Tuesday, April 30, 2024

What is the rhythm?

A patient was found down approximately 30 minutes after taking methamphetamine.  Bystander CPR.  Medics found patient in PEA arrest.  He was resuscitated into a perfusing rhythm.  He went in and out of arrest until arrival at the ED.  

Here is the only prehospital 12-lead:

Sinus tachycardia, somewhat wide QRS, Ischemia

Here is the first ED ECG:

What is the rhythm here?

This ECG is pathognomonic of hyperkalemia, with wide QRS, very SHARPLY peaked T-waves, flat ST segments, RBBB pattern and large R-wave in aVR.  

What does that say about the rhythm?  It is regular.  It is supraventricular.  It is not tachycardic.  

Is this an accelerated Junctional rhythm?  Junctional rhythm is possible, but most likely is "Sinoventricular rhythm".  Sinoventricular rhythm is a supraventricular rhythm that is initiated by the sinus node but does not manifest with P-waves because the hyperkalemia completely flattens the P-wave.

The K returned at 7.8 mEq/L.

Core temp was 40 degrees C.  

The remaineder of the case was complicated and the patient ultimately died.

See here another case of sinoventricular rhythm:

And more cases discussing Sinoventricular Rhythm:


Ken Grauer (below) has a different opinion; I'm not sure I agree but it's good to have multiple viewpoints!


MY Comment, by KEN GRAUER, MD (4/30/2024):

Today's case relates the unfortunate events of metamphetamine toxicity, resulting in multiple complications and the patient's ultimate demise. That said — I found this case highly insightful regarding a number of ECG manifestations of hyperkalemia.
  • For clarity in Figure-1 — I've labeled the 2 ECGs in today's case.

I focus my comments on: i) The initial rhythm; andii) Reasons for the dramatic changes in ST-T wave appearance between ECG #1 and ECG #2.
  • I fully acknowledge some speculation — given that we lack precise timing of these serial tracings, as well as not knowing the corresponding serum K+ level at the time each tracing was recorded.

  • To EMPHASIZE: The points that I discuss below that relate to the rhythm in ECG #1 and ECG #2 — are advanced concepts that go beyond-the-Core!

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

MY Initial Thoughts on ECG #1:
Before delving into specifics of ECG #1 — it's important to appreciate that there is a limit to the amount of voltage that prehospital ECGs in most EMS systems are able to display. As a result — QRS amplitudes are automatically truncated once they exceed that limit (which as per the dotted RED lines in Figure-1 — is 10 mm for the deepest S wave in leads V3,V4 — and, for the tallest R wave in lead V4).
  • Whereas this truncation of QRS amplitudes does not affect clinical management in today's case — we have shown a number of examples in which anterior lead ST elevation might suggest acute LAD OMI if one was not aware that such ST-T waves would not be disproportionate IF full anterior lead S wave amplitude was recorded (See My Comment at the bottom of the page in the November 29, 2023 post and in the June 20, 2020 post in Dr. Smith's ECG Blog).

The RHYTHM: When I first saw ECG #1 — I wondered IF the rhythm might be either AFlutter or ATach with 2:1 conduction — as the upright peaked deflections marked by the RED and dark BLUE lines in lead II of ECG #1 looked similar in morphology (as P waves with 2:1 AFlutter or ATach should look) — and the spacing between these upright peaked deflections looked to be almost equal.
  • PEARL #1: With an SVT rhythm — Consider the possibility of 2:1 conduction IF you see equally spaced, similar P-wave-looking deflections. Use of calipers immediately provides the answer — that these upright, peaked deflections seen in each of the inferior leads are not equally spaced (measuring 360 msec. vs 320 msec.) — and therefore, the dark BLUE line deflection in lead II is not an "extra" P wave.
  • Similarly — the upright peaked light BLUE line deflection immersed within the depressed ST segment in lead II also can not be an "extra" P wave — because there clearly is no way this peaked light BLUE line deflection could produce a regular tachycardic P wave rate with other pointed deflections in this rhythm.

  • PEARL #2: At times like this, when I am initially uncertain whether the upright peaked deflections are part of the ST-T wave vs "extra" P waves — LOOK for the "break" in the rhythm (which occurs after the 3rd beat) Doing so should make it clear that the peaked light and dark BLUE deflections in Figure-1 are related to the preceding QRS complex (and not to the next QRS complex)

  • BOTTOM Line: As bizarre as it initially might seem — these extra upright peaked deflections seen in each of the inferior leads of ECG #1 do not represent atrial activity. Instead — these peaked deflections represent part of the ST-T wave! This is relevant to interpretation of the initial (EMS) ECG in today's case — as I explain momentarily!

I refer the interested reader to My Comment in the February 27, 2023 post in Dr. Smith's ECG Blog — in which I review the challenges in determining the cardiac rhythm with hyperkalemia — as well as reviewing the sequence of expected ECG changes with this electrolyte disorder.

PEARL #3: Much attention focuses on the appearance of tall, peaked and pointed T waