Wednesday, August 30, 2023

A woman in her 70s with chest pain

Case sent by Logan Stark MD, written by Pendell Meyers 

A woman in her 70s presented with acute chest pain. It started 10 hours prior to arrival, then had improved, then recently returned. No prior ECG was available. 

Here is her triage ECG:

What do you think?

The ECG was sent to me with no information, and I replied "OMI".

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

V1 and V2 have abnormal STE, and V2 has a hyperacute T wave. There is reciprocal STD in II, III, and aVF. 

One more thing that should be mentioned: since there are only Q waves from V1 to V3, it is possible that there was an old anterior wall MI, or that the current event is subacute, or acute on top of an old Q wave. Regardless, V2 with a hyperacute T wave and abnormal T/S ratio means there must be acute OMI, regardless of prior events. The pattern overall is similar to the "South African flag sign".

The initial high sensitivity troponin I returned at only 19 ng/L (which is elevated in this assay, as the URL is 12 ng/L for women). Does that change your interpretation??


Hopefully it confers even more benefit to reperfusion, since the troponin has not risen very high yet. Notice how the patients onset of symptoms (10 hours ago) is potentially misleading if you ignore the intermittent nature of her symptoms.

The cath lab was activated immediately (before the troponin of course), and the patient was taken to cath and found to have acute proximal LAD occlusion (unknown initial TIMI flow, but corrected to TIMI 3 with PCI). 

Here are her ECGs after cath over the next 12 hours:

The repeat ECGs alone prove that the initial ECG shows OMI, since there are reperfusion findings in the same leads as the initial OMI findings. There is deflation of the hyperacute T waves and then progressive terminal T wave inversion. 


If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

MY Comment, by KEN GRAUER, MD (8/30/2023):
The 2 Key Questions regarding today’s presentation are the following:
  • Question #1: Is the ECG in Figure-1 likely to represent an ongoing or recent OMI in need of prompt cath and PCI?
  • Question #2: How fast can we answer Question #1?

For clarity in Figure-1 — I’ve reproduced the initial tracing in today’s case.

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

Addressing the 2 KEY Questions:
For followers of Dr. Smith’s ECG Blog — it will often be easy and quick to answer these 2 Questions:
  • Point #1: Is the history worrisome? Obviously a history of new-onset CP (Chest Pain) in a patient of a certain age and risk profile would immediately place the patient in a “higher-risk” group. Today's case involves a woman in her 70s who describes "acute CP" that began ~10 hours earlier — so this history clearly increases our concern.

  • Point #2: Followers of Dr. Smith's ECG Blog who have long ago replaced the outdated "STEMI paradigm" with the much more sensitive and specific OMI Paradigm (most recently reviewed in Dr. Smith's OMI Lecture — and in Dr. Mark Hellerman's OMI Pocket Guide— will immediately recognize the other critical piece of information in the history from today's patient = The patient's CP improved — and then returned, at which time she presented to the ED.

  • The OMI Paradigm integrates the clinical reality that acute coronary occlusion may be punctuated by periods during which CP decreases as a result of spontaneous reopening of the "culprit" vessel — but that such spontaneous reopening may be followed at any point by spontaneous reclosure, sometimes with the "culprit" vessel spontaneously opening and closing a number of times until a final state is reached. 
  • As a result, marked ST elevation that may have been present at the onset of symptoms — may be greatly reduced (or even "pseudo"-normalized) — IF the initial ECG is obtained after a reduction of symptoms!

  • Point #3: Ideally — We would have more information regarding the specifics correlating the timing and relative severity of this patient's symptoms — with the timing of when ECG #1 was obtained (ie, Had this patient's CP returned minutes — or an hour or more, before this initial ED ECG was recorded?)
  • That said, even without that information — the history provided above by today's patient is potentially consistent with such spontaneous reopening of the "culprit" vessel — which means that despite a lack (or a minimal amount) of frank ST elevation — in this higher-risk patient with a very worrisome history for a recent or ongoing acute coronary event — even subtle signs of OMI suffice to warrant prompt cardiac catheterization!

