Cardiac preload

Cardiac preload describes the degree of stretch or initial tension in myocardial fibers caused by ventricular filling at the end of diastole, just before contraction. It is a determinant of stroke volume according to the Frank-Starling law: the greater the stretch (within physiological limits), the stronger the subsequent contraction. Preload is affected by blood volume, venous return, heart rate, rhythm, and ventricular compliance. Clinically, it is estimated by ventricular end-diastolic pressure or volume. Preload manipulation is important in managing fluid balance, heart failure, and shock, but it is not a discrete molecular or receptor target for drugs.

Other names

Left ventricular end-diastolic pressure (LVEDP)Ventricular end-diastolic volume (EDV)Initial myocardial stretch

Drugs that reduce preload generally decrease blood volume (diuretics), increase venous dilation (nitrates), or alter cardiac filling pressures; Drugs that increase preload may include fluids/blood products