Posts tagged “Pacemaker

Littmann’s Sign

In 2007, Littmann and colleagues presented a novel EKG indicator of hyperkalemia based on the computerized “double counting” of heart rate. Over a 13-year period they identified 33 cases in which the GE-Marquette computerized 12SL EKG interpretation algorithm “double counted” or “near double counted” the actual heart rate seen on electrocardiogram. All 33 patients had hyperkalemia (between 5.3-8.8 mEq/L K+) as confirmed by serology taken within two hours of the double-counted EKG recording.

Littmann’s sign can be seen in the following EKG, initially presented here as a study in hyperkalemia in September of 2010.

A 65 year-old Caucasian man with sepsis and HHNKC; the potassium was 7.7mEq/L. The heart rate is 72 bpm; the computer counts 137 bpm.

Although the GE algorithm is proprietary and unavailable for analysis, they argue that, “The QRS width and axis measurement by the interpretation software suggested that, on many occasions, the computer recognized the T waves as being the QRS complexes….” (p.586)

Littmann et al. conclude stating, “Although interpretation software double counting of heart rate appears to be quite specific for hyperkalemia, its sensitivity is almost certainly very low.” (p.586)

While this research represents an intriguing new insight, it leaves many open questions. How were these 33 EKG cases identified? Were certain populations screened for this anomaly? How many total EKGs were reviewed in the course of this investigation?

Littmann claims that double counting “appears to be quite specific” presumably because all 33 EKGs were associated with underlying hyperkalemia. Yet without insight into the methods used to assemble this case series, I remain skeptical that these investigators did not succumb to confirmation bias in the process of collecting their EKGs. The existence of non-hyperkalemic double counting is not discussed in this publication and no differential diagnosis is presented regarding alternative etiologies.

In fact, concerning alternative etiologies and the specificity of double QRS counting, it turns out that this phenomenon has been extensively described in the pacemaker literature for over a decade. A Pubmed search using the combined terms “double counting QRS” produces numerous references. (Al-Ahmad A, Barold SS, Boriani G)

I reviewed 22 pacemaker EKGs collected over a 10 month period, recorded pre-hospitaly using the same GE-Marquette algorithm. This is what I found:

Looking further through ~50 EKGs collected over the same 10 months I found this as well:

In the first pair of EKGs, the computer appears to be confusing the pacemaker spike for a QRS complex; this is clearly “double counting of the QRS.”

The second pair is more complicated. This is not technically “double counting” of the QRS; there is not a 1:1 relationship between each QRS and a particular artifactual deflection. This is over-counting with a coincidental but not precise 2:1 relationship between the total count made by the computer and the total number of true QRS complexes. The interpretation of “Atrial Fibrillation” supports this in that it suggests that numerous complexes are counted during the first 5 seconds and then much fewer in the last 5. Although Littmann’s sign is not technically present here, the 12-lead EKG must be scrutinized to reach this conclusion. This seems problematic given Littmann’s stated goal of elucidating an “objective”, and “easily identifiable” indicator. (p.586)

No clinical data is available on these EKGs and it cannot be proven that these patients did not in fact have elevated potassium.

While producing these two hypothetical “false positives” hardly constitutes significant evidence, it is interesting that such counterpoints to Littmann’s specificity claims were so easily identified. Of further concern is the distinction between perfect double counting as seen in the pacemaker case and “near double counting” as seen in both the hyperkalemia case from Sept. 2010 and artifact case. What bearing this has on Littmann’s argument remains unclear.

Although a novel indicator, I am not sure that there is as yet persuasive evidence for what exactly Littmann’s sign indicates or how often this indication is specific for any one underlying clinical etiology.


Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007;25:584-90.

Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med. 2007 Nov;25(9):1077-8.

Al-Ahmad A, Wang PJ, Homoud MK, Estes NA 3rd, Link MS. Frequent ICD shocks due to double sensing in patients with bi-ventricular implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2003 Dec;9(3):377-81.

Barold SS, Herweg B, Gallardo I. Double counting of the ventricular electrogram in biventricular pacemakers and ICDs. Pacing Clin Electrophysiol. 2003 Aug;26(8):1645-8.

Boriani G, Biffi M, Frabetti L, Parlapiano M, Galli R, Branzi A, Magnani B. Cardioverter-defibrillator oversensing due to double counting of ventricular tachycardia electrograms. Int J Cardiol. 1998 Sep 1;66(1):91-5.


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.


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

Wikipedia. (2011) Trifascicular Block. Retrieved from