Harvey > Arrhythmias & Antiarrhythmics Flashcards
1
Q
what is phase 0?
A
upstroke
2
Q
what is phase 1?
A
early-fast repolarization
3
Q
what is phase 2?
A
plateau
4
Q
what is phase 3?
A
repolarization
5
Q
what is phase 4?
A
diastole
resting membrane potential
6
Q
what is the p wave?
A
atrial activation
7
Q
what is QRS?
A
ventricular activation
8
Q
what is the T wave?
A
ventricular repolarization
9
Q
are all action potentials in the heart the same?
A
NO
10
Q
what are the 2 types of APs in the heart?
A
slow response
fast response
11
Q
how many phases does fast response have?
A
5 (phase 0 1 2 3 4)
12
Q
how many phases does slow response have?
A
3 (phase 0 3 4)
13
Q
what parts of the heart fire spontaneously?
A
SA node
AV node
purkinje fibers
14
Q
what types of channels are involved in fast response?
A
sodium
15
Q
what types of channels are involved in slow response?
A
calcium
16
Q
the FASTER the upstroke velocity, the FASTER the _________
A
propagation/conduction velocity
17
Q
what 3 ions are important in the heart?
A
potassium
sodium
calcium
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!
19
Q
what happens in phase 0 of fast response?
A
activation of Na channels
deactivation of inward rectifier K channels
20
Q
what happens in phase 1 of fast response?
A
inactivation of Na channels
21
Q
what happens in phase 2 of fast response?
A
activation of Ca channels
22
Q
what happens in phase 3 of fast response?
A
inactivation of Ca channels
activation of delayed rectifier K channels
23
Q
what happens in phase 4 of fast response?
A
deactivation of delayed rectifier K channels
reactivation of inward rectifier K channels
24
Q
what are the phase 3 K channels?
A
IKr & IKs
25
what is the heart's resting membrane potential due to?
potassium conductance
26
what is IKr?
the rapid component of the delayed rectifier channels
27
what makes up IKr?
hERG + MiRP1
28
what makes up IKs?
KvLQT1 + minK
29
what happens in phase 0 of slow response?
activation of Ca channels
30
what happens in phase 3 of slow response?
inactivation of Ca channels
| activation of delayed rectifier K channels
31
what happens in phase 4 of slow response?
deactivation of delayed rectifier K channels
| activation of pacemaker channels
32
what is effective refractory period (ERP)?
stimulus cannot generate another AP
33
what is relative refractory period (RRP)?
stimulus can generate an abnormal AP
34
when does ERP occur?
btwn phase 0 and the middle of phase 3 in fast response
35
when does RRP occur?
halfway thru phase 3 until phase 4 starts in fast response (some excitability has recovered)
36
recovery from excitability is a function of what?
recovering the Na channels from their inactivated state
37
if you get another AP during RRP, will it be fast or slow?
slower than normal
| slower conduction velocity
38
what is the definition of arrhythmia?
disruption of RATE, RHYTHM, OR PATTERN of electrical activity
39
what are the 2 dangers assoc w/ arrhythmias?
vascular stasis
| loss of CO
40
what % of pts that suffer from MI have an arrhythmia?
80%
41
what % of pts that undergo anesthesia have an arrhythmia?
50%
42
what % of pts treated w/ cardiac glycosides have an arrhythmia?
25%
43
what are the 2 mechanisms of arrhythmias?
disturbance in electrical IMPULSE FORMATION (automaticity)
AND
disturbance in CONDUCTION of electrical activity
44
what is tachycardia?
anything over 100bpm
45
what is bradycardia?
anything under 60bpm
46
T/F: rhythm in tachy & bradycardia is regular
TRUE
47
T/F: atrial & ventricular rates are the same in atrial tachycardia
FALSE
| ventricular is slower
48
what is the atrial rate in atrial tachycardia?
250-350
49
what is the ventricular rate in atrial tachycardia?
80-150
50
which arrhythmias have variable rhythms?
atrial tachycardia
| ventricular tachycardia
51
what is the ventricular rate in afib?
variable
52
what is the rhythm like in afib?
very irregular!
53
what is the atrial rate in ventricular tachycardia?
variable
54
what is the ventricular rate in ventricular tachycardia?
