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Pharm II > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What do antiarrhythmic agents focus on?

A

Cardiac ion channels (Na, Ca, K)

Adrenergic receptors

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2
Q

What is the receptor target for class IA drugs and what EKG changes will you see?

A

Na and K channels

QRS and QT prolonged

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3
Q

What is the receptor target for class IB drugs and what EKG changes will you see?

A

Na channels

QRS prolonged

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4
Q

What is the receptor target for class II drugs and what EKG changes will you see?

A

Beta receptors

PR prolonged

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5
Q

What is the receptor target for class III drugs and what EKG changes will you see?

A

K channels

QT prolonged

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6
Q

What is the receptor target for class IV drugs and what EKG changes will you see?

A

Ca channels

PR prolonged

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7
Q

Which antiarrhythmics are class IA?

A

Procainamide
Amiodarone
Moricizine

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8
Q

Which antiarrhythmics are class IB?

A

Lidocaine

Phenytoin

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9
Q

Which antiarrhythmics are class II?

A 
Esmolol
Amiodarone
Propranolol
Atenolol
Labetalol
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10
Q

Which antiarrhythmics are class III?

A 
Bretylium
Ibutilide
Amiodarone
Sotalol
Dofetilide
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11
Q

Which antiarrhythmics are class IV?

A

Verapamil
Diltiazem
Amiodarone

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12
Q

What is the resting membrane potential?

A

Resting transmembrane concentration gradients for K and Na are maintained by active ion pumps and selective membrane conductance
-90 mV

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13
Q

T/F: Sarcolemma is more permeable to K than to Na

A

True

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14
Q

What are the phases of the cardiac action potential?

A 
Phase 0: rapid depolarization
Phase 1: Early rapid repolarization
Phase 2: Plateau
Phase 3: Rapid repolarization
Phase 4: Spontaneous diastolic depolarization
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15
Q

What happens during phase 0?

A

Action potential is initiated by an increase in Na conductance through ion-specific fast channels
vM becomes positive quickly

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16
Q

What happens during phase 1?

A

Na permeability is rapidly inactivated over 1-2 ms

The cell starts to repolarize

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17
Q

What happens during phase 2?

A

Repolarization is delayed by an increase in conductance of Ca through slow channels

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18
Q

What happens during phase 3?

A

Complete repolarization due to inactivation of Ca conductance and an increase in K permeability

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19
Q

What happens during phase 4?

A

Slow depolarization characteristic of all pacemaker cells

Results from a complex interaction between inward and outward currents of Ca and K during diastole

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20
Q

These channels are responsible for phase 0 is SA and AV nodes, contribute to phase 2 in ventricular contractile cells, and affects phase 4

A

Slow channels, Ca mediated

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21
Q

These channels are responsible for phase 0 (sharp upstroke in the His-purkinje system and atrial and ventricular muscle, rapid conduction velocity

A

Fast channels, Na mediated

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22
Q

T/F: cells that do no undergo spontaneous phase 4 depolarization are automatic and capable of impulse generation

A

False: cells that undergo spontaneous phase 4…

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23
Q

Factors that reduce ___ at the higher pacemaker sites will ___ favor the movement of the pacemaker to lower sites

A

Automaticity

passively

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24
Q

What are the vagal influences that contribute to automaticity?

A

Digitalis drugs
Parasympathomimetic drugs
Halothane

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25
Q

What must happen for re-entry to occur?

A

Unidirectional block of impulse conduction (area of injury)
Slow conduction via an alternate pathway
Impulse finds the unidirectional block repolarized and able to conduct the impulse retrograde
Impulse reactivates the alternate pathway and repeats the process

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26
Q

Where can re-entry occur?

A

SA node
Atrium (aflutter, afib)
AV node
Ventricle (VT)

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27
Q

What does pharmacologic arrhythmia management rely on?

A

The different ion channels responsible for impulse generation in the atria and ventricles versus the SA and AV nodes

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28
Q

Which ion channels are responsible for impulse generation in the atria and ventricles?

A

Na channels

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29
Q

Which ion channels are responsible for impulse generation in the SA and AV nodes?

A

Ca channels

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30
Q

Which class of antiarrhythmic drugs are calcium channel blockers?

A

Class IV

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31
Q

Which class of antiarrhythmic drugs block fast Na channel with or without K channel blockade

A

Class I

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32
Q

Which class of antiarrhythmic drugs are beta blockers?

A

Class II

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33
Q

Which class of antiarrhythmic drugs are K channel blockers?

