Tuesday, March 20, 2018

Hypotensive and Tachycardic in Clinic: A Quick Ticket to the ED and Lewis Leads

This was contributed by one of our fine interns, Aaron Robinson.

A 40-something male cancer patient presented to clinic for a routine follow up and stated he was feeling “tired.” He was just finishing a course of antibiotics for bacteremia. 

His BP was found to be 60 systolic with a heart rate in the 170s.  He was moved to the Emergency Department.

He appeared ill, but was not acutely in distress. He showed signs of volume depletion.

His initial ECG is shown below. What do you see?
Initial ECG: This is a regular narrow complex tachycardia at a rate of 157 BPM. 

There is no obvious atrial activity prior to the QRS. There seems to be some perturbation of the T wave (inverted retrograde P-waves, seen in PSVT) in the inferior leads making SVT very likely. 

Smith comment: The differential of regular narrow complex tachycardia at a rate of 157 is: 
1. sinus tach
2. paroxysmal SVT (PSVT, due to AVNRT or WPW)
3. atrial flutter with 2:1 conduction, and 
4. very rarely, junctional tachycardia. 

You can see what appear to be small negative waves after nearly every QRS.  This would indicate PSVT  When you become accustomed to seeing these, you can readily recognized them as retrograde P-waves.

We have seen many instances in which sinus tachycardia was misdiagnosed as SVT.  Here is one:

A Relatively Narrow Complex Tachycardia at a Rate of 180.

So if you're uncertain whether these are retrograde P-waves, and are wondering if you are missing sinus tachycardia, and the patient is stable (as here), you can try Lewis leads to see if sinus P-waves appear.  

It takes about 30 seconds to align Lewis leads and then switch to lead I to see the result.

Aaron continues: Bedside cardiac US demonstrated a hyperdynamic and tachycardic heart with IVC variation with each breath, suggesting volume depletion, as we initially suspected. 

Fluid resuscitation was started but the rate stayed between 160 and 170. 

Smith comment: assessing response to volume repletion is a great way to confirm sinus tach.  Sinus is an automatic rhythm with varying rate, where re-entrant rhythms such as PSVT are always at a constant rate.  If the rate slowly drifts down, this confirms sinus.  If the rate does not change, you have not confirmed a non-sinus rhythm, but you have made it far more likely.

Aaron continues:  The physicians then re-arranged the limb leads of the 12-lead ECG in the Lewis Leads pattern, in order to better identify P-waves, or lack thereof.   

Smith comment: it is much easier to use the monitor leads for Lewis lead placement than to use the 12-lead.   

For a quick review on Lewis Lead Placement, check out this post.

  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.
Aaron continues: The 12-lead ECG using Lewis Leads is below. What do you see?  Remember, look at Lead I. In this example, Lead II is helpful too.
In this ECG, retrograde atrial activity is more obvious in the Lewis Leads.  Do you notice anything weird about the P-waves? They are upright, with 2 humps! The Lewis Leads were reversed on this 12-lead EKG, such that retrograde P-waves appeared upright.  

Just as importantly, the Lewis leads did not uncover normal upright P-waves in front of the QRS.  Thus, Lewis leads did not reveal sinus rhythm; at the same time, they did confirm retrograde P-waves, but because the leads were reversed, it was somewhat confusing!   

Regardless, this Lewis Lead ECG helped the physicians confirm the diagnosis of SVT with retrograde P waves.

The patient was given 6mg adenosine and converted to a rate in the 110’s. His post-adenosine ECG is below.
Normal sinus rhythm

Learning Points:
1.     The most important takeaway from this case is that you should use Lewis Leads on the monitor, not on the 12-lead EKG (even though limb leads on the 12-lead will suffice). You will be able to have a live view of the appropriate leads on the monitor. You don’t need all 12 leads!
2.     Lewis Leads can help to ascertain atrial activity by focusing the electrodes on the atria.
3.     Be mindful of lead reversal. If something doesn’t make sense, consider reversed leads. Check out this LITFL page for a quick summary on lead reversal. In our case, it caused the P waves to be upright, not negative like we expected. 

Here is another very nice case using Lewis leads:

Wide Complex Tachycardia. What is the Diagnosis?

Friday, March 16, 2018

Are these Wellens' waves?

