Wednesday, April 16, 2014

Chest pain in a middle-aged male

A middle-aged male presented with acute onset of typical ischemic type chest pain.

Here is his initial ECG:
What do you see?

He had a previous ECG from 10 years prior:
This shows either subaute anterior MI (Q-waves, ST Elevation, T-wave inversion) or acute MI superimposed on previous MI.  LV aneurysm is possible but unlikely (no QS-waves, significant T-wave amplitude, even though largely negative).

So we know he has LAD disease and previous MI.

The acute ECG (first one at top) clearly shows the previous MI (Q-waves).  The T-waves are upright.  Is this pseudonormalization?  No.  Over weeks to months and certainly years, inverted T-waves of MI normalize as part of the natural history of the ECG in MI (Although, in LV aneurysm, they often remain with shallow invertion).  So before this acute event the T-waves were likely upright.

But these previous T-waves were not upright and hyperacute, as they are here in the top ECG: the T-waves in that first ECG are suspiciously large, and there is some hint of reciprocal ST depression in inferior leads.  These findings need aggressive investigation with frequent serial ECGs or immediate echocardiography.  They could represent LAD occlusion.

The pain continued and another ECG was recorded 1 hour later:
What is the diagnosis?

These are now subtle de Winter's hyperacute T-waves; see the subtle ST depression in V3.

These were not seen or appreciated.  The initial troponin returned at less than 0.04 ng/mL.  The patient was admitted to the hospital without angiography in spite of continued chest pain.  

A second troponin at 6 hours returned at 0.7 ng/mL (elevated).  He was diagnosed with NonSTEMI.  The pain continued.

A third ECG was recorded at 7 hours:
Now the T-waves are less acute, but there are deepening Q-waves and loss of R-wave height

The troponin I was 16 ng/mL at hour 13.  

Here is the 13 hour ECG:
T-waves are smaller yet, especially in V4

He went for cath and it showed 100% ostial LAD occlusion.  There was no mention of collateral circulation.

Echo: Anterior wall motion abnormality with EF of 35-40%, although it is unknown what the EF was before this event.  There was no myocardial wall thinning to suggest that this WMA was due to old MI, though the previous ECG is fairly conclusive about that.

Here is a post cath ECG at 26 hours:
Now there is also some inferior ST elevation with reciprocal ST depression in aVL.  This is highly suggestive of inferior MI.  The RCA was anomolous, arising from the left coronary cusp, and it is possible (though not mentioned) that it was affected during the procedure.  There is no more information on this.

Diagnosis: LAD occlusion in the context of previous MI, and manifesting subtle de Winter's T-waves. 

Here are some more examples of the wide variety of de Winter's T-waves from LAD occlusion:

Monday, April 14, 2014

Anterior STEMI?

The patient presents to the emergency Department with complaints of substernal left-sided chest pain present for 4 days but worse in the last 24 hours.

Here is his ED ECG:

The computerized QTc is 451.  What do you think?  The previous ECG, with interpretation, is below.

Here is the Previous ECG.
My reading was printed on the ECG as "probable benign T-wave inversion."    I had discharged the patient at his previous visit.  His presentation had not been concerning for ACS and his ECG was, to me, a benign variant.

The physicians were appropriately worried about the previous ECG and used the formula (see sidebar Excel applet) and came out with a value above 23.4  (I cannot remember what the value was, but they did use 3 mm for the STE variable).

When I apply the formula, even if I use 3 mm as the ST elevation as 60 ms after the J-point, and use R amplitude in V4 at 22 mm, I get 23.03 (which is less than 23.4 and thus indicates early repol).  Furthermore, the morphology of V4 is nearly diagnostic of "Benign T-wave inversion."

In general, if there is T-wave inversion, I do not recommend using the formula. Patients whose ECGs had T-wave inversion in V2-V5 were excluded from the study because T-wave inversion, as a general rule, should imply MI.  However, if you are familiar with the morphology of Benign T-wave Inversion (BTWI), then you would see that these ECGs manifest probable BTWI and be less worried about the ST Elevation.

As for the formula, when you get a value that is close to 23.4, it is wise to not rely on it too heavily.  The sensitivity and specificity of 23.4 was close to 90%, but I the closer the value is to 23.4, the less sensitive and specific it is.

Appropriately, they ordered a 2nd ED ECG about 20 minutes later:
QTc is 445

They thought there might be more STE in lead V3.  I do not see any significant change.

They were still worried, but instead of activating the cath lab, they appropriately consulted the cardiologist and together decided on an immediate formal echocardiogram.

The echo showed:

--Normal left ventricular size, mild concentric left ventricular hypertrophy and hyperdynamic systolic function.
--The estimated left ventricular ejection fraction is 75 %.
--No left ventricular wall motion abnormality identified.
--Normal right ventricular size and function.

The patient was admitted and ruled out for MI.

Benign T-wave Inversion (this link takes you to many examples)

There are many etiologies of T-wave inversion.  We are most worried about ischemic T-wave inversion.  Wellens' syndrome is particularly dangerous, as it signifies an unstable critical LAD stenosis.  I have several posts on this; here is one that shows the entire evolution.

Another etiology is "Benign T-wave Inversion", which has long been recognized. I first saw it described in Chou's textbook.  It is a normal variant associated with early repolarization.  K. Wang recently studied it.  He reviewed ECGs from all 11,424 patients who had at least one recorded during 2007 at Hennepin County Medical Center (where I work) and set aside the 101 cases of benign T-wave inversion.  97 were black.  3.7% of black men and  1% of black women had this finding.  1 of 5099 white patients had it.  Aside from an 8.8% incidence (9 of 109) black males aged 17-19, it was evenly distributed by age group.

I have reviewed these 101 ECGs, and what strikes me is:

1. There is a relatively short QT interval (QTc < 425ms)  (this case would be an exception!)
2. The leads with T-wave inversion often have very distinct J-waves.
3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves).
5. The leads with T-wave inversion (left precordial) usually have some ST elevation
6. Right precordial leads often have ST elevation typical of classic early repolarization
7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
9. II, III, and aVF also frequently have T-wave inversion. 

Friday, April 11, 2014

Unstable Angina: Dr. Braunwald asks if it is time for a Requiem

In a recent commentary, Dr. Eugene Braunwald asked if it is time for a Requiem for Unstable Angina (ACS without a positive troponin, as defined by a rise and/or fall with at least one level above the 99% reference value).

Here is a quote:

"Indeed, in its 2008–2009 report, the World Health Organization revision of the definition of MI stated: 'Many patients who in the past would have been diagnosed as having unstable angina will now be diagnosed as having had an MI.'  In the next few years, there will likely be much wider use of higher-sensitivity assays for cTn and acceptance of the universal definition of MI.  As a consequence, UA is likely to be further marginalized, its definition will become highly dependent on the particular assay for cTn used, and the term will become ever more ambiguous and cause confusion because it will mean different things to different people. Indeed, it is not clear that ACS events can occur without some increase in circulating cTn when measured by a high sensitivity assay."

This article prompted some recent Tweets about whether Unstable Angina (UA) still exists in the age of sensitive biomarkers. Don't all ACS rule in by serial trops now?

UA certainly does still exist, at least for now, because in the U.S. we do not yet have FDA approval for high sensitivity troponin (hscTnI).  And we do not yet know for certain whether hscTnI will abolish UA, or just diminish the number of patients with troponin (-) ACS.

Perhaps when we get hs troponin in the U.S. (not yet), it will be exceedingly uncommon, but with the use of contemporary troponin assays, it is an important phenomenon still.

Below are some old examples, and one new one:

Here are several previously posted cases.  

Here is another that was just posted on April 4.

Now I have yet another to post:

A patient with DM and, it seems, heavy alcohol use had also been recently admitted for chest pain: she ruled out for MI (sorry, I do not have the ECGs from that presentation), then had a positive stress test, which led to an LAD stent (thus, she had unstable angina, but that is only the first of two episodes for her).

She presented to the ED some time after the stent, complaining of fatigue and chest pain.  She had stopped taking her Clopidogrel.  She had also stopped her propranolol.  She was dehydrated and ketotic.  BP was normal and she was tachycardic.  There was a systolic murmur.

Here is her ED ECG:
There is sinus tach, perhaps due to both dehydration and possibly also to some propranolol withdrawal.  It is abnormal, but there is nothing specific for ischemia.  It certainly could represent ischemia, but no definite active ongoing ischemia.  The QT appears to be about 380 ms and thus QTc = 570ms (see leads II and III).  This QT is very long and suggests that the "T" waves in II, and III are really U-waves.  I strongly suspect hypokalemia, but (oddly) no K was measured until over 24 hours later.  

She had a stat formal echo which showed hyperdynamic heart and anterior wall motion abnormality but with EF of 85%.  There was no serious valvular disorder.

Her pain resolved.  She ruled out for MI with contemporary high sensitivity troponins.

The next morning she had a VT arrest and was resuscitated.  Here is her post resus ECG:
Large ST elevation.  It has a very odd morphology, even mimicking Brugada and Hyperkalemia, but it must be assumed to be LAD occlusion

She was taken for cath and had a 100% LAD occlusion that was stented.

She did well.


Unstable Angina still exists.  It is dangerous.  It may be missed by both ECG and (by definition) troponin.  It happened twice in this patient.  It is too early for a Requiem.

Wednesday, April 9, 2014

Chest pain in a patient with previous inferior STEMI. Scrutinize both the ECG and the history!

I was looking through a stack of ECGs (I can't help myself) and saw this one, which caught my eye:
What do you think?  Computerized QRS duration is 120 ms.

My thought was that it looked like there was likely very subtle anterior injury.  In spite of the slightly prolonged conduction, I applied the anterior STEMI calculator (see sidebar excel applet, or "subtleSTEMI" iphone app), using:

1. ST elevation at 60 ms after the J-point in lead V3: 2 mm (it is probably really 2.5 mm, but I wanted to be conservative)
2. computerized QTc = 413 ms
3. R-wave amplitude in V4 = 9 mm

Result = 23.83 (greater than 23.4 and thus indicating likely LAD occlusion)

One reader thought this was LBBB and that the modified Sgarbossa rule should apply instead.
My answer: It is not a true LBBB.  The intrinsicoid inflection in V5 and V6 is only about 30 ms and must be 50 ms to be LBBB.  That is to say, it must take a long time for the left ventricle to depolarize.  Furthermore, it just doesn't "look" like LBBB.  It is simply a slightly wide QRS.

He did come in by EMS and the prehospital ECG was identical.

Here is his previous ECG:
Note the inferior ST elevation that was present even after opening the infarct artery causing the inferior STMEI.  But also look at V1 and V2.  The ST segments and T-waves are different from the ED ECG.  Thus there is new ST elevation, suggesting anteroseptal STEMI and greatly increasing the suspicion for LAD occlusion.

So I went to look at the chart:

He was a male in his 60s who complained of chest pain.  He had h/o inferior STEMI which was stented.

As I suspected, these ST and T-wave changes were not seen.  Most physicians do not see such abnormalities, even if they are changes, as in this case.  They are extremely subtle.  That is why I recommend scrutinizing them, comparing carefully with the previous ECG, and using the formula to see if your suspicions are worth pursuing.

A positive result with such scrutiny does NOT mandate cath lab activation, but does require further intense scrutiny.

One area of further scrutiny is to look at the previous cath findings:  was there LAD or left main disease?  Is LAD ischemia a real possibility?  If they had looked, they would have found that the left main had a 50% lesion and the LAD had a 90% distal stenosis.  The distal stenosis does not fit with this ECG which looks like septal STEMI, but the left main does.

This patient was treated for unstable angina medically.  His initial troponin was negative.

However, he did not get evaluated for possible acute LAD occlusion.


Later, his next troponin 3 hours later was 1.3 ng/mL.  At this time, he underwent another ECG, five hours after the first:
The ST elevation is resolved.  This again strongly supports that the first one had acute ischemia causing ST elevation

The next day he went for an angiogram and was found to have severe 3 vessel disease involving the left main and the LAD.  The LAD had a new, open, 80% ostial lesion.  The left main had a new 60-70% stenosis.  I am not sure which (or both?) was the culprit, but either could have resulted in death.

