Monday, January 8, 2024

What do you suspect from this ECG in this 40-something with SOB and Chest pain?

I was reviewing ECGs for a study, and came across this one, and was able to get all the clinical information:

What do you think?

The Queen diagnosed "OMI with high confidence" due to the ST Elevation in V1-V3.

Smith interpretation:  This is highly likely to be due to extreme right heart strain and is nearly diagnostic of pulmonary embolism.

Let me tell you about her hospitalization, discharged 1 day prior, but it was at another hospital (I wish I had the ECG from that hospitalization):

The patient is 40 years old and presented to another hospital with chest pain and SOB.  She had been sitting doing work when she experienced "waves of chest tightness".  Since that moment, she had had shortness of breath as well as pressure-like chest pain. Any kind of exertion made the shortness of breath considerably worse. She also has had some coughing at night. She notes slight bilateral ankle swelling. 

I do not have the EKG, but it was described as "non-diagnostic" (that probably means that the physician did not know how to diagnose it).  

Her troponin I returned at 900 ng/L.  She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram.  On formal echo, she had a normal LV and "right ventricular prominence."  

"Patient was given aspirin, sublingual nitro as well as heparin. Patient did have a considerable relief of pain with the nitro and was placed on a nitro drip. I discussed all results with patient. I discussed the case with Cardiology will admit to their service."

She went to angio and had normal coronaries.  

Yet she was discharged with a diagnosis of NSTEMI!

What was the actual diagnosis?  

How did they anchor on NSTEMI?  

Probably because of a high troponin with chest pain.  

The next day she called 911 for worse Chest pain and SOB.  

Paramedics found her semi-conscious, pale, cool, diaphoretic, tachypneic, very hypotensive.  Sats were 88%. Lungs were clear to auscultation.

Medics recorded the above ECG and called a STEMI alert.  The patient went into arrest pre-hospital.   She was briefly resuscitated and made it to the ED alive, long enough to have another ECG:

This could be all due to RV strain or the STE in inferor leads could also be due to supply demand mismatch (type II STEMI)

She was given 100 mg of tPA but arrested again and could not be resuscitated.

What is the clear diagnosis and reason for arrest?

It is of course pulmonary embolism.  No d-dimer or CT pulmonary angiogram was done when they discovered that she had normal coronary arteries.

Diagnostic anchoring due to chest pain and elevated troponin

Tragic case.

Other cases of Pulmonary Embolism with ST elevation in V1

Chest pain, ST Elevation, and tachycardia in a 40-something woman

A man in his 40s w a highly specific ECG (there are several other ECGs at this post)

Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

Sudden Severe SOB and ST Segment Elevation: What is the Diagnosis and Treatment?

A man in his 30s with cardiac arrest and STE on the post-ROSC ECG


MY Comment, by KEN GRAUER, MD (1/8/2024):

My only hope about today's tragic case — is that the involved providers learn from mistakes made.
  • The 2 ECGs that were recorded in today's case are insightful. For clarity in Figure-1 — I've reproduced and labeled these tracings.

The best way to avoid missing the diagnosis of acute PE (Pulmonary Embolism) — is to remember to think of this diagnosis.
  • Think of this diagnosis when your patient presents with a chief complaint of SOB (Shortness Of Breath) — or when in addition to CP (Chest Pain), the patient has SOB. 
  • Think of this diagnosis when a patient with CP and SOB + elevated troponin — has normal coronary arteries on cardiac cath.
  • Think of this diagnosis when a patient with CP and SOB again calls EMS for CP the day after acute coronary occlusion is ruled out (ie, by cath done the day before) — especially when O2 saturation is reduced.
  • And especially — Think of the diagnosis of acute PE when the patient's ECG looks like the initial tracing in today's case ( = ECG #1 in Figure-1).

  • KEY Point: Along the way — Count the patient's respirations yourselfThe simple act of counting a patient's breathing rate is so often underestimated — yet so helpful when rapid at highlighting the need for pulmonary evaluation.


The 2 ECGs in Today's CASE:

Figure-1: I've labeled the 2 ECGs shown in today's case.

