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Cardio > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What is the most common cause of death in patients with MI or terminal heart failure?

A

cardiac arrhythmias

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2
Q

How do you define an arrhythmia?

A

any rhythm that is not normal sinus rhythm

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3
Q

What are the two major mechanisms for arrhythmias?

A

1) Abnormal automaticity

2) Abnormal (reentrant) conduction

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4
Q

Why is Torsades de pointes unique in the clinically important arrhythmias?

A

it is often INDUCED by antiarrhythmic and other drugs that change the shape of the AP and prolong the QT interval (ex. quinidine and other class III drugs)

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5
Q

What is the other cause (not drug induced) of Torsades de pointes?

A

long QT syndrome (heritable abnormal prolongation of QT interval caused by mutations in the Ik or Ina channel proteins

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6
Q

What dominates the AP upstroke in most parts of the heart?

A

sodium current

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7
Q

What dominates the AP upstroke in the AV nodal cells?

A

calcium current

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8
Q

What is “abnormal automaticity”? What is it caused by?

A

spontaneous depolarization of cells without “pacemaker” current (ex. atrial and ventricular myocytes). Can be seen with ischemia, stretch of myocardial fibers, hypoxia, low ions, increased SNS activity

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9
Q

What is “abnormal conduction”?

A

conduction of an impulse that does not follow the normal path OR that reenters tissue previously excited

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10
Q

What does the PR interval signify?

A

measure of the conduction time from atrium to ventricle through the AV node

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11
Q

What does the QRS duration signify?

A

time required for all of the ventricular cells to be activated (intraventricular conduction time)

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12
Q

What does the QT interval reflect?

A

duration of ventricular AP

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13
Q

What does recovery from inactivation in sodium-dependent cardiac cells depend on?

A

1) membrane potential (varies with repolarization time and extracellular K+ conc)
2) Sodium channel blocking drugs

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14
Q

Antiarrhythmic drugs act on what 4 targets?

A

1) Sodium current
2) Calcium current
3) Potassium current
OR
4) Beta adrenoceptors that modulate the currents

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15
Q

Describe antiarrhythmic drug classification.

A

Divided into 4 groups or classes with one miscellaneous group

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16
Q

What are the class I antiarrhythmic agents? What do they do?

A

Sodium channel blockers- slow conduction in ischemic and depolarized cells and slow/abolish abnormal pacemakers that are dependent on sodium channels by increasing threshold potential and hyperpolarizing

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17
Q

What are the class II antiarrhythmic agents?

A

Beta-adrenoceptor blockers

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18
Q

What are the class III antiarrhythmic agents?

A

Potassium channel blockers

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19
Q

What are the class IV antiarrhythmic agents?

A

Calcium channel blockers

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20
Q

What are the class V antiarrhythmic agents?

A

Adenosine, potassium ion, magnesium ion

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21
Q

Group 1 antiarrhythmic drugs are divided into what subclasses? What are these based on?

A

Group 1A-1C

Based on dissociation rate

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22
Q

What do group 1A drugs do? What is the prototype?

A

Prolong the AP- intermediate dissociation rate

Procainamide

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23
Q

What do group 1B drugs do? What is the prototype?

A

shorten AP in some cardiac tissues (ventricle only)- rapid dissociation
Lidocaine

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24
Q

What do group 1C drugs do? What is the prototype?

A

have no effect on AP duration- very slow depolarization

Flecainide

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25
Q

What are the most selective antiarrhythmic agents?

A

Group 1B (affect ischemic tissue but has negligible effects on sodium channels)

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26
Q

How do sodium channel-blocking drugs target abnormal tissue?

A

“Use-dependent”- bind to receptors more readily when the voltage channel is open or just inactivated (must bind to the inside of the channel) than when it is fully repolarized and resting (normal cells)

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27
Q

List the group 1A antiarrhythmics.

A

Procainamide, quinidine, disopyramide

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28
Q

What are the clinical applications for group 1A antiarrhythmics?

A

Atrial and ventricular arrhythmias, especially after MI

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29
Q

What do group 1A antiarrhythmics do the the PR interval, QRS duration, and the QT interval?

A

PR: increase owing to channel blocking or decrease owing to antimuscarinic action
QRS: increase
QT: increase

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30
Q

What are the adverse effects of group 1A antiarrhythmics?

