Friday, February 12, 2016

Pericarditis? Or STEMI? The difference can be fatal.

This was sent by a reader who wishes to remain anonymous.  Details are at a bare minimum, but it remains instructive.

An elderly patient had a good reason for demand ischemia and there was no suspicion of ACS.  This ECG was recorded:
There is sinus tachycardia.  Complexes 3, 6, 12, & 15 appear to have some pre-excitation, with secondary repolarization changes.
In leads without pre-excitation, there is
diffuse ST depression consistent with demand ischemia

Clinical Course

The pathology leading to the ischemia was treated and resolved.  Later, what may have been simply a routine ECG was recorded.  If the patient had symptoms at the time of this 2nd ECG, they were not documented.  It also is unclear if anyone involved with the patient saw the ECG at the time it was recorded -- no clinician commented on it in the chart.

Here it is:
The cardiologist who read the ECG on the system (who probably did not know the patient or the reason for the recording) read this as "Diffuse Nonspecific ST Elevation, consider Pericarditis"
What do you think?

There is subtle ST elevation in inferior and lateral leads, and subtle reciprocal ST depression in lead aVL and also subtle ST depression in lead V2.  This is highly suspicious for acute STEMI, and even meets STEMI criteria in leads V4-V6.  It is very unlikely to be pericarditis.


Not long after the ECG was recorded, the patient arrested.  She was unable to be resuscitated.  The autopsy showed an acute RCA thrombosis with 90% occlusion.

Learning Points:
1. You diagnose pericarditis at your (or your patient's) peril
2. Pericarditis does not have reciprocal ST depression, not in either lead aVL or in V2.  This ECG is very specific for STEMI.
3. Even when patients are asymptomatic, or apparently so, they can have life threatening MI.  If the ECG has specific signs of MI, as this one does, then do not be fooled by the absence of symptoms.
4. It is very easy to overlook ECG findings if you are interpreting a routine ECG, without knowledge of the patient's condition (this includes over-reading of ECGs from a list, as was done in this case).

Monday, February 8, 2016

Subacute STEMI. Should the patient go for emergent PCI, or can he wait until the next day?

This was sent by a very good medical student, who had a very good question.  He wishes to remain anonymous.

A 56 y/o male presented with Chest Pain radiating to the left jaw, starting at 8pm the previous night (15 hours prior), which was 10/10 at that time.  He decided to wait it out at home, then presented at around 11 AM, pain now reported at 2/10.

Here is the initial ECG (see the patient's previous ECG below for comparison):
There is sinus rhythm and new inferior QS-waves with less than 1 mm of inferior ST elevation, and reciprocal ST depression in aVL, and T-wave inversion.  
Such T-wave inversion is common not only in reperfusion, but in persistent and prolonged occlusion after formation of Q-waves, especially QS-waves.

Here is the patient's previous ECG:
This old ECG confirms that the first ECG shows a new MI

So this patient has a subacute STEMI.   

The initial troponin T returned at 0.47 ng/mL (quite high for Troponin T) and rose from there to 0.81, then 1.96 (typical of a large STEMI).  Whether the troponin continues to rise or not says nothing about ongoing ischemia: it takes time for complete troponin rise and fall even after infarction is completed.  Only the ECG and pain can tell you prospectively whether ischemia is ongoing.

The patient was admitted with "NonSTEMI" and did not undergo emergent angiogram and PCI.  He went the next day.

This is a nearly completed STEMI (a very advanced subacute STEMI). To call it a NonSTEMI is misleading.

Is it too late for emergency cath lab activation?  Should he go now, or with less urgency (tomorrow)?

My answer is this: 

If there is:
1) persistent ST elevation (as there is here) or 
2) persistent pain (as there is here)

Then the patient should go emergently.

But I know of no data to support this.

There are 2 excellent articles addressing whether a patient with completed MI should undergo PCI at all (vs. medical therapy alone), but none addressing this situation.

Schomig et al. published this in JAMA in 2005:  
Data presented shows benefit of PCI (vs. medical therapy alone) for patients who present between 12-48 hours after STEMI if there was persistent STE, or simply new Q-waveseven in the absence of pain.  But they did not assess the urgency of PCI.

Hochman et al. published the Occluded Arteries Trial (in the New England Journal).  
In this article, they assessed arteries occluded for 3 days or more, and found that PCI resulted in worse outcomes than medical therapy.

The question this student posed was slightly different: beyond 12 hours, is emergent PCI better than delayed PCI (both groups getting PCI).

ACC/AHA 2013 STEMI guidelines say this:

Primary PCI is reasonable in patients with STEMI if there is clinical and/or ECG evidence of ongoing ischemia between 12 and 24 hours after symptom onset (94,95). (Level of Evidence: B).  This means if there is chest pain, persistent ST elevation, or especially upright T-waves.

But the ACC/AHA guidelines do NOT address the timing (emergent vs. urgent) and they reference two studies, one of which is the Schomig article above, and the other of which also does not address emergent vs. urgent PCI.  

94. Schömig A, Mehilli J, Antoniucci D, et al. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. JAMA. 2005;293: 2865–72.

95. Gierlotka M, Gasior M, Wilczek K, et al. Reperfusion by primarypercutaneous coronary intervention in patients with ST-segment elevationmyocardial infarction within 12 to 24 hours of the onset ofsymptoms (from a prospective national observational study [PL-ACS]). Am J Cardiol. 2011;107:501–8.

Learning Points
1. I think if there is ongoing pain or ST Elevation, it is wise to go emergently to the cath lab to save any remaining viable myocardium.  Randomized data on this is lacking.  Probably, most researchers would be reluctant to test such management.  Similarly, no one has ever conducted a randomized trial of emergent vs. delayed PCI for NonSTEMI with refractory (continued) symptoms.
2. PCI at some point within the first 12-48 hours of STEMI is definitely indicated.

Dr. Goldsmith of our Cardiology Department added his opinion in an email:

This is a gray zone. Apropos of your general thinking that we should act to make a clinical difference and not just on the basis of guidelines (!) the issue of timing here relates to how much salvage is likely. Points in favor of going now: the relatively low trop on presentation (suggests possible opening/closing of an artery) with pain. If the trop had been 20 I probably would not have gone.....pain and ST elev are problematic guides because both can persist for many hours after there is no chance of successful reperfusion (MI pain in the old days required morphine for 24 hours, usually, as I remember from my residency!). So these are tough, and as you say there is no firm guidance. The low trop with a rise suggest a new event or recurrent event to me, rather than a done deal, so I probably would have argued for earlier study knowing it might or might not help but would not likely hurt. Perfect Pathway B case, by the way!

Saturday, February 6, 2016

What is going on here? There is more than immediately meets the eye.

This is a repost, but it was only posted as a video presentation on hqmeded:

A patient presented with chest pain:
What do you see? (Sorry for the obscured V6.  It doesn't show anything)

There is an obvious inferior STEMI.  The cath lab was activated.  I saw the ECG later and called the interventionalist to hear the outcome.  He said there was a mid-RCA occlusion.  I said, "That is strange, because the ECG has ST elevation in V1 and indicates a right ventricular MI."

He went back to look at the angiogram.  He then saw that the culprit was in the proximal RCA, proximal to the RV marginal branch, and that there had, indeed, been an RV MI.  The mid-RCA occlusion was an embolus from the proximal RCA.  Fortunately, the patient was still on the table and he could go back and place the stent at the correct lesion in the ulcerated plaque in the proximal RCA.

Learning Points:

1.  In inferior STEMI, ST elevation in V1 is a very specific finding for right ventricular MI.  We have studied this and are near completion of a manuscript on it.

2. In inferior STEMI, it pays to record a right sided ECG.

Friday, February 5, 2016

Apparent Pseudo-STEMI patterns are not necessarily Pseudo. Beware.

This was contributed by an ECG enthusiast who wishes to remain anonymous.

LVH is a well-described “mimic” of STEMI. However, a diagnosis of LVH does not exclude an acute coronary occlusion, and the clinical context, including symptoms and old ECGs, must be taken into account.

A 50 year-old woman came to the ED with recent-onset chest pain.:
She had a history of hypertension, as well as concentric LVH on a very recent echo. Furthermore, she had markedly elevated systolic BP > 200 mm Hg.

Her initial ECG:
There is STE in lead III, < 1 mm, as well as STD with inverted T waves in leads I and aVL. This pattern of STE and STD could represent an early or subtle inferior coronary occlusion. However, the R wave in aVL is ≥ 11 mm, basically diagnostic for LVH.  

Smith comment: the voltage only barely meets LVH criteria, but the morphology of the T-wave inversion in aVL has the "hockey stick" shape often seen in LVH.  Furthermore, the inferior T-waves are not as large as one would suspect with a coronary occlusion (see example at bottom).  I would agree with the contributor that it does not look like the typical ST-T of subtle inferior MI.  But, remember, coronary occlusion can show almost nothing on the ECG.  If it can show nothing, then very subtle abnormalities could be something.

The ECG raised concerns for inferior MI, but it was decided that the STE and STD were due to repolarization changes of LVH. Nonetheless, a repeat ECG was obtained 1 hour later:
Not significantly evolved from the prior ECG.

These ECGs were compared with an ECG from 1 week prior:
Although there is T wave flattening in leads I and aVL, there is no suggestion of LVH on this ECG. In fact, the ST segments in I and aVL are slightly elevated, and those in the inferior leads II and aVF subtly depressed.

Smith comment: The change from one month ago is diagnostic of ischemia.  

I very much doubt that LVH on the ECG, with ST-T repolarization abnormalities, can develop over one month.  Serial ECGs are very helpful, but frequently show no or minimal evolution over one hour.  One need only see this recent case I posted for another example of absence of evolution.

Contributor continued:
Given the previously documented LVH on echo, as well as the lack of evolution over 1 hour, the new ECG changes were attributed to a combination of acute hypertension, LVH, and different patient and limb-lead positioning. The patient received aspirin, morphine, and nitroglycerin. The first troponin was below the 99% cut off, and she was admitted to telemetry for serial troponins.

Smith comment: I think it would have been appropriate to dial up the Nitro until the BP is normal, then repeat the ECG.  If the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated.  If they resolve, then perhaps the findings are due to the severe hypertension.  That is exactly what happened in this really interesting case.

Contributer continued
Wait, why did she have an ECG from a week ago?
She had been admitted earlier in the month for an NSTEMI without ECG changes. On angiography, a drug-eluting stent was used to open a total RCA occlusion. (The ECG above was post-PCI.)

With this knowledge that she had received PCI to the coronary region of concern on the ECG (the RCA typically supplies the inferior wall) only weeks ago, the plan was made to manage her ongoing pain medically, and she was admitted to a telemetry bed.

ECGs were repeated at 5 hours post-arrival: 
Although the R wave in aVL is still diagnostic for LVH, the STD/TWI in leads I and aVL have resolved, as has the STE in III and aVF. This proves that they were due to ACS, not LVH.

And 6 hours post-arrival:
The R wave in aVL has regressed to her baseline height, while T wave inversions in III and aVF suggest spontaneous reperfusion of the inferior wall. 

The 8-hour troponin returned at 6.7 ng/mL. (Smith comment: we don't know the peak, and it is not a reliable indicator of infarct size as it depends on reperfusion, which makes it rise high and quickly, infarct size, collateral circulation, and assay.  However, this certainly is consistent with an acute coronary occlusion, although her ECGs did not meet criteria for STEMI).  She went to angiogram the next day and the RCA was indeed (persistently) occluded.  The RCA territory, however, was now well supplied by left to right collaterals, so that the damage was not extensive.  No PCI was done except for on two unrelated diagonals (off the LAD).

Why did she have an acute occlusion after getting stented?
Unfortunately, after her PCI earlier in the month, she had been discharged home without a Plavix prescription. In combination with aspirin, this medication is essential for preventing in-stent thrombosis. Her echo, which during her earlier admission had shown only concentric LVH, now had an akinetic basal inferior segment. She was presumed to have had an early in-stent thrombosis of the RCA DES due to insufficient platelet inhibition.

Brief review: LVH and inferior STEMI
LVH is well appreciated as producing STE in leads V1-V3, mimicking anterior STEMI. However, no proven criteria permit a clear distinction between acute anterior ischemia and LVH.

This situation is even less clear for inferior STE when LVH criteria are met. A recent review of LVH and STEMI highlights that “there is confusion whether the exclusion of STE thresholds in patients with LVH is limited to leads V2-V3 or applies to all leads.”

On the one hand...

On the one hand, LVH frequently manifests ST changes that mimic inferior STEMI. 
For example:
Example 2 from Life in the Fast Lane:

Case 4 from this post on Dr. Smith's ECG blog:

Case 6 from this post on Dr. Smith's ECG Blog:

On the other hand...
On the other hand, these clear examples of LVH easily met precordial-lead criteria for LVH, as well as limb-lead criteria. Our patient, however, only met limb-lead criteria, and just barely.

Furthermore, it is plausible that the change in axis was because the limb-lead electrodes had been placed differently (e.g. on chest instead of arms) than the prior ECG, or the patient positioned differently (e.g. seated versus supine). However, such changes would not produce the ST changes we see, especially over so short a period of time.

Dr Smith has a great case that also demonstrates the peril of attributing new inferior ST changes to LVH. A patient with chest pain had this ECG:
It meets criteria for LVH based on aVL, but the ST-T are far out of proportion to the QRS amplitude.  This was diagnosed as MI by the emergency physician, but the interventionalist would not take the patient to the cath lab because he was convinced it was due to LVH.
Furthermore, there was a previous ECG for comparison:
Again, the previous ECG makes the diagnosis definite

Sunday, January 31, 2016

The Electrocardiographically Silent Circumflex Artery

A 39 yo otherwise healthy man with no risk factors was walking at the mall when he developed chest pressure.  He presented to the ED after 30 minutes, now also feeling weak.  He was diaphoretic.  Here was his initial ECG:
There is sinus rhythm.  There is abnormal T-wave inversion in V2 which is abnormal and very suspicious There is minimal, nondiagnostic ST elevation in inferior leads with possibly a suggestion of reciprocal ST depression in aVL.  There are thin and normal inferior Q-waves. Thus, there are some suspicious abnormalities, but no definite signs of ischemia.   There is also minimal, nondiagnostic ST elevation in V5 and V6. 
Because of persistent symptoms, another ECG was recorded 30 minutes later:
There is only one new finding on this ECG which suggests ischemia.  It is very subtle but real.  What is it?  

See V3, where there is now some ST depression.  The previous ECG has a small amount of appropriate ST elevation in V3; any ST depression in a young male is abnormal, especially if changed from previous.  This is worrisome when combined with the abnormal T-wave in V2.

Let's look at both V3's, magnified:
The later ECG (bottom panel) shows minimal ST depression in V3.  The top shows minimal ST elevation (normal).  The difference is significant and highly suggests posterior ischemia.

This abnormality in V3 was apparently not seen by the treating MD, who is a nationally recognized expert in STEMI care (showing how difficult these diagnoses can be).

The initial troponin was negative. The patient was admitted to telemetry.  At 4 AM, his second troponin returned at 1.8 ng/mL.  Another ECG was recorded:
T-waves in V2 and V3 are now upright and larger, evolving. 
Are these posterior reperfusion T-waves?

He went for cath at 6 AM because of ongoing symptoms and a "positive" troponin.  He had an occluded OM-2 that was opened and stented.  

Troponin I peaked at 99 ng/mL (large MI)!

So this is a NonSTEMI, right?  Technically, yes, because there is not 1 mm of STE in 2 consecutive leads.  But the definition misses the point.  It is a coronary occlusion with a substantial myocardial territory at risk, that showed only very subtle ST changes.

Should you activate the cath lab for this?

Not from the ECG alone.  However, if you notice the ST depression, you then realize that this is ischemic chest pain, not esophageal spasm.  Once you know that the chest pain is ischemic in origin, and you cannot control it medically, then you must go urgently to the cath lab.

The patient should be treated with NTG, Aspirin (and clopidogrel, if your institution allows), metoprolol, antithrombotics, and GP IIb IIIa inhibitors.  If the pain persists, and the ST depression persists, then talk to your interventionalist immediately.

Here is the followup ECG:
The ST abnormalities have resolved.  There are new inferior Q-waves diagnostic of inferior MI.  The R-wave is increased in V2, consistent with posterior (now called lateral, to my dismay) MI (analog of a Q-wave).  There is no apparent resolution of the minimal and non-diagnostic inferior ST elevation.
Notice the T-waves are smaller in V5 and V6 now.

I don't have all the data on this case, and do not know if there is an inferior wall motion abnormality, or if this OM-2 supplied the inferior wall.  It  probably did, as evidenced by the Q-waves; but it is very interesting that during the acute phase, there were no diagnostic ST changes in inferior leads, and the minimal ST elevation that was present did not evolve.

Many MIs are electrocardiographically "silent," especially when in the circumflex territory.  I do wonder whether, in the studies that show this phenomenon, if an ECG expert evaluated the ECG for the subtle signs of ischemia.  I suspect that many or most that are thought to be "silent" are really just "subtle."  But many show nothing!

Here are more electrocardiographically subtle MI.

Why is the lateral wall, and the circumflex artery territory, electrocardiographically silent?

1. The lateral wall stretches far around to the posterior wall.  I, aVL, V5, and V6 just don't go posterior enough.  Posterior leads may help with this.
2. As you go lateral, the heart has more lung between it and the chest wall, so lead strength is buffered by air.

Anterior ST depression can help with assessing the posterior wall.   The combination of 1) accepting a lower threshold in lateral leads (0.5 mm), 2) considering ST depression in V1-V4 as posterior STEMI, and 3) using posterior leads at a threshold of 0.5 mm, will all improve the sensitivity.

Friday, January 29, 2016

Looking for a wall motion abnormality can lead you astray

A Middle-aged male presented with chest pain of 3 hours duration. He has a history of hyperlipidemia only.  There is pressure to mid-chest, radiating to the right arm, associated with diaphoresis.   He never had this before.  It was not related to eating.  There was no cough or fever, nor trauma.  There was no recent surgery, and no h/o thromboembolism.

Exam and BP were normal.

Here is the first ECG:  0526
There is ST elevation in V1-V4, with concave ST segments.  Is it ischemic, or is it early repol?
It does not meet STEMI "criteria," but we know they are insensitive
First, look for any reciprocal ST depression and you see it in lead III, plus some subtle STD in II and aVF.
There is a bit of ST elevation in I and aVL as well.
When there is reciprocal ST depression, it is likely to be LAD occlusion and the LAD occlusion formula may be falsely negative.
Indeed, if you do make the calculation, with STE60V3 = 4, QTc was 385, and R-wave amplitude in V4 = 20 results in 20.98, which is quite low

There was a previous ECG for comparison:
This is truly normal, without any significant ST elevation
You can see that the T-wave are now much larger than on the previous ECG.
These changes are diagnostic!

But the clinicians were not convinced.

So they did a bedside echo.  Here are 3 parasternal short axis views:

They read the echo as normal, without a wall motion abnormality.

Is it normal?

Comment: I think I see a clear wall motion abnormality of the anterior wall (closest to the transducer), but wall motion abnormalities are hard to see, especially for the non-expert, and especially without contrast or stress echocardiography (speckle tracking -- see these cases).

And then a repeat ECG at 0540
Not much different.

They proceeded to look for other pathology with ultrasound:

A bedside ultrasound showed a normal aortic root and distal aorta.  The gall bladder had no stones and a normal duct.  There was no abdominal free fluid and no hydronephrosis.  Chest X-ray showed no infiltrate and a normal mediastinum.  D Dimer was normal, and lipase was minimally elevated.

Cardiology was consulted by our Pathway B, and Nitroglycerine (NTG) initiated with a plan to maximize it to eliminate pain.

Another ECG was recorded at 0556:

Then the first troponin returned at 0.036 ng/mL (99% reference = 0.030 ng/mL).

Comment: A negative troponin does not help in acute coronary occlusion, because it may be too early to be "positive."  But a positive one in a patient with no baseline pathology (heart failure, renal failure) or reason for demand ischemia (sepsis, resp failure, etc.), but only with ischemic symptoms such as chest pain, tells you that an equivocal ECG is a positive ECG.

With a nitroglycerine dose titrated up to 60 mcg/min and a systolic BP of 90-100, the nitro could not be increased further.

The decision was made to activate the cath lab in the setting of elevated troponin, concerning ECGs, refractory typical pain, and no alternative explanation such as pericarditis or aortic dissection.

Another ECG was recorded at 0629:
Now there is more ST elevation and the change in the ECG itself is clearly diagnostic.


At angiogram, there was a 100% mid-LAD occlusion, without good collateral circulation.  It was stented.

Here is the troponin profile:
Notice how the troponin suddenly rises after reperfusion and  release of troponin from the cardiac circulation.
The levels are quite high, consistent with a very large infarction.

Here is the ECG the next morning:
There is still significant ST elevation, now with T-wave inversion.  The persistent STE suggests that there is continued microvascular obstruction and is not a good sign.

An echo the next day showed:
Normal left ventricular size, thickness and systolic function.
The estimated left ventricular ejection fraction is 56%.
Regional wall motion abnormality-distal septum anterior and apex

Learning Points:

1. In a patient with real suspicion of MI and anterior ST elevation that does not meet STEMI "criteria," if there is inferior reciprocal ST depression, it is LAD occlusion until proven otherwise.  This is true even if the "early repol -- LAD occlusion" formula value is less than 23.4 (specific) or even if less than 22 (otherwise, a very sensitive cutpoint).

