Unit 6 - Cardiac Rhythm Monitors & Equipment Flashcards
(242 cards)
1
Q
normal path of cardiac conduction
A
SA node - internodal tracts - AV node - bundle of His - bundle branches - Purkinje fibers
2
Q
quantifies how fast an electrochemical impulse propagates along neural pathway
A
Conduction Velocity
3
Q
normal conduction velocity of SA and AV nodes
A
0.02 – 0.10 m/sec (slow conduction)
4
Q
normal conduction of myocardial muscle cells
A
0.3 – 1 m/sec (intermediate conduction)
5
Q
normal conduction velocity of His bundle, bundle branches, and Purkinje fibers
A
1 – 4 m/sec (fast conduction)
6
Q
what 3 things is conduction velocity a function of
A
1) RMP
2) AP amplitude
3) rate of change in membrane potential during phase 0
7
Q
what is conduction velocity affected by
A
- ANS tone
- hyperkalemia-induced closure of fast Na+ channels
- ischemia
- acidosis
- antiarrhythmic drugs
8
Q
what are accessory pathways
A
- Band of connective tissue that electrically isolates atria from ventricles
- preserves AV synchrony by preventing atrial tissue from prematurely exciting ventricular tissue
9
Q
“gatekeeper” of electrical transmission between atria and ventricles
A
AV node
10
Q
accessory pathway assoc. with connection from atrium to AV node
A
James Fiber
11
Q
accessory pathway assoc. with connection from atrium to His bundle
A
Atrio-hisian fiber
12
Q
accessory pathway assoc. with connection from atrium to ventricle
A
Kent’s bundle
13
Q
accessory pathway assoc. with connection from AV to ventricle
A
Mahaim bundle
14
Q
event, ion movement, and key EKG event assoc with phase 0 of cardiac conduction
A
depolarization
Na+ in
QRS
15
Q
event, ion movement, and key EKG event assoc with phase 1 of cardiac conduction
A
initial repolarization
Cl- in, K+ out
QRS
16
Q
event, ion movement, and key EKG event assoc with phase 2 of cardiac conduction
A
plateau
Ca2+ in, K+ out
ST segment
17
Q
event, ion movement, and key EKG event assoc with phase 3 of cardiac conduction
A
final repolarization
K+ out
T wave
18
Q
event, ion movement, and key EKG event assoc with phase 4 of cardiac conduction
A
resting phase
K+ leak
end of T wave
19
Q
part of EKG assoc. with beginning of atrial depolarization
A
P wave
20
Q
what part of EKG is atrial depolarization complete
A
PR interal
21
Q
represents atrial repolarization, ventricular depolarization begins on EKG tracing
A
QRS
22
Q
part of EKG assoc. with beginning of ventricular repolarization
A
T wave
(complete at end of T wave)
23
Q
normal duration and amplitude of P wave
A
duration: 0.08-0.12 sec
amplitude: < 2.5 mm
24
Q
what do biphasic P waves suggest
A
LA enlargement
think mitral stenosis
25
what do biphasic P waves suggest
LA enlargement
| think mitral stenosis
26
normal duration of PR interval
0.12-0.2 sec
27
causes of PR interval depression
* viral pericarditis
* atrial infarction
28
normal duration and amplitude of Q wave
duration < 0.04 sec
amplitude < 0.4-0.5 mm
29
characteristics of pathologic Q wave (possible MI)
* amplitude > 1/3 of R wave
* duration > 0.04 sec
* depth > 1 mm
30
normal QTC
Men < 0.45
Women < 0.47
31
characteristic of ST segment seen with MI
elevation or depression > 1 mm
32
when might ST be increased
MI
hyperkalemia
endocarditis
33
normal amplitude of T wave
< 10 mm in precordial
< 6 mm in limb leads
34
normal direction of T wave
Usually points in same direction as QRS
points opposite if repolarization prolonged by myocardial ischemia, BBB
35
causes of peaked T waves
myocardial ischemia
LVH
intracranial bleed
36
EKG changes with hyperkalemia
* peaked T waves
* short QT
* prolonged PR
* wide QRS
* low P amplitude
* nodal block
## Footnote
order of appearance early to late
37
u wave with hypokalemia
> 1.5 mm
38
what is an Osborn wave and what is it assoc with
Small positive deflection immediately after QRS may occur with hypothermia
39
EKG reference point for measuring ST elevation and depression
PR segment
40
what is the J point of EKG tracing
point where QRS complex ends, ST segment begins
41
how can J point be used to quantify ST elevation or depression
Measuring this point relative to PR segment can quantify amount of ST elevation and depression
42
as a general rule, when is J point significant
> +1 or < -1 are significant
43
EKG changes with hypokalemia
* u wave
* ST depression
* flat T wave
* long QT
44
EKG changes with hyper or hypocalcemia
* hyper = short QT
* hypo = long QT
45
EKG changes with hyper or hypomagnesemia
* hyper = not significant unless very high; heart block & arrest
* hypo = not significant unless very low; long QT
46
what region of the heart does lead I monitor
what's the corresponding coronary artery
lateral
circumflex a.