This ECG was sent to me by one of my residents, who was puzzled by it:

This ECG is from a 21 yo M with PMH of poly-substance abuse.  He presented with nausea and vomiting after drinking the night before.  He denied any chest pain or shortness of breath.  He has no other significant medical history he does not take any medications.

This one was read by the computer as "Acute STEMI" (!!)
What do you think?
My resident thought this looked like Wellens' pattern in lead V2

Some hours later, this was recorded:
Now there is resolution of the inverted T-wave in V2

Electrolytes were normal.

My response:

I looked at the ECGs before reading anything.

The one read as acute STEMI was clearly early repol to me.  

What particularly confuses one would be the T-wave inversion in V2.  However, also notice that there is an rSr' in both V1 and V2.  Notice that in the second ECG, these are gone and the T-wave inversion is not present.  Both of these findings (rSr' and T-wave inversion in lead V2) are seen if V1 and V2 are recorded too high on the chest, which is a very common recording error, but not well known among physicians.  The second ECG is normalized.  I strongly suspect that they were not recorded with the leads in the same position.  Or the patient was lying down for the first one and sitting up for the second, which changes the position of the heart in the chest.

I showed this to Brooks Walsh, see below.  He added this important aspect:

There is one complication: normally, the P-wave in V1 is biphasic.  When the leads are placed too high, the P-wave in V1 is all negative, because all atrial depolarization is moving down, away from the highly placed leads.

In this case, there are all upright P-waves in V1 in both ECGs.  But look also at limb leads: the P-wave is inverted!  Thus, in this case, there is an ectopic atrial rhythm, not sinus rhythm.  This ectopic atrial rhythm accounts for the upright P-waves in V1 and V2, even though the leads were placed too high.

In other words, if you depend on P-wave morphology in lead V1 to tell you if the leads are placed too high, you would be misled!

Learning Points:

1. rSr' in lead V1 is often a result of leads placed too high

2. this also results in T-wave inversion in lead V2.

3. this should also result in an all negative P-wave in V1, unless there is a co-existing ectopic atrial rhythm, as in this case.

My friend, co-author and frequent blog poster, Brooks Walsh, just wrote a great article on this topic.

Here it is:

Wednesday, March 14, 2018

Syncope, History of Coronary Disease, and ST Elevation: Should Medics Activate the Cath Lab?

A 60-something male had a syncopal episode.  911 was called.   The patient had no complaint of chest pain or shortness of breath. A prehospital ECG was recorded:

Limb leads
Precordial Leads
There is ST Elevation in V1-V3, and in aVL, with reciprocal ST depression in II, III, and aVF.
There is also some ST depression in V5 and V6, and ST elevation in aVR.
What do you think?

The medics interpreted the ST elevation, with reciprocal ST depression, as STEMI, and activated the cath lab.

Note that you cannot see the entire QRS on the prehospital ECG.  The R-waves in leads II and III are cut off.  The S-waves in V1-V3 are cut off.  There is likely to be very high voltage that is cut off.

It is important to remember that not all ST elevation with reciprocal ST depression is a manifestation of STEMI.   LVH, LBBB, and WPW can all have ST Elevation with reciprocal ST depression. Especially LVH.

On arrival, I looked at the ECG and immediately knew it was a false positive due to LVH.

An ECG was recorded in the ED:
This confirms high voltage. QRS is 118 ms.
There is no evidence of STEMI.
All ST deviation is a result of LVH with secondary repolarization abnormalities
These are secondary to abnormal depolarization due to LVH, with high voltage.
These are expected ST-T abnormalities given the high voltage abnormal QRS.
They are not "primary" ST-T abnormalities of ischemia.

This ECG has similarities to Left Bundle Branch Block (LBBB), but it is NOT LBBB because the QRS is not long enough and there is not enough delay from onset of the QRS to peak of R-wave in lateral leads.  Q-waves in V5 and V6, and absence of monophasic R-wave in aVL also argue against LBBB.  See more on LBBB and LVH at the bottom of the post.

The cath lab was de-activated.

There was further history:

The patient had not anything to eat or drink all day long and felt subjectively dehydrated. He had been walking much of the day, then went to the bathroom and after urinating became light headed and fell w/ brief loss of consciousness.

There was never any chest pain or dyspnea.

He had a history of CABG and ischemic cardiomyopathy.

A repeat ECG 3 hours later was not different.


The troponins were slightly positive, peaking at 0.52 ng/mL (not consistent with STEMI).  Cr. was elevated, consistent with dehydration.

Echo showed:

Decreased left ventricular systolic performance, moderately-severe, EF about 35%, with LV enlargement.
Asynchronous interventricular septal motion consistent with left bundle branch block (although the ECG did not show LBBB).
Regional wall motion abnormality-distal septum and apex.
Evidence for dilated left ventricle with regional dysfunction in the LAD distribution. 
Markedly dysynchronous septal motion consistent with LBBB.

Thus, there is echo evidence of myocardial infarction (new or old), thought to be old.  Syncope could have been vasovagal (neurocardiogenic, triggered by dehydration), but with poor LV function, it could also have been due to ventricular tachycardia.  Acute type I MI is much less likely.  Troponin elevation is probably due to type II MI: underperfusion in the setting of chronic coronary disease.

The patient refused further investigations and was discharged.

Learning Points:

1. Syncope alone is an uncommon presentation of STEMI.  Any ECG finding with ST elevation should be approached with skepticism if there is no chest pain or chest discomfort.

Corollary: It should be very unusual for medics to activate the cath lab for syncope alone, without chest pain, as any associated ST Elevation is likely to be a false positive.

2. LVH is a common cause of false positive ST elevation, and often has reciprocal ST depression.

LBBB has recently been re-defined:

Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the era of cardiac resynchronization therapy. Am J Cardiol. 2011;107(6):927–34.

Here is a quote from the abstract: 

"Three key studies over the past 65 years have suggested that 1/3 of patients diagnosed with LBBB by conventional electrocardiographic criteria may not have true complete LBBB, but likely have a combination of left ventricular hypertrophy and left anterior fascicular block. On the basis of additional insights from computer simulations, the investigators propose stricter criteria for complete LBBB that include a QRS duration ≥140 ms for men and ≥130 ms for women, along with mid-QRS notching or slurring in ≥2 contiguous leads. Further studies are needed to reinvestigate the electrocardiographic criteria for complete LBBB and the implications of these criteria for selecting patients for CRT." 

One more very short article with full text: 

Int Cardiovasc Res J. 7(2):39-40.LBBB: State of the Art Criteria.

Monday, March 12, 2018

A crashing patient with an abnormal ECG that you must recognize

Written by Pendell Meyers, with edits from Steve Smith

Let's consider this nearly pathognomonic ECG without the clinical context (because sometimes the clinical context will not be as easy as in this case).
What is the answer?

This ECG is diagnostic of hemodynamically significant acute right heart strain. Notice I did not say "pulmonary embolism," because any form of severe acute right heart strain may produce this ECG. This includes, but is not limited to, PE, asthma/COPD exacerbation, hypoxic vasoconstriction from pneumonia, acute pulmonary hypertension exacerbation.  It has even been seen anecdotally in acute cessation or discontinuation of continuous IV pulmonary vasodilator.

The findings include sinus tachycardia, characteristic QRS morphology most diagnostic in V3 with a small R wave followed by a very large S wave with a convex upward ST segment morphology, ST segment strain morphology in the inferior and anterior leads leading to deep symmetric T-wave inversion.

Why is it not Wellens??? (Wellens pattern is a term which refers to coronary reperfusion morphology in the anterior leads)

The best answer is because the entire gestalt of the ECG shows acute right heart strain instead, and just does not look like Wellens after you've seen Wellens hundreds of times. It is true that the morphology of the T-wave inversions can be very similar in anterior reperfusion syndrome (Wellens). It is also true that anterior and inferior T-wave inversion could be consistent with reperfusion of a type III wraparound LAD occlusion, despite the fact that Kosuge et al showed that T-wave inversion in lead III is much more likely to be PE than ACS if your differential contains nothing else.  However, in reperfusion (Wellens'), the symptoms are resolved at the time of the ECG.  Thus, it is critical to compare the ECG with the symptomatic state of the patient!  

Differences of Pulmonary Embolism T-waves from Wellens' T-waves:
1. Wellens' is a syndrome of a painless period following an anginal (chest pain) event.  Coronary reperfusion changes on ECG should be accompanied by significant reduction or resolution of symptoms. In this case we have a crashing patient while T-wave inversion is ongoing!

