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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
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]
Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.
The CIVD increases blood flow and subsequently the temperature of the fingers. This can be painful and is sometimes known as the 'hot aches' which can be painful enough to bring on vomiting. [citation needed] A new phase of vasoconstriction follows the vasodilation, after which the process repeats itself. This is called the Hunting reaction ...
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.
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.
This obstruction increases the pulmonary vascular resistance. If large enough, the clot increases the load on the right side of the heart. The right ventricle must work harder to pump blood to the lungs. With back-up of blood, the right ventricle can begin to dilate. Right heart failure can ensue, leading to shock and death. [18]