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Anti-arrhythmics Flashcards

1
Q

Rapid depolarization due to influx of Na ions.

Action potential -> cell depolarizes and contraction begins

A

Phase 0

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2
Q

Early rapid depol due to K+ moving out of the cell

Contraction is in process

A

Phase 1

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3
Q

Plateau phase mainly due to inward mvmt of Ca+ into muscle cell

A

Phase 2

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4
Q

Repolarizaion, as K+ moves out of cell

A

Phase 3

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5
Q

K+ flows out and Na+ seeps into cell (return to resting level)

A

Phase 4

Sympathetic stimulation increases the rate of pahse 4 depol, increasing HR

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6
Q

Interval during which a 2nd action potential cannot be initiated, no matter size

A

Absolute refarctory period

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7
Q

Interval following the relatiev refractory period when a second action potential is inhibited, but not impossivle

A

Relative refractory period

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8
Q

Electrical impulses travel through AV node slowly, but reach ventricles

Results in PR prolongation

A

1st degree heart block

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9
Q

Impulses travel slowly and occasionally get blocked, causing ventricles to beat out of sequence

A

2nd degree heart block

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10
Q

Atrial impulses do not reach ventricles so ventricles create their own impulse, cause them to beat out of sequence

Life threatening

A

3rd degree heart block

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11
Q

Torsades de Pointes typically occurs at QT interval > 500 ms.

What are some causes of TDP?

A

Hypokalemia

Hypomagnesemia

Drugs (see next slide/card)

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12
Q

Anti-arrhythmics that cause TDP?

A

Sotalol
Amiodarone
Quinidine

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13
Q

Abx that cause TDP?

A

Macrolides (Azithromycin!, Clarithromycin, Erythromycin)

Fluoroquinolones (Moxifloxacin)

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14
Q

Anti-nausea drugs that cause TDP?

A

Odansetron

Granisetron

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15
Q

Antidepressants that cause TDP?

A

Citalopram
Fluoxetine
Amitriptyline

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16
Q

Antipschotics that casue TDP?

A

Typical anti-psychotics (Haloperidol, chiefly)

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17
Q

Can sumatriptan cause TDP?

A

Yes

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18
Q

Supraventricular arrhythmias?

A

AFib (Fast/irregular, HF, Ischemic stroke)

Aflutter (Fast/regular, reentrant rhythm)

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19
Q

Paroxysmal SVTs can occur due to?

A

digitalis toxicity, caffeine intake, anxiety, alcohol, WP

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20
Q

V Tach?

A

More than 3 straight beats at a rate > 120

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21
Q

Lengthen refractory period

Decrease automaticity

Decrease conduction velocity

A

Class 1A (Na channel blocker)

Procainamide
Disopyramide
Quinidine

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22
Q

Weak Na channel blocker

Shorten phase 3 repolarization

Possess local anesthetic acitivity

A

Class 1B (Fast Na channel blocker)

Lidocaine
Mexiletine

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23
Q

Slow conduction velocity with little effect on refractory period

Useful in supraventricular and ventricular arrhythmias (caution w/ ventriculars, however?)

A

class 1C (potent Na channel blocker)

Flecainide
Propafenone

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24
Q

Block catecholamines

Lengthen refractory period

Decrease automaticity

A

Class 2 (beta b’s)

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25
Q

Prolongs phase 3

K channel blcoker

A

Class 3

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26
Q

Inhibits SA/AV node, prolonging refarctory period

SLows conduction

Decrease automaticity

A

Class 4 (CCBs)

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27
Q

Increase QRS and QT

Used for Atrial/Ventricular arrhythmias

A

class 1A

Procainamide
Disopyramide
Quinidine

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28
Q

Decrease QT interval

Used for ventricular arrhythmias

A

Class 1B

Lidocaine
Mexiletine

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29
Q

Increase QRS

USed for Atrial and ventricular arrhythmias

A

Class 1C

Flecainide
Propafenone

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30
Q

Decrease HR and increase PR

Used for Tachyarrhythmias caused by sympathetic activity and Supraventricular/ventricular arrhythmias

A

Class 2 (beta b’s)

Metoprolol
Atenolol
Propranolol
Esmolol

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31
Q

Increase QT interval

Used for Atrial and ventricular arrhythmias

(note that these DO NOT increase QRS like the class 1As… otherwise very similar)

A

Class 3 (K-channel blocker)

Amiodarone
Sotalol (beta-ish)
Ibutilide
Difetilide
Dronedarone
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32
Q

