Antiarrhythimics Flashcards
Decreased automaticity Restoration of conduction (restore depressed conduction and reverse re-entry) Decreased conduction (Covert 1-way to 2-way block and block re-entry) Decreased/Increased ERPs (reverse or block re-entry) Homogeneity of ERPs
Antiarrhythmics
Most arrhythmias caused by
Abnormal conduction pathway
Class ___ drugs good at increasing ERP
3
Class _____ drugs good at decreasing conduction velocity
1
Na channel blockers - slow conduction
Class 1
Beta-receptor blockers
Inhibit sympathetic input to AV node
Class 2
Prolong APD
Increase ERP
Class 3
Ca channel block
Class 4 drugs
Class one drugs bind to Na channels in their ______ state and dissociate in their _____ closed
Open
Closed
Class 1A
Class 1B
Class 1C
Moderate dissociation
Fast dissociation
Slow dissociation
Good for tachycardia, hypoxia, ischemia
Class 1B
A lot of drug stays bound from one AP to next. Most profound effect on slowing conduction
Class 1C
Associate during
Dissociation during
Systole
Diastole
Procainamide is a class _____ drug
1A
Decrease automaticity
Decrease conduction velocity
Increase APD and ERP
Procainamide
Has some Anticholinergic effects
Procainamide
Has unpredictable effects on the AV node
Class 1A
Procainamide
Directly will decrease AV node conduction
Anticholinergic effects increase AV node conduction
Increase/Decrease AV node conduction
Procainamide
Class 1A
Avoid in prolonged QT syndrome because can cause torsades de pointes
Procainamide
Used for life threatening ventricular arrhythmias
Orally and IV
Hepatic and renal metabolism
Procainamide
Class 1A
Has active metabolite NAPA
Procainamide
Causes ANA formation and a lupus like syndrome
Procainamide (Class 1A)
Hydralazine
Causes agranulocytosis and leukopenia early in treatment
Procainamide
Has proarrhythmic effects
Procainamide
Avoid in prolonged QT, lupus, and hypokalemia
Procainamide (Class 1A)
Lidocaine and mixiletine
Class 1B drugs
Have minimal effects in normal myocardium, and class 1A like action in diseased myocardium
Class 1B drugs
Use in life threatening ventricular arrhythmias and digoxin-induced arrhythmias
Lidocaine
Hepatic metabolism- first pass elimination
IV only
Must decrease dose in liver disease & CHF
Lidocaine
Can cause seizures with CNS
Lidocaine
Has hypersensitivity to other amides, causes severe hepatic dysfunction
Lidocaine
Similar to lidocaine
Orally effective
Causes GI, CNS, tremors, and thrombocytopenia
Mexiletene (Class 1B)
Flecainide and Propafenone
Class 1C drugs
Markedly slow conduction, decrease automaticity
Flecainide and Propafenone
Used in life threatening ventricular arrhythmias and disabling supra ventricular arrhythmias IN the ABSENCE of organic heart disease
Flecainide (Class 1C)
Increases mortality post MI
Avoid in pre-existing heart probes
Flecainide (Class 1C)
Conduction block
Flecainide
Similar to Flecainide
Propafenone
Inhibit sympathetic input (Decreases automaticity and conduction velocity, increases refractories)
Prominent effects in SA and AV nodes
Decrease contractility
Class 2 beta blockers
Used in supraventricular arrhythmias, a flutter and a fib, symptomatic PVCs, post MI, and CHF
Class 2 (beta blockers)
Can cause bronchoconstriction, CHF, AV block, cold extremities
Increase insulin-induced hypoglycemia b/c they block the reflexive increase in HR
Class 2 beta blockers
Propanolol is
Nonspecific beta blocker
Metoprolol is
Cardioselective beta blocker
Esmolol is
Cardio selective beta blocker
Short half life (mins). Control ventricle rate in Afib and a flutter. Control sinus tachycardia
Esmolol
Homogenous prolongation of APD (proarrhythmic).
Class 3
Treat refractory life threatening ventricular arrhythmias
Class 3
Increased automaticity
Conduction block or slowing
Decreased/Increased ERPs
Heterogeneity of ERPs
Proarrhythmics
