Even when the story is obvious, with intractable pain, the STEMI paradigm can cause preventable delays

 Written by Pendell Meyers

A man in his early 60s presented with acute chest pain rated 10/10 with associated nausea and vomiting with known history of multivessel CAD. He presented at 2300 with onset of symptoms at 2230. He was awoken from sleep by the symptoms, which were identical to prior MI for which he received a stent years ago. On arrival his heart rate was 43 bpm and blood pressure 91/62. Atropine and IV fluid was given.

Here was his triage ECG:

What do you think? Baseline below for comparison, but try first without it.

His baseline ECG was available on file:

The presentation ECG shows diagnostic evidence of posterolateral OMI. There is sinus bradycardia with a relatively normal QRS complex, followed by some STE in aVL, with upright hyperacute T wave, with reciprocal STD in the inferior leads and negative hyperacute T waves. The posterior involvement is suggested by STD in V3-V4, which is highly specific for posterior OMI in the setting of ACS and no QRS explanation (RVH, RBBB, etc.) for such STD. 

This ECG is very easy for readers of this blog. But it does not meet STEMI criteria. 

The EM providers evaluated the patient and concluded, easily, that the patient was having ACS. But they did not understand the ECG, documenting "no clear STEMI." 

CT pulmonary angiogram was chest negative for PE.

Initial troponin I was 15 ng/L (99% upper reference limit for men is 20 ng/L for this assay). Remember how his symptoms started just 30 minutes prior to arrival!

Repeat troponin I was 21 ng/L (delta = 6 ng/L, dangerously close to our departmental delta value of 4 ng/L!)

Another ECG was obtained at 2330:

Ongoing posterolateral OMI.

ASA and heparin were started, as well as nitroglycerin drip, none of which controlled his ongoing chest pain. He was then given 4 mg morphine x 2. 

The EM physician then initiated code STEMI due to "continued minimal ST elevation in aVL and ongoing pain and vomiting." An emergent transfer is initiated to the nearby cath center. Cardiology "canceled" the code STEMI, but accepted the patient for urgent transfer.

Cardiology documents:

"ECG was not definitive for STEMI but there was concern for an acute circumflex lesion given the lack of definitive ECG changes but typical presentation."

"NSTEMI with unstable angina. EKG with NSR with ST depression in III and aVF. Chest pain starting at 2230 and remaining constant despite nitrates, heparin, aspirin, and morphine."

Angiogram at 0230 (4 hours after arrival):  

LCX proximal 99% stenosis with thrombus, TIMI 3 flow, at the edge of a previously placed stent. The lesion was stented with excellent angiographic result. EF at cath was 55%. 

"To be clear this was not a STEMI presentation given the lack of ST elevations and TIMI-3 flow on angiography but an emergency procedure was indicated as the patient had intractable chest pain with non-STEMI with intractable unstable angina. Patient does not need to go to an ICU."

Meyers comment: There are several problems with this cardiologist's last comment that reveal significant gaps in understanding of AMI and ACS. The cardiologist states very clearly that he or she believes TIMI-3 flow is not possible with "STEMI." This is obviously false, here is an excerpt from our recent study:

Outcomes used to ascertain the presence of OMI on the ECG cannot be based solely on TIMI flow of the lesion at the time of the angiogram because the state of the artery frequently differs between the time of the ECG and the time of the angiogram. Proven STEMI has an open artery in 19% to 36% of cases, depending on whether it is TIMI −1, −2, or −3 flow. Karwowski et al showed that only 64% of 4581 STEMIs had TIMI 0 flow on angiogram. [25] Stone et al found that 72% have TIMI 0 or 1 flow. [26] Finally, Cox et al found that 80% had TIMI 0, 1, or 2 flow.[26]  Thus, approximately 20% of true, obvious STEMIs have TIMI 3 flow at immediate angiogram. [27]

25. Karwowski J, Gierlotka M, Gasior M, Polonski L, Ciszewski J, Beckowski M, Kowalik I, Szwed H. Relationship between an in-farct related artery, acute total coronary occlusion, and mortality in patients with ST-segment and non-ST-segment myocardial infarction. Pol Arch Intern Med. 2017;127:401–411.