100-250
55
what is the atrial rate in vfib?
variable
56
what is the atrial rate in afib?
there isn't one
57
what causes bradycardia?
XS parasympathetic tone
| sick sinus syndrome
58
what causes tachycardia?
XS sympathetic tone
59
what are the 2 disturbances in impulse FORMATION at the sinus node?
bradycardia
| tachycardia
60
T/F: breathing can cause arrhythmias
TRUE
| SA node generates impulses at a varying rate depending on inspiration & expiration
61
what is responsible for arrhythmia generated during breathing?
parasympathetic/vagal tone
62
where are the 2 ectopic nodes that can exhibit disturbances in impulse FORMATION?
AV node/bundle of His
| Purkinje fibers
63
what happens in hypokalemia?
purkinje firing is increased
64
what is a junctional rhythm?
impulses originate at the AV node w/ retrograde & anterograde transmission
65
what happens w/ the p wave in junctional rhythm?
inverted, happens after QRS
66
what are the 2 impulse FORMATION defects in the atrial or ventricular myocardium (ectopic)?
early after-depol (EADs)
| delayed after-depol (DADs)
67
when do EADs occur?
phase 3 repolarization
68
when do DADs occur?
resting membrane potential AFTER the cell is fully repolarized
69
T/F: EADs & DADs act as ectopic pacemakers
TRUE
70
what can trigger EADs?
prolonging ventricular AP duration (i.e. QT)
71
what are EADs assoc w/?
prolonged QT
72
what can EADs lead to?
torsade de pointes (type of vtach)
73
what are the risk factors for TdP?
```
pharmacologic
genetic
electrolyte imbalances
female
bradycardia
sympathetic stimulation
```
74
what drugs can lead to TdP?
anything that prolongs the QT interval > specifically drugs that act on K channels (IKr HERG)
75
what genetic condition can lead to TdP?
inherited long QT syndrome
76
what is the antihistamine that was taken off the market because it caused long QT syndrome bc it acted on the HERG channel?
terfenadine (and astemizole)
77
T/F: there are no drugs on the market now that cause prolonged QT interval
FALSE
| there are a ton that potentially can cause prolonged QT but when managed effectively do not
78
what do the genetic syndromes assoc w/ inherited long QT affect in your body?
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
what electrolyte imbalances are risk factors for TdP?
HYPOKALEMIA
hypomagnesemia
hypocalcemia
80
why does hypokalemia cause arrhythmias/long QT syndrome/TdP?
when K levels decrease, ventricular AP duration INCREASES
81
T/F: usually one thing is enough to cause an arrhythmia & death
FALSE
| usually it's a combo of factors (i.e. a gene + a new abx or something)
82
what leads to DADs (ions)?
XS Ca in SR causes spontaneous release > subsequent removal of Ca by Na/Ca exchanger generates inward depolarizing current
83
what causes DADs?
```
DIGOXIN!
catecholamines
hypercalcemia
increased HR
genetic defect
```
84
what ion movement specifically causes the DAD?
1 Ca out for every 3 Na in
| the Na IN causes the depolarization
85
what is CPVT?
catecholaminergic polymorphic ventricular tachycardia
| i.e. genetic thing that can cause DADs
86
what 2 gene pdts, if defective, can lead to DADs?
```
ryanodine receptor (GAIN of fxn)
calsequestrin (LOSS of fxn)
```
87
what are the 2 types of disturbances in CONDUCTION of electrical activity?
slowed conduction WITH OR WITHOUT reentry
88
where is the dysfxn in slowed conduction W/O reentry?
AV node
89
what is 1st degree slowed conduction w/o reentry? (i.e. 1st degree block)
prolonged PR interval
90
what is 2nd degree slowed conduction w/o reentry? (i.e. 2nd degree block)
intermittent failure of AV conduction
91
what is 3rd degree slowed conduction w/o reentry? (i.e. 3rd degree block)
complete failure of AV impulse conduction
92
where does slowed conduction WITH reentry act?
atrial
AV node
ventricular
93
what are the 3 requirements for reentry?
multiple parallel conduction pathways
area of unidirectional block
slowed conduction
94
ischemia causes what?
depolarization
| no O2 > no ATP > no Na/K pump > no normal K gradient > increased K outside cell
95
what are ATP-sensitive K channels?
when ATP levels go down, they open > HUGE increase in K conductance & K leaks OUT of the cell
96
what is the normal resting membrane potential value of K?
