Table 2.
Antiarrhythmic drugs. VT = ventricular tachycardia, VPB = ventricular premature beat, LQTS = long QT syndrome, CPVT = catecholaminergic ventricular tachycardia, BB = Betablocker, AVN = atrio-ventricular node, VF = ventricular fibrillation, TdP = Torsade de pointes tachycardia, LVEF = left ventricular ejection fraction, HFrEF = heart failure with reduced ejection fraction.
| Antiarrhythmic drug (Vaughan Williams Class) Dose | Special feature | Indication | Important side effects or contraindications |
|---|---|---|---|
|
Ajmaline (IA) i.v. single dose 1 mg/kg till max. 100 mg Infusion: speed max. 10 mg/min; continuous infusion: 10–50 mg/h |
short half-life, easy titration | VT, VF, malignant arrhythmias triggered by short coupled VPBs, (Ajmaline-test to unmask Brugada-syndrome) | QRS widening, PQ-prolongation, QT-prolongation, pro-arrhythmic effect (stop therapy in case of QRS widening > 25%, PQ-prolongation > 50%, QTc prolongation > 500 ms) |
|
Quinidine (IA) p.o. sulfate 200–600 mg every 6-12hrs gluconate 324–648 mg every 8-12hrs i.v. total 800 mg, rate 50 mg/min |
strong blocker of transient K-efflux | VF, Brugada syndrome, SQTS, VF in acute MI, malignant arrhythmias triggered by short coupled VPBs | syncope, TdP, AV-block, nausea, vomiting, QRS widening, QTc prolongation |
|
Lidocaine (IB) i.v. 1–1,5mg/kg bolus, then 0,5–0,75 mg/kg bolus every 5–10 min, max. dose 3 mg/kg Infusion: 1–4 mg/min |
advantage of stronger binding and effect in low pH and membrane potential in case of ischemia triggered VTs | VTs caused by acute myocardial ischemia | proarrhythmic, bradycardia, delirium, psychosis |
|
Mexiletine (IB) p.o. 150–300 mg every 8-12hrs |
especially as add-on in inefficiency of amiodarone | VT, LQTS3 | heart failure, sinus node dysfunction, AV-block |
|
Flecainide (IC) p.o. 50–200 mg every 12hrs Propafenone (IC) p.o. 150–300 mg every 8hrs |
PQ-prolongation, QRS-prolongation | VPBs, VT, flecainide also for CPVT | bradycardia, med. induced Brugada syndrome, monomorphic VTs due to myocardial scar, eventually acute reduction of LVEF in HFrEF |
|
Beta-Blocker (II) Propranolol: i.v. 1–3 mg every 5 min max. 5 mg if necessary repeated after 4hrs Esmolol: i.v. 0,5mg/kg bolus, then 0,05 mg/kg/min Landiolol: i.v. 0,1–0,3mg/kg bolus, then 0,01–0,04 mg/kg/min |
cornerstone of VT therapy advantage of non-selective BB is suppression of adrenergic tonus (e.g. propranolol) in case of severely reduced LVEF BB with short half-life (e. g. esmolol, landiolol). reduction in sinus rate, increase of AVN refractoriness ultra-short half-life (3–5 min), advantage of less pronounced neg. inotrope effect and reduced risk of hypotension [9], [36]. |
VPB, VT, LQTS, CPVT | hypotension, bradycardia, AV-block, bronchospasm |
|
Sotalol (III) p.o. 160 – 320 mg/day |
betablocker and class III antiarrhythmic drug | VT, 2nd line drug in ARVC | QT-prolongation, TdP, bradycardia, AV-block, depression |
|
Amiodarone (III) i.v. 150–300 mg bolus; 1 mg/min for 6hrs, then 0,5mg/min for 18 h p.o. 3x200-400 mg/day, if 10 g total dose 200 mg/day |
most important emergency antiarrhythmic drug, even more effective, if combined with BB reduction of sinus rate, QRS prolongation, QTc prolongation, increase of AVN-refractoriness |
VT, VF | bradycardia, AV-block, QT-prolongation (proarrhythmic effect, if QTc > 500 ms TdP) contraindication: LQTS, TdP, bradycardia induced VTs |
|
Verapamil (IV) i.v. 2,5–5 mg every 15–30 min p.o.: 240–480 mg/day |
reduction of sinus rate and AV-conduction, PQ-prolongation | VT, VPBs, fascicular VT | hypotension, edema, aggravation of HFrEF, AV-block, bradycardia |
|
Isuprenaline (other) i.v. 0.5–20 μg/min |
cardiac acceleration to suppress ectopic VPBs, enhancement of the inward calcium current to eliminate the transmural voltage gradient | Electrical Storm in Brugada syndrome, early repolarization syndrome and short QT syndrome |
hypotension, tachycardia, hypokalemia |