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18 Antiarrhythmics
Chapter 18 Pharmacology of Cardiac Rhythm
Question | Answer |
---|---|
Class IA Antiarrhythmics | Block of voltage-gated Na+ channels and K+ channels in vent. myocytes (decr. phase 0 upstroke velocity and prolongs repolar.) and SA nodal cells (shifts threshold to more + potentials and decr. slope of phase 4 depolar.) CONTRA: Prolonged QT interval |
Quinidine | + Vagolytic effect ADV: torsades de pointes, complete AV block, vent. tachycardia, agranulocytosis, thrombocytopenia, hepatotoxicity, acute asthma attack, resp. arrest, angioedema, rare occurrence of systemic lupus *Quinidine-induced digoxin toxicity |
Procainamide | ADV: Same as quinidine, except fewer anticholinergic effects. Lupus-like syndrome may occur after prolonged use. |
Disopyramide | Same as quinidine, except more profound anticholinergic effects and fewer GI effects. |
Class IB Antiarrhythmics | Use-dependent block of voltage-gated Na+ channels in ventricular myocytes (decreases phase 0 upstroke velocity); may also shorten repolarization CONTRA: Stokes-Adams syndrome |
Lidocaine | √Ventricular arrhythmias in the context of MI ADV: Seizures, asystole, bradycardia, cardiac arrest, new or worsened arrhythmias, respiratory depression, anaphylaxis, status asthmaticus |
Mexiletine | Oral analogue of lidocaine. |
Phenytoin | √Seizures ADV: Agranulocytosis, leukopenia, pancytopenia, thrombocytopenia, hepatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis. *Inducer of P450 3A4 |
Class IC Antiarrhythmics | Marked block of voltage-gated Na+ channels in ventricular myocytes (decreases phase 0 upstroke velocity) |