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Pharm II Exam 2 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

PSVT

A

paroxysmal supraventricular tachycardia

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2
Q

predominant pacemaker

A

SA node

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3
Q

lethal arrhythmia

A

v. fib

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4
Q

causes of arrhythmia

A

digoxin (25%)
anesthesia (50%)
AMI (80%)

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5
Q

Slow response fibers

A

SA node

AV node

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6
Q

fast response fibers

A

Atria
Ventricles
Bundle of His
Purkinje cells

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7
Q

Highest automaticity

A

SA node (sets HR)

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8
Q

lethal arrhythmias can be causes by

A

antiarrhythmic agents

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9
Q

Channels for slow acting fiber (SA and AV)

A

calcium channels

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10
Q

ERP

A

shortest interval at which a premature stimulus results in a propagated response (phase 0., 1, 2, and most of 3)

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11
Q

ERP length of ADP

A

ERP is ~85% of APD

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12
Q

AP in purkinje cell phases

A

Phase 0: opening of Na channels, rapid depol, inactivaiton of Na channels

Phase 1: rapid partial repol due to inactivation of fast Na channels and increased K+c channel permeability

Phase 2: plateau: Ca (L-type) and some Na (“window” or late current” channels are open)

Phase 3: Repolarization: Ca channels inactivated and K+ channels open, Na channels turning to rest

Phase 4: resting membrane potential

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13
Q

SA node AP phases

A

Phase 4: funny sodium current (spontaneous depol)
Phase 0: T-type Ca open and start to depol, then L-type Ca cause AP
Phase 1: Ca channels close, K+ activated
Phase4: spontaneous regeneration via Na funny channels

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14
Q

Causes of arrhythmia

A

distrbuance in impulse generation
impulse conduction
both

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15
Q

Precipitating factors of arrhythmias

A 
ischemia, hypoxemia
alkalosis, electrolyte abrnomalities
Excess catecholamines
Drug toxicity (digoxin, antiarrhythmic)
Overstretched fiber
scarred/diseased tissue
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16
Q

Factors that decreases rate of pacemaker cells

A

Increase depol potential (more neg)
Increase AP duration
Increase slope of phase 4 depol (K+)
Increase threshold hypotential

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17
Q

Simple blocks

A

AV block

Bundle branch Block

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18
Q

Reentry mechanism

A

obstacle to homogenous conduction; unidirectional block; conduction time long enough to find excitable tissues

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19
Q

Aims of antiarrythmic therapy

A

reduce ectopic pacemaker activity

modify conduction or refractoriness to disable reentry

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20
Q

Mechanism of antiarrhythmic (sodium channel blockade)

A

Sodium channel block
block sympathetic effects (BB)
prolong ERP
Calcium channel blockade

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21
Q

Lengthen ERP

A

Active Na channel blockers (class 1a: quinidine, procainamide)

K+ channel blockers amiodarone, sotalol)

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22
Q

K+ channel blockers

A

amiodarone

sotalol

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23
Q

1a drugs

A

block activated Na channels; lenghten AP, inc. ERP

Quinidine, Procainamide

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24
Q

1b drugs

A

block inactivated Na channels
dec AP, dec ERP

Lidocaine

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25
Q

1c drugs

A

block all Na channels
no effect on AP, or ERP

Flecainide

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26
Q

Quinidine MOA

A

slows rate of rise (Vmax) in normal cells by blocking active Na+ channels
No depolarization in damaged cells

2ndary: Inhibits K+ channels (prolong AP and ERP)

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27
Q

When is quinidine used

A

“BROAD SPECTRUM”
acute and chronic supra and ventricular arrhythmias

rarely used due to effects

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28
Q

SE of quinidie

A

Cardiotoxic: SA, AV block, ventricular arrhythmia
Low therapeutic index
Cinchonism
DIARRHEA, n/v
block alpha rec: hypotension and reflex tach
paradoxical tach: “anticholinergic like effect”
Quinidine syncope - prolonged QRS and QT
TORSADES (inc. AP)

29
Q

Torsades due to

A

increasing AP

30
Q

Cinchonism

A 
loss of hearing
angioedema
vertigo
visual distrubance
thrombocytopenic purpura
tinnitus
vascular collapse
31
Q

Procainamide

A

hepatic metabolism – slow, fast acetylators

less alpha block - less atropine like effects

32
Q

SE of procainamide

A

LUPUS: slow acetylators (NAT2 gene)

