Permanent pacemakers (PPMs) were introduced in the 1950s for use in patients with pathologic conditions of the sinus node, atrioventricular (AV) node, or His–Purkinje system. Since that time they have been refined to allow more complex programming. In addition, periprocedural morbidity has been reduced significantly. As a result, the number of devices implanted has increased steadily, with over 150,000 new pacemakers implanted in the United States each year.¹

The sinus node is an oval piece of tissue in the roof of the right atrium that is 10 to 20 mm long and 2 to 3 mm wide. It is less than 1 mm from the epicardial surface between the superior and inferior venae cavae.^2,3 Its blood supply is derived from the right coronary artery (RCA) 55 to 60 percent of the time and from the circumflex coronary artery 40 to 45 percent of the time.²

The atria are anatomically complex structures and differ significantly from each other. The right atrium is heavily trabeculated over the lateral wall and appendage and is characterized by significant heterogeneity, with abrupt changes in muscle fiber orientation over short distances. In contrast, the left atrium is a more uniform structure. Unlike ventricular myocardium, which contains Purkinje fibers, it now is generally accepted that the atria do not contain specialized conduction tissue. Instead, the spread of the impulse depends on the properties of the atrial muscle bundles. Simultaneous electrical mapping of canine left and right atria demonstrate that the left atrium consistently activates approximately 10 ms later than does the right atrium. Rapid activation of the anterior surface of the left atrium is facilitated by a muscle bundle known as Bachmann bundle. The wave fronts then converge in the posterior left atrium inferior to the pulmonary veins. Human atria demonstrate similar activation patterns, although the activation times are twice as long because of the larger atrial surface area.³

The compact portion of the AV node (AVN) is just beneath the right atrial endocardium anterior to the coronary sinus ostium and directly above the insertion of the septal leaflet of the tricuspid valve (TV). The AVN is located at the apex of the triangle of Koch, which is defined by the TV inferiorly, the tendon of Todaro superiorly, and a line drawn between the coronary sinus and the tricuspid annulus posteriorly. Of note, the node is well removed anteriorly from the coronary sinus. The AVN becomes the penetrating bundle of His at the central fibrous body. In 85 to 90 percent of people, the blood supply to the AVN is via the RCA; in the remainder, blood is supplied via the circumflex coronary artery.²

The branching portion of the His bundle begins at the muscular intraventricular septum and becomes the left bundle branch (LBB) and the right bundle branch (RBB). The LBB arises and continues onto the septum beneath the noncoronary cusp of the aortic valve. The LBB may divide into anterior and posterior branches or may have a different branching pattern. The RBB continues as an unbranched extension of the AVN and continues along the right side of interventricular septum to the apex of the right ventricle (RV) and the base of the anterior papillary muscle. Purkinje fibers continue from the bundle branches as networks of conduction fibers on the endocardial surface of both ventricles.²

The conducting tissues of the heart may be divided into fast-response and slow-response tissues. The distribution of ions and their associated electrical voltage gradients are responsible for the cardiac action potential. The baseline of this potential is −90 mV, and the peak is +20 mV for fast-response tissues (Fig. 44-1). The depolarization of fast-response tissues such as the atria, the bundle of His, bundle branches, and Purkinje fibers is due to an inward sodium current, whereas repolarization of those tissues is due primarily to outward potassium currents. In slow-response tissues such as the sinus node and the AVN, the baseline is about −70 mV and depolarization depends primarily on the L-type calcium current.

Cardiac pacing is based on the principle that myocardial cells can be depolarized repeatedly by electrical stimulation. In cardiac pacing, voltage is applied across two electrodes, at least one of which is in contact with myocardium. In bipolar leads, the two electrodes usually are separated from each other on the lead by about 1 cm. In unipolar leads, only one electrode is in contact with the myocardium, and the other electrode is typically the outer can of the pacemaker generator.

The voltage, current, resistance, and energy of a pacing system are related to one another according to the following equations:

V = I × R

where V = voltage (volts), I = current (milliamperes), and R = resistance (kilohms).

E = V × I × t (time the current is applied) or E = (V²/R) × t

Electrical sensing is based on the detection of the intrinsic current between the two electrodes on bipolar leads or between the lead tip and the pacemaker generator in a unipolar system, with a filter system in place. Unipolar systems are subject to much more noise and/or cross talk than are bipolar leads because the distance between the two electrodes is greater.

