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Intraoperative or Procedural Management of Pacemakers

Although no special monitoring or anesthetic technique is required for the patient with a pacemaker, attention must be given to a number of concerns. First, electrocardiographic monitoring of the patient must include the ability to detect pacemaker discharges. Currently, most electrocardiographic monitors in both the operating room and the intensive care unit perform digital acquisition and analysis of electrocardiographic signals. As a result, in their default settings, these monitors will filter the pacemaker artifacts, and no pacemaker "spikes" will


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TABLE 35-6 -- Makers and models of pacemakers with minute ventilation sensors *
ELA Medical
  Brio (212, 220, 222)
  Chorus RM (7034, 7134)
  Opus RM (4534)
  Talent (130, 213, 223)
Guidant Medical and CPI Cardiac Pacemakers, Inc.
  Pulsar (1172, 1272)
  Pulsar Max (1170, 1171, 1270)
  Pulsar Max II (1180, 1181, 1280)
  Insignia Plus (1194, 1297, 1298)
Medtronic
  Kappa 400 series (KDR401, KDR403, KSR401, KSR403)
Telectronics/St. Jude
  Meta (1202, 1204, 1206, 1230, 1250, 1254, 1256)
  Tempo (1102, 1902, 2102, 2902)
*Pacemakers with minute ventilation (bioimpedance) sensors frequently respond to electromagnetic interference with pacing at the upper sensor rate.[46] [50] These tachycardias also can be produced by connection to an operating room electrocardiographic monitor because many of these devices inject electrical signals through the electrocardiographic leads to determine respiratory rate or a lead disconnection.[45] [47] In 1998, the U.S. Center for Devices and Radiologic Health issued a safety alert calling for the deactivation of any minute ventilation sensor before exposing a patient to a potential source of electromagnetic interference or connection to medical devices. [48]




be shown. This filtering must be disabled so that the monitor will "paint" pacemaker spikes onto the display. Even with the filtering disabled, though, pacemaker artifacts do not always appear. Atrial signals are weak, and current monitors do a poor job detecting them. Also, since the digital monitors generally analyze only one lead for these signals (and then "paint" on artifacts on every lead), placement of the electrocardiographic leads can markedly affect the detection axis. In practice, when a patient with known pacing is monitored, sometimes changing the "analysis" lead on the monitor will result in the appearance of pacing signals. Unfortunately, when the ESU artifact filter is disabled, any use of the monopolar ESU unit can lead to inappropriate "painting" of pacemaker artifacts on the monitor ( Fig. 35-5 ).

Second, patient monitoring must include the ability to ensure that paced electrical activity is converted to mechanical systoles. Mechanical systoles are best evaluated by pulse oximetry plethysmography or arterial pressure waveform display.

Third, there is limited experience with intraoperative BiV pacing at this time. These patients often have ejection fractions less than 30%, and they depend on pacing in both ventricles to improve their cardiac output. Loss of ventricular pacing from any cause (AV dyssynchrony [atrial fibrillation, atrial flutter, appearance of junctional rhythm], myocardial ischemia, acid-base disturbance, change in pacing threshold, ESU interference, and so on) can cause an immediate decrease in cardiac output. Monitoring of these patients probably should include beat-to-beat monitoring of cardiac output. The patient with HOCM pacing is also dependent upon forced ventricular pacing to limit left ventricular outflow tract obstruction.

Fourth, some patients might need an increased pacing rate during the perioperative period to meet an increased oxygen demand. This subject is often not addressed. Pacemaker patients reportedly have high postoperative morbidity and mortality,[51] and failure to address tissue oxygen demands and cardiac output needs might contribute to this problem.

Fifth, appropriate equipment must be on hand to provide backup pacing and/or defibrillation to the patient who might need it. The literature and anecdotal experience suggest that cardiac generators, while hardy, occasionally perform some untoward maneuver or fail, even in the absence of EMI.[52] Acceptable, but inappropriate behavior of a pacemaker or ICD can create an inhospitable situation. Even a properly working, dual chamber pacemaker can produce R-on-T pacing, especially in the setting of a junctional rhythm or PVCs ( Fig. 35-6 ).

The medical team caring for the patient with an implanted cardiac pulse generator must understand that the patient has been deemed needy of this device by a physician who is an expert in the diagnosis and management of cardiac rhythm issues. Few anesthesiologists are qualified to contradict this diagnosis, yet some persist in providing an anesthetic without appropriate backup pacing and defibrillation equipment on hand.

Monopolar "Bovie" electrosurgery (ESU) use remains the principal intraoperative issue for the patient with a pacemaker. Between 1984 and 1997, the U.S. FDA was notified of 456 adverse events with pulse generators, 255 from electrosurgery, and a "significant number" of device failures.[53] Monopolar ESU is more likely to cause problems than bipolar ESU, and patients with unipolar electrode configuration are more sensitive to electromagnetic interference than those with bipolar configurations.[54] The most common effect of ESU on pacemakers is ventricular oversensing which causes pacemaker inhibition (see Fig. 35-5B ). Sometimes, the pacemaker determines that significant EMI is present and begins pacing asynchronously at the programmed lower rate.[55] This behavior is called "noise reversion mode pacing," even though the pacemaker does not actually change "modes."

Magnet placement during electrosurgery might prevent aberrant pacemaker behavior, and it might allow reprogramming of an older (pre-1990) generator. Note that not all generators "open" their programming window during placement of a magnet (for example, devices from Guidant and/or CPI cannot be programmed in the presence of a magnet). Newer generators are believed to be relatively immune to spurious reprogramming from EMI.

If monopolar electrosurgery is to be used, then the electrosurgical current-return pad (often misidentified as the "grounding pad") must be placed to ensure that the electrosurgical current path does not cross the pacemaking system. Some authors recommend placement of this pad on the shoulder for head and neck procedures or the distal arm (with sterile draping of the wire) for breast and


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Figure 35-5 Disabling the pacemaker artifact filter on a digitally processed electrocardiographic (ECG) monitor results in the "painting" of environmental interference (EMI) as pacemaker artifacts. A, The patient's underlying rate exceeded the pacemaker's programmed lower rate limit, and no pacing took place. However, activation of the monopolar electrosurgical unit (ESU) in the "cut" mode produced sufficient electromagnetic noise that the monitor began painting pacemaker artifacts at a rate of about 20 Hz. The top tracing is ECG lead II, the middle tracing is ECG lead V5, and the bottom tracing is the invasive arterial pressure waveform. B, "Coagulation" ESU produced ventricular oversensing with pacemaker inhibition and left this patient with a compromised cardiac output. There is also evidence of inappropriate monitor painting of pacemaker artifacts from the EMI. The top tracing is ECG lead II, the middle tracing is the pulse oximeter plethysmogram, and the bottom tracing is the invasive arterial pressure waveform. (Adapted from Rozner MA: [untitled letter]. Pacing Clin Electrophysiol 26:923–925, 2003.)


Figure 35-6 Normal dual chamber pacemaker timing can produce R-on-T pacing. A, This strip demonstrates functional ventricular undersensing of a premature ventricular contraction (PVC) with a resultant R-on-T pace leading to torsades de pointes. This patient had a dual chamber pacemaker in the DDD mode with a programmed lower rate of 70 beats/min (R-R interval is 857 msec) and an atrioventricular delay of 200 msec. With these parameters, the pacemaker paces the atrium at 657 msec after any previous ventricular event. Atrial pacing (A) and ventricular pacing (V) are indicated. The top tracing is electrocardiographic (ECG) lead II, the middle tracing is ECG lead V5, and the bottom tracing is the invasive arterial blood pressure. Approximately 660 msec after the first QRS (1) on the strip (which was adequately sensed by the pacemaker), an atrial stimulus is emitted. At 200 msec after this atrial pace, a ventricular stimulus is emitted, appearing to depolarize the ventricle (2). About 660 msec later (3), the patient had a PVC. Because the pacemaker was preparing to emit the atrial stimulus, it had disabled its ventricular sensing element and failed to sense this PVC (i.e., functional undersensing). At 200 msec after the atrial stimulus, no ventricular event had been sensed, and the pacemaker emitted a ventricular stimulus on the T wave. Because the ventricle was in a refractory period from the PVC, there was no depolarization of the ventricle (i.e., functional noncapture). At 660 msec from this attempted ventricular pacing, the pacemaker again paces the atrium (4), and it appears that the next ventricular pacing impulse captures the ventricle. At (5), there is a repeat of the events at (3); the pacemaker disabled its sensing elements in preparation to pace the atrium and failed to detect the PVC. This time, however, the ventricular pace on the T wave produced torsades de pointes. B, This strip was obtained from a Medtronic programmer during interrogation of a Kappa 700 dual-chamber pacemaker. The top tracing is ECG lead II, and the bottom tracing is the marker channel, which shows the pacemaker's interpretation of events. This pacemaker was programmed to the DDD mode with a lower rate of 60 beats/min. The atrioventricular (AV) delay was 200 msec. As a result, after any ventricular event, the pacemaker will emit an atrial pulse at 800 msec if no intervening atrial or ventricular event takes place. This patient had a junctional rhythm at 75 beats/min (corresponding to an R-R interval of 800 msec), and the pacemaker emitted an atrial pulse just as the junctional event occurred. Because the pacemaker disables its ventricular sensing element when emitting the atrial pulse, it failed to detect the ventricular event and emitted the ventricular pulse 200 msec later, falling on the T wave. This inappropriate pacing takes place every other cycle, because every other junctional event is sensed about 600 msec after the previous ventricular pace. Decreasing the AV delay decreases the likelihood of pacing during the vulnerable period of the ventricle. Atrial pace (AP), ventricular pace (VP), and ventricular sensed event (VS) are indicated. The third complex deserves comment. The pacemaker sensed this ventricular event as it re-enabled its sensing element, and the pacemaker could not tell whether the sensed event was a true ventricular depolarization or an echo of the atrial pace (called far-field oversensing). When a signal from the ventricle is sensed within 30 to 90 msec after an atrial pace, many pacemakers immediately emit a ventricular pacing stimulus. Called a ventricular safety pace, this pacing stimulus is designed to protect the patient from inappropriate sensing of the atrial signal by the ventricular channel, which would then inhibit the ventricular output. The safety pace is emitted at 110 msec to prevent R-on-T pacing. This feature is also called nonphysiologic AV delay by some manufacturers. R-on-T pacing can be appropriate (but not ideal) behavior of a DDD or DDI pacemaker in the setting of PVCs or a junctional rhythm. It can also be seen with atrial or ventricular undersensing.


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axillary procedures.[54] [56] Procedures using only monopolar ESU or with special pacing ramifications include the following:
Lithotripsy: The cardiac generator must be excluded from the lithotripter field. Since some lithotripters trigger their output on the sensed electrocardiographic "R" wave, atrial pacing should be disabled to prevent the lithotripter from inappropriately firing on the atrial pacing artifact;

Transurethral Resection and Uterine Hysteroscopy: TUR of the bladder or prostate and hysteroscopic procedures generally use monopolar ESU, and device reprogramming might be needed to prevent pacemaker oversensing with resultant pacemaker inhibition. A new resectoscope is in clinical trial that includes the current-return electrode on the shaft (the irrigation medium will be normal saline) which might limit EMI to the generator;

Magnetic Resonance Imaging (MRI)—Absolutely contraindicated by most device manufacturers, and deaths have been reported. * According to physicians' manuals from most manufacturers, MRI can lead to reed switch closure (magnet mode activation), reprogramming, inappropriate high rate pacing, generator damage, myocardial injury, or generator movement within the pocket, causing pain or lead failure. Nevertheless, safe performance of MRI with pacemakers has been reported[57] ;

Electroconvulsive Therapy—ECT requires non-sensing (asynchronous) mode to prevent myopotential-induced oversensing with resultant pacemaker inhibition [58] ;

Nerve Stimulator Testing/Therapy—Nerve stimulators can cause pacemaker oversensing with resultant pacemaker inhibition and cardiac arrest.[59] Nerve stimulators have been used intraoperatively to inhibit undesired cardiac pacing. [10] For the patient with an ICD, inappropriate detection of neuromuscular stimulators, TENS, and chiropractic electrical muscle stimulation as VT or VF has been reported[60] [61] ;

Succinylcholine Use—There is one report of a problem in a pacemaker-dependent patient upon administration of succinylcholine.[62] In this case, muscle fasciculations might have caused ventricular oversensing with resultant pacemaker inhibition, but the case is difficult to interpret. No electrocardiographic tracings were published, and the pacemaker was damaged during a subsequent defibrillation. Using programmers, I have witnessed succinylcholine administration to over 50 patients with pacemakers or defibrillators, and I have not observed any myopotential oversensing. However, myopotential oversensing (in the absence of succinylcholine) has been observed to interfere with pacemaker function[63] or cause inappropriate ICD therapy.[64]

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