47
what region of the heart is monitored by lead II
corresponding coronary artery?
inferior
RCA
48
what region of the heart is monitored by lead III
corresponding coronary artery?
inferior
RCA
49
what region of the heart is monitored by aVL
corresponding coronary artery?
lateral
circumflex
50
what region of the heart is monitored by aVF
corresponding coronary artery?
inferior
RCA
51
what region of the heart is monitored by V1
corresponding coronary artery?
septum
LAD
52
what region of the heart is monitored by V2
corresponding coronary artery?
septum
LAD
53
what region of the heart is monitored by V3
corresponding coronary artery?
anterior
LAD
54
what region of the heart is monitored by V4
corresponding coronary artery?
anterior
LAD
55
what region of the heart is monitored by V5
corresponding coronary artery?
lateral
circumflex
56
what region of the heart is monitored by V5
corresponding coronary artery?
lateral
circumflex
57
what is mean electrical vector
avg current flow of all APs at given time
58
measure of mean electrical vector
EKG waveform
59
when does positive deflection occur in EKG Lead
when the vector of depolarization travels towards + electrode
60
when does negative deflection occur in EKG lead
occurs when the vector of depolarization travels away from + electrode
61
when does biphasic deflection occur with EKG waveform
when vector of depolarization travels perpendicular to + electrode
62
what is the vector of depolarization
QRS Complex
63
direction heart depolarizes
from the base - apex and endocardium - epicardium
64
vector of repolarization
T wave
65
direction of heart repolarization
opposite depolarization:
apex - base
epicardium - endocardium
66
what explains why T wave usually points in the same direction as the R wave
The “double negative” (opposite direction + negative current)
67
what does axis represent
the direction of the mean electrical vector in the frontal plane
68
lead I and aVF in normal axis
lead I +
lead aVF +
69
lead I and aVF in LAD
lead I +
lead aVF -
## Footnote
extreme RAD: lead I, aVF -
70
lead I and aVF in RAD
lead I -
aVF +
71
normal axis
-30 to +90 degrees
72
axis in LAD and RAD
* LAD is more negative than -30 degrees
* RAD is more positive than 90 degrees
73
causes of axis deviation
hypertrophy, conduction block, or a physical change in heart position
74
causes of RAD
COPD, acute bronchospasm, cor pulmonale, pHTN, PE
75
causes of LAD
chronic HTN, LBBB, aortis stenosis or insufficiency, mitral regurgitation
76
direction of mean electrical vector in hypertrophy vs infarction
tends to point towards areas of hypertrophy (more tissue to depolarize) and away from areas of infarction (vector has to move around these areas)
77
how does the bainbridge reflex affect HR
* Inhalation = ↓ intrathoracic pressure = ↑ venous return = ↑ HR
* Exhalation = ↑ intrathoracic pressure = ↓ venous return = ↓ HR
78
adverse effect of giving < 0.5 mg atropine
can cause paradoxical bradycardia (probably mediated by presynaptic muscarinic receptors)
79
treatment of bradycardia assoc. with beta blocker or CCB overdose
**glucagon**
50-70 mcg/kg q 3-5 min
can follow with 2-10 mg/hr gtt
80
MOA of glucagon for beta blocker induced bradycardia
stimulates receptors in myocardium, increasing cAMP
increased HR, contractility, AV conduction
81
what usually causes sinus tachycardia
increased intrinsic firing rate of the SA node or SNS stimulation
82
characteristics of A fib
Irregular rhythm with absent P wave
Chaotic electrical activity in the atrium is conducted to ventricle at a varied and irregular rate.
