Sudden Cardiogenic Shock

An elderly woman presented with rather sudden altered mental status, hypoxia, and hypotension.  She had no significant past medical history except for cognitive decline.  She was cool and mottled with thready pulses.  BP was 54/32.  No murmurs were heard.  Tissue perfusion monitor recorded 33% (very low) [see this explanation of StO2 by our new chief and prolific researcher, Jim Miner]

She was immediately intubated by blind nasotracheal technique (very fast, no complications).

Immediate ultrasound showed good sliding signs and B-lines (a sign of pulmonary edema) only on the right.

Here was her initial cardiac ultrasound, parasternal short axis:

This shows decreased LV function, but only moderate, not clearly bad enough to account for severe shock.  There seems to be an anterior wall motion abnormality.  What else is there?  Look at the density moving in the LV.  See below for further interpretation.

Here is a parasternal long axis view:

Again, there is moderately decreased LV function.  The base of the heart appears to be contracting well.  What else do you see?  (It is pointed out in the still picture with arrow below)

This is a flopping papillary muscle.  The first ultrasound (short axis) also shows this flopping.

Here is the inferior vena cava (IVC):

The echogenicity of the blood in the IVC is a sign of profound stasis.  You can see the blood moving not forward, but both forward and backward.  Thus, there are very high right sided pressures.

So there is right sided failure.
What is the etiology?  The most common etiology of acutely elevated right sided pressures is left sided failure.  Of course pulmonary embolism is a relatively common cause as well.  Right sided MI can give high right sided pressures with low pulmonary artery pressures.

B-lines suggest pulmonary edema and suggest left sided failure, not right side only failure.

How about the ECG? (this is an ECG blog, after all!):

This shows acute on old, or subacute (more likely) inferior MI.  There are Q-waves, minimal ST elevation with reciprocal ST depression in aVL.  There is also evidence of diffuse subenocardial ischemia with ST depression in V4-V6.

 A right-sided ECG was recorded:

No evidence of RV MI

A chest X-ray was done:

This shows a very significant finding which I had never known about before: right side pulmonary edema, which correlates with the right sided B-lines on pulmonary ultrasound.  The radiology boards use this image for one particular diagnosis.

Initial troponin I was 13 ng/mL.  K was 7.0. HyperK was treated but with no clinical improvement of the patient.  Lactate was 17 mEq/L.  She was started on Norepinephrine and the tissue perfusion (StO2 monitor) rose to 58%.  (significantly better, but still below the goal of 75%).  BP was 89/72.

Let's put this all together:
1. Sudden decompensation into shock
2. Pulmonary Edema on the right
3. LV function not so bad that she should necessarily be in cardiogenic shock
4. Subacute inferior MI, probably was a STEMI at onset
5. Very high right sided pressures


What is it?

Echo: this shows a loose papillary muscle
CXR: right upper lobe pulmonary edema is highly suggestive of severe mitral regurgitation.  It just so happens that when there is severe mitral regurg, the jet is directed exactly at the pulmonary veins that drain the right upper lobe!  Thus, it causes worse pulmonary edema in the right upper lobe than elsewhere.  The radiologist noted this finding.
ECG: Papillary muscle rupture is most commonly associated with posterior MI, which is very closely associated with inferior MI.

Outcome:

A formal echo was immediately done and confirmed papillary muscle rupture with severe mitral regurgitation.

Here is the report:
--Partial rupture of the posterolateral papillary muscle with chordae to the anterior mitral valve leaflet with resultant partial flail and eccentric moderately severe mitral regurgitation.
--Decreased LV systolic performance severe.  Estimated left ventricular ejection fraction is 27%.  The LV function may be worse because of the pressors.
--Regional wall motion abnormality-inferoposterior, akinetic.
--Regional wall motion abnormality-distal septum, apex and anterolateral, akinetic.

