Monday, November 2, 2015

Paramedics make a great call

A middle-aged male called 911 for chest pain.

Here was the first prehospital ECG with pain at 5/10:
Computerized QTc is 418 ms.  There is nondiagnostic ST elevation in V1-V4.
If you use the formula, you get 25.15, (> 23.4, which is all but diagnostic of LAD occlusion).
The medics did not use the formula, as far as I know.

Medics were worried, and gave nitroglycerine, then repeated the ECG at 5 minutes with pain at 2/10:
 Less ST elevation
And they repeated again with pain at 1/10 at 9 minutes:
Near Normal 

Medics asked for physician interpretation on arrival. Physicians were worried and activated the cath lab.   The first (and only) ED ECG is here:
QTc 386.  Most ST elevation is resolved.  Formula value is now down to a very low value of 19.352

A 90% thrombotic LAD lesion was found and stented.  There was pre-procedure TIMI-3 flow (perfect flow)

Door to balloon time was 25 minutes.

Peak troponin I was 17 ng/mL.

Subsequent Echo showed EF of 56% and distal septal, anterior, apical, and
anteroseptal hypokinesis (wall motion abnormality).

Here are post PCI EKGs, this one at 29 minutes after arrival:
You can see the beginning of terminal T-wave inversion in V2 and V3.
Had there been no prior ECGs, this patient who is now pain free would be suspected of Wellens' syndrome

The next one was done at 10 hours after the first:
Evolving T-wave inversion, classic Wellens pattern B morphology

And then the next day:
Full blown Wellens' Pattern B terminal T-wave inversion.

Learning Points

1. This was diagnosed as a NonSTEMI.
2. The artery was occluded, or nearly so, at the time of the first ECG.
3. Serial ECGs demonstrated dynamic changes diagnostic of ACS (transient STEMI)
4. This facilitated rapid treatment of a potentially life threatening LAD thrombus.
5. This also demonstrates how Wellens' ECG morphology is a representation of the post occlusion state, after spontaneous reperfusion (although it also looks that way after therapeutic reperfusion)
6. Finally, Transient STEMI should be taken emergently to the cath lab.  Failure to do so can result in Disaster: Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

Here is a similar case and its learning points, with a reference to an article by my partner, Brian Mahoney, on use of prehospital nitroglycerin:

Wait until after the ECG to give Nitroglycerine

Learning points:
1. NTG may cause reperfusion
2. Record an ECG before NTG
3. Always look at prehospital ECGs
4. Even after STEMI (if reperfused, with small amount of myocardium infarcted), and even when the ECG is diagnostic of ACS (as it was the next day), the simultaneous echocardiogram may be normal.

Here is an interesting abstract regarding NTG after the EKG:

Mahoney BD, Hildebrandt DA, Allegra P. Normalization of Diagnostic For STEMI Prehospital ECG with Nitroglycerin Therapy. Prehospital Emergency Care 2008;15:105, Abstract 24.

 Hypothesis. The decision to take a patient for emergent reperfusion therapy is largely determined by an ECG diagnostic for ST Elevation Myocardial Infarction (STEMI). Hildebrandt et al have proven that  prehospital 12 Lead ECGs followed by an immediate call for reperfusion team mobilization reduce door to balloon times.We hypothesize that prehospital ECGs will normalize in some STEMI patients after  nitroglycerin (NTG)therapy or due to spontaneous reperfusion.  NTG therapy before an ECG, or the absence of a prehospital ECG capacity in some services may lead to missing the early diagnosis of STEMI thus delaying reperfusion therapy. Methods. A prospective analysis of consecutive adult patients  presenting to an urban/suburban two paramedic ambulance service fromJuly 15, 2006, to August 15, 2007, who have diagnostic ECGs for STEMI.  Paramedics managing a possible myocardial infarction patient were instructed to obtain rapidly an ECG prior to treatment with NTG. If the initial ECG was diagnostic for STEMI the paramedic called to mobilize the reperfusion team. A second ECG was done prior to arrival at the ED. The ECGs were later reviewed by emergency physicians and cardiologists who confirmed the presence of a diagnostic prehospital ECG and STEMI.  Results. During the 13 month interval, 87 patients had an initial ECG that was diagnostic for STEMI. These patients received no NTG from the paramedics prior to obtaining the first ECG. An average of 16 minutes 42 seconds later, 3 patients had an ECG that was no longer diagnostic for STEMI and 3 had a partial normalization in their ECG that made diagnosis of STEMI more difficult. Conclusions. Prehospital ECGs diagnostic for STEMI can normalize or become nondiagnostic after NTG administration or due to spontaneous reperfusion or evolution. In the absence of a prehospital ECG, it is possible that 6 of 87 (7%) of STEMI patients in this study would have had reperfusion delayed due to a rapid change in their ECG. Limitations include no control group receiving NTG prior to the first ECG.


  1. Very good case again; I would also point out, in regards to your excellent post on QRS distortion last month, that the QRS segments in all consecutive ECGs look fragmented, specifically in the inferior leads II, III and aVF, therefore excluding any early repolarization hypothesis.

    N.B: please note I am a different 'Olivier' from the one who posted a comment on this very same topic. I think you mistook him for me in your reply for the '40-something with chest pain" post ;-)


    1. Olivier,
      Thanks, and thanks for letting me know that you are not the Olivier I met on Tuesday!


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