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Cardiovascular - Pharmacology > Antiarrythmics > Flashcards

Antiarrythmics Flashcards

1
Q

What are Class I antiarrhythmics?

A

sodium channel blockers

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2
Q

What are Class II antiarrhythmics?

A

beta blockers

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3
Q

What are Class III antiarrhythmics?

A

potassium channel blockers

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4
Q

What are Class IV antiarrhythmics?

A

calcium channel blockers

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5
Q

What are two other antiarrhythmics?

A

Adenosine and Magnesium.

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6
Q

What are the Class IA antiarrythmics?

A

Quinidine, Procainamide, Disopyramide

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7
Q

What is the mechanism of action of Class IA antiarrhythmics?

A

Slows conduction velocity in atria and his/purkinje fibers. Increases AP duration, increases effection refractory period. Increases QT interval.

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8
Q

What are the clinical uses for Class IA anti-arryhthmics?

A

Useful for atrial and ventricular arryhthmias, especially reentrant and ectopic SVT and VT; depresses automaticity of ectopic foci

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9
Q

What are the important toxicities of Class IA antiarrythmics? What is one important toxicity associated iwth each one.

A

Torsades (long QT), thrombocytopenia.
Quinidine: Cinchonism (headache, tinnitus)
Procainamide: Reversible SLE-like syndrome
Disopyramide: heart failure

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10
Q

What are the Class IB antiarrythmics?

A

Lidocaine, Mexilitine

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11
Q

What is the mechanism of action of Class IB antiarrythmics?

A

 Decreases AP duration; increases conduction velocity of AV node/his-purk. Preferentially affect ischemic or
depolarized Purkinje and ventricular tissue.
Phenytoin can also fall into the IB category.

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12
Q

What is the clinical uses of Class IB antiarrhythmics?

A

Acute ventricular arrhythmias (especially postMI), digitalis-induced arrhythmias. IB is Best
post-MI.

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13
Q

What are toxicities associated with Class IB antiarrhythmics?

A

CNS stimulation/depression, cardiovascular

depression.

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14
Q

What are the Class IC antiarrhythmics?

A

Flecainide, Propafenone.

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15
Q

What is the mechanism of action of Class IC antiarrythmics?

A

Significantly prolongs ERP in AV node and
accessory bypass tracts. No effect on ERP in
Purkinje and ventricular tissue.
Minimal effect on AP duration.

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16
Q

What is the clinical uses of Class IC antiarrhythmics?

A

SVTs, including atrial fibrillation. Only as a last

resort in refractory VT.

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17
Q

What are toxicities associated with Class IC antiarrhythmics?

A

Proarrhythmic, especially post-MI
(contraindicated). IC is Contraindicated in
structural and ischemic heart disease.

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18
Q

How do Class II antiarrhythmics work?

A

Beta blockers. Decreased beta receptor activation, decreased cAMP, decreased Ca2+ current. Thereby decrease SA and AV nodal activity.

19
Q

How do Class II antiarrhythmics affect the slope of phase 4 in pacemaker cells?

A

Decrease the slope; it takes longer to reach threshold. Suppress abnormal pacemakers.

20
Q

Why does the PR interval increase with Class II antiarrhythmics?

A

The AV node is particularly sensitive.

21
Q

Which Class 2 antiarryh is shortest acting?

A

esmolol

22
Q

What are the clinical uses for class II antiarrhythmics?

A

SVT, ventricular rate control for atrial fibrillation and atrial flutter.

23
Q

What is the toxicity associated with Class 2s?

A 
Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), 
CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.
24
Q

Which beta blocker can cause dyslipidemia?

A

Metoprolol

25
Q

Which beta blocker can exacerbate vasospasm in Prinzmetal’s angina?

A

propanolol

26
Q

Which happens if you give beta blockers alone for pheo or cocaine toxicity?

A

There will be unopposed alpha agonism, will result in hypertension (soemtimes emergency)

27
Q

How to treat beta blocker overdose?

A

Saline, atropine, glucagon

28
Q

Which drugs are class III antiarrhythmics?

A

Amiodarone, Ibutilide, Dofetilide, Sotalol.

29
Q

What is the mechanism of Class III antiarrhythmics?

A

 Increase AP duration,  ERP,  and QT interval; prolongs phase 3.

30
Q

What are the clinical uses for Class III antiarrhythmics?

A

Atrial fibrillation, atrial flutter; ventricular

tachycardia (amiodarone, sotalol).

31
Q

What are the toxicities associated with sotalol?

A

Sotalol—torsades de pointes, excessive β

blockade.

32
Q

What are the toxicities associated with ibutilide?

A

torsades

33
Q

What are the toxicities associated with amiodarone?

A

Amiodarone—pulmonary fibrosis,
hepatotoxicity, hypothyroidism/
hyperthyroidism (amiodarone is 40% iodine by
weight), acts as hapten (corneal deposits, blue/
gray skin deposits resulting in photodermatitis),
neurologic effects, constipation, cardiovascular
effects (bradycardia, heart block, HF).

34
Q

What are the tests you must order before starting amiodarone?

A

PFTs, LFTs, TFTs

35
Q

Is amiodarone lipophilic?

A

yes

36
Q

What are the Class IV antiarrhthymics?

A

Verapamil, diltiazem

37
Q

What is the mechanism of Class IV antiarrhthymics?

A

decreases conduction velocity,  prolongs ERP,  prolongs PR interval.

38
Q

What is the clinical use of Class IV antiarrhthymics?

A

Prevention of nodal arrhythmias (e.g., SVT), rate control in atrial fibrillation.

39
Q

What is the toxicity associated with Class IV antiarrhthymics?

A

Constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression).

40
Q

How does adenosine work?

A

 K+ out of cells Žhyperpolarizing the cell and decreasing I
Ca. Drug of choice in diagnosing/abolishing
supraventricular tachycardia. Very short acting (~ 15 sec).

41
Q

What drugs blunt the effects of adenosine?

A

Effects blunted by theophylline and

caffeine (both are adenosine receptor antagonists).

42
Q

What are the adverse effects of adenosine?

A

Adverse effects include flushing, hypotension,

chest pain, sense of impending doom, bronchospasm.

43
Q

When is Mg2+ used as an antiarrhythmic?

A

With torsades de pointes and digoxin toxicity.

Cardiovascular - Pharmacology (3 decks)

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