2. Acute coronary occlusion (especially during reperfusion) is very rarely accompanied by tachycardia.  When there is tachycardia, the patient is in cardiogenic shock with very poor LV function on bedside echo.

3. The T-waves simply look different in Wellens'.  Here is an example of Wellens'.  We hope you can see the difference:

See these cases for more examples: 

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

Please notice in particular the morphology in V2-V3, as I believe this is particularly helpful to describe as evidence of acute right heart strain, including:

- Generally much bigger S-wave than R-wave
- Usually either isoelectric J-point or some small J-point elevation followed by convex upward ST segment elevation rollercoastering into T-wave inversion
- Usually some ST segment depression in the more lateral leads V4-V6 and the inferior leads, also with T-wave inversion
- Please note that these QRS characteristics will not apply in the not-uncommon scenario that the patient develops acute RBBB because of the strain on the RV

Here are the blown up images of V2-V3 from several of the cases on this blog with acute right heart strain (all but one of which was due to pulmonary embolism, and the other was due to acute severe asthma exacerbation)

Now that we've learned the lesson, let's watch this very interesting case play out:

A female in her 40s with history of HTN and obesity presented with progressively worsening dyspnea with mild exertion, and now with dyspnea at rest over the past 4 days. She also complained of generalized weakness, lightheadedness, diaphoresis, chest pain, and cough. On initial exam she appeared acutely ill, with initial vitals showing tachycardia, hypoxia, and borderline hypotension.

Here is her initial ECG, followed by her repeat ECG approximately 15 minutes later:

Bedside echo was done.  This one is from a previous case on this blog,  but is similar to this patient:

This shows impressively obvious right heart strain.  The LV is small (underfilled) with good function. 

She was appropriately anticoagulated immediately with heparin before going to CT scan.
There are filling defects in both main pulmonary arteries. The pulmonary artery trunk is dilated at 35mm per radiology report.

Filling defects are seen to extend to bilateral lobar, interloper, and segmental branches diffusely throughout both lungs. This is a very large clot burden. Radiology commented that the inter ventricular septum is bowed towards the left ventricle, suggestive of right heart strain.

Troponin T returned elevated at 0.12 ng/mL. NT pro BP returned at 10,676 pg/mL.

Despite heparin and supportive care, the patients mental status and blood pressure worsened. She was diagnosed with massive PE and given intravenous tPA with rapid improvement in hemodynamics and mental status.

She had an uneventful ICU course and improved steadily over the course of a week. She was discharged and did well.

Here is her ECG on day 2 after much improvement in hemodynamics and oxygenation:
Tachycardia has resolved. ST and T-wave abnormalities evolving appropriately.

Here is her ECG on day 4:
Almost entirely back to normal.

 Learning Points:

1) The history and exam will not always be this obvious, yet in cases this severe, the ECG findings often are obvious if you know what to look for.

2) The cells of the right ventricle do not know why they are having such a hard time when they report their acute strain on the ECG. Whether it's a PE or a severe asthma attack, the cellular physiology of these cells is acutely the same. Therefore the ECG is also indistinguishable between acute right heart strain etiologies.

3) Reperfusion T-wave inversion should be present in the pain free state. These T-wave inversions in the anterior and inferior leads during pain are likely to be due to acute right heart strain from PE.

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 

Friday, March 9, 2018

A patient with a "seizure" and a completely "normal" ECG

I happened on this ECG while walking by, and read it with no clinical information, remarked on it, and discussed it with the physicians caring for the patient.
The computer read the ECG as completely normal.

I heard this clinical information: This patient presented with a "seizure," and was to be worked up by neurology for new onset of seizures.

What do you think?

The computer measured the QT at 420 ms, and QTc at 445 ms.

Let's magnify V2 and V3:

Here I put lines in at the onset of the QRS and end of the T-wave (or is it a U-wave?)
Approximately 595 ms

Here I point out an apparent U-wave in V1
So it is possible that the T-wave is really a U-wave
A long QU interval is just as dangerous.

The K returned at 2.5 mEq/L and it turns out that the patient had been having diarrhea.

There was a previous ECG recorded with K = 3.6 mEq/L
Much more normal, although has some nonspecific ST depression

The patient did not likely have a seizure, but more likely had an episode of VT (Torsades de Pointes) which resulted in tonic clonic activity.