2. Compare with a previous ECG.  If there is a marked change, then it is likely to be due to ACS/coronary occlusion.    

Unfortunately, early repol is not completely stable: Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

3. Bedside echo has many great uses.  In suspected ACS, visualization of a wall motion abnormality may help to make the diagnosis of coronary occlusion, especially with speckle tracking; the positive predictive value is probably good.  But it is hazardous to try to rule out MI with limited bedside echo.  In this case, its use delayed care.

4.  Finally, the clinicians did a superb job by remaining vigilant, continuing to search for alternative causes and to monitor for ACS through serial ECGs, troponin, Nitroglycerine use and more.  This patient could easily have been just admitted for "rule out MI" and been left with a crippling cardiac injury.

5. Many NonSTEMI are due to coronary occlusion.  Early angiography with PCI saves myocardium.

Monday, January 25, 2016

Atrial Fib with RVR. What treatment? Then SVT. Is it sinus? Use ultrasound and Lewis leads!

An elderly man with a history of diabetes and HTN presented with lethargy and weakness.  He had no CP or SOB, and it was unknown if there was a previous history of atrial fib.  He was on atenolol, but it was not known if this was simply for hypertension, or for atrial fib.  He was not anticoagulated.  He also had decreased urine output.  There was no history of any GI bleeding or other hemorrhage.  There was no fever.  He had an ECG recorded upon arrival:
There is atrial fibrillation with a rapid ventricular response (rate of approximately 120).  There are aberrantly conducted beats (Ashmann's phenomenon), which are easily confused with runs of VT.
There is ST depression in V2-V6 that is clearly ischemic.
The ischemia on the ECG could be of several possible etiologies: 
1) New atrial fib with RVR causing demand ischemia (but the rate is not terribly fast).
2) Old atrial fib with poor rate control causing demand ischemia.
3) ACS with possible additional ischemia from atrial fib with RVR
4) Hemorrhage/dehydration/sepsis/etc., with new or old atrial fib, resulting in reflexive tachycardia and demand ischemia.

To find the answer, it is wise to assess volume status, which can be done with ultrasound:

A bedside ultrasound was done from the subcostal view, concentrating on the IVC.  If this is due to etiologies 1-3, one would expect a full IVC.  If etiology 4, then one expects a flat and/or collapsing IVC:

This shows a collapsing inferior vena cava (IVC), consistent with volume depletion

Another with a better view of the heart.  RV is on upper part of the view, next the liver:

RV is quite small.  LV is also small and has good contractility.  This supports volume depletion.

The appropriate therapy would be fluids and further workup for hemorrhage/dehydration/sepsis/etc.

However, BOTH an esmolol bolus and drip, and IV fluids were started.

But beta blockade should NOT be given, at least not yet.  In a volume depleted state, this patient needs the reflexive tachycardia for cardiac output.

By the time I arrived and was involved, the esmolol had not been at a high enough dose to do any harm.

In the meantime, the first troponin I returned at 0.562 ng/mL.  I was fairly certain that this was a type II (demand ischemia) MI and that this patient was not having ACS.

I stopped the esmolol and gave the patient 2 liters of fluid.  After fluids, the IVC was less collapsing:

But the patient monitor then showed a regular tachycardia without any P-waves.  The rate was very constant at 140 and so I wondered if this was SVT or sinus tach.  Another ECG was recorded:
Now there is a regular supraventricular rhythm.  There are probable P-waves, but I wasn't entirely certain.
What to do?
Lewis Leads!!

I went into the patient's room, and, according to the interview with Christopher Watford on EMCrit, I changed the monitor leads around (this is not a 12-lead!)

  1. Place the Right Arm electrode on the patient’s manubrium.
  2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
  3. Place the Left Leg electrode on the right lower costal margin.
  4. Monitor Lead I.
I printed it out.  This is what I recorded:
Now the P-waves are obvious

So the patient now has sinus tachycardia.

The next troponin returned at 5.0 ng/mL.

I gave more fluids and the heart rate came down.  Here is the next ECG:

He developed a fever and urine showed WBC's.  He was treated for urosepsis and did well.  He did not have ACS.

