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Action Potential of Cardiac Muscle & Pacemaker Cells | CVS Physiology | USMLE Step 1 & Step 2 CK | Dr G Bhanu Prakash

In this high-yield lecture on Cardiovascular Physiology, Dr G Bhanu Prakash explains the detailed action potential of cardiac muscle cells and pacemaker cells, a frequently tested topic in both USMLE Step 1 and Step 2 CK. Understanding the electrophysiological differences between ventricular myocytes and SA/AV nodal cells is crucial for mastering cardiac conduction, arrhythmia mechanisms, and the pharmacologic actions of antiarrhythmic drugs.

We begin with the action potential of ventricular contractile cells (non-pacemaker cells), which follows five distinct phases:

Phase 0 (Rapid Depolarization) ⚡ – Due to a fast influx of Na⁺ through voltage-gated sodium channels.

Phase 1 (Initial Repolarization) 🧲 – Transient K⁺ efflux through Ito channels.

Phase 2 (Plateau Phase) ➖ – Unique to cardiac muscle, maintained by a balance between Ca²⁺ influx (via L-type calcium channels) and K⁺ efflux, allowing sustained contraction necessary for effective blood ejection.

Phase 3 (Repolarization) 🔋 – Closure of Ca²⁺ channels with continued K⁺ efflux, restoring resting membrane potential.

Phase 4 (Resting Phase) 💤 – Maintained by inward rectifier K⁺ channels.

We then compare this with the action potential of pacemaker cells (SA node and AV node), which display spontaneous depolarization and lack a true resting membrane potential:

Phase 4 (Slow Depolarization) 🔁 – Driven by “funny” If Na⁺ channels, gradually bringing the membrane to threshold.

Phase 0 (Depolarization) 📈 – Slower Ca²⁺ influx via L-type channels (no fast Na⁺ channels).

Phase 3 (Repolarization) 🧲 – Due to K⁺ efflux.

Key concepts covered include:
_______________________________
Why the SA node is the dominant pacemaker due to its fastest phase 4 depolarization

The role of the AV node in conduction delay

How drugs like beta blockers, calcium channel blockers, and class I/III antiarrhythmics target specific phases of the action potential

The basis of reentry circuits, ectopic pacemakers, and arrhythmogenesis


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