What is Preload?

The best way to think of preload is as a volume.

Essentially, preload is the VOLUME of blood in the ventricles at the end of diastole.  This is termed End Diastolic Volume (EDV), thus at the very end of diastole, if you look at that volume of blood sitting in the ventricles . . . that is your PRELOAD.

Measuring Preload

That volume is measured as the pressure that it exerts on the walls of the ventricles in mmHg.

There are two numbers that we can use to indirectly measure or estimate preload: CVP and PAOP

CVP is central venous pressure and provides an indirect measure of the EDV in the right ventricle.  This is a parameter that a nurse can view using a flowtrac or other system that allows this number to be viewed.

PAOP is pulmonary artery occlusion pressure provides an indirect measure of the EDV in the left ventricle. This number can aid in evaluating preload status of the left side of the heart.

Preload Highs and Lows

Preload is essentially (in basic terms) a measure of volume status within the body.  In states that lead to low volume (shock, hypotension, tamponade) you will also see decrease preload.  In states that create excessive volume ( heart failure, brady-arrhythmias) , you will notice increased preload. Therefore treating the underlying cause should result in alleviating the problem.  If preload is low due to a volume issue volume can be added through fluids or blood.  If preload is high due to poor pump function diuretics or alternative medication therapy might be considered.

What is Afterload?

The best way to think of afterload is pressure.

Essentially, afterload is the PRESSURE that ventricles must exert to open the semilunar (aortic/pulmonic) valves.  Vessels distal to the ventricles exert a pressure due to vasoconstriction or vasodilation.  This pressure maintains the valves closed.  In order to open the valves a specific pressure within the ventricles must be reached . . . this pressure is the AFTERLOAD.  This number is represented by SVR and PVR (systemic and pulmonary vascular resistance respectively).

Afterload Highs and Lows

While afterload can be effected by volume status it is basically a result of vascular resistance within the aorta and lungs.  These numbers are further a result of vasoconstriction and vasodilation.  So if afterload is too high (HTN, aortic stenosis, SNS stimulation) the patient may benefit from vasodilators.  In cases of decreased afterload, overdilation of the vasculature (sepsis, hypotension),  the patient might benefit from vasopressors.

Conclusion

This is a basic introduction to preload and afterload to help clarify the difference between the two.  Please post any questions or thoughts below.