Rapid Review·Cardiovascular

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PHARMACOLOGY

T1Must know

Class IV & Other Antiarrhythmics

FA P328

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diltiazem and verapamil.
block L-type calcium channels, so spontaneous depolarization slows; conduction velocity falls, the effective refractory period lengthens, and the PR interval lengthens.
rate control in atrial fibrillation and flutter, and prevention of nodal arrhythmias.
constipation, gingival hyperplasia, flushing, edema, plus heart failure, AV block, and sinus node depression.
slows the pacemaker action potential, lowering heart rate and AV nodal conduction. Very short acting, about 15 seconds.
  • Less cAMP: the funny current (HCN) slows, phase 4 flattens, and the rate falls.
  • Less cAMP also shuts L-type calcium channels: less calcium influx, a slower phase 0, and slower AV conduction.
  • Direct opening of K+ channels: K+ leaves the cell, hyperpolarizing it and lengthening the pacemaker's refractory period.
drug of choice for diagnosing and terminating certain forms of SVT.
flushing, hypotension, chest pain, a sense of impending doom, and bronchospasm.
both are adenosine receptor antagonists.
effective in torsades de pointes and in digoxin toxicity.
selectively inhibits the funny sodium channels (I_f), prolonging slow depolarization in phase 4. "IVabradine works on phase IV."
chronic HFrEF. Adverse: luminous phenomena, i.e. visual brightness (the same channels sit in the retina), plus hypertension and bradycardia.
ivabradine slows the heart without touching contractility or blood pressure, because it acts purely on the SA node's pacemaker current. That is what makes it useful once beta-blockers are maxed out or not tolerated.

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Why are class IV antiarrhythmics prescribed for patients with atrial fibrillation?

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