This was texted to me. An 80-something woman who presented with chest pain and dyspnea.
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:
- 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.
- For clarity — I've reproduced today's ECG in Figure-1, having 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). |
- 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).
- 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.
- 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).
- 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.
- 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).
- 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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