This ECG was handed to one of my partners who was working in triage.
My partner immediately diagnosed inferior OMI. (Do you see: the subtle STE in III and aVF? The terminal QRS distortion in aVF? The ST depression in aVL? The ST depression in V2-V4 of posterior OMI? There is terminal T-wave inversion in III with terminal upright T-wave in aVL -- This strongly suggests reperfusion IF the patient's symptoms have subsided. But they had not.)
This was read by the conventional algorithm as "Nonspecific ST-T abnormalities". It was overread by an interventional cardiologist also as nonspecific.
He went to find the patient: Middle-aged man was working this afternoon when he developed sudden onset lightheadedness with diaphoresis, nausea, and had multiple episodes of emesis. The symptoms persisted for several hours, so his wife convinced him to come to the hospital. He has no history of similar symptoms.
This ECG is diagnostic regardless of whether the patient has chest pain or not.
He specifically denies chest pain or trouble breathing. This was confirmed over and over with the patient.
All of my partners are good at recognizing OMI on the ECG.
He sent it to the Queen of Hearts:
The patient was taken to the critical care area. His systolic blood pressure was 80 mmHg and his lactate was 6 mEq/L. The patient is in shock.
Why was he in shock? ---The answer is on the ECG.
If you are not sure, maybe you will understand after seeing this ECG recorded 17 minutes later:
There is much more obvious STE in V1 that, especially in the context of inferior OMI, is diagnostic of right ventricular (RV) OMI (RV MI). This implies a proximal RCA occlusion, proximal to the RV marginal branch which supplies the RV. Not all proximal RCA OMI cause RV MI physiology (decreased RV cardiac output) and RV ECG ischemia: often the RV gets collateral circulation from the LAD which protects it from events like this.
He was taken to the cath lab and a total occlusion of the proximal RCA was found.
Angiographic findings:
1. Left main: no stenosis.
2. LAD: 40-50% ostial stenosis, otherwise luminal irregularities.
3. LCX: Large, nondominant. Supplies a large OM. Luminal irregularities,
but no stenosis.
4. RCA: proximal thrombotic or embolic occlusion with TIMI 0 flow. It
supplies an RPDA (inferior OMI) and RPLA (posterior OMI) without stenoses.
A post PCI ECG was recorded:
Another similar ECG was recorded an hour later:
--Normal left ventricular cavity size, wall thickness and systolic function; estimated ejection fraction is 55-60%.
--Regional wall motion abnormality in the mid to basal inferior segments.
--Moderately dilated right ventricle with moderately reduced right ventricular systolic function.
The estimated pulmonary artery systolic pressure is 17 mmHg + RA pressure.
Based on the appearance of the IVC, the RA pressure is significantly elevated. (Smith: this is because of decreased RV output, so it backs up into the RA)
So this too supports RV infarction.
Right Ventricular infarction (RV OMI)
Treatment of RV infarction prior to reperfusion: possibly some gentle hydration (see below) and norepinephrine to keep systolic BP high. Unlike the LV which is perfused during diastole (because of very high chamber pressure during systole), the low pressure RV is perfused best in systole. Keeping the systolic BP normal is very important for mitigating RV ischemia. Even with an occluded RV marginal branch, collateral circulation can save the RV if the systolic pressure is high enough.
Gentle hydration: Caution to avoid excessive volume administration; overdistension of the ischemically dilated RV can lead to pressure on the septum and decreased LV output, similar to PE. It can also result in the descending limb of the Starling curve, resulting in further depression of RV pump performance.
The best single lead for RV infarction on the normal 12-lead is V1. If there is not STD in V2, V1 has moderate sensitivity for proximal RCA occlusion. But if there is any STD in V2, there is posterior OMI which "pulls down" the ST in V1 also, hiding the RV infarction.
More articles on danger of RV OMI:
Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. New Engl Journal. You can support the diagnosis of RV MI using Right Ventricular Leads, particularly V4R, but Kosuge (above) showed that even V4R ST segment can be pulled down by the ST depression of posterior MI, leading to a false negative.
Right ventricular dysfunction and risk of heart failure and mortality after myocardial infarction. JACC
MY Comment, by KEN GRAUER, MD (5/10/2024):
- I focus my comments on this story — in which I'll add some thoughts to Dr. Smith's excellent discussion. For clarity — I've labeled the 4 serial tracings in today's case.
- Did YOU Notice the rhythm in ECG #1?
- HINT: The rhythm in ECG #1 is not sinus!
- For the rhythm to be sinus — the P wave should be upright in lead II. The only 2 exceptions to this statement are dextrocardia and lead misplacement.
- The YELLOW arrows in lead II of ECG #1 show that no P wave is present in this lead. Instead — a small, upright P wave is seen in leads I and aVL (BLUE arrows in these leads). There is no lead reversal. This pattern, in which no definite P wave is seen in lead II — but an upright P wave is seen in leads I and aVL — is consistent with a low atrial rhythm.
- KEY Point: A low atrial rhythm is most often a common normal variant — although in today's case, it may convey similar implications as would a junctional escape rhythm. That said, while clinical management of today's patient is not altered by not having a sinus rhythm — You can simplify life (and never overlook sinus rhythm again) by routinely spending the first 2-3 seconds of your inspection of every ECG you encounter by scanning the long lead II rhythm strip with your educated "eye" to make sure that each QRS is preceded by an upright P wave.
- NOTE: ECG #2 was obtained 17 minutes later. RED arrows in ECG #2 show the return of sinus rhythm (RED arrows in the long lead II of ECG #2). Beats #9 and 10 in ECG #2 occur early, and are probably PACs (with beat #10 probably being conducted with aberration).
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| Figure-1: I've labeled the first 2 ECGs in today's case. |
- Once we've established that the rhythm in ECG #1 is supraventricular (ie, a low atrial rhythm, as noted above) — my "eye" was immediately drawn to lead III (within the RED rectangle), which shows a large Q wave, ST segment coving with subtle-but-definite ST elevation, and terminal T wave inversion.
- Confirmation that the subtle ST segment elevation in lead III is real and acute — is forthcoming within seconds from the 2 frontal plane leads enclosed within the BLUE rectangles: i) In lead aVF — the Q wave and ST segment straightening with slight ST elevation conveys support from this neighboring lead to lead III; and, ii) In high-lateral lead aVL — we see the precise mirror-image opposite ST-T wave picture as we see in lead III. This reciprocal change is also seen in the other high-lateral limb lead ( = lead I) — and verifies the diagnosis of acute inferior OMI until proven otherwise.
- We've emphasized on multiple occasions that the ST-T wave in leads V2 and V3 should normally show slight, gentle-upsloping ST segment elevation. Instead, lead V2 in ECG #1 (within the RED rectangle) jumps out as manifesting a flat (straight) ST segment without any ST elevation. Given that we've already established the diagnosis of acute inferior OMI — the ST-T wave appearance within this RED rectangle establishes the diagnosis of associated posterior OMI (which is further supported by abrupt transition to a predominant R wave already by lead V2).
- Within the BLUE rectangle in neighboring lead V3 — we see ST segment flattening and slight-but-real ST depression — thus providing further evidence of acute infero-postero OMI.
- NOTE: The time it should take for an "educated eye" to appreciate the above ECG findings within the 2 RED and 3 BLUE rectangles should be less than 20 seconds.
- KEY Point: As soon as the acute infero-postero OMI was recognized in ECG #1 — our "eye" should be drawn to the disproportionately tall and "fat" T wave in lead V1 of this tracing (within the PURPLE rectangle). As per Dr. Smith — the clinical importance of appreciating that the tiny QRS complex in lead V1 should not display a disproportionate hypervoluminous T wave — is that this finding is diagnostic of acute RV MI (thereby explaining this patient's hypotension). In addition, this finding localizes the "culprit" artery to the proximal RCA.
- In ECG #1 — ST segment flattening with slight depression from posterior OMI was most marked in leads V2 and V3.
- 17 minutes later with the recording of ECG #2 — we see marked increase in the ST elevation from the RV MI in leads V1,V2 — such that lead V2 no longer shows ST-T wave changes of posterior OMI (within the PURPLE rectangles in ECG #2). In contrast — the limb leads in ECG #2 show no significant serial change.
- I completely agree with Dr. Smith — that the "theme" of these post-PCI rhythms is the development of variations of AIVR (Accelerated IdioVentricular Rhythm) — which given the timing of this rhythm, suggests this is a reperfusion arrhythmia (that is often associated with successful reperfusion from PCI).
- AIVR is most often a transient occurrence in the post-PCI setting. Although the "atrial kick" is lost — most patientts will be hemodynamically stable (from the successful PCI), in which case no intervention is needed!
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| Figure-2: I've labeled the 3rd and 4th ECGs in today's case. |
- I did not think any P waves were present in ECG #3 for the first 10 beats in the long lead II rhythm strip. I dropped a vertical RED line from the onset of the very wide QRS in lead I. This told me that the initial slurring and notching in lead II did not represent atrial activity — but instead formed the inital part of the QRS complex in this lead.
- Despite the resemblance to LBBB morphology in the first 10 beats (ie, with an all-upright R wave in lateral leads I and aVL — and a predominantly negative QRS in anterior leads V1,V2,V3) — the lack of atrial activity overwhelmingly favored a ventricular rhythm (rather than a junctional rhythm with LBBB) as the cause for QRS widening.
- KEY Point: AIVR with LBBB-like morphology suggests that this ventricular rhythm is arising from the right ventricle — which is consistent with the acute RV MI producing shock in today's case.
- Beats #12 and 13 — are sinus conducted (RED arrows highlighting definite sinus P waves in front of beats #12 and 13).
- Working backward — I thought the RED arrow in front of beat #11 was also a sinus P wave, albeit with a shorter PR interval than that seen before beats #12 and 13.
- The QRS complex of beat #11 is clearly wider than the QRS of sinus beats #12 and 13 — but not as wide as the 10 QRS complexes that preceed beat #11 (This is perhaps easier to appreciate by looking at the simultaneously-recorded beats in the 12-lead tracing above the long lead II rhythm strip). Therefore — beat #11 is a fusion beat! (a determination that further supports our deduction that beats #1-thru-10 are ventricular in etiology = AIVR).
- The confusing part to me in ECG #3 — was the changing QRS morphology for beats #1-thru-10 in the long lead II rhythm strip. For clarity — I labeled the wide, equiphasic complexes with an "X" ( = beats #1-thru-7; #9) — and the wide predominantly negative complexes with a "Y" ( = beats #8 and 10).
- Whereas the R-R interval for complexes "X" were equal to each other — the 2 "Y" complexes were preceded by a slightly shorter R-R interval.
- MY THEORY: I suspect there are 2 ventricular sites, each producing their own version of AIVR. In support of my theory — Note that ~1 hour later, ECG #4 now shows all beats in the long lead II of this 2nd post-PCI tracing with the same QRS morphology — that is consistent with the predominantly negative morphology of complex "Y" (and with a slightly faster AIVR rate than was seen for AIVR by the "X" complexes in ECG #3).
- The rate of AIVR with the "X" complexes is ~75/minute (an R-R interval = 4 large boxes).
- The rate of AIVR with the "Y" complexes is 85-90/minute (an R-R interval = 3.4 large boxes — and similar to the shorter coupling interval for the 2 "Y" complex beats in ECG #3).
- It is because the rate of AIVR with the "Y" complexes is slightly faster than the rate of the "X" complexes — that we see dominance of the "Y" AIVR in ECG #4.
- While clearly more difficult to assess ST-T wave morphology when confronted with 2 different AIVR morphologies — the coved and markedly elevated ST segment in lead III of ECG #3 and ECG #4 simply should not be there!
- In the chest leads — Note the dramatic difference in the shape of the coved and markedly elevated ST segment in lead V1 of these 2 post-PCI tracings — compared to the upward concavity and much less elevated ST segments in lead V2 and V3. Isn't this similar to the "interplay" we saw in ECGs #1 and #2 between lead V1 ST elevation from RV MI — and lack of ST elevation in leads V2,V3 from the posterior OMI?
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