26. Stone GW, Cox D, Garcia E, Brodie BR, Morice MC, Griffin J, Mattos L, Lansky AJ, O’Neill WW, Grines CL. Normal flow (TIMI-3) before mechanical reperfusion therapy is an independent determinant of survival in acute myocardial infarction: analysis from the primary angioplasty in myocardial infarction trials. Circulation. 2001;104:636–641. doi: 10.1161/ hc3101.093701

27. Cox DA, Stone GW, Grines CL, Stuckey T, Zimetbaum PJ, Tcheng JE, Turco M, Garcia E, Guagliumi G, Iwaoka RS, et al. Comparative early and late outcomes after primary percutaneous coronary intervention in ST-segment elevation and non–ST-segment elevation acute myocardial infarction (from the CADILLAC Trial). Am J Cardiol. 2006;98:331–337. doi: 10.1016/j.amjcard.2006.01.102

Case Continued:

Echo next morning:

EF 50%. Akinesis of the basal-mid anterolateral, inferolateral, and inferior myocardium.

Repeat troponin I in AM: greater than 25,000 ng/L (our lab's upper reporting limit)

The patient had an uncomplicated hospital course and was discharged. 

Learning Points:

Expert ECG diagnosis could have dramatically improved the patient's time to reperfusion.

LCX OMIs are the most frequently missed. NSTEMI patient with missed OMI have double the mortality compared to NSTEMI patients without OMI. This patient was not completely "missed", but significantly delayed (approximately 3.5 hours) due to lack of expert ECG interpretation, and potentially sluggish recognition of refractory angina and ECG ischemia, and cancellation of emergent transport.

This patient provides an example of OMI with an initial high sensitivity troponin I less than the 99%ile upper reference limit, as happens in 1/4 of all true STEMI (Wereski et al.--Smith is a co-author).

ACS with ongoing pain and/or ECG ischemia despite medical management has always been an indication for emergent (less than 2 hours) cath, in all guidelines; however, this guidelines is not frequently followed.

I will repeat this important point: "STEMI" does not require TIMI 0 flow. About 20% of obvious STEMI(+) OMI patients have TIMI 3 flow at the time of angiogram. TIMI 3 flow at the time of cath cannot be used as a reason why a patient didn't have OMI or STEMI.

A Pathognomonic ECG. What is it? (Hint: 2 diagnoses in one)

I was reading through the list of EKGs and saw this one.  What is it diagnostic of? (hint: 2 diagnoses in one)

There is a very long, flat, ST segment, resulting in a long QT (most long QT is due to a wide T-wave, not a long ST segment).  This is diagnostic of hypocalcemia.  There are also peaked T-waves of hyperkalemia.  This is a common combination in dialysis patients.

The ionized calcium was 2.29 mg/dL (normal is 4.40-5.20).  The K was 6.2 mEq/L.

Here are the symptoms she had (very typical for hypocalcemia):

Dialysis patient with left upper extremity numbness and tingling, lightheadedness, perioral numbness and tingling, and bilateral lower extremity stocking glove numbness and tingling. 

She was given 6 grams of calcium gluconate and K was shifted.

Here is the subsequent ECG:

All findings are corrected

A man in his 40s with epigastric pain and a dynamic ECG

 Case written and submitted by Dr. Arjun J V, peer reviewed by Meyers, Smith, Grauer

A 49 year male patient was brought to our ED at around 9 PM on with complaints of epigastric pain since that afternoon. The patient had the same complaints on and off for many years which would resolve on taking OTC antacids. However, this time the pain was persistent and included new diaphoresis, so he presented to an outside facility where this ECG was recorded:

What do you think?

There is sinus rhythm with a narrow QRS complex with normal axis. There is slight PR depression in III, followed by some STE with upright T wave. Lead aVL shows a negative QRS complex with a seemingly large negative T wave. Lead I also has a negative T wave. 

There is STE in the anterior leads but with reassuring large voltage QRS and reassuring morphology; to me it fits with normal variant anterior STE, not concerning for OMI. 

