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PMCOL 343 > 3-cardio > Flashcards

3-cardio Flashcards

1
Q

what are 4 causes of dysrhythmia

A

delayed after depolarization
abnormal pacemaker activity
heart block
circus movement/ re-entry

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2
Q

what can cause delayed after depolarization

A

catecholamine action or digitalis toxicity (ca2+ overload)

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3
Q

what can cause abnormal pacemaker activity

A

altered autonomic effects or long QT syndrome

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4
Q

what is heart block/ what can cause it

A

conduction block of AV node

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5
Q

what are 3 pathological requirements for circus movement

A

circular conducting pathway
branch of circuit with UNIDIRECTIONAL conduction block
refractory period of re-entry region < propogation time around pathway

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6
Q

draw the circus movement pathway

A

yes

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7
Q

what do you want to do to the refractory period to reduce circus movement

A

increase refractory period (so it cant double back)

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8
Q

what are 5 desirable features of antidysrhythmic drugs

A 
1-convert 1 way block to 2 way block
2-increase refractory period
3-block effects of catecholamines
4-reduce excitability and rhythmicity (without reducing contractility)
5-produce "use-dependent" block
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9
Q

what is use dependent block

A

so first impulse gets through but impulses generated rapidly after first impulse are blocked

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10
Q

is it hard to reduce excitability and rhythmicity without reducing contractility

A

yes because they are intimately linked

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11
Q

how do doctors choose which antidysrhythmics to give the patient

A

its empirical - based on experience not so much theory

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12
Q

why can antidysrhythmics create more issues

A

because precise rates and routes of conduction determine cardiac function, any type of disturbance easily promotes arrhythmia

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13
Q

how do you want to best treat supraventricular dysrhythmias +what drug is best

A

increase AV block

something like propranolol

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14
Q

how do you want to best treat ventricular dysrhythmias

A

best to preserve AV conduction to increase chance of sinus rhythm taking over

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15
Q

what is another name for cardioversion

A

defibrillation

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16
Q

what is another name for defibrillation

A

cardioversion

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17
Q

why can defibrillation be better than antidysrhythmics drugs

A

because all antidysrhythmics have effects on other tissue that produce undesirable side effects

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18
Q

why can cardioversion be better than antidysrhythmics drugs

A

because all antidysrhythmics have effects on other tissue that produce undesirable side effects

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19
Q

what is an example of an undesirable effect of antidysrhythmics

A

lidocaine is a CNS depressant

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20
Q

what can general anesthetics do to dysrhythmia

A

sensitive the myocardium to catecholamines (like beta1 adrenergics), which could cause a dysrhythmia

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21
Q

who classified the antidysrhythmic drugs

A

vaughan-williams

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22
Q

how did vaughan-williams base his drug classes

A

in vitro electrophysiological effects (in glass/ test tube)

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23
Q

what do class 1A drugs do GENERALLY

A

membrane stabilizers which prolong refractory period

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24
Q

what drug is a class 1A

A

quinidine

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25
Q

what is quinidine

A

class 1A

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26
Q

how do patients typically use quinidine

A

prophylactically for atrial and ventricular dysrhythmia

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27
Q

what do class 1A do to refractory period

A

increase

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28
Q

how does quinidine work

A

blocks na+ and k+ channels

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29
Q

what does quinidine do to threshold

A

increases

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30
Q

how does quinidine slow rate of rise of Na+ dependent phase 0

A

use dependent effect

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31
Q

how does quinidine effect phase 4

A

decreases slope (Na/K dependent)

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32
Q

what are some off target effects in all class 1A agents

A

anticholinergic (like atropine)

-independent of antidysrhythmic action

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33
Q

which drugs have anticholinergic effects that are independent of antidysrhythmic action

A

class 1A agents

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34
Q

what does quinidine do to conduction velocity

A

decrease

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35
Q

what does quinidine do to automaticity

A

decrease

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36
Q

what does quinidine do to action potential duration

A

increase

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37
Q

what does quinidine do to QT interval

A

increase

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38
Q

what does quinidine do to refractory period

A

increase

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39
Q

what does quinidine do to one-way conversion blocks

A

abolished re-entry - turns it into a two way block

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40
Q

what does quinidine do to contractility and HOW

A

decrease via negative ionotropic effect

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41
Q

what is the negative inotropic effect

A

SA node slows sinus rate, GIRK channels hyperpolarized Sa node, decrease slope in phase 4