A

Class III

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34
Q

Which drugs are in class IC?

A

Flecainide

Propafenone

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35
Q

How do class II antiarrhythmics work?

A

Decrease rate of depolarization

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36
Q

What are the effects on the action potential for type IA drugs?

A

Slows phase 0, prolongs 3

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37
Q

What are the effects on the action potential for type IB drugs?

A

Slows phase 0, shortens 3

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38
Q

What are the effects on the action potential for type IC drugs?

A

Very slow phase 0, no 3 effects

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39
Q

What are the effects on the action potential for type II drugs?

A

Reduces slope of 4

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40
Q

What are the effects on the action potential for type III drugs?

A

Prolongs phase 3

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41
Q

What are the effects on the action potential for type IV drugs?

A

Reduces slope of 4

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42
Q

What is the mechanism of action of Procainamide?

A

Na & K channel blocker
Depresses automaticity by decreasing the slope of phase 4 depolarization, increases refractoriness
Prevent re-entry by converting unidirectional to bidirectional block

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43
Q

What are the indications for Procainamide?

A

Ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
SVT, afib, PVCs, and VT

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44
Q

What happens if you rapidly infuse Procainamide?

A

Severe hypotension from myocardial depression and vasodilation

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45
Q

T/F: There is a toxic metabolite with Procainamide

A

True

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46
Q

S/S of toxicity of Procainamide

A 
Myocardial depression
Hypotension
QRS complex and QT prolongation
Heart block
Ventricular ectopy
Systemic lupus erythematosus-like syndrome possible with chronic administration
47
Q

What is the mechanism of action of Lidocaine?

A

Na channel blocker

Decrease the slope of phase 4 depolarization in purkinje fibers, reduce automaticity

48
Q

What are the indications for Lidocaine?

A

First choice for ventricular arrhythmias particularly re-entry dysrthymias (PVCs and vtach)
Ineffective against supraventricular arrhythmias

49
Q

What is the therapeutic concentration of Lidocaine?

A

1.5-5 mg/L

50
Q

What are the s/s of toxicity of Lidocaine?

A

CNS: depression to stimulation (convulsions)
CV: may depress LV performance in pre-existing LV dysfunction, rarely cause further slowing in patients with SB

51
Q

What is the mechanism of action of Dilantin?

A

Na channel blocker
Depresses phase 4 diastolic depolarization
Abolishes activity triggered by digitalis-induced after depolarizations (automaticity) in Purkinje fibers

52
Q

What are the indications for Dilantin?

A

Useful in the suppression of ventricular dysrhythmias associated with dig toxicity
Paradoxical vtach or torsades de pointes that is associated with prolonged QTc interval

53
Q

Why do you have to administer Dilantin via a central line?

A

Drug is highly alkaline and can cause phlebitis when administered through a peripheral IV

54
Q

What are the s/s of toxicity of Dilantin?

A 
Rapid administration assoc. with resp arrest, severe hypotension, vent ectopy and death
Drowsiness
Nystagmus
Nausea
Vertigo
Other cerebella signs
55
Q

What is the mechanism of action of Flecainide?

A

Depresses action potential phase 0
Prolongs QRS and to a lesser extent PR interval
May suppress SA node like BBs and Ca channel blockers
Delays conduction in bypass tracts

56
Q

What are the indications for Flecainide?

A

Effective in suppressing PVS and vtach

Atrial tachydysrhythmias including WPW (delays conduction in bypass tracts)

57
Q

What are the side effects for Flecainide?

A

Moderate negative inotropic effect
Vertigo
Difficulty in visual accommodation

58
Q

What is the mechanism of action with Propranolol?

A

Beta blockade leads to slowing of the SA node (decreased slope of phase 4 depolarization)
Slow the rate depolarization of ectopic pacemakers
Prolonged AV nodal conduction
Increased refractoriness of AV node

59
Q

What are the indications for Propranolol?

A

Control of SVT
Convert atrial tachyarrhythmias to SR
Slow ventricular response to afib and flutter

60
Q

What are the toxicity effects of Propranolol?

A

Primarily due to beta blockade
Profound bradycardia or asystole
LV failure
Acute bronchospasm

61
Q

How do Type III Antiarrhythmic drugs (K channel blockade) work?

A

Interrupts reentry by slowing conduction or increasing the refractory period
Prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT (torsades)

62
Q

What is the structural analog of thyroid hormone?

A

Amiodarone

63
Q

What is the mechanism of action for Amiodarone?

