LVH with anterior ST Elevation. When is it anterior STEMI?

This is another great case and discussion was contributed by Brooks Walsh, with some additions by Smith.   

Here we discuss the differentiation of true positive from false positive ST elevation in the setting of LVH.

What do you think of this ECG in a patient with chest pain?

There is ST elevation, but also high voltage (though the high voltage is NOT in the leads with worrisome STE, rather, it is in aVL).  Is the ST elevation due to LVH?

Case history

A middle-aged woman with a history of HTN, but no prior CAD, presented to the ED with chest pain. The pain had been mild and intermittent for 2 weeks, but had become more intense on the night of presentation. Her vitals signs were remarkable for marked hypertension.  An ECG was obtained at triage: 

ECG #1 at 0000 hours.

If you ignore the baseline wander, there is non-significant STE in V1 and V2. The QRS in aVL varies in height, but one complex has an R-wave amplitude greater than 11 mm, which is very specific for LVH. The ST depression in V6, and T wave flattening/inversion in V6 and aVL, also support LVH

The ECG was repeated to get a clearer tracing and because her pain increased to 10/10 at that moment. 

ECG #2 at 0004 hours (this is the one at the top of the post).

Only 4 minutes after ECG #1, there is greater STE in V1-V3, although it is concave-upwards. The T-waves in those leads have also significantly increased. There is ST depression in leads I, II, and aVL. The computer  displayed an *** ACUTE AMI SUSPECTED*** alert.
However, computers are often fooled by LVH.  
The criteria of Armstrong et al. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH.  This is the same number used for the modified Sgarbossa criteria for LBBB.  But here the ratio is only 14% - 18%, so those criteria would say that this is not LAD occlusion.

 

The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic."

In spite of those worries, she activated the cath lab.

A bedside echo was performed:


There is LVH, but also a septal wall motion abnormality.
 No prior echocardiogram was available for comparison.


The ECG was repeated when the patient reported her pain had decreased.

ECG #3 at 0018 hours.

Similar to ECG #1, there is non-significant STE in V1- V2, and R in aVL greater than 11 mm. Also note the prolonged R-wave peak time in V5, V6, and the ST depression in lead I, and small amount of T-wave inversion in aVL. All these factors, again, support an ECG diagnosis of LVH

The patient was nonetheless taken for emergency angiography, and a 99% mid-LAD lesion was found and stented.

ECG #4, 24 hours later

Anterior T-wave inversion, indicating reperfusion. Interestingly, few signs of LVH at this point.

Can you diagnose an ACO (STEMI) when you also have LVH?

LVH can mimic an acute anterior coronary occlusion (ACO) on the ECG.1 Emergency physicians and cardiologists can have difficulty distinguishing these,4 and LVH is often cited as a cause of “false-positive” emergent angiography for ACO.5,6

A number of approaches have been suggested to differentiate the ECG of chronic LVH from that of a patient with a superimposed ACO, but none of them have proven satisfactory. For example, the ECG can be compared with older tracings. However, the ST segments in patients with LVH may show significant variation over time in the absence of ischemia.3 Some have also suggested that the typically asymmetric T wave inversion (TWI) of LVH might be distinguished from the typically symmetric TWI of cardiac ischemia. However, no evidence is cited to support this.3

Is the STE concave or convex?

LVH usually has concave-upwards ST segments, but conVEX-upwards can also be seen, e.g. in these cases from Dr Smith’s book: The ECG in Acute MI:

Case 22-1. Chest pain in known LVH, negative troponins and stress test, no wall motion abnormality.

Case 22-4. Received fibrinolytics twice, but negative troponins both times. Echo showed LVH only, no wall motion abnormality.
Note also that the T-waves are not tall!

Conversely, an ACO of the LAD will usually produce STE in the anterior leads with convex-upwards ST segments. Smith, however, showed that many ACOs of the LAD (without LVH) had conCAVE-upwards morphology on the initial ECG.8 (This was likely a function of time: patients with a shorter time between symptom onset and ECG were less likely to show convexity.)

