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APEX > Unit 6 - Cardiac Rhythm Monitors & Equipment > Flashcards

Unit 6 - Cardiac Rhythm Monitors & Equipment Flashcards

1
Q

normal path of cardiac conduction

A

SA node - internodal tracts - AV node - bundle of His - bundle branches - Purkinje fibers

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2
Q

quantifies how fast an electrochemical impulse propagates along neural pathway

A

Conduction Velocity

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3
Q

normal conduction velocity of SA and AV nodes

A

0.02 – 0.10 m/sec (slow conduction)

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4
Q

normal conduction of myocardial muscle cells

A

0.3 – 1 m/sec (intermediate conduction)

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5
Q

normal conduction velocity of His bundle, bundle branches, and Purkinje fibers

A

1 – 4 m/sec (fast conduction)

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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

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7
Q

what is conduction velocity affected by

A
  • ANS tone
  • hyperkalemia-induced closure of fast Na+ channels
  • ischemia
  • acidosis
  • antiarrhythmic drugs
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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
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9
Q

“gatekeeper” of electrical transmission between atria and ventricles

A

AV node

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10
Q

accessory pathway assoc. with connection from atrium to AV node

A

James Fiber

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11
Q

accessory pathway assoc. with connection from atrium to His bundle

A

Atrio-hisian fiber

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12
Q

accessory pathway assoc. with connection from atrium to ventricle

A

Kent’s bundle

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13
Q

accessory pathway assoc. with connection from AV to ventricle

A

Mahaim bundle

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14
Q

event, ion movement, and key EKG event assoc with phase 0 of cardiac conduction

A

depolarization
Na+ in
QRS

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15
Q

event, ion movement, and key EKG event assoc with phase 1 of cardiac conduction

A

initial repolarization
Cl- in, K+ out
QRS

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16
Q

event, ion movement, and key EKG event assoc with phase 2 of cardiac conduction

A

plateau
Ca2+ in, K+ out
ST segment

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17
Q

event, ion movement, and key EKG event assoc with phase 3 of cardiac conduction

A

final repolarization
K+ out
T wave

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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

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19
Q

part of EKG assoc. with beginning of atrial depolarization

A

P wave

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20
Q

what part of EKG is atrial depolarization complete

A

PR interal

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21
Q

represents atrial repolarization, ventricular depolarization begins on EKG tracing

A

QRS

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22
Q

part of EKG assoc. with beginning of ventricular repolarization

A

T wave
(complete at end of T wave)

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23
Q

normal duration and amplitude of P wave

A

duration: 0.08-0.12 sec
amplitude: < 2.5 mm

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24
Q

what do biphasic P waves suggest

A

LA enlargement

think mitral stenosis

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25
Q

what do biphasic P waves suggest

A

LA enlargement

think mitral stenosis

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26
Q

normal duration of PR interval

A

0.12-0.2 sec

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27
Q

causes of PR interval depression

A
  • viral pericarditis
  • atrial infarction
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28
Q

normal duration and amplitude of Q wave

A

duration < 0.04 sec
amplitude < 0.4-0.5 mm

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29
Q

characteristics of pathologic Q wave (possible MI)

A
  • amplitude > 1/3 of R wave
  • duration > 0.04 sec
  • depth > 1 mm
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30
Q

normal QTC

A

Men < 0.45
Women < 0.47

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31
Q

characteristic of ST segment seen with MI

A

elevation or depression > 1 mm

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32
Q

when might ST be increased

A

MI
hyperkalemia
endocarditis

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33
Q

normal amplitude of T wave

A

< 10 mm in precordial
< 6 mm in limb leads

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34
Q

normal direction of T wave

A

Usually points in same direction as QRS

points opposite if repolarization prolonged by myocardial ischemia, BBB

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35
Q

causes of peaked T waves

A

myocardial ischemia
LVH
intracranial bleed

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36
Q

EKG changes with hyperkalemia

A
  • peaked T waves
  • short QT
  • prolonged PR
  • wide QRS
  • low P amplitude
  • nodal block

order of appearance early to late

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37
Q

u wave with hypokalemia

A

> 1.5 mm

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38
Q

what is an Osborn wave and what is it assoc with

A

Small positive deflection immediately after QRS may occur with hypothermia

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39
Q

EKG reference point for measuring ST elevation and depression

A

PR segment

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40
Q

what is the J point of EKG tracing

A

point where QRS complex ends, ST segment begins

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41
Q

how can J point be used to quantify ST elevation or depression

A

Measuring this point relative to PR segment can quantify amount of ST elevation and depression

