Couldn’t Find a Catchy Title, But We Tri(fascicular)ed

Co-authors: Balal Aslam MD, Esteban Davila MD

Edited by: Alec Feuerbach MD

Case:

An 82-year-old female with a past medical history of diabetes and hypertension presented to the ED after a syncopal episode. The patient stated that she was walking to the shower when she felt weak, had a “strange feeling in her belly”, and then lost consciousness. Her nephew caught her before she fell to the ground. There was no witnessed shaking during the episode and she quickly returned to baseline. The patient denied feeling any chest pain, nausea, vomiting, exertional chest pain, dyspnea on exertion, orthopnea, or lower extremity swelling. She denied any recent infectious symptoms. However, she did endorse a similar episode two months prior. 

Vital signs were normal. The physical exam revealed a normal S1 and S2 without murmurs, lungs that were clear to auscultation, a neurological exam without focal deficits and steady gait, and there was no lower extremity edema. 

Her ECG is below.

Figure 1: Initial ECG

ECG Interpretation: Rate 75/min, sinus rhythm, left axis deviation, 1st degree AV block (PR 240 ms) and right bundle branch block (RBBB) and left anterior fascicular block (LAFB) (QRS 140-150 ms). 

The treating physicians obtained labs that were unremarkable. What caused this patient’s syncope? Let’s take a closer look at the conduction abnormalities in this ECG to figure it out.

Ventricular Conduction

The electrical conduction system of the heart distal to the bundle of His is divided into a left and right bundle branch (LBB and RBB). The LBB further separates into the less talked about left septal, left anterior, and left posterior fascicles. Both the left fascicles and RBB continue to branch into Purkinje fibers which innervate the entire myocardium.[1] 

The conduction system of the heart utilizes a complex combination of cellular excitability, specialized gap junctions in specific locations, cell size and architecture, and ion channels to provide an orderly spread of electrical conduction and coordinated contraction of the ventricles.[2,3] Connexin protein Cx40, a gap junction with high conductance found in higher proportion in Purkinje fibers, is essential to the accelerated electrical conduction of the His-Purkinje system.[4]

If one of the RBB, LBB, or fascicles is blocked – meaning there is altered conduction of the electrical impulse down the cardiac tissue containing the affected bundle branch – the cells in that region of the heart will be depolarized through cell-to-cell transmission. These cardiac myocytes do not have access to the specific gap junctions found in Purkinje fibers and atrial tissue (like Cx40) which can conduct faster. As a result, there is a much slower, less synchronized contraction of the ventricles.  The unaffected bundle branch, however, would continue to propagate rapid, coordinated conduction. Because of this slow method of cell-to-cell transmission, distinct, wide QRS complexes are seen on the ECG. 

Figure 2: RBBB.[5] This causes a change in the direction of the transmission of the depolarization vectors. More discussion on RBBB and the ECG criteria can be found here.

Right Bundle Branch Block

Our patient has evidence of RBBB. The differential for RBBB includes normal variants, hypertension, structural heart disease, pulmonary embolism, pulmonary hypertension, and Brugada syndrome. The prevalence of RBBB is age and gender-dependent, ranging from 0.6% in women less than 40 years old to 14.3% in men above 80 years old,[6] with a prevalence in general populations between 2% to 3%.[7] RBBB alone, in the absence of significant heart disease or suspected inciting underlying pathology, usually does not require treatment. However, our patient had other conduction abnormalities in addition to RBBB. 

Left Anterior Fascicular Block

A LAFB is caused by impaired conduction of the left anterior fascicle which manifests on an ECG as a pathologic left axis deviation (axis between -30 to -90 degrees), qR complexes in leads I and AVL, and rS complexes in leads II, III, and AVF.

Figure 3: LAFB. Source: https://litfl.com/left-anterior-fascicular-block-lafb-ecg-library/

The figure above demonstrates left axis deviation (LAD). This is seen on the ECG as a net positive complex in lead I and a net negative complex in AVF. We can further characterize this axis as pathologic LAD if there is a negative complex in lead II.[8] With the left anterior fascicle blocked, depolarization of the anterior portion of the left ventricle comes from the interventricular septum and inferior/posterior regions of the LV leading to a shift in axis. 

Trifascicular Block?

If we refer back to our patient’s ECG we can see that our patient has RBBB, LAFB, and 1st degree AV block (PR > 200 ms without dropped QRS complex). This combination is often called a trifascicular block as there are three areas of impaired conduction – more examples can be found here. However, this is a misnomer. From a structural standpoint, the AV node, the site of 1st degree AV block, is not a fascicle. In addition, the 2009 AHA/ACCF/HRS joint recommendation advised against the use of the terms bifascicular and trifascicular block, noting the “great variation in anatomy and pathology producing such patterns.” The recommendation is to describe each conduction defect separately.[9] 

This ECG finding is relevant to emergency physicians. In the presence of multiple blocks, there are fewer pathways through which conduction can occur to the ventricles. In our patient with RBBB and LAFB, theoretically, only the LPF (and possibly the septal fascicle) is available to conduct through the ventricles. A transient block in the LPF could induce a complete heart block and subsequent syncope, as junctional and ventricular escape rhythms do not always occur.[10,11] Naturally, the question we want to know is, “does this patient need a pacemaker?” Let’s tackle this question with these blocks separately.

Before wading into this guideline, we will define what constitutes severe symptoms according to the ACC/AHA/HRS: bradycardia directly responsible for syncope/presyncope, transient dizziness or lightheartedness, heart failure symptoms, or confusional states resulting from cerebral hypoperfusion. Emergency clinician readers will recognize the difficulty in attributing these common presenting symptoms to bradycardia that may transient and resolve before ED presentation. Without a cardiac monitor of the event, physicians are left with a good history, exam, ECG interpretation, and gestalt. 

1st Degree AV Block 

AV Blocks can generally be thought of as at the AV node, intra-Hisian (meaning within the bundle of His), and infra-Hisian (meaning below the bundle of His). 1st degree AV block, actually a misnomer given all P waves are conducted, is generally located in the AV node, causing the prolonged PR interval. It is generally considered low-risk for progression to clinically important, higher grade AVB, though recent studies have challenged this belief.[12-14] If there is both prolonged PR interval and a widened QRS in the absence of prior BBB, it can be inferred that the block is intra-Hisian, though this is best evaluated with an Electrophysiology study (EPS). Therefore, the decision for pacemaker placement is contingent on both symptoms and the location of the block. 

According to the 2018 ACC/AHA/HRS Guideline on the evaluation and management of cardiac conduction delays, asymptomatic patients with 1st degree AVB believed to be at the level of the AV node or symptomatic patients whose symptoms don’t correspond to the AV block should not receive a permanent pacemaker, citing evidence of harm. 

If it is unclear if symptoms are related to the type I AVB, outpatient ambulatory ECG monitoring is recommended and Cardiology referral is warranted. Any patient with infra-Hisian 1st degree AVB or severe symptoms requires Cardiology evaluation for a permanent pacemaker.[15] 

RBBB and LAFB 

Patients with chronic RBBB and LAFB or LPFB have an increased probability of advanced AV block (AVB) and ventricular arrhythmias compared to the general population.[16] Though asymptomatic patients have rates of AVB or ventricular arrhythmia of 0.6% to 0.8%,[17] those that present with syncope have an annual incidence of 5% to 11%.[18] With this in mind, let’s go to the guidelines. 

The decision for evaluation for pacemaker once again hinges on symptoms, but in this patient population, there is more nuance. In asymptomatic patients with bifascicular or trifascicular block (ACC/AHA guidelines use this terminology), both a transthoracic echocardiogram, if structural heart disease is suspected, and an ambulatory ECG recording to document higher degree AVB are recommended. 

In asymptomatic patients with RBBB and LAFB/LPFB with additional 1st degree AV block, the assumption is that the AV block is located in the AV node and is not concerning for progression. Therefore, the presence of 1st degree AV block with RBBB and LAFB by itself does not automatically determine the need for pacemaker.[15] 

However, in patients presenting with RBBB and LAFB/LPFB and unexplained syncope, patients require an EPS to evaluate AV conduction and extent of infranodal disease. The presence of syncope, as mentioned above, implies a higher risk of AVB or ventricular arrhythmia, hence the recommendation.  

Those with syncope, RBBB, LAFB/LPFB, and 1st degree AVB need an EPS as well. The benefit of a pacemaker for these patients is decreased rates of syncope,[19,20] though rates of mortality are unchanged.[21] In addition, those with alternating BBB, such as those with alternating LBBB and RBBB, require a pacemaker, as this demonstrates unstable conduction through both bundles, putting the patient at risk for complete heart block. 

Figure 4: recommendations for evaluation of conduction disorders with 1:1 AV conduction.[15] HV: his-ventricle interval, measured during an EPS; AV: atrioventricular; BBB: bundle branch block; HF: heart failure; LBBB: left bundle branch block; and LVEF: left ventricular ejection fraction

Back to the Patient

Having taken a deep dive into the guidelines, let’s return to our patient. She was admitted to the hospital for telemetry monitoring and Cardiology evaluation. She underwent a transthoracic echocardiogram that revealed no abnormalities. She was discharged home without inpatient EPS, in contrast to the ACC/AHA guidelines, but returned a few days later with recurrent syncope. She was again admitted to the hospital and underwent an EPS that revealed an HV interval > 70 ms, and a dual chamber pacemaker was placed without complication

Take Home Points: 

– Given the variability in underlying pathology, describe each conduction abnormality separately instead of using terms, bifascicular and trifascicular block

– 1st Degree AVB: unless there is a new wide QRS or severe symptoms, these patients do not need a pacemaker 

– RBBB and LAFB/LPFB in an asymptomatic patient = outpatient Cardiology referral for TTE and ambulatory ECG 

– RBBB and LAFB/LPFB and unexplained syncope = admission for EPS and possible pacemaker placement