A

Potent inhibitor of abnormal automaticity
Prolongs the effective refractory period and action potential duration in all cardiac tissues including accessory bypass tracts (blocks inactivated Na channels and K movement, prolongs PR, QRS, and QT intervals)
May potentiate slowing of the SA node and AV conduction (may potentiate BBs and CCBs)

64
Q

What are the indications for Amiodarone?

A

IV for the acute termination of ventricular and supraventricular arrhythmias

  • Recurrent vfib or recurrent unstable vtach in pts unresponsive to or unable to tolerate other agents
  • Effective in maintaining SR in patients with afib
  • Suppression of tachydysrhythmias associated with WPW
65
Q

What is the half life for Amio?

A

Prolonged t 1/2 of weeks to months in patients on the oral agent for several years
Omission of 1 or 2 doses unlikely to result in recurrence of arrhythmia

66
Q

What are the toxicity effects of Amio?

A 
-Resp: ARDS, pulmonary fibrosis
CV: bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
Heme: coagulation abnormalities
Hepatic: increased LFTs, liver failure
Endo: hypo or hyperthyroidism
67
Q

What are you at risk for with Ibutilide (Corvert)?

A

Risk of prolonged QT

68
Q

What are the indications for Corvert?

A

Conversion of afib/aflutter
Less hypotension than amio, but still prodysrhythmic
More rapid conversion that procainamide or sotalol

69
Q

Are there renal and hepatic dosing adjustments of Corvert?

A

No

70
Q

What is an alternative multichannel blocking antiarrhythmic?

A

Dronedarone (Multaq)

Similar properties to amio but is structurally noniodinated

71
Q

What is the indication for MULTAQ?

A

For a fib to maintain NSR

Less efficacious but with less undesirable side effects or deaths

72
Q

What are the contraindications for Dronedarone?

A

Increased risk of death stroke and heart failure in patients with decompensated heart failure or permanent afib
Second/third degree heart block, HR <50 bpm
Meds that inhibit CYP3A4, prolong QTc
Pregnancy
Significant liver disease

73
Q

What is Sotalol?

A

Oral non-selective beta antagonist
Lengthens repolarization and effective refractory period in all cardiac tissues (prolongs action potential phase 3)
Lowers blood pressure

74
Q

What are the uses for Sotalol?

A

PSVT
Vtach and vfib
Antihypertensive

75
Q

How do calcium channel blockers work?

A

Inhibit inward slow Ca currents

Slow the atrial rate (SA node effect) and slow conduction through the AV node (prolonging the PR interval)

76
Q

What is the mechanism of action for Verapamil?

A

Selectively blocks slow channels by inhibiting the normal Ca influx into the cell
Slow channel activity is most important in SA and AV nodes (prolongs AV nodal conduction and refractoriness, depresses the rate of SA node discharge)

77
Q

What are the indications for Verapamil?

A

Treat SVT

Slow ventricular rate in afib and flutter

78
Q

T/F: Verapamil has an effect on accessory tracts

A

False: No effect on accessory tracts

79
Q

What are the toxicity side effects for Verapamil?

A

HYPOTENSION
Bradycardia, asystole, and AV block
Myocardial depression is uncommon in pts with reasonable LV function

80
Q

What is the mechanism of action for Cardizem?

A

slow channel blocking prolongs AV nodal conduction and refractoriness

81
Q

What are the indications for Cardizem?

A

Ventricular rate control in afib or aflutter

82
Q

What is the mechanism of action for Digoxin?

A

Inhibits Na/K ATPase
Directly prolongs the effective refractory period in the AV node (slows the ventricular response rate in afib)
Indirectly increases vagal activity and reduces sympathetic activity

83
Q

T/F: Digoxin enhances conduction through accessory pathways

A

True, can enhance ventricular response in WPW

84
Q

What are the indications for Digoxin?

A

Ventricular rate control in afib, aflutter, and SVT

85
Q

What are the toxicity side effects for Digoxin?

A

Alterations in cardiac rate and rhythm may stimulate almost every known rhythm disturbance but PVCs most common

86
Q

What is the mechanism of action for Adenosine?

A

Activates K channels that hyperpolarize nodal tissue causing a transient 3rd degree AV block

  • Less effect in the atrium
  • Depression of the action potential in the AV node
  • Methyxanthines inhibit the action of adenosine (bind to the adenosine receptor)
  • Dipyridamole (adenosine uptake inhibitor) and cardiac transplantation (denervation hypersensitivity) potentiate adenosine’s effects
87
Q

What are the indications for adenosine?

