Written by Bobby Nicholson MD, with edits by Meyers
A man in his early 30s presented at 7:35am to the ED with chest pain (7/10) beginning suddenly at 7:30pm the night prior. The note did not specify whether the pain had been truly constant for 12 hours, or whether it had been intermittent. He had associated nausea, vomiting, hot flashes, chills, dyspnea, and cough. He had uncontrolled type 1 diabetes and smoking history. Vitals were normal. Physical exam was unremarkable. No prior ECG was on file.
At 0742, this ECG was obtained in triage:
|What do you think?|
- Sinus rhythm
- QRS is narrow with normal frontal plane axis, but with deep QS waves in V2-V4, and small Q waves in V5 and V6
- STE in V1-V5, meeting STEMI criteria in multiple leads
- Also a tiny amount of STE in I and aVL (with terminally inverted T-wave in aVL), with tiny reciprocal STD in III
- Upright and large T waves in leads with STE
Assuming he did not have a prior LAD territory OMI, this ECG shows acute LAD Occlusion MI, with a very significant amount of damage already done (very deep QS waves in multiple leads), but also with ongoing viable tissue that is actively infarcting (this is known because of the large upright hyperacute T waves in the same leads).
The pitfall I see for this ECG is that many providers will believe that there is no benefit to emergent reperfusion due to the presence of Q waves and the description of pain that started 12 hours ago. This ECG makes me certain that there is still remaining salvageable myocardium, and the patient should get emergent reperfusion as soon as possible.
Should the patient get emergent PCI according to the ECG? YES
Should the patient get emergent PCI according to the current ACC/AHA STEMI guidelines? YES
The ACC/AHA guidelines state that
Immediate PCI is recommended if available for STEMI patients with ischemic symptoms for <12 h in duration (class I, level A) and those with ongoing ischemia at 12-24 h after the onset of symptoms (class IIa, level B).
Below is some reference information from our EMRAP Corependium chapter regarding the acuity of OMI, hyperacute T waves, and Q waves:
Back to the case:
The cath lab was activated and the patient was found to have 100% occlusion of the mid-LAD, which was stented successfully.
The initial hs troponin I returned at 2,478 ng/L, and would later peak greater than 25,000 ng/L (our lab does not report higher).
His echo showed EF 42%, "akinesis of the mid-apical and apical inferoseptal myocardium."
At 9:00, after his cath and stent, a repeat ECG was obtained:
|Consistent with initial reperfusion compared to the presentation ECG. STE has reduced, and there is expected terminal T wave inversion.|
Later that afternoon at 1400:
|Similar to prior.|
Next day at 0700:
|Progression of reperfusion. Again, there has been significant anterior wall loss, but also a significant amount saved (if not, there would not be such significant reperfusion progression).|
Young people can have classic type 1 ACS and OMI.
The timing of OMI is much more complicated than the time since onset of symptoms reported by the patient. The ECG is much better at estimating acuity and viability.
Q waves can be present in the first hour of OMI, but deep QS waves usually are not present in the first few hours of persistent OMI.
The viable but at-risk myocardium shows up in the T wave. Upright T waves mean there is still viable tissue to save or lose.
Persistent symptoms or persistent ECG ischemia is an indication to perform primary PCI even after 12 hours of reported symptoms per the ACC/AHA guidelines (with other guidelines around the world being even more aggressive).