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Cardiac Rhythm Disturbance
Section I Bradycardia
Definition
Abnormal bradycardia is a slow cardiac rate that results chronically or episodically in inadequate cardiac output or life-threatening ventricular arrhythmias.
Historical Note
During the early 1700s, peripheral pulsations of the circulation began to be timed, and in 1717 Gerbezius recognized bradycardia as a deviation from the usual pulse rate. Morgagni is believed to have surmised the relationship between bradycardia and syncope in 1761, but he attributed both to melancholy. In 1827, Adams accurately described what became known as Adams-Stokes syndrome and proposed that it had a cardiac origin. This idea was not well accepted until Stokes, in 1846, collected reports of seven patients with the condition and agreed with Adams’ concepts. The phrase maladie de Adams-Stokes was originated in 1899 by Huchard.
Understanding the morphologic basis of Adams-Stokes syndrome began after Harvey's description of the cardiac cycle. Cardiac conduction tissues were first described by Purkinje in 1845, which he mistook as cartilage tissue. The atrioventricular (AV) conduction bundle was described by His in 1893 and in 1896, Aschoff and Tawara described the AV node and its connection to the His bundle. Then in 1907, Keith and Flack described the sinoatrial, or sinus, node ; its function was demonstrated in 1906 by Einthoven.
It has long been known that the heart responds to external electrical stimulation. As long ago as 1804, Aldini successfully stimulated systole in the hearts of decapitated criminals. Apparently it was known during the late 1800s that direct heart puncture with or without injecting drugs would occasionally produce effective cardiac contractions. Mond reported that in 1929, Lidwill in Australia successfully paced the heart of a stillborn infant for a time by direct ventricular puncture. In 1932, Hyman atrially paced several patients with what he termed an artificial pacemaker , and Bigelow and colleagues in Toronto paced canine hearts by esophageal and precordial electrodes in 1950.
In 1952 in Boston, Zoll reported successfully pacing hearts of patients with complete heart block with external cutaneous electrodes and a large and relatively nonmobile pulse generator. This method was the only one available when intracardiac surgery came into existence during the mid-1950s, and although stimulation of each heartbeat was accompanied by skeletal muscle contractions, and skin under the electrodes quickly became excoriated, this method kept some cardiac surgical patients alive until sinus rhythm returned. However, for patients in whom sinus rhythm did not return, the agony of skeletal muscle contractions and skin excoriations increased as the days passed. Sheer terror developed with approach of the surgeon who would each day provoke an Adams-Stokes episode by turning off the pacer to see whether an adequate idioventricular rhythm, let alone sinus rhythm, would replace the electrocardiographic image of P waves without any QRS complex.
Change began when Lillehei, in Minneapolis, enlisted the help of Earl Bakken, a television engineer and later founder of Medtronics Corporation, in developing a small portable pacemaker. More importantly, he devised the technique of leaving a wire attached to the ventricular epicardium at operation and bringing it out externally. The external electrode was used to pace the heart with minimal patient discomfort. Later, Thevenet, Hodges, and Lillehei devised a method of inserting the wire into the ventricle through a needle passed through the skin over the precordium without an operation. These systems used a portable pacemaker system devised by Bakken.
In 1959, Elmquist and Senning in Stockholm reported placing the first totally implantable pacemaker system using epicardial electrodes. This advance was made possible by invention of transistors during the 1950s. In 1960, Chardack, Gage, and Greatbatch described a self-contained, implantable pulse generator driven by a mercury cell battery for use with implanted epicardial leads.
During the previous year, Furman and Robinson had reported the use of endocardial electrodes introduced transvenously rather than epicardially. Their data supported the idea that endocardial and epicardial electrodes perform similarly. This led to widespread availability by 1961 of both endocardial electrodes inserted transvenously and epicardial electrodes inserted by thoracotomy. These early pacemakers paced at a set rate and did not sense spontaneous cardiac activity. They were crude by present standards but allowed 85% of patients having Adams-Stokes episodes to survive for at least 1 year, in contrast to less than 50% before their introduction.
Rapid developments followed, and pulse generators that sensed the QRS and fired only when no spontaneous QRS occurred within a specified time became available during the mid-1960s. Much work led by Greatbatch during the late 1960s and early 1970s to improve the cells (batteries) resulted in commercial availability of lithium cell–powered pulse generators during the early 1970s. The lithium cells were much more reliable and, with hydrogen gas no longer being liberated in the pulse generator, hermetic sealing of the entire device became possible. More complicated electronic circuits were developed to permit programming of rate and stimulus duration as well as better QRS sensing as transistorized circuits with a few components evolved into hybrid circuits with more components, into integrated circuits, and finally into implantable pulse generators containing microprocessors.
Further improvements permitted atrial sensing and pacing as well as ventricular sensing and pacing (universal pacing) and ventricular pacing synchronized with the patient's atrial contractions, and sequential AV pacing. Currently available pacemakers provide sensing of either body motion or increase in respirations and use the information to alter pacing rate appropriate for patient activity. Finally, the combination of multiprogrammability with diagnostic radio and telephonic transmission has permitted accurate evaluation of pacemaker function and noninvasive adjustment of pacemaker variables for optimal treatment of the patient.
Improvements in pacing electrodes have been made through the years in the form of better wire alloys, antifracture characteristics, electrode pacing threshold properties, and lead insulation. These improvements have diminished the occurrence of high pacing thresholds and lead fracture.
Morphology
Abnormal bradycardia may be the result of complete heart block, a condition in which P waves (atrial depolarization) occur at a constant interval but are unrelated to the less frequently occurring or absent and often broad QRS complexes (ventricular depolarization).
Heart Block
Complete heart block may be present at birth or develop later in life.
Congenital Complete Heart Block
Musculature of the atrial septum may be congenitally deficient near the AV valves, such that there is a diminished or absent connection between the atria and the AV node. Lev described morphologic discontinuity between AV node and bundle of His as another basis for congenital complete heart block in otherwise normal hearts. In hearts with AV discordant connections, complete heart block may be present at birth, presumably related to these same mechanisms.
Spontaneously Developing Complete Heart Block
Some congenital anomalies of the bundle of His may predispose patients to developing complete heart block. Thus, in hearts with AV discordant connection, unusually long length of the bundle of His is believed to predispose it to fibrosis and loss of function.
Certain disease processes may damage the conduction system. Calcification of the aortic valve may extend into the underlying ventricular septum and damage the bundle of His by a shearing effect during certain phases of the cardiac cycle. Mitral calcification does the same less commonly. Acute coronary occlusions resulting in posteroinferior myocardial infarctions may be associated with temporary AV node ischemia and heart block.
An increase in fibrous tissue of the bundle of His and its branches, accompanied by a decrease in number of conduction fibers, seems to be part of the aging process. Progressive fibrosis and fiber loss in left and right bundle branches and resultant heart block (Lev disease, Lenegre disease) may represent acceleration of this process. Anteroseptal myocardial infarctions produce ischemic necrosis in and around right and left bundle branches and may result in permanent heart block. Chronic ischemic heart disease can gradually result in septal fibrosis, with loss of function in both bundle branches. Dilated cardiomyopathy (see “Dilated Cardiomyopathy” in Section II of Chapter 20 ) may be associated with long-standing left ventricular fibrosis that may involve the bundle branches and produce complete heart block.
Surgically Induced Complete Heart Block
During surgical procedures for repair of ventricular septal defects (isolated or as part of tetralogy of Fallot and other complexes; see Chapter 35, Chapter 38, Chapter 52, Chapter 53, Chapter 54, Chapter 55, Chapter 56 ) or AV septal defects (see Chapter 34 ), resection of discrete subvalvar aortic stenosis (see Chapter 47 ), and replacement of the mitral, aortic, or tricuspid valves (see Chapter 11, Chapter 12, Chapter 13, Chapter 14 ), the bundle of His or contiguous AV node may be severed or sutured. In the absence of such direct injuries, the conduction bundle or AV node may be functionally damaged by hemorrhage, with resultant complete heart block. Although fibrosis must develop in these surgical areas late postoperatively, it is interesting that complete heart block is rare late after operation.
Other Bradycardias
Sinus Node Dysfunction
Important sinus node dysfunction may develop without identifiable morphologic changes in the node. Loss of sinus node cells normally associated with aging may accelerate and cause dysfunction, especially in patients with a subnormal nodal cell population at birth. Amyloid deposition may occur within the sinus node and produce dysfunction.
Direct damage to the sinus node by surgical procedures occurs but is uncommon. Damage to the sinus node can result in a junctional rhythm that becomes slower as time passes. In the absence of direct injury, surgical procedures in the region of the sinus node, such as the atrial switch operation (see “Atrial Switch Operation” under Technique of Operation in Chapter 52 ) and Fontan operation (see “Technique of Operation” in Section IV of Chapter 41 ), may result in late perinodal fibrosis, with consequent loss of sinus node function. This process may be due to damage to the sinus node artery. The transseptal approach to the left atrium, which often involves an incision in the roof of the right atrium and division of the sinus node artery, can also result in temporary or permanent sinus node dysfunction.
Dysfunction of Pathways between Sinus and Atrioventricular Nodes
Preferential conduction pathways between the sinus and AV nodes may be interrupted by congenital absence of electrical continuity in these areas.
Surgical procedures, especially atrial switch and Fontan operations, may rarely damage preferential conduction pathways immediately. More commonly, late postoperative fibrosis develops and interferes with conduction along these pathways, and a slow junctional rhythm results.
Clinical Features and Diagnostic Criteria
Pathophysiology
Hemodynamic Effects
Although blood flow into the aorta and large arteries is intermittent (pulsatile), the combined effects of the aortic valve, elasticity of the aorta and great arteries, and characteristics of the arterial distributing system make flow rate relatively constant in capillaries. Thus, cells of the brain and other organs receive continuous nutrient flow. The magnitude of this flow is related to, among other things, net forward flow across the aortic valve with each ventricular systole and heart rate. When the stroke volume is large and heart rate slow, as in trained athletes at rest, elasticity of the aorta and its filling during systole are sufficient to maintain an adequate volume of runoff during a long diastolic period, and thus an adequate nutrient flow to cells of the brain and other organs. When stroke volume is not large, runoff during the late part of chronically long diastolic periods may be inadequate to maintain the proper internal milieu of cells of the brain and other organs. Because the brain is particularly sensitive to hypoxia, cerebral symptoms usually develop before those from dysfunction of other organs.
Cardiac Electrophysiologic Effects
The longer the intervals between periodic depolarizations of ventricular myocardium, the greater the degree of QT prolongation and the higher the likelihood of developing ventricular extrasystoles or tachycardia or both, especially of the torsades de pointes variety (long QT syndrome). Thus, bradycardia predisposes the patient to life-threatening ventricular arrhythmias. Furthermore, with complete heart block, there is the possibility of prolonged ventricular asystole.
Symptoms
Clinical manifestations of first-degree heart block (PR interval > 0.2 second in adults) are rare. Second-degree heart block (intermittent lack of AV conduction 1 ) may be manifested by bradycardia and symptoms. In third-degree (complete) heart block (all atrial impulses fail to be conducted to the ventricle), bradycardia is present, and symptoms are frequent.
1 The two types of second-degree heart block are Mobitz I, in which AV conduction time is progressively prolonged (Wenckebach period) until one atrial impulse is not conducted to the ventricle, and Mobitz II, in which AV conduction times are constant, but episodically an atrial impulse is not conducted to the ventricles.
About 80% of patients (particularly those with sinoatrial disorder [sick sinus syndrome]) have no symptoms when first seen, but eventually become symptomatic. Syncope is the predominant symptom, but palpitations, dyspnea, and angina also occur. Approximately a quarter of patients with sinus node dysfunction have ischemic heart disease.
Diagnostic Criteria
Bradycardias are diagnosed largely by electrocardiographic (ECG) criteria.
Atrioventricular Block
Complete AV block and symptomatic incomplete AV block (such as 2 : 1 second-degree AV block) are diagnosed by standard ECG. When paroxysmal AV block is suspected as the cause of symptoms, prolonged ambulatory ECG monitoring may provide confirmation of the diagnosis (see “ Indications for Intervention ” later in this section).
Sick Sinus Syndrome
Symptomatic arrhythmias in sick sinus syndrome include profound sinus bradycardia, junctional bradycardia, sinus arrest, sinus node exit block, and the so-called tachycardia-bradycardia syndrome in which paroxysmal atrial tachycardia, flutter, or fibrillation is followed by symptomatic pauses caused by overdrive suppression of the sinus node and subsidiary pacemakers. In most of these patients, the resting ECG may not be diagnostic, and prolonged ambulatory ECG monitoring is required to document the abnormal rhythm. Electrophysiologic study is of limited help because abnormal sinus node recovery times or sinoatrial conduction times are demonstrable in only a small minority of symptomatic patients.
Carotid Sinus Syndrome
A hyperactive carotid sinus reflex is said to be present when digital stimulation of the carotid sinus results in cardiac asystole lasting 3 or more seconds. Carotid sinus syndrome is diagnosed when, in addition to the presence of a hyperactive reflex, the patient's spontaneous symptom complex can be reproduced by stimulation of one or both (not simultaneously) carotid sinuses. Pacemaker therapy may completely relieve symptoms in patients with only a cardioinhibitory response. However, the presence of a simultaneous vasodepressor response should also be sought by repetition of massage after intravenous atropine and measurements of the blood pressure. Preservation of the heart rate may not prevent symptoms caused by hypotension in such patients.
Natural History
Bradycardia from both spontaneous heart block and spontaneous sinus node dysfunction tends to occur in elderly patients. The mean age of patients at the time of diagnosis of spontaneously occurring heart block is 70 years.
Spontaneously Developing Complete Heart Block
The proportion of patients with complete heart block developing spontaneously who remain asymptomatic is not known. The most common clinical manifestation is an Adams-Stokes episode. This syndrome is part of the history in 60% to 70% of patients. Symptoms probably eventually develop in most patients. The exact proportion of symptomatic patients is in part determined by functional status of the heart as a whole. Likewise, the tendency toward premature death is related to functional status of the myocardium along with other risk factors.
Patients with Adams-Stokes episodes as a manifestation of complete heart block and who are not paced have a 1-year survival of 50% to 75%, much less than that of an age-sex-race–matched general population. One-year survival is said to be 70% to 80% in patients with complete heart block but without a history of syncope. These differences persist with follow-up to 15 years and appear to be related to the considerably higher prevalence of sudden death in the patients who have syncopal attacks. Syncopal attacks, as well as sudden death, in patients with idioventricular or bundle of His rhythm usually result from sudden ventricular asystole. Syncopal attacks also may be precipitated by a sudden reduction in stroke volume or increased metabolic demands.
Congenital Complete Heart Block
Infants born with congenital complete heart block and hearts that are otherwise normal have a prognosis that may be somewhat better than that for patients with spontaneously developing complete heart block. Ten-year survival for congenital complete heart block is about 85%, with most deaths occurring in the first month of life. Deaths occurring after this time are related to Adams-Stokes episodes.
Surgically Induced Complete Heart Block
In the early years of cardiac surgery when epicardial and transvenous pacing was not possible, hospital mortality was greatly increased in patients in whom complete heart block developed perioperatively. Unpaced hospital survivors had a 1-year survival of about 40%.
Sinus Node Dysfunction
The natural history of patients with this type of bradycardia has not been clearly described.
Technique of Intervention
Development of techniques and devices for cardiac pacing has involved surgeons, physicians, interventional cardiologists, and industry, and advances continue to be made. Methods of insertion and the devices implanted are constantly being improved. Whereas in the 1960s pacemakers were usually inserted by cardiothoracic surgeons, currently in many parts of the world they are inserted, managed, and followed by cardiologists, and often by cardiologists with specialized knowledge of cardiac electrophysiology. Because of these developments, it is no longer practical to include detailed descriptions in a textbook of cardiac surgery. Instead, only general information regarding cardiac pacemaking and basic device insertion procedures are discussed.
Pacing Modes
There are a number of pacing modes. In addition to the basic characteristics described here, many pacemakers have special tachyarrhythmia functions and other programmable functions. Also, some pacemakers sense some surrogates of increased metabolic activity (e.g., body motion, increased rate or volume of respiration) and increase pacing rate accordingly.
VVI
In VVI mode, the ventricle is paced (V), sensing is from the ventricle (V), and response to a sensed spontaneous ventricular depolarization is inhibition (I) of delivering the next electrical stimulus by the pulse generator. The disadvantage of this pacing mode is lack of atrial contributions to ventricular filling. The advantage is simplicity of electrode placement and a relatively long life of the pulse generator.
AAI
In AAI mode, the atrium (A, usually the right) is paced, sensing is from the atrium (A), and sensed atrial depolarization inhibits (I) the next programmed electrical impulse. The AAI mode requires normal AV conduction and functioning atrial pathways to the AV node. This type of pacing mode was anticipated and pioneered by Lillehei and colleagues as early as 1963.
The AAI mode is seldom used (<5%), primarily because many patients with sinus node dysfunction ultimately require ventricular pacing. Its advantage is preservation of atrial contribution to ventricular filling.
VDD
VDD mode, as well as DVI and DDD modes described subsequently, requires both atrial and ventricular electrodes. It also requires relatively normal sinus node function. In VDD mode, the ventricle is paced (V), both the atrium and ventricle are sensed ( D denotes dual chamber or dual function), and the response of the pulse generator may be either the triggering or inhibiting (D) of the next electrical pulse. Generally, sensed atrial depolarization triggers a stimulating pulse to the ventricular electrode at a preset or variable PR interval. Ventricular stimulus is inhibited when spontaneous ventricular depolarization follows atrial depolarization within the set PR interval of the pulse generator. The pulse generator is programmed so that when the PP interval becomes excessively long, the pulse generator functions in VVI mode.
Advantages of the VDD mode are preserved atrial contribution to ventricular filling and ventricular rate that follows the patient's own atrial rate, thereby responding appropriately to stress and exercise. Disadvantages are need for both atrial and ventricular electrodes and the possibility of producing a reciprocating (loop) tachycardia by retrograde conduction.
DVI
Both atrium and ventricle (D) are paced in DVI mode, with an appropriate interval between the stimuli to each. Ventricular (V) but not atrial depolarization is sensed. A sensed ventricular depolarization inhibits (I) the next dual pacing stimulus in noncommitted DVI mode; it does not do so in committed DVI mode.
The advantage is maintaining atrial contribution to ventricular filling even when sinus node function fails. Raza and colleagues, Raichlen and colleagues, and others have documented the hemodynamic advantages of this arrangement. The disadvantage is that AV synchronization is lost when the atrial rate increases during exercise or stress.
DDD
DDD mode, or universal pacing mode, can pace both atrium and ventricle (D), sense both atrial and ventricular depolarization (D), and either trigger or inhibit (D) an electrical pacing pulse. Its advantage is universality of application. Disadvantages are that dual stimulation reduces battery lifetime, and loop tachycardia can occur with variations in retrograde conduction from ventricles to atria. These disadvantages can be eliminated or reduced by programming the pacemaker pulse generator characteristics according to changes in the patient's AV and ventriculoatrial conduction characteristics.
Electrode Testing
Each electrode placed is tested at the time of insertion. The pacing threshold , or the lowest delivered voltage at which myocardial depolarization occurs, is tested first. For ventricular electrodes, a threshold of 0.3 V or less (usually at 0.5-ms pulse duration) is optimal. A threshold of 0.3 to 0.5 V is frequently observed, and a threshold as high as 1.0 V is acceptable. Higher thresholds are undesirable because they reduce pulse generator life. For atrial electrodes, a stimulating threshold of 1.0 V or less is acceptable. In open chest insertion, use of the electrocautery tends to increase the stimulating threshold.
The electrode is then tested for its sensing capabilities . For both endocardial and epicardial ventricular electrodes, a QRS complex in the electrogram of 5 mV or more is desirable. For atrial electrodes, a P wave with peak-to-peak amplitude of 2 mV or more is acceptable.
Other important testing for a transvenously placed electrode includes determining that (1) it does not provoke ventricular tachycardia by its position, (2) its position is mechanically stable, and (3) it does not pace the diaphragm or skeletal muscle. Bipolar electrodes are generally used; they are less subject to interference by skeletal muscle contraction than unipolar electrodes. The latter are sometimes used when the pulse generator surface serves as the indifferent electrode.
Transvenous Electrode Insertion and Pulse Generator Placement
After the patient is positioned on the operating table, temporary pacing wires, if present, are secured with their tips outside the operative field and attached to an external pulse generator. The operative field is prepared and draped, including the lower neck and anterior chest wall. Wires are passed from the surgical field for emergency pacing, obtaining endocardial electrograms, pulse generator testing, and lead threshold measurement. An adjustable constant-current, dual-channel, external pulse generator is used to determine atrial capture when simultaneous atrial and ventricular pacing are necessary.
Local anesthesia is administered to achieve a field block. An oblique or transverse incision is made below the clavicle, generally on the left side (on the right for left-handed individuals). A subcutaneous pocket is created over the pectoralis major fascia. The pocket should be appropriate for size of the pulse generator. If no permanent pacing electrodes are in place, electrocautery may be used for the dissection and to achieve hemostasis.
Edges of the incision are retracted to expose the space between first rib and clavicle for access to the subclavian vein. A needle with a syringe attached is used to locate and penetrate the vein. A flexible J-tip guidewire is passed through the needle into the subclavian vein and advanced into the superior vena cava. Position of the guidewire is confirmed by fluoroscopy, and the needle is withdrawn and replaced with a peel-away sheath catheter. The distal 5 cm of the stylet for the ventricular electrode is bent into a small curve and inserted into the electrode. The electrode and stylet are placed into the sheath catheter and advanced into the right atrium, after which the sheath catheter is peeled away and removed. Under fluoroscopic control, the electrode is advanced through the tricuspid valve into the right ventricle and further advanced into the pulmonary trunk to ensure that the coronary sinus has not been entered. The curved stylet is replaced with a straight one that is not fully inserted, leaving the electrode flexible in its distal 5 to 10 cm. The electrode is withdrawn along the ventricular septum until an appropriate anatomic position has been found among the trabeculations near the ventricular apex. The stylet is advanced to the tip of the electrode to stiffen the electrode. It is advanced gently among the trabeculations and “seated.” It is secured passively by the tines on the electrode or by extruding its attachment coil. The stylet is removed.
The electrode is then tested (see “ Electrode Testing ” earlier in this section). Testing with deep breathing is done to judge and set the final length of catheter within the ventricle when the diaphragm is in its most inferior position. Once a suitable anatomic and functional position has been located, the lead is secured with a small plastic sleeve to the pectoral fascia to prevent inadvertent displacement.
Placing the atrial electrode, if one is to be used, is done after inserting the ventricular electrode. Penetrating the subclavian vein for inserting the atrial electrode is preferentially performed at the beginning of the procedure. After the guidewire for the ventricular electrode is inserted, a second guidewire is inserted into the subclavian vein. Separate penetration of the subclavian vein is desirable to prevent dislodging the ventricular electrode while manipulating the atrial electrode. Alternatively, the guidewire used for ventricular electrode insertion may be withdrawn and used subsequently for atrial electrode insertion. Bleeding from the subclavian vein puncture site, however, may be a problem.
A second peel-away sheath catheter is inserted into the subclavian vein over the guidewire and the atrial electrode inserted through it over the guidewire. The electrode is advanced into the right atrium with stylet in place. The stylet is withdrawn, permitting the pre-formed J-curve to appear in the electrode. Manipulation of the stylet and gentle rotation of the electrode permit positioning of its tip into the atrial appendage. This position is verified by the lateral to-and-fro motion of the tip and may be confirmed by lateral fluoroscopy. The electrode tip is secured to atrial endocardium by extruding the screw-in coil. The electrode is then tested (see “ Electrode Testing ” earlier in this section). After a satisfactory position is achieved, the electrode is secured to the pectoralis fascia by a suture.
The appropriate pulse generator is selected, inspected, and checked by the pacemaker system analyzer. The ends of the pacing leads are cleaned to remove blood or tissue and are inserted into the pulse generator. Satisfactory function of the pacing system is verified by ECG before wound closure. The wound is inspected for hemostasis and irrigated with antibiotic solution. The pacing system is cleaned with antibiotic solution, placed in the pocket, and secured with nonabsorbable sutures. The pacing leads are kept away from the anterior surface of the pulse generator to prevent injury during subsequent pulse generator replacement. The wound is closed in layers, with the first layer isolating the pulse generator pocket from the remainder of the incision.
Electrode Insertion by Thoracotomy and Pulse Generator Placement
When an open technique is necessary, the patient is positioned on the operating table for a sternotomy, left anterior thoracotomy, or epigastric incision. For single-chamber (ventricular pacing) insertion, anterior thoracotomy or epigastric incisions are adequate. When dual-chamber pacing is contemplated or when pacing is required early after a cardiac operation, a median sternotomy is used. Procedures regarding temporary pacing wires, skin preparation, and draping are the same as for the transvenous approach.
In adults, a separate transverse left upper quadrant abdominal or infraclavicular incision is made and a pocket developed in the prefascial space. In infants and usually in children, the pocket is created behind the rectus abdominis muscle. A site for electrode attachment to the right or left ventricle is identified in a region of myocardium uncovered by fat, away from any coronary arteries and from the phrenic nerve, and if possible, not directly under the sternum. If there is uncertainty about the site, an electrode probe can be used to locate an appropriate site for placing the electrode. Screw-in electrodes are commonly used for ventricular pacing because of ease of insertion. They are secured by clockwise rotation of the corkscrew electrode with gentle pressure on the myocardium. Electrodes that lie on the epicardial surface, held in place with fine sutures, are preferable for atrial pacing even though they are more difficult to insert. If space permits, two electrodes are placed in each location. The electrodes are tested as previously described.
A tunnel is created from the pericardial cavity to the previously formed subcutaneous pocket. An appropriate pulse generator is selected, tested, and connected to the electrodes.
Wounds are closed in layers, and one chest tube is left for closed drainage.
Permanent Pacing after Intracardiac Surgery
Complete heart block occurring during cardiac operation is managed by placing temporary pacing electrodes on the right ventricle and right atrium so that AV sequential pacing can be performed using an external pulse generator. The pacing threshold of the temporary electrodes should be tested daily. When it appears that complete heart block or profound bradycardia is likely to be permanent, an implantable pacing system is inserted by the transvenous or open route.
The notable exception to this strategy is when there is a high probability of complete heart block developing at operation or when heart block may develop later and access to the right ventricle by the transvenous route is not possible. This includes patients who have replacement of the tricuspid valve with a mechanical prosthesis. These patients should have permanent epicardial electrodes placed at the time of the cardiac operation. Bioprosthetic valves in the tricuspid position may be crossed by a transvenous electrode without important impairment of prosthetic valve function.
Before discontinuing cardiopulmonary bypass (CPB), cardiac action is established by AV sequential pacing through two temporary right atrial and two temporary ventricular wires attached to an external pulse generator. Single bipolar temporary wires may also be used. Preferably, permanent ventricular electrodes are placed after discontinuing CPB and completing hemostasis, because electrocautery tends to increase the pacing threshold of already implanted leads. Permanent atrial electrodes should also be placed if dual chamber pacing is desired. The ends of the permanent leads are capped and placed subcutaneously in the left upper quadrant of the abdomen or brought through the anterior chest wall to a subcutaneous position below the left clavicle. A loop of lead is left within the pericardial cavity.
If heart block persists, the patient is returned to the operating room. With the patient under local anesthesia and conscious sedation, the surgical field is prepared. A transverse incision is made over the left upper quadrant of the abdomen (or below the clavicle), and the electrode ends are retrieved. The electrodes are tested and attached to the pulse generator, a pocket is created for it, and the incision is closed. The temporary wires are withdrawn.
Alternatively, the pulse generator can be attached to the electrodes and implanted at the time of cardiac repair. The disadvantage is that sinus rhythm may return in a few days, and the pulse generator may no longer be essential. There is also risk of bleeding into the pulse generator pocket, with formation of a hematoma.
Special Features of Postoperative Care
Usual care for cardiac surgical patients is given early postoperatively (see Chapter 5 ). In addition, a chest radiograph is obtained to ascertain position of the leads. Pacing threshold is usually not determined by noninvasive testing prior to hospital discharge, because thresholds obtained at this time are always higher than those obtained 6 weeks to 3 months later. Reprogramming of the pulse generator at an appropriate voltage is best done later, leaving the relatively higher and safer pacing voltage until that time.
The electrodes are considered to have become stable by about 6 months after implantation. Around that time they are rechecked, and the pulse generator is set at the lowest output considered to be safe.
Results
Survival
It is generally agreed that survival of patients with bradycardia is improved by permanent pacing. Death early after pacemaker insertion is unusual, and when it occurs it is usually due to coexisting cardiac problems. This is true for children as well as adults. Ten-day mortality is 1.6%, and 30-day mortality is 2.7% ( Fig. 16-1 ).
Survival late after pacemaker insertion is satisfactory, with 5- and 10-year survival of 59% and 39%, respectively (see Fig. 16-1 ). Survival is similar in those whose bradycardia is from heart block and those in whom it is related to sinus node dysfunction. Advanced age decreases late survival ( Table 16-1 ), as does chronic heart failure and presence of ischemic heart disease.
Table 16-1
Survival by Patient Age after Pacemaker Implantation
Data from 1068 patients at UAB, 1961-1984, and Shepard RB: personal communication; 1985.
| Age | ||
|---|---|---|
| ≤Years | < | 5-Year Survival |
| 40 | 50 | 83 |
| 50 | 60 | 66 |
| 60 | 70 | 67 |
| 70 | 80 | 62 |
| 80 | 90 | 51 |
Infection and Pulse Generator Erosion
Infection and pulse generator erosion are not always identified separately as complications of pacemaking, and they must therefore be considered together.
Even with meticulous surgical technique and prophylactic antibiotic therapy, infection in the wound and around the pulse generator and leads occurs in 0.5% to 2% of cases. Treatment consists of inserting an entirely new pacemaker system at a different site and complete removal of the old system.
Excessive pressure of the pulse generator or wire against the overlying skin or subcutaneous tissue can cause necrosis and permit their exposure. The true prevalence of this condition is unknown because it is often considered infection. Insertion of pulse generators in small pockets with skin closure under tension increases the chance of skin necrosis. When the pulse generator and leads become exposed as a result of pressure necrosis, treatment is the same as for an infected pacemaker. Preventing this problem is best achieved by forming the pulse generator pocket in the immediate prefascial space to permit as much tissue as possible to come between pulse generator and skin.
Lead and Electrode Malfunction
Time-Related Variability of Pacing Thresholds
The lowest possible initial pacing and sensing thresholds are sought at the time of placing the electrodes, because thresholds frequently rise later. One or more months after insertion, more than half the leads have a threshold pacing level greater than any level measured initially or during the first month of use. Forty-five percent of epicardial electrode leads have either a grossly unstable threshold pacing level or a gradually increasing level ( Fig. 16-2 ) for as long as 10 years after insertion ( Fig. 16-3 ). These “spikes” in the threshold pacing level may be associated with episodes of intercurrent infection. Such changes probably account for at least some of the sudden deaths that occur late after initiating pacing for complete heart block after repair of congenital heart disease.
Undersensing
Undersensing, or lack of recognization of the heart's depolarization, is related most commonly to inadequate placement of the electrode. At times it can result from fibrosis at the electrode-myocardial junction. This complication leads to competitive pacing. Undersensing can generally be treated by noninvasive programming to increase sensitivity of the pulse generator.
Electrode Dislodgment
Electrode dislodgment, with or without right ventricular or atrial perforation, is the most common complication of inserting either ventricular or atrial endocardial leads. Dislodgment occurs in less than 2% of cases.
Lead Fracture
Lead fracture, with consequent loss of pacing, is an infrequent early complication of pacemaking but is not uncommon years after implantation.
New Symptoms from Pacing in VVI Mode
Syncope or near-syncope is one of the most important symptoms resulting from pacing. Syncope as a manifestation of pacemaker syndrome occurs in less than 10% of patients being paced in VVI mode. Arterial hypotension may also develop. These symptoms usually occur when ventriculoatrial conduction is intact and the indication for pacing has been sinus node dysfunction. The exact etiology of symptoms is uncertain, but they may be due to lack of atrial contribution to ventricular filling secondary to AV asynchrony, with or without atrial contraction against a closed AV valve. Also, AV valve regurgitation may be caused by asynchronous contraction of atria and ventricles. Diagnosis is suspected when those symptoms and signs are present and can sometimes be verified by an increase in blood pressure when pacing is stopped and a decrease when it is restarted. Treatment is VDD or DDD pacing.
Dizziness occurs in about one third of patients. Because both dizziness and syncope are common in elderly patients, these symptoms may not be the result of pacing per se. Palpitations are noted by about one third of patients, sometimes due to awareness of ventricular pacing. They are noted frequently at night when sinus slowing in patients with VVI units results in pacemaker activation. They may be eliminated by AAI or DDD pacing or minimized by programming hysteresis into a VVI system.
Indications for Intervention
The most common indication for permanent cardiac pacing is symptomatic bradycardia. It may be intermittent or permanent and due to complete heart block, second-degree AV block, or sinus node dysfunction. Symptoms must be directly attributable to the bradycardia and may include syncope, dizziness, exercise intolerance, and heart failure. When ambulatory ECG monitoring is negative for abnormal bradycardia, electrophysiologic study is indicated in patients with unexplained transient neurologic symptoms. The finding of prolongation of the HV interval (time from onset of activation of the bundle of His to the earliest onset of ventricular depolarization) of at least 70 milliseconds supports a diagnosis of paroxysmal AV block as the cause of the symptoms and justifies elective pacemaker implantation. In the absence of neurologic symptoms, however, the finding of such HV prolongation rarely if ever warrants prophylactic pacemaker implantation.
Another indication is surgically induced complete heart block, because of the risk of an Adams-Stokes episode. Patients in sinus rhythm after repair of congenital malformations, but in whom complete heart block follows repair and persists for a number of days before reversion to sinus rhythm, are at increased risk for developing late symptomatic heart block. These patients should be considered for prophylactic pacemaker implantation before hospital discharge, particularly when subsidiary escape pacemakers have been absent or unreliable.
In some situations, permanent pacing may be indicated in asymptomatic patients because of risk of an Adams-Stokes episode. These situations include profound bradycardia (ventricular rate < 40 beats · min −1 ) , second-degree AV block at the infra-His level, advanced second-degree AV or complete heart block after myocardial infarction, and congenital heart block with a wide QRS escape rhythm. Other rhythms may be an indication for pacing in asymptomatic patients. These include new bundle-branch block with transient second-degree AV block postmyocardial infarction, bifascicular bundle-branch block with intermittent type II second-degree AV block, sinus node dysfunction, and transient postsurgical AV block that reverts to bifascicular block in children. In sinus node dysfunction, for example, when symptoms are relatively infrequent, the decision to advise permanent pacing may rest on the demonstration of asymptomatic sinus pauses, sinoatrial exit block, or both.
A special situation is extensive intraatrial operations such as the Senning or Mustard operation (see “Senning Technique” and “Mustard Technique” under Technique of Operation in Chapter 52 ) or the Fontan operation (see Chapter 41 ). Junctional rhythm often develops late postoperatively with the potential of tachybradycardia and sudden death. This situation is an indication for atrial pacing (AAI).
In response to publication of studies advancing the knowledge of the natural history of cardiac arrhythmia optimally treated by cardiac pacing and important advances in pacing device technology, the American College of Cardiology (ACC), the American Heart Association (AHA), the North American Society for Pacing and Electrophysiology (NASPE), and the Heart Rhythm Society (HRS) appointed a committee of physicians to develop guidelines for implanting cardiac pacemakers and arrhythmia devices. The most recent version of the guidelines appeared in 2008. This comprehensive document is the definitive statement on indications for cardiac pacing. A summary of these indications for commonly occurring conditions is shown in Boxes 16-1 through 16-3 . As new information accumulates, other indications for cardiac pacing are being identified ( Box 16-4 ).
Box 16-1
Modified from Epstein and colleagues.
Indications for Permanent Pacemaker Insertion Based on ACC/AHA/HRS Guidelines
Acquired Atrioventricular Block in Adults
Class I a
a Class I = conditions for which there is evidence and/or general agreement that treatment is beneficial, useful, and effective. Class II = conditions for which there is conflicting evidence and/or divergence of opinion about benefit, usefulness, or efficacy or treatment (a = weight of evidence favors, b = usefulness less well established). Class III = conditions for which the procedure is not useful and/or effective or is harmful.
- 1
Third-degree and advanced second-degree atrioventricular (AV) block at any anatomic level associated with:
- a
Bradycardia with symptoms or ventricular arrhythmias presumed to be due to AV block
- b
Arrhythmias and other medical conditions requiring drug therapy that result in symptomatic bradycardia
- c
No symptoms, but with documented periods of asystole ≥ 3 seconds or any escape rhythm < 40 beats · min −1 or with an escape rhythm below the AV node
- d
No symptoms but with atrial fibrillation and bradycardia with 1 or more pauses of at least 5 seconds
- e
Catheter ablation of the AV junction
- f
Postoperative AV block that is not expected to resolve after cardiac surgery
- g
Neuromuscular diseases with AV block (myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy, peroneal muscular dystrophy)
- h
Exercise in the absence of myocardial ischemia
- a
- 2
Second-degree AV block with associated symptomatic bradycardia
- 3
Asymptomatic persistent third-degree AV block with average awake ventricular rates of 40 beats · min −1 or faster if cardiomegaly or left ventricular dysfunction is present, or if site of block is below the AV node
Class IIa
- 1
Third-degree AV block with escape rate ≥ 40 beats · min −1 in asymptomatic patients without cardiomegaly
- 2
Asymptomatic second-degree AV block at intra- or infra-His levels at electrophysiologic study
- 3
First- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise
- 4
Asymptomatic type II second-degree AV block with narrow QRS
Class IIb
- 1
May be considered for neuromuscular diseases (see above) with any degree of AV block with or without symptoms
Class III (Pacemaker Not Indicated)
- 1
Asymptomatic first-degree AV block
- 2
Asymptomatic type I second-degree AV block at the supra-His (AV node) level or that level not known to be intra- or infra-Hisian
- 3
AV block that is expected to resolve and unlikely to recur
Key: ACC, American College of Cardiology; AHA, American Heart Association; HRS, Heart Rhythm Society.
Box 16-2
Modified from Epstein and colleagues.
Indications for Permanent Pacemaker Insertion Based on ACC/AHA/HRS Guidelines
Chronic Bifascicular Block a
a Bifascicular block refers to electrocardiographic evidence of impaired conduction below the AV node in two or three fascicles of the right and left bundles; it is commonly associated with syncope and precedes third-degree AV block associated with increased incidence of sudden death.
Class I b
b Class I = Conditions for which there is evidence and/or general agreement that treatment is beneficial, useful, and effective. Class II = Conditions for which there is conflicting evidence and/or divergence of opinion about benefit, usefulness, and/or efficacy of treatment; a = weight of evidence favors. Class III = Conditions for which the procedure is not useful and/or effective or is harmful.
- 1
Advanced second-degree atrioventricular (AV) block or intermittent third-degree AV block
- 2
Type II second-degree AV block
- 3
Alternating bundle-branch block (Level of evidence: C)
Class IIa
- 1
Reasonable for syncope not demonstrated to be due to AV block when other likely causes have been excluded, specifically ventricular tachycardia
- 2
Reasonable for an incidental finding at electrophysiologic study of a markedly prolonged HV interval (≥100 ms) in asymptomatic patients
- 3
Reasonable for an incidental finding at electrophysiologic study of pacing-induced infra-His block that is not physiologic
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