Even after the K returned low, no clinician went back to look at the ECG to see if there were any findings.  No clinician questioned the symptom of "seizure."   The faculty physician involved is one of the smartest and best clinicians I've ever worked with, and very good at ECG interpretation.  Yet he did not scrutinize the ECG.

This is the problem with computerized interpretations.  People tend to trust them implicitly, and turn off their critical faculties.

Learning Points:

1. Always look at the QT interval.  If it looks long, you must measure it.  Do not trust the computer.  On the other hand, when it looks normal, it is usually accurate.  (That is why it works in the formula for differentiating subtle LAD occlusion from normal variant ST elevation.)

2.  A long QT could be a long QU interval (prominent U-wave), but the danger of polymorphic ventricular tachycardia (Torsades de Pointes) is just as high.

3.  Even when the computer states the ECG is completely normal, it may be very abnormal.

There was a paper last year contending that if the computer reads the ECG as normal, the physician need not look at it, at least not in triage.

I discuss this paper here:

A middle-aged woman with chest pain and a "normal" ECG in triage

Read these:

In depth on QT correction and QT in general:

QT Correction Formulas Compared to The Rule of Thumb ("Half the QT")

I just posted this case yesterday.  Both of these cases were this week.

Thursday, March 8, 2018

Alcohol withdrawal and sinus tachycardia

This patient with alcohol withdrawal and tachycardia had an ECG recorded:
What do you think?

There is sinus tachycardia.

Look at the QT interval: it is far more than half the QT.  The computer reads the QT at 386 ms, and QTc of 462 (proprietary correction formula unknown!)

Read this article: 

QT Correction Formulas Compared to The Rule of Thumb ("Half the QT")

I measure the QT at 440 ms.  RR interval is 470 ms.  It is possible that what we are seeing is a fusion of the T- and U-wave, but the consequences are similar.

Here is the QTc:
Very long QT !!
(Fridericia is best; at heart rates over 60, Bazett results in a QT that is too long)

The magnesium returned at 1.2 mEq/L  (low).

There was also a profound metabolic alkalosis, with K = 3.0 mEq/L.

The patient is at high risk of Torsades.

Learning Point:

Do not trust the computer measurement of the QT interval when it looks long!

Monday, March 5, 2018

To activate or not to activate?

Written by Pendell Meyers, with edits by Steve Smith

I was texted this ECG with no clinical information:
(This will be called ECG-2)
What do you think?

I replied "Actually I think this might be a false positive."

The ECG shows sinus rhythm with relatively normal QRS complex followed by large STE in V1-V3, with ~4mm STE in V2. There are no pathologic Q-waves, no terminal QRS distortion. I do not think there is any STD in the inferior leads; there is a tiny amount of PR depression (normal) and the J-point is exactly on line with the PR interval. In lead III the T-wave does slope downward at first, but I just didn't think this was convincing morphology to be called reciprocal STD.

I was left with concerning anterior STE which may be a normal variant or may be LAD occlusion, so I used the SubtleSTEMI app on my phone:

3 variable


I sent it immediately to Dr. Smith with no clinical information. He saw it on his phone without the QT (so could not use the formulas), and responded: "That is a really tough one. But I think it is actually a normal variant. My best guess, but I am not sure. Did you use the formulas?"

It turns out this was from a male in his 50s with history of smoking and HTN but no known CAD who presented due to chest pain radiating to the right cheek and right arm, which had awoken him from sleep early in the morning. By the time he arrived in the ED, his pain had apparently spontaneously resolved.

Here was his initial ED ECG earlier that morning (ECG-1):

There is a small amount of STE in V1 and V2, but much less than the ECG above. This ECG is easily within normal limits.

The patient had an initial undetectable troponin and was placed in the observation unit for serial troponins and CTCA vs. stress test.

While waiting in the observation unit, the patient suddenly complained of returning chest pain.  This is when ECG-2 was recorded; here it is again:

The following ECG (ECG-3) was recorded 10 minutes later:
Similar findings with dramatic STE in V2. There is no reciprocal STD.

The treating clinicians interpreted his return of pain with dynamic ECG changes and dramatic STE in the anterior leads as a "STEMI," and activated the cath lab (appropriately).

Here is the result:
Normal left circulation (except for a 40% D1 nonculprit stenosis according to the report).