83
Most common postoperative tachydysrhythmia
A fib
## Footnote
usually between POD 2-4. Most common in older patients after cardiothoracic surgery.
84
treament of acute A fib
cardioversion (start with 100 joules)
85
when should TEE be obtained with A fib
onset > 48 hours or undetermined
86
when is A fib an indication to cancel surgery
new onset or undiagnosed
87
characteristics of A flutter waveform
Organized supraventricular rhythm with classic “sawtooth” pattern
## Footnote
Each atrial depolarization produces an atrial contraction, but not all atrial depolarizations are conducted past the AV node
88
rate with A flutter
Fast atrial rate (250-350)
89
ratio of atrial to ventricular contractions with A flutter
usually defined - ex 3:1
90
treatment of A flutter
rate control or cardioversion (HD unstable - cardioversion starting @ 50 joules)
91
prevents all atrial impulses from being transmitted to ventricles in A flutter
Effective refractory period
92
when should TEE be obtained in A flutter
If onset is > 48 hours or undetermined
93
when do junctional rhythms occur
when AV node functions as the dominant pacemaker
94
HR in junctional rhythm
40-60 because rate 4 depolarization of AV node is slow
95
causes of junctional rhythm
* SA node depression (volatiles)
* SA node block
* prolonged AV node conduction
96
treatment of junctional rhythm
Can give atropine 0.5 mg IV can be given if HD impacted by slow HR
97
what causes wide QRS with PVCs
Originate from foci below AV
98
unifocal PVCs
arise from a single location (same morphology)
99
multifocal PVCs
arise from multiple locations (different QRS morphologies)
100
EKG changes with digoxin toxicity
* down-sloping ST segment
* shortened QT interval
* T waves that are flat, inverted, or biphasic
101
when can PVCs precipitate R on T phenomenon
landing on the 2nd half of the T wave (during relative refractory period),
102
causes of PVCs
* SNS stimulation
* myocardial ischemia/infarction
* valvular heart disease
* cardiomyopathy
* prolonged QTc
* hypokalemia
* hypomagnesemia
* digoxin toxicity
* caffeine
* cocaine
* alcohol
* mechanical irritation (CVL insertion)
103
when should PVCs be treated
when frequent (> 6/min), polymorphic, or occur in runs of > 3
Symptomatic: lidocaine 1-1.5 mg/kg (can give infusion 1-4 mg/min)
104
Most common cause of sudden cardiac death
V fib
105
what is Brugada syndrome
Sodium ion channelopathy in the heart
pseudo-BBB & persistent ST elevations in V1-V2
106
EKG changes in type 1 brugada syndrome
* ST elevations 2 mm or greater
* downsloping ST segment
* inverted T wave
107
EKG changes in brugada syndrome type 2
* ST elevation 2 mm or greater
* "saddle back" ST-T wave configuration
* upright or biphasic T wave
108
Common cause of sudden nocturnal death d/t Vtach or fibrillation
Brugada syndrome
109
patient population Brugada syndrome is most common in
males from southeast Asia
110
characteristics of 1st degree heart block
* PR interval is > 0.2 seconds
* usually asymptomatic
111
etiologies of 1st degree heart block
* age-related degenerative changes
* CAD
* digoxin
* amiodarone
112
characteristics of 2nd degree heart block type 1
| (Mobitz Type 1)
PR interval becomes progressively longer with each cycle but the last P wave does not conduct to the ventricles - cycle repeats
113
affected region in 1st degree heart block
AV node or bundle of His
114
affected region in 2nd degree heart block type 1
AV node
115
etiologies of 2nd-degree heart block type 1
* structural conduction defect
* myocardial injury/infarction, beta blockers, CCBs, digoxin, sympatholytics
116
treatment of 2nd degree heart block type 1
* monitor if asymptomatic
* give atropine if symptomatic
117
affected regions with 2nd degree heart block type 2
