INDICATIONS FOR PERMANENT PACING

The indications for permanent pacemakers can be divided into three classifications (Table1) and are listed in Table 2 (below) according to the most recent indications published by a joint task force by the American College of Cardiology and American Heart Association in 1998.

 

TABLE 1- Consensus for Appropriateness of Pacer Implant Indication

Class I Conditions for which there is general agreement that permanent pacemakers should be implanted.

Class IIa Conditions for which permanent pacemakers are frequently used but there is divergence of opinion with respect to the necessity of their insertion. Weight of evidence/opinion is in favor of pace-maker use.

Class IIb Conditions for which permanent pacemakers are frequently used but there is divergence of opinion with respect to the necessity of their insertion. Weight of evidence/opinion is in favor of pace-maker use.

Class III Conditions for which there is general agreement that devices are unnecessary.

	Class I	Class II	Class III
Acquired AV block	Third-degree AV block with: Bradycardia and symptoms due to AV block Requirement of drugs that result in symptomatic bradycardia After catheter ablation of the AV junction or after postoperative AV block not expected to resolve Neuromuscular diseases with AV block Escape rhythm <40 bpm or asystole >3 s in awake symptom-free patients Second-degree AV block. permanent or intermittent- with symptomatic bradycardia	Asymptomatic complete AV block with average awake ventricular rate >40 bpm Asymptomatic type 11 second-degree AV block (permanent or intermittent) Asymptomatic type I second-degree AV block at or below the bundle of His (documented by electrophysiologic studies) First degree AV block with symptoms suggestive of pacemaker syndrome and documented alleviation of symptoms with temporary pacing Class IIb Marked first-degree AV block in patients with congestive heart failure	Asymptomatic first-degree AV block Asymptomatic type I second-degree AV block above the level of the bun dle of His AV block expected to resolve
After myocardial infarction	Persistent second- or third-degree AV block in the His-Purkinje system or Transient advanced infranodal AV block and associated BBB Symptomatic second- or third-degree AV block at any level	Class IIb Persistent advanced AV block at the AV node level	Transient AV conduction disturbances without intraventricular conduction defects or with isolated left an- terior fascicular block Acquired left anterior fascicular block Persistent first-degree AV block in the presence of old or age-indeteminate BBB
Bifascicular or trifasicular block	Intermittent complete heart block associated with symptoms Type II second-degree AV block	Class IIa Bifascicular or trifascicular block with syncope not proven to be due to AV block but other causes of syncope not identifiable HV interval >100 ms or pacing-induced infra-His block	Fascicular block without AV block or symptoms Fascicular block with first-degree AV block without symptoms
Sinus node dysfunction	Sinus node dysfunction with documented symptomatic bradycardia (in some patients, this will occur as a result of long-term essential drug therapy of a type and dose for which there is no acceptable alternative) Symptomatic chronotropic incompetence	Class IIa Sinus node dysfunction. occurring spontaneously or as a result of necessary drug therapy with heart rates <40 bpm without clear association between significant symptoms and bradycardia Class IIb In minimally symptomatic patients, chronic heart rate <30 bpm while awake	Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia is a consequence of long-term drug treatment Sinus node dysfunction in patients in whom symptoms suggestive of bradycardia are clearly documented not to be associated with a slow hear rate. Sinus node dysfunction with symptomatic bradycardia due to nonessential drug therapy
Hypersensitive carotid sinus and neurocardiac syndromes	Recurrent syncope associated with clear, spontaneous events provoked by carotid sinus stimulation: minimal carotid sinus pressure induces asystole of >3 s duration in the absence of any medication that depresses the sinus node or AV conduction	Class IIa Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response Class IIb Syncope with associated bradycardia reproduced by head-up tilt (with or without provocative maneuvers or isoproterenol )	A hyperactive cardioinhibitorv response to carotid sinus stimulation in the absence of symptoms Vague symptoms (dizziness or light-headedness) with a hyperactive cardioinhibitory response to carotid sinus stimulation Recurrent syncope, light-headedness, dizziness in the absence of a cardioinhibitory response

Table 2

These recommendations serve as guidelines, and there are other clinical factors that may affect the decision to implant a pacer. Many indications for pacemaker implantation are predicated by the presence of symptoms. However, many symptoms such as fatigue or subtle symptoms of congestive heart failure may be recognized only in retrospect, after placement of a permanent pacemaker.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992

Pacing in Acquired Atrioventricular Block

It is generally agreed that complete heart block, permanent or intermittent, at any anatomic level associated with symptoms such as dizziness, lightheadedness, syncope, congestive heart failure, or confusion is an indication for a permanent pacemaker. In the absence of symptoms, pacing is indicated for patients with third-degree AV block, especially with awake heart rates of less than 40 beats per minute or pauses of longer than 3 s.

In the presence of bifascicular or trifascicular block, intermittent third-degree or type II second-degree AV block usually indicates the need for a permanent pacemaker. When patients with these conduction patterns present with syncope, a pacemaker is usually required. However, an electrophysiology study may be useful to rule out other causes of syncope (e.g., ventricular tachycardia) particularly if structural heart disease is present. Additionally, during electrophysiology study, permanent pacing may be indicated if there is a markedly prolonged HV interval (>100 ms) or nonphysiologic pacing or drug-induced infranodal His block.

Second-degree AV block associated with symptomatic bradycardia is an indication for pacing. In asymptomatic pattients with second-degree AV block, type II, cardiac pacing may be required if the level of block is infranodal because the progression to complete heart block is common. Although type I second degree AV block is usually located at the AV nodal level,there are patients with bundle branch block or intraventricular conduction delays in whom type I second degree AV block is located at an infranodal level. These patients should be approached similar to second-degree type II AV block, since the risk of progression to complete heart block remains high. Lastly, with 2:1 AV block, the level of block may be difficult to determine.
In the presence of a bundle branch block or intraventricular conduction delay and 2;1 Av block, the level of block is usually infranodal and therefore may be an indication for pacing.

In asymptomatic and otherwise healthy patients, the presence of intermittent second-degree, type I AV maybe due to enhanced vagal tone. In asymptomatic elderly patients with daytime type I second degree AV block and strutural heart disease, however, there is some divergence of opinion as to whetheher permanent pacing should or should not be considered. Many patients may become symptomatic during clinical follow-up.

Due to the benign prognosis first-degree AV block is not considered an indication for permanent pacing. However, marked first-degree AV block (PR > 0.30 s), inappropriate1y timed atrial systole that occurs after ventricular systole can lead to symptoms similar to having retrograde ventriculoatrial conduction. This may be of hemodynamic connsequence in some patients. particularly with left ventricular systolic or diastolic dysfunction. Additionally, because there is not an appropriately timed ventricular systole occurring at the end of atrial sysole, end diastolic mitral regurgitation develops, which may be of clinical signifance in patients with left ventricular systolic dysfunction. Therefore, dual chamber pacing may be indicated in select patients with marked first dgree AV block in whom hemodynamic improvement can be demonstrated by temporary pacing to resynchronize the atrium and the ventricles.

Of note, patients with neuromuscular diseases with AV block should be considered for DDDpacing, since progression of conduction system disease is not uncommon.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992

Pacing in Congenital Atrioventricular Block

Congenital heart block is usually due to AV nodal block. Patients tend to be asymptomatic and typically have narrow QRS complex rhythms. However, congenital AV block is associated with serious and possible fatal complications, including syncope and sudden death. In one study, a mean daytime heart rate less than 50 beats per minute was associated with sudden death or need for pacemaker. Exercise testing is useful to assess response at rest and exercise. Other indicators of poor outcome include prolonged QT interval (corrected for heart rate), cardiomegaly. atrial enlargement. decreased left ventricular systolic function, mean ventricular rates lower than median for age, periods of junctional exit block, and mitral regurgitattion.
Therefore, cardiac pacing is indicated in all symptomatic patients with congenital AV block. Furthermore, cardiac pacing is now recommended even for symptom-free adults. In the largest series published to date, there was reported a 5 percent mortality risk in adults older than 15 years with congenital AV block in the absence of heart disease. Eight of 102 patients whose cases were followed for 7 to 30 years had fatal Stokes-Adams attacks. Syncope, mitral regurgitation, and/or heart failure occurred in 30 percent of this cohort.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992

Pacing in Sinus Nodal Dysfunction

Sinus nodal dysfunction has become the most common indication for pacing in the United States. Pacing therapy has been demonstrated to be superior to medical therapy with theophylline for patients with sinus nodal dysfunction. The guidelines (Table 1 and Table 2 above) stress the importance of correlating symptoms with bradyarrhythmias. Often, it is difficult to correlate ECG findings with symptoms. Furthermore, symptoms may be nebulous. For instance, the presence of fatigue and dyspnea may be due to a bradyarrhythmia but may also be duee to lack of conditioning or other cardiac dysfunction.

The presence of the tachycardia/bradycardia syndrome is especially common in patients with paroxsymal atrial arrhythmias (Fig. 16 fourth illustration). The bradyarrhythmia often occurs at the termination of tachycardia and can lead to pauses of several seconds.
Drugs used to suppress tachyarrhythmias may lead to symptomatic bradycardia, in which case a bradycardia pacemaker would be required.

Patients with asymptomatic bradyarrhythmias should be evaluated carefully prior to placing a pacemaker. In general, an absolute heart rate of less than 30 beats per minute is an indication for pacemaker placement, even in the absence of symptoms. An exercise test can demonstrate intact sinus nodal function in patients with otherwise asymptomatic bradyarrhythmias who do not require pacing therapy. Atheletes commonly have physiologic bradycardia. even with heart rates of less than 40 beatd per minute, due to enhanced vagal tone. Finally, it should be noted that sleep apnea may cause asymptomatic, nocturnal bradyarrhythmias, in which case pacing therapy is not indicated.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Pacing in Carotid Sinus Syndrome

The diagnosis for carotid sinus syndrome (CSS) is typically made by demonstrating asystolic pauses of longer than 3 s with carotid sinus massage or a vasodepressor response of greater than 50 mmHg associated with clear symptoms provoked by carotid sinus stimulation, such as wearing a tight shirt or turning one's head. Vague symptoms such as dizziness associated with a hyperactive cardioinhibitory response to carotid sinus stimulation do not represent an indication for permanent pacing.
Improvement of symptoms and suppression of syncope have been demonstrated by treating patients with cardiac pacing, particularly dual-chamber pacing. Single-chamber atrial pacing is contraindicated because of the increased risk of transient AV block. Some studies suggest that hemodynamic evaluation of patients may enable them to be stratified into groups among whom VVL pacing would be sufficient. However, DDD pacing is probably better in most patients with CSS, because of the presence of vasodepressor and cardioinhibitory reflexes.

Cardiac Pacing in Neurocardiogenic Syncope

The role of pacing for neurocardiogenic syncope is controversial. Because these are younger patients who generally respond to medication, pacing is not required in most patients. Cardiac pacing has been shown to prevent the bradycardia and AV block associated with neurocardiogenic syncope, but patients still typically experience hypotension, vasodilatation, and other associated symptoms. The Vasovagal Pacemaker Study demonstrated a role for pacing in patients with vasovagal syncope refractory to standard medical therapy. Therefore, patients with refractory neurocardiogenic syncope may benefit from pacing, especially if they have a predominant cardioinhibitory component.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Pacing in Hypertrophic Cardiomyopathy

In patients with hypertrophic cardiomyopathy (HCM) and left ventricular outflow tract (LVOT) gradients, DDD pacing with a programmed short AV interval has been proposed as therapy to reduce LVOT gradient and improve symptoms. This concept is based on early studies where it was shown that DDD pacing with short AV interval decreased the LVOT gradient by a mean of 35 mmHg, and there was improvement of symptoms associated with HCM. An observational study involving 84 patients whose cases were followed for a mean of 2.3 years showed improvement of symptoms in nearly all patients, and there was reduction in the left ventricular wall thickness by more than 4 mm in a subgroup of patients. However, 15 percent of the patients required AV junction ablation to allow ventricular preexcitation by the pacer.
The mechanism by which DDD pacing reduces LVOT gradient remains controversial. With ventricular pacing at short AV interval, the right ventricular apex is preexcited by the pacemaker, causing alteration of the left ventricular activation sequence and paradoxical septal motion. This causes the septum to move away from the posterior left ventricular wall in early systole, thereby widening the LVOT during systole. It is also possible that ventricular pacing alters myocardial perfusion, decreases mitral valve systolic anterior motion, and/or decreases inotropy, which may also contribute to the effects of pacing in this disorder.
Therefore, if DDD pacing is used as terapy for obstructive hypertrophic cardiomyopathy, placement of pacing lead and programming of the AV interval are crucial for a beneficial effect. The AV interval should be programmed to the interval that still allows for left ventricular preexcitation,which would decrease but not eliminate the deleterious pacing with very short AV intervals. Echocardiography may help select the optimal pacing AV interval.
The long-term clinical effectiveness of DDD pacing in patients with obstructive HCM remains controversial. Some recent and randomized studies cast some doubt as to the clinical effectiveness of pacing for objectively improving functional capacity, quality of life, and LVOT gradient. One small randomized study failed to demonstrate improvement in exercise response to DDD pacing. Another study in patients with obstructive HCM showed that when patients were randomized to backup AAI pacing versus DDD pacing with short AV interval, there was no difference in subjective improvement. LVOT gradient was reduced by 40 percent in 57 percent of patients and remained unchanged in the other 43 percent of patients. Only 12 percent of patients (all older than age 65) showed improvement in functional capacity after 12 months in the study. Therefore, based on this randomized double-blind study,pacing could not be routinely recommended for drug-refractory patients with obstructive HCM but, rather, may be considered for select patients with medically refractory obstructive HCM as an alternative to surgical myectomy.
Patients with hypertensive cardiac hypertrophy with cavity obliteration may also show clinical improvement with DDD pacing. In contrast to obstructive HCM, patients with nonobstructive symptomatic HCM experience limited symptomatic improvement and no objective evidence of hemodynamic benefit with DDD pacing and short AV interval.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Pacing in Dilated Cardiomyopathy and Congestive Heart Failure

Initial reports suggested that patients with congestive heart failure and dilated cardiomyopathy may benefit from dual chamber pacing by altering and optimizing timing of left atrial to left ventricular activation or improving left ventricular contractile function. There was initial enthusiasm that pacing with a short AV interval may improve hemodynamic function and that the patients with first-degree AV block derived the most benefit. An acute hemodynamic study demonstrated that pacing with a short AV interval could eliminate presystolic mitral regurgitation in patients with first-degree AV block, restore normal AV relationships, and improve hemodynamic function. Subsequent studies showed that standard DDD pacing does not improve hemodynamic function in patients with physiologic PR intervals. On this basis, DDD pacing is possibly indicated in patients with dilated cardiomyopathy or marked first-degree AV block and where acute hemodynamic studies demonstrate improvement by dual chamber pacing.

Whereas pacing the ventricles with short AV interval may have limited benefit, the ability to pace the ventricles in a more synchronous manner to improve mechanical efficiency has also been studied. Ventricular pacing typically is achieved by pacing through a lead placed in the right ventricular apex, which may not produce the most efficient ventricular mechanical function. Pacing through the His-Purkinje system in theory may provide more physiologic ventricular activation patterns but is currently not readily available. Pacing from the right ventricular septum or outflow track may enable earlier left ventricular activation and, hence, more simultaneous contraction. However the results of hemodynamic improvement using right ventricular outflow tract pacing has shown a trend for improvement in some studies,whereas other studies show no benefit at all compared ventricular apical (RVA) pacing. It has been proposed that left ventricular or biventricular pacing may optimize hemodynamic function in patients with dilated congestive cardiomyopathY, particularly those patients with intraventricular conduction delay. Left ventricular pacing can be accomplished by either an epicardial lead or a transvenous lead through the coronary sinus venous system. An acute hemodynamic study was performed on patients with severe heart failure, intraventricular conduction delay (usually bundle branch block), and increased capillary wedge. These patients had measurement of hemodynamic parameters during either right ventricular pacing or biventricular pacing, which was compared with AAI pacing (control values). These results showed improvement of cardiac index and decrease in capillary wedge pressure with either right ventricular pacing or biventricular pacing, which was compared with AAI (control values). These results showed improvement of cardiac index and decrease in capillary wedge with either right ventricular pacing or biventricula pacing compared with AAI pacing. Furthermore, biventricular pacing showed more hemodynamic benefit compared with right ventricular pacing. Another study on patients with congestive heart failure and wide duration showed that epicardial left ventricular pacing, with or without concurrent right ventricular pacing, mproved hemodynamic function at optimized AV intervals compared with controls values. Therefore, left ventricular pacing may evolve as a therapeutic pacing technique in patients with congestive dilated cardiomyopathy and intraventricular conduction delay.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Another study has recently shown that biventricular pacing may improve maximal and submaximal exercise capacity in patients with advanced heart failure and intraventricular conduction delay.

Varma,C.,MD,and others,JACCC,Vol.41,No.4,2003,PP582-588.

It has been recently reported that functional mitral regurgitation is reduced by cardiac resynchronizatio therapy (implantation of a biventricular pacing device with a right ventricular apical lead and a LV pacing electrode implanted through the coronary sinus and positioned in an LV epicardial vein) in patients with heart failure (HF) and left bundle branch block (LBBB). This effect is directly related to the increased closing force (LV+dP/dt max. The results support the hypothesis that an increase in transmitral pressure gradient(TMP),mediated by a rise in LV+dp/dtmax due to more coordinated LV contraction, may facilitate effective mitral valve closure.

Breithhardt,MD,and others,Acute Effects of Cardiac Resynchronization Therapy on Functional Mitral Rgurgitation in Advanced Systolic Heart Failure,JACCC,Vol.41,No.5,2003,PP 765-770.

PACEMAKER HARDWARE

Implant and Explant

Nearly all pacemakers are implanted through a transvenous approach by either cardiologists or surgeons. The choice of using an operating room or a catheterization Iaboratory for the implant procedure probably plays little role in procedural-related complications but a cardiac catheterization laboratory involves lower hospital costs.

A full description of the surgical procedure has been reviewed elsewhere. Venous access for lead placement is through a subclavian venipuncture or a cephalic vein cutdown. The use of subclavian venipuncture is technically easier, and this vein can almost always accommodate two leads. With the subclavian venipuncture, there exists the risk of subclavian artery puncture, pneumothorax, or air embolus. Furthermore, pacing leads placed medially incur an additional risk of being "crushed" by the clavicle and first rib leading to lead insulation breaks or fractures (Fig. 16b). Lateral puncture of the subclavian or axillary vein using intravenous contrast may allow for safe lateral subclavianl venous puncture. A cephalic vein cutdown may also avoid some of the risk associated with subclavian vein puncture; however, this vein is not always accessible and cannot always accommodate two pacing leads.

Explanations of pacemaker generators are routinely performed during pacemaker generator changes. However, removal of pacemaker leads can be difficult due to fibrosis between chronically implanted leads and surrounding cardiac, valvular, and vascular structures. Traditional methods for extraction of chronically implanted leads involve specialized extraction sheaths that are glided over implanted leads to tear and peel away the encapsulating tissue. Recently, a technique using ultraviolet excimer laser light has been introduced to facilitate lead extraction by allowing advancement of sheaths over pacer leads without excessive mechanical tearing of fibrotic tissues. Compared with mechanical extraction, laser-assisted extraction demonstrated a greater success rate in lead removal (94 percent versus 64 percent) and less time to remove leads, with no difference in complications.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Hardware

The pacemaker system consists of a pulse generator and the pacing lead(s). Pacemaker system selection should be primarily based on the medical and surgical requirements of the patient. It is unusual that one pacemaker system would be most optimal and cost effective for all patients. An algorithm for choosing a pacemaker system and pacing mode is presented in Fig. 16c. Pacemaker leads can be unipolar or bipolar (Fig. 16d and Fig. 16e). Unipolar leads use a distal electrode in the catheter as the cathode and the shell of the pacemaker generator as the anode. Therefore, the myocardium and adjacent tissue complete the circuit. A bipolar lead consist of two separate conductors and electrodes within the lead. Since the electrodes for sensing in a bipolar lead are much closer together, bipolar signals are sharper with less extraneous noise (Fig. 16f).

