Pulmonary edema, with tachycardia and OMI on the ECG -- what is going on?

This was written by Hans Helseth.

A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chest pain and shortness of breath. She awoke in the morning with sharp chest pain which worsened throughout the morning. As her pain worsened, so did her dyspnea. She was found by paramedics with an oxygen saturation of 64%, but could not tolerate BiPAP during transport due to claustrophobia. She arrived to the ED with a nonrebreather mask. Her blood pressure on arrival was 153/69. An EKG was immediately recorded. The status of the patient’s chest pain at this time is unknown:

EKG 1, 1300:

There is sinus tachycardia and artifact of low and high frequency. The high frequency artifact may be caused by the patient shivering or tensing her muscles. A patient in acute distress may not be able to relax during the recording of their EKG, causing high frequency artifacts that give the waveform a fuzzy look. The low frequency artifact is caused by respiration which shifts the isoelectric baseline up and down with inspiration and expiration. It is best seen in V1 and V5 in this EKG. In fact, the patient’s respiratory rate can be calculated by measuring the time from peak to peak of the baseline in V5 at around 37 respirations per minute.

This EKG is also diagnostic of acute inferior OMI. There is tachycardia, but beneath the artifact, the ST segments in leads III and aVF are elevated, and the T waves are concave and terminally inverted, suggesting the possibility of reperfusion Leads I and aVL show ST depression with a terminally upright T wave, a morphology typically reciprocal to inferior ST elevation representing transmural ischemia of the inferior wall.

Smith: I would say this STE with T-wave inversion (suggesting reperfusion) is "between" active and reperfused inferior OMI, and with persistent symptoms or instability, it is active and acute until proven otherwise. There are no Q-waves to suggest old inferior MI, or inferior aneurysm as the etiology of the ST Elevation. However, there is also significant tachycardia, with heart rate of 116, and known hypoxia. Whenever there is tachycardia, I am skeptical of OMI unless it has led to severely compromised ejection fracction with cardiogenic shock. Or I suspect that there is OMI simultaneous with another pathology. We certainly know that there is hypoxia. I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. What other pathology is possible? Anything that causes pulmonary edema: poor LV function, fluid overload, previous heart failure (HFrEF or HFpEF), valvular disease. Summary: it is hard to say whether this ST Elevation was initiated by 1) something which led to pulmonary edema, then hypoxia, then supply-demand mismatch, or 2) whether ACS with OMI combined with some other pre-existing condition led to a decrease in LV function and pulmonary edema. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). See reference and discussion below. Also see these posts of Type II STEMI. Management?: stabilize the patient and repeat the ECG.

An EKG from a year prior was available for comparison:

The ED physician noted “Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. She was quite tremulous and short of breath when this EKG was obtained.”

Truly, the Marquette 12 SL algorithm correctly identifies this “STEMI”. Of course, the Queen of Hearts also recognizes it:

While this EKG did not convince the attending physician, a repeat EKG was obtained an hour later once the patient’s respiratory status improved:

EKG 2, 1415:

Now the ST elevation is decreased. The inferior leads have T wave inversion, consistent with reperfusion. There is still ST depression in leads I and aVL, and in the lateral leads.

Now the Marquette 12 SL algorithm does not identify “STEMI”, but the Queen of Hearts can see past the lack of ST elevation. She still calls this a “STEMI equivalent” in need of emergent reperfusion:

This version of the Queen of Hearts will call a reperfused OMI "OMI."  She does not distinguish.  PMCardio will correct that in the future.

The ED physician noted “Once her respiratory status improved, her EKG looks much improved with no evidence of STEMI”.

Two high sensitivity troponin T values returned:

1307- 138 ng/L

1511- 120 ng/L

A chest X-Ray showed pulmonary edema. A CT scan showed no PE but showed bilateral pleural effusions and aortitis. She was started on lasix. Cardiology services were consulted at a PCI capable hospital. They recommended transfer for admission, but did not recommend emergent angiography. The patient was started on heparin “for possible NSTEMI vs demand ischemia”.

More troponin values were measured at the cardiac center:

2327- 267 ng/L

0821- 355 ng/L

1108- 305 ng/L

An echocardiogram on day three of the patient’s admission showed an ejection fraction of 46% with abnormal basal inferior and basal lateral segments, and severe aortic stenosis. (Smith: "decompensation" of aortic stenosis might have initiated this entire cascade. What "initiates" the aortic stenosis cascade? --increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.)

The patient was finally weaned to room air on day 4 and taken for a CT scan to evaluate the possibility of aortic valve replacement. The scan showed a bicuspid aortic valve with severe stenosis and coronary artery disease. A lesion in the mid LAD was described as moderate, and a mid RCA stenosis was described as “probably severe”.

