Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 9 Week 2 > Harvey > Arrhythmias & Antiarrhythmics > Flashcards

Harvey > Arrhythmias & Antiarrhythmics Flashcards

1
Q

what is phase 0?

A

upstroke

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

what is phase 1?

A

early-fast repolarization

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

what is phase 2?

A

plateau

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

what is phase 3?

A

repolarization

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

what is phase 4?

A

diastole

resting membrane potential

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

what is the p wave?

A

atrial activation

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

what is QRS?

A

ventricular activation

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

what is the T wave?

A

ventricular repolarization

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

are all action potentials in the heart the same?

A

NO

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

what are the 2 types of APs in the heart?

A

slow response

fast response

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

how many phases does fast response have?

A

5 (phase 0 1 2 3 4)

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

how many phases does slow response have?

A

3 (phase 0 3 4)

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

what parts of the heart fire spontaneously?

A

SA node
AV node
purkinje fibers

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

what types of channels are involved in fast response?

A

sodium

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

what types of channels are involved in slow response?

A

calcium

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

the FASTER the upstroke velocity, the FASTER the _________

A

propagation/conduction velocity

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

what 3 ions are important in the heart?

A

potassium
sodium
calcium

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

T/F: sodium channels in the heart stay open for a long time

A

FALSE

stay open for a short time & close quickly!

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

what happens in phase 0 of fast response?

A

activation of Na channels

deactivation of inward rectifier K channels

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

what happens in phase 1 of fast response?

A

inactivation of Na channels

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

what happens in phase 2 of fast response?

A

activation of Ca channels

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

what happens in phase 3 of fast response?

A

inactivation of Ca channels

activation of delayed rectifier K channels

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

what happens in phase 4 of fast response?

A

deactivation of delayed rectifier K channels

reactivation of inward rectifier K channels

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

what are the phase 3 K channels?

A

IKr & IKs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the heart’s resting membrane potential due to?

A

potassium conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is IKr?

A

the rapid component of the delayed rectifier channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what makes up IKr?

A

hERG + MiRP1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what makes up IKs?

A

KvLQT1 + minK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what happens in phase 0 of slow response?

A

activation of Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what happens in phase 3 of slow response?

A

inactivation of Ca channels

activation of delayed rectifier K channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what happens in phase 4 of slow response?

A

deactivation of delayed rectifier K channels

activation of pacemaker channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is effective refractory period (ERP)?

A

stimulus cannot generate another AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is relative refractory period (RRP)?

A

stimulus can generate an abnormal AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

when does ERP occur?

A

btwn phase 0 and the middle of phase 3 in fast response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

when does RRP occur?

A

halfway thru phase 3 until phase 4 starts in fast response (some excitability has recovered)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

recovery from excitability is a function of what?

A

recovering the Na channels from their inactivated state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

if you get another AP during RRP, will it be fast or slow?

A

slower than normal

slower conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is the definition of arrhythmia?

A

disruption of RATE, RHYTHM, OR PATTERN of electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the 2 dangers assoc w/ arrhythmias?

A

vascular stasis

loss of CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what % of pts that suffer from MI have an arrhythmia?

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what % of pts that undergo anesthesia have an arrhythmia?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what % of pts treated w/ cardiac glycosides have an arrhythmia?

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the 2 mechanisms of arrhythmias?

A

disturbance in electrical IMPULSE FORMATION (automaticity)
AND
disturbance in CONDUCTION of electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is tachycardia?

A

anything over 100bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is bradycardia?

A

anything under 60bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

T/F: rhythm in tachy & bradycardia is regular

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

T/F: atrial & ventricular rates are the same in atrial tachycardia

A

FALSE

ventricular is slower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the atrial rate in atrial tachycardia?

A

250-350

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is the ventricular rate in atrial tachycardia?

A

80-150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

which arrhythmias have variable rhythms?

A

atrial tachycardia

ventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the ventricular rate in afib?

A

variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the rhythm like in afib?

A

very irregular!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is the atrial rate in ventricular tachycardia?

A

variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the ventricular rate in ventricular tachycardia?

A

100-250

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is the atrial rate in vfib?

A

variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is the atrial rate in afib?

A

there isn’t one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what causes bradycardia?

A

XS parasympathetic tone

sick sinus syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what causes tachycardia?

A

XS sympathetic tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what are the 2 disturbances in impulse FORMATION at the sinus node?

A

bradycardia

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

T/F: breathing can cause arrhythmias

A

TRUE

SA node generates impulses at a varying rate depending on inspiration & expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is responsible for arrhythmia generated during breathing?