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42
Q

as a general rule, when is J point significant

A

> +1 or < -1 are significant

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43
Q

EKG changes with hypokalemia

A
  • u wave
  • ST depression
  • flat T wave
  • long QT
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44
Q

EKG changes with hyper or hypocalcemia

A
  • hyper = short QT
  • hypo = long QT
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45
Q

EKG changes with hyper or hypomagnesemia

A
  • hyper = not significant unless very high; heart block & arrest
  • hypo = not significant unless very low; long QT
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46
Q

what region of the heart does lead I monitor

what’s the corresponding coronary artery

A

lateral
circumflex a.

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47
Q

what region of the heart is monitored by lead II

corresponding coronary artery?

A

inferior
RCA

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48
Q

what region of the heart is monitored by lead III

corresponding coronary artery?

A

inferior
RCA

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49
Q

what region of the heart is monitored by aVL

corresponding coronary artery?

A

lateral
circumflex

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50
Q

what region of the heart is monitored by aVF

corresponding coronary artery?

A

inferior
RCA

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51
Q

what region of the heart is monitored by V1

corresponding coronary artery?

A

septum
LAD

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52
Q

what region of the heart is monitored by V2

corresponding coronary artery?

A

septum
LAD

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53
Q

what region of the heart is monitored by V3

corresponding coronary artery?

A

anterior
LAD

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54
Q

what region of the heart is monitored by V4

corresponding coronary artery?

A

anterior
LAD

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55
Q

what region of the heart is monitored by V5

corresponding coronary artery?

A

lateral
circumflex

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56
Q

what region of the heart is monitored by V5

corresponding coronary artery?

A

lateral
circumflex

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57
Q

what is mean electrical vector

A

avg current flow of all APs at given time

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58
Q

measure of mean electrical vector

A

EKG waveform

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59
Q

when does positive deflection occur in EKG Lead

A

when the vector of depolarization travels towards + electrode

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60
Q

when does negative deflection occur in EKG lead

A

occurs when the vector of depolarization travels away from + electrode

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61
Q

when does biphasic deflection occur with EKG waveform

A

when vector of depolarization travels perpendicular to + electrode

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62
Q

what is the vector of depolarization

A

QRS Complex

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63
Q

direction heart depolarizes

A

from the base - apex and endocardium - epicardium

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64
Q

vector of repolarization

A

T wave

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65
Q

direction of heart repolarization

A

opposite depolarization:
apex - base
epicardium - endocardium

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66
Q

what explains why T wave usually points in the same direction as the R wave

A

The “double negative” (opposite direction + negative current)

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67
Q

what does axis represent

A

the direction of the mean electrical vector in the frontal plane

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68
Q

lead I and aVF in normal axis

A

lead I +
lead aVF +

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69
Q

lead I and aVF in LAD

A

lead I +
lead aVF -

extreme RAD: lead I, aVF -

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70
Q

lead I and aVF in RAD

A

lead I -
aVF +

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71
Q

normal axis

A

-30 to +90 degrees

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72
Q

axis in LAD and RAD

A
  • LAD is more negative than -30 degrees
  • RAD is more positive than 90 degrees
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73
Q

causes of axis deviation

A

hypertrophy, conduction block, or a physical change in heart position

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74
Q

causes of RAD

A

COPD, acute bronchospasm, cor pulmonale, pHTN, PE

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75
Q

causes of LAD

A

chronic HTN, LBBB, aortis stenosis or insufficiency, mitral regurgitation

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76
Q

direction of mean electrical vector in hypertrophy vs infarction

A

tends to point towards areas of hypertrophy (more tissue to depolarize) and away from areas of infarction (vector has to move around these areas)

