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PCM Exam 2 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

The ______ node causes slowing of the heart contraction

A

AV

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2
Q

Atrial vs ventricular tachyarrythmia

A
  • atrial: not as dangerous. The biggest concern is the formation of a clot due to blood stasis in the atria
  • ventricular: very dangerous can can be lethal
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3
Q

The bundle of Kent/ bypass tract allow impulses to travel more quickly from __________ to ________ than the _____ node

A

Atria to ventricles; AV node

Common cause of arrhythmias

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4
Q

The rapid upstroke in phase 0 of the myocardial action potential is due to _____

A

Opening of sodium channels and ends as the sodium channels are inactivated

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5
Q

What happens in phase 1 of the myocardial action potential?

A

Phase 1: initial repolarization

  • sodium channels inactivate
  • K channels rapidly open and close → transient outward current
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6
Q

What causes the plateau in phase 2 of the myocardial action potential?

A

Balance of the opening of voltage sensitive calcium channels (depolarization) and slow outward movement of K (repolarization)

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7
Q

The repolarization phase (phase 3) is due to:

A

Opening of K and the outward current (polarizing) and calcium channels close

Gain of Na and loss of K (imbalance corrected by Na/K ATPase)

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8
Q

What is phase 4 of the myocardial action potential?

A

Resting potential in which there is a small gradual increasing depolarizing to eventually reach threshold of the next AP

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9
Q

Where do you see pacemaker action potential?

A

SA and AV nodes

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10
Q

The phase 0 upstroke in the pacemaker action potential is due to ________

A

Calcium; (in myocardial AP, the upstroke is due to sodium)

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11
Q

Phase 3’s repolarization in the pacemaker action potential is due to ________

A

Inactivation of calicum channels and ↑ activation fo K channels → ↑ efflux fo K

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12
Q

___________ channels causes the slow spontaneous depolarization in phase 4 of pacemaker action potential

A

Funny channels (mixed Na/K inward current)

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13
Q

Drugs that slow conduction through the _____ node are going to ______ the PR nterval

A

AV node; ↑ PR interval

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14
Q

What it’s he QT interval?

A

The time from ventricular depolarization to ventricular repolarization

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15
Q

What would affect the QT interval?

A

Extending the acting potential of ventricular myocytes wll extend QT interval

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16
Q

Mechanisms of arrhythmias

A
  • disturbances in impulse formation
  • disturbance in impulse conduction
  • mixture of both
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17
Q

What are the two classifications for arrhythmias

A
  • supraventricular (atrial or AV junctional)

- ventricular

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18
Q

What is the leading cause of arrhythmias

A

Drug toxicity, especially from antiarrhythmics

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19
Q

What are common causes of arrhythmias

A

Most arise from either abnormal automaticity or from defects in impulse conduction

  • abnormal automaticity (generates complete stimuli)
  • re-entrant circuits
  • afterdepolarizations
  • accessory tract pathways
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20
Q

_____ node sets the pace of myocardium contraction

A

SA

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21
Q

Most antiarrhymtics suppress automaticity by blocking either _______ or ________ and what phase is affected in the action potential?

A

Na and Ca;

  • ↓ slope of phase 4 depolarization and/or ↑ threshold of discharge to a less negative voltage

Above two lead to a ↓ frequency of discharge

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22
Q

Most antiarrythmics cause a decrease in the slope of phase ____ depolarization

A

Phase 4

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23
Q

________ is the most common cause of arrhythmias

A

Re-entry; occurs if there is a unidirectional block. The problem here is that the impulses will travel backwards via the dead/non excitable area and re enter the tissues that have already been stimulated

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24
Q

What are mechanisms that antiarrhythmics can prevent re-entry?

A
  • slowing conduction

- ↑ the refractory period

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25
Q

After treatment of re-entrant circuits, a _________ conduction block becomes a __________ conduction block

A

Unidirectional; bidirectional

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26
Q

Early afterdepolarizations occur during phase ________ of the AP and are triggered by conditions that ___________

A

Phase 2 or 3; conditions that prolong action potential such as drugs that prolong QT interval

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27
Q

Drugs that prolong ______ interval can trigger early afterdepolarizations

A

QT

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28
Q

When digoxin causes early afterdepolarizatoins, it is due to ________

A

Changes in calcium and sodium ions

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29
Q

_________ afterdepolarizations arises from the plateau

A

Early;

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30
Q

Delayed afterdepolarizations occur shortly after __________ so it arises from the _______

A

Completion of depolarization; resting potential

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31
Q

________ has been used to treat bradyarrhythmias

A

Atropine;

cardiac pacemakers are the treatment of choice

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32
Q

Class 1-4 antiarrhythmic drugs

A

Class I: Na channel blockers
Class II: β blockers
Class III: K channel blockers
Class IV: Calcium channel blockers

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33
Q

What are the class IV anti-arrhythmic drugs?