What About Today's ECG?
Given the above history in today's case — I viewed ECG #1 asking myself, "Are there any ECG findings that are definitely abnormal enough to merit prompt cath?" While completely agreeing with Dr. Meyers' interpretation and the High-Confidence OMI interpretation by QOH (Queen OHearts) — I'll add the following perspective:
  • As per Dr. Meyers — there are QS complexes in leads V1,V2,V3 (as well as an r wave that is still of small amplitude in lead V4). This lack of anterior forces could be an acute finding — and/or — indicative of an acute event superimposed on prior anteroseptal infarction.
  • As per Dr. Meyers — the ST-T wave in lead V2 looks hyperacute (definite straightening of the ST segment takeoff in this lead — with a disproportionate amount of ST elevation given tiny size of the QRS — with a wider-than-expected ST segment base). But as potentially ominous as the ST-T wave in lead V2 looks — I wanted more evidence before concluding that ECG #1 represented definite indication for prompt cath.
  • The ST segment in lead V1 is coved, with slight elevation and surprisingly deep T wave inversion — so clearly suspicious in association with lead V2 findings of proximal LAD occlusion — but I still wanted a bit more.
  • Unfortunately — lead V3 is uninterpretable for assessing acute changes because of artifactual distortion of the ST-T wave in this lead. IF I were to still be in doubt about my interpretation after looking at all 12 leads — then the uninterpretable nature of this very important neighboring lead V3 could justify immediately repeating the ECG.

That said — Repeating ECG #1 was not necessary ...
  • There is simply NO way that the ST-T waves in each of the inferior leads is a "normal" finding. Note that each of the ST segments in leads II,III,aVF are abnormally straight, slightly depressed — and finish with a disproportionately tall terminal T wave. Whether this is all a reflection of reciprocal changes to acute LAD OMI, or perhaps reflects some component of reperfusion change in this patient with waxing and waning CP, is uncertain. What is certain — is that these inferior lead ST-T wave changes + the hyperacute ST-T wave in lead V2 + the history in this 70s woman are diagnostic of recent and/or ongoing acute LAD OMI in need of prompt cath.

  • Additional Findings in ECG #1: Completing my survey of all 12 leads in today's initial tracing — there is: i) A surprisingly unimpressive ST-T wave in lead aVL (I suspect that some of the ST elevation that usually accompanies acute proximal LAD OMI has "pseudo"-normalized because of a component of spontaneous reperfusion)ii) The T wave in lead V4 (and to a lesser extent — probably also the T waves in leads V5,V6) is also probably hyperacute (ie, disproportionately hypervoluminous compared to the small size of the QRS)andiii) I suspect that if the artifact in lead V3 was eliminated — that the ST-T wave in this lead would manifest a "transition" appearance between the hyperacute T wave with ST elevation in lead V2 — and the non-elevated but hyperacute T wave in lead V4.

  • BOTTOM Line: The decision that prompt cath is needed in today's case is one that can (should) be reached within the very few minutes needed to establish the history of waxing and waning CP over the previous 10 hours — and the minute or two that it takes to record this 1st ECG. Experienced providers versed in the OMI paradigm will recognize the above ECG changes I describe in less than 1 minute. 

ADDENDUM: What is the Rhythm in ECG #3 ???

Did YOU notice that the 3rd ECG shown above in today's case has group beating? (ie, Alternating short-long R-R intervals for beats #1-2; 3-4; 5-6; 7-8; and 9-10 in Figure-2)
  • As I've often emphasized in my comments in Dr. Smith's ECG Blog — the presence of group beating in association with an acute (or recent) MI should suggest the possibility of 2nd-degree AV Block, Mobitz Type I ( = AV Wenckebach). Is Mobitz I the cause of the group beating that we see in Figure-2?

Figure-2: I've reproduced the 3rd ECG shown above by Dr. Meyers in today's case. Does the group beating that we see represent Mobitz I, 2nd-degree AV block?

Mobitz I, 2nd-degree AV block ( = AV Wenckebach) — is probably the most common AV conduction disturbance seen in association with acute or recent inferior MI. It is not nearly as common with acute LAD occlusion, as was seen on cath in today's case.
  • The group beating seen in the long lead II rhythm strip of ECG #3 is unlikely to be the result of chance — since with the exception of the last 2 beats in the tracing, the shorter R-R intervals are of similar (albeit not exact) duration — and the longer R-R intervals are also of similar duration.

  • We can definitely rule out 2nd-degree AV block of the Mobitz I type — because: i) The atrial rhythm is not regular; ii) The PR interval is not increasing from the 1st-to-the-2nd beat in each group; andiii) There is no dropped (non-conducted) on-time P wave during the pauses, as there has to be with Mobitz I.

  • The rhythm in Figure-2 is also not Mobitz II because: i) The QRS is not wide (as it usually is with Mobitz II); andii) There is no dropped (non-conducted) on-time P wave during the pauses, as there should be with Mobitz II.

  • Although sinus arrhythmia may sometimes occur in a pattern that resembles "group beating" — I thought the difference in R-R interval duration between shorter and longer cycles in Figure-2 was much greater than would be expected with sinus arrhythmia.

