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![Summary of Pacemaker Indications
• Sinus node dysfunction
• AV block (Congenital, acquired, surgical)
• Bifascicular and trifascicular block
• Hypersensitive Carotid Sinus Syndrome (CSS)
• [ Malignant Vasovagal Syncope (MVVS) ]
• Pacing after cardiac transplantation
• Heart Failure / HOCM / AF
• ( AHA/ACC and BPEG indications )](https://image.slidesharecdn.com/pacemakeroverview-180209135913/85/Pacemaker-overview-71-320.jpg)
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Pacemaker overview
- 1.
- 2. Indications for PacingIndicationsfor Pacing The normal & pathological ECG
- 3. Impulse Formation and ConductionDisturbances
- 4. ““Normal Heart Rhythm”NormalHeart Rhythm” (Function)(Function)
- 5.
- 6.
- 7. Bundle of HIS Normal HeartFunction
- 8. Normal Heart Function LeftBundle Branch (LBB) Anterior Fascicle of LBB Posterior Fascicle of LBB Right Bundle Branch (RBB)
- 9.
- 10. Normal Heart Function Vent.Systole
- 11. Normal Heart Function Vent.Diastole
- 12.
- 13. Normal Values • PRInterval: 120 to 210 msec • QRS Interval: 80 to 110 msec
- 14. 60,000 Interval = Heart Rate Rate:IntervalRelationship
- 15. The Rate isTheRate is : ? ?: ? ? Interval : 750 msecInterval : 750 msec Rate:Interval Relationship
- 16. The Rate isTheRate is :: 750750 Interval : 750 msecInterval : 750 msec 60,00060,000 80 bpm80 bpm Rate:Interval Relationship
- 17. The interval is:The interval is : 5050 Rate : 50 bpmRate : 50 bpm 60,00060,000 1200 ms1200 ms Rate:Interval Relationship
- 18. Interval (ms) 200400 600 800 1000 1200 1400 1600 Rate (bpm/ppm) 300 150 100 75 60 50 43 37.5 Interval (ms) 200 400 600 800 1000 1200 1400 1600 Rate (bpm/ppm) 300 150 100 75 60 50 43 37.5 At a paper speed of 25mm/sec Rate:Interval Relationship
- 19. 25 mm is1 sec. 5 mm = 0.2 sec. 1 mm = 0.04 sec. 25 mm/second Rate:Interval Relationship
- 20. ““Abnormal Heart Rhythm”AbnormalHeart Rhythm” (Indications for Pacing)(Indications for Pacing)
- 21. Definitions.... • Bradycardia: R< 60 bpm • Tachycardia: R > 100 bpm • Flutter: R > 250 bpm • Fibrillation: R > 350 bpm
- 22. Pacemaker Indication Classifications ClassI – Conditions for which there is evidence and/or general agreement that permanent pacemakers should be implanted Class II – Conditions for which permanent pacemakers are frequently used but there is divergence of opinion with respect to the necessity of their insertion – Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy – Class IIb: Usefulness/efficacy is less well established by evidence/opinion Class III – Conditions for which there is general agreement that pacemakers are unnecessary JACC Vol. 31, no. 5 April 1998, 1175-1209
- 23. Pacemaker Indication Classifications •Evidence supporting current recommendations are ranked as levels A, B, and C: – Level A: Data derived from multiple randomised clinical trials involving a large number of individuals – Level B: Data derived from a limited number of trials involving comparatively small numbers of patients or from well-designed data analysis of nonrandomised studies or observational data registries – Level C: Consensus of expert opinion was the primary source of recommendation JACC Vol. 31, no. 5 April 1998, 1175-1209
- 24. Sinus Node Dysfunction •Sick Sinus Syndrome • Sinus bradycardia • Sinus arrest • SA block • Brady-tachy syndrome • Chronotropic incompetence (CI)
- 25. Class I Indications •Sinus node dysfunction with documentedSinus node dysfunction with documented symptomatic sinussymptomatic sinus bradycardiabradycardia • Symptomatic chronotropic incompetence Class II Indications • Class IIa: Symptomatic patients with sinus node dysfunction and with no clear association between symptoms and bradycardia • Class IIb: Chronic heart rate < 30 bpm in minimally symptomatic patients while awake Class III Indications • Asymptomatic sinus node dysfunction Sinus Node Dysfunction – Indications for Pacemaker Implantation JACC Vol. 31, no. 5 April 1998, 1175-1209
- 26. Sinus Node Dysfunction– Sinus Bradycardia • Persistent slow rate from the SA node. The parameters from this waveform include: – Rate = 55 bpm – PR interval = 180 ms (0.18 seconds)
- 27. Sinus Node Dysfunction– Sinus Arrest • Failure of sinus node discharge resulting in the absence of atrial depolarisation and periods of ventricular asystole – Rate = 75 bpm – PR interval = 180 ms (0.18 seconds) – 2.8 second arrest 2.8-second arrest
- 28. 2.1-second pause Sinus NodeDysfunction – SA Exit Block • Transient blockage of impulses from the SA node – Rate = 52 bpm – PR interval = 180 ms (0.18 seconds) – 2.1-second pause
- 29. Sinus Node Dysfunction– Brady-Tachy Syndrome • Intermittent episodes of slow and fast rates from the SA node or atria – Rate during bradycardia = 43 bpm – Rate during tachycardia = 130 bpm
- 30.
