- Email: [email protected]
Bradycardia pacing
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Bradycardia pacing
suddenly from one to the other, is termed ‘tachy-brady syndrome’. Though abnormalities of AV conduction can often be demonstrated patients with SND, only 1% of patients per year will develop significant AV block.1
Benjamin D Brown David J Fox
AV node disease Acquired AV block is the second most common indication for permanent pacemaker placement. Three degrees of heart block are described, according to site and severity (see Table 1 for classification of heart block). Many disorders can cause acquired AV block, although it is most commonly idiopathic. Nodal conduction can also result from ischaemia (after MI), toxicity (bblockers, calcium channel antagonists, digoxin), infection (brucellosis, Lyme disease) and cardiac surgery (most commonly following aortic valve surgery, given the proximity of the AVN to the aortic valve).
Abstract Pacemakers though technologically complex are fundamentally simple once an understanding of the components and language is achieved. This review aims to provide that knowledge to reassure the clinician over a device that is frequently found on medical and surgical wards. Despite pacemakers being cost effective and increasingly commonplace they remain underutilized. Therefore we also aim to equip the reader with the key principles to identify individuals who may benefit from pacemaker implant.
Neurocardiogenic (vasovagal) syncope Syncope as a symptom is most often (50e60% cases) caused by neurocardiogenic syncope. Neurocardiogenic syncope (also known as vasovagal syncope) is a benign condition characterized by a self-limited episode of systemic hypotension, during which increased vagal tone results in a reduction of cardiac filling, bradycardia and hypotension with ensuing loss of consciousness. Differential diagnoses include carotid sinus hypersensitivity (resulting from an extreme reflex response to carotid sinus stimulation) and orthostatic hypotension (failure of the autonomic reflex response). The mainstay of management is education of the patient to avoid situations that predispose to syncope, coping skills, and reassurance of the patient and others that this is a benign condition, though pacing for the bradycardia component is occasionally helpful in selected patients.2
Keywords bradycardia; heart block; pacemaker; pacemaker programming; pacing indication
Since the first human pacemaker in the 1950s, there has been rapid development in the technology of cardiac devices for rhythm management and the equipment to facilitate their implantation. As a result, the number of patients with devices has soared and the indications for their use have increased. This review aims to provide a practical review of pacemaker indications, and an overview of pacemaker function and malfunction, to demystify a device that has become commonplace in medical practice.
Failure of the cardiac conduction system Pacing indications Despite the many clinical situations in which permanent pacing is considered, two factors guide many decisions: the association
Impulse generation is chiefly from the sino-atrial node (SAN) and propagates across the atrium to the atrioventricular node (AV node) prior to rapid transit down the HisePurkinje network to the ventricles. Failure of impulse generation (SAN) or impulse propagation (AV node, HisePurkinje network) will result in bradycardia; if this is sufficiently slow or prolonged, it will result in symptoms.
Classification of heart block First degree
Sinus node disease (SND) Sinus node disease is the commonest reason for pacemaker implant. It is most often idiopathic and most frequently seen in the elderly. SND refers to a broad array of abnormalities in the sinus node resulting in sinus bradycardia, chronotropic incompetence and sinus arrest. The frequent association of paroxysmal atrial fibrillation (AF) and sinus bradycardia, which may oscillate
Second degree
Benjamin D Brown MBChB MRCP MD is a Consultant Cardiologist/Electrophysiologist, University Hospital of South Manchester NHS Trust, Manchester, UK. Competing interests: none declared.
Third degree
David J Fox MBChB MRCP MD is a Consultant Cardiologist/Electrophysiologist, University Hospital of South Manchester NHS Trust, Manchester, UK. Competing interests: Dr Fox has previously received research funding from Medtronic Inc.
MEDICINE 38:9
Fixed but prolonged PR interval (200 ms) 1:1 AV relationship Some atrial activity is not conducted through to the ventricles (intermittent but complete failure of AVN conduction). Further classified into Mobitz I (Wenckebach) e progressive prolongation of PR interval until P wave fails to be conducted and cycle starts again; or Mobitz II e PR interval constant but ventricular activation fails either intermittently or in a fixed ratio to the P wave rate (e.g. 2:1, 3:1, 4:1). Complete AV block or AV dissociation. Atrial activity independent of ventricular activity (ventricular activity provided by escape rhythm of around 30-40 bpm).
Table 1
526
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
of symptoms with an arrhythmia and the location of the conduction abnormality.
Pacemaker indications (adapted from ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm abnormalities)
Symptoms: patients are often considered for pacemaker placement because of symptoms that may have resulted from bradyarrhythmias (e.g. dizziness, light-headedness, syncope, fatigue, and poor exercise tolerance). Frequently, evidence of mild or intermittent sinus node dysfunction or conduction abnormalities is found and it is crucial to attempt to establish a direct correlation between symptoms and bradyarrhythmias by a careful history and ambulatory monitoring.
Class I (good evidence) C Complete (third degree) AV block. C Advanced second-degree AV block (block of two or more consecutive P-waves). C Symptomatic Mobitz I or Mobitz II second-degree AV block. C Mobitz II second-degree AV block with a widened QRS or chronic bifascicular block, regardless of symptoms. C Exercise-induced second- or third-degree AV block (in the absence of myocardial ischaemia). C POST MI C Third-degree AV block within or below the HisePurkinje system. C Persistent second-degree AV block in the HisePurkinje system, with bilateral bundle branch block. C Transient advanced infranodal AV block with associated bundle branch block. C Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually a heart rate below 40 beats/min or frequent sinus pauses). C Symptomatic chronotropic incompetence. C Significant carotid sinus hypersensitivity (syncope and >3 s of asystole following minimal carotid sinus massage).
Location of conduction abnormality: the location of an atrioventricular (AV) conduction abnormality (within the AV node or in the HisePurkinje system) is an important determinant of both the probability and the likely pace of progression of conduction system disease. Disease below the AV node in the HisePurkinje system is generally considered to be less stable and as a result, permanent pacemaker placement is more likely to be recommended (Table 2). Guidelines for implantation of cardiac pacemakers have been established by a task force formed jointly by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society.3 Although occasional cases cannot be categorized according to these guidelines, they are, for the most part, all-encompassing and have been widely endorsed (see Table 3).
Class IIa/IIb (some evidence in favour though some divergence of opinion) C Asymptomatic Mobitz II second-degree AV block with a narrow QRS interval C First-degree AV block when there is haemodynamic compromise because of effective AV dissociation secondary to a very long PR interval. C Bifascicular or trifascicular block associated with syncope that can be attributed to transient complete heart block, based upon the exclusion of other plausible causes of syncope (specifically ventricular tachycardia) C Sinus bradycardia (heart rate <40 beats/min) in a patient with symptoms suggestive of bradycardia, but without a clearly demonstrated association between bradycardia and symptoms. C Sinus node dysfunction in a patient with unexplained syncope. C Chronic heart rates <40 beats/min while awake in a minimally symptomatic patient. C Patients with syncope without clear provocative events and with a hypersensitive cardio-inhibitory response of 3 s or longer. C Patients with recurrent neurocardiogenic syncope associated with bradycardia, documented spontaneously or at the time of tilt-table testing.
Other indications Neuromuscular diseases A number of neuromuscular diseases including myotonic muscular dystrophy, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy are associated with AV block. Patients with these disorders have a class I indication for pacemaker placement once any evidence of second- or third-degree block develops. This is true even if the patient is asymptomatic, because AV conduction disease can progress rapidly and unpredictably. Long QT syndrome Because of their ability to prevent bradycardia e and hence, ventricular arrhythmias e pacemakers have been used in highrisk patients with long QT syndrome. However, many high-risk long QT patients are now treated with an implantable cardioverter-defibrillator, which also has pacing capability.
ECG characteristics of nodal vs infranodal conduction abnormality
Table 3
AV nodal pathology
Significant PR prolongation or Mobitz type I (AV Wenckebach). Disease below the AV Normal/minimally prolonged PR interval, node (infrahisian) Mobitz type II (fixed degree AV block), QRS complex abnormalities (bundle branch block and/or fascicular block).
Hypertrophic cardiomyopathy Pacing for medically refractory, symptomatic hypertrophic cardiomyopathy with significant resting or provoked LV outflow obstruction is now considered a class IIb indication and is not generally recommended. It was previously thought that pacing in the right ventricular apex with a short AV delay would alleviate a proportion of
Table 2
MEDICINE 38:9
527
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Common pacemaker modes Though many different pacing modes are possible, DDD pacing is most commonly employed e in around two-thirds of patients. The majority of the remainder will receive a ventricular-based pacing system with <1% receiving a system with an atrial lead only.5 DDD e dual-chamber pacing, dual-chamber sensing and inhibited pacing in either atrium or ventricle if impulse sensed in that chamber. Physiological pacing/maintaining AV synchrony. VVI e device paces in the ventricle, senses in the ventricle and is inhibited in response to a ventricular-sensed event. Also known as ventricular demand pacing or ventricular inhibited pacing.
the outflow tract gradient, but these patients would now be considered for either surgical myomectomy or alcohol septal ablation.
Pacemaker function Components A pacemaker consists of three components e battery (generally lithium iodide), circuitry (determines what the pacemaker can do) and lead connectors (International standard for all manufacturers (‘IS1’)). Pacing leads Pacing leads have an electrode at the tip secured within the heart by either active or passive fixation (see Figure 1). Passive leads secure themselves within the myocardial trabeculae by use of tines (like a soft anchor), whereas active leads have a small helical screw that is deployed into the myocardium. Pacing leads have two basic but crucial functions e (1) they are required to see or ‘sense’ a cardiac impulse and be able to pace appropriately, (2) they must be able to pace the myocardium in the absence of a cardiac impulse. A pacing lead in good contact with the heart will see/sense a clear intracardiac signal and will require a lower voltage to initiate cardiac depolarization (good sensing ¼ clear signal seen, good threshold ¼ low voltage required to initiate depolarization). These parameters are checked at the time of implant and at each clinic visit.
Pacemaker features The first pacemakers offered only fixed rate pacing compared to the modern device, which has a bewildering array of programmable features. Though these may vary subtly from one manufacturer to another, their core behaviours are the same. Upper and lower rate The device is programmed to the minimum or lower rate that the pacemaker will allow and, accordingly, the upper rate is the maximum rate the pacemaker will pace. These two values are often set to 60/120 bpm but can be varied according to the patient’s age and pacing requirements (upper limit increased for younger individual).
Confusion over sensing Ideal sensing will result in appropriate sensing of a cardiac impulse. If a pacemaker is undersensing, it will not sense all cardiac events and may pace when this is not required. Conversely, a device that is oversensing (physiological or non-physiological signals) will withhold pacing or track inappropriately (e.g. atrial oversensing would detect too many atrial events and try to pace or track this signal down to the ventricle). This can be corrected by altering the sensitivity. For oversensing, increasing the sensitivity will make the device less sensitive and fewer events will be sensed. For undersensing, the sensitivity can be reduced making the device more sensitive so that more events will be sensed.
AV delay This clearly applies only to dual-chamber pacemakers and is the pacemaker equivalent of the PR interval. The optimal AV delay varies but is in the range of 120e200 ms. Newer devices allow the programming of a rate-adaptive AV delay that shortens with higher heart rates, mimicking normal exercise physiology. In an attempt to reduce ventricular pacing (to preserve battery and allow intrinsic conduction) several manufacturers have developed algorithms that attempt to minimize ventricular pacing by progressive prolongation of the AV delay to enable intrinsic conduction. Rate response A common indication for pacemaker implantation is SAN disease, which is often associated with chronotropic incompetence/ a failure to increase heart rate in response to exercise. Most devices are fitted with a sensor (accelerometer, piezo-electric activity sensor) that detects movement/activity and increases the base rate of the pacemaker, to raise heart rate and therefore cardiac output during exercise. The rate response can be assessed by looking at a device-generated histogram at pacing clinic follow-up.
Pacing nomenclature Pacemaker mode is described by a five-letter alphabetic code4 (see Table 4).
Hysteresis This feature prolongs battery life by allowing the heart rate to fall just below the lower rate, enabling intrinsic conduction to continue. For example, a pacemaker set at 60 bpm with a hysteresis rate of 50 bpm would allow the heart rate to fall to 50 bpm before pacing at 60 bpm and would continue pacing until the heart rate returned above 60 bpm once more. Mode switching Many patients with a dual-chamber device will have paroxysms of atrial fibrillation that could theoretically be tracked to the ventricle, resulting in rapid ventricular pacing. Mode switching allows the automatic detection of atrial arrhythmias to prevent
Figure 1 Passive/tined pacing lead a and active fixation lead with screw deployed b.
MEDICINE 38:9
528
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Pacemaker code describing type of pacemaker and its programming First letter Chamber(s) paced A ¼ atrium V ¼ ventricle D ¼ dual (both A & V)
Second letter Chamber(s) sensed A ¼ atrium V ¼ ventricle D ¼ dual (both A & V) O ¼ no sensing
Third letter Response to sensed event I ¼ inhibited T ¼ triggered (pacing) D ¼ both (inhibited and/or triggered) O ¼ no action
Fourth letter If present R ¼ rate response
Fifth letter If present, indicates multisite pacing A ¼ atrium V ¼ ventricle D ¼ dual (both A & V)
Table 4
2 Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ 2004; 329: 336e41. 3 Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation 2008; 117: e350. 4 Bernstein AD, Daubert JC, Fletcher RD, et al. The North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group. The NASPE/BPEG generic code for antibradycardia, adaptive rate and multisite pacing. Pacing Clin Electrophysiol 2002; 25: 260e4. 5 Network Devices Survey Group. National Pacemaker survey from 2007. Available at: www.devicesurvey.com. 6 Tops LF, Schalij MJ, Bax JJ. The Effects of right ventricular apical pacing on ventricular function and dyssynchrony: implications for therapy. J Am Coll Cardiol 2009; 54: 764e76. 7 Thackray SD, Witte KK, Nikitin NP, Clark AL, Kaye GC, Cleland JG. The prevalence of heart failure and asymptomatic left ventricular systolic dysfunction in a typical regional pacemaker population. Eur Heart J 2003; 24: 1143e52. 8 Thambo JB, Bordachar P, Garrigue S, et al. Detrimental ventricular remodeling in patients with congenital complete heart block and chronic right ventricular apical pacing. Circulation 2004; 110: 3766e72. 9 Kypta A, Steinwender C, Kammler J, Leisch F, Hofmann R. Long-term outcomes in patients with atrioventricular block undergoing septal ventricular lead implantation compared with standard apical pacing. Europace 2008; 10: 574e9. 10 Cleland JGF, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539.
this. For example, mode switching would occur when the sensed atrial rate exceeded a preset rate and the device would switch from DDD mode to VVI. Where to put the ventricular pacing lead? Right ventricular leads have traditionally been positioned at the right ventricular apex (RVA). Chronic RVA pacing increases morbidity and mortality, mostly because it increases the incidence of heart failure.6e8 These data have contributed to the investigation of alternative RV pacing sites and algorithms to minimize ventricular pacing. Currently, the alternative site undergoing most investigation is the RV septum. There are suggestions that many of the acute adverse haemodynamic effects of RVA pacing are abrogated when the RV lead is placed on the septum. However, studies looking at clinical outcomes in the short-to-medium term have failed to show superiority of nonapical versus RVA pacing, partly because many patients do not develop heart failure despite RVA pacing. A recently published, longer-term study has again failed to demonstrate improved outcomes from pacing the RV septum rather than the RVA.9 The outcome of Protect PACE, evaluating pacing at the high outflow tract compared with RVA, is awaited. For those individuals with impaired left ventricular systolic dysfunction and breathlessness, there is a well-established role for biventricular pacing with a lead placed in the coronary sinus via the right atrium, allowing simultaneous pacing of the left and right ventricles, which reduces mechanical dyssynchrony. Pacing impaired ventricles in this manner leads to an improvement in symptoms and a reduction in mortality.10 This will be discussed in more detail under heart failure treatment. A
REFERENCES 1 Menozzi C, Brignole M, Alboni P, et al. The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavourable outcome. Am J Cardiol 1998; 82: 1205e9.
MEDICINE 38:9
529
Ó 2010 Published by Elsevier Ltd.
Bradycardia pacing
suddenly from one to the other, is termed ‘tachy-brady syndrome’. Though abnormalities of AV conduction can often be demonstrated patients with SND, only 1% of patients per year will develop significant AV block.1
Benjamin D Brown David J Fox
AV node disease Acquired AV block is the second most common indication for permanent pacemaker placement. Three degrees of heart block are described, according to site and severity (see Table 1 for classification of heart block). Many disorders can cause acquired AV block, although it is most commonly idiopathic. Nodal conduction can also result from ischaemia (after MI), toxicity (bblockers, calcium channel antagonists, digoxin), infection (brucellosis, Lyme disease) and cardiac surgery (most commonly following aortic valve surgery, given the proximity of the AVN to the aortic valve).
Abstract Pacemakers though technologically complex are fundamentally simple once an understanding of the components and language is achieved. This review aims to provide that knowledge to reassure the clinician over a device that is frequently found on medical and surgical wards. Despite pacemakers being cost effective and increasingly commonplace they remain underutilized. Therefore we also aim to equip the reader with the key principles to identify individuals who may benefit from pacemaker implant.
Neurocardiogenic (vasovagal) syncope Syncope as a symptom is most often (50e60% cases) caused by neurocardiogenic syncope. Neurocardiogenic syncope (also known as vasovagal syncope) is a benign condition characterized by a self-limited episode of systemic hypotension, during which increased vagal tone results in a reduction of cardiac filling, bradycardia and hypotension with ensuing loss of consciousness. Differential diagnoses include carotid sinus hypersensitivity (resulting from an extreme reflex response to carotid sinus stimulation) and orthostatic hypotension (failure of the autonomic reflex response). The mainstay of management is education of the patient to avoid situations that predispose to syncope, coping skills, and reassurance of the patient and others that this is a benign condition, though pacing for the bradycardia component is occasionally helpful in selected patients.2
Keywords bradycardia; heart block; pacemaker; pacemaker programming; pacing indication
Since the first human pacemaker in the 1950s, there has been rapid development in the technology of cardiac devices for rhythm management and the equipment to facilitate their implantation. As a result, the number of patients with devices has soared and the indications for their use have increased. This review aims to provide a practical review of pacemaker indications, and an overview of pacemaker function and malfunction, to demystify a device that has become commonplace in medical practice.
Failure of the cardiac conduction system Pacing indications Despite the many clinical situations in which permanent pacing is considered, two factors guide many decisions: the association
Impulse generation is chiefly from the sino-atrial node (SAN) and propagates across the atrium to the atrioventricular node (AV node) prior to rapid transit down the HisePurkinje network to the ventricles. Failure of impulse generation (SAN) or impulse propagation (AV node, HisePurkinje network) will result in bradycardia; if this is sufficiently slow or prolonged, it will result in symptoms.
Classification of heart block First degree
Sinus node disease (SND) Sinus node disease is the commonest reason for pacemaker implant. It is most often idiopathic and most frequently seen in the elderly. SND refers to a broad array of abnormalities in the sinus node resulting in sinus bradycardia, chronotropic incompetence and sinus arrest. The frequent association of paroxysmal atrial fibrillation (AF) and sinus bradycardia, which may oscillate
Second degree
Benjamin D Brown MBChB MRCP MD is a Consultant Cardiologist/Electrophysiologist, University Hospital of South Manchester NHS Trust, Manchester, UK. Competing interests: none declared.
Third degree
David J Fox MBChB MRCP MD is a Consultant Cardiologist/Electrophysiologist, University Hospital of South Manchester NHS Trust, Manchester, UK. Competing interests: Dr Fox has previously received research funding from Medtronic Inc.
MEDICINE 38:9
Fixed but prolonged PR interval (200 ms) 1:1 AV relationship Some atrial activity is not conducted through to the ventricles (intermittent but complete failure of AVN conduction). Further classified into Mobitz I (Wenckebach) e progressive prolongation of PR interval until P wave fails to be conducted and cycle starts again; or Mobitz II e PR interval constant but ventricular activation fails either intermittently or in a fixed ratio to the P wave rate (e.g. 2:1, 3:1, 4:1). Complete AV block or AV dissociation. Atrial activity independent of ventricular activity (ventricular activity provided by escape rhythm of around 30-40 bpm).
Table 1
526
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
of symptoms with an arrhythmia and the location of the conduction abnormality.
Pacemaker indications (adapted from ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm abnormalities)
Symptoms: patients are often considered for pacemaker placement because of symptoms that may have resulted from bradyarrhythmias (e.g. dizziness, light-headedness, syncope, fatigue, and poor exercise tolerance). Frequently, evidence of mild or intermittent sinus node dysfunction or conduction abnormalities is found and it is crucial to attempt to establish a direct correlation between symptoms and bradyarrhythmias by a careful history and ambulatory monitoring.
Class I (good evidence) C Complete (third degree) AV block. C Advanced second-degree AV block (block of two or more consecutive P-waves). C Symptomatic Mobitz I or Mobitz II second-degree AV block. C Mobitz II second-degree AV block with a widened QRS or chronic bifascicular block, regardless of symptoms. C Exercise-induced second- or third-degree AV block (in the absence of myocardial ischaemia). C POST MI C Third-degree AV block within or below the HisePurkinje system. C Persistent second-degree AV block in the HisePurkinje system, with bilateral bundle branch block. C Transient advanced infranodal AV block with associated bundle branch block. C Sinus bradycardia in which symptoms are clearly related to the bradycardia (usually a heart rate below 40 beats/min or frequent sinus pauses). C Symptomatic chronotropic incompetence. C Significant carotid sinus hypersensitivity (syncope and >3 s of asystole following minimal carotid sinus massage).
Location of conduction abnormality: the location of an atrioventricular (AV) conduction abnormality (within the AV node or in the HisePurkinje system) is an important determinant of both the probability and the likely pace of progression of conduction system disease. Disease below the AV node in the HisePurkinje system is generally considered to be less stable and as a result, permanent pacemaker placement is more likely to be recommended (Table 2). Guidelines for implantation of cardiac pacemakers have been established by a task force formed jointly by the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society.3 Although occasional cases cannot be categorized according to these guidelines, they are, for the most part, all-encompassing and have been widely endorsed (see Table 3).
Class IIa/IIb (some evidence in favour though some divergence of opinion) C Asymptomatic Mobitz II second-degree AV block with a narrow QRS interval C First-degree AV block when there is haemodynamic compromise because of effective AV dissociation secondary to a very long PR interval. C Bifascicular or trifascicular block associated with syncope that can be attributed to transient complete heart block, based upon the exclusion of other plausible causes of syncope (specifically ventricular tachycardia) C Sinus bradycardia (heart rate <40 beats/min) in a patient with symptoms suggestive of bradycardia, but without a clearly demonstrated association between bradycardia and symptoms. C Sinus node dysfunction in a patient with unexplained syncope. C Chronic heart rates <40 beats/min while awake in a minimally symptomatic patient. C Patients with syncope without clear provocative events and with a hypersensitive cardio-inhibitory response of 3 s or longer. C Patients with recurrent neurocardiogenic syncope associated with bradycardia, documented spontaneously or at the time of tilt-table testing.
Other indications Neuromuscular diseases A number of neuromuscular diseases including myotonic muscular dystrophy, Erb’s dystrophy (limb-girdle), and peroneal muscular atrophy are associated with AV block. Patients with these disorders have a class I indication for pacemaker placement once any evidence of second- or third-degree block develops. This is true even if the patient is asymptomatic, because AV conduction disease can progress rapidly and unpredictably. Long QT syndrome Because of their ability to prevent bradycardia e and hence, ventricular arrhythmias e pacemakers have been used in highrisk patients with long QT syndrome. However, many high-risk long QT patients are now treated with an implantable cardioverter-defibrillator, which also has pacing capability.
ECG characteristics of nodal vs infranodal conduction abnormality
Table 3
AV nodal pathology
Significant PR prolongation or Mobitz type I (AV Wenckebach). Disease below the AV Normal/minimally prolonged PR interval, node (infrahisian) Mobitz type II (fixed degree AV block), QRS complex abnormalities (bundle branch block and/or fascicular block).