33
Q

Class 1B drug

A

lidocaine

34
Q

MOA of Lidocaine

A

inhibits inactive Na channels
preferentially effects damaged cells (more inactive Na channels) – blocks the slow Na “window” current

dec. APD and ERP - via window current block

fast binding and dissociation

35
Q

Use of Lidocaine

A

acute ventricular arrhythmia

36
Q

why is lidocaine only used for ventricular arrhythmias

A

blocks Na window current – only present in purkinje and ventricular wall cells

37
Q

Why is lidocaine good

A

preferential for damaged cells (inactive Na channels)

least negative inotropic antiarrhythmic

38
Q

SE of lidocaine

A

bradycardia
paresthesia, convulsions

(lightheaded, tinnitus, mm. twitch, blurred vision, euphoria, hypotension)

39
Q

How often is lidocaine used?

A

ACUTE ONLY – prophylactice use can increase mortality

40
Q

Contra for lidocaine

A

caution in hepatic failure and HF (metabolized in liver)

41
Q

Worst drug for inducing arrhythmias

A

Flecainide

42
Q

Drugs for PSVT

A
  1. Adenosine
  2. Esmolol (IV)
  3. Verapimil
43
Q

Blocks K+ channels

A

Amiloride (main action)
Quinidine, Procainamide (2ndary action)

both thus increase APD

44
Q

All jobs of amiodarone

A 
K+ channel blocker (mainly)
Na+ channel blocker (class I)
BB (class II)
Some Ca channel blocking (IV)
Alpha blocker
45
Q

Alpha blockers

A

Amiodarone

Quinidine, procainamide

46
Q

DOC for ventricular arrhythmias

A

Amiodarone

47
Q

Amiodarone Use

A

supra and ventricular arrhythmias

DOC: Ventricular arrhythmias

48
Q

SE of amiodarone

A

dec sinus rate and conduction – prolonged QT w/o TORSADES**
Bradycardia, heart block HF
Deposits in tissue: brown/yello cornea, blue/gray skin, photodermatitis
Thyroid dysfunction
PULMONARY FIBROSIS

49
Q

Prolong QRS drugs

A

Quinidine, procainamide

Amiodarone

50
Q

sotalol MOA

A

class III - K+ channel blocker, BB (non-specific)

51
Q

Contraindications for sotalol

A 
BB contras:
Asthma
DM
end-stage HF
Bradycardic
Heart Block
52
Q

SE of sotalol

A

prolong QT - TORSADES!

53
Q

Cause Torsades

A

Quinine, procainamide

sotalol

54
Q

Class IV Drugs

A

Verapamil, Diltiazem

55
Q

MOA of verapamil

A

block L-type calcium channels; slows AV conduction (dec. HR)

56
Q

Use of verapamil

A

suptraventricular arrhythmias: a. flutter, a. fib

PVST (3rd line)

57
Q

SE of verapamil

A

negative inotrope
constipation
avoid combo w/ BB (bradycardia)

58
Q

Cause constipation

A

Verapamil, Diltiazam

Bile-acid sequesterants

59
Q

Adenosine MOA

A

increases K conductance and decreases cAMP-induce Ca influx – HYPERPOLARIZES and RESETS heart

only used in reentry arrhtythmias

60
Q

Adenosine is DOC for

A

PSVT

WPW Syndrome

61
Q

SE for adenoside

A 
SOB
chest burning
flush
hypotension
H/a, nausea
62
Q

Magnesium use

A

DOC: torsades
Seizures, HTN – eclampsia
Digital induced arrhythmias

63
Q

Potassium levels and arrhythmia

A

Both hypokalemia and hyperkalemia are arrhythmogenic

64
Q

MOA of potassium

A

makes resting potential more positive (depolarizes)
increases K+ has membrane stabilizing action by increasing K+ permeability, and this action predominates (HYPERPOLARIZES) – decreased APD

65
Q

Not effective for both supra and ventricular

A 
Class IV (Supra - CCB)
Class Ib (ventricular - inactive)
66
Q

Safest for prophylactic therapy

A

BB and CCB

67
Q

IV only drugs

A

lidocaine
adenosine
Mg

68
Q

Broadest drug w/ most effefcts

A

Flecainide

Pharm II Exam 2 (4 decks)

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