- 31. AV Block • First-degreeAV block • Second-degree AV block – Mobitz types I and II • Third-degree AV block
- 32. Class I Indications •3rddegree AV block associated with: – Symptomatic bradycardia (including those from arrhythmias and other medical conditions) – Documented periods of asystole > 3 seconds – Escape rate < 40 bpm in awake, symptom-free patients – Post AV junction ablation – Post-operative AV block not expected to resolve • Second degree AV block regardless of type or site of block, with associated symptomatic bradycardia AV Block – Indications JACC Vol.. 31, no. 5 April 1998, 1175-1209
- 33. AV Block –Indications JACC Vol. 31, no. 5 April 1998, 1175-1209 Class II Indications • Class IIa: – Asymptomatic CHB with a ventricular rate > 40 bpm – Asymptomatic Type II 2nd degree AV block – Asymptomatic Type I 2nddegree AV block within the His-Purkinje system found incidentally at EP study – First-degree AV block with symptoms suggestive of pacemaker syndrome and documented alleviation of symptoms with temporary AV pacing • Class IIb: – First degree AV block > 300 ms in patients with LV dysfunction in whom a shorter AV interval results in haemodynamic improvement
- 34. AV Block –Indications Class III Indications • Asymptomatic 1stdegree AV block • Asymptomatic Type I 2nd degree AV block at supra-Hisian level • AV block expected to resolve and unlikely to recur (e.g., drug toxicity, Lyme Disease) JACC Vol. 31, no. 5 April 1998, 1175-1209
- 35. First-Degree AV Block •AV conduction is delayed, and the PR interval is prolonged (> 210 ms or 0.21 seconds) – Rate = 79 bpm – PR interval = 340 ms (0.34 seconds) 340 ms
- 36. Second-Degree AV Block– Mobitz I (Wenckebach) • Progressive prolongation of the PR interval until a ventricular beat is dropped – Ventricular rate = irregular – Atrial rate = 90 bpm – PR interval = progressively longer until a P-wave fails to conduct 200 360 400 ms ms ms No QRS
- 37. Second-Degree AV Block –Mobitz II • Regularly dropped ventricular beats – 2:1 block (2 P waves to 1 QRS complex) – Ventricular rate = 60 bpm – Atrial rate = 120 bpm P P QRS
- 38. Third-Degree AV Block •No impulse conduction from the atria to the ventricles – Ventricular rate = 37 bpm – Atrial rate = 130 bpm – PR interval = variable
- 39.
