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Bradycardia and Permanent Pacemakers
DISORDERS OF CARDIAC RHYTHM
Sinus node disease is also known as sino-atrial node disease, ‘sick sinus syndrome’ and tachy/brady syndrome. The aetiology is most commonly idiopathic, probably related to conduction tissue fibrosis, though the condition may occur in association with myocardial infarction (MI), cardiomyopathy or infiltrative conditions such as amyloidosis. It is most likely to occur in the seventh or eighth decade, but may occur at any age. Sinus node disease is the most common indication for pacing in young individuals. Subsequent development of AV node disease is reported in 10–20% of those with sinus node disease; the incidence increases with age. AV node disease – the aetiology of AV node disease can be: • idiopathic (most common – likely to result from conduction tissue fibrosis) • acute MI • congenital (in isolation or with other congenital defects) • post-cardiac surgery (particularly aortic and less commonly mitral valve replacement) • deposition diseases (amyloidosis, sarcoidosis) • infections (e.g. Lyme disease, chronic brucellosis) • drug toxicity (e.g. digoxin, β-blockers, verapamil). The classification of AV block is shown in Figure 1. Neurocardiogenic syncope – the most widely recognized forms of neurocardiogenic syncope are as follows.
Bradycardia and Permanent Pacemakers Mark J Mason Vince Paul
The investigation and management of bradycardia is an increasingly complex topic, but with the development of pacemakers there are few areas of medicine that offer such substantial improvements in patients’ quality of life. About 400,000 pacemakers are implanted worldwide per year; about 270 are implanted per million population in the UK, 370 per million in Europe as a whole and 434 per million in the USA. The use of pacing varies, however, depending on the availability of expertise to recognize the potential benefits of pacing, to select an appropriate type and to implant the device. This contribution focuses on the investigation of patients with bradycardia and the subsequent indications for pacing. The indications are based on the recommendations of the American College of Cardiology/American Heart Association.
Bradycardia North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group recommendations on general indications for pacing
The pathophysiology of bradycardia may be divided into: • failure to initiate a cardiac impulse – sinus node disease • failure to conduct the cardiac impulse – atrioventricular (AV) node disease • ‘neurocardiogenic’ syncope.
Class 1 – acceptable and necessary • Acquired symptomatic complete AV block (unpaced 1-year mortality is 30–35%, compared with 5% if paced) • Symptomatic congenital complete heart block (decisions regarding timing may be difficult in children and teenagers who are still growing – seek expert advice) • Symptomatic second-degree AV block (Mobitz I or II) • Symptomatic sinus bradycardia • When accompanied by significant symptoms, sinus bradycardia that is the consequence of long-term drug treatment for which there is no acceptable alternative • Sinus node dysfunction ± tachyarrhythmia or AV block • Sinus node dysfunction ± symptoms in patients with potentially life-threatening ventricular arrhythmia or tachycardia secondary to bradycardia • Bradycardia associated with significant symptoms and with supraventricular tachycardia and high-degree AV block unresponsive to appropriate pharmacological management Class 2 – may be acceptable or necessary • Asymptomatic acquired third-degree AV block with ventricular rate > 40 beats per minute • Bifascicular or trifascicular block accompanied by syncope that is attributed to transient complete heart block after other plausible causes of syncope have been reasonably excluded • Asymptomatic Mobitz II second-degree AV block • Asymptomatic Mobitz I second-degree AV block within the His–Purkinje system (requires electrophysiological evaluation)
ClassiÞcation of atrioventricular block First-degree AV block is identified by prolongation of the PR interval to > 200 milliseconds. Second-degree AV block may be classified as: • Mobitz type 1 (‘Wenckebach’) block – progressive lengthening of the PR interval with each successive complex until a P wave is not conducted and a QRS complex is ‘dropped’ • Mobitz type II block – PR interval is constant, but QRS complexes are dropped either intermittently or in a fixed ratio to the P wave rate (e.g. 2:1, 3:1, 4:1) Third-degree ʻcompleteʼ AV block: there is complete dissociation of atrial and ventricular electrical activity. P waves remain regular at a rate determined by the sinus node and QRS complexes ‘march through’ independently in an idioventricular ‘escape’ rhythm. The rate is typically 30–50 per minute (higher levels of block lead to faster rates and narrower QRS complexes).