Indications for Permanent Pacing

Current indications for permanent pacing are based on the 2008 consensus guidelines published by the ACC/AHA/HRS.⁴ The indications follow the standard evidence-based tiered system. A class I indication means that a procedure generally is agreed to be beneficial; class IIa indications are those for which there is conflicting evidence or a divergence of opinion but the weight of evidence is in favor of a procedure. Class IIb is similar to class IIa except that the efficacy of a procedure is less well established.

Permanent pacing should be considered for all patients with irreversible symptomatic bradycardia and selected patients with asymptomatic bradycardia. In addition, indications for cardiac resynchronization therapy (CRT) via biventricular pacing in patients with dilated cardiomyopathies have increased significantly in recent years. Pacing needs in specific cardiac operations are considered individually later in this section but are based on the general indications given below.

Common causes of symptomatic bradycardia include sinus node dysfunction (SND), third degree or advanced second degree AV block (AVB), and carotid sinus hypersensitivity (CSH). The following is a summary of the recommendations for PPM implantation in each of these conditions⁴:

• 
  

  Class I recommendations for pacing in SND:

  
  
  
  
  • 
    

    SND with documented symptomatic bradycardia

    
    
  • 
    

    Symptomatic chronotropic incompetence

    
    
  • 
    

    Symptomatic bradycardia that results from required drug therapy for medical conditions

  
  
• 
  

  Class I recommendations for pacing in acquired AVB:

  
  
  
  
  • 
    

    Third degree or advanced second degree AVB with symptomatic bradycardia

    
    
  • 
    

    Third degree AVB that results from required drug therapy for medical conditions

    
    
  • 
    

    AVB in symptom-free patients in sinus rhythm with asystole >3 s, escape rhythm <40 bpm, or infranodal escape

    
    
  • 
    

    AVB in symptom-free patients in AF with pauses >5 s

    
    
  • 
    

    Postoperative AVB that is not expected to resolve after surgery

    
    
  • 
    

    Mobitz II second degree AVB

    
    
  • 
    

    Alternating bundle branch block

  
  
• 
  

  Class I recommendations for pacing for CSH:

  
  
  
  
  • 
    

    Syncope occurring due to spontaneous CSH and carotid sinus pressure that induces ventricular asystole >3 s

Permanent Pacing After Coronary Artery Bypass Grafting

After coronary artery bypass grafting (CABG) or valve surgery, patients may develop a number of conduction disturbances, including a left hemiblock, right bundle branch block (RBBB), left bundle branch block (LBBB), bifascicular block, and AVB. The overall incidence of conduction disturbances after CABG is reported to be 10 to 15 percent.^5,6. The significance of the various fascicular blocks after CABG has been controversial. In contrast to some early studies from the 1970s and 1980s, more recent studies of patients after CABG have not demonstrated any association between bundle branch block or intraventricular conduction defects and cardiac mortality over 3 to 5 years^7–9 even though these conduction disturbances probably indicate some degree of intraoperative myocardial damage.

It has been estimated that overall, 0.4 to 1.1 percent of patients who undergo CABG will require permanent pacing.⁶ This risk is roughly doubled for patients undergoing repeat operations.¹⁰ Risk factors for AVB and other conduction disturbances include advanced age, the number of vessels bypassed, left main coronary artery stenosis accompanied by total occlusion of a dominant RCA, the presence of an ungraftable RCA, proximal left anterior descending artery (LAD) stenosis involving the first septal perforator, aortic cross-clamp time, and prolonged hypothermic cardioplegia.^11–15 In one series of 120 consecutive cardiac surgery patients, the risk of postoperative pacemaker implantation was higher for patients with preexisting clinical or electrocardiogram (ECG) evidence of a conduction disturbance. In this study, predictors of long-term pacemaker dependency were postoperative complete AVB and bypass time >120 min.¹⁶ Of note, the use of normothermic cardioplegia for shorter periods may be responsible for the decreased incidence of AVB after CABG in some series.¹⁷

