Antiarrhythmic agent resident survival guide

Template:Antiarrhythmic agent Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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

Arrhythmia (more β1)

*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).

Don'ts

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