This left 2 additional considerations. I've drawn laddergrams in Figure-3 and Figure-4 to illustrate these 2 remaining possibilities.
  • As I emphasize in my September 26, 2020 post of Dr. Smith's ECG Blog — the most common cause of a pause is a blocked PAC (and not some form of AV block).
  • IF the cause of the group beating that we see in ECG #3 is blocked PACs — then a laddergram of this would look like Figure-3, in which the early-occurring PACs would be hiding under the BLUE arrows. When PACs occur very early during the cycle — they may fall within the ARP (Absolute Refractory Period), and therefore not be conducted
  • That said — I simply can not convince myself that there is any evidence of "tell-tale" notching indicative of a hidden PAC within any of the even-numbered beat T waves in any of the simultaneously-recorded leads seen in Figure-2.

Figure-3: Laddergram showing what blocked PACs would look like.

As I discuss in My Comment at the bottom of the page in the May 25, 2022 post in Dr. Smith's ECG Blog — SA Block is a potential cause of repetitive group beating in which the atrial rhythm is not regular — the PR interval does not increase — and the in which there is no non-conducted P wave within the longer R-R intervals.
  • IF the cause of the group beating that we see in ECG #3 is SA block — then a laddergram of this might look like Figure-4in which the rate of impulse formation from the SA node remains regular (with minimal variation due to sinus arrhythmia) — but only 2 out of every 3 SA nodal impulses are able to make it out of the SA node into the atria.
  • That said — SA block is rare. I would simply not expect to see it in the very last ECG in today's case at a time when PCI successfully reestablished flow to the "culprit" artery, and the patient was otherwise doing well.

Figure-4: Laddergram showing what SA block would look like.

BOTTOM Line regarding the Rhythm in ECG #3:
I fully acknowledge not knowing the cause of the group beating that we see in ECG #3
  • Perhaps the most common cause of short pauses is operative — with blocked PACs being completely hidden within the T waves under the BLUE arrows in Figure-3?
  • Or perhaps the group beating is simply the result of sinus arrhythmia that by chance results in alternating R-R intervals of very similar size?

  • MY Hunch: I suspect that the cause of the group beating we see in ECG #3 is benign, whatever the specific etiology turns out to be. I wish a little longer period of monitoring would have been obtained — which I suspect would have told us what the true cause is. That said — the sharp clinician who does not want to overlook rhythm disorders will be systematic in the assessment of every rhythm encountered — and will not overlook the  group beating present in today's 3rd ECG.

  • P.S.: I'll close with this link to My Comment in the April 6, 2023 post in Dr. Smith's ECG Blog — in which I illustrate how failure to be systematic in rhythm assessment (with failure to recognize group beating) — resulted in overlooking an AV block that was clinically significant.

Saturday, August 19, 2023

75 year old dialysis patient with nausea, vomiting and lightheadedness

Written by Jesse McLaren


A 75 year-old patient with diabetes and end stage renal disease was sent to the ED after dialysis for three days of nausea, vomiting, loose stool, lightheadedness and fatigue. RR18 sat 99% HR 90 BP 90/60, afebrile.  Below is the 15 lead ECG. What do you think? 

There’s normal sinus rhythm, normal conduction, normal axis, normal R wave progression and normal voltages. There’s subtle inferior ST elevation with straightening of the ST segment, reciprocal ST depression and T wave inversion in aVL, and ST depression in V2. This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R).


Because the patient had no chest pain or shortness of breath, they were initially diagnosed as gastroenteritis. Potassium was normal. The ECG above was only done an hour after arrival, when the first high sensitivity troponin I returned at 300ng/L (normal <26 in males and <16 in females). But because the patient had no chest pain or shortness of breath, it was not deemed to be from ACS.


This is not unusual. In a large database of patients with MI, those on dialysis had greater frequency of comorbidities but only 44% presented with chest pain. They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. They had had twice the rate of cardiac arrest and twice the in-hospital mortality[1] In another study of patients diagnosed with STEMI, those on dialysis experienced delayed reperfusion and double the mortality.[2]


Two hours after arrival another ECG was done:

Now STEMI(+)OMI, but the patient still had no chest pain or shortness of breath, so the ED physician requested a stat cardiology consult. Cardiology did not think it was "STEMI", but repeated the troponin.


Four hours after arrival, the second troponin rose to 700, and another 12 and 15 lead ECG were done:

Still OMI but not STEMI on anterior or posterior leads.