A

parasympathetic/vagal tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

where are the 2 ectopic nodes that can exhibit disturbances in impulse FORMATION?

A

AV node/bundle of His

Purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what happens in hypokalemia?

A

purkinje firing is increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what is a junctional rhythm?

A

impulses originate at the AV node w/ retrograde & anterograde transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what happens w/ the p wave in junctional rhythm?

A

inverted, happens after QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the 2 impulse FORMATION defects in the atrial or ventricular myocardium (ectopic)?

A

early after-depol (EADs)

delayed after-depol (DADs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

when do EADs occur?

A

phase 3 repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

when do DADs occur?

A

resting membrane potential AFTER the cell is fully repolarized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

T/F: EADs & DADs act as ectopic pacemakers

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what can trigger EADs?

A

prolonging ventricular AP duration (i.e. QT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are EADs assoc w/?

A

prolonged QT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what can EADs lead to?

A

torsade de pointes (type of vtach)

73
Q

what are the risk factors for TdP?

A 
pharmacologic
genetic
electrolyte imbalances
female
bradycardia
sympathetic stimulation
74
Q

what drugs can lead to TdP?

A

anything that prolongs the QT interval > specifically drugs that act on K channels (IKr HERG)

75
Q

what genetic condition can lead to TdP?

A

inherited long QT syndrome

76
Q

what is the antihistamine that was taken off the market because it caused long QT syndrome bc it acted on the HERG channel?

A

terfenadine (and astemizole)

77
Q

T/F: there are no drugs on the market now that cause prolonged QT interval

A

FALSE

there are a ton that potentially can cause prolonged QT but when managed effectively do not

78
Q

what do the genetic syndromes assoc w/ inherited long QT affect in your body?

A

an ion channel
K channels LOSS of fxn (think of Karlie Kloss)
Na channel GAIN of fxn (doesn’t inactivate)
Ca channel GAIN of fxn

79
Q

what electrolyte imbalances are risk factors for TdP?

A

HYPOKALEMIA
hypomagnesemia
hypocalcemia

80
Q

why does hypokalemia cause arrhythmias/long QT syndrome/TdP?

A

when K levels decrease, ventricular AP duration INCREASES

81
Q

T/F: usually one thing is enough to cause an arrhythmia & death

A

FALSE

usually it’s a combo of factors (i.e. a gene + a new abx or something)

82
Q

what leads to DADs (ions)?

A

XS Ca in SR causes spontaneous release > subsequent removal of Ca by Na/Ca exchanger generates inward depolarizing current

83
Q

what causes DADs?

A 
DIGOXIN!
catecholamines
hypercalcemia
increased HR
genetic defect
84
Q

what ion movement specifically causes the DAD?

A

1 Ca out for every 3 Na in

the Na IN causes the depolarization

85
Q

what is CPVT?

A

catecholaminergic polymorphic ventricular tachycardia

i.e. genetic thing that can cause DADs

86
Q

what 2 gene pdts, if defective, can lead to DADs?

A 
ryanodine receptor (GAIN of fxn) 
calsequestrin (LOSS of fxn)
87
Q

what are the 2 types of disturbances in CONDUCTION of electrical activity?

A

slowed conduction WITH OR WITHOUT reentry

88
Q

where is the dysfxn in slowed conduction W/O reentry?

A

AV node

89
Q

what is 1st degree slowed conduction w/o reentry? (i.e. 1st degree block)

A

prolonged PR interval

90
Q

what is 2nd degree slowed conduction w/o reentry? (i.e. 2nd degree block)

A

intermittent failure of AV conduction

91
Q

what is 3rd degree slowed conduction w/o reentry? (i.e. 3rd degree block)

A

complete failure of AV impulse conduction

92
Q

where does slowed conduction WITH reentry act?

A

atrial
AV node
ventricular

93
Q

what are the 3 requirements for reentry?

A

multiple parallel conduction pathways
area of unidirectional block
slowed conduction

94
Q

ischemia causes what?

A

depolarization

no O2 > no ATP > no Na/K pump > no normal K gradient > increased K outside cell

95
Q

what are ATP-sensitive K channels?

A

when ATP levels go down, they open > HUGE increase in K conductance & K leaks OUT of the cell

96
Q

what is the normal resting membrane potential value of K?

A

4mV

97
Q

how does ischemia affect the resting membrane potential?

A

slows Na channel recovery from inactivation

prevents some channels from recovering at all

98
Q

how much do extracellular K levels increase w/i minutes of a coronary occlusion?

A

10-20 mM

99
Q

ischemia/hypoxia reduces cellular ATP, which does what 2 things?