It is all but certain that one of them was occluded, or nearly so, when the patient was having chest pain and ST elevation.

Fortunately for all involved, this LAD (or left main) reperfused spontaneously, with the aid of aspirin, plavix, and heparin.  Had it not done so, it could have been disastrous for the patient.

He went for CABG.


Scrutinize the ECG
Scrutinize the History

These findings are discoverable: I found them by just glancing at the ECG in a random stack, without any other information.  They are there on the ECG.  You just have to get good at looking for them, use the formula, compare with the previous, and look at the previous angiogram results.  If suspicion persists, pursue even further scrutiny.

Tuesday, April 8, 2014

Waxing and Waning Chest Pain

A male in his 50s presented with Chest pain on and off during the day.  At the time of presentation, he had only some jaw pain.  An ECG was recorded:
What do you think?

There are inferior and lateral T-wave inversions (reperfusion T-waves, analogous to Wellens' waves which were described in the LAD distribution, V2-V4, but this also applies also to other coronary distributions).  There is also ST depression in V2 and V3: this is of course really ST elevation of the posterior wall, as recorded from the anterior wall.  

T-waves are upright in V2 and V3 because, just like the inferior and lateral walls, the posterior wall is also reperfused.  If we had posterior leads, it would show posterior T-wave inversion.  Instead, we have anterior lead recordings, which superimpose a positive anterior T-wave with the opposite (because recorded from the opposing anterior chest) of a negative posterior T-wave (reperfusion of the posterior wall).  Thus, we have the oppositve of a negative, which is positive; this positive is added to the anterior positive, which is two positives, and so the T-wave is upright with some added voltage.

This had me very worried, so even though the patient had no new symptoms, within 15 minutes I recorded another ECG to be certain that the artery was not re-occluding.  Here it is:
What do you think?

Now the T-waves are upright in inferior and lateral leads (pseudonormalization), indicating re-occlusion of the infarct-related artery.   There is new minimal ST elevation in II, III, aVF and reciprocal ST depression in aVL.  This is diagnostic of inferior MI (though technically not a "STEMI" because it does not meet the artibrary "criteria" for STEMI which we know are useless numerical cutoffs.

This is another NonSTEMI that needs the cath lab now, as the ECG shows signs of coronary occlusion even without 1 mm of ST elevation.

The T-waves in V2 and V3 are still upright. The predominant forces are still from the anterior wall, which is closest to the overlying leads, so any small amount of posterior positivity (which would result in a negative T-wave as recorded anteriorly) is overwhelmed by the anterior wall positive T-waves.

I activated the cath lab immediately.

Shortly thereafter, the patient reported no pain at all, including absence of neck pain.  We recorded this ECG:
Now the T-waves are inverted again, the ST segments have all but normalized, and the precordial T-waves are much larger becuase of the addition of anterior wall positive T-waves to the negative of posterior negative T-waves (see explanation above).


On arrival in the cath lab he was pain free.  The angiogram showed an ulcerated thrombotic plaque in the distal RCA with good flow, plus a very tight lesion in a right posterolateral branch to the posterior and lateral walls.

Diagnosis: Infero-postero-lateral MI due to dynamic ACS of the RCA.

Peak troponin I was 1 ng/mL.  

Standard management in these cases is to admit the patient on medical management for ACS: aspirin, heparin or LMWH, P2Y12 inhibitor.  If the patient rules in, then he/she goes to the cath lab the next day.  But this is not adequate for a significant percentage of NonSTEMI patients; namely, those who have evidence of coronary occlusion or an artery that is opening and closing.  There are no randomized trials of this management strategy, but there are several studies showing that when NonSTEMI patients do get their next day cath after a rule in by troponins, the infarct related artery is closed about 25-30% of the time.  These patients have higher biomarkers, worse LV function, and higher mortaility than patients whose artery is open.

1. Wang T et al.  Am Heart J 2009;157(4):716-23.
2. From AM, et al. Am J Cardiol 2010;106(8):1081-5.
3. Pride YB et al.  JACC: Cardiovasc Interventions 2010; 3(8):806-11.


1. Wellens' syndrome has analogous findings in the inferior and/or lateral walls.
2. T-wave changes of the posterior wall record in the opposite direction from the anterior wall.
3. Reperfusion T-waves indicate a very unstable plaque that can instantly re-occlude at any moment. The re-occlusion is signaled by a "pseudonormalization" of T-waves.  
4. Many coronary occlusions do not have 1 mm of ST segment elevation
5. Many NonSTEMIs need the cath lab now.

Sunday, April 6, 2014

Prehospital Inferior STEMI: Bedside Echo in ED is normal

A woman in her 60's complained of chest pain.  911 was called.  She had this prehospital ECG:
Obvious Infero-posterior and lateral STEMI

The cath lab was activated.

While waiting for the cath team to be ready, I recorded this bedside echo:

This shows excellent wall motion everywhere.  I was amazed and realized that she must have had spontaneous reperfusion.  (I cannot say for certain that a high quality echo with contrast would have been normal)

So I recorded an ED ECG:
This is near normal, except for the abnormal T-waves (down up in aVL, and note the abnormal T-wave in V2).

Here is an enlargement of V1-V3:

Note the morphology of V2, because this is a one of the typical morphologies seen early after reperfusion of the posterior wall. As time goes on, the T-wave will become fully upright and taller then normal, unless there is re-occlusion

So this patient had spontaneous reperfusion.  She went to the cath lab and by the time she arrived, the RCA was again 100% occluded.  There was ruptured plaque and thrombus.  It was opened rapidly.

Peak troponin I was 0.60 ng/ml.  Formal echo was normal except for a probable anterior wall motion abnormality, only seen on one view, and possibly pre-existing.  EF 66%.

Here was the post cath ECG:
Note the tall T-wave in V3.  This is tall because the an opposite view of an inverted posterior T-wave (which is positive) is superimposed on a normal upright anterior wall T-wave.  I call this "posterior reperfusion T-waves."  There is a Q-wave in V2 which would correlate with the echo finding.


1. Spontaneous reperfusion normalizes BOTH the ECG and the echocardiogram.  Only if there is persistent myocardial stunning from ischemia (which usually is present with prolonged severe ischemia) is wall motion persistently affected.  If we had done an echo during the ST elevation, there would have been a wall motion abnormality, but it disappeared with reperfusion.
2.  Learn this reperfusion morphology in lead V2 from reperfused posterior STEMI. It is important in recognizing ACS if you do not have a recording during pain.
3. Down-up T-waves (e.g., aVL here) is almost always a reperfusion morphology (alternatively, it can be a U-wave masquerading as a T-wave)

Friday, April 4, 2014

A Very Unstable Angina. No STEMI present, but needs the cath lab now.

An elderly woman with h/o diabetes and hypertension but no prior cardiac history had been having exertional chest pain for months, though with a normal stress test.  She had onset at rest of severe substernal chest pressure radiating to the neck.   There was associated SOB and diaphoresis. EMS came and recorded this ECG:

What is it?  See annotated ECG below.

I have put arrows where I think the P-waves are.  They march out regularly, but are non-conducting.  This is complete, 3rd degree, AV block.  The escape is regular at a rate of about 36 and looks like a right bundle branch block and left anterior fascicular block, which means that the escape originates from the posterior fascicle.  (Another possibility would be junctional escape with RBBB/LAFB, but this should be faster).  There are no clear ischemic ST segments or T-waves, though the expected discordant ST depression in V2 is not there, and there is a hint of upwardly sloping ST elevation in V1.

She received nitroglycerin and aspirin and her pain very much improved. She arrived in the ED with a pulse of 81 and very elevated BP at 200/90.

This ECG was recorded:
Now there is sinus rhythm with LBBB.  The only hint of ischemia are concordant T-waves in V5 and V6 (these were quite specific for MI - but not STEMI - in Sgarbossa's study).  This ECG also confirms that the previous escape was NOT junctional because nodal escape would also have associated LBBB.

The transcutaneous pacer was placed, she was given clopidogrel and heparin, and the cath lab was activated.  Electrolytes and CBC were normal.  A formal echo was done which showed an anterior and apical wall motion abnormality consistent with LAD ischemia.  The EF was about 40%.

She became bradycardic again and this was recorded:
The first half of the ECG has second degree block Mobitz II (by ECG alone, this could be Mobitz I; but in this clinical context, with previous complete AV block, it must be Mobitz II), then changing to normal rhythm with every P-wave conducted.  All conducted beats have LBBB morphology and there is no clear evidence of ischemia.

Here is a third ED ECG:
There is 2:1 AVblock for 3 beats, with every 2nd P-wave conducting to LBBB.  Then there are 3 P-waves that do not conduct, followed by an RBBB escape (just like on the prehospital ECG).  Then 2:1 block resumes.

The patient went to cath and had severe 3 vessel disease.  She ruled out for MI!!  Maximum troponin I was 0.016 ng/mL (99% reference = 0.030 ng/mL.

She had a pacer placed and went for CABG, successful.  Here is her paced ECG after surgery:
Paced rhythm with no evidence of ischemia

Later, she was in sinus rhythm:
Sinus with LBBB, again, no ischemia.


1. Ischemia can be severe enough to result in low EF, wall motion abnormality, and heart block, but with negative troponins.
2. There are other indications for the cath lab than ST segment or T-wave abnormalities.  These include hemodynamic instability, heart failure, dysrhythmias, heart block, and ischemic chest pain that cannot be controlled by medical means.

Wednesday, April 2, 2014

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:


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.


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


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.

Sunday, March 30, 2014

New ACC poster: many STEMI patients present with subtle ST elevation.

New ACC poster: many STEMI patients present with subtle ST elevation. Their prognosis is similar to those who meet STEMI "criteria". They need early reperfusion.

However, this study could have missed many occlusions because they only studied patients who did get immediate primary PCI.  They did not study the NonSTEMI patients who were later found to have limited coronary flow and might have benefited from immediate reperfusion.

The ECG told the whole story, but no one listened: ECG interpretation skills are critical to patient outcomes.


This was sent by a medical student somewhere in the world who will remain anonymous.  Details are scant so that it cannot be recognized.

The minute this medical student saw the first ECG, he knew the diagnosis without any further information.  Reading ECGs is hard, but can be done with commitment to learning, which comes from an awareness of its importance.  My most talented blog readers are paramedics because they have to put themselves on the line every time they activate the cath lab.  And they teach me a lot.  One of my most talented readers is a health care assistant (a nursing assistant) who has taken a keen interest in ECGs.  He can beat nearly anyone.  So you don't have to be highly trained.  You don't have to be a genius. You need to be interested and understand the value of the ECG.   It is not the ECG which is nonspecific, it is the interpreter.


A female in her 60s presented with 3 days of nausea, vomiting, and diarrhea, and not feeling well.  She complained of jaw pain and shortness of breath.  There was a 30 second episode of syncope, and another one the previous evening, without any tonic clonic movements, tongue-biting, or incontinence. She was ill appearing.  She had a remote history of lung cancer many years ago, cured.  She had no other medical  history.

She had this ECG recorded:
ECG 1: QTc is 484.  What do you think, especially compared to the previous, pasted below?

Previous ECG. completely normal

The diagnostic features of the first ECG were entirely missed by a whole team of emergency physicians, cardiologist, surgeons and others, even as the patient became increasingly hypotensive to a systolic BP of 60.  The lactate was elevated and pH low.  They were worried that the syncope was seizure and that she had brain mets.  Then they were worried about sepsis as an etiology of hypotension.  Then the notes mention "cardiogenic shock" but without any reference to a cardiac echo or to a chest x-ray.  Was there pulmonary edema?  Not mentioned in physicians'  notes.  Then she had some RUQ tenderness which led to a long process of evaluation for an abdominal source of sepsis, which turned up negative.  Initially fluids were given, then stopped in favor of pressors, as a CVP line showed CVP = elevated.

Another ECG was recorded:
ECG 2: Findings are still present and have evolved to a small degree

At time 6 hours, Troponin T returns at between 0.50 and 1.00 ng/mL (not giving exact number, but significantly high)

Now having frequent PVCs.

