Tuesday, August 1, 2017

ST Elevation in I and aVL: do prehospital cath lab activation on these cases?

Case 1.

A 50-something year old man with 2 cardiac risk factors had a syncopal episode associated with diaphoresis.  There was no chest pain and no dyspnea.

A prehospital ECG was recorded:
There is some ST elevation in leads I and aVL, though not 1 mm.
If you've been reading this blog, you know that an acute coronary occlusion may present with less than 1 mm of STE.
Does this ST Elevation in I and aVL represent a high lateral MI or is it normal variant?

There is also ST Elevation in leads V1-V5.
Is all this ST Elevation normal variant?  Or is it due to ischemia?
What do you think?

Below I have put dark lines in which show exactly how much ST Elevation there is in leads I and aVL, and how much reciprocal ST depression, if any, in leads II, III, and aVF.
STE is greatest in lead I, and there is zero ST depression in II and aVF, and very little in lead III, which is the most important lead for assessing reciprocal ST depression in high lateral MI.
What do you think?
QTc = 392

Answer: It is normal variant ST Elevation.

I was presented with this ECG on patient arrival and I immediately de-activated the cath lab, recognizing that the ECG (shown above) is a normal variant.

Sometimes normal variant ST Elevation is in leads V2-V4, sometimes in V5 and V6, sometimes in II, III, and aVF, and sometimes in I and aVL.  There may be any combination of the above normal variant ST Elevation findings.

You can determine whether ST Elevation in V2-V4 is normal variant or is due to LAD occlusion by using the 3- or 4- variable formula.  The 4-variable is more accurate but not validated. See the formulas here: http://hqmeded-ecg.blogspot.com/p/rules-equations.html

The 3-variable comes to 23.23 (slightly below 23.4)
The 4-variable comes to 17.15 (very low and below the most accurate cutoff of 18.2)
Unlikely to be LAD occlusion.

We recorded an ED ECG:
The STE in I and aVL is about the same.
The prehospital ECG has a bit more STE in V5 than this one, but I did not think it significant.

And compared it to one from a month prior:
Notice that there is STE at baseline, though maybe not quite as obvious here as on the prehospital ECG recorded one month later (first ECG above)

Clinical Course

Serial troponins were negative.  The patient was dehydrated as the etiology of syncope.  a 3 hour troponin was below the level of detection.  The patient was discharged.

Prehospital Cath Lab activation

Below is the prehospital activation plan that we have at Hennpin County Medical Center:  

1. The patient must have chest pain or chest discomfort.
2. The computer must interpret ***STEMI***

1. Many MI do NOT present with any chest discomfort.  However, in the absence of chest discomfort, you should only do prehospital activation if the ECG is unequivocal (clearly a STEMI, clearly diagnostic).

2. The computer is about 60% sensitive and 90% specific for STEMI.  So, if you are expert in reading the ECG, as many paramedics are (but many are not), then you can overrule the computer.  But if you are not expert, you will have many false positive activations.

My last post was a false positive activation:

Chest Pain and ST Elevation on the Monitor

Case 2

A 60-something woman presented to urgent care with substernal chest discomfort that radiates to left arm and back.  She had an episode of vomiting while at urgent care.  She denied SOB or lightheadedness.  There was no diaphoresis, the skin was warm and dry.  Only past history was hypertension.  BP 158/100.

Here was the prehospital ECG:

What do you think?

(The computer did NOT read ***STEMI***, but it did mention possible ischemia.)

Interpretation: This clearly shows significant inferior reciprocal ST depression, even though there is very little ST Elevation in leads I and aVL.  There is also confirmatory ST depression in V4 -V6.

One other big difference between this and case 1: the patient primarily had chest discomfort!  

The cath lab was activated, and there was a 100% occlusion of the first diagonal (high lateral MI, just as the ECG would predict), and severe stenosis of other unspecified coronary arteries.

One third of MI, and even one third of STEMI, present without chest pain (Canto JG. JAMA. 2000;283(24):3223-3229).  But you don't get to know the diagnosis before the symptoms; you are presented with a symptomatic patient.  And if the patient has acute chest discomfort, the probability of acute coronary occlusion is far higher than if he/she presents with dyspnea only, or epigastric pain, or shoulder pain, or syncope.  These may be the only presenting symptoms, but to activate the cath lab when they are the only symptoms, there must be a clearly diagnostic ECG.

Case 3.

This is another case of ST elevation in leads I and aVL.

A colleague sent it without any other information and asked "Do you think this is STEMI in a patient with chest pain?"
What do you think?

Here was my answer:

"No, this is not STEMI. These are particularly confusing cases for people because early repol is usually in II, III, aVF and precordial leads. But it can be limited to I and aVL and the giveaway is the prominent J-waves in these 2 leads. And even a bit if reciprocal ST depression in III is ok. But one must be very careful with these, as especially if one is not expert at recognition, it can be easily confused for high lateral MI, and vice versa. Tell me more!"

He replied:

"You're spot on with the explanation. It was not a STEMI."

Learning Point:

If the paramedic is worried about coronary occlusion, and:

1. the patient does not have chest pain, or
2. the ECG is not clearly diagnostic.


1. Obtain serial prehospital ECGs, and activate if they become diagnostic, or
2. Wait until ED arrival for more information.

More similar cases:

True + vs. False + high lateral MI. ST depression does not localize.


  1. Thanks for the post.... 🙂

  2. In case 3, lead V3 is suggestive of short PR with a hint of pre-excitation. Overall also, PR interval also appears to be short. Kindly enlighten Sir !

    1. Rajiv,
      I see what you mean, but PR is still > 120 and it was not WPW.
      Steve Smith

  3. What was it that ruled out an ACS? The EKG alone? In small rural canada we have no ability for assessing wall motion abnormality. After reading your blogs I would have done serial EKG and Trops to rule out ACS as this EKG would be very suspicious to my perspective and being an hour away from a PCI facility would have made transfer to a PCI facility something to consider immediately.

    1. Kent,
      I did not mean to imply that ACS is rule out by the EKG. That is never the case. Just that there is no indication for emergent reperfusion therapy.
      ACS and even MI can have a totally normal EKG.
      The only way to rule out MI is with serial troponins.
      ACS cannot even be ruled out with serial troponins, as unstable angina still exists.
      These patients may need further risk stratification with stress test or CTCA.


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