Updated: 4/1/2018

Sites of Action for Cardiac Drugs

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Snapshot
  • A 24-year-old woman presents with tachycardia. She reports that this happens every few years without any identifiable causes. Her pulse is 200/min. Her other vital signs are stable. An electrocardiogram shows a patient with narrow complex QRS, tachycardia to 204/min, and a regular rhythm. She is given a medication to slow down the atrioventricular node and attempt to end the narrow complex tachycardia. (Adenosine)
Introduction
  • Adenosine
    • mechanism of action
      • ↑ K+ out of the cells, which hyperpolarizes the cell and causes ↓ AV nodal conduction
    • background
      • action potential is initiated by the sinoatrial (SA) node
        • slowed by the atrioventricular (AV) node
        • allows for ventricular filling prior to contraction
  • Calcium channel blockers
    • mechanism of action
      • directly blocks L-type voltage-gated Ca2+ channels (dihydropyridine receptors)
    • background
      • action potential causes a rush of Ca2+ into the cell
      • Ca2+ enters via L-type voltage-gated Ca2+ channels
      • this triggers the release of more Ca2+ from the sarcoplasmic reticulum
        • via ryanodine receptors
          • blocked by the ryanodine toxin
  • Digoxin
    • mechanism of action
      • 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
    • background
      • contractility is determined by intracellular Ca2+
        • positive inotropic agents increase intracellular Ca2+
  • β-blockers
    • mechanism of action
      • indirectly blocks L-type voltage-gated Ca2+ channels (dihydropyridine receptors) via ↓ cAMP
    • background
      • positive inotropy by ↑ sympathetic nervous system is mediated by β1 receptors at the SA and AV nodes
 

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