The stroke volume is dependent on venous return to the heart
CO = HR x SV
SV = ml blood/min
BP = HR x SV x TPR
TPR = (MAP-CVP)/CO (Ohm's Law)
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
Increasing the preload increases the tension developed by the muscle fibre and increases the velocity of fibre shortening.
This assumes that afterload and inotropic states remain constant - if not, the curve alters shape.
Dr. David Lyness
Beyond a certain point contractility falls and the clinical state of cardiac failure occurs
In clinical practice it is difficult to measure end diastolic volume (preload)
Surrogate estimates include:
- Central venous pressure (CVP) gives an estimate of the right ventricular EDV,
- Pulmonary artery occlusion pressure (PAOP, sometimes called the “wedge pressure”)
gives an estimate of the left ventricular EDV (clinically the side we are more often
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 STRESSAfterload 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.
Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber.
In health, afterload is determined predominantly by vascular tone, or the degree of vasoconstriction (or dilatation) of the arteries and arterioles.
PRELOAD = END-DIASTOLIC VOLUMEPreload 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.
This refers to the intrinsic ability of the cardiac muscle fibres to contract and is independent of the degree of preload and after load.
Factors affecting this property are called inotropes; positive and negative.
Largest determinant of contractility = sympathetic nervous system - acts directly, or via catecholamines from the adrenal gland. (+ve)
Many factors cause a decrease in contractility (-ve); examples would be an acidosis, hypoxia, hypocalcaemia, and many drugs (particularly anaesthetics and antiarrhythmic drugs).
Factors that increase preload:
↑ Ventricular Compliance
↑ Atrial Contractility
↑ Aortic Pressure
↑ CVP via ↑thoracic venous blood volume & venous return
↓ Venous Compliance leads to ↑CVP
Venous return is affected by respiration, muscle contraction and gravity.
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.