The natural history of AVB in patients after CABG is that it may resolve within hours after the surgery; last for days, weeks, or months and then resolve; or persist.^11,12 In a series of 348 consecutive patients undergoing CABG, 56 of whom developed AVB postoperatively, the AVB lasted for less than 6 h in 32 (57 percent) and for more than 6 h in 24 (43 percent).¹³ In another series of 93 consecutive patients undergoing CABG, all four patients who developed third-degree AVB after the operation were no longer in AVB after 2 months (AVB resolved in one patient on the second postoperative day; the other three patients had PPMs implanted before discharge).¹¹ Another study evaluated 26 patients who had a PPM implanted for AVB and 10 patients with a PPM implanted for SND after CABG. The pacemaker dependency rate (defined as the need for pacing with mode set to VVI 50) after 3 years was 65 percent for the AVB group and 30 percent for the SND group.¹² If the AVB resolves, permanent pacing is unnecessary. Although it may be reasoned that selected patients may not need a generator change at the time of battery end of life because of potential recovery of the conduction system, the authors generally maintain the PPM in most patients because it is difficult to establish with certainty that these patients will not require pacing at some point in the future. Furthermore, it should be noted that a generator change is a very low-risk procedure.

Permanent Pacing After Valvular Surgery

Compared with the approximately 1 percent of patients undergoing CABG who have a need for permanent pacing, 3 to 6 percent of patients undergoing valve surgery require permanent pacing.^6,18 The most likely reason for the increased need for permanent pacing after valve surgery is the risk of trauma to the conduction system with this procedure. An estimation of the likelihood of the need for permanent pacing at the time of surgery informs the choice of the temporary epicardial pacing configuration. Since temporary leads may be associated with bleeding, tamponade, bypass graft injury, and infection, only the necessary number of leads should be implanted. For example, whereas a single ventricular epicardial lead may be appropriate for a low-risk patient, a dual-lead configuration with an additional ventricular lead (in case one lead fails) may be appropriate for higher risk patients.

In a series of 4694 patients undergoing valve surgery between 1992 and 2002 at the Brigham and Women’s Hospital, a multivariate analysis established the following as risk factors for conduction disturbances requiring PPM implantation: RBBB [odds ratio (OR) 3.6], LBBB (OR 2.0) and PR interval more than 200 ms (OR 1.9) on the preoperative ECG, multivalve surgery involving the TV (OR 3.7) or not involving it (OR 2.1), advanced age (OR 1.4), and a history of prior valve surgery (OR 1.8).¹⁸ For surgery involving only one valve, the risk was lowest for mitral valve surgery (3.5 percent), somewhat higher for aortic valve surgery (5.1 percent), and highest for TV surgery (12 percent). On the basis of the preoperative ECG, the need for permanent pacing was greatest in those with a preexisting isolated RBBB (18 percent) or an RBBB accompanied by a left hemiblock (bifascicular block; 16 percent) and somewhat lower in those with a preexisting LBBB (10 percent). A prediction rule for the need for permanent pacing was developed according to the point system shown in Table 44-1. The need for permanent pacing for total point scores of 0, 1, 2, 3, 4, 5, and 6 was 1.9, 5.2, 8.7, 12, 21, 36, and 50 percent, respectively.¹⁸ In a recent retrospective review of 4999 patients undergoing cardiac surgery between 1993 and 2005, the strongest predictors of pacemaker implantation were LBBB and aortic valve surgery. TV repair was not associated with an increased rate of pacemaker implantation, though these patients made up a minority of the cases (7 percent).¹⁹ Similar to coronary bypass surgery, repeat valve replacement operations are associated with increased risk of long-term conduction disturbance, requiring a PPM in as many as 16 percent of patients.¹⁰ A better understanding of what constitutes a high-risk patient will help providers avoid delays in PPM implantation and facilitate patient mobilization and discharge.

