A 58-year-old man has a prolonged PR interval of 240 ms. Which ion channel abnormality is most directly responsible for slow conduction through the AV node?
- A Reduced L-type Ca2+ channel (ICaL) current, which drives AV nodal action potential upstroke ✓
- B Reduced INa (fast sodium current), slowing phase 0 in the AV node
- C Increased IK1 (inward rectifier), hyperpolarising AV nodal cells
- D Reduced IKs current, prolonging action potential duration globally
Correct answer: A. Reduced L-type Ca2+ channel (ICaL) current, which drives AV nodal action potential upstroke
Explanation
Unlike ventricular myocytes, AV nodal cells are 'slow response' fibres whose action potential upstroke (phase 0) is generated primarily by ICaL (L-type Ca2+ channels), not INa. Reduced ICaL directly slows conduction velocity through the AV node and prolongs the PR interval. Ca2+-channel blockers (verapamil, diltiazem) exploit this mechanism to increase AV nodal refractoriness. INa blockade would preferentially affect atrial/ventricular fast fibres.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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