In 1899, 4 years prior to the invention of the EKG, Karel Wenckebach utilized arterial kymographs to characterize a clinical presentation of regular irregularity in cardiac systoles. This entity was to become one of most well known eponyms in medicine– what we now know as the Wenckebach phenomenon.
With this case, I want to call attention not to the rhythm itself, but to an unusual feature seen here in conjunction with the Wenckebach: look closely at the 4th QRS complex– how do we know this is a junctional escape and not simply a grossly prolonged PR interval? If such a distinction can be made, what clinical significance should we ascribe to the finding?
In normal cardiac physiology, as the impulse descends from the His bundle, the first portion of myocardium to be activated is the septum; thus the initial deflection of the QRS complex reflects the vector of septal depolarization. Further, given that the septum is predominantly supplied by the posterior fascicle of the LBB, the septal myocardium depolarizes from left to right; it is therefore not pathological to note an initially negative deflection in lead II.
Graphic courtesy of http://www.cvphysiology.com/Arrhythmias/A016.htm
What is noteworthy about the complexes on these tracings, however, is not that there is an initial Q-wave in II, but that the escape complexes in the lead II tracing reveal a conspicuously more pronounced initial Q wave deflection than that present in the normative systoles. Although the QRS morphology and R-wave axis here remain consistent, pointing into the lower left quadrant (~+60°), in the escape complex there is a greater mass of initial electrical activity dissipating away from the lead II electrode (~–120°). This suggests that the ectopic focus responsible for these junctional escape beats is slightly more inferior relative to that authoring the normative QRS signals. In short, due to a more inferior position in the AV nodal tissue, a greater portion of myocardium would depolarize backwards towards the superior and rightward hexaxial quadrant, thus giving rise to the slightly greater Q wave in the escape complexes.
Although these observations on the initial deflection axis suffice to demonstrate a junctional rather than sinus origin to the complexes in question, it should be emphasized that alternative, “markedly slow pathways” through the junctional tissue may mimic this finding. Shinji Kinoshita et al. have recently presented an interesting and more sophisticated analysis of how to approach this issue in their article, Apparent AV Junctional Escape in Wenckebach AV Block: Markedly Slow Conduction Through The Slow AV Pathway, which can be found in the Journal of Cardiovascular Medicine 2009, 10:161–166.
Given that the existence of a junctional focus can be positively or negatively established, however, we might propose a risk stratification dichotomy between Wenckebach pts demonstrating a functional escape pacemaker (as seen above) and those with “escape failure” who must endure QRS dropping without junctional compensation. While systematic study and clinical correlates remain necessary to validate this hypothesis, pts in this latter category would presumably carry greater risk of symptomatic bradycardia than those in the former, and the absence of junctional escape activity might therefore be a positive predictor of greater morbidity in this population.