Anti-Arrhythmic Flashcards

1
Q

4 ways of decreasing spontaneous activity

A

Decrease phase 4 slope
Increase threshold
Increased maximum diastolic potential (hyperpolarize)
Increase APD

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2
Q

2 ways of increasing refractoriness

A

Na channel blockers - shift voltage dependence of recovery - delay Na recovery
AP prolonging drug - extend ERP w/out interacting w/Na channels

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3
Q

State dependent blockade

A

block fast inward Na channels when in open/inactivated but not resting

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4
Q

MOA Class I agents

A
Block fast inward Na channels to varying degrees in conductive tissue
Decrease Vmax 
Reduce automaticity
delay conduction
prolong ERP
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5
Q

Class 1a Na targets

A

open > inactive

dissociation in seconds

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6
Q

MOA Quinidine

A

moderate binding to Na = decrease Vmax
block K = increase APD
block alpha adrenergic = decrease BP
block M2 = increase HR

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7
Q

TX Quinidine

A

Mainly used in refractory pts to:
convert AF/AFl
prevent recurrence of AF
Treat life-threatening ventricular arrhythmias

Also atrial/ventricular arrhythmias (re-entrant SVT, VT)

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8
Q

AE Quinidine

A

N/V/D - most common
cinchonism
hypotension (adrenergic)
proarrhythmic - TdP (QT)

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9
Q

1a agents

A

Quinidine
Procainamide
Disopyramide

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10
Q

MOA Procainamide

A

block Na = slow conduction, automaticity, excitability of A/V/Purk
block K = prolong APD and refraactoriness

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11
Q

Quinidine vs Procainamide

A

Procainamide has little vagolytic activity and does not prolong QT as much

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12
Q

TX Procainamide

A

Life-threatening ventricular arrhythmias**
Ventricular arrhythmias immediately post MI
convert VT

Acute supraventricular:
Re-entrant SVT
A fib
A flutter w/WPW

Requires adequate time - not emergency

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13
Q

AE Procainamide

A
Arrhythmia aggravation
TdP - contraindicated in long QT, HX of TdP, hypo-K
heat block/sinus node dysfunction
SLE like syndrome
GI N/V - common
Decrease kidney fx
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14
Q

1b Na channel

A

inactive&raquo_space;» open

dissociate in under 1s

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15
Q

1b agents

A

Lidocaine

Mexiletine

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16
Q

MOA Lidocaine

A

block inactivated&raquo_space; open Na = reduced Vmax
shorten AP
more effective in ischemic tissue
lower slop of phase 4 = lower threshold for excitability
slows ventricular rate
potentiates infranodal block

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17
Q

TX Lidocaine

A

Used to be first-line for ventricular arrhythmias (post MI)
Now - second choice for immediate life-threatening or symptomatic arrhythmias
Ineffective:
prophylaxis after MI
Atrial tissue

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18
Q

PKX Lidocaine

A

Extensive first pass - IV use

Multiple loading doses and maintenance infusion

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19
Q

AE Lidocaine

A

Rapid bolus: tinnitus, seizure
High dose: drowsy, confused, hallucination
CV decreased

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20
Q

1c agents

A

Propafenone

Flecainide

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21
Q

1c Na channels

A

Strongest binding to Na channels
O state
slow dissociation = strong effects on p0 depol

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22
Q

MOA Propafenone

A

strong inhibitor of Na channel
can inhibit B-adrenergic
structurally similar to propranolol

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23
Q

TX Propafenone

A
Ventricular arrhythmias in pts w/ no HD and preserved ventricular fx
atrial arrhythmias (Afib, PSVT)
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24
Q

MOA Flecainide

A

potent Na channel blockade = prolonged p0 + wide QRS

markedly slows intraventricular conduction**

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25
Q

TX Flecainide

A

ONLY life-threatening ectopic ventricular arrhythmias

Not first line agent - fatal proarrhythmic

26
Q

AE 1c

A

proarrhythmic especially post-MI

Contraindicated in structural and ischemic HD

27
Q

MOA Class II agents

A

B-blockers

decrease cAMP/Ca = decrease SA node automaticity, AV node conduction, ventricular contractility

28
Q

TX Class II

A

Supraventricular arrhythmias (sympathetic)
ONLY drug effective in preventing sudden cardiac death post-MI
NOT effective in severe arrhythmias (recurrent VT)

