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Cardiovascular Exam II > Drugs for Cardiac Arrhythmia > Flashcards

Drugs for Cardiac Arrhythmia Flashcards

1
Q

Types of Anti-arrhythmic drugs

A

Class 1 = Na+ channel blockers

Class 2 = Beta blockers

Class 3 = K+ channell blockers

Class 4 = Cardioactive Ca++ channel blockers

Miscellaneous = Adenosine

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2
Q

Class 1 antiarrhythmics are Na+ channel blocking drugs. What drugs are included in this class?

A

Class 1A = quinidine, procainamide, disopyramide

Class 1B = lidocaine, mexiletine

Class 1C = flecainide, propafenone

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3
Q

Class 2 anti-arrhythmics are beta blockers. What drugs are included in this class?

A

Esmolol

Propranalol

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4
Q

Class 3 antiarrhythmics are K+ channel blockers. What drugs are included in this class?

A

Amiodarone
Sotalol
Dofetilide
Ibutilide

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5
Q

Class 4 antiarrhythmics are the cardioactive calcium channel blockers. What drugs are included in this class?

A

Verapamil

Diltiazam

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6
Q

Ions responsible for phases of fast APs in cardiac muscle (ventricles, atria, purkinje fibers)

A

Phase 0: Na+ in (via voltage-dependent fast Na channels)

Phase 1: K+ out

Phase 2: plateau d/t K+ out = Ca++ in

Phase 3: K+ out (Ca channels close)

Phase 4: resting potential restored by Na/K pump

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7
Q

Ions responsible for phases of slow APs in cardiac pacemaker(s) — SA and AV node

A

Phase 4: slow spontaneous depol d/t slow Na leak in (some slow Ca influx via T-type channels)

Phase 0: Ca influx through L-type Ca channels

Phase 3: repolarization via K+ efflux

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8
Q

Factors that determine firing rate or automaticity of pacemaker AP

A

Rate of spontaneous depol in phase 4 (i.e., slope) — decreased slope = decreased rate; need more time to reach threshold

Threshold potential — potential at which AP is triggered

Resting potential — if potential is less negative, firing rate increases

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9
Q

In terms of class 1 antiarrhythmics (sodium channel blockers), most therapeutically useful drugs block ______ or ______ Na channels, with very little affinity towards channels in a _____state

A

Activated; inactivated; resting

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10
Q

MOA of Class 1A drugs

A

Block sodium channels, slow impulse conduction, reduce automatism of latent (ectopic) pacemakers

State-dependent block —preferentially bind to open (activated) sodium channels); ectopic pacemaker cells with faster rhythms will be preferentially targeted!

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11
Q

The kinetics of dissociation determine how quickly drugs dissociate from the channel and thus the duration of the block. Class 1A drugs dissociate from Na channel with ____ kinetics; they also block _____ channels

A

Intermediate; K+

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12
Q

Effect of class 1A drugs on ECG

A

Prolong AP duration —> prolonged QRS and QT intervals

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13
Q

Which of the class 1A drugs directly depresses the activities of the SA and AV nodes, possesses antimuscarinic activity and ganglion-blocking properties, and is used to tx sustained ventricular tachycardias, and may be used in arrhythmias associated with MI?

A

Procainamide

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14
Q

The active metabolite of procainamide has class ____ activity, _____ half life, and accumulates in ____ dysfunction. Measurements of both parent drug and metabolite are necessary in pharmacokinetic studies

A

3; longer; renal

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15
Q

Since procainamide has ganglion-blocking properties, it reduces peripheral vascular resistance and may cause _____

A

Hypotension

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16
Q

Adverse effects of Procainamide

A

Cardiac = QT prolongation, induction of torsade de pointes arrythmias and syncope, excess inhibition of conduction

Extracardiac = lupus erythematosus syndrome with arthritis, pleuritis, pulmonary dz, hepatitis, and fever; also nausea, diarrhea, agranulocytosis

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17
Q

Class 1A antiarrhythmic that is natural alkaloid from cinchona bark, used occasionally for restoring rhythm in atrial flutter/fibrillation in pts with otherwise normal hearts; may also be used for sustained ventricular arrhythmia

A

Quinidine

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18
Q

In clinical trials, pts on quinidine were 2x as likely to have normal sinus rhythm, but the risk of ____ was 2-3 fold

A

Death

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19
Q

Quinidine has _____ effects (may enhance AV conductance) and exhibits ______ activity (effect on PR interval is variable)

A

Antimuscarinic; beta-blocking

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20
Q

AEs of quinidine

A

Cardiac: QT prolongation, induction of torsade de pointes arrhythmia and syncope, excess slowing of conduction through heart

Extracardiac: GI (diarrhea, N/V), HA, dizziness, tinnitisu (cinchonism), thrombocytopenia, hepatitis, fever