Unipolar leads are simpler to design, smaller in diameter and, because of their simplicity, probably less likely to fail. Because of their small size, it is easier to pass two unipolar leads through a cephalic venous approach. However there are several disadvantages to unipolar lead systems. Because the unipolar lead uses body tissue to complete the circuit, there is the possibility of causing muscle stimulation. Most pacemakers avoid this by placing the stimulating surface of anterior such that it interfaces with subcutaneous tissue and not the pectoralis muscle. Unipolar sensing is fa to pick up extracardiac signals, including myopotentials (Fig. 16f), far-field sensing of remote cardiac potentials and electromagnetic interference. Finally, unipolar pacing is generally contraindicated in patients with a concomitant implantable defibrillator. Therefore, most leads implanted today are bipolar.

Leads are attached to the heart by active or passive fixation. Active fixation involves the use of some type of exposed or retractable screw within the lead system that fixes the lead to the heart (Fig. 16e). Passive fixation involves the use of tines, which are short protuberances that extend proximal to the distal electrode and interact with myocardial tissue to hold the lead in place. Active fixation leads are used more in the atrrium and allow fixation of the leads almost anywhere within the right atrium or ventricle. The use of either type of lead probably has little effect on complication rate or lead dislodgment rate when used by experienced operators.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Lead Placement and Acute Threshold Testing

Atrial and ventricular leads are placed into the appropriate chambers after ensuring adequate pacing and sensing thresholds.

Table 3

The basic premise in obtaining acute pacing and sensing thresholds during implant is that these thresholds may degenerate over time, and adequate safety margins need to be obtained to ensure safe long-term pacing and sensing. Furthermore, one should be aware of the type of unit implanted, its capabilities for pacing outputs, programmed sensitivities,and pacing modality (bipolar versus unipolar). The indication for pacing may also affect decisions about acceptable pacing thresholds, because of the inverse relationship between current drain and battery life. In patients who only require occasional backup pacing, higher pacing thresholds may be acceptable. Therefore, pacing thresholds should be optimized at the time of implant as influenced by the patient's pacing requirements and capabilities of the pacemaker. For sensing functions, ventricular electrograms measure at least 5 mV at frequently measure in excess of 10 to 20 mV. Ventricular sensitivity is generally programmed between 2 to 3 mV so that adequate safety margin exists for intrinsic ventricular depolarizatlion without the risk of oversensing T waves or other artifacts. Atrial electrograms are lower in amplitude than ventricularelectrograms; however, a minimum atrial electrogram to 2 mV should be obtained. In unipolar systems, a largei electrogram is important because of the increased risk ol sensing myopotentials or other artifactual signals if the sensitivity is programmed to less than 1 mV. In patients paroxysmal atrial fibrillation or flutter, the atrial during tachycardia might be smaller than during sinw Conversely, in patients with marked sinus bradycardia it is expected that there will be nearly 100 percent atriai atnal sensing thresholds may not be as important. Finalbi minimum programmed sensitivity available by the pacer I 0.5 mV) may influence acceptable sensing thresholds al Many factors may affect atrial or ventricular pacing sensing thresholds. There is variation to these threshold pending on the autonomic tone or the electrolyte status is an expected rise in acute thresholds within 1 to following implant due to acute inflammation, which be more exaggerated with active fixation lead syste] drugs, particularly antiarrhythmic medications, may ing thresholds. The presence of new myocardia around the leads would be expected to lead to dete pacing and/or sensing thresholds. Leads that are steroid eluting generally limit the acute rise in pacing threshold. Long-term thresholds appear to stabilize sometime after 3 to 6 months.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

PACEMAKER FOLLOW-UP

The goal for pacemaker follow-up should be to perform a systematic evaluation of the pacemaker as it relates to and functions with the patient and his or her individual needs. These goals are outlined in Table 4. Complete guidelines for pacemaker follow-up have been described.
In the first several months after pacer implant, several evaluations of pacer function may be required in order to optimize pacing outputs, rate responsiveness, and other features. There is a stable period of pacer function starting 6 to 12 month following implant until the expected time for battery depletion. Therefore, direct evaluations of pacer function may be performed once or twice per year during this time, depending on whether the patient is pacer dependent and depending on the pacer type and whether any of the pacer components are under any advisory warnings.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Transtetephonic Monitoring

Technology is available for simple devices used by patients to transmit their ECG by telephone to a receiving station so that their ECG rhythm may be analyzed to detect normal or abnormal pacemaker function. In this way, a spontaneous pacing rhythm can be assessed for normal or abnornal pacing function. More importantly, by applying a magnet to the pacemaker and observing the magnet rate during the transtelephonic monitoring (TTM), the battery status can be assessed During TTM, changes in pacing rate or loss of output could always be detected. Ventricular oversensing or atrial pace/sense problems can sometimes be detected during TTM. Follow-up using TTM should be used to supplement and replace direct evaluation of pacer function. The frequency of follow-up should be individualized according to the type of pacemaker, whether the patient is pacemaker dependent, age of puIse generator and expected longevity, presence of any pacemaker component under advisory or warning, and patient clinical factors. As depletion of pacer battery occurs, TTM may used as often as every month to appropriately determine timing for pacer replacement.

Components for Direct Evaluation of Pacemaker Systems

CHECKING PACING THRESHOLDS AND PROGRAMMING PACING OUTPUTS

Pacemakers should always be programmed for maximal safety particularly in patients who are pacemaker dependent. To understand how to program pacemakers safely and efficiently, basic principles are reviewed.

Current Drain

Ultimately, the longevity of the battery will be function of the current drain versus battery capacity. There is nominal current drain for operating pacemaker circuitry, which varies according to the pacer type; however, most current drain results from pacing output.
The current delivered per pacing pulse is a function of the voltagedivided by the lead impedance (I=V/R)-Ohm's law. Therefore, it is desirable to be able to implant leads with low pacing voltage thresholds. Additionally, leadsdesigned to have high impedance appear to decrease long term current drain.

Strength-Duration Curve

The strength-duration curve (Fig. 16g) relates voltage and pulse width. This curve is dynamic during the first 2 to 3 months following implant. With an acute rise in threshold, the curve is expected to shift upward two to four times and then subsequently shift back downward at a level greater than the initially obtained values. At pulse widths less than 0.2 ms, the curve is steep; at pulse widths exceeding 1.0 ms, the curve is flat. With this kind of relationship, programming pulse widths greater than 1 ms generally does not add safety margin to the pacing output but does substantially increase battery current drain. Similarly, programming pacing pulse widths less than 0.2 to 0.3 ms may not allow sufficient safety margin at even high voltage amplitudes.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .

Total Energy Expenditure of the Pacemaker

This is defined as energy = (voltage)2 multiplied by pulse width divided by impedance. According to this relationship, the energy expenditure has an exponential relationship to voltage output but has a linear relationship to pulse width. Therefore, it is preferable to reduce voltage output rather than pulse width to conserve battery life.

Calculating Pacing Threshold

At implant, it is standard to fix the pulse width at 0.5 ms and reduce the voltage until the lowest voltage that maintains consistent pacing-which is the pacing threshold (Fig. 16h). One can fix the pulse width at any value, however (usually between 0.3 and 1.0 ms), and calculate a voltage threshold. Similarly, one can fix the voltage at a certain value and reduce the pulse width to the lowest value that maintains consistent pacing, which would also define the pacing threshold. Either method is acceptable to define a pacing threshold.

Safety Margin

The safety margin for pacing outputs can be calculated by multiples of either the pulse width or the voltage threshold. For example, if the voltage threshold at 0.5 ms is 1.5 V, then a pacing output of o.5 ms and 3.0 V would yield an energy safety margin of fourfold, given the relationship between energy and voltage. Similar, if pulse-width threshold at 3.0 V. is 0.15 ms, then a pacing output of 3.0 V and 0.6 ms would provide an energy safety margin of fourfold.

Acute Pacing Outputs

Because the extent of the acute rise in pacing thresholds may be difficult to predict, it is better to program high pacing outputs at implant and during the first 6 to 24 weeks after implant. A greater safety margin may be desired in patients who are pacemaker dependent. Typically, greater safety margins are also desired in ventricular leads rather than atrial leads. Steroid-eluting leads generally result in blunting of the acute rise in threshold, which may allow for lower pacing outputs early after implant.

Chronic Pacing Outputs

In the time frame of 2 to 6 months, the pacing thresholds stabilize. Therefore, chronic pacing outputs may be programmed.

Table 5

Almost all pacing batteries consist of lithium-iodide systems, which generate 2.8 V. It is most efficient to pace at the voltage of the battery (2.5 to 2.8 V). Therefore, longevity of pacemakers can be improved if pacing outputs are reduced to 2.5 V with pulse widths programmed 2 to 4 times pulse-width thresholds. Finally, some newer pacemakers have the ability to confirm capture on a beat-by-beat basis. Using algorithms to automatically check pacing capture thresholds, these pacers adjust pacing voltages just above the pacing threshold in order to reduce curent drain and prolong battery longevity.