It would have been easy for this patient to be admitted as “non-STEMI” with further delay to angiogram. Fortunately, the cath lab was activated: 99% proximal RCA occlusion with TIMI 2 flow. Peak troponin was 4,000 and echo revealed basal/inferior wall hypokinesis.


Discharge ECG showed inferior Q waves and infero/posterior reperfusion T waves:


ECG interpretation vs clinical application


It’s common for the clinical picture to cloud ECG interpretation. As with any test, the ECG is a tool for clinical decision-making and needs clinical correlation. But the first step is correct ECG interpretation, in isolation. You don’t need clinical assessment to know the troponin because it has a specific value that doesn’t depend on patient symptoms. The lab interprets the troponin in isolation, and then you correlate the results clinically. It didn’t matter that the patient had no chest pain, because their first troponin was 300; Similarly, it didn’t matter that the patient had no chest pain, because their ECG showed OMI. But ECGs interpretation is often conflated with clinical assessment, so if patients don’t present with chest pain the ischemic changes are not seen or are attributed to something other than ischemia.


Instead, ECGs need to be interpreted in isolation and then applied to the patient. This is how OMI can be taught to AI, which can help identify patients at risk of missed occlusions. I sent the first ECG to the Queen of Hearts app:

With this high confidence on ECG interpretation in isolation, the clinician could then apply this to the clinical picture: a dialysis patient with GI symptoms and lightheadedness (potential anginal equivalents), without any clinical evidence for this being a type 2 OMI, and with myocarditis being a diagnosis of exclusion. This could have expedited cath lab activation and saved myocardium.



Take home

1.     Dialysis patients have a high rate of ACS without chest pain and high rate of delayed diagnosis and delayed reperfusion

2.     Primary ST depression in aVL reciprocal to subtle inferior ST elevation can identify inferior STEMI(-)OMI

3.     Ischemic ST depression max V1-4 is highly specific for posterior OMI, and posterior leads can be falsely negative

4.     ECG interpretation needs to be done in isolation and then applied to the patient, and this way AI can help identify patients at risk of missed occlusions



1.     Herzog et al. Clinical characteristics of dialysis patients with acute myocardial infarction in the United States. A collaborative project of the United States Renal Data System and the National Registry of Myocardial Infarction. Circulation 2007

2.     Khan et al. Contemporary trends and outcomes in patients with ST-segment elevation myocardial infarction and end-stage renal disease on dialysis: insights from the National Inpatient Sample. Cardiovasc Resvasc Med 2020


MY Comment, by KEN GRAUER, MD (8/19/2023):


Today's case has similarities to other cases we frequently present in Dr. Smith's ECG Blog — namely despite clear signs on the initial ECG suggesting acute coronary occlusion — this stemi-negative but OMI-positive tracing was not only discounted after the initial ECG, but still not acted on even after the initial troponin assay came back elevated primarily because the patient did not have chest pain (See this December 6, 2022 casealso by Dr. McLaren — as well as others on Dr. Smith's ECG Blog).
  • In the hope of constructive commentary — I focus my observations on a number of Problems in Management that today's case illustrates — which can (and hopefully will) be corrected.

For clarity in Figure-1 — I've labeled today's initial tracing. 

Figure-1: The initial ECG in today’s case.

Problem #1: 
As I emphasized in My Comment in the December 6, 2022 post — Not all patients with acute MI report chest pain. The Framingham studies from many years ago taught us that the incidence of Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

  • The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
  • But in the other half of this 30% (ie, in ~15% of all patients with MI) — although these patients found on follow-up ECG to have had infarction did not have chest pain — they did have "something else" thought to be associated with their MI.
  • The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).

  • BOTTOM Line: Be aware of the entity of Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is often appreciated. We need to remember that not all patients with acute (or recent) MI have chest pain with their event.

  • Application to Today's Case: As an older (ie, 75 years old) patient with diabetes (as well as end-stage renal failure) — who presented because of a several day history including GI symptoms, lightheadedness and fatigue, but no fever — today's patient had a host of features that might predispose to an infarction without chest pain.

Problem #2:
As should be evident in Figure-1 — Today's initial ECG is diagnostic of acute OMI.
  • All 3 inferior leads not only demonstrate subtle-but-real ST elevation — but also hyperacute T waves (especially in lead III — in which there should be no doubt that the ST segment takeoff is overly straight — with a "fatter"-than-it-should-be T wave peak and, a wider-than-it-should-be ST-T wave base).
  • In addition — infarction Q waves are seen in all 3 inferior leads (ie, Given modest QRS amplitude — each of these inferior Q waves is wider than I would expect for a septal or normal variant Q wave).
  • The above said — the reason to emphasize that ECG #1 is diagnostic of acute OMI until you prove otherwise — is the mirror-image opposite (reciprocal) ST-T wave changes seen in lead aVLNothing else is needed — since these 4 leads definitively say, "Acute OMI until proven otherwise".