Prophylaxis for Postoperative Atrial Fibrillation

Postoperative atrial fibrillation occurs in 10 to 40 percent of all patients undergoing open heart surgery.^20–23 The issue of prophylactic pacing after cardiac surgery as prophylaxis for atrial fibrillation was addressed in a meta-analysis of eight trials that enrolled a total of 776 patients and compared control patients with patients randomized to right atrial, left atrial, or biatrial pacing.²⁴ The patients could be paced at a fixed high rate (fixed high-rate pacing) or at a rate just fast enough to overcome the intrinsic rate (overdrive pacing). Risk reductions for postoperative atrial fibrillation of 2.6-fold and 1.8-fold were found for overdrive biatrial and right atrial pacing, respectively, and there was a 2.5-fold reduction for fixed high-rate biatrial pacing. Whether biatrial pacing confers an advantage over right atrial pacing is controversial.^25,26 Ongoing studies should help clarify these issues. Although temporary atrial pacing to decrease atrial fibrillation after cardiac surgery has gained general acceptance, the data supporting permanent pacing are not well established.

Although medical therapy with prophylactic β-blockers, amiodarone, and sotalol has been shown to reduce postoperative atrial fibrillation, pacing therapy offers several advantages, including minimal expense; no association with ventricular proarrhythmia, bradycardia, or hypotension; and no need for the initiation of therapy before surgery. In summary, the approximately 2.5-fold risk reduction associated with biatrial pacing (either overdrive or fixed high rate) and overdrive right atrial pacing makes pacing an attractive nonpharmacologic method for preventing atrial fibrillation after cardiac surgery, particularly since atrial epicardial wires are in place.

Pacing in Cardiac Transplantation

Bradycardia after cardiac transplantation is common, usually temporary, and often due to SND. Although the most common cause for this SND is probably surgical trauma at the time of transplantation,²⁷ several other causes have been implicated, including disruption of the blood supply to the sinus node,²⁸ ischemic time,²⁹ rejection,³⁰ donor age,³¹ and pretransplant amiodarone use.³²

Until the early 1990s, the standard anastomosis between the recipient and donor hearts was a biatrial anastomosis, as originally described by Lower and Shumway in the canine heart in 1960.³³ As the biatrial anastomosis requires opening the recipient right atrium from the inferior vena caval (IVC) orifice with transection and oversewing of the recipient superior vena cava (SVC), the suture line may result in direct damage to the donor sinus node as well as the blood supply to the sinus node.³⁴ In the bicaval anastomosis, which came into widespread use in the 1990s, there are direct donor–recipient anastomoses of the IVC and SVC, although the left-sided anastomosis may occur at the level of the pulmonary vein or left atrium, depending on the technique used.^35,36 As might be expected, several studies have documented a decreased need for pacing with the use of the bicaval anastomosis compared with the standard biatrial anastomosis.^34,37–39 In the two randomized studies that compared the need for permanent pacing on the basis of the type of anastomosis used, permanent pacing was required in 5 (6.5 percent) of 75 patients with the biatrial anastomosis but was not required in any of the 81 patients with the bicaval anastomosis. According to a compilation of six studies, permanent pacing was required in 60 (9.2 percent) of 651 patients with biatrial anastomoses compared with only 1 (0.3 percent) of 340 patients with bicaval anastomoses. Although the incidence of prolonged SND has been reduced with bicaval anastamoses, this benefit may be attenuated in the era of extended donor criteria. Posttransplant PPM requirements were examined in 88 patients who underwent a bicaval anastamotic approach between 2000 and 2004. Ultimately, 18 of the 88 (20.5 percent) required PPM implantation. Mean donor age was the major risk factor for postoperative pacemaker requirement (44.7 years vs 35.7, p = 0.0289) and may suggest a predilection for increased susceptibility to perioperative ischemia and a higher incidence of underlying conduction and coronary disease in older hearts.⁴⁰

The initial approach to a cardiac transplant patient with postoperative bradycardia resulting from SND is medical therapy with chronotropic agents and the use of operatively placed temporary epicardial leads if necessary. Theophylline has been shown to improve prolonged chronotropic dysfunction in transplant recipients and is the drug of choice.⁴¹ Isoproterenol and terbutaline also may be used. Published commentaries generally have recommended permanent pacing if bradycardia caused by SND persists for 2 to 3 weeks.^34,42 Ambulatory Holter monitoring may aid in the decision whether to implant a PPM. The reason to wait as long as possible to implant a permanent system is that SND after transplantation is usually manifest by the first week and resolves over 1 to 3 months. Serial electrophysiologic studies in 40 posttransplant patients demonstrated that the sinus node recovery time (SNRT) became abnormal by the first week in 6 (15 percent) patients and by 3 months in 1 other patient. In all six patients with early SND, the SNRT returned to normal by 6 weeks, although sinoatrial conduction abnormalities persisted in two patients.⁴³ Because maintaining AV synchrony will maximize cardiac output, a dual-chamber pacemaker system usually is used and programmed to DDDR, although permanent atrial pacing without a ventricular lead is an option (albeit one rarely used in the United States) if AV conduction is intact. One advantage of using an atrial lead only is the decreased likelihood of dislodgment with biopsy, although this is uncommon with experienced operators. If a biatrial anastomosis is present, the pacemaker lead should be implanted in the anteroseptal right atrium rather than the lateral right atrium near the anastomosis.