1
Mark J Mason is a Locum Consultant Cardiologist at Harefield Hospital, Harefield, UK. Vince Paul is Consultant Cardiologist at St Peter’s Hospital, Chertsey, UK. 2 MEDICINE
137
© 2002 The Medicine Publishing Company Ltd
DISORDERS OF CARDIAC RHYTHM
Atrioventricular block associated with myocardial infarction Site of infarction
Level of AV block
Management Acute
Chronic
Inferior
Second-degree – Mobitz I Second-degree – Mobitz II Third-degree (complete)
Conservative (unless compromised) Temporary pacing Temporary pacing
Sinus rhythm may recover after up to 6 weeks; in practice, probably wait 1 week
Anterior
Second-degree – Mobitz I Second-degree – Mobitz II Third-degree (complete)
Temporary pacing Temporary pacing Temporary pacing
Recovery unlikely; early permanent pacing is therefore recommended
3
• In vasovagal syndrome, patients experience syncope or presyncope associated with a sudden increase in vagal activity. This may occur in response to stress or emotional precipitants, or there may be no identifiable provocation. Patients present with profound peripheral vasodilatation leading to hypotension during which the heart rate remains unchanged, with bradycardia and consequent haemodynamic compromise, or with a combination of these responses. The response is sometimes preceded by tachycardia, which in a few patients is the only clinical manifestation. • Carotid sinus hypersensitivity is a similar clinical entity in which stimulation of the carotid sinus (e.g. by a tight collar or turning the head) in susceptible individuals leads to vasodilatation, bradycardia or both.
Cardiac pacing Cardiac pacing may be temporary (usually an emergency measure to provide support until a permanent device can be implanted) or permanent. Temporary pacing The indications for temporary pacing can be broadly described as any bradyarrhythmia presenting with evidence, or a high likelihood, of haemodynamic compromise (including syncope or presyncope). Modes of temporary pacing External pacing – adhesive pads are positioned on the skin either postero-anteriorly (lower aspect of the left scapula posteriorly and the apex anteriorly) or anteriorly using the conventional paddle positions for defibrillation. External pacing may be useful in acute situations. To minimize discomfort in conscious patients, the output should be the minimum required to achieve capture. Transvenous temporary pacing – a temporary pacing wire is advanced to the right ventricular apex via a large vein under local anaesthetic. The internal jugular or subclavian route is usually used, though it is preferable to avoid the subclavian route because this is a potential site for permanent pacemaker implantation. In an emergency, the femoral vein may be used.
Clinical features of bradyarrhythmias: the symptoms of bradyarrhythmia are most commonly intermittent syncope or presyncope, but may be more general (e.g. tiredness, lethargy). Many patients present with symptoms of the underlying cause (e.g. MI, drug toxicity). In sino-atrial node disease, symptoms of the tachycardic elements of the rhythm may also occur. These are detected by the patient as palpitations, which may be difficult to control with drug therapy without potentiating bradyarrhythmias. Investigations: the mainstay of investigation is 24-hour Holter monitoring. AV block may be obvious on 12-lead ECG, and in sinus node disease extreme bradycardia at rest or sinus arrhythmia (which would be deemed inappropriate in older age groups) may be seen. Use of an event recorder triggered by the patient may be indicated when symptoms are intermittent.
Permanent pacing Conventional permanent pacemakers are either singlechamber (atrial or ventricular) or dual-chamber (both). In the past, most implanted devices paced only the ventricle. Increasing recognition of the importance of synchronized atrial and ventricular contraction has led to greater use of dual-chamber pacing with its presumed ‘physiological’ benefits,
Management: pacing recommendations are shown in Figure 2. The role of pacing after MI is summarized in Figure 3.
North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group pacemaker codes
Designation Letters used
First Chambers paced V, ventricle A, atrium D, dual (both)
Second Chambers sensed V, ventricle A, atrium D, dual (both) O, none
Letter position Third Type of response T, triggered (paced) I, inhibited D, dual (either)
Fourth Programmable functions R, rate responsive (Others available but seldom used)
Fifth Tachyarrhythmia functions Seldom used
4 MEDICINE
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© 2002 The Medicine Publishing Company Ltd
DISORDERS OF CARDIAC RHYTHM
though these may be overstated. The indications for each type of device are summarized below, though given the variation between patients, this list cannot be exhaustive: • sinus node disease – either atrial single-chamber (in relatively young patients in whom development of AV node disease is unlikely for some time) or (usually) dual-chamber • AV node disease – usually dual-chamber • bradycardia with underlying atrial fibrillation – there is no organized atrial activity and therefore single-chamber ventricular pacing is appropriate. Occasionally, single-chamber ventricular pacing is appropriate for symptomatic benefit in those in whom ‘physiological’ pacing is not deemed important. The type of pacing system is described by a five-letter code agreed by the North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group (Figure 4). Only the first three letters are commonly used; the fourth is sometimes used to denote rate-responsive capabilities (R, see below). The most commonly used devices are single-chamber atrial (AAI) or ventricular (VVI), and dual-chamber (DDD). Patients with isolated AV block may be adequately managed with sensing of atrial activity and subsequent pacing of the ventricle as appropriate (VDD). This can be achieved by programming a conventional dual-chamber device with atrial and ventricular leads, or by using a single specific VDD lead positioned in the ventricle with a sensor along its length on the portion of the lead within the right atrium. However, the lack of contact between the atrial sensor and the myocardium means that the lead can erroneously sense electrical activity from elsewhere (e.g. ventricular or chest muscles – ‘far-field’ sensing).
Upper rate – the maximum paced rate is determined by several factors, including the activity and general health of the patient. An initial estimate is calculated in the same manner as the target rate for exercise testing (e.g. 200 minus age, in an 80-year-old, gives an upper rate of 120 beats per minute). AV delay (or interval) is the time a dual-chamber device allows following a sensed or paced atrial impulse before pacing the ventricle. This may vary according to circumstances; for example, in patients with AV conduction problems, a long AV interval is programmed to allow an inherent ventricular impulse, thereby inhibiting ventricular pacing and preserving battery life. There is evidence to suggest that a subgroup of patients with heart failure may benefit from a very short AV interval, such that all ventricular impulses are paced. ‘Mode switching’ is a feature of some dual-chamber generators designed to overcome the potential problem of the onset of atrial fibrillation or flutter. If the atrial rate is detected to be above a certain (programmable) limit, the device reverts to VVI mode and then rechecks intermittently (again after a programmable interval). Rate response – some devices can increase the paced rate in an attempt to reflect a normal physiological response to activity. Various types of sensor within the device are available. The most common are: • physical activity (‘movement’) – detects the amount and speed of body motion • minute volume – detects increases in respiratory activity and uses this as a gauge of increased physical activity • QT interval – decreases during exercise due to catecholamine release (probably the most physiological of sensors). Many devices now have a combination of two or more sensors, which allows cross-checking to ensure that any change in pacing rate is appropriate. u
Pacemaker programming Pacing mode – single-chamber devices offer relatively little scope for change of mode. If appropriate (which is rare), they can be reprogrammed to fixed-rate (non-sensed) pacing (denoted AOO or VOO) (e.g. before general surgical procedures to allow use of diathermy, which may otherwise interfere with pacemaker sensing function). Dual-chamber devices may be reprogrammed to sense or pace within a single chamber. This is most commonly used in patients who develop atrial fibrillation, in whom the device is programmed to VVI mode such that it disregards the atrial activity. Lower rate is the minimum heart rate that the pacemaker allows. If the inherent rate of the relevant cardiac chamber is above this figure, the device senses the impulse and inhibits pacing. If the rate falls below this figure, the device adds a paced beat. Many factors determine the programmed lower rate, including the age and general activity of the patient and the indication for pacing. The lower rate is often a compromise, reducing the amount of time spent pacing in the interests of increasing battery life. Hysteresis may further increase battery life by allowing the patient’s own rhythm to function down to the programmed hysteresis rate (e.g. 50 beats per minute), before the device commences pacing at the programmed lower rate (e.g. 60 beats per minute). This reduces the time spent in paced rhythm if the patient experiences transient decreases in heart rate.
MEDICINE
REFERENCES Cowell R, Morris-Thurgood J, Ilsley C, Paul V. Septal Short Atrioventricular Delay Pacing: Additional Hemodynamic Improvements in Heart Failure. Pacing Clin Electrophysiol 1994; 17(11): 1980–3. Gregoratos G, Cheitlin M, Conill A et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol 1998; 31: 1175–209. Lamas G A, Orav E J, Stambler B S et al. Quality of Life and Clinical Outcomes in Elderly Patients Treated with Ventricular Pacing as Compared with Dual Chamber Pacing. Pacemaker Selection in the Elderly Investigators. N Engl J Med 1998; 338: 1097–104.
Practice points • Bradycardias are significant causes of morbidity, and occasionally mortality • Many patients with bradycardia who might benefit from pacing remain undetected • New developments in pacing for heart failure (e.g. biventricular pacing) may offer substantial benefits in both quality of life and survival
139
© 2002 The Medicine Publishing Company Ltd
Sinus node disease is also known as sino-atrial node disease, ‘sick sinus syndrome’ and tachy/brady syndrome. The aetiology is most commonly idiopathic, probably related to conduction tissue fibrosis, though the condition may occur in association with myocardial infarction (MI), cardiomyopathy or infiltrative conditions such as amyloidosis. It is most likely to occur in the seventh or eighth decade, but may occur at any age. Sinus node disease is the most common indication for pacing in young individuals. Subsequent development of AV node disease is reported in 10–20% of those with sinus node disease; the incidence increases with age. AV node disease – the aetiology of AV node disease can be: • idiopathic (most common – likely to result from conduction tissue fibrosis) • acute MI • congenital (in isolation or with other congenital defects) • post-cardiac surgery (particularly aortic and less commonly mitral valve replacement) • deposition diseases (amyloidosis, sarcoidosis) • infections (e.g. Lyme disease, chronic brucellosis) • drug toxicity (e.g. digoxin, β-blockers, verapamil). The classification of AV block is shown in Figure 1. Neurocardiogenic syncope – the most widely recognized forms of neurocardiogenic syncope are as follows.
Bradycardia and Permanent Pacemakers Mark J Mason Vince Paul
The investigation and management of bradycardia is an increasingly complex topic, but with the development of pacemakers there are few areas of medicine that offer such substantial improvements in patients’ quality of life. About 400,000 pacemakers are implanted worldwide per year; about 270 are implanted per million population in the UK, 370 per million in Europe as a whole and 434 per million in the USA. The use of pacing varies, however, depending on the availability of expertise to recognize the potential benefits of pacing, to select an appropriate type and to implant the device. This contribution focuses on the investigation of patients with bradycardia and the subsequent indications for pacing. The indications are based on the recommendations of the American College of Cardiology/American Heart Association.
Bradycardia North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group recommendations on general indications for pacing
The pathophysiology of bradycardia may be divided into: • failure to initiate a cardiac impulse – sinus node disease • failure to conduct the cardiac impulse – atrioventricular (AV) node disease • ‘neurocardiogenic’ syncope.
Class 1 – acceptable and necessary • Acquired symptomatic complete AV block (unpaced 1-year mortality is 30–35%, compared with 5% if paced) • Symptomatic congenital complete heart block (decisions regarding timing may be difficult in children and teenagers who are still growing – seek expert advice) • Symptomatic second-degree AV block (Mobitz I or II) • Symptomatic sinus bradycardia • When accompanied by significant symptoms, sinus bradycardia that is the consequence of long-term drug treatment for which there is no acceptable alternative • Sinus node dysfunction ± tachyarrhythmia or AV block • Sinus node dysfunction ± symptoms in patients with potentially life-threatening ventricular arrhythmia or tachycardia secondary to bradycardia • Bradycardia associated with significant symptoms and with supraventricular tachycardia and high-degree AV block unresponsive to appropriate pharmacological management Class 2 – may be acceptable or necessary • Asymptomatic acquired third-degree AV block with ventricular rate > 40 beats per minute • Bifascicular or trifascicular block accompanied by syncope that is attributed to transient complete heart block after other plausible causes of syncope have been reasonably excluded • Asymptomatic Mobitz II second-degree AV block • Asymptomatic Mobitz I second-degree AV block within the His–Purkinje system (requires electrophysiological evaluation)
ClassiÞcation of atrioventricular block First-degree AV block is identified by prolongation of the PR interval to > 200 milliseconds. Second-degree AV block may be classified as: • Mobitz type 1 (‘Wenckebach’) block – progressive lengthening of the PR interval with each successive complex until a P wave is not conducted and a QRS complex is ‘dropped’ • Mobitz type II block – PR interval is constant, but QRS complexes are dropped either intermittently or in a fixed ratio to the P wave rate (e.g. 2:1, 3:1, 4:1) Third-degree ʻcompleteʼ AV block: there is complete dissociation of atrial and ventricular electrical activity. P waves remain regular at a rate determined by the sinus node and QRS complexes ‘march through’ independently in an idioventricular ‘escape’ rhythm. The rate is typically 30–50 per minute (higher levels of block lead to faster rates and narrower QRS complexes).
1
Mark J Mason is a Locum Consultant Cardiologist at Harefield Hospital, Harefield, UK. Vince Paul is Consultant Cardiologist at St Peter’s Hospital, Chertsey, UK. 2 MEDICINE
137
© 2002 The Medicine Publishing Company Ltd
DISORDERS OF CARDIAC RHYTHM
Atrioventricular block associated with myocardial infarction Site of infarction
Level of AV block
Management Acute
Chronic
Inferior
Second-degree – Mobitz I Second-degree – Mobitz II Third-degree (complete)
Conservative (unless compromised) Temporary pacing Temporary pacing
Sinus rhythm may recover after up to 6 weeks; in practice, probably wait 1 week
Anterior
Second-degree – Mobitz I Second-degree – Mobitz II Third-degree (complete)
Temporary pacing Temporary pacing Temporary pacing
Recovery unlikely; early permanent pacing is therefore recommended
3
• In vasovagal syndrome, patients experience syncope or presyncope associated with a sudden increase in vagal activity. This may occur in response to stress or emotional precipitants, or there may be no identifiable provocation. Patients present with profound peripheral vasodilatation leading to hypotension during which the heart rate remains unchanged, with bradycardia and consequent haemodynamic compromise, or with a combination of these responses. The response is sometimes preceded by tachycardia, which in a few patients is the only clinical manifestation. • Carotid sinus hypersensitivity is a similar clinical entity in which stimulation of the carotid sinus (e.g. by a tight collar or turning the head) in susceptible individuals leads to vasodilatation, bradycardia or both.
Cardiac pacing Cardiac pacing may be temporary (usually an emergency measure to provide support until a permanent device can be implanted) or permanent. Temporary pacing The indications for temporary pacing can be broadly described as any bradyarrhythmia presenting with evidence, or a high likelihood, of haemodynamic compromise (including syncope or presyncope). Modes of temporary pacing External pacing – adhesive pads are positioned on the skin either postero-anteriorly (lower aspect of the left scapula posteriorly and the apex anteriorly) or anteriorly using the conventional paddle positions for defibrillation. External pacing may be useful in acute situations. To minimize discomfort in conscious patients, the output should be the minimum required to achieve capture. Transvenous temporary pacing – a temporary pacing wire is advanced to the right ventricular apex via a large vein under local anaesthetic. The internal jugular or subclavian route is usually used, though it is preferable to avoid the subclavian route because this is a potential site for permanent pacemaker implantation. In an emergency, the femoral vein may be used.
Clinical features of bradyarrhythmias: the symptoms of bradyarrhythmia are most commonly intermittent syncope or presyncope, but may be more general (e.g. tiredness, lethargy). Many patients present with symptoms of the underlying cause (e.g. MI, drug toxicity). In sino-atrial node disease, symptoms of the tachycardic elements of the rhythm may also occur. These are detected by the patient as palpitations, which may be difficult to control with drug therapy without potentiating bradyarrhythmias. Investigations: the mainstay of investigation is 24-hour Holter monitoring. AV block may be obvious on 12-lead ECG, and in sinus node disease extreme bradycardia at rest or sinus arrhythmia (which would be deemed inappropriate in older age groups) may be seen. Use of an event recorder triggered by the patient may be indicated when symptoms are intermittent.
Permanent pacing Conventional permanent pacemakers are either singlechamber (atrial or ventricular) or dual-chamber (both). In the past, most implanted devices paced only the ventricle. Increasing recognition of the importance of synchronized atrial and ventricular contraction has led to greater use of dual-chamber pacing with its presumed ‘physiological’ benefits,
Management: pacing recommendations are shown in Figure 2. The role of pacing after MI is summarized in Figure 3.
North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group pacemaker codes
Designation Letters used
First Chambers paced V, ventricle A, atrium D, dual (both)
Second Chambers sensed V, ventricle A, atrium D, dual (both) O, none
Letter position Third Type of response T, triggered (paced) I, inhibited D, dual (either)
Fourth Programmable functions R, rate responsive (Others available but seldom used)
Fifth Tachyarrhythmia functions Seldom used
4 MEDICINE
138
© 2002 The Medicine Publishing Company Ltd
DISORDERS OF CARDIAC RHYTHM
though these may be overstated. The indications for each type of device are summarized below, though given the variation between patients, this list cannot be exhaustive: • sinus node disease – either atrial single-chamber (in relatively young patients in whom development of AV node disease is unlikely for some time) or (usually) dual-chamber • AV node disease – usually dual-chamber • bradycardia with underlying atrial fibrillation – there is no organized atrial activity and therefore single-chamber ventricular pacing is appropriate. Occasionally, single-chamber ventricular pacing is appropriate for symptomatic benefit in those in whom ‘physiological’ pacing is not deemed important. The type of pacing system is described by a five-letter code agreed by the North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group (Figure 4). Only the first three letters are commonly used; the fourth is sometimes used to denote rate-responsive capabilities (R, see below). The most commonly used devices are single-chamber atrial (AAI) or ventricular (VVI), and dual-chamber (DDD). Patients with isolated AV block may be adequately managed with sensing of atrial activity and subsequent pacing of the ventricle as appropriate (VDD). This can be achieved by programming a conventional dual-chamber device with atrial and ventricular leads, or by using a single specific VDD lead positioned in the ventricle with a sensor along its length on the portion of the lead within the right atrium. However, the lack of contact between the atrial sensor and the myocardium means that the lead can erroneously sense electrical activity from elsewhere (e.g. ventricular or chest muscles – ‘far-field’ sensing).
Upper rate – the maximum paced rate is determined by several factors, including the activity and general health of the patient. An initial estimate is calculated in the same manner as the target rate for exercise testing (e.g. 200 minus age, in an 80-year-old, gives an upper rate of 120 beats per minute). AV delay (or interval) is the time a dual-chamber device allows following a sensed or paced atrial impulse before pacing the ventricle. This may vary according to circumstances; for example, in patients with AV conduction problems, a long AV interval is programmed to allow an inherent ventricular impulse, thereby inhibiting ventricular pacing and preserving battery life. There is evidence to suggest that a subgroup of patients with heart failure may benefit from a very short AV interval, such that all ventricular impulses are paced. ‘Mode switching’ is a feature of some dual-chamber generators designed to overcome the potential problem of the onset of atrial fibrillation or flutter. If the atrial rate is detected to be above a certain (programmable) limit, the device reverts to VVI mode and then rechecks intermittently (again after a programmable interval). Rate response – some devices can increase the paced rate in an attempt to reflect a normal physiological response to activity. Various types of sensor within the device are available. The most common are: • physical activity (‘movement’) – detects the amount and speed of body motion • minute volume – detects increases in respiratory activity and uses this as a gauge of increased physical activity • QT interval – decreases during exercise due to catecholamine release (probably the most physiological of sensors). Many devices now have a combination of two or more sensors, which allows cross-checking to ensure that any change in pacing rate is appropriate. u
Pacemaker programming Pacing mode – single-chamber devices offer relatively little scope for change of mode. If appropriate (which is rare), they can be reprogrammed to fixed-rate (non-sensed) pacing (denoted AOO or VOO) (e.g. before general surgical procedures to allow use of diathermy, which may otherwise interfere with pacemaker sensing function). Dual-chamber devices may be reprogrammed to sense or pace within a single chamber. This is most commonly used in patients who develop atrial fibrillation, in whom the device is programmed to VVI mode such that it disregards the atrial activity. Lower rate is the minimum heart rate that the pacemaker allows. If the inherent rate of the relevant cardiac chamber is above this figure, the device senses the impulse and inhibits pacing. If the rate falls below this figure, the device adds a paced beat. Many factors determine the programmed lower rate, including the age and general activity of the patient and the indication for pacing. The lower rate is often a compromise, reducing the amount of time spent pacing in the interests of increasing battery life. Hysteresis may further increase battery life by allowing the patient’s own rhythm to function down to the programmed hysteresis rate (e.g. 50 beats per minute), before the device commences pacing at the programmed lower rate (e.g. 60 beats per minute). This reduces the time spent in paced rhythm if the patient experiences transient decreases in heart rate.
MEDICINE
REFERENCES Cowell R, Morris-Thurgood J, Ilsley C, Paul V. Septal Short Atrioventricular Delay Pacing: Additional Hemodynamic Improvements in Heart Failure. Pacing Clin Electrophysiol 1994; 17(11): 1980–3. Gregoratos G, Cheitlin M, Conill A et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol 1998; 31: 1175–209. Lamas G A, Orav E J, Stambler B S et al. Quality of Life and Clinical Outcomes in Elderly Patients Treated with Ventricular Pacing as Compared with Dual Chamber Pacing. Pacemaker Selection in the Elderly Investigators. N Engl J Med 1998; 338: 1097–104.
Practice points • Bradycardias are significant causes of morbidity, and occasionally mortality • Many patients with bradycardia who might benefit from pacing remain undetected • New developments in pacing for heart failure (e.g. biventricular pacing) may offer substantial benefits in both quality of life and survival
139
© 2002 The Medicine Publishing Company Ltd