Introduction to Endocardial and Epicardial Pacing
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1 Introduction to Endocardial and Epicardial Pacing Impulse Formation and Conduction Disturbances Frank Ngo, MD Cardiac Conduction Sinus Node Cardiac Conduction AV Node Sinus Node (SA Node) Atrioventricular Node (AV Node) The Heart s Natural Rate of bpm at rest Receives impulses from SA node Delivers impulses to the His- Purkinje System Delivers rates between bpm if SA node fails to deliver impulses Cardiac Conduction HIS Bundle Cardiac Conduction Purkinje Fibers Bundle of His Begins conduction to the ventricles AV Junctional Tissue: Rates between bpm Purkinje Network Bundle Branches and Purkinje Fibers Moves the impulse through the ventricles for contraction Escape Rhythm : Between bpm 1
2 Normal Sinus Rhythm Impulse Formation in SA Node Atrial Depolarization Delay at AV Node Conduction through Bundle Branches Conduction through Purkinje Fibers 2
3 Ventricular Depolarization Plateau Phase of Repolarization Final Rapid (Phase 3) Repolarization Normal ECG Activation This pattern of depolarization results in efficient mechanical contraction which is the purpose to pump blood. ECGs Annotation Normal Ranges in Milliseconds: PR Interval ms QRS Complex ms QT Interval ms Symptoms Syncope or pre-syncope Dizziness Congestive heart failure Mental confusion Palpitations Shortness of breath Exercise intolerance 3
4 ACC/AHA Classification of Indications Class I Conditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective. ACC/AHA Classification of Indications Class II Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment. Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy. Class IIb: Usefulness/efficacy is less well established by evidence/opinion. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: ACC/AHA Classification of Indications Class III Conditions for which there is evidence and/or general agreement that a procedure or treatment is not useful/effective and in some cases may be harmful. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: ACC/AHA Classification of Clinical Evidence Evidence supporting current recommendations are ranked as levels A, B, and C: Level A: Data derived from multiple randomized 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 nonrandomized studies or observational data registries. Level C: Consensus of expert opinion was the primary source of recommendation. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: Sinus Node Dysfunction Chronotropic Incompetence Sinus bradycardia Sinus arrest SA block Brady-tachy syndrome Chronotropic incompetence Max Heart Rate Rest Slow Start Activity Unstable Time Stop Activity Quick 4
5 Sinus Node Dysfunction Sinus Node Dysfunction symptomatic: bradycardia or pauses chronotropic incompetence due to required drug therapy Ia unassociated symptoms (HR<40bpm) unexplained syncope with SND (discovered or provoked) Ib HR<40 bpm while awake Asymptomatic SND unrelated symptoms (Symptoms occur also in absence of Bradycardia) Drug related Due to nonessential drug therapy Sinus Node Dysfunction Sinus Bradycardia Sinus Node Dysfunction Sinus Arrest 2.8-second arrest Persistent slow rate from the SA node. The parameters from this waveform include: Rate = 55 bpm PR interval = 180 ms (.18 seconds) Failure of sinus node discharge resulting in the absence of atrial depolarization and periods of ventricular asystole Rate = 75 bpm PR interval = 180 ms (.18 seconds) 2.8-second arrest Sinus Node Dysfunction SA Exit Block Sinus Node Dysfunction Bradycardia-Tachycardia (Brady-Tachy) Syndrome 2.1-second pause Transient blockage of impulses from the SA node Rate = 52 bpm PR interval = 180 ms (.18 seconds) 2.1-second pause Intermittent episodes of slow and fast rates from the SA node or atria Rate during bradycardia = 43 bpm Rate during tachycardia = 130 bpm 5
6 AV Block First-degree AV block Second-degree degree AV block Mobitz types I and II Third-degree degree AV block Bifascicular and trifascicular block AV Block (Adults) 3rd, advanced 2nd with symptoms drug-related related Escape rate < 40bpm or any rate below AV node >3 sec pause >5 sec pause and AF AV junction ablation/surgery neuromuscular diseases exercise related (not ischemic) AV Block (Adults) AV Block (Adults) 2nd type II with wide QRS (RBBB included) 3rd LV dysfunction Block below the AV node Ia 3rd persistent 2nd (intra- or infra-his) found during EPS 1st and 2nd with symptoms (PM-syndrome syndrome-like or hemodynamic) 2nd type II with narrow QRS Ib Any AVB + neuromuscular disease Any AVB due to drug use, expected to recur after drug withdrawal AV Block (Adults) Second-Degree AV Block Mobitz I (Wenckebach) 1st asymptomatic 2nd supra-his type I asymptomatic any transient ms ms ms No QRS 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 P fails to conduct 6
7 Second-Degree AV Block Mobitz II Third-Degree AV Block Regularly dropped ventricular beats 2:1 block (2 P waves to 1 QRS complex) Ventricular rate = 60 bpm Atrial rate = 110 bpm P P QRS No impulse conduction from the atria to the ventricles Ventricular rate = 37 bpm Atrial rate = 130 bpm PR interval = variable Chronic Bifascicular Block Fascicular Block advanced 2nd intermittent 3rd 2nd type II alternating BBB Ia syncope with other reasons excluded HV time during EPS>100ms pacing-induced induced infra-his block Ib neuromuscular diseases no AVB or symptoms 1st AVB no symptoms Right bundle branch block and left posterior hemiblock Right bundle branch block and left anterior hemiblock Complete left bundle branch block After the Acute Phase of MI 2nd with alternating BBB 3rd after STEMI 2nd or 3 rd infranodal AVB and associated BBB 2nd or 3rd with symptoms Ib 2nd and 3rd at AVN level asymptomatic After the Acute Phase of MI transient without intraventricular conduction defects transient with isolated left anterior FB new BBB or FB without AVB 1st asymptomatic with BBB or FB 7
