Antiarrhythmic drugs

Question 1

Drug classes for arrythmia

Answer 1

1 - Na channel blocker
2 - B blocker
3 - K channel blocker
4 - Ca channel blocker

Question 2

Name class 1 antiarrhythmic drugs

Answer 2

1A: procainamide
1B: lidocaine
1C: flecainide

Question 3

procainamide MOA

Answer 3

Na channel blocker, slows phase 0 depolarisation.

• reduces automaticity, reduce conductivity
• increase APD, increase ERP

Question 4

lidocaine MOA

Answer 4

Na channel blocker, shortens phase 3 repolarisation and APD

• reduce automaticity, no change in conductivity
• decrease APD, no change in ERP

Question 5

flecainide MOA

Answer 5

Na channel blocker, slows phase 0 depolarisation (markedly), some shortening of phase 3 repolarisation

• reduce automaticity, reduce conductivity
• no change in APD, no change in ERP

Question 6

flecainide clinical uses

Answer 6

refractory ventricular tachycardias (these tend to progress to VF)

Question 7

flecainide adverse effects

Answer 7

potentially lead to sudden death if there is IHD

only use when other drugs dont work

Question 8

Which Na channel blocker reduces APD

Answer 8

lidocaine

Question 9

what is effect of Na channel blocker on ERP

Answer 9

no change, except procainamide which increases ERP

Question 10

Which antiarrhythmic drugs ahve no effect on ERP?

Answer 10

1B (lidocaine), 1C (flecainide), 2 (B blockers)

Question 11

B blocker MOA

Answer 11

1. indirectly block Ca channels –> take longer to reach threshold potential due to reduced Ca influx –> reduce and prolong phase 4 depolarisation –> reduce automaticity
2. prolong AV conduction –> reduce HR
3. reduce contractility
   - no change in APD, no change in ERP

Question 12

B blocker clinical uses

Answer 12

1. tachycardia caused by sympathetic activation
2. AF
3. AV nodal re-entry tachycardia
4. post MI to reduce sudden arrhythmic death

Question 13

Name 1 K channel blocker

Answer 13

amiodarone

Question 14

amiodarone MOA

Answer 14

prolong phase 3 repolarisation (no phase 0 effect):

• main effect: blockade of Ik (phase 3)
• also blocks Na and Ca channels, B adrenoceptors
• increase APD, increase ERP

Question 15

amiodarone PK

Answer 15

1. low bioavailability 35-65%
2. hepatic metabolism to desethylamiodarone (bioactive)
3. elimination half life 3-10 days, takes several weeks to completely eliminate
4. effects maintained for 1-3 months after discontinuation

Question 16

amiodarone clinical uses

Answer 16

1. AF to maintain normal sinus rhythm

2. prevention of re-entry ventricular tachycardia

Question 17

amiodarone adverse effects

Answer 17

1. symptomatic bradycardia

2. heart block

Question 18

name 2 non DHP Ca channel blockers

Answer 18

verapamil, diltiazem

Question 19

verapamil, diltiazem MOA

Answer 19

1. block Ca channels –> take longer to reach threshold optential due to reduced Ca influx –> reduce and prolong phase 4 depolarisation –> reduce automaticity
2. prolong AV conduction –> reduce HR

• increase APD, increase ERP

Question 20

verapamil, diltiazem clinical uses

Answer 20

1. supraventricular tachycardia

2. re-entry tachycardia

Question 21

adenosine MOA

Answer 21

1. stimulate cardiac K channel (Kach)
2. inhibiting Ca current
   => suppress AV nodal conduction + increase AV nodal refractory period

Question 22

adenosine PK

Answer 22

half life in blood less than 10s, infusion

Question 23

adenosine clinical use

Answer 23

emergency situation of supraventricular tachycardia

Question 24

adenosine adverse effects

Answer 24

1. flushing
2. shortness of breath or chest burning
3. induction of AV block or AF
4. headache, hypotension, etc.