4mV
97
how does ischemia affect the resting membrane potential?
slows Na channel recovery from inactivation
| prevents some channels from recovering at all
98
how much do extracellular K levels increase w/i minutes of a coronary occlusion?
10-20 mM
99
ischemia/hypoxia reduces cellular ATP, which does what 2 things?
reduces Na/K ATPase activity
| activates ATP-sensitive K channels
100
are premature contractions significant?
nope
101
what are the 2 types of premature contractions?
PVC & PAC
| premature ventricular/atrial contractions
102
what induces PVCs & PACs?
reentry
103
what is the mechanism for atach or vtach?
one sustained reentrant circuit
104
what is the mechanism for paroxysmal supraventricular tachycardia (PSVT)?
AV node reentry
105
what is the mechanism for nonsustained ventricular tachycardia (NSVT)?
one transient circuit
106
what is the mechanism for aflutter?
one large reentrant circuit
107
what is the mechanism for afib or vfib?
lots of reentrant circuits
108
why is the hallmark of PVC a WIDE QRS?
impulse is started in ventricular myocardium and spreads slowly
109
what does the ECG for vfib look like?
rapid wide irregular ventricular complexes (just like you're scribbling something out)
110
what does vtach look like on ECG?
wide ventricular complexes (like lots of PVCs) w/ a rate >120 bpm
111
what does the ECG for aflutter look like?
rapid flutter waves w/ irregular ventricular response
| so like 3 P waves btwn QRS complexes
112
what does the ECG for afib look like?
baseline irregular w/ irregular ventricular response
113
what are the 3 indications for treating cardiac arrhythmias?
if the arrhythmia decreases CO
if it is likely to precipitate a more serious arrhythmia
if it is likely to precipitate an embolism
114
what arrhythmias decrease CO?
severe bradycardia
vtach
vfib
115
what arrythmias are likely to precipitate more serious arrhythmias?
afib > sustained vtach
| vtach > vfib
116
what arrhythmia is likely to precipitate an embolism?
chronic afib
117
what are the therapeutic modalities for treating arrhythmias?
```
drugs
correct electrolyte imbalances
DC cardioversion
pacemaker
carotid sinus massage/Valsalva
ablation of ectopic foci
lifestyle mods
```
118
how do MOST antiarrhythmic drugs act?
by directly blocking or altering the kinetics of CARDIAC ION CHANNELS
119
how do drugs interact w/ ion channels (what manner)?
state-dependent manner
| affinity for channels in OPEN/INACTIVATED state is HIGHER than affinity for channels in a resting state
120
T/F: drug affinity is HIGHER for OPEN/INACTIVE channels than for resting channels
TRUE
121
why do antiarrhythmic agents preferentially target the ions?
bc conditions that precipitate arrhythmias affect the state of ion channels
122
what can antiarrhythmic agents ALSO affect?
ion channels in normal tissue
| so they may be proarrhythmic
123
what do type I drugs affect?
Na channels
124
what drugs are in class Ia?
procainamide & quinidine
125
what is the mechanism of class Ia drugs?
Na channel blockers that increase AP duration
126
what drugs are in class Ib?
lidocaine
127
what is the mechanism of class Ib drugs?
Na channel blockers that slightly decrease AP duration
128
what drugs are in class Ic?
flecainide
129
what is the mechanism of class Ic drugs?
Na channel blockers that don't change AP duration
130
what drugs are in class II?
propranolol & metoprolol
131
what is the mechanism of class II drugs?
beta blockers
132
what drugs are in class III?
amiodarone
133
what is the mechanism of class III drugs?
K channel blockers that increase AP duration
134
what is the mechanism of class IV drugs?
L-type Ca channel blockers
135
what drugs are class IV drugs?
verapamil
136
what drugs are in the Misc class?
adenosine & digoxin
137
what is the mechanism of adenosine?
adenosine receptor agonist
138
what is the mechanism of digoxin?
parasympathomimetic
139
how do class Ia drugs impact ECG?
increase QRS
| increase QT
140
how do class Ib drugs impact ECG?
decreased QT
141
how do class Ic drugs impact ECG?
widened QRS
142
how do class Ia drugs impact AP & upstroke velocity?
increase AP duration
| slows upstroke velocity
143
how do class Ib drugs impact AP & upstroke velocity?
shortened AP duration
| no impact on upstroke velocity
144
how do class Ic drugs impact AP & upstroke velocity?
no effect on AP duration
| slows upstroke velocity
145
why do the sodium channel blockers prolong action potential duration?
because they ALSO impact K channels
146
How do class 1 drugs reduce the excitability of ectopic pacemakers (esp Purkinje fibers)?
raise the threshold of excitability to prolong the time btwn APs
147
how do class 1 agents block reentry?
increase ERP duration & convert unidirectional block to bi
148
how do class 1 agents increase ERP duration?
make the tissue TOTALLY inexcitable so that no reentry can occur
149
what are the clinical indications for class Ia drugs?
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
what are the clinical indications for class Ib drugs?
drug of 2nd choice for terminating vtach & preventing vfib after DC cardioversion (1st: amiodarone)
INEFFECTIVE against atrial arrhythmias!!
151
what are the clinical indications or class Ic drugs?
supraventricular arrhythmias in pts w/o hx of ischemic heart disease
152
what do class 1 drugs have NO ROLE in?
PREVENTION of cardiac arrhythmias & sudden cardiac death in post-MI pts
153
routine use of class I drugs in high risk pts (MI survivors) increased the risk of what?
DEATH
154
class Ic drugs suppress asymptomatic ventricular arrhythmias, but increased what?
arrhythmia-induced deaths (3.6x placebo)
155
what is the proarrhythmic mechanism of class I agents?
converts slowed conduction to unidirectional block via reduced Na current
156
when should you use class II agents?
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
what types of rhythms do beta blockers reduce?
normal pacemaker automaticity
incidence of DADs
CPVT
158
what is the most common cardiac arrhythmia?
afib
159
what % of ppl over 80yo have afib?
~10%
160
T/F: afib is usually one-time
FALSE
| pts who develop it once are predisposed to develop it again
161
WHY are pts that get afib predisposed to get it again?
electrical remodeling of the atria
162
what are the 3 Ps of afib?
paroxysmal > persistent > permanent
163
what are the sx of afib?
palpitations, dyspnea, fatigue, decreased exercise tolerance, chest pain
164
what are the risk factors for afib?
hyperthyroidism, HTN, age, CHF, previous afib
165
what are the complications of afib?
stroke, vtach, tachycardia-induced heart failure, ventricular bradycardia
166
what are the 3 types of treatment for afib?
rate control
rhythm control
anticoagulant therapy
167
what does rate control do in afib?
allows afib to persist but controls the ventricular rate
168
T/F: rate control is easy to achieve in most pts
TRUE
169
why would you try to control rate in afib?
avoids use of treatments w/ lots of side effects
170
what does rate control in afib do for the risk of stroke?
reduces it if you also do concomitant anticoagulant therapy
171
how does rhythm control work in afib?
eliminates atrial arrhythmia & converts to normal sinus rhythm (cardioversion)
172
what 2 good things happen w/ rhythm control?
reduced risk of stroke
| better exercise tolerance
173
how do rate & rhythm control in afib affect mortality?
they don't!
174
what can you give your pt to achieve rate control?
```
class II agent
class IV agent
and/or digoxin
pacemaker
AV node ablation w/ pacemaker
```
175
what pts should get a pacemaker in afib?
pts w/ slow ventricular response
176
what pts should get AV node ablation w/ pacemaker in afib?
pts w/ fast ventricular response
177
how can you achieve cardioversion in rhythm control of afib?
```
direct current (DC)
class Ic agent (flecainide)
class III agent (amiodarone)
```
178
how can you maintain normal sinus rhythm in afib?
```
class III agent (amiodarone)
class Ic agent (flecainide)
```
179
what are the 3 ways you can achieve rhythm control in pts w/ afib?
cardioversion
maintenance of normal sinus rhythm
catheter ablation
