Antiarrhythmic agent resident survival guide
Template:Antiarrhythmic agent Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Definition
Causes
Life Threatening Causes
Common Causes
Prognosis
Vaughan-Williams classification of antiarrhythmic agents
| Vaughan-Williams classification of antiarrhythmic agents | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Class IA | Class IB | Class IC | Class II | Class III | Class IV | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Mechanism | Predominantly sodium channel blocker with some potassium channel blocking activity | Sodium channel blocking activity | *V1 receptor of GIT vasculatures *Antidiuretic effects | *Pure α1 agonist(Vasoconstrictive) *No β1 | *Predominant β1 agonist (↑contractility) *β2 arterial smooth muscle (Hypotensive) | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Agents | Quinidine, procainamide, disopyramide | Lidocaine, mexiletine, phenytoin | 2nd line septic shock | 1st line Neurogenic shock 3rd-4th line septic shock | *1st line cardiogenic shock * low output septic shock | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Effect | Slows conduction, & prolongs repolarization | Slow conduction in diseased tissues, shorten repolarization | 0.03 unit/min | 20-300 mcg/kg/min | 2.5-20 mcg/kg/min | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Indications | Pre-excited atrial arrhythmias PSVT, Ventricular tachycardia | Ventricular arrhythmia | *Coronary spasm *Splanchnic vasoconstriction | Reflex bradycardia (only α1) | Hypotension (β2) | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Complications | Abdominal cramping, diarrhea, rash, cinchonism (hearing decrease, tinnitus, and blurred vision), thrombocytopenia, hemolytic anemia, lupus syndrome , granulomatous hepatitis, QRS widening and ventricular arrhythmias. | *Not in cardiogenic shock *Arrhythmia *Ischemia induced cardiotoxicity | *Ischemic heart *Gut ischemia | *Bradycardia *Heart block | *Hypotension (add α1 agonist) | ||||||||||||||||||||||||||||||||||||||||||||||||||||
Do's
- Toxic levels of quinidine cause severe QRS widening and ventricular arrhythmias. (may reverse with the infusion of sodium lactate or sodium bicarbonate).
- Quinidine syncope most frequently due to VT (incidence 0.5 to 4.4%).VF (median occurence 3 days after initiation of drug) is common to all Class 1A drugs (concordance rate ~ 30%). In other words, if Torsade de Pointes or VF is observed with one class 1A agent all other class 1A agents should be avoided due to high incidence of Torsade de Pointes. Because of risk of proarrhythmia all class 1A drugs should be initiated in hospital. If QTC > 500 msec stop drug.
Don'ts
- Do not start with low dose Dopamine dose to perfuse the kidney.