Antiarrhythmic agent resident survival guide

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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
 
Quinidine - 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

  • 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.
  • Disopyramide side-effects include anticholinergic effects (30%) including dry mouth, blurred vision, constipation, and urinary retention. Pyridostigmine (90 mg twelve hourly to 180 mg every eight hours) prevents or diminishes the anticholinergic effect of disopyramide and allows high tolerated doses of the drug.
  • Disopyramide-induced hypoglycemia has been noted. Other reported side effects includes nausea, vomiting, rash, cholestatic jaundice, and agranulocytosis. It prolongs repolarization and may cause proarrhythmia (VF, Torsade de Pointes)
  • Procainamide has gastrointestinal side effects, ANA, lupus like syndrome and pro-arrhythmiagenic (Torsade de Pointes)

Dose independent (similar to Quinidine).

Don'ts

  • Do not start with low dose Dopamine dose to perfuse the kidney.

References

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