- 40. Class I Indications •Intermittent 3rddegree AV block • Type II 2nd degree AV block Class II Indications • Class IIa: – Syncope not proved to be due to AV block when other causes have been exluded, specifically VT – Prolonged HV interval ( >100 ms) – Pacing-induced infra-Hisian block that is not physiological • Class IIb: None Class III Indications • Asymptomatic fascicular block without AV block • Asymptomatic fascicular block with 1st degree AV block Bifascicular and Trifascicular Block (Chronic) – Indications JACC Vol. 31, no. 5 April 1998, 1175-1209
- 41. Bifascicular Block Right bundlebranch block and left posterior hemiblock
- 42. Bifascicular Block Right bundlebranch block and left anterior hemiblock
- 43. Bifascicular Block Complete left bundlebranch block
- 44. Trifascicular Block • Completeblock in the right bundle branch and complete or incomplete block in both divisions of the left bundle branch
- 45. ECG Recording: • Rate •Rhythm –regular or irregular? –if irregular, is there a pattern? (e.g. 2:1 or 3:1 block or Wenckebach) • QRS-complexes? Width? • P-waves? In what relation to QRS-complexes? • PR-Interval with normal duration (120-210 ms) or irregular? Continuously increasing P-R interval?
- 46. What is aPacemaker?What is a Pacemaker?
- 47. What is aPacemaker?What is a Pacemaker? A Pacemaker System consists of a Pulse Generator plus Lead (s)
- 48. What is aPacemaker?
- 49. • Pulse generator:power source or battery • Leads or wires • Cathode (negative electrode) • Anode (positive electrode) • Body tissue IPG Lead Anode Cathode Implantable Pacemaker Systems Contain the Following Components:
- 50. • Contains abattery that provides the energy for sending electrical impulses to the heart • Houses the circuitry that controls pacemaker operations Circuitry Battery The Pulse Generator:
- 51. Battery Connector Hybrid Telemetry antenna Output capacitors Reed(Magnet) switch Clock Defibrillation protection Atrial connector Ventricular connector Resistors Anatomy of a Pacemaker
- 52.
- 53. What is aPacemaker?
- 54. • Deliver electrical impulsesfrom the pulse generator to the heart • Sense cardiac depolarisation Lead Leads Are Insulated Wires That:
- 55. ConductorTip Electrode InsulationConnector Pin Pacing Lead Components • Conductor • Connector Pin • Insulation • Electrode
- 56. How do pacemakerswork?How do pacemakers work?
- 57. How do pacemakerswork? • Modes and Codes – NBG Code – Mode Selection – Indications for Pacing – Pacing Modes • Sensing & Pacing • Pacemaker Timing • Pacemaker Therapies (Operation) & Diagnostics
- 58. Modes and CodesModesand Codes
- 59. NBG Code I Chamber Paced II Chamber Sensed III Response to Sensing IV Programmable Functions/Rate Modulation V Antitachy Function(s) V:Ventricle V: Ventricle T: Triggered P: Simple programmable P: Pace A: Atrium A: Atrium I: Inhibited M: Multi- programmable S: Shock D: Dual (A+V) D: Dual (A+V) D: Dual (T+I) C: Communicating D: Dual (P+S) O: None O: None O: None R: Rate modulating O: None S: Single (A or V) S: Single (A or V) O: None
- 60. Mode Selection forOptimalMode Selection for Optimal Pacing TherapyPacing Therapy
- 61. Providing Optimal Pacing Therapy •Heart rate increase • Stroke volume maximisation • Atrial based pacing • Normal ventricular activation sequence • (Patient outcomes and costs if optimal pacing therapy/mode is not chosen)
- 62. Cardiac OutputCardiac Output CardiacOutput (l/min)= Heart Rate x Stroke Volume
- 63. Heart Rate x x x x SV x HR Age65-80 (N=16) 130 120 110 100 90 80 70 HeartRate(BPM) StrokeVolume(mL/Min) Cardiac Output (L/Min) Rodehefer RJ, Circ.; 69:203, 1984. 6 7 8 9 10 11 12 13 14 15 1613 17 18 70 80 90 100 110 120 130 140 150 160 x