A
  • verapamil and diltiazem
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34
Q

Class I antiarrhythmic drugs block ________ and thus affects phase ______

A

Inward Na channels;

Slows the rate of rise of phase 0 depolarization

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35
Q

Antiarrhymic drugs possess use/state dependence. What is this?

A

These drugs bind to channels when they are open or closed NOT very well in their resting state → have more effect when there is arrhythmia (adds to selectivity)

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36
Q

What are the class 1A antiarrhythmics

A
  • quinidine
  • procainamide
  • disopyramide
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37
Q

Procainamide and other similar drugs (class ________ antiarrhythmics) affect: __________ and _________ phases

A
  • Slows rate of change of phase 0 by acting on the sodium channels (↑ QRS)
  • prolongs phase 3 by inhibiting K channels and thus ↑ the ventricular effective refractory period (inc. QT → early afterdepolarizations causing more Na channels to open)

Class 1A

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38
Q

Quinidine can also block K channels and affects _______ and ______ but NOT _______

A

Atrial and ventricular AP’s BUT NOT the nodal action potential

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39
Q

What are the presenting features of cinchonism and what drug is this group of adverse effects associated with?

A
  • blurred vision, tinnitus, headache and pscyhosis

- associated with quinine and quinidine

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40
Q

What are some adverse effects of quinidine?

A
  • SA/AV block
  • thrombocytopenic purpura
  • ventricular tachycardia in toxic doses
  • cinchonism: blurred vision, tinnitus, headache and psychosis
  • mixed α adrenergic block and antimuscarinic properties
  • can ↑ concentration of digoxin by ↓ renal clearance
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41
Q

________ can ↑ concentration of digoxin by _______

A

Quinidine; ↓ renal clearance of digoxin

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42
Q

Quinidine should not be given to patients with _____

A

Heart block

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43
Q

________ and _______ are class 1A antiarrhythmic drugs that have anti-muscarinic properties but _______ has the most severe antimuscarinic effects

A

Quinidine and procainamide; disopyramide

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44
Q

_________ and _______ are drugs that are associated with reversible lupus like syndrome

A

Hydralazine and procainamide

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45
Q

The acetylation of _________ produces NAPA which prolonged the _________ blockade

A

Procainamide; potassium channel

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46
Q

Which class 1A antiarrhythmic is contraindicated in patients with lupus?

A

Procainamide; this drug also causes reversible lupus like syndrome

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47
Q

Which class 1A drug has the strongest negative ionotropic effect?

A

Disopryamide

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48
Q

Dispyramide causes peripheral _________

A

Vasoconstriction; class 1A antiarrhythmic

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49
Q

What are the class 1B antiarrhythmics

A

Lidocaine and mexiletine

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50
Q

What phases do the class 1B antiarrhythmic drugs affect?

A

Slows phase 0 and ↓ slow of phase 4
Shortens phase 3 repolarization (this is not clinically significant and is actually pro-arrhythmic and has no adverse effects)

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51
Q

If you give a person without an arrhythmia lidocaine, would you see any changes on the EKG?

A 
NO 
(Same with class 1A drugs)
52
Q

Class 1B drugs are used specifically for _________ arrhythmias

A

VENTRICULAR

53
Q

Class ____ drugs are used for both atrial and ventricular arrhythmias

A

1A

54
Q

Which class 1 antiarrhythmic sub class as a milder sodium channel block?

A

Class 1B

55
Q

1st treatment for ventricular tachyarrhythmias is _________ and the second line is ________

A

1st line: amiodarone

2nd line: lidocaine

56
Q

What are some symptoms you see in a lidocaine OD?

A

Convulsions and coma

57
Q

Does lidocaine have any ionotropic effect?

A

NO

58
Q

________ is the oral version of lidocaine and thus can expect to see more _____ adverse effects

A

Mexitene; GI

59
Q

Which class 1 drug rapidly associated and disassociated with sodium channels?

A

Class 1B: lidocaine and mexiletine

60
Q

What can you expect to see on the AP graph of a class 1C drug?