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77
Q

how does the bainbridge reflex affect HR

A
  • Inhalation = ↓ intrathoracic pressure = ↑ venous return = ↑ HR
  • Exhalation = ↑ intrathoracic pressure = ↓ venous return = ↓ HR
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78
Q

adverse effect of giving < 0.5 mg atropine

A

can cause paradoxical bradycardia (probably mediated by presynaptic muscarinic receptors)

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79
Q

treatment of bradycardia assoc. with beta blocker or CCB overdose

A

glucagon
50-70 mcg/kg q 3-5 min
can follow with 2-10 mg/hr gtt

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80
Q

MOA of glucagon for beta blocker induced bradycardia

A

stimulates receptors in myocardium, increasing cAMP

increased HR, contractility, AV conduction

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81
Q

what usually causes sinus tachycardia

A

increased intrinsic firing rate of the SA node or SNS stimulation

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82
Q

characteristics of A fib

A

Irregular rhythm with absent P wave

Chaotic electrical activity in the atrium is conducted to ventricle at a varied and irregular rate.

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83
Q

Most common postoperative tachydysrhythmia

A

A fib

usually between POD 2-4. Most common in older patients after cardiothoracic surgery.

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84
Q

treament of acute A fib

A

cardioversion (start with 100 joules)

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85
Q

when should TEE be obtained with A fib

A

onset > 48 hours or undetermined

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86
Q

when is A fib an indication to cancel surgery

A

new onset or undiagnosed

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87
Q

characteristics of A flutter waveform

A

Organized supraventricular rhythm with classic “sawtooth” pattern

Each atrial depolarization produces an atrial contraction, but not all atrial depolarizations are conducted past the AV node

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88
Q

rate with A flutter

A

Fast atrial rate (250-350)

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89
Q

ratio of atrial to ventricular contractions with A flutter

A

usually defined - ex 3:1

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90
Q

treatment of A flutter

A

rate control or cardioversion (HD unstable - cardioversion starting @ 50 joules)

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91
Q

prevents all atrial impulses from being transmitted to ventricles in A flutter

A

Effective refractory period

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92
Q

when should TEE be obtained in A flutter

A

If onset is > 48 hours or undetermined

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93
Q

when do junctional rhythms occur

A

when AV node functions as the dominant pacemaker

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94
Q

HR in junctional rhythm

A

40-60 because rate 4 depolarization of AV node is slow

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95
Q

causes of junctional rhythm

A
  • SA node depression (volatiles)
  • SA node block
  • prolonged AV node conduction
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96
Q

treatment of junctional rhythm

A

Can give atropine 0.5 mg IV can be given if HD impacted by slow HR

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97
Q

what causes wide QRS with PVCs

A

Originate from foci below AV

98
Q

unifocal PVCs

A

arise from a single location (same morphology)

99
Q

multifocal PVCs

A

arise from multiple locations (different QRS morphologies)

100
Q

EKG changes with digoxin toxicity

A
  • down-sloping ST segment
  • shortened QT interval
  • T waves that are flat, inverted, or biphasic
101
Q

when can PVCs precipitate R on T phenomenon

A

landing on the 2nd half of the T wave (during relative refractory period),

102
Q

causes of PVCs

A
  • SNS stimulation
  • myocardial ischemia/infarction
  • valvular heart disease
  • cardiomyopathy
  • prolonged QTc
  • hypokalemia
  • hypomagnesemia
  • digoxin toxicity
  • caffeine
  • cocaine
  • alcohol
  • mechanical irritation (CVL insertion)
103
Q

when should PVCs be treated

A

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
Q

Most common cause of sudden cardiac death

105
Q

what is Brugada syndrome

A

Sodium ion channelopathy in the heart

pseudo-BBB & persistent ST elevations in V1-V2

106
Q

EKG changes in type 1 brugada syndrome

A
  • ST elevations 2 mm or greater
  • downsloping ST segment
  • inverted T wave
107
Q

EKG changes in brugada syndrome type 2

A
  • ST elevation 2 mm or greater
  • “saddle back” ST-T wave configuration
  • upright or biphasic T wave
108
Q