- 64. Proven Benefits ofAtrial Based Pacing Study Results Higano et al. 1990 Gallik et al. 1994 Santini et al. 1991 Rosenqvist et al. 1991 Sulke et al. 1992 Improved cardiac index during low level exercise (where most patient activity occurs) Increase in LV filling 30% increase in resting cardiac output Decrease in pulmonary wedge pressure Increase in resting cardiac output Increase in resting cardiac output, especially in patients with poor LV function Decreased incidence of mitral and tricuspid valve regurgitation
- 65. Proven Benefits ofAtrial Based Pacing Study Results Rosenquist 1988 Santini 1990 Stangl 1990 Zanini 1990 Less atrial fibrillation (AF), less CHF, improved survival after 4 years compared to VVI Less AF, improved survival after 5 years average Less AF, improved survival after 5 years compared to VVI Suppression of atrial dysrhythmias Improved morbidity (less AF, CHF, embolic events) after 3 plus uears, compared to VVI
- 66. Patient Mode Preference DDDR59% DDIR 13% Any Dual 9% No Preference 9% DDD 5% VVIR 5% Sulke N, et al. J AM Coll Cardiol; 17(3):696-706, 1991
- 67. Optimal Pacing Mode(BPEG) • Sinus Node Disease - AAI (R) • AVB - DDD • SND + AVB - DDDR + DDIR • Chronic AF + AVB - VVI (R) • CSS / MVVS - DDI
- 68. Alternative Pacing Mode •Sinus Node Disease - AAI • AVB - VDD • SND + AVB - DDD + DDI • Chronic AF + AVB - VVI • CSS - DDD / VVI • MVVS - DDD
- 69. Inappropriate Pacing Mode •Sinus Node Disease - VVI + VDD • AVB - AAI + DDI • SND + AVB - AAI + VVI • Chronic AF + AVB - AAI/DDD/VDD • CSS - AAI+VDD • MVVS - AAI/VVI/VDD
- 70. Mode Selection DecisionTree DDIR with SV PVARP DDDR with MS N VVI VVIR Are they chronic? Y Y N DDD, VDD DDDR DDDR Y N Is AV conduction intact? Is SA node function presently adequate? Symptomatic bradycardia Are atrial tachyarrhythmias present? Is SA node function presently adequate? Is AV conduction intact? Y Y N AAIR DDDR DDD, DDI with RDR N N(SSS) (CSS, VVS) N
- 71. Summary of PacemakerIndications • Sinus node dysfunction • AV block (Congenital, acquired, surgical) • Bifascicular and trifascicular block • Hypersensitive Carotid Sinus Syndrome (CSS) • [ Malignant Vasovagal Syncope (MVVS) ] • Pacing after cardiac transplantation • Heart Failure / HOCM / AF • ( AHA/ACC and BPEG indications )
- 72.
- 73.
- 74. Programmed lower rate50 mm/s VVI Pacing Modes
- 75.
- 76. Programmed lower rate50 mm/s Sensor indicated rate VVIR Pacing Modes
- 77. Programmed lower rate50 mm/s Sensor indicated rate VVIR Pacing Modes
- 78.
- 79. Programmed lower rate50 mm/s AAI Pacing Modes
- 80.
- 81. Programmed lower rate50 mm/s AAIR Sensor indicated rate Pacing Modes
- 82.
- 83. Output circuit DVI AMP A-V Sequential Outputcircuit Output circuit VDD AMP AMP Pacing Modes
- 84. = Refract.Sensing = Blanking =Refract.periode= Stimulatie = Sensing V A Pacing Modes VDD
- 85. Output circuit DVI AMP A-V Sequential Outputcircuit Pacing Modes
- 86. Programmed lower rate50 mm/s DVI Pacing Modes
- 87. Output circuit DVIR AMP A-V Sequential Outputcircuit Sensor Pacing Modes
- 88. Output circuit DDI(R) AMP Output circuit Timing& Control AMP A-V UniversalSensor Pacing Modes
- 89. Output circuit DVI AMP A-V Sequential Outputcircuit Output circuit DDD AMP A-V Universal Output circuit Timing & Control AMP Pacing Modes
- 90. Output circuit DVI AMP A-V Sequential Outputcircuit Output circuit DDDR AMP A-V Universal Output circuit Timing & Control AMP Sensor Pacing Modes
- 91. Pacing Modes -Summary Output circuit VAT AMP Atrial Synchronised Output circuit AAI AMP Atrial Demand Output circuit DVI AMP A-V Sequential Output circuit Output circuit VDD AMP Atrial synchronised Ventricular Inhibited AMP Output circuit DDD AMP A-V Universal Output circuit Timing & Control AMP Output circuit VVI AMP Ventricular Demand
Editor's Notes
- #4 We will start by discussing normal impulse fomation and then move into common conduction disturbances. As abnormal conduction is discussed we will correlate the AHA/ACC guidelines for pacemaker implantation related to that particular rhythm.
