmonary Hypertension (PH) is increased blood pressure within the right heart leading to the lungs. PH indicates a regionally applied increase in Afterload dedicated to the right side of the heart, divided and isolated from the left heart by the intraventricular Cardiac Septum.

Aortic stenosis increases afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 110 mmHg in order to open the aortic valve and eject blood into the aorta.

Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure. The diastolic blood pressure would fall, due to regurgitation. This would result in an increase pulse pressure.

Mitral regurgitation decreases the afterload. During ventricular systole, regurgitant blood flows backwards through a leaking mitral valve in addition to blood that is properly ejected through the aortic valve. With an extra pathway for blood flow through the mitral valve, the left ventricle does not have to work as hard to eject its blood, i.e. there is a decreased afterload.[2] Afterload is largely dependent upon aortic pressure.

See also


  1. ^ afterload at Dorland's Medical Dictionary
  2. ^ Klabunde RE (2007-04-05). "Mitral Regurgitation". Cardiovascular Physiology Concepts. Richard E. Klabunde. Retrieved 2010-01-01. 

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