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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
Effect of class 1B drugs on AP and ECG
May shorten AP More specific action on Na channels —> do NOT block K+ channels, do not prolong AP or QT duration on ECG
26
MOA of lidocaine (class 1B antiarrhythmic)
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
27
Clinical use for lidocaine
Used in mono- and polymorphic ventricular tachycardias — very efficient in arrhythmias associated with AMI
28
Lidocaine has extensive ____ metabolism, and thus is only given ____
First-pass; IV
29
AEs of lidocaine
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
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
Mexiletine
31
AEs of mexilitine
Tremor, blurred vision, nausea, lethargy
32
MOA of class 1C antiarrhythmics
Block Na channels and slow impulse conduction State-dependent block: preferentially bind to open (activated) Na channels
33
Class 1C antiarrhythmics dissociate from channel with ____ kinetics and block certain ____ channels
Slow; K
34
Class 1C antiarrhythmics effect on AP and ECG
Do NOT prolong AP duration, but may prolong QRS interval duration on ECG
35
Class 1C antiarrhythmic that blocks Na and K channels and has no antimuscarinic effects
Flecainide
36
Clinical use of flecainide (class 1C)
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
AEs for Flecainide
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
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
Propafenone
39
AEs of propafenone
Exacerbation of ventricular arrhythmias Metallic taste Constipation
40
Propafenone should not be combined with the ____ and ____ inhibitors, as the risk of proarrhythmia may be increased
CYP2D6; CYP3A4
41
MOA of class 2 antiarrhythmics
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
Clinical indications for propranalol use in cardiac arrhythmias
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
Short-acting selective beta-1 blocker with half life of 10 min d/t hydrolysis by blood esterases; thus given has continuous IV infusion
Esmolol
44
Clinical use of esmolol
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
AEs of beta blockers used as antiarrhythmics
Reduced CO, bronchoconstriction, impaired liver glucose mobilization, unfavorable lipoprotein profile (increase VLDL, decrease HDL), sedation, depression, withdrawal syndrome associated with sympathetic hyperresponsiveness
46
Contraindications to use of beta blockers
Asthma Peripheral vascular disease Raynaud’s syndrome Type 1 diabetics on insulin Bradyarrhythmias and AV conduction abnormalities Severe depression of cardiac function
47
What K channels are open in the resting state?
Inwardly rectifying K+ channels
48
Class 3 antiarrhythmics are K+ channel blockers. What effect do they have on the AP and ECG?
Prolong AP duration as well as refractory period Prolong QT interval on ECG
49
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
Amiodarone
50
Clinical use of amiodarone
Tx of ventricular arrhythmias, afib
51
Amiodarone is metabolized by ____, thus its half-life is affected by inhibitors of this enzyme (cimetidine) or inducers (rifampin)
CYP3A4
52
How long-lasting are the effects of amiodarone?
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
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
Inhibitor
54
Adverse effects of amiodarone
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
Antiarrhythmic that acts as class 2 non-selective beta-blocker and class 3 agent (prolongs APD)
Sotalol
56
Clinical use of sotalol
Tx of life-threatening ventricular arrhythmias Maintenance of sinus rhythm in pts with afib
57
AEs of sotalol
Depression of cardiac function Provokes torsade de pointes
58
Class 3 antiarrhythmic that specifically blocks rapid component of the delayed rectifier K+ current; effect is more pronounced at lower heart rates
Dofetilide
59
Dofetilide is eliminated by the _____, has a very narrow therapeutic window and dose has to be adjusted based on _________
Kidneys; creatinine clearance
60
Clinical use of dofetilide
Used to convert AF to sinus rhythm and maintain sinus rhythm after cardioversion
61
AEs of dofelitide
QT prolongation and increased risk of ventricular arrhythmias
62
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
Ibutilide
63
Clinical use of ibutilide
Used to convert atrial flutter and atrial fibrillation to sinus rhythm
64
AEs of ibutilide
QT prolongation and increased risk of ventricular arrhythmias Pts require continuous ECG monitoring until QT returns to baseline
65
MOA of class 4 antiarrhythmics
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
Clinical use of class 4 antiarrhythmics (verapamil, diltiazem)
Prevention of paroxysmal SVT Rate control in AF and atrial flutter
67
AEs of class 4 antiarrhythmics
Cardiac: negative inotropy, AV block, SA node arrest, bradyarrhythmias, hypotension Extracardiac: constipation (verapamil)
68
MOA of adenosine
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
Clinical use of adenosine
Conversion to sinus rhythm in paroxysmal SVT
70
AEs of adenosine
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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