A 
increased arrhythmias (Torsades de Pointes, only at high doses does it show class III activity)
hypotension
lupus-like syndrome (with prolonged PO use, especially if slow acetylator in liver)
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31
Q

What do group 1B antiarrhythmics target?

A

ischemic/depolarized Purkinje and ventricular tissue (little effect on atrial tissue)

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32
Q

What is the effect of group 1B antiarrhythmics?

A

1) reduce AP duration (sometimes)

2) Slow recovery of sodium channels from inactivation

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33
Q

True or false: group 1B drugs have major effects that can be seen on the EKG.

A

FALSE: they do not harm normal cardiac cells so they have little effect on ECG

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34
Q

What are the clinical applications for group 1B antiarrhythmics?

A

ventricular arrhythmias (tachycardia) and VPBs

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35
Q

What are the adverse effects of group 1B antiarrhythmics?

A

CNS sedation or excitation

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36
Q

What do group 1C antiarrhythmics do the the PR interval, QRS duration, and the QT interval?

A
  • NO effect on QT interval or AP duration
  • Slow conduction velocity in atrial and ventricular cells

QRS: increase
PR: slight increase

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37
Q

What group 1A antiarrhythmic can you not use with digoxin?

A

quinidine (reduces it clearance and increases serum concentration)

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38
Q

What usually exacerbates the toxicity of group 1 drugs?

A

hyperkalemia

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39
Q

How do you reverse an overdose on group 1 antiarrhythmics?

A

sodium lactate

pressor sympathomimetics

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40
Q

Lidocaine has what ROA? Why?

A

IV or IM but NEVER orally, because of high first-pass effect and cardiotoxic metabolites. However, really lipophilic, so it will distribute into fat tissue when given IV and needs 2-phase loading protocol.

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41
Q

What is the group 1b antiarrhythmic that can be taken orally? What is the down side?

A

mexiletine- GI distress common and limits usefulness

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42
Q

What are the clinical indications of flecainide?

A

approved only for refractory ventricular tachycardias and certain intractable supraventricular arrhythmias (that fail to respond to other drugs)

43
Q

Flecainide is more likely than any other antiarrhythmic drug to have what effect?

A

proarrhythmic (exacerbate or precipitates arrhythmias). this was shown in CAST to actually increase chance of death after MI

44
Q

What is the mechanism of group 2 antiarrhythmics?

A

cardiac beta receptor blockage and reduction in cAMP which reduces both sodium and calcium currents and suppresses abnormal pacemakers

45
Q

What are the beta-blockers used in arrhythmia treatment? What types?

A

Propranolol (atrial/ventricular arrhythmia)
Metoprolol (off label for arrhythmias)
Acebutolol (ventricular arrhythmia)
Esmolol (supraventricular arrhythmia)

46
Q

What part of the heart is very sensitive to beta blockers? What do group 2 antiarrhythmics do the the PR interval, QRS duration, and the QT interval?

A

AV node
prolong the PR interval (decrease phase 4 slope)
no effect on QRS or QT

47
Q

What is the clinical use for esmolol in arrhythmia treatment?

A

IV administration in acute supraventricular arrhythmias

48
Q

What is the clinical use oral beta blockers in arrhythmia treatment?

A

prophylactic drugs in patients who have had an MI

49
Q

What are the adverse effects of beta blockers?

A
  • bronchospasm
  • cardiac depression
  • AV block
  • Hypotension
50
Q

List the group 3 antiarrhythmics.

A 
Dofetilide
Ibutilide
Sotalol (chiral compound)
Amiodarone
Dronedarone
51
Q

What is the hallmark of group 3 antiarrhythmics?

A

prolongation of AP duration (and ERP) due to blockage of IKr (responsible for repolarization)

52
Q

What does amiodarone do the the PR interval, QRS duration, and the QT interval? Why?

A

PR: increase slightly (beta)
QRS: increase
QT: LARGE increase (Ik)
Blocks sodium, calcium, potassium channels and beta receptors.

53
Q

What do ibutilide and dofetilide do the the PR interval, QRS duration, and the QT interval?

A

large QT increase

54
Q

What does sotalol do the the PR interval, QRS duration, and the QT interval?

A

Increase PR interval (beta block)

Increase QT interval (Ik block)

55
Q

What drug is considered to be the most efficacious of all antiarrhythmic drugs?