ECG Findings that Suggest Acute PE:
We have presented numerous cases of acute PE in multiple posts in Dr. Smith’s ECG Blog. I’ve previously reviewed specific ECG findings to look for (See My Comment at the bottom of the page in the September 1, 2020 post — the March 4, 2023 post — and, in the March 6, 2022 postamong others. I include a summarizing Table of ECG Findings in Figure-2 of the ADDENDUM below)
  • There is no single ECG finding that is diagnostic of acute PE. That said, given the suggestive clinical setting in today's case — it's important to recognize the combination of diagnostic findings that point to this diagnosis in both of the ECGs recorded.

The Initial ECG:
As per Dr. Smith — ECG #1 was recorded by the EMS team the day after this 40-year old woman had been discharged from the hospital with a diagnosis of NSTEMI, but with normal coronary arteries on cath. Her symptoms at the time ECG #1 was obtained were CP and SOB — yet interpretation of this initial tracing prompted a STEMI alert. KEY Findings in ECG #1 include the following:
  • Sinus tachycardia at ~110/minute.
  • Suggestion of a rightward axis (surprisingly deep S wave in lead I ).
  • Peaked P waves in the inferior leads (not quite satisfying the 2.5 mm amplitude criterion for true RAA — but still suggestive given the clinical setting).
  • Suggestion of RV "strain" (as shown within the BLUE rectangle — ST segment coving with slight elevation and fairly deep, symmetric anterior T wave inversion).
  • ST elevation in lead aVR.
  • Diffuse ST depression (seen in 6 leads = II,III,aVF; and V4,5,6).

COMMENT: While understandable how QS complexes with associated ST segment coving and elevation in ECG #1 might prompt concern about acute MI — cardiac cath done a day or two earlier revealed normal coronary arteries — and SOB was a major presenting symptom. In view of this clinical presentation — the combination of ECG findings noted above should instead immediately prompt concern about acute PE.
  • KEY Point: The most convincing ECG finding is seen within the BLUE rectangle — namely ST coving with prominent, symmetric T wave inversion in the anterior leads. In a tachycardic patient with SOB — acute RV "strain" from PE will be a much more likely explanation for this finding than reperfusion T waves from recent infarction.


The 2nd ECG (after Pre-Hospital Resuscitation):
As noted above — ECG #2 was a pre-hospital tracing recorded following resuscitation — presumably just a short while after ECG #1. Remarkable findings include the following:
  • Tachycardia persists — but P waves are no longer seen! The overall rhythm is quite regular, albeit with some irregularity in simultaneously-recorded leads V1,V2,V3.
  • The QRS complex has widened — consistent with RBBB. The S wave in lead I has deepened — consistent with either LPHB vs an increase in right axis deviation from acute RV "strain".
  • Despite QRS widening in ECG #2 — I strongly suspect a supraventricular rhythm because the initial deflection of the QRS (both direction and slope) is so similar in so many leads to the initial QRS deflection in ECG #1 ( ? Junctional tachycardia?).
  • An S1Q3T3 is now seen (In the interim since ECG #1 was recorded — we now see a definite q wave in lead III — and despite the artifact, apparent symmetric T wave inversion in lead III).
  • qRR' pattern is seen in lead V1. While consistent with RBBB (wide terminal S waves being seen in lateral leads I and V6) — the qR in V1 is probably an indicator of increased pulmonary pressure from severe RV "strain" (See My Comment in the March 28, 2022 post in Dr. Smith's ECG Blog).
  • Despite the artifact — inferior and anterior T wave inversion indicative of RV "strain" are present.
  • There is ST elevation in leads III and aVR.

COMMENT: Given that ECG #2 was obtained following cardiopulmonary arrest — I interpreted this tracing as showing progression of findings since ECG #1, and all but confirming massive acute PE as the cause.


Awareness of the constellation of ECG findings shown in Figure-2 (many of which are present in subtle or less-subtle form) — is why within seconds of hearing the history in today's case, we should immediately suspect massive acute PE as the cause.

Figure-2: ECG findings associated of acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).

NOTE: The ECG is far less likely to help in the diagnosis of relatively small (ie, subsegmental) PEs that are not hemodynamically significant, and which are often only discovered on Chest CT performed on patients with less convincing symptoms. 
  • This is probably a “good thing” — since evidence is lacking that treatment of incidentally discovered, non-hemodynamically significant subsegmental PEs is beneficial (and it certainly is not without potential for harm). 
  • Perhaps it is a “benefit-in-disguise” that the ECG is unlikely assist in detection of relatively smaller pulmonary emboli.

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