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42
Q

what happens with block by quinidine with more activity

A

increases the degree of block

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43
Q

what do class 1B drugs do GENERALLY

A

membrane stabilizers which shorten refractory period

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44
Q

what is an example of 1B drug

A

lidocaine

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45
Q

what class is lidocaine

A

1B

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46
Q

when is lidocaine used

A

emergency treatment of ventricular dysrhythmias

47
Q

how does lidocaine work

A

blocks Na channels

48
Q

what does lidocaine do to threshold

A

increase

49
Q

what does lidocaine do to phase 4

A

decreases rate of rise of NaK dependent phase 4 pacemaker

50
Q

what does lidocaine do to phase 3

A

shorten

51
Q

what does lidocaine do to phase 0

A

slows rate of rise ONLY IN DAMAGED TISSUE

52
Q

how does lidocaine affect phase 0

A

use dependent effect - inactivated state blocker

53
Q

what does lidocaine do to ECG in healthy people

A

little effect

54
Q

what does lidocaine do to automaticity and where

A

decreases automaticity and especially in purkinje fibres

55
Q

what does lidocaine do to automaticity

A

decreases automaticity and especially in purkinje fibres

56
Q

does lidocaine have the same effects on healthy and ischemic tissues

A

no

57
Q

what does lidocaine do to one way block and where

A

converts it into a two way block in ischemic tissue

58
Q

what does lidocaine do to one way block

A

converts it into a two way block in ischemic tissue

59
Q

what does lidocaine do to ADP

A

decrease

60
Q

what does lidocaine do to ERP

A

decrease

61
Q

why do you use lidocaine if it decreases ADP and ERP

A

because its still a really good antidysrhythmic

62
Q

what do class 1C drugs do GENERALLY

A

membrane stabilizers which do not affect refractory period

63
Q

what is an example of a 1C drug

A

flecanide

64
Q

what is flecanide

A

1C

65
Q

when do you use flecanide

A

prophylaxis of atrial dysrhythimas

66
Q

what does flecanide do to phase 0

A

slows rate of rise

67
Q

what does flecanide do to APD

A

nothing

68
Q

what does flecanide do to ERP

A

nothing

69
Q

what does flecanide do to ventricular dysrhythmias

A

worsen

70
Q

what are class 2 drugs GENERALLY

A

anti adrenergics and membrane stabilizers

71
Q

what are 2 examples of class 2 drugs

A

propranolol and acebutolol

72
Q

what is acebutolol

A

b1 blocker, class 2

73
Q

how are class 2 drugs used

A

in adjunct to other therapies

74
Q

what 4 catecholamine effects to anti-adrenergics antagonize

A

1-delayed afterdepolarizations
2-purkinje fibre automaticity
3-increased AV conduction
4-shortened ventricular AP

75
Q

what do class 2 do to delayed afterdepolarizations

A

stops them

76
Q

what do class 2 do to purkinje fibre automaticity

A

reduce

77
Q

what do class 2 do to AV conduction

A

decrease

78
Q

what do class 2 do to ventricular AP

A

increase

79
Q

what 3 situations are B blockers contraindicated

A

severe heart failure
asthma
dysrhythmias with AV block

80
Q

why dont you use B blockers in dysrhythmias with AV block

A

because beta blockers already decrease AV

81
Q

which class of drugs is beta blockers

A

2

82
Q

what do class 3 drugs do GENERALLY

A

prolong ADP and ERP, no effect on rise time

83
Q

what is amiodarone (class)

A

class 3

84
Q

what is sotalol

A

b blocker AND class 3

85
Q

what are examples of class 3 drugs

A

amiodarone and sotalol

86
Q

how does amiodarone work

A

thyroxine antagonist which prolongs refractory period

87
Q

what is the duration of action for amiodarone

A

long, more than 30 days

88
Q

what does sotalol do to heart AP

A

prolongs the ERP and APD

89
Q

what kind of beta blocker is sotalol

A

non selective

90
Q

why would amiodarone be a thyroxine antagonist/ what is this good for

A

thyroxine usually juices things up, so its an antagonist so it will downregulate the sympathetic effects

91
Q

what are class 4 drugs GENERALLY

A

slow channel blockers

92
Q

what are 2 class 4 drugs

A

verapamil and diltiazem

93
Q

what kind of dysrhythmia are class 4 drugs good for

A

supraventricular dysrhythmias (not ventricular)

94
Q

are class 4 drugs good for ventricular dysrhythmias

A

noooo

95
Q

how do class 4 drugs work

A

cardioselected L-type calcium channel blocker to block AV conduction

96
Q

what are the 2 main types of class 5 drugs

A

cardiac glycosides and adenosine

97
Q

what is an example of cardiac glycosides

A

digoxin

98
Q

what is another name for the cardiac glycosides

A

digitalis glycosides

99
Q

what is the therapeutic action of cardiac glycosides

A

decrease conduction through the AV node

100
Q

what class is diltiazem

A

4

101
Q

what class is verapamil

A

4

102
Q

what class are cardiac glycosides

A

5

103
Q

what class is adenosine

A

5

104
Q

where does adenosine occur naturally

A

in blood

105
Q

what does adenosine do to the heart

A

decrease sinus rate and decrease AV conduction

106
Q

what are the electrophysiological effects of adenosine similar to

A

ACh

107
Q

what do class 6 drugs do

A

enhance vagal activity

108
Q

what are “channelopathies”

A

individuals with genetic disorders with mutations in cardiac potassium channels

109
Q

what are 3 types of people with long Q-T syndrome

A

people with “channelopathies”, some diabetics and people with cardiovasc disorders

110
Q

what does long Q-T mean/entail

A

prolonged ventricular action potentials

111
Q

what can long Q-T syndrome cause

A

fatal dysrhythmias

112
Q

can people with long Q-T take sotalol and why

A

no becaus it increases refractory period

113
Q

why do people with long Q-T have to be careful with lots of drugs

A

because lots of eve non-cardiovasc drugs can precipitate long Q-T in susceptible individuals

114
Q

how can fibres with long Q-T cause dysrhythmias

A

if they are adjacent to fibres with normal refractory period, they can be re-excited by the fibre with a long refractory period

PMCOL 343 (31 decks)

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