A

MARKED depression of phase 0 action potential AND NO EFFECT ON PHASE 3 because no effect on K channels

Class 1C drugs: flecainide and propafenone

61
Q

Class ____ drugs associates and reassociates slowly with Na channels

A

1C: flecainide and propafenone

62
Q

A large ↑ in QRS is seen with _______

A

Class 1C drugs: flecainide and propafenone

63
Q

What are some clinical applications of flecainide

A

Class 1C drug;

  • severe symptomatic ventricular arrhythmias
  • premature ventricular contraction
  • ventricular tachycardia resistant to other therapy
  • supraventricular arrhythmias
64
Q

Flecainide has _______ inotropic effects

A

NEGATIVE

65
Q

Which drug is useful to treat arrhythmias in people with CHF and why?

A

Lidocaine because it does not have any negative inotropic effects

66
Q

Which class 1 drug is associated with β booking activity and thus can cause bronchospasm or aggravate underlying heart failure?

A
  • propafenone (class 1C)
67
Q

Lidocaine and mexiletine _____ QRS and ______ QT

A

Slight ↑ in QRS and slight ↓ in QT (QT ↓ is clinically insignificant)

68
Q

Class 1 drugs that ↑ both QRS and QT:

A

Quinidine, procainamide, and disopyramide (1A)

69
Q

Class II drugs are _____ blockers

A

β1 (↓ HR and contractility)

70
Q

Class ___ affects the SA and AV node

A

Class II (β blockers)

71
Q

Class II has its main effects on the ____ tissues

A

Nodal; little effect on the action potential in most myocardial cells

Mainly AV node

72
Q

An ↑ in _____ interval is seen on EKG when given β blockers

A

PR

73
Q

What drug is given to reduce the incidence of sudden arrhythmic death following an MI?

A

β blocker

74
Q

_______ drugs are used to CONTROL supraventricular tachycardias (prevent the atrial tachycardia from developing into a ventricular one)

A

Class 2 drugs (β blocker)

75
Q

What is the β blocker of choice to be given during surgery for a true arrhythmias and given via IV and has short acting β1 selective antagonist?

A

Esmolol

76
Q

Beta blockers are used to threat ______ but are contraindicated in _____

A

Chronic heart failure; contraindicated in acute decompensated HF

77
Q

Class III antiarrythmics extend ______ interval because they ______

A

QT; block repolarizing K channels

78
Q

The arrhythmias caused by amiodarone are the ____________ due to the class ____ activity

A

Early afterdepolarizations; class 3 activity (blockade of K channels)

79
Q

Which drug extends QT but DOES NOT ↑ risk for ventricular arrhythmias?

A

Amiodarone

80
Q

Dominant effect of amiodarone

A 
K channel blockade; 
Has class 1,2 and 3 activity
81
Q

Amiodarone blocks mostly ______ sodium channels

A

Inactivated

82
Q

MOA of amiodarone

A
  • blocks inactivated sodium channels
  • blocks K channels (dominant effect)
  • weak calcium channel blocker
  • inhibits α and β receptors
  • anti-anginal
  • anti-arrhythmic
83
Q

The DOC for acute ventricular tachyarrhythmia is _______

A

Amiodarone

2nd line: lidocaine

84
Q

Interstitial pulmonary fibrosis is an AE of __________

A

Amiodarone

85
Q

What are some adverse effects of amiodarone?

A
  • Hyper or hypothyroidism (thyroxine)
  • INTERSTITIAL PULMONARY FIBROSIS
  • blue skin discoloration (iodine accumulation)
86
Q

Amiodarone is contraindicated in patients taking:

A
  • digoxin
  • theophylline
  • warfarin
  • quinidine
87
Q

What conditions are amiodarone contraindicated in?

A
  • bradycardia
  • SA/AV block
  • severe hypotension
  • severe respiratory failure
88
Q

Sotalol is a class ____ drug that also acts as a _______

A

Class 3 (potassium blcoker) that is also a potent NON selective β blocker

89
Q

Sotalol affects what phase of the AP?

A
  • extends QT (K channel blocker)

- extends PR (β blocker)

90
Q

Which drug is used to maintain sinus rhythm in patients with atrial fibrillation and flutter?

A

Sotalol (class 3 with also β blocker activity); given as prophylactic to prevent moving out of sinus rhythm

91
Q

Which anti-arrhythmic drug has the lowest rate of acute/long term adverse effects?