- #6 Initiation of the cardiac cycle normally begins with initiation of the impulse at the sinoatrial (SA) node. A resulting wave of depolarization passes through the right and left atria, which produces the P wave on the surface ECG and stimulates atrial contraction.
- #7 Following activation of the atria, the impulse proceeds to the atrioventricular (AV) node, which is the only normal conduction pathway between the atria and the ventricles. The AV node slows impulse conduction which allows time for contraction of the atria and the pumping of blood from the atria to the ventricles prior to ventricular contraction. Conduction time through the AV node accounts for most of the duration of the PR interval.
- #8 Just below the AV node, the impulse passes through the bundle of His. A small portion of the last part of the PR interval is represented by the conduction time through the bundle of His.
- #9 After the impulse passes through the bundle of His, it proceeds through the left and right bundle branches. A small portion of the last part of the PR interval is represented by the conduction time through the bundle branches.
- #10 Next the impulse passes through the Purkinje fibers (interlacing fibers of modified cardiac muscle). A small portion of the last part of the PR interval is represented by the conduction time through the Purkinje system.
- #11 The impulse passes quickly through the bundle of His, the left and right bundle branches, and the Purkinje fibers leading to depolarization and contraction of the ventricles. The QRS complex on the ECG represents the depolarization of the ventricular muscle mass.
- #12 The T wave on the ECG represents the repolarization and relaxation of the ventricles. Atrial repolarization and relaxation occurs during the QRS complex.
- #23 The American College of Cardiology and the American Heart Association have determined guidelines for pacemaker implantation. These 1998 guidelines are divided into three classes. Class II has subcategories A and B. Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #24 In addition to classification, recommendations that are evidence based were added to descriptions. For example: Class I indication for symptomatic third-degree AV block was designated with a “level of evidence: C” For the sake of brevity, this presentation will not include evidence based recommendations. For a complete listing of recommendations, consult JACC , April 1998. Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #25 Sinus node dysfunction encompasses a variety of impulse formation and conduction problems, including: sinus bradycardia sinus arrest sinoatrial block supraventricular tachycardias alternating with periods of bradycardia or asystole chronotropic incompetence When symptoms are present, the term sick sinus syndrome (SSS) is also used. Note: As many as 30% of patients will have additional conduction abnormalities elsewhere in the conduction system.
- #26 Class I Indication(s): 1. Documented symptomatic sinus bradycardia, including frequent sinus pauses that produce symptoms. May be due to long-term drug therapy of a type and dose for which there is no accepted alternative 2. Symptomatic chronotropic incompetence (of the sinus node) Class II Indication(s): 1a.Symptomatic patients with sinus node dysfunction and documented rates of &lt; 40 bpm without a clear-cut association between significant symptoms and the bradycardia 1b.In minimally symptomatic patients, chronic heart rate &lt; 30 bpm while awake Class III Indication(s): 1. Asymptomatic sinus node dysfunction (sinus bradycardia, SA block, or sinus arrest). Also, sinus node dysfunction with symptomatic bradycardia due to nonessential drug therapy 2. Sinus node dysfunction in patients with symptoms suggestive of bradycardia that are clearly documented as not associated with a slow heart rate Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #27 Sinus bradycardia occurs when the SA node fires at a slow (&lt; 60 bpm) rate.
- #28 Sinus arrest occurs when there is a pause in the rate at which the SA node fires. With sinus arrest there is no relationship between the pause and the basic cycle length.
- #29 SA exit block occurs when the SA node fires, but the impulse does not conduct to the pathways that cause the atrium to contract. In SA exit block there is a relationship between the pattern and the basic cycle length (because the sinus node continues to fire regularly), approximately two, but less commonly three or four times the normal P-P interval.