The question is: is this concerning for subtle inferior OMI? On on hand, the T wave in III is not definitively hyperacute, but the T wave in aVL may be fairly big for its QRS complex. We have shown many examples of this. 

At the outside hospital, the patient was given DAPT and was referred to a higher centre with Cath lab facilities. The providers were concerned for inferior OMI. The patient was hemodynamically stable but had persistent discomfort. An ECG was obtained at the receiving facility on arrival: 

What has changed compared to the first ECG? What does it mean?

Now the STE and T wave in III seem to be less elevated than before. The deep TWI in I and aVL are replaced by upright T waves. In the first ECG, aVR has a slightly upright T wave (a red flag for this condition, by the way), whereas now it is depressed.

Does it mean that the inferior OMI is starting to reperfuse? Does it mean that the high lateral area is showing pseudonormalization??

NO!

Neither of these are correct. All changes between the two ECGs are explained completely by reversal of the LA and RA electrodes on the first ECG.

Look at the differences:

 - Lead I (defined by RA negative, LA positive) is perfectly inverted between the two ECGs: in the first ECG (with lead reversal) we see qR then negative T wave. In the second ECG (with correct leads) we see rS with positive T.

 - Lead "aVL" in the first ECG is actually lead aVR, and it matches lead aVR of the second (correct leads) ECG

 - Lead "aVR" in the first ECG is actually lead aVL, and it matches aVL in the second (correct leads) ECG

 - aVR should not generally have a positive T wave if the leads are correct and the QRS is narrow and overall leftward

Below is Ken Grauer's excellent diagram showing the effects of LA/RA reversal:

Here they are side by side:

Here is the initial ECG before and after correcting the leads as per Dr. Grauer's diagram:

Unfortunately the lead reversal was not noticed by the treating team, who was still worried about OMI.

The patient’s ROS was unremarkable and POCUS did not show any RWMA. Both the ED team and Cardiology team were not completely convinced for the need for an emergent CAG but erred on the side of caution, possibly because of the following reasons:

 - Initial ECG showed perceived changes of inferior wall MI 

 - Young MIs can present with atypical changes

 - The recent & sudden death of a 45 year old male celebrity due to MI who was known to be extremely fit and health conscious. The untimely death shook the whole state to the core which witnessed an increase in the number of patients getting health check-ups[1]

Troponins were not awaited and emergent angiogram was done which was completely normal, with no evidence of CAD. No complications of the angiogram were experienced.

Labs were unremarkable. Troponin-I, Lipase & Amylase were negative.

CT abdomen showed possible changes of acute calculous cholecystitis. Patient was advised surgery but the patient did not go through with it. Patient was discharged against medical advice. Further follow up is unavailable.

Learning Points:

Lead reversal is common and can create scenarios like this one, in which a well meaning physician looking for signs of OMI can be fooled into concern for a dynamic ECG finding, leading to unnecessary concern and possibly an unnecessary angiogram. Learning the most common forms of lead reversal can help prevent this.

LA/RA reversal causes lead I to become inverted, and switches the places of leads II/III and aVL/aVR, while lead aVF remains unchanged.

When the QRS and T waves are otherwise normal, a positive QRS and/or T wave in aVR can be a red flag for lead misplacement.

Human factors and recency bias can affect patient management.

References:

1. https://bangaloremirror.indiatimes.com/bangalore/others/a-not-so-hearty-tale/articleshow/87475651.cms

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MY Comment by KEN GRAUER, MD (11/27/2021):

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Lead misplacement is easy to overlook! This is because of the tendency to "assume" that routine normal placement of extremity electrode leads will automatically happen. And because it almost always does happen — we are not used to recognizing lead misplacement when it does occur. There are several additional reasons why the LA-RA lead reversal may have been missed in today's case:

• This patient has RAD (Right Axis Deviation) on his baseline tracing — with a small amplitude QRS complex showing predominant negativity in lead I. LA-RA lead reversal is usually picked up because of the finding of "global negativity" (of the P wave, QRS and T wave) in lead I. But because of the RAD — the QRS complex in today's initial tracing was predominantly positive! (and therefore simulated a high lateral Q wave infarction with deep T wave inversion).
• Global negativity (ie, negative P wave, QRS and T wave) is normally seen in lead aVR — because this most remote electrode lead normally views the heart's electrical activity as traveling away from its distant perspective (looking down from the right shoulder). But because of the baseline RAD — we did not see an all upright R wave as a "tip-off" to LA-RA lead reversal in lead aVR.
• Small amplitude P wave activity in lead I on the initial tracing in today's case did not clearly suggest a negative P wave in lead I, that also would have been a "tip-off" to LA-RA lead reversal.
• Finally — the P wave in lead II was upright, so that sinus rhythm was assumed.

