Pacing by Hussam Tayeb - SMACC ECG Workshop 2014


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PowerPoint presentation from Dr Hussam Tayeb's talk on pacemakers at the SMACC Gold ECG Workshop, March 2014.

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  • 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
  • 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
  • The solution: Pacing either permanent or temproary
  • Pacing nomenclature when describing pacing modes:Rate responsiveness: Movement sensor and breathing sensor to allow matching the pacing rate to the physiological demands
  • 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:
  • 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
  • Undersensing leads tooverpacing
  • Oversensing leads to underpacing
  • Conductionpropogates through the myocardium rahter than through the his-purkinje system resulting in slow and heterogenouspropogation of current
  • Functional MRIncreased Strain and oxygen demansDecreased CO, increased filling pressures Long term effects: remodelling, heart failure, AF, and death
  • Functional MRIncreased Strain and oxygen demansDecreased CO, increased filling pressures Long term effects: remodelling, heart failure, AF, and death
  • 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.
  • 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
  • Dual chamber pacing can ensue in 4 different configurations depending on patient and set pacing parameters
  • Concept of maximal tracking rate
  • 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
  • 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
  • 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
  • 1/3 rd non responders
  • LV pacing from posterolateral vein
  • 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
  • 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,
  • Identify the type and make of device, Phone a friend
  • Pacing by Hussam Tayeb - SMACC ECG Workshop 2014

    1. 1. Pacing Hussam Tayeb
    2. 2. Cardiac Conduction: P Wave
    3. 3. Cardiac Conduction: AV Node
    4. 4. Cardiac Conduction: Bundle Branches
    5. 5. The Solution
    6. 6. Capture
    7. 7. QRS Morphologies
    8. 8. Undersensing
    9. 9. Oversensing
    10. 10. RV Pacing is Bad Really Bad
    11. 11. RVOT Pacing
    12. 12. Dual Chamber Pacing Lower Rate Upper Tracking Rate
    13. 13. AP VP AS VP PAV SAV 200 ms 170 ms AV Intervals
    14. 14. SENSE! Blanking Refractory Time 5.0 mV 2.5 mV 1.25 mV Sensing
    15. 15. Refractory Periods The VRP is intended to prevent self-inhibition such as sensing of T-waves AP VP Ventricular Refractory Period (VRP) VRP
    16. 16. Post Ventricular Atrial Refractory Period (PVARP) Refractory Periods AP VP A-V Interval (Atrial Refractory) Total Atrial Refractory Period (TARP)
    17. 17. Dual Chamber Pacing AP-VP AP-VS AS-VS
    18. 18. Dual Chamber Pacing AS-VP What to do when intrinsic rate becomes higher than the upper tracking rate?
    19. 19. 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
    20. 20. Wenkebach P P
    21. 21. 2:1 Block
    22. 22. Mode Switching DDD to DDI or VVI
    23. 23. Kenny ; The nuts and bolts of Paced ECG Interpretation Mode Switch Shortening SAV Lengthening SAV
    24. 24. Dual Chamber Pacemakers Try to Minimise Ventricular Pacing
    25. 25. Hysteresis
    26. 26. Normal Algorithms
    27. 27. Biventricular Pacing CRT
    28. 28. Biventricular Pacing CRT
    29. 29. CRT algorithms are designed to maximise ventricular pacing
    30. 30. 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
    31. 31. 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