A 52-year-old man with chronic hypertension presents with dyspnea on exertion. Echocardiography reveals left ventricular hypertrophy with preserved ejection fraction. Which of the following is the most common mechanism by which increased afterload reduces cardiac output in this patient?

Explanation

## Mechanism of Afterload-Induced Reduction in Cardiac Output **Key Point:** Afterload is the ventricular wall stress (tension) during systolic ejection, determined by the Laplace law: $\sigma = \frac{Pr}{2h}$, where P = pressure, r = radius, h = wall thickness. ### Why Increased Afterload Reduces Stroke Volume When afterload increases (e.g., in hypertension): 1. **Increased wall stress** → greater force required to eject blood 2. **Energy cost rises** → myocardium must perform more work at the same contractile state 3. **Stroke volume decreases** → at any given preload and contractility, the ventricle ejects less blood 4. **Cardiac output falls** → CO = HR × SV **Clinical Pearl:** This is the fundamental Frank-Starling principle applied inversely: increased afterload shifts the SV-preload curve downward and rightward, meaning the same preload now generates less stroke volume. ### Why Hypertrophy Develops The ventricle compensates by increasing wall thickness (h), which reduces wall stress and partially restores ejection fraction—hence "preserved EF" in this case. However, if afterload remains chronically elevated, eventual systolic dysfunction ensues. **High-Yield:** The relationship between afterload and stroke volume is **inverse and non-linear**. Small increases in afterload have modest effects; large increases (e.g., acute hypertensive crisis) can precipitate acute decompensation. ### Relevant Equation $$\text{Cardiac Output} = \text{Heart Rate} \times \text{Stroke Volume}$$ Stroke volume is determined by: - **Preload** (venous return, LVEDV) — positive relationship - **Afterload** (LV wall stress) — negative relationship - **Contractility** (inotropic state) — positive relationship [cite:Guyton & Hall Ch 9]