- David Didlake
Formula Utilization
David Didlake
Firefighter / Paramedic
Acute Care Nurse Practitioner
@DidlakeDW
Peer review provided by Dr. Steve Smith
@SmithECGblog
I was conducting QA/QI on two very recent cases and was struck by the uniqueness of both.
CASE 1
A 45 y/o Male called 911 for new onset central chest discomfort, non-radiating, 5/10 pain scale, and without any vomiting, diaphoresis, or pallor. Moreover, he had no pertinent medical history to report in terms of CAD, HTN, HLD, or DM, for example. His vital signs were unremarkable, and the lung fields were free of fluid congestion during auscultation.
A 12 Lead ECG was recorded.
Raw findings include Sinus Rhythm amidst an otherwise normal QRS. I initially suspected V2 as being placed too high on the chest, but there is no accompanying inverted P wave here, so the positioning is sound.
It’s important to stress the presence of a normal QRS (i.e., no gross evidence of LVH, LBBB, WPW, or Pacemaker, etc) because any derangement of the ST/T potentially signifies a primary change due to the presence of ischemia – especially when the clinical circumstance is consistent with Acute Coronary Syndrome (ACS) – as opposed to a secondary phenomenon of abnormal repolarization in the setting of abnormal depolarization.
This ECG immediately struck me as an LAD occlusion.
According to the EMS narrative, this patient initially refused hospital transport and advised that he would seek evaluation at a later time with his personal physician. Although the attending crews did not consider the ECG pathognomonic for occlusive thrombosis, they nonetheless considered the patient high-risk for ACS and implored him to reconsider.
As the conversation progressed, another ECG spontaneously printed.
The pathology is now painfully evident. A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered.
Briefly, I think the conversation merits addressing the importance of serial ECG’s. As for this case, I can’t say with certainty if the crews intended on doing such amidst the discussion of transport refusal. As previously mentioned, ECG 2 was spontaneously ejected from the LifePak 15. Why? It’s because the computer’s internal algorithm noticed the dramatic ST/T shift and subsequently flagged it as “MEETS ST ELEVATION MI CRITERIA.”
One cannot rely on this feature as a means of detecting changes – subtle, or dramatic – for volatile occlusive coronary thrombus. Refer to the below case as an example in which the LP15 utterly failed to recognize the ST/T changes, and had it not been for aggressive, proactive monitoring with serial ECG’s, the acute LAD occlusion may have gone undetected:
Now, back to today’s case.
Upon hospital arrival, the patient verbalized slight attenuation of pain. Here is the final ECG just prior to ED transfer.
There is some “deflation” of the ST/T configuration upon juxtaposition with ECG 2. This is to suggest improved TIMI flow – most likely a combination of the ASA administration in tandem with the body’s own natural tPA – yet the ECG still retains signatures of an active thrombus.
He was rushed to the Cath Lab where an LAD culprit lesion was stented. This first image shows turbulent flow through stenotic narrowing of the vessel.
Here is the LAD after stent placement.
CASE 2
A 55 y/o Male suddenly awoke from sleep in the early morning hours with intense 10/10 epigastric pain. He called 911, and EMS crews subsequently found him diaphoretic and vomiting. He reported a medical history of DM, HTN, and HLD. His vital signs were otherwise stable.
A 12 Lead ECG was recorded.
Similar to Case 1, raw findings include Sinus Rhythm with an otherwise normal QRS. Again, emphasis is placed on the fact that this ECG is not grossly imperiled by abnormal depolarization – such as LVH, LBBB, WPW, etc – that would necessarily beget abnormal repolarization and thus directly influence the contour of the ST/T by secondary means rather than primary.
Still, the robust volume T waves of V2 and V3 necessarily mandate scrutinizing attention as their voltage is disproportionately large upon juxtaposition with the respective paired QRS amidst demonstrable ST elevation. Moreover, there is the appearance of reciprocal ST depression in Lead III.
The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center.
But this ECG did not strike me as an LAD occlusion during QA/QI.
No serial ECG’s were recorded. Attached below is the initial ED tracing upon hospital arrival, approximately 25 minutes after the prehospital ECG.
There is no dramatic change, or evolution. There is increase R wave voltage in V3, which could be the result of variance in lead placement, or subtle changes in body positioning. The total R wave voltage in V4 clearly exceeds the grid lines as its height is cropped.
The patient was admitted for cholelithiasis and did well. There were no changes in serial Troponins.
Discussion
When the QRS is normal, is the encountered ST/T changes that beget suspicion for LAD ACS (as in both of these cases) the result of occlusive coronary thrombus, or simply a normal variant? Clinically, both patients presented with complaints, and presentations, worrisome for ACS during the initial encounter; and in both cases much decision-making trajectory came down to the ECG.
We can use the formulas for differentiating LAD occlusion versus Normal Variant as a useful guide. [1-3]
Case 1
QTc 386 ms
ST elevation in V3 (60 ms after the J-point) 3 mm
R wave amplitude in V4 5 mm
QRS amplitude in V2 5 mm
21.16 and supports LAD occlusion
Case 2
QTc 441 ms
ST elevation in V3 (60 ms after the J point) 2.5 mm
R wave amplitude in V4 23 mm
QRS amplitude in V2 16 mm
17.01 and does not support LAD occlusion
The reason why Case 1 immediately struck me as LAD occlusion and, simultaneously, Case 2 did not – even in the absence of technical 3-variable/4-variable equation results – was the overall distribution of T wave voltage to R wave voltage across the precordium. This is appreciable to the naked eye.
Both cases display large T waves. And by voltage alone, Case 2 is actually the more worrisome in terms of average T wave height to suggest hyperacuity. But in Case 1, the T waves are wider at the base, and equally less concave during the upward slope.
Ultimately, it’s the T-to-R ratio that makes the difference, and that’s because a smaller R wave amplitude is the best variable predicting OMI versus Normal Variant.
In Case 1, there is poor R wave progression in V1-V3, and this pattern lingers in V4 such that the T wave amplitude to R wave amplitude is incredibly high. Whereas, in Case 2, the poor R wave progression of V1-V3 explosively rises to dramatic voltage in V4. The T wave here is large, but it’s the low ratio to R wave height that discriminates this as Normal Variant versus OMI.
Benign ST/T configuration can be dramatic, and many times frightening. When the differential is LAD occlusion versus Normal Variant, use the formula as an assistive tool – only exercise extreme caution when reclassifying what you believe to be LAD occlusion as Normal Variant. With deliberate practice, spot diagnosis of T-to-R ratio will come with time.
References
1] Smith, S. W., et al. (2012). Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardial infarction. Annals of Emergency Medicine, 60(1), 45-56.
2] Driver, B. E., et al. (2017). A new 4-variable formula to differentiate normal variant ST-segment elevation in V2-V4 (early repolarization) from subtle left anterior descending coronary occlusion – adding QRS amplitude of V2 improves the model. Journal of Electrocardiology, 50, 561-569.
3] Aslanger, E., et al. (2018). A tale of two formulas: Differentiation of subtle anterior MI from benign ST-segment elevation. Annals of Noninvasive Electrocardiology, 23(6), 1-6.