An example of acute LAD occlusion with upwardly concave ST segments in every lead of V2-V6:

Note again that the T-waves are not tall

Is there a “Smith-modified-Sgarbossa” rule for ST elevation in LVH?

Similar to the anterior STE seen with LBBB, the degree of STE in leads V1-V3 of patients with LVH is generally proportional to the depth of the proceeding S wave. In the case of LBBB, it has been shown that STE that exceeds 25% of the proceeding S-wave depth is disproportionately high, and identifies ACO with excellent specificity.9 Could this also work in LVH?

One retrospective analysis by Armstrong et al. suggested that, with LVH, STE in V1-V3 that exceeds 25% of the preceding QRS complex could be an accurate means for ruling out ACO, and fairly sensitive for identifying ACO. 

Smith comment: The Armstrong paper did not have appropriate methods to study this.  The appropriate methods would be to take consecutive ECGs with high voltage and ST elevation in the leads with ST elevation, separate them into those with and without LAD occlusion, and see what are the differences in ST/S ratio.  I have inserted at the bottom of this post some examples from Armstrong's paper.  You will see that they are not cases that you would have difficulty with.  I have tried to study this topic twice and failed because there are very few cases of high voltage in V1-V4 and LAD occlusion.   In fact, even this case does not fit, as the voltage in the affected leads does not meet LVH criteria!

Most importantly, since STE in LVH rarely exceeds 4 mm in height, the 25% criterion is likely far too insensitive. For example, in a patient with an S-wave 30 mm in depth, the STE would have to exceed almost 7 mm.  

In our case, Lead V3 in ECG #2 shows STE/QRS = 3-4/22-24 for a maximum ratio of 17%, far short of the 25% criterion.  Yet the LAD was occluded, or nearly so, at this time.

Use the T wave, not the ST segment?

It is unclear if ischemia modifies T wave height or morphology in LVH.3 In our case, the dynamic rise and fall of the anterior T waves is striking, suggesting hyperacute T waves.10

See all three compared.  The middle one is during LAD occlusion.

However, it has been difficult to define hyperacute T-waves in patients with normal baseline ECGs, let alone those with LVH.  Unfortunately, while some authors have suggested that certain criteria (T-wave amplitude/QRS amplitude greater than 75%) could differentiate ACO from LVH,11 their cited study excluded patients with LVH.10

Now we know that Hyperacute T-waves are defined more by their "bulk" as defined by 1) "area under the curve relative to QRS size" and 2) by symmetry (hyperacute T-waves are more symmetric than normal T-waves.  Area under the curve is dependent on 3 elements: 1) height or amplitude 2) QT interval and 3) shape of the upsloping ST segment (very concave results in low AUC, very convex in high AUC.

Is LVH like left ventricular aneurysm?

The repolarization behavior of LVA is likely distinct from that of LVH. However, an analogous rule for identifying superimposed ACO of the LAD in the presence of persistent STE after prior MI (aka “left ventricular aneurysm,” or LVA) was just validated.12 An acute MI is likely if the T-wave amplitude to QRS amplitude ratio exceeds 0.36 in any of leads V1-V4 when a patient has ECG signs of LVA.

It’s unclear if we can use the same analysis in patients with LVH. However, it is clear that, in lead V3 in Figure 2, the Tamp/QRSamp exceeds 0.36 by a significant margin.  (It also does so in lead V2, at 7/14 = 50%).

Conclusion

It is complete conjecture at this point, but perhaps we should be measuring T-wave heights more often in suspected ACO. Close scrutiny of T-waves have anecdotally been useful when no diagnostic ST elevation is seen, and even when a ventricular pacer has obscured the ST segment.


Illustration of why Armstrong's paper does not help us with the question at hand:
These two ECGs are from Armstrong's paper (5) and are supposed to illustrate how the ST/S ratio of greater than 25% works to differentiate LVH from STEMI

You can see that, in neither of these cases of anterior STEMI would you be asking whether the ST elevation is due to LVH or not.  A rule that is useful would help you differentiate the ST elevation due to LVH from that which is due to STEMI superimposed on LVH.

