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Postoperative Episodic Left Bundle Branch Block

Elterman, Kelly G. MD; Mallampati, Seshagiri Rao MD; Tedrow, Usha B. MD, MS; Urman, Richard D. MD, MBA

doi: 10.1097/ACC.0b013e3182a963be
Case Reports: Case Report

Transient left bundle branch block (LBBB) associated with physical exertion has been described in patients with and without coronary artery disease. A 64-year-old woman with no history of coronary artery disease underwent Nissen fundoplication under general anesthesia. Preoperatively, an exercise-tolerance test revealed LBBB, without ischemic symptoms. Intraoperatively, the electrocardiogram revealed normal sinus rhythm. Postoperatively, LBBB appeared in the absence of clinical symptoms or physiologic stress. The patient reported several similar episodes previously. Cardiac enzymes were negative. Subsequent electrocardiograms revealed persistence of LBBB. Anesthesiologists should be aware of the possibility of perioperative transient LBBB in the absence of cardiac ischemia.

From the Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women’s Hospital, Boston, Massachusetts.

Accepted for publication August 12, 2013

Funding: Not funded.

This report was previously presented, in part, at the American Society of Anesthesiologists.

The authors declare no conflicts of interest.

Address correspondence to Kelly G. Elterman, MD, Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women’s Hospital, 75 Francis St., CWN-L1, Boston, MA 02115. Address e-mail to

Transient left bundle branch block (LBBB) is a phenomenon in patients with a history of coronary heart disease (CHD), particularly with physical exertion or in the perioperative period.1 Cases of exercise-related or intraoperative transient LBBB, accompanied by tachycardia or hypertension, in patients with and without coronary artery disease (CAD), have been described.2–4 We present a case of postoperative recurrence of an episodic temporary LBBB in the absence of associated tachycardia or hypertension in a patient with no known CHD.

The patient and her family were not contacted, and the IRB determined that approval was not required.

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A 64-year-old woman with a medical history of obstructive sleep apnea, hypothyroidism, hyperlipidemia, gastroesophageal reflux disease, and a hiatal hernia presented to our institution for a laparoscopic Nissen fundoplication. Her medications consisted of levothyroxine, atorvastatin, lithium, and duloxetine. She had no known history of CHD. As part of her preoperative evaluation, she underwent an exercise-tolerance test (ETT) with echocardiographic imaging to assess nonanginal chest pain, during which her baseline heart rate was 86 bpm. She was in normal sinus rhythm (NSR), and her electrocardiogram (ECG) demonstrated a LBBB at rest. During exercise, her maximal heart rate was 137 bpm, without symptoms of cardiac ischemia. The ECG response to stress was uninterpretable given the LBBB. Echocardiographic images revealed an ejection fraction of 65% to 70%, without regional wall motion or valvular abnormalities, and appropriate augmentation with exercise.

The patient was asymptomatic and presented in NSR with evidence of borderline interventricular conduction delay (IVCD), as suggested by a QRS duration of 112 milliseconds but no LBBB on the day of her operation (Fig. 1). Her intraoperative course was uneventful. Before anesthetic induction, her heart rate was 85 bpm, and arterial blood pressure was 144/76 mm Hg. She received fentanyl 100 mcg and propofol 250 mg on induction. She was subsequently paralyzed with 100 mg succinylcholine, and her trachea successfully intubated. During the case, anesthesia was maintained with a propofol infusion, and paralysis was continued with vecuronium. Her heart rate ranged from 60 to 70 bpm, the ECG revealed NSR without LBBB, and her systolic blood pressures ranged from 85 to 140 mm Hg throughout the case. Before tracheal extubation, neuromuscular blockade was reversed with glycopyrrolate and neostigmine. She received ondansetron for nausea prophylaxis, and ketorolac for pain control.

Figure 1

Figure 1

Postoperatively, she was transferred to the postanesthesia care unit, where she reported feeling comfortable. The anesthesia team was called when her nurse noted the sudden appearance of LBBB (Fig. 2). On examining the patient’s telemetry strip, we noticed an acute change in QRS complex duration. At baseline, the complex appeared to have a duration of approximately 110 milliseconds, perhaps indicative of a borderline IVCD, and after 2 narrower complexes of approximately 80 milliseconds duration, the QRS complex became obviously prolonged with a duration of approximately 130 milliseconds. On evaluation, the patient denied chest pain, dyspnea, nausea, or dizziness. Her heart rate was 90 bpm, and arterial blood pressure was 108/45 mm Hg. In addition, she reported previous episodes of transient LBBB, without associated symptoms and with subsequent negative clinical investigations. A 12-lead ECG was obtained and revealed a LBBB, at a rate of 93 bpm (Fig. 3).

Figure 2

Figure 2

Figure 3

Figure 3

Review of previous ECGs revealed NSR without LBBB on the morning before the ETT (at a rate of 85 bpm), presence of LBBB at rest and with exercise during the ETT (at a rate of 86 bpm), borderline IVCD but no LBBB 2 days before surgery (at a rate of 73 bpm), and NSR without LBBB intraoperatively and postoperatively before the abrupt change (at rates ranging 60–70 bpm).

Serum markers of cardiac ischemia, including creatine kinase, creatine kinase MB, and troponin, were negative. Serum electrolytes were unremarkable. Subsequent ECGs also revealed LBBB with heart rates of 80 to 89 bpm. She remained asymptomatic throughout her hospital course and was discharged home the following day.

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LBBB occurs when normal conduction through the His-Purkinje system is disturbed due to slowing of anterograde conduction or retrograde invasion of the left bundle, leading to prolongation of ventricular depolarization and widening of the QRS complex. The etiology of this entity is multifold and includes structural heart disease, abberant conduction in the absence of structural heart disease, and electrolyte abnormalities. The appearance of LBBB may be transient, intermittent, or permanent. Transient LBBB is defined as block which subsequently reverts to normal conduction. Intermittent LBBB is defined as the appearance of blocked and normal conduction on the same ECG tracing.5 The appearance of permanent conduction delay is more common than either transient or intermittent bundle branch block (BBB).

The appearance of LBBB has significant clinical implications. In 1 study, women with known cardiovascular disease and BBB were at greater risk for CHD-related death. Those with a LBBB had a higher all-cause mortality. LBBB in women without cardiovascular disease was also predictive of CHD-related death.6 Perhaps of even greater clinical relevance is the finding by Aro et al.7 that not only LBBB but also prolongation of the QRS beyond 110 milliseconds in the absence of BBB is significantly associated with arrythmia-related and all-cause mortality. Zhang et al.6 identified a similar phenomenon, demonstrating that women with QRS prolongation 110 to 119 milliseconds but without BBB had a 71% increased risk for CHD-related death and 27% increase in all-cause mortality.

Sudden onset of LBBB is usually concerning for acute cardiac ischemia, infarction, or previously undiagnosed CHD, particularly in the setting of stress. Grady et al.8 demonstrated that exercise-induced LBBB was independently associated with increased cardiovascular mortality and morbidity, in both patients with and without documented CAD. García Pascual et al.9 showed that exercise-induced LBBB may be rate-related and could be due to coronary vasospasm, amenable to treatment with calcium channel blockers, particularly in the absence of fixed coronary lesions. Similarly, Vasey et al.2 suggested that exercise-induced LBBB is not necessarily indicative of CAD, particularly at a heart rate >125 bpm, and may instead be a developing cardiomyopathy.

However, LBBB may also appear in the absence of heart rate or arterial blood pressure increase. Shimamoto et al.10 were able to induce LBBB on introduction of a catheter into the left ventricle during cardiac catheterization in 3 patients without CAD or previous IVCD. In 2 of these patients, LBBB was transient and resolved the same day. In the third patient, however, the LBBB persisted for months. Chow et al.11 reported predictable appearance of LBBB induced by laughing, presumably due to transient ischemia caused by increased intrathoracic pressure. Bauer12 described 5 cases of LBBB induced and abolished at will using physiologic maneuvers such as straining, breath-holding, deep inspiration, or carotid stimulation. Edelman and Hurlbert5 reported a case of transient and intermittent LBBB which occurred intraoperatively in the absence of hypertension or tachycardia. Similarly, Domino et al.13 and, more recently, Tyagi et al.14 reported cases of benign perioperative rate-related LBBB which resolved with pharmacologic control of heart rate or carotid massage.

In this case, we present postoperative recurrence of an episodic LBBB in the absence of electrolyte abnormality,15 myocardial infarction, medication administration,16 hypertension, or tachycardia in a patient with no known CAD. There are several possible mechanisms for this rare occurrence. First, it could be that the patient did indeed have undiagnosed CAD. Without cardiac catheterization, it is not possible to know her coronary anatomy. However, the absence of ischemic symptoms and laboratory tests suggestive of ischemia, as well as the lack of associated hypertension or tachycardia, argue against this possibility.

Another possibility is that the LBBB is transient ischemia or vasospasm, in the absence of a coronary lesion, not significant enough to result in symptoms. Transient ischemia could result from increased intrathoracic pressure, as has been previously described,11,12 and in this patient could have resulted from transmission of increased intra-abdominal pressures secondary to laparoscopy. However, if this were the case, the LBBB would have likely appeared intraoperatively rather than in the postanesthesia care unit. Furthermore, negative cardiac enzymes argue against any clinically significant ischemia. Alternatively, it could be that retrograde invasion of the left bundle, initiated by ectopic beats, resulted in a complete LBBB pattern.

While the lack of obvious tachycardia argues against ischemia as the cause of the LBBB, a rate-related cause cannot be entirely discounted. Recall that the patient presented to her preoperative ETT with a heart rate of 86 bpm and a LBBB. Intraoperatively, her heart rate ranged from 60 to 70 bpm without LBBB. When the LBBB appeared postoperatively, her heart rate was 93 bpm. Perhaps for this patient, a heart rate of 80 to 90 bpm is a relative tachycardia, a rate that is within normal limits, but for her, it is sufficient to elicit a conduction delay. As Bauer described, it is possible to have a “critical rate” above which conduction through the affected bundle is blocked.12

Given the patient’s history of episodic transient LBBB, concern for an acute event was decreased but not dismissed. Despite the history of recurrence and lack of associated symptoms, an ECG was obtained, and cardiac enzymes were assessed; because, even in the setting of episodic LBBB, a recurrence due to transient conduction delay could not be differentiated from that of a recurrence due to ischemia without investigation. Further immediate clinical intervention, such as cardiology consultation and initiation of treatment for acute myocardial infarction which would have been appropriate had this been the patient’s first presentation of LBBB, was not considered necessary. Similarly, pharmacologic intervention or clinical maneuvers to alter the heart rate were not attempted because the patient was hemodynamically stable. The patient was instructed to follow up with her cardiologist; however, the exact etiology of her transient conduction defect, whether it be functional or neurogenic nature,12 remains unidentified. Because the presence of transient LBBB can evolve into permanent LBBB, increases the risk of all-cause mortality, and may herald the onset of ischemic heart disease,2,5 further investigation, including cardiac catheterization, is certainly warranted for this patient.

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While the sudden appearance of LBBB is often a sign of cardiac ischemia, it may also be vasospasm, a rate-related BBB, or recurrence of an episodic conduction delay. In a hemodynamically stable patient without known CHD or evidence of acute ischemia, recurrence of a transient conduction delay may have no immediate clinical consequences. It does, however, have significant prognostic implications. Over time, these patients are at increased risk for development of permanent BBB, CAD, cardiomyopathy, and CHD-related as well as all-cause mortality. Anesthesiologists should be aware of the possibility of episodic LBBB and its clinical significance so as to be able to manage and educate their patients appropriately.

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