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8. ECG > Pacemaker > Flashcards

Pacemaker Flashcards

1
Q

Common PM implanted in vet practice

A
  • Single transvenous lead pacing in RV apex most commonly
    o Easy to place
    o Alternative sites: bundle of His, biventricular
  • Single epicardial lead pacing on LV apex
    o Alternative for unsuitable to transvenous pacing
  • Dual chamber may provide superior performance → DDD mode
    o Favorize AV synchrony → improve hemodynamics
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2
Q

Risk epicardial pacing

A

↑ risk for bacteremia, thrombosis, embolism

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3
Q

Consequences of long term RV pacing

A

 Asynchronous ventricular contraction
 Impaired cardiac performance
 Deleterious myocardial remodeling

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4
Q

Advantage of Dual ch

A

o Favorize AV synchrony → improve hemodynamics

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5
Q

CO depends on

A

o Ventricular rate and physiologic HR variation
o Synchrony of atrial/ventricular contraction
 Can be attained by
* Pacing atrium
* Endogenous atrial depol → AV delay → ventricular pacing
 Hu: improve CO, BP, quality of life
o Ventricular activation sequence

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6
Q

Modes of dual chamber pacing

A
  • DDD mode: 2 leads (1 atrial, 1 ventricular)
  • VDD mode: 1 lead in RV with floating electrodes
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7
Q

Disadvantages of dual pacing

A

o Complex programming,
o ↑ expense, ↑ implantation time
o Technical challenge of placing atrial lead in small patiens
o ↑ complications post op

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8
Q

Define the NASPE/BPEG classification.

A

1- Chamber paced
O none
A atrium
V ventricle
D dual

2- Chamber sensed
O none
A atrium
V ventricle
D dual

3- response to sensing
O none
T triggered
I inhibited
D dual

4- rate modulation
O non
R rate modulation

5- multisite pacing
O none
A atrium
V ventricle
D dual

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9
Q

What are the typical modes used in veterinary practice?

A

Most commons: VVI and VVIR

AAI/AAIR
VDD
DDD

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10
Q

VVI modality

A
  • Ventricular depolarization in absence of inherent beat
  • Sensing ventricular signal → inhibit PM output
    o Important feature to prevent competitive rhythms and trigger arrhythmias if pacing during vulnerable period of cardiac cycle
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11
Q

Disadvantages

A

o Preset pacing rate (non physiological pacing)
o Asynchronous contraction of A and V → can lead to PM syndrome

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12
Q

VVIR

A
  • Similar to VVI + rate responsiveness (chronotropic competence)
  • Stimulation frequency ↑ in response to physical activity/respiration
    o Sensors: motion, minute ventilation
  • AV asynchrony persists
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13
Q

AAI/AAIR

A
  • Single chamber, atrial inhibited +/- rate responsiveness
    o Stimulus delivered to atrium
    o PM output inhibited by atrial events
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14
Q

AAI/AAIR pacing indications

A

SSS and normal AV node function

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15
Q

AAI/AAIR pacing advantages

A

o Maintain AV synchrony
o Synchronous ventricular contraction
o Avoid retrograde conduction through AV node and echo beats

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16
Q

AAI/AAIR pacing disadvantages

A

lack of depol if AVB occurs
o 24h Holter and Weckenbach testing recommended

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17
Q

VDD

A
  • Atrial synchronous pacing
    o Single pacing lead w sensing electrodes in atrial portion of lead
     Pacing in ventricle
     Sensing in atria and ventricle → input inhibited by ventricular beat but stimulated by atrial beat
    o Sensed atrial events → AV delay
     Intrinsic ventricular beat during AV delay → inhibit pacing, reset timing cycle
     No intrinsic ventricular beat → paced beat at end of AV delay
     No intrinsic atrial event → PM escape w paced ventricular depol at lower rate
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18
Q

Upper tracking rate

A

upper limit of atrial depol permitted to trigger ventricular depol

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19
Q

Requirement for VDD pacing

A
  • Need normal SA node function
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20
Q

DDD

A
  • Dual chamber pacing + sensing with inhibition and tracking → fully automatic PM
  • Similar to VDD but atrium is paced
    o No intrinsic atrial depol → atrial paced beat → tracked → ventricular paced beat
  • ECG can vary → normal sinus rhythm, atrial pacing only, AV sequential pacing, atrial synchronous pacing
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21
Q

DDD pacing advantages

A

preserve AV synchrony

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22
Q

PM refractory periodq

A
  • Pacemaker is refractory for specific (pragrammable) period after paced or sensed depol
    o Ventricular events during refractory period = will not reset PM
    o Ventricular event after refractory period → sensed and inhibit output
     Restart timing cycle
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23
Q

Pacemaker syndrome c/s

A
  • Vasovagal syncope, pre-syncope, shortness of breath, dyspnea with exertion
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24
Q

Mechanism of c/s w/ PM syndrome

A

o ↑LAP/RAP with atrial contraction against closed AV valve during ventricular contraction
 Release of ANP → vasodilation and diuresis
o Stretch of atrial baroR → vagally mediated hypotension
o Stimulation of cardiopulmonary baroR from canon V wave

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25
Q

Cause of c/s w/ PM syndrome

A
  • Caused by improper timing btw atrial and ventricular contraction
    o Atrial contraction: 15-25% of CO
    o Hemodynamic consequence: ↓CO, BP, ↑PAP/PVP
    o Suspect if BP ↓ >20mmHg with paced beats compared to sinus rhythm
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26
Q

Treatment PM syndrome

A

should resolve with restoration of AV synchrony
o VVIR should help → allow underlying sinus rate to predominate
o Dual chamber PM to insure AV sequential pacing

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27
Q

Ventriculoatrial conduction

A
  • Retrograde depolarization of atria
    o Hu: 90% of SSS and 30% of AVB cases
  • Long term effects in dogs not established
    o Hu: ↑ susceptibility to adverse circulatory reflexes from atrial R
     Atrial, PVs, venoatrial jct distension → vagal afferent → vasodepressor response → ↓BP and HR
     Associated with ↑ R sided and pulmonary filling P
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28
Q

Components of pacing system

A

Pulse generator
Pacing lead

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29
Q

Pulse generator

A

o Lithium iodide battery w electronic circuitry connected to lead
 D/c pacing impulses of different voltage/duration
 Sense intracardiac signals, filter signals, rate response fct, store rhythms data
o Can test battery life, lead impedance, retrograde ventriculoatrial conduction, pacing thresholds

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30
Q

Asynchronous mode

A

magnet in close proximity

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31
Q

Pacing lead: how is it made

A

o Insulated wire that conduct impulse from generator to myocardium
 Conductor + lead insulation + lead connector + electrode

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32
Q

Types of leads and fixation

A

o Epicardial: pacing wires sutured to heart → atrium +/- ventricle

o Transvenous endocardial: RA, RV
 Passive fixation: collar of tines at tip of lead → anchors lead in RV trabeculae
 Active fixation: screw into myocardium

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33
Q

Pacing circuit

A

o Anode → + pole, cathode → - pole
 Cathode is always tip of lead

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34
Q

Circuit unipolar lead

A

cathode = lead tip, anode = generator
 Impulse travels from generator → myocardium in lead
 Myocardium → generator via soft tissues
* Proximity to skeletal muscles → can cause twitching

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35
Q

ECG unipolar lead

A

large pacing spikes

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36
Q

Advantages unipolar lead

A
  • Smaller diameter pacing leads
  • Single attachment site
  • Superior sensitivity for sensing intrinsic beats
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37
Q

Disadvantages unipolar lead

A
  • More susceptible to oversensing
  • Can detect skeletal muscle potentials
  • Generator in contact w/ body/tissues → can cause muscle twitching
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38
Q

Circuit bipolar lead

A

2 spaced electrodes distally on lead, distal = cathode, proximal = anode

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39
Q

Advantages bipolar lead

A
  • Greater signal to noise ratio
  • Less sensitivity to extraneous interference
  • Avoid skeletal muscle stimulation
  • Generator does not have to touch body tissue
  • Less susceptible to oversensing
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40
Q

ECG bipolar lead

A

Smaller pacing spikes

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41
Q

Why choose epicardial PM

A

o Usually if lead dislodgement or animal too small for transvenous

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42
Q

ECG epicardial PM

A

larger pacing spikes
 Wide QRS

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43
Q

Disadvantages epicardial PM

A

 More inflammation vs transvenous
 Invasive: intercostal or diaphragmatic approach

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44
Q

Advantages epicardial PM

A

 Can be considered for pts at higher risk for endocardial complications due to pt size, pre-existing infections, or hypercoagulability
 Pacing from L ventricle might be associated with better cardiac systolic fct (compared to RV)
 Avoid contact of lead w/ blood and intra cardiac structures

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45
Q

Factors involving lead system in clinic

A

o Output voltage
 Certain magnitude of voltage must be applied to induce depol of myocytes
 Stimulation threshold: min voltage required to stimulate heart outside its refractory period

o Lead resistance

o Pulse duration (width)

o Pacing rate

o % pacing time

o Battery capacity

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46
Q

Ohm’s law

A

V = IR

V: stimulus voltage
I: current
R: resistance

47
Q

Strength duration curve

A
  • Relationship btw voltage and pulse duration → exponential

o Pulse width <0.25ms → steep curve
o Pulse width >1ms → flat curve

48
Q

Energy (E) of pacing stimulus: determined by

A
  • To stimulate the heart → certain amount of voltage must be applied for a certain time
    o Energy (E) of pacing stimulus: determined by
     V: voltage
     t: duration of voltage applied → pulse width
     R: resistance
    o ↑ voltage with ↓ pulse width OR ↓ voltage but ↑ pulse width

E = (V^2 t)/R

49
Q

PM programming w/ strength duration curve

A

o If short pulse duration: short error margin if stimulation threshold ↑
o If long pulse width: no more effect on heart stimulation → drain battery

50
Q

What is rheobase

A

o Lowest voltage resulting in capture
o Usually pulse width <1.5ms

51
Q

What is chronaxie

A

o Pulse width required to capture at 2x rheobase voltage
o Approximate minimum threshold stimulation energy

52
Q

Safety margin for programming

A

o Voltage: 2x voltage at chronaxie pulse width
o Pulse width: 3x pulse width at chronaxie if <0.2ms
 If >0.2ms → voltage should be ↑ or lead repositioned

53
Q

Ideal chronic settings

A
  • Chronic leads: should not have stimulation thresholds >2.5V at pulse width of 0.5ms
    o ↓ longevity of pulse generator
54
Q

Threshold tests

A

After PM implantation and at rechecks
* ↓ voltage at given pulse width (0.5ms) until loss of capture
* ↓ pulse width at given voltage (5V) until loss of capture

55
Q

What is Wendensky’s effect

A

capture hysteresis
o Testing from capture → loss of capture, not lack of capture → capture
o > energy required to gain capture

56
Q

What is impedance

A
  • Total resistance to current flow
    o Excessive resistance → generates heat → not efficient to generate current for pacing
    o ↓ acutely after implantation, then ↑ and stabilizes
57
Q

Factors influencing impedance

A

Resisance of
o Conducting lead → conductor resistance
 Bipolar leads: ↑ conductor impedance → 2 conducting wires
 Unipolar leads: ↓ impedance → large surface area of anode (pulse generator)

o Electrode and tissue → electrode resistance
 Small electrode tip: ↑ resistance but more efficient use of E

o Accumulation of charge at electrode tip interface → polarization resistance
 Minimized by
* Optimizing pulse width to lowest values
* Small tips electrode

58
Q

Goal for impedance

A

250-1000 ohms
o Can help detect complications
 ↑ impedance >1200  + ↑ voltage threshold → lead fracture
 ↓ impedance <250  + ↓/normal voltage threshold → insulation breakage
 Normal impedance + ↑ voltage threshold → lead dislodgement/exit block

59
Q

Complications

A

Lead dislodgement
Pacemaker malfunction
Absence of pacing spikes and capture failure
Presence of spikes and capture failure
presence of spikes w/ improper sensing
Extracardiac stim
Infection

60
Q

Most common complication

A

Lead dislodgement
usually w/i days to wks ater implantation

61
Q

Causes of lead dislodgment

A

o Improper fixation: screwing of active lead or lodging of passive lead
o Excessive neck motion in post op period
o Too little/much slack in lead
o Excessive mvt of pulse generator

62
Q

ECG lead dislodgement

A

o Complete/intermittent loss of pacing/sensing
o Change in QRS morphology compared to implantation → suspect lead dislodgement

63
Q

PM interrogation lead dislodgement

A

↑ voltage threshold and normal impedance

64
Q

Causes of Pacemaker not pacing as programmed

A

o Battery depletion → runaway PM phenomenon (see question 37)
o Magnet mode: reed switch
o Defibrillation
o Inadvertent reprogramming
 Cold climates: reset pulse generator 2nd to battery voltage drop

65
Q

Causes for Absence of pacing spikes and capture

A

o Battery failure
o Circuit failure
o Lead fracture
o Unipolar lead placed in a bipolar device
o Incompatible connection btw lead/pulse generator
o Oversensing: detection of extracardiac potentials
o Unipolar PM not in contact w tissue
o Cross-talk in dual chamber device
o Loose connection
o Insulation failure

66
Q

Troubleshoot Absence of pacing spikes and capture

A
  • ECG: determine if lack of PM capture is associated with loss of pacing spikes
    o Bipolar leads: small pacing artifacts can be difficult to visualize
67
Q

Most common cause of Presence of pacing spikes and failure to capture

A

lead dislodgement

o Inadequate stimulus
o Exit block
o Inappropriate lead placement
o Lead fracture → ↑ lead impedance
o Insulation failure → ↓ lead impedance
o Battery failure
o Circuit failure
o Improper contact/lead perforation

68
Q

Explain how exit block from PM can occur

A

↑ pacing threshold
 Fibrous tissue at electrode/myocardium surface
* ↑ voltage/pulse width can help, but usually requires repositioning the lead
* Systemic steroids can have some beneficial effects
 No change in QRS morphology
 Rare complication with steroid eluting leads
 Other causes: electrolyte disturbances (hyperK+) or drugs (class Ic anti arrhythmic)

69
Q

Extracardiac stimulation

A
  • Thumping, mvt of neck/diaphragm with each pacing stimulus
  • Causes: most commonly from unipolar device w high output
    o Close proximity of electrode w diaphragm
    o Phernic nerve stimulation
    o Lead insulation failure
    o Device placed upside down
    o Lead perforating the heart
70
Q

Define sensitivity and its importance

A
  • How easily PM can see R wave
    o Important feature to avoid pacing during vulnerable period of T wave
     Prevent Vfib
71
Q

Ability to sense depend on

A

o Type of lead
o Electrode size
o Lead contact to myocardium
o Tissue reaction around electrode
o Position of electrode
o Physiologic factors: repiration, exercise, catecholamines, body position
o Drugs

72
Q

Programmable determinant of sensing

A

amplitude
filtering
slew rate of intracardiac electrocardiogram

73
Q

Amplitude of signal and sensitivity

A

 ↑ sensitivity: more sensitive to detect ↓ amplitude signals (lower mV)
* Overpacing, compete with intrinsic rhythm
 ↓ sensitivity: less sensitive → only detect larger/↑amplitude signals (higher mV)
* Prevent oversensing of waveforms (T wave) or myopotentials

74
Q

Sensing threshold

A

progressive ↓ sensitivity until sensed signal is lost
* Should be programmed ½ of sensing threshold (2x more sensitive)

75
Q

Filtering of intracardiac signals and sensitivity

A

must have higher amplitude to be sensed
 Low frequency signals → T wave
 High frequency signals → myopotentials

76
Q

Slew rate and sensitivity

A

slope/rate of change in voltage
 ↓ slew rate → gradual increase in amplitude = more difficult to sense
 If amplitude is large → less important

77
Q

Importance of adequate RP settings

A
  • Refractory period after sensed beat → 25 to 100ms after pacing spike
    o Too short: T wave sensing
    o Too long: no sensing of VPC if occurs
78
Q

Oversensing def

A
  • Inappropriate signal is sensed
79
Q

ECG feature oversensing

A

loss of capture w/o pacing spike on ECG
o To distinguish from other forms of loss of capture → restore VOO mode with magnet and see if pacing resume

80
Q

Causes of oversensing

A

o Sensing of myopotentials with unipolar pacing
o Sensing P or T waves
o Afterpotentials: electrical signal after delivery of stimulation impulse
 Usually not sensed being in blanking (RP) period

81
Q

Undersensing def

A
  • Failure to recognize intrinsic cardiac beats
    o Impulse delivered at inappropriate time
    o Timing of pacing spikes vs paced/intrinsic beats
82
Q

ECG findings undersensing

A
  • Fusion: paced + intrinsic beat
  • Pseudofusion: pacing spike superimposed to intrinsic QRS
    o Stimulus too late to cause true fusion
    o Stimulation occur during RF of ventricle
83
Q

Causes undersensing

A

o Improper programming: ↑ sensitivity, magnet application (asynchronous pacing)
o Lead dislodgement, malpositioning
o Battery failure
o Poor slew rate
o Intrinsic beat failure in the device RP

84
Q

How does a VVI ventricular pacemaker set at 90 ppm with a refractory period of 320 msec respond to a premature ventricular complex occurring at 250 msec after the last paced beat?

A

The VPC occurring at 250 milliseconds after the last paced beat will be ignored by the pacemaker due to the ongoing refractory period, and the pacemaker will continue its pacing cycle as programmed.
* Ventricular events during ventricular RP → not reset ventricular timing
o Ventricular beat will occur at normal interval → pacing after 333ms in that case (1/90)
o PM in refractory state will not respond to any sensed events
* Ventricular event after ventricular RP → sensed → inhibit output and reset timing cycle
o Cardiac rhythms may be irregular with VVI/VVIR pacing and RR interval can vary

85
Q

What causes a runaway pacemaker?

A

Low battery voltage

  • Intermittent burst of extremely rapid low amplitude pacing spikes (2000/min)
    o Low battery voltage
    o Modern PM: limit runaway PM by
     Hermetic sealing
     Fixed maximal rate
     ↓ pulse amplitude at rapid rates
86
Q

2 types of response to runaway PM

A

o ↓mA as rate ↑ → partial/complete loss of effective pacing → reversion to underlying rhythm
o Sufficient amplutide with ↑ PM d/c rate →rapid ventricular depol → tachycardia/fibrillation

87
Q

DDX runaway PM

A

pacemaker mediated tachycardia

88
Q

Tx runaway PM

A

interruption of retrograde impulses from ventricles → atria
o Excision of pulse generator or transection of pacing wires
o Vagal maneuver, chemical interventions, defibrillation will not help

89
Q

What causes Twiddler’s syndrome?

A
  • Uncommon malfunction cause
  • Manipulation of PM generator → coiling/dislodgement of lead → failure of ventricular pacing
    o Scratching of cranial chest or neck
    o Local muscular action during exercise
90
Q

What is hysteresis

A
  • Programmable function with single chamber pacing
  • Favor intrinsic beats over paced beats
    o Slight delay in lower pacing rate after each sensed intrinsic beat
    o Give opportunity for another intrinsic beat
  • Interval btw sensed beat and paced beat > than 2 paced beats
  • SSS or 2AVB: ↓ # of non physiological beats
91
Q

PM mediated tachy

A
  • Re-entry tachycardia: PM is antegrade pathway, AV node is retrograde pathway
    o When ventriculoatrial conduction is present with dual chamber device (VDD or DDD)
    o Retrograde P wave sensed as atrial activity → subsequent ventricular pacing
  • Paced tachycardia with rate limit = PM maximal pacing rate
92
Q

Termination of PM mediated tachy

A

o Programmed algorithms designed to terminate tachycardia
o Impulse interrupted in AV node
o Sensing of retrograde P wave is blocked

93
Q

Define noise reversion

A
  • Switch to asynchronous pacing
    o Sensing of rapid repetitive events over a short period of time
    o Repetitive refractory sensing → >1 beat sensed in RP
  • Safety feature to maintain pacing activity when electrical interference affects sensing fct
94
Q

Causes of noise reversion

A

o Electromagnetic interference
o Myopotentials
o Electrocautery
o Shorter RR, shorter QT, large T waves → can be misdiagnosed by PM as noise when sensed during RP

95
Q

What are two ways of adjusting pacing settings to alleviate noise reversion?

A

o Shorten RP → ↓ refractory sensed events
o ↓ sensitivity (↑ sensed mA)

96
Q

Ideal RP programming

A

o Include T wave
o Slightly longer than QT interval
 QT interval → related to HR
 QT of paced beat will be longer vs VPC or tachycardia

97
Q

2 parts of RP

A

Blanking period
Noise sampling period

98
Q

Blanking period of RP

A

PM is blind of any activity
 Can be programmed in AAI, dual chamber mode but not in VVI/VVIR
 Disabled sensing period = NO SENSING OCCURS

99
Q

Noise sampling period RP

A

 Sensing occurs
 If intrinsic beat is sensed = restart refractory period but not pacing interval
* Vs if not in RP = will restart pacing interval
 If too long → single or multiple cardiac events can be sensed → multiple restart of RP
* Can cause noise reversion and asynchronous pacing