His bundle or bundle branches
118
etiologies of 2nd degree heart block type 2
structural conduction defect, infarction
119
treatment of 2nd degree heart block type 2
pacemaker (atropine is not effective)
120
characteristics of 2nd degree heart block type 2
* Some P’s conduct to ventricles while others don’t - P arrives on time after dropped QRS
* Usually set ratio 2:1 or 3:1
121
common symptoms of 2nd degree heart block
palpitations
syncope
122
characteristics of 3rd degree heart block
* AV dissociation: atria & ventricles each have their own rate
* Block in AV node has narrow QRS (rate 45-55)
* Block below AV node has wide QRS (rate 30-40)
123
etiologies of 3rd degree heart block
* fibrotic degeneration of atrial conduction system
* Lenegre’s disease
124
common symptoms of 3rd degree heart block
dyspnea, syncope, weakness, vertigo
125
treatment of 3rd degree heart block
pacemaker, isoproterenol
126
what is a Stoke-Adams attack
decreased CO assoc. with 3rd degree heart block can cause decreased cerebral perfusion & syncope
127
how are antiarrythmic meds classified
according to ability to block specific ion channels & currents of cardiac AP
128
MOA of class 1 antiarrythmics
Na+ channel blockers
129
MOA of 1A antiarrythmics
moderate phase 0 depression
prolongs phase 4 repolarization (K+ block = increased QT)
130
MOA of 1B antiarrythmics
* Weak depression of phase 0
* Shortened phase 3 repolarization
131
Weak depression of phase 0
Shortened phase 1C repolarization
* Strong depression of phase 0
* Little effect on phase 3 repolarization
132
examples of 1A antiarrythmics
quinidine, procainamide, disopyramide
133
examples of 1B antiarrhythmics
Lidocaine, phenytoin
134
examples of 1C antiarrhythmics
Flecainide, Propafenone
135
MOA of class 2 antiarryhthmics
(beta blockers)
Slow phase 4 depolarization in SA node
136
MOA of class 3 antiarrhythmics
(K+ channel blockers)
Prolongs phase 3 repolarization
Increased effective refractory period
137
examples of class 3 antiarrhythmics
Amiodarone, Bretyrium
138
MOA of class 4 antiarrhythmics
(Calcium channel blockers)
Decreased conduction velocity through AV node
139
examples of class 4 antiarrhythmics
Verapamil, Diltiazem
140
endogenous nucleoside that slows conduction through AV node
adenosine
141
MOA of adenosine
* Stimulates cardiac adenosine-1 receptor
* potassium efflux = cell membrane hyperpolarized = AV node conduction slowed
142
uses of adenosine
* SVT
* WPW with narrow QRS
| Not useful for A-fib, A-flutter, or V-tach
143
dosing adenosine
* PIV: 1st dose 6 mg, 2nd dose 12 mg
* CVL: 1st dose 3 mg, 2nd dose 6 mg
144
patient population that may have adverse effect with adenosine
Can cause bronchospasm in asthmatics
145
normal conduction through the heart
SA node - AV node - His bundle - bundle branches - purkinje fibers
146
most common cause of tachyarrhythmias
reentry pathways
147
EKG findings consistent with WPW
* Delta wave caused by ventricular preexcitation
* Short PR interval (< .12 seconds)
* Wide QRS
* Possible T wave inversion
148
what is a reentry pathway
single cardiac impulse can move backwards and keep exciting the same part of the myocardium
149
how does normal conduction protect against reentry
* impulse can't move backwards (tissues behind the impulse remain in absolute refractory)
* impulses travel along right and left pathways at same speed & meet along connecting pathways but cancel each other out
* no opportunity for re-entry to occur
150
how does a reentry pathway occur
single cardiac impulse can move backwards and keep exciting the same part of the myocardium
One pathway is normal and the other has a bidirectional block. Impulse in normal pathway continues through circuit.
