Afterload is the tension in the ventricular wall that is generated during ventricular systolic ejection. This tension is determined by the sum of forces preventing ejection of blood from the ventricle. Afterload can be increased by several factors, all having to do with a decrease in ventricular outflow tract resistance and/or arterial vascular resistance:
- Aortic stenosis: the left ventricle has to overcome the pressure gradient caused by the stenotic aortic outflow tract or valve
- Hypertension: the left ventricle has to work harder to eject blood into the aorta
- Ventricular dilation: afterload is increased by an increase in ventricular radius and a decrease in emptying efficiency
Afterload can also be decreased by:
- Ventricular hypertrophy: a thickened wall reduces wall stress and afterload
- Mitral insufficiency: during ventricular systole, blood can regurgitate back into the left atrium through the diseased mitral valve as well as be ejected through the aortic valve, leading to a decrease in outflow tract resistance
When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.