8 HCSS and NCGS recurrent syncope and inducible pause > 3 sec Ia inducible pause longer than 3 sec Ib symptomatic NCGS with bradycardia no symptoms effective avoidance behavior Mechanisms of Neurocardiogenic Syncope Cardioinhibitory Initiated by inappropriate drop in heart rate Vasodepressor Symptomatic decrease in systolic blood pressure due to vasodilation Mixed Includes components of cardioinhibitory and vasodepressor Vasovagal Syncope (VVS) Vasovagal Syncope (VVS) Neurally mediated transient loss of consciousness Can be precipitated by: Fear, anxiety Physical pain or anticipation of trauma/pain Prolonged standing Symptoms include: Dizziness Blurred vision Weakness Nausea, abdominal discomfort Sweating Pacing in Patients with Vasovagal Syncope (VVS) Because cardioinhibitory VVS is associated with bradycardia or asystole, high-rate pacing may be an effective therapy I indication Pacing is not indicated for pure vasodepressor VVS Pacing in CSS and VVS Class I Indications 1. Recurrent syncope caused by carotid sinus stimulation; minimal carotid sinus pressure induces ventricular asystole >3 sec duration in absence of any medication that depresses the sinus node or AV conduction. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106:
9 Pacing in CSS and VVS Class IIa Indications 1. Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response. 2. Significantly symptomatic and recurrent neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table table testing. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: Pacing for CSS and VVS Class III Indications 1. Hyperactive cardioinhibitory response to CS stimulation in absence of symptoms or in the presence of vague symptoms such as dizziness, lightheadedness, or both. 2. Recurrent syncope, lightheadedness or dizziness in absence of hyperactive cardioinhibitory response. 3. Situational vasovagal syncope in which avoidance behavior is effective. Gregoratos G. et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac s and Antiarrhythmia Devices: a Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2002;106: S/P Cardiac Transplant Devices with Automatic Detection and Pacing to Terminate Tachycardias Ia all other class I indications Ib bradycardia, limiting rehabilitation syncope Symptomatic recurrent SVT terminated by pacing when ablation and drugs fail rapid anterograde conducting ng accessory pathway is present 9
10 Hypertrophic Cardiomyopathy SND or AVB as described before Ib medically refractory symptoms with LV outflow tract obstruction (check SCD risk) asymptomatic (or medically controllable) no LV outflow tract obstruction Pacing to prevent VT pause-dependent VT Ia High risk congenital long-qt Ib Recurrent drug refractory symptomatic AF & SND ectopic ventricular activity torsade, reversible caused Pacing to prevent AF if no other pacing indication Pacing Lead Activity 70 bpm 100,000 beats / day 37,000,000 beats / year 10
11 Pacing Lead Components Conductor Connector Pin Insulation Electrode Lead Assembly Conductor -- Unipolar Construction Unipolar lead 1 pacing conductor IPG case ( can( can ) for sensing Tip Electrode Conductor Insulation Connector Pin Conductor -- Bipolar Construction Bipolar 1 pacing conductor 1 sensing conductor Transvenous Leads Have Different Fixation Mechanisms Passive fixation The tines become lodged in the trabeculae (fibrous meshwork) of the heart Electrodes Fixation Mechanism Active Fixation Mechanism Endocardial Fixed screw Extendable/retractable Electrodes -- Fixation Mechanism Fixation Mechanism Myocardial/Epicardial Stab-in Screw-in Suture-on 11
12 Ventricular Activation Sequence Mode Selection for Optimal Pacing Therapy Normal Sequence Paced Sequence NBG Code Paced Rhythm Recognition I Chamber Paced II Chamber Sensed III Response to Sensing V: Ventricle V: Ventricle T: Triggered A: Atrium A: Atrium I: Inhibited IV Programmable Functions/Rate Modulation P: Simple programmable M: Multiprogrammable V Antitachy Function(s) P: Pace 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 AAI / 60 Paced Rhythm Recognition Dual-Chamber Systems Have Two Leads: One lead implanted in the atrium One lead implanted in the ventricle VVI / 60 12
13 Paced Rhythm Recognition Paced Rhythm Recognition DDD / 60 / 120 (p-wave tracking ) DDD / 60 / 120 Paced Rhythm Recognition Paced Rhythm Recognition DDD / 60 / 120 DDD / 60 / 120 s Perform Four Functions: Pacing Technologies for Newer Pacing Indications Stimulate cardiac depolarization Sense intrinsic cardiac function Respond to increased metabolic demand by providing rate responsive pacing Provide diagnostic information stored by the pacemaker 13
14 Pacing in Patients with Hypersensitive Carotid Sinus Syndrome (CSS) Rate Drop Response Therapy AAI pacing is contraindicated because 70% of CSS patients exhibit reflex AV block VVI is prone to causing pacemaker syndrome in CSS patients DDD or DDI pacing are better modes for most CSS patients because they maintain AV synchrony and rate support Summary of Indications and Mode Selection Module Impulse formation and conduction disturbances Indications for pacing therapy Mode selection for optimal pacing therapy New indications and technologies available for pacing therapy Malfunctions Loss of Capture Atrial Oversensing 14
15 Atrial Undersensing Atrial Undersensing Ventricular Oversensing 15
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