Friday, July 7, 2023

This was texted to me by a former resident. An 80-something woman who presented with chest pain and dyspnea.

This was texted to me.  An 80-something woman who presented with chest pain and dyspnea.

What do you think?







The rhythm appears to be atrial fibrillation.  In any case, it is clearly a supraventricular rhythm.  There is significant ST depression in V2-V4.  Is this posterior OMI?

Before jumping to any conclusions about the significance of ST-T abnormalities, you must first be certain that they are not a result of (secondary to) any QRS abnormalities. Do you see any such abnormalities?

There is a large R-wave in V1.  Is this RBBB?  No, it is not RBBB.  The QRS is not wide enough, there are no wide S-waves in V5 and V6.

Is it perhaps right ventricular hypertrophy (RVH)?  

Look for right axis deviation.  Indeed, there is a deep S-wave in lead I: Right axis.

This is RVH.  And RVH often has such secondary repolarization abnormalities: STD in V1-V3, usually also with T-wave inversion.

See these cases of RVH:  

Elderly woman w shortness of breath and an ECG that helps to understand it


So I texted back:

"All the ST depression is due to RVH. See the right axis?? And R/S in V1 > 1.  (Large R wave in V1)"

And he responded:

"Ah yeah. That fits. Had big RV on my bedside US. Thanks!!" 

An old formal echo was found from 6 mo ago:

 Dilated right ventricle with septal flattening and estimated right ventricular systolic pressure of 70 mmHg (significant pulmonary hypertension). 

She ruled out for acute MI by troponins.  

See further discussion of R/S ratio greater than 1 in lead V1 by Ken below.


I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:







===================================
MY Comment, by KEN GRAUER, MD (7/7/2023):
===================================
I found today's case extremely interesting as a "follow-up" to our July 5, 2023 post — in which the QOH (Queen OHearts) AI algorithm mistakenly thought the ECG it was given represented OMI with "high confidence", whereas in fact an acute MI was ruled out by serial troponins. The "lesson learned" — was that QOH is not yet flawless in its rulings for all types of tracings.
  • As per My Comment on that July 5 post — I did not view this mistaken judgment by QOH as an "error" in the usual sense of the word — because there simply is not yet a sufficient data bank of similar cases representing the unique ECG pseudo-infarction pattern that we saw in that July 5 post.
  • That said — QOH is already highly sophisticated and accurate in her assessment of ECGs from acute chest pain patients, in which the ECG is not complicated by uncommon OMI mimics.
  • With time (and the ever increasing data bank of more and more ECGs that we do have definitive clinical follow-up for) — the accuracy of the QOH AI algorithm for determining acute OMI vs "no-OMI" will continue to expand in its scope of ECG types that it has been trained to accurately assess.

What is Different about Today's Tracing?
Today's ECG presents QOH with a different type of sophisticated challenge. As per Dr. Smith's above discussion — He was texted today's tracing, told only that this ECG was obtained from an 80-something year old woman who presented with chest pain and dyspnea. 
  • For clarity — I've reproduced today's ECG in Figure-1having deleted the distraction of the 3 long lead rhythm strips that appeared below the original tracing. 

  • NOTE: I was less certain than Dr. Smith that today's tracing did not represent an acute MI in association with "something else". Why might I have thought this?


Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on Today's ECG:
As per Dr. Smith — the rhythm in ECG #1 appears to be AFib with a controlled ventricular response (ie, irregularly irregular without clear sign of P waves).
  • The QRS complex "looks" slightly widened in a number of leads — but does not measure more than 0.10 second in duration, therefore not widened.
  • The frontal plane axis appears to be slightly rightward (ie, with an S wave in lead V1 that is slightly deeper than the R wave is tall).
  • There is no LVH. On the contrary — Overall QRS amplitude in ECG #1 appears to be reduced, especially in all 6 of the chest leads (ie, there is generalized low voltage).

Regarding
 Q-R-S-T Changes:
  • There are small Q waves in leads III and aVF. These are probably not significant.
  • KEY Point: Regarding R wave progression — the QRS complex in lead V1 is not "normal". Instead — there is what appears to be an rsR' configuration, with essentially no negative deflection following the R'. As per Dr. Smith — the Question arises as to WHY this is so?

  • PEARL #1: There clearly are ST-T wave abnormalities in ECG #1 — but I find it far more time-efficient before honing in on ST-T wave abnormalities — to work through the most likely reason for the abnormal QRS complex in lead V1.


Considerations when there is a Tall R in Lead V1:
In my experience — one of the greatest benefits of being systematic in 12-lead ECG interpretation — is that use of the Q-R-S-T memory aid prompts (ie, forces) you to always assess the "R" (ie, R wave progression— and clearly, we have predominant positive forces in lead V1 of ECG #1.
  • PEARL #2: In adults — it is not normal for the R wave in right-sided lead V1 to be taller than the S wave is deep. This is because of left ventricular predominance in adults. As a result — the finding of a Tall R Wave in Lead V1 (ie, R=S or R>S in V1) should prompt the following diagnostic considerations: i) WPW; ii) RBBB; iii) RVH; iv) Posterior MI; v) HCM (Hypertrophic CardioMyopathy); and, vi) Normal Variant (which is a diagnosis of exclusion!).

  • As I discussed in My Comment in the December 10, 2022 post of Dr. Smith's ECG Blog — Once we recognize the abnormal predominant positivity of the QRS in lead V1 of today's tracing — We can run through the above LIST of common potential Causes of a Tall R in Lead V1.

  • Since there are no delta waves and the QRS is not wide in ECG #1 — we are not dealing with WPW.

  • Since the QRS is not wide — there is no "complete" RBBB. That said — there is an rsR' complex in lead V1 — and there are narrow (but deep) terminal S waves in both of the high lateral limb leads ( = leads I and aVL). Although typically, there should also be a terminal S wave in lateral chest lead V6 — not all rbbb conduction defects "read the textbook" — so I would classify the QRS appearance in leads I, aVL and V1 as consistent with incomplete RBBB.

  • As per Dr. Smith — there also appears to be RVH in ECG #1 — because there is a predominant R wave in lead V1 + a rightward axis + incomplete RBBB + low voltage + ST-T wave abnormalities in anterior leads potentially consistent with RV "strain" — with this making 4 ECG findings potentially consistent with RVH in this patient who presented with acute dyspnea (For review on "My Take" for the ECG diagnosis of RVH — Please see My Comment at the bottom of the page in the March 6, 2022 post and in the September 1, 2020 post of Dr. Smith's ECG Blog).

Continuing with the 6 common potential causes of a Tall R in V1:
  • Could there be posterior MI? (After all, this patient did also present with chest pain ...) — See below.

  • Could there be HCM? I'd say probably not given overall reduced voltage (though Echo at the bedside will provide a definitive answer to this question).

  • Finally — today's tracing is clearly not a normal variant.

Putting It All Together: 
Today's ECG shows AFib with a controlled ventricular response — with incomplete RBBB and a number of findings that strongly suggest RVH. What else?
  • I was bothered by the shape of the ST-T wave in leads V1,V2,V3. Typically with incomplete RBBB — the ST-T wave is not nearly as deeply inverted as it is in lead V1 of ECG #1.
  • Typically with RV "strain" — ST-T wave depression is also seen in the inferior leads (but this is not the case in ECG #1).
  • Typically with pure RV "strain" — the ST segment in leads V2,V3 and especially V4 will not be as flattened as it is in ECG #1 — nor will there be the flat ischemic-looking ST segments that we see in leads I and aVL.

  • BOTTOM Line: Until I have more data — I favor open consideration of all possibilities. The only information I had at the time I evaluated ECG #1 — was that this 80-year old woman presented with dyspnea and chest pain  — and that she had an ECG showing AFib with probable RVH and some ST-T wave abnormalities that I felt were not completely typical for incomplete RBBB and RV "strain". Therefore — I was not yet ready to rule out the possibility that this patient might not also have had recent posterior MI (especially given the ST-T wave appearance in leads V3,V4). 

CASE Follow-Up:
As per Dr. Smith — the clinician caring for today's patient did an Echo showing a large RV — and apparently ruled out the possibility of recent infarction.
  • P.S.: On my "Wish List" for QOH — I'd LOVE to see her eventually incorporate a more extensive differential diagnosis beyond simply declaring "OMI" or "No OMI". That said — I already LOVE the QOH AI application! 
 

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