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NAPLEX Content > Anti-arrhythmics > Flashcards

Anti-arrhythmics Flashcards

1
Q

What’s heart rate (u)

A

HR describes the frequency of depolarization of the ventricles

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2
Q

What’s the normal resting HR (normal sinus rhythm - NSR)? (U)

A

60-100 beats per minute

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3
Q

Can Arrythmias be silent? (U)

A

Yes

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4
Q

In most pts that experience sx, what do they experience?

A

Palpitations (feeling like there’s fluttering or racing)

Dizziness

Lightheadedness

SOB

Chest pain

Fatigue

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5
Q

In severe cases, what sx may one experience?

A

Syncope

Heart failure

Death

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6
Q

What’s the most common etiology of arrhythmias?

A

Myocardial ischemia

OR

Infarction secondary to coronary artery dx

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7
Q

List the non-cardiac conditions that may trigger arrhythmias.

A

Electrolyte imbalances especially those involving potassium, magnesium, sodium and calcium

Elevated sympathetic states such as hyperthyroidism and infection

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8
Q

List the electrolytes that may trigger arrhythmias when they are out of balance

A

Potassium

Magnesium

Sodium

Calcium

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9
Q

What’s QT prolongation?

A

Drug- induced slowing of repolarization, which can result in a particularly dangerous ventricular tachyarrhythmia called Torsade de Pointes (TdP)

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10
Q

What’s the resting value?

A

-90 mV

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11
Q

What happens in phase 0 of action potential?

A

Depolarization (determines conduction velocity)

Na channels OPEN (entering cell)

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12
Q

What determines conduction velocity?

A

Depolarization

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13
Q

What’s the value of phase 1 of action potential?

A

+ 10mV

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14
Q

What happens in phase 1 of action potential?

A

PEAK

Na channels CLOSE

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15
Q

What happens in phase 2 (plateau)?

A

PLATEAU

Ca channels OPEN (entering cell)

K channels OPEN (EXITING cell)

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16
Q

What happens in phase 3?

A

Repolarization

Ca2+ channels CLOSE
K channel stays open (continue exiting cells)
Na may enter cell (late inward Na current)

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17
Q

What happens in phase 4?

A

Automaticity

Slow increase in potential

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18
Q

When is refractory period of action potential?

A

Phase 1 to end of phase 3

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19
Q

How’s arrhythmias classified?

A

Based on their location of origin into:

Supraventricular

OR

Ventricular

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20
Q

What’s Supraventricular arrhythmias?

A

Arrhythmias originating ABOVE atrioventricular node

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21
Q

What’s ventricular arrhythmias?

A

Originating BELOW the atrioventricular node

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22
Q

What’s the most common Supraventricular arrhythmias? (U)

A

Atrial fibrillation (AFib)

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23
Q

What’s AFib?

A

Results from multiple waves of electrical impulses in the atria, resulting in an irregular and usually RAPID VENTRICULAR RESPONSE

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24
Q

Why does the mgt of AFib involve anticoagulation?

A

Due to disorganized depolarization of the atria, coordinated atrial contraction is impaired, which increases the risk of thromboembolism and stroke

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25
Q

What type of ventricular tachycardia is a medical emergency?

A

Ventricular tachycardia without a pulse

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26
Q

What’s a risk factor for Torsade De Pointes (TdP)? (U)

A

Prolongation of the QT prolongation

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27
Q

What’s Torsade de Pointes (TdP)? What can it result in?

A

TdP is a particularly lethal ventricular tachyarrhythmia which is most commonly ass. with drugs and can result in SUDDEN CARDIAC DEATH

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28
Q

How is QT interval measured? What’s the measured space define?

A

From beginning of the QRS complex to the end of the T wave

Reflect ventricular depolarization and repolarization

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29
Q

What pre-existing condition may cause additive QT prolongation?

A

Any pre-existing cardiac condition

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30
Q

What class of antiarrhythmics also result in additive QT prolongation? (U)

A

Class Ia (Disopyramide, Quinidine, Procainamide) double quarter pounder

Class III (Amiodarone, Ibutilide, Dofetilide, Dronedarone, Sotalol) AIDDS

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31
Q

Name main antibiotics that may cause additive QT prolongation. (U)

A

Quinolones (Ciprofloxacin, Levo, Moxi, Nor, Ofloxacin, Gemi, Spar)

Macrolides (Azithromycin, Erythromycin, Clarithromycin, Telithromycin)

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32
Q

Which Azole antifungal is most responsible for causing additive QT prolongation? (U)

A

Voriconazole

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33
Q

Which anticancer is most responsible for causing additive QT prolongation? (U)

A

Nilotinib

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34
Q

Which SSRI is most responsible for causing additive QT prolongation? (U)

A

Citalopram (Celexa)

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35
Q

What’s the max dose of citalopram to prevent additive QT prolongation?