Common cause of sudden nocturnal death d/t Vtach or fibrillation

A

Brugada syndrome

109
Q

patient population Brugada syndrome is most common in

A

males from southeast Asia

110
Q

characteristics of 1st degree heart block

A
  • PR interval is > 0.2 seconds
  • usually asymptomatic
111
Q

etiologies of 1st degree heart block

A
  • age-related degenerative changes
  • CAD
  • digoxin
  • amiodarone
112
Q

characteristics of 2nd degree heart block type 1

(Mobitz Type 1)

A

PR interval becomes progressively longer with each cycle but the last P wave does not conduct to the ventricles - cycle repeats

113
Q

affected region in 1st degree heart block

A

AV node or bundle of His

114
Q

affected region in 2nd degree heart block type 1

115
Q

etiologies of 2nd-degree heart block type 1

A
  • structural conduction defect
  • myocardial injury/infarction, beta blockers, CCBs, digoxin, sympatholytics
116
Q

treatment of 2nd degree heart block type 1

A
  • monitor if asymptomatic
  • give atropine if symptomatic
117
Q

affected regions with 2nd degree heart block type 2

A

His bundle or bundle branches

118
Q

etiologies of 2nd degree heart block type 2

A

structural conduction defect, infarction

119
Q

treatment of 2nd degree heart block type 2

A

pacemaker (atropine is not effective)

120
Q

characteristics of 2nd degree heart block type 2

A
  • 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
Q

common symptoms of 2nd degree heart block

A

palpitations
syncope

122
Q

characteristics of 3rd degree heart block

A
  • 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
Q

etiologies of 3rd degree heart block

A
  • fibrotic degeneration of atrial conduction system
  • Lenegre’s disease
124
Q

common symptoms of 3rd degree heart block

A

dyspnea, syncope, weakness, vertigo

125
Q

treatment of 3rd degree heart block

A

pacemaker, isoproterenol

126
Q

what is a Stoke-Adams attack

A

decreased CO assoc. with 3rd degree heart block can cause decreased cerebral perfusion & syncope

127
Q

how are antiarrythmic meds classified

A

according to ability to block specific ion channels & currents of cardiac AP

128
Q

MOA of class 1 antiarrythmics

A

Na+ channel blockers

129
Q

MOA of 1A antiarrythmics

A

moderate phase 0 depression

prolongs phase 4 repolarization (K+ block = increased QT)

130
Q

MOA of 1B antiarrythmics

A
  • Weak depression of phase 0
  • Shortened phase 3 repolarization
131
Q

Weak depression of phase 0
Shortened phase 1C repolarization

A
  • Strong depression of phase 0
  • Little effect on phase 3 repolarization
132
Q

examples of 1A antiarrythmics

A

quinidine, procainamide, disopyramide

133
Q

examples of 1B antiarrhythmics

A

Lidocaine, phenytoin

134
Q

examples of 1C antiarrhythmics

A

Flecainide, Propafenone

135
Q

MOA of class 2 antiarryhthmics

A

(beta blockers)

Slow phase 4 depolarization in SA node

136
Q

MOA of class 3 antiarrhythmics

A

(K+ channel blockers)

Prolongs phase 3 repolarization
Increased effective refractory period

137
Q

examples of class 3 antiarrhythmics

A

Amiodarone, Bretyrium

138
Q

MOA of class 4 antiarrhythmics

A

(Calcium channel blockers)