151
2 Ways to Break the Reentry Circuit:
1. Slow conduction velocity through circuit
2. Increase refractory period of cells at location of unidirectional block
152
causes of reentry pathways
* Conduction occurs over a long distance: LA dilation d/t mitral stenosis
* Conduction velocity is low: ischemia, hyperkalemia
* Refractory period is shorter: epinephrine, electric shock from alternating current
153
Most common pre-excitation syndrome
WPW
154
Defining feature of WPW
accessory conduction pathway (Kent's bundle) that bypasses AV node
155
how is WPW usually diagnosed
routine EKG or during workup for history of tachyarrhythmia
156
what is a delta wave in WPW
after SA depolarizes, impulse travels through AV node and accessory pathway at the same time
Accessory pathway doesn’t delay the impulse - arrives at ventricle early (causes characteristic delta wave)
157
Most common tachydysrhythmia assoc. with WPW
AV Nodal Reentry Tachycardia
158
incidence of orthodromic vs. antidromic AVNRT
Orthodromic = 90% of cases
159
reentry conduction pathway in orthodromic AVNRT
**Signal passes through AV first**
Atrium - AV node - ventricle - accessory pathway - atrium
160
reentry conduction pathway in antidromic AVNRT
Signal passes through accessory 1st
Atrium - accessory pathway - ventricle - AV node - atrium
161
QRS complex in orthodromic AVNRT
Narrow – ventricular depolarization occurs normally via His-Purkinje
162
QRS complex in antidromic AVNRT
Wide – depolarization slower because His-Purkinje is bypassed
163
treatment of Orthodromic AVNRT
Block conduction at AV node by increasing AV’s refractory period:
* Cardioversion
* Vagal maneuvers
* Adenosine
* Beta blockers
* Verapamil
* Amiodarone
164
treatment of antidromic AVNRT
Block conduction at accessory pathway by ↑ accessory pathway refractory pd:
* Cardioversion
* Procainamide
165
medications to avoid in antidromic AVNRT
Do NOT give agents that increase refractory period of AV node (will favor conduction through accessory pathway)
166
type of AVNRT that's the most dangerous
Antidromic
167
type of AVNRT that's the most dangerous
Antidromic
168
why is antidromic AVNRT more dangerous than orthodromic
gatekeeper function of AV node is bypassed, HR can increase well beyond heart’s pumping ability (dramatically ↓ filling time)
169
adverse effect of giving an AV blocking drug in antidromic AVNRT
* If you give a drug that preferentially blocks AV node, will force conduction along accessory pathway
* can induce ** V-fib**
## Footnote
Avoid adenosine, digoxin, CCBs, beta blockers, lidocaine
170
treatment of A-fib in WPW patient
* Treatment of choice: procainamide (increases refractory period in accessory pathway
* Cardiovert if hemodynamically unstable
171
definitive treatment for WPW
Radiofrequency Ablation
172
risks of Radiofrequency Ablation
thermal injury to LA and esophagus
closely monitor esophageal temp
173
Underlying cause of Torsades
delay in ventricular repolarization (phase 3 of AP)
174
what is Torsades usually associated with
prolonged QT interval
175
mnemonic for factors assoc. with prolonged QT interval and Torsades
PONTES:
* Phenothiazines,
* Other meds
* Intracranial bleed
* No known cause
* Type 1 antiarrhythmics
* Electrolyte disturbances
* Syndromes
176
metabolic disturbances assoc. with prolonged QT/Torsades
hypokalemia, hypocalcemia, hypomagnesemia
177
drugs assoc. with prolonged QT/Torsades
* methadone
* droperidol
* haloperidol
* ondansetron
* halogenated agents
* amiodarone (especially with hypokalemia)
* quinidine
178
med that has FDA requirement for 12 lead EKG before use
droperidol
179
genetic syndromes assoc with long QT/Torsades
Romano-Ward syndrome, Timothy syndrome
180