OTHER FEATURES

Sensing

Sensing of atrial and ventricular intracardiac electrograms can be evaluated by different algorithms. To test atrial sensing, the pacemaker needs to be programmed temporarily at a programmed atrial rate less than the intrinsic sinus rate. To test ventricular sensing, the pacer can be temporarilly regrammed to the VVI mode if the programmed rate is less than the intrinsic heart rate. Alternatively, with intact AV conduction, the delay can be increased to allow AV conduction and thereby allow for ventricular sensing in the DDD mode. Increasing the programmed sensitivity until the intrinsic P or R wave is no longer sensed (Fig. 16i) is another method to test sensing threshold. Telemetry of atrial or ventricular electrograms allows for direct measurement of the amplitude (Fig. 16f). Lastly, some pacemakers have algorithms whereby the pacemaker automatically measures atrial and ventricular electrograms.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992

Lead Function

Lead function is assessed by pacing and sensing function and by measuring impedance. Although there is a wide variability of normal lead impedances, chronic lead impedances should not widely vary between outpatient follow-up visits. A fractured lead exhibits a markedly elevated lead impedance. Insulation breaks manifest by reduced lead impedances. Lead fractures or insulation breaks often are intermittent problems. Therefore, normal lead impedances and pacing and sensing thresholds do not rule out these problems. The leads can be stressed by having the patient change position and do various provocative arm movements to facilitate diagnosis of lead-related problems that are not otherwise observed.

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992

Battery function

Almost all pacemakers use lithium-iodide batteries, which have an initial battery voltage of 2.8 V. Battery voltages can be directly measured and, at a certain level (elective replacement index, ERI), the pacemaker unit requires elective generator change. At a lower voltage (end of life, EOL), there is potential loss of pacemaker function; therefore immediate generator change is mandated.
Battery function can also be assessed without formal interrogation. Many pacemakers reset to a VVI mode at a preset pacing rate, or the pacing rate decreases to less than the programmed lower rate of the pacermaker when battery reaches the ERI or EOL stage. Additionally, the magnet mode causes asynchronous pacing at a preset magnet rate for particular pacemaker model. This magnet rate varies according to whether the battery status is adequate or not.

Rate Responsiveness

Rate-responsive pacemakers require periodic adjustments of the rate-responsive features to optimize clinical responsiveness. The programmable variables include a rate-responsive upper pacing rate, which may be a separate programmable variable than the upper tracking rate. A rate-response slope may be programmed to determine the pacing rate at a certain activity level. Some pacemakers store data with respect to the use of rate responsiveness over a certain period. Otherwise, one can simply have the patient walk briskly for 2 to 3 mm and assess the heart rate to determine whether it is appropriate given the patient's age and clinical status. Some pacemakers offer algorithms whereby the physician chooses the appropriate heart rate for "brisk walking," and the pacemaker automatically calculates the optimal rate-responsive programming.

Pacer Diagnostic Function

Modern pacemakers have increased memory capabilities to store diagnostic information. The basic diagnostic feature displays counts or percentages of pacing versus sensing in the atrial and ventricular chambers. If a patient has complete heart block but has intact sinus nodal function, it would be expected that there be 100 percent ventricular pacing with predominant atrial sensing. The breakdown of pacing and sensing in each chamber can be stratified according to the heart rate that can give the clinician some clues as to the presence of chronotropic incompetence or appropriateness of rate responsiveness.
With respect to arrhythmia monitoring, the presence and quantity of premature ventricular and atnal complexes are presented. For patients with mode-switching pacemakers, the number of mode switches probably represents a marker for the number of atrial arrhythmias. However, these data do not provide information with respect to duration and timing of these atrial arrhythmias. One study showed that most of these atrial arrhythmias are very brief, lasting only a few seconds in many cases More information about the occurrence, timing, and duration of arrhythmias, including stored intracardiac electrograms, is available in some pacers. This type of information may facilitate diagnosis of arrhythmias without the need for ancillary testing (Fig. 16j). Furthermore, when patients complain of symptoms such as palpitations, these diagnostic features may enablediagnosis of, or rule out, atrial or ventricular tachyarrhythmias.

Chest Radiograph (Posteroanterior and Lateral)

A standard chest x-ray is recommended as part of the predischarge evaluation to ensure appropriate placement of leads, rule out lead migration, and serve as a baseline.

PACEMAKER FUNCTION AND MODES

Magnet Mode

Virtually all pacemakers pace in an asynchronous mode when they come into contact with a magnetic field. The response to a magnet varies according to manufacturer, pacemaker model, and sometimes even the mode in which a pacer is programmed. Single-chamber pacers respond to magnets by asynchronous pacing at either the programmed rate or a special magnet rate (Fig. 16k). This allows a simple noninvasive method to assess pacing at the bedside, office, or by TTM. In patients who are pacemaker dependent and experiencing oversensing thereby inhibiting pacemaker output, a magnet is a convenient short-term method to ensure pacing. Furthermore, pacemakers usually have one magnet rate for a battery that is intact and another one for a battery that is at ERI or at EOL. If these rates are known, applying a magnet to a pacemaker is an easy noninvasive method to assess battery status.

VVI Mode

In the VVI mode, a pacemaker operates as shown in Fig. 16l The lower rate is converted to an interval (milliseconds). After a paced or sensed ventricular event, a programmable refractory period prevents inappropriate sensing of T waves. After the pacemaker ventricular refractory period, there is an interval extending to the escape interval during which time the pacemaker senses a ventricular event, if one occurs before the end of the interval; otherwise, there is ventricular pacing output.
Hysteresis is a programmable function in which the ventricular escape interval is longer after a sensed ventricular event than after a paced ventricular event. This feature can be used in patients with sinus rhythm so that VVI pacing would not initiate until the sinus rate drops below the hysteresis rate, which is lower than the pacemaker rate (Fig. 16m ).

AAI Pacing

AAIR is an excellent mode of pacing in patients with sinus node dysfunction and normal AV nodal and His-Purkinje function.The timing sequences are the same for AAI as for VVI pacing. Atrial sensitivities are programmed at lower values (increased sensitivity) to sense intrinsic P waves safely. This frequently leads to oversensing of far-field ventricular electrograms, which can be avoided by programming a longer refractory period.
Patients with sinus nodal dysfunction may develop AV block, which may be a source of concern when using AAI pacing. However, with careful selection of patients, including normal PR intervals, absence of bundle branch block, and AV Wenckebach occurring at atrial pacing rates of more than 120 beats per minute, the risk of development of second- or third-degree AV block is less than 0.6 percent per year.

DDD Pacing

DDD pacing is the most common pacing mode for dual-chamber pacemakers. The timing sequences for DDD pacing are described in Fig. 16n. This mode is used for patients with AV node and/or sinus node dysfunction.

DDD PACING IN PATIENTS WITH SINUS NODE DYSFUNCTION

Patients with sinus node dysfunction may have intermittent or chronic sinus bradycardia requiring intermittent or continuous atrial pacing. If patients have intact AV conduction, the pace-maker functions as an AAI pacer. Due to medications that slow AV conduction and/or intrinsic AV nodal or His-Purkinje disease, however, patients with DDD pacemakers frequently demonstrate fused ventricular complexes originating from ventricular stimulation and through the AV conduction system. The degree of fusion of the ventricular complex between pacing from a right ventricular lead and conduction down the AV nodal-His-Purkinje system depends in large part on the difference between the programmed AV interval and the intrinsic AV conduction time.
For ventricular output to be inhibited in patients with DDD pacemakers, the pacemaker AV interval must be longer than the conduction time between the sensed or paced atrial complex to the right ventricular lead. A very long AV interval (more than 0.25 s) may decrease the benefit of AV synchrony when AV pacing does occur. It is not uncommon that pacemakers sense the ventricular electrogram late during ventricular depolarization especially with right ventricular conduction delay or right bundle branch block. Pacemaker pseudofusion occurs when there is ventricular pacing within the QRS complex (Fig. 16o).

PATIENTS WITH ATRIO VENTRICULAR BLOCK AND NORMAL SINUS NODE FUNCTION

In the DDD mode, if the lower rate of the pacer is programmed at a sufficiently low value to permit atrial tracking, the pacemaker stimulates the ventricle synchronous with intrinsic P waves. If a patient does not require atrial pacing, it may be reasonable to implant a dual-chamber pacer with a single tripolar or quadripolar lead that allows atrial sensing and ventricular pacing and sensing (Fig. 16p). These VDD pacing systems allow for ease of implant and for bipolar atrial sensing. Atrial sensing may not be as reliable compared to a fixed atrial lead, which may lead to occasional atrial undersensing.80'81 In a recent prospective comparison between single-lead VDD systems to DDD leads, however, there were lower P-wave amplitudes in the group with VDD systems, but no significant clinical differences with respect to atrial undersensing.

DDD versus VVI Pacing

Multiple retrospective and observational studies and a few 'rospective studies demonstrate hemodynamic, clinical, and quality-of-life benefits of dual-chamber or atrial-based pacing versus ventricular pacing. Therefore, it appears prudent to implant DDD pacers in most patients with intact atrial function but not all patients.
In patients with congestive heart failure due to left ventncular systolic dysfunction, the dependence of cardiac output to AV synchrony appears to decrease secondarily to the already increased left ventricular filling pressures. Patients with fixed stroke volume (i.e., left ventricular systolic dysfunction) may depend almost exclusively on heart rate for cardiac output and, therefore, may have limited benefit from AV synchrony. However, any improvement in cardiac output with restoration of AV synchrony may be clinically significant. Additionally, clinical conditions such as left ventricular hypertrophy or diastolic dysfunction generally are dependent on adequate preload to maintain cardiac output. Restoration of AV synchrony appears to be particularly significant for these patients.

