Wednesday, July 17, 2019

A Text Message in the Middle of the night. Do you give thrombolytics?

I awoke in the morning and discovered a text with this ECG that was sent 6 hours prior by a former resident:

"60 year old with classic chest pain.  The cath lab is occupied for the next 90 minutes.  Cards says "not a STEMI".  Thinking of giving lytics."
What do you think?
What do you do?













I texted back: "Sorry for delay!  Was sleeping.  This is OMI!!  Did you give lytics?  Proximal LAD.  Great catch!"

There is 0.5 mm of ST Elevation in V3-V6.  The T-wave in V4 is far too large for the QRS.  The LAD occlusion formula would be very high due to the extremely small R-wave in V4 and QRS in V2, but without the QT I cannot calculate it exactly.

This ECG is diagnostic of LAD OMI.  Occlusion Myocardial Infarction.

I continued:

"Cards was right.  It is not a STEMI.  But the new paradigm is OMI.  And that is what is important.  ST Elevation is a very poor way to define myocardial infarction. We have a couple articles, one in press and one in review, that we hope will continue to prompt a change in that inadequate paradigm."

More about the case:

History: 60 yo woman w/ history of smoking but no other cardiac risks who presented to triage w/ CP. She had awoken in the morning w/ bilateral arm paresthesias and by evening called a nurse advice line who told her she may be having a heart attack and to go to ED to be evaluated.

While in her car she developed central chest pressure radiating to right shoulder about 20 min prior to arrival.

She was seen in triage where she had an ECG recorded at T0:
What do you think?
(The dx can be made without looking at the baseline ECG, but it is below if you want to see it)?














A baseline ECG was available and is also attached.


Now you know the diagnosis.  Acute LAD occlusion.

But the ED is a busy place:
"She was hypertensive in the 190s-200s systolic but otherwise had normal VS. The ED was very busy and there were no open rooms.

"The triage ECG was shown to a physician, I don't honestly recall if it was me or one of my partners and labs and CXR were ordered by the provide in triage.

"By the time she was roomed and I assigned myself to her care it was about 1 hr later. She remained very hypertensive and had a nursing note that said she had been too anxious to get a repeat ECG and requesting an order for Ativan.

"As I was reviewing her triage information and initial ECG another pt was roomed who appeared to be critically ill with an STEMI.

"I ordered her aspirin, NTG, fentanyl, a repeat ECG and walked into the room w/ the new STEMI pt.

"As I walked into that room that lab called w/ her initial troponin value of 1.0 (LOD < 0.03). The repeat ECG I ordered is attached here as ECG #2 and was done at T+70."

Tough to interpret

"I activated the cath lab for my 2nd pt and was not able to get to her bedside until about 30 min later. Her pain and HTN were improved but she was still having active CP. I ordered more NTG and fentanyl and obtained another repeat ECG."

(ECG 3-2 at T+100 attached here).

This is the ECG at the top


"I activated the cath lab at this point.


"Our cardiologist came back down to the ED looked at the most recent ECG and said, "That's not a STEMI".  I told him I disagreed and thought the patient needed emergent catheterization. He told me that regardless they would be unable to take her for at least 90 min b/c they were just starting the other case I had sent them.

"That's the point at which I texted you. 

"We gave heparin, started nitro gtt and was considering giving thrombolytics but our unit coordinator was able to find an accepting cardiologist at the hospital down the street in about 5 minutes. 

"She went emergently to cath (not able to figure out exact timing from my chart review) and was found to have 100% thrombotic distal LADD1 which was stented. Her troponin I there was >50 (they don't measure higher). No post cath echo yet."



The question still remains (thrombolytics?):

If there is no cath lab, are thrombolytics indicated?  If I were the treating physician, I would give thrombolytics. But that is because I am so certain that this is an LAD occlusion that there is no doubt in my mind that the benefit/risk ratio of thrombolytics favors treatment.

A careful read of all the original thrombolytic literature shows that the "criteria" for giving thrombolytics are extremely inaccurate.  Moreover, there is much recent literature showing that acute coronary occlusion frequently does not meet criteria.  In the best study to date, published last month, ST Elevation was 35% sensitive for adjudicated STEMI (51% on serial ECGs) and 21% sensitive for OMI (30% on serial ECGs).  Cardiologists were 49% sensitive for OMI.

