What are afterload and preload in cardiovascular physiology?

Preload and Afterload in Cardiovascular Physiology

Preload is all factors contributing to passive ventricular wall stress at end-diastole (essentially the stretch on the myocardium before contraction), while afterload is all factors contributing to total myocardial wall stress during systolic ejection (the resistance the ventricle must overcome to eject blood). 1

Preload: The Diastolic Loading Condition

Preload represents the ventricular wall tension at the end of diastolic filling, determined primarily by end-diastolic volume and ventricular compliance. 1

• The best clinical measure of preload is end-diastolic volume, which can be assessed by ventriculography, echocardiography, or indicator dilution techniques 2
• At the sarcomere level, preload determines the initial muscle fiber length before contraction, which directly influences contractile force through the Frank-Starling mechanism 3
• According to the Law of LaPlace, preload-related wall stress equals (pressure × radius) / (2 × wall thickness) at end-diastole 1
• In chronic heart failure, sarcomere length reaches maximum and changes little, meaning the failing heart does not truly operate on a descending limb of the Frank-Starling curve 4
• Preload is acutely load-dependent—the end-diastolic pressure-volume relation shifts with changes in both afterload and preload itself, making it not entirely load-independent 5

Afterload: The Systolic Loading Condition

Afterload is the ventricular wall stress during ejection, fundamentally determined by arterial pressure, arterial stiffness, and vascular resistance. 6

Left Ventricular Afterload

• LV afterload is the aortic input impedance, composed of both steady and pulsatile components that cannot be characterized by a single number 6
• The steady component is systemic vascular resistance (SVR), determined by arteriolar caliber and number 6
• The pulsatile component depends on arterial stiffness, total arterial compliance, wave reflection amplitude, and reflected wave transit time 6
• Brachial arterial pressure alone inadequately describes LV afterload—proper assessment requires central aortic pressure-flow relations 6
• For clinical purposes, afterload can be reasonably monitored by arterial blood pressure, though this is an oversimplification 2
• Increased pulsatile afterload creates ventricular-vascular mismatch, increasing myocardial oxygen demand, decreasing cardiac efficiency, and promoting left ventricular hypertrophy 6

Right Ventricular Afterload

• RV afterload is wall stress during systolic ejection, estimated by summation of resistive and pulsatile blood flow components 6
• Commonly used measures like pulmonary artery systolic pressure and pulmonary vascular resistance inadequately describe RV afterload because they ignore pulsatile loading contributions 6
• The RV is highly sensitive to afterload changes—minor increases in afterload cause large decreases in stroke volume due to its shallower end-systolic pressure-volume slope compared to the LV 6
• Elevated left heart filling pressures directly increase RV afterload by reducing pulmonary artery compliance and increasing pulmonary vascular resistance 6

Clinical Implications and Therapeutic Considerations

Afterload Reduction in Heart Failure

• In chronic severe aortic regurgitation with poor surgical candidacy, vasodilator therapy (particularly nifedipine and hydralazine) reduces end-diastolic volume and increases ejection fraction over 1-2 years 7
• LV systolic dysfunction from aortic regurgitation is initially reversible when related to afterload excess, with potential for full recovery after appropriate intervention 6, 7
• Afterload reduction in acute decompensated heart failure requires exceptional caution in patients with chronic anemia (like thalassemia major) who have baseline low systemic vascular resistance—titrate carefully against urine output and clinical response rather than target pressures 6

Preload Management Pitfalls

• In patients with chronic anemia, baseline preload is already elevated—overdiuresis can precipitate acute renal failure by excessive preload reduction, especially with compromised oncotic status from chronic liver disease 6
• Older patients with restrictive physiology tolerate neither overfilling nor underfilling 6

Ventricular-Vascular Coupling

• Optimal ventricular efficiency occurs when end-systolic elastance (Ees) matches arterial elastance, with a ratio of 1.0; uncoupling occurs below 0.6-1.0 6
• When afterload increases acutely, arterial elastance increases disproportionately to Ees, making ventricular function inefficient with more energy expended to maintain output 6