Antiarrhythmic Drugs

Question 1

Class I Drugs

Answer 1

Depresses the rate of rise of phase 0 AP by inhibiting fast Na+ channels and stabilizing membrane potential. Increases threshold for firing in abnormal pacemaker cells, so good tx for tachycardias. Hyperkalemia causes increased toxicity for all class I drugs.
IA--prolongs duration of AP
IB--shortens duration of AP
IC--no change in duration of AP

Question 2

Class IA Drugs

Answer 2

Quinidine, procainamide, and disopyramide.
“The Queen Proclaims Diso’s pyramid.”
Prolong duration of AP, increases effective refractory period (ERP), increases QT interval. Wide spectrum–affects atrial and ventricular arrhythmias, esp reentrant and ectopic supraventricular and ventricular tachycardias.

Question 3

Class IB Drugs

Answer 3

Lidocaine, mexiletine, Tocainide (and diphenylhydantoin–phenytoin).
“I’d Buy Lidy’s Mexican Tacos.” “IB is Best post-MI”.
Shortens duration of AP. Best effects on ischemic or depolarized Purkinje and ventricular tissue. Used to tx acute ventricular arrhythmias (esp post-MI) and digitalis-induced arrhythmias. Also used to tx long QT w/ attacks of torsade de pointes VT and effort-induced VT. No effect on SVT’s.

Question 4

Class IC Drugs

Answer 4

Propafenone and flecainide.
Do not change duration of AP. Wide spectrum–used to tx ventricular tachycardias that progress to VF and intractable SVT. Considered most effective (along with amiodarone) in tx of WPW tachycardias. IC is contraindicated in structural heart dz and s/p MI.

Question 5

Class II Drugs

Answer 5

Beta blockers that neutralize/inhibit effects of sympathomimetic agents by decreasing rate of rise of phase 0 and flattening phase 4 of pacemaker AP.

Question 6

Class III Drugs

Answer 6

Amiodarone, (Ibutilide), Dronedarone, and Sotalol. “AIDS”.
K+ channel blockers that prolong duration of AP w/o affecting rate of rise of phase 0. Increases ERP. Used when other antiarrhythmics fail. Increases QT interval.

Question 7

Class IV Drugs

Answer 7

Verapamil, diltiazem.
Ca2+ channel blockers that affect SA and AV nodal arrhythmias, primary effects on SVT (not VT). Decrease conduction velocity, increase ERP, increase PR interval.

Question 8

Adenosine

Answer 8

Coronary artery vasodilator; increased K+ flux out of cell which hyperpolarizes cell and decreases Ca2+ flux. Blocks AV node and terminates AV node reentry arrhythmias and slows ventricular response rate to AF and AFL. Useful in dx’ing wide complex tachycardias.

Question 9

Amiodarone

Answer 9

Class III antiarrhythmic; wide spectrum—tx’s both VT and SVT’s. Drug of choice for life threatening cardiac arrhythmias such as cardiomyopathy, WPW syndrome (with AF and AFL), in chronic ischemic heart dz w/ VT and VF when can’t use ICD implant.

Question 10

Lidocaine

Answer 10

Class IB antiarrhythmic; drug of choice for acute tx of VT due to high efficacy, low toxicity, and short t1/2. Administered via IV only.

Question 11

Digoxin

Answer 11

Cardiac glycoside, most widely used digitalis compound; directly inhibits Na/K/ATPase which indirectly inhibits Na/Ca antiport leading increase in intracellular Ca2+ and positive inotropy. Digoxin increases vagal tone and decreases sympathetic tone to AV and SA nodes, thus decreasing HR.

• Drug of choice to slow ventricular response to AF and AFL. Also used to tx CHF (by increasing contractility).
• Never give digoxin to adult pt with WPW syndrome (accelerates conduction through accessory AV pathway).

Pharmacology: long t1/2 of 1.5 days, renal excretion

Side effects: N/V/D, blurry yellow vision (Van Gogh), rarely gynecomastia. At increased risk for digitalis toxicity in pt w/ hypokalemia (low serum K+), high serum magnesium, and high serum calcium.