A

reduces Na/K ATPase activity

activates ATP-sensitive K channels

100
Q

are premature contractions significant?

A

nope

101
Q

what are the 2 types of premature contractions?

A

PVC & PAC

premature ventricular/atrial contractions

102
Q

what induces PVCs & PACs?

A

reentry

103
Q

what is the mechanism for atach or vtach?

A

one sustained reentrant circuit

104
Q

what is the mechanism for paroxysmal supraventricular tachycardia (PSVT)?

A

AV node reentry

105
Q

what is the mechanism for nonsustained ventricular tachycardia (NSVT)?

A

one transient circuit

106
Q

what is the mechanism for aflutter?

A

one large reentrant circuit

107
Q

what is the mechanism for afib or vfib?

A

lots of reentrant circuits

108
Q

why is the hallmark of PVC a WIDE QRS?

A

impulse is started in ventricular myocardium and spreads slowly

109
Q

what does the ECG for vfib look like?

A

rapid wide irregular ventricular complexes (just like you’re scribbling something out)

110
Q

what does vtach look like on ECG?

A

wide ventricular complexes (like lots of PVCs) w/ a rate >120 bpm

111
Q

what does the ECG for aflutter look like?

A

rapid flutter waves w/ irregular ventricular response

so like 3 P waves btwn QRS complexes

112
Q

what does the ECG for afib look like?

A

baseline irregular w/ irregular ventricular response

113
Q

what are the 3 indications for treating cardiac arrhythmias?

A

if the arrhythmia decreases CO
if it is likely to precipitate a more serious arrhythmia
if it is likely to precipitate an embolism

114
Q

what arrhythmias decrease CO?

A

severe bradycardia
vtach
vfib

115
Q

what arrythmias are likely to precipitate more serious arrhythmias?

A

afib > sustained vtach

vtach > vfib

116
Q

what arrhythmia is likely to precipitate an embolism?

A

chronic afib

117
Q

what are the therapeutic modalities for treating arrhythmias?

A 
drugs
correct electrolyte imbalances
DC cardioversion
pacemaker
carotid sinus massage/Valsalva
ablation of ectopic foci
lifestyle mods
118
Q

how do MOST antiarrhythmic drugs act?

A

by directly blocking or altering the kinetics of CARDIAC ION CHANNELS

119
Q

how do drugs interact w/ ion channels (what manner)?

A

state-dependent manner

affinity for channels in OPEN/INACTIVATED state is HIGHER than affinity for channels in a resting state

120
Q

T/F: drug affinity is HIGHER for OPEN/INACTIVE channels than for resting channels

A

TRUE

121
Q

why do antiarrhythmic agents preferentially target the ions?

A

bc conditions that precipitate arrhythmias affect the state of ion channels

122
Q

what can antiarrhythmic agents ALSO affect?

A

ion channels in normal tissue

so they may be proarrhythmic

123
Q

what do type I drugs affect?

A

Na channels

124
Q

what drugs are in class Ia?

A

procainamide & quinidine

125
Q

what is the mechanism of class Ia drugs?

A

Na channel blockers that increase AP duration

126
Q

what drugs are in class Ib?

A

lidocaine

127
Q

what is the mechanism of class Ib drugs?

A

Na channel blockers that slightly decrease AP duration

128
Q

what drugs are in class Ic?

A

flecainide

129
Q

what is the mechanism of class Ic drugs?

A

Na channel blockers that don’t change AP duration

130
Q

what drugs are in class II?

A

propranolol & metoprolol

131
Q

what is the mechanism of class II drugs?

A

beta blockers

132
Q

what drugs are in class III?

A

amiodarone

133
Q

what is the mechanism of class III drugs?

A

K channel blockers that increase AP duration

134
Q

what is the mechanism of class IV drugs?

A

L-type Ca channel blockers

135
Q

what drugs are class IV drugs?

A

verapamil

136
Q

what drugs are in the Misc class?

A

adenosine & digoxin

137
Q

what is the mechanism of adenosine?

A

adenosine receptor agonist

138
Q

what is the mechanism of digoxin?

A

parasympathomimetic

139
Q

how do class Ia drugs impact ECG?

A

increase QRS

increase QT

140
Q

how do class Ib drugs impact ECG?

A

decreased QT

141
Q

how do class Ic drugs impact ECG?

A

widened QRS

142
Q

how do class Ia drugs impact AP & upstroke velocity?

A

increase AP duration

slows upstroke velocity

143
Q

how do class Ib drugs impact AP & upstroke velocity?

A

shortened AP duration

no impact on upstroke velocity

144
Q

how do class Ic drugs impact AP & upstroke velocity?

