The following was recorded from a 90 year-old Caucasian man with shortness of breath.
This is very suspicious for second degree block; bigeminal PACs or PJCs with compensatory pauses are also possibilities. There is poor visualization of atrial activity due to background noise and intrinsic low voltage. The 12-lead is referenced for the best lead to visualize:
V1 seems promising; a V1 rhythm strip is acquired:
Worse still. Next, the Lewis lead:
Now the diagnosis is transparent. Before resorting to the placement of Lewis electrodes, the voltage gain can be doubled and noise reduction strategies applied. These were not utilized here.
12-lead under Lewis electrode placement:
There is diminished QRS voltage, new inferior Q-waves and ST-segment abnormalities. This could easily be misinterpreted, but it is an artifact of the lead system.
Switching back to standard placement. Different electrodes were used at this time and the voltage is altered; the background noise has faded but the atria remain quiet:
This patient was ultimately found to be pancytopenic (WBCs 3.1, RBCs 1.17, Hem 4.8, Crit 13.0, Platelets 96, Neu 23, Lym 60, Monos 16) and was worked up for myelodysplastic syndrome. The electrocardiographic findings may be associated with the anemia; they may also be incidental.
Christopher Watford brought the Lewis lead to my attention; he has described its physiology and advantages extensively in his blog post, Highlighting Atrial Activity on an ECG: The S5 Lead, as well as via audio on the EMCrit Podcast with Scott Wiengart.
There are numerous alternative lead systems: Brughada leads, high and low precordial placements for visualizing poorly represented territories, systems designed to emphasize pacemaker activity, etc. Body surface mapping technologies (e.g. The 80-Lead Prime ECG) have also shown promise. Some of these lead systems are described on this site under EKG Resources.
Bakker, A., et al. (2009). The lewis lead: Making recognition of P waves easy during wide QRS tachycardia. Circulation, (2009), 119; e592-e593. [Free Full Text] doi: 10.1161/CIRCULATIONAHA.109.852053
Lewis T. (1931). Auricular fibrillation. Clinical Electrocardiography. 5th ed. London, UK: Shaw and Sons; 1931: 87–100.
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.
New EKGs and new insights on a 2010 cold case. To recap:
While vacationing in Saigon a 57 year-old Caucasian female presented to the local emergency center with complaints of nausea and light-headedness. She experienced cardiac arrest, was resuscitated, and was found to have a persistent idioventricular rhythm coupled with significant acidosis and hypotension. She required multiple pressors and ultimately recovered despite a syndrome of multi-system organ failure. She was stabilized and transferred back to the states to a medical rehab facility. Infectious disease work up revealed only Candida Pelliculosa.
After several weeks in rehab, she again presented to the ED with complaints of nausea and light-headedness. Her past medical history included an aortic valve replacement (secondary to aortic stenosis), paroxysmal a-fib, diabetes, and depression. She was taking coumadin, flecainide, lexapro, januvia, and lopressor. Her BP on arrival was 81/44; the following EKG was recorded:
She had no complaints of chest discomfort or shortness of breath. At this time the potassium was 4.1, sodium 133, chloride 104, creatinine 3.1, BUN 31, glucose 114, and lactic acid 1.4. The white blood count was elevated at 15.6k. Amylase, lipase, AST and ALT were all mildly above normal. The pH was 7.01.
Her mental status deteriorated; she was intubated in the ED and transferred to the ICU. That night she suffered a PEA arrest and was resuscitated; multiple pressors were added sequentially for homodynamic support and a dialysis catheter and arterial line were placed. Peri-arrest bradyarrythmias were frequent and a transvenous pacemaker was inserted.
On the second hospital day the following EKG was recorded:
The potassium was 4.9, the sodium 135, chloride 101, creatinine 3.9, BUN 41, glucose 187, and lactic acid 13.