Patients with Sick Sinus Syndrome

In patients with sick sinus syndrome, dual-chamber pacing has been shown to be superior to VVI pacing Many studies have demonstrated that atrial-based pacing (DDD) is associated with decreased clinical events, including atrial fibrillation, congestive heart failure, stroke, and death, mainly but not exclusively in patients with sick sinus syndrome. Several mechanisms by which atrial-based pacing is beneficial in patients with sick sinus syndrome may not apply to the subset of patients with ciegree or complete AV blocK. VVI pacing in patients with retrograde VA conduction causes atrial contractions against closed AV valves, leading to atrial distension and transient increases in pulmonary capillary wedge and jugular venous pressures. Increased atrial distension may predispose individuals to atrial fibrillation. This is apt to be more evident in the patients with sick sinus syndrome who already have paroxysmal atrial fibrillation or are at risk for such arrhythmias. Sympathetic activity is elevated during VVI versus dual-chamber pacing, which contributes to increased morbidity and possible mortalityY9 Even in the absence of retrograde conduction, VVI pacing with VA dissociation leads to atrial systoles throughout the cardiac cycle, which can also lead to a similar deleterious effect on atrial size and function. Therefore, dual-chamber pacing appears to reduce the incidence of atrial fibrillation and embolic complications.
Andersen and colleagues published short- and long-term reports on a randomized study comparing single- and dual-chamber pacing in patients with sick sinus syndrome. In their long-term study, they reported a reduction of embolic events, atrial fibrillation, and mortality with use of atnal-based pacing. Additionally, they found progressive benefit from atnal pacing compared with ventricular pacing, which resulted in overall improvement of survival based on total mortality and death from cardiovascular causes. Additionally, many studies have shown that maintenance of AV synchrony improves quality of life particularly at rest. In fact, many patients who have VVI pacers may not recognize the extent of their symptoms until they have an upgrade to a DDD system.

Atrioventricular Block

In patients with AV block, the advantage of dual-chamber pacing has been demonstrated by some authors but not by others. In a retrospective study from the Mayo Clinic on an elderly population, long-term survival was not affected by the mode of pacing. Lamas et al published a series on 407 elderly patients (older than age 65) who were randomized to have a dual-chamber pacer programmed to either VVI~RJ or DDD~R] modes. These authors concluded that the main quality-of-life benefits associated with DDDR pacing were noted in the group of patients with sick sinus syndrome, and there were no quality-of-life benefits noted in the patients with pacers implanted for AV block.
Therefore, there now appear to be adequate data supporting the use of atrial-based pacing (AAI, DDI, and DDD) in patients with sick sinus syndrome. The benefit of dual-chamber versus ventricular pacing in patients with advanced or complete AV block appears to be controversial. In patients with intact sinus node function and AV block, however, it is prudent to at least implant a single-lead VDD system, if not a complete dual-chamber pacing system, to restore AV synchrony in order to restore physiologic pacing.

PACING TIMING INTERVALS AND UPPER RATE BEHAVIOR

Atrioventricular Interval

The Av interval is divided into three zones.The first 20 t0 40ms of this interval is the atrial blanking period.The ventricular channel is blanked during this period to prevent inappropriate sensing of atrial output (crosstalk). Crosstalk is a greater problem in unipolar than in bipolar systems. The next part of the AV interval occurs from the end of the blanking period to approximately 100 to 120 ms after the atrial pacing output. If a ventricular sensed event occurred at this point, it would be nonphysiologic because of the short elapsed AV interval. The pacemaker responds with a ventricular output at a short AV interval (100 to 120 ms), which is a safety feature (ventricular safety pacing (Fig. 16q).Ventrcular safety pacing is a feature that ensures ventricular pacing in case the sensed event was not a ventricular depolarization;instead, pacing occurs at a short interval so that the pacing output falls before the T wave.

Finally, if there is a sensed event in the latter part of AV interval, the pacemaker response is to inhibit ventricular pacing output.

Upper Rate Behavior

The total atrial refractory period (TARP) consists of the AV interval and the postventricular atrial refractory period (PVARP). The TARP is a programmable value that can be calculated in milliseconds. Ventricular tracking of atnal events cannot exceed a frequency shorter than the TARP. By dividing 60,000 by the TARP, a rate can be calculated that is the upper rate at which a pacemaker can track atrial events at a 1:1 ratio. At atrial rates exceeding this value, every other atrial event will fall within the pacemaker refractory period (PVARP) and there will be 2:1 pacemaker AV block. Therefore, the rate corresponding to the TARP corresponds to the pacemaker 2:1 rate.
The upper tracking rate is a separate programmable value. The upper tracking rate is generally programmed at a rate less than that corresponding to the TARP. This leads to pacemaker Wenckebach behavior when the patient's atnal rate exceeds the programmed upper rate (Fig. 16r). The Wenckebach interval is defined as the difference between the programmed upper rate and the rate corresponding to the TARP.
Therefore, when a patient has a sinus or other atrial tachycardia, the pacemaker can track the P waves in a 1:1 fashion up to either the upper programmed rate of the pacer or to the pacemaker 2:1 rate, which ever is lower. If the 2:1 pacemaker rate is lower, there may be deleterious hemodynamic consequences for an exercising patient in whom the ventricular response would abruptly drop by nearly half. For this reason, a Wenckebach interval is preferred by programming the TARP to a sufficiently short interval or the upper rate of the pacemaker to a rate that is less than the 2:1 AV block rate.
Various strategies are available for active patients with DDD pacemakers who require physiologic upper rates. Many pacemakers offer autoadjusting AV intervals that shorten with increasing rates. By shortening the AV interval, the TARP decreases, which allows greater upper tracking rates before reaching the rate of 2:1 AV block. Another strategy involves sensor-driven rate smoothing. The rate-responsive features are activated, and, in fact, a separate upper sensor-driven rate, different than the upper atrial tracking rate, may be programmed. This enables maintenance of increased ventricular pacing rates driven by the sensor when the pacer would otherwise respond with AV Wenckebach or 2:1 AV block.

USE OF PACEMAKERS IN DIFFERENT CLINICAL SITUATIONS

Paroxysmal Atrial Fibrillation, FLutter, and Other Tachyarrhythmias

DDD pacing is problematic in the presence of atrial tachyarrhythmias. During atrial fibrillation, there are so many sensed atrial events occurring at rapid rates that a DDD pacemaker responds with an attempt to track these electrograms up to but not exceeding the upper rate (Fig. 16s and Fig. 16t). The ECG hallmark is an irregularly irregular ventricular paced rhythm at a mean rate just below the upper rate. Of course, if the patient has intrinsic AV conduction, the patient's ventricular rate is not controlled by the pacemaker but rather by the intrinsic AV nodal conduction.
There are various strategies for preventing inappropriate upper tracking behavior during atrial tachyarrhythmias. In a patient with intact AV conduction and paroxysmal atrial tachyarrhythmias, DDI or DDIR modes would be appropriate (Fig. 16s). In this mode of pacing, there is no tracking of atrial events. If there is a sinus or other atnal sensed electrogram, the pacer will inhibit atrial pacing output. Ventricular pacing occurs only at the lower rate interval. For patients with sick sinus syndrome, the clinical problem necessitating a pacemaker is the bradycardia resulting from intrinsic sinus node dysfunction or the bradyarrhythmias resulting from therapy to suppress the tachyarrhythmias. Therefore, DDIR is a very effective pacing mode for patients with sick sinus syndrome who have intrinsic AV conduction.
At the initiation of atrial fibrillation or other atrial tachyarrhythmia, many pacers can automatically switch pacer modes from DDD(R) to VVI(R) or DDI(R) (Fig. 16t ). The automatic mode switch may occur at the upper rate of the pacemaker or at a separate programmable mode switch rate. It may occur with single or multiple sequential premature atrial complexes, depending on the pacemaker model. Mode switching appears to be a clinically effective method of pacing in patients with AV block and paroxysmal atrial arrhythmias.
Mode switching reduces symptoms associated with atrial fibrillation only if patients have adequate control of intrinsic AV conduction during atnal fibrillation. For this reason, a strategy of AV junction ablation with implantation of a mode-switching dual-chamber pacemaker can provide symptomatic relief for those patients with medically refractory paroxysmal atrial fibrillation with rapid ventricular response.

Prevention of Atrial Fibrillation by Pacing

The initiation and maintenance of atrial fibrillation involve several pathophysiologic mechanisms, the most dominant of which is multiple reentrant pathways (see http://www.rjmatthewsmd.com/ re animation of mechanism of atrial fibrillation). Pacing therapy may reduce dispersion of refractoriness in the atrium, a feature in reentry, or eliminate pause-dependent initiation of arrhythmias. As discussed above atnal-based pacing (AAI or DDD) reduces the incidence of atrial fibrillation compared with VVI pacing in those patients who require pacing; it is unknown, however, whether atrial pacing in itself may reduce the occurrence of atrial fibrillation. In patients with sick sinus syndrome who require bradycardia pacing support, it has been suggested that standard atrial pacing reduces the frequency of atrial fibrillation. These studies examined the arrhythmia-free interval before and after atrial pacing. In another study of patients who had atrial fibrillation without sinus nodal dysfunction, however, DDD pacers were implanted 3 months prior to planned AV junction ablation, and these pacers were programmed to DDD pacing at 70 beats per minute or to backup DDI pacing at 30 beats per minute.The patients who were actively paced did not have fewer episodes of atrial fibrillation. Therefore, pacing in itself may not reduce the occurrence of atrial fibrillation but may be helpful in the management of those patients who have sinus nodal dysfunction.
It has been reported that dual-site atrial pacing may reduce the occurrence of episodes of atrial fibrillation. One lead is placed in the right atrium and a second lead is placed in the coronary sinus ostium or inside the coronary sinus to advance left atrial depolarization. In theory, synchronization of the atria may reduce dispersion of refractoriness and thereby reduce the occurrence of atrial fibrillation.

Pacing in Chronic Atrial Fibrillation or Other Atrial Tachyarrhythmia

Patients with persistent atrial tachyarrhythmias and high-degree or complete AV block generally require a VVIR pacemaker unless their functional status is limited, in which case a VVI pacemaker would suffice. DDD(R) may be implanted in select patients with persistent atrial fibrillation in whom cardioversion to sinus rhythm is expected.