Problem #3:
Although no additional leads beyond leads II,III,aVF and aVL should be needed to justify (and activate) prompt cath — the remaining 9 leads on this initial 15-lead ECG provide more incontrovertible evidence:
  • When doubt exists about the acuity of inferior OMI — ST-T wave changes in selected chest leads may suggest acute (or recent) posterior MI that reinforces an already decisive OMI diagnosis.
  • As I've often emphasized — use of the Mirror Test facilitates rapid recognition of acute (or recent) posterior MI. This is based on the principle that ST depression maximal in leads V2-thru-V4 (especially when the shape of this ST depression is a mirror-image opposite of what acute stemi-elevation looks like) — strongly suggests posterior MI (See My Comment at the bottom of the page in the September 21, 2022 post).

  • Chest lead ST-T wave findings in Figure-1 are admittedly subtle — but undeniably present. There normally is slight (usually 1-2 mm) upward-sloping ST elevation in anterior leads V2,V3. Not only do the BLUE arrows in these leads show a lack of this normal upward-sloping ST elevation — but the coved and depressed ST segment in lead V2 conveys a positive Mirror Test. Support to this diagnosis of presumed posterior MI is added by the abnormal J-point ST depression in lead V4.
  • BOTTOM Line: Problem #3 is not using these subtle-but-real ST-T wave abnormalities in selected chest leads of Figure-1 to solidify the diagnosis of acute (or recent) inferior OMI.

Problem #4:
Even before we get to assessing the 3 additional leads in this 15-lead ECG — Problem #4 is the failure to consider acute RV involvement. After all — this elderly patient is predisposed to potentially having a "silent" MI with non-chest-pain symptoms as the presenting complaint. 
  • IF the inferior OMI that we've already diagnosed in today's case is associated with a significant component of acute RV involvement — then navigating optimal treatment in this elderly patient becomes that much more challenging (ie, This dialysis patient presented with 3 days of nausea, vomiting, diarrhea and now lightheadedness with fatigue — which if associated with volume-dependent acute RV involvement will make for a series of difficult-to-balance issues).

  • Typically with acute infero-postero OMI in which we see hyperacute inferior lead ST-T waves in association with mirror-image opposite reciprocal changes as marked as we see in lead aVL — I would expect more ST depression than we see in leads V1-thru-V4. In particular in Figure-1 — right-sided lead V1 manifests no ST depression at all. So even before looking at lead V4R — I suspected acute proximal RCA occlusion with at least possible (if not probable) RV involvement.

  • As good as it is that a 15-lead ECG was obtained as part of today's initial tracing (including right-sided lead V4R) — the fact that there is clear ST elevation in lead V4R (BLUE arrow in this lead highlighting J-point ST elevation) — was apparently discounted, again "because today's patient did not have chest pain".

Problem #5:
There apparently was dependence on posterior leads for the diagnosis of posterior infarction. As we've often emphasized in Dr. Smith's ECG Blog — Posterior leads often provide false reassurance (See My Comment at the bottom of the page in the September 21, 2022 post). As occurred in today’s initial ECG — despite our recognition of posterior OMI by the ST-T wave appearance in leads V2-thru-V4 in Figure-1 — no ST elevation at all is seen in posterior leads V8,V9.
  • Failure of posterior leads to consistently demonstrate ST elevation in association with subtle posterior OMI — should not be surprising. This is because posterior placement of leads V7, V8 and V9 situates these leads in a position from which electrical activity must pass through the thick musculature of the back before being recorded on the ECG. As a result — even under optimal circumstances, QRST amplitudes (and therefore the amount of ST-T wave elevation) in posterior leads is often modest.
  • In contrast — because you are not having to traverse the thick back musculature to record a standard ECG (as you have to do when recording posterior leads) — the relative amplitude of ST-T wave segment deviations in anterior chest leads on a standard 12-lead ECG tends to be significantly larger than the ST-T wave amplitude seen with posterior leads. This is why I believe the Mirror Test is superior to use of posterior leads.

  • EDITORIAL Note: I do not believe I have ever seen a case in which a posterior infarction diagnosed by posterior leads was not evident by use of the Mirror Test on the standard 12-lead ECG.  

Monday, August 14, 2023

What does the ECG show in this patient with chest pain, hypotension, dyspnea, and hypoxemia?

