Preload, Afterload and Contractility

PRELOAD, AFTERLOAD AND CONTRACTILITY

Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.

Afterload is the force or load against which the heart has to contract to eject the blood.

Contractility is the intrinsic strength of the cardiac muscle independent of preload, but a change in preload will affect the force of contraction.

Afterload is the ‘load’ to which the heart must pump against. Afterload goes down when aortic pressure and systemic vascular resistance decreases through vasodilation.

Decreasing afterload will affect the Doppler numbers in a number of ways. Peak velocity (PV) may increrase as the heart finds it easier to  pump against decreasing pressures. This will also affect corrected flow times (FTc), as the duration of aortic blood flow will increase as afterload decreases.

Poor Left Ventricular Function

The waveform below demonstrates the response to a positive inotrope. In the first (left) screenshot, the patient had a ‘rounded’ flow waveform, with a low Peak velocity (PV) and stroke volume (SV), possibly indicating left ventricular failure. The patient was not fluid responsive and following administration of a positive inotrope, both PV and SV increase (right screenshot). ​

Systemic Vascular Resistance

Systemic vascular resistance (SVR) is the resistance to blood flow offered by all of the systemic vasculature [2]. An increase in SVR depends on the degree of sympathetic stimulation which itself depends on the degree of sympathetic activation, responsiveness of the vasculature, the number of vascular beds involved and the relative series and parallel arrangement of these beds to each other. Changes in blood viscosity also affect SVR.

SVR is an unreliable indicator of left ventricular afterload [2] since it reflects only peripheral vasomotor tone and not left ventricular systolic wall force. Discordant changes in left ventricular afterload and SVR can occur during pharmacological interventions as shown by Lang et al. They conclude “In the clinical setting, changes in SVR do not necessarily reflect left ventricular loading conditions since the true measure of ventricular afterload must consider the interaction of factors internal and external to the myocardium.”

References

1. Klabunde, R.E., Cardiovascular Physiology Concepts. 2005.Philadelphia. Lippincott Williams & Wilkins
2. Lang et al 1986​. Systemic vascular resistance: an unreliable index of left ventricular afterload. Circulation 74:1114-1123