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Pharm 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What 4 ways can you change the rate of pacemaker cells?

A

1) maximum diastolic potential
2) slope of phase 4 depolarization
3) threshold potential
4) duration of action potential

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2
Q

What are the two goals of antiarrhythmics?

A

1) Reduce ectopic pacemaker activity

2) Modify conduction or refractoriness to disable reentry

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3
Q

What are the 4 mechanisms to treat arrhythmias?

A

1) Sodium channel blockade
2) Blockade of sympathetic effects
3) Prolongation of the effective refractory period
4) Calcium channel blockade (slows repolarization)

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4
Q

What is the major mechanism of disturbance of impulse conduction?

A

reentry mechanism

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5
Q

What are class 1 antiarrhythmics?

A

Sodium channel blockers

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6
Q

What are the mechanisms of class 1a drugs? What drugs are they?

A

blocks open or activated Na+ channels to lengthen the duration of the action potential (increase ERP); quinidine, procainamide

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7
Q

What is the MOA of class 1c drugs? What drugs are they?

A

binds to all sodium channels, no effect on the duration of action potential (no change in ERP); flecainide

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8
Q

What is the MOA of class 1b drugs? What drugs are they?

A

blocks inactivated sodium channels to shorten the duration of the AP (decrease ERP); lidocaine

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9
Q

What drugs are in class II? What is their main property?

A

Beta blockers, reduce adrenergic activity on the heart

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10
Q

What drugs are in class III? What is their main property?

A

K+ channel blockers to increase ERP; amiodorone and sotalol

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11
Q

What drugs are in class IV? What is their main property?

A

CCBs to decrease HR and contractility; verapamil and diltiazem

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12
Q

What are the drugs in the misc category of antiarrhythmics? What is their route of administration?

A

adenosine, magnesium, potassium, digoxin; all IV only

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13
Q

What drug is used for acute and chronic treatment of SVT and ventricular arrhythmias?

A

Quinidine (cardioquin)

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14
Q

What 3 actions does quinidine have?

A

decreases automaticity, decreases membrane response, increases diastolic threshold (the threshold needed to reach relaxation phase)

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15
Q

What does the muscarinic receptor blockade of quinidine cause?

A

increased HR and AV node conduction

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16
Q

What are some adverse effects of quinidine?

A

Low therapeutic index, cardiac toxicity, SA/AV block, ventricular arrhythmia and severe hypotension at toxic doses
WIDENING OF QRS AND QT INTERVAL, causes QUINIDINE SYNCOPE, TORSADE DE POINTES
DIARRHEA
CINCHONISM

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17
Q

What other drug, when give with quinidine, increases chance for quinidine syncope?

A

digitalis

18
Q

What is a benefit to procainamide over quinidine use?

A

Less prominent antimuscarinic effects, potential to cause LUPUS, other adverse effects similar to quinidine

19
Q

What is the MOA for lidocaine?

A

rapidly blocks inactivated Na+ channels, shortens APD

20
Q

What is the DOC for ventricular arrhythmias? How is it administered?

A

lidocaine; IV

21
Q

What are two common adverse effects of lidocaine?

A

High contractility, CONVULSIONS

22
Q

What is the last ditch effort drug binds to all sodium channels?

A

Flecainide

23
Q

What is the non-specific BBlocker for arrhythmias?

A

Propranolol

24
Q

What is the B1-blocker with a normal half-life for arrhythmias?

A

acebutolol

25
Q

What is the B1-blocker with a short half-life? What is it used for?

A

Esmolol; Chronic treatment of PVST

26
Q

What is the MOA of amiodarone?

A

Blocks K+ channels (hence class III), binds to inactivated Na+ channels, and binds to some calcium channels, thereby INCREASING APD SIGNIFICANTLY!

27
Q

What is the overall effect of amiodarone?

A

Slows sinus rate, conduction, and prolongs QT and QRS (like a beta blocker). It has a much longer APD and MUCH LONGER ERP, which makes it the jack of all antiarrhymics.

28
Q

What drug has a half-life of 13-103 days and an extra long loading period?

A

Amiodarone

29
Q

What fact about amiodorone makes it the DOC for ventricular arrhythmias for ACLS? What else is it effective against?

A

It does not cause torsade de points; supraventricular and ventricular arrhythmias; oral

30
Q

What are two major side effects of amiodarone, one of which is cause for removal?

A

Pulmonary fibrosis in 5-15%, thyroid dysfunction

31
Q

Which drug is a non-selective BB that is a class III antiarrhymic? What is it used for? What is one potential adverse side effect?

A

Sotalol; same indications as amiodarone; Torsade de pointes

32
Q

What drug blocks slow L-type cardiac Ca2+ channels, has indication for atrial and supraventricular tachycardias due to marked effect on the SA and AV nodes? What drugs should you not combine it with?

A

Verapamil (cardio specific); beta blockers

33
Q

What drug inhibits calcium influx in both myocardial and vascular smooth muscle cells, causing vasodilation?

A

Diltiazem

34
Q

What are some indications for diltiazem use?

A

to decrease heart rate, PSVT and to control ventricular rate in a fib

35
Q

What is the order of drug usage for PSVT?

A

Acute: Adenosine (IV) then Esmolol then Diltiazem (IV)

36
Q

Which drug enhances K+ conductance and inhibits cAMP-induced calcium influx?

A

Adenosine (hyperpolarizes everything and “resets” the heart, so it literally stops the heart for a matter of seconds)

37
Q

What is adenosine used to treat?

A

PSVT and WPW, has a very short half life

38
Q

What is the DOC for torsade de pointes?

A

Magnesium

39
Q

What is useful for the management of seizures and/or hypertension in eclampsia?

A

Magnesium

40
Q

What is useful for treating digitalis induced arrhymias?

A

Magnesium

41
Q

What is the MOA of potassium?

A

increased serum K+ can both depolarize and hyperpolarize the membrane, but it has the tendency to hyperpolarize so it decreases the APD, conduction, pacemaker rate, and pacemaker arrhythmogenesis

Pharm 2 (11 decks)

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