A Practical Approach to Cardiac Anesthesia (Practical Approach Series) 5th Ed.

17 Arrhythmia, Rhythm Management Devices, and Catheter and Surgical Ablation

Soraya M. Samii and Jerry C. Luck, Jr.

KEY POINTS

 1. Patients with moderate to severe left ventricular dysfunction are at a higher risk for sustained monomorphic VT than those with preserved left ventricular function.

 2. VT more commonly causes syncope and when it is associated with structural heart disease it is also associated with a high risk of sudden cardiac death.

 3. Symptomatic patients with SND or evidence of conduction disease such as second- or third-degree AV block almost always need a permanent pacemaker preoperatively.

 4. For VT, IV amiodarone is the initial drug of choice, but lidocaine is also considered especially if there is concern for ongoing ischemia. For torsades de pointes, management includes eliminating offending drugs in the setting of the long QT syndromes. Correcting electrolyte deficiencies with IV magnesium and potassium are particularly helpful in correcting the prolonged QT interval, as possibly stopping medications contributing to bradycardia. Amiodarone in the setting of torsades de pointes can prolong the QT interval and make the problem worse.

 5. Bifascicular block with periodic third-degree AV block and syncope is associated with an increased incidence of sudden death. Prophylactic permanent pacing is indicated in this circumstance.

 6. The requirement for temporary pacing with acute MI by itself does not constitute an indication for permanent pacing.

 7. Sensor-driven tachycardia may occur with adaptive-rate devices that sense vibration, impedance changes, or the QT interval if they sense mechanical or physiologic interference, which leads to inappropriate high-rate pacing. Thus, it is advised that ARP be disabled in perioperative settings.

 8. Because of the unpredictable interaction between the MRI and CIEDs, MRIs are generally contraindicated in individuals with CIEDs. There is now an approved compatible pacemaker generator and lead system for individuals likely to need MRI.

 9. Most contemporary pacemaker devices respond to magnet application by a device-specific single- or dual-chamber asynchronous pacing mode. Adaptive-rate response is generally suspended with magnet mode as well. With asynchronous pacing, the pacemaker will no longer be inhibited by sensed activity and instead pace at a fixed rate regardless of underlying rhythm.

10. Some manufacturers, Biotronik, St. Jude Medical, and Boston Scientific devices, have a programmable magnet mode that may make response to magnet application different than anticipated. Although rarely used, this feature may be programmed to save patient-activated rhythm recordings with magnet application rather than revert the pacemaker to asynchronous pacing.

11. EMI signals between 5 and 100 Hz are not filtered, because these overlap the frequency range of intracardiac signals. Therefore, EMI in this frequency range may be interpreted as intracardiac signals, giving rise to abnormal behavior. Possible responses include (i) inappropriate inhibition or triggering of stimulation, (ii) asynchronous pacing (Fig. 17.5), (iii) mode resetting, (iv) direct damage to the pulse generator circuitry, and (v) triggering of unnecessary ICD shocks.

12. Treatment options for VT include antitachycardia pacing, cardioversion, or defibrillation. Up to 90% of monomorphic VTs can be terminated by a critical pacing sequence, reducing the need for painful shocks and conserving battery life. With antitachycardia pacing, trains of stimuli are delivered at a fixed percentage of the VT cycle length.

13. Acute MI, severe acute acid–base or electrolyte imbalance, or hypoxia may increase defibrillation thresholds, leading to ineffective shocks. Any of these also could affect the rate or morphology of VT and the ability to diagnose VT.

14. Response of an ICD to magnet application [8]. Magnet application does not interfere with bradycardia pacing and does not trigger asynchronous pacing in an ICD. Magnet application in contemporary ICDs causes inhibition of tachycardia sensing and delivery of shock only. All current ICDs remain inhibited as long as the magnet remains in stable contact with the ICD. Once the magnet is removed, the ICD reverts to the programmed tachyarrhythmia settings.

15. Baseline information about the surgery is needed by the CIED team (cardiologist, electrophysiologist, and pacemaker clinic staff managing the device) such as (i) type and location of the procedure, (ii) body position at surgery, (iii) electrosurgery needed and site of use, (iv) potential need for DC cardioversion or defibrillation, and (v) other EMI sources.

16. For pacemaker-dependent patients: These patients are at particular risk of asystole in the presence of EMI. If EMI is likely (e.g., unipolar cautery in the vicinity of the pulse generator or leads and surgery above the umbilicus), then the device should be programmed to an asynchronous mode. In the case of pacemakers, this can be done with magnet application in most situations, which will also inactivate the rate-responsive pacing.

17. In cases where the pacemaker-dependent patient has an ICD or the location of surgery precludes placement of a magnet, consideration of programming the device to asynchronous mode with the proprietary programmer is recommended. The other alternative if reprogramming is not an option is to limit the EMI to short bursts while watching the response of pacing and minimize episodes of asystole. For patients with adaptive-rate pacemakers (including some ICDs), this capability should be programmed off if EMI causes inappropriate rate response.

18. Use of a magnet eliminates the complexity of reprogramming the CIED in the operating room. The magnet can be easily removed when competing rhythms develop with asynchronous pacing.

19. In a situation with an ICD and no device information, a magnet should not be placed over the ICD pulse generator unless EMI is unavoidable. If EMI is unavoidable, then the patient needs to be placed on cardiac monitor and a magnet will need to be placed on (and kept on) the ICD generator during cautery or RF therapy.

ANY DISTURBANCE OF RHYTHM OR conduction, or arrhythmia that destabilizes hemodynamics perioperatively will need to be addressed. Treatment with antiarrhythmic agents has been the standard approach to manage symptomatic arrhythmias acutely. More recently, electrical therapies have gained wider acceptance in rhythm management. They presently play a premiere role in patients undergoing cardiac surgery and greatly impact a growing number of noncardiac surgery cases. The emphasis in this chapter is on perioperative management of patients with implanted devices. Concepts of arrhythmogenesis, antiarrhythmic action, and drug selection are discussed only briefly. The reader is referred to Chapter 2 for discussion of specific antiarrhythmic drugs and their pharmacology and to Chapter 1 for a discussion of arrhythmogenesis.

I. Concepts of arrhythmogenesis

   A. Basic electrophysiology

     1. Action potential (AP). A ventricular muscle cell’s AP has five phases caused by changes in the cell membrane’s permeability to sodium, potassium, and calcium (Fig. 17.1). Phase 0 represents depolarization and is characterized by a rapid upstroke as sodium rapidly enters the cell. There is a rapid drop in the cell’s impedance from a resting state at 80 to 85 mV. Phase 1 is an early rapid repolarization period caused by potassium egress from the cell. Phase 2 is a plateau phase representing a slow recovery phase: The slow inward calcium current is counterbalanced by outward potassium current. Phase 3 is a rapid repolarization phase as a result of accelerated potassium efflux. The diastolic interval between APs is termed Phase 4 and is a cell’s resting membrane state in atrial and ventricular muscle.

Figure 17.1 Action potential (AP) and resting membrane potential (RMP) of a quiescent Purkinje fiber. Extracellular and intracellular ion concentrations during Phase 4, and the active and passive ion exchangers that restore intracellular ion concentrations during Phase 4 are shown to the right of the AP. Inward depolarizing and outward repolarizing currents are shown below the AP. The adenosine triphosphate (ATP)-dependent Na/K pump maintains steep outwardly and inwardly directed gradients (arrows) for K+ and Na+, respectively, and generates small net outward current. The passive Na/Ca exchanger generates small net inward current. A small, inward “leak” of Na+ keeps the RMP slightly positive to the K equilibrium potential (96 mV). AP Phase 0 is the upstroke, Phase 1 is initial rapid repolarization, Phase 2 is the plateau, and Phase 3 is final repolarization. The cell is unresponsive to propagating AP or external stimuli during the absolute refractory period. A small electrotonic potential (A) occurs in response to a propagating AP or external stimulus during the relative refractory period (RRP). It is incapable of self-propagation. A normal AP is generated at the end of the RRP (B), when the Na channels have fully recovered from inactivation. It is capable of propagation. Note that threshold potential (TP) for excitation is more positive during the RRP.

     2. Ion channels. Electrical activation of cardiac cells is the result of membrane currents crossing the hydrophobic lipid membranes through their specific protein channel. Opening and closing of gates in these channels are determined by the membrane potential (voltage dependence) and by the time elapsed after changes in potential (time dependence). Membrane channels cycle through the “activated,” “inactivated,” and “recovery” stages with each AP. Inward currents of sodium and calcium ions enter the cell using this gating mechanism. On the surface electrocardiogram (ECG), rapid-acting sodium currents contribute to the “P” and the “QRS” complexes. Depolarization of the sinoatrial (SA) node and the atrioventricular (AV) node, in contrast, occurs as a result of the slower-opening calcium-dependent channels. The slowly conducting calcium channel in the AV node creates the delay in the node and is responsible for nearly two-thirds of the PR interval during normal conduction. A group of potassium channels are responsible for repolarization and the “T” wave on the electrocardiogram (ECG).

          Cardiac arrhythmias occur when abnormal channel proteins are substituted for the normal protein and the ion channel is altered. For example, QT prolongation may be inherited as a result of encoding an altered gene or it may be acquired as a consequence of an antiarrhythmic agent inhibiting a specific ion channel [1].

     3. Excitability. Reducing the cell’s transmembrane potential to a critical level will initiate a propagated response and this level is termed the threshold potential. There are two mechanisms by which a propagated AP is developed: (i) a natural electrical stimulus and (ii) an applied electrical current. For an applied stimulus, threshold of a tissue is defined as the minimum amount of energy that will elicit a response. When external electrodes are used, only that part of the stimulus which penetrates the cell membrane contributes to excitation. The size of the stimulating electrode is critical to threshold. Reducing the size of the stimulating electrode (from 3 mm to 0.5 mm) will increase the current density over a smaller area and decrease the amount of energy needed to achieve threshold. It is common practice in pacing to use a small stimulating electrode and a larger indifferent electrode to reduce threshold and facilitate excitation.