Decreased conduction velocity through AV node

139
Q

examples of class 4 antiarrhythmics

A

Verapamil, Diltiazem

140
Q

endogenous nucleoside that slows conduction through AV node

141
Q

MOA of adenosine

A
  • Stimulates cardiac adenosine-1 receptor
  • potassium efflux = cell membrane hyperpolarized = AV node conduction slowed
142
Q

uses of adenosine

A
  • SVT
  • WPW with narrow QRS

Not useful for A-fib, A-flutter, or V-tach

143
Q

dosing adenosine

A
  • PIV: 1st dose 6 mg, 2nd dose 12 mg
  • CVL: 1st dose 3 mg, 2nd dose 6 mg
144
Q

patient population that may have adverse effect with adenosine

A

Can cause bronchospasm in asthmatics

145
Q

normal conduction through the heart

A

SA node - AV node - His bundle - bundle branches - purkinje fibers

146
Q

most common cause of tachyarrhythmias

A

reentry pathways

147
Q

EKG findings consistent with WPW

A
  • Delta wave caused by ventricular preexcitation
  • Short PR interval (< .12 seconds)
  • Wide QRS
  • Possible T wave inversion
148
Q

what is a reentry pathway

A

single cardiac impulse can move backwards and keep exciting the same part of the myocardium

149
Q

how does normal conduction protect against reentry

A
  • 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
Q

how does a reentry pathway occur

A

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
Q

2 Ways to Break the Reentry Circuit:

A
  1. Slow conduction velocity through circuit
  2. Increase refractory period of cells at location of unidirectional block
152
Q

causes of reentry pathways

A
  • 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
Q

Most common pre-excitation syndrome

154
Q

Defining feature of WPW

A

accessory conduction pathway (Kent’s bundle) that bypasses AV node

155
Q

how is WPW usually diagnosed

A

routine EKG or during workup for history of tachyarrhythmia

156
Q

what is a delta wave in WPW

A

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
Q

Most common tachydysrhythmia assoc. with WPW

A

AV Nodal Reentry Tachycardia

158
Q

incidence of orthodromic vs. antidromic AVNRT

A

Orthodromic = 90% of cases

159
Q

reentry conduction pathway in orthodromic AVNRT

A

Signal passes through AV first

Atrium - AV node - ventricle - accessory pathway - atrium

160
Q

reentry conduction pathway in antidromic AVNRT

A

Signal passes through accessory 1st

Atrium - accessory pathway - ventricle - AV node - atrium

161
Q

QRS complex in orthodromic AVNRT

A

Narrow – ventricular depolarization occurs normally via His-Purkinje

162
Q

QRS complex in antidromic AVNRT

A

Wide – depolarization slower because His-Purkinje is bypassed

163
Q

treatment of Orthodromic AVNRT

A

Block conduction at AV node by increasing AV’s refractory period:
* Cardioversion
* Vagal maneuvers
* Adenosine
* Beta blockers
* Verapamil
* Amiodarone

164
Q

treatment of antidromic AVNRT

A

Block conduction at accessory pathway by ↑ accessory pathway refractory pd:
* Cardioversion
* Procainamide

165
Q

medications to avoid in antidromic AVNRT

A

Do NOT give agents that increase refractory period of AV node (will favor conduction through accessory pathway)

166
Q

type of AVNRT that’s the most dangerous

A

Antidromic

167
Q

type of AVNRT that’s the most dangerous

A

Antidromic

168
Q

why is antidromic AVNRT more dangerous than orthodromic

A

gatekeeper function of AV node is bypassed, HR can increase well beyond heart’s pumping ability (dramatically ↓ filling time)

169
Q

adverse effect of giving an AV blocking drug in antidromic AVNRT

A
  • If you give a drug that preferentially blocks AV node, will force conduction along accessory pathway
  • can induce ** V-fib**

Avoid adenosine, digoxin, CCBs, beta blockers, lidocaine

170
Q

treatment of A-fib in WPW patient

A
  • Treatment of choice: procainamide (increases refractory period in accessory pathway
  • Cardiovert if hemodynamically unstable
171
Q

definitive treatment for WPW

A

Radiofrequency Ablation

172
Q

risks of Radiofrequency Ablation

A

thermal injury to LA and esophagus

closely monitor esophageal temp

173
Q

Underlying cause of Torsades

A

delay in ventricular repolarization (phase 3 of AP)

174
Q

what is Torsades usually associated with

A

prolonged QT interval

175
Q

mnemonic for factors assoc. with prolonged QT interval and Torsades

A

PONTES:

  • Phenothiazines,
  • Other meds
  • Intracranial bleed
  • No known cause
  • Type 1 antiarrhythmics
  • Electrolyte disturbances
  • Syndromes
176
Q

metabolic disturbances assoc. with prolonged QT/Torsades

A

hypokalemia, hypocalcemia, hypomagnesemia

177
Q

drugs assoc. with prolonged QT/Torsades

A
  • methadone
  • droperidol
  • haloperidol
  • ondansetron
  • halogenated agents
  • amiodarone (especially with hypokalemia)
  • quinidine
178
Q

med that has FDA requirement for 12 lead EKG before use

A

droperidol

179
Q

genetic syndromes assoc with long QT/Torsades

A

Romano-Ward syndrome, Timothy syndrome

180
Q

cardiac conditions assoc with long QT/Torsades

A

hypertrophic cardiomyopathy, SAH, bradycardia

181
Q

how can prolonged QT result in Torsades

A

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
Q

relationship between QT intercal and HR

A

QT interval varies inversely with HR

183
Q

how to prevent Torsades with long QT syndrome:

A

may require beta blocker prophylaxis and/or ICD placement, avoid SNS stimulation

184
Q

acute treatment of Torsades

A

focuses on reversing underlying cause and/or shorten QT interval
* Magnesium sulfate
* Pacing to increase HR will decrease AP duration and QT interval

185
Q

5 pacemaker indications

A
  • 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
Q

what does the circuit board of pacemaker do

A

processes electrical info from the heart and responds to signals based on programmed settings

187
Q

EKG appearance with atrial pacing and capture

A

atrial artifact (vertical line) followed by P wave

pacing spike precedes P wave, QRS is normal

188
Q

EKG appearance with ventricular pacing and capture

A

ventricular artifact (vertical line) followed by wide QRS

pacing spike precedes QRS

189
Q

where is the atrial lead. of apacemaker placed

A

right atrial appendage

190
Q

placement of pacemaker ventricular lead

A

apex of RV

191
Q

what do the letters of the 5-letter pacemaker code describe

A

each letter describes a function performed by that particular pacemaker

192
Q

what do the letters of a pacemaker stand for

A
  • Position 1 = chamber paced
  • Position 2 = chamber sensed
  • Position 3 = response to sensor
  • Position 4 = programmability
  • Position 5 = can pace multiple sites
193
Q

what does position 4 of pacemaker code describe

A

programmability

describes the ability to adjust HR in response to physiologic need

194
Q

what does position 3 of pacemaker code describe

A
  • 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
Q

EKG appearance of AV Sequential Pacemaker (dual chamber)

A

pacing spike stimulates the atria and another that stimulates ventricles

ex: DDD pacing

196
Q

EKG appearance of AV Sequential Pacemaker (dual chamber)

A

pacing spike stimulates the atria and another that stimulates ventricles

ex: DDD pacing

197
Q

when is risk of EMI greatest

A

coagulation setting on monopolar electrocautery and radiofrequency ablation

198
Q

characteristics of asynchronois pacing

AOO, VOO, DOO

A
  • Pacemaker delivers constant rate
  • No sense or inhibition
  • Can be underlying competitive rhythm
199
Q

adverse effect of pacer spike delivered during ventricular repolarization with asynchronous pacing

A

“R on T”

200
Q

what is single-chamber demand pacing

ex- AAI, VVI

A

Backup mode – only fires when native heart rate falls below predetermined rate

201
Q

what is single-chamber demand pacing

ex- AAI, VVI

A

Backup mode – only fires when native heart rate falls below predetermined rate

202
Q

most common mode of pacing

A

Dual-Chamber AV Sequential Demand Pacing

Makes sure the atrium contracts 1st, followed by ventricle

203
Q

most common mode of pacing

A

Dual-Chamber AV Sequential Demand Pacing

Makes sure the atrium contracts 1st, followed by ventricle

204
Q

what happens to a pacemaker in the presence of a magnet

A

usually but not always converts to asynchronous mode

consult manufacturer

205
Q

what happens to ICD in presence of a magnet

A

suspends ICD and prevents shock delivery

206
Q

what happens to a pacemaker + ICD in presence of a magnet

A

suspends ICD & prevents shock delivery; NO effect on pacemaker function

207
Q

3 types of pacemaker failure

A
  1. Failure to sense
  2. Failure to capture
  3. Failure to output
208
Q

3 types of pacemaker failure

A
  1. Failure to sense
  2. Failure to capture
  3. Failure to output
209
Q

pacemaker letters:
O =
A =
V =
D =
T =
I =
R =

A

O = none
A = atrium
V = ventricle
D = dual
T = triggered
I = inhibited
R = rate modulation

