Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PMCOL 343 > 3-cardio > Flashcards

3-cardio Flashcards

(113 cards)

Start Studying
1
Q

what can cause delayed after depolarization

A

catecholamine action or digitalis toxicity (ca2+ overload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what can cause abnormal pacemaker activity

A

altered autonomic effects or long QT syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is heart block/ what can cause it

A

conduction block of AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

draw the circus movement pathway

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

increase refractory period (so it cant double back)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is use dependent block

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

is it hard to reduce excitability and rhythmicity without reducing contractility

A

yes because they are intimately linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how do doctors choose which antidysrhythmics to give the patient

A

its empirical - based on experience not so much theory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

increase AV block

something like propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how do you want to best treat ventricular dysrhythmias

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is another name for cardioversion

A

defibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is another name for defibrillation

A

cardioversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why can defibrillation be better than antidysrhythmics drugs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why can cardioversion be better than antidysrhythmics drugs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is an example of an undesirable effect of antidysrhythmics

A

lidocaine is a CNS depressant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what can general anesthetics do to dysrhythmia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

who classified the antidysrhythmic drugs

A

vaughan-williams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how did vaughan-williams base his drug classes

A

in vitro electrophysiological effects (in glass/ test tube)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do class 1A drugs do GENERALLY

A

membrane stabilizers which prolong refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what drug is a class 1A

A

quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is quinidine

A

class 1A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how do patients typically use quinidine
prophylactically for atrial and ventricular dysrhythmia
26
what do class 1A do to refractory period
increase
27
how does quinidine work
blocks na+ and k+ channels
28
what does quinidine do to threshold
increases
29
how does quinidine slow rate of rise of Na+ dependent phase 0
use dependent effect
30
how does quinidine effect phase 4
decreases slope (Na/K dependent)
31
what are some off target effects in all class 1A agents
anticholinergic (like atropine) | -independent of antidysrhythmic action
32
which drugs have anticholinergic effects that are independent of antidysrhythmic action
class 1A agents
33
what does quinidine do to conduction velocity
decrease
34
what does quinidine do to automaticity
decrease
35
what does quinidine do to action potential duration
increase
36
what does quinidine do to QT interval
increase
37
what does quinidine do to refractory period
increase
38
what does quinidine do to one-way conversion blocks
abolished re-entry - turns it into a two way block
39
what does quinidine do to contractility and HOW
decrease via negative ionotropic effect
40
what is the negative inotropic effect
SA node slows sinus rate, GIRK channels hyperpolarized Sa node, decrease slope in phase 4
41
what happens with block by quinidine with more activity
increases the degree of block
42
what do class 1B drugs do GENERALLY
membrane stabilizers which shorten refractory period
43
what is an example of 1B drug
lidocaine
44
what class is lidocaine
1B
45
when is lidocaine used
emergency treatment of ventricular dysrhythmias
46
how does lidocaine work
blocks Na channels
47
what does lidocaine do to threshold
increase
48
what does lidocaine do to phase 4
decreases rate of rise of NaK dependent phase 4 pacemaker
49
what does lidocaine do to phase 3
shorten
50
what does lidocaine do to phase 0
slows rate of rise ONLY IN DAMAGED TISSUE
51
how does lidocaine affect phase 0
use dependent effect - inactivated state blocker
52
what does lidocaine do to ECG in healthy people
little effect
53
what does lidocaine do to automaticity and where
decreases automaticity and especially in purkinje fibres
54
what does lidocaine do to automaticity
decreases automaticity and especially in purkinje fibres
55
does lidocaine have the same effects on healthy and ischemic tissues
no
56
what does lidocaine do to one way block and where
converts it into a two way block in ischemic tissue
57
what does lidocaine do to one way block
converts it into a two way block in ischemic tissue
58
what does lidocaine do to ADP
decrease
59
what does lidocaine do to ERP
decrease
60
why do you use lidocaine if it decreases ADP and ERP
because its still a really good antidysrhythmic
61
what do class 1C drugs do GENERALLY
membrane stabilizers which do not affect refractory period
62
what is an example of a 1C drug
flecanide
63
what is flecanide
1C
64
when do you use flecanide
prophylaxis of atrial dysrhythimas
65
what does flecanide do to phase 0
slows rate of rise
66
what does flecanide do to APD
nothing
67
what does flecanide do to ERP
nothing
68
what does flecanide do to ventricular dysrhythmias
worsen
69
what are class 2 drugs GENERALLY
anti adrenergics and membrane stabilizers
70
what are 2 examples of class 2 drugs
propranolol and acebutolol
71
what is acebutolol
b1 blocker, class 2
72
how are class 2 drugs used
in adjunct to other therapies
73
what 4 catecholamine effects to anti-adrenergics antagonize
1-delayed afterdepolarizations 2-purkinje fibre automaticity 3-increased AV conduction 4-shortened ventricular AP
74
what do class 2 do to delayed afterdepolarizations
stops them
75
what do class 2 do to purkinje fibre automaticity
reduce
76
what do class 2 do to AV conduction
decrease
77
what do class 2 do to ventricular AP
increase
78
what 3 situations are B blockers contraindicated
severe heart failure asthma dysrhythmias with AV block
79
why dont you use B blockers in dysrhythmias with AV block
because beta blockers already decrease AV
80
which class of drugs is beta blockers
2
81
what do class 3 drugs do GENERALLY
prolong ADP and ERP, no effect on rise time
82
what is amiodarone (class)
class 3
83
what is sotalol
b blocker AND class 3
84
what are examples of class 3 drugs
amiodarone and sotalol
85
how does amiodarone work
thyroxine antagonist which prolongs refractory period
86
what is the duration of action for amiodarone
long, more than 30 days
87
what does sotalol do to heart AP
prolongs the ERP and APD
88
what kind of beta blocker is sotalol
non selective
89
why would amiodarone be a thyroxine antagonist/ what is this good for
thyroxine usually juices things up, so its an antagonist so it will downregulate the sympathetic effects
90
what are class 4 drugs GENERALLY
slow channel blockers
91
what are 2 class 4 drugs
verapamil and diltiazem
92
what kind of dysrhythmia are class 4 drugs good for
supraventricular dysrhythmias (not ventricular)
93
are class 4 drugs good for ventricular dysrhythmias
noooo
94
how do class 4 drugs work
cardioselected L-type calcium channel blocker to block AV conduction
95
what are the 2 main types of class 5 drugs
cardiac glycosides and adenosine
96
what is an example of cardiac glycosides
digoxin
97
what is another name for the cardiac glycosides
digitalis glycosides
98
what is the therapeutic action of cardiac glycosides
decrease conduction through the AV node
99
what class is diltiazem
4
100
what class is verapamil
4
101
what class are cardiac glycosides
5
102
what class is adenosine
5
103
where does adenosine occur naturally
in blood
104
what does adenosine do to the heart
decrease sinus rate and decrease AV conduction
105
what are the electrophysiological effects of adenosine similar to
ACh
106
what do class 6 drugs do
enhance vagal activity
107
what are "channelopathies"
individuals with genetic disorders with mutations in cardiac potassium channels
108
what are 3 types of people with long Q-T syndrome
people with "channelopathies", some diabetics and people with cardiovasc disorders
109
what does long Q-T mean/entail
prolonged ventricular action potentials
110
what can long Q-T syndrome cause
fatal dysrhythmias
111
can people with long Q-T take sotalol and why
no becaus it increases refractory period
112
why do people with long Q-T have to be careful with lots of drugs
because lots of eve non-cardiovasc drugs can precipitate long Q-T in susceptible individuals
113
how can fibres with long Q-T cause dysrhythmias
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions