A 64 yr old white female presented to EMS with n/v/d times three days and a recent episode of orthostatic syncope. She had no complaints of chest discomfort or shortness of breath. She was pale in apearance and found to be hypotensive on exam.
Although AV dissociation can be appreciated in the first three tracings, the fourth appears consistent with undifferentiated 2nd degree conduction block and prolonged (>200 ms) PR interval with bigeminal junctional escape. Close examination of II and V4-6 reveal a subtle morphological variation in the complexes, supporting the argument for multiple depolarization foci. A narrow-complex junctional escape rhythm is typical of a culprit RCA lesion resulting in often transient ischemia to the superior portion of the nodal tissue. Wide-complex 3rd degree block more frequently reflects a significant LCA infarction which has resulted in distal, more inferior conduction system damage that is less likely to recover. Note that the ST elevation in III is greater than that in II— a finding that has been correlated with RV involvement, although I know of no EBM trials to support this. It is regrettable that right-sided and posterior leads were not recorded.
AV conduction abnormalities can be appreciated in as much as 30% of inferior wall MIs owing to the ~70% prevalence of the RCA as the dominant vessel supplying the AV nodal branch. Left dominant coronary systems present a variation to the predictability of progressive conduction pathway ischemia but constitute only 10% of the populace. This leaves 20% with co-dominant systems. In the absence of confounding factors, it would be interesting if there has been a study demonstrating a decreased incidence of AV conduction blocks in pts with redundant AV nodal circulation who present with acute coronary syndrome.
Despite what appear to be convalescent ECG changes over the course of these three 12-leads, the pt. deteriorated rapidly in the ED and required pressor support and intubation before she could be transported to the cath lab. The outcome is unknown.
A 68 year old white male presenting to EMS with chest pain and a history of HTN. No further on this case in known at this time.
This ECG demonstrates a 3:2 Wenkibach phenomenon with an initial inconsistency, possibly due to an A:V ratio shift or artifactual event. Note the subtle elevation in V6; again, a 15lead tracing would have been optimal here.
It should not be forgotten that although inferior wall STEMI typically results from RCA occlusion, it may also arise from a lesion in the Circumflex; in the latter case, the right heart is spared and RCA dependent conduction system elements remain unaffected. Dr. Smith has recently presented an example of this phenomenon as well as a review of a risk stratification ECG algorhythm recently proposed to deliniate RCA vs CLX lesions on ECG. While the case above meets several of these criteria (aVR depression and V6 eleveation), the manifest conduction system involvment all but eliminates the possibility of a CLX eitiology. I hope to post a better example of the DeVerna RCA/CLX decision tool in the near future; see Dr. Smith’s ECG site for a superior and more appropriately exemplified discussion of this new research.
A 52yr old hispanic male with history of hyperlipidemia, IDDM, hypertension, and 30 pack/yr smoking presents to the ED with c/o nausea and diaphoresis. His mother had an MI at 50, and he has two sisters– one suffered an MI at 52 with subsequent CABG, and the other had an MI at 49. His BP on arrival was 92/48.
Another 3:2 Wenkibach; the second ECG shows the pathology resolving slightly to a 1st degree conduction delay, perhaps reflecting beneficial pharmacotherapy.
This pt. received medical management at an outside facility until he could be transported to the cath lab. His Pro-BNP on admission to CCU was 4668, and his Troponin peaked at 8.36ng/ml. No further is known.
A 59 yr old white male presented to his primary care physician with complaints of weakness and exertional dyspnea. The following ECG was recorded by EMS called to the scene.
Again we see the preference in RCA occlusion for a junctional rather than ventricular escape pacemaker. The low voltage baseline activity in leads I, II, and III appears artifactual, however a close examination of the precordial leads demonstrates a small blip consistantly 200ms after the beginning of the QRS, suggesting the possibility of retrograde atrial depolarization buried within the ST-segment. These findings have been marked with the red arrows below.
The disturbances marked with the blue arrows should also be noted, perhaps representing atrial depolarizations with “P-mitrale” morphology. Under this interpretation, the EKG in fact demonstrates a sinus rhythm with marked 1st degree block. Unfortunately, no additional tracings are available for study.
This pt survived to reach the cath lab, but no further is known.
A 52 yr old man, transfered from an outside hospital, pain free at this time and resting comfortably.
Included for completeness, this ECG demonstrates no AV block but is a distractor from the previous series. Individual P-waves cannot be identified; the rhythm is irregularly irregular. In the context of inferior wall MI, this pt is experiencing slow ventricular response a-fib with an associated digitalis-type ST-segment morphology.
Again, unfortunately, no follow up was possible regarding this pt’s outcome.