Getting this diagnosis right is critical not just to surgical therapy, but to medical as well: severe mitral regurgitation is treated with afterload reduction such as nitroprusside, to promote forward flow of blood.  This is just the opposite of using pressors!

The patient's wishes were to not have aggressive intervention and she was made comfort cares only.


Comment:

This is an incredibly hard diagnosis to make without doppler ultrasound.  One MUST keep it in mind in any kind of shock.  Even shock in trauma can be due to valvular disruption.  When I question providers about etiologies of cardiogenic shock, they almost NEVER mention valvular disorders.

Always keep valvular disorders in mind with cardiogenic shock!

Incredible Case Demonstrating the Value of Frequent Serial ECGs

This case is presented and written by Vince DiGiulio, (EMT-Critical Care and emergency department tech).  As his title shows, he is a tech.  Not a paramedic.  Not a nurse.  Not a doctor.  He is a wizard at reading ECGs and is entirely self-taught.  He was the ECG tech on this case, and his skills mean that he recognized the pathology on the ECG and could stand there and keep recording them.

A 75 year old female presents with a chief complaint of “reflux.” 

Starting about five days ago, a couple of times each day she has experienced a burning sensation behind the lower third of her sternum that is relieved within 10-15 minutes of taking an over-the-counter antacid. She has been diagnosed with GERD in the past and always carries a roll of calcium-carbonate chewables in her purse.

Today she woke with the same pain, but this time it lasted at least an hour before subsiding. A couple of hours later the pain returned, and when it had not diminished after another hour she decided to come to the ED.

The following ECG is captured on arrival, approximately 90 minutes after onset of the latest episode of pain. The pain has been constant and she rates it as a 4/10.

Is this ECG diagnostic of any abnormality? A previous EKG will be available but it will take a few minutes to pull up.

There is a poor R-wave progression across the precordials (transition is between V4 and V5); subtle ST-elevation in V2-V4, I, and aVL; and reciprocal ST-depression in II, III, and aVF. Additionally, using the BER vs. anterior STEMI calculator on the right side of this page, the equation value of this tracing is 25.4, greater than 23.4 (using measurements of 2.7 mm, 400 ms, and 4.4 mm, respectively). This tracing is diagnostic of anterior subepicardial ischemia, almost always due to LAD occlusion.

As the tech running this EKG, at this point I recognized our patient was almost certainly experiencing a STEMI but knew I would have a tough time convincing our emergency physician, let alone the cardiologist. So, wanting to be sure I was getting the best data possible and not seeing a falsely poor R-wave progression due to incorrect precordial electrode placement, I double checked my stickers (that were all fine) and ran a second ECG exactly 90 seconds later…

After only 90 seconds the anterior STEMI is now obvious, enough so that it even triggers the machine’s ***ACUTE MI*** alert.

That’s all it took, 90 seconds, with absolutely no change in patient symptoms or condition, and now we have a clearly diagnostic tracing. At this point the cath lab was activated and we finally had time to pull up the patient’s old ECG.


Here is the patient's basline ECG:

Normal

While preparing the patient for transfer, I kept the patient wired and shot the following tracings:

Only 4 minutes after the first ECG and the ST-elevation keeps growing. Her heart rate has also increased, probably because around this time the doctor was giving the, “I’m concerned about your heart” speech all emergency care providers know so well. 

We’re now 8 minutes after ECG 01 and the ST-elevation in V3 is almost taller than the R-wave.

Watch what happens after Nitroglycerin:

Only minutes after the first SL nitro tablet (0.4 mg) and suddenly the ST/T abnormalities have almost entirely resolved (though the patient is still experiencing the same symptoms). Compared to ECG 01, her anterior T-waves are much more normal in size. The only hints of ischemia are the reciprocal ST- depression in the inferior leads (probably most obvious in aVF) and the upright T-wave in V1, new from her old ECG but very non-specific outside of this scenario. Her equation value is now 23.3, less than 23.4 (using measurements of 1.0 mm, 403 ms, and 5.0 mm).  

Then the T-waves enlarge again!

This ECG is very similar to ECG 05, but worryingly her anterior T-waves have increased in size again. The patient is still symptomatic, although less so, and there are still the same subtle signs of ischemia present as in ECG 05. Of note, her rate has also slowed significantly secondary to 5mg of metoprolol. Her equation value is now 23.8, greater than 23.4 (using measurements of 1.4 mm, 401 ms, and 4.7 mm).

Then after another Nitro:

This tracing is following the second dose of nitro with nearly complete resolution of the patient’s symptoms. Compared to ECG 06, her T-waves have decreased in size again and there seems to be less ST- depression evident in the inferior leads. Even V1 is starting to invert as a return to the patient’s baseline. Outside of the setting of the prior ECG’s, this tracing would be perfectly normal, though there is still some clockwise-rotation of the Z-axis. 

Outcome:

The patient was quickly transferred to the cath lab where a culprit lesion of a large obtuse-marginal artery (surprisingly, it was not LAD, though it would be useful to know more specifics about the coronary anatomy and culprit lesions) was successfully stented with a good outcome. Multi-vessel CAD was also noted, with plans made for CABG sometime after discharge from this hospitalization. After departing the ED, her first troponin-I, drawn eight minutes in at the time of ECG 04, came back at 0.49 ng/mL (ref  is less than 0.04 ng/mL)


There are several important take-home points from this case.

First, the ECG 01 was diagnostic of anterior STEMI right from the start. While there might be a couple of true STEMI mimics that can create this picture (stress cardiomyopathy is the best candidate), in the patient presenting with chest pain, this ECG is their ticket to the cath lab.

Second, acute coronary syndrome and myocardial infarction are incredibly dynamic processes, with vessels occluding, de-occluding, and spasming on a sometimes rapid basis. In this case it took only 90 seconds, with no change in patient symptoms, for her ECG abnormalities to progress from very subtle to markedly  abnormal. Don’t be afraid of serial ECG’s, even if the patient’s symptoms are constant.

Related to that, and this is especially directed towards prehospital providers, don’t ever give nitro without first running a 12-lead. It only took one SL nitro for this patient’s ECG to go from an obvious anterior STEMI in ECG 04 to completely non-diagnostic in ECG 05. If you only had the latter ECG to go on, you would never know that this patient was actually experiencing a true anterior MI. It might not happen too often (see this case: http://hqmeded-ecg.blogspot.com/2011/07/wait-until-after-ecg-to-
give.html), but it’s vitally important information.

Finally, one of the nurses working on this case was shocked when I showed her the rapid changes in the patient’s ST-elevation after the patient had been transferred. She had been closely following the rhythm strip on the three-electrode, three-lead cardiac monitor, and had noticed absolutely no changes or even abnormalities aside from a small amount of ST-depression. This is because she was monitoring lead II, which, if you look back, was equally unimpressive across every ECG I shot. You cannot monitor just a single lead in ACS patients, especially when anterior MI is a concern. These patients need, at the very least, five-electrode cables capable of monitoring the augmented leads along with a chosen precordial lead, if not continuous 12-lead monitoring. As this case demonstrates, the ECG’s of ACS patients can change too rapidly, independent of patient symptoms, to warrant anything less.

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:

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:

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. 

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).

http://circ.ahajournals.org.ezp2.lib.umn.edu/content/127/24/2452.full.pdf+html

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.

Lesson:

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.

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.

Outcome:

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.

Lesson:

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.

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.

Lessons:

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.

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.

 Lessons:

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)

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.

Lessons:

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.

A Non STEMI that needs the cath lab now.

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

Diagnosis? 

He had an immediate ED ECG:

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

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

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

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

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

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

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

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

Then the patient complained of increasing pain again:

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

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

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

Amazingly, the bedside echo showed very good LV function.

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

Outcome:

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

Both!

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

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