Cardiac afterload (null)

Cardiac afterload is a term describing the pressure or resistance that the heart, particularly the left ventricle, must overcome to eject blood into the aorta during systole. It is primarily determined by systemic vascular resistance and aortic pressure for the left heart, and pulmonary artery pressure for the right heart. Quantitatively, afterload can be estimated using formulas derived from the Law of Laplace, involving ventricular wall stress, chamber radius, and wall thickness. Physiologically, increased afterload reduces stroke volume and cardiac output, and persistent elevation contributes to pathological cardiac hypertrophy and heart failure. Afterload is not a molecular or pharmacological target itself, but it is influenced by various drugs used in the management of cardiovascular diseases, mainly by reducing vascular resistance.

Other names

AfterloadVentricular afterloadVascular afterload

Drugs affecting afterload generally act by decreasing systemic vascular resistance or reducing aortic/pulmonary pressure, thereby lowering the "load" the heart must overcome to eject blood