Afterload Effect on Stroke Volume

Afterload Effect on Stroke Volume is the inverse relationship describing how the resistance and pressure the ventricle must overcome to eject blood into the arterial circulation influences the volume ejected during a single contraction, with increased afterload, at constant preload and contractility, reducing the extent of myocardial fiber shortening achieved during ejection and thereby decreasing stroke volume.

Defining Afterload

The Load Opposing Ejection

Afterload refers to the force, or wall tension, that the ventricular myocardium must generate and sustain in order to overcome the resistance of the arterial circulation and open the semilunar valve, a load that continues to oppose the muscle throughout the entirety of the ejection phase rather than being encountered only at its onset.

Relationship to Arterial Pressure and Resistance

Afterload is closely related to, though not identical with, arterial pressure, since the wall tension the ventricle must generate depends not only on the pressure within the artery but also on the geometry of the ventricular chamber itself, as expressed through the relationship between wall tension, pressure, and chamber radius.

Mechanistic Link to Stroke Volume

Force-Velocity Relationship of Cardiac Muscle

Cardiac muscle, like other muscle types, exhibits an inverse relationship between the load against which it contracts and the velocity and extent of shortening it can achieve, meaning that as afterload increases, the myocardial fibers shorten less rapidly and to a lesser extent during a contraction of fixed intrinsic strength.

Effect on End Systolic Volume

Because reduced fiber shortening at higher afterload leaves a greater residual volume of blood within the ventricle at the conclusion of ejection, increased afterload raises end systolic volume, and since stroke volume is calculated as the difference between end diastolic and end systolic volume, this rise in end systolic volume directly reduces stroke volume when end diastolic volume remains constant.

Representation on the Pressure-Volume Loop

Rightward Shift Along the End Systolic Relationship

An increase in afterload, at constant preload and contractility, shifts the end systolic pressure-volume point rightward and upward along the fixed end systolic pressure-volume relationship, reflecting the larger residual ventricular volume remaining after a contraction that reached a higher peak systolic pressure but achieved less shortening.

Preserved End Systolic Pressure-Volume Relationship

Because the end systolic pressure-volume relationship itself reflects contractility rather than loading conditions, a change in afterload alone moves the end systolic point along this fixed line rather than shifting the line itself, distinguishing the effect of afterload from the effect of a true change in contractility.

Interaction With Compensatory Mechanisms

Frank-Starling Compensation for Elevated Afterload

Because increased afterload initially raises end systolic volume without an immediate compensatory change in venous return, the larger residual volume combines with normal venous inflow during the subsequent diastole to increase end diastolic volume in the following cycle, and this increased preload can partially restore stroke volume toward its original value through the Frank-Starling mechanism over subsequent beats.

Limits of Compensation

This compensatory lengthening of the myocardial fibers can offset only a portion of the reduction in stroke volume caused by sustained elevation in afterload, since the length-tension relationship governing the Frank-Starling mechanism has physiological limits beyond which further fiber stretch does not yield proportional increases in contractile force.

Physiological Determinants of Afterload

Arterial Resistance and Compliance

The resistance offered by the systemic or pulmonary arterioles, together with the compliance, or distensibility, of the large elastic arteries receiving the ejected stroke volume, jointly determine the pressure the ventricle must overcome throughout ejection, with reduced arterial compliance or increased peripheral resistance both raising afterload.

Ventricular Wall Geometry

Consistent with the relationship between wall tension, pressure, and chamber radius, a dilated ventricular chamber experiences greater wall tension, and therefore greater afterload, for any given intraventricular pressure compared to a normally sized chamber, illustrating how chamber geometry itself contributes to the overall afterload the myocardium must overcome.

Functional Significance of the Representation

Inverse Determinant of Ejection Performance

Afterload functions as an inverse determinant of stroke volume, meaning that all else held constant, any physiological or pathological process that raises the resistance or pressure opposing ventricular ejection tends to reduce the volume of blood delivered during each contraction.

Basis for Distinguishing Loading-Dependent From Intrinsic Changes in Ejection

Because the effect of afterload on stroke volume operates through the force-velocity properties of muscle contraction rather than through any change in the muscle's intrinsic contractile capacity, this relationship provides the conceptual basis for distinguishing reductions in stroke volume attributable to increased arterial resistance from those attributable to a genuine decline in myocardial contractility.