The cardiology consultant believed this to be an idioventricular rhythm of likely metabolic origin, secondary to electrolyte disturbance, possible flecainide or lexapro toxicity, or sepsis. Despite a widened QRS, the echocardiogram revealed a normal EF. Lexapro and flecainide were discontinued at this time.
On the third hospital day this EKG was recorded:
Labs from this date show a potassium of 3.5, sodium 143, chloride 97, creatinine 4.1, BUN 30, glucose 256, and lactic acid 23.
The blood pressure and electrocardiogram gradually stabilized; all cardiac enzyme assays were negative. By the seventh day she was extubated and transferred back to the hospital at which she had been originally treated returning from Vietnam. No bacteria, fungus, or parasites were isolated during this admission, however, she did have a positive hep-c antibody. Prior to discharge this EKG was recorded:
Labs from this date indicate a potassium of 3.4, sodium of 142, chloride 110, creatinine 2.4, BUN 40, glucose 303, and lactic acid 2.4.
She was subsequently lost to follow up.
The differential diagnosis for a sinusoidal, wide complex rhythm between 80-120bpm with QRST fusion includes hyperkalemia, sodium channel blocker toxicity, aberrant QRS AIVR, and tachycardia with aberrant conduction and massive ST elevation. In 2010, when I first presented these EKGs, I believed that this case (in the acute phase) represented AIVR.
The dominant pacemaker may in fact be idioventricular. The presence of AV dissociation would confirm this, but I do not see P waves. The third EKG (hospital day 3) is equivocal. This could also be a-fib with AIVR and dissociation.
Even if the rhythm is AIVR, there is still a more important diagnosis at stake.
For comparison, and to illustrate this, here are some exemplars:
This is typical AIVR:
Image courtesy of Life In The Fast Lane
This is RBBB with LAFB and massive STE:
Image courtesy of Dr. Smith’s ECG Blog
Hear are three cases of sodium channel blockade with TCA cardio-toxicity:
Unknown TCA toxicity. Image courtesy of EB Medicine.
This is purported cocaine cardiotoxicity with features of sodium channel blockade:
Image courtesy of ECGpedia.
Two cases of flecainide toxicity:
Image courtesy of Bond et. al., Heart 2010.
Image courtesy of EB Medicine.
Sodium channel blocker and specifically flecainide toxicity has been covered extensively in the literature; the following excerpts are particularly relevant in light of this case.
“Flecainide is an increasingly used class 1C antiarrhythmic drug used for the management of both supra-ventricular and ventricular arrhythmias. It causes rate-dependent slowing of the rapid sodium channel slowing phase 0 of depolarization and in high doses inhibits the slow calcium channel.” (Timperley, 2005)
“Cardiac voltage-gated sodium channels reside in the cell membrane and open in response to depolarization of the cell. The sodium channel blockers bind to the transmembrane sodium channels and decrease the number available for depolarization. This creates a delay of sodium entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens.” (Hollowell, p.880– graphic and text.)
“Bradydysrhythmias are rare in sodium channel blocking agents because many of these also possess anticholinergic or sympathomimetic properties. These agents can, however, affect the pacemaker cells that are dependent on sodium entry, thus causing bradycardia. In severe poisoning, the combination of a wide QRS complex and bradycardia is a sign of overwhelming sodium channel blockade of all channels, including the pacemaker cells.” (Delk, p.683)
“Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. ….In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.” (Giardina, G. 2010)
“Impending cardiovascular toxicity in adult patients [with TCA poisoning] is usually preceded by specific ECG abnormalities: the majority of pateints at significant risk will have a QRS duration >100ms or a rightward shift (130-270) of the terminal 40ms of the frontal plane QRS vector. The later finding is characterized by a negative deflection of the terminal portion of the QRS complex in lead I and a positive deflection of the same portion in lead avR.” (Van Mieghem, p.1569)
“In severe cases [of sodium channel blocker toxicity], the QRS prolongation becomes so profound that it is difficult to distinguish between ventricular and supraventricular rhythms. Continued prolongation of the QRS complex may result in a sine wave pattern and eventual asystole.” (Holstege, p166.)
There are multiple mechanisms for flecainide toxicity in this case.
- Reduced metabolism and elimination due to impairment of liver and renal function.
- Significant acidosis resulting in a decrease in protein bound flecainide and an increase in the free (active) agent in the blood stream.
- Borderline hyponatremia as a potential predisposing condition for over-therapeutic sodium channel blockade.
Bond, R., et al. (2010). Iatrogenic flecainide toxicity. Heart (2010), 96:2048-2049 doi:10.1136/hrt.2010.202101
Delk, C., et al. (2007). Electrocardiographic abnormalities associated with poisoning. American Journal of Emergency Medicine, (2007), 25, 672-687.
Giardina, G. (2010). Major side effects of flecainide. UpToDate.
Harrigan, R., et al. (1999). ECG abnormalities in tricyclic antidepressant ingestion. American Journal of Emergency Medicine, (1999), July 17(4), 387 – 393.
Hollowell, H. et al. (2005) Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. American Journal of Emergency Medicine, (2005), 23, 876 – 889.
Holstege, C., et al. (2006). ECG manifestations: The poisoned patient. Emerg Med Clin N Am, 24 (2006) 159–177. Free full text.
Timperley, J., et al. (2005). Flecainide overdose– support using an intra-aortic balloon pump. BMC Emergency Medicine, (2005), 5: 10. doi: 10.1186/1471-227X-5-10
Van Mieghem, C., et al. (2004). The clinical value of the ECG in noncardiac conditions. Chest (2004), 125, 1561-1576.
Williamson, K., et al. (2006). Electrocardiographic applications of lead aVR. American Journal of Emergency Medicine (2006), 24, 864-874.
In 2010, as part of a case series exploring the presentation of AV block in the setting of inferior wall STEMI, I discussed the following EKGs:
It was hypothesized from these tracings that a proximal RCA lesion was responsible for the manifest inferior wall and right ventricular involvement, likely in the setting of a right dominant coronary system owing to the AV nodal dysfunction.
Recently I was able to follow up on this case.
This was a 64 year-old Caucasian female complaining of nausea, vomiting, and a syncopal episode while attempting to ambulate. Her history was significant for HTN, hyperlipidemia, breast cancer, and a mechanical aortic valve replacement in 2005. At that time a presurgical cath had identified a 70% ostial RCA stenosis. This baseline EKG was recorded on admission:
In 2008, on the date the case study EKGs were recorded, she became progressively hypotensive while in the emergency department and required intubation and vasopressor circulatory support. During emergent catheterization stents were placed across a 99% diffuse ostial RCA lesion and a further stenosis of the distal RCA. The interventionalist described a right dominant coronary system with a small LAD and circumflex. On arrival in the ED, a troponin of 0.14ng/mL was recorded. At noon on the following day the value had climbed to 55.20 and peaked at over 90 later that evening.
Due to cardiogenic shock, both an IABP and temporary pacemaker were placed. A long ICU course ensued during which numerous abnormalities were identified and addressed including but not limited to severe sepsis, a ruptured breast implant, gall bladder disease, elevated LFTs, and a renal mass suspicious for carcinoma. The following EKGs were recorded on ICU days 2, 3, and 4.
In June of 2009 she was again admitted to the hospital, at this time with a primary diagnosis of aspirational pneumonia complicated by renal insufficiency.
A tracheotomy was placed. Respiratory failure and sepsis were treated in the ICU and ventilator weaning was begun only to rebound with recurrent episodes of septic shock. This was repeated four times over a two-month period. Renal function progressively declined, as did her baseline mental status. This is the last EGK on file for this patient:
She experienced asystolic arrest and died the next day.
Persistent ST-segment elevation following PCI has been shown to closely reflect the presence of microvascular reperfusion injury as demonstrated by impairment of microcirculatory flow on PET imaging and intracoronary contrast echocardiography. Mechanisms of reperfusion injury include neutrophil infiltration, tissue edema, and direct mivrovascular damage following tissue hypoxia. Impaired microcirculatory reperfusion resulting from these mechanisms has been correlated with more extensive infarction and a worse clinical outcome. Roughly 30%-40% of patients undergoing PCI demonstrate persistent STE on hospital discharge.
In their 1999 publication, Claeys et al. utilized persistent ST-segment elevation following PCI to identify patients at risk for reperfusion injury. They report, “Patients >55 years of age with systolic pressures <120mmHg were at high risk for development of impaired reperfusion compared with patients not meeting these criteria (72% versus 14%, P<0.001).” (Claeys et al., 1999, p.1972)
Also in 1999, Matetzky et al. demonstrated similar findings comparing clinical outcomes in patients with comparable angiographic results following PCI but contrasting presentations on ECG regarding the persistence of ST-segment elevation. Results of this research indicated that, “…ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction…. Group B patients [those with persistent STE], as compared with those of Group A [those with early resolution of STE], had a higher incidence of in-hospital mortality (11% vs. 2%, p 0.088), congestive heart failure (CHF) (28% vs. 19%, odds ratio (OR) 4, 95% conﬁdence interval (CI) 1 to 15, p 0.04), higher long-term mortality (OR 7.3, 95% CI 1.9 to 28, p 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR 6.5, 95% CI 1.3 to 33, p 0.016 with logistic regression).” (Matetzky et al., 1999, p.1932)
In 2007, Galiuto et al. investigated the clinical correlates found in patients demonstrating persistent STE following primary or rescue PCI. They report, “Such an ECG sign at hospital discharge may be considered associated with a large infarct size, and, in 30% of cases, with LV aneurysm formation and with continuing LV remodeling.” (Galiuto et al., 2007, p.1380)
These three studies reviewed between 100-150 patients each.
In 2010, however, Verouden et al. reviewed over 2100 patients undergoing PCI with the intent of further characterizing the clinical and demographic determinants of persistent ST-elevation after coronary intervention. They report that, “Incomplete ST-segment recovery was a strong predictor of long-term mortality…,” and, “…incomplete ST-segment recovery at the end of PCI occurred signiﬁcantly more often in the presence of an age >60 years, nonsmoking, diabetes mellitus, left anterior descending coronary artery–related STEMI, multivessel disease, and preprocedural Thrombolysis In Myocardial Infarction grade 3 ﬂow.” (Verouden et al., 2010, p.1692)
Claeys, M., et al. (1999). Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. Circulation. 1999;99:1972-1977, doi: 10.1161/01.CIR.99.15.1972
Galiuto, L., et al. (2007). Functional and structural correlates of persistent ST elevation after acute myocardial infarction successfully treated by percutaneous coronary intervention. Heart. 2007; 93: 1376-1380, doi: 10.1136/hrt.2006.105320
Matetzky, S., et al. (1999). The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA. Journal of the American College of Cardiology. Vol. 34, No. 7, 1999.
Verouden, N., et al. (2010). Clinical and angiographic predictors of ST-segment recovery after primary percutaneous coronary intervention. American Journal of Cardiology. 2010;105:1692-1697.
A 37 year-old Caucasian male presents to the emergency department with palpitations of two hours duration. A 12-lead EKG is recorded.
This 12-lead demonstrates an irregularly irregular, polymorphic wide complex tachycardia; this can only be atrial fibrillation with frequent conduction through a Wolf-Parkinson-White accessory pathway system.
The differential diagnosis for this presentation principally consists of polymorphic VT, RVR a-fib with ventricular conduction aberrancy, and a-fib with underlying WPW. The presence of multiple wide complex QRS morphologies excludes the diagnoses of a-fib with BBB, and, as Mattu and Brady have pointed out, polymorphic VT will typically hold a constant rate while this EKG shows significant variance between R-R intervals– from >450ms to <240ms. (Mattu, 2003, p.138)
RVR a-fib with aberrant conduction and gross ST-segment abnormalities but uniform QRS morphology. (EMS 12-Lead: http://ems12lead.com/2011/09/68-year-old-male-cc-chest-pain/)
Polymorphic VT of Torsades de Points in the setting of hypokalemia and prolonged QT; multiple QRS morphologies but uniform rate. (LITFL: http://lifeinthefastlane.com/ecg-library/tdp/)
Note that due to the fixed duration of the AV nodal refractory period, synchronized atrio-ventricular conduction is typically limited to below 200 impulses per minute. It is for this reason that RVR a-fib very rarely exceeds 180-200bpm. The bypass tract in WPW, however, has a dangerously short refractory period and thus can support re-entrant tachycardias well above this limit. As Chou has stated, “…the presence of the WPW syndrome can be suspected from the rhythm strip alone if the atrial fibrillation is accompanied by a ventricular rate greater than 200bpm. Such a rapid ventricular response would be highly unusual if the conduction is by way of the normal AV conduction system.” (Chou, 1996, p.480)
Antiarrhythmic agents which slow or block AV nodal conduction are contraindicated in this setting as they can enhance conduction through the accessory pathway and accelerate ventricular response. Procainamide and related sodium channel antagonists have therefore been used with favorable results.
Regarding amiodarone, although numerous case reports have tracked poor outcomes, it remains a popular treatment modality for this syndrome and may statistically be a safe alternative. In 2005, for example, Tijunellis and Herbert demonstrated a case-series of 10 patients in which amiodarone was malignantly proarhythmic; in half of these, the initial arrhythmia was v-fib. Nonetheless, case-series can be misleading and I do not know of definitive research in this area.
In light of this, judicious use of electrical therapy is often considered the safest and most reliable approach.
Mortality associated with the Wolf-Parkinson-White syndrome remains at <1% and is thought to result from rapid response a-fib degenerating into v-fib arrest (Ellis, 2011). This outcome can be fostered through inappropriate pharmacological management if the initial presentation is misunderstood. Fortunately, once this dramatic EKG signature has been appreciated, it is unlikely to go unrecognized.
Dr. Stephen Smith has discussed this syndrome and the treatment risks, and his insights can be found here. Among other remarks, he states, “Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals. If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous.” (Smith, 2011)
I wish also to excerpt Dr. Johnson Francis of Cardiophile MD who has addressed this topic directly. Dr. Francis states, “The shortest RR interval gives an estimate of the ventricular refractory period. If it is below 250 msec, it is ominous as the ventricular rates can go very high and it can degenerate into ventricular fibrillation.” (Francis, 2008) Note that in this particular case, the overall ventricular rate is not excessively fast and perhaps speaks to the relative clinical stability of the patient.
Additional case studies of WPW a-fib can be found in the Case Library.
Chou, T. and Knilans, T. (1996). Electrocardiography in Clinical Practice: Adult and Paediatric, 4th Ed. W.B. Saunders Co.
Ellis, C., et al. (2011). Wolff-Parkinson-White Syndrome. Medscape eMedicine. Retrieved from: http://emedicine.medscape.com/article/159222-overview
Mattu, A. and Brady, W. (2003). ECGs for the emergency physician, V.1. BMJ Publishing Group.
Tijunelis, M. and Herbert, M. (2005). Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. Canadian Journal of Emergency Medicine. (4): No.4, p262. Retrieved from: http://www.cjem-online.ca/v7/n4/p262
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:
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.
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.
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
A 59 year-old white female presents to EMS with two hours of 9/10 substernal chest pressure radiating into her left arm. Her history is significant for HTN, hyperlipidemia, and 30 pack-years smoking. The blood pressure is 90/50; she is diaphoretic and pale.
1st degree AV block can be seen complicating this inferolateral MI. Note that the STE in lead III is greater than that in II and caution should therefore be observed regarding right ventricular involvement. Of additional note is the unexpectedly tall R-wave in V2, a remarkable finding when met with right sided ST-depression.
In light of the ST elevations in V5 and 6, II, III, avF, and right precordial depressions suggestive of posterior wall infarction, it might seem reasonable to assume that a proximal culprit lesion is placing a large territory of myocardium at risk. In the past, however, there has been a lack of consensus among investigators with regard to whether either the number of leads demonstrating STE or the net magnitude of STE can be reliably correlated with the extent of myocardial injury. (Birnbaum and Drew, 2003, 492-493)
Without engaging the question of how myocardial injury can or should be quantified, it is clear that the 12-lead EKG does not equitably represent all myocardial territories. Not only are some regions better visualized than others, but electrical vectors can augment and dampen one another. This phenomenon is of particular interest when we consider that ST elevation in V4R, V1, and V2 due to right ventricular involvement may be canceled from view by the opposing vectors of a concomitant posterior wall infarction. Posterior forces may be likewise mitigated, even as they already demonstrate proportionally lower voltage due to the greater distance of the surface electrodes from the depolarizing myocardium.
Case reports of “normalization” resulting from the opposition of two independent currents of injury have been described. Wang and colleagues present a case in which the electrocardiographic evidence of acute anteroseptal infarction suddenly disappeared from view, they contend, as a direct result of a new, electrically oppositional, infarction of the posterior wall. Their abstract is as follows:
In a 76-year-old man an electrocardiographic pattern of acute anteroseptal myocardial infarction disappeared suddenly. At necropsy, a more recent posterior myocardial infarct was found, in addition to an acute anteroseptal infarct. “Normalization” of the electrocardiogram from the pattern of anteroseptal myocardial infarction in this case resulted from the loss of opposing electromotive forces in the posterior wall because of posterior infarction. (Wang, K., et al., 1976)
Thus, when considering the “rear view” leads, there is a real sense in which things “may be larger than they appear.” Therefore, regardless of ones skepticism as to the proportionality between ST elevation and actual myocardial tissue necrosis (Birnbaum), a high index of suspicion should be maintained when a pattern of acute changes implicates an arterial lesion likely placing two ischemic myocardial territories opposite one another (Wang).
Although this 15-lead EKG shows only non-specific T-wave inversion in V4R, the posterior leads V7 and V8 demonstrate subtle ST elevation, thus confirming what can be suspected from the initial tracing. The 1st degree block has resolved, and the magnitude of ST elevation has diminished.
Despite what appeared to be an initially positive response to medical management, the final pre-hospital tracing recorded from this patient shows unifocal PVCs in the pattern of bigeminy.
This was to prove an ominous sign in this case, as shortly after arrival in the ED the patient became unconscious and was noted to be in ventricular tachycardia. Pulses were initially present and cardioversion was performed. Sinus rhythm resumed briefly but again gave way to VT, this time without pulses. Despite aggressive efforts, refractory VF persisted for over 30 minutes and the patient could not be resuscitated.
Dr. Stephen Smith has discussed the issue of posterior wall STEMI through a series of case presentations and his insights on this topic can be found here.
Tom Bouthillet also has a superior set of case studies addressing the issue of posterior STEMI; the category “Acute Posterior STEMI” can be found here, in his site index.
Of additional note, AV block is a frequent finding in inferior wall MI and further case studies illustrating this and discussing the mechanism involved can be found on this site in the case series of September, 2010.
Birnbaum, Y. and Drew, B. 2003. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad. Med. J. 2003;79;490-504. doi:10.1136/pmj.79.935.490
Wang, K., et al. 1976. Sudden disappearance of electrocardiographic pattern of anteroseptal myocardial infarction. Result of superimposed acute posterior myocardial infarction. Chest. 1976;70;402-404. doi: 10.1378/chest.70.3.402