Pacing in Complete or Intermittent Third-Degree Atrioventricular Block

Patients with one of the neurally mediated syncope syndromes generally have intact sinus and AV nodal function. Because of combined vasodepressor and cardioinhibitory responses, patients usually require dual-chamber pacing when a pacer is irnplanted. Additionally, these patients benefit from an interventional pacing rate (80 to 100 pulses per minute) during their vasovagal episodes and only require backup pacing at rates of 4O to 50 pulses per minute during other times. Therefore, one algorithm is to use dual-chamber hysteresis so that when a patient's heart rate drops to the lower rate, pacing is initiated at the interventional rate. This algorithm has limitations, since i patient's heart rate needs to exceed the interventional pacing Lefore inhibiting the pacer. Some pacemakers now offer rate drop response pacing, which involves interventional pacing (80 to 110 pulses per minute with gradual decline in paced rate at 1 to 5 minutes) that is triggered by a steep drop in a patient's intrinsic heart rate. Based on the North American Vasovagal Pacing Study, there was a reduction in syncope from 70 percent in the control group to 22 percent in patients who had pacers implanted with the rate-drop response feature.

Pacing in Cardiac Transplant Patients

After orthotopic cardiac transplant, there is a high incidence of chronotropic incompetence resulting in slow junctional rhythm, sinus arrest, or sinus bradycardia. Bradycardia tends to resolve spontaneously in most patients, but 6 to 21 percent of patients may require permanent pacing. Although symptomatic bradycardia is generally an early finding after transplantation, up to 5 percent of patients following transplant may have symptomatic bradycardia as a late finding.During the implant, the atrial lead is positioned in the donor atrium. A DDDR or AAIR pacer is placed, depending on whether AV conduction is intact.

HEMODYNAMICS OF CARDIAC PACING

In theory. a pacemaker optimizes and maintains AV synchrony and optimizes ventricular activation and heart rate to enable cardiac output to meet the metabolic needs of the patient, whether he or she is resting, sleeping, or exercising. There are many variables involved in determining cardiac output through an effect on stroke volume, such as the autonomic tone, physical condition of the patient, left ventricular diastolic and systolic function, and peripheral vascular resistance. As seen in Table 6, many variables in pacing systems can affect cardiac hemodynamic function.

TABLE 6 Effects of Cardiac Pacing Variables on Hemodynamic Function

Atrioventricular Interval

The role of the AV interval and the optimal AV interval for improving hemodynamic function has been studied. For most patients, the optimal AV interval corresponds to the physiologic range (i.e., an AV interval of approximately 150 ± 50 ms). In clinical practice, however, most patients' quality of life is not significantly different between AV intervals that are optimized by noninvasive assessment versus AV intervals that are suboptimal.
There are other considerations when programming AV intervals. With AV sequential pacing, the start of the P wave corresponds to the start of the AV interval while, with P-wave synchronous ventricular pacing, the start of the P wave begins approximately 20 to 70 ms prior to the start of the AV interval, depending on the conduction time from the sinus node to the atrial electrodes. The optimal AV interval for P-wave synchronous ventricular pacing would be shorter than the optimal AV interval for AV sequential pacing."2 Therefore, to achieve similar hemodynamic effects from ventricular pacing following a sensed or paced P wave, the sensed AV interval should be programmed approximately 40 to 50 ms shorter than the paced AV interval. Additionally, left ventricular cardiac function is more dependent on left atnal to left ventricular relationships rather than right atrial to right ventricular AV interval. For this reason, there is much variability between patients with respect to programming AV intervals.

Pacemaker Syndrome

The pacemaker syndrome is a constellation of signs and symptoms representing adverse reaction to VVI pacing. Most of the symptoms relate to loss of AV synchrony and also to retrograde conduction. These include orthostatic hypotension, near syncope, fatigue, exercise intolerance, malaise, weakness, cough, awareness of heartbeat, chest fullness, neck fullness, headache, chest pain, and other symptoms that may be nonspecific. On exam, these patients may have intermittent or persistent cannon A waves and possible liver pulsation. ECG demonstrates VVI pacing present at the time of the symptoms.
The basis for pacemaker syndrome is not only loss of AV synchrony but also the presence of ventricular-atrial conduction. Atrial contraction against closed AV valves leads to increases in jugular and pulmonary venous pressure causing cough and m alaise in patients with intact cardiac function and congestive heart failure in other patients with structural heart disease. Distended atria can lead to reflex vasodepressor effects mediated by the autonomic nervous system and diuresis mediated by elevated levels of atnal natriuretic malaise in patients with intact cardiac function and peptide. Therefore, if patients have decreased cardiac output and arterial pressure secondary to VVI pacing, autonomic and humoral reflexes can lead to further hypotension and hemodynamic deterioration.
DDI pacing may produce pacemaker syndrome if the sinus rate exceeds the lower rate. DDD pacing can lead to pacemaker syndrome in select patients with severe intraatrial conduction delay who experience inappropriate timing between left atrial systole and left ventricular contraction. This may necessitate the addition of a coronary sinus pacing lead to advance left atrial systole.
The management of pacemaker syndrome usually requires restoration of AV synchrony. In many patients, an upgrade to a dual-chamber pacer is indicated. In some patients with intact sinus and AV conduction, lowering the pacing rate in VVI mode and using the hysteresis mode may promote sinus rhythm, lessening the symptoms associated with pacemaker syndrome. Using the VVIR mode by itself will not prevent or reduce symptoms from the pacemaker syndrome. Many patients may experience mild symptoms of the pacemaker syndrome and not recognize the symptoms until after an upgrade to a dual-chamber pacemaker. Most patients prefer DDD pacing to VVI pacing in various clinical and hemodynamic studies.

RATE-RESPONSIVE PACEMAKERS

The ability of a pacemaker to increase the lower rate in response to a physical or physiologic stimulus is termed rate-responsive, rate-adaptive, or sensor-driven pacing. The letter R in the fourth position of the NASPE/BPEG pacing code indicates rate-responsive pacing. Sensor systems that respond to parameters or activities that correlate with physiologic need for increased cardiac pacing rate provide input to the pacer, which increases the pacer lower rate. Numerous sensors have been developed with the goal of providing sensor input into the pacemaker, which can be then used to provide rate-adaptive pacing.

Hemodynamic Evaluation of Rate-Adaptive Pacing

Cardiac output is a function of ventricular rate and stroke volume, modified by variables such as AV synchrony, ventricular preload, ventricular afterload, and autonomic state. In normal individuals at rest, pacing-induced increase in ventricular rate usually results in a transient increase in cardiac output followed by decrease in stroke volume, returning cardiac output toward normal. When there is a physiologic need for increased cardiac output, however, such as during exercise, stroke volume is maintained during increased ventricular pacing rate.
The role of the atrium and the need for AV synchrony remain less certain during faster rates compared with heart rates under 100 beats per minute. In patients with AV and ventricularatrial block, pacing in the VDD mode compared with VVI pacing matched to the atrial rate (without AV synchrony) appears to provide similar cardiac output. Multiple studies have shown that the change in work capacity correlates with ventricular rate during exercise whether the ventricular rate is triggered by spontaneous atrial activity or by a pacemaker sensor. Therefore, AV synchrony may be less important in patients during exercise who achieve or require heart rates in excess of 120 beats per minute. Nevertheless, VVIR pacing is not a substitute for DDD pacing.
If a patient has a VVI pacemaker and ventriculoatrial conduction, or a DDD pacing programmed with long AV intervals such that the P wave is closer to the preceding R wave, deleterious hemodynamic consequences may result. In this circumstance, there would be a decrease in cardiac output, since the atrium would consistently pace against closed AV valves, producing increases in the pulmonary and jugular venous pressures. This would also produce symptoms of the pacemaker syndrome. Dual-chamber pacemakers currently available often have options of rate-adaptive AV intervals. This provides the advantage of maintaining normal AV relationships during exercise and prevent retrograde atrial contraction.

RATE-ADAPTIVE SENSORS

Multiple rate adaptive sensors are available or under development. Actively based sensors are used most commonly. These are piezoelectric crystal systems that are very sensitive to detection of vibration induced by up-down motion (activity) or acceleration, particularly (forward-backward motion).
The drawback of activity-based pacers is that they do not provide feedback that is proportional to physiologic need. For instance, climbing up stairs requires more work than going down stairs; however, going down stairs is usually faster and would activate the sensor more than climbing up stairs. This leads to faster-paced rates while going down stairs. Similarly, other activity with little body vibrations may produce ineffective rate adaptation from the pacemaker. Therefore, true physiologic sensors are desirable for rate-responsive pacing. The role of physiologic sensors is to provide some measurable index of activity, exercise, or catecholamine state that can provide a more accurate input to the pacemaker for rate-adaptive pacing. The QT interval is affected by heart rate but also independently by catecholamines. Therefore, pacers can measure the interval from the ventricular stimulus to the end of the sensed T wave and modulate heart rate based on this measurement. The drawback of this technique is that the patient has to be ventricular paced in order to measure the QT, or stimulus-T, interval.
Since there exists a close relationship between respiratory rate or minute ventilation and heart rate, various sensors incorporate measurements of respiratory effort. These systems are based on measurement of transthoracic impedance between the pacemaker lead and the pulse generator. The impedance increases with inspirations and decreases with expiration; the amplitude of the impedance change is proportional to the tidal volume. Minute ventilation is the product of the tidal volume and respiratory rate. Thus, minute ventilation can provide an accurate physiologic estimate of metabolic needs. One of the disadvantages of this system is that energy is required to measure impedance, which increases current drain from the pacemaker.
A number of other sensor systems are available or under development. Many use physiologic parameters, such as pH, oxygen saturation, stroke volume, or temperature. The premise behind all of these are that the measured parameters can provide an accurate measure of a patient's metabolic needs, which can be used to guide rate responsiveness. There are various benefits and drawbacks to the different methods.