 

 

The diagram Dr. Meyers credited me above, showing the effects of LA-RA lead reversal on the ECG is adapted from the LITFL ( = Life-In-The-Fast-Lane) web site — which is my "Quick GO-TO" reference for the most common types of lead misplacement. Simply put in, "LITFL lead reversal" in your on-line Search bar — and this KEY link comes up instantly!

• LA-RA lead reversal is by far the most common technical mishap. It is usually EASY to recognize, because we are likely to see: i) Global negativity in lead I — which should never normally be seen — and which tells you there is either lead misplacement or dextrocardia; ii) The QRS in lead aVR is upright; and, iii) The P wave in lead II will often be negative.
• For another example of LA-RA Lead Reversal with more detailed discussion of this entity — CLICK HERE.

 

In Summary:

There are several reasons the LA-RA lead reversal was easy to overlook in today's case. The reason I immediately picked it up — is that today's initial ECG simply "looked funny" to me — because:

• It is highly unusual to see a very wide Q wave with such disproportionately large T wave inversion in lead I (even when you have acute high lateral infarction).
• We do not see global negativity in lead aVR (ie, the P wave is flat and the T wave is definitely positive).
• Although positive — the P wave in lead II is smaller than the P wave in lead III (which would be unusual for normal sinus rhythm).
• Lead aVL "looks funny" (ie, it shows "global negativity" — that is usually seen in lead aVR).
• KEY Point: Whenever I see an ECG that "looks funny" — I verify lead placement and then immediately repeat that tracing (especially when my differential diagnosis is "Rule Out" acute MI)!

 

 

Any ST depression in V2 and V3 is posterior OMI until proven otherwise, especially if downsloping

A middle aged male presented after onset, approximately 50 minutes prior, of constant crushing 10/10 substernal chest pain, radiating into right arm associated with shortness of breath. He had never felt this way before. There was a history of HTN but he was not taking any medicines.

Prehospital ECG was recorded approximately 20 minutes after pain onset and 20 minutes prior to ED arrival:

There are somewhat large T-waves in II and aVF and a sagging ST segment in aVL, suggestive of inferior OMI.  

There is some minimal downsloping ST depression in V2 and V3, which is suggestive of posterior OMI. 

The ECG is not diagnostic however.

This first ED ECG was recorded approximately 10 minutes after ED arrival, and about 30 minutes after the prehospital ECG:

There is downsloping minimal STD in V2 and V3.  

The T-wave in lead II is somewhat suspicious, but is not a diagnostic OMI finding.

This is highly suspicious for isolated posterior OMI

Here are the precordial leads magnified, and the ST segments in V2 and V3 highlighted

There is perhaps a 0.5 mm of ST depression in leads V2 and V3, and it is downsloping.

In our recent research, published in November 2021 in The Journal of the American Heart Association, any ST depression maximal in V1-V4 is 96% specific for OMI requiring PCI (assuming, of course the patient has symptoms compatible with ACS).  

It is important to remember that the ECG in normal people without ischemia and without an abnormal QRS such as RBBB never has more than 0.5 mm of STD, and rarely has any STD at all.  The vast majority have some STE in V2 and V3.  (Macfarlane PW. Age, sex, and the ST amplitude in health and disease. J Electrocardiol [Internet] 2001;34 Suppl:235–41.)

