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This is the ejection stage of the cardiac cycle; it is depicted (see circular diagram) as the ventricular systole–first phase followed by the ventricular systole–second phase. [2] After ventricular pressures fall below their peak(s) and below those in the trunks of the aorta and pulmonary arteries, the aortic and pulmonary valves close ...
The isovolumetric contraction phase lasts about 0.05 seconds, [1] but this short period of time is enough to build up a sufficiently high pressure that eventually overcomes that of the aorta and the pulmonary artery upon opening of the semilunar valves. This process, therefore, helps maintain the correct unidirectional flow of blood through the ...
The Purkinje fibers transmit the signals more rapidly to stimulate contraction of the ventricles. [2] The conduction system consists of specialized heart muscle cells, situated within the myocardium. [3] There is a skeleton of fibrous tissue that surrounds the conduction system which can be seen on an ECG.
The standard model used to understand the cardiac action potential is that of the ventricular myocyte. Outlined below are the five phases of the ventricular myocyte action potential, with reference also to the SAN action potential. Figure 2a: Ventricular action potential (left) and sinoatrial node action potential (right) waveforms.
Electrical waves track a systole (a contraction) of the heart. The end-point of the P wave depolarization is the start-point of the atrial stage of systole. The ventricular stage of systole begins at the R peak of the QRS wave complex; the T wave indicates the end of ventricular contraction, after which ventricular relaxation (ventricular diastole) begins.
Consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction. [1] In the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the ...
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
As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, [2] without depending upon external regulation to make ...