A

amiodarone: used with atrial and ventricular arrhythmias, and as drug of choice in cardiac rescuscitation

56
Q

What are the toxicities of amiodarone?

A 
Thyroid abnormalities (structural analog of thyroid hormone)
Deposits in skin and cornea
Pulmonary fibrosis
Optic neuritis (blindness)
RARE torsades
57
Q

What is the clinical application for sotalol?

A

atrial, ventricular AV nodal reentrant arrhythmias (including v tach). Less effective but less toxic than amiodarone

58
Q

What are the AAs of sotalol? Contraindications?

A

dose related torsades
Cardiac depression
Contraindications: QT>450msec, Renal insufficiency, asthma, CHF, AV block, bradycardia, MI

59
Q

What is the clinical application for ibutilide? Adverse effects?

A

treatment of acute atrial fibrillation and atrial flutter

AE: torsade de pointe, not for patients iwth long QT

60
Q

What is the clinical application for dofetilide? Adverse Effects?

A

treatment and prophylaxis of atrial fibrillation (interrupts re-entry in atrium)
AE: torsades de pointes, transient asystole

61
Q

True or false: all L-type calcium channel blockers are useful in antiarrhythmic therapy.

A

FALSE: dihydropyridines are NOT useful, because they actually stimulate reflex sympathetic heart stimulation which could worsen arrhythmias

62
Q

What are the effects of group 4 antiarrythmics?

A
  • State and use-dependent selective depression of calcium current
  • AV conduction velocity is decreased
  • Effective refractory period and PR interval is increased
63
Q

What is the major clinical use of group 4 antiarrhythmics?

A

Verapamil and Diltiazem prevent and converting AV nodal reentry (nodal tachycardia) to normal sinus rhythm

64
Q

What are the major adverse effects of group 4 antiarrhythmics?

A

depression of contractility
reduce AV node automaticity
depress AV conduction
decrease BP

65
Q

Group 4 antiarrhythmics should be avoided with what condition?

A

ventricular tachycardias, CHF, sinus bradycardia, or AV block

66
Q

How does adenosine work in treatment of arrhythmias?

A

given in high doses as IV bolus and blocks conduction of AV node by hyperpolarizing tissue through increased Ik1 and reducing calcium current

67
Q

What is the drug of choice for AV nodal arrhythmias (PSVT)?

A

adenosine

68
Q

What is the half-life of adenosine?

A

around 10 s (must give IV)

69
Q

What are the adverse effects of adenosine?

A

flushing, hypotension, transient asystole (<3s) transient chest pain and dyspnea

70
Q

What is the use of potassium in treating arrhythmias?

A

Hypokalemia- increased incidence of arrhythmias (especially in patients on digitalis)
Hyperkalemia- depress conduction and can cause reentry arrythmias
*Need to balance and normalize

71
Q

What is the use of magnesium ion in treating arrhythmias?

A

poorly understood, possibly increase sodium potassium ATPase activity

72
Q

What are the adverse effects of Mg ion?

A

muscle weakness

if too high, respiratory paralysis

73
Q

List the non-pharmacologic treatment options for arrhythmias.

A

1) external defibrillation
2) implanted defibrillators
3) implanted pacemakers
4) radiofrequency ablation of arrhythmogenic foci via catheter

74
Q

What is propafenone? What is it used for?

A 
class 1C agent with beta-adrenergic properties.
A fib, A flutter in patients WITHOUT heart disease
75
Q

What are the drugs of choice for interrupting re-entry?

A

Class 1A and 1B
Class III
NOT class 1C, ventricular problem so contraindicated!!

76
Q

When do you use dronedarone?

A

paroxysmal atrial fibrilliation and maintenance of sinus rhythm after cardioversion in people without CHF!

77
Q

What is “triggered automaticity”?

A

“echo” depolarization in response to preceding depolarization. Can be early afterdepolarization (EAD) or delayed afterpolarization (DAD)

78
Q

What is an APB?

A

premature atrial beat

79
Q

What might cause APBs in a healthy 21 year old?

A

enhanced automaticity of an atrial conducting fiber (probably due to increased intake of caffeine)

80
Q

Pacemaker channels are linked to what other systems?

A

1) muscarinic receptors (parasympathetic nervous system)
2) sympathetic nervous system
3) adenosine receptors

81
Q

How would you treat reduced automaticity of the SA node (sinus arrest)?