Learning Points:

1. Not all myocardial infarction is due to ACS
2. Atrial fibrillation with RVR may be a consequence, not a cause of, illness
3. Volume status is critical in the management of Atrial fibrillation with RVR
4. If you are not certain of a source of SVT, do Lewis leads

Wednesday, January 20, 2016

Inferior STEMI with AV Block, Cardiogenic Shock and ST elevation in V1

This is a case I had with one of our superb internal medicine/emergency medicine residents, Marco Salmen, MD.  He wrote it up for this blog, with some help from me.


An elderly woman called 911 for acute onset of nausea and chest pain of 30 minutes duration.  A prehospital ECG was identical to this first ED ECG

Rhythm: There is a regular, narrow complex bradycardia, with ventricular rate of ~43 bpm. There appear to be P-waves at irregular intervals, but without relationship to the QRS.  Thus, there is third degree (complete) AV block.  The escape is narrow, thus junctional or from the bundle of HIS.  

QRST: The QRS is narrow, so any ST-T abnormalities are primary: there is significant ST elevation in leads II, III, and AVF, with reciprocal ST depression in leads I and AVL, all suggestive of an inferior STEMI. Note that the ST elevation in lead III is greater than that in lead II, but that this is not specific for culprit artery (RCA vs. Left Circumflex).  However, there is ST elevation in lead V1, the furthest right pre-cordial lead, which lies directly over the RV free wall and highly suggests a Right Ventricular MI

The medics activated the cath lab from prehospital.

The patient arrived awake, alert, with only mild chest pain.  The BP was 136/91 with SpO2 of 100% and StO2 (tissue oxygenation) of 69% (slightly below lower limits of normal at 70%).  She had no past medical history.  

Inferior STEMI with RV infarction was diagnosed, IV fluids were hung wide open, Aspirin, Ticagrelor and Heparin were given, and a cardiac ultrasound was performed. 

What do you see?

There is a large, dilated right ventricle with significantly reduced systolic function, with bulging into the left ventricle known as the “D sign”.  There is diffuse hypokinesis that appears to spare the RV apex.  This is known as “McConnell’s sign”, and is seen in both acute PE and RV MI equally. 1  Although not seen well in this view, the left ventricle appears to have mildly reduced systolic function as well.

Additionally, there were no B-lines (with RV MI, one may get cardiogenic shock but without pulmonary edema), as the shock is due to right ventricular failure, which does not lead to the elevated pulmonary capillary pressure that causes pulmonary edema. 

A confirmatory Right Sided EKG was obtained. 

Increasing ST elevation is seen in Leads VR3 through VR6 confirm Right Ventricular MI. 

While preparing for catheterization, the patient's BP dropped to 54/25, with StO2 still at 69%.  Fluids were continued.  1 mg of atropine was given without effect.  Then there was an acute change in mental status with BP 66/53 and congruent with an acute drop in StO2 to 60% (low, indicative of inadequate perfusion).  With this cardiogenic shock, she required intubation for airway protection, as well as transient vasopressors (push dose epinephrine), sedation with ketamine, paralysis with atracurium, and transcutaneous cardiac pacing, which improved her heart rate and perfusion. 

A chest x-ray was done, again with only mild pulmonary edema:

Coronary angiography revealed an acute thrombus with 100% occlusion of the proximal Right Coronary Artery (proximal to the right ventricular marginal branch), successfully stented and reduced. The left coronary arteries were clean.  She required approximately 12 hours on a vasopressor infusion and with an intra-aortic balloon pump, but was successfully weaned, extubated, and left the hospital on Day 4. Her formal echocardiogram revealed full right ventricular function, LVEF of ~50%, and small persistent wall motion abnormality.

Right Coronary Artery Occlusion and Right Ventricular Infarction by ECG
            This patient’s first ECG clearly demonstrated STEMI and the need for cath lab activation.  The right coronary artery is the most common culprit artery in acute inferior MI, but a lesion in the left circumflex artery (LCx) can produce a similar pattern of ST elevation in inferior leads.  Distinguishing an RCA lesion from LCx lesion by early electrocardiogram is often important given the unique consequences of right coronary ischemia, particularly SA node ischemia causing bradycardia and AV nodal ischemia causing AV block, as well as right ventricular MI with dysfunction. Because RV dysfunction can lead to reduced LV filling (pre-load), with resultant hypotension and potentially shock (with greatly increased mortality over isolated LV inferior STEMI)2, it is important for first-line providers to quickly recognize the presence of RV dysfunction in the setting of MI.  Clinically significant RV dysfunction occurs likely in only a minority of inferior myocardial infarctions, due in part to its smaller mass, thinner walls, and extensive collateral circulation 3, 4. When RV dysfunction is observed or suspected, nitrate administration must be avoided, and instead, augmentation of pre-load must be given, commonly through IV fluids.

            In addition to ST elevation in inferior leads, there are several features of the ECG that suggest an RCA lesion and RV ischemia.   Commonly referenced standard of ST elevation in Lead III greater than in Lead II suggests an RCA lesion, but is not specific or sensitive for RV infarction.  Similarly, ST depression in lead aVL is very sensitive and specific for inferior MI, but non-specific for culprit artery (RCA vs. LCx) or the presence of RV infarct 5. Some series suggest the magnitude of ST depression in aVL can be more specific for RCA occlusion, while the absence of any ST depression in lead I is highly suggestive of a Left Circumflex lesion over a RCA lesion 6, 7.  However, claims that ST depression in I is indicative of RV MI are incorrect except to the extent that, by indicating RCA etiology, it makes RVMI possible (circumflex occlusion does NOT cause RV MI).

           Among precordial leads, ST elevation in lead V1, the furthest right precordial lead which lies directly over the RV free wall, is nearly diagnostic of RV STEMI. Investigators have looked at the ratio of ST depression in Lead V3 compared to ST elevation in Lead II (V3:III ratio), finding that a V3:III ratio of less than 0.5 suggests a proximal RCA occlusion8.

Right-sided ECG:           

Confirmation of suspected RV infarction can be seen on right-sided ECG, by placing precordial leads over the right chest, as seen here:

ST elevation in Lead V4R is highly sensitive for an RV infarct, as confirmed by multiple studies.   Specificity for RV infarction approaches 100% if ST elevation in V4R is greater than any ST elevation in V1-V39. One must remember, however, that a right-sided ECG should be obtained early in suspected inferior MI, as the right-sided ST elevation is transient and most prominent early in the course of infarction.

            Not all proximal RCA occlusions result in significant RV MI, especially not in hemodynamically significant RV MI. This is due to extensive collaterals from the LAD to the right ventricle.  In patients with collaterals from the LAD, a high degree of obstructive coronary disease in the LAD can limit the left to right collateral circulation and result in larger RV MI.(10) 

Learning Points:

1. In acute inferior STEMI, on the standard left-sided ECG, STE in Lead V1 predicts RV MI. 

2. Early in the course of an MI, findings on right-sided EKG, particularly ST elevation in Lead V4R, can confirm RV infarction.

3. McConnell's sign and D-sign are not specific to pulmonary embolism, but are equally suggestive of RV MI

4. RV MI can lead to profound shock and death

5. Moderate IV fluid administration can ameliorate the shock and hypotension.

6.  Intubation and paralysis lowers the metabolic needs in cardiogenic shock.

7.  External pacing improves perfusion in shock with bradycardia


            Birnbaum Y, Drew BJ. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad Med J 2003, Vol 79: 490-504

            Birnbaum Y et al. ST segment depression in AVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart Journal, 1993. Vol. 14 (1) 4-7.

                        1 Casazza F et al. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarctions. European Journal of Echocardiography, 2005, Vol. 6: 11-14 

              4 Haupt H, Hutchins G, & Moore G. Right Ventricular Infarction; Role of the Moderator Band Artery in Determining Infarct Size.  Circulation, 1983, 67: 1268-1271

              8Kosuge M et al. New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction. Am J Cardiol 1998, Vol 82: 1318–22.

            9Lopez-Sendon J, Coma-Canella I, Alcasena S, et al. Electrocardiographic findings in acute right ventricular infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2, and V3. J Am Coll Cardiol 1985, Vol 6:1273–9

            3Ondros et al. Right ventricular myocardial infarction: from pathophysiology to diagnosis. Exp Clin Cardiology, 2013. 18 (1): 27-30.

              7Turban et al. Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction.  Ann Noninvasive Electrocardiology, 2003, Vol.8 (3):185-8.

              2Zehender et al. Right Ventricular Infarction as an independent predictor of prognosis after acute inferior myocardial infarction. NEJM, 1993, Vol 328 

                     10.  Haupt HM et al.  Right Ventricular Infarction: Role of the Moderator Band Artery in Determining Infarct Size.  Circulation 1983;67:12168-1272.