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Updated: Mar 31 2018

Myocardial Action Potential

  • Snapshot
    • A 60-year-old man presents to his cardiologist for a follow-up of newly diagnosed diastolic heart failure. He has a history of asthma and chronic obstructive lung disease. He reports that his pulmonologist does not want him to take β-blockers. However, his cardiologist wants to start him on a medication to slow the heart rate. He reassures the patient that this drug acts not on β-receptors but on a Ca2+ channel. (Verapamil)
  • Introduction
    • Ions responsible for the action potential of atria, ventricles, and Purkinje fibers are the same
      • upstroke
        • inward Na+ current
      • plateau
        • slow inward Ca2+ current via L-type voltage-gated Ca2+ channels
        • a sustained period of depolarization
          • allows for ventricular filling
  • Ventricular Action Potential
    • Resting membrane potential
      • -85 mV resting membrane potential is maintained by inward rectifier K+ channels
        • inward rectifier K+ channels open at rest and close with depolarization
    • Phase 0, upstroke
      • rapid depolarization
        • caused by the opening of voltage-gated Na+ channels and inward Na+ current
          • Na+ current depolarizes cell membrane, which closes inward rectifier K+ channels
    • Phase 1, initial repolarization
      • brief repolarization and net outward current
        • inactivation gates on Na+ channels close
        • Na+ current is decreased
        • outward K+ current down an electrochemical gradient
    • Phase 2, plateau
      • stable, long period of depolarized membrane potential
      • inward and outward current are equal, with no net current flow
        • inward Ca2+ current (slow inward current)
          • opened L-type Ca2+ channels
            • blocked by Ca2+ channel blockers
          • entry of Ca2+ also triggers the release of more Ca2+ from sarcoplasmic reticulum in the cell (Ca2+-induced Ca2+ release)
        • outward K+ current
          • driven by electrochemical driving force
    • Phase 3, repolarization
      • net outward current
        • L-type voltage-gated Ca2+ channels close
          • a decrease in inward Ca2+ current
        • delayed rectifier K+ channels open completely and repolarize the membrane
          • increase in outward K+ current
      • inward rectifier K+ channels re-open
    • Phase 4, resting membrane potential
      • inward and outward currents are equal
      • delayed rectifier K+ channels close
      • inward rectifier K+ channels are fully open, resetting resting membrane potential at -85 mV
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