What is afterload?

What is Afterload

Afterload is the ventricular wall stress during systolic ejection—the resistance the ventricle must overcome to eject blood—determined by intracavitary pressure, ventricular diameter, and wall thickness according to the law of LaPlace. 1

Fundamental Definition

Afterload represents the force opposing ventricular contraction during systole, most accurately defined as ventricular wall stress rather than simply arterial pressure or vascular resistance. 1

• According to the law of LaPlace, wall stress (afterload) is directly proportional to intracavitary pressure and internal ventricular diameter, and inversely related to ventricular wall thickness 1
• For the left ventricle, afterload remains within normal range when the hypertrophic process adequately increases wall thickness to counter elevated intracavitary systolic pressure 1
• The inverse relationship between systolic wall stress and ejection fraction is maintained—as long as wall stress is normal, ejection fraction is preserved 1

Right Ventricular Afterload: A More Complex Picture

RV afterload is most appropriately defined as RV wall stress during systolic ejection, estimated by the summation of resistive AND pulsatile components of blood flow—not just pulmonary artery pressure or pulmonary vascular resistance alone. 1

• Commonly used measures like PA systolic pressure and pulmonary vascular resistance provide inadequate descriptions of RV afterload because they fail to account for pulsatile loading contributions 1
• As blood ejects from the RV into the lungs, antegrade flow encounters waves of retrograde flow generated by multiple bifurcations throughout the pulmonary vasculature, creating impedance waves that reduce antegrade flow and increase peak PA systolic pressure 1
• Elevated left heart filling pressures directly increase RV afterload, secondarily reduce PA compliance, and increase PA resistance through acute vasoconstriction and chronic vascular remodeling 1

Clinical Significance: RV vs LV Sensitivity

The RV is extraordinarily sensitive to afterload changes—minor increases in afterload cause large decreases in stroke volume, unlike the LV which tolerates pressure increases much better. 1

• The RV has a shallower end-systolic pressure-volume slope than the LV, resulting in lesser change in end-systolic pressure but greater change in end-systolic volume 1
• When PA systolic pressure increases acutely, RV stroke volume decreases significantly and arterial elastance increases out of proportion to end-systolic elastance, making RV function inefficient 1
• In contrast, an increase in aortic systolic pressure results in smaller decreases in LV stroke volume, maintaining near-normal ventriculo-arterial coupling 1

Common Clinical Pitfall: Confusing Afterload with Resistance

Systemic vascular resistance is an unreliable index of left ventricular afterload because it reflects only peripheral arteriolar tone rather than true ventricular systolic wall force. 2

• SVR underestimated the magnitude of change in LV wall stress by 22% when afterload was decreased with nitroprusside, 54% when afterload was increased with methoxamine, and 50% when afterload was decreased with dobutamine 2
• Most critically, discordant changes can occur—during norepinephrine infusion, SVR increased by 21% while actual wall stress fell by 9% 2
• A true measure of left ventricular afterload must consider the interaction of factors both internal (chamber pressure, dimension, wall thickness) and external (arterial impedance) to the myocardium 2, 3

Afterload in Disease States

In aortic stenosis, LV systolic wall stress (afterload) remains normal as long as the hypertrophic process adequately increases relative wall thickness to counter high intracavitary pressure. 1

• If hypertrophy is inadequate and relative wall thickness does not increase proportionally to pressure, wall stress increases and high afterload causes decreased ejection fraction 1
• In chronic aortic regurgitation, the enlarged chamber size with associated increase in systolic wall stress results in increased LV afterload, representing a condition of combined volume and pressure overload 1

In acute right heart failure, abruptly increased RV afterload from pulmonary embolism, hypoxia, or acidemia can precipitously decrease RV stroke volume with minimal increase in RV systolic pressure. 1

• The RV is coupled to high-compliance, low-resistance pulmonary circulation and adapts to volume changes rather than pressure changes 1
• Acute reductions in RV contractility combined with increased afterload promote RV dilation, tricuspid regurgitation, and ventricular interdependence effects that impede LV filling 1