A

Sotalol

92
Q

_______ is a potent and PURE K channel blocker

A

Dofetilide

93
Q

________ is a classs 3 drug given to convert atrial fibrillation/flutter to normal sinus rhythm

A

Dofetilide

94
Q

Class IV antiarrhythmics block ______ channels leading to ↓ rate of phase _____

A

Calcium; phase 0 depolarization in nodal tissues (similar to class 2 drugs by slowing conduction in SA and AV nodes)

95
Q

With class IV drugs, there is a ↑ in _____ interval

A

PR

96
Q

What are the two class IV drugs ?

A
  • verapamil

- diltiazem

97
Q

Major effects of diltiazem and verapamil

A

These two drugs are class IV antiarrhythmic drugs that are calcium channel blockers

  • ↓ contractility
  • ↓ HR
  • ↓ conduction velocity
98
Q

Verapamil and diltiazem bind to _____ calcium channels

A

Open, depolarized; (prevents repolarization before the drug dissociates)

99
Q

Class IV is more effective in ______ arrhythmias

A

Atrial

Class IV drugs: verapamil and diltiazem

100
Q

High risk of constipation is an AE of what drug?

A

Verapamil (class IV)

101
Q

Doses of _______ must be altered when giving what class IV drug?

A

Doses of: digoxin, dofetilide, simvastatin, and lovastatin

When giving verapamil

102
Q

What drug SHORTENS the refractory period in atrial and ventricular myocardial cells?

A

Digoxin

103
Q

Digoxin ________ the refractory period in _______

A

PROLONGS in the AV node

104
Q

Digoxin _______ refractory period in the atrial and myocardial cells

A

SHORTENS

105
Q

What is the pro-arrhythmic effect of digoxin?

A

Shortening the refractory period in the atrial and ventricular myocardial cells

106
Q

Clinical application of digoxin?

A
  • control of ventricular resisters rate in atrial fibrillation with impaired left ventricular function or HF
107
Q

What drug is best to give to treat atrial fibrillation when they patient also has left ventricular dysfunction or HF

A

Digoxin

108
Q

Which drugs slow the concussion through the AV node and ↑ PR interval?

A
  • β blockers
  • calcium channel blockers
  • digoxin
109
Q

Digoxin treats atrial fibrillation by controlling ________

A

Ventricular rate; (β blockers and calcium channel blockers do the same)

110
Q

What is used to treat the ventricular arrhythmias caused by digoxin?

A
  • lidocaine OR magnesium
111
Q

DOC for acute supraventricular tachycardia?

A

ADENOSINE

112
Q

What is the effect of high doses of adenosine?

A
  • ↓ conduction velocity
  • prolongs refractor period
  • ↓ automaticity in AV node
113
Q

Adenosine leads to ___________ of the AV node via:

A

Hyperpolarization of the AV node; enhancing K conduction and inhibits cAMP mediated calcium influx

114
Q

DOC for acute ventricular tachycardia

A

Amiodarone

115
Q

Magnesium is a _______ antagonist

A

Calcium

116
Q

Magnesium is used for the treatment of: (3)

A
  • trades de pointes
  • digitalis induced arrhythmias
  • prophylaxis of arrhythmia in acute MI
117
Q

Which classes of anitarrhythmics act on the SA node?

A
  • Class 2 (β blockers)
  • class IV (calcium channel blockers)
  • digoxin
118
Q

What class of drugs affects the AV node?

A
  • Class IV (calcium channel blockers)
  • Class II (β blockers)
  • digoxin
119
Q

Which anti arrhythmic drugs affect the atrial myocytes?

A
  • Class 1A and 1C

- Class III (K channel blockers)

120
Q

Which classes of antiarrhythmics affects the ventricular myocytes?

A
  • class I (Na channel blockers, includes 1B because 1B only works on ventricles while 1A and 1C works on both atria and ventricles)
  • Class III (K channel blockers)
121
Q

Which antiarrythmics affect the accessory pathways?

A
  • Class 1A

- Class III (K channel blockers)

122
Q

_______ channel blockade seems to have an affect on the accessory pathway

A

Potassium

123
Q

What drugs are used to treat ventricular and supraventricular arrhythmia ?

A

Class 1A and 1C, and Class III (K channel blockers)

124
Q

What drugs are used to treat mainly ventricular arrhythmias?:

A

Class 1B: lidocaine and mexiletene

125
Q

What drugs are used to treat mainly supraventricular arrhythmias

A 
- class IV drugs (calcium channel blockers) 
Class II drugs (β blockers)

PCM Exam 2 (32 decks)

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