No more EKGs were recorded during the patient’s admission. The final impression was that the troponin elevation represented type 2 MI with a fixed RCA and LAD stenosis after the respiratory distress caused by acute pulmonary edema. The EKGs from the ED presentation were felt by cardiology to represent "subendocardial ischemia."

Smith: these ECGs do NOT show subendocardial ischemia. They show transmural injury (OMI). Now, it is conceivable to have ST Elevation due to type 2 MI (supply demand mismatch), but it is VERY unusual. I studied this over 10 years ago and published this abstract. In our data, only 4% of Type 2 MI had new ST Elevation. The vast majority of ischemia from supply demand mismatch is diffuse ST depression, with ST Elevation in aVR. The top ECG is diagnostic of thrombotic type 1 OMI until proven otherwise.

Case Continued

The patient was discharged from the hospital with a plan for a scheduled coronary angiogram to assess the coronary arteries and the possibility of aortic valve replacement.

A month later, she presented again to the emergency department with a few hours of chest pain that resolved before ED presentation. An EKG was recorded in the ED:

EKG 3, a month later:

This EKG represents reperfusion of the inferior wall with terminal T wave negativity. But there are new Q-waves, indicating intervening infarction -- uncertain when. There is still slight ST depression in leads I and aVL.

A troponin T resulted at 24 ng/L.

This EKG was interpreted as showing no signs of ischemia, the troponin was interpreted as having “improved from previous” (meaning improved from the 305 ng/L value a month prior) and the patient was no longer in pain. She was discharged again from the emergency department without a second EKG or troponin. 

Another week and a half later (about 6 weeks after her original presentation for chest pain and shortness of breath) the patient presented to the hospital for her scheduled angiogram:

There is total occlusion of the middle segment of the RCA (Picture A, annotated in D). The RAO views above show the LAD and LCx arteries (pictures B and C, annotated in pictures E and F respectively). The green line in picture F shows contrast filling the PDA, representing left to right collateral circulation.

The full key to the annotations made by Willy Frick on these cath images can be found in his great guide to coronary angiography.

The RCA lesion was treated as a CTO and not intervened upon. The angiographer also noted all other vessels to have "mild disease".

Smith: I'm confused as to why it was called "CTO" (chronic total occlusion) if just a month prior it was only "severe stenosis."

The patient was again sent home with a plan for surgical aortic valve replacement and coronary artery bypass grafting to the PDA. Two months later, she had her surgery, which was successful. An EKG was recorded after her surgery:

Since the baseline EKG at the beginning of the post, the Q waves in lead III have increased in size. There are also inferior and lateral T wave inversions, but this could be an effect of the surgery.

Learning points:

• While OMI rarely presents with tachycardia, inferior OMI complicated by another cardiopulmonary pathology like pulmonary edema and aortic stenosis can show tachycardia.
• Acute coronary occlusion and acute pulmonary edema can coexist. Pulmonary edema caused by acute MI is especially worrisome.
• Chest pain patients should not be discharged without serial troponin measurements, especially if their EKG shows T wave inversion. In a patient with OMI, the first troponin value may be low or normal.
• A low troponin value should not be compared with an elevated troponin value a month old.
• EKGs obscured by artifact should be promptly repeated in critical patients, especially if the provider feels that the artifact is impeding the interpretation of an EKG in a patient with new chest pain.

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MY Comment, by KEN GRAUER, MD (2/27/2025):

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Today's case reminds me of a selected number of cases I have had during my career in which the patient teaches the doctor. Fortunately, over the ensuing weeks after she was first seen — this patient survived despite a recurrence of her initial presentation. 

• The "good news" — is that this patient ultimately underwent successful surgical aortic valve replacement and coronary artery bypass grafting (albeit this wasn't until 3+ months after her initial presentation — with several providers not appreciating that rather than a "NSTEMI" or a "Type II MI", this patient's first ECG was clearly diagnostic of an acute coronary occlusion MI).
• For clarity in Figure-1 — I've reproduced and labeled that initial ECG. I focus my comments on assessment during that first hospital admission.

The Initial ECG in Today's CASE:

As per Hans Helseth — ECG #1 is diagnostic of acute inferior OMI.

