Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

A male in his 50's called 911 for constant 8/10 midsternal chest pressure.  Here was his prehospital ECG:
Computerized QTc is 423 ms.  The ST elevation at the J-point was measured by the computer (see right side), and is less than the "criteria" for anterior STEMI (2 mm in males over age 40).  There is also almost a saddleback morphology in V2.  I say "almost" because the R' wave is not tall enough to be a typical saddleback.
By the subtle LAD occlusion vs. Early Repol formula, this is clearly LAD occlusion: STE60V3 = 2, RAV4 = about 7, value = 25.07 (greater than 23.4 indicates probable LAD occlusion)

Here is a typical saddleback morphology, which is rarely due to STEMI:
This saddleback ST elevation prompted a false positive cath lab activation.  It was due to LVH.  Notice how tall the R' wave is.  Such saddleback ST elevation is rarely due to STEMI (I have never seen one that was!).

This nearly meets ECG criteria for type 2 Brugada morphology (I will post on that difficult topic soon).  Full text link:  Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Case continued:

He was given 2 sublingual NTG, with improvement of pain to 4/10.  Here was the second prehospital ECG:
Computerized QTc is 421 ms.  There is no significant change.

He arrived in the ED and had this ECG recorded:
QTc is 435 ms.  There is still less than 2 mm STE at the J-point, so it does not meet STEMI criteria.  The formula, using 1.5, 435, and 11 gives a value of 23.8, which, greater than 23.4 is unequivocally positive.  LAD occlusion must be assumed until proven otherwise.

The ECG was read as normal by both the computer and the physician.

Comment: Readers of this blog may be critical of this, but that is because you have been sensitized to this diagnosis.  This is the normal assessment throughout the world!  To do better than this is the exception, not the norm.

That is why in study after study, 20-30% of angiograms done for "rule-in MI" by troponins find an 100% occluded artery at next day angiogram.

Don't be critical of this assessment; rather, pass the word and help your fellow emergency physicians and cardiologists to see these findings.

The initial contemporary, sensitive troponin (but not high sensitivity troponin -- these are not yet available in the U.S.) was less than 0.10 ng/mL (undetectable).

The first troponin is negative in 50% of acute STEMI.

A repeat ECG was done 140 minutes later:
QTc is 444 ms.  There is no more STE than before.  T-waves are slightly different, but not larger.
Q-waves are beginning to form in V2 and V3.  This proves it is an acute anterior MI.

A troponin drawn almost 4 hours after the first one was 0.18 ng/mL.  It doesn't sound very high, does it?  The Q-waves were not noticed.

Case continued

At 4.5 hours, another ECG was recorded:

At this point, the Q-waves were noticed and the cath lab was activated.

A 100% LAD occlusion was stented.

No further followup is available.

Learning point

I repeat this theme over and over: Acute coronary occlusion may be very subtle.  It is frequently missed.  Readers of this blog probably would not miss this.  The person who sent it to me does read the blog, and he was doing QA when he noticed this and immediately recognized that it was a missed subtle occlusion.  It would be classified as a NonSTEMI.  He states that it is difficult to convey to his colleagues how to recognize these.

Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology

A male in his early 30s was playing soccer when the ball hit him in the chest.  At some point after this, he began having chest pain.  The pain radiated into the L arm, and was 8/10 in severity. The pain was similar to pain he had with a previous STEMI, for which he received a bare metal stent in the LAD a couple years prior.  He was on no medications.  
BP was 160/100. 

Here was his first ED ECG with 8/10 pain:
There is sinus rhythm.  There is minimal ST Elevation in anterior leads.  There is a QS-wave in V2, due to the old anterior MI.  The T-wave is taller than expected for old MI.  In V4, the T-wave size is far out of proportion to the QRS.  There is minimal STE in aVL with reciprocal ST depression in lead III.

Here is the last ECG from 3 years prior:
There are QS-waves in V2 and V3.  The terminal part of the T-wave in V3 is inverted, and the T-wave in V2 is not tall.
This is typical of LV aneurysm morphology (persistent ST elevation after previous MI)

We have derived and validated a rule to differentiate "LV aneurysm" ST elevation from STEMI (just finishing validation manuscript).  The rule depends on the principle that acute STEMI has a tall T-wave and LV aneurysm does not.  There are two versions:

In the first rule, if there is any single T/QRS ratio in V1-V4 that is greater than 0.36, it is likely STEMI:  for the ECG from 3 years prior, that would be lead V2.  At 5mm/21mm, the ratio is less than 0.36 and would indicate LV aneurysm.  But for the first acute ECG above, lead V2 is 8.5/15 which is 0.56 and would NOT indicate LV aneurysm.

