Which mechanism explains why increasing preload can increase stroke volume in a healthy ventricle?

• A. It increases sarcomere stretch, enhancing contractility and increasing stroke volume.
• B. It reduces cross-bridge formation, decreasing stroke volume.
• C. It is independent of venous return.
• D. It decreases LV afterload.

Answer: (A)

This tests the length–tension relationship of cardiac muscle, known as the Frank-Starling mechanism. Preload is the end-diastolic stretch of the left ventricle. When you increase preload, the sarcomeres are stretched closer to their optimal length, which increases the likelihood of cross-bridge formation between actin and myosin for a given Ca2+ level. The result is a stronger contraction and a larger stroke volume in a healthy ventricle.

Other ideas don’t fit this mechanism: reducing cross-bridge formation would lower stroke volume, not increase it. Preload is inherently tied to venous return, so it isn’t independent of venous return. And preload changes are about filling (and stretch), not about actively lowering afterload; afterload is the pressure the ventricle must overcome to eject blood.