All of the following are mechanisms by which increased sympathetic nervous system activity increases cardiac output EXCEPT:

Explanation

## Mechanisms of Sympathetic Stimulation on Cardiac Output **Key Point:** Sympathetic activation increases cardiac output (CO = HR × SV) through three primary mechanisms: increased heart rate, increased contractility, and increased venous return — NOT decreased venous return. ### Correct Mechanisms of Sympathetic Action | Mechanism | Receptor | Effect on CO | |-----------|----------|-------------| | Increased HR | β₁ on SA node | ↑ HR component | | Increased contractility | β₁ on ventricular myocardium | ↑ SV via ↑ force of contraction | | Increased venous return | α₁ on veins (venoconstriction) | ↑ SV via Frank-Starling mechanism | | Faster AV conduction | β₁ on AV node | ↑ HR, optimizes ventricular filling | **High-Yield:** Sympathetic nervous system increases cardiac output through the **fight-or-flight response** — all three components (HR, contractility, venous return) must increase together. Venoconstriction of capacitance vessels **increases** venous return by reducing the venous capacitance pool, shifting blood centrally. ### Why the Distractor Is Wrong **Clinical Pearl:** The option stating "decreased venous return due to venoconstriction" contradicts basic cardiovascular physiology. Venoconstriction of capacitance vessels (which hold ~60% of blood volume) **reduces venous capacitance**, thereby **increasing** venous return to the heart. This is a critical mechanism for augmenting stroke volume during sympathetic activation. **Mnemonic:** **SCAT** — Sympathetic activation increases: **S**troke volume (via venoconstriction + contractility), **C**ontractility (β₁), **A**trial rate (β₁ on SA node), **T**ransmission speed (β₁ on AV node). [cite:Guyton & Hall Textbook of Medical Physiology 14e Ch 9]