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