Decrease HR and increase PR

USed for Atrial arrhythmias (fib/flutter) and reentrant Supraventricular

A

Class 4 (CCBs)

Verapamil
Diltiazem

33
Q

Class 1A drug

Anticholinergic properties

Atrial flutter/A-fib

Metabolized by CYP3A4

Inhibited by CYP450

A

Quinidine

by inhibiting CYP450 = increase digoxin effects/toxicity as well as anticoagulation effects of warfarin

34
Q

Diarrhea

Anticholinergic properties

Skeletal muscle weakness

High doses -> fatal v-tac and arrhythmias

Cinchonism

35
Q

Most frequently used 1A agent

Used after lidocaine/amioadarone for ventricular arrhythmias associated w/ MI

Oral route common – IV can lead to HOTN

Short half life

NAPA (prolongs AP)

A

Procainamide

36
Q

QT interval prolongation

Long term = lupus-like syndrome (increases ANAs)

Arthralgia/arthritis

A

procainamide

37
Q

Reserved only for tx of ventricular arrhythmias unresponsive to procainamide/quinidine

(fallen out of favor)

A

disopyramide

38
Q

USed in v-tac w/ a pulse

Alternative agent for pulseless VT/VF (if amiodarone isn’t available)

IV/IM only (extensive first pass effect)

Adjusts dose in CHF/hepatic dz

A

Lidocaine (class 1B)

39
Q

Least cardio toxic of Na channel blockers

BUT contraindicated in 3rd degree HB

A

Lidocaine (class 1B)

40
Q

Orally active form of Lidocaine

Narrow therapeutic index

Dyspepsia (most common SE)

Contraindicated in 3rd degree HB (like lido)

(off label for diabetic neuropathy/nerve injury)

A

mexiletine (class 1B)

41
Q

Class 1C “pill in pocket”

Possesses neg inotrope effects which can exacerbate HF

Contraindicated in HF, CAD, valvular dz

A

Flecainide

42
Q

Class 1C w/ weak beta-blocking properties

“pill in pocket approach”

metallic taste

A

Propafenone

43
Q

DOC in a-fib/a-flutter?

What else should a pt w/ a-fib be started on?

A

Class 2 (beta b’s)

Also start on anticoagulation therapy to prevent clot prevention

44
Q

Caution w/ DM, asthma, lipid abnormalities

DO NOT use acutely to control ventricular response in HF

A

Class 2 (beta b’s)

Metoprolol
Atenolol
Propranolol
Esmolol

45
Q

Given its very short half life (IV only), what would you use for an emergency (e.g., aortic dissection)?

Also used intraoperatively for BP/HR?arrhythmias

Metabolized extensively by esterase (no drug interaction)

46
Q

Prolongs phase 3 - block K-channel

Used for rhythm control, rate control and atrial/ventricular arrhythmias

A 
Amiodarone
Sotalol
Ibutilide
Dofetilide
Dronedrone
47
Q

Related to iodine/thyroxine

DOC in pulseless v-tac (cardiac arrest)

BUT contraindicated in:

  • iodine sensitivty/hyperthyroidism
  • 3rd degree HB
A

amiodarone (class 3)

48
Q

LONNNNGGGG half life (1-3 month effect)

Inhibits CYP3A4 (so increases statins, digoxin, warfarin)

Additive brady w/ (nonDHP CCBs, b-blockers)

A

amiodarone (class 3)

49
Q

Adverse effects…

CNS, liver toxicity (monitor), hypo/hyperthyroidism (monitor), **BLUE GRAY SKIN

***PULMONARY FIBROSIS (CXR, pulmonary function test q 6-12 months)

A

amiodarone (class 3)

50
Q

derivative of amiodarone

Shorter half life

Inhibitor of CYP3A4

QT prolongation

A

dronedarone (class 3)

51
Q

Contraindicated:

higher level HF

QT>500

Severe hepatic impairment

2nd, 3rd degree HB (like sotalol)

Bradycardia

A

dronedarone (class 3)

52
Q

Used for Life-threatening ventricular tachyarrhythmia and supraventricular arrhythmias and maintenance of sinus rhythm in pts w/ a fib

A

sotalol (beta blocker properties, BUT classified as a K channel blocker)

53
Q

BLACK BOX warning: if initiated on this drug, should be be monitored in a facility that can provide cardiac resuscitation for 3 days

A

Sotalol (k-channel blocker)

Also be wary of bronchospam

54
Q

Contraindicated in:

HFrEF<40

CrCl < 40

Sinus bradycardia

2nd/3rd degree HB (like dronedrone)

A

Sotalol (k-channel blocker)

55
Q

Indicated for conversion of a-fib/a-flutter and maintenance of normal sinus rhythm

100% bioavailable

Black box: must be hospitalized for initiation and obtain a QTc 2-3 hours after first 5 doses

A

Dofetilide

56
Q

Contraindicated in pts w/ CrCl < 20 or QTc>400

TDP risk is high

A

Dofetilide

57
Q

Effect on the SA node is to slow depolarization and decrease HR

But more importantly, it slows conduction at the AV node

More effective agaisnt atrial (than ventricular) arrhythmias

A

CCB (class 4)

Verapamil
Diltiazem

Both nonDHPs

58
Q

Cardiac glycoside slightly increasing cardiac contractility

Stimulates vagus nerve

SO, slows SA/AV nodes -> slowing HR

59
Q

Positive inotrope that is rec’d to cotnrol ventricular respone to a-fib/a-flutter

CYP3A4 (minor substate)

60
Q

Potassium and digoxin… sup with it?

A

They compete for binding sites. So, hypokalemia results in increased digoxin effects (and hyperkalemia decreases digoxin effects)

61
Q

Concentration greater than 2ng/ml can cause ectopic ventricular bears -> v-tac -> fibrillation -> cardiac arrest

Also, Xanthopsia, anorexia, HA, disorientation

62
Q

DOC for acute covnersion of regular rhythm paroxysmal supvraventricular tachycardia

Increases K efflux, decreases Ca influx (SO, causes a slowing of HR)

Only used in acute/emergencies

63
Q

***Super mega ultra short half life

FOllow each dose with a NaCl push!!

6 then 12 mg dose

A

Adenosine

can lead to asystole

64
Q

Most common arrhythmia… prevalence increases w/ age

can develop from a flutter

A

A fib (ventricular rate > 140)

65
Q

Paroxysmal a fib?

Persisent a fib?

A

Paroxysmal = self resolves w/ in 7 days

Persistent > days

66
Q

Rate control vs rhythm control?

A

Rate is AT LEAST as good as rhythm, but rhythm drugs have more risks than risk drugs

67
Q

In patients w/ HF, what arrhythmia drugs should be avoided?

A

Class 1A, 1C (also avoid these in acute MI)

Dronedarone is also CI

68
Q

For ventricular rate control, beta blockers are effective for controlling exercise-associated HR increases… What three beta blockers can be considered in pts w/ stable HF?

BUT avoid these in WPW

A

Bisoprolol
Carvedilol
Metoprolol

69
Q

Given beta blockers pulmonary effects, what could we use for ventricular rate control in pts w/ COPD/asthma?

A

Class 4 (nonDHP CCBs)

Verapamil
Diltiazem

70
Q

Can be used as an additional HR control measure (w/ b-blocker, diltiazem, or verapamil) but never alone?

71
Q

Amiodaraone can be use for ventricular control when?

A

AFTER trying b-blockers, non-DHP CCBs, and digoxin

72
Q

If patients have a-fib, what what to determine reisk of stroke?

A

CHA2DS2VASc (>2 = anticoagulant warfarin; less than 2 cosnider aspirin)

73
Q

Electrical cardioversion is first line for stable pts in A-Fib . What should you ensure absence of?

A

Ensure absence of atrial thrombi! (use a transesophageal echocardiogram)

74
Q

Chemical cardioversion for A-fib?

A

Pill in pocket approach…

Class 1C antiarrhythmics (flecainamide, propafenone)

Contraindicated in patients w/ structural heart dz

75
Q

Another method for chemical cardioveaion of A-Fib if Class 1C drugs don’t work… (or if they’re contraindicated)

A

Amiodarone

76
Q

What coudl we use in symptomatic bradycardia?

A

Atropine

Blocks effects of Ach on vagus nerve. Elevates sinus rate and AV nodal/SA conduction

77
Q

In an acute setting, what could we use for Paroxysmal supraventricular tachycardia?

A

Adenosine

alternatively, try a vagal maneuver, verapamil, diltizaem, beta-blockers, or digoxin

78
Q

Drugs for v-tac/pulseless fibrillation

A

Epi (NOT an antiarrhytmic)

  1. Amiodarone (slow IV)
  2. Lidocaine
  3. Procainamide
79
Q

Drugs for TDP?

A
  1. Magnesium (IV!)

slows rate of SA node

Pharm 2 (5 decks)

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