A

Atropine (if too much vagal tone)

Epinephrine (beta agonist)

82
Q

What is a VPB?

A

premature ventricular beat

83
Q

Does a VPB count as normal or abnormal automaticity?

A

abnormal (ventricular myocytes do not normally have “pacemaker” activity)

84
Q

How do sodium channel blockers stop re-entry?

A
  • Decreased rate of depolarization (phase 0)
  • Increased effective refractory period, because there is a slower voltage-dependent recovery of the Na+ channels with the drug bound
85
Q

Ventricular tachycardia is most commonly due to what?

A

organized re-entry of impulses around an anatomic barrier (ex. area of myocardial infarction or ischemia)

86
Q

What conditions are required for re-entry to occur?

A

1) Anatomic or physicologic obstacle
2) Unidirectional block
3) Conduction time exceeds effective refractory period in “slow” circuit

87
Q

What typically triggers re-entry?

A

premature impulse (automaticity)

88
Q

How do K+ channel blockers stop re-entry?

A

prolongation of the ERP in the slow conducting limb prevents re-entry back into the “slow side”

89
Q

Describe the pharmacokinetics of amiodarone.

A
  • Highly lipophillic
  • Eliminated VERY slowly (t1/2 = 20-100 days)
  • Oral or IV loading dose needed for rapid onset
  • CYP3A4 metabolized and inhibitor
90
Q

What are the top 3 drugs for treating ventricular tachycardia?

A

1) Amiodarone
2) Lidocaine
3) Procaineamide

91
Q

Having an EF below what percentage places a person at high risk of sudden cardiac death due to ventricular tachycardia/fibrillation?

A

<35%

92
Q

How would you treat someone at high risk of sudden cardiac death due to ventricular tachycardia/fibrillation?

A

Implantable cardiac defibrillator

93
Q

What are the two strategies for treating arrhythmias due to re-entry into the atrium (a fib)?

A

1) Rhythm control strategy

2) Rate control strategy

94
Q

What is the rhythm control strategy?

A

Interrupting re-entry within the atria using Class I and III antiarrhythmic drugs as with ventricular tachycardia

95
Q

What is the rate control strategy?

A

Controlling rate of ventricular activation from atrial re-entry by slowing conduction of the atrial impulses through the AV node

96
Q

What did the AFFIRM trial discover in the comparison of rhythm versus rate control of atrial fibrillation?

A

Rate control (digoxin, beta blocker, diltiazem and verapamil + warfarin) is better than rhythm control.

97
Q

What 3 drugs slow conduction through the AV node to prevent supraventricular arrhythmias?

A

1) Calcium channel blockers (verapamil/diltiazem)
2) Beta blockers (propranolol/metoprolol)
3) Digoxin (vagal effect)

98
Q

What is the MOA of digoxin?

A

Inhibits Na+/K+ ATP pump, reduces SA node automaticity (increases intracellular calcium)

99
Q

What are the conflicting effects of digoxin?

A

Vagal= antiarrhythmic effects (reduce SA automaticity and AV conduction, interrupts reentry in AV node)
Arrhythmogenic effets= increased normal automaticity, may lead to DADs from calcium overload

100
Q

Arrhythmias originating in the AV node are called what? What does this look like on an ECG?

A

paroxysmal supraventricular tachycardia (simultaneous activation of ventricle and atria (retrograde)).
Narrow QRS, regular rhythm, no p waves

101
Q

What problems can Wolff Parkinson White Syndrome cause?

A

Direct connection from atria to ventricle leads to:
Ventricular fibrillation (from multiple atrial signalling)
Supraventricular tachycardias

102
Q

What effect does vagal stimulation have on atrial tissue?

A

“Paradoxical effect” where it shortens AP duration, increases conduction velocity, and decreases ERP

103
Q

What is contraindicated in Wolf-Parkinson white syndrome?

A 
Digoxin (increases vagal afferents to heart which will result in increased conduction velocity and a potential for induction of ventricular fibrillation)
Do not use class IV or Ib either!  (could cause v fib as well)
104
Q

What is the best way to treat someone with WPW syndrome arrhythmias (a fib and a flutter)?

A

1) combination therapy (Class Ia and II)

2) single agent (Class III or class Ic)

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