In our study: There were 118 patients with "suspected ischemic ST depression maximal in V1-V4" (45 with less than 1 mm).  I blindly read ECGs of all 808 patients, and called OMI in 112 of these 118 patients; 99 had OMI and, of these, 34 had less than 1 mm STD.  Of these 34, 12 had STEMI in other leads, but 22 did not.  Of these 22, every one had some other subtle OMI findings in other leads.  In other words, we did not have a single patient with STD maxV1-4, AND less than 1 mm who did not have some subtle finding elsewhere, as is the case here.  On the other hand, we did have 2 patients with less than 0.5 mm STD and no other OMI findings whom I interpreted as "no OMI" who indeed had no OMI.  

So the finding of less than 1 mm in V2 and V3 which is completely isolated (no OMI findings elsewhere on the 12-lead) remains highly suspicious, but not diagnostic.  

However, downsloping STD in V2 and V3 is, in my experience, diagnostic.  

Case continued

I was very worried about about OMI from the crushing chest pain alone, even without the ECG, and I was specifically worried about posterior OMI for the above reasons. 

6 minutes later, we recorded posterior leads:

This shows a trace of STE in V4, but not up to 0.5 mm.  

I think the STD in V2 and V3 may have deepened a bit, but I did not notice it at the time.

Case continued

The blood pressure was 175/125.  This made aortic dissection a possibility as well.  We started him on high dose IV nitroglycerin up to 200 mcg/min, with sublingual NTG every 5 minutes, and this brought his BP down to 120/73. The pain persisted.  This is important: ACS with pain that can't be controlled with NTG should go emergently to the cath lab "regardless of ECG or biomarker findings!" (Eur Soc of Cardiology guidelines)

I called the cardiologist directly and stated that I thought this was ACS/OMI.  He agreed and we decided to do a CT for dissection.  If that was negative, the patient would go emergently to the cath lab.

While I was on the phone with him, we recorded this ECG 17 minutes after the 2nd one (23 minutes after the first), with posterior leads still attached:

This one has evolved and is now definitely diagnostic.  

Increased STD in V2 and V3

New STE in I and aVL

New hyperacute T-wave in I

Increased T-wave size in aVL

New inferior reciprocal ST depression.  

Greater than 0.5 mm of STE in posterior leads V8 and V9 (labelled V5 and V6)

The cath lab was activated.

While waiting for the cath team, another ECG was recorded at 37 minutes after the first, standard 12 lead (not posterior):

Now there are additionally hyperacute T waves in V4-V6, with some new ST elevation

The initial troponin I returned at 10 ng/L, which is within the normal range.

Aside: In our study of 925 patients with STEMI, using the same assay, the initial troponin was below the 99th percentile in 14.4%  Here is the reference: Wereski et al. (including Smith).  High-Sensitivity Cardiac Troponin Concentrations at Presentation in Patients With ST-Segment Elevation Myocardial Infarction

Angiogram and PCI

1. Acute coronary syndrome.

2. Thrombotic D1 occlusion 100% (this is the culprit vessel).

3. Multivessel coronary artery disease 

4. Successful D1 stenting with a drug eluting stent.

Post PCI

Next morning

The troponin I peaked at greater than 50,000 ng/L, a very large acute OMI.

Echo:

Mildly increased LV wall thickness with normal LV cavity size and an estimated ejection fraction of 45%.

Regional wall motion abnormality--mid anterolateral and mid inferolateral hypokinesis.

This is consistent with posterior OMI ("posterior" is now classified as "lateral" -- this is complicated and explained in the article).

Learning points:

1. Any ST depression that is not explained by RBBB or other QRS findings, in a patient with symptoms suggestive of ACS, is posterior OMI until proven otherwise.

2. Unexplained chest pain that is typical of ACS, and is not controlled with medical therapy, needs an angiogram even in the absence of ECG or biomarker proof of ACS.

3.  ST depression of posterior OMI is almost always accompanied by some other subtle OMI finding in inferior or lateral leads.

4. ST depression that is downsloping, even if less than 0.5-1.0 mm, is particularly worrisome, even in the absence of other subtle OMI findings.

5. When there is severe hypertension, all chest pain might be due to supply demand mismatch.  Therefore, one must lower the BP before activating the cath lab.

Shark fin post arrest: do you understand the ECG?