A

40mg/d

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36
Q

When is 20mg citalopram the max dose to prevent additive QT prolongation?

A 
60+ years
Liver impairment
HF 
S/P MI
2C19 poor metabolizer
Pt on 2C19 inhibitors
Taking QT prolonging drugs
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37
Q

Whats the max dose in for Escitalopram (Lexapro) to prevent additive QT prolongation?

In the elderly?

A

20mg/d

Don’t exceed 10mg/d

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38
Q

What’s the preferred antidepressant in cardiac pts to prevent QT prolongation?

A

Sertraline (Zoloft)

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39
Q

What antidepressant should be avoided if pt has cardiac risk?

A

Citalopram

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40
Q

Which antiemetic agent is most responsible for causing additive QT prolongation? (U)

A

5-HT3-receptor antagonists (Dolasetron, Ondansetron, Granisetron, Palonosetron)

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41
Q

Which antipsychotic is most responsible for causing additive QT prolongation? (U)

A

Thioridazine

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42
Q

Which other agent is most responsible for causing additive QT prolongation? (U)

A

Methadone

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43
Q

What’s the 2 main reasons antiarrhythmic drugs are used?

A

Class I and III (used to terminate arrhythmias and restore and maintain normal sinus rhythm)

Class II and IV and Digoxin (used to slow ventricular rate during a Supraventricular arrhythmias)

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44
Q

What class of antiarrhythmic drugs is used to terminate arrhythmias and restore and maintain normal sinus rhythm?

A

Class I and III
Disopyramide, Quinidine, Procainamide,
Lidocaine, Mexiletine, Phenytoin,
Flecainide, Propafenone,

Amiodarone, Ibutilide, Dofetilide, Dronedarone, Sotalol (AIDDS)

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45
Q

What class of antiarrhythmic agent is used to slow ventricular rate during a Supraventricular arrhythmias?

A

Class II
Beta-blockers e.g. Esmolol, Propranolol)

Class IV
Verapamil, Diltiazem

Digoxin

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46
Q

What must be done prior to starting any medication for NON-LIFE-THREATENING arrhythmia? (U)

A

Check pts electrolytes

AND

Run a toxicology screen

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47
Q

What’s the Vaughan Williams classification of antiarrhythmics?

A

Class I a, b, c

Class II

Class III

Class IV

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48
Q

List drugs that are listed as class Ia.

A

Double Quarter Pounder

Disopyramide

Quinidine

Procainamide

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49
Q

List drugs that are listed as class Ib

A

Lettuce, Mayo, Pickles

Lidocaine

Mexiletine

Phenytoin

50
Q

List drugs that are listed as class Ic

A

Fries Please

Flecainide

Propafenone

51
Q

List drugs that are listed as class II

A

Beta-blockers e.g. Esmolol, Propranolol

52
Q

List drugs that are listed as class III

A

AIDDS

Amiodarone

Ibutilide

Dofetilide

Dronedarone

Sotalol

53
Q

List drugs that are listed as class IV

A

Verapamil

Diltiazem

54
Q

How are class I antiarrhythmics sub-classified?

A

They are Na channel blockers.

They are divided based on the DURATION of time they bind to Na channel

Ia - Intermediate Na channel blockers and they also block K channel

Ib - Fast Na channel blockers

Ic - Long Na channel blockers

55
Q

Define class Ia antiarrhythmics

A

INTERMEDIATE Na + K channel blockers

Double Quarter Pounder

Disopyramide

Quinidine

Procainamide

56
Q

Define class Ib antiarrhythmics

A

FAST Na channel blockers

Lettuce, Mayo, Pickles

Lidocaine

Mexiletine

Phenytoin

57
Q

Define class Ic antiarrhythmics

A

LONG Na channel blocker

Fries Please

Flecainide

Propafenone

58
Q

Which class I sub- Grp especially have a black box warning?

A

Class Ic (fries pls - Flecainide, Propafenone)

59
Q

MOA of class Ia antiarrhythmics?

A

REDUCE conduction velocity and automaticity

INCREASE refractory period

60
Q

What’s the black box warning associated with Quinidine (class Ia)? (U)

A

Control AV conduction BEFORE initiating

61
Q

SE of quinidine (class Ia)? (U)

A

Diarrhea (35%)

Stomach cramping (22%)

QT prolongation

Nausea/vomiting

Anorexia

Lightheadedness

Cinchonism (tinnitus, hearing loss, blurred vision, headache, delirium)

62
Q

Are the different salts of quinidine interchangeable

A

No!

