CV Anti-tachyarrhythmics Flashcards
Class IA
block Na channel - decreases conduction + automaticity increases QRS. block K channel - increases refractoriness + QT. effective against supra/ventricular arrhythmias caused by re-entry or ectopic, terminate A-fib. decrease ventricular contractility, clinical use decreasing causing arrhythmias
Class IB
block Na channel when HR high or ischemia. doesn’t really change EKG, slight decrease QT in patients with long QT. effective against ventricular arrhythmia caused by re-entry or ectopic. useful against digoxin induced arrhythmia. given IV
Class IC
strongest Na channel block - decrease conduction and prolongs QRS a lot. used for serious ventricular arrhythmia caused by re-entry, A-fib, AV nodal re-entry. prone to cause arrhythmias, decrease ventricular contractility
Class II
β blockers. decrease AV conduction - increase PR. treat those involved with anesthesia, surgery, exercise, cocaine. control ventricular rate in A-fib. treat long QT. proven to decrease sudden cardiac death after MI
Class III
block K channels - increase refractoriness + QT. effective against supra/ventricular arrhythmias caused by re-entry or ectopic, terminate A-fib. drug of choice for post-cardiac resuscitation and HF. less likely to cause arrhythmias
Class IV
block L-type Ca channels. decrease AV conduction - increase PR. act similar to β blockers but better at treating AV nodal re-entry tachycardia, ventricular rate control and A-fib
Digoxin
blocks Na/K ATPase. decrease sympathetic, increase parasympathetic. ventricular rate control in HF + A-fib patients. propensity to cause arrhythmias
Adenosine
increase K channel opening, decrease intracellular cAMP - decrease AV conduction, increase PR. slows heart. treat AV nodal re-entry tachycardia. short duration, given IV