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Updated: Aug 5 2019

Cardiac Myocyte Physiology

Images
https://upload.medbullets.com/topic/108014/images/excitation contraction coupling.jpg
https://upload.medbullets.com/topic/108014/images/cardiomyocyte physiology.jpg
https://upload.medbullets.com/topic/108014/images/cmp.jpg
  • Snapshot
    • A 64-year-old man with chronic obstructive pulmonary disease presents with palpitations and lightheadedness. In his chart, there are documented allergies to calcium channel blockers. He is tachycardic (160/min). An electrocardiogram reveals an irregular supraventricular rhythm with polymorphic P waves. A medication that increases contractility is given. (Digoxin)
  • Introduction
    • Generation of action potential
      • initiated by the sinoatrial (SA) node
      • delayed by the atrioventricular (AV) node
        • allows for ventricular filling prior to contraction
    • Excitability and refractory periods
      • excitability
        • myocytes are able to generate an action potential in response to depolarization
        • cells must reach the threshold potential to achieve an action potential
        • note, myocytes are electrically coupled via gap junctions that allow propagation of the action potential
      • refractory period
        • occurs after depolarization
        • prevents further depolarization as the inactivation gates on the Na+ channels are closed and no current can flow through them
        • once a cell is repolarized, the inactivation gates on the Na+ channels re-open
          • a cell is once again excitable
  • Excitation-Contraction Coupling
    • The action potential causes a rush of Ca2+ into the cell
      • via L-type voltage-gated Ca2+ channels
        • indirectly blocked by β-blockers via ↓ cAMP
        • directly blocked by non-dihydropyridine Ca2+ channel blockers
    • This triggers the release of more Ca2+ from the sarcoplasmic reticulum
      • via ryanodine receptors
        • blocked by the ryanodine toxin
    • Ca2+ binds to troponin C
      • tropomyosin is moved out of the way
    • Actin and myosin can now bind
      • cross-bridges are formed and broken, and thin and thick filaments slide past each other creating tension
    • Contraction occurs
  • Contractility
    • Contractility, or level of tension generated, is determined by intracellular Ca2+
      • positive inotropic agents increase intracellular Ca2+
      • digoxin
        • inhibits extracellular K+ binding site of the Na+-K+ ATPase on myocyte cell membrane
          • when the ATPase is inhibited, ↑ Na+ intracellular concentration
          • Ca2+-Na+ exchanger decreases the amount of Ca2+ it pumps out of the cell
          • ↑ Ca2+ intracellular concentration
  • Relaxation
    • Relaxation and repolarization of the cell membrane occurs when ↓ intracellular Ca2+ concentration back to resting levels
      • Ca2+ ATPase on sarcoplasmic reticulum membrane
        • Ca2+ returns to sarcoplasmic reticulum
      • Ca2+ ATPase on cell membrane
        • Ca2+ extruded out of the cell
      • Ca2+-Na+ exchange on cell membrane
        • exchanges 1 Ca2+ out of the cell for 3 Na+ into the cell
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