Posts tagged “bundle branch block

STEMI seen in PVC

Although the previous case study was written for formalistic reasons and is admittedly neither very interesting nor particularly original, there is one interesting feature here worthy of note:

The arrows indicate complexes resulting from intermittant LBBB or PVCs with LBBB morphology. The latter is more likely given that their differing frontal plane axes (-60 vs +60) implicate two separate foci.

Despite aberrant conduction, the current of injury resulting from the anterior infarct remains explicit and is diagnostic of coronary occlusion.

In the first EKG (04:15) the complexes in V2 and V3 show appropriately discordant STE, but the ST/S ratio is groselly excessive. In 2010, Dodd and colegues demonstrated that an ST/S ratio >0.2 carries high specificity for LAD occlusion (1). Note the ratios in this case:

V2:    ST/S = 6mm/7mm = ~0.86

V3:    ST/S = 5.5mm/11mm = 0.5

In the second EKG (07:10) there is >1mm concordant STE in V4 and V6. In LBBB, the ST segments should always be discordant, and, when the terminal R wave is positive, they should show an appropriate proportion of ST depression. Thus, even in V6 where the J-point is isoelectric, there is a conspicuous absence of ST depression. This is a STEMI equivalent (2). Even if this patient had a baseline LBBB and the entire EKG showed wide-complex aberrancy, the MI would not be hidden.

These features as illustrated here closely reflect the more thorough and authoratative work of Dr. Smith in his May 21, 2011 blog post, “LBBB: Is There STEMI?

Reproduced from his text:

Smith modified Sgarbossa rule:

  1. At least one lead with concordant STE (Sgarbossa criterion 1) or
  2. At least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
  3. Proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)

References

  1. Dodd KW. Aramburo L. Broberg E. Smith SW. For Diagnosis of Acute Anterior Myocardial Infarction Due to Left Anterior Descending Artery Occlusion in Left Bundle Branch Block, High ST/S Ratio Is More Accurate than Convex ST Segment Morphology (Abstract 583).  Academic Emergency Medicine 17(s1):S196; May 2010.
  2. Dodd KW. Aramburo L. Henry TD. Smith SW. Ratio of Discordant ST Segment Elevation or Depression to QRS Complex Amplitude is an Accurate Diagnostic Criterion of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block (Abstract 551).  Circulation October 2008;118 (18 Supplement):S578.
  3. Dr. Stephan Smith. “LBBB: Is There STEMI?” Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html

In re Littmann et al. (2007)…

For background regarding EKG double counting and Littmann’s sign of  hyperkalemia, see March, 2012.

The following was recorded from an 82 year-old female with lethargy and malaise; electrolyte status is unknown, as is any further clinical data.

This is a 10 second strip with 9 QRS complexes; the true heart rate is thus 54bpm. The GE-Marquette 12SL interpretation algorithm has counted 163bpm, (3 x 54 = 162). Assuming that this is a result of systematic error and not coincidence, both the mechanism and significance of triple counting remain unclear.


Case No. 15: So it’s a “Trifascicular Block”?

In 2009 the AHA released recommendations for the standardization and interpretation of the electrocardiogram stating that, “The terms atypical LBBB, bilateral bundle-branch block, bifascicular block, and trifascicular block are not recommended because of the great variation in anatomy and pathology producing such patterns. The committee recommends that each conduction defect be described separately in terms of the structure or structures involved instead of as bifascicular, trifascicular, or multifascicular block.” (Rautaharju, P., et al., 2009)

Despite the ambiguity and referential instability of the term, however, the so-called “trifascicular block” remains at large in many clinical settings. So much so, in fact, that it has its own Wikipedia page: “Trifascicular block… has three features: prolongation of the PR interval (first degree AV block), right bundle branch block, and either left anterior fascicular block or left posterior fascicular block.” Wikipedia makes no mention, however, of the AHA guidelines or ongoing controversy surrounding this set of electrocardiographic features. Wikipedia concludes by stating that, “The treatment for diffuse distal conduction system disease is insertion of a pacemaker.” (Wikipedia, 2011)

The idea of “trifascicular block”, however, is not only problematic due to its potential reference to a multiplicity of histopathological substrates, but even assuming a trifascicular model of the sub-Hisian conduction system, the concept of “trifascicular block” cannot be distinguished from complete heart block. If there are only three fascicles leading into the ventricles and all three are blocked, then there is de facto complete heart block. Rather what seems to be meant by the term “trifascicular block” is a situation in which the traditional three fascicles of the left and right bundle branches all demonstrate some degree of disease or dysfunction. For example, typically a RBBB with a left anterior fascicular block and 1° AV block is considered a trifascicular block. Yet even here the situation is unclear: the 1° AV block may be due to disease in the remaining posterior left fascicle or a pathological process above the bifurcation of the His bundle resulting in an AV conduction delay.

Regardless of this semantic debate, it has been known since the early 1900s that in the predominance of human subjects the left bundle branch splits into three rather than two fascicles. Disease of the left septal fascicle has been extensively characterized electrocardiographically, histologically, and otherwise. (Riera, A., et al., 2008)

In fact, extensive individual variance complicates the branching and interconnection of the fascicles of the LBB. This is further confused by evidence indicating that fascicular blockade can occur in the absence of identifiable histological lesions. When making the diagnosis of acquired advanced distal conduction system disease, therefore, toxicological, infectious, and other reversible etiologies must first be ruled out.

Left, Diagrammatic sketches of the LBB reconstructed from transverse sections of the LBB of human hearts. Right, 4 prototypes of LBB dissected from adult normal human hearts. Note that each of these prototypes has a similar pattern among those obtained histologically. (Rautaharju, P., et al., 2009)

While the polyfascicular nature of the LBB remains largely an academic observation with limited utility in most clinical settings, this anatomical variance certainly speaks to the rationale behind the AHA recommendations. The pragmatic concern remains not whether the term “trifascicular block” is semantically sound or anatomically appropriate, however, but whether the electrocardiographic features of “trifascicular block” are sufficient evidence of advanced distal conduction system disease to warrant pacemaker implantation or prophylactic measures in anticipation of complete heart block (for example application of external pacing pads, observational admission, or specialty consultation).

I will examine three case studies exploring the utility of a “trifascicular block” nomenclature, and some treatment indications when faced with “trifascicular” disease.

Case No. 1: Mr. A, a 79 year-old Caucasian man, presents to EMS with complaints of syncope and superficial facial injuries from the subsequent fall. He reports a similar episode of “passing out” once before, but did not follow up on the incident. His medical history consists of glaucoma and a distant history of smoking.

This EKG, recorded by EMS providers at the scene, demonstrates 3rd degree heart block. An atrial rate of ~90bpm persists discontinuously behind a sub-Hisian ventricular escape rhythm of ~ 25-30bpm with LBBB morphology.

On arrival in the ED this EKG was recorded:

The P-R intervals here are constant and non-lengthening; the R-R intervals are constant and not decreasing. Both of these features are consistent with Mobitz II rather than the Wenkebach phenomenon.

This interpretation aligns well with the known pathophysiology of intermittent 3rd degree block. Lipman and Massie state that, “Clinically, [Mobitz type II] often is associated with RBBB and left axis deviation. Thus, Mobitz type II block with wide QRS complexes is often associated with lesions below the AV node. This has been confirmed by His’ bundle electrocardiograms… Mobitz type II block [is] associated with incomplete trifascicular block, is considered more serious, and is much more likely to produce Stokes-Adams attacks and necessitate pacemaker insertion.” (Lipman-Massie, 1989, p.453.)

Given symptoms suggesting Stokes-Adams syncope and evidence of advanced AV block, this patient was admitted for cardiology consultation. Several days later this EKG was obtained.

Here we see RBBB with left anterior fascicular block (R-axis at -52°, small Q in I and avL, and small R in III and avF)—exactly the findings predicted by the quotation from Lipman-Massie.

As seen here, electrocardiographic proof of intermittent sub-Hisian 3rd degree heart block may be considered evidence of poly-fascicular disease with likely future Stokes-Adams events. Current AHA guidelines regarding acquired AV block in adults state that, “Permanent pacemaker implantation is indicated for third degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block.” (Epstien, A., et al., 2008, e358.) In light of this, a pacemaker was placed and the patient was discharged without complications.

Case No. 2: Mr. B, a 90 year-old Caucasian man with multiple medical problems, was brought in by ambulance with reports of increased lethargy and possible altered mental status as per his nursing home care providers. A routine EKG was recorded.

This EKG demonstrates the classic “trifascicular block” features of RBBB, LAFB, and 1st degree HB. Interestingly, there is inappropriate T-wave concordance in some leads of the inferior and high lateral distribution. A previous EKG was not available for comparison and no follow up EKG was recorded, making the significance of these findings difficult to ascertain.

After sleeping for six hours in the emergency department, Mr. B was found walking to the bathroom, articulate but confused, awake and alert to his surroundings, in no ostensible distress. All laboratory assays returned within normal limits and his relatives at the bedside testified that he was behaving and mentating normally. He was discharged without follow up back to his allied nursing facility.

Case No. 3: Ms. C, a 66 year old Hispanic woman with IDDM and known coronary artery disease, presented to the emergency department with sweats, chills, dysuria, and an oral temperature of 101.4° F.

This EKG demonstrates 1st degree HB in the presence of LBBB, another classic pattern of “trifascicular” disease. Incidentally, the 0.04ms notching of the S-wave upstroke in V3 represents Cabrera’s sign, one of several types of QRS fragmentation seen in LBBB and paced rhythms, known typically to be highly specific (~90%) for prior MI, but lacking in sensitivity (~60%) (Mithilesh K., et al., 2008). This ECG feature was consistent in this case with a prior anterior wall MI in 2005.

Unsurprisingly, urinanalysis in this case confirmed the clinical suspicion of UTI and the patient was discharged on antibiotics with follow up to her primary.

Both the cases of Mr. B and Ms. C  involve patients with histories consistent with extensive distal conduction system disease and incidental electrocardiographic findings revealing “textbook” “trifascicular block”. Yet neither of these patients’ symptoms or clinical presentation was in any way correlated with the disease process manifest on EKG, and neither warranted intervention.

The initial case of Mr. A, however, involves a patient with a known pathophysiological disease model (ref. Lipman-Massie) and both electrocardiographic proof of intermittent high degree AV block and Stokes-Adams symptoms circumstantially linked to the arrhythmic disturbance. Both of these features are independent absolute indications for pacemaker therapy.

The term “trifascicular block” does not appear in the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. Regarding indications for pacing in acquired distal conduction system disease as represented by chronic bifascicular block, the 2008 Guidelines make the following recommendations:

  • Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent third-degree AV block.
  • Permanent pacemaker implantation is indicated for type II second-degree AV block.
  • Permanent pacemaker implantation is indicated for alternating bundle-branch block.
  • Permanent pacemaker implantation is not indicated for fascicular block without AV block or symptoms.
  • Permanent pacemaker implantation is not indicated for fascicular block with first-degree AV block without symptoms. (Epstein A., et al., 2008, e360.)

Although case-specific, well reasoned clinical judgment is the best guiding principle of any treatment, the hope in presenting these three cases is to call into question not simply the histopathological verisimilitude of the “trifascicular block” nomenclature but to examine the case for this term’s pragmatic utility. In all three cases, the concept of “trifascicular block” proves to be a misleading descriptor, failing to capture the therapeutic relevance of the EKGs in question.

The remarks presented here are entirely the opinion of the author and should not represent advice or guidelines for any treatment, diagnosis, or test. My ambition has been to address specifically the issue of a “trifascicular block” nomenclature in device-based therapy for distal conduction system disease. There do exist contexts in which this term can be of significant value; of note is this fascinating case report from Tom Buthillet discussing a WCT, classic “trifascicular block”, and the risks of antiarrhythmic administration.

References

Dunn, M., and Lipman, B. (1989). Lipman-Massie Clinical Electrocardiography, 8th ed. Yearbook Medical Publisher Inc.

Epstein, A., et al. (2008). ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. Circulation, 2008, 117:e350-e408. doi: 10.1161/CIRCUALTIONAHA.108.189742

Marcelo, E., et al. (2007). Hemiblocks revisited. Circulation, 2007, 115:1154-1163. doi: 10.1161/CIRCULATIONAHA.106.637389

Mithilesh, K., et al. (2008). Fragmented wide QRS on a 12-lead ECG: a sign of myocardial scar and poor prognosis. Circulation Arrhythmia and Electrophysiology, 2008, 1:258-268. DOI: 10.1161/CIRCEP.107.763284

Rautaharju, P., et al. (2009). AHA/ACCF/HRS Recommendation for the standardization and interpretation of the electrocardiogram. Circulation, 2009, 119:e241-e250. doi: 10.1161/CIRCULATIONAHA.108.191096

Riera, A., et al. (2008). The history of left septal fascicular block: chronological consideration of a reality yet to be universally accepted. Indian Pacing and Electrophysiology Journal, 2008, 8(2):114-128. Retrieved from http://www.ipej.org/0802/riera2.htm

Wikipedia. (2011) Trifascicular Block. Retrieved from http://en.wikipedia.org/wiki/Trifascicular_block


Case No. 3: Status Post Cardiac Arrest

An 84yr old white female, s/p VT/PEA arrest.

This ECG demonstrates AV dual sequenced pacing with loss of atrial capture. Note the high left axis in the x-y plane, consistent with typical pacer findings, but an atypical rightward shift of electrical forces across the precordial z-axis (inverse R-wave progression). Traditionally ventricular pacing electrodes are deployed in the right heart and result in a LBBB ECG morphology as the myocardial tissue depolarizes from right to left. Yet in this case we see a dramatic RBBB pattern, raising concerns about displacement or septal perforation, particularly given that the pt. has received CPR. The etiology of RBBB pacer morphology is not exclusively pathological, however, and receives a good discussion on Dr. S. Venkatesan’s Cardiology Blog. Note that the QRS in this case is elongated above 160ms, and necessarily reflects slow and poorly coordinated ventricular contraction, perhaps betraying a newly aberrant interventricular conduction pathway, even for this 100% paced patient.

Another interesting example of a similar RBBB effect can be seen at Dr. M. Rosengarten’s electrocardiography site, and there is a thorough case report and research analysis of the phenomenon in The Journal of Electrocardiography Vol.6 No. 1, 2003.

Shortly after this 12-lead was captured, the pt. again deteriorated into PEA and was lost to resuscitative efforts.