References

1.         Huang HD, Birnbaum Y. ST elevation: differentiation between ST elevation myocardial infarction and nonischemic ST elevation. J Electrocardiol. 2011;44(5):494.e1-e494.e12. doi:10.1016/j.jelectrocard.2011.06.002.

2.         Brady WJ, Chan TC, Pollack M. Electrocardiographic manifestations: patterns that confound the EKG diagnosis of acute myocardial infarction—left bundle branch block, ventricular paced rhythm, and left ventricular hypertrophy1. J Emerg Med. 2000;18(1):71-78. doi:10.1016/S0736-4679(99)00178-X.

3.         Birnbaum Y, Alam M. LVH and the diagnosis of STEMI - how should we apply the current guidelines? J Electrocardiol. 2014;47(5):655-660. doi:10.1016/j.jelectrocard.2014.06.001.

4.         Brady WJ. Electrocardiographic left ventricular hypertrophy in chest pain patients: Differentiation from acute coronary ischemic events. Am J Emerg Med. 1998;16(7):692-696. doi:10.1016/S0735-6757(98)90179-6.

5.         Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic Criteria for ST-Elevation Myocardial Infarction in Patients With Left Ventricular Hypertrophy. Am J Cardiol. 2012;110(7):977-983. doi:10.1016/j.amjcard.2012.05.032.

6.         Shamim S, McCrary J, Wayne L, Gratton M, Bogart DB. Electrocardiograhic findings resulting in inappropriate cardiac catheterization laboratory activation for ST-segment elevation myocardial infarction. Cardiovasc Diagn Ther. 2014;4(3):215-223. doi:10.3978/j.issn.2223-3652.2014.05.01.

7.         Schocken DD. Electrocardiographic left ventricular strain pattern: Everything old is new again. J Electrocardiol. 2014;47(5):595-598. doi:10.1016/j.jelectrocard.2014.06.005.

8.         Smith SW. Upwardly concave ST segment morphology is common in acute left anterior descending coronary occlusion. J Emerg Med. 2006;31(1):69-77. doi:10.1016/j.jemermed.2005.09.008.

9.         Meyers HP, Limkakeng Jr. AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-1264. doi:10.1016/j.ahj.2015.09.005.

10.        Collins MS, Carter JE, Dougherty JM, Majercik SM, Hodsden JE, Logue EE. Hyperacute T-wave criteria using computer ECG analysis. Ann Emerg Med. 1990;19(2):114-120. doi:10.1016/S0196-0644(05)81792-5.

11.        Sovari AA, Assadi R, Lakshminarayanan B, Kocheril AG. Hyperacute T wave, the early sign of myocardial infarction. Am J Emerg Med. 2007;25(7):859.e1-e859.e7. doi:10.1016/j.ajem.2007.02.005.

12.        Klein LR, Shroff GR, Beeman W, Smith SW. Electrocardiographic criteria to differentiate acute anterior ST-elevation myocardial infarction from left ventricular aneurysm. Am J Emerg Med. 2015;33(6):786-790. doi:10.1016/j.ajem.2015.03.044.

13.        Neuman Y, Cercek B, Aragon J, et al. Comparison of frequency of left ventricular wall motion abnormalities in patients with a first acute myocardial infarction with versus without left ventricular hypertrophy. Am J Cardiol. 2004;94(6):763-766. doi:10.1016/j.amjcard.2004.05.061.

14.        Smith SW, Meyers HP. Hyperacute T-waves Can Be a Useful Sign of Occlusion Myocardial Infarction if Appropriately Defined. Ann. Emerg. Med. [Internet]. 2023;Available from: http://dx.doi.org/10.1016/j.annemergmed.2023.01.011

Chest pain with New LBBB: It helps to actually measure the ST/S ratio

An elderly male presented with 48 hours of off and on chest pain.  This ECG was recorded with pain:

The QRS is 130 ms.  It is essentially LBBB, though some might quibble with the tiny Q-wave in aVL or the fact that the intrinsicoid deflection (onset to peak of R-wave in V5, V6) is not quite 60 ms (it is at least 55 ms).
When I first glanced at this, I did not think it looked like STEMI (that is, I did not think it met the modified Sgarbossa criteria)

But then I measure it.  Here is V3 magnified:

Here I point out where the J-point and the PQ junction are:

You can see that, no matter which complex you measure, the ST elevation at the J-point is at least 3.5 mm.  The S-wave is no more than 13 mm.
Thus, the ST/S ratio in V3 is greater than 0.25.
There is thus proportionally excessively discordant ST elevation.
Only one lead is required!

The cath lab was activated.

Another ECG was recorded, with reportedly ongoing chest pain:

Now the ST elevation is less.  The ratio is about 3/15 = 0.20.
0.20 is still very good for diagnosing coronary occlusion.
However, look at lead V4: there is 1.5/5.0 = 0.30 ratio (the QRS is so different from the first ECG that I suspect some lead placement changes)
This improving ECG makes it appear as if there is some reperfusion of the artery.

At angiogram, a 90% thrombotic lesion was found and stented.  I suspect that the artery had spontaneously reperfused prior to the angiogram.  That is why the ST segments were falling.

Here is the post-PCI ECG:

It is now much more atypical for LBBB and should be called a nonspecific intraventricular conduction delay.  QRS is 126 ms.
The disproportionally excessive discordant ST elevation is gone.

This is 2 days later:

LBBB is gone.  There is normal conduction and anterior reperfusion T-waves.

Learning Point:

In LBBB, measure the ST elevation at the J-point and the PQ junction.  In a patient with the right clinical scenario, if there is one lead with a ratio greater than 0.25, then there is occlusion until proven otherwise.

A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia

This case was contributed by one of my talented colleagues, Johanna Moore, MD.  She is our research director and is doing some great research on cardiac arrest.  Check out her research on Head-up CPR!

There is more interesting stuff on Head up CPR here.  And here.

Case

A patient with a history of CABG in 1998, with subsequent ischemic cardiomyopathy, called his clinic to report he had a few minutes of burning chest and epigastric pain, associated with walking, that was now gone.  They told him to call 911.  Medics arrived and recorded this ECG (pain free) about 15 minutes after the resolution of chest discomfort:

Left Bundle Branch Block, but with both S-waves and T-waves cut off due to high voltage. 
You can see quite a bit of discordant ST depression in V5 and V6, but not out of proportion

The paramedics were worried by his ECG and had a physician check the patient and ECG at the door.

The patient arrived and was free of discomfort. 

After briefly reviewing the patient's previous ECG, the physicians decided to expedite the patient's care by placing him in a critical care area despite the patient's well appearance.   This first ED ECG was recorded at 15 minutes after the previous prehospital ECG and 30 minutes after resolution of discomfort.

There is LBBB with 7.5 mm of STE in lead V2 (the lead with the highest ST/S ratio)
The S-wave is 43 mm.  The ratio is 7.5/43 = 0.174.
This is below the Modified Sgarbossa cutoff of 0.25
In Smith's studies, 0.20 was more sensitive but less specific than 0.25; 0.17 is less than either.
Nevertheless, there is a big and scary change from the previous ECG (below).

1 year prior

LBBB with a relatively narrow QRS and much less ST deviation

The physicians were concerned regarding the change from the patient's previous ECG and degree of absolute ST segment elevation on the new ECG. 

On further history, the patient reported no associated symptoms. He was a reticent historian, and only after repeated pointed questioning was better history obtained.  He stated that the discomfort was brought on by walking, lasted for "just a few minutes" and relieved with rest. When asked more about the duration of the pain, the patient stated the pain lasted for 15-20 minutes. When specifically asked if he had any recent episodes like this, he stated he had a few similar pains in recent weeks, but was unable to state how this episode was different today.

He looked very comfortable, and stated he felt back to normal. He had a blood pressure of 137/85, pulse of 77, and O2 sat of 95%.

The patient reported he had not had an angiogram since the CABG was performed in 1998. The last echocardiogram on file from 2012 showed an EF of 43%, with inferior, septal, and posterior wall motion abnormalities. The ED physicians performed a bedside echo:



This shows globally severe systolic dysfunction.

Based on the history, ECG, and bedside echo, the ED physicians called the on call cardiologist for an emergent consult. The cardiologist was present within 10 min and also performed a history and physical.

This repeat ECG was performed 16 min later, and 31 min after the prehospital ECG:

There is slightly less ST elevation in V2, at 6 mm, for a ratio of 6/38 = 0.158.
The ST segment, and the ratio, are falling.
Now there is also much less ST depression in V5 and V6

The cardiologist and ED physician debated what to do. Both thought the patient would eventually need an angiogram either later that day or the next. It was reassuring to them the patient appeared well, but he had a concerning medical history and HPI for unstable angina, especially taking his cardiac ultrasound and ECG into account as well. As they were talking with the patient, the troponin I returned at 0.516 ng/mL.

At this point, the physicians did not have a good alternative explanation to ACS for why this troponin would be positive and both agreed he should go to the cath lab.

The angiogram showed a "99%" LAD lesion that was hazy, but had TIMI-3 flow.

Here is the post PCI ECG:

5 mm STE in lead V2.  Ratio = 5/38 = 0.132
The ratio is still falling

Troponin I peaked at 1.390 ng/mL the next AM, and this ECG was recorded:

4 mm of STE in lead V2.  Ratio = 4/35 = 0.114 (normal)

Smith comment

What happened here?

This is the most likely scenario:

The patient had a completely occluded LAD, or nearly so, at the time of the chest discomfort.  The flow was less than TIMI 3 at that moment.  If an ECG had been recorded, the ST Elevation would have been even higher (or the S-wave amplitude lower), and it would probably have been high enough to meet the Modified Sgarbossa criteria.

However, the artery opened, the ischemia was resolving, and the pain resolved.  By the time of the first ECG, it was no longer diagnostic (no longer met Modified Sgarbossa criteria).  Nevertheless, the physicians used very good judgment to take the patient to the cath lab, where although there was TIMI-3 flow, there was an acute lesion due to ACS.

As the ischemia resolved, the ST/S ratio fell from 0.174 to 0.158 in just 16 minutes, then to 0.132, then 0.114

In spite of Occlusion, the troponin I peaked at only 1.390 ng/mL.  By our research methods, this would not qualify as an Occlusion MI (OMI), even though it is!!  Even though this OMI put a lot of myocardium at risk, reperfusion was so fast that only a small amount of myocardium actuallly died

Learning Point:

There can be severe ACS, even with "99%" stenosis, and TIMI-3 flow at the same time.  The ECG will not be diagnostic of occlusion when there is TIMI-3 flow, even if the artery is severely narrowed by thrombus.

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

An elderly male had a syncopal episode.  911 was called.  When medics arrived, the patient was alert and following commands.  In the presence of the medics, he lost consciousness and became apneic and underwent 30 seconds of chest compressions, after which he started moaning and was again able to communicate and follow commands.   No shock was ever delivered.

A 12-lead was recorded:

Without a rhythm strip, this rhythm is difficult.  In any case, there is bradycardia.  There is either RBBB (see rSR' in V1) or there is a left sided escape rhythm that gives RBBB morphology.
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia.  There is no ST elevation.

The patient was moaning upon arrival to the ED, looked ashen, and had agonal respirations.  He was unresponsive to painful stimuli.

He was in profound shock.

He was intubated.

A bedside cardiac ultrasound was recorded:

Here is a still image of the echo:

The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber.
What do you think?

There is no pericardial fluid to account for shock.  The RV is huge.  This essentially rules out hypovolemia as the etiology (no GI bleed, no ruptured AAA, etc.).  It makes pulmonary embolism (PE) very likely.  It also makes large right ventricular infarct possible, but much less likely than PE.  The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure.  RV pressure appears to be high (large RV), so there is obstruction between the RV and LV (PE).

Alternatively, the RV is so ischemic as to be unable to generate high pressures (RVMI).  This is much less likely than PE.

Along with supportive cares, this first ED ECG was recorded:

What do you think?

Annotated with arrows:

The arrows show what I believe are P-waves.  So this is third degree AV block.  There is a wide QRS, so there is infra-HIS escape.  It is RBBB morphology (left bundle escape).
There is obvious ischemic ST elevation in V1-V3, maximal in V1.
There are slightly large T-waves inferior, with ST depression in aVL

There is "Precordial Swirl" pattern (STE V1 with STD V5,6 usually due to LAD occlusion proximal to Septal perforator.  It can also be due to RV MI.

What is going on?

First, what kind of arrest was this?  It was a PEA or bradyasystolic arrest, not a shockable rhythm.  There is 3rd degree heart block.  Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI.

Second: what does the ultrasound tell us about the condition? Is this an anterior (LV) MI?  No!          --The large RV and small LV on ultrasound make this a right ventricular process.  A standard anterior MI would have a large LV with poor function, not a small LV.  This LV is not filling.

Third: what does the ECG tell us about the left ventricle?  It is anterior, but is it anterior LV or anterior RV????   LV anterior STEMI does not give maximal ST elevation in V1.  So this ECG is typical of right ventricular (RV) STEMI.

Fourth:   RV STEMI is almost always accompanied by profound inferior STEMI.  Though there is some evidence of this in inferior leads, it is not convincing.

          Therefore, the ultrasound looks like PE, and the location of the ST elevation tell us that it is an RV STEMI (which manifests in "anterior" leads, as they overlie the anterior RV).

Fifth: the ultrasound in RV MI can look identical to that of PE: there can be both McConnell's sign and "D" sign, as well as enlarged RV with poor function.

Sixth:  Severe shock (e.g., due to PE) may result in STEMI (and, if anterior, it can be from anterior LV or anterior RV ischemia, or both) from low coronary pressure and flow, simply due to the shock.  Here we have evidence of massive RV dysfunction.

Seventh: When the severe shock that is the etiology of STEMI is due to PE, the ST elevation likely reflects the RV, as there is both low coronary flow in the RV marginal branch, and very high RV pressures (low supply and high demand).

Eighth: STEMI even if from low flow, not ACS, can cause ischemia of the conduction system and result in complete AV block, even infra-HIS AV block.

All of this favors PE with resulting RV STEMI, but initiated by PE.

Summary:
1.  If this had been a shockable rhythm, STEMI would be most likely.  But it is bradyasystolic, so pulmonary embolism must be high on the differential.
2.  The echo shows that, if this is MI, it is most likely an RV MI.  It is not an (LV) anterior MI.
3.  The ECG also shows RV MI, not LV anterior MI
4.  So is this an isolated RV MI with shock?  Possible, but huge pulmonary embolism is more likely.

In a patient with such a differential diagnosis, and in profound shock, near death, the treatment is IV thrombolytics.  A 1/2 dose (50mg) of full dose (100 mg) bolus may be given when the patient is in extremis as this patient is.

Such isolated RV STEMI is rare, but pulmonary embolism is not.  Thus, this is most likely pulmonary embolism, not STEMI.  However, thrombolytics will treat both.  Lytics are very effective early in the course of STEMI.  Moreover, their use does not precluded subsequent angiography and PCI if this turns out to be RV STEMI.

Clinical course

The clinicians thought this was LV STEMI due to the "anterior" ST elevation.  The cath lab was activated.  In the cath lab, the coronaries were clean.  Pulmonary embolism was suspected a right side cath with pulmonary angiogram confirmed it.



Here is the left pulmonary artery



There is extensive clot in the main pulmonary artery






Here is the right pulmonary artery


Less thrombus here


Catheter-Based thrombectomy was undertaken.