In the second rule, one takes the sum of T-wave amplitudes in V1-V4 and divides by the sum of the QRS amplitude in V1-V4.  A value less than 22 indicates LV aneurysm.  In the second ECG from 3 years ago, that comes to 10/47 = 0.215, consistent with LVA.


Records showed that his STEMI was anterior and resulted in an EF of 40%, an anterior wall motion abnormality, and peak troponin I of over 100 ng/mL.

He was given sublingual NTG with some pain relief.  Here is the second ECG 13 minutes after the first, with 6/10 pain:
There is decreasing T-wave amplitude, consistent with some reperfusion.  

The cath lab was activated.  The interventionalist did not think the ECGs were different from before, but he was glad to take the patient for an angiogram.

In the meantime, the patient was given aspirin, clopidogrel, and a heparin bolus.  While waiting for cath, a NTG drip was started.

At 27 minutes after the first ECG, the patient had 5/10 pain on a Nitroglycerine drip at 200 mcg/min, with a BP of 130/80, and had this ECG recorded:
The T-waves are beginning to invert.  This is consistent with some reperfusion.


There was an in-stent thrombosis in the mid LAD with with 90% thrombotic occlusion and an embolism to the distal LAD.  Plain old balloon angioplasty (POBA) was performed, and the patient was put on aggressive antiplatelet and antithrombotic therapy.

Here is the post cath ECG:
T-waves are fully inverted now.

The troponin peaked at 12 ng/mL (not very high).  The formal echo showed dense anterior, septal, and apical wall motion abnormality, with an EF of only 29%.  This probably indicates "stunning," and there will probably be recovery of wall motion and EF, as reperfusion was quick.

Stunning may take up to 6 weeks to recover.

Learning Points

1. T-wave height correlates with acute infarction.
2. Absence of tall or large upright T-waves in the presence of QS-waves correlates with large old infarction, or LV Aneurysm morphology.
3. Acute STEMI can be superimposed on LV aneurysm morphology.  When it is, the T-wave turns upright with higher amplitude.  

Dyspnea on Exertion in a Middle Aged Woman.

A middle-aged woman presented to the ED with increasing dyspnea on exertion.  She had a normal physical exam except for a heart rate slightly over 100.  No other history or vitals are provided.  This ECG was recorded:
What do you see?  Answer below.

The patient was admitted to the hospital for rule out MI.  A later cardiology read of the ECG identified electrical alternans and the patient was re-examined and found to be hypotensive.  An echo confirmed tamponade.   Pericardiocentesis was performed and the patient improved.

No more details are available.

Notice that not only does the voltage alternate, but the QRS morphology also alternates, with slight changes in QRS axis, especially in precordial leads (see lead V3).

Electrical Alternans (EA):

Here is a great old review (full text pdf):

EA is relatively rare, and only about 1/3 of EA is associated with pericardial effusion.  Total electrical alternans (involvement of both atrial and ventricular components) is diagnostic of tamponade, but only a fraction of tamponade manifests this (low sensitivity, high specificity).

In patients in sinus rhythm, EA is almost never found in simple pericardial effusion (without tamponade: thus, EA in sinus rhythm is almost always due to tamponade).

Patients with PSVT frequently have EA without any effusion or tamponade, so this rule only applies to patients in sinus rhythm.

Bottom line: do an echo whenever you see EA.

Massive Osborn Waves of Severe Hypothermia (23.6 C), with Cardiac Echo

This patient was found down in the Minnesota Winter.  He felt cold and was unresponsive.  He had palpable pulses at a rate of 30, and his BP was 65/45.  A core temperature was 23.6 degrees Celsius.   Here is his first ECG.
Regular rate of about 30 beats per minute.  It appears to be atrial fibrillation, though it is possible that P-waves are hidden.  If atrial fibrillation, there is AV block and a junctional escape.  
There are MASSIVE Osborn Waves

Here is the bedside echo (this is not slowed down!):

There are very slow contractions with bradycardia, but the ejection fraction is good enough.

Although the patient is hypotensive and has a very low cardiac output, little cardiac output is required in a hypothermic patient with very slow metabolism.  The Postassium was not elevated.

Internal Rewarming was started with an intravascular catheter.  One hour later, the temp was 25.2 and this was the ECG:
The first complex is sinus with a narrow QRS and an Osborn wave.  The subsequent beats appear to be wide ventricular escape beats.  Beats 3, 4, and 5 appear to occur immediately after a P-wave; they appear to have escaped before the P-wave had a chance to conduct.   

Another 1/2 hour after that, the temp was 26.4
Sinus rhythm with 2:1 AV block, with Osborn waves

3 hours later, the temp was 29.0:
Sinus rhythm with 2:1 AV Block.  The heart rate is increasing.

The patient completely rewarmed and did well.

You Must Read the ECG in Clinical Context….

An elderly male presented with cough and dyspnea, progressive for several days.  He had no chest pain.  Among his many tests, the ECG was done first, and was handed to me before I ever saw the patient:
There is minimal ST elevation in inferior leads, with reciprocal ST depression in aVL and marked ST depression in V2-V5.

This is consistent with inferior and posterior MI (posterior STEMI), but also with subendocardial ischemia.  The clinical context is critical.  Although a patient with acute chest pain and this ECG is likely to have a posterior MI, a complex medical patient may have reasons for supply/demand cardiac ischemia that are not related to ACS.

Such "demand ischemia" is usually diffuse and subendocardial, but it may be focal, especially if there is a coronary stenosis in a particular territory.  In such a case, it may present with ST elevation.

Subendocardial demand ischemia may have ST depression that mimics posterior STEMI.  But the minimal ST elevation in lead III suggests that this really is transmural ischemia generating ST elevation of inferior and posterior walls.

On exam, the patient was slightly hypoxic and very pale; he appeared to be anemic. His hemoglobin was 4.8 g/dL and so he was transfused.  He had heme + stools but no melena or gross blood.  He also had pneumonia, and a core temperature was 38.5.

I knew this was not a typical ACS and so I activated our "Pathway B", which is a compromise between activating the cath lab ("Pathway A") and not activating.  It is for emergent cardiologic evaluation for patients who might need emergent angiogram and PCI, but are complicated by an equivocal ECG or complicated medical problems.

The cardiologist came immediately.  An emergency formal echo showed an inferolateral wall motion abnormality.  In the record, an old angiogram reported a chronically occluded obtuse marginal (OM).  The previous echo was normal, but a stress echo had shown induced inferolateral hypokinesis.  Thus, there was prior proof that this area was vulnerable to stress; the territory of this artery was reliant on collateral circulation for oxygen delivery.

The first troponin I returned at 3.9 ng/mL.

The etiology of these ECG findings was not ACS, but rather transmural ischemia (with resulting ST elevation) in the territory of the chronically occluded OM due to poor oxygen delivery in this vulnerable area.

After resuscitation, especially with blood products, the hemoglobin was 8.8 and the ST depression was resolved.  The troponin I peaked at 12 ng/mL and then fell.  Here is the next day ECG:
Still abnormal but no severe ischemia remains

The patient did not undergo an angiogram.  He did well.

Learning Points:

Type 1 MI (due to ACS) vs. Type 2 MI (due to poor oxygen delivery and/or high oxygen demand)

1. Don't automatically activate the cath lab for ischemic ST elevation on the ECG (in this case is was posterior ST elevation).  Think first about why there is ischemia.

2. Don't forget Type 2 MI as the etiology of ischemia (ECG or troponin elevation).  In our studies at HCMC, 65-75% of all MI are type 2 MI.

3.  Most ischemia from type 2 supply demand mismatch is subendocardial.  It will usually have more diffuse ST depression.

4.  The echo is likely to have no new wall motion abnormality when there is subendocardial ischemia.

5.  Even MI with ST elevation may be Type 2 MI.

6.  From 2-5% of Type 2 MI have ischemic ST Elevation.  We believe it should not be called STEMI.  See this article by Sandoval, Smith and Apple.

7.  Here is the most recent review of Type II MI, by Sandoval, Smith, Thordsen, and Apple.

Here are 3 more examples of type II MI with ST elevation.

Cardiac arrest, severe acidosis, and a bizarre ECG

A middle aged male had an unwitnessed PEA arrest associated with cocaine use.  Whether there was a shockable rhythm prior to PEA is unknown, but he was never defibrillated.  He received chest compressions with LUCAS and 3 doses of epinephrine, and was intubated by prehospital providers.  He had intermittent pulses.  Here is his initial ECG, with a pH of 6.50:
The rhythm is uncertain: probably an accelerated junctional rhythm with RBBB and PVCs, but it could be an accelerated rhythm initiated in the left bundle, mimicking RBBB.  It is important to ascertain the end of the QRS, which I attempt to do below.
Also present are 6 PVCs: complexes 3, 6, 7, 9, 10 (second PVC morphology), and 13  

With this wide complex, hyperkalemia should be high on the differential diagnosis

Here I try to find the end of the QRS:
Try to find the end of the QRS in any lead.  If you use lead II, it appears as if the blue line is at the end of the QRS. But it is uncertain.  The black line may represent the end of the QRS in leads V5 and V6, but I don't think so.
If the QRS end is represented by the blue line, then there is quite a bit of ST elevation (V1-V4) and ST depression (V5 and V6).

I was very suspicious of hyperkalemia, so we gave 3 g of calcium gluconate.  But the K returned at 4.5 mEq/L.

So is this STEMI?

Some clinical context is important:

1. It was not ventricular fibrillation, but PEA.  This suggests another mechanism other than ischemia.
2. We found that the pH was 6.50 (pCO2 100, HCO3 8).  Severe acidosis can result in very deranged ECGs.
3. Cocaine complicates the clinical picture.  As he had zero neurologic function after resuscitation, we were suspicious of possible cocaine associated head bleed followed by resp arrest then PEA arrest.

I did not think this was STEMI, but rather the consequences of cocaine, acidosis, and cardiac arrest.

The patient was ventilated and another ECG was recorded at 15 minutes, at a pH of 6.70 (pCO2 50, HCO3 5):
 I believe it is easier to find the end of the QRS in this one.  See below.
Also, it now it resembles Brugada Type 1 pattern ECG, which can be induced by cocaine, a sodium channel blocker (like all ***caines, including lidocaine).

Here I draw lines again:
The end of the QRS is indicated by the blue lines.  There still appears to be some ST elevation and depression, but it is less.  There is a Brugada Type 1 morphology in V1-V3.

The patient was in cardiogenic shock, partly due to bradycardia and partly due to presumed low SVR, as the ejection fraction by bedside ultrasound was excellent.  He was put on an epinephrine drip to increase heart rate and Systemic Vascular Resistance.  75 minutes later, the pH was 7.00 and this was the ECG:
Still bizarre, and Brugada-like, but normalizing.

Further information:
It turns out he had had a bradycardia arrest 7 weeks prior, also associated with cocaine, and with apparent status epilepticus.  In that case, there probably was never a shockable rhythm.  This was his first ECG at that time (pH 6.68)
Again, it is a bizarre RBBB pattern with Brugada type 1 morphology.  There is ST elevation but it does not look like the ST elevation of STEMI as it is downsloping with a negative T-wave.

7 minutes later, this ECG was recorded:
It is narrowing a bit but still bizarre with RBBB morphology and downsloping STE.

And yet another had been recorded at 24 minutes after the 1st (17 after the 2nd)

At that visit, he had been cooled. Angiogram had shown no Coronary disease.  He had awoken and been discharged.  His cardiac arrest had been attributed to status epilepticus and polysubstance abuse.

Further Events on this Presentation:

Pupils were still fixed and dilated. Even with the ambient lights off, there was no response to light.  Since PEA arrest with severe neurologic deficits may be due to intracranial bleed, including subarachnoid hemorrhage (and SAH may be caused by cocaine), we obtained a head CT before initiating cooling.  It was negative.

He was cooled and admitted to the ICU.

The next day he was moving all extremities, had a peak troponin of 0.50 ng/mL, and had a normal echocardiogram.

Here was the next day ECG at a temp of 33 degrees:
I am uncertain, but I suspect that he is shivering.  All the bizarre findings are gone.

He awoke fully and neurologically intact (so much for GCS 3 with fixed and dilated pupils!).

We consulted the electrophysiologist, who plans to do a workup for occult Brugada syndrome.  The workup may include family history, provocative testing with Na channel blocking agents, and ECGs of family members.

1. Cocaine-induced myocardial infarction in patients with normal coronary arteries probably involves adrenergically mediated increases in myocardial oxygen consumption, vasoconstriction of large epicardial arteries or small coronary resistance vessels, and coronary thrombosis.  Such ischemia may cause cardiac arrest.

2. But cocaine can also cause cardiac arrest from its sodium channel (local anesthetic) properties. There need not be an underlying sodium channel defect (e.g., Brugada) for cocaine to result in arrhythmic cardiac arrest.

3. Furthermore, these same Na channel blocking effects can unmask underlying Brugada syndrome, just like any Na channel blocker.  Electrophysiologists perform provocative testing with Na channel blockers to help diagnose Brugada syndrome.

Literature on Cocaine and Brugada Pattern ECG is limited to case reports:

1. Here is one case report in which the ECG looks like hyperkalemia, but the author assures me the K was only 4.5 mEq/L: Cardiac arrest from cocaine with Brugada pattern (full text)

2. Here is another full text case: Brugada Pattern ECG and cardiac arrest in cocaine toxicity: reading between the white lines.

3. Aborted Sudden Death, Transient Brugada Pattern, and Wide QRS Dysrrhythmias After Massive Cocaine Ingestion

4Hyperkalemia and cocaine induced dynamic Brugada-type electrocardiogram


Severe Acidosis may also affect the ECG, but this pattern was quite specific and unlikely to be due to acidosis alone.