Now chest pain free.  Cardiologist note says: "Elevated troponin explained by type II MI due to her shock."  "Repeat ECG showing no STEMI, only non-specific ST-segment and T-wave abnormalities, unchanged from prior"

Transferred to surgery for exploration but diagnostic studies were too indeterminate to be certain of intra-abdominal pathology.  Besides, the surgeons say she is "too unstable for surgery."

Day 2:

A cardiac echo was done which showed normal LV function but moderate RV systolic dysfunction and diastolic septal flattening consistent with right ventricular volume overloadRight ventricle: moderately enlarged, hypocontractile free wall, moderate global decrease function.

Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI.

Still the pieces were not put together.

Another ECG is recorded:

ECG 3: More evolution, but not recognized.

I have only shown you 3 of the many ECGs recorded over the 3 days, all of which were diagnostic but not diagnosed.

After midnight (now day 3), she complains of shoulder pain and dyspnea.  Troponin was repeated and returned higher still.

She was taken to the cath lab.

What was the diagnosis?  See below.

Outcome and Analysis:

ECG 1 is diagnostic of inferior and right ventricular MI.  There is a junctional bradycardia.  There is less than 1 mm of STE in inferior leads with diagnostic reciprocal ST depression in aVL.  Additionally, there is ST elevation in V1 which, in the presence of inferior MI is diagnostic of Right ventricular MI.  This is the etiology of the syncope and hypotension and shock and elevated CVP. and right ventricular echo findings..  Furthermore, there are T-wave changes in V2 and V3 which are highly suggestive of ischemia, but difficult to localize: anterior? posterior? right ventricular?  In any case, these further support the diagnosis of coronary occlusion or near occlusion.  ECG 2 is similar, also with a junctional rhythm that is resulting in inverted P-waves in inferior leads (retrograde).  ECG 3 is yet more evolved.

When they finally did it, the cath showed a 100% RCA thrombotic occlusion at the ostium (proximal, before the RV marginal branch), confirming all clinical and ECG findings (except for diarrhea).  There was also disease of the LAD and Left circ.

She turned out to not have any abdominal pathology.
All cultures were negative.
There were multiple complications.

This was an inferior and right ventricular MI and once the first ECG was recorded, the diagnosis could have been made: everything about the presentation, after the ECG, screamed this diagnosis.


I cannot read the minds of the physicians involved, but I suspect there were two components to the delayed diagnosis:

1. Atypical presentation (nausea, vomting, and diarrhea)
2. Failure to regognize subtle but diagnostic features of the ECG.

Many say generally that the ECG is often a "non-diagnostic" test, or a nonspecific test.  Most often, it is the interpreter who is nondiagnostic and nonspecific.  The ECG here told the whole story, very specifically.  It was the failure of accurate interpretation which led to a 2 day delay in diagnosis and significicant myocardial loss and much unnecessary diagnostic and therapeutic intervention.

The ECG told the whole story, but no one listened.

Friday, March 28, 2014

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

A male in his 60s presented complaining of dysnpea and chest pain.  He was tachypneic and ill appearing.

I was texted this ECG.  The physician worried about PE mostly, but also MI:
My response was: "incomplete RBBB.  No evidence of acute MI.  Certainly could be PE.  What does the cardiac echo show?"

The bedside echocardiogram showed a serpiginous echogenic structure in the right atrium that was also flowing in and out of the right ventricle.  The RV was enlarged.

I am sorry that I had to take this video down because my colleague wants to submit it to an academic journal.  I have left the still frame in.

Still frame of the video: Blue circle show thrombus snaking throughout right atrium and right ventricle.

The patient was given IV tPA and rapidly improved.  A subsequent ultrasound showed no more thrombus.

Thursday, March 27, 2014

COPD exacerbation, what do the ECG and bedside echo show?

A woman in her 60s presented with a COPD exacerbation.  She also complained of some sharp chest pain with coughing. She was in moderate distress consistent with a moderate COPD exacerbation.  An ECG was recorded:

The computer reading was: "Anterior ST elevation due to early repolarization."