210
Q
A

atrial pacing

211
Q
A

ventricular pacing

212
Q
A

AV Sequential Pacemaker (dual chamber)

213
Q
A

Torsades de Pointes

214
Q
A

1st Degree Heart Block

215
Q
A

2nd Degree Heart Block (Mobitz Type 1)

216
Q
A

Second Degree Heart Block (Mobitz Type 2)

217
Q
A

Third Degree Heart Block

218
Q

when does failure to sense occur

aka undersensing

A

when pacemaker doesn’t sense native cardiac rhythm

219
Q
A

pacemaker failure to sense

220
Q

how can failure to sense cause V fib

A

Can cause “R-on-T” phenomenon if it fires during ventricular repolarization

221
Q

EKG findings with failure to sense

A

Pacemaker sends impulse at sporadic times = pacing spikes in unexpected places

Results in asynchronous pacing

222
Q

what causes failure to capture

A
  • electrode displacement
  • wire fracture
  • conditions that make myocardium more resistant to depolarization (↑/↓ K+, hypocapnia, hypothermia, MI, fibrotic tissue around leads, antiarrythmics)
223
Q

EKG findings with failure to capture

A

Will see pacing spikes on EKG but they aren’t followed by QRS (ventricular depolarization)

224
Q

what is failure to capture

A

ventricle doesn’t depolarize in response to a pacing stimulus

225
Q

med that could theoretically cause pacemaker failure to capture

A

succs

could make myocardium less resistant to depolarization (transient ↑ in K

226
Q

med that could theoretically cause pacemaker failure to capture

A

succs

could make myocardium less resistant to depolarization (transient ↑ in K

227
Q

what is failure to output

A

pacing stimulus not produced in a situation when it should be

228
Q

causes of failure to output

A

oversensing, pulse generator failure, or lead failure

229
Q

which electrocautery setting causes more EMI

A

“Coagulation” setting uses more EMI than “cutting” setting

230
Q

which type of cautery causes more EMI - monopolar or bipolar

A

Monopolar

if surgeon insists, make sure they use short bursts (< 0.5 seconds)

231
Q

which type of cautery causes more EMI - monopolar or bipolar

A

Monopolar

if surgeon insists, make sure they use short bursts (< 0.5 seconds)

232
Q

when is risk of EMI greatest with pacemaker

A

when tip used within 15 cm radius of pulse generator

233
Q

where should electrocautery pad be placed when pt has pacemaker

A

ace electrocautery return pad far away from pulse generator and location that prevents a direct line of current through the pulse generator

234
Q

medications to treat pacemaker failure

A

Consider isoproterenol, epinephrine, and/or atropine

235
Q

is MRI contraindicated in pt with an ICD/pacemaker?

236
Q

are lithotropsy or ECT contraindicated with pacemaker?

237
Q

what conditions increase the risk of failure to capture

A
  • hyper/hypokalemia
  • hypocapnea (intracellular K shift)
  • hypothermia
  • MI
  • fibrotic tissue buildup around pacing leads
  • antiarrythmic medications
238
Q

3 internodal tracts that travel from SA to AV node

A
  1. anterior nodal tract (gives rise to Bachmann bundle)
  2. middle internodal tract (Wenkebach tract)
  3. posterior internodal tract (Thorel tract)

Bachmann pathway depolarizes LA

239
Q

what is the only electrical pathway betwen cardiac chambers

240
Q

reference point for measuring changes in ST segment

A

PR interval

241
Q

reference point for measuring changes in ST segment

A

PR interval

242
Q

what is the J point

A

where QRS ends and ST segment begins

APEX (54 decks)

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