Infection and DKA, then sudden dyspnea with chest pain while in the ED

A 63 year old male with PMH of CAD and peripheral vascular disease from type I DM presented to clinic and was found to have a very high blood sugar and so was sent to the ED.

Patient stated that he has had glucose over 400 even though he has not missed any doses of insulin.  He also endorses fatigue, upset stomach, frequent urination, increased thirst, and decreased appetite over the past 2 days. 

Pulse was 115, BP 140/65, and afebrile

He was found to have cellulitis and to be in diabetic ketoacidosis, with bicarb of 14, pH of 2.27, glucose of 381, anion gap of 18, and lactate of 2.2 mEq/L.

He was treated for infection and DKA, and admission to hospital was planned.

While in the ED, patient developed acute dyspnea while at rest, initially not associated with chest pain. He later developed mild continuous chest pain, that he describes as the sensation of someone standing on his chest. 

This ECG was recorded: 

What do you think?

There is widespread ST depression.  This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was also tachycardia prior to development of chest pain.

Bedside echo showed no evidence of reduced EF, no signs of right heart strain, no regional wall abnormality. Lung exam showed diffuse B lines bilaterally. Xray was consistent with pulmonary vascular congestion. 40 mg of furosemide was given.

Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present.  See this post: What do you think the echocardiogram shows in this case?

Shortly thereafter, the troponin came back at 3,129 ng/L (very high).  Aspirin was given and cardiology was consulted.  But due to the absence of significant ST elevation, the cath lab was not activated.  They agreed ischemia was likely in the setting of demand given DKA and infection. EKG showed sinus rhythm at 100 BPM with a normal axis and diffuse ST depressions.

That this is all demand ischemia is unlikely.  The patient had no chest symptoms until he had been in the ED for many hours and had been undergoing management of his DKA.  

Another ECG was recorded:

What do you think?

This is diagnostic of Occlusion MI (OMI) as Aslanger's pattern (Diagnostic of OMI).  Aslanger's is a combination of inferior OMI with widespread ST depression and is due to BOTH occlusion of one artery (usually the circumflex, but sometimes the RCA) AND simultantous 3 vessel disease.  

Because there is an ST depression vector towards leads V5 and II, leads aVF and II cannot manifest ST elevation or hyperacute T-wave from the inferior OMI.  The ST depression vector includes these leads and cancels out the STE of the inferior OMI.  Only lead III can have STE (and, of course, aVR, which is opposite, reciprocal to, the ST depression in I, II, V5).

Not knowing anything about the patient, I saw this ECG on our system just as I was leaving the dept.  The patient was under the care of another ED physician.

Here was the interpretation I put into the system, and told the physicians about it:

Inferior Occlusion MI with diffuse subendocardial ischemia.  Aslanger's pattern.  Hyperacute T-wave in lead III, with reciprocal findings in aVL -- single lead OMI in the setting of multivessel disease.

Aslanger's pattern (Smith was co-author on this): A new electrocardiographic pattern indicating inferior myocardial infarction

The next troponin returned at 8822 ng/L.

The emergency physicians advocated for the cath lab but she was not taken until the morning because this was a "NonSTEMI."

Here is the troponin profile:

Here is the Queen of Hearts assessment:

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  

For Americans, you need to wait for the FDA.  But in the meantime:

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

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Case continued

After about 8 hours of pain, the patient's pain resolved spontaneously, probably aided by the aspirin and heparin.  Here is the ECG at that point in time: 

The ischemia is mostly resolved.  One would expect that the angiogram would show open arteries with normal TIMI-3 flow and culprit lesions.  20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later.

So the presence of an open artery does not tell you anything about the state of the artery at the time of the ECG.

Angiogram:

Severe two-vessel coronary artery disease with possible co-culprits (90% proximal circumflex, 70% mid/distal RCA) in the setting of non-ST elevation myocardial infarction. 

Previously placed stents in the LAD (multiple) and mid circumflex and patent

Formal echocardiogram:

Normal left ventricular size and wall thickness.

Mildly decreased left ventricular systolic function with an estimated EF of 48%.

Regional wall motion abnormality--basal to mid inferior and inferolateral hypokinesis.

This was the previous echo just 3 months before

Normal left ventricular chamber size. Normal left ventricular wall thickness. 

Ejection fraction of 66%. 

No regional wall motion abnormalities. 

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MY Comment, by KEN GRAUER, MD (11/21/2023):

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Today's case provides an excellent example of Aslanger's Pattern — as well as an astute test in the "art" of comparing serial ECGs. 

• For clarity in Figure-1 — I've reproduced the first 2 ECGs in today's case. It could be all-too-easy to overlook the subtle-but-real ECG changes that occurred during the 4 hours that passed between the recording of these 2 tracings.

Figure-1: Comparison of the first 2 ECGs in today's case.

Comparison Between ECGs #1 and #2:

As per Dr. Smith — ECG #1 shows sinus tachycardia with the pattern of DSI (Diffuse Subendocardial Ischemia) — in that there is ST depression in multiple leads with ST elevation in lead aVR>V1.

• PEARL #1: The BEST way to compare 2 serial ECGs — is to put both tracings next to each other — and then to compare lead-by-lead to note any subtle changes that may have occurred. 
• It is all-too-easy to overlook subtle changes if you simply look at one entire tracing — and then look at the 2nd tracing, but without specifically looking lead-by-lead to see if there are any changes.

Applying this technique to the 2 tracings in Figure-1:

• Lead III in ECG #2 now shows a Q wave — as well as ST segment coving with slight ST elevation that replaces the ST depression that was seen in ECG #1.
• Lead aVL in ECG #2 now shows subtle-but-real coved ST depression, that is the mirror-image opposite picture of the new coved ST elevation that we now see in lead III.
• 
  
• In the chest leads in ECG #2 — there is now a definite increase in R wave amplitude in leads V1,V2,V3 and V4 — compared to relative R wave amplitude that was previously seen in these leads in ECG #1

IMPRESSION: As per Dr. Smith — the findings now seen in ECG #2 are perfectly consistent with Aslanger's Pattern — which in today's case, strongly suggests an acutely evolving infero-postero OMI. The reason these ECG changes are so challenging to recognize — is that this patient has severe underlying multi-vessel coronary disease that masks some of the acute findings.

• Inferior OMI — is suggested by the new ST coving with elevation in lead III, in association with mirror-image opposite reciprocal ST depresstion in lead aVL.
• Posterior OMI — is suggested by the increased R wave amplitude in leads V1-thru-V4.
• The combination of new persistent chest pain + the above-described ECG changes between the 2 tracings shown in Figure-1 — constitute "dynamic" ECG changes.

PEARL #2:  = Aslanger's Pattern:

Examples of Aslanger's Pattern appear in a number of cases in Dr. Smith's ECG Blog (This pattern is very nicely described by Dr. Smith in the January 4, 2021 post). The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

 

Isn't it interesting how closely ECG #2 in today's case follows the above description of Aslanger's Pattern!