Therapeutic summary of selected drugs used to treat arrhythmias: (Table 12-2)

Table 12-2. Therapeutic Summary of Selected Drugs used to Treat Arrhythmias

CLINICAL
DRUGS
APPLICATIONS
ADVERSE EFFECTS
CONTRAINDICATIONS
Mechanism: Bind to open sodium channels and also block potassium channels; prolong ERP
Class IA
Disopyramide
Procainamide
Quinidine

Atrial arrhythmias
Ventricular
arrhythmias

Hypotension
Syncope
Anticholinergic
Wide QRS complex
Prolonged QT
(Torasade de
pointes)
Cinchonism
(quinidine)
Thrompcytopenia
(quinidine)
SLE-like syndrome
(procainamide)

Hypersensitivity
With drugs that
prolong QT
Thrombocytopenia
(quinidine)

Mechanism: Bind to inactivated sodium channels; decrease ERP

Class IB
Lidocaine (IV
only)
Mexiletine
Tocainide

Ventricular
arrhythmias from
myocardial
infarction
Local anesthetic
Neuropathic pain
(mexiletine)

Many CNS effects

Arrhythmias
Seizures

Hypersensitivity
Severe degrees of
SA, AV, or
intraventricular
heart block

Mechanism: Bind to all sodium channels; minimal effect on ERP

Refractory ventricular
Class IC
arrhythmias
Flecainide
Propafenone

Increased mortality
with chronic use
Very proarrhythmogenic

Hypersensitivity
Pre-existing
second- or thirddegree AV block
Coronary artery
disease

Bradycardia
Hypotension
Bronchoconstriction
Hyperlipidemia
Hyperkalemia
Fatigue

Hypersensitivity
Severe
hyperactive airway
disease
Cardiogenic shock
Severe sinus
bradycardia
Heart block

Mechanism: -Adrenergic receptor blockers

Class II
Esmolol (IV
only)
Metoprolol
Propranolol

Tachycardia
Control ventricular
rate in atrial
fibrillation
Intraoperative or
postoperative
arrhythmias
(esmolol)

Mechanism: Potassium channel blockers

Class III
Amiodarone
Dofetilide
Ibutilide
Sotalol

Life-threatening
recurrent
ventricular
fibrillation
Hemodynamicallyunstable VT
Heart rate control
in patients with
atrial fibrillation
Conversion of
atrial fibrillation to
sinus rhythm
(ibutilide)

Torsades de
pointes
Pulmonary toxicity
(amiodarone)
Bradycardia
Arrhythmias
Thyroid dysfunction
(amiodarone)

Hypersensitivity
Cardiogenic shock
Pregnancy
(amiodarone)

Mechanism: Calcium channel blockers: slow action potential upstroke in SA and AV nodal
tissue
Class IV
Diltiazem
Verapamil

Supraventricular
tachyarrhythmias
Control ventricular
rate in atrial
fibrillation
Migraine
(verapamil)

Constipation
Bradycardia
Hypotension

Hypersensitivity
Second- or thirddegree AV block
Wolff-ParkinsonWhite syndrome
Cardiogenic shock
Congestive heart
failure

Mechanism: Slows conduction through AV node, interrupts re-entry pathways through the AV
node, restores normal sinus rhythm
Adenosine

Conversion of PSVTs to
normal sinus rhythm

Facial flushing
Dyspnea
Discomfort of neck,
throat, jaw
Headache

Hypersensitivity
Second- or thirddegree AV block
or sick sinus
syndrome

Flushing
Hypotension
Diarrhea

Hypersensitivity
Heart block
Myocardial
damage

Mechanism: Unknown, but anti-calcium effect

Magnesium

Torsade de
pointes
Prevention and
treatment of
seizures in severe
pre-eclampsia or
eclampsia
Treatment of
cardiac
arrhythmias
(VT/VF) caused
by
hypomagnesemia

Mechanism: Suppression of the AV node conduction; increases effective refractory period;

decreases conduction velocity; enhances vagal tone
Digoxin

Control ventricular
rate in atrial
fibrillation
Congestive heart
failure

All types of
arrhythmias
Gastrointestinal
distress
Visual disturbances
(blurred or yellow
vision)

Hypersensitivity
Heart block
Wolff-ParkinsonWhite syndrome

Mechanism: Potassium, major cation; essential for the conduction of nerve impulses in heart,
brain, and skeletal muscle; contraction of cardiac, skeletal and smooth muscles; maintenance
of normal renal function, acid-base balance, carbohydrate metabolism, and gastric secretion
Potassium

Treatment or
prevention of
hypokalemia
Treatment of
digoxin
cardiotoxicity

Hyperkalemia

Hyperkalemia

AV, atrioventricular; ERP, effective refractory period; PSVTs paroxysmal supraventricular tachycardias; SA,
sinoatrial; SLE, systemic lupus erythematosus; VF, ventricular fibrillation; VT, ventricular tachycardia.