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21
Q

Class 1A antiarrhythmic used for tx of recurrent ventricular arrhythmias and affords potent antimuscarinic effect on the heart

A

Disopyramide

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22
Q

AEs of disopyramide

A

Cardiac: QT prolongation, induction of torsade de pointes and syncope, negative inotropic effect — may precipitate heart failure, excessive depression of cardiac conduction

Extracardiac: atropine-like symptoms —urinary retention, dry mouth, blurry vision, constipation, exacerbation of glaucoma

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23
Q

MOA of class 1B antiarrhythmics

A

Block Na channels

State-dependent block — bind to inactivated sodium channels (preferentially bind to depolarized cells)

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24
Q

Class 1B drugs dissociate from Na channel with ____ kinetics

A

Fast — thus they have no effect on conduction in normal tissue

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25
Q

Effect of class 1B drugs on AP and ECG

A

May shorten AP

More specific action on Na channels —> do NOT block K+ channels, do not prolong AP or QT duration on ECG

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26
Q

MOA of lidocaine (class 1B antiarrhythmic)

A

Blocks inactivated Na channels (use-dependence) — selectively blocks conduction in depolarized tissue, making damaged tissue “electrically silent”

Rapid kinetics results in recovery from block between AP, with no effect on cardiac conductivity in normal tissue

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27
Q

Clinical use for lidocaine

A

Used in mono- and polymorphic ventricular tachycardias — very efficient in arrhythmias associated with AMI

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28
Q

Lidocaine has extensive ____ metabolism, and thus is only given ____

A

First-pass; IV

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29
Q

AEs of lidocaine

A

Cardiovascular: may cause hypotension in pts with heart failure by inhibiting cardiac contractility, proarrhythmic effects are uncommon

Neurologic: paresthesias, tremor, slurred speech, convulsions

[note that lidocaine is least toxic of ALL class 1 antiarrhythmics]

30
Q

Orally active drug with electrophysiological and antiarrhythmic effects similar to lidocaine, used for ventricular arrhythmias and to relieve chronic pain, especially due to diabetic neuropathy and nerve injury

A

Mexiletine

31
Q

AEs of mexilitine

A

Tremor, blurred vision, nausea, lethargy

32
Q

MOA of class 1C antiarrhythmics

A

Block Na channels and slow impulse conduction

State-dependent block: preferentially bind to open (activated) Na channels

33
Q

Class 1C antiarrhythmics dissociate from channel with ____ kinetics and block certain ____ channels

A

Slow; K

34
Q

Class 1C antiarrhythmics effect on AP and ECG

A

Do NOT prolong AP duration, but may prolong QRS interval duration on ECG

35
Q

Class 1C antiarrhythmic that blocks Na and K channels and has no antimuscarinic effects

A

Flecainide

36
Q

Clinical use of flecainide (class 1C)

A

Used in pts with normal hearts for tx of supraventricular arrhythmias including AF, paroxysmal SVT (AVNRT, AVRT)

Also for life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia

37
Q

AEs for Flecainide

A

May be very effective in suppressing PVCs, but may cause severe exacerbation of ventricular arrhythmias when administered to:

Pts with pre-existing ventricular tachyarrhythmias

Pts with a previous MI

Pts with ventricular ectopic rhythms

38
Q

Class 1C antiarrhythmic with weak beta-blocking activity, used to prevent paroxysmal AF and SVT in pts without structural dz, as well as in sustained ventricular arrhythmias

A

Propafenone

39
Q

AEs of propafenone

A

Exacerbation of ventricular arrhythmias

Metallic taste

Constipation

40
Q

Propafenone should not be combined with the ____ and ____ inhibitors, as the risk of proarrhythmia may be increased

A

CYP2D6; CYP3A4

41
Q

MOA of class 2 antiarrhythmics

A

Beta-blockers!

Decrease SA and AV nodal activity by decreasing cAMP, and decreasing Ca currents

Suppress abnormal pacemakers by decreasing the slope of phase 4

The AV node is particularly sensitive — increased PR interval

42
Q

Clinical indications for propranalol use in cardiac arrhythmias

A

Arrhythmias associated with stress

Re-entrant arrhythmias that involve AV node (AVNRT, AVRT)

Afib and flutter

Arrhythmias associated with MI — decreased mortality in pts with AMI

43
Q

Short-acting selective beta-1 blocker with half life of 10 min d/t hydrolysis by blood esterases; thus given has continuous IV infusion

A

Esmolol

44
Q

Clinical use of esmolol

A

Supraventricular arrhythmias

Arrhythmias associated with thyrotoxicosis

Myocardial ischemia or AMI with arrhythmia

As an adjunct drug in general anesthesia to control arrhythmias in perioperative period

45
Q

AEs of beta blockers used as antiarrhythmics

A

Reduced CO, bronchoconstriction, impaired liver glucose mobilization, unfavorable lipoprotein profile (increase VLDL, decrease HDL), sedation, depression, withdrawal syndrome associated with sympathetic hyperresponsiveness

46
Q

Contraindications to use of beta blockers

A

Asthma

Peripheral vascular disease

Raynaud’s syndrome

Type 1 diabetics on insulin

Bradyarrhythmias and AV conduction abnormalities

Severe depression of cardiac function

47
Q

What K channels are open in the resting state?

