Friday, June 12, 2020

Serial ECGs highly suspicious for inferior OMI: Give thrombolytics prior to transfer for PCI?

One of my former residents texted this info to me with the EKGs:

"I have here a 50 something-year-old female with multiple stents who presents with a concerning pain history. Pain relief with nitroglycerin, and I am starting a nitroglycerin drip. 

"I’m worried about a hyperacute RCA infarct. 

"There is no old ECG available.

"I have to transfer for PCI, and am wondering if I should give thrombolytics first."

Here is the initial ECG:
Inferior STE less than 1 mm, with reciprocal inverted T-wave and STD in aVL  

I recorded this one 15 minutes later:

Now with straightening of the ST segments

Looking at it now, it looks like an obvious inferior OMI, but I could not see it as well on my phone, and certainly could not compare them easily on my phone.

This was my response:
"It is suspicious for sure. But I am not totally convinced. It just does not look entirely right and it could be that there is some LVH.  Is there a history of hypertension?"

"Yes. History of Hypertension."

Then I would just activate the cath lab, but I'm not certain enough to give thrombolytics.

So he did not give thrombolytics, but did activate the helicopter and cath lab.

Then he obtained this just before transfer:
Now it has evolved and is diagnostic of inferior OMI
This is clearly a right sided ECG: see the absence of R-waves in V4-V6, and the negative T-waves.
It shows no evidence of RV MI

The physician saw this, and was then going to give tenecteplase, except that he then discovered that the patient had a history of a subdural hemorrhage.

Patient was transferred and had an RCA occlusion.

Learning points:

1. Thrombolytics should only be given when very certain of the diagnosis of OMI.

2.  Thrombolytics prior to transfer: If OMI is diagnosed, you should give thrombolytics prior to transfer for PCI (for STEMI) if the "FMC to Balloon Time" (first medical contact to balloon time - FMC-BT) is greater than 120 minutes, or the time from arrival at the first ED to balloon will be greater than 90 minutes.  "First medical contact" would be the medics arriving at the patients home.  

The fact is that the majority of transfers do not get a FMC-BT so short.  The data shows that if the transport time itself is greater than 30 minutes, fewer than half get a FMC to balloon time of less than 120 minutes.

3. You should not give thrombolytics at all if there are any absolute contraindications. 

Absolute contraindications are:
  • Prior intracranial hemorrhage (ICH)
  • Known structural cerebral vascular lesion
  • Known malignant intracranial neoplasm
  • Ischemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (excluding menses)
  • Significant closed head trauma or facial trauma within 3 months
  • Intracranial or intraspinal surgery within 2 months
  • Severe uncontrolled hypertension (unresponsive to emergency therapy) > 185/110
  • For streptokinase, prior treatment within the previous 6 months

MY Comment by KEN GRAUER, MD (6/12/2020):
THIS is a subtle case! As per Dr. Smith — the initial ECG was texted to him for an opinion. The patient was a 50-something woman with a history of multiple stents + worrisome new chest pain, relieved by NTG.
  • I focus My Comment on the initial 2 ECGs, done 15-minutes apart. For clarity — I have put both tracings together in Figure-1.

  • Given the above history — HOW would YOU interpret ECG #1?
  • Knowing that ECG #2 was obtained just 15 minutes after ECG #1 — Does this 2nd tracing assist in YOUR diagnosis? IF so — WHICH LEAD(s) convinced you?

Figure-1: The 2 ECGs in today’s case (See text).

My THOUGHTS on ECG #1: This case is challenging as it is — and it is made more difficult by the less than optimal quality of the tracings. More than just angulation in certain leads — there is baseline artifact that impedes assessment of ST-T wave morphology. Looking first at ECG #1:
  • The rhythm is sinus at ~85/minute. All intervals are normal. The axis is close to zero degrees. There is no chamber enlargement.
  • Regarding Q-R-S-T Changes — there is a tiny q wave in lead aVL. There appears to be a tiny initial r wave in lead V1, which is lost in V2 — but returns in lead V3. Transition is slightly delayed, and occurs between leads V5-to-V6.
  • The difficulty in interpreting this tracing lies with assessment of ST-T waves — especially in the inferior leads. Because of the artifact — ST-T wave morphology in each of the inferior leads changes from one-beat-to-the-next.
  • My Confession — I didn’t know how to interpret the ST-T waves in the inferior leads of ECG #1. In some of the leads — it looks like there is J-point ST elevation. Some complexes almost look hyperacute. Others look normal. And, ST-T wave morphology changes from one beat-to-the-next.
  • That said — lead aVL in ECG #1 is clearly abnormal. Although ST-T wave morphology in lead aVL also changes from one beat to the next — what is consistent is the ST-T wave depression in this lead. The other high lateral lead (ie, lead I) shows nonspecific ST-T wave flattening.
  • I see no acute changes in the chest leads — although the T wave in lead V6 is clearly flatter than is typically expected in this lead.

My Clinical Impression of ECG #1 — We are clearly dealing with a “high-prevalence” situation, in that this patient has known severe coronary disease — and she presented to the ED with worrisome new-onset chest pain. As a result — our threshold is lowered for interpreting subtle ST-T wave changes as abnormal.
  • While some beats in the inferior leads do suggest ST elevation — and, the ST-T wave depression in lead aVL could reflect reciprocal changes — I felt the inferior lead findings to be too inconsistent to form a definite opinion. More information (and a repeat ECG in no more than a few minutes) is needed. In the meantime, given the history of severe coronary disease, and the presentation of new-onset chest pain — We need to consider that this patient may be having an acute event until we can prove otherwise.

My THOUGHTS on the ECG #2: I was pleased to learn that a 2nd ECG was obtained shortly after ECG #1 (Bottom tracing in Figure-1). Although baseline artifact again impedes assessment of inferior lead ST-T wave morphology — I thought there were significant changes in some leads.
  • The rhythm in ECG #2 is once again sinus at about the same rate as was seen in ECG #1. The frontal plane axis is slightly more negative in ECG #2 (since the QRS complex is now predominantly negative in lead aVF) — but the predominantly positive QRS in lead II tells us that LAHB is not present. Transition occurs a bit earlier in ECG #2 (ie, between leads V4-to-V5).
  • PEARL — Because of the inferior lead artifact and beat-to-beat variation in ST-T wave morphology that is seen in both tracings — we need to accept that our judgement as to whether there has been significant change during the 15 minutes between ECG #1 and ECG #2 will be a subjective one. I made this judgement by “stepping back” a bit from the ECGs — eyeing all beats in each of the inferior leads (II, III, aVF) at the same time in ECG #1 — and then doing the same for ECG #2 while comparing the 2 tracings. My sense was that the take-off of ST segments in leads II and III is a bit straighter in ECG #2 — and, that the T waves in leads III and aVF of ECG #2 are fatter at their peak and wider at their base. The J-point in each of the inferior leads seems more convincingly elevated than it did in ECG #1.
  • I do not think there has been any change in ST-T wave appearance in lead aVL between the 2 tracings.
  • On the other hand, there has been a definite change in lead V2 — which now clearly manifests a straight ST segment in ECG #2. In contrast — the ST segment was gently upsloping in ECG #1. This change appears to be “real” — and is consistent with probable acute posterior involvement in this patient with suspicious inferior lead changes.
  • I thought there was no significant change in ST-T wave appearance in the other chest leads.

My Clinical Impression of ECG #2 Compared to ECG #1: My sense is that there has been some “dynamic” change in ST-T wave appearance between the 2 tracings during the 15 minutes since ECG #1 was recorded.
  • While hard for me to put my finger on “why” this is so ... — the ST-T waves in the inferior leads of ECG #2 just look more hyperacute than they did in ECG #1. The ST-T wave depression in lead aVL has to be taken as an acute reciprocal change. And there is no doubt that the ST segment in lead V2 of ECG #2 is flatter than it was in ECG #1.
  • Given the history in this patient with known severe coronary disease — one has to assume acute infero-postero OMI until you prove otherwise.


  1. What's the explanation for the complete loss of R waves in the chest leads in ECG #3? This isn't typical of an RCA occlusion!

    1. Dave,
      Sorry, forgot to mention chest leads. He never said, but I assume that those were right sided leads on the last EKG.


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