     4. Conduction. There are regions of cells with specialized conduction characteristics within the heart that propagate conduction in a preferential direction, spreading to adjacent areas faster though the preferential sites. This allows for a more organized direction of conduction so that, for example, both atria are depolarized prior to the stimulus reaching the AV node to depolarize the ventricles. In the sinus and AV nodes, L- and T-type calcium channels are the source of the propagated current [2]. In the Purkinje fiber the sodium channel is the source of the conducted current. Conduction velocity is much slower at about 0.2 m/s in the node versus 2 m/s in the Purkinje cells. These different characteristics explain the effects of certain antiarrhythmic medications. For instance, blocking the sodium channel with a Class I antiarrhythmic agent will preferentially reduce the conduction velocity in the Purkinje cells compared to the AV node because of this agent’s primary effect on sodium channels.

   B. Mechanism of arrhythmia (Table 17.1)

Table 17.1 Confirmed or postulated electrophysiologic mechanisms for clinical arrhythmias

     1. Automaticity. Automaticity is a unique property of an excitable cell allowing spontaneous depolarization and initiation of electrical impulse in the absence of external electrical stimulation. The SA node serves as the primary automatic pacemaker for the heart. Subsidiary pacemakers exhibiting automaticity are also found along the crista terminalis, the coronary sinus ostium, within the AV junction and in the ventricular His–Purkinje system. They may assume control of the heart if the SA node falters. Automaticity is either normal or abnormal. Alterations in automaticity due to changes in the ionic currents normally involved in impulse initiation are considered normal. Examples of normal automaticity include sinus tachycardia and junctional tachycardia during catecholamine states that increase current through the T-type calcium channels in the nodal cells. Abnormal automaticity occurs when ionic currents not normally involved in impulse initiation cause spontaneous depolarizations in atrial and ventricular muscle cells that normally do not have pacemaker activity. An example of abnormal automaticity occurs during ischemic injury causing muscle cells to shift their maximum diastolic potential to a more positive resting level and thus facilitate spontaneous depolarization [3].

     2. Triggered activity. Triggered activity is the result of abnormal oscillations in membrane potential reaching the threshold to induce another AP following a normal AP depolarization. These after depolarizations can occur before full repolarization has occurred, known as early after depolarizations (EADs), or late after repolarization has occurred, known as delayed after depolarization (DAD). Oscillations of either type of after depolarizations that exceed the threshold potential may trigger an abnormal tachycardia.

          EADs occur most frequently with delays in repolarization and prolongation of the QT interval. Acquired and congenital QT prolongation syndromes are predisposed to EADs and can result in torsades de pointes sometimes known as polymorphic ventricular tachycardia (VT) and sudden death. The torsades de pointes, triggered in prolonged QT syndromes, is facilitated by bradycardia and adrenaline. Examples of inherited predisposition to triggered initiation include defects in genes encoding Na and K ion channels that produce a net reduction in outward positive current during repolarization resulting in prolongation of the QT interval. Acquired prolongation of the QT interval from hypokalemia, pharmacologic agents including class IA and III antiarrhythmics, antibiotics such as erythromycin and antifungal agents, antihistamines, and the phenothiazine piperidine class can cause EADs.

          Delayed after depolarization potentials cause arrhythmias related to calcium overload. Digoxin toxicity is the most common agent causing DAD, and triggered activity is the common mechanism for digitalis-induced accelerated junctional rhythm and bidirectional VT. Catecholamines facilitate calcium loading and the development of DADs.

     3. Re-entry. For either anatomical or functional re-entrant excitation to occur, the electrical wave front must circle around a core of inexcitable tissue at a rate that preserves an excitable gap. For initiation, there must be (i) an area of unidirectional conduction block, (ii) two conduction pathways that are connected at each end, and (iii) an area of slow conduction. Anatomical re-entrant circuits are common to several supraventricular tachycardias (SVTs) including Wolff–Parkinson–White syndrome, with an accessory AV pathway, and typical and atypical AV nodal re-entrant tachycardia. Classic atrial flutter has an anatomical right atrial loop classically involving the area of slow conduction known as the cavotricuspid isthmus. Pathologic sustained monomorphic VT is commonly due to anatomic re-entry from and is frequently associated with scarring from a prior myocardial infarction or fibrosis associated with dilated nonischemic cardiomyopathy.

          A functional re-entrant loop involves a small circuit around an area of tissue with an inexcitable core. Functional re-entry may occur with some forms of atrial tachycardia and is a mechanism for the multiple wavelet theory of atrial fibrillation.

   C. Anatomical substrates and triggers

     1. Supraventricular. The highly complex atria have a heterogeneous branching network of subendocardial muscle bundles that create functional areas of block as well as preferential planes of excitation. Longitudinal connected myocardial fibers conduct faster than fibers connected along transverse or parallel lines (so-called anisotropic conduction). In the right atrium, the crista terminalis and Eustachian ridge tend to act as anatomical barriers that help to facilitate a single re-entrant loop during atrial flutter. An area of slow conduction can usually be found in the isthmus of atrial tissue between the tricuspid annulus and the inferior vena cava. This is a frequent anatomical area for ablation of both clockwise and counterclockwise atrial flutter. The ostia of the pulmonary veins are frequently the sites of the initiation of atrial fibrillation. This chaotic atrial rhythm can be triggered by a single focus frequently localized to a pulmonary vein. Once initiated by a premature depolarization, the multiple wavelets are facilitated by the complex nature of the atria.

     2. Ventricular. Myocardial ischemia and infarction can create both acute and chronic substrates for VT and fibrillation. As discussed above, scar from previous infarction can create an anatomic re-entrant circuit providing the substrate for re-entrant VT. In the acute events such as acute coronary occlusion, metabolic derangements occur including local hyperkalemia, hypoxia, acidosis and an increase in adrenergic tone increasing the likelihood for automaticity, triggered activity, and functional re-entry. With acute coronary occlusion, ventricular fibrillation (VF) is common and is directly related to an increase in sympathetic tone. Accelerated idiopathic ventricular rhythm is frequently seen with acute myocardial infarction and is attributed to abnormal automaticity. In the chronic phase, the infarct becomes mottled and over several weeks islands of viable muscle cells are surrounded by electrically inert barriers of scar tissue. Slow conduction is present and allows for unidirectional block. These factors are conducive to re-entry which is the mechanism for sustained monomorphic VT in about 6% to 8% of survivors of myocardial infarction. Myocardial remodeling as a consequence of infarction provides a classic substrate for arrhythmias. Patients with moderate to severe left ventricular dysfunction are at a higher risk for sustained monomorphic VT than those with preserved left ventricular function.

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   D. Neural control of arrhythmias

     1. b-Adrenergic modulation. Increased sympathetic tone increases the susceptibility to VF in the early stage of myocardial infarction. In the chronic phase it facilitates initiation of sustained monomorphic VT. β-Adrenergic blocking drugs, propranolol, metoprolol, and nadolol significantly reduce the incidence of VF during acute infarction and reduce the risk of sudden death later. Also, β-blockers do not prevent reperfusion arrhythmias.

     2. Parasympathetic activation. During acute infarction, vagal activation exerts a protective effect against VF. Bradycardia appears necessary for this protective effect. Increasing heart rate by pacing will negate this protective effect. Vagal stimulation does little to protect against reperfusion arrhythmias.

   E. Clinical approach to arrhythmias

     1. Syncope is defined as the loss of consciousness and muscle tone with spontaneous resolution. It may occur in up to 40% of the general population. The most common is vasovagal or neurally mediated syncope which is quite common in the young. This type of syncope is not associated with increased risk of death. Syncope occurs at an annual rate of 6% in patients 75 yrs old or older, but in only 0.7% of those below age 45. The goal is to determine if syncope is of the benign vasovagal variety or of the more dangerous cardiac type [4]. The 1-yr mortality from syncope of a cardiac cause can range from 18% to 33% while the noncardiac group has 0% to 6% mortality. Patients with vasovagal mediated syncope do not die from syncope. The anatomical cardiac causes of syncope result in obstruction to cardiac output, such as aortic stenosis and outflow obstruction in hypertrophic cardiomyopathy. Arrhythmias that suddenly reduce cardiac output and profoundly affect blood pressure can cause syncope. Sinus node dysfunction (SND) and AV block are common causes of bradyarrhythmias that can cause syncope. SVT causes syncope less often. VT more commonly causes syncope and when it is associated with structural heart disease it is also associated with a high risk of sudden cardiac death. In patients with syncope, check the ECG for arrhythmias such as atrial fibrillation, evidence of myocardial infarction, or conduction disease such as bundle branch block. Other important features to evaluate include pre-excitation (delta waves), the QT interval, and ectopy. Any of these abnormalities may predict a greater risk of mortality and a need for further evaluation.

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     2. Bradycardia. Heart rates less than 60 bpm are considered bradycardic. Slow heart rhythms become an issue generally in older patients who may be asymptomatic. Resting slow heart rates in young patients are most likely a result of high vagal tone and are not pathologic. Heart rates greater than 50 tend to be hemodynamically stable while those less than 40 bpm while the patient is awake often are not. If the asymptomatic bradycardic patient has no evidence of conduction disease (normal QRS morphology) and a chronotropic response to exercise, atropine or Isoproterenol, a pacemaker is rarely indicated. On the other hand, symptomatic patients with SND or evidence of conduction disease such as second- or third-degree AV block almost always need a permanent pacemaker preoperatively. Bradycardia secondary to neurocardiogenic syncope, medications, or increased vagal tone will not generally require a pacemaker. Simply removing the offending medicine or treating the inciting condition will be sufficient.

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     3. Tachycardia. Heart rates above 100 bpm are termed “tachycardia.” These can be sinus, a pathologic SVT, or VT. Sinus tachycardia rarely exceeds 140 bpm at rest unless the patient is in distress, shock, acute respiratory failure, or thyroid storm. In adults not in distress, a narrow, regular QRS tachycardia at rates above 150 bpm is rarely sinus. Regular and narrow QRS tachycardia at these rapid rates are frequently paroxysmal supraventricular tachycardia (PSVT) or atrial flutter with 2 to 1 conduction. Irregular SVTs are either the more common atrial fibrillation or multifocal atrial tachycardia. The later is seen in elderly patients with severe chronic pulmonary disease.

