Pharmacology: anti dysrhythmias

Question 1

Do risks of dysrhythmias need to be weighed with benefits of giving them?
Can some dysrhythmias be benign?
Can some anti dysrhythmias reduce efficacy of drugs patient may be taking to treat heart condition?
Can some anti dysrhythmics be pro dysrhythmic - especially in combination?

Answer 1

Yes
Yes
Yes
Yes
YEs

Question 2

General principles of treating bradydysrhythmias?

Answer 2

Stop using bradycardic medicines
Only use anti dysrhythmic drugs acutely - eg. atropine and adrenaline. If bradycardia is persistent, use a pacemaker - not drugs.

Question 3

When treating tachydysrhythmias, do you target rate or rhythm first?

Answer 3

Rate

Question 4

What are the aims in treating AF?

Answer 4

Control ventricular rate. Then, control sinus rhythm
Prevent tachycardia induced heart failure
Prevent thromboembolism (with anti coagulants)

Question 5

What are the 4 Singh Vaughan Williams classifications of anti dysrhythmic drugs?
How to remember?

Answer 5

Na bitch, oK cool.
Class I: sodium channel blockers
Class II: beta blockers
Class III: potassium channel blockers
Class IV: calcium channel blockers

Question 6

What phases of the cardiac action potential do the following impact:
Class I: sodium channel blockers
Class II: beta blockers
Class III: potassium channel blockers
Class IV: calcium channel blockers

Answer 6

Class I: phase 0
Class II: phase 2 and 4
Class III: phase 3
Class IV: phase 2

Question 7

What are the 3 subtypes of Class I drugs (sodium channel blockers?)

Answer 7

1a: intermediate dissociation
1b: fast dissociation
1c: slow dissociation

Question 8

Class 1a: intermediate dissociation
- What indication?
- Is it commonly used?
- ADRs?
- Example?

Answer 8

• Narrow indication: life threatening ventricular arrhythmias which have been refractory to other treatments
• Not common
• Significant anticholinergic activity - hence ADRs of blurred vision, dry mouth, constipation, urinary retention
• Eg. disopyramide

Question 9

Class 1b: fast dissociation
- Indication?
- Formulation?
- Example?

Answer 9

• Indication: serious ventricular arrhythmias, particularly after MI
• Formulation: injectable
• Eg. lidocaine (lignocaine)

Question 10

Class 1c: slow dissociation
- MOA?
- Is it short or long acting?
- ADRs?
- Example?

Answer 10

• Reduces frequency of ventricular ectopic beats, slows cardiac conduction by increasing refracctory period
• Long acting
• ADRs: pro dysrhythmic –> new/worsed dysrhythmias possible –> limits its use
• Eg. flecainide

Question 11

Class II: beta blockers
- MOA?

Answer 11

Reduces pro dysrhythmic effects of (NA) and sympathetic tone
–> (N)A acts on B1 adrenoceptors to increase rate of depolarisation during phase 4 - can cause normally quiescent parts of the heart to take on a spontaneous rhythm

Recrease SA node automaticity

Question 12

Class II: beta blockers
- Indications?
- Example

Answer 12

AF/flutter post AMI
Atenolol

Question 13

Class: potassium channel blockers
MOA?
Examples:

Answer 13

By blocking outwards potassium current, increases QT interval –> prolong refractory period
Amiodarone, sotalol

Question 14

Amiodarone
- Describe distribution, half life, accumulation?
- ADRs?

Answer 14

Very tissue bound, long elimination half life, accumulation with repeat dosing (avoid with loading dose + maintenance doses)

Deposits in thyroid (toxicity), lung (pulmonary fibrosis), liver (hepatotoxicity), skin, eye deposits
Prodysrhythmic

Question 15

Sotalol
Is it non selective?

Answer 15

Yes

Question 16

Class IV: calcium channel blockers
- MOA?
- Examples?

Answer 16

Blocks calcium channels in heart –> suppresses normal and abnormal activity

Verapamil and ilpiazim

Question 17

Particular indications for verapamil?

Answer 17

used for AF and to prevent paroxysmal supraventricular tachycardia

Question 18

2 additional drugs?

Answer 18

Adenosine
Digoxin

Question 19

Digoxin:
- MOA?
ADRs?

Answer 19

Blocks AV conduction –> slows ventricular rate in AF
AV block with toxic levels, ectopic beats

Question 20

Adenosine:
- MOA?
- Formulation

Answer 20

MOA
○ Converts supraventricular tachycardia to sinus rhythm when administered by IV
○ Binds to A1 adenosine receptors –> act on the AV node, stimulating a pathway similar to M2 muscarinic receptors (because the same cardiac potassium channel is also activated by Ach). Leads to hyperpolation of conduction tissue –> converts supraventricular tachycardia to sinus rhythm when administered by IV
§ These recepts are absent in ventricles, meaning the drug has more of an atrial action.

Formulation: IV