cardiac conditions assoc with long QT/Torsades
hypertrophic cardiomyopathy, SAH, bradycardia
181
how can prolonged QT result in Torsades
An electrical stimulus (PVC, poorly timed pacer discharge) during relative refractory period (2nd half of T wave) can cause torsades (R-on-T phenomenon)
182
relationship between QT intercal and HR
QT interval varies inversely with HR
183
how to prevent Torsades with long QT syndrome:
may require beta blocker prophylaxis and/or ICD placement, avoid SNS stimulation
184
acute treatment of Torsades
focuses on reversing underlying cause and/or shorten QT interval
* Magnesium sulfate
* Pacing to increase HR will decrease AP duration and QT interval
185
5 pacemaker indications
* Symptomatic SA node disease (disease of impulse formation)
* Symptomatic AV node disease (disease of impulse conduction)
* Long QT syndrome
* Dilated cardiomyopathy
* Hypertrophic obstructive cardiomyopathy
186
what does the circuit board of pacemaker do
processes electrical info from the heart and responds to signals based on programmed settings
187
EKG appearance with atrial pacing and capture
atrial artifact (vertical line) followed by P wave
| pacing spike precedes P wave, QRS is normal
188
EKG appearance with ventricular pacing and capture
ventricular artifact (vertical line) followed by wide QRS
| pacing spike precedes QRS
189
where is the atrial lead. of apacemaker placed
right atrial appendage
190
placement of pacemaker ventricular lead
apex of RV
191
what do the letters of the 5-letter pacemaker code describe
each letter describes a function performed by that particular pacemaker
192
what do the letters of a pacemaker stand for
* Position 1 = chamber paced
* Position 2 = chamber sensed
* Position 3 = response to sensor
* Position 4 = programmability
* Position 5 = can pace multiple sites
193
what does position 4 of pacemaker code describe
programmability
describes the ability to adjust HR in response to physiologic need
194
what does position 3 of pacemaker code describe
* T = sensed activity tells pacemaker to fire
* I = sensed activity tells pacemaker NOT to fire
* D = if native activity is sensed, pacing is inhibited. If not sensed, pacemaker fires.
195
EKG appearance of AV Sequential Pacemaker (dual chamber)
pacing spike stimulates the atria and another that stimulates ventricles
| ex: DDD pacing
196
EKG appearance of AV Sequential Pacemaker (dual chamber)
pacing spike stimulates the atria and another that stimulates ventricles
| ex: DDD pacing
197
when is risk of EMI greatest
coagulation setting on monopolar electrocautery and radiofrequency ablation
198
characteristics of asynchronois pacing
| AOO, VOO, DOO
* Pacemaker delivers constant rate
* No sense or inhibition
* Can be underlying competitive rhythm
199
adverse effect of pacer spike delivered during ventricular repolarization with asynchronous pacing
“R on T”
200
what is single-chamber demand pacing
| ex- AAI, VVI
Backup mode – only fires when native heart rate falls below predetermined rate
201
what is single-chamber demand pacing
| ex- AAI, VVI
Backup mode – only fires when native heart rate falls below predetermined rate
202
most common mode of pacing
Dual-Chamber AV Sequential Demand Pacing
## Footnote
Makes sure the atrium contracts 1st, followed by ventricle
203
most common mode of pacing
Dual-Chamber AV Sequential Demand Pacing
## Footnote
Makes sure the atrium contracts 1st, followed by ventricle
204
what happens to a pacemaker in the presence of a magnet
usually but not always converts to asynchronous mode
consult manufacturer
205
what happens to ICD in presence of a magnet
suspends ICD and prevents shock delivery
206
