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.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

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):

===================================

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!

Why do we liberally record ECGs? And what do you think the angiogram showed?

A 40 something complained of 1 week of constipation and eructation after a "bad batch of enchiladas."  He stated all of this was causing abdominal pain, which he indicated was in the epigastrium.

On exam, he had Right Upper Quadrant tenderness.

A point of care right upper quadrant ultrasound showed + gallstones but no wall thickening or pericholecystic fluid.  No etiology of the pain was established, but a gastric acid related etiology was suspected.

The providers decided after a while that it would be advisable to record an ECG, just in case.  

Here it is:

This ECG was texted to me.  What do you think?  What was my answer?

I said that "This is Aslanger's pattern.  You'd better get an angiogram or at least a stat echo.  It looks like Occlusion MI (OMI)." See below for description of Aslanger's pattern.

There is single lead STE in III, with recipocal STD in aVL (inferior OMI).  There is STD in V3-V6 diagnostic of subendocardial ischemia.

The first troponin returned at 3000 ng/L.

Angiogram:

Severe 3 vessel Coronary artery disease involving the LAD

100% mid LCX occlusion.

Formal Echo:

Regional wall motion abnormality--very mild apical septal and apical anterior hypokinesis.

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

Discussion:

This ECG is Aslanger's pattern, and the angiogram is exactly what you expect with this ECG pattern, including the inferior OMI attributed to circumflex (more often than RCA).

This pattern was recently published in J Electrocardiology: Aslanger and others (including Smith).  A new electrocardiographic pattern indicating inferior myocardial infarction.  https://pubmed.ncbi.nlm.nih.gov/32526537/

This newly recognized ECG pattern is defined as:

(1) any STE in III (with reciprocal STD in aVL), but not in other inferior leads, 

(2) STD in any of leads V4 to V6, (but not in V2) with a positive or terminally positive T-wave, 

(3) ST in lead V1 higher than ST in V2."  

The subendocardial ischemia, with an ST depression vector towards lead II, prevents ST elevation in II and aVF, leaving only lead III to manifest single lead ST Elevation.

Learning Points:

1. Upper abdominal pain may be due to acute MI.  If there is no definite diagnosis (and sometimes even if there is), and ECG and possibly also troponin should be ordered for upper abdominal pain.

2. Aslanger pattern, even if the STE is less than 1 mm (with reciprocal STD in aVL), is diagnostic of OMI in the right clinical situation.   This presentation has a low pretest probability, so obtaining an echo is wise, UNLESS the troponin comes back diagnostic, as in this case.

EKGs filed under "atypical symptoms"

Full echo results:

Decreased left ventricular systolic performance, moderate.

The estimated left ventricular ejection fraction is 35%.

Regional wall motion abnormality-distal septum and apex akinetic.

Regional wall motion abnormality-inferolateral, base.

Regional wall motion abnormality-basal inferior/inferior septum.

Normal right ventricular size with probable RV hypertrophy.

No evidence for left ventricular thrombus.

ECG with Aslanger's Pattern. CT Pulmonary Angiogram Reveals LAD Ischemia (Septal Transmural). But this is not Contradictory.

A 52 y.o. male presented with persistent central chest pressure, without radiation, SOB or diaphoresis, which began at rest approximately one hour prior to arrival.   He had never had pain like this before.  He felt slightly nauseous earlier but no vomiting.  He is denying any back pain or abdominal pain.  

An ECG was recorded during pain:

What do you think?

This shows significant ST depression in I, II, and V4-V6, with reciprocal ST Elevation in aVR.  This suggests diffuse subendocardial ischemia.  

However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1.  These suggest inferior OMI with possible RV involvement.

Both of these patterns together suggest Aslanger's pattern, recently published in J Electrocardiology: A new electrocardiographic pattern indicating inferior myocardial infarction.  https://pubmed.ncbi.nlm.nih.gov/32526537/

This newly recognized ECG pattern is defined as "(1) any STE in III, but not in other inferior leads, (2) STD in any of leads V4 to V6, (but not in V2) with a positive or terminally positive T-wave, (3) ST in lead V1 higher than ST in V2."  

