## Electrophysiological Comparison: SA Node vs AV Node **Key Point:** The SA and AV nodes differ fundamentally in their intrinsic firing rates, conduction velocities, and refractory periods — properties that define their roles in the conducting system. ### Comparative Electrophysiology | Property | SA Node | AV Node | | --- | --- | --- | | **Intrinsic rate** | 60–100 bpm (fastest) | 40–60 bpm | | **Conduction velocity** | 1 m/s | 0.02–0.05 m/s (slowest) | | **Refractory period** | Shorter (~150 ms) | Longer (~300 ms) | | **Action potential** | Slow diastolic depolarization (Phase 4) | Slow diastolic depolarization | | **Primary ion channels** | L-type Ca²⁺ and HCN (funny current) | L-type Ca²⁺ (minimal fast Na⁺) | | **Autonomic sensitivity** | High (β-adrenergic, vagal) | High (β-adrenergic, vagal) | ### Physiological Significance **High-Yield:** The SA node is the pacemaker because: - Its intrinsic rate (60–100 bpm) is faster than the AV node (40–60 bpm) and Purkinje system (20–40 bpm) - It depolarizes first, suppressing slower subsidiary pacemakers (overdrive suppression) **Clinical Pearl:** The AV node's slow conduction velocity and long refractory period serve a critical function: - They delay impulse transmission from atria to ventricles, allowing atrial contraction to complete before ventricular activation - This delay is visible as the PR interval on ECG (normal 120–200 ms) - Without this delay, atrial and ventricular contractions would occur simultaneously, reducing cardiac output **Mnemonic: SAVE** — SA node is Superior (location), Accelerated (fastest rate), Very fast to fire; AV node is Accessory (secondary pacemaker), Velocity slow, Vital delay. ### Clinical Applications - **Atropine** (vagolytic) increases SA node rate more than AV node rate - **Adenosine** blocks AV node conduction (used to terminate SVT) - **Beta-blockers** slow both nodes but may preferentially affect AV node in some contexts - **Digoxin** enhances vagal tone, slowing AV node conduction 
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