- #30 Brady-tachy syndrome occurs when the SA node has alternating periods of firing too slowly (&lt; 60 bpm) and too fast (&gt; 100 bpm). Brady-tachy syndrome often manifests itself in periods of atrial tachycardia, flutter, or fibrillation. Cessation of the tacycardia is often followed by long pauses from the SA node.
- #31 It is important to be able to able to increase heart rate with activity (chronotropic competence). The pacemaker and mode selected should provide the ability to increase rate with activity either by “tracking” the sinus node or, if the sinus node is not chronotropically competent, by providing the rate response via a sensor.
- #32 AV block can manifest in the following ways listed above.
- #33 Class I Indication(s): In addition to those listed, other indications for 3rd degree block include: Neuromuscular diseases with AV block such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb’s dystrophy, and peroneal muscular atrophy. Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #34 In addition to those listed, other indications include: Class II Indication(s): IIa: Asymptomatic Type II 2° AV block. If not paced, asymptomatic Type II 2° AV block patients should be followed very closely because Type II 2° AV block patients with symptoms are at a high risk for developing CHB. Most patients with type II block are symptomatic, which is a Class I indication. True asymptomatic Type II block is rare and pacemaker therapy is generally recommended. IIb: Marked first-degree AV block in patients with LV dysfunction and symptoms of congestive heart failure in whom a shorter AV interval results in hemodynamic improvement, presumably by decreasing left atrial filling pressure. Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #36 AV block can be described as a prolongation of the PR interval. The PR interval is the interval from the onset of the P wave to the onset of the QRS complex. First-degree AV block is defined by a PR interval greater than 0.20 seconds (200 msec). First-degree AV block can be thought of as a delay in AV conduction, but each atrial signal is conducted to the ventricles (1:1 ratio).
- #37 Second-degree AV block is characterized by intermittent failure of atrial depolarizations to reach the ventricle. There are two patterns of second-degree AV block. The first, Type I, is marked by progressive prolongation of the PR interval in cycles preceding a dropped beat. This is also referred to as Wenckebach or Mobitz Type I block. The AV node is most commonly the site of Mobitz I block. The QRS duration is usually normal.
- #38 Mobitz Type II second-degree AV block refers to intermittent dropped beats preceded by constant PR intervals. To differentiate Mobitz I from Mobitz II, note the PR interval in the beats preceding and following the dropped beat. If a difference between these two PR intervals is more than 0.02 seconds (20 msec), then it is Mobitz I. If the difference is less than 0.02 seconds, then it is Mobitz II. The infranodal (His bundle) tissue is most commonly the site of Mobitz II block. Note: Advanced second-degree block refers to the block of two or more consecutive P waves (i.e., 3:1 block).
- #39 Third-degree AV block is also referred to as complete heart block. It is characterized by a complete dissociation between P waves and QRS complexes. The QRS complexes are not caused by conduction of the P waves through the AV node to the ventricles, but rather the QRS is initiated at a site below the AV node (such as in the His bundle or the Purkinje fibers). This “escape rhythm” is normally 40–60 bpm if initiated by the His bundle (a junctional rhythm) and &lt;40 bpm if initiated by the Purkinje fibers.
- #40 After the impulse passes through the bundle of His, it proceeds through the left and right bundle branches. A small portion of the last part of the PR interval is represented by the conduction time through the bundle branches.
- #41 Symptomatic advanced AV block that develops in patients with underlying bifascicular and trifascicular block is associated with a high mortality rate and a significant incidence of sudden death, though there is evidence of a slow rate of progression to 3rd degree AV block. Syncope is common in patients with bifascicular block, and evidence proves an increased incidence of sudden cardiac death. Therefore, if the cause of syncope in the presence of bi/trifascicular block cannot be determined, prophylactic pacing is indicated. PR and HV intervals have been identified as possible predictors of 3rd degree AV block and sudden death in the presence of underlying bifascicular block. However, the prolongation is often at the level of the AV node, and frequently there is no correlation between the PR and HV intervals and progression to 3rd degree AV block and the incidence of sudden cardiac death. Gregoratos G, et al. ACC/AHA guidelines for Implantation of cardiac pacemakers and antiarrhythmia devices: a report of the ACC/AHA Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol. 1998:31; 1175-1206.