267mg of gluconate = 200mg of sulfate form

63
Q

What’s unique about Procainamide injection metabolite? (U)

A

Has a active metabolite - N-acetyl Procainamide (NAPA)

64
Q

What’s the black box warning associated with Procainamide injection?

A

Fatal blood dyscrasias e.g. Agranulocytosis

Long-term use -> Positive antibody (ANA) in 50% of pts which may result in DRUG-INDUCED LUPUS ERYTHEMATOSUS-like syndrome

65
Q

SEs of Procainamide injection?(u)

A

Hypitension

Rash

Lupus-like syndrome

QT prolongation

Agranulocytosis

66
Q

What’s the SE of Disopyramide?

A

Anticholinergics effect (xerostomia, constipation, urinary constipation)

67
Q

Effect of class Ia agents (double quarter pounder) on QT prolongation?

A

ALL class Ia can have additive QT prolongation with other agents that also prolong the QT interval

68
Q

What are class Ib agents (Mayo, Lettuce, Pickles) ONLY used for?

A

Ventricular arrhythmias (no efficacy for Supraventricular arrhythmias such as AFib)

69
Q

T/F? All class Ib antiarrhythmics can’t cross the blood-brain barrier.

A

False.

All can cross the blood-brain-barrier

70
Q

When are class Ic agents absolutely contraindicated?

A

Patients with heart failure (HF)

OR

Those who just experienced an acute myocardial infarction (MI)

71
Q

MOA of class II antiarrhythmics (Esmolol, Propranolol)?

A

Block beta-blockers

AND

Indirectly block Ca channels in the SA and AV nodes

72
Q

What are class II antiarrhythmics (Esmolol, Propranolol) used for? (U)

A

To slow the ventricular rate in Supraventricular tachyarrhythmia (eg. AFib)

73
Q

MOA of class III agents? (AIDDS)

A

Blocks K channels -> significant increase in refractory period

74
Q

What’s the exception to the MOA of class III agents?

A

Ibutilide - works by activating the late inward Na current which also results in increased refractory period

75
Q

In addition to blocking K channel, what other channels/receptors do Amiodarone and Dronedarone act on?

A

They also block

Alpha-adrenergic receptors

Beta-adrenergic receptors

Ca channels

Na channels

76
Q

In addition to blocking K channel, what other channels/receptors do Soltalol act on?

A

Significant B-adnerergic receptor blocker

77
Q

What’s the class of amiodarone? And brand name?

A

Class III

Cordarone
Pacerone
Nexterone

78
Q

What’s the black box warning of amiodarone?

A

Pts should be hospitalized when therapy is initiated becuz of (pulmonary toxicity, liver toxicity, proarrhythmic)

79
Q

SE of amiodarone (cordarone/pacerone/nexterone)

A

Hypotension (IV only)

GI upset

Hypo/hyperthyroidism (more hypo than hyper)

Dizziness

Bradycardia

Peripheral neuropathy/paresthesias

Ataxia

Tremor

Corneal microdeposits, Optic neuritis

Pulmonary fibrosis

Photosensitivity

Increased LFTs

Slate blue (blue-grayish) skin discoloration

80
Q

What considerations are taken when amiodarone (cardarone, pacerone, nexterone) will be infused over 2 hrs?

A

Should be admin in a non-polyvinyl chloride (non-PVC) container should as polyolefin or glass

Recommended to be added to D5W

81
Q

What’s the advantage of premixed IV bag? (U)

A

Longer stability

PVC bag not an issue

Available in most commonly used conc

If hypotension occurs, can slow rate or d/c

82
Q

What’s the half- life of amiodarone?

A

40-60 days

83
Q

When’s amiodarone recommended? (U)

A

Drug of choice I pts with concomitant heart failure

84
Q

Which is the class III agent has to be given with meals?

A

Dronedarone - 400mg PO BID with meals

85
Q

What’s the black box warning of Dronedarone?

A

HF (class IV or any class with a recent hospitalization)

AND

In pts with permanent AFib

86
Q

SE of Dronedarone? (U)

A

QT prolongation

Bradycardia

Increased SCr (and possibly BUN)

Diarrhea

Nausea

Hypokalemia

Hypomagnesemia

87
Q

What’s the pregnancy cat. of Dronedarone?

88
Q

When’s Dronedarone used?

A

Only in pts who can be converted to normal sinus rhythm

89
Q

Which class III agent requires a REMS program?

A

Dofetilide (Tikosyn)

90
Q

What’s T.I.P.S?