Hypertrophic cardiomyopathy Pacing for medically refractory, symptomatic hypertrophic cardiomyopathy with significant resting or provoked LV outflow obstruction is now considered a class IIb indication and is not generally recommended. It was previously thought that pacing in the right ventricular apex with a short AV delay would alleviate a proportion of
Table 2
MEDICINE 38:9
527
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Common pacemaker modes Though many different pacing modes are possible, DDD pacing is most commonly employed e in around two-thirds of patients. The majority of the remainder will receive a ventricular-based pacing system with <1% receiving a system with an atrial lead only.5 DDD e dual-chamber pacing, dual-chamber sensing and inhibited pacing in either atrium or ventricle if impulse sensed in that chamber. Physiological pacing/maintaining AV synchrony. VVI e device paces in the ventricle, senses in the ventricle and is inhibited in response to a ventricular-sensed event. Also known as ventricular demand pacing or ventricular inhibited pacing.
the outflow tract gradient, but these patients would now be considered for either surgical myomectomy or alcohol septal ablation.
Pacemaker function Components A pacemaker consists of three components e battery (generally lithium iodide), circuitry (determines what the pacemaker can do) and lead connectors (International standard for all manufacturers (‘IS1’)). Pacing leads Pacing leads have an electrode at the tip secured within the heart by either active or passive fixation (see Figure 1). Passive leads secure themselves within the myocardial trabeculae by use of tines (like a soft anchor), whereas active leads have a small helical screw that is deployed into the myocardium. Pacing leads have two basic but crucial functions e (1) they are required to see or ‘sense’ a cardiac impulse and be able to pace appropriately, (2) they must be able to pace the myocardium in the absence of a cardiac impulse. A pacing lead in good contact with the heart will see/sense a clear intracardiac signal and will require a lower voltage to initiate cardiac depolarization (good sensing ¼ clear signal seen, good threshold ¼ low voltage required to initiate depolarization). These parameters are checked at the time of implant and at each clinic visit.
Pacemaker features The first pacemakers offered only fixed rate pacing compared to the modern device, which has a bewildering array of programmable features. Though these may vary subtly from one manufacturer to another, their core behaviours are the same. Upper and lower rate The device is programmed to the minimum or lower rate that the pacemaker will allow and, accordingly, the upper rate is the maximum rate the pacemaker will pace. These two values are often set to 60/120 bpm but can be varied according to the patient’s age and pacing requirements (upper limit increased for younger individual).
Confusion over sensing Ideal sensing will result in appropriate sensing of a cardiac impulse. If a pacemaker is undersensing, it will not sense all cardiac events and may pace when this is not required. Conversely, a device that is oversensing (physiological or non-physiological signals) will withhold pacing or track inappropriately (e.g. atrial oversensing would detect too many atrial events and try to pace or track this signal down to the ventricle). This can be corrected by altering the sensitivity. For oversensing, increasing the sensitivity will make the device less sensitive and fewer events will be sensed. For undersensing, the sensitivity can be reduced making the device more sensitive so that more events will be sensed.
AV delay This clearly applies only to dual-chamber pacemakers and is the pacemaker equivalent of the PR interval. The optimal AV delay varies but is in the range of 120e200 ms. Newer devices allow the programming of a rate-adaptive AV delay that shortens with higher heart rates, mimicking normal exercise physiology. In an attempt to reduce ventricular pacing (to preserve battery and allow intrinsic conduction) several manufacturers have developed algorithms that attempt to minimize ventricular pacing by progressive prolongation of the AV delay to enable intrinsic conduction. Rate response A common indication for pacemaker implantation is SAN disease, which is often associated with chronotropic incompetence/ a failure to increase heart rate in response to exercise. Most devices are fitted with a sensor (accelerometer, piezo-electric activity sensor) that detects movement/activity and increases the base rate of the pacemaker, to raise heart rate and therefore cardiac output during exercise. The rate response can be assessed by looking at a device-generated histogram at pacing clinic follow-up.
Pacing nomenclature Pacemaker mode is described by a five-letter alphabetic code4 (see Table 4).