The treating physicians were alarmed by the first ECG due to the apparent hyperacute T-wave in V3.  They applied the LAD occlusion vs. early repol formula (see sidebar for excel applet and see previous posts), using computerized QTc of 416, STE60V3 of 3.0 (it may be 3.5) and R amplitude in V4 of 13, and found a value of 23.9 which is greater than 23.4 and indicates LAD occlusion.

So they sought out a previous ECG:

Here is one from 2 weeks prior:
What do you think?

Now they were even more worried, as the acute ECG is much different.  However, this patient did not have chest pain that was in any way typical.  They were appropriately reluctant to activate the cath lab, but did call the cardiologist, who was also appropriately worried.

A bedside ED cardiac echo was done during the evaluation:

The embed code has stopped working consistently.  You can see the video by clicking here:

First bedside ultrasound, subcostal view from Stephen Smith on Vimeo.

Here is an annotated still picture of one frame from above:
The blue arrow points toward the tricuspic valve and the base of the RV.  The red arrow points toward the mitral valve and the base of the LV

Second ultrasound, apical view from Stephen Smith on Vimeo.

What do these cardiac echo clips show?

First video clip: This clearly shows the bases of both the right and left ventricles are beating vigorously, but the apex is hardly moving at all.

Second clip: It is easy to see the base of the heart contracting, but although the image quality of the apex is poor, one does not see much motion there

At this point, the patient started having crushing chest pain and another ECG was recorded:
Now there is increased ST elevation in V3. See outcome below.

A formal ultrasound with Definity contrast was being done at approximately the same time as the onset of severe chest pain.  It showed:

--Regional wall motion abnormality-distal septum anterior and apex akinetic, large.
--Regional wall motion abnormality-distal inferior wall akinetic.
--Regional wall motion abnormality-lateral akinetic.
--There good contractility of the base of the heart.

--Normal left ventricular size.

--Decreased right ventricular systolic performance severe.
--Regional wall motion abnormality-right ventricle .


This ultrasound and the bedside ultrasounds show "apical ballooning", all highly suggestive of Takotsubo stress cardiomyopathy (which is likely to accompany a stressful event such as a COPD exacerbation), but it is also compatible with acute LAD occlusion.  The crushing chest pain, wall motion abnormalities, hyperacute T-waves and ST elevation were possibly due to takotsubo stress cardiomyopathy but also possibly due to LAD occlusion.  The patient was taken to the cath lab and had no obstructive LAD lesion and no culprit.  The troponin I peaked around 1.5 ng/ml.

Can one distinguish on the ECG between takotsubo stress cardiomyopathy (SCM) and acute STEMI???  Not reliably!  There are some ECGs that are clearly due to stress cardiomyopathy (widespread T-wave inversion).  But when the ECG is recorded during the ST elevation phase, I know of no reliable way to differentiate these.  I reviewed this topic in this post.  To sum it up very briefly, if it appears to be an infero-antero-lateral STEMI, it is more likely to be SCM than if the ST elevation is in one coronary distribution (e.g., anterior, as in this case); however, again, this is not more than 80% reliable.  The cellular pathophysiology of SCM is identical to STEMI (severe transmural ischemia), but it is due to catecholamine stress and small vessel constriction (NOT due to epicardial coronary flow obstruction); and that is why the ECG is nearly identical.

Here are several more cases of SCM.

Does cardiac ultrasound definitively differentiate the two entities?  In the acute phase, apical ballooning is highly suspicious for SCM, but large wall motion abnormalities may also be seen in patients with proximal LAD occlusion in a type III (wraparound) vessel, affecting anterior, lateral, and inferior walls.  These STEMI cases also have widespread ST elevation as in SCM.

Is the Right Ventricle involved in Takotsubo Stress Cardiomyopathy?

RV SCM has been described, appears to accompany LV takotsubo cardiomyopathy up to 25% of the time and be associated with worse LV function.   See this article: and also this article:


There is no more vexing ECG mimic of acute STEMI than SCM because the underlying cellular pathophysiology is the same.  It is unusual to make the diagnosis without an angiogram.