## Sympathetic vs. Parasympathetic Effects on Cardiac Output **Key Point:** Cardiac output (CO) = Heart Rate (HR) × Stroke Volume (SV). The discriminating feature between sympathetic and parasympathetic stimulation lies in their opposing effects on both HR and SV. ### Sympathetic Stimulation - **Heart rate:** Increases (via β₁ receptors on SA node) - **Stroke volume:** Increases (via β₁ receptors on ventricular myocardium → increased contractility) - **Net effect:** CO increases significantly - **Mechanism:** Norepinephrine/epinephrine bind β₁ receptors → ↑ cAMP → ↑ Ca²⁺ influx ### Parasympathetic Stimulation - **Heart rate:** Decreases (via M₂ muscarinic receptors on SA node) - **Stroke volume:** Decreases (minimal direct effect on ventricles; AV nodal slowing reduces diastolic filling) - **Net effect:** CO decreases - **Mechanism:** Acetylcholine bind M₂ receptors → ↓ cAMP → ↓ Ca²⁺ influx | Feature | Sympathetic | Parasympathetic | |---------|-------------|------------------| | Heart Rate | ↑ | ↓ | | Contractility | ↑ | ↓ (minimal on ventricles) | | Stroke Volume | ↑ | ↓ | | Cardiac Output | ↑↑ | ↓ | | Conduction velocity (AV node) | ↑ | ↓ | **High-Yield:** The **simultaneous increase in both HR and SV** is the hallmark of sympathetic activation and distinguishes it from all other regulatory mechanisms. Parasympathetic effects are primarily chronotropic (rate-lowering) with secondary reduction in SV. **Clinical Pearl:** During exercise, sympathetic dominance increases CO by 4–5 fold. In vagal maneuvers (Valsalva), parasympathetic activation reduces CO acutely, causing orthostatic symptoms. **Mnemonic:** **SYMPATHETIC = SPEED & STRENGTH** (↑ HR, ↑ contractility). **PARASYMPATHETIC = PAUSE & PUTTER** (↓ HR, ↓ contractility).
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