pharmacology: antiarrhythmics

Question 1

what are the class 1 antiarrhythmic drugs?

Answer 1

Na+ channel blockers

Question 2

what are the class 1a antiarrhythmic drugs? mechanism?

Answer 2

quinidine, procainamide

mechanism: block fast Na+ channel in the open or activated - state “state dependent” blockade
- increases action potential duration and effective refractory period

Question 3

quinidine uses and side effects

Answer 3

use: atrial fibrillation but need initial digitalization to slow AV conduction
side effects: hyperkalemia and also displaces digoxin
- may have some reflex tachycardia due to alpha block vasodilation and increased HR and AV conduction due to muscarinic receptor blockade

Question 4

procainamide metabolized by

Answer 4

N-acetyltransferase to N-acetyl procainaide (can have slow and fast metabolizers

Question 5

procainamide side effects

Answer 5

SLE like syndrome in slow acetylators
hematotoxicity (thrombocytopenia and agranulocytosis)
CV effects (torsades)

Question 6

what are the class 1B drugs and mechanism?

Answer 6

lidocaine and mexiletine
mechanism: block INACTIVATED CHANNELS which DECREASES action potential duration (gives more time for filling which improves CO)

Question 7

what are the class 1B drugs good for?

Answer 7

slow conduction in hypoxic and ischemic tissues - preference for these tissues

Question 8

lidocaine and mexiletine side effects

Answer 8

CNS toxicity (seizures)
least cardiotoxic
first-pass metabolism (IV)
digoxin toxicity

Question 9

class 1C drugs and mechanism?

Answer 9

flecainide
blocks fast Na channels especially in His-Purkinje tissue
no effect on APD or ANS effects
(only used as last stitch effort)

Question 10

what are the class II antiarrhythmic drugs? mechanism?

Answer 10

beta blockers

mechanism: prevent beta receptor activation, decreasing SA and AV nodal activity
- decreases slope of phase 4 of AP in pacemakers

Question 11

which beta blocker is nonselective? selective?

Answer 11

nonselective: propranolol
cardioselective: acebutolol and esmolol

Question 12

beta blocker uses

Answer 12

prophylaxis post-MI and in supraventricular tachyarrhythmias (SVTs)
ESMOLOL FOR ACUTE SVTs

Question 13

what are the class III antiarrhythmic drugs? mechanism?

Answer 13

amiodarone and sotalol
K channel blockers which increase action potential duration and effective refractory period (esp in Purkinje and ventricular fibers)

Question 14

amiodarone uses

Answer 14

mimics class I, II, III, IV
increased APD and ERP in all cardiac tissues and are used in any arrhythmias
*has long long long half live - binds extensively to tissues

Question 15

amiodarone side effects

Answer 15

pulmonary fibrosis
blue pigmentation of skin
phototoxicity
corneal deposits
hepatic necrosis
thyroid dysfunction (iodination)

Question 16

sotalol mechanism and use

Answer 16

decreases K current, slowing phase III
also a non-selective beta blocker leading to decreased HR, AV conduction
used in life-threatening ventricular arrhythmia

Question 17

sotalol side effects

Answer 17

torsades

Question 18

what are the class IV antiarrhythmic drugs? mechanism?

Answer 18

verapamil and diltiazem

mechanism: block slow cardiac Ca channel, decreasing phase 0 and phase 4

Question 19

verapamil and diltiazem uses and side effects

Answer 19

uses: supraventricular tachycardias

side effects: constipation (verapamil), dizziness, flushing, hypotension, AV block

Question 20

adenosine

Answer 20

activates adensoine receptors causing Gi coupled decrease in cAMP (M2) - causes a decrease in SA and AV nodal activity

Question 21

adenosine uses

Answer 21

DOC for paroxysmal supraventricular tachycardias and AV nodal arrhythmias

Question 22

adenosine side effects

Answer 22

flushing, sedation, dyspnea
SHORT HALF LIFE!!!!
antagonized by methylxanthines (theophylline and caffeine)

Question 23

magnesium use

Answer 23

torsades (competes with Ca)

Question 24

what drugs cause torsades?

Answer 24

potassium channel blockers (class 1A and III)
antipsychotics (thioridazine)
TCA