Written by Pendell Meyers, with some edits by Smith

A man in his 40s with many comorbidities presented to the ED with chest pain, hypotension, dyspnea, and hypoxemia.

The bedside echo showed a large RV (Does this mean there is a pulmonary embolism as the etiology?)

Here is his triage ECG:

What do you think? Lots of info here.

The rhythm is 2:1 atrial flutter.   The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia.

The QRS is around 100 msec wide (narrow), but with very abnormal morphology including a large R-wave in V1, deep S-wave in I, R-wave in aVR.  If this were RBBB, it would need to be incomplete, as the QRS duration is less than 120 ms.

However,  V1 does NOT have an rSR' as one would see in either complete or incomplete RBBB.  Rather, there is a qR.  (Exception: One might see a qR in RBBB if there is an old septal MI).  There are also large R-waves in V2 and V3, all indicating right ventricular hypertrophy.  

The ST depression in V1-V3 might make you think of posterior OMI; however, these are all discordant to the abnormal R-wave.  The repolarization abnormalities are all secondary (as a result of) the abnormal QRS (RVH).  These are very typical repol abnormalities for RVH.

When you suspect pulmonary embolism due to large RV on POCUS, always look for right axis deviation and a large R-wave in V1 because the large RV may be entirely due to chronic RVH, not acute PE.  PE does not manifest a large R-wave in V1 unless it is RBBB or iRBBB.  

Chronic RVH is due to chronic pulmonary hypertension, and these patients are extremely difficult to manage when they are acutely ill.

There is also a suggestion of hyperkalemia with peaked T waves, but I was not able to get a potassium level in this case. 

A prior ECG was available for comparison:

There is sinus rhythm here; the QRS is the same

We can see that the QRS is essentially the same as prior. The RVH is not new. Notice the STD maximal in V3-4. This is NOT indicative of posterior OMI because it is secondary to this very abnormal QRS made by RVH. 

OMI recognition cannot be learned well by reading text, but our best "sentence" or "criteria" for helping learners see posterior OMI is: In the context of acute symptoms suspicious for ACS, ST depression maximal in V1-V4 (without an abnormal QRS cause) is specific for posterior OMI until proven otherwise. This is one of the times when the abnormal QRS is causing the STD maximal in V1-V4, by the principle of appropriate discordance.

The electronic medical record revealed that this patient had known history including pulmonary hypertension, sickle cell disease with frequent transfusions, CHF, restrictive lung disease with chronic hypoxic respiratory failure on oxygen at home, CKD, OSA on nightly BIPAP, and chronic pulmonary embolism. Obviously he has multiple reasons to have pulmonary hypertension.

How about management?  

1) It would help to cardiovert to sinus rhythm

------This would improve the atrial contribution to ventricular filling.  

2) Norepinephine to support Blood Pressure.    

------This is critical for supporting RV perfusion. The RV is normally a low pressure chamber, and perfusion happens in both systole and diastole (unlike the LV, which only perfuses in diastole when the pump is not squeezing).  But in pulmonary hypertension, RV perfusion is greatly diminished, especially when there is hypotension.  This leads to a "vicious circle" in acute on chronic RV failure.

CT pulmonary angiogram revealed only his known chronic PE burden, no acute PE.

He was critically ill with a complex course, and ultimately did not do well.

See these other cases of RVH:

An elderly woman with shortness of breath and an ECG that helps understand it

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

What is going on in V2 and V3, with a troponin I rising to 1826 ng/L at 4 hours?

55 year old woman with chest pain and precordial T-wave Inversions

MY Comment, by KEN GRAUER, MD (8/14/2023):
Today's initial tracing is challenging— especially given that my first impression was made without the benefit of clinical information. I focus my comments on a number of additional points to those brought out in Dr. Meyers discussion.
  • For clarity in Figure-1 — I've reproduced and labeled the 2 ECGs in today's case.

  • NOTE: The reason I find today's initial ECG so challenging — is that both for the rhythm, as well as for the rest of this 12-lead tracing — there is a differential diagnosis, and not a single definite answer. Rather than a single diagnosis for the rhythm and the 12-lead — optimal interpretation in my opinion entails awareness of the need for additional clinical information before we can settle on "the Answer".  

Figure-1: I've labeled the 2 ECGs in today's case.

