Snapshot A 56-year-old man recently had a myocardial infarction. While in the hospital, he reported being lightheaded. An electrocardiogram revealed a ventricular arrhythmia. His past medical history included hypertension, diabetes mellitus type 2, and chronic kidney disease. He was initially given amiodarone with no effect. He was then given a medication known to be effective in post-myocardial infarction arrhythmias. (Mexiletine) Introduction Anti-arrhythmic medications are divided into 4 classes class I drugs are Na+ channel blockers class II drugs are β-blockers class III drugs are K+ channel blockers class IV drugs are Ca2+ channel blockers AntiarrhythmicsClassMneumonicMechanismClass IANa+ channel blockersDoubleQuarterPounderDisopyramideQuinidineProcainamide↑ Action potential (AP)↑ Effective refractory period (ERP)↑ QT intervalClass IBNa+ channel blockersLettuce andMayoLidocaineMexiletine↓ AP↓ ERPAffects ischemic or depolarized tissuehence, great for post-myocardial infarction arrhythmiasClass ICNa+ channel blockersFriesPleaseFlecainidePropafenone↑ ERP in atrioventricular node but not in ventricular tissueClass II β-blockersDrug name - lolSelective β-blockersmetoprolol, esmolol, propranolol, atenolol, and timololesmolol is the most short-actingNonselective α- and β-blockerscarvedilollabetalol↓ Sinoatrial and atrioventricular nodal activity↓ cAMP and ↓ Ca2+ currents↓ slope of phase 4↑ PR intervalClass III K+channel blockersAIDSAmiodaroneIbutilideDofetilideSotalol↑ AP↑ ERP↑ QT intervalClass IV Ca2+channel blockersClass IVDrugsVerapamilDiltiazem↑ ERP↑ PR interval↓ Conduction velocity Class I - Na+ Channel Blockers Double Quarter Pounder, with Lettuce and Mayo, and Fries Please for classes IA, IB, and IC respectively these drugs slow down conduction and ↓ slope of phase 0 depolarization Class IA (disopyramide, quinidine, and procainamide) clinical use atrial and ventricular arrhythmias re-entrant and ectopic supraventricular tachycardias (SVTs) and ventricular tachycardias (VTs) toxicity thrombocytopenia torsades de pointes from ↑ QT interval heart failure (disopyramide) headache (quinidine) tinnitus (quinidine) reversible systemic lupus erythematosus-like syndrome (procainamide) Class IB (lidocaine and mexiletine) clinical use post-myocardial infarction and other ventricular arrhythmias digitalis-induced arrhythmias toxicity cardiovascular depression central nervous system effects Class IC (flecainide and propafenone) clinical use SVTs, including atrial fibrillation toxicity proarrhythmic contraindicated in structural and ischemic heart disease, especially post-myocardial infarction Class II - β-Blockers Clinical use SVTs, including atrial fibrillation and atrial flutter Toxicity impotence exacerbation of lung disease (chronic obstructive pulmonary disease and asthma) cardiovascular effects bradycardia atrioventricular block heart failure central nervous system effects sedation sleep disturbance dyslipidemia (metoprolol) exacerbate Prinzmetal angina (propranolol) Treatment for overdose of β-blockers saline atropine glucagon Class III - K+ Channel Blockers Clinical use atrial fibrillation atrial flutter VTs especially amiodarone and sotalol Toxicity torsades de pointes (sotalol and ibutilide) excessive β-blockade (sotalol) amiodarone no risk of torsades de pointes check pulmonary function tests (PFTs), liver function tests (LFTs), and thyroid function tests (TFTs) pulmonary fibrosis and interstitial pneumonitis hepatotoxicity thyrotoxicity, leading to hypo- or hyperthyroidism depending on patient's baseline thyroid function or any pre-existing thyroid disease blue/gray skin deposits and photodermatitis corneal deposits neurologic effects gastrointestinal effects cardiovascular depression bradycardia heart block heart failure Class IV - Ca2+ Channel Blockers Clinical use atrial fibrillation prevention of SVT Toxicity constipation flushing edema cardiovascular depression heart failure atrioventricular block sinus node depression Other Anti-Arrhythmics Adenosine mechanism ↑ K+ out of cells causes hyperpolarization of the cell and decreased atrioventricular node conduction very short-acting (approximately 15 seconds) clinical use diagnosing and/or terminating SVT toxicity flushing hypotension chest pain sense of impending doom bronchospasm Mg2+ clinical use torsades de pointes digoxin toxicity toxicity lethargy bradycardia