Antiarrhythmic Drugs

Question 1

What two conditions must be met for AAD treatment of Reentry pathways?

Answer 1

Unidirectional block and an area of slowed conduction

Question 2

What AAD class’s mostly contribute to prolonged QT?

Answer 2

IA, IC, III

Question 3

Where is the QT interval best measured on a 12-lead ECG?

Answer 3

II, V5 or V6

Question 4

QTc Framingham:

Answer 4

QTc = QT + 0.154(1-RR)

Question 5

7 causes of prolonged qt:

Answer 5

1. Electrolyte abnormalities (⬇️k, mg, ca)
2. Hypothermia
3. Myocardial ischemia
4. Post-cardiac arrest
5. High intracranial pressure
6. Congenital Long Qt syndrome
7. Drugs

Question 6

3 causes of shortened qtc (<350 ms)

Answer 6

1. Hypercalcemia
2. Digoxin
3. Congenital short qt syndrome

Question 7

Mechanism of class IA AADs:

Answer 7

Moderate Na blockade, prolonged AP duration

Question 8

Mechanism of class IB AADs:

Answer 8

Mild Na blockade, shortened AP duration

Question 9

Mechanism of class IC AADs:

Answer 9

Strong Na blockade, no AP effect

Question 10

What AP phase do class I AADs primarily effect?

Answer 10

Phase 0 depolarization

Question 11

Class IA drugs (3):

Answer 11

Procainamide
Disopyramide
Quinidine

Question 12

Class IB drugs (2):

Answer 12

Lidocaine

Mexiletine

Question 13

Class IC drugs (2):

Answer 13

Flecainide

Propafenone

Question 14

Which class IA drug has the side effects of + ANA (80%) and drug induced lupus (30%)?

Answer 14

Procainamide

Question 15

What is the main metabolite of Procainamide and how is it formed?

Answer 15

NAPA - acetylation in liver

Question 16

Which class IA drug should be avoided in a-fib patients?

Answer 16

Quinidine

Question 17

What is the mechanism of class IB AADs?

Answer 17

Shorten phase 3 depolarization and lower AP duration

Question 18

What is the primary usage of IB AADs?

Answer 18

Ventricular tachycardia

Question 19

What are the primary uses of IB AADs?

Answer 19

Paroxysmal SVT, A-fib, vent. Tachycardia

Question 20

Class IC contraindications (2):

Answer 20

Ischemic heart disease (CAD, MI)

CHF

Question 21

How are class IB AADs metabolized?

Answer 21

Liver - 1st pass

Question 22

What is a contraindication to propafenone?

Answer 22

Asthma bc it is a weak B blocker

Question 23

What is the mechanism of class II AADs?

Answer 23

B-Blockers: inhibition of cardiac sympathetic pathway.

Lowered phase 4 slope

Prolonged repolarization of AV node

Question 24

Use of class II AADs

Answer 24

Supra ventricular arrhythmias

Vent. Arrhythmias, long QT syndrome

Post MI, low O2 demand

Question 25

B1-selective class II AADs: (5)

Answer 25

``` Acebutolol Atenolol Bisprolol Esmolol Metoprolol ```

Question 26

Which b1 selective class II aad is IV only?

Answer 26

Esmolol

Question 27

Which b1 selective class II AAD is membrane stabilizing for isi?

Answer 27

Acebutolol

Question 28

Non-b1-selective class II AADs:

Answer 28

Nadolol | Propanolol

Question 29

Non-B selective and a-receptor blocking class II AADs:

Answer 29

Carvedilol | Labetalol

Question 30

What is carvedilol used for?

Answer 30

HF management

Question 31

What is Labetalol used for?

Answer 31

Acute hypertensive crisis

Question 32

Contraindication to class II AADs: (3)

Answer 32

1. High degree AV block (2nd degree type 2, 3rd degree) 2. Bradycardia, hypotension 3. Asthma, wheezing

Question 33

Adverse effects of type II AADs:

Answer 33

Cold hands/feet Fatigue GI upset Low HR, bradycardia

Question 34

What is the mechanism of class III AADs?

Answer 34

Outwards K+ channel blockers in phase 3 repolarization (no phase 0).

Question 35

What are the uses (2) of class III AADs?

Answer 35

A-fib/flutter, vent arrhythmias

Question 36

6 class III AADs:

Answer 36

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