Afterload refers to the resistance the heart must overcome to eject blood during systole. It is closely approximated by mean arterial pressure (MAP) and influenced by vascular resistance and ventricular wall stress.
Factors Affecting Afterload:
✅ Increased Afterload With:
- Higher Wall Tension (Laplace’s Law): Increased ventricular pressure leads to greater wall tension, raising afterload.
- Chronic Hypertension (↑ MAP): Persistent high blood pressure forces the left ventricle (LV) to work harder, leading to LV hypertrophy as a compensatory response to reduce wall stress.
✅ Decreased Afterload With:
- Arterial Vasodilators (e.g., Hydralazine): Reduce systemic vascular resistance, lowering afterload.
- ACE Inhibitors & ARBs: Lower both preload and afterload, improving cardiac efficiency.
Left Ventricular Adaptation to Increased Afterload:
When afterload increases, the LV compensates by thickening (hypertrophy) to reduce wall stress and maintain function. However, prolonged hypertrophy can lead to heart failure with preserved ejection fraction (HFpEF) due to stiffened myocardium.
Managing afterload is crucial in conditions like hypertension, heart failure, and aortic stenosis to prevent excessive cardiac strain.