Source / episode info
- **Episode:**55
- **Title:**Divine Intervention Episode 55 – Cardiac Pharmacology for the USMLE Step 1 (Part 1)
- **Published:**2018-10-04
- Source:Episode page
One-liner
This episode details the five phases of the myocardial action potential and three phases of the pacemaker potential, focusing on Class I antiarrhythmics (sodium and potassium channel blockers) and emphasizing critical management principles for Wolff-Parkinson-White syndrome (WPW).
High-yield summary
- Myocardial AP: Phase 0 (Fast Na+ influx/Depolarization); Phase 2 (Ca++ influx + Na+ influx); Phase 3 (Delayed rectifier K+ efflux/Repolarization).
- Pacemaker Potential: Automaticity is driven by the "funny current" (I_f) in Phase 4. Sympathetic stimulation increases I_f slope; Parasympathetic decreases it.
- Class I Antiarrhythmics: These drugs block Na+ channels and are classified based on their specific effect: Class IA (Na+ & K+ blocker, prolongs QT); Class IB (Phase 2 Na+ blocker, shortens APD); Class IC (Pure Na+ blocker, no change in APD).
- EKG Correlation: QRS complex reflects ventricular depolarization (fast); QT interval reflects ventricular repolarization (slow). Prolonging the action potential duration primarily prolongs the QT interval.
- WPW Syndrome Management: Never use AV nodal blockers (e.g., Beta-blockers, non-dihydropyridine CCBs) in suspected WPW because they increase conduction through the accessory pathway (Bundle of Kent), risking rapid ventricular rates and sudden death.
Learning objectives
- Describe the electrophysiology of the myocardial action potential and pacemaker potential phases.
- Differentiate the mechanisms of Class I antiarrhythmics (IA, IB, IC) based on their specific ion channel blockade.
- Predict the resulting changes in QRS width versus QT interval duration following drug administration.
- Identify contraindications for rate control agents in patients with Wolff-Parkinson-White syndrome (WPW).
- Recognize and manage the clinical manifestations of Digoxin toxicity.
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