MY Thoughts on Today's Rhythm:
I think the rhythm in today's initial tracing ( = ECG #1 in Figure-1) is best described as a regular SVT (SupraVentricular Tachycardia) at ~140/minute.
  • Although the QRS complex in ECG #1 looks a little wide — I measure QRS duration = 0.10 second (ie, half of a large box on ECG grid paper) — which is at the upper limit of normal for QRS duration.
  • There is atrial activity in ECG #1 — in the form of a negative deflection that occurs near the mid-point of the R-R interval in lead II (BLUE arrows).
  • There is 1 different-looking beat beat #6 in the long lead II rhythm strip of ECG #1). Presumably beat #6 is a PVC (Premature Ventricular Contraction) — since it is wider and very different-looking than the other beats in this tracing. Presumably there is also some fusion of this PVC with the underlying supraventricular beats.

KEY Point: Rather than jumping to a specific rhythm diagnosis — I favor formulation of a differential diagnosis. For practical purposes — the overwhelming majority of regular SVT rhythms seen in an emergency setting will turn out to be one of the following 4 diagnoses on this LIST: i) Sinus Tachycardia; ii) A reentry SVT rhythm (ie, AVNRT or AVRT)iii) ATach ( = Atrial Tachycardia)oriv) AFlutter (Atrial Flutter).
  • As I've often reviewed in my comments on Dr. Smith's ECG Blog (See the May 1, 2023 post, among many others) — review of a few considerations will usually narrow down this differential diagnosis within seconds.

  • The rhythm in ECG #1 is not Sinus Tachycardia — because there is no upright P wave in lead II. Instead, we see a negative deflection (highlighted by the BLUE arrows) — as well as a rounded upright deflection to the right of the blue arrows that looks to broad too be a sinus P wave.

  • doubt that the rhythm is a reentry SVT. As I review in my comment at the bottom of the page in the March 6, 2020 post of Dr. Smith's ECG Blog — the negative atrial activity highlighted by the BLUE arrows looks to be misplaced for either AVNRT (in which the RP' interval is very short, usually not passing beyond the S in the QRS) — or for AVRT (in which the RP' interval usually does not pass beyond the midpoint of the ST segment). While possible that this rhythm could reflect the "fast-slow" form of AVNRT (ie, as shown in my Figure-3 of the March 6, 2020 post) — this "fast-slow" form of AVNRT is very uncommon, and usually manifests a sharper and deeper negative deflection for the retrograde P wave.

  • It's possible that the rhythm could be ATach. That said — strict 1:1 conduction with ATach is a relatively uncommon form of SVT in an unselected emergency setting (ie, there more often will be group beating with Wenckebach conduction and/or some pause in the SVT).

  • This leaves us with AFlutter. In my experience — AFlutter with 2:1 AV conduction is by far the most commonly overlooked cause of an undiagnosed SVT rhythm — especially when sinus P waves are absent, and the ventricular rate of the rhythm is close to ~150/minute (ie, usual range ~130-160/minute).

  • The EASIEST way to avoid overlooking the diagnosis of AFlutter is to: i) Remind yourself that AFlutter is by far the most commonly overlooked SVT rhythm — such that we need to always think of this diagnosis whenever we see any regular SVT rhythm at ~130-160/minute, in which sinus P waves are absent; ii) Remember that when you see atrial activity near the midpoint of the R-R interval in a fast rhythm (as highlighted by the BLUE arrows) — that there very often will be 2:1 atrial activity (with a 2nd P wave hidden within the QRS complex)andiii)  Use calipers! (ie, Set your calipers to precisely 1/2 the R-R interval — and then search all 12 leads to see IF there is any kind of deflection that you can walk out with this 2:1 ratio).

BOTTOM Line Regarding the Rhythm in ECG #1:
Although I was not 100% certain regarding the rhythm diagnosis after reviewing ECG #1 — I knew the rhythm was not sinus tachycardia — and thought that both a reentry SVT and ATach were unlikely — leaving me with AFlutter being the most likely diagnosis.
  • Setting my calipers to precisely 1/2 the R-R interval — I was able to walk out 2:1 atrial activity for the rounded positive deflections in leads III and aVF (RED lines) — as well as for the rounded negative deflections in lead aVL (PURPLE lines). 
  • Although not quite in the usual "sawtooth" pattern of typical AFlutter — this 2:1 atrial conduction — which given the ventricular rate of ~140/minute — would yield an atrial rate of ~140 X 2 ~ 270-280/minute, virtually confirming the diagnosis of AFlutter even before treatment (ie, reentry SVTs and ATach generally don't go quite this fast).

  • Final Point regarding the Rhythm: I always look for a "break" in an SVT rhythm — as the slight change in the cadence of the rhythm often provides a "tell-tale" clue to etiology. I believe the BLUE lines in the long lead II rhythm strip support the diagnosis of AFlutter — by showing what appears to be uninterrupted flutter waves before and after the PVC.

