A 16 year old girl with altered mental status and possible overdose

A 16 year old girl presented with altered mental status, probably due to alcohol intoxication, but also with possible overdose.

As part of her workup, she had an ECG:
The computer interpreted this as Left Bundle Branch Block
The overreading physician confirmed this read.
2 subsequent identical ECGs were confirmed as left bundle branch block, by different physicians.
What do you think?

























This ECG was texted to me in real time by the resident, asking what it was.
My immediate reply: WPW

Notice the very short PR interval and the profound delta waves.  This is clearly NOT left bundle branch block.

Case continued

The patient awoke from her intoxication without complications.  She and her mother denied ever having palpitations, tachycardia, chest pain, or shortness of breath.

Diagnosis:

Asymptomatic WPW.


Management:

The management of asymptomatic WPW is beyond the scope of this blog.  Suffice it to say that there is a very high incidence of serious events in untreated children with this ECG finding.

See this publication: 

The Natural History of Asymptomatic Ventricular Pre-Excitation: A Long-Term Prospective Follow-Up Study of 184 Asymptomatic Children.  Journal of the American College of Cardiology.  Volume 53, Issue 3, 20 January 2009, Pages 275–28.



Such cases should all be referred to cardiology, pediatric cardiology, or an electrophysiologist, avoid exercise until follow up, and call 911 for chest pain, SOB, or palpitations.


Computer interpretations:

The computer is often wrong, but leads to serious diagnostic momentum.  What would the overreading physicians have interpreted had the computer:

1) Given some other diagnosis?  
2) Given no diagnosis at all?  
3) Or if the physicians read the ECG first, then looked at the computer interpretation?

I don't know. How did you interpret it?  Correctly?  Or as LBBB?


I will be presenting an abstract at SAEM on the diagnosis of atrial dysrhythmias by computer and by overread, compared to a new neural network, machine-learning algorithm.  When the standard diagnostic algorithm falsely diagnosed atrial fibrillation, the physician corrected it only half the time.  By the way, the new algorithm performed far better.


Learning Point

1.  Blind yourself to the computer interpretation until you make your own.
2. Only then look at the computer interpretation.
3. Then look back at the ECG if the computer sees something (accurate or not) that you did not.























ST Elevation and QS-waves in a patient with Dyspnea

I was shown this ECG of a patient with dyspnea:
My interpretation: "Subacute STEMI"
In other words, STEMI of at least 6 hours duration, and more typically greater than 12 hours.


ECG differential may include: Old anterior MI with persistent ST Elevation (LV aneurysm morphology).

Which is it?

My rule for differentiating acute STEMI from LV aneurysm really only reliably distinguishes between:
1. acute STEMI on the one hand
2. subacute STEMI or LV aneurysm on the other.

What is the rule?

First, there must be ST Elevation.
Second, the ECG differential diagnosis much be LV aneurysm vs. acute STEMI.

This rule should not be used for early repol vs. acute STEMI.  Conversely, if the differential is LV aneurysm vs. acute STEMI, then you should NOT use the early repol formula.

When should LV aneurysm be on the ECG differential diagnosis?  Primarily when there are well-formed Q-waves, with at least one QS-wave, in V1-V4.  A QS-wave is defined by absence of any R-wave or r-wave of at least 1 mm.  (If there is an R-wave or r-wave, we call the whole wave a QR-wave, Qr-wave, or qR-wave, depending on the relative size of the Q-wave vs. R-wave.)

The rule: If there is one lead of V1-V4 in which the T/QRS ratio is greater than 0.36, then acute STEMI is the likely diagnosis, though subacute STEMI is also possible.  Since both require the cath lab, if the ratio is greater than 0.36, and the clinical situation is right (i.e., unexplained chest discomfort), then cath lab activation is indicated.  I both derived and validated this formula, for which the cutoff has good sensitivity and specificity:
Derivationhttp://www.sciencedirect.com/science/article/pii/S0735675705000811
(accuracy of formula = 93.2%)
Validationhttp://www.sciencedirect.com/science/article/pii/S0735675715001904
Validation full text
Sensitivity 91%, specificity 81%

False negatives had pain duration greater than 6 hours. Thus, it may classify those patients with prolonged chest pain as LV aneurysm when they are really subacute STEMI.

This case

If the formula were used here, then lead V4 would have a T/QRS ratio of 5/11.5 = 0.43.  Only one lead is needed, so the criterion is met for acute STEMI.

Really, however, LV aneurysm was never on my differential diagnosis when I glanced at this ECG.

Why?     It is true that there are QS-waves in all of V1-V4, which might lead you to believe it is LV aneurysm.  However, this ECG has up to 4 mm of ST elevation (in V4, 4 mm STE is relative to an 11.5 mm S-wave), and I have never seen an LV aneurysm case with this much ST elevation.


This is a typical LV aneurysm:





Then my partner told me about the case:

A middle aged woman presented in pulmonary edema. She had suffered from chest pain 2 weeks earlier.

She had an immediate bedside ultrasound:


Many B-lines of pulmonary edema



Here is a view of her left ventricle:



Akinetic Septum and Apex.  Echo differential is large anteroseptal MI vs. Takotsubo.


Short axis view:

Akinetic septum.  Since this is more focal, takotsubo is much less likely.



Here is a view using Speckle tracking strain echocardiography, which can be done on our ED POCUS machines.






There is a surprising amount of collapse of the inferior vena cave (IVC):




She was stabilized on noninvasive positive pressure ventilation and was able to lie flat for an angiogram.

The patient was taken to the cath lab and a 100% thrombotic mid-LAD occlusion was found.



Troponin I profile:
This troponin profile is consistent with an MI that occurred many days ago and was much higher then.  The slight rise may be due to the additional stress of acute pulmonary edema. 


Echo on day 3:
38% ejection fraction
Anteroapical Wall motion abnormality.
ECG:
Now the T/QRS ratio is 4/13,which is less than 0.36
But it is more than it should be after successful reperfusion.
This is a bad sign and indicates poor microvascular reperfusion.
Such persistent ST elevation after reperfusion is an ECG sign that an LV aneurysm will develop.

















What is the culprit artery? Not what you think.


An elderly woman who was quite healthy except for some chronic renal insufficiency and hypertension had 3 days of classic angina lasting only 10-15 minutes at a time, but which became more constant on the day of presentation.

She called 911.  Medics palpated a pulse of 80 and a BP of 140 systolic, and recorded this prehospital ECG (day 1):

Atrial Fibrillation at a rate of about 120.
Profound ST depression: leads I, II, III, aVF, V3-V6.
There is STE in aVR (reciprocal ST elevation, reciprocal to the ST depression)
This is classic diffuse subendocardial ischemia.


She was given a sublingual nitroglycerin and her BP dropped to 80 systolic.

On arrival, she still had chest pressure and this ECG was recorded:
Atrial fibrillation with rapid ventricular response
Diffuse ST depression, as with prehospital ECG


Is the ischemia a result of atrial fib with RVR, or is atrial fib with RVR just exacerbating ischemia whose source is acute coronary syndrome?

The history is highly suggestive of ACS.

The patient was given a diltiazem bolus and drip, her pulse slowed, and her chest pain completely resolved.  Another ECG was recorded:
Atrial Fib with a controlled rate
The ST Depression is mostly resolved with this slower rate

The first troponin was, not surprisingly, elevated at 1.07 ng/mL.  

The blood pressure was well maintained.  The patient was started on heparin and aspirin, and coronary angiography was planned for the next morning but also with plans to take her emergently to the cath lab if her pain recurred or if the ST depression recurred.

She did well overnight.  The troponin peaked on day 2 at 3.0 ng/mL (expected with complete resolution of ischemia -- this rise is due to ischemia that occurred before the rate control).

The ECG showed near complete resolution of ischemia on day 2:
Now converted to sinus rhythm.
Only minimal residual ST depression


Formal Echo showed a subtle inferior wall motion abnormality.

For various reasons, partly due to her calculated risk of angiography, she did not go to the cath lab that day.

The next day (day 3), the pain recurred and another ECG was recorded:
Inferior-posterior-and lateral subtle STEMI


At this point, she went emergently to the cath lab and had a circumflex occlusion with thrombus.


Comment 1:

You thought it was going to be LAD or Left Main, right?  It certainly could have been.  But it is important to remember that ischemic ST depression does not localize.  When there is diffuse subendocardial ischemia, it can be due to any culprit artery.  This is proven in stress testing, in which the location of the ST depression during stress does not predict the stenosed artery.  Why is this?  Uncertain.

In this case, the thrombus in the circumflex on day 1 was non-occlusive, resulting in subendocardial ischemia that manifested as ST depression in many leads.  It is tempting to say that the ST depression was "posterior STEMI" on these initial ECGs, but that is not so.  The ST depression was not V1-V3 (as in posterior STEMI), but rather V3-V6 (which is what is seen in subendocardial ischemia).  Furthermore, there was ST depression in I, II, III, and aVF.  The ST depression vector was inferior and anterior, with a reciprocal ST elevation vector that is superior (resulting in STE in aVR).

2 days later, when the artery completely occludes, real STEMI results, with an ST elevation vector towards inferior and posterior walls.  Complete occlusion reverses the ST vector! 


Comment 2:

This is a great example of how the dichotomy between STEMI and Non-STEMI is false.  They are both due to thrombus in the coronary artery and both are very dangerous.  STEMI and NonSTEMI exist on a spectrum.  Thrombus can lyse and propagate, and NonSTEMI can convert to STEMI.

Ten cases of hyperacute T-waves in V4-V6

Here are 10 cases with hyperacute T-waves in V4-V6.

Each case is interesting and you can click on the link to read the entire case.

1.

Chest pain relieved by Maalox and viscous lidocaine





3.
http://hqmeded-ecg.blogspot.com/2014/11/an-elderly-man-with-severe-chest.html




4.
http://hqmeded-ecg.blogspot.com/2015/04/ventricular-fibrillation-resuscitation.html




5.
http://hqmeded-ecg.blogspot.com/2011/12/subtle-inferoposterolateral-stemi.html



6.
http://hqmeded-ecg.blogspot.com/2012/01/subtle-anterior-transient-injury.html


7.
http://hqmeded-ecg.blogspot.com/2016/03/this-case-was-sent-by-one-of-our-great.html


8.
http://hqmeded-ecg.blogspot.com/2014/08/poor-microvascular-reperfusion-no.html


9.
http://hqmeded-ecg.blogspot.com/2011/06/unstable-angina-then-prehospital-subtle.html



10.
http://hqmeded-ecg.blogspot.com/2016/11/what-are-these-wide-complexes.html


8 year-old with report of "syncope and an abnormal ECG".

This case was contributed by John Dunbar, an outstanding Hennepin EM Resident.

A previously healthy, fully immunized 8 year-old African American boy presented with a report of "syncope and abnormal ECG" by EMS.  

On arrival to the ED, he was awake but lethargic with EMS report of normal prehospital glucose by EMS, HR in the 90s and BP's in the 110s/70s and O2 sats of at least 98% on room air.  Immediately, a bedside cardiac ultrasound was performed while the ECG was being setup and this showed good global function, no effusion, no overt ventricular enlargement or septal hypertrophy (measurements not taken) and a normal caliber IVC without B-lines bilaterally.  A 12-lead ECG was performed as below and looked similar to the prehospital ECG (not available): 
Figure 1.
Sinus rhythm with normal axis.
Biphasic T-waves with asymmetric T-wave inversion in V1-V4
ST elevation in V1, V2, V3.
Unusual T-wave inversion in V2 and V3

The ECG was texted to Dr. Smith contemporaneously with the patient's ED evaluation and this is what Smith wrote:"Is he African American?  This is a different kind of normal variant.  This is not a case of classic juvenile T-waves.  Check out the following blog post which shows some other normal variants, of which this is one: Persistent Juvenile T-wave Pattern. This post has examples of various benign T-wave patterns."

Normal variants T-wave inversion includes, but is not limited to:
1.  ST-T Normal Variation (STTNV) 
2. "Persistent" Juvenile T-waves 
      --As they're not really "persistent," it is more appropriately called Juvenile T-W Pattern (JTWP) because this T-wave pattern is normal for the very young and up until adolescence, but it is not necessarily persistent, in that it may come and go.
3.  Benign T-wave Inversion (BTWI), which is often lumped together with STTNV (1).  

I like to differentiate BTWI from STTNV.  BTWI, which Dr. Smith first learned about in Chou's textbook "Electrocardiography in Clinical Practice," has STE and T-wave inversion primarily in V3-V6; STTNV primarily in V2 and V3. 


The pattern in this 8 yo is consistent with ST-T Normal Variation (STTNV), also called “ST Elevation and Inverted T Wave.”  It is a normal variant of early repolarization that can persist just like Juvenile T-wave Pattern (JTWP).
Here are two examples of STTNV from the earlier post which was written largely by Brooks Walsh (http://hqmeded-ecg.blogspot.com/2015/01/persistent-juvenile-t-wave-pattern.html):

Choo 2002 (2)
T-wave inversion is mostly in V2 and V3
STTNV
Figure 2.

2009 Papadakis (3)
STTNV
Again, mostly in V2 and V3
Figure 3.

1. The ST elevation in V1-V3 with the asymmetric t-wave inversions is what makes this STTNV. This pattern is less commonly seen in children. Some consider it a variant of JTWP, though others feel it is a separate entity (1).  This pattern is subtly different from Benign T-Wave Inversion, which is primarily in V3-V6 (see 3 examples below) and this post: Benign T-wave Inversion: view video or read text


2. Juvenile T-wave pattern (JTWP) does have asymmetric inverted T-waves in V1-V3, as in this normal ECG from a 3 year old, borrowed from Chan et al. (10).  These T-wave inversions can extend to V4.
Juvenile T-wave Pattern
Figure 4: ECG of 3 year-old girl showing characteristics of JTWP:
Shallow T-wave inversions, limited to V1-V3, V4
Assymetric morphology of the inverted T-wave
No significant ST Elevation


Here is are 3 examples of Benign T-wave Inversion:
Notice the precordial T-wave Inversion is primarily in V3-V6.  There is typical STE of early repol in V2.  There is a small S-wave and large R-wave in V4.  Often there is also T-wave inversion in inferior leads.









Commentary

JTWP, BTWP, and STTNV can persist into adulthood and complicate presentations for chest pain, syncope, palpitations, SOB, etc. as these patterns have to be differentiated from ACS, PE, ARVD, etc.

- PJTWP typically resolves by age 19 in males and age 30 in women and is more common in women (4, 5, 6, 7, 8, 9)  

- BTWI is more common in African American males and athletes. (1).

Dr. K. Wang has shown that STTNV (which Smith calls BTWI, as the ECGs in this cohort all had T-wave inversion in V3-V6) is by far most common in African American males.   Smith has studied all the EKGs in his cohort and found that:

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

Case Continued

With respect to this specific case, the history was more consistent with a seizure: while at the store, he reported to his mother he didn't feel well with a mild frontal headache. He then collapsed and was noted by an EMT bystander to have eye deviation, rhythmic tongue movements and increased tonic activity.  When EMS arrived 6 minutes later, he remained confused with his eyes open unable to follow commands more consistent with postictal state than syncope. On arrival to the ED he was drowsy with a non-focal exam and persistence of his mild headache that resolved over 30 minutes or so. He had no prodromal symptoms other than headache, no antecedent illness and no fevers.

However, given the perceived ECG abnormalities, Peds Cardiology was asked to review the ECG and reported it was normal but did not expand.  When sent to Dr. Smith, he immediately recognized the T-wave inversions are a normal variant similar to STTNV.  This has been reviewed in the blog before and you can explore the prior posts (http://hqmeded-ecg.blogspot.com/search?q=juvenile) for more details.  Differentiating pathologic findings from normal variants among both adult and pediatric ECGs is paramount both for rapid diagnosis and prevention of therapeutic delay on the one hand, and avoiding excessive downstream testing on the other. 

After normal labs and period of observation patient was discharged with close follow up with pediatric neurology and diagnosis of first time seizure.  

References:
(1) Roukoz H.  Wang K.  ST Elevation and Inverted T Wave as Another Normal Variant Mimicking Acute Myocardial Infarction: The Prevalence, Age, Gender, and Racial Distribution.  Annals of Noninvasive Electrocardiology 16(1):64-69, January 2011.   doi:10.1111/j.1542-474X.2010.00410.x.
This is Benign T-wave Inversion

(2) Choo JK, Abernethy III WB, Hutter Jr. AM. Electrocardiographic observations in professional football players. Am. J. Cardiol.2002;90(2):198-200. doi:10.1016/S0002-9149(02)02454-2.

(3) Papadakis M, Basavarajaiah S, Rawlins J, et al. Prevalence and significance of T-wave inversions in predominantly Caucasian adolescent athletes. Eur. Heart J. 2009;30(14):1728-1735. doi:10.1093/eurheartj/ehp164.

(4)  Marcus FI.  Prevalence of T-Wave Inversion Beyond V1 in Young Normal Individuals and Usefulness for the Diagnosis of Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia.  Am J Cardiol 2005;95:1070-1071.

(5) Kaid KA, Maqsood A, Cohen M, Rothfeld E. Further characterization of the “persistent juvenile T-wave pattern” in adults. J. Electrocardiol. 2008;41(6):644-645. doi:10.1016/j.jelectrocard.2008.08.028.

(6) Aro AL, Anttonen O, Tikkanen JT, et al. Prevalence and Prognostic Significance of T-Wave Inversions in Right Precordial Leads of a 12-Lead Electrocardiogram in the Middle-Aged Subjects. Circulation 2012;125(21):2572-2577. doi:10.1161/CIRCULATIONAHA.112.098681.

(7) Assali A-R, Khamaysi N, Birnbaum Y. Juvenile ECG pattern in adult black arabs. J. Electrocardiol. 1997;30(2):87-90. doi:10.1016/S0022-0736(97)80014-3.

(8) Malhotra A, Dhutia H, Gati S, et al. 103 Prevalence and significance of anterior T wave inversion in females. Heart Br. Card. Soc.2014;100 Suppl 3:A60. doi:10.1136/heartjnl-2014-306118.103.

(9).  Rawlins J, Carre F, Kervio G, et al. Ethnic Differences in Physiological Cardiac Adaptation to Intense Physical Exercise in Highly Trained Female Athletes. Circulation 2010;121(9):1078-1085. doi:10.1161/CIRCULATIONAHA.109.917211.

(10).  Chan TC, Sharieff GQ, Brady WJ. Electrocardiographic Manifestations: Pediatric ECG. J. Emerg. Med. 2008;35(4):421-430. doi:10.1016/j.jemermed.2007.09.039.