- #42 Bifascicular block is defined as one of the following: Right bundle branch block and left posterior hemiblock (highlighted in red) Right bundle branch block and left anterior hemiblock Complete left bundle branch block Bifascicular block is marked by prolonged QRS (&gt; 120 ms or .12 seconds or longer).
- #43 Bifascicular block Right bundle branch block and left anterior hemiblock (highlighted in red and yellow)
- #44 Bifascicular block Complete left bundle branch block (highlighted red)
- #45 Trifascicular Block has the appearance of AV nodal block. Combinations that constitute trifascicular block are: Right bundle branch block, complete left anterior fascicular block and complete left posterior fascicular block. Combination of complete block in one or two subdivisions of the common bundle and incomplete block in one or two subdivisions.
- #51 Lithium-iodine is the most commonly used power source for today’s pacemakers. Microprocessors (both ROM and RAM) control sensing, output, telemetry, and diagnostic circuits.
- #54 The first implantable pacemakers, developed in 1960, were asynchronous pacemakers, i.e., pacing without regard to the heart’s intrinsic action (VOO). Single-chamber “demand” pacemakers were introduced in the late 1960s. In 1979, the first dual chamber pacemaker (DVI) was introduced, followed closely by the 1981 release of the first DDD pacemaker, the Versatrax. The first single chamber, rate responsive pacemaker, Activitrax, was released in 1985. Today, dual-chamber pacemakers use rate responsive pacing to mimic the heart’s rate response to provide/meet metabolic needs, most recently using a combination of sensors to best accomplish this task… Pictured above: (upper left) One of the first implantable devices. The device is coated with epoxy. (upper right) Chardack Greatbatch device, late 1960’s. (lower left) Model 5943, a VVI device with titanium case (1974). (Middle) One of the first DDD devices, model number 7004. (lower right) Early 1998: Kappa 400!
- #56 This slide illustrates the essential components of a pacing lead. The following topics will be discussed for each component: · Purpose · Design factors · Performance factors
- #60 The first letter refers to the chamber(s) being paced The second letter refers to the chamber(s) being sensed The third letter refers to the pacemaker’s response to a sensed event: T = TriggeredD = Dual (inhibited and triggered*) I = InhibitedO = No response *In a single chamber mode, “triggered” means that when an intrinsic event is sensed, a pace is triggered immediately thereafter. In a dual chamber mode, “triggered” means that a sensed atrial event will initiate (trigger) an A-V delay. The fourth letter denotes the pacemaker’s programmability and whether it is capable of rate response: P = Simple Programmable (rate and/or output) M = Multiprogrammable (rate, output, sensitivity, etc.) C = Communicating (pacemaker can send/receive information to/from the programmer) R = Rate Modulation O = None Note that this sequence is hierarchical. In other words, it is assumed that if a pacemaker has rate modulation capabilities, “R”, that it also can communicate, “C”. The fifth letter represents the pacemaker’s antitachycardia functions: P = PaceD = Dual (pace and shock available) S = ShockO = None You may want to test the audience by having them describe different pacing modes. More modes and ECG strips are found in Module 2.
- #62 In order to choose the mode for the patient that will optimize pacing therapy, we need to think about four factors which can be influenced by the pacemaker: Heart rate Stroke volume Atrial electrical stability Ventricular activation sequence
- #63 Cardiac output is the result of heart rate (HR) times stroke volume (SV). In most cases, pacemaker patients have diseased hearts, and cardiac output has been compromised by reduced heart rate and/or stroke volume. Improved (ideally, normal) cardiac output is the primary goal of optimal pacing therapy. When selecting lower rate and rate response parameter values, it is important to select rates that are appropriate for the condition of the patient. If paced rates are too fast, it is possible to overload the venous system, which may cause negative results such as stretching of the atrium, increased edema, and increased congestion (patients may complain of palpitations or their hearts “racing”). If paced rates are achieved that are not fast enough for a given activity, the peripheral demands will exceed the cardiac output that is provided and the patient will have to curtail activity.