MY Thoughts on the 12-Lead ECG:
As per Dr. Meyers — Flutter waves may alter the appearance of underlying ST-T waves — sometimes mimicking or concealing ischemic or other cause of abnormal ST-T wave changes.
  • For example — Doesn't it look like there is ST coving with some inferior lead ST elevation in ECG #1 during AFlutter? Although we do not have a follow-up ECG on today's patient — I suspect that once the rate slows and the rhythm converted to sinus, that this "pseudo-ST-elevation pattern" will resolve.

What About the Tall R Wave in Lead V1 of ECG #1?
I thought the most interesting finding on today's 12-lead tracing was the tall R wave in lead V1.
  • This patient has IRBBB (Incomplete Right Bundle Branch Block) — as determined by the qR pattern in right-sided lead V1 with predominant positivity in this lead — in association with slightly widened terminal S waves in all lateral leads (ie, in leads I, aVL, V6).
  • As I mentioned above — the QRS is of upper normal duration, but not widened (ie, ~0.10 second) — which is why this is "incomplete" (and not complete) RBBB.

  • As I've discussed in detail in my comment at the bottom of the page of the February 12, 2023 post of Dr. Smith's ECG Blog — the ECG diagnosis of RVH (Right Ventricular Hypertrophy) is difficult to make. This is because no single ECG finding by itself is diagnostic — but instead, the ECG diagnosis of RVH is made by identifying a combination of ECG findings in a patient with a clinical history consistent with RVH.
  • IRBBB itself is one of the ECG findings consistent (suggestive) of RVH.
  • While difficult to sort out potential ST-T wave inversion in the inferior and anterior leads in ECG #1 given the rhythm of AFlutter at a rapid rate, and the absence of a follow-up tracing — I suspect the negative deflections seen in leads III, aVF and V3 may persist following conversion to sinus rhythm, therefore suggesting the possibility of RV "strain".
  • Although difficult to sort out from IRBBB (which by definition produces a terminal S wave in lead V1) — there appears to be an S1Q3T3 pattern in ECG #1.

  • PEARL: Although possible for a RBBB conduction disturbance (complete or incomplete RBBB) to lose the initial positive deflection (r wave) in lead V1 because of septal infarction — in the presence of other ECG findings suggestive of RVH — a qR pattern in lead V1 often serves as a marker for pulmonary hypertension (illustration of the pathophysiology for this ECG finding in Figure-2 of my comment from the February 12, 2023 post).

Putting It All Together:
The initial ECG in today's case strongly suggested that the rhythm was AFlutter with 2:1 AV conduction, at a ventricular rate of ~140/minute. Although 1st priority will be to control the ventricular response (and ideally convert the rhythm to sinus) — the findings of IRBBB with a qR pattern in lead V1 — with an S1Q3T3 pattern and possible RV strain — suggest RVH as a unifying diagnosis, potentially with pulmonary hypertension if not also acute RV "strain".
  • At this point — I got to see a prior ECG on this patient ( = ECG #2 in Figure-1— and learned about the patient's History (ie, Sickle Cell Disease with frequent emergency visits for blood transfusions, heart failure, renal insufficiency and pulmonary hypertension from restrictive lung disease with chronic hypoxemic respiratory failure and a history of prior pulmonary embolisms).

Comparison of ECG #1 with a Prior Tracing:
I found it insightful to compare the 2 tracings in Figure-1:
  • Sinus rhythm is present in the prior ECG (RED arrow in lead II of ECG #2). Note how this upright P wave with normal PR interval in ECG #2 contrasts with the negative deflection in the mid-point of the R-R interval in ECG #1 (BLUE arrow). Remember that atrial activity near the mid-point of the R-R interval in a fast rhythm often signals the presence of 2:1 atrial activity!
  • Note that the precisely regular 2:1 atrial activity seen in ECG #1 (ie, the RED and PURPLE lines seen in leads III,aVF and aVL) were not seen in the prior ECG — supporting our impression that these rounded deflections represented 2:1 flutter activity.

  • IRBBB with a qR pattern in lead V1 (YELLOW arrows in both tracings) + ST-T wave inversion in leads V1-thru-V4 were present in the prior ECG — consistent with this patient's longstanding history of end-stage pulmonary disease with pulmonary hypertension. This confirmed that none of these ECG findings were new.

  • The T waves in leads I and V3-thru-V6 were not nearly as pointed in the prior tracing compared to ECG #1 — in support of Dr. Meyers concern that this chronically ill patient with longstanding renal disease may be hyperkalemic.

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