DUAL SENSORS

Some sensors systems provide the advantage of more physiologic pacing during steady state but have a slow response time during initiation of exercise. Other sensors, particularly activity sensors, have fast response times at initiation of activity but may not produce physiologic responses during peak or steady-state activity. Pacers with dual sensors can provide patients with rapid responses during the start of exercise to augment the heart rate and a more physiologic sensor (QT, minute ventilation) to provide more proportional heart rate response during steady state. The benefit of dual sensors has not been conclusively demonstrated in long-term randomized studies, and, in fact, one acute exercise study demonstrated no clinical advantage of dual sensor over single-sensor rate-responsive pacing.

Programming Rate-Adaptive Parameters

The parameters for programming rate responsiveness include the lower and upper activity rates, which may be separate from the upper tracking rate. A treadmill test may be required to optimize pacemaker programming. In practice, it is often sufficient to have the patient walk for a few minutes and program the rate-responsive features to achieve what would be expected to be a physiologic pacing rate for that patient. Different pacers have different algorithms that can automate the adjustments of the rate responsiveness. In most patients, it is difficult to demonstrate clinical effectiveness of automatic rate-response optimization versus fixed rate-responsive programming in the office or clinic.

PACEMAKER COMPLICATIONS

Pacemaker complications can occur at the time of implantation or, less likely, can occur late after implantation (Table 7). Overall, early complications have been reported in the range of 3 to ii percent, depending on the definition of complication, duration, and intensity of follow-up.

TABLE 7 Complications Related to Pacemakers

Complications of Pacemaker Implant

Cardiac perforation is a potentially serious and often unrecognized complication of pacemaker lead insertion. This may be recognized at the time of lead insertion by fluoroscopic position of the lead, a paced QRS complex having right bundle branch block pattern, diaphragmatic stimulation, or hypotension resulting from cardiac tamponade. In the absence of anticoagulation, perforation usually does not lead to tamponade if the lead is withdrawn and repositioned. After implantation, cardiac perforation may be recognized by pericardial pain, friction rub, increasing ventricular pacing threshold, diaphragmatic stimulation, or pericardial effusion. The presence of these signs is not diagnostic of cardiac perforation, and echocardiograms should be performed to examine the lead position. If perforation is suspected, and the patient is hemodynarnically stable, clinical observation is often the prudent course.
Other implant-related complications include subclavian arterial puncture, pneumothorax, hemothorax, and air embolus. Rarely, a lead may be introduced into the left ventricle through an inadvertent subclavian arterial puncture or through an unrecognized atrial or ventricular septal defect.
Complications of venous leads include venous occlusion with resulting superior vena cava syndrome or thrombosis of the subclavian vein with ipsilateral arm edema. Acute thrombosis may be treated with heparin and warfarin and managed conservatively if the patient responds to anticoagulation. Invasive and surgical interventions, including venoplasty and stent placement, have been described. Most occlusions, partial or complete, may occur over time and tend to be asymptomatic because of the formation of venous collaterals.
Infections related to pacemaker implantation are rare. The use of prophylactic antibiotics and irrigation of the pacemaker pocket with antibiotic solution may help prevent infection, especially from local flora. Early infections may be caused by Staphylococcus aureus and can be aggressive. Late infections are commonly related to Staphylococcus epidermidis and may have a more indolent course. Occasionally, pacemaker infections are misdiagnosed as pacemaker allergy. Other signs of infection include local inflammation and abscess formation, erosion of the pacer, and fever with positive blood culture without an identifiable focus of infection. Transesophageal echocardiography may help determine whether vegetations are present on the pacemaker lead. If the pacemaker is infected, removal of the pacemaker leads and generator is usually required.

Mechanical Complications

During implant, the leads are connected to the pulse generator by a setscrew mechanism. If the setscrew is loose (Fig. 16d), then pacemaker malfunction may occur, manifested by increased impedance and intermittent or complete failure to capture.
The pacemaker leads are subject to long-term complications. The insulation of the leads may break, leading to problems with oversensing (due to electrical noise), undersensing, and failure to capture (due to current leak). This problem often manifests intermittently and may be difficult to detect during a routine pacer check. The patient may complain of pectoral muscle stimulation due to current leak around an insulation break. An abnormally low impedance with demonstrable lead malfunction is diagnostic for insulation break. Subtle insulation breaks may be detected by having the patient perform provocative maneuvers while monitoring an ECG (and marker channels) and or measuring impedances.
Leads may also fracture over time (Fig. 16b). Early lead fractures lead to increased impedances associated with failure to capture, oversensing, and undersensing. Some leads use retention wires to preform an atrial lead so that it is more likely to attach and remain within the atrial appendage. Fracture of a retention wire does not cause any pacemaker malfunction, but it can lead to serious complications, including cardiac perforation and death, when it penetrates through the insulation into the atrial cavity.
Twiddler's syndrome is a term applied to patients who intentionally or unintentionally manipulate their pulse generator, causing twisting of the entire pacemaker system. This leads to lead dislodgment or fracture. This may also result from an excessively large pacemaker pocket allowing rotation of the pacemaker.

Electromagnetic Interference of Pacemaker Function

In general, electromagnetic interference (EMI) can originate from a variety of sources that have the potential to affect pacemaker function adversely. In Table 8 are listed some of the more common sources of EMI with potential pacemaker effects.

TABLE 8 Sources of Electromagnetic Interference and Potential Effects

Unipolar pacemakers are usually more susceptible to EMI interference than are bipolar pacemakers because the sensing circuit encompasses a larger area compared with bipolar sensing. Factors that affect EMI interference have to do with the source of the interference and the proximity to the pacemaker generator. Many of these sources are located in a hospital environment or specialized places such as construction sites. Magnetic resonance imaging scans are contraindicated in patients with pacemakers, although there are case reports of patients with pacers undergoing MRI scans without adverse events. Sources of EMI at home and the office usually do not pose a problem for patients. There is concern, however, that electronic article surveillance devices, found commonly in retail establishments, can interfere with pacemaker function, if patients linger by these devices.
The effects of EMI vary according t o its source and the type of pacemaker. Inhibition of pacing output can potentially be life threatening for patients who are pacemaker dependent. If the EMI is interpreted as atrial events by the pacemaker, then inappropriate ventricular pacing may occur in patients with DDD pacemakers, since these pacemakers attempt to track these events, which are interpreted as atnal. EMI often causes electrical noise that causes the pacemaker to function in a noise reversion mode. The actual function of this mode differs among the different pacemakers, but this mode involves switching to an asynchronous pacing mode. After elimination of this interference, pacers generally revert to the previously programmed mode; however, it is possible for EMI to cause pacemakers to revert to a backup pacing mode. Backup pacing in some models is unipolar VVI pacing at a preset rate.
Occasionally, EMI causes permanent damage to the pulse generator. Therapeutic radiation can damage the complementary metal oxide semiconductors (CMOS) that are part of most modern pacemakers. Generally, doses in excess of 5000 rad, but as little as 1000 rad, may induce pacemaker circuitry damage, which in turn can cause pacemaker failure or even induce a runaway pacemaker. If the pacemaker cannot be shielded from the field of radiation, then consideration should be given to reimplanting the pacemaker at a distant site.
In studies examining interactions between pacemakers and cellular telephones, it was noted that digital telephones may cause intermittent pacemaker dysfunction. These adverse effects observed included pacemaker inhibition, inappropriate ventricular tracking (in VDD or DDD pacemakers), or resetting the pacemaker to a backup asynchronous mode. Factors associated with interference include unipolar pacing systems, digital cellular phones, increased output by the cellular phone, and close proximity of the cellular phone to the pacer. Because of the diversity of cellular phones and pacemakers that have different shielding capabilities against electromagnetic interference, it is difficult to draw firm conclusions on the use of digital cellular telephones.159 No consistent problems have been detected with analog telephones. It is advisable that patients use cellular telephones that are analog or to keep digital cellular (with power outputs greater than 3 W) phones 20cm away from their pacemaker generator.

Medtronic Standard GuideLines Regarding Electrosurgery and Pacemakers

Message of 9/11/01 Regarding Phacoemulsion Procedures and Pacemakers:
Regarding phacoemulsification procedures and pacemaker dependent patients this procedure should pose no problems given that the energy is sound waves and not generation of an electric current.

 

ELECTROSURGERY AND PACEMAKERS

Essentially, any type of interference has the possibility of causing reversion to asynchronous pacing or possibly pacemaker inhibition. Interference could cause complete inhibition. Electrosurgery and defibrillation have the potential to cause either of these things to happen.

Since electrosurgery and especially defibrillation are generally necessary procedures, Medtronic makes recommendations on how to minimize the possible pacemaker interference problems. The remainder of this letter will contain these recommendations.

Effects of electrosurgical currents upon implanted pulse generators can be controlled by the location of the electrosurgical electrode in respect to the implanted pacemaker system, the orientation of the surgical electrodes to the pacing system, the spacing of the surgical electrodes from the pacemaker, and the frequency of application of the electrosurgical currents. I will describe these four areas first and then discuss other factors which I feel may influence how electrosurgery is used.

If possible, the return or ground electrodes should be placed so that the pacing system is not directly in the current path between the active and return electrodes on the arm, leg, neck, etc., may help to position the electrodes away from the pacing system.

Electrosurgical effects are reduced if the current is flowing perpendicular to the electrodes of the pacemaker lead. In a bipolar pacemaker, the orientation of the pacing lead electrodes within the heart may be difficult to determine. A unipolar pacing system orientation is easier to determine with one pacing electrode in the heart while the pulse generator itself acts as the indifferent electrode. Unipolar systems are more susceptible to external interference due to the larger "antenna effect" they present. It is more important to have a perpendicular current flow past the electrodes of a unipolar pacing system than in a bipolar system.

Very high current densities are generated at the active electrosurgical electrode. Placement of this electrode near the implanted pulse generator may induce sufficient current to the pulse generator to cause it to revert to a fixed rate or inhibit. Placement of the active electrode as far away as possible from the pulse generator will minimize the effects of these induced currents. Currents at the active electrode disperse rapidly so that at a distance of only a few centimeters the effects on the pulse generator will be substantially reduced.