- #64 In a healthy heart, cardiac output at maximum workload can reach a level approximately 4.5 times that at rest. Increases in heart rate (workload) alone can increase cardiac output by 300% (3 times), and increases in stroke volume can increase cardiac output by 50%. In the pacing population, ability to increase SV is usually diminshed. Therefore, it is important to be able to increase heart rate with activity or to meet metabolic need. Rodeheffer R, et al. Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilation and increased stroke volume compensate for a diminished heart rate. Circulation, 1984; 69(2), 203-213.
- #65 Included is a summary of some studies depicting long-term results of AV synchronous (atrial based) and non-synchronous (VVI/R) pacing In addition to heart rate and stroke volume, the propensity for development of atrial fibrillation with the associated risks of thromboembolic events, stroke, and reduced survival is an important issue. Studies have shown that atrial-based pacing modes (modes that can sense and respond to P waves) have a much lower incidence of developing atrial fibrillation than modes that only pace and sense in the ventricle. For this reason, as well as the increase in cardiac output due to AV synchrony, it is advantageous to use atrial-based pacing modes whenever possible. Note: Exceptions include instances when it is not possible to sense the atrium or conditions in which it would not be beneficial to sense the atrium, such as chronic atrial fibrillation or flutter, inability to achieve adequate pacing/sensing thresholds, or an inexcitable atrium. Higano, et al. Hemodynamic importance of atrioventricular synchrony during low levels of exercise. PACE, 1990; 13:509 Abstact. Gallik DM, et al. Comparison of ventricular function in atrial rate adaptive versus dual chamber rate adaptive pacing during exercise. PACE, 1994; 17(2):179-185 Santini, et al. New Perspectives in Cardiac Pacing. Mount Kisco, NY: Futura Publishing, 1991. Rosenquist M, et al. Relative importance of activation sequence compared to atrioventricular synchrony during low levels of exercise. AM J Cardiology, 1991;67:148-156. SulkeN, et al. “Sbuclinical pacemaker syndrome: A randomized study of symptom free patients with ventricular demand (VVI) pacemakers upgraded to dual chamber devices. Brit Heart J, 1992; 67(1):57-64.
- #66 In addition to heart rate and stroke volume, the propensity for development of atrial fibrillation with the associated risks of thromboembolic events, stroke, and reduced survival is an important issue. Studies have shown that atrial-based pacing modes (modes that can sense and respond to P waves) have a much lower incidence of developing atrial fibrillation than modes that only pace and sense in the ventricle. For this reason, as well as the increase in cardiac output due to AV synchrony, it is advantageous to use atrial-based pacing modes whenever possible. Note: Exceptions include instances when it is not possible to sense the atrium or conditions in which it would not be beneficial to sense the atrium, such as chronic atrial fibrillation or flutter, inability to achieve adequate pacing/sensing thresholds, or an inexcitable atrium. Rosenquist M, et al. Long-term pacing in sinus node disease: Effects of stimulation mode on cardiovascular morbidity and mortality. AM Heart J. 1988; 116(1 pt.1): 16-22. Santini M., et al. Relation of prognosis in sick sinus syndrome to age, conduction defects, and modes of permanent cardiac pacing. AM J Cardiol. 1990; 65(11):729-735. Stangl K, et al. Differences between atrial single chamber pacing (AAI) and ventricular single chamber acing (VVI) with respect to prognosis and antiarrhythmic effect in patients with SSS. PACE, 1990; 13(12):863-868. Zanini R, et al. Morbidity and mortality of patients with sinus node disease: comparative effects of atrial and ventricular pacing. PACE, 1990; 13(12): 2076-2079.
- #67 Subjective Patient Improvement Several studies have compared dual chamber and/or atrial pacing to ventricular pacing in terms of patient preference and other quality of life indicators. Overwhelmingly, patients choose dual chamber pacing over VVI/R, and conversely, most patients identify VVI/R as the least acceptable pacing mode. Sulke N, et al. A randomized double-blind crossover comparison of four rate-reponsive pacing modes. JACC, 1991; 17(3):696-706.
- #71 This is the decision tree that we will be using to (practice) determine the optimal pacing mode for five example patients. When evaluating which pacing mode would provide optimal pacing therapy for each patient, we must ask ourselves three questions: Are atrial tachyarrhythmias present? (Can the atrium be paced and sensed reliably?) Is AV conduction intact? Is SA node function presently adequate?