          Wide QRS tachycardia may be ventricular or supraventricular in origin. In general, if the patient has underlying heart disease, the mechanism of the wide complex tachycardia is VT until proven otherwise. However, there are several conditions in which the mechanism may be SVT including (i) SVT with an underlying or functional bundle branch block, (ii) SVT with nonspecific intraventricular conduction delay, or (iii) pre-excitation syndrome. The ECG diagnosis of VT hinges on seeing AV dissociation or fusion or capture beats. Intraventricular conduction delay can occur with the use of Class I antiarrhythmic agents or in the setting of extreme hyperkalemia. Wolff–Parkinson–White syndrome should be considered in a young healthy individual presenting with atrial fibrillation and a wide QRS rhythm. Functional bundle branch block is seen in the young and rarely in the elderly.

II. Treatment modalities

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   A. Pharmacologic treatment. Algorithms are now in place for acute treatment of SVTs. SVT is usually treated with intravenous (IV) adenosine acutely in the symptomatic patient. For atrial fibrillation the initial focus is on rate control. Agents that are effective acutely include IV diltiazem and the β-blockers metoprolol and esmolol. Esmolol has an extremely short half-life. Digoxin is of little use acutely and is very unpredictable. IV amiodarone is now being used more frequently in the acute management of patients with poor ventricular function and atrial fibrillation with rapid ventricular rates. This medication should be infused through a central line given the risk for tissue necrosis with extravasation. The pharmacologic treatment of ventricular arrhythmias in the hemodynamically stable patient involves treating the underlying causes. For VT, IV amiodarone is the initial drug of choice, but lidocaine is also considered especially if there is concern for ongoing ischemia. For torsades de pointes, management includes eliminating offending drugs in the setting of the long QT syndromes. Correcting electrolyte deficiencies with IV magnesium and potassium are particularly helpful in correcting the prolonged QT interval, as possibly stopping medications contributing to bradycardia. Amiodarone in the setting of torsades de pointes can prolong the QT interval and make the problem worse. For the hemodynamically unstable patient with sustained ventricular arrhythmias, pharmacologic management would follow the current advanced cardiac life support (ACLS) protocols.

   Proarrhythmia. Although drugs have proved safe and effective in the normal heart, their safety and efficacy have proved worrisome in the structurally abnormal heart. Chronic drug therapy for arrhythmias in patients with structural heart disease is associated with increased mortality due to proarrhythmic effects. Class IA antiarrhythmic agents are contraindicated in individuals with congestive heart failure and poor left ventricular function (ejection fraction below 0.30). Class IC agents should be avoided in individuals with a prior myocardial infarction because of the increased risk of sudden death [5]. Class III agents will prolong the QT interval and increase the risk of torsades de pointes.

   B. Nonpharmacologic treatments. The emphasis on the chronic treatment for arrhythmias, especially ventricular arrhythmias in patients with structural heart disease, has moved from drugs to electricity. Because of technologic advances, cardiac implantable electrical devices (CIEDs) have become smaller and increasingly complex. This complexity has greatly expanded therapeutic options, but it has greatly increased the potential for malfunction in the perioperative setting. Except in infants and small children, a formal thoracotomy is no longer used for implantation of a CIED. Contemporary devices are small enough to be suitable for pectoral implantation.

     1. External cardioversion and defibrillation. External direct-current (DC) cardioversion differs from defibrillation only in that the former incorporates a time delay circuit for shock synchronization to the QRS complex of the surface ECG. Current devices employ universal use of biphasic shocks, which lower shock current requirements for DC cardioversion and defibrillation. Automated external defibrillators self-analyze and give instructions for defibrillation [6].

        a. Indications: Synchronized shocks are used for most pathologic hemodynamically unstable tachycardias, except VF or VT when the QRS complex cannot be distinguished from T waves. Automatic rhythm disturbances (e.g., accelerated AV junctional or accelerated idioventricular rhythms) are not amenable to DC cardioversion.

        b. Procedure: Synchronized cardioversion with the largest R or S wave on the ECG will prevent inadvertent triggering of VF. Improper synchronization may occur when there is bundle branch block with a wide R wave, when the T wave is highly peaked, and with pacing artifacts from a malfunctioning pacemaker (i.e., failure to capture). Synchronization should be checked after each discharge. Electrodes are placed in an anterior-lateral, posterior-lateral, or an anteroposterior (AP) position. Current should pass though the heart’s long axis, depolarize the bulk of myocardium, and minimize flow through high-impedance bony tissue. Electrode paste or gel is used to reduce transthoracic impedance. Bridging of the electrodes by conductive paste or gel should be avoided, because this will reduce the amount of energy delivered to the heart. Present-day units automatically boot to an energy setting of 200 J. This is the starting energy dosage for defibrillating adults. For cardioversion, energy titration (initially use only the lowest possible energies) reduces both energy use and complications. Initial settings of 20 to 50 J may be successful for terminating typical atrial flutter or stable monomorphic VT. DC cardioversion is extremely painful. Patients must be sedated for DC cardioversion at any power setting. Generally, an anesthesiologist or nurse anesthetist will administer a short-acting sedative such as IV propofol or etomidate. The combination of midazolam and fentanyl can be an alternative but is not ideal due to the prolonged duration of action.

        c. CIEDs and cardioversion. Older and especially unipolar devices could be easily affected by DC cardioversion. Transient loss of capture and electrical reset were not uncommon. This interference does not happen with modern bipolar and well- protected devices. Using the anterior–posterior pads position and the anterior pad location at least 8 cm from the CIED will prevent malfunction or damage to the device. Directly applied currents of 10 to 30 J to the ventricles during cardiac surgery on occasion can cause reset of the pulse generator.

     2. Temporary pacing. Compared to drugs for treating cardiac rhythm disturbances, temporary pacing has several advantages. The effect is immediate, control is precise, and there is reduced risk of untoward effects and proarrhythmia.

        a. Indications. Temporary pacing is indicated for rate support in patients with symptomatic bradycardia or escape rhythms. Prophylactic or stand-by pacing is indicated for patients at increased risk for sudden high-degree AV heart block. Temporary pacing can be used to overdrive or terminate atrial flutter and some sustained monomorphic VT. More specific established and emerging indications for temporary pacing are shown in Table 17.2. The endpoint for temporary pacing is resolution of the indication or implantation of a permanent pacemaker for a continuing indication.

Table 17.2 Usual and less-established indications for temporary cardiac pacing

        b. Technology. Transvenous endocardial or epicardial leads are usually used for temporary pacing. Temporary endocardial bipolar active fixation wires are available for both atrial and ventricular pacing. Single- or dual-chamber pacing can be achieved. Transvenous leads are passed from above using the internal jugular or subclavian approaches or from below using a femoral vein. Epicardial leads are routinely used in patients having cardiac surgery. The noninvasive transcutaneous and transesophageal routes are also available. Transcutaneous pacing is uncomfortable and used in emergency situations. In the operating room it is for transient backup pacing only. It produces ventricular capture and does not preserve optimal hemodynamics in patients with intact AV conduction. With available technology for transesophageal pacing, only atrial pacing is reliable. Thus, the method is not suitable for patients with advanced AV block or atrial fibrillation.

     3. Permanent pacing. Permanent pacemakers are no longer prescribed simply for rate support. They have become an integral part of treatment, along with drugs and other measures, to prevent arrhythmias and improve quality of life in patients with heart failure [7].

        a. Indications. The presence or absence of symptoms directly attributable to bradycardia has an important influence on the decision to implant a permanent pacemaker. There is increasing interest in multisite pacing as part of the management for patients with structural heart disease and heart failure. In the past, pacemakers were prescribed to treat re-entrant tachyarrhythmias. Today, this capability can be programmed for either the atrium or ventricle as part of “tiered therapies” with an internal cardioverter–defibrillator (ICD).

           (1) AV block. Patients may be asymptomatic or have symptoms related to bradycardia, ventricular arrhythmias, or both. There is little evidence that pacing improves survival with isolated first-degree AV block. With Type I, second-degree AV block due to AV nodal-conduction delay, progression to higher-degree block is unlikely. Pacing is usually not indicated unless the patient has symptoms. With Type II, second-degree AV block within or below the His bundle, symptoms are frequent, prognosis is poor, and progression to third-degree AV block is common. Pacing is recommended for chronic Type II second-degree AV block. It is recommended for Type I second-degree AV block in the presence of symptoms such as syncope. Pacing improves survival in both types of second-degree AV block. Nonrandomized studies strongly suggest that pacing improves survival in patients with third-degree AV block.

           (2) Bifascicular and trifascicular block. Although third-degree AV block is commonly preceded by bifascicular block, the rate of progression is slow (years). Further, there is no credible evidence for acute progression to third-degree AV block during anesthesia and surgery. Bifascicular block with periodic third-degree AV block and syncope is associated with an increased incidence of sudden death. Prophylactic permanent pacing is indicated in this circumstance.

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           (3) AV block after acute MI. The requirement for temporary pacing with acute MI by itself does not constitute an indication for permanent pacing. The long-term prognosis for survivors of acute MI is related primarily to the extent of myocardial injury and nature of intraventricular conduction defects, rather than to AV block itself. Acute MI patients with intraventricular conduction disturbances have unfavorable short- and long-term prognoses, with increased risk of sudden death. This prognosis is not necessarily due to the development of high-grade AV block, although the incidence of such block is higher in these patients.

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           (4) SND. SND may manifest as sinus bradycardia, pause or arrest, or SA block, with or without escape rhythms. It often occurs in association with atrial fibrillation or atrial flutter (tachycardia–bradycardia syndrome). Patients with SND may have symptoms due to bradycardia, tachycardia, or both. Correlation of symptoms with arrhythmias is essential and is established by ambulatory monitoring. SND also presents as chronotropic incompetence (inability to increase rate appropriately). An adaptive-rate pacemaker may benefit these patients by restoring more physiologic heart rates. Although symptomatic SND is the primary indication for a pacemaker, pacing does not necessarily improve survival, but it can improve the quality of life.

           (5) Hypersensitive carotid sinus syndrome or neurally mediated syndrome. Hypersensitive carotid sinus syndrome is manifest by syncope due to an exaggerated response to carotid sinus stimulation. It is an uncommon cause of syncope. If purely cardioinhibitory (asystole, heart block) and without vasodepressor components (vasodilatation), then a pacemaker can be prescribed. A hyperactive response is defined as asystole for longer than 3 s due to sinus arrest or heart block and an abrupt decrease in blood pressure. With the more common neurally mediated mixed response, attention to both components is essential for effective therapy. Neurally mediated (vasovagal) syncope accounts for nearly 25% of all syncope. The role of permanent pacing is controversial but probably limited.

           (6) Pacing in children and adolescents. Indications for pacing are similar in children and adults, but there are additional considerations. For example, what is the optimal heart rate for the patient’s age? Further, what is optimal given ventricular dysfunction or altered circulatory physiology? Hence, pacing indications are based more on correlation of symptoms with bradycardia, rather than arbitrary rate criteria, and include the following:

             (a) Bradycardia only after other causes (e.g., seizures, breath holding, apnea or neurally mediated mechanisms) are excluded.

             (b) Symptomatic congenital third-degree AV block

             (c) Persistent advanced second- or third-degree AV block after cardiac surgery. However, for patients with residual bifascicular block and intermittent AV block, the need is less certain.

             (d) Use along with β-blockers in patients with congenital long QT syndrome, especially with pause-dependent VT.

           (7) Miscellaneous pacing indications

             (a) A dual-chamber pacemaker with short AV delay reduces left ventricular outflow tract obstruction, alleviates symptoms in obstructive hypertrophic cardiomyopathy in some cases, and may improve functional status. Permanent pacing does not reduce mortality or prevent sudden death in this disease.

             (b) Bradyarrhythmias after cardiac transplantation are mostly due to SND. Cardiac transplantation today preserves the sinus node so SND is much less likely. Most patients with bradycardia show improvement by 1 yr so that long-term pacing is unnecessary.

             (c) A combination of pacing and β-blockers may be used for prophylaxis for tachyarrhythmias in congenital long QT syndrome. Pacing therapy alone is not recommended. Backup dual-chamber defibrillator therapy is now preferred.

        b. Technology. Contemporary single- and dual-chamber pacemakers are sophisticated devices, with multiple programmable features, including automatic mode switching, rate adaptive pacing, automatic threshold pacing, and programmable lead configuration. Pacemakers are powered by lithium iodide batteries, with an expected service life of 5 to 12 yrs, depending on device capabilities, need for pacing, and programmed stimulus parameters. Most systems use transvenous leads. Lead configuration is programmable. With the unipolar configuration, the pacemaker housing (can) serves as anode (+) and the distal electrode of the bipolar pacing lead as cathode (–). With the bipolar configuration, proximal and distal lead electrodes serve as anode and cathode, respectively. The ability to program unipolar pacing is necessary if lead insulation or conductor failure occurs in a bipolar lead system. Also, it permits exploitation of either configuration while minimizing its disadvantages (e.g., oversensing with unipolar leads). A dual-chamber pacemaker with automatic mode switching is optimal for patients with AV block and susceptibility to paroxysmal atrial fibrillation. Algorithms detect fast, nonphysiologic atrial rates and automatically switch the pacing mode to one that excludes atrial tracking and the associated risk of upper-rate ventricular pacing.

     4. Implantable cardioverter—defibrillator. Contemporary ICDs are multiprogrammable, are longer lived, use transvenous leads, and may incorporate all capabilities of a modern dual-chamber pacemaker. ICDs are powered by combination of both batteries and capacitors. Many current models also have wireless technology that allows patients to have remote follow-up via their home phone lines for routine ICD evaluations limiting the in-person visits to the pacer clinic or doctor’s office to annual or bi-annual evaluations. Additionally, ICDs have multiple tachycardia detection zones, with programmable detection criteria and “tiered therapy” for each (antitachycardia pacing → cardioversion shocks → defibrillatory shocks if necessary). ICDs also store arrhythmia event records and treatment results. Future devices will be tailored to meet all nonpharmacologic aspects of cardiac rhythm management for individual patients. Finally, ICDs have undergone significant downsizing (50 mL or smaller) and nearly all are prepectoral implants.

        a. Indications. ICDs are used for secondary or primary prevention of sudden death.

           (1) Secondary prevention. ICDs are used for secondary prevention in patients who have survived a cardiac arrest from sustained ventricular arrhythmias. Most commonly these are patients with heart failure and reduced left ventricular systolic function. Of this population, coronary artery disease and ischemic cardiomyopathy are the most common etiologies of the heart failure. Secondary prevention indications for ICDs also include individuals with structural heart disease who have documented sustained ventricular tachyarrhythmias or inducible sustained ventricular tachyarrhythmias by electrophysiologic testing. ICDs are widely accepted for improving outcomes in these patients by preventing sudden cardiac death. Other indications for secondary prevention include patients with long QT syndrome and recurrent syncope, sustained ventricular arrhythmias, or sudden cardiac arrest despite drug therapy. ICD plus Class IA drugs are prescribed for patients with idiopathic VF and Brugada syndrome with recurrent ventricular arrhythmias. Other indications are (i) sudden death survivors with hypertrophic cardiomyopathy; (ii) prophylaxis for syncope and sudden death with drug-refractory arrhythmogenic right ventricular dysplasia; and (iii) children with malignant tachyarrhythmias or sudden death and congenital heart disease, cardiomyopathies, or primary electrical disease (e.g., long QT syndrome).

           (2) Primary prevention. ICDs are used for primary prevention of sudden death in patients who are at high risk for sudden cardiac death. This population mainly includes those with systolic heart failure with ejection fractions 35% that has not improved despite medical therapy. The cause of heart failure may be from coronary artery disease or of nonischemic origin. Other indications for primary prevention ICDs include patients with high risk features with inherited or acquired conditions that place them at increased risk for life-threatening ventricular arrhythmias including long QT syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, cardiac sarcoid, Brugada syndrome, and congenital heart disease.

        b. Technology. The ICD pulse generator is a self-powered minicomputer with one or two (in series) batteries that power the pulse generator, circuitry, and aluminum electrolytic capacitors. The batteries may be lithium–silver vanadium oxide or evolving hybrid technology and vary between the manufacturers. A major challenge in ICD design is the large range of voltages within a very small package. Intracardiac signals may be as low as 100 μV, and therapeutic shocks approach 750 V. Further, ICD batteries contain up to 20,000 J, and a potential hazard exists if the charging and firing circuits were to electrically or thermally unload all this energy into the patient in a brief time period. The number of shocks delivered during treatment is usually limited to five or six per arrhythmia. The expected service life is 5 to 8 yrs.

III. Device function, malfunction, and interference [8]

   A. Pacemakers. A single-chamber pacemaker stimulates the atria or ventricles at programmed timing intervals. Sensing spontaneous atrial or ventricular depolarizations inhibit the device from delivering unnecessary or inappropriate stimuli. Dual-chamber devices time the delivery of ventricular stimuli relative to sensed atrial depolarizations to maintain proper AV synchrony. Figure 17.2 illustrates how a pacemaker might be configured to pace in patients with SND or atrioventricular heart block (AVHB).

   In Figure 17.2 and throughout this chapter, the North American Society for Pacing and Electrophysiology–British Pacing and Electrophysiology Group (NASPE/BPEG) pacemaker code (also known as the NBG code) is used as a short-hand to describe pacing modes (Table 17.3).

Table 17.3 NASPE/BPEG (NBG) pacemaker code used as shorthand to designate pacing modes

Figure 17.2 Bradycardia pacing modes. A dysfunctional sinoatrial node (SAN), atrium, or atrioventricular node (AVN) is indicated by white circles or rectangles. Normal impulse transmission between these structures and the ventricles (VENT) is indicated by solid lines, with blocked or ineffective conduction indicated by hashed lines. An arrow pointing toward the pulse generator (blue) indicates sensing, whereas one pointing toward the atrium or ventricle indicates pacing in that chamber. Top left: AAI pacing for sinus arrest or bradycardia. There is a single atrial lead for both sensing and pacing. Atrial pacing occurs unless inhibited by a sensed spontaneous atrial depolarization. Top right: VVI pacing for AV heart block with atrial fibrillation. There is a single ventricular lead for both sensing and pacing. Ventricular pacing occurs unless inhibited by a sensed spontaneous ventricular depolarization. Bottom left: VDD pacing for AV heart block with normal SAN and atrial function. The atrial lead is for sensing only, and the ventricular lead is for both pacing and sensing. After a sensed atrial depolarization, the ventricle is paced after the programmed AV interval (i.e., atrial-triggered ventricular pacing [VAT]), unless first inhibited by a sensed ventricular depolarization (i.e., the VVI component of the VDD mode). Bottom right: Dual-chamber sequential or AV universal (DDD) pacing for sinus bradycardia with AV heart block. Both atrial and ventricular leads are for sensing and pacing. This mode incorporates all of the preceding pacing capabilities (AAI, VVI, and VAT).

     1. Function. Today, most US pacemakers are dual-chamber (DDD or DDDR) devices with rate-adaptive features (rate response) that can be activated if clinically indicated. Single-chamber pacemakers may pace either the atrium or ventricle depending on lead placement and also may have rate-adaptive features turned on. Dual-chamber pacemakers may also be programmed to act like a single-chamber pacer activating either the atrial or ventricular lead through the use of the proprietary programmer. For example, in individuals with normal conduction and sinus node function, dual-chamber pacemakers may operate as a single-chamber device in the AAI (AAIR, AAI) or VVI (VVIR) modes (Fig. 17.2).

        a. Single-chamber pacemaker. These devices have a single timing interval, the atrial or ventricular escape interval, between successive stimuli in the absence of sensed depolarization. In the AAI or VVI mode (Fig. 17.3), pacing occurs at the end of the programmed atrial or ventricular escape interval unless a spontaneous atrial or ventricular depolarization is sensed first, resetting these intervals. If the device has rate hysteresis as a programmable option, then the atrial or ventricular escape interval after a sensed depolarization is programmed longer than that after a paced depolarization to encourage emergence of intrinsic rhythm and prolong battery life.

Figure 17.3 Top: AAI pacing, as for a patient with sinus bradycardia and intact AV conduction. The atrium is paced (beats 1 and 3)—arrow pointing toward the ECG in the atrial channel (AC) timing diagram—unless inhibited by sensed spontaneous atrial depolarization (beat 2)—arrow pointing away from the ECG in the AC timing diagram. The atrial refractory period (AtRP) prevents R and T waves from being sensed by the AC and inappropriately resetting the atrial escape timing (AA interval). Note that spontaneous atrial depolarization (beat 2) occurs before the AA interval times out, resetting the AA interval. The short vertical line in the AC timing diagram above beat 2 shows where the stimulus would have occurred had the previous AA interval timed out. In the absence of subsequent spontaneous atrial depolarization (beat 3), the AA interval times out with delivery of a stimulus. Bottom: VVI pacing, as for a patient with atrial fibrillation and AV heart block. Beats 1 and 3 are paced, and beat 2 is spontaneous. The latter resets the ventricular escape interval (VV), which otherwise would have timed out with delivery of a stimulus, indicated by the short vertical line in the ventricular channel (VC) timing diagram above beat 2. The new VV interval times out with stimulus delivery (beat 3), because there is no sensed ventricular depolarization to reset the timing. VRP, ventricular refractory period.

        b. Dual-chamber pacemaker. A DDD (“AV universal”) pacemaker can pace and sense in both the atrium and the ventricle. It has two basic timing intervals whose sum is the pacing cycle duration (Fig. 17.4). The first is the AV interval, which is the programmed interval from a paced or sensed atrial depolarization to ensuing ventricular stimulation. Some devices offer the option of programmable AV interval hysteresis. If so, the AV interval after paced atrial depolarization is longer than that after sensed depolarization to maintain greater uniformity between atrial and ventricular depolarizations. The second interval is the VA interval, the interval between sensed or paced ventricular depolarization and the next atrial stimulus. During atrial and ventricular refractory periods (Fig. 17.4), sensed events do not reset the device escape timing. During the ventricular channel blanking period (Fig. 17.4), ventricular sensing is disabled to avoid overloading of the ventricular sense amplifier by voltage generated by the atrial stimulus, thereby inappropriately resetting the VA interval. Sensing during the alert periods outside the ventricular blanking and postventricular atrial and ventricular refractory periods initiates new AV or VA intervals (Fig. 17.4). Operationally, depending on sensing patterns, a DDD pacemaker can provide atrial, ventricular, dual-chamber sequential, or no pacing (Fig. 17.4).

Figure 17.4 AV universal (DDD) pacing, as for a patient with sinus node dysfunction and atrio-ventricular (AV) heart block. The atrium is paced (beat 1)—arrow pointing toward the ECG in the atrial channel (AC) timing diagram above beat 1—unless inhibited by sensed atrial depolarization (beats 2 and 3)—arrows pointing away from the ECG in the AC timing diagram. The AC is refractory during the AV interval and from delivery of the ventricular stimulus until the end of the postventricular atrial refractory period (PVARP). This prevents atrial sensing from resetting the escape timing (i.e., AV interval). The ventricular channel (VC) blanking period (BP) prevents sensing of the atrial pacing stimulus, thereby resetting the AV interval and delaying ventricular stimulus delivery. However, sensed ventricular depolarization or noise (e.g., electrocautery) in the alert period (VC) after the blanking period also could inhibit ventricular stimulation. As shown, this does not occur, so the AV interval times out with delivery of a ventricular stimulus. The ventricular refractory period (VRP) prevents sensed T waves from inappropriately resetting the ventriculo-atrial (VA) interval. However, sensing during the alert periods after the PVARP or VRP will reset basic timing, initiating new AV and VA intervals, respectively. Since the first beat is fully paced, it is an example of asynchronous AV sequential pacing (i.e., DOO). With the second beat, a sensed spontaneous atrial depolarization initiates a new AV interval, inhibiting the atrial stimulus that would have occurred, indicated by the short vertical line in the AC timing diagram. Subsequently, there is spontaneous ventricular depolarization before the AV interval times out. The ventricular stimulus that otherwise would have occurred at the end of the AV interval is indicated by the short vertical line in the VC timing diagram below beat 2. The third beat begins with a sensed atrial depolarization. As with beat 2, this also occurs before the VA interval times out. In the absence of sensed ventricular depolarization (beat 3), the new AV interval times out with ventricular stimulus delivery. Beat 3 is an example of atrial-inhibited, ventricular-triggered pacing (i.e., VDD).

        c. Adaptive-rate pacing (ARP). ARP is a programmable feature in nearly all implanted devices (both pacemakers and ICDs) in service today. In patients with chronotropic incompetence, ARP has been shown to improve exercise capacity and quality of life. Activity-based sensors are used most commonly to determine the paced heart rate. These are piezoelectric crystals that sense vibration (up-and-down motion) or acceleration (forward–backward movement) as an index of physical activity. However, they do not provide feedback proportional to physiologic need. A better alternative is the QT interval, in which a QT-sensing device measures the stimulus to T wave interval during ventricular pacing. However, this measure is affected by changes in heart rate and catecholamines. Minute ventilation sensors measure changes in transthoracic impedance with respiration (i.e., increase with inspiration and decrease with expiration) and provide an estimate of metabolic need that is more proportional to exercise. However, they increase current drain on the device. Other sensors in use or under development measure O2 saturation, pH, stroke volume, or temperature. Finally, because ARP sensors may have a disproportionate response time at the beginning of exercise versus steady-state exercise, a dual-sensor ARP device may provide a more proportional response. Obviously, such complexity and the use of multiple physiologic sensors increase the potential for device malfunction in the perioperative setting.

     2. Malfunction. Primary pacemaker malfunction is rare (less than 2% of all device-related problems). Pacing malfunction can occur with ICDs, because all ICDs today include a pacing function which can pace at least the ventricle. Some devices have programmed behavior that simulates malfunction, termed pseudomalfunction. For example, failure to pace may be misdiagnosed with programmed rate hysteresis. Also, apparent device malfunction in response to electromagnetic interference (EMI) may be normal device operation, as described later in this chapter.

          Pacemaker malfunction is classified as failure to pace, failure to capture, pacing at abnormal rates, failure to sense, oversensing, and malfunction unique to dual-chamber devices (Table 17.4). Among the causes for failure to capture are drugs or conditions that affect pacing thresholds (Table 17.5). To diagnose malfunction, it is necessary to obtain a 12-lead ECG and chest X-ray film and to interrogate the device for pacing and sensing thresholds, lead impedances, battery voltage, and magnet rate.

Table 17.4 Categories of pacemaker malfunction, ECG appearance, and likely cause for malfunction

Table 17.5 Drugs and conditions that affect or have no proven effect on pacing thresholds

          Malfunctions unique to dual-chamber devices are crosstalk inhibition and pacemaker-mediated tachycardia (PMT).

        a. Crosstalk inhibition. Crosstalk refers to the oversensing of atrial signals from atrial stimulation on the ventricular sense channel or circuit of a dual-chamber pacemaker. This oversensing has the potential of inhibiting ventricular output. Crosstalk is prevented by increasing the ventricular sensing threshold, decreasing atrial stimulus output, or programming a longer ventricular blanking period (Fig. 17.4), so long as these provide adequate safety margins for atrial capture and ventricular sensing. If crosstalk cannot be prevented, many dual-chamber devices have a feature referred to as nonphysiologic AV delay or ventricular safety pacing. Whenever the ventricular channel senses anything early during the AV interval, a ventricular stimulus is triggered after an abbreviated AV interval. This either will depolarize ventricular myocardium or will fail to do so if myocardium is refractory due to spontaneous depolarization. The premature timing of the triggered ventricular stimulus prevents it from occurring during the vulnerable period of the T wave.

        b. Pacemaker-mediated tachycardia (PMT). PMT is undesired rapid pacing caused by the device or its interaction with the patient. PMT includes sensor-driven tachycardia, tachycardia during magnetic resonance imaging (MRI), tachycardia due to tracking of myopotentials or atrial tachyarrhythmias, pacemaker re-entrant tachycardia, and runaway pacemaker.

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            Sensor-driven tachycardia may occur with adaptive-rate devices that sense vibration, impedance changes, or the QT interval if they sense mechanical or physiologic interference, which leads to inappropriate high-rate pacing. Thus, it is advised that ARP be disabled in perioperative settings.

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            MRI. Powerful forces exist in the MRI suite, including static and gradient magnetic fields, and radiofrequency (RF) fields. The static magnetic field may exert a torque effect on the pulse generator or close the magnetic reed switch to cause asynchronous pacing. The gradient magnetic field may induce voltage large enough to inhibit a demand pacemaker but is unlikely to cause pacing. The RF field may generate enough current in the leads to cause pacing at the frequency of the pulsed energy (60 to 300 bpm). Because of the unpredictable interaction between the MRI and CIEDs, MRIs are generally contraindicated in individuals with CIEDs. There is now an approved compatible pacemaker generator and lead system for individuals likely to need MRI.

            Tachycardia due to myopotential tracking occurs in a dual-chamber device when the atrial sense channel is programmed unipolar and the device programmed to VAT, VDD, or DDD modes. Sensed myopotentials from pectoral muscle beneath the pulse generator can trigger ventricular pacing up to the maximum atrial tracking rate.

            Tachycardia due to tracking atrial tachyarrhythmias has a similar explanation. Medication to suppress the arrhythmia (often atrial fibrillation) or cardioversion may be necessary. Placing a magnet over the pulse generator to disable sensing in most instances (see response to magnet, later) will terminate high-rate atrial tracking. Newer dual-chamber devices with automatic mode switching detect fast, nonphysiologic atrial tachycardia and automatically switch the device to a nontracking mode.

            Finally, pacemaker-re-entrant tachycardia can occur in a device programmed to an atrial tracking mode. Up to 50% of patients with dual-chamber devices are susceptible to PRT because they have retrograde (VA) conduction via the AVN or an accessory AV pathway. PRT occurs when spontaneous or paced ventricular beats are conducted back to the atria to trigger ventricular pacing. To prevent PRT, a longer postventricular atrial refractory period is programmed (Fig. 17.4). Also, placing a magnet over the pulse generator will terminate PRT in most devices by disabling sensing. However, PRT may recur after the magnet is removed.

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     3. Response of pacemaker to magnet application. Most contemporary pacemaker devices respond to magnet application by a device-specific single- or dual-chamber asynchronous pacing mode. Adaptive-rate response is generally suspended with magnet mode as well. With asynchronous pacing, the pacemaker will no longer be inhibited by sensed activity and instead pace at a fixed rate regardless of underlying rhythm. The first few magnet-triggered beats may occur at a rate and output other than that seen later. Pacing amplitudes remain constant at the programmed output in Biotronik, Boston Scientific, and Medtronic pacemakers. The pacing amplitude with magnet application in ELA/Sorin and St. Jude pacemakers may be higher than the programmed output settings. The response to a magnet should be determined prior to an anticipated surgical procedure and is predicted by the brand of the pacemaker in most circumstances. However, some manufacturers, Biotronik, St. Jude Medical, and Boston Scientific devices, have a programmable magnet mode that may make response to magnet application different than anticipated. Although rarely used, this feature may be programmed to save patient-activated rhythm recordings with magnet application rather than revert the pacemaker to asynchronous pacing. To confirm that the typical magnet response is “‘on,” place magnet on the device and evaluate if there is a change to asynchronous pacing on telemetry. The magnet-triggered rate and the duration of pacing do vary based on manufacturer and battery status. For example, Biotronik pacemakers have a magnet rate at 90 bpm for 10 beats only while all other manufacturers pace asynchronously as long as the magnet is in contact with the pacemaker. The fixed magnet rate for Boston Scientific pacemakers is 100 bpm; St. Jude is 98.6 bpm; ELA/Sorin is 96 bpm. Medtronic pacemakers are triggered for three beats at 100 bpm then default to 85 bpm. However, with impending power source depletion, the magnet rate will approach the programmed rate of the end-of-life (EOL) or elective replacement indicator (ERI) and is usually a slower pacing interval than the standard magnet rate (Table 17.6).

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          In a patient whose intrinsic rhythm inhibits the device, magnet application may serve to identify the programmed mode when the correct programmer is not available for telemetry. Also, with device malfunction due to malsensing, magnet-initiated asynchronous pacing may temporarily correct the problem, confirming the presence of far-field sensing, crosstalk inhibition, T-wave sensing, or PMT. Finally, in pacemaker-dependent patients, magnet application may ensure pacing if EMI inhibits output (e.g., surgical electrocautery).

     4. Interference. CIEDs are subject to interference from nonbiologic electromagnetic sources. In general, devices in service today are effectively shielded against EMI. Increasing use of bipolar sensing has further reduced the problem. EMI frequencies above 109 Hz (i.e., infrared, visible light, ultraviolet, X-rays, and gamma rays) do not interfere with pacemakers or ICDs, because the wavelengths are much shorter than the device or lead dimensions. High-intensity therapeutic X-rays and irradiation can directly damage circuitry. EMI enters a device by conduction (direct contact) or radiation (leads acting as an antenna). Devices are protected from EMI by (i) shielding the circuitry, (ii) using a bipolar versus unipolar lead configuration for sensing to minimize the antenna, and (iii) filtering incoming signals to exclude noncardiac signals. If EMI does enter the pulse generator, noise protection algorithms in the timing circuit help reduce its effect on the patient. However, EMI signals between 5 and 100 Hz are not filtered, because these overlap the frequency range of intracardiac signals. Therefore, EMI in this frequency range may be interpreted as intracardiac signals, giving rise to abnormal behavior. Possible responses include (i) inappropriate inhibition or triggering of stimulation, (ii) asynchronous pacing (Fig. 17.5), (iii) mode resetting, (iv) direct damage to the pulse generator circuitry, and (v) triggering of unnecessary ICD shocks (Table 17.7).

Table 17.6 Elective replacement indicators that may affect the nominal rate of pacing

Figure 17.5 VVI pacemaker to continuous EMI. Temporary asynchronous pacing stimulation (Stim) occurs at the programmed basic rate interval. The ventricular refractory period (rectangles) begins with the noise (N) sampling period (blue rectangles), during which time there is no sensing. During the remainder of this refractory period, repeated noise (N) sensing above a specified minimal frequency (e.g., 7 Hz) is interpreted as EMI. This restarts the ventricular refractory period. Portions of the previous refractory period pre-empted by the newly initiated ventricular refractory period are indicated by hashed rectangles. Therefore, so long as interference persists, the pacemaker remains refractory and escape timing is determined entirely by the programmed basic rate interval. In this example, the second paced R wave falls in the noise sampling period. It is not sensed, but it initiates a new ventricular refractory period. The spontaneous R wave is not sensed and does not affect escape timing.

Table 17.7 Perioperative EMI sources and their potential effects on implanted pacemakers or implantable cardioverter–defibrillators

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          Finally, with EMI and inappropriate device behavior, it is widely assumed that placing a magnet over a pulse generator invariably will cause asynchronous pacing as long as the magnet remains in place. However, this is not always the case. Although used rarely, some devices (see above in Section III.A.3.) may have programmed magnet response off. In contrast to pacemakers, magnet application on ICDs will not alter the pacing mode and will not change the mode to asynchronous pacing (see below). Thus, if possible, one should determine before EMI exposure what pulse generator is present and what must be done to provide protection. If this is not possible preoperatively, then one must observe the magnet response during EMI to ascertain whether there is protection from EMI sensing. For example, if a pacemaker-dependent patient has inappropriate inhibition or triggering of output during electrosurgery even with magnet application, then electrosurgery must be limited to short bursts.

   B. ICD. An ICD consists of a pulse generator and leads for tachyarrhythmia detection and therapy. Modern ICDs use transvenous lead systems for sensing, pacing, and biphasic shock delivery. Epicardial leads are still used in infants and small children. Use of biphasic compared to monophasic shocks has greatly lowered defibrillation energy requirements and has led to development of smaller ICDs.

     1. Sensing ventricular depolarizations. Reliable sensing is essential. The sense amplifier must respond quickly and accurately to rates of 30 to 360 bpm or greater, and to the varying amplitude and morphology of intracardiac signals during VT or VF. Unfiltered intracardiac electrograms are sent to the sense amplifier. This has a band-pass filter to reject low-frequency T waves and high-frequency noise. There is automatic gain control (auto-gain), a rectifier to eliminate polarity dependency, and a fixed or auto-adjusting threshold event detector. The sense amplifier produces a set of R–R intervals for the VT/VF detection algorithms to use.

     2. VF detection. ICDs use rate criteria as the sole method for detecting VF. Due to the circumstances of VF, the detection algorithms must have high sensitivity and low specificity. If criteria for detection are too aggressive, the ICD likely will oversense T waves during sinus rhythm, leading to spurious shocks. If too conservative, it likely will undersense some VF but work very well during sinus rhythm. An ICD X/Ydetector triggers when X of the previous Y sensed ventricular intervals are shorter than the VF detection interval. Typically, this is 70% to 80% of intervals in a sliding window of 10 to 24. This approach is very good at ignoring the effect of a small number of undersensed events due to the small amplitude of VF intracardiac signals. Any tachycardia with a cycle length less than the VF detection interval will initiate VF therapy. After capacitor charging but before shock delivery, an algorithm confirms the presence of VF. After shock delivery, redetection and episode-termination algorithms determine whether VF has terminated, continued, or changed.

     3. Tachycardia detection and discrimination (single-chamber ICD). Most VT algorithms require a programmable number of consecutive R–R intervals shorter than the VT detection interval. A longer R–R interval, as might occur during atrial fibrillation, would reset the VT counters. In patients with both supraventricular and ventricular tachyarrhythmias, up to 45% of ICD discharges may be inappropriate if rate is used as the sole criterion for VT therapy.

          To increase specificity, VT detection algorithm enhancements are programmed for one or more VT zones in single-chamber ICDs, including criteria for stability of rate, suddenness of onset, and intracardiac QRS morphology.

        a. The rate stability criterion is used to distinguish sustained monomorphic VT with little cycle length variation from atrial fibrillation with much greater cycle length variation. Such enhancement criteria are not available in the VF zone, where maximum sensitivity is required. Also, they are programmed only in rate zones that correspond to VT hemodynamically tolerated by the patient.

        b. The suddenness of onset criterion is used to distinguish sinus tachycardia from VT, because VT has a more sudden rate increase.

        c. Finally, morphology algorithms discriminate VT from SVT based on morphology of intracardiac electrograms.

     4. Tachycardia detection and discrimination (dual-chamber ICD). Inadequate specificity of VT detection algorithms, despite enhancements, has been a significant problem with single-chamber ICDs. Dual-chamber ICDs use an atrial lead, which is used for bradycardia pacing and sensing for tachycardia discrimination. Detection algorithms use atrial and ventricular timing data to discriminate SVT from VT. For example, the algorithm in devices of one manufacturer has several key elements: (i) the pattern of atrial and ventricular events; (ii) atrial and ventricular rates; (iii) regularity of R–R intervals; (iv) presence or absence of AV dissociation; and (v) atrial and ventricular pattern analysis.

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     5. Tiered therapy. Treatment options for VT include antitachycardia pacing, cardioversion, or defibrillation. Up to 90% of monomorphic VTs can be terminated by a critical pacing sequence, reducing the need for painful shocks and conserving battery life. With antitachycardia pacing, trains of stimuli are delivered at a fixed percentage of the VT cycle length. Repeated and more aggressive trains result either in termination of VT or progression to cardioversion or defibrillation.

     6. ICD malfunction. Malfunctions specific to ICD include inappropriate shock delivery, failure to deliver therapy, ineffective shocks, and interactions with drugs or devices affecting the efficacy of therapy. There is potential for pacing malfunction as well since all ICDs have a pacemaker function.

        a. Inappropriate delivery of shocks. Artifacts created by lead-related malfunction may be interpreted as tachycardia, with inappropriate shock delivery. Electrocautery artifact may be similarly misinterpreted. Rapid SVT or nonsustained VT may be misdiagnosed as sustained VT or VF, especially if rate-only criteria are used for diagnosis. R- and T-wave oversensing, causing double counting during bradycardia pacing, has led to inappropriate shocks.

        b. Failure to deliver therapy or ineffective shocks. Especially after repeated shocks for VF, tachyarrhythmias may be undersensed with failure to deliver therapy. Exposure to diagnostic X-rays or computed tomographic scans does not adversely affect shock delivery. Acute MI, severe acute acid–base or electrolyte imbalance, or hypoxia may increase defibrillation thresholds, leading to ineffective shocks. Any of these also could affect the rate or morphology of VT and the ability to diagnose VT. Finally, isoflurane and propofol do not affect defibrillation thresholds. The effect of other anesthetics or drugs used to supplement anesthesia is unknown.

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        c. Drug–device interactions affecting efficacy of ICD therapy. Antiarrhythmic drugs are used along with ICD to suppress (i) recurring sustained VT and the need for shocks; (ii) nonsustained VT that triggers unnecessary shocks; and (iii) atrial fibrillation with inappropriate shocks. Also, they may be used to slow VT to make it better tolerated or more amenable to termination by antitachycardia pacing and to slow AV nodal conduction with atrial fibrillation.

            Possible adverse effects of combined drug and ICD therapy are (i) slowing of VT to below the programmed rate-detection threshold; (ii) proarrhythmia, increasing the need for shocks; (iii) increased defibrillation thresholds; (iv) reduced hemodynamic tolerance of VT; (v) increase in PR, QRS, or QT intervals, causing multiple counting and spurious shocks; and (vi) altered morphology or reduced amplitude of intracardiac electrograms and failure to detect VT/VF. Lidocaine, chronic amiodarone, Class IC drugs (e.g., flecainide), and phenytoin can increase defibrillation thresholds. Class IA drugs (e.g., quinidine) generally do not affect defibrillation thresholds.

        d. Device–device interactions affecting efficacy of therapy. In the past, pacemakers were used for bradycardia and antitachycardia pacing in ICD patients. Today, ICD incorporates both pacing capabilities, but still there may be occasional patients with an ICD and a pacemaker. More common today may be the consideration of brain or nerve stimulators in a patient with an ICD or pacemaker. Regardless of the type of pulse stimulators, possible adverse interactions between two devices include (i) sensed pacing artifacts or depolarizations that may lead to multiple counting, misdiagnosis as VT/VF, and spurious shocks; and (ii) ICD shocks that may reprogram a pacemaker or cause failure to capture or sense. The use of only bipolar pacing from the other device will minimize such interference, but must be fully evaluated prior to permanent implantation.

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     7. Response of an ICD to magnet application [8]. Magnet application does not interfere with bradycardia pacing and does not trigger asynchronous pacing in an ICD. Magnet application in contemporary ICDs causes inhibition of tachycardia sensing and delivery of shock only. All current ICDs remain inhibited as long as the magnet remains in stable contact with the ICD. Once the magnet is removed, the ICD reverts to the programmed tachyarrhythmia settings. One deviation from this is in some Biotronik ICD platforms where a magnet placed in direct contact with the ICD will inhibit continuously up to 8 hrs. After 8 hrs, the programmed tachycardia therapy will be reactivated even with the magnet is still in contact. This universal response to magnet across all manufacturers has not always been the case and has caused confusion on how to deal with ICDs in the operative setting. Older platforms manufactured by Boston Scientific/Guidant Corp. had a programmable response to magnet application, most commonly programmed to Magnet Use Enable, but there were exceptions. Most of these device platforms are no longer in service.

          With an appropriately placed magnet, Boston Scientific (Guidant) ICDs have R-synchronous beeping followed by a continuous sound that indicates inactivation of tachyarrhythmia function. Medtronic devices emit a continuous sound for 20 to 30 s to indicate inactivation of tachyarrhythmia sensing. ICDs by St. Jude Medical, Biotronik, and ELA/Sorin do not emit sounds in the presence of a magnet. These different audible responses to magnets may continue to be a source of confusion. Regardless of the audible response, all ICDs turn off tachycardiac sensing and therapy when a magnet remains applied to the generator.

     8. Interference and ICD. Reports of inappropriate ICD shocks due to EMI oversensing are infrequent. EMI initially might be misinterpreted as VF, but spurious shocks will not occur unless it continues beyond the capacitor charging period (see Section III.A.4 and Table 17.7). Magnet application does not interfere with bradycardia pacing and does not trigger asynchronous pacing in an ICD.

IV. Perioperative considerations for the patient with a CIED [8]

   A. Preoperative patient evaluation. Patients with pacemakers or ICDs, especially the latter, often have serious cardiac functional impairment. Many have debilitating coexisting systemic disease as well. Special attention is paid to progression of disease and functional status, current medications, and compliance with treatment. No special testing is required just because the patient has an implanted device. However, baseline information about the surgery is needed by the CIED team (cardiologist, electrophysiologist, and pacemaker clinic staff managing the device) such as (i) type and location of the procedure, (ii) body position at surgery, (iii) electrosurgery needed and site of use, (iv) potential need for DC cardioversion or defibrillation, and (v) other EMI sources.

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   B. CIED team evaluation. Most surgical facilities today have an onsite CIED clinic or service (or access to one) that should be consulted to provide preoperative consultation on the management of the device. If not, the next best strategy is to identify the device and contact the manufacturer for advice. All patients should carry a card that identifies the model and serial numbers of the device, the date of implantation, and the implanting physician or clinic. Unless the planned surgery is truly emergent or poses little risk of EMI-related device malfunction (e.g., bipolar cautery will be used; the surgical field is far removed from the device, leads and grounding plate), it is imperative to (i) identify the device (manufacturer, model, leads, battery status), (ii) determine the date and indication(s) for its implantation, and (iii) to check its function. If a recent device check (for pacemakers <12 mos and for ICDs <6 mos) is not available, then the CIED team should perform a check. The data to be provided by this interrogation are (i) type of device (single, dual, biventricular), (ii) programmed mode, (iii) programmed rates, energy, sensing, tachyarrhythmia settings for an ICD, (iv) pacemaker-dependent status, (v) underlying rhythm, (vi) specifics about magnet response, and (vii) pacing safety margin and battery longevity. If the CIED has no recent device check data and it cannot be interrogated, then obtain (i) a 12-lead ECG (for pacemakers, with and without a magnet) and (ii) an X-ray film of the pulse generator area which may reveal a unique radiopaque code (“signature”) that identifies the manufacturer and model of the device (Table 17.8). If the surgery is truly emergent and it is not possible to identify the device, the basic function of most suppressed pacemakers is confirmed by placing a magnet over the pulse generator to establish the asynchronous pacing rate, provided the magnet function has not been programmed off. Cholinergic stimulation (e.g., Valsalva maneuver, carotid sinus massage, adenosine, or edrophonium) might be useful to slow the intrinsic rate sufficiently to show the presence of pacing stimuli.

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   C. Device management. A qualified physician with device expertise must supervise the recommended preoperative prescription for device management. The prescription should not be provided by industry-employed representatives.

   For pacemaker-dependent patients: These patients are at particular risk of asystole in the presence of EMI. If EMI is likely (e.g., unipolar cautery in the vicinity of the pulse generator or leads and surgery above the umbilicus), then the device should be programmed to an asynchronous mode. In the case of pacemakers, this can be done with magnet application in most situations, which will also inactivate the rate-responsive pacing, but confirmation of the magnet response is recommended prior to the surgical procedure if possible. In cases where the pacemaker-dependent patient has an ICD or the location of surgery precludes placement of a magnet, consideration of programming the device to asynchronous mode with the proprietary programmer is recommended. The other alternative if reprogramming is not an option is to limit the EMI to short bursts while watching the response of pacing and minimize episodes of asystole. For patients with adaptive-rate pacemakers (including some ICDs), this capability should be programmed off if EMI causes inappropriate rate response. As stated above, for pacemakers, magnet application will inactivate this feature, but ICDs will need to be reprogrammed (Table 17.7). In ICDs, tachycardia sensing and therapy should be turned off. This can be accomplished with magnet application or with reprogramming. If any reprogramming is planned, then patients must stay on monitored telemetry until the CIED is reprogrammed back to baseline settings.

   In an emergency, if the patient is 100% pacing on the 12-lead ECG and on telemetry, then the assumption is that the patient is pacemaker dependent. In this situation, there needs to be continuous hemodynamic monitoring that will not be distorted with EMI such as a pulse wave form from an arterial line or plethysmography. A form of backup pacing should also be considered such as anterior–posterior transcutaneous pacing pads.

   If intrinsic conduction (i.e., no pacing) is seen on the 12-lead ECG, then proceed with surgery and have a magnet available.

   Magnet versus reprogramming: If the CIED is reprogrammed then continuous monitoring is mandated. In the operating room, it is difficult to reverse reprogramming. If spontaneous heart rates exceed the asynchronous programmed pacing rate then both deleterious hemodynamic and arrhythmia events may develop. Likewise, post procedure, the ICD antitachyarrhythmia therapies must be reactivated. This does not always occur and is a possible source of medical error. Use of a magnet eliminates the complexity of reprogramming the CIED in the operating room. The magnet can be easily removed when competing rhythms develop with asynchronous pacing. However, the magnet behavior of the specific CIED needs to be known preoperatively.

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Table 17.8 North American manufacturers of pacemakers and implantable cardioverter–defibrillators

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   D. Precautions: Surgery unrelated to device. The chief concern is to reduce risk of hemodynamic instability due to inappropriate inhibition or triggering of output (pacing stimuli or shocks), or upper-rate pacing behavior (adaptive-rate devices). If EMI is likely to cause device malfunction and the patient does not have an adequate intrinsic rhythm, a pacemaker should be programmed to an asynchronous mode and tachycardia sensing disabled for ICD. If the device features ARP, this should be programmed off. If ICD sensing is disabled, continuous cardiac monitoring must be maintained and an external cardioverter–defibrillator must be available.

     1. Surgical sources for EMI. Technology has provided a variety of new surgical tools to assist in a variety of procedures. Many of these new technologies create EMI. It is this EMI that can cause erratic behavior in pacemakers and ICDs. Any tool that uses electricity or uses a magnet field can emit interfering signals when close to the device or heart. Locating the grounding plate as far as possible from the cautery tool reduces EMI from unipolar cautery. The pulse generator and leads should not be between the Bovie tool and grounding plate (i.e., in the current pathway). Pacing function is confirmed by monitoring heart sounds or the pulse waveform. Only the lowest possible energies and brief bursts of electrocautery or other sources of EMI such as RF should be used, especially with instability due to device malfunction. If cautery must be used in the vicinity (less than 15 cm) of the pulse generator or leads and there is significant hemodynamic instability due to EMI, then it is reasonable to place a magnet directly over the pulse generator of a pacemaker. This will cause most devices to pace asynchronously until the magnet is removed, unless the magnet mode has been programmed off. In a situation with an ICD and no device information, a magnet should not be placed over the ICD pulse generator unless EMI is unavoidable. If EMI is unavoidable, then the patient needs to be placed on cardiac monitor and a magnet will need to be placed on (and kept on) the ICD generator during cautery or RF therapy. In this case, EMI has a potential to trigger antitachycardia pacing or shocks that may destabilize the patient. By placing the magnet over the generator, the device will no longer sense or treat tachyarrhythmias. It will not react to EMI or to a real tachyarrhythmia. However, as discussed above, the magnet will not affect the pacing programming including rate response of the ICD.

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     2. External cardioversion or defibrillation. Shocks probably will not cause temporary inhibition or transient loss of capture. Today’s devices are better shielded and nearly all have a backup bradycardia pacing capability and a reset mode. Pulse generator damage is related to the distance of the external paddles from the pulse generator. All device manufacturers recommend the AP paddle configuration, with the paddles located at least 10 cm from the pulse generator. Further, it is advised that the lowest possible energies be used for cardioversion or defibrillation. After cardioversion or defibrillation, the device must be interrogated to assure proper function.

   E. Management for system implantation or revision. Except in infants and small children, in whom epicardial leads are widely used, most CIED systems use transvenous leads. The pulse generator and leads are often implanted using local anesthesia and sedation. For epicardial lead placement with a thoracotomy, general anesthesia is needed. General anesthesia or monitored anesthesia care with heavy sedation may be requested for some pacer and ICD system implants especially if the patient has significant advanced comorbidities.

      1. Lead extraction [9]—General anesthesia is often recommended for cases involving lead extractions especially in leads that are more than 10 yrs old. Cases involving lead extraction are often more prolonged procedures and carry additional procedural risk, the most concerning being catastrophic bleeding. Indications for lead extraction have expanded with recent updates in the HRS Guidelines. Class I indications for lead extraction mainly involve infected pacemaker and ICD systems and symptomatic occlusion of central veins. Other important indications involve removing nonfunctional leads to avoid future complications of superior vena cava syndrome, especially in young patients. In the case of device infection, these patients may have sepsis and are certainly at risk of becoming septic during the lead extraction. The potential bleeding sites include tearing of the superior vena cava and intracardiac perforation or avulsion. This type of procedure also involves the use of large-bore central venous sheaths up to 18F in size that may be used from both the subclavian and femoral venous sites. The prolonged procedure time involving large sheaths also places the patients at risk for pulmonary embolism or stroke caused by either air or clot. Fortunately, enhanced tools have been devised that improve patient safety and ease of extraction, including Eximer laser tools and cutting sheaths. Even with these enhanced tools, the risk of life-threatening bleeding is real and requires immediate recognition and action. Cardiothoracic surgeons and facilities need to be available within minutes if there are complications. In these situations there is an emergent need for thoracotomy and surgical repair. Tools for pericardiocentesis and chest tube insertion must be in arms reach. In addition, these cases may be further complicated by the patient being pacemaker dependent. This situation will require the use of temporary pacing that may become dislodged during the intracardiac manipulation of the leads. Because of the potential complications that can occur in lead extraction it is imperative to have continuous hemodynamic monitoring. A sudden drop in blood pressure may be the only warning signs to alert clinicians of pending circulatory collapse due to a complication from lead extraction.

      2. For all procedures requiring general anesthesia or monitored anesthesia care, consider the following:

        a. Most patients with symptomatic bradycardia will have temporary pacing. Otherwise, chronotropic drugs with backup external pacing should be available. Sedation may make an escape rhythm due to conduction disease worse.

        b. Have reliable plethysmography waveform or direct arterial blood pressure monitoring.

        c. Select the best surface ECG leads for P waves (II, V1) and for ischemia diagnosis (V5).

        d. Pulmonary artery catheters are seldom used or needed today. They may interfere with ICD lead positioning.

        e. An external cardioverter–defibrillator must be available and functioning. Defibrillator patches should be applied to the patient in the anterior–posterior configuration.

        f. With an ICD, tachycardia sensing should be disabled by a magnet or with reprogramming when unipolar electrosurgery is used.

        g. Contemporary inhalation and IV anesthetics are not known to increase defibrillation thresholds and are selected more with a view to hemodynamic tolerance. Inhalation agents and propofol may affect the morphology of sensed intracardiac electrograms and inducibility of tachyarrhythmias, which is a consideration during EP testing. Contemporary inhalation anesthetics (sevoflurane, desflurane) and small amounts of lidocaine for vascular access are not known to affect defibrillation thresholds.

        h. Paralytic agents must be used with caution during lead implant procedures. It is customary to assure that lead placement does not cause diaphragmatic or chest wall stimulation during pacing. This avoidable extracardiac stimulation will be inhibited by paralytic agents. If extracardiac stimulation occurs, the pacemaker lead usually requires repositioning.

V. Catheter or surgical modification of arrhythmia substrates.

RF catheter ablation has replaced antiarrhythmic drug therapy for treatment of many types of chronic or recurring cardiac tachyarrhythmias. Tachyarrhythmias amenable to this form of treatment include those shown at EP study to have a focal origin (triggered or automatic) or are sustained by fixed, defined re-entry circuits. Surgical ablation may be performed for these same arrhythmias if catheter ablation has failed or is not feasible. In addition, a catheter or surgical maze procedure may be used to interrupt multiple re-entry circuits associated with atrial fibrillation [10].

   A. RF catheter ablation [11]. RF catheter ablation procedures are performed in an EP laboratory using conscious sedation (generally with midazolam, fentanyl, and/or propofol). Usually, both tachyarrhythmia diagnosis and RF ablation can be performed in a single session. Three to five electrode catheters are inserted percutaneously into the femoral, internal jugular, or subclavian vein, or via a retrograde aortic or transseptal approach, and positioned within the heart to allow pacing and recording at key sites. The efficacy of RF catheter ablation depends on accurate identification of the site of origin of the arrhythmia. Once this site has been identified and the electrode catheter is positioned in direct contact with the site, RF energy is delivered through the catheter to eliminate the source or circuit of the arrhythmia. Arrhythmias that can be “cured” by RF catheter ablation and the success rates are listed in Table 17.9. RF ablation of the AV node is effective in controlling the ventricular rate in severely symptomatic patients with atrial fibrillation or multifocal atrial tachycardia when drug therapy has failed or is poorly tolerated. After AV nodal ablation all patients require a permanent pacemaker because of AV block. Pulmonary vein isolation with RF energy or cryoablation with transvenous catheters is used generally for younger patients with recurrent paroxysmal and persistent atrial fibrillation [12].

   For CIED patients undergoing RF catheter ablation, RF energy may cause electrical reset, reprogramming, over- or undersensing, and inappropriate inhibition. Rarely does RF energy lead to reset or damage at the lead–tissue interface.

Table 17.9 Tachyarrhythmias that can be “cured” by catheter RF ablation

   B. Arrhythmia surgery [13]. The potential morbidity of open chest surgery, as well as associated high costs, length of hospitalization, and delayed functional recovery, fostered the development of percutaneous catheter ablation. Nonetheless, direct surgical approaches continue to have an important role for patients with arrhythmogenic conditions refractory to catheter ablation or with associated surgical abnormalities. Surgical procedures have been designed for almost all supraventricular tachyarrhythmias but today have application primarily to the treatment of atrial fibrillation.

     1. Surgical approaches to therapy of atrial fibrillation [14]. To maintain atrial contraction and AV synchrony, preserve sinus node function, and provide symptomatic relief, Cox et al. devised the surgical MAZE procedure. With this procedure, both atrial appendages are excised and a pattern of incisions is made in the right and left atria. The maze procedure (i) eliminates most opportunities for re-entry, (ii) reduces the likelihood of fibrillation in any remaining tissue segment due to myocardial mass reduction, (iii) allows the sinus impulse to be conducted to the AV node in proper sequence via tissue strips joining adjacent segments (i.e., preserves atrial transport function), and (iv) eliminates blood stasis to reduce the risk of thromboembolism. As an isolated procedure for treating atrial fibrillation, the maze procedure has the limitation of requiring cardiopulmonary bypass and cardioplegic circulatory arrest. However, it has been used in conjunction with other cardiac operations, notably mitral valve surgery. The most recent modification of the procedure uses minimally invasive surgery and either RF current or cryoablation, resulting in fewer atriotomies.

     2. Accessory AV pathway. There are essentially two surgical approaches to division of accessory AV pathways: The endocardial and epicardial approaches. Both require a median sternotomy. With the aid of multiple-electrode recording, EP mapping of the pathways is accomplished off cardiopulmonary bypass. This is particularly attractive when the epicardial approach is to be used for division of the accessory pathway, because this technique is feasible off pump. The endocardial approach involves a supra-annular incision within the left atrium for left-sided pathways (requires aortic cross-clamping and cold cardioplegia) and from within the right atrium for pathways crossing the tricuspid annulus (requires only cardiopulmonary bypass). Accessory pathways are divided using sharp dissection. The epicardial approach does not require opening the atria. It is carried out on a normothermic beating heart without cardiopulmonary bypass. Lesions are created by cryoablation. No clear-cut superiority has been demonstrated for the endocardial or epicardial approach, at least in terms of clinical results.

     3. Other supraventricular and ventricular arrhythmias. For other supraventricular arrhythmias amenable to cure by focal ablation, surgery is reserved for patients with associated cardiac surgical abnormalities, intractable arrhythmias after failed RF catheter ablation, or arrhythmias not amenable to RF catheter ablation [15]. For patients with ventricular arrhythmias, the role of surgery must be reconsidered in view of the dramatic advances in ICD technology. Nonetheless, in selected circumstances, surgical ablation may lead to the best quality of life (e.g., spurious shocks with ICD). Patients with preserved left ventricular function have the lowest surgical risk but also good long-term survival, whatever the therapy. The surgical technique is a compromise between preservation of cardiac function and neutralization of the current or future arrhythmogenic substrates. It is based on two surgical concepts: Exclusion and ablation. Exclusion is aimed at isolating the arrhythmogenic mechanism from the rest of heart. Ablation is aimed at neutralizing the arrhythmogenic foci. Surgical techniques include ventriculotomy, transmural resection, endocardial resection, cryoablation, and laser photocoagulation. The latter two methods produce a well-demarcated mass of neutralized tissue that accomplishes the treatment goal without undue myocardial functional impairment. Cryosurgery is enhanced by cold cardioplegia, whereas laser photocoagulation can be accomplished on the normothermic, beating heart. Another surgical issue is the value of intraoperative mapping which can lead to inordinately prolonged pump times.

     4. Perioperative considerations. Whether arrhythmia surgery is performed on or off pump, the requirement for cardioplegic circulatory arrest is dictated by the surgical procedure. Arrhythmia surgery can be accomplished safely with total IV anesthesia, obviating the need for volatile inhalation anesthetics that might modify arrhythmia substrates or the results of EP testing during the surgical procedure.

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