• The history immediately places this patient at extremely high risk for OMI. She is older (69yo) — and she woke up with new chest pain that continually worsened throughout the morning. As a result — any potentially acute abnormality on ECG has to be taken as an acute OMI until proven otherwise.
• In addition — the patient was markedly dyspneic and tachypneic (RR >35/minute) — hypoxemic (O2 sat = 64%) — and tachycardic (~110-115/minute). This presentation clearly indicates more than simple ACS (Acute Coronary Syndrome).
• It is true that sinus tachycardia sometimes results in ST elevation from the tachycardia (with return to normal of ST segments once heart rate slows). That said — there is no mistaking the J-point elevation with ST segment coving in lead III and lead aVF (within the RED rectangles). Terminal T wave inversion in leads III and aVF (RED arrows) not only supports the legitimacy of ST elevation in these leads — but suggests that there may already be some element of spontaneous reperfusion (especially since by history, at least several hours have passed since onset of CP).
• Although true that there is much artifact on this initial tracing — this same obviously abnormal ST elevation is seen in all 7 complexes in leads III and aVF. This uniformity of ST elevation in every beat in these 2 leads does not happen if "artifact" is the cause.
• Any doubt about the legitimacy of this ST elevation in leads III and aVF should be instantly eliminated on seeing shelf-like reciprocal ST depression in all 7 complexes in high-lateral leads I and aVL.
• Further confirmation of the legitimacy of the diagnosis of acute OMI is forthcoming from lack of the normally expected, slight gently upsloping ST elevation in lead V2. Because of respiratory motion artifact (due to this patient's distress and tachypnea) — none of the 4 ST segments in lead V2 look the same. But the fact that all 4 of these ST segments lack the normal, slight gently upsloping ST elevation in lead V2 tells us this is a real effect indicative of associated posterior OMI (and not the result of artifact).
• I'll note that assessment of ST-T waves in lead V3 is more difficult to ascertain — but in the context of clear inferior OMI in the limb leads — lead V2 alone is diagnostic of associated posterior OMI.
• Perhaps part of the reason for the subtlety of ST-T wave changes in leads V2,V3 and the flattened ST-T wave in lead V1 — is that this patient with probable acute RCA occlusion may have associated RV involvement that attenuates the amount of ST depression usually expected with posterior OMI. Right-sided leads should be obtained.
• Finally — there is abnormal ST-T wave flattening in leads V4,V5,V6, as well as in lead II. I interpreted this ST-T wave flattening in these 4 leads as suggestive of multi-vessel coronary disease in the context of acute infero-postero OMI.

Figure-1: I've labeled the initial ECG in today's case.

Respiratory Motion Artifact:

As per Hans Helseth — Today's ECG provides unique insight regarding how we know this patient's respiratory rate is so fast. Note the uniform 8.2 large box interval between the respiratory motion peaks that we see in beats #3,6,9,12,15 and 18.

• The easy way to determine heart rate is to divide 300 by the number of large boxes for the R-R interval — and, 300 ÷ 8.2 = 37 breaths/minute (as noted by Hans Helseth).
• PEARL: Obviously we do not need this insight in today's case, because we are told about this patient's dyspnea and tachypnea. But many of us are charged with overseeing the ECGs of patients that we do not have in front of us — and being able (with ECGs such as today's 1st tracing) to tell how very fast a patient is breathing could be a clue to how sick that patient is likely to be.

Insight's from Today's CASE:

• The artifact in today's initial ECG should not prevent a diagnosis of acute OMI in this older woman with sudden onset new, severe CP.
• If ever in doubt about the validity of ECG findings in a patient with new CP and artifact — Don't wait! Immediately repeat that ECG.
• When the patient presents with new, severe CP and is high risk for acute MI (as today's patient clearly was on this initial admission) — the initial ECG should be repeated within no more than 15-30 minutes.
• The diagnosis of acute OMI was confirmed in today's case in multiple ways (the abnormal initial ECG — evolutionary changes suggesting reperfusion on the repeat ECG — obvious ECG changes compared to the prior tracing from a year earlier — positive troponins — tachycardia, tachypnea, hypoxemia and pulmonary edema). Cardiac cath should have promptly been done.
• NOTE: When you don't cath the patient in a timely manner — then you will miss identifying the "culprit" artery a certain percentage of the time. When you wait 6 weeks after the event to do the cath (as was done in today's case) — then you will not know what things looked like 6 weeks earlier.

KEY Point: Today's patient had severe AS (Aortic Stenosis) complicating all of the above. From what we are told — the severity of her AS was not known prior to her initial hospitalization, especially given her apparent history of hypertension. And, especially in a patient with acute pulmonary edema — a bedside diagnosis of severe AS may be extremely difficult to pick up on auscultation. But at least on Day #3 — Echo did identify severe AS.

• Severe AS markedly complicates management and portends poorer longterm outcome when associated with acute MI (Abraham et al — Cath Cardiovasc Interv 102(1): 159-165, 2023 — Paquin et al — Open Heart 9(1):e002046, 2022 ).
• Critical AS complicates hemodynamics of the coronary circulation — including hemodynamics of collateral flow (Wiegerinck et al — Circ: Cardiovasc Interven 8(8): e002443, 2015). 
• 
  
• Looking at the case (admittedly in retrospect, and in the comfort of my desk chair) — One has to wonder about the time until cath was done, and about the time until surgery.