A

Inwardly rectifying K+ channels

48
Q

Class 3 antiarrhythmics are K+ channel blockers. What effect do they have on the AP and ECG?

A

Prolong AP duration as well as refractory period

Prolong QT interval on ECG

49
Q

Class 3 antiarrhythmic that blocks K channels and inactivated sodium channels as well as some calcium channel blocking activities, prolongs QT interval and APD uniformly over a wide range of heart rates, possesses adrenolytic activity resulting in bradycardia and slowed AV conduction and peripheral vasodilation

A

Amiodarone

50
Q

Clinical use of amiodarone

A

Tx of ventricular arrhythmias, afib

51
Q

Amiodarone is metabolized by ____, thus its half-life is affected by inhibitors of this enzyme (cimetidine) or inducers (rifampin)

A

CYP3A4

52
Q

How long-lasting are the effects of amiodarone?

A

Its major metabolite is active with very long elimination half life of weeks to months; effects are maintained 1-3 months after discontinuation, and metabolites are found in tissues 1 year after discontinuation

53
Q

Amiodarone itself is a ______ of many CYP enzymes - thus it may affect the metabolism of many other drugs, and all medications should be carefully reviewed in
patients on amiodarone – dose adjustments may be necessary

A

Inhibitor

54
Q

Adverse effects of amiodarone

A

Cardiac: AV block and bradycardia; incidence of torsade de pointes is low as compared to other class 3 drugs

Extracardiac: fatal pulmonary fibrosis, hepatitis, photodermatitis (blue-grey skin discoloration in sun-exposed areas), deposits of drug in cornea and other eye tissues — optic neuritis, blocks peripheral conversion of thyroxine to triiodothyronine, also a source of inorganic iodine in the body (may cause hyper or hypothyroid)

55
Q

Antiarrhythmic that acts as class 2 non-selective beta-blocker and class 3 agent (prolongs APD)

A

Sotalol

56
Q

Clinical use of sotalol

A

Tx of life-threatening ventricular arrhythmias

Maintenance of sinus rhythm in pts with afib

57
Q

AEs of sotalol

A

Depression of cardiac function

Provokes torsade de pointes

58
Q

Class 3 antiarrhythmic that specifically blocks rapid component of the delayed rectifier K+ current; effect is more pronounced at lower heart rates

A

Dofetilide

59
Q

Dofetilide is eliminated by the _____, has a very narrow therapeutic window and dose has to be adjusted based on _________

A

Kidneys; creatinine clearance

60
Q

Clinical use of dofetilide

A

Used to convert AF to sinus rhythm and maintain sinus rhythm after cardioversion

61
Q

AEs of dofelitide

A

QT prolongation and increased risk of ventricular arrhythmias

62
Q

Class 3 antiarrhythmic similar to dofelitide that slows cardiac repolarization by blockade of the rapid component of the delayed rectifier K+ current; administered IV and rapidly cleared by hepatic metabolism

A

Ibutilide

63
Q

Clinical use of ibutilide

A

Used to convert atrial flutter and atrial fibrillation to sinus rhythm

64
Q

AEs of ibutilide

A

QT prolongation and increased risk of ventricular arrhythmias

Pts require continuous ECG monitoring until QT returns to baseline

65
Q

MOA of class 4 antiarrhythmics

A

Block both activated and inactivated L-type calcium channels

Active in slow response cells — decrease slope of phase 0 depolarization and increase L-type Ca channel threshold potential refractory period in AV node

[Slow SA node depolarization —> bradycardia; prolong AP duration and conduction time in AV node]

66
Q

Clinical use of class 4 antiarrhythmics (verapamil, diltiazem)

A

Prevention of paroxysmal SVT

Rate control in AF and atrial flutter

67
Q

AEs of class 4 antiarrhythmics

A

Cardiac: negative inotropy, AV block, SA node arrest, bradyarrhythmias, hypotension

Extracardiac: constipation (verapamil)

68
Q

MOA of adenosine

A

Activates K+ current and inhibits Ca++ and funny currents, causing marked hyperpolarization and suppression of action potentials in slow cells

Inhibits AV conduction and increases nodal refractory period

69
Q

Clinical use of adenosine

A

Conversion to sinus rhythm in paroxysmal SVT

70
Q

AEs of adenosine

A

Shortness of breath

Bronchoconstriction (both A1 and A2B adenosine receptors cause bronchoconstriction)

Chest burning

AV block

Hypotension

Cardiovascular Exam II (11 decks)

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