Here is the post thrombectomy angiogram:


There is now good flow in both trunks.


Unfortunately, the patient was too ill to survive.

Briefly without pulse, has pulmonary edema and LBBB with 10 mm of ST Elevation

A middle-aged male was found down.  EMS was able to get the patient to climb onto the ambulance by himself, then during transport he became less responsive.  They briefly could not find pulses, and gave a short period of CPR with ROSC, but he did not require a shock. They gave Narcan without improvement.  An oral airway was placed and BVM oxygenation provided.  The patient arrived unable to provide any further history.

BP was 180/100, HR 130, Oxygen saturations 84%.

He was intubated.  A bedside ultrasound showed poor global function and B-lines of pulmonary edema.

Here was the first ECG:

There is sinus tach and left bundle branch block (LBBB).
There is massive ST Elevation in V2 and V3
The ST segment in V3, as I measure it, is 10 mm, with a 38 mm S-wave.
The ratio is 10/38, which is greater than 0.25, consistent with LAD occlusion.
This meets the modified Sgarbossa criteria, which have been derived and validated.
Should we diagnose anterior STEMI?
Should we activate the cath lab?

Here is the chest x-ray, in case you don't believe in B-lines:

Profound Pulmonary Edema

Remember:

In both of the studies of the Modified Sgarbossa criteria, we excluded patients with extremely elevated BP, pulmonary edema, extreme tachycardia, or hyperkalemia.

That is because these patients need supportive care and then, subsequently, a decision on the cath lab.

This patient would have been excluded from the studies.

The blood gas returned with severe acidemia, with both metabolic and respiratory acidosis:
pH 6.8, pCO2 = 86, HCO3 = 14
Lactate was greater than 15.
K was normal.

The patient was stabilized with supportive care.  The respiratory acidosis improved with good ventilation.  The lactate had time to metabolize.  The patient was well oxygenated.  The elevated BP resolved with propofol.

By the time of the second ECG, the pulse was about 100, O2 sats 95%, BP 144/80.

100 minutes after first:

Supportive Care has resolved all the pathologic ST elevation.

The Peak troponin I overnight was 2.382 ng/mL, consistent with NonSTEMI.

An ECG was recorded the next AM:

Remains without obvious ischemia.  It does not even show reperfusion T-waves.

Case continued

The next AM more data revealed a history of coronary disease with stent placement in the circumflex 3 years prior.  Since then, he has had progressively worsening dyspnea on exertion, and orthopnea.

Echo the following AM showed EF 35%, asynchronous interventricular septal motion (due to LBBB), inferior wall motion abnormality, LV enlargement, and LVH.

It was unclear exactly what had caused acute decompensation.  Hypotheses included brief dysrhythmia or ACS leading to shock and pulmonary edema.  

Given the coronary history and findings on TTE (inferior wall motion abnormality), ACS was high on the differential, and so he went for cath later that day.

Cath result:  total occlusion of a small right posterior descending artery (RPDA) which filled by left to right and right to right collaterals.  No intervention was done because the artery was too small and the territory it supplied had good collateral circulation.

The patient was later able to relate that he was having some SOB and trying to contact his doctor when he decompensated.

The explanation of his deterioration:

He has baseline poor LV function with increasing heart failure symptoms, then had an acute occlusion of a very small RPDA which affected his LV function just enough to tip him over the edge into acute pulmonary edema.

He was managed medically and did well.  He was scheduled for cardiac resynchronization therapy (a biventricular pacemaker which improves cardiac output in patients who have LBBB with a QRS greater than 130 ms).

Learning Point:

Respiratory failure with hypoxia, hypertension, tachycardia, and acidosis can lead to profound ECG changes, in both LBBB and in normal conduction.  Before making the reperfusion decision, stabilize the patient.

Although in this case he did have a coronary occlusion, it was small and neither needed PCI, nor could be intervened upon.

It was not the LAD, so these ECG findings had nothing to do with the very small coronary occlusion.