One might argue that this case does not apply because of the ST depression in V2, but 1) V2 is probably misplaced and 2) it is not enough ST depression to negate the rule.

Here, we will ignore lead V2 because it doesn't make any sense at all: the R/S ratio is higher than in either V1 or V3, which suggests misplacement.

Here is an illustration of the ST vector in Aslanger's pattern:

The label of leads II and III are reversed -- Sorry

The right side of the inferior wall manifests ST Elevation, resulting in an ST vector directly to the right. Thus, even though there is inferior OMI, there is no STE in II or aVF, only in III.  Moreover, this means there will be MORE reciprocal STD in lead I than in lead aVL, and this is indeed the case with our ECG above.  If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.  With the ST vector all to the right, the only leads with ST Elevation are III, aVR and V1.

Thus, this pattern was associated with simultaneous inferior MI AND diffuse ischemia due to LAD, Left Main, or 3 vessel disease.

HOWEVER, there is yet another entity which could produce this, and it is transmural septal ischemia.  Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), with ADDED STE in III?  

Aslanger added in the limitations in his article: 

"Theoretically, an isolated basal inferoseptal infarction or an acute inferior MI in the presence of previous infarctions that may change the orientation of lesion vector can also cause a similar picture. Lastly, this pattern may represent a chronic change from a previous ischemic insult as seen in a limited number of the patients in the control group".

Vectors: 

In diffuse subendocardial ischemia, which when due to ACS, is usually from LAD or Left Main insufficiency, all walls would have a negative vector pointing from the endocardium to the epicardium (positive vector from epicardium to endocardium, the opposite of OMI).  Since there is no ventricular wall at the top ("base") of the heart (there are only atria), then the addition of all those negative vectors points towards the apex; if the entire heart has subendocardial ischemia, then the ST depression vector points towards the apex (II, V5), with a reciprocal STE vector towards aVR (and even V1).   

In Septal STEMI, transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation.  aVR is similarly (but not exactly) placed and can show STE.  Lead III is also on the right and might manifest ST Elevation in Septal STEMI.

It is important to remember that the ST depression of subendocardial ischemia does not localize.  Here, the ST depression is in "lateral" leads, but this does not mean there is "lateral" ischemia.  It may either be reciprocal to Septal STEMI, or due to subendocardial ischemia from the LAD insufficiency.

Case Continued

Bedside ultrasound was performed:

This shows an anterior wall motion abnormality, and highly suggests the LAD as the infarct artery.  Often patients with subendocardial ischemia on the ECG do NOT have a wall motion abnormality, which contrasts with patients with OMI/STEMI who always have a wall motion abnormality, at least if the echo is of high enough quality and uses bubble contrast.

The patient was slightly tachypneic and mildly hypoxic in the stabilization room and therefore the physicians obtained a CT pulmonary angiogram as well as aortogram to rule out dissection and PE.

The initial Abbott hs troponin I returned at 52 ng/L (Upper reference limit for males is less than or equal to 34 ng/L).  FYI: 52 ng/L is the threshold for "rule in" by European studies as it has a high positive predictive value in the setting of chest pain.

The D dimer was undetectable, so CTPA was probably unnecessary, but it did have interesting findings:

Top left: conventional CT.  

Top right is colored iodine overlay; Blue areas of myocardium are ischemia.  

Bottom left is plain iodine map.  

Bottom right is low Kilo Electron Volt image which brings out iodine.  See the 2 very dark areas, one in the septum and one near the apex.  Notice that they correlate with blue on the colored spectral CT (blue is ischemia on spectral CT).

These areas of hypoperfusion are in the septum and apex, strongly suggesting LAD ischemia.  In addition, they are indeed transmural!

This CT interpretation was made with moderate certainty

Contrast this CT transmural ischemia here with this CT subendocardial ischemia. 

Below we can see a coronal image of the heart:

Notice the inferior wall (lower part of image) is subtly transmurally darker than the remainder.

If prospectively interpreted in blinded fashion, this is not definitively diagnostic, according to our CT Guru, Gopal Punjabi (https://twitter.com/CtSpectral)

This suggests inferior OMI but is by no means diagnostic.

