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Pharmacology > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

Class IA drugs?

A

Quinidine, disopyramide, procainamide

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2
Q

Class IB drugs?

A

Lidocaine, mexiletine, tocainimide

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3
Q

Class IC drugs?

A

Flecainide, propafenone

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4
Q

Class II drugs?

A

Metoprolol, propranolol, esmolol, atenolol, timolol

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5
Q

Class III drugs?

A

Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)

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6
Q

Class IV drugs?

A

Verapamil > diltiazem

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7
Q

Which drugs are state dependent (selectively depress tissue that is frequently depolarized such as tachycardia?

A

Class I drugs

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8
Q

What do all class I drugs have in common?

A

Decrease slope of phase 0, decreasing conduction of AP and thus rate of contraction

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9
Q

MOA of class IA?

A

Increase AP duration, delays phase 3 repolarization (increases ERP and prolonged QTi)

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10
Q

MOA of class IB?

A

Preferentially affects ischemic or depolarized tissue, phase 3 (ERP) is shortened as well as the entire AP

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11
Q

MOA of class IC?

A

NO effect on AP

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12
Q

AEs of HA, tinnitus, vertigo and psychosis?

A

Quinidine - cinchonism

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13
Q

Drug induced lupus?

A

Procainamide

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14
Q

Best for post-MI?

A

Class IB drugs

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15
Q

Contraindicated post-MI as it may cause arryhthmias?

A

Class IC drugs

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16
Q

May exacerbate heart failure?

A

Class IC drugs (watch out in pts with low ejection fraction)

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17
Q

MOA of class II drugs?

A

Decreases SA and AV node activity by decreasing cAMP, decreasing Ca current, decreasing contractility and HR. Suppress abnormal pacemakers by decreasing slope of phase 4. Increases PR interval by affecting AV node particularly.

18
Q

1st line for persistent a-fib in presence of structural heart damage?

A

B-blockers

19
Q

AEs of B-blockers?

A

Impotence, exacerbation of asthma, bradycardia, AV block, CHF, sedation/sleep alterations, may mask signs of hypoglycemia

20
Q

Tx for B-blocker OD?

A

Glucagon

21
Q

MOA of class III drugs?

A

Block K efflux, increases AP duration and ERP (prolonged QTi)

22
Q

AEs of sotalol?

A

Torsades, excessive B-block

23
Q

AEs of ibutilide?

A

Torsades

24
Q

AEs of amiodarone?

A

Pulmonary fibrosis, hepatotoxicity, thyroid toxicity, corneal deposits, blue/gray skin deposits resulting in photodermatitis, ataxia, CV effects

25
Q

Why can amiodarone block Na, K, and C and have alpha and B-blocking effects?

A

It alters the lipid membrane

26
Q

MOA of class IV drugs?

A

Block Ca channels in SA and AV nodes, slowing phase 4 depolarization, decreasing conduction velocity, prolonging PR interval and ERP

27
Q

MOA of adenosine?

A

Increase K efflux out of SA and AV nodal cells, hyperpolarizing the cell and decreasing HR

28
Q

Use for adenosine?

A

Dx/abolishing SVTs

29
Q

DOA for adenosine?

A

VERY short (15 secs)

30
Q

AEs of adenosine?

A

Flushing, hypotension, chest pain, dyspnea

31
Q

What blocks the effects of adenosine?

A

Theophylline and caffeine

32
Q

MOA of K?

A

Increases threshold for cardiac APs, decreasing excitation and thus HR

33
Q

Use for K?

A

Suppresses ectopic pacemakers, esp those assoc with digoxin toxicity

34
Q

Use for Mg?

A

Torsades, digoxin toxicity

35
Q

MOA of digoxin?

A

Inhibits Na/K ATPase, which inhibits the Na/Ca exchanger causing increased contractility; stimulates vagus nerve causing decreased HR

36
Q

Use for digoxin?

A

CHF, a-fib

37
Q

AEs of digoxin?

A

N/V/D, blurry yellow vision, ECG changes (increased PRi, decreased QTi, ST-scooping, T-wave inversion), cardiac arrythmias, hyperkalemia

38
Q

What exacerbates digoxin AEs?

A

1) Hypokalemia
2) Renal failure
3) Quinidine

39
Q

Digoxin toxicity tx?

A

Tx the hypokalemia, anti-dig Fab, lidocaine, Mg

40
Q

Worst AE of digoxin?

A

Ventricular tachyarrhythmias

Pharmacology (24 decks)

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