Pulsing modes of interference typically have more effect on pulse generators than do continuous sources. Pulses may be generated by turning the electrosurgical equipment on and off or by removing and reapplying the active electrode while the equipment is turned on. This type of effect can be reduced by minimizing the number of times the surgical equipment is activated. If inhibition is suspected, use of electrosurgery should be limited to one second with a rest period of approximately 10 seconds. This procedure allows the pulse generator to function properly for a greater portion of the time, therefore, permitting the patient's cardiac output to be properly maintained.
Excessive power usage also contributes to effects upon pulse generators. Maintaining equipment in good working conditions will help reduce the power required and also minimize the emission of spurious interference.

Placing a magnet over a demand nonprogramrnable pulse generator will cause it to operate asynchronously at a fixed rate. This will also eliminate the effects of external interference by disabling the sensing amplifier of the pulse generator. If the patient can tolerate the competitive pacing of asynchronous pacing, then I would suggest placing the magnet over a nonprogrammable demand pulse generator when using electrosurgical currents.

Do not place a magnet over a demand programmable pulse generator when an external source of interference is present. The magnet will cause the pulse generator to operate asynchronously, but also activates the programming circuitry. Reprogramming may occur if the external interference is of sufficient amplitude to affect the pulse generator while the programming circuit is activated by a magnet. Reprogramming will not occur as readily in the new multiprogrammable pulse generators. These units require a special digital series of codes before access can be made to the programming circuitry.

Inadvertent touching of the active electrode to the implanted pulse generator may result in excessive current conducted into the pacing lead system. Repositioning of the lead may be required if tissue is damaged at the pacing electrode site.

In summary, unipolar pacing systems are more susceptible to external interference. Being aware of the location, orientation, spacing, and application procedure of the electrosurgical electrode may help minimize effects on the pulse generator. Do not use a magnet over a programmable demand pulse generator in the presence of strong interference fields. Proper maintenance and use of power of the surgical equipment will reduce undesirable effects on the pulse generator.

Defibrillation concerns for implantable pulse generators are very similar to those stated for use with electrosurgery. If possible, position the electrodes so that currents are not passing through the pacing system. Place the defibrillator electrodes at least thirteen centimeters or five inches from the implanted pulse generator and use the least amount of energy to satisfactorily revert the patient. Repeated discharges to the implanted pulse generator will not have the cumulative damaging affects.

lmplantable Medtronic pulse generators are designed to withstand 400 watt-seconds of defibrillation energy. The functional operation of the pulse generator may be verified following defibrillatory discharges.
Rev. 10.95

ELECTROSURGERY RECOMMENDATIONS

1. Do not perform electrosurgery within six inches of the pulse generator.

2. Use the minimum electrosurgical power settings required.

3. Use short bursts (preferably less than one second in duration) spaced more than five seconds apart. If electrosurgery is causing inhibition of the pacemaker, a longer time between bursts will minimize hemodynamic effects.

4. If the patient can tolerate asynchronous pacing, the pacemaker mode can be changed to either VOO or AOO. In the case of a nonprogrammable pacemaker, simply place a magnet over the IPG. Do not place a magnet over a programmable pulse generator, rather program the pacemaker to asynchronous operation prior to surgery. Asynchronous operation eliminates the potential for reversion or inhibition due to oversensing.

5. If possible, a bipolar cautery should be used. A bipolar system has a definite, short current path which greatly reduces the area of interference to roughly a six-inch circle centered around the electrosurgical site. If a unipolar device is used, the indifferent electrode should be placed such that the current flowing between the electrosurgical site and the indifferent electrode (ground plate) will not intersect the pacing system.

6. Always monitor pacemaker patients during electrosurgery. If, because of interference, the ECG tracing is not clear, the patients pulse generator should be monitored manually or by some other means such as ear or finger plethosgraphy, Doppler pulse detection, or arterial pressure display.

7. Emergency pacing equipment as well as an appropriate programmer should be readily available.

8. Verify function of IPG after procedure. Remember to reprogram out of VOOIAOO modes if that was done prior to the procedure.
Rev. 10.95

PACEMAKER MALFUNCTION

Pacemaker malfunction can be categorized as loss of capture, abnormal pacing rate, undersensing, oversensing, or other erratic behavior. The approach to diagnosing pacemaker malfunction is to inspect the ECG carefully, interrogate the pacemaker; check pacing and sensing thresholds, lead impedances, and battery voltage/ magnet rate; and perform a chest x-ray. Many instances of pacemaker malfunction actually represent normal function of the pacemaker (Table 9). Usually, causes of pacer malfunction may be diagnosed noninvaasively, but, occasionally, surgery is required to diagnose problems..

TABLE 9 Suspected Malfunction Occurring During Normal Pacer Function

TABLE 10. Causes of Upper Rate Behavior in DDD Pacemakers (and Atrioventricular Block)

	ECG Characteristics	Response to Magnet
Sinus tachycardia	1:1 Atrioventricular pacing, pacemaker Wenckebach or 2:1 block depending on the PVARP, upper rate, and sinus rate	No change in paced rhythm after magnet removed
Atrial fibrillation	Irregularly irregular paced ventricular rhythm up to but not exceeding the upper rate	No change in paced rhythm after magnet removed
Pacemaker-mediated	Regular paced ventricular rhythm equal to or less than upper rate	Termination of tachycardia

ABBREVIATION: PVARP = postventricular atrial refractory period.

Abnormal Pacing Rates

Abnormal pacing rates can be due to normal or abnormal pacing function (Table 9). Failure of the pacemaker to output is usually due to oversensing. Occasionally, there is pacemaker output that is not visible because of bipolar pacing producing very low amplitude pacing artifacts (artifacts from digital ECG recording are commonly difficult to visualize). Conversely, absence of pacing stimuli may be due to interruption of current flow from a lead fracture, insulation break, or a loose setscrew.
Abnormally fast pacing rates usually are due to normal pacing function. They may be in response to rate-adaptive sensors. In DDD pacemakers, upper rate pacing may be due to sinus tachycardia, atrial tachyarrhythmias, or pacemaker-mediated tachycardia (Table 10). In ei ther case, the pacemaker function is normal and is responding either to a rapid atrial rate or to retrograde atrial activity. Rarely, very rapid ventricular pacing ("runaway pacemakers") can cause life-threatening problems requiring disconnection of the pacemaker. Occasionally, abnormal pacing rates can be due to an unstable lead position where the lead is swinging between heart chambers.

Loss of Capture

The loss of pacemaker capture occurs when there is a visible pacing stimulus and no atrial or ventricular depolarization. This may be intermittent or persistent. Most problems occur at the pacemaker lead/tissue interface. For instance, lead dislodgment can cause obvious failure to capture. An increase in the pacing threshold above the pacing output can occur as part of the rise above initial threshold within a few weeks following lead placement (Fig. 16u) or because of drug therapy, electrolytes, myocardial infarction, or ischemia. Fracture of the lead, insulation breaks, and loose setscrews are mechanical problems that can cause failure to capture. Lastly, battery depletion may cause the pacing output to decline sufficiently such that pacing failure occurs.
Loss of capture requires a check of pacing threshold and of pacing lead impedance and a chest x-ray. For instance, if the problem is an elevated pacing threshold, pacing outputs must be increased. Abnormal lead impedances may confirm a lead failure and the need for lead replacement.

Oversensing

This problem leads to abnormal pacing rates with pacemaker pauses. Generally, unipolar lead systems are more susceptible to oversensing. The sources for oversensing can be intracardiac, extracardiac, or due to EM!. Analysis of ECG, especially with pacemaker interrogation and pacemaker marker channels, may help to determine the cause. If the oversensing is regular, analysis of the pauses may suggest T-wave or P-wave oversensing. T-wave oversensing usually can be eliminated by decreasing the sensitivity (increasing the millivoltage required to sense electrical activity) or increasing the ventricular refractory period.
Oversensing due to lead fracture, insulation break, or other electrode problems will usually be random and erratic (Fig. 16v). With early lead problems, the malfunction is intermittent and may be exacerbated by certain body positions or motions. In later stages, the combination of oversensing, undersensing, and failure to capture is almost always diagnostic of a lead-related problem. Programming to an asynchronous mode may temporarily control this problem while awaiting a lead replacement, which should be carried out as promptly as possible.
Crosstalk inhibition is a phenomena usually seen in unipolar pacers. It is due to ventricular sensing of atrial output. This is currently a rare problem because UI blanking periods 41IU ventricular safety pacing.
Myopotential oversensing is usually a problem in umpolar but not bipolar systems. These skeletal myopotentials generate interference, which tends to correspond to certain activity. The optimal solution is reprogramming the sensitivity to a level high enough to avoid myopotential sensing while preserving adequate safety margin to sense intrinsic cardiac depolarizations.

Undersensing

An inadequate intracardiac signal can lead to undersensing (Fig. 16q). The intracardiac electrograms can deteriorate due to inflammation or scar formation at the tissue lead interface. Additionally, certain drugs, electrolyte abnormalities, infarction, ischemia, lead fracture, or insulation breaks can lead to undersensing. Cardioversion or defibrillation can also cause attenuation of intracardiac electrograms.Usually,undersensing is a greater problem in the atrium than in the ventricle. The optimal solution is to program an enhanced sensitivity (decrease sensing level). With bipolar systems, the programmed sensitivity can usually be reduced to 0.18 mV in the atrium, without oversensing of myopotentials or other extraneous signals.
Other etiologies for undersensing occur when intrinsic atrial or ventricular complexes fall within one of the programmed refractory periods. Undersensing can also result from a pacer that was inadvertently programmed to an asynchronous mode (occasionally occurring with battery depletion or pacemaker generator reset).

Mitrani,R.D. and others,Cardiac Pacemakers,Hurst's The Heart,10th edition,Vol.1,pp.963-992 .