29
Q

Esmolol

A

very short t.5 - only IV
No ISA, no membrane depressant
little/no bronchospasm
useful for short term B-blockade (aortic dissection, critically ill, post-op HTN)

30
Q

Class II AE

A

Impotence
COPD/asthma exacerbation
Bradycardia, AV block, HF - mask signs of hypo-G
CNS sedation
Dyslipidemia (metoprolol)
Exacerbation of angina (propranolol)
contraindicated in pheochromocytoma or cocaine (except carvedilol and labetalol)

31
Q

TX of B-blocker overdose

A

Saline
Atropine
Glucagon

32
Q

MOA class III

A

Multiple effects at K, Ca, Na and autonomic

Main: prolong phase 3 repol = increased QT

33
Q

Class III agents

A
Amiodarone
Ibutilide
Dofetilide 
Dronedarone
Sotalol
34
Q

MOA Amiodarone

A
block K = long APD/refractory
Block Na (inactivated)
block Ca = slow SA P4 
Slow AV node conduction
noncompetitive blockade of a, B, M
35
Q

TX Amiodarone

A

Widely used
Conversion of AF - maintain sinus rhythm - DOC*
AVNRT*
WPW tachycardia
Oral - LT VT or resistant VF
IV - acute termination of VT/VF - replacing lidocaine for out-of-hospital cardiac arrest

36
Q

PKX Amiodarone

A

Lipophilic
metabolized to DEA - potent
responsible for early arrhythmias after discontinuation

37
Q

AE Amiodarone

A

Lethal pulmonary fibrosis
Hyper/hypothyroidism
Elevated hepatic enzymes
Check PFTs, LFTs, TFTs

38
Q

MOA Ibutilide

A

Block rapid component of delayed rectifier K = slow repol

Activate slow inward Na = prolong AP

39
Q

TX Ibutilide

A

IV - acute conversion of AF/AFl to NSR (20 min)

40
Q

AE Ibutilide

A

Excessive QT prolongation

TdP - continuous ECG monitoring for 4h

41
Q

MOA Dofetilide

A

Block delayed rectifier K current

does not block other K

42
Q

PKX Dofetilide

A

100% bioavailable
Verapamil - increased peak plasma
Cimetidine - prolong t.5

43
Q

TX Dofetilide

A

Restore/maintain NSR in A-fib

44
Q

AE Dofetilide

A

dose-dependent QT prolongation

ventricular proarrhythmia

45
Q

MOA Sotalol

A
B-blocker
AP prolonging (K)
46
Q

TX Sotalol

A

Life-threatening ventricular arrhythmias

Children SV/V arrhythmias

47
Q

AE Sotalol

A

TdP

LV depression w/HF

48
Q

Class IV agents

A

Verapamil

Diltiazem

49
Q

MOA Class IV

A

Ca channel antagonists
Similar to Class II w/ primary effects on nodal p0
Incomplete blockade

50
Q

Major CV actions of Class IV

A

Negative chronotrope, dromotrope, inotrope

51
Q

Class IV TX

A

Systemic HTN
Angina pectoris
SVT
Post-infarct protection

52
Q

Verapamil MOA

A

block slow inward Ca channels in nodal tissue
Decrease SA automaticity, HR, AV conduction (increase PR), increase ERP
Ineffective on ventricular arrhythmia

53
Q

Verapamil TX

A
PO - prevention
IV - conversion 
nodal arrhythmias (PSVT)
Rate control - A-fib
angina pectoris
HTN
54
Q

AE Verapamil

A
HA
Constipation
Exacerbate CHF
Hypotensino
AV block w/B-blocker
55
Q

Contraindication Verapamil

A

Sick sinus syndrome
Pre-existing AV nodal dz
WPW w/Afib
V-tach

56
Q

MOA Adenosine

A

A1 receptor in SA/AV = increase K =
SA node hyperpol and low firing rate
Short APD
Depression of AV conduction velocity

A2 receptor
Increase endothelial Ca
Increase NO
Vasodilation

57
Q

TX Adenosine

A

Acute conversion of paroxysmal supraventricular tachycardia cause by reentry bypass

58
Q

PKX Adenosine

A

IV bolus to central vein

Blunted by adenosine antagonist - caffeine, theophylline

59
Q

TX Mg

A

TdP

Digitalis arrhythmias

60
Q

TX Bradycardia

A

Atropine - vagal block
Isoproterenol - B1 agonist
Pacemaker

61
Q

TX Sinus Tachycardia, PSVT

A

vagal stimulation
carotid massage
Valsalva