The stroke volume is dependent on venous return to the heart
CO = HR x SV
Increasing venous return (preload) to the left ventricle increases left ventricular end-diastolic pressure and volume.This results in an increase in stroke volume - which is a determinant in cardiac output & therefore oxygen delivery
Dr. David Lyness
In clinical practice it is difficult to measure end diastolic volume (preload)Surrogate estimates include:
If the ventricles are OVER FILLED, the fibres are stretched beyond the maximal point for optimal contraction - this decreases SV, perfusion and oxygen delivery because there is a reduction on the force of contractions. Beware in cardiac patient with CHF/dialysis pt's.
AFTERLOAD = END SYSTOLIC WALL STRESS
Afterload is the pressure in the wall of the left ventricle during ejection. In other words, it is the end load against which the heart contracts to eject blood. Afterload is readily broken into components: one factor is the aortic pressure the left ventricular muscle must overcome to eject blood.
PRELOAD = END-DIASTOLIC VOLUME
Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. Preload, therefore, is related to muscle sarcomere length. Because sarcomere length cannot be determined in the intact heart, other indices of preload are used such as ventricular end-diastolic volume or pressure.
Myocardial contractilityThis refers to the intrinsic ability of the cardiac muscle fibres to contract and is independent of the degree of preload and after load.
Factors that increase preload:
↑ Ventricular Compliance
Preload, Myocardial Contractility and Afterload
are the three components contributing to stroke volume
TPR = Total Peripheral Resistance (or SVR)CVP is close to 0, so often just MAP is used.