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Cardiology > Anti-arrhythmic drugs > Flashcards

Anti-arrhythmic drugs Flashcards

1
Q

What are the class IA vaughn williams class drugs? What channels are affected?

A

Disopyramide, Quinidine, Procainamide

(Double quarter pounder); Sodium and potassium channels blocked

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2
Q

What are the class IB Vaughn williams class drugs? Channel affected?

A

Lidocaine and Mexiletine

(Lettuce and mayo); Sodium channel blocked

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3
Q

What are the Class IC VW class drugs? Channel affected?

A

Propafenone and Flecainide

(Pepsi and fries); Sodium channel blocked

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4
Q

What are the Class II VW class drugs? Channel affected?

A

Metoprolol, propranolol, atenolol, timolol, esmolol

(Beta blockers); B1 receptor blocked

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5
Q

What are the Class III VW class drugs? Channel affected?

A

Amiodarone, dronaredone, dofelitide, sotalol, Ibutilide

(A drooling dog is sleeping); Potassium channel blocked

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6
Q

What are the Class IV VW class drugs? Channel affected?

A

Verapamil, diltiazem; Calcium channel blocked

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7
Q

What channels are blocked by adenosine?

A

Potassium and calcium

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8
Q

Which VW drugs decrease automaticity?

A

All of them (including adenosine)

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9
Q

Which VW drugs increase action potential duration, thus increasing refractory period?

A

Class IA and Class III

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10
Q

What VW drugs increase REFRACTORY PERIOD WITHOUT INCREASING ACTION POTENTIAL DURATION?

A

Class IA, IB, IC and Adenosine

Class IA increases refractory pd with and without APD

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11
Q

Which VW drugs decrease conduction velocity?

A

Class IA, IC, II, IV, and Adenosine

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12
Q

How do Class I VW drugs work by decreasing automaticity?

A

They block sodium channels, INCREASING THRESHOLD POTENTIAL

Note: Class IA drugs also increase AP duration via potassium channel blockage

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13
Q

How do Class II VW drugs work by decreasing automaticity?

A

They are B-anatagonists, DECREASING PHASE 4 SLOPE

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14
Q

How do Class III VW drugs work by decreasing automaticity?

A

They block potassium channels, INCREASING AP DURATION

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15
Q

How do Class IV drugs work by decreasing automaticity?

A

They block calcium channels, SLOWING SA/AV NODE DEPOLARIZATION

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16
Q

How does adenosine decrease automaticity?

A

INCREASES MAXIMUM DIASTOLIC POTENTIAL; I.e. making interior of the cell more negative between APs. It does this by promoting Potassium efflux in SA and AV nodes

17
Q

Do class I drugs work on resting/closed, activated, or inactivated sodium channels?

A

Class IA: Activated/Open
Class IB: Inactivated/closed
Class IC: Activated/open

18
Q

Class IA drugs have what effects on depolarization and refractory period?

A

They have a moderate affinity for blocking sodium channels and block potassium channels. They therefore prolong repolarization, prolong phase 2 and 3, leading to PROLONGED REFRACTORY PERIOD

19
Q

Class IB drugs have what effects on depolarization and refractory period?

A

They have a weak affinity for sodium channels, and shorten repolarization. Shorten phase 2 and 3.

20
Q

Class IC drugs have what affect on depolarization and refractory period?

A

They have a strong affinity for blocking sodium channels, but do not affect action potential duration.

21
Q

What are some toxicities of Class IA VW drugs?

A

For a drug like procainamide, they prolong Action potential, leading to prolonged QT interval, which can lead to Torsade de pointes

22
Q

What are some toxicities of Class IC VW drugs?

A

For flecainide and propafenone, they should not be used in patients with structural abnormalities

23
Q

What are some toxicities with Class III VW drugs?

A

Prolonged AP, which can lead to Prolonged QT, which can lead to Torsade depointes (Note: Amiodarone is not associated with TdP)

24
Q

Non-dihydropyridines act on which cells?; What are some examples?

A

Vascular smooth muscle AND Cardiac tissue; Verapamil, diltiazem

25
Q

Dihydropyridines act on which cells?; Examples?

A

Vascular smooth muscle; Amlodipine, nifedipine

26
Q

What are some PK issues with adenosine?

A

Short half-life: Less than 30 seconds. Administered by RAPID IV Bolus

27
Q

How do Antiarrhythmic drugs increase refractory period of cardiac myocytes?

A
  1. Increase length of action potential (Class IA and Class III)
  2. They slow the recovery of sodium channels during repolarization (Class IA/B/C, adenosine- Do not lengthen APD)
28
Q

How do class IA/B/C drugs increase refractory period?

A

They do not change length of APD, but slow the reset of Sodium channels. So it takes longer for enough resting channels to be available to imitate new AP

29
Q

How does adenosine increase refractory period?

A

It does not affect APD, but slows calcium influx

30
Q

What are some AV blocking drugs (Nodal agents)

A
  • Class II drug: Slows sodium influx (reduces phase 4 slope)
  • Class IV: Slows calcium influx
  • adenosine (increases maximum diastolic potential)

All slow conduction through AV node

31
Q

What are the PR interval, QRS, and QT effects of Class IA drugs?

A
  • No effect on PR interval
  • Increases QRS complex
  • - INCREASES QT INTERVAL*
32
Q

What are the PR interval, QRS, and QT effects of Class IB drugs?

A
  • No effect on PR interval, QRS, and no effect/decreased QT interval
33
Q

What are the PR interval, QRS, and QT effects of Class IC drugs?

A
  • Increases PR interval
  • Increases QRS Complex
  • No effect or increased QT Interval
34
Q

What are the PR interval, QRS, and QT effects of Class II drugs?

A
  • No effect or increased PR interval
  • No effect on QRS complex
  • No effect on QT interval
35
Q

What are the PR interval, QRS, and QT effects of Class III drugs?

A
  • No effect or increased PR interval
  • No effect or increased QRS complex
  • -INCREASED QT INTERVAL*
36
Q

What are the PR interval, QRS, and QT effects of Class IV drugs?

A
  • Increased PR interval
  • No effect on QRS complex
  • No effect on QT interval

Cardiology (18 decks)

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