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Pacing
Hussam Tayeb
Cardiac Conduction: P Wave
Cardiac Conduction: AV Node
Cardiac Conduction: Bundle
Branches
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
The Solution
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Capture
QRS Morphologies
Undersensing
Oversensing
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
RV Pacing is Bad
Really Bad
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
RVOT Pacing
Dual Chamber Pacing
Lower Rate
Upper Tracking Rate
AP
VP
AS
VP
PAV SAV
200 ms 170 ms
AV Intervals
SENSE!
Blanking Refractory
Time
5.0 mV
2.5 mV
1.25 mV
Sensing
Refractory Periods
The VRP is intended to prevent self-inhibition such
as sensing of T-waves
AP
VP
Ventricular Refractory
Period
(VRP)
VRP
Post Ventricular Atrial
Refractory Period (PVARP)
Refractory Periods
AP
VP
A-V Interval
(Atrial Refractory)
Total Atrial Refractory Period (TARP)
Dual Chamber Pacing
AP-VP AP-VS AS-VS
Dual Chamber Pacing
AS-VP
What to do when intrinsic rate
becomes higher than the upper
tracking rate?
PVARP
Wenckebach Operation
Prolongs the SAV until upper rate limit expires
AS AS AR AP
VPVP VP
TARP
SAV PAV PVARPSAV PVARP
P Wave Blocked (unsensed or unused)
TARP TARP
Upper Tracking
Rate
Wenkebach
P P
2:1 Block
Mode Switching
DDD to DDI or VVI
Kenny ; The nuts and bolts of Paced
ECG Interpretation
Mode
Switch
Shortening
SAV
Lengthening
SAV
Dual Chamber
Pacemakers Try to
Minimise Ventricular
Pacing
Hysteresis
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Normal Algorithms
Biventricular Pacing
CRT
Biventricular Pacing
CRT
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
Pacing by Hussam Tayeb - SMACC ECG Workshop 2014
CRT algorithms are
designed to maximise
ventricular pacing
Magnets
Pacemaker
ICD
Asynchronous pacing at 85 or 65 bpm
ICD detection temporarily inhibited
No permanent changes to device
programming
No effect on pacing therapy
RV pacing is bad
CRT is good …………….mostly
Dual Chamber and CRT
troubleshooting can be very complex
make it easy on yourself and call a
friend

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Pacing by Hussam Tayeb - SMACC ECG Workshop 2014

Notas del editor

  1. My only disclosure is that although cardiology trained I am not an electrophisiologistThe second point is that the professor of EP upon hearing of my intention to train in ICU half jokingly told me that I am devolving into an inferior specialty
  2. At its most extreme we end up with completeav nodal dissociation and resultant escape beats being generated from the his-purkinje system or the ventricular myocardium
  3. The solution: Pacing either permanent or temproary
  4. Pacing nomenclature when describing pacing modes:Rate responsiveness: Movement sensor and breathing sensor to allow matching the pacing rate to the physiological demands
  5. In order to make the heart beat,the pacemaker produces an electricalpacing stimulus. The pacing stimulus,also called ‘‘spike,’’ ‘‘impulse,’’ or‘‘output,’’ can be described in termsof its amplitude (most commonly volts[V]) and pulse width (milliseconds[ms]). Both of these parameters maybe programmed. Whether a stimulusactually makes the heart beat dependson a few factors:
  6. Paced QRS: pacing spike proceeds and generatedventricular depolarisationFusion: intrinsic depolarisation proceeds pacing spike, but pacing spike occurs early and contributes to the ventricular depolarisation (the QRS is narrower than a fully paced beat) Fusion usually is not hazardous and does not necessarily indicate pacemaker dysfunctionPseudofusion: intrinsic depolaristion proceeds pacing spike, ventricular tissue is in an absolte refractory phase and as such the pacing spike does not contribute to ventricular depolarisation
  7. Undersensing leads tooverpacing
  8. Oversensing leads to underpacing
  9. Conductionpropogates through the myocardium rahter than through the his-purkinje system resulting in slow and heterogenouspropogation of current
  10. Functional MRIncreased Strain and oxygen demansDecreased CO, increased filling pressures Long term effects: remodelling, heart failure, AF, and death
  11. Functional MRIncreased Strain and oxygen demansDecreased CO, increased filling pressures Long term effects: remodelling, heart failure, AF, and death
  12. RV lead is placed in the septal portion of RVOT resulting in more physiological propogation of current. The evidence about these benefits is not very strong but it remains the preferred site in many centres.
  13. Atrial lead in the right atrial appendage, Right ventricular lead (apex or RVOT), More parameters to control and program.The lowest rate the pacemaker will pace the atrium in the absence of intrinsic atrial eventsThe maximum rate the ventricle can be paced in response to a sensed atrial event
  14. Dual chamber pacing can ensue in 4 different configurations depending on patient and set pacing parameters
  15. Concept of maximal tracking rate
  16. This graph shows how the dual chamber pacemakers respond to increasing atrial sensed ratesInitially it starts by shortening the SAV interval , with further increases in the atrial rate the device reaches the wenkebachplateu where now the SAV interval is lengthened and ventricular pacing rate is maintained reasonably constant. When every second arial impulse falls into the TARP we end up with 2:1 block and ventricular pacing rate drops
  17. Programmable feature that periodically extends the pacing interval to look for intrinsic cardiac activity. Usually set ~ 10bpm less than pacing rate Longer time delay between sensed (intrinsic complexes) as opposed to a shorter time delay between paced complexes
  18. CRT has really revolutionised the treatment of heart failure with LBBB, with improved clinical and QOL outcomes. unfortunately up to a 1/3rd of patients do not benefti “non responders”Implantors aim for the basal and mid anterolateral or posterolateral regions. Apical vein placement has been shown to increase mortality
  19. 1/3 rd non responders
  20. LV pacing from posterolateral vein
  21. This is the same patient with activation of the RV apical lead. Notice the right superior (westward) axis , the significant narrowing of the qrs, and the ongoing dominance of R wave dominance in v1
  22. RV lead in RVOTOther causes of loss of dominant R wave in V1: Failure of LV capture we would expect a left axis and positive QRS in V5-V6LV lead placed in the anterior veinProlonged latency of LV pacing due to anatomical reasons or previous scarring,
  23. Identify the type and make of device, Phone a friend