Which of the following is the primary mechanism by which increased venous return leads to increased cardiac output according to the Frank-Starling law?

Explanation

## Frank-Starling Mechanism **Key Point:** The Frank-Starling law (also called the length-tension relationship) states that cardiac output is directly proportional to the initial length of cardiac myocytes, within physiological limits. ### Mechanism 1. **Venous return increases** → ventricular filling increases → ventricular end-diastolic volume (VEDV) increases 2. **Myocardial fiber stretch increases** → optimal spacing of actin and myosin filaments 3. **Cross-bridge formation improves** → greater force of contraction (increased stroke volume) 4. **Cardiac output increases** (CO = SV × HR) ### Why This Is Intrinsic **High-Yield:** This mechanism is **independent of neural or hormonal input** — it is a purely mechanical property of the heart. The stretched sarcomere generates more force because: - Actin and myosin filaments are positioned optimally for cross-bridge cycling - Calcium sensitivity of troponin C is enhanced - Geometric arrangement of thick and thin filaments is ideal **Clinical Pearl:** This is why a patient in supine position (increased venous return) has higher cardiac output than when standing upright — no sympathetic activation needed. ### Limits **Warning:** Beyond optimal stretch (VEDV ~130 mL in left ventricle), further stretch **decreases** force of contraction (descending limb of Starling curve) — seen in acute severe volume overload or dilated cardiomyopathy. [cite:Guyton & Hall Ch 9]