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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 ...
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.
The net result is that, while contraction causes ventricular pressures to rise sharply, there is no overall change in volume because of the closed valves. 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 ...
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 ...
Coordinated contraction of ventricular cells. The ventricles must maximize systolic pressure to force blood through the circulation, so all the ventricular cells must work together. Ventricular contraction begins at the apex of the heart, progressing upwards to eject blood into the great arteries.
The left ventricular muscle must relax and contract quickly and be able to increase or lower its pumping capacity under the control of the nervous system. In the diastolic phase, it has to relax very quickly after each contraction so as to quickly fill with the oxygenated blood flowing from the pulmonary veins. Likewise in the systolic phase ...
An increase in sympathetic stimulation to the heart increases contractility and heart rate. 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.
A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis). The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism ) represents the relationship between stroke volume ...