Pacemaker Flashcards
Common PM implanted in vet practice
- 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
Risk epicardial pacing
↑ risk for bacteremia, thrombosis, embolism
Consequences of long term RV pacing
Asynchronous ventricular contraction
Impaired cardiac performance
Deleterious myocardial remodeling
Advantage of Dual ch
o Favorize AV synchrony → improve hemodynamics
CO depends on
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
Modes of dual chamber pacing
- DDD mode: 2 leads (1 atrial, 1 ventricular)
- VDD mode: 1 lead in RV with floating electrodes
Disadvantages of dual pacing
o Complex programming,
o ↑ expense, ↑ implantation time
o Technical challenge of placing atrial lead in small patiens
o ↑ complications post op
Define the NASPE/BPEG classification.
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
What are the typical modes used in veterinary practice?
Most commons: VVI and VVIR
AAI/AAIR
VDD
DDD
VVI modality
- 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
Disadvantages
o Preset pacing rate (non physiological pacing)
o Asynchronous contraction of A and V → can lead to PM syndrome
VVIR
- Similar to VVI + rate responsiveness (chronotropic competence)
- Stimulation frequency ↑ in response to physical activity/respiration
o Sensors: motion, minute ventilation - AV asynchrony persists
AAI/AAIR
- Single chamber, atrial inhibited +/- rate responsiveness
o Stimulus delivered to atrium
o PM output inhibited by atrial events
AAI/AAIR pacing indications
SSS and normal AV node function
AAI/AAIR pacing advantages
o Maintain AV synchrony
o Synchronous ventricular contraction
o Avoid retrograde conduction through AV node and echo beats
AAI/AAIR pacing disadvantages
lack of depol if AVB occurs
o 24h Holter and Weckenbach testing recommended
VDD
- 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
Upper tracking rate
upper limit of atrial depol permitted to trigger ventricular depol
Requirement for VDD pacing
- Need normal SA node function
DDD
- 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
DDD pacing advantages
preserve AV synchrony
PM refractory periodq
- 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
Pacemaker syndrome c/s
- Vasovagal syncope, pre-syncope, shortness of breath, dyspnea with exertion
Mechanism of c/s w/ PM syndrome
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
Cause of c/s w/ PM syndrome
- 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
Treatment PM syndrome
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
Ventriculoatrial conduction
- 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
Components of pacing system
Pulse generator
Pacing lead
Pulse generator
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
Asynchronous mode
magnet in close proximity
Pacing lead: how is it made
o Insulated wire that conduct impulse from generator to myocardium
Conductor + lead insulation + lead connector + electrode
Types of leads and fixation
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
Pacing circuit
o Anode → + pole, cathode → - pole
Cathode is always tip of lead
Circuit unipolar lead
cathode = lead tip, anode = generator
Impulse travels from generator → myocardium in lead
Myocardium → generator via soft tissues
* Proximity to skeletal muscles → can cause twitching
ECG unipolar lead
large pacing spikes
Advantages unipolar lead
- Smaller diameter pacing leads
- Single attachment site
- Superior sensitivity for sensing intrinsic beats
Disadvantages unipolar lead
- More susceptible to oversensing
- Can detect skeletal muscle potentials
- Generator in contact w/ body/tissues → can cause muscle twitching
Circuit bipolar lead
2 spaced electrodes distally on lead, distal = cathode, proximal = anode
Advantages bipolar lead
- 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
ECG bipolar lead
Smaller pacing spikes
Why choose epicardial PM
o Usually if lead dislodgement or animal too small for transvenous
ECG epicardial PM
larger pacing spikes
Wide QRS
Disadvantages epicardial PM
More inflammation vs transvenous
Invasive: intercostal or diaphragmatic approach
Advantages epicardial PM
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
Factors involving lead system in clinic
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
Ohm’s law
V = IR
V: stimulus voltage
I: current
R: resistance
Strength duration curve
- Relationship btw voltage and pulse duration → exponential
o Pulse width <0.25ms → steep curve
o Pulse width >1ms → flat curve
Energy (E) of pacing stimulus: determined by
- 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
PM programming w/ strength duration curve
o If short pulse duration: short error margin if stimulation threshold ↑
o If long pulse width: no more effect on heart stimulation → drain battery
What is rheobase
o Lowest voltage resulting in capture
o Usually pulse width <1.5ms
What is chronaxie
o Pulse width required to capture at 2x rheobase voltage
o Approximate minimum threshold stimulation energy
Safety margin for programming
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
Ideal chronic settings
- Chronic leads: should not have stimulation thresholds >2.5V at pulse width of 0.5ms
o ↓ longevity of pulse generator
Threshold tests
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
What is Wendensky’s effect
capture hysteresis
o Testing from capture → loss of capture, not lack of capture → capture
o > energy required to gain capture
What is impedance
- Total resistance to current flow
o Excessive resistance → generates heat → not efficient to generate current for pacing
o ↓ acutely after implantation, then ↑ and stabilizes
Factors influencing impedance
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
Goal for impedance
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
Complications
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
Most common complication
Lead dislodgement
usually w/i days to wks ater implantation
Causes of lead dislodgment
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
ECG lead dislodgement
o Complete/intermittent loss of pacing/sensing
o Change in QRS morphology compared to implantation → suspect lead dislodgement
PM interrogation lead dislodgement
↑ voltage threshold and normal impedance
Causes of Pacemaker not pacing as programmed
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
Causes for Absence of pacing spikes and capture
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
Troubleshoot Absence of pacing spikes and capture
- 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
Most common cause of Presence of pacing spikes and failure to capture
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
Explain how exit block from PM can occur
↑ 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)
Extracardiac stimulation
- 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
Define sensitivity and its importance
- How easily PM can see R wave
o Important feature to avoid pacing during vulnerable period of T wave
Prevent Vfib
Ability to sense depend on
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
Programmable determinant of sensing
amplitude
filtering
slew rate of intracardiac electrocardiogram
Amplitude of signal and sensitivity
↑ 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
Sensing threshold
progressive ↓ sensitivity until sensed signal is lost
* Should be programmed ½ of sensing threshold (2x more sensitive)
Filtering of intracardiac signals and sensitivity
must have higher amplitude to be sensed
Low frequency signals → T wave
High frequency signals → myopotentials
Slew rate and sensitivity
slope/rate of change in voltage
↓ slew rate → gradual increase in amplitude = more difficult to sense
If amplitude is large → less important
Importance of adequate RP settings
- 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
Oversensing def
- Inappropriate signal is sensed
ECG feature oversensing
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
Causes of oversensing
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
Undersensing def
- Failure to recognize intrinsic cardiac beats
o Impulse delivered at inappropriate time
o Timing of pacing spikes vs paced/intrinsic beats
ECG findings undersensing
- 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
Causes undersensing
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
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?
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
What causes a runaway pacemaker?
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
2 types of response to runaway PM
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
DDX runaway PM
pacemaker mediated tachycardia
Tx runaway PM
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
What causes Twiddler’s syndrome?
- 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
What is hysteresis
- 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
PM mediated tachy
- 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
Termination of PM mediated tachy
o Programmed algorithms designed to terminate tachycardia
o Impulse interrupted in AV node
o Sensing of retrograde P wave is blocked
Define noise reversion
- 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
Causes of noise reversion
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
What are two ways of adjusting pacing settings to alleviate noise reversion?
o Shorten RP → ↓ refractory sensed events
o ↓ sensitivity (↑ sensed mA)
Ideal RP programming
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
2 parts of RP
Blanking period
Noise sampling period
Blanking period of RP
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
Noise sampling period RP
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
Clinical scenarios of noise reversion
- External factors: electrocautery, defibrillation, MRI, KT ablation, dental equipment
- Concomitant bradycardias and tachycardias
Guidelines to adjust sensitivity and RP to avoid complications
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
Ventricular refractory period
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
Post ventricular atrial refractory period
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
Post ventricular atrial blanking period
- Portion of the post-ventricular atrial RP
o Absolute RP disabling atrial sensing after paced/sensed/refractory sensed ventricular events
Total atrial RP
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
Lower rate interval
- Lowest rate that will trigger a paced beat
Upper tracking rate
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
Programming upper tracking rate
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
What is PM Wenckebach response
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
Upper rate behavior
- 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
Upper rate behavior determined by
o Total atrial RP
o Maximum tracking rate
PM Wenckebach
- 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
What parameters would you alter to create pacemaker Wenckebach?
- 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
What parameters would you alter to create 2:1 AVB?
- 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