what happens to a pacemaker + ICD in presence of a magnet
suspends ICD & prevents shock delivery; NO effect on pacemaker function
207
3 types of pacemaker failure
1. Failure to sense
2. Failure to capture
3. Failure to output
208
3 types of pacemaker failure
1. Failure to sense
2. Failure to capture
3. Failure to output
209
pacemaker letters:
O =
A =
V =
D =
T =
I =
R =
O = none
A = atrium
V = ventricle
D = dual
T = triggered
I = inhibited
R = rate modulation
210
atrial pacing
211
ventricular pacing
212
AV Sequential Pacemaker (dual chamber)
213
Torsades de Pointes
214
1st Degree Heart Block
215
2nd Degree Heart Block (Mobitz Type 1)
216
Second Degree Heart Block (Mobitz Type 2)
217
Third Degree Heart Block
218
when does failure to sense occur
| aka undersensing
when pacemaker doesn’t sense native cardiac rhythm
219
pacemaker failure to sense
220
how can failure to sense cause V fib
Can cause “R-on-T” phenomenon if it fires during ventricular repolarization
221
EKG findings with failure to sense
Pacemaker sends impulse at sporadic times = pacing spikes in unexpected places
Results in asynchronous pacing
222
what causes failure to capture
* electrode displacement
* wire fracture
* conditions that make myocardium more resistant to depolarization (↑/↓ K+, hypocapnia, hypothermia, MI, fibrotic tissue around leads, antiarrythmics)
223
EKG findings with failure to capture
Will see pacing spikes on EKG but they aren’t followed by QRS (ventricular depolarization)
224
what is failure to capture
ventricle doesn’t depolarize in response to a pacing stimulus
225
med that could theoretically cause pacemaker failure to capture
succs
| could make myocardium less resistant to depolarization (transient ↑ in K
226
med that could theoretically cause pacemaker failure to capture
succs
| could make myocardium less resistant to depolarization (transient ↑ in K
227
what is failure to output
pacing stimulus not produced in a situation when it should be
228
causes of failure to output
oversensing, pulse generator failure, or lead failure
229
which electrocautery setting causes more EMI
“Coagulation” setting uses more EMI than “cutting” setting
230
which type of cautery causes more EMI - monopolar or bipolar
Monopolar
## Footnote
if surgeon insists, make sure they use short bursts (< 0.5 seconds)
231
which type of cautery causes more EMI - monopolar or bipolar
Monopolar
## Footnote
if surgeon insists, make sure they use short bursts (< 0.5 seconds)
232
when is risk of EMI greatest with pacemaker
when tip used within 15 cm radius of pulse generator
233
where should electrocautery pad be placed when pt has pacemaker
ace electrocautery return pad far away from pulse generator and location that prevents a direct line of current through the pulse generator
234
medications to treat pacemaker failure
Consider isoproterenol, epinephrine, and/or atropine
235
is MRI contraindicated in pt with an ICD/pacemaker?
yup
236
are lithotropsy or ECT contraindicated with pacemaker?
nope
237
what conditions increase the risk of failure to capture
* hyper/hypokalemia
* hypocapnea (intracellular K shift)
* hypothermia
* MI
* fibrotic tissue buildup around pacing leads
* antiarrythmic medications
238
3 internodal tracts that travel from SA to AV node
1. anterior nodal tract (gives rise to Bachmann bundle)
2. middle internodal tract (Wenkebach tract)
3. posterior internodal tract (Thorel tract)
## Footnote
**Bachmann pathway** depolarizes LA
239
what is the only electrical pathway betwen cardiac chambers
AV node
240
reference point for measuring changes in ST segment
PR interval
241
reference point for measuring changes in ST segment
PR interval
242
what is the J point
where QRS ends and ST segment begins