A

Treatment of PSVT including those that involve accessory pathways

88
Q

Is Adenosine useful in the treatment of arrhythmias originating distal to the AV node or afib or flutter?

A

No

89
Q

What is the half life of Adenosine?

A

1.5 seconds

90
Q

How is Adenosine inactivated?

A

By cellular uptake

91
Q

What are the toxicity effects of Adenosine?

A

Facial flushing, dyspnea, and chest pressure most common but subside in <60 seconds
May exacerbate bronchoconstriction in asthmatic patients

92
Q

What are the Prodysrhythmic effects?

A

Brady or tachydysrhythmias that represent new cardiac dysrhythmias associated with chronic antidysrhythmic drug treatment

93
Q

What are the types of prodysrhythmic effects?

A

Torsades de pointes
Increased ventricular tachycardias
Wide complex ventricular rhythm

94
Q

What is the mechanism of action of Torsades?

A

K channel blockade may prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT or vfib

95
Q

What is the treatment of Torsades?

A

Discontinue the offending agents
Correct electrolyte disturbances
Give 2 gm Mag
Increase HR if low with temp pacing or isoproterenol
Cardiovert only if hemodynamically compromised

96
Q

What is incessant ventricular tachycardia precipitated by?

A

Class IA and IC drugs that slow conduction of cardiac impulses sufficiently to create a continuous ventricular tachycardia circuit (re-entry)

97
Q

What is wide complex ventricular rhythm associated with?

A

Class 1C drugs in the setting of structural heart disease

98
Q

What are the treatment goals of antiarrhythmic drugs?

A

Restore NSR
Abolish ectopic beats
Control HR

99
Q

What inhalational agent sensitizes the myocardium to catecholamines that can lead to ventricular arrhythmias

A

Halothane

100
Q

Affect conduction and cause junctional rhythms

A

Inhalational agents

101
Q

A repeated dose of this muscle relaxant can lead to SB, junctional rhythms, ventricular arrhythmias and asystole

A

Succinylcholine

102
Q

What might be a first sign of myocardial ischemia under anesthesia?

A

PVCs or changes in conduction

103
Q

What are some therapeutic alternatives to treating arrhythmias?

A 
Slowing the HR
-Treat underlying cause
-Overdrive pacing
-DC shock for severe hemodynamic impairment
Increasing the HR
-Stop manipulation
-Pancuronium
-Isoproterenol gtt
-Pacing
104
Q

What is the treatment for intra-op bradycardia?

A

Lighten anesthesia
Anticholinergic agent
Beta agonist
Pacemaker

105
Q

What is the treatment for intraop SVT?

A

Cardioversion if SBP <80 and ischemia to prevent irreversible complications (MI, stroke)
Focus on reversible causes

106
Q

T/F: Most intraop supraventricular tachyrhythms are hemodynamically unstable and cardioversion is needed

A

False, most are hemodynamically stable and don’t need cardioversion

107
Q

What is the drug therapy for intraop SVT?

A

Adenosine (useful for PSVT)

108
Q

What is the drug therapy for orthodromic conduction (QRS complex <120 ms)?

A

Vagal maneuvers or AV nodal blocking agents
IV adenosine
DC cardioversion for hemodynamically unstable pt

109
Q

What is the drug therapy for AVRT and antidromic conduction (wide QRS complex)?

A

Procainamide, Amio or Ibutilide, slow conduction over pathways
AV nodal blocking agents could induce VT/VF because they could increase conduction in the accessory pathway
DC cardioversion with hemodynamic instability

110
Q

T/F: You want to avoid Procainamid, Amio and Ibutilide in patients with antegrade accessory pathway conduction

A

True

111
Q

What is the drug therapy for afib/aflutter?

A

Controlling ventricular rate is the mainstay of therapy
-AV nodal blockers Class II or IV (esmolol, metoprolol, propranolol, diltiazem or verapamil)
-Tensilon or Neostigmine
-Dig
-Vagal maneuvers, over-drive pacing, DC cardioversion
Class IA or III drugs more likely to terminate the arrhythmia

112
Q

Giving this prior to DC countershocks may improve chances of sustained cardioversion

A

IV procainamide or amio

113
Q

What is the treatment of sustained VT or VF?

A

DC countershocks

Resistant VT or VF: IV lido or procainamide, IV amio

114
Q

How do you treat polymorphic VT?

A 
Asynchronous DC countershocks in patients with hemodynamic collapse
-IV mg, K repletion, increase HR, class IB antiarrhythmic drugs

Pharm II (8 decks)

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