Anti-arrythmia drugs Flashcards

1
Q

How long is a normal P wave?

A

0.08 - 0.1s

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2
Q

How long is the PR interval?

A

0.12 o 0.2s

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3
Q

How long is a normal QRS complex?

A

0.06 to 0.1s

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4
Q

How long is a normal QT interval?

A

0.2 to 0.4s

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5
Q

What is the mechanism of action of Class 1 Anti-arrythmics?

A

Sodium Channel Blockers

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6
Q

Give examples of Class 1A, 1B and 1C anti-arrythmics.

A

1A - Procainamide
1B - lidocaine
1C - Flecainide

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7
Q

How does procainamide work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Class 1A Anti arrythmic, Sodium Channel Blocker, reduces rate of phase 0 - increases ERP and APD; Reduces both conductivity and automaticity

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8
Q

How does lidocaine work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Class 1B anti-arrythmic, sodium channel blocker, reduces rate of phase 0 rise & shortens phase 3 repolarisation; Reduces APD, no effect in ERP; reduces automaticity, no effect on conductivity

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9
Q

How does flecainide work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Class 1C anti-arrythmic, sodium channel blocker, reduces rate of phase 0 rise & shortens phase 3 repolarisation; no effect in ERP & APD; reduces automaticity & conductivity

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10
Q

When to use Class 1 anti-arrythmics?

A

Refractory VTs that tend to progress to VF

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11
Q

What are two examples of class 2 anti-arrythmics?

A

Beta Blockers. Metoprolol, Propanolol

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12
Q

How do class 2 anti-arrythmics work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Reduces phase 4 depolarisation via indirect effect on calcium channels (less calcium, not hitting the depolarisation threshold so fast) & AV conduction prolonged; no change to APD and ERP; reduces automaticity

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13
Q

What are clinical uses of class 2 anti-arrythmics?

A
  1. Tachycardia caused by sympathetic activation
  2. AF
  3. AV nodal reentry tachycardia
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14
Q

How do class 3 anti-arrythmics work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Potassium channel blocker. Prolongs phase 3 repolarisation. Increases ERP and APD

also blocks sodium channels, adrenergic receptors and calcium channels

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15
Q

What is an example of a class 3 antiarrythmic?

A

Amiodarone

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16
Q

What is the bioavailability, elimination t1/2, and metabolism method for amiodarone?

A

35-65%, 3-10days for first 50% & several weeks for next 50%; hepatic metabolism into desethylamiodarone

17
Q

How long do effects of amiodarone last?

A

1-3m

18
Q

What is amiodarone used for?

A

AF

Reentry Ventricular tachycardia

19
Q

Adverse effects of amiodarone?

A

Bradycardia and heart block

20
Q

How do class 4 anti-arrythmics work? What is its effect on effective refractory period & duration of action potential? Effect on conductivity and automaticity?

A

Calcium Channel Blocker. Prolongs phase 4 depolarisation & reduces AV node conductivity; increase ERP and APD

21
Q

Examples of anti arrythmic Class 4 drugs?

A

Verapamil, Diltiazem

22
Q

What are the uses of class 4 antiarrythmics?

A

HTN, Angina, Supraventicular Tachycardia

23
Q

What are adverse effects of class 4 antiarrythmics?

A

Patients with pre-existing depressed cardiac function contraindicated

Hypotension
HR
MI

24
Q

What is the mechanism of action of adenosine?

A

Suppression of AV node conduction and increase AV node refractory period
- stimulates K+ channel
- inhibits calcium current

25
Q

What is the T1/2 of adenosine?

A

Less than 10s

26
Q

What is the clinical use of adenosine?

A

Supraventricular Tachycardia