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The stroke volume is affected by changes in preload, afterload, and inotropy (contractility). In normal hearts, the SV is not strongly influenced by afterload, whereas, in failing hearts, the SV is highly sensitive to afterload changes. Stroke volume relative to EDV is Ejection Fraction.
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.
The three curves illustrate that shifts along the same line indicate a change in preload, while shifts from one line to another indicate a change in afterload or 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 ...
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]
Afterload is a determinant of stroke volume (in addition to preload, and strength of myocardial contraction). [ 1 ] Following Laplace's law , the tension upon the muscle fibers in the heart wall is the pressure within the ventricle multiplied by the volume within the ventricle divided by the wall thickness (this ratio is the other factor in ...
Many of the factors that regulate the heart rate also affect cardiac function by altering the stroke volume. While a number of variables are involved, stroke volume is dependent upon the difference between end diastolic volume and end systolic volume. The three primary factors involved are preload, afterload and contractility. [1]
By contrast, the Anrep effect occurs at constant preload, triggered solely by afterload. [1] [2] [3] It is characterized by increased contractility (steeper end-systolic pressure-volume relationship) and higher stroke work, without changes in stroke volume or end-diastolic volume. [3] [4]
Preload can still be approximated by the inexpensive echocardiographic measurement end-diastolic volume or EDV. Preload increases with exercise (slightly), increasing blood volume (as in edema, excessive blood transfusion (overtransfusion), polycythemia) and neuroendocrine activity (sympathetic tone). An arteriovenous fistula can increase ...