Antiarrhythmics

Question 1

Class 1

Answer 1

sodium channel blockers

• slow or block conduction (especially in depolarized cell)
• decrease slope of phase 0 depolarization
• state dependent (selectively depress tissue that is frequently depolarized [e.g. tachy])

Question 2

Class 1A
Drugs 
MOA
Clinical Use
Toxicity

Answer 2

the Queen Proclaims Diso’s pyramid
Quinidine
Procainamide
Disopyramide

MOA:
Increase AP duration
Increase effective refractory period in ventricular action potential
Increase QT interval

Clinical Use:
Atrial and Ventricular Arrhythmias
-Reentrant and ectopic SVT and VT

Toxicity:

1. Cinchonism (headache, tinnitus with quinidine)
2. Reversible SLE-like syndrome (procainamide)
3. Heart failure (disopyramide)
4. thrombocytopenia
5. torsades de pointes due to increased QT interval

Question 3

Class 1B

Answer 3

I’d Buy Liddy’s Mexican Tacos
Lidocaine, Mexiletine
(Phenytoin can also fall in this category)

MOA

1. decrease AP duration
2. preferentially affect ischemic or depolarized purkinje and ventricular tissue

Clinical Use
1. Acute ventricular arrhythmias (especially post MI)
2. Digitalis induced arrhythmias
IB is Best post-MI

Toxicity

1. CNS stimulation/depression
2. cardiovascular depression

Question 4

Class 1C

Answer 4

Can i have Fries Please
Flecainide Propafenone

MOA

1. Prolongs effective refractory period in AV node and accessory bypass tracts
2. No effect on ERP in purkinje and ventricular tissue
3. minimal effect on AP duration

Clinical Use

1. SVTs including atrial fibrillation
2. only as last resort in refractory VT

Toxicity

1. Proarrhythmic, especially post MI
   (contraindicated) . 1C is Contraindicated in structural and ischemic heart disease

Question 5

Class 2

Answer 5

Beta Blockers
Metoprolol, Propranolol, esmolol, atenolol, timolol, carvedilol

MOA: Decrease SA and AV nodal activity by decreasing cAMP and Ca currents. Suppress abnormal pacemaker by decreasing phase 4 slope
AV node particularly sensitive–>increase in PR interval
Esmolol very short acting

Clinical Use:

1. SVT
2. Ventricular rate control for atrial fibrillation and atrial flutter

Toxicity:

1. Impotence
2. exacerbation of COPD and asthma
3. Cardiovascular effects (brady, AV block, HF_
4. CNS effects (sedation, sleep alterations)
5. May mask signs of hypoglycemia
6. cause unopposed Alpha1 agonism if given alone for pheochromocytoma or cocaine toxicity

Metoprolol can cause dyslipidemia
Propranolol can exacerbate vasospasm in Prinzmetal angina

Treat B blocker overdose with saline, atropine and glucagon

Question 6

Class 3

Answer 6

Potassium channel blockers
AIDS
Amiodarone 
Ibutilide
Dofetilide 
Sotalol 

MOA
Increase AP duration
Increase Effective refractory period
Increase QT interval

Clinical Use
Atrial fibrillation
Atrial flutter
Ventricular Tachycardia (amiodarone, sotalol)

Toxicity

1. Sotalol-torsades de pointes, excessive Beta blockade
2. Ibutilide-torsades de pointes
3. Amiodarone
   - pulmonary fibrosis
   - hepatotoxicity/hyperthyroidism
   - hapten
   - neurological effects
   - constipation
   - cardiovascular effects (brady, HB, HF)
   - check PFTs, LFTs, TFTs
   - lipophilic and has class 1,2,4, and IV effects

Question 7

Class 4

Answer 7

Calcium channel blockers
Verapamil and diltiazem

MOA
Decrease conduction velocity
Increase Effective refractory period
Increase PR interval

Clinical USe
Prevention of nodal arrhythmias (e.g. SVT)
Rate control in atrial fibrillation

Toxicity
Constipation, flushing, edema, cardiovascular effects ( HF, AV block, sinus node depression)

Question 8

Adenosine

Answer 8

MOA
Increase K+ out of cells–> hyperpolarization of the cell and decreased Ca current

Clinical Use

• drug of choice for diagnosing/abolishing supraventricular tachycardia
• very short acting (15 sec)
• effects blunted by theophylline and caffeine (both are adenosine receptor antagonists)

Toxicity
-flushing, hypotension, chest pain, sense of impending doom, bronchospasm

Question 9

MG

Answer 9

Effective in torsades de pointes and digoxin toxicity