Case submitted by Dr. Daryl Williams, written by Pendell Meyers, peer reviewed by Smith and Bracey

A physician bystander witnessed a middle-aged or slightly elderly man suddenly collapse while walking down the street, very close to the hospital. The physician immediately started CPR and called EMS. EMS arrived quickly and found the patient to be in VFib. After several shocks the patient achieved ROSC.

A minute or so after arrival to the ED, he went back into VFib and was immediately shocked back out into sinus rhythm.

His EMS ECG during initial ROSC was available for the ED team:

Here is his ED ECG:

What do you think?

Both ECGs above show RBBB + LAFB, with massive concordant STE in leads V2-V6 as well as I and aVL. There is shark fin morphology (aka "Giant R wave", or "Lambda wave"), in which the wide complex QRS appears to fuse with the massive STE, causing confusion as to where the J point actually is, and where the QRS ends and the ST segment begins. This pattern is diagnostic of at least LAD occlusion (which of course supplies the anterolateral walls and the RBB and LAF), but given how severe the findings are even out into the high lateral wall, the occlusion may even be more proximal, such as the left main. This pattern is more commonly seen in LAD occlusion simply because persistent left main occlusion is rare, probably because it such patients rarely survive long enough to obtain an ECG and/or angiogram.

Below, I have placed red vertical lines at the J points.

I was sent the above ECG with no clinical information, and my response was: "Should be a huge LAD or theoretically even left main occlusion."

The cath lab was activated immediately. At this time the patient had stable ROSC, was intubated, and did not require pressors.

The LV EF was estimated at 20%. An Impella was placed for hemodynamic support. 

Angiogram:

Acute thrombotic culprit lesion of the distal left main coronary artery and proximal LAD with 80% stenosis, also at the time of angiogram. There was also 80-90% stenosis of the proximal D1, and 90% at the ramus intermedius. It is not completely clear whether these were also thrombotic extensions of the distal left main lesion, but these are probably all part of the same acute culprit left main lesion, or downstream showering from it. 

There was mild diffuse (non-quantified) CAD of the LCX, otherwise no evidence of CAD in any other part of the coronaries.

As predicted from the ability to obtain ROSC, there is not full occlusion at the time of cath. There is flow in each vessel distally. 

For a patient who suffers cardiac arrest with recurrent or refractory VF due to left main occlusion, it is very unlikely to get stable ROSC unless the lesion opens up at least a little bit. And that is what we see here. The post cath ECG below confirms reperfusion including resolution of RBBB and LAFB:

In fact, now there is more of a LBBB pattern, but a bit odd because I and aVL are not all upright.

Initial contemporary troponin T was 0.11 ng/dL (reference range less than 0.01 ng/dL). Troponin rose to 2.10 ng/dL but then no further measurements were recorded, so the peak troponin was not measured.

He had a long and rocky course in the ICU. Brain MRI showed multiple areas of restricted diffuse and acute cerebral infarct consistent with hypoxic encephalopathy. Despite ideal cardiac arrest conditions (immediate professional CPR, near the hospital, quick response time, seemingly zero no-flow time, and aggressive immediate cath lab activation), it seems that there will be at least some element of permanent neurologic injury, but the severity is yet to be determined.

Learning Points:

You must understand the shark fin morphology, and the fact that the LAD supplies the right bundle branch and the left anterior fascicle, if you want to be able to diagnose the most severe OMIs that exist like this one! STEMI criteria do not apply here, and many providers will not even know where to measure the ST segment at all.

In this case, we see lead aVR has ST and T wave depression in lead aVR, NOT ST elevation. This is because aVR simply shows the reciprocal findings of the many other leads which are oriented in the opposite direction. With widespread STE in many leftward leads, it is inevitable that lead aVR must show reciprocal STD. If there had been better coronary perfusion and more collateral circulation at the time of these ECGs, then instead of an anterolateral OMI pattern, we may have seen the pattern of diffuse subendocardial ischemia, with diffuse STD and reciprocal STE in aVR. The key is that aVR has no new or primary information. I teach that "aVR" stands for the "aVerage Reciprocal" lead, because it shows the reciprocal findings of the average of all the other leads on the 12-lead, which are largely oriented in the opposite general direction from lead aVR.