Case continued

The patient was placed on a nitroglycerin drip and chest pain gradually resolved.  The emergency medicine faculty spoke directly with cardiology faculty and the decision was made to activate the cath lab via "pathway B."  (Our "Pathway A" is for clear STEMI; "Pathway B" is intensive evaluation and discussion for patients who might need the cath lab emergently for possible OMI, but it is not as clear as with STEMI).  The patient was subsequently given 5000 units of heparin, 180 mg of ticagrelor, and defib pads were placed on the patient in the event that he should have a cardiac arrest. 

Angiogram

Culprit Lesion: 90% mid LAD stenosis with evidence of plaque rupture, TIMI III flow on angiography.

Troponin profile:

Unfortunately, they were not measured to peak, which would help determine if this was indeed Septal STEMI or Non-Occlusive Subendocardial Ischemia.

ECG after PCI:

Left axis deviation, but otherwise normal

Formal Echo:

The estimated left ventricular ejection fraction is 71%.

There is no left ventricular wall motion abnormality identified.

So the wall motion has recovered (remember we showed a definite WMA during the ischemia).  Such quick recovery is uncommon in STEMI/OMI unless there is very quick reperfusion.  If this case was indeed OMI, then there was very fast spontaneous reperfusion, as in indicated by the open artery with TIMI III flow.  When reperfusion is not so fast, wall motion recovery may require many days to weeks.  When recovery is delayed, it is often called "myocardial stunning."

A Non STEMI that needs the cath lab now.

A male in his 60's called 911 for chest pain.  He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease.   His pain was intermittent and he was vague about when it was present and when it was resolved.  Here is his prehospital ECG:

Diagnosis? 

He had an immediate ED ECG:

There is artifact, but the findings appear to be largely gone now

The diagnosis is acute MI, but not STEMI.  There is slight ST elevation in lead III with reciprocal ST depression in aVL.  The T-wave is inverted in III, indicating reperfusion (what I like to call "inferior Wellens' syndrome).  There is no Q-wave, so this is unlikely to be old MI, and more likely to be acute NonSTEMI of the inferior wall.

I saw these ECGs, and since there was no immediate urgency, allowed the resident to manage it without any comment.  However, he did not see the abnormality on the prehospital ECG, so I finally said something like: "What are you going to do about the MI patient?".    When I pointed out the findings, we recorded another ECG:

Now there is increased ischemia, but where is it? My interpretation was that this is an inferior MI with posterior extension, as the ST depression in the precordial leads was maximal in V3 (opposite the posterior wall). There is about  1 mm of STE in aVR  I considered but rejected subendocardial ischemia.  

The ST elevation vector is posterior, inferior, and right, to the right of lead III and also posterior.  Is it subendocardial ischemia, or inferior MI?  See this post on the (Five primary patterns of ischemic ST depression, without ST elevation)

Because of the dynamic ACS, we activated the cath lab in the middle of the night.  Aspririn, Plavix (in spite of STE in aVR, because I thought this was inferior MI), Heparin were given.  The BP was elevated, so we gave metoprolol 5 mg IV x3 + 50 mg po.

His pain resolved and another ECG (but with precordial leads on the right) was recorded:

ST Depression is Resolved in V2 (=V1 R).  No evidence of RV MI.

Then the patient complained of increasing pain again:

There is now profound ST depression and STE in aVR, and the ST depression extends deeply in V5 and V6.  There is little ST elevation in inferior leads.

This time, the ST vector is more rightward, toward aVR and also posterior.

Now I regretted giving Plavix, as the probability of 3 vessel disease or left main insufficiency (not occlusion!) was much higher.  Thus, the chance of needing CABG was higher and Plavix can cause much operative bleeding.

Amazingly, the bedside echo showed very good LV function.

A nitro drip and sublingual nitro was given, the drip rapidly titrated to 80 mcg/min.  The BP came under better control and the patient was moved to the cath lab.

Outcome:

Was it RCA or LCX with inferior MI?  Or was it 3 vessel disease/left main insufficiency?

Both!

The active culprit was an RCA thrombus with 99% occlusion, but there was severe LAD and circumflex disease as well (severe 3 vessel disease).

The RCA was opened with POBA ("plain old balloon angioplasty") and eptifibatide was started.  The patient was referred for CABG and did well.