Antiarrhythmics

Question 1

Class 1a

Answer 1

Blocks Na and K+ channels
Increased QRS and QT

Question 2

Class 1b

Answer 2

blocks Na+ channels
Rapid dissociation rate
Narrower QT interval

Question 3

Class 1c

Answer 3

Blocks Na channels
Slow dissociation rate (>10sec)
Increased QRS
Not as steep depolarization phase

Question 4

Class 1a drugs

Answer 4

Quinidine
Procainamide
Disopyramide

Question 5

Class 1a side effect

Answer 5

torsades de pointes

Question 6

Class 1b drugs

Answer 6

Lidocaine
Mexiletine
Increased potency in ischemic tissue

Question 7

Class 1b drug indications

Answer 7

ventricular tachycardia, ventricular fibrillation (not useful in atrial arrhythmias

Question 8

Class 1c drugs

Answer 8

Flecainide
Propafenone
Not for people with heart disease and ischemia

Question 9

Class 1c indications

Answer 9

A-fib in patients without CAD; and SVT’s

Question 10

Class 2 antiarrhthmics

Answer 10

beta-blockers (metoprolol, propranolol, esmolol)
Slows down Ca-channel during funny phase (T-type). decreased slope of phase 4 depolarization (funny channel) and prolonged depolarization at AV node

Question 11

Class 2 indications

Answer 11

Treat/prevent supraventricular and ventricular arrhythmias
A-fib/flutter - control ventricular rate
Supraventricular tachycardias
(slows HR to control symptoms; not convert them out of a-fib)
Ventricular arrythmia prevention (raise the threshold for v-fib in ischemic myocardium and reduce vent. arrhythmias and cardiac arrest after ACS and in patients with HF

Question 12

Class 2 adverse effects

Answer 12

fatigue, bronchospasm, hypotension, impotence, depression, aggravation of HF, masking of symptoms of hypoglycemia in diabetic patients

Question 13

Class 3 antiarrhythmics

Answer 13

Block K+ delayed rectifier current
Prolonged repolarization (Longer QT interval)
Keeps inside positive longer to give Na channels in refractory period

Question 14

Class 3 adverse effects

Answer 14

Tossed de pointes

Question 15

Class 3 drugs

Answer 15

Dronedarone, amioderone, sotalol, ibutilide, dofetilide

Question 16

Amioderone

Answer 16

Closest to ideal antiarrhythmics
K+ channel blocker (prolongs action potential duration)
Na+ channel blocker (blocks inactivated Na+ channels; relatively rapid rate of recovery)
L-type Ca+ channel blocker and non-selective beta blocker (slows sinus node and AV conduction)
Works best at a high heart rate
Rarely pro arrhythmic

Question 17

Amioderone

Answer 17

Highly lip-philic - large volume of distribution
Unusual pharmacokinetics (delayed onset, loading doses required (10 grams) and half life of around 2 months)
Hepatic metabolism by CYP3A4 and 2C8 to desethyl-amiodarone (active metabolite)
Inhibits CYP3A4, CYP2C9, and P-glycoprotein (drug interactions with digoxin, warfarin, and statins)

Question 18

Amioderone black box warning

Answer 18

Pulmonary toxicity (10-17%)
Liver injury (mild)
Worsening of cardiac dysrhythmias (2-5% heart block or sinus bradycardia)

Question 19

Amioderone contraindications

Answer 19

Known hypersensitivity to amioderone, including iodine
Cardiogenic shock
Marked sinus bradycardia
2nd or 3rd degree AV block unless pacemaker is available

Question 20

Class 4 antiarrhythmics

Answer 20

Non-dihydropyridine calcium channel blockers
Verapamil and diltazem
Block l-type calcium channels
Slow action potential rise and prolonged repolarization at AV node

Question 21

Class 4 indications

Answer 21

IV and PO
Supraventricular tachyarrhythmias (afib/flutter - reduce ventricular rate and SVTs)

Question 22

Class 4 adverse effects

Answer 22

hypotension, bradycardia, AV block, and negative inotropy

Question 23

Adenosine MOA

Answer 23

activates K+ current in the atrium and sinus and AV nodes
Causes hyper polarization and suppression of calcium action potentials
Causes a temporary AV block (goal)
Onset and duration is very fast so it is safe

Question 24

Adenosine indications

Answer 24

paroxysmal supraventricular tachy

Question 25

Adenosine adverse effects

Answer 25

flushing, dyspnea, bronchospasm, chest pressure/filling (all short lived because of short duration of action)

Question 26

Digoxin MOA

Answer 26

Enhances central and peripheral vagal tone
Hyperpolarization causes slower depolarization and HR is decreased
sensitization of baroreceptors and increases parasympathetic tone (decreases sinus node automaticity and prolongs AV node)
Inhibits Na/K pump (increases intracellular Ca+ and increases contractility and proarrhythmic potential)

Question 27

Digoxin indications

Answer 27

A-fib/flutter - control ventricular rate (only reduces resting HR, good in combination with BB/CCB, and HRrEF)
Narrow therapeutic window (0.5-2.0ng/ml (<1 in HF)

Question 28

Digoxin toxicity

Answer 28

GI upset, altered color perception (halo vision), malaise, bradycardia, AV block, v-tach/fib

Question 29

Anti-muscarinic MOA

Answer 29

Blocks acetylcholine receptors on muscarinics
Alters parasympathetic functions

Question 30

Anti-muscarinic effects

Answer 30

Increases HR, decreases smooth muscle motility, and decreases exocrine gland secretion.

Question 31

Antimuscarinic indications

Answer 31

Short term relief of hemodynamically significant bradycardia or AV block (useful in post intubation related bradycardia)

Question 32

Anti-muscarinic adverse effects

Answer 32

Dry mouth, blurred vision, photophobia, and tachycardia