Cardiac Resynchronization Therapy (Biventricular Pacing)

Heart failure is the fastest growing cardiovascular diagnosis in the United States with an estimated prevalence of 2.5 percent in adults and an estimated cost of over $39.2 billion in 2010.⁴⁴ Heart failure syndromes represent a constellation of molecular, anatomic, and neurohormonal perturbations. One downstream effect of neurohormonal regulation includes the alteration of myocardial membrane properties leading to action potential prolongation, an imbalance of calcium homeostasis, and cell–cell coupling. These changes ultimately lead to interventricular dyssynchrony (often LBBB) and greater arrhythmogenicity. Although great strides have been made using medications to target and attenuate the negative remodeling process that ensues with heart failure, biventricular pacing to restore cardiac synchrony provides another arrow in the quiver to combat heart failure morbidity and mortality.

CRT has proven beneficial for patients with dilated cardiomyopathy, intraventricular conduction delay, and heart failure. The objective is to correct dyssynchrony by pacing the left ventricle alone or both ventricles (biventricular).

The Multisite Stimulation in Cardiomyopathy (MUSTIC) study showed statistically significant improvements in the 6-min walk and quality of life (but not mortality) with biventricular pacing,⁴⁵ and the Multisite InSync Randomized Clinical Evaluation (MIRACLE) study has shown improvements in functional class, quality of life, and left ventricular (LV) dimensions.⁴⁶ Resynchronization therapy in the COMPANION (Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure) trial directly compared pacing with (CRT-D) and without (CRT-P) defibrillation capability with optimal medical therapy.⁴⁷ CRT-D reduced mortality by 36 percent compared with medical therapy, but there was insufficient evidence to conclude that CRT-P was inferior to CRT-D. The effects of CRT on mortality were further evaluated in the CARE-HF trial. Enrollment criteria included New York Heart Association (NYHA) class III/IV heart failure, LVEF <35 percent, QRS ≥120 ms. In both trials the risk of death was reduced with CRT versus no pacing; however, only CARE-HF demonstrated statistical significance (HR 0.64, p <0.002).^47,48 No large trial has yet demonstrated clinical benefit among patients without QRS prolongation, even when they have been selected for echocardiographic measures of dyssynchrony.⁴⁹

The benefit for implantable cardioverter-defibrillator (ICD) implantation in heart-failure patients has been well established based on SCDHeFT and MADIT-II data showing a survival benefit with defibrillators in patients with class II or III heart failure and a severely depressed ejection fraction.^50–52 More recently, the MADIT-CRT trial compared the use of a CRT plus an ICD device versus an ICD alone in 1820 patients with NYHA class I or II heart failure, LVEF ≤30 percent, and QRS ≥130 ms. This study included both ischemic and nonischemic cardiomyopathy patients and demonstrated a reduction in the primary combined endpoint of death or heart failure events in the CRT-D group (17.2 vs 25.3 percent, p = 0.001). This was driven primarily by a 41 percent reduction in heart failure events.⁵³

Based on these data, current guidelines recommend CRT with biventricular pacing in patients with NYHA class III or ambulatory class IV heart failure, LVEF of 35 percent or less, and a QRS duration greater than 120 ms,⁴ or NYHA class I or II with LVEF ≤30 percent and QRS ≥130 ms.