Hysteresis This feature prolongs battery life by allowing the heart rate to fall just below the lower rate, enabling intrinsic conduction to continue. For example, a pacemaker set at 60 bpm with a hysteresis rate of 50 bpm would allow the heart rate to fall to 50 bpm before pacing at 60 bpm and would continue pacing until the heart rate returned above 60 bpm once more. Mode switching Many patients with a dual-chamber device will have paroxysms of atrial fibrillation that could theoretically be tracked to the ventricle, resulting in rapid ventricular pacing. Mode switching allows the automatic detection of atrial arrhythmias to prevent
Figure 1 Passive/tined pacing lead a and active fixation lead with screw deployed b.
MEDICINE 38:9
528
Ó 2010 Published by Elsevier Ltd.
ARRHYTHMIAS AND ELECTROPHYSIOLOGY
Pacemaker code describing type of pacemaker and its programming First letter Chamber(s) paced A ¼ atrium V ¼ ventricle D ¼ dual (both A & V)
Second letter Chamber(s) sensed A ¼ atrium V ¼ ventricle D ¼ dual (both A & V) O ¼ no sensing
Third letter Response to sensed event I ¼ inhibited T ¼ triggered (pacing) D ¼ both (inhibited and/or triggered) O ¼ no action
Fourth letter If present R ¼ rate response
Fifth letter If present, indicates multisite pacing A ¼ atrium V ¼ ventricle D ¼ dual (both A & V)
Table 4
2 Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ 2004; 329: 336e41. 3 Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation 2008; 117: e350. 4 Bernstein AD, Daubert JC, Fletcher RD, et al. The North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group. The NASPE/BPEG generic code for antibradycardia, adaptive rate and multisite pacing. Pacing Clin Electrophysiol 2002; 25: 260e4. 5 Network Devices Survey Group. National Pacemaker survey from 2007. Available at: www.devicesurvey.com. 6 Tops LF, Schalij MJ, Bax JJ. The Effects of right ventricular apical pacing on ventricular function and dyssynchrony: implications for therapy. J Am Coll Cardiol 2009; 54: 764e76. 7 Thackray SD, Witte KK, Nikitin NP, Clark AL, Kaye GC, Cleland JG. The prevalence of heart failure and asymptomatic left ventricular systolic dysfunction in a typical regional pacemaker population. Eur Heart J 2003; 24: 1143e52. 8 Thambo JB, Bordachar P, Garrigue S, et al. Detrimental ventricular remodeling in patients with congenital complete heart block and chronic right ventricular apical pacing. Circulation 2004; 110: 3766e72. 9 Kypta A, Steinwender C, Kammler J, Leisch F, Hofmann R. Long-term outcomes in patients with atrioventricular block undergoing septal ventricular lead implantation compared with standard apical pacing. Europace 2008; 10: 574e9. 10 Cleland JGF, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539.
this. For example, mode switching would occur when the sensed atrial rate exceeded a preset rate and the device would switch from DDD mode to VVI. Where to put the ventricular pacing lead? Right ventricular leads have traditionally been positioned at the right ventricular apex (RVA). Chronic RVA pacing increases morbidity and mortality, mostly because it increases the incidence of heart failure.6e8 These data have contributed to the investigation of alternative RV pacing sites and algorithms to minimize ventricular pacing. Currently, the alternative site undergoing most investigation is the RV septum. There are suggestions that many of the acute adverse haemodynamic effects of RVA pacing are abrogated when the RV lead is placed on the septum. However, studies looking at clinical outcomes in the short-to-medium term have failed to show superiority of nonapical versus RVA pacing, partly because many patients do not develop heart failure despite RVA pacing. A recently published, longer-term study has again failed to demonstrate improved outcomes from pacing the RV septum rather than the RVA.9 The outcome of Protect PACE, evaluating pacing at the high outflow tract compared with RVA, is awaited. For those individuals with impaired left ventricular systolic dysfunction and breathlessness, there is a well-established role for biventricular pacing with a lead placed in the coronary sinus via the right atrium, allowing simultaneous pacing of the left and right ventricles, which reduces mechanical dyssynchrony. Pacing impaired ventricles in this manner leads to an improvement in symptoms and a reduction in mortality.10 This will be discussed in more detail under heart failure treatment. A
REFERENCES 1 Menozzi C, Brignole M, Alboni P, et al. The natural course of untreated sick sinus syndrome and identification of the variables predictive of unfavourable outcome. Am J Cardiol 1998; 82: 1205e9.
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