A

no effect on AP duration

slows upstroke velocity

145
Q

why do the sodium channel blockers prolong action potential duration?

A

because they ALSO impact K channels

146
Q

How do class 1 drugs reduce the excitability of ectopic pacemakers (esp Purkinje fibers)?

A

raise the threshold of excitability to prolong the time btwn APs

147
Q

how do class 1 agents block reentry?

A

increase ERP duration & convert unidirectional block to bi

148
Q

how do class 1 agents increase ERP duration?

A

make the tissue TOTALLY inexcitable so that no reentry can occur

149
Q

what are the clinical indications for class Ia drugs?

A

most atrial & ventricular arrhythmias in pts w/o hx of ischemic heart disease
drug of 2nd or 3rd choice for RX of sustained ventricular arrhythmias after MI (amiodarone & lido preferred)

150
Q

what are the clinical indications for class Ib drugs?

A

drug of 2nd choice for terminating vtach & preventing vfib after DC cardioversion (1st: amiodarone)
INEFFECTIVE against atrial arrhythmias!!

151
Q

what are the clinical indications or class Ic drugs?

A

supraventricular arrhythmias in pts w/o hx of ischemic heart disease

152
Q

what do class 1 drugs have NO ROLE in?

A

PREVENTION of cardiac arrhythmias & sudden cardiac death in post-MI pts

153
Q

routine use of class I drugs in high risk pts (MI survivors) increased the risk of what?

A

DEATH

154
Q

class Ic drugs suppress asymptomatic ventricular arrhythmias, but increased what?

A

arrhythmia-induced deaths (3.6x placebo)

155
Q

what is the proarrhythmic mechanism of class I agents?

A

converts slowed conduction to unidirectional block via reduced Na current

156
Q

when should you use class II agents?

A

to prevent arrhythmias & sudden death in pts w/ hx of CHF & MI
AND
to control ventricular rate in pts w/ supraventricular tachyarrhythmias (afib)
AND
catecholaminergic polymorphic ventricular tachycardia (CPVT)

157
Q

what types of rhythms do beta blockers reduce?

A

normal pacemaker automaticity
incidence of DADs
CPVT

158
Q

what is the most common cardiac arrhythmia?

A

afib

159
Q

what % of ppl over 80yo have afib?

A

~10%

160
Q

T/F: afib is usually one-time

A

FALSE

pts who develop it once are predisposed to develop it again

161
Q

WHY are pts that get afib predisposed to get it again?

A

electrical remodeling of the atria

162
Q

what are the 3 Ps of afib?

A

paroxysmal > persistent > permanent

163
Q

what are the sx of afib?

A

palpitations, dyspnea, fatigue, decreased exercise tolerance, chest pain

164
Q

what are the risk factors for afib?

A

hyperthyroidism, HTN, age, CHF, previous afib

165
Q

what are the complications of afib?

A

stroke, vtach, tachycardia-induced heart failure, ventricular bradycardia

166
Q

what are the 3 types of treatment for afib?

A

rate control
rhythm control
anticoagulant therapy

167
Q

what does rate control do in afib?

A

allows afib to persist but controls the ventricular rate

168
Q

T/F: rate control is easy to achieve in most pts

A

TRUE

169
Q

why would you try to control rate in afib?

A

avoids use of treatments w/ lots of side effects

170
Q

what does rate control in afib do for the risk of stroke?

A

reduces it if you also do concomitant anticoagulant therapy

171
Q

how does rhythm control work in afib?

A

eliminates atrial arrhythmia & converts to normal sinus rhythm (cardioversion)

172
Q

what 2 good things happen w/ rhythm control?

A

reduced risk of stroke

better exercise tolerance

173
Q

how do rate & rhythm control in afib affect mortality?

A

they don’t!

174
Q

what can you give your pt to achieve rate control?

A 
class II agent
class IV agent
and/or digoxin
pacemaker
AV node ablation w/ pacemaker
175
Q

what pts should get a pacemaker in afib?

A

pts w/ slow ventricular response

176
Q

what pts should get AV node ablation w/ pacemaker in afib?

A

pts w/ fast ventricular response

177
Q

how can you achieve cardioversion in rhythm control of afib?

A 
direct current (DC)
class Ic agent (flecainide)
class III agent (amiodarone)
178
Q

how can you maintain normal sinus rhythm in afib?

A 
class III agent (amiodarone)
class Ic agent (flecainide)
179
Q

what are the 3 ways you can achieve rhythm control in pts w/ afib?

A

cardioversion
maintenance of normal sinus rhythm
catheter ablation

Block 9 Week 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions