- David Didlake
Syncope and Block
Firefighter / Paramedic
Acute Care Nurse Practitioner
Peer review provided by Dr. Steve Smith
A 72 y/o Male experiences a syncopal episode while seated. This occurred in a public place, so bystanders rushed to his aid and provided immediate assistance to protect against any associated fall or head strike. It’s reported that he regained consciousness after 30 seconds, approximately.
EMS finds him supine, alert and oriented, and without any gross distress. Crew members note residual pallor and clammy skin. He reports a vague description of feeling ill just prior to the incident, however denies any specific prodrome of chest discomfort, difficulty breathing, abdominal pain, or palpitations. Pertinent medical history includes HTN, HLD, and DM – all of which are optimally controlled with medication. He advises, however, recurrent syncopal episodes for the past six months, some of which have resulted in ED admission, yet no identifying mechanism could be determined. He is due for a cardiologist appointment in five days.
A 12 Lead ECG is captured:
This was initially interpreted as Sinus Brady with “block.” Closer inspection, however, will show that this is high grade AVB (possibly pathological third degree) with, most likely, a Junctional Escape.
The RBBB-like configuration in V1-V3, as a whole, displays dramatic T wave inversion. In V1, the ST segment of the singular QRS complex might be suffering from wavering baseline, but at least appears to show appropriate slight discordant ST depression subsequent to the R’ wave. Lead V2 shows RR’ QRS configuration, and although ST depression is otherwise expected here, the discordance is a bit excessive.
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Moreover, the overall clinical presentation (syncope with advanced AVB) is consistent with Stokes-Adams, and it is not uncommon to encounter bizarre ST/T changes during the attack episodes.
A telemetry strip was recorded:
There is changing QRS morphology, specifically alternation between RBBB-like and LBBB-like configuration (based on the characteristic Lead I patterns). The LBBB-like complexes come earlier than expected. Are these PVC’s? Below I have annotated the strip:
The black arrows in Lead II denote recurring Sinus P waves at 100 bpm, approximately. In Lead I the horizontal blue arrows reflect a basic RR cycle length of 1600ms (38 bpm) that recurs, but is interrupted by the more-wide, and morphologically different, QRS complexes (orange arrows, beats 3 and 6).
The RR coupling interval between Beat 2 and 3 is 800ms, and 840ms between Beat 5 and 6. As along as the coupling intervals do not exceed 80ms, generally speaking, we can say that they are fixed and unlikely to suggest a parasystolic focus (in the specific context of PVC evaluation).  The unique feature of Beats 3 and 6, however, is that they share a similar PRi, and anytime a QRS comes unexpectedly early amidst AVB one must entertain the prospect of legitimate Sinus capture amidst AV dissociation. Still, the AVB is severely high-grade and could lead to death.
Attending crews recorded another 12 Lead ECG:
These LBBB-like complexes are now appearing more frequent. Below is the same ECG with annotations:
As previously depicted, the black arrows show continuous Sinus P waves with persistent QRS dissociation, except for the beats marked with orange arrows (Leads I, V1, and V6) – they all share similar PR intervals and maintain classic LBBB configuration respective to the leads in question (rS in V1, and monomorphic R in Leads I and V6). It’s important to emphasize this otherwise “classic” behavior as I think it further supports the prospect of Sinus capture, as opposed to the escape mechanism that twists the morphological rules inherent to RBBB with direct supraventricular influence.
The patient was assisted to an upright seated position and tolerated this change well. Attending crews then brought the stretcher close and further assisted him to a reclined position of comfort. It was during this time that a sudden increase in pulse rate was noted, so another 12 Lead ECG was recorded upon docking the stretcher in the ambulance:
There is now 1:1 P:QRS ratio with LBBB. The patient advised overall improvement with complete resolution of symptoms. Hospital transport was unremarkable. The patient care narrative states no further changes in heart rate with persistent LBBB morphology. He received a permanent pacemaker during the subsequent inpatient stay.
LBBB and Myocardial Infarction
In the emergent setting it’s important to assess LBBB through the lens of the Smith-modified Sgarbossa criteria, especially in a context that is clinically consistent with Acute Coronary Syndrome. In isolation, however, syncope does not hold significant weight for OMI – as opposed to something like crushing chest discomfort, for example – although stereotypical ACS might become blurry in both the elderly and diabetic populations.
This is important because we must rely on the ECG to further elucidate the story when the patient cannot. The final ECG in today’s case shows terminally concordant T wave inversions in Leads III, aVL, and I. How do T waves in LBBB specifically manifest signatures of occlusion, or reperfusion, and is any T wave configuration superior to the m-Sgarbossa criteria?
Smith and Myers found that in otherwise classic Wellens syndrome – that is, prior anginal chest pain that resolves with subsequent dynamic T wave inversions on the ECG – even the T waves of LBBB behave similarly.  Although the clinical context in today’s case does not fit these descriptors for Type I OMI (e.g. plaque disruption), the T waves still manifest markings of a previous state of suboptimal coronary flow that resolved: Type II supply-demand mismatch in the setting of extreme bradycardia.
In LBBB, concordant T wave morphology has high specificity for predicting coronary reperfusion, but does not otherwise yield any useful benefit in predicting MI, and equally underperforms in comparison to the m-Sgarbossa criteria. [3,4] The final 12 Lead ECG does not meet any Smith-modified Sgarbossa criteria, so the T wave signatures are characteristic of improved coronary flow, but not necessarily MI.
LBBB and Heart Failure
ECG findings of uncomplicated LBBB (that is, no criteria met for m-Sgarbossa criteria) are so ubiquitous in clinical medicine that it’s easy to overlook the nefarious sequelae of this pathology when no circumstance of OMI are present.
LBBB is typically the result of preexisting hypertrophy, ischemic heart disease, or cardiomyopathy. In the absence of these disease states, there may be primary degenerative changes to the conduction system (Lenegre disease), or sclerotic calcification of the cardiac skeleton (Lev disease). Regardless of inciting mechanism, LBBB induces ventricular wall motion abnormalities that ultimately yield mechanical dyssynchrony. 
The patient may experience pernicious exertional dyspnea, exercise intolerance, cough, or discrete fluid consolidation in the periphery – all red flag markers of clinical heart failure. LBBB may be the precipitating cause of the heart failure syndrome, or may portend high mortality when identified in preexisting heart failure. Although no strict correlation exists between QRS prolongation and left ventricular dysfunction, a duration >180ms suggests severe structural abnormalities. Furthermore, excessive QRS fragmentation equally suggests significant myocardial scarring. 
Chronic vs Transient LBBB
Permanence of LBBB is predicated on many of the disease states listed above. Transient manifestation, however, is possible during states cycle length variation (e.g. Phase IV block, or concealed transeptal conduction).
Let’s revisit the initial telemetry strip (with markings) during gross bradycardia:
The LBBB morphology appears when the Sinus P waves capture the ventricles in Beats 3 and 6. Note that this occurs only after a very long RR cycle length.
These bradycardic changes are consistent with Phase IV (or, deceleration-dependent) conduction block of the His-Purkinje (His-P) system. In general, the refractory period of the bundle branches is dependent on the preceding RR cycle length. Thus, proclivity for block is established at low rates with progressive increases in cycle length. Moreover, diseased His-P cells have a less negative resting membrane potential during Phase IV of the conduction cycle, which inactivates sodium channels and renders them refractory to subsequent impulses with failure to fully depolarize. 
Phase IV block is, indeed, abnormal and should alert the clinician to the presence of severely diseased His-P cells, although its manifestation on the ECG can be transient with restoration to narrow QRS duration upon normalization of heart rate.
Here again is the 12 Lead ECG upon heart rate normalization:
The fact that LBBB persists at increased heart rate (and shorter RR cycle lengths) strongly suggests that the patient’s conduction disturbance is preexisting (for any of the pathological reasons listed above) and merits cardiology consultation. It’s possible that LBBB perpetuation here is the result of concealed transeptal conduction, but given predilection of said phenomenon for structurally normal hearts, I think the prospect of such is unlikely.
 Surawicz, B. & Knilans, T. K. (2008). Chou’s Electrocardiography in Clinical Practice (6th ed). Chapter 17: Ventricular Arrhythmias. Saunders-Elsevier: Philadelphia, PA.
 Meyers, H. P. & Smith, S. W. (2017). Dynamic T-wave inversions in the setting of left bundle branch block. American Journal of Emergency Medicine, 35, 938(e5)-938(e7).
 Meyers, H. P., et al. (2016). Evaluation of T-wave morphology in patients with left bundle branch block and suspected acute coronary syndrome. The Journal of Emergency Medicine, 51(3), 229-237.
 Dodd, K. W., et al. (2016). Comparison of the QRS complex, ST-segment, and T-wave among patients with left bundle branch block with and without acute myocardial infarction. The Journal of Emergency Medicine, 51(1), 1-8.
 Isnard, R. & Pousset, F. (2020). Left bundle branch block-induced cardiomyopathy: Myth or reality? International Journal of Cardiology, 300, 201-202.
 Tabrizi, F., et al. (2007). Influence of left bundle branch block on long-term mortality in a population with heart failure. European Heart Journal, 28, 2449-2455.
 Callans, D. J. (2021). Josephson’s Clinical Cardiac Electrophysiology: Techniques and Interpretations (6th ed). Chapter 4: Intraventricular Conduction Disturbances. Wolters-Kluwer: Philadelphia, PA.