Since the left ventricle is usually paced via the coronary sinus, transvenous LV pacing is more technically difficult than is endocardial right ventricular pacing. A number of challenges exist with coronary sinus lead placement including difficulty accessing the coronary sinus ostium, unfavorable venous anatomy, and poor pacing parameters owing to myocardial fibrosis, or extracardiac stimulation. Transvenous coronary sinus leads can ultimately be placed successfully about 90 percent of the time. For the remaining cases, an alternative approach may be used such as surgical epicardial placement or transseptal or transapical LV endocardial placement, as discussed below.

Hypertrophic Obstructive Cardiomyopathy

The objective of permanent pacing in patients with hypertrophic obstructive cardiomyopathy is to improve outflow obstruction with early stimulation of the right ventricular apex. The pacemaker is generally programmed to DDD mode with leads in the right atrium and RV. Randomized clinical studies^54–56 have shown statistically significant reductions in the LV outflow tract pressure gradient but only mild improvement in functional status and generally no improvement in quality of life. There are currently no data available to suggest that pacing changes the natural history of hypertrophic cardiomyopathy (HCM). Therefore, routine implantation of dual-chamber pacemakers should not be advocated in all patients with symptomatic obstructive HCM. Patients who may benefit the most are those with significant gradients (more than 30 mm Hg at rest or more than 50 mm Hg provoked). Myomectomy and ethanol septal ablation are probably more effective treatment options for patients with hypertrophic obstructive cardiomyopathy. Complete heart block can develop after transcoronary alcohol ablation of septal hypertrophy in patients with HCM and should be treated with permanent pacing. The decision whether to implant a pacemaker alone or a pacemaker–defibrillator is based on clinical judgment but may be guided by several factors that, if present, favor a pacemaker–defibrillator. These factors are a personal history of syncope or sudden cardiac death, a family history of sudden cardiac death, nonsustained ventricular tachycardia (VT), massive hypertrophy (wall thickness of 30 mm or more), a pathologic drop in blood pressure with exercise, and HCM mutations associated with an increased risk for sudden cardiac death.

Pacing After a Myocardial Infarction

In patients who have had a myocardial infarction, temporary pacing is a class I indication for the following conditions⁴:

1. 
   

   Asystole

   
   
2. 
   

   Symptomatic bradycardia

   
   
3. 
   

   Bilateral BBB [alternating BBB or RBBB with alternating left anterior/posterior fascicular block (LAFB/LPFB)]

   
   
4. 
   

   Asymptomatic Mobitz 2 AVB

   
   
5. 
   

   New bifascicular block (LBBB or RBBB with left hemiblock)

Permanent pacing is a class I indication for the following conditions⁴:

1. 
   

   Persistent second-degree AVB in the His–Purkinje system with alternating bundle branch block or third-degree AVB within or below the His–Purkinje system after ST-segment elevation MI. (Level of Evidence: B)

   
   
2. 
   

   Transient advanced second- or third-degree infranodal AVB and associated bundle branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evidence: B)

   
   
3. 
   

   Persistent and symptomatic second- or third-degree AVB. (Level of Evidence: C)

Permanent pacing usually is not indicated after a myocardial infarction for transient second- or third-degree AVB in the absence of a wide QRS (e.g., with an isolated LAFB). The long-term prognosis for survivors of myocardial infarction who have had AVB is related primarily to the extent of myocardial injury and the character of intraventricular conduction disturbances rather than the AVB itself.

Temporary Endocardial Leads

Temporary endocardial leads usually are introduced via a sheath system in a jugular or subclavian vein. The right internal jugular vein is generally the vein of choice, as it allows for easy passage of the pacing lead through the right atrium and into the RV. As these leads usually are placed in the intensive care unit, often without the aid of fluoroscopy, the position of the lead initially is gaged by viewing the intracardiac electrogram (the distal end of the pacing lead is attached to a cardiac monitoring system). As the lead traverses the right atrium and tricuspid annulus, a large amplitude P wave will transition to a large R wave. Premature ventricular beats and injury current indicate that the lead is in contact with the right ventricular myocardium. A common pitfall is pacing the tricuspid annulus. Because this is an unstable position, the lead should be advanced amply into the RV. After the introduction of the lead and verification of appropriate pacing thresholds, the lead should be locked into place in the sheath and its position should be verified with chest radiography.

