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Determinants of Contractile Function in the Intact Heart
Cardiac Output = Stroke Volume x Heart Rate CO = SV x HR
The three major determinants of stroke volume are preload, afterload, and contractility.
Preload: stretch on the myocardial fibers before contraction. In a healthy heart, the higher the preload, the higher the SV.
Afterload: the load or force the ventricle must contract against. For the LV, the afterload is the pressure in the aorta that the ventricle must overcome to open the aortic valve and eject blood. Afterload is independent from preload. The higher the afterload, the lower the SV.
Afterload is also defined as the wall stress that develops during systolic ejection. Represented by the LaPlace relationship: σ= P r/ 2 h (wall tension = LV pressure x LV radius / 2 x LV wall thickness) Increased arterial pressure increases wall tension. Increased wall thickness decreases wall tension.
Contractility (inotrophy): the contractile force of the ventricles at a given preload and afterload. Can be enhanced physiological or pharmacologically. The higher the CTY, the higher the SV. Increased CTY shifts the Frank-Starling curve upwards, which increases SV for a given preload and afterload. (See second figure above)
A few more terms:
Ejection Fraction: fraction of end-diastolic volume ejected during systole (normal 55-75%)
Compliance: ease or difficulty with which the chamber can be filled. If ventricular compliance is reduced, as in severe LVH, then it accepts less volume from the atria, resulting in lower end-diastolic volume (AKA lower preload) and subsequently, a lower SV.
Three important concepts:
Ventricular SV is a function of preload, afterload, and contractility. SV rises with an increase in preload and contractility and a decrease in afterload.
Ventricular end-diastolic volume is a measure of preload and is influenced by a compliance of the atria and ventricles.
Ventricular end-systolic volume depends on afterload and contractility, but not on preload (because of Frank-Starling relationship.)