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Pharm Block 2 > Anti-arrhythmic > Flashcards

Anti-arrhythmic Flashcards

1
Q 
Sodium channel open
inward sodium depolarization
class 1 drugs affect this phase
A

phase 0 - fast response

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2
Q

sodium channel inactivated

outward K+ & inward chloride current contribute to notch & overshoot

A

phase 1 - fast response

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3
Q

inward L type Calcium and outward K+ current from plateau

A

phase 2 - fast response

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4
Q 
repolarization by outward K+ current, note that a slow inward Na+ current (window current) prolonging APD
class 3 drugs affect this phase
A

phase 3 - fast response

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5
Q

returning to resting potential by Na+/K+ ATPase

A

phase 4 - fast response

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6
Q

absolute no response to any stimuli

A

effective refractory period

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7
Q

strong stimulus can elicit a response, but not sync with rest of heart

A

relative refractory period

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8
Q

1) bradycardia, occurs with AV block

2) tachycardia, occurs when a reentrant circuit develops

A

mechanisms for arrhythmia

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9
Q

V max decrease

decrease conduction velocity

A

rate of phase 0 depolarization

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10
Q

less negative

slower conduction velocity

A

threshold potential

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11
Q

more negative the RP

faster conduction velocity

A

resting potential

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12
Q

pacemaker phase

inward Na+ funny & Ca2+ (T type) and inward K+ current

A

phase 4 - slow response

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13
Q 
inward Ca2+ (L type)
class 4 affect this phase
A

phase 0 - slow response

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14
Q

outward K+ current

classes 2 & 3 affect this phase

A

phase 3 - slow response

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15
Q

is innervated by PANS & SANS activated by M2 & B1 receptors

A

SA Node

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16
Q

In what phase is slope increased by increase in cAMP resulting from B1 activation and slowed by decrease in cAMP resulting from M2 activation

A

phase 4 of slow response

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17
Q

1) Increase upstroke velocity in pacemakers by increase calcium L type
2) shorten APD by increase K+
3) Increase HR by increase of funny Na thus increase slope of phase 4

A

Results of Increase cAMP

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18
Q

1) does opposite of increase cAMP
2) also produces K+ current, which slows the rate of diastolic depolarization and decrease HR
3) B Blockers prevent cAMP formation, with primary effects on SA and AV node tissues

A

Results of decrease cAMP

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19
Q

treats sinus bradycardia
makes slope steeped
blocks M2 causing increase cAMP, PKA & HR

A

Atropine

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20
Q

causes bradycardia

treats sinus tachycardia

A

Ivabradine

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21
Q

decrease slope of phase 0 upstroke (slows conduction of cardiac AP) AP will almost look tipped over with decrease slope by blocking sodium channels

A

Class 1

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22
Q

bind to open or inactivated sodium channels

A

class 1

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23
Q

use dependence - have greater effect on rapidly depolarizing tissues (increase heart rate causes slower phase 0 upstroke)

A

class 1

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24
Q

affect the sodium dependent cardiac AP (no action at the SA and AV nodes)

A

class 1

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25
Q

widen QRS complex (decrease AP conduction velocity) this will happen when the HR increases b/c that will increase effect of the drug

A

class 1

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26
Q

1) intermediate binding to Na channel
2) increase APD (dec phase 0)
3) block K+ ch prolonging phase 2 & 3 of AP = prolonged refractory period
4) treat SVT and ventricular arrhythmias

A

class 1A

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27
Q

1) use to treat atrial, AV juntion and ventricular tachycardia
2) block M receptor - increase HR & AV cond
3) block alpha 1 - postural hypotension and reflex tachycardia
4) effect dec by P450 inducers and enhance by P450 inhibitors

A

quinidine

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28
Q

1) cinchonism
2) severe headache
3) hypotension
4) prolong QT interval

A

ADR of quinidine

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29
Q

no anti M and anti alpha effect

metabolized by acetyltransferase

A

procainamide

30
Q

reversible lupus erythematous like synd.

prolong QT - torsades de point

A

procainamide ADR

31
Q

used to treat ventricular arrhythmias

contraindicated in HF

A

Disopyramide

32
Q

anticholinergic

negative inotropic effect (dec contractility)

A

Disopyramide ADR

33
Q

have low binding affinity to Na ch (dec APD)

shorten phase 2 & 3 of AP - shorten refractory period = no chance of tornadoes de point

