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Rate-Dependent Left Bundle Branch Block in an Ambulatory Surgery Patient: A Case Report

Farag, Ashraf MD, MBBS*; Tsai, Justin MD*; Deeb, Sam MD; Putman-Garcia, Deidre MSNA*; Wasnick, John D. MD, MPH*; Conlay, Lydia A. MD, PhD*

doi: 10.1213/XAA.0000000000000435
Case Reports: Case Report

A 52-year-old woman, ASA II (American Society of Anesthesia classification II) scheduled for cholecystectomy in an ambulatory center, exhibited a wide-complex tachycardia with ectopy on the monitor after induction with propofol and succinylcholine. Blood pressure remained stable; amiodarone was administered for presumed ventricular tachycardia. A 12-lead electrocardiogram (ECG) showed a new left bundle branch block (LBBB) at 98 beats per minute (bpm), which resolved when the heart rate slowed. Surgery was postponed, and both the LBBB and ectopy recurred frequently during the next 24 hours in the intensive care unit, particularly at heart rates >90 bpm. Troponins were normal, and the patient was diagnosed with a rate-dependent LBBB and cleared for surgery.

*Department of Anesthesiology, Texas Tech School of Medicine, Lubbock, Texas; and Department of Surgery, Texas Tech School of Medicine and Swat Surgical Associates, Lubbock, Texas.

Accepted for publication August 30, 2016.

Funding: None.

The authors declare no conflicts of interest.

Address correspondence to Lydia Conlay, MD, PhD, Department of Anesthesiology, Texas Tech School of Medicine, 3601 4th St, STOP 8182, Lubbock, TX 79430. Address e-mail to

The sudden onset of wide-complex cardiac rhythms can be an unsettling event, particularly in an ambulatory setting, where resources for a complex assessment and interventions may be limited. Moreover, it can be difficult to differentiate a new left bundle branch block (LBBB) from other potentially more serious arrhythmias on a monitor, particularly if the rhythm is rapid and accompanied by frequent premature ventricular contractions (PVCs). Previous reports have described the onset of a rate-responsive LBBB associated with both general and epidural anesthesia, as well as after the administration of a variety of drugs, including succinylcholine and pancuronium.1,2 In general, this rhythm has been described as benign, mainly because of the lack of cardiac enzyme elevation.2–4 However, the measurement of troponins, a more sensitive indicator of ischemia, was not available at the time of previous clinical reports.

We describe a case of a new-onset LBBB accompanied by significant ectopy in an apparently previously healthy ambulatory surgery patient. We discuss the challenges with the differential diagnosis, the treatments, and the evaluations for ischemia with troponins.

The patient was offered an opportunity to review the case report, and she gave written permission to the authors for its publication.

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A 52-year-old woman presented to an ambulatory center for an elective cholecystectomy. Her past medical history was remarkable for morbid obesity (115 kg, body mass index [BMI], 42.2 kg/m2), reflux, depression, and chronic back pain. The patient’s medications included 60 mg daily of dexlansoprazole, 5/325 mg of Norco every 4 hours, and 150 mg of venlafaxine HCl XR daily. She had previously undergone a hysterectomy, a tonsillectomy, a carpal tunnel release, an unknown type of back surgery, and 3 cesarean deliveries without known problems with anesthesia. A preoperative complete blood count and basic metabolic panel were within the normal range. An electrocardiogram (ECG) performed 6 days before surgery showed sinus rhythm at a rate of 88 beats per minute (bpm), with a moderate intraventricular conduction delay (QRS interval, 115 milliseconds). This finding was not present on an ECG performed 5 years earlier. Her physical exam was unremarkable.

The patient was premedicated with 1 mg of midazolam, transported to the operating room, and connected to standard American Society of Anesthesiologists monitors. Her initial vital signs showed a sinus rhythm with a heart rate (HR) of 75 bpm, and a blood pressure (BP) of 123/82 mm Hg. A wide-complex couplet was noted on the monitor before the administration of any additional medications. During preoxygenation, 2 wide-complex couplets were again observed. Approximately 25 mcg of fentanyl and 60 mg of lidocaine were administered intravenously, and anesthesia was induced with 180 mg of propofol followed by 100 mg of succinylcholine to facilitate tracheal intubation.

Immediately after laryngoscopy, the patient’s HR and BP increased from 85 bpm and 115/90 mm Hg to 109 and 161/123, respectively. Approximately 6% desflurane was begun. A wide-complex tachycardia at approximately 98 bpm with numerous PVCs was observed on the monitor. The pulse was palpable, the BP was 90/45, and no P waves were discernible (printed rhythm strips are not available in our ambulatory unit). With a presumptive diagnosis of ventricular tachycardia, 2 successive doses of IV lidocaine, 40 mg and 100 mg were administered when the crash cart containing other resuscitative drugs and an ECG machine were obtained. As her BP declined to 86/47 mm Hg, the desflurane was reduced to 2.5%, and 50 mcg of phenylephrine was administered IV. Upon arrival of the crash cart, the arrhythmia was treated with 150 mg of IV amiodarone over several minutes as a 12-lead ECG was performed. This ECG showed sinus rhythm at a rate of 98 bpm and a new complete LBBB (Figure 1). The patient’s HR slowed to 77 bpm shortly after treatment with amiodarone, both the LBBB and the ectopy resolved, and a second 12-lead ECG showed a moderate intraventricular conduction delay and a sinus rhythm with nonspecific T-wave abnormalities (Figure 2). Troponins were sent for analysis.

Figure 1.

Figure 1.

Figure 2.

Figure 2.

Given the appearance of a new LBBB with ectopy, options such as continuing with the surgery, rescheduling the case for later in the afternoon (after the patient had been seen by a cardiologist), and postponing the surgery were discussed. The surgeon was reluctant to proceed until the patient had undergone a comprehensive cardiac evaluation and workup. Thus, desflurane was discontinued, and the patient emerged from anesthesia uneventfully. She was transferred to the cardiac care unit (CCU) for further evaluation.

During the next 24 hours, the patient repeatedly exhibited multiple episodes of a LBBB and ectopy, particularly when her HR increased to more than the mid 90s (Figure 3). These arrhythmias were asymptomatic and not accompanied by hemodynamic instability. Serial troponin levels remained below the detectable limit, <.01 ng/L, and cardiac enzymes including creatine phosphokinase, lactic dehydrogenase, and serum glutamic oxaloacetic transaminase were normal. The patient was discharged from the hospital with the diagnosis of an intermittent rate-dependent LBBB, and no further workup was deemed necessary.

Figure 3.

Figure 3.

The patient was subsequently admitted to another institution by the surgeon, and an electrophysiologic evaluation was completed showing a rate-responsive LBBB. Her gallbladder was removed uneventfully there, although similar arrhythmias reportedly appeared repeatedly throughout the perioperative period.

Approximately 1 year after the removal of her gallbladder, the patient reportedly underwent an attempted esophagogastroduodenoscopy and colonoscopy in a doctor’s office. She was told that she flat-lined during that procedure and was transferred emergently to the institution where her gallbladder had been removed. She was diagnosed with severe nonischemic cardiomyopathy and systolic congestive heart failure with an ejection fraction of 20%, and a biventricular implantable cardioverter defibrillator was placed. She has resumed normal activities, which include working full time and mowing the lawn.

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The phenomenon of a rate-dependent LBBB is not commonly encountered during anesthesia. It is most easily diagnosed by directly observing the emergence and disappearance of the LBBB on a 12-lead ECG as the patient’s heart rate crosses over the critical rate. Although generally thought of as benign, it has been associated with pre-existing bundle branch disease, chronic hypertension, myocardial infarction, and/or ischemia, it and may eventually result in a permanent LBBB.1,5–7 Various treatments have been used to terminate a rate-responsive LBBB, including carotid massage, neostigmine, and propranolol.2

The rate-related LBBB observed in the operating room may resemble the exercise-induced transient LBBB, observed in .4% to .5% of patients undergoing an exercise tolerance test.8,9 Although often benign, it can also be associated with coronary artery disease, or it can represent an early manifestation of diffuse heart disease.10 When associated with another cardiac pathology, a rate-related LBBB is associated with a poorer prognosis compared with other intraventricular conduction defects without concomitant cardiac disorders.11,12 If an exercise-induced transient LBBB occurs frequently, it is thought to contribute to left ventricular dyssynchrony and to possibly lead to congestive heart failure.13 This may well have occurred in our patient.

A LBBB can occur, albeit infrequently, in young healthy patients with no apparent structural heart disease. For an asymptomatic patient with an isolated LBBB and no other evidence of cardiac disease, no specific treatment is required, and there is a minimal, if any, effect on outcome.14 However, a LBBB occurs most often in patients with underlying heart disease, and it typically reflects a slowly progressive degeneration of the conduction system leading to myocardial fibrosis. Hypertension, coronary artery disease, and cardiomyopathy are examples of conditions that may progress to a LBBB by this mechanism.11 A LBBB may also follow myocardial ischemia, myocardial infarction, or myocarditis, and it can likewise complicate the diagnosis of these conditions. It can also lead to left ventricular (LV) dyssynchrony, and in patients with LV dysfunction, it can exacerbate heart failure.12,13 Pacemaker insertion is indicated for patients with LBBB who develop a symptomatic conduction system disturbance such as a third-degree or Mobitz type II heart block, and to remodel the left ventricle.12,13 In older patients, a LBBB is associated with increased mortality.14

This patient had some electrocardiographic evidence of an interventricular conduction defect nearly 5 years before the procedure, suggesting the presence of pre-existing bundle branch disease, although she was asymptomatic and functionally very active. But in contrast to previous reports in which the LBBB was an isolated event, she exhibited not only a rate-dependent LBBB in the operating room, but also frequent PVCs that were absent in her baseline ECG. Given the presence of PVCs, ischemia was a concern, so troponins were sent for analysis. In previous reports, serial cardiac enzymes, including creatine phosphokinase, lactic dehydrogenase, and serum glutamic oxaloacetic transaminase, were noted to be normal after the rate-dependent LBBB was observed.1,2 Troponin levels, a more sensitive marker of myocardial necrosis,15 were not measured because the technical means to do so was not available at the time.1,2 Troponins were undetectable in our patient, suggesting that no myocardial damage had occurred.

Although a LBBB has a fairly characteristic appearance on ECG, there are other conditions with a similar appearance that should be excluded from the differential before its diagnosis. For example, ventricular tachycardia (HR, >100 bpm) and accelerated idioventricular rhythm (HR, 60-100 bpm) may both resemble a LBBB, although these rhythms are associated with atrioventricular dissociation. Other conditions that may mimic LBBB include Wolff–Parkinson–White Syndrome, in which the pre-excitation pattern from a right-sided accessory pathway can mimic LBBB.16 Similarly, right ventricular pacing can cause left bundle branch morphology; the presence of pacemaker spikes could differentiate this complex from a LBBB.16 However, pacing spikes are not always present or visible on an ECG monitor.

Moreover, differentiating ventricular arrhythmias from supraventricular arrhythmias or other aberrant rhythms is notoriously difficult when viewing the rhythm on a monitor screen. In our case, the arrhythmia presented as a wide-complex tachycardia accompanied by PVCs. A wide-complex tachycardia can be a ventricular tachycardia, a supraventricular tachycardia with aberrancy, or a pre-excited tachycardia (perhaps mediated by an accessory pathway).16 Ventricular tachycardia is by far the most common in patients with pre-existing heart disease, accounting for approximately 80% of cases.17–19 Because the diagnosis of a wide-complex tachycardia cannot always be made with certainty, even when using multiple ECG criteria, an unknown or uncertain rhythm should be presumed to be ventricular tachycardia in the absence of contrary evidence.16

Because our patient’s tachycardia was accompanied by multifocal PVCs and the rapid heart rate obscured any P waves on the 5-lead monitor, the presumptive diagnosis was ventricular tachycardia. Lidocaine was administered because it was immediately available in the room. Amiodarone was administered for presumed ventricular tachycardia, or an uncertain rhythm.18,20,21 After amiodarone administration, the patient’s LBBB and PVCs resolved, although both recurred repeatedly during the next 24 hours in the CCU. It is interesting that our patient’s arrhythmias resolved so quickly with the amiodarone bolus. The antiarrhythmic properties of amiodarone are thought to be largely related to prolongation of the action potential.22 But it also exerts an antiadrenergic effect by noncompetitively inhibiting α-receptors and β-receptors.23,24 The response we observed may thus have reflected a beta-blocking effect of amiodarone. In retrospect, it is also likely that simply slowing the patient’s heart rate in another manner would have resulted in a resolution of the arrhythmia as well.

Another therapeutic strategy would have been to administer adenosine initially to differentiate between superventricular and ventricular tachycardia and to potentially disrupt a superventricular tachycardia if it existed. An atrial reentry tachycardia such as atrial fibrillation or atrial flutter has a transient response to adenosine, but adenosine does not terminate the arrhythmia. On the other hand, a nodal reentry tachycardia is terminated by adenosine. Ventricular arrhythmias do not respond to adenosine because these arrhythmias originate in tissues distal to the conduction system. However, it should be noted that adenosine is recommended for ventricular tachycardias only if the tachycardia is regular and monomorphic, and its use should only be considered to differentiate ventricular tachycardia from supraventricular tachycardia.16,17 Other antiarrhythmic agents useful for hemodynamically stable ventricular tachycardia include 20 to 50 mg/min of IV procainamide or 1.5 mg/kg of IV sotalol administered during a 5-minute period, although these drugs should generally be administered with caution and by experts.20,21

This case demonstrates several points. First, although a rate-responsive LBBB in the operating room may be benign, it may also be the harbinger of additional pathology, particularly if the LBBB is accompanied by another abnormal rhythm. Second, a rate-responsive LBBB can occur without demonstrable myocardial ischemia, as indicated by sensitive measures of ischemia (troponin) not available for previously published reports. Third, a rate-responsive LBBB can masquerade as a wide-complex tachycardia and can be difficult to diagnose accurately, particularly on a monitor screen. And although amiodarone is known to be an effective treatment for ventricular arrhythmias, it may also be useful for the treatment of other rhythms as well.

A rate-responsive LBBB can be benign, or it can represent an early manifestation of more extensive heart disease, in which case it is associated with a poorer prognosis when compared with intraventricular conduction defects without concomitant cardiac disorders.10–12 Thus, it is our recommendation that patients with pre-existing cardiac pathology who develop an intraoperative LBBB and healthy patients who exhibit a new LBBB plus an additional cardiac arrhythmia (possibly suggesting other cardiac pathology) be further evaluated. This could include transthoracic echocardiography, if it is available.

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Name: Ashraf Farag, MD, MBBS.

Contribution: This author helped complete the manuscript.

Name: Justin Tsai, MD.

Contribution: This author helped complete the manuscript.

Name: Sam Deeb, MD.

Contribution: This author helped complete the manuscript.

Name: Deidre Putman-Garcia, MSNA.

Contribution: This author helped complete the manuscript.

Name: John D. Wasnick, MD, MPH.

Contribution: This author helped complete the manuscript.

Name: Lydia A. Conlay, MD, PhD.

Contribution: This author helped complete the manuscript.

This manuscript was handled by: Raymond C. Roy, MD.

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