If I diagnose an acute Coronary occlusion, regardless of "STEMI criteria" of an artery that supplies a significant myocardial territory,  and the cath lab is not available, I will give thrombolytics if there are not any really serious contraindications.  I am not going to recommend that everyone do it because it is very dependent on ECG and other skills to be certain of the diagnosis.

Prospective validation of current quantitative electrocardiographic criteria for ST-elevation myocardial infarction


Pendell and I wrote an Editorial on this, but we cannot reproduce it here:
H. Pendell Meyers.  Stephen W. Smith.  Prospective, real-world evidence showing the gap between ST elevation myocardial infarction (STEMI) and occlusion MI (OMI)



===================================
Comment by KEN GRAUER, MD (7/18/2019):
===================================
This case was made especially challenging by small size of QRS complexes, baseline artifact in a number of leads, and continued use of the outdated “stemi” paradigm for defining acute coronary.
  • I focus my attention on interpretation of the ECG that was texted to Dr. Smith ( = ECG #1 in Figure-1).
  • NOTE: There is low voltage in all 12 leads. In my attempt to facilitate interpretation — I’ve relabeled this tracing, and have removed some of the excess spacing in between lead groups. I believe doing so makes it easier to appreciate the acute ST-T wave changes.
Figure-1: The ECG that was texted to Dr. Smith in this case (See text).



MTHOUGHTS on ECG #1: The patient in question was a 60yo woman with typical new-onset chest pain. As per Dr. Smith — the ECG in Figure-1 that was texted to him is diagnostic of acute OMI.

Descriptive Analysis of ECG #1:
  • Low voltage! There is baseline artifact in several limb leads. The rhythm is sinus at ~80/minute. The PR interval is normal. All intervals (PR, QRS, QTc) are normal. The frontal plane axis is slightly leftward (ie, more negative than positive in lead aVF) — but not negative enough to qualify as LAHB (left anterior hemiblock), because the QRS is not predominantly negative in lead II. I estimate the axis to be about -15 degrees. There is no chamber enlargement.
Regarding Q-R-S-TChanges:
  • There are small, narrow Q waves in leads aVL, V5 and V6. These Q waves are of uncertain significance.
  • The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed (ie, it occurs between leads V4-to-V5). More importantly — the R wave remains tiny until lead V5This most probably is related to the acute ongoing process.
As has already been noted — ST-T wave Changes are diagnostic:
  • Considering the tiny size of QRS complex — there is significant Selevation in leads V3-thru-V6. This is associated with hyperacute waves (that are disproportionately taller and fatter-then-they-should-be-at-their-peakin leads V3V4V5, and probably also V6.
  • In the limb leads — there is ST elevation in lead aVL reciprocal ST-T wave changes in each of the inferior leads. While more difficult to appreciate because of artifact and small QRS complex size — the ST segment is conspicuously straightened in leads II and aVF; slightly depressed in lead III; and, associated with disproportionate T wave size in all 3 inferior leads.
  • Personal Observation: Doesn’t doubling the size of the QRST complex in certain leads of ECG #1 facilitate appreciation of a definite acute OMI(See Figure-2).
Figure-2: I’ve doubled the size of 1 complex in leads III, aVL, aVF, and V3-thru-V6. I have not changed proportions of the ECG grid within the RED rectangles. Doesn’t this facilitate diagnosis of acute OMI? (See text).



COMMENT: Regardless of whether the millimeter definition of acute “STEMI” is or is not met — the ECG in Figure-1 is diagnostic of acute OMI in this patient with new onset typical chest pain. Acute reperfusion is indicated.
  • The ECG in Figure-1 is consistent with acute mid- or distal-LAD occlusion — since ST elevation does not really begin until lead V3, and is maximal in leads V4 and V5 (ie, ST elevation typically begins sooner with proximal LAD occlusion).
  • From an ECG terminology standpoint — preservation of the initial r wave in leads V1 and V2 suggests that this is not anteroseptal infarction, but rather anterior infarction (ie, from a terminology standpoint — the initial r wave should be lost in lead V1 when there is “septal” infarction).
  • That said, persistence of no more than a tiny r wave until lead V5, and then no more than relatively small R waves in leads V5 and V6 — is consistent with the extensive area of jeopardized myocardium suggested by the number of leads in ECG #1 that show acute ST-T wave deviation.
  • P.S.: Taking another look at the magnified complexes within the RED rectangles in Figure-2 — perhaps the definition of acute “STEMI” is met after all in this case?

Our THANKS to Dr. Smith for presenting this case!



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