A

Tikosyn (Dofetilide) in pharmacy system - allows retail pharmacies to stock and dispense Tikosyn

91
Q

What’s the monitoring parameters for Tikosyn (Dofetilide)?

A

ECG

Renal fxn

K

Mg

HR

BP

In the first few days

92
Q

What’s the effect of ALL class III agents on QT prolongation?

A

Can have additive QT prolongation with other agents that also prolong the QT interval

93
Q

What should be considered wrt to electrolytes and ALL anti-arrhythmic?

A

Electrolyte abnormalities (k, Na, Ca, Mg) should be corrected before any antiarrhythmics is initiated

94
Q

What’s the consequence of not correcting electrolyte before initiating antiarrhythmics?

A

Risk of arrhythmia is increased

95
Q

What should be avoided with use of class III antiarrhythmics?

A

Grapefruit juice/pdts

Ephedra

St. John’s wort (P-glycoprotein inducer)

96
Q

What meds should be reduced when starting amiodarone? By how much?

A

Digoxin (reduce by 50%) and Warfarin (reduce by 30%-50%)

97
Q

What class of drugs should use lower doses with amiodarone?

A

Simvastatin, Lovastatin, Atorvastatin

98
Q

T/F? Monitor INR after initiating Dronedarone in pts with Warfarin

99
Q

MOA of class IV agents?

A

They block L-type Ca channels, slowing SA and AV nodal conduction velocity

100
Q

Uses of class IV agents?

A

Used to slow ventricular rate in Supraventricular tachyarrhythmia

101
Q

List agents under class IV antiarrhythmics?

A

Diltiazem (Cardizem)

Verapamil (Calan/ Verelan/ Covera HS)

102
Q

What type of CCBs are used in antiarrhythmics?

A

Only non-dihydropyridine CCBs are used

103
Q

When is CCB is preferred over b-blocker in pts with arrhythmias?

A

If co- existing asthma/COPD in pts

104
Q

Other antiarrhythmics not included in Vaughan Williams classification?

A

Adenosine (Adenocard)

Digoxin (Lanoxin)

105
Q

MOA of adenosine?

A

Slows conduction through the AV node via activation of adenosine-1 receptors

106
Q

Uses of adenosine in arrhythmias?

A

Used to restore normal sinus rhythm in Supraventricular re-entrant tachyarrhythmia

107
Q

Effects of digoxin?(u)

A

Digoxin enhances vagal tone, resulting in decrease ventricular rate in atrial tachyarrhythmia

108
Q

What’s the brand name of digoxin? (U)

109
Q

What’s the therapeutic range of digoxin (lanoxin) for AFib?

A

0.8-2 ng/mL

110
Q

What’s the antidote for Digoxin (lanoxin)?

111
Q

Whats the first signs of digoxin (lanoxin) toxicity? (U)

A

Nausea/vomiting

Loss of appetite

Bradycardia

112
Q

Other signs of digoxin (lanoxin) toxicity? (U)

A

Blurred/ double vision

Altered color perception

Greenish-yellow halos around lights or objects

Abdominal pain

Confusion

Delirium

Arrhythmia (prolonged PR interval, accelerated junctional rhythm, bidirectional ventricular tachycardia)

113
Q

Is digoxin (lanoxin) used alone?

A

No!

Used in combo with b-blockers or CCB

114
Q

Since digoxin is mostly renally cleared, whats the concern with digoxin (lanoxin) use here?

A

In decreased renal fxn -> reduce digoxin dose

In acute renal failure -> hold digoxin

115
Q

What increases risk of digoxin (lanoxin) toxicity?

A

Hypokalemia (K < 3.5 mEq/L)

Hypomagnesemia

Hypercalcemia

116
Q

Role of medication guide in amiodarone dosing?

A

Dispense medication guide with amiodarone

117
Q

Should amiodarone be taken with food?

A

Amiodarone can be taken with/ without food.

BUT, if you should stick to which ever method you use e.g. If you start taking amiodarone with food, then you need to continue taking it with food, while on the med

118
Q

What body organs need to be monitored while in amiodarone?

A

Eyes - vision should be checked before and during the time you’re using amiodarone

Blood - blood should be checked regularly

Chest x-ray during tx

Thyroid

Liver

Lungs

119
Q

Photosensitivity and amiodarone?

A

Amiodarone may cause your skin to be more sensitive to the sun.

Stay out of the sun

120
Q

What’s the brand name for Dronedarone?

121
Q

What’s the potassium safe range for pt on digoxin?

A

3.5-5 mEq/L

122
Q

What’s arrhythmias?

A

Caused by abnormalities in the formation and/or conduction of these electrical impulses

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