100
Q

Clinical scenarios of noise reversion

A
  • External factors: electrocautery, defibrillation, MRI, KT ablation, dental equipment
  • Concomitant bradycardias and tachycardias
101
Q

Guidelines to adjust sensitivity and RP to avoid complications

A

o RP should be approx 20-30 msec greater than QT interval
o Sensitivity should be determined by threshold test or measurement from intracardiac lead recording of the R wave and A wave
o Sensitivity should be programmed to ½ to ⅓ intrinsic atrial signal
o Blanking period should be programmed to duration 20-30 msec greater than pacing spike to R wave duration

102
Q

Ventricular refractory period

A

All pacing modes
* Interval initiated by paced/sensed ventricular events
o Refractory ventricular channel
 Improve signal discrimination
 Avoid sensing T waves
o VDD/DDD = or < than post ventricular atrial RP
* Blanking period: 25-100ms after pacing spike, duration 20-30ms > than pacing spike-R wave interval;
* Noise sampling period: include T wave, slightly longer than QT interval

103
Q

Post ventricular atrial refractory period

A

VDD or DDD
* Interval initiated by paced/sensed ventricular events
o Prevent atrial sensing of retrograde P waves, APCs, far filed QRS complexes
* Programmed = to QRS-T duration
o Should not be shorter than ventricular RP
o Long atrial RP limits upper rate response by extending total atrial RP

104
Q

Post ventricular atrial blanking period

A
  • Portion of the post-ventricular atrial RP
    o Absolute RP disabling atrial sensing after paced/sensed/refractory sensed ventricular events
105
Q

Total atrial RP

A

VDD or DDD
* Sum of AV interval + post ventricular atrial RP
* Determines fastest rate associated w 1:1 AV synchrony
o If atrial rate ↑ and PP < total atrial RP → 2:1 AVB

106
Q

Lower rate interval

A
  • Lowest rate that will trigger a paced beat
107
Q

Upper tracking rate

A

Shortest ventricular paced interval
o Fastest rate paced when tracking atrial rate
 VDD: paced complex are initiated by atrial sensing
 Ventricular paced rhythm limited to programmed parameters for atrial sensing
o Equal or < than total atrial RP → 2:1 AVB

108
Q

Programming upper tracking rate

A

o Upper tracking rate < total atrial RP
 If HR ↑ above tracking limit → induce 2:1 AVB
o Upper tracking rate = total atrial RP
 Upper tracking rate = 60 000/total atrial RP
o Upper tracking rate > total atrial RP
 Upper tracking rate define fastest pacing
 Atrial events can still be sensed
* Produce ventricular stimulation by Wenckebach upper rate response
* Smoother transition with fast atrial rates vs abrupt 2:1 AVB

109
Q

What is PM Wenckebach response

A

o Variability/prolongation of AV interval
o Sustained upper rate limit ventricular paced complexes
o Occasional abrupt change in ventricular beat to beat interval when P wave in post-ventricular atrial RP

110
Q

Upper rate behavior

A
  • Response of a dual chamber PM in tracking mode to ↑ HR > max tracking rate
    o 1:1 tracking
    o Pacemaker Wenckebach
    o 2:1 block
  • Only observed in devices tracking intrinsic P waves
    o Most apparent in patients dependent on PM AV conduction
    o Patients with intact AV conduction may mask it
111
Q

Upper rate behavior determined by

A

o Total atrial RP
o Maximum tracking rate

112
Q

PM Wenckebach

A
  • Mobitz type I: progressive lengthening of AV interval until dropped ventricular beat
    o Because UPPER TRACKING RATE LIMIT PACING
    o PM needs to wait until UTR is done before pacing
113
Q

What parameters would you alter to create pacemaker Wenckebach?

A
  • Adjust AV delay (AV interval)
    o ↑ atrial rate → AV delay progressively ↑ until dropped beat
    o Progressive ↑ PR until non conducted P wave
  • Upper tracking rate > total atrial RP
    o Shorten post ventricular atrial RP
    o Shorten sensed AV period
    o Program rate adaptative AV interval
     Shorten interval with ↑HR
114
Q

What parameters would you alter to create 2:1 AVB?

A
  • Adjust TARP
    o Total atrial RP = AV interval + post ventricular atrial RP (PVARP)
    o ↑ atrial rate exceeding PM ability to track → every other atrial impulse is blocked → 2:1 conduction pattern

8. ECG (19 decks)

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