Cardiovascular Implantable Electronic Device Management in Noncardiac Surgery

Pacemaker Indications

Common indications for permanent pacing include symptomatic bradycardia from sinus node or atrioventricular (AV) node disease, long QT syndrome, hypertrophic obstructive cardiomyopathy (HOCM), and dilated cardiomyopathy.

Pacemaker Leads

Although knowledge regarding the exact type of leads implanted is not often necessary for the safe and appropriate perioperative management of CIEDs, a basic understanding of the lead types makes chest radiograph interpretation easier and helps determine the potential effects of electromagnetic interference (EMI). Furthermore, lead type can be very important during lead removal.

Pacemaker leads can be either bipolar or unipolar, with bipolar leads being more common in the United States. The chest radiograph in Fig. 4.1 is an example of a dual-chamber pacemaker with bipolar leads in the right atrium (RA) and right ventricle (RV). Bipolar leads contain both the anode and cathode within the lead itself, but in a unipolar system, the lead contains the cathode and the pulse generator itself functions as the anode. The shorter distance between the anode and cathode in a bipolar system reduces susceptibility to EMI specifically with regard to sensing. This shorter distance between anode and cathode can also result in smaller amplitude or even unrecognized pacer spikes on the intraoperative electrocardiogram (ECG). In contrast, the unipolar system results in electricity traveling a longer distance from the lead or cathode to the pulse generator or anode. This configuration requires the generator or “can” be positioned in the left pectoral region as well as an increased susceptibility to EMI.

Although bipolar leads are less susceptible to EMI, they have historically been larger in diameter and less durable than unipolar leads. However, durability in recent years has become closer to equivalent. Additional quoted advantages of bipolar leads include less pectoral muscle stimulation because they do not use an “active can” configuration and the ability to convert to unipolar pacing if indicated by the clinical situation.

Leads can also be broken down by their fixation mechanism. Fixation mechanism is important as active fixation leads are at risk of perforating thin-walled structures like the RA ( Fig. 4.2 ) during placement. Perforation can result in significant pain, pneumomediastinum, or effusions. Occasionally, diaphragmatic pacing is associated with lead perforation. This can involve either diaphragm by direct stimulation of the diaphragm (left hemidiaphragm) or via stimulation of the phrenic nerve by the right atrial (right hemidiaphragm) or the coronary sinus (left hemidiaphragm) leads. Diaphragmatic pacing can be quite uncomfortable for the awake patient and may only require an alteration in voltage/pulse width or lead repositioning. However, it can be a sign of lead perforation and should elicit an investigation.

In preparation for lead removal, the length of time in situ and the fixation mechanism are vitally important. For example, tined leads are passive fixation leads ( Fig. 4.3 ) that are difficult to reposition or remove if ineffective because of their fixation mechanism and scar tissue formation. Luckily, they have fallen out of favor with most electrophysiologists. An additional type of passive fixation lead that is still in use today is covered in the discussion of CRT.

Rate Modulation

Rate modulation and rate adaptation, denoted by an R in the fourth position of the NBG code (see Table 4.1 ), are terms used to describe a pacemaker's ability to automatically change the heart rate in response to certain monitored parameters. Given that an estimated 85% of pacemakers implanted in the United States are rate responsive and 99% have this capability, anesthesiologists should be familiar with rate modulation in case an experienced programmer is not available preoperatively.

The monitored physiologic parameters that can induce rate changes include acceleration caused by motion; patient movement; QT interval; central venous temperature, oxygen saturation, or pH; right ventricular pressure; minute ventilation via thoracic impedance; physiologic impedance; heat; or a combination of acceleration and minute ventilation. When required, a pacemaker with rate modulation enabled can alter the heart rate and thus the cardiac output to meet metabolic demand.

Specifically, pacemakers that correlate an increase in respiratory rate and tidal volume with exercise and a need for increased cardiac output pose a challenge for anesthesiologists. The paced rate in these devices may inappropriately increase in response to mechanical hyperventilation, external respiratory rate monitoring, or even electrocautery. This results from monitoring respiratory rate and tidal volume via thoracic impedance between the lead and generator. On inspiration, the distance between the generator and the lead increases. In addition, the inspired gas in the thorax results in greater impedance to the small electrical signals emitted from the lead. The device then correlates the increase in thoracic impedance caused by distance as well as inspired gas with an increased respiratory rate or tidal volume and a need for greater cardiac output. Interestingly, patients with an exacerbation of congestive heart failure may present with a decrease in thoracic impedance as a result of associated pulmonary edema.

The American Society of Anesthesiologists (ASA) and Heart Rhythm Society (HRS), in the 2011 ASA Practice Advisory, provide a recommendation that rate-adaptive therapy should be disabled preoperatively if “advantageous.” Intraoperative rate changes, which result from elective continuation of rate modulation or a lack of CIED programming resources, are usually benign. However, an increase in heart rate may be hemodynamically significant, unfavorable for certain comorbidities (e.g., coronary artery disease), or misinterpreted as patient discomfort. Therefore it is not surprising that device manufacturers have previously made more definitive recommendations that minute ventilation-driven rate-adaptive therapy should be programmed “off” during mechanical ventilation. Changes in rate because of active rate modulation can result from succinylcholine-induced muscle fasciculations, an oscillating saw, myoclonic jerks, postoperative shivering, electroconvulsive therapy (ECT), and QT alterations from medications, pH, or electrolytes. However, the most commonly encountered stimuli for rate changes in the operating room (OR) are electrocautery, external respiratory rate monitoring, and mechanical hyperventilation.

If active rate modulation results in an intolerable or undesirable increase in heart rate, a number of treatment options are available. The eliciting stimulus (e.g., hyperventilation or electrocautery) can be withdrawn, a magnet can place the pacemaker into an asynchronous mode (some caveats are discussed later), or CIED programming can disable rate modulation. Thankfully, minute ventilation rate modulation is only commonly found in the Boston Scientific and Sorin devices ( Table 4.2 ). These Boston Scientific and Sorin devices may require perioperative programming given their rate modulation monitor in conjunction with their magnet mode rates of 100 beats/min and 96 beats/min, respectively. Magnet application as a means of addressing rate modulation in these devices may risk ischemia in patients with coronary artery disease. Therefore disabling this function via programming may be more appropriate. Given that rate modulation via any monitored parameter offers no advantage to the patient in the OR, strong consideration should be given to disabling rate-adaptive therapy in the perioperative period ( Box 4.1 ).

Box 4.1

Methods to Disable Rate Modulation

• Cardiac implantable electrical device programming to disable rate modulation (preferred).

• Apply a magnet, which will place the pacemaker into an asynchronous mode.

• Remove the eliciting stimulus (e.g., hyperventilation or electrocautery).

Multisite Pacing

At first glance, the fifth position of the NBG code (see Table 4.1 ) appears redundant given the possibility of “D” (dual) in the first position. Furthermore, the information conveyed by the fifth position is frequently omitted from notes regarding a device's mode (e.g., DDDR). However, the fifth position of the NBG code conveys unique and valuable information to the practitioner regarding either multiple leads in a single chamber or leads in multiple chambers. For example, in CRT, there are leads “in” both the RV and left ventricle (LV). This information would not be communicated by a “D” in the first position, which would simply denote leads in both the atrium and the ventricle (i.e., a dual-chamber pacemaker).

The goal of CRT is twofold: (1) to maintain sequential AV contraction and (2) to synchronize ventricular contraction of the RV and LV. A dual-chamber pacemaker successfully maintains sequential AV contraction between the RA and the RV; however, RV pacing often results in delayed depolarization of the LV inferior or inferolateral wall because of a conduction delay. CRT attempts to address this phenomenon in certain patient populations by placing a lead in the coronary sinus. The coronary sinus lead can then be used to pace the left ventricle from that inferolateral location with the goal being synchronized ventricular contraction and increased cardiac output. Interestingly, the coronary sinus or “CS lead” is another passive fixation lead that is frequently maintained in place by removing a guide, which allows the lead to take a bent shape in the vessel lumen. Given that this lead is placed in the coronary sinus, it results in epicardial pacing in contrast to the RA or RV leads, which are endocardial. The ultimate location of this coronary sinus lead has been generalized to the posterior or basal inferolateral location, but in fact optimization does vary (the process of optimization is beyond the scope of this text). However, despite optimal coronary sinus lead placement, approximately 30% of patients with severe LV systolic dysfunction do not respond to CRT. Determination of which patients will respond to CRT is an active field of investigation.

Indications for CRT, which is also frequently described as biventricular pacing, have expanded in recent years ( Table 4.3 ). In 2012, an American College of Cardiology (ACC)/American Heart Association (AHA)/HRS update extended a class I indication to New York Heart Association (NYHA) class II patients with a left bundle branch block (LBBB) and QRS greater than 150 ms. A class IIa indication was also given to patients with an LBBB with QRS 120 to 149 ms or non-LBBB pattern with QRS greater than 150 ms. Therefore patients with CRT devices will likely become more common in the OR. A small but sometimes confusing point is the documentation of either CRT-D or CRT-P. Although the indications are essentially the same (see Table 4.3 ), CRT-D implies pacing for CRT plus an automatic implantable cardioverter defibrillator (AICD), but CRT-P implies no AICD component. Because most patients who qualify for CRT also meet indications for AICD therapy, the majority of CRT patients will have CRT-D devices.

The CRT-D devices pose a unique problem for perioperative management because a magnet application will only succeed in deactivating the ICD portion of the device. Given that the goal of CRT is the synchronization of ventricular contraction and the associated increase in cardiac output, these patients might be considered “functionally” pacemaker dependent. This is a debatable position because CRT patients often have an “adequate” underlying rhythm. However, given the goal is to promote pacing, inhibition caused by EMI may result in a reduction in cardiac output. Therefore reprogramming CRT-D devices to an asynchronous mode would be required to guarantee continued pacing in the perioperative period when EMI is anticipated ( Box 4.2 ).

Box 4.2

Cardiac Resynchronization Therapy With Defibrillation Capability (CRT-D Devices) and Magnet Application

• Because CRT-D devices contain an automatic implantable cardioverter-defibrillator, magnet application will only disable tachyarrhythmia therapies and NOT result in asynchronous pacing.

• Inhibition of biventricular pacing may result in a reduction in cardiac output and hypotension.

Mode Switching

Although it is not present in the NBG code, mode switching can often be found in an interrogation note. Mode switching allows for device identification of atrial tachyarrhythmias and the automatic conversion of pacemaker settings. For example, atrial fibrillation can result in ventricular tachycardia in patients with a dual-chamber pacemaker. Without mode switching enabled, a DDDR pacemaker would track the atria (e.g., atrial fibrillation) and pace the ventricle resulting in ventricular tachycardia. This may be misdiagnosed as a run of ventricular tachycardia given the new wide complexes. With mode switching enabled, the pacemaker would automatically switch from DDDR to a VVIR mode and thus eliminate the atrial tracking function.

In certain situations, intraoperative mode switching can have significant hemodynamic consequences. For example, EMI (e.g., electrocautery) in the OR can be misinterpreted by the device as a supraventricular tachyarrhythmia. With mode switching enabled, the pacemaker may inappropriately switch to a VVIR setting. The subsequent loss of AV synchrony can result in a significant reduction in cardiac output and deterioration in hemodynamics. Although mode switching does not usually present significant challenges in the perioperative period, it can be used to a clinician's advantage. For example, the atrial tachyarrhythmia burden can be determined preoperatively from the number of mode switches listed in an interrogation note.

Pacemaker Failure

Pacemaker failure has three causes: (1) failure of capture, (2) lead failure, or (3) generator failure. Failure of capture secondary to a myocardial defect (i.e., no myocardial depolarizations despite generator output) is the most difficult problem to solve. Myocardial changes that can result in noncapture include myocardial ischemia or infarction, acid-base disturbances, electrolytes abnormalities, or abnormal antiarrhythmic drug levels. Sympathetic drugs, however, tend to lower pacing thresholds and therefore promote depolarization. Luckily, the other two causes of pacemaker failure—outright generator or lead failure—remain rare.