Permanent Endocardial Leads

Endocardial leads may be fixated actively or passively. The technique for the introduction of permanent endocardial leads is discussed in detail below. In active fixation, a screw mechanism attaches the lead to the endocardium. Passive fixation leads have polyurethane or silicon tines that facilitate attachment to trabeculae. Passive atrial pacemaker leads are designed for placement in the trabeculations of the right atrial appendage. Passive ventricular leads are designed for placement in the apex of the RV with its trabeculations. Placement of leads in other areas of the atrium and ventricle generally requires active fixation for stabilization. Pacing thresholds may be slightly higher with active fixation, although this is rarely of any consequence. Pacing thresholds may increase after active fixation as a result of inflammation and fibrosis at the site of injury. Most leads are now laden with steroids to minimize the inflammatory response. Active fixation leads are more likely to perforate, particularly at the RV apex, but passive leads may have higher rates of acute dislodgement, particularly in the atrium. Active fixation leads are thought to be easier to extract, though little data exists to support this. In general, the two leads have similar sensing characteristics.

Technique for Implantation of Permanent Endocardial Leads

The subclavian approach is currently the standard approach for the placement of endocardial leads and is used for the placement of over 75 percent of those leads.¹ This approach has evolved since Furman and Schwedel⁵⁷ reported successful transvenous endocardial pacing via the brachial vein in 1959. Because of a high rate of lead dislodgement, this approach was replaced briefly by the external jugular vein approach.⁵⁸ The cephalic cut-down approach became the standard in the late 1960s⁵⁹ and remained the standard for over a decade. As a result of the introduction of the peel-away sheath for the percutaneous introduction of leads, the subclavian approach emerged and remains the standard.⁶⁰ In a series of 200 consecutive patients randomized to endocardial lead insertion via a subclavian approach or a cephalic approach, successful lead placement was achieved in 99 percent randomized to the subclavian approach and 64 percent of cases with the cephalic approach.⁶¹ The total procedure time was 86 ± 22 min with the subclavian approach and 98 ± 35 min with the cephalic approach (p <0.01). Blood loss was also less with the subclavian approach (55 ± 13 mL vs 115 ± 107 mL; p <0.01).

The following approach is adapted from Calkins and coworkers and is used at the authors’ institution⁶¹:

1. 
   

   The patient is positioned supine on the fluoroscopy table and a venogram is performed to guide vascular access. Approximately 10 mL of 1:1 contrast dye and normal saline solution is injected via an intravenous (IV) line placed distally in an ipsilateral vein and then flushed with 25 to 50 mL of saline.

   
   
2. 
   

   A sterile field is created.

   
   
3. 
   

   Generous local anesthesia is given (this may be sufficient, but light sedation often is needed).

   
   
4. 
   

   A subcutaneous generator pocket is created by an incision 2 cm below and parallel to the clavicle. The pocket is created along the pectoralis fascia (Fig. 44-2).

   
   
5. 
   

   Once the axillary and subclavian veins have been opacified, a 5F-micropuncture needle attached to extension tubing and a 10-mL syringe is positioned at a 60° angle to the plane of the skin and parallel to the axillary vein (Figs. 44-3 and 44-4). Adjustment of the site of needle entry may be necessary to ensure that the needle enters the vein as it crosses over the first rib.

   
   
6. 
   

   A micropuncture guidewire is advanced through the needle to the SVC and is replaced by a 5F-micropuncture sheath that allows the introduction of a 50-cm, 0.035-in J-tipped guidewire.

   
   
7. 
   

   A peel-away sheath (generally 7–9F) is advanced over the 0.035-in guidewire.

   
   
8. 
   

   The ventricular lead is advanced through this sheath, and the sheath then is peeled and removed. The ventricular lead is advanced into the right ventricular apex under fluoroscopy.

   
   
9. 
   

   If an atrial lead is planned as well, a second subclavian venipuncture is made, and the atrial lead is placed with the use of the same technique.

   
   
10. 
    

    The leads are connected to the generator, and then pacing and sensing measurements are obtained.

    
    
11. 
    

    If measurements are satisfactory, the lead is screwed in (active fixation) or securely placed among trabeculae (passive fixation). The leads are secured by suture sleeves within the device pocket.

    
    
12. 
    

    The pocket is irrigated with antibiotic solution.

    
    
13. 
    

    The excess lead is coiled and placed into pocket along with the generator.⁶¹