A

class 1B

34
Q

treat ventricular arrhythmias (ischemic tissues) in Na ch. spending more time in open and resting state b/c of longer AP

A

class 1B

35
Q

greater tendency to work with ischemic heart problems

A

class 1B

36
Q

treats ventricular arrhythmias by IV
not useful in atrial arrhythmias
decreases APD
SE: CNS toxicity

A

lidocaine

37
Q

similar to lidocaine in action but given orally

A

Mexiletine

38
Q

other drugs in class 1B

A

phenytoin and tocainide

39
Q

strong binding affinity for Na ch (drastic slowing go phase 0) effects QRS, prolongs ERP in Av node, no change in APD

A

class 1C

40
Q

treats supraventricular (a fib) and ventricular arrhythmias; can restore and maintain normal sinus rhythm in a fib and flutter

A

class 1C

41
Q

Class 1C drugs

A

Flecainide

Propafenone

42
Q

Class 1B drugs

A

Lidocaine
Mexiletine
Phenytoin
Tocainide

43
Q

Class 1A drugs

A

Quinidine
Procainamide
Disopyramide

44
Q

decrease cAMP - leads to closure of membrane Ca2+ ch preventing upstroke of AV node AP

A

Class 2

45
Q

prolong phase 4 of nodal AP
decrease pacemaker activity
prolong conduction time and refractory period

A

class 2

46
Q

can cause heart block

A

class 2

47
Q

treats arrhythmias blocking SANS inout to SA and AV node

supra ventricular arrhythmias (A fib/ flutter

A

class 2

48
Q

prevents rapid ventricular response in atrial fib/ flutter “rate control” but does not fix the atrial fib

A

class 2

49
Q

class 2 drugs

A

beta blockers

50
Q

Class 3 drugs

A

Amiodarone

Sotalol

51
Q

block K+ ch prolonging phase 2 and 3 of AP - prolong refractory period
widen QT interval
induce torsades

A

Class 3

52
Q

treats both SVT and ventricular arrhythmias and A fib / flutter

A

Class 3

53
Q

can restore and maintain normal sinus rhythm in a fib and flutter

A

Class 3 (class 1C can also)

54
Q 
neurological SE
grey corneal deposits 
hyperthyroidism 
hypothyroidism 
pulmonary fibrosis - restrictive lung dz
induces HF
hyposensitivity hepatitis 
grey blue skin discoloration
photodermatitis 
inhibits cytochrome P450 inhibition
A

ADR of Amiodarone

55
Q

Class 4 drugs

A

Diltiazem

Verapamil

56
Q 
blocks L type calcium channels 
blocks phases 4 and 0
prolong conduction 
prolong PR interval 
prevents RVR in A fib and flutter
A

Class 4

57
Q

exert a greater effect on tissues that fire more freq. that use calcium current

A

class 4

58
Q

treats SVT

use as IV to treat PSVT

A

Class 4

59
Q

can cause heart block if used with a drug like digoxin

A

class 4

60
Q

constipation
AV block
HF

A

class 4 ADR

61
Q

Class 5 drugs

A

digoxin
magnesium
adenosine

62
Q

exerts direct PANS effect by stimulating vagus nerve - AV nodal inhibition; useful in A fib (not 1st line); prevents RVR in A fib “rate control”

A

digoxin

63
Q

treats torsades

A

magnesium

64
Q

causes peak T waves and shortens QT interval

A

hyperkalemia

65
Q

induces U waves at end of T waves on EKG
severe muscle weakness
abnorm glucose

A

hypokalemia

66
Q

inhibitory A1 receptor on myocardium @ SA & AV nodes (outward increase K+ current(hyper polarize) and suppresses Ca2+ inward current)
prolongs AV refractory period

A

Adenosine

67
Q

causes transient high grade heart block (direct AV node inhibition for about 10s)

A

Adenosine

68
Q

1st line agent for acute treatment for PVST

A

Adenosine

69
Q

causes coronary dilation (mediated by A2 receptor)

A

Adenosine

70
Q

cutaneous flushing
SOB, chest pain and impending sense of doom
fainting, headache and hypotension

A

Adenosine ADR

71
Q

inhibited by caffeine and theophylline

A

Adenosine

Pharm Block 2 (22 decks)

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