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Temporary Pacing: Indications, Modes, and Techniques
Medical Emergencies I
0025-7125/86 $0.00
+ .20
Temporary Pacing Indications, Modes, and Techniques
Robert C. Hauser, M.D., * and Ralph M. Vicari, M.D. t
Emergency temporary pacing is a routine procedure that is performed in all medical centers and in most community hospitals. It is not only an accepted and widely applied form of therapy, but is also safe when used in the proper setting. Temporary pacing has been integral to the success of intracardiac surgery and its role in the management of medical emergencies, including acute myocardial infarction, has been established over several decades of vigorous investigation and scholarly debate. Today, temporary pacing is being used to diagnose and control acute rhythm disturbances, such as atrial flutter and ventricular tachycardia, and new leads for dual chamber applications are being introduced for physiologic pacing. Novel insertion techniques have been devised to facilitate the employment of multiple leads and single catheters are being perfected that can perform several functions. New external pacemakers will not only provide sophisticated bradyarrhythmia pacing, but will also contain antitachycardia programs, including low-energy cardioversion and defibrillation. Accordingly, the goals of this chapter are: (1) to review the indications for temporary pacing; (2) to describe and illustrate the techniques; (3) to discuss the fundamentals of electrical stimulation; and (4) to explore special applications, such as overdrive and dual chamber DDD pacing. PACING FOR BRADYARRHYTHMIAS INDICATIONS
Acute Myocardial Infarction Temporary pacing during acute myocardial infarction (AMI) may be therapeutic or prophylactic. Therapeutic pacing is always indicated when
*Associate
Professor of Medicine, Rush Medical College; and Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois tInstructor, Department of Medicine, Rush Medical College; and Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois
Medical Clinics of North America-Vol. 70, No. 4, July 1986
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814
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M.
VICARI
Figure 1. Blood supply of the conduction system. SAN = sinoatrial node. AVN = atrioventricular node. RBB = right bundle branch. LAF = left anterior fascicle. LPF = left posterior Llscicle. HB = bundle of His.
RBB
the patient has disquieting symptoms that are attributable to a bradyarrhythmia, while prophylactic pacing is warranted when certain rhythm and/or conduction disturbances appear during the early hospital phase of AMI. In all cases, the need for pacing must be weighed against the known and potential risks . The latter are directly related to the patient's clinical status, the experience of the operator, and the ability of the hospital staff to recognize and manage complications. It clearly is unwise to subject a patient to the anxiety and discomfort of a procedure for marginal indications in the midst of an AMI. It is equally imprudent, however, to withhold pacing in any circumstance when the potential benefits are well established. Thus, the decision to insert a temporary pacemaker may be influenced by local factors, including physician coverage and expertise and the availability of skilled nursing and adequate equipment. In some situations, it1llay be more sensible to use a standby external transcutaneous pacemaker, discussed below, in an asymptomatic patient than to assume the risks of pacemaker insertion under suboptimal conditions. Blood Supply of the Conduction System The blood supply of the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His (HB), and bundle branches is shown in Figure 1. The right coronary artery supplies the SA and AV nodes in 90% of patients. The SA node often receives nourishment from the left coronary system as well; thus , sinoatrial ischemia or infarction is relatively uncommon. The AV nodal artery, however, usually is the sole blood supply to the AV node, and hence AV block is three to four times more frequent during inferior than anterior infarction. The HB and left posterior fascicle (LPF) receive a dual supply from the right and left coronary arteries, while the right bundle branch block (RBBB) and left anterior fascicle (LAF) are supplied by septal perforators from the left anterior descending coronary artery. By implication, only extensive anterior infarction produces complete AV block, and proximal occlusion of the left anterior descending coronary artery may
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result in RBBB and LAF block (bifascicular block). Similarly, in the absence of preexisting disease, isolated conduction disorders involving the HB and LPF are observed infrequently in acute myocardial infarction. Atrioventricular Block First degree block alone does not require pacing, but may be a harbinger of complete AV block, which usually is preceded by type I or 11 second-degree AV block. Prophylactic pacing may be indicated if firstdegree block is associated with new onset bundle branch block. Also, it is conceivable that marked first-degree block may produce hypotension or low cardiac output by compromising atrial transport in susceptible individuals; such patients may benefit from the restoration of normal AV sequencing with dual-chamber pacing. Type I (Wenckebach) second-degree AV block is common and type 11 block is rare. Type I usually is due to block in the AV node, is almost always transient (seldom lasting longer than 48 hours), and requires pacing only if it results in symptoms. Occasionally, when type I block occurs more than 24 hours after onset of AMI, it may persist 48 hours or more. Late onset type I block generally is unresponsive to atropine, and may require temporary pacing if symptoms occur. In contrast, type 11 mandates prophylactic temporary pacing because the site of block is most often within the His-Purkinje system and unheralded asystole can occur. It may be difficult or impossible to differentiate type I from type 11 block in the presence of 2:1 conduction; in such a circumstance, it is reasonable to pace if the QRS duration is prolonged. Temporary pacing usually is indicated for complete (third-degree) AV block during AMI. Pacing may not improve survival, but it will prevent asystole, bradycardia-dependent arrhythmias or ischemia, and permit the use of drugs that affect the automaticity of the escape focus. Some physicians may elect to observe patients with complete AV block if the rate of the escape rhythm is greater than 50 beats/min and if the QRS is narrow (AV node or proximal HB block). Others may argue that the prognosis of patients who have an anterior AMI complicated by complete AV block is so poor that temporary pacing is not justified. The most common errors, however, are due to misinterpretation of the electrocardiogram (ECG). Nonconducted, premature atrial contractions may be erroneously read as second-degree AV block. Accelerated junctional or idioventricular rhythms with wide QRS complexes may masquerade as advanced or complete AV block, and concealed extrasystoles from a ventricular or HB focus may mimic AV block, especially on single-lead tracings. Intraventricular Conduction Defects The rationale and results of pacing for intraventricular conduction defects (IVCDs) have been the subjects of a recent review. 4 HB recordings play no Significant role in the decision to pace. One patient in four who presents with a new onset right bundle branch block plus left anterior or posterior fascicular block will progress to complete AV block during AMI; the risk is reduced by half if this bifascicular block is old. Nevertheless, prophylactic temporary pacing is recommended for both new and old RBBB
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+ LAFB or RBBB + LPFB. Pacing is not required for isolated RBBB, LBBB, LAFB, or LPFB. A temporary pacemaker is warranted in patients who have LBBB and who need hemodynamic monitoring, eg, Swan-Canz catheterization, because there is a small but significant risk of causing RBBB, and hence, bilateral BBB during catheter manipulation. Sinoatrial Dysfunction Sinus bradycardia is seen frequently during the early phase of AMI and usually is associated with ischemic pain. In the intensive care setting, sinus bradycardia is a relatively benign rhythm disturbance, although it has been correlated with a higher incidence of ventricular fibrillation. 1 Sinus arrest or sinoatrial block is far less common. Since most of these disturbances of sinus function are vagally mediated, atropine is the treatment of choice and temporary pacing is needed only if symptoms persist or if these bradycardias become progenitors of potentially lethal ventricular arrhythmias. BRADYARRHYTHMIAS NOT ASSOCIATED WITH MYOCARDIAL INFARCTION Acquired Atrioventricular Block The first temporary transvenous pacemaker was inserted for StokesAdams syncope due to acquired complete (third-degree) AV block (CHB) and this is still the most common indication for pacing a bradyarrhythmia that is not related to an AMI. Acute AV block may be due to drug intoxication, metabolic disturbances, connective tissue disorders, or inflammatory disease and it may occur as the result of intracardiac surgery or trauma. Acquired chronic AV block usually is of the primary idiopathic type with sclerosis of the cardiac skeleton (Lev's disease). Other common causes of chronic AV block include coronary artery disease and calcific aortic stenosis. Temporary pacing is not indicated for first-degree or type I (Wenckebach) second-degree AV block unless significant symptoms persist despite drug therapy. Likewise, pacing is not necessary for asymptomatic 2: 1 AV block with a narrow QRS. Acute type 11 or complete AV block should be paced if: (1) the patient is symptomatic, (2) QRS is wide, (3) ventricular rate is less than 50 beats/min; or (4) circumstances require drugs that may suppress escape focus automaticity. Most chronic type 11 or complete AV blocks will need permanent pacing and a temporary pacemaker may be warranted prior to implant for rate support during the insertion of the permanent lead electrodes. Intraventricular Conduction Defects As noted previously, temporary pacing is warranted prior to insertion of a balloon-tip catheter for pulmonary artery pressure monitoring in patients who have LBBB. Otherwise, prophylactic temporary pacing is not recommended for asymptomatic acute or chronic IVCDs that are not
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associated with AMI. ~oreover, temporary pacing is not indicated as a precautionary measure prior to major surgery. 1.5 Sinoatrial Dysfunction Symptomatic sinoatrial dysfunction occasionally necessitates temporary rate support while reversible causal factors, such as drug toxicity or inflammatory disease, are excluded. Most patients who have chronic symptomatic sinoatrial dysfunction do not need prophylactic temporary pacing prior to permanent pacemaker insertion. Some individuals who have paroxysmal atrial fibrillation with a slow ventricular response and/or markedly abnormal sinus function require therapeutic temporary pacing before and during the implant procedure. Such patients often do not exhibit an adequate response to atropine and electrical stimulation is necessary to ensure a stable perioperative rhythm. TECHNIQUES Pacing Modes and Pulse Generators Single and dual chamber temporary pacing may be applied using any one of the pacing modes and a variety of pulse-generator and lead systems. The type of pacing is best described by the International Classification of Heart Diseases (ICHD) code, which was developed to facilitate communication. 14 As illustrated in Figure 2, the first letter of the code signifies the chamber(s) paced, ie, V for ventricle, A for atrium, and D for both atrium and ventricle; the second letter represents the chamber(s) sensed (A, V, or D). The third letter describes the mode of response to a sensed P or R wave: I for inhibited, T for triggered, and D for dual mode of response. Additional letters and positions are intended primarily for permanent pacemakers. The most common pacing mode is VVI, or R-wave-inhibited, where pacing and sensing occur via a single lead in the ventricle and the pacemaker's output is inhibited when an R wave is sensed during the pacemaker's escape interval. Similarly, the AAI mode is P-wave-inhibited pacing; obviously, the pacing lead must be in the atrium. The triggered mode of response (AAT or VVT) rarely is used for single-chamber applications. A number of single-chamber external pulse generators are commercially available. Dual chamber pacing requires two leads, atrial and ventricular, and a pulse generator capable of functioning in one or more dual chamber modes. The AV sequential (DVI) mode paces in the atrium and the ventricle but senses only in the ventricle; since it does not sense in the atrium, competitive rhythms, including atrial fibrillation and supraventricular tachycardia (SVT), may occur in individuals who are prone to these dysrhythmias. A commercially available external DVI AV sequential pulse generator (~edtronic Model 5330, ~edtronic, Inc., Minneapolis, Minnesota) also can be used for single-chamber pacing. Adjustable settings include rate (ppm), AV interval (ms), ventricular sensitivity (m V), and stimulus output amplitude (volts) in both chambers.
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TYPE
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VrCARI
MODE OF RESPONSE
CHAMBER SENSED
VENTRICULAR f----------l~V INHIBITED
INHIBITED BY R-WAVE
VENTRICULAR f----------l~V TRIGGERED
TRIGGERED BY R-WAVE
VVI
VVT
ATRIAL INHIBITED
AAI
.-------------------------------------- V
.-------------------------------------- V
INHIBITED BY P-WAVE
I-------~A
.-------------------------------------- A
INHIBITED BY R-WAVE
1--------l~A AV SEQUENTIAL 1------l~V
OVI
----------------------------------- --- V
~--~--~--------.A AV DELAY V UNIVERSAL • ______________________________________
TRIGGERED BY P-WAVE
A
INHIBITED BY R-WAVE
'---__ 0_0_0_---->.-------------------------------------- V Figure 2. Types of pacing modes and associated codes. A text for discussion.
=
atrium. V
=
ventricle. See
Temporary fully automatic AV universal (DDD) pacing is possible using functional implantable DDD models that have been removed from patients for reasons other than pulse generator failure l2 (Fig. 3). Commercial external DDD pulse generators also are being introduced. As the code implies, DDD pacemakers sense and pace in both chambers; it will inhibit when a spontaneous QRS is sensed in the ventricle and a native P wave will trigger a ventricular output stimulus following the electronic AV interva1. 9 Thus, the DDD ECG may show atrial pacing (Fig. 4), AV sequential pacing (Fig. 4), or P-wave-triggered ventricular pacing (Fig. 5). DDD pacemakers have lower and upper rate settings, eg, 70 ppm and 150 ppm respectively, and between these two settings, the sinus or atrial rate will govern the frequency of ventricular stimulation. If the sinus rate falls below the lower rate, then atrial or AV sequential pacing will occur. When the sinus rate exceeds the upper rate (Fig. 6), varying degrees of electronic AV block will appear in order to limit the rate of ventricular pacing. No pacemaker stimuli will be observed if the patient's sinus rate is faster than the lower rate and if the AV conduction time is less than the electronic AV interval; similarly, a sinus or supraventricular tachycardia with intact AV conduction will not be affected by the pacemaker. Pacemaker-mediated tachycardia (PMT) is the principal electrophysiologic complication of DDD pacing. PMT is an artificial re-entrant tachycardia wherein the pacemaker is the antegrade limb and the ventriculoatrial
TEMPOHAHY PACING
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Figure 3. Adaptation of permanent unipolar dual-chamber pulse generator for temporary applications. The cathode (distal tip) electrodes of the atrial and ventricular leads are connected to the pulse generator using the existing set screws. An anode clip connector can be fabricated by most hospital biomedical staffs. The anode (proximal ring) electrodes of both leads are grounded to the pulse generator housing using the anode clip. For bipolar pulse generators (not shown), the cathodes and anodes of both leads are connected directly to the pulse generator. The pulse generator and lead connector should be isolated from the environment by a plastic bag or rubber glove.
(V A) pathway is the retrograde limb of the tachycardia circuit (Fig. 7). Most PMTs are initiated by a ventricular ectopic beat that is conducted retrogradely to the atrium, where the ectopic P wave is sensed by the DDD atrial sensing circuit; in turn, the P wave triggers ventricular pacing after the programmed AV interval. This endless loop tachycardia will persist until the VA pathway is blocked or until the retrograde P wave fails to trigger a ventricular stimulus. P:\1T will be observed most frequently in patients who have intact AV conduction; however, approximately 15% of individuals who have ante grade block will conduct retrogradely over a VA pathway. A PMT can be abolished by prolonging the postventricular atrial refractory period (PVARP) so that the retrograde P wave is not sensed; a PVARP of 300 ms will prevent or terminate the vast majority of PMTs. Alternatively, the pacemaker can be set to the DVI or VVI mode. Some DDD models have a DDI mode that does not produce P-wave-triggered ventricular pacing and hence PMTs are not possible. 6 Further, DDI pacing is useful in patients who have paroxysmal atrial fibrillation/flutter or SVT; in this mode, sinus rhythm or atrial tachyarrhythmias will inhibit atrial stimulation, thereby preventing competition, and they will not trigger ventricular pacing. When using an implantable DDD pulse generator as a temporary external pacemaker, it is necessary to have the associated programmer in order to adjust the various p'lrameters to the desired settings. In most
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VA VV
AV ----.----
AV_
AV~
AR- - + ........
~
VR
VR
LRL
• _ LRL
URL
URL
-------.
AR ..................
AR . .... ......... .
VR •
LRl
URL
Figure 4. Diagram of a DDD pulse generator's response to a conducted sinus beat (1), and in the presence of sinus bradycardia, with intact AV conduction (2), and sinus bradycardia with AV block (3). VA = interval between ventricular sensed and atrial paced events. VV = interval between ventricular sensed and paced events. AV = atrioventricular delay. AR = atrial refractory period. VR = ventricular refractory period. LRL = lower rate limit. URL = upper rate limit. The postventricular atrial refractory period (also known as PVARP) is that portion of the atrial refractory period following a ventricular sensed or paced event. Solid horizontal arrows, beginning and end of the AV, AR, VR, LRL, and URL intervals. Dashed lines, the potential durations of these intervals if sensed or paced ventricular events had not reset the intervals. Dotted lines, portions of the AR intervals initiated by the atrial event. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
2
-
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VR
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.............
..
VR
_L_R_L_ _ _ _ _ _ _ _ _ _ .. URL
-
AV-----
..
..
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LRL
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n
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•
Figure 5. Diagram of DDD pulse generator behavior during sinus rhythm, with intact AV conduction (beats 1 and 2), and a paced ventricular beat (3) that is triggered by a spontaneous P wave. For definition of abbreviations, see legend to Figure 4. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
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SINUS RATE
LOWER RATE =60bpm UPPER RATE =150bpm AV INTERVAL = 150msec = 83 bpm SINUS RATE = 140 bpm
SINUS RATE
=152 bpm
SINUS RATE
=163 bpm
Figure 6. This DDD pacemaker was programmed to the settings shown. As the sinus rate exceeds the upper rate of 150 beats/m in (bpm), electronic AV block occurs because the P waves fall during the atrial refractory periods (arrows).
situations, the following values are appropriate: (1) lower rate = 60 beats/min; (2) upper rate = 130 beats/min; (3) AV interval = 150 to 200 ms; (4) PVARP = 300 ms; (5) ventricular refractory period = 300 ms; (6) atrial sensitivity = 0.5 to 1.0 mY; (7) ventricular sensitivity = 1.5 to 2.5 mY; (8) atrial and ventricular output = 5 V and 0.5 ms or 6 mA and 0.6 ms. Inhibition of ventricular pacing by an atrial stimulus (crosstalk) may occur if the atrial output and/or ventricular sensitivity are high. The incidence of all types of electrical interference with pacemaker function can be reduced by using bipolar lead systems.
Figure 7. (A) DDD pacemaker-mediated tachycardia initiated by P-wave-conducted retrograde to the atria following a ventricular premature beat. AR = atrial refractory period of pulse generator's atrial sensing circuit. A = atrium. V = ventricle. (B) Prevention of endless loop DDD pacemaker tachycardia by extension of the atrial sensing circuit's refractory period (AR) to prevent detection of retrograde P wave following VPC. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
A
B
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Selection of Pacing Mode Selection of thc most suitable temporary pacing mode is based on four considerations, including: (1) therapcutic objectives; (2) electrophysiologic findings, ie, rhythm and conduction; (3) hemodynamic needs; and (4) technical factors. If the object of temporary pacing is to provide prophylactic rate support, then single-chamber ventricular pacing usually will suffice. Examples of such patients include those who have suffered an AMI that is complicated by RBBB + LAFB, or individuals who need temporary pacing prior to permanent pacemaker insertion for acquired complete AV block. In general, therefore, the routine use of prophylactic, dual-chamber tempor;lry pacing cannot bc justified. If a goal of temporary pacing is to preserve function, however, one should select the most physiologic approach. The patient's clinical electrophysiology dictates certain pacing requirements. Single-chamber, atrial pacing (AAI) may be adequate for individuals who have slow sinus rates; atrial pacing is contraindicated in the presence of AV block and it is ineffective in the presence of atrial fibrillation or atrial paralysis. As will be discussed, rapid atrial pacing may be applied to terminate atrial flutter or SVT. The AV sequential (DVI) or DDD mode may be employed for sinus bradyarrhythmias complicated by AV block; DVI pacing should be avoided if atrial competition is likely to produce atrial dysrhythmias. The DDD mode is the most adaptable of all the pacing modalities; it not only provides basic rate support in both chambers but also responds to atrial activity. Except for established atrial fibrillation, there are no contraindications to DDD pacing. Hemodynamically, atrial pacing maintains AV synchrony and preserves the normal sequence of ventricular depolarization. In the presence of AV block, AV sequential pacing coordinates atrial and ventricular systole, but right ventricular stimulation may decrease stroke volume. Compared with ventricular pacing, atrial and AV sequential pacing increase stroke volume 10% to 20% by augmenting preload, and they reduce mean atrial pressures by eliminating AV dissociation (Fig. 8). The DDD mode not only offers the same hemodynamic advantages of atrial or AV sequential pacing, but also provides rate responsiveness. Rate responsive pacing is the major mechanism by which large increments in cardiac output are achieved. Thus, the DDD pacemaker varies its pacing rate based on a physiologic marker, ie, sinus node activity, that reflects an increased need for blood flow. It may be concluded that the AAI mode is satisfactory for therapeutic pacing if AV conduction is normal and that DDD pacing provides optimum hemodynamic benefits in the presence of AV block. New sensors (stroke volume, dp/dt), so-called artificial sinus nodes, are being developed to provide rate responsiveness when sinus activity is impaired. R Therapeutic pacing is indicated in patients who havc acute myocardial infarction, including right ventricular infarction, ischemic heart disease, hypertrophic cardiomyopathy, hypertensive heart disease, aortic stenosis, and in any circumstance where ventricular pacing produces circulatory embarrassment. Technical obstacles may intervene to preclude atrial or dual-chamber
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TE:\IPORAI\Y PA-CI"!G
LV
Dimensions
Stroke Volume
10-20%
~
Contractilityf-----
Myocardial Fiber Shortening
Cardiac Output
Afterload Peripheral Circulation
Figure 8, Atrial and AV sequential pacing preserves AV synchrony, which accounts for 10% to 20% of the stroke volume, by increasing the extent of myocardial fiher shortening via the Frank-Starling mechanism, Cardiac output is the product of the stroke volume and the heart rate, DDD pacing improves cardiac output hy preserving AV synchrony and hy adjusting the pacing rate in response to sinus activity, LV = left ventricle, (From Hallser, It G,: Techniques for improving cardiac performance with implantahle devices, P,A,C,E., 7:1234, 1984; with permission,)
pacing, but the number of such difficulties are decreasing as new leads and pulse generators are introduced, The most common problems are: (1) venous access; (2) lead stability; (3) atrial sensing; (4) high threshold(s); (,5) arrhythmias; and (6) interference with or by a balloon-tipped catheter in the pulmonary artery. While these technical considerations are dcalt with elsewhere in this chapter, they are mentioned here because each may influence the selection of pacing mode.
LEADS AND INSERTION TECHNIQUES Venous Access Virtually any lead can be inserted into a major vein using a needle, guidewire, and sheath-dilator set. Multiple leads or catheters may be introduced with a single venous puncture and a sufficiently large diameter sheath or with two smaller, peel-away sheaths. The guidewire is not removed until all leads or catheters arc in satisfactory position so that recannulation can be performed without a second venous puncture,2 Although attempts to enter the subclavian or internal jugular vein involve certain risks, pacing leads that are inserted via these routes arc readily positioned in either chamber. Further, subclavian and internal jugular leads tend to be more stable and they allow greater patient mobility, Access to
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the central venous circulation hom the brachial vein is more difncult, particularly ff)r multiple leads, and thus this approach generally is unsuitable for emergency pacing. Similarly, femoral leads are difficult to position quickly and stable atrial pacing is not easy to maintain. It is rarely necessary to insert an emergency pacing lead via the percutaneous, transthoracic route/ 6 coronary laceration and hemopericardium are recognized complications of this method. Nevertheless, transthoracic pacing may be lifesaving in the presence of asystole when the right ventricle cannot be accessed by safer methods. Pacing Leads A variety of temporary leads or catheters are available for single and dual-chamber pacing. 1 The semifloating or floating types have largely replaced the stiff woven Dacron catheters because the latter require fluoroscopy during placement while the former may be positioned using only electrocardiographic monitoring. Moreover, stiff catheters are more likely to perforate or displace and their long-term threshold behavior is unsatisfactory. Flow-directed, balloon-tipped pacing leads are easy to locate in the right ventricular apex and they are so flexible that malposition and exit block are infrequent problems. A preformed, atrial J temporary pacing lead has been designed to be passed via the subclavian vein into the right atrium without fluoroscopic guidance;l3 it can be used together with any ventricular lead for dualchamber pacing. A single catheter with fixed or moveable flared atrial electrodes that are mounted on a straight ventricular lead may simplify the placement of a dual chamber system. While pacing Swan-Canz catheters may be used for temporary AY stimulation, the results are mixed because balloon inflation may displace the electrodes and, consequently, capture may be lost. Novel Swan-Canz catheters that contain a separate lumen for independent pacing probes are being evaluated. Transthoracic ventricular pacing leads are notoriously unstable, but a recently introduced, flared model may impart some security.] Another design incorporates a channel that allows the instillation of intracardiac drugs. Pacing Threshold and Electrogram Measurements Satisfactory lead performance cannot be obtained unless the acute threshold of stimulation is low and the intracardiac signal (R wave or P wave) has sufficient amplitude for sensing. Thresholds of less than 1 Yor 1 mA should be sought for atrial and ventricular leads. The P wave and R wave peak-to-peak amplitudes should be greater than 1 and 6 mY, respectively. Thresholds can be assessed with variable-output, external pulse generators and the intracardiac signals may be measured from recordings that are made directly from the electrodes. Both threshold and electrogram values can be acquired using commercial pacing system analyzers. Failure to obtain an adequate threshold or intracardiac signal may be due to: (1) poor contact between the electrode and endocardium; (2) local endocardial necrosis or fibrosis; (3) hypoxia or acidosis; (4) hypokalemia; and (5) drug effects, particularly type I antiarrhythmics. The former is by
TE"IPORARY PACIKC
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far the most common cause and the only solution is to reposition the lead. Endocardial necrosis or fibrosis may he encountered in patients with right ventricular AMI and fluoroscopy may be needed to find an acceptable pacing site. A low amplitude R or P wave can result when the electrodes of the temporary bipolar lead are oriented perpendicular to the depolarization wave front in the ventricle or atrium. When this occurs, a satisfactory signal can be obtained by relocating the electrodes, perhaps in a different plane, while monitoring the intracardiac signal. It is rarely necessary to unipolarize the electrodes hy using a skin or subcutaneous electrode as the anode. The threshold of stimulation rises after lead insertion because an inflammatory response occurs at the electrode-tissue interface. Thus, the current (mA) or voltage (V) required to capture increases as the stimulating electrode is separated from excitable myocardium. The magnitude of the threshold rise may be three- to four-fold over a period of hours or days. Accordingly, if the acute threshold is 0.7 V, a safety margin of 2 to 3 V is warranted. The important characteristics of the intracardiac electrogram do not change significantly after lead insertion, provided the electrodes remain stable. Nevertheless, a sensing safety margin that is twice the measured P or R wave amplitude is recommended. Complications The most common complications include: (1) lead displacement, (2) thrombophlebitis, (3) infection, and (4) extracardiac muscle stimulation. Other complications are related to the method used to gain venous access, cg, subclavian puncture. Backward displacement of the lead results in pacing malfunction; in addition, an unstable lead may induce arrhythmias. Myocardial perforation is rare with the softer, more compliant leads, but woven catheters are particularly prone to this complication. Perforation may be heralded hy extracardiac muscle stimulation and the paced ECG may show RBBB because the electrode is stimulating the left ventricular epimyocardium. Tamponade is infrequent, but it may be delayed. Management includes lead withdrawal and replacement, usually with a soft catheter under fluoroscopic control and subsequent surveillance for evidence of hemodynamic compromise. Thrombophlebitis is associated with femoral and brachial vein insertion sites. Lead removal and reinsertion via a different venous system usually are indicated. While brachial vein thrombophlebitis may be treated without anticoagulation, femoral vein involvement requires heparinization unless it is contraindicated. External Transcutaneous Pacing The external transcutaneous pacemaker (ETCP), originally described by Zoll in 1952, has been reintroduced in the form of an improved device that operates in the demand mode. 5 Stimuli are delivered via two large surfllCe area electrodes that are applied to the skin of the chest wall. Although long constant current pulses are used, some patients cannot tolerate the discomfort and a smaller proportion cannot be paced. Despite these potential disadvantages, ETCP is useful in a number of situations. Emergency pacing can be instituted by paramedical personnel or in
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hospitals that lack the resources required to insert temporary pacemakers. A standby ETCP may be a reasonable alternative to prophylactic transvenous pacing in the intensive care unit, emergency room, operating room, or cardiac catheterization laboratory. PACING FOR TACHYARRHYTHMIAS Temporary cardiac pacing has been used to correct and control a variety of atrial and ventricular tachyarrhythmias. Its effectiveness is well established, particularly in the postoperative cardiac surgical patient in whom, due to prior placement of temporary epicardial electrodes, it is often the preferred mode of therapy. 17 Temporary antitachycardia pacing has been applied to arrhythmias refractory to medical treatment and those associated with digitalis intoxication. In the latter case, the hazards associated with DC cardioversion can be avoided. The most frequent therapeutic mode of antitachycardia pacing is overdrive burst termination. Two general principles of this type of pacing are: (1) effective pacing rates for termination of tachycardias generally are 110% to 140% of the spontaneous rate of the tachycardia, and (2) catheter proximity to the origin of the tachycardia influences success rates for conversion. An effective technique for interruption of most tachyarrhythmias is to position the pacing catheter in the right atrium or right ventricle and initiate stimulation at 10 to 20 beats/min above the intrinsic rate. Pacing rates are increased progressively by 10 beats/min, unless hemodynamic instability results, until successful conversion ensues. Type I atrial flutter (atrial rate 230-350 beats/min and negative flutter waves leads 11, Ill, and a VF) usually can be successfully interrupted by positioning the pacing catheter high in the right atrium. Burst pacing is initiated as described above and continued for 20 to 30 seconds. The hallmark of successful conversion is a change in polarity of atrial complexes from negative to positive in the inferior leads. Occasionally, atrial fibrillation may be precipitated by this technique. This rhythm, however, usually is transient and, if persistent, generally is easier to treat medically than atrial flutter. A variety of other supraventricular tachyarrhythmias are amenable to overdrive burst pacing with techniques similar to those described above. Ventricular tachycardia can be interrupted by application of single or double extrastimuli in the majority of patients who can remain hemodynamically stable during programmed testing. 11 Overdrive burst pacing also has been successful in converting ventricular tachycardia; however, pacing rates above 135% of the intrinsic rate increase the risk of ventricular fibrillation. It is recommended that standby DC cardioversion units be available immediately in any patient undergoing anti tachycardia pacing. Ventricular tachyarrhythmias associated with a prolonged QT interval, also known as "torsades de pointes," have been controlled effectively by temporary cardiac pacing. 10 This arrhythmia is most likely the result of excessive dispersion of ventricular refractory periods, and often is associated with drug toxicity, particularly the type I antiarrhythmic agents. The right atrium is the preferred site of stimulation, unless AV block is present, since
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TEMPOHARY PACING
normal AV synchrony is preserved. Pacing at heart rates above the intrinsic rate, especially in patients with sinus bradycardia, shortens cycle length and QT interval, providing more uniformity of ventricular refractory periods. A specially designed catheter recently was devised that allows successful transvenous cardioversion of ventricular tachycardia and fibrillation in the majority of patients tested. 18 The future of anti tachycardia pacing may include devices able to overdrive pace ventricular tachycardia with backup cardioversion and perhaps defibrillation.
REFERENCES 1. Adgey, A. A. J., Geddes, J. S., Webb, s. W., et aI.: Acute phase of myocardial infarction. Lancet, 2:501, 1971. 2. Belott, P. H.: Retaining guidewire, introducer technique for unlimited access to the central circulation: A review. Clin. Prog. Pacing ElectrophysioI., 1 :59, 1983. 3. Billhardt, R. A.: Temporary pacing. Clin. Prog. Pacing ElectrophysioI., 2:305, 1984. 4. Codini, M. A.: Conduction disturbances in acute myocardial infarction: The use of pacemaker therapy. Clin. Prog. Pacing EledrophysioI., 1:142, 1983. 5. Falk, R. H., Zoll, P. M., and Zoll, R. H.: Safety and efficacy of non-invasive cardiac pacing. N. EngI. J. Med., 309:1166, 1983. 6. Floro, V., Castellanet, M., Florio, J., et al.: DOl: A new mode for cardiac pacing. Clin. Prog. Pacing ElectrophysioI., 2:255, 1984. 7. Furman, S., and Fisher, J. D.: Endless loop tachycardia in an AV universal (ODD) pacemaker. PACE, 5:486, 1982. 8. Hauser, R. G.: Techniques for improving cardiac performance with implantable devices. PACE, 7:1234, 1984. 9. Hauser, R. G.: The electrocardiography of AV universal ODD pacemakers. PACE, 6:399, 1983. 10. Kahn, M. M., Logan, K. R., McComb, J. M., et aI.: Management of recurrent ventricular tachyarrhythmias associated with Q-T prolongation. Am. J. CardioI., 47:1301, 1981. 11. Kastor, J. A., Horowitz, L. N., Harken, A. H., et al.: Clinical electrophysiology of ventricular tachycardia. :'11. EngI. J. Med., 304:1004,1981. 12. Littleford, P. 0.: Physiologic temporary pacing: Techniques and indications. Clin. Prog. Pacing ElectrophysioI., 2:236, 1984. 13. Littleford, P. 0., and Pepine, C. J.: A new temporary atrial pacing catheter inserted percutaneously into the subclavian vein without fluoroscopy. PACE, 4:458, 1981. 14. Parsonnet, V., Furman, S., Smith, N. P. D., et al.: Optimal resources for implantable cardiac pacemakers. Circulation, 68:277A, 1983. 15. Pastore, J. 0., Yurchak, P. M., Janis, K. M., et aI.: The risk of advanced heart block in surgical patients with right bundle branch block and left axis deviation. Circulation, 57:677, 1978. 16. Roberts, J. R., and Greenberg, M. I.: Emergency transthoracic pacemaker. Ann. Emerg. Med., lO:600, 1981. 17. Waldo, A. L., Wells, J. L., Cooper, T. B., et al.: Temporary pacing: Applications and techniques in the treatment of cardiac arrhythmias. Prog. Cardiovasc. Dis., 23:451, 1981. 18. Zipes, D. P., Jackman, W. M., Heger, J. J., et al.: Clinical transvenous cardioversion of recurrent life threatening ventricular tachyarrhythmias: Low energy synchronized cardioversion of ventricular tachvcardia and termination of ventricular fibrillation in patients using a catheter electrod~. Am. Heart J., 103:789, 1982. Section of Cardiology Rush-Presbyterian-St. Luke's Medical Center 1753 West Congress Parkway Chicago, IL 60612
0025-7125/86 $0.00
+ .20
Temporary Pacing Indications, Modes, and Techniques
Robert C. Hauser, M.D., * and Ralph M. Vicari, M.D. t
Emergency temporary pacing is a routine procedure that is performed in all medical centers and in most community hospitals. It is not only an accepted and widely applied form of therapy, but is also safe when used in the proper setting. Temporary pacing has been integral to the success of intracardiac surgery and its role in the management of medical emergencies, including acute myocardial infarction, has been established over several decades of vigorous investigation and scholarly debate. Today, temporary pacing is being used to diagnose and control acute rhythm disturbances, such as atrial flutter and ventricular tachycardia, and new leads for dual chamber applications are being introduced for physiologic pacing. Novel insertion techniques have been devised to facilitate the employment of multiple leads and single catheters are being perfected that can perform several functions. New external pacemakers will not only provide sophisticated bradyarrhythmia pacing, but will also contain antitachycardia programs, including low-energy cardioversion and defibrillation. Accordingly, the goals of this chapter are: (1) to review the indications for temporary pacing; (2) to describe and illustrate the techniques; (3) to discuss the fundamentals of electrical stimulation; and (4) to explore special applications, such as overdrive and dual chamber DDD pacing. PACING FOR BRADYARRHYTHMIAS INDICATIONS
Acute Myocardial Infarction Temporary pacing during acute myocardial infarction (AMI) may be therapeutic or prophylactic. Therapeutic pacing is always indicated when
*Associate
Professor of Medicine, Rush Medical College; and Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois tInstructor, Department of Medicine, Rush Medical College; and Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois
Medical Clinics of North America-Vol. 70, No. 4, July 1986
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814
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M.
VICARI
Figure 1. Blood supply of the conduction system. SAN = sinoatrial node. AVN = atrioventricular node. RBB = right bundle branch. LAF = left anterior fascicle. LPF = left posterior Llscicle. HB = bundle of His.
RBB
the patient has disquieting symptoms that are attributable to a bradyarrhythmia, while prophylactic pacing is warranted when certain rhythm and/or conduction disturbances appear during the early hospital phase of AMI. In all cases, the need for pacing must be weighed against the known and potential risks . The latter are directly related to the patient's clinical status, the experience of the operator, and the ability of the hospital staff to recognize and manage complications. It clearly is unwise to subject a patient to the anxiety and discomfort of a procedure for marginal indications in the midst of an AMI. It is equally imprudent, however, to withhold pacing in any circumstance when the potential benefits are well established. Thus, the decision to insert a temporary pacemaker may be influenced by local factors, including physician coverage and expertise and the availability of skilled nursing and adequate equipment. In some situations, it1llay be more sensible to use a standby external transcutaneous pacemaker, discussed below, in an asymptomatic patient than to assume the risks of pacemaker insertion under suboptimal conditions. Blood Supply of the Conduction System The blood supply of the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His (HB), and bundle branches is shown in Figure 1. The right coronary artery supplies the SA and AV nodes in 90% of patients. The SA node often receives nourishment from the left coronary system as well; thus , sinoatrial ischemia or infarction is relatively uncommon. The AV nodal artery, however, usually is the sole blood supply to the AV node, and hence AV block is three to four times more frequent during inferior than anterior infarction. The HB and left posterior fascicle (LPF) receive a dual supply from the right and left coronary arteries, while the right bundle branch block (RBBB) and left anterior fascicle (LAF) are supplied by septal perforators from the left anterior descending coronary artery. By implication, only extensive anterior infarction produces complete AV block, and proximal occlusion of the left anterior descending coronary artery may
TEMPORARY PACING
815
result in RBBB and LAF block (bifascicular block). Similarly, in the absence of preexisting disease, isolated conduction disorders involving the HB and LPF are observed infrequently in acute myocardial infarction. Atrioventricular Block First degree block alone does not require pacing, but may be a harbinger of complete AV block, which usually is preceded by type I or 11 second-degree AV block. Prophylactic pacing may be indicated if firstdegree block is associated with new onset bundle branch block. Also, it is conceivable that marked first-degree block may produce hypotension or low cardiac output by compromising atrial transport in susceptible individuals; such patients may benefit from the restoration of normal AV sequencing with dual-chamber pacing. Type I (Wenckebach) second-degree AV block is common and type 11 block is rare. Type I usually is due to block in the AV node, is almost always transient (seldom lasting longer than 48 hours), and requires pacing only if it results in symptoms. Occasionally, when type I block occurs more than 24 hours after onset of AMI, it may persist 48 hours or more. Late onset type I block generally is unresponsive to atropine, and may require temporary pacing if symptoms occur. In contrast, type 11 mandates prophylactic temporary pacing because the site of block is most often within the His-Purkinje system and unheralded asystole can occur. It may be difficult or impossible to differentiate type I from type 11 block in the presence of 2:1 conduction; in such a circumstance, it is reasonable to pace if the QRS duration is prolonged. Temporary pacing usually is indicated for complete (third-degree) AV block during AMI. Pacing may not improve survival, but it will prevent asystole, bradycardia-dependent arrhythmias or ischemia, and permit the use of drugs that affect the automaticity of the escape focus. Some physicians may elect to observe patients with complete AV block if the rate of the escape rhythm is greater than 50 beats/min and if the QRS is narrow (AV node or proximal HB block). Others may argue that the prognosis of patients who have an anterior AMI complicated by complete AV block is so poor that temporary pacing is not justified. The most common errors, however, are due to misinterpretation of the electrocardiogram (ECG). Nonconducted, premature atrial contractions may be erroneously read as second-degree AV block. Accelerated junctional or idioventricular rhythms with wide QRS complexes may masquerade as advanced or complete AV block, and concealed extrasystoles from a ventricular or HB focus may mimic AV block, especially on single-lead tracings. Intraventricular Conduction Defects The rationale and results of pacing for intraventricular conduction defects (IVCDs) have been the subjects of a recent review. 4 HB recordings play no Significant role in the decision to pace. One patient in four who presents with a new onset right bundle branch block plus left anterior or posterior fascicular block will progress to complete AV block during AMI; the risk is reduced by half if this bifascicular block is old. Nevertheless, prophylactic temporary pacing is recommended for both new and old RBBB
816
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,\;1. VICARI
+ LAFB or RBBB + LPFB. Pacing is not required for isolated RBBB, LBBB, LAFB, or LPFB. A temporary pacemaker is warranted in patients who have LBBB and who need hemodynamic monitoring, eg, Swan-Canz catheterization, because there is a small but significant risk of causing RBBB, and hence, bilateral BBB during catheter manipulation. Sinoatrial Dysfunction Sinus bradycardia is seen frequently during the early phase of AMI and usually is associated with ischemic pain. In the intensive care setting, sinus bradycardia is a relatively benign rhythm disturbance, although it has been correlated with a higher incidence of ventricular fibrillation. 1 Sinus arrest or sinoatrial block is far less common. Since most of these disturbances of sinus function are vagally mediated, atropine is the treatment of choice and temporary pacing is needed only if symptoms persist or if these bradycardias become progenitors of potentially lethal ventricular arrhythmias. BRADYARRHYTHMIAS NOT ASSOCIATED WITH MYOCARDIAL INFARCTION Acquired Atrioventricular Block The first temporary transvenous pacemaker was inserted for StokesAdams syncope due to acquired complete (third-degree) AV block (CHB) and this is still the most common indication for pacing a bradyarrhythmia that is not related to an AMI. Acute AV block may be due to drug intoxication, metabolic disturbances, connective tissue disorders, or inflammatory disease and it may occur as the result of intracardiac surgery or trauma. Acquired chronic AV block usually is of the primary idiopathic type with sclerosis of the cardiac skeleton (Lev's disease). Other common causes of chronic AV block include coronary artery disease and calcific aortic stenosis. Temporary pacing is not indicated for first-degree or type I (Wenckebach) second-degree AV block unless significant symptoms persist despite drug therapy. Likewise, pacing is not necessary for asymptomatic 2: 1 AV block with a narrow QRS. Acute type 11 or complete AV block should be paced if: (1) the patient is symptomatic, (2) QRS is wide, (3) ventricular rate is less than 50 beats/min; or (4) circumstances require drugs that may suppress escape focus automaticity. Most chronic type 11 or complete AV blocks will need permanent pacing and a temporary pacemaker may be warranted prior to implant for rate support during the insertion of the permanent lead electrodes. Intraventricular Conduction Defects As noted previously, temporary pacing is warranted prior to insertion of a balloon-tip catheter for pulmonary artery pressure monitoring in patients who have LBBB. Otherwise, prophylactic temporary pacing is not recommended for asymptomatic acute or chronic IVCDs that are not
817
TEVlPOHAHY PACI:-.!G
associated with AMI. ~oreover, temporary pacing is not indicated as a precautionary measure prior to major surgery. 1.5 Sinoatrial Dysfunction Symptomatic sinoatrial dysfunction occasionally necessitates temporary rate support while reversible causal factors, such as drug toxicity or inflammatory disease, are excluded. Most patients who have chronic symptomatic sinoatrial dysfunction do not need prophylactic temporary pacing prior to permanent pacemaker insertion. Some individuals who have paroxysmal atrial fibrillation with a slow ventricular response and/or markedly abnormal sinus function require therapeutic temporary pacing before and during the implant procedure. Such patients often do not exhibit an adequate response to atropine and electrical stimulation is necessary to ensure a stable perioperative rhythm. TECHNIQUES Pacing Modes and Pulse Generators Single and dual chamber temporary pacing may be applied using any one of the pacing modes and a variety of pulse-generator and lead systems. The type of pacing is best described by the International Classification of Heart Diseases (ICHD) code, which was developed to facilitate communication. 14 As illustrated in Figure 2, the first letter of the code signifies the chamber(s) paced, ie, V for ventricle, A for atrium, and D for both atrium and ventricle; the second letter represents the chamber(s) sensed (A, V, or D). The third letter describes the mode of response to a sensed P or R wave: I for inhibited, T for triggered, and D for dual mode of response. Additional letters and positions are intended primarily for permanent pacemakers. The most common pacing mode is VVI, or R-wave-inhibited, where pacing and sensing occur via a single lead in the ventricle and the pacemaker's output is inhibited when an R wave is sensed during the pacemaker's escape interval. Similarly, the AAI mode is P-wave-inhibited pacing; obviously, the pacing lead must be in the atrium. The triggered mode of response (AAT or VVT) rarely is used for single-chamber applications. A number of single-chamber external pulse generators are commercially available. Dual chamber pacing requires two leads, atrial and ventricular, and a pulse generator capable of functioning in one or more dual chamber modes. The AV sequential (DVI) mode paces in the atrium and the ventricle but senses only in the ventricle; since it does not sense in the atrium, competitive rhythms, including atrial fibrillation and supraventricular tachycardia (SVT), may occur in individuals who are prone to these dysrhythmias. A commercially available external DVI AV sequential pulse generator (~edtronic Model 5330, ~edtronic, Inc., Minneapolis, Minnesota) also can be used for single-chamber pacing. Adjustable settings include rate (ppm), AV interval (ms), ventricular sensitivity (m V), and stimulus output amplitude (volts) in both chambers.
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HAUSER AND RALPH
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VrCARI
MODE OF RESPONSE
CHAMBER SENSED
VENTRICULAR f----------l~V INHIBITED
INHIBITED BY R-WAVE
VENTRICULAR f----------l~V TRIGGERED
TRIGGERED BY R-WAVE
VVI
VVT
ATRIAL INHIBITED
AAI
.-------------------------------------- V
.-------------------------------------- V
INHIBITED BY P-WAVE
I-------~A
.-------------------------------------- A
INHIBITED BY R-WAVE
1--------l~A AV SEQUENTIAL 1------l~V
OVI
----------------------------------- --- V
~--~--~--------.A AV DELAY V UNIVERSAL • ______________________________________
TRIGGERED BY P-WAVE
A
INHIBITED BY R-WAVE
'---__ 0_0_0_---->.-------------------------------------- V Figure 2. Types of pacing modes and associated codes. A text for discussion.
=
atrium. V
=
ventricle. See
Temporary fully automatic AV universal (DDD) pacing is possible using functional implantable DDD models that have been removed from patients for reasons other than pulse generator failure l2 (Fig. 3). Commercial external DDD pulse generators also are being introduced. As the code implies, DDD pacemakers sense and pace in both chambers; it will inhibit when a spontaneous QRS is sensed in the ventricle and a native P wave will trigger a ventricular output stimulus following the electronic AV interva1. 9 Thus, the DDD ECG may show atrial pacing (Fig. 4), AV sequential pacing (Fig. 4), or P-wave-triggered ventricular pacing (Fig. 5). DDD pacemakers have lower and upper rate settings, eg, 70 ppm and 150 ppm respectively, and between these two settings, the sinus or atrial rate will govern the frequency of ventricular stimulation. If the sinus rate falls below the lower rate, then atrial or AV sequential pacing will occur. When the sinus rate exceeds the upper rate (Fig. 6), varying degrees of electronic AV block will appear in order to limit the rate of ventricular pacing. No pacemaker stimuli will be observed if the patient's sinus rate is faster than the lower rate and if the AV conduction time is less than the electronic AV interval; similarly, a sinus or supraventricular tachycardia with intact AV conduction will not be affected by the pacemaker. Pacemaker-mediated tachycardia (PMT) is the principal electrophysiologic complication of DDD pacing. PMT is an artificial re-entrant tachycardia wherein the pacemaker is the antegrade limb and the ventriculoatrial
TEMPOHAHY PACING
819
Figure 3. Adaptation of permanent unipolar dual-chamber pulse generator for temporary applications. The cathode (distal tip) electrodes of the atrial and ventricular leads are connected to the pulse generator using the existing set screws. An anode clip connector can be fabricated by most hospital biomedical staffs. The anode (proximal ring) electrodes of both leads are grounded to the pulse generator housing using the anode clip. For bipolar pulse generators (not shown), the cathodes and anodes of both leads are connected directly to the pulse generator. The pulse generator and lead connector should be isolated from the environment by a plastic bag or rubber glove.
(V A) pathway is the retrograde limb of the tachycardia circuit (Fig. 7). Most PMTs are initiated by a ventricular ectopic beat that is conducted retrogradely to the atrium, where the ectopic P wave is sensed by the DDD atrial sensing circuit; in turn, the P wave triggers ventricular pacing after the programmed AV interval. This endless loop tachycardia will persist until the VA pathway is blocked or until the retrograde P wave fails to trigger a ventricular stimulus. P:\1T will be observed most frequently in patients who have intact AV conduction; however, approximately 15% of individuals who have ante grade block will conduct retrogradely over a VA pathway. A PMT can be abolished by prolonging the postventricular atrial refractory period (PVARP) so that the retrograde P wave is not sensed; a PVARP of 300 ms will prevent or terminate the vast majority of PMTs. Alternatively, the pacemaker can be set to the DVI or VVI mode. Some DDD models have a DDI mode that does not produce P-wave-triggered ventricular pacing and hence PMTs are not possible. 6 Further, DDI pacing is useful in patients who have paroxysmal atrial fibrillation/flutter or SVT; in this mode, sinus rhythm or atrial tachyarrhythmias will inhibit atrial stimulation, thereby preventing competition, and they will not trigger ventricular pacing. When using an implantable DDD pulse generator as a temporary external pacemaker, it is necessary to have the associated programmer in order to adjust the various p'lrameters to the desired settings. In most
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VA VV
AV ----.----
AV_
AV~
AR- - + ........
~
VR
VR
LRL
• _ LRL
URL
URL
-------.
AR ..................
AR . .... ......... .
VR •
LRl
URL
Figure 4. Diagram of a DDD pulse generator's response to a conducted sinus beat (1), and in the presence of sinus bradycardia, with intact AV conduction (2), and sinus bradycardia with AV block (3). VA = interval between ventricular sensed and atrial paced events. VV = interval between ventricular sensed and paced events. AV = atrioventricular delay. AR = atrial refractory period. VR = ventricular refractory period. LRL = lower rate limit. URL = upper rate limit. The postventricular atrial refractory period (also known as PVARP) is that portion of the atrial refractory period following a ventricular sensed or paced event. Solid horizontal arrows, beginning and end of the AV, AR, VR, LRL, and URL intervals. Dashed lines, the potential durations of these intervals if sensed or paced ventricular events had not reset the intervals. Dotted lines, portions of the AR intervals initiated by the atrial event. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
2
-
AR .............
VR
AV-
AR
.............
..
VR
_L_R_L_ _ _ _ _ _ _ _ _ _ .. URL
-
AV-----
..
..
n_nn_n_n
URL
LRL
..
..
n
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URL
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•
Figure 5. Diagram of DDD pulse generator behavior during sinus rhythm, with intact AV conduction (beats 1 and 2), and a paced ventricular beat (3) that is triggered by a spontaneous P wave. For definition of abbreviations, see legend to Figure 4. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
821
TEMPORARY PACING
SINUS RATE
LOWER RATE =60bpm UPPER RATE =150bpm AV INTERVAL = 150msec = 83 bpm SINUS RATE = 140 bpm
SINUS RATE
=152 bpm
SINUS RATE
=163 bpm
Figure 6. This DDD pacemaker was programmed to the settings shown. As the sinus rate exceeds the upper rate of 150 beats/m in (bpm), electronic AV block occurs because the P waves fall during the atrial refractory periods (arrows).
situations, the following values are appropriate: (1) lower rate = 60 beats/min; (2) upper rate = 130 beats/min; (3) AV interval = 150 to 200 ms; (4) PVARP = 300 ms; (5) ventricular refractory period = 300 ms; (6) atrial sensitivity = 0.5 to 1.0 mY; (7) ventricular sensitivity = 1.5 to 2.5 mY; (8) atrial and ventricular output = 5 V and 0.5 ms or 6 mA and 0.6 ms. Inhibition of ventricular pacing by an atrial stimulus (crosstalk) may occur if the atrial output and/or ventricular sensitivity are high. The incidence of all types of electrical interference with pacemaker function can be reduced by using bipolar lead systems.
Figure 7. (A) DDD pacemaker-mediated tachycardia initiated by P-wave-conducted retrograde to the atria following a ventricular premature beat. AR = atrial refractory period of pulse generator's atrial sensing circuit. A = atrium. V = ventricle. (B) Prevention of endless loop DDD pacemaker tachycardia by extension of the atrial sensing circuit's refractory period (AR) to prevent detection of retrograde P wave following VPC. (From Hauser, R. C.: The electrocardiography of AV universal DDD pacemakers. P.A.C.E., 6:399, 1983; with permission.)
A
B
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Selection of Pacing Mode Selection of thc most suitable temporary pacing mode is based on four considerations, including: (1) therapcutic objectives; (2) electrophysiologic findings, ie, rhythm and conduction; (3) hemodynamic needs; and (4) technical factors. If the object of temporary pacing is to provide prophylactic rate support, then single-chamber ventricular pacing usually will suffice. Examples of such patients include those who have suffered an AMI that is complicated by RBBB + LAFB, or individuals who need temporary pacing prior to permanent pacemaker insertion for acquired complete AV block. In general, therefore, the routine use of prophylactic, dual-chamber tempor;lry pacing cannot bc justified. If a goal of temporary pacing is to preserve function, however, one should select the most physiologic approach. The patient's clinical electrophysiology dictates certain pacing requirements. Single-chamber, atrial pacing (AAI) may be adequate for individuals who have slow sinus rates; atrial pacing is contraindicated in the presence of AV block and it is ineffective in the presence of atrial fibrillation or atrial paralysis. As will be discussed, rapid atrial pacing may be applied to terminate atrial flutter or SVT. The AV sequential (DVI) or DDD mode may be employed for sinus bradyarrhythmias complicated by AV block; DVI pacing should be avoided if atrial competition is likely to produce atrial dysrhythmias. The DDD mode is the most adaptable of all the pacing modalities; it not only provides basic rate support in both chambers but also responds to atrial activity. Except for established atrial fibrillation, there are no contraindications to DDD pacing. Hemodynamically, atrial pacing maintains AV synchrony and preserves the normal sequence of ventricular depolarization. In the presence of AV block, AV sequential pacing coordinates atrial and ventricular systole, but right ventricular stimulation may decrease stroke volume. Compared with ventricular pacing, atrial and AV sequential pacing increase stroke volume 10% to 20% by augmenting preload, and they reduce mean atrial pressures by eliminating AV dissociation (Fig. 8). The DDD mode not only offers the same hemodynamic advantages of atrial or AV sequential pacing, but also provides rate responsiveness. Rate responsive pacing is the major mechanism by which large increments in cardiac output are achieved. Thus, the DDD pacemaker varies its pacing rate based on a physiologic marker, ie, sinus node activity, that reflects an increased need for blood flow. It may be concluded that the AAI mode is satisfactory for therapeutic pacing if AV conduction is normal and that DDD pacing provides optimum hemodynamic benefits in the presence of AV block. New sensors (stroke volume, dp/dt), so-called artificial sinus nodes, are being developed to provide rate responsiveness when sinus activity is impaired. R Therapeutic pacing is indicated in patients who havc acute myocardial infarction, including right ventricular infarction, ischemic heart disease, hypertrophic cardiomyopathy, hypertensive heart disease, aortic stenosis, and in any circumstance where ventricular pacing produces circulatory embarrassment. Technical obstacles may intervene to preclude atrial or dual-chamber
823
TE:\IPORAI\Y PA-CI"!G
LV
Dimensions
Stroke Volume
10-20%
~
Contractilityf-----
Myocardial Fiber Shortening
Cardiac Output
Afterload Peripheral Circulation
Figure 8, Atrial and AV sequential pacing preserves AV synchrony, which accounts for 10% to 20% of the stroke volume, by increasing the extent of myocardial fiher shortening via the Frank-Starling mechanism, Cardiac output is the product of the stroke volume and the heart rate, DDD pacing improves cardiac output hy preserving AV synchrony and hy adjusting the pacing rate in response to sinus activity, LV = left ventricle, (From Hallser, It G,: Techniques for improving cardiac performance with implantahle devices, P,A,C,E., 7:1234, 1984; with permission,)
pacing, but the number of such difficulties are decreasing as new leads and pulse generators are introduced, The most common problems are: (1) venous access; (2) lead stability; (3) atrial sensing; (4) high threshold(s); (,5) arrhythmias; and (6) interference with or by a balloon-tipped catheter in the pulmonary artery. While these technical considerations are dcalt with elsewhere in this chapter, they are mentioned here because each may influence the selection of pacing mode.
LEADS AND INSERTION TECHNIQUES Venous Access Virtually any lead can be inserted into a major vein using a needle, guidewire, and sheath-dilator set. Multiple leads or catheters may be introduced with a single venous puncture and a sufficiently large diameter sheath or with two smaller, peel-away sheaths. The guidewire is not removed until all leads or catheters arc in satisfactory position so that recannulation can be performed without a second venous puncture,2 Although attempts to enter the subclavian or internal jugular vein involve certain risks, pacing leads that are inserted via these routes arc readily positioned in either chamber. Further, subclavian and internal jugular leads tend to be more stable and they allow greater patient mobility, Access to
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.\1. VICAHI
the central venous circulation hom the brachial vein is more difncult, particularly ff)r multiple leads, and thus this approach generally is unsuitable for emergency pacing. Similarly, femoral leads are difficult to position quickly and stable atrial pacing is not easy to maintain. It is rarely necessary to insert an emergency pacing lead via the percutaneous, transthoracic route/ 6 coronary laceration and hemopericardium are recognized complications of this method. Nevertheless, transthoracic pacing may be lifesaving in the presence of asystole when the right ventricle cannot be accessed by safer methods. Pacing Leads A variety of temporary leads or catheters are available for single and dual-chamber pacing. 1 The semifloating or floating types have largely replaced the stiff woven Dacron catheters because the latter require fluoroscopy during placement while the former may be positioned using only electrocardiographic monitoring. Moreover, stiff catheters are more likely to perforate or displace and their long-term threshold behavior is unsatisfactory. Flow-directed, balloon-tipped pacing leads are easy to locate in the right ventricular apex and they are so flexible that malposition and exit block are infrequent problems. A preformed, atrial J temporary pacing lead has been designed to be passed via the subclavian vein into the right atrium without fluoroscopic guidance;l3 it can be used together with any ventricular lead for dualchamber pacing. A single catheter with fixed or moveable flared atrial electrodes that are mounted on a straight ventricular lead may simplify the placement of a dual chamber system. While pacing Swan-Canz catheters may be used for temporary AY stimulation, the results are mixed because balloon inflation may displace the electrodes and, consequently, capture may be lost. Novel Swan-Canz catheters that contain a separate lumen for independent pacing probes are being evaluated. Transthoracic ventricular pacing leads are notoriously unstable, but a recently introduced, flared model may impart some security.] Another design incorporates a channel that allows the instillation of intracardiac drugs. Pacing Threshold and Electrogram Measurements Satisfactory lead performance cannot be obtained unless the acute threshold of stimulation is low and the intracardiac signal (R wave or P wave) has sufficient amplitude for sensing. Thresholds of less than 1 Yor 1 mA should be sought for atrial and ventricular leads. The P wave and R wave peak-to-peak amplitudes should be greater than 1 and 6 mY, respectively. Thresholds can be assessed with variable-output, external pulse generators and the intracardiac signals may be measured from recordings that are made directly from the electrodes. Both threshold and electrogram values can be acquired using commercial pacing system analyzers. Failure to obtain an adequate threshold or intracardiac signal may be due to: (1) poor contact between the electrode and endocardium; (2) local endocardial necrosis or fibrosis; (3) hypoxia or acidosis; (4) hypokalemia; and (5) drug effects, particularly type I antiarrhythmics. The former is by
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far the most common cause and the only solution is to reposition the lead. Endocardial necrosis or fibrosis may he encountered in patients with right ventricular AMI and fluoroscopy may be needed to find an acceptable pacing site. A low amplitude R or P wave can result when the electrodes of the temporary bipolar lead are oriented perpendicular to the depolarization wave front in the ventricle or atrium. When this occurs, a satisfactory signal can be obtained by relocating the electrodes, perhaps in a different plane, while monitoring the intracardiac signal. It is rarely necessary to unipolarize the electrodes hy using a skin or subcutaneous electrode as the anode. The threshold of stimulation rises after lead insertion because an inflammatory response occurs at the electrode-tissue interface. Thus, the current (mA) or voltage (V) required to capture increases as the stimulating electrode is separated from excitable myocardium. The magnitude of the threshold rise may be three- to four-fold over a period of hours or days. Accordingly, if the acute threshold is 0.7 V, a safety margin of 2 to 3 V is warranted. The important characteristics of the intracardiac electrogram do not change significantly after lead insertion, provided the electrodes remain stable. Nevertheless, a sensing safety margin that is twice the measured P or R wave amplitude is recommended. Complications The most common complications include: (1) lead displacement, (2) thrombophlebitis, (3) infection, and (4) extracardiac muscle stimulation. Other complications are related to the method used to gain venous access, cg, subclavian puncture. Backward displacement of the lead results in pacing malfunction; in addition, an unstable lead may induce arrhythmias. Myocardial perforation is rare with the softer, more compliant leads, but woven catheters are particularly prone to this complication. Perforation may be heralded hy extracardiac muscle stimulation and the paced ECG may show RBBB because the electrode is stimulating the left ventricular epimyocardium. Tamponade is infrequent, but it may be delayed. Management includes lead withdrawal and replacement, usually with a soft catheter under fluoroscopic control and subsequent surveillance for evidence of hemodynamic compromise. Thrombophlebitis is associated with femoral and brachial vein insertion sites. Lead removal and reinsertion via a different venous system usually are indicated. While brachial vein thrombophlebitis may be treated without anticoagulation, femoral vein involvement requires heparinization unless it is contraindicated. External Transcutaneous Pacing The external transcutaneous pacemaker (ETCP), originally described by Zoll in 1952, has been reintroduced in the form of an improved device that operates in the demand mode. 5 Stimuli are delivered via two large surfllCe area electrodes that are applied to the skin of the chest wall. Although long constant current pulses are used, some patients cannot tolerate the discomfort and a smaller proportion cannot be paced. Despite these potential disadvantages, ETCP is useful in a number of situations. Emergency pacing can be instituted by paramedical personnel or in
826
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G.
HAUSER A:-.ID RALPI! ~. VICAR!
hospitals that lack the resources required to insert temporary pacemakers. A standby ETCP may be a reasonable alternative to prophylactic transvenous pacing in the intensive care unit, emergency room, operating room, or cardiac catheterization laboratory. PACING FOR TACHYARRHYTHMIAS Temporary cardiac pacing has been used to correct and control a variety of atrial and ventricular tachyarrhythmias. Its effectiveness is well established, particularly in the postoperative cardiac surgical patient in whom, due to prior placement of temporary epicardial electrodes, it is often the preferred mode of therapy. 17 Temporary antitachycardia pacing has been applied to arrhythmias refractory to medical treatment and those associated with digitalis intoxication. In the latter case, the hazards associated with DC cardioversion can be avoided. The most frequent therapeutic mode of antitachycardia pacing is overdrive burst termination. Two general principles of this type of pacing are: (1) effective pacing rates for termination of tachycardias generally are 110% to 140% of the spontaneous rate of the tachycardia, and (2) catheter proximity to the origin of the tachycardia influences success rates for conversion. An effective technique for interruption of most tachyarrhythmias is to position the pacing catheter in the right atrium or right ventricle and initiate stimulation at 10 to 20 beats/min above the intrinsic rate. Pacing rates are increased progressively by 10 beats/min, unless hemodynamic instability results, until successful conversion ensues. Type I atrial flutter (atrial rate 230-350 beats/min and negative flutter waves leads 11, Ill, and a VF) usually can be successfully interrupted by positioning the pacing catheter high in the right atrium. Burst pacing is initiated as described above and continued for 20 to 30 seconds. The hallmark of successful conversion is a change in polarity of atrial complexes from negative to positive in the inferior leads. Occasionally, atrial fibrillation may be precipitated by this technique. This rhythm, however, usually is transient and, if persistent, generally is easier to treat medically than atrial flutter. A variety of other supraventricular tachyarrhythmias are amenable to overdrive burst pacing with techniques similar to those described above. Ventricular tachycardia can be interrupted by application of single or double extrastimuli in the majority of patients who can remain hemodynamically stable during programmed testing. 11 Overdrive burst pacing also has been successful in converting ventricular tachycardia; however, pacing rates above 135% of the intrinsic rate increase the risk of ventricular fibrillation. It is recommended that standby DC cardioversion units be available immediately in any patient undergoing anti tachycardia pacing. Ventricular tachyarrhythmias associated with a prolonged QT interval, also known as "torsades de pointes," have been controlled effectively by temporary cardiac pacing. 10 This arrhythmia is most likely the result of excessive dispersion of ventricular refractory periods, and often is associated with drug toxicity, particularly the type I antiarrhythmic agents. The right atrium is the preferred site of stimulation, unless AV block is present, since
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TEMPOHARY PACING
normal AV synchrony is preserved. Pacing at heart rates above the intrinsic rate, especially in patients with sinus bradycardia, shortens cycle length and QT interval, providing more uniformity of ventricular refractory periods. A specially designed catheter recently was devised that allows successful transvenous cardioversion of ventricular tachycardia and fibrillation in the majority of patients tested. 18 The future of anti tachycardia pacing may include devices able to overdrive pace ventricular tachycardia with backup cardioversion and perhaps defibrillation.
REFERENCES 1. Adgey, A. A. J., Geddes, J. S., Webb, s. W., et aI.: Acute phase of myocardial infarction. Lancet, 2:501, 1971. 2. Belott, P. H.: Retaining guidewire, introducer technique for unlimited access to the central circulation: A review. Clin. Prog. Pacing ElectrophysioI., 1 :59, 1983. 3. Billhardt, R. A.: Temporary pacing. Clin. Prog. Pacing ElectrophysioI., 2:305, 1984. 4. Codini, M. A.: Conduction disturbances in acute myocardial infarction: The use of pacemaker therapy. Clin. Prog. Pacing EledrophysioI., 1:142, 1983. 5. Falk, R. H., Zoll, P. M., and Zoll, R. H.: Safety and efficacy of non-invasive cardiac pacing. N. EngI. J. Med., 309:1166, 1983. 6. Floro, V., Castellanet, M., Florio, J., et al.: DOl: A new mode for cardiac pacing. Clin. Prog. Pacing ElectrophysioI., 2:255, 1984. 7. Furman, S., and Fisher, J. D.: Endless loop tachycardia in an AV universal (ODD) pacemaker. PACE, 5:486, 1982. 8. Hauser, R. G.: Techniques for improving cardiac performance with implantable devices. PACE, 7:1234, 1984. 9. Hauser, R. G.: The electrocardiography of AV universal ODD pacemakers. PACE, 6:399, 1983. 10. Kahn, M. M., Logan, K. R., McComb, J. M., et aI.: Management of recurrent ventricular tachyarrhythmias associated with Q-T prolongation. Am. J. CardioI., 47:1301, 1981. 11. Kastor, J. A., Horowitz, L. N., Harken, A. H., et al.: Clinical electrophysiology of ventricular tachycardia. :'11. EngI. J. Med., 304:1004,1981. 12. Littleford, P. 0.: Physiologic temporary pacing: Techniques and indications. Clin. Prog. Pacing ElectrophysioI., 2:236, 1984. 13. Littleford, P. 0., and Pepine, C. J.: A new temporary atrial pacing catheter inserted percutaneously into the subclavian vein without fluoroscopy. PACE, 4:458, 1981. 14. Parsonnet, V., Furman, S., Smith, N. P. D., et al.: Optimal resources for implantable cardiac pacemakers. Circulation, 68:277A, 1983. 15. Pastore, J. 0., Yurchak, P. M., Janis, K. M., et aI.: The risk of advanced heart block in surgical patients with right bundle branch block and left axis deviation. Circulation, 57:677, 1978. 16. Roberts, J. R., and Greenberg, M. I.: Emergency transthoracic pacemaker. Ann. Emerg. Med., lO:600, 1981. 17. Waldo, A. L., Wells, J. L., Cooper, T. B., et al.: Temporary pacing: Applications and techniques in the treatment of cardiac arrhythmias. Prog. Cardiovasc. Dis., 23:451, 1981. 18. Zipes, D. P., Jackman, W. M., Heger, J. J., et al.: Clinical transvenous cardioversion of recurrent life threatening ventricular tachyarrhythmias: Low energy synchronized cardioversion of ventricular tachvcardia and termination of ventricular fibrillation in patients using a catheter electrod~. Am. Heart J., 103:789, 1982. Section of Cardiology Rush-Presbyterian-St. Luke's Medical Center 1753 West Congress Parkway Chicago, IL 60612