A 49-year-old male with no reported past medical history presents to the emergency department (ED) with a 5-day history of chest pain. He reports a history of intense, substernal chest pain yesterday that was unrelieved, leading him to schedule a clinic appointment for the next day. At the clinic, his primary care doctor advised him to come straight to the ED after completing a “strange EKG.” On arrival in the ED, the patient denies any active chest pain in triage. However, he states that he has some mild pain in the middle of his upper back, “probably just from mowing my lawn the other day.”
An ECG is obtained in triage, with a computer interpretation read as “Type III Brugada pattern” (Figure 1). The triage team is instructed to bring the patient directly back to the ED. What is your interpretation of this ECG? What is on your differential?
Interpretation:
Rate: 108 bpm; Rhythm: Sinus tachycardia. Axis: Left axis deviation (I: positive, II: negative, aVF: negative); Intervals: PR: 148ms, normal; QRS: 132ms, prolonged; QTc: 429, normal; P-Waves: present and inverted in V1-V2; QRS Complex: Wide (>120) with qR segments in V1-V3; ST Segment/T-Waves: 1 mm ST elevation in V1-V2, 1 mm ST depression in II, III, aVF, V6. T wave inversions seen in aVL, V1-V3.
The patient had labs completed in triage. Ten minutes after being roomed in the ED, a troponin of 42.5 was reported. The ED team consulted Cardiology, who advised that they would arrive at bedside shortly to evaluate the patient.
To address the back pain in consideration of possible acute aortic pathology, bilateral upper extremity blood pressures were completed and noted to be similar and normotensive. The patient was also noted to have 2+ and equal radial pulses bilaterally. Point-of-care ultrasound revealed no evidence of pericardial effusion or aortic dissection flap in the aortic root. However, diffuse hypokinesis was appreciated.
Cardiology arrived at bedside and interpreted the ECG as a bifascicular block with a new right bundle branch block (RBBB) and a left anterior fascicular block (LAFB). The cath lab was activated for percutaneous coronary intervention (PCI), and the patient was found to have 100% occlusion of the proximal left anterior descending (LAD) artery requiring stent placement. The patient was ultimately admitted to the Cardiac ICU for post-PCI care.
Discussion:
RBBB is identified by its signature RSR’ pattern or wide, notched R waves in leads V1-V2, along with a wide QRS complex and slurred S waves in lateral leads (Figure 2).
Figure 2. RBBB diagnostic criteria (Life in the Fast Lane).
RBBB is understood to be caused by a delay in depolarization of the right ventricle. The atrioventricular (AV) node conducts through the bundle of His and down the left bundle branch. Then, the right ventricle depolarizes following this event.
Reviewing Figure 1, an RSR’ pattern is present. However, the patient has a left axis deviation; typically, a right axis deviation is expected with RBBB. And, why are there large S waves in the inferior leads (II, III, aVF)?
Isolated LAFBs are caused by a delay in depolarization of the left side of the left ventricle. An impulse travels via the posterior fascicle down the interventricular septum, ultimately terminating at the inferior septal wall of the left ventricle (Figure 3). The impulse then immediately depolarizes downwards and towards the right, only later depolarizing toward the left, producing the findings that we see in the inferior leads. These findings include small R waves in leads II, III and aVF and small Q waves in lateral leads, 1 and aVL (Figure 4).
Figure 3. Fascicular anatomy (CanadiEM).
Figure 4. LAFB diagnostic criteria (Life in the Fast Lane).
This patient’s pathology is best described as a bifascicular block (Figure 5). The 2 most common types of bifascicular blocks include:
RBBB with LAFB, usually with left axis deviation (most common)
RBBB and left posterior fascicular block (LPFB), which typically is manifested with a right axis deviation (less common, not an ED diagnosis)
In patients with a previous LAFB who then develop a RBBB, conduction to the ventricles is only possible through the remaining posterior fascicle. Because of this, the ECG typically demonstrates RBBB pathological changes on ECG with an imposed left axis deviation, as seen in this patient.
Etiologies for bifascicular blocks include:
Ischemic heart disease
Aortic stenosis
Degenerative conduction system disease
Structural heart disease
Occlusive myocardial infarction
Figure 5. Bifascicular block (Life in the Fast Lane).
If patients are asymptomatic with bifascicular blocks - with no evidence of syncope, fatigue, or chest pain - no intervention is necessary at that time. However, a common presentation in patients with symptomatic bifascicular blocks is syncope, which can be recurrent. In these cases, pacemaker implantation may be indicated, but notably, there is no increased incidence of sudden cardiac death in these patients. Guidance and management of care in patients with bifascicular blocks can better be assessed by an electrophysiologic study and monitoring with Cardiology.
In a patient presenting with bifascicular block and chest pain, acute coronary syndrome should be considered as an etiology. Although the patient above met criteria for RBBB with LAFB, the evidence that this is due to an acute occlusive myocardial infarction (OMI) is because there are new ischemic ST segment and T-wave changes.
Take Away Points:
A new bifascicular block in the setting of an acute OMI should raise concern for an LAD obstruction.
In the setting of a RBBB, the ST segments in leads V1-V3 should be depressed. ST elevation in leads V1-V3 in the setting of a RBBB should raise concern for an acute LAD obstruction.
Consider the causes of a bifascicular block in patients with RBBB and a left axis deviation. A LAFB may also be present.
While ECG computer interpretation is often helpful, it cannot reliably interpret all irregularities, and thus, the emergency physician should remain vigilant to appropriate ECG interpretation.
Authored by Austin Reynolds, DO; Michael Hohl, MD; Taylor Wahrenbrock, MD; Erica Dolph, MD; and Ari Edelheit, MD.
References:
Epstein AE, DiMarco JP , Ellenbogen KA, et al. 2012 ACCF/ AHA/ HRS Focused Update Incorporated Into the ACCF/ AHA/ HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2013; 127(3):e283-352.
Sclarovsky S, Lewin RF, Strasberg B, Agmon J.Left Anterior Hemiblock Obscuring the Diagnosis of Right Bundle Branch Block in Acute Myocardial Infarction. Circulation. 1979;60(1):26-32.
Zimmerman FH. ECG Core Curriculum. McGraw Hill Professional; 2023.
Strauss DG, Loring Z, Selvester RH, et al. Right, but Not Left, Bundle Branch Block Is Associated With Large Anteroseptal Scar. Journal of the American College of Cardiology. 2013;62(11):959-67.
Image Sources:
Figure 2: Burns, E., Buttner, R., & Buttner, E. B. and R. (2024, October 8). Right bundle branch block (RBBB). Life in the Fast Lane • LITFL.
Figure 3: Jones, T . (2015, December 18). The Boring Guide to ECG’s: Fascicular Blocks. CanadiEM.
Figure 4: Larkin, J., Buttner, R., & Buttner, J. L. and R. (2025, February 18). Left anterior fascicular block (LAFB). Life in the Fast Lane • LITFL.
Figure 5: Burns, E., Buttner, R., & Buttner, E. B. and R. (2024a, October 8). Bifascicular Block. Life in the Fast Lane • LITFL.