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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 ...
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]
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.
However, the relationship is not simple because of the restriction of the term preload to single myocytes. 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 ...
The right ventricular end-diastolic volume (RVEDV) ranges between 100 and 160 mL. [5] The right ventricular end-diastolic volume index (RVEDVI) is calculated by RVEDV/BSA and ranges between 60 and 100 mL/m 2. [5]
In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from the ventricle per beat. Stroke volume is calculated using measurements of ventricle volumes from an echocardiogram and subtracting the volume of the blood in the ventricle at the end of a beat (called end-systolic volume [note 1]) from the volume of blood just prior to the beat (called end-diastolic volume).
Stroke volume (= end-diastolic volume − end-systolic volume) Ejection fraction (= stroke volume / end-diastolic volume) Cardiac output is mathematically ` to systole [clarification needed] Inotropic, chronotropic, and dromotropic states; Cardiac input (= heart rate * suction volume Can be calculated by inverting terms in Fick principle)
Note that, for cardiac function curve, "central venous pressure" is the independent variable and "systemic flow" is the dependent variable; for vascular function curve, the opposite is true. Venous return curves showing the normal curve when the mean systemic filling pressure (Psf) is 7 mm Hg and the effect of altering the Psf to 3.5, 7, or 14 ...