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Afterload is largely dependent upon aortic pressure. Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). Afterload is proportional to the average arterial pressure. [1] As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles respectively.
Afterload is the mean tension produced by a chamber of the heart in order to contract. It can also be considered as the ‘load’ that the heart must eject blood against. Afterload is, therefore, a consequence of aortic large vessel compliance, wave reflection, and small vessel resistance (LV afterload) or similar pulmonary artery parameters (RV afterload
End-systolic volume (ESV) is the volume of blood in a ventricle at the end of contraction, or systole, and the beginning of filling, or diastole.. ESV is the lowest volume of blood in the ventricle at any point in the cardiac cycle.
An increase in contractility tends to increase stroke volume and thus a secondary increase in preload. An increase in preload results in an increased force of contraction by Starling's law of the heart; this does not require a change in contractility. An increase in afterload will increase contractility (through the Anrep effect). [4]
Since increasing afterload will prevent blood from flowing in a normal forward path, it will increase any murmurs that are due to backwards flowing blood. [3] This includes aortic regurgitation (AR), mitral regurgitation (MR), and a ventricular septal defect (VSD).
The Anrep effect describes the rapid increase in myocardial contractility in response to the sudden rise in afterload, the pressure the heart must work against to eject blood. [ 1 ] [ 2 ] This adaptive mechanism allows the heart to sustain stroke volume and cardiac output despite increased resistance.
An increase in the volume or speed of venous return will increase preload and, through the Frank–Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume. [9] Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume.
An increase in the age and also in the systolic blood pressure (SBP) is accompanied with decrease on arterial compliance. [6] Endothelial dysfunction results in reduced compliance (increased arterial stiffness), especially in the smaller arteries. This is characteristic of patients with hypertension. However, it may be seen in normotensive ...