Sometimes even with the best possible conditions, the neurologic outcome of cardiac arrest can eclipse the cardiac salvageability.

Some of the most severe LAD or left main occlusions present with acute RBBB and LAFB, and these findings carry the highest risk for acute ventricular fibrillation, acute cardiogenic shock, and highest in-hospital mortality when studied by Widimsky et al. (in-hospital mortality was 18.8% for AMI with new RBBB alone). Additionally, the RBBB and LAFB make the recognition of the J-point and STE more difficult and more likely to be misinterpreted (when the QRS is wide, the J-point will hide!). Upon successful and timely reperfusion, the patient may regain function of the previously ischemic or stunned fascicles.

Widimsky PW, Rohác F, Stásek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86–95. 

https://pubmed.ncbi.nlm.nih.gov/21890488/

See these other related posts:

A deadly alcohol binge: a man in his 30s with chest pain and initial high sensitivity troponin I within normal limits

See 7 more cases of true total Left main occlusion here:

How does Acute Total Left Main Coronary occlusion present on the ECG?

Here is a post on RBBB + LAFB and its significance, with links to many more such cases:

Cardiac Arrest at the airport, with an easy but important ECG for everyone to recognize

A woman in her 60s with 6 hours of chest pain, dyspnea, tachycardia, and hypoxemia

Ventricular Fibrillation, ROSC after perfusion restored by ECMO, then ECG. Protocols can be overridden by Physician Judgment.

What is the Diagnosis in this 70-something with Chest Pain?

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

A man in his 80s with chest pain

What, besides large anterior STEMI, is so ominous about this ECG?

Chest Pain and Right Bundle Branch Block

See other "shark fin" morphology cases here:

Fascinating case of dynamic shark fin morphology - what is going on?

1 hour of CPR, then ECMO circulation, then successful defibrillation....

Persistent Ventricular Fibrillation, ED ECMO, ED TEE, ROSC, Shark Fin ECG (also called "Giant R-wave"), Postinfarction Regional Pericarditis. What a Case!

Shark Fin morphology recognized only by EM physician

"Shark Fin": A Deadly ECG Sign that you Must Know!

"Shark fin" ECG in I, aVL, V4 and V5. Which artery? Hint: patient is in shock and was put on ECMO

Refractory V FIb Arrest, put on ECMO, regains an organized rhythm, and a 12-lead is recorded.

Giant R-waves. What are they?

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Bracey, A., Meyers, P., & Smith, S. W. (2020). Post-arrest wide complex rhythm: What is the cause of death? The American Journal of Emergency Medicine. https://doi.org/10.1016/j.ajem.2020.12.028

But don't be fooled by the other etiologies of shark fin morphology:

Another Shark Fin. With a twist.

A woman in her 60s with syncope and vomiting. Does she need a pacemaker?

 Written by Pendell Meyers with some edits by Steve Smith

A woman in her 60s on chemotherapy presented to the Emergency Department for a syncopal episode just prior to arrival. She was walking to the bathroom when she suddenly felt nauseous and passed out. EMS was called by the patient's daughter, and en route to the ED she vomited twice. On arrival to the ED, she adamantly denies chest pain but says she's "just still not feeling well." She had no prior known cardiac disease.

Triage at 0755:

The rhythm is most either atrial fibrillation with complete heart block and resulting junctional escape, or atrial flutter with very high degree (but constant) block. Remember, atrial fibrillation cannot result in regular ventricular rhythm if it is conducted through the AV node.

The QRS has narrow normal morphology. There is almost 1 mm STE in III, but no STE at all in II or aVF. The T wave in III is hyperacute, and is biphasic up-down. Leads aVL and I show reciprocal findings (STD and TWI biphasic down-up). Through the baseline wander, you can see the impression of downsloping STD in V2 indicating posterior extension. Interestingly, V3 then appears to have a hyperacute biphasic down-up T wave, with hyperacute Ts in V3 and V4, but then V5 and V6 do not.  All the biphasic T-waves suggest that there is some early spontaneous reperfusion happening.

Overall, it is diagnostic of inferoposterior OMI, likely RCA occlusion, likely also explaining the acute bradydysrhythmia.

The rhythm was noticed as pathologic, but none of the ischemic findings discussed above were initially noticed. It seems as though the providers felt that the problem was a primary bradydysrhythmia.

Initial troponin returned at 520 ng/L, and another ECG is recorded at that time (0900):

Findings are very similar to the first ECG. There is ongoing active transmural (full thickness) infarction. Still no STEMI criteria.

Anther ECG was done at 1000 (reason unknown):

This ECG shows some interval reperfusion compared to the prior ones, including slight deflation of the hyperacute T waves and terminal T wave inversion in III, and the opposite in V2.

At this point the patient was persistently hypotensive and bradycardic requiring epinephrine drip to maintain heart rate above 50 bpm. She was described as uncomfortable and short of breath. She continued to deny chest pain. 

The ED team consulted cardiology for symptomatic bradycardia, asking whether the patient should go for an emergent pacemaker. The cardiology team evaluated the patient, reviewed all the ECGs above, and apparently found no concern for ischemia and agreed that the primary problem was just the bradydysrhythmia.

They were in the process of consenting the patient for a pacemaker when I contacted the ED provider in real time (I happened to be actively reading ECGs for the department from home at that time). I explained my concern for RCA occlusion as the cause of her OMI findings on ECG, and as the cause for her bradydysrhythmia (because the RCA almost always supplies the AV node).

The ED team performed a bedside echo which showed an inferior wall motion abnormality.

The repeat troponin I was 595 ng/L.

Another ECG was performed at 1055:

The end of the T wave in III is difficult to see through the atrial waves. There are some features of reperfusion, but also some leads that seem to show ongoing ischemia.

I was told the patient was still persistently symptomatic despite some features of reperfusion on ECG. She still required epinephrine and norepinephrine drip and was short of breath.

The ED provider was  able to convince the skeptical cardiologist to perform an angiogram before placing a pacemaker. 

The angiogram showed an acute thrombotic proximal RCA occlusion (TIMI 0 flow). After PCI, there was 0% residual stenosis with TIMI 3 flow.  

Comment: TIMI-0 flow does not rule out some degree of microvascular reperfusion; collateral flow may account for the minimal ECG features of reperfusion.  In fact, in Wellens' studies which established Wellens' syndrome, in all cases there was perfusion, but 20% of these cases were in spite of an occluded artery, but through collateral circulation.) This is precisely the reason why we conceptually define OMI as: "Acute coronary occlusion or near-occlusion with insufficient collateral circulation, resulting in imminent full-thickness myocardial infarction."

The first ECG after cath was performed hours later, in the cardiac ICU:

Sinus rhythm with PACs. There is resolution of the STE and hyperacute T waves, as well as terminal T wave inversion in III. This confirms reperfusion. Not to mention the dramatic improvement in AV node function.

The ICU staff noted that, after PCI, her heart rate rapidly improved and she never required even a temporary pacemaker. Her epinephrine and norepinephrine requirement resolved within hours of PCI. 

In fact, within 24 hours the patient required metoprolol and amiodarone for rate control of intermittent atrial fibrillation with rapid ventricular response:

Later she was back in sinus rhythm:

She had several minor complications unrelated to ACS during her stay, but was ultimately discharged on day 5.

Learning Points:

The most important, deadly, reversible causes of bradycardia include acute RCA occlusion (OMI), hyperkalemia, and toxicity from beta blockers, calcium channel blockers, or digoxin. We in the ED must be the experts at recognizing these conditions on the ECG. 

If this patient had instead received a pacemaker rather than RCA reperfusion, her ECG would have shown a ventricular paced rhythm. Providers who cannot recognize OMI in normal QRS conduction may be even less likely to recognize it in ventricular paced rhythm, although we have shown that it can be reliably done with proper training: 

New Review: Diagnosis of Occlusion Myocardial Infarction in Patients with Left Bundle Branch Block and Paced Rhythms

Until we get AI that can learn ECG patterns, we might need human ECG experts to act like radiologists, so that EM physicians and cardiologists can have access to expert interpretation.

You must learn to recognize hyperacute T waves. 

This patient is STEMI(-) OMI that clearly benefits from emergent reperfusion.