Normal right circulation.

Non-obstructive CAD, no coronary occlusion. Repeat ECG after cath was unchanged. Serial troponins were all undetectable. Echo was done and was unremarkable.

What do you think the final diagnosis was in the chart?

"Pericarditis," of course. He was treated with colchicine and discharged. This patient likely did not have pericarditis. It is much more likely that this ECG is simply a normal variant. Normal variants can change dramatically and dynamically as above. It is an unfortunate truth that we have shown on this blog many times.

Let me be clear: we are not advocating that this patient should not have been cathed emergently. Any patient with a concerning clinical picture or ECG may deserve emergent cath. Dynamic and dramatic STE in general does in fact have a significant rate of true positive acute coronary occlusion. Additionally, diagnostic cath (without any coronary intervention) is a very low risk procedure. But expert ECG interpretation can often predict the false positives in the group of dramatic ECG findings.

Would I have activated the cath lab? Assuming his clinical appearance was as concerning as it sounds on paper, I still think it would have been perfectly reasonable to do so, although in the back of my mind I would suspect a false positive. And that is completely acceptable and likely good care, because the ECG cannot identify all acute coronary occlusion. I would make sure that I am not overlooking the possibility of other dangerous etiologies of chest pain including dissection and PE before letting the patient roll away to the cath lab.

When this specific population (benign early repolarization vs. subtle LAD occlusion) was studied, R-wave amplitude in V4 was the most important predictor variable, more important than STE. QRS amplitude in V2 and QTc were also as important as STE. This is because acute coronary occlusion does not follow the rules of the "STEMI criteria." Instead, you must become expert in ECG interpretation by learning from cases such as these.

Smith comment: 

1. Is there an alternative to activating the cath lab if you suspect normal variant?  Yes. If you can get a rapid high quality, bubble contrast enhanced echocardiogram, read by an expert, and, while the patient has symptoms and ECG findings, it shows no wall motion abnormality (WMA), then you can be certain that it is normal variant.

2.  Caveat: However, frequently clinicians do such an echocardiogram after symptoms and ECG findings have resolved. This is hazardous! Although there is usually some residual stunning (WMA),  sometimes the ischemia was so brief that the wall motion completely recovers.  This would be a false negative echo and leave the patient with an unstable plaque and thrombus in the coronary artery that would then not be intervened upon.

Friday, March 2, 2018

Scary ST Elevation. What is it?

911 was called for an 18 year old who had altered mental status after using K2 (a recreational drug).  The medics put the patient on the monitor and saw ST elevation.  They then recorded a prehospital 12-lead (not shown, as it is identical to the ED ECG), which showed marked ST Elevation.  The computer diagnosed "Pericarditis."  They were very worried, and brought the patient to the "Stabilization Room" for critically ill patients.

On arrival, I looked at the prehospital ECG (again, identical to the ED ECG shown below):
What did I think?

I immediately said "Normal Variant ST Elevation," and directed the patient to our "Special Care Unit" for altered mental status from drugs and alcohol.

This is not pericarditis, nor is it STEMI.  Get to know this pattern just like you would get to know a friend.  I called him "Jack," and told the residents to get to know Jack.

Jack often has high voltage QRS, has marked J-waves (they look almost like Osborn waves).  There is a relatively short QT interval.  The ST Elevation is towards leads II and V5.  Thus, there is no reciprocal ST depression in aVL. [In fact, these could be Osborn waves, but they were not: the patient was not hypothermic.]

Although the T-wave is negative in aVL, it is NOT T-wave inversion, as the QRS-T angle is narrow (QRS axis is 85 degrees, almost directly inferior; T-wave axis is 68 degrees -- angle is only 17 degrees.  Both these measurements are accurately made by the computer algorithm.)

How do I know it is not pericarditis?  First, the patient denied any chest pain!  Second, normal variant STE is far more common that pericarditis.  There are J-waves, no PR depression, and no Spodick's sign (downsloping T-P segment -- of questionable reliability).

It is very common for Normal Variant STE to be misdiagnosed as pericarditis.  Does this have adverse consequences??  It may.  Take a look at this case that was written by Pendell Meyers when he was a medical student: due to misdiagnosis of the ECG as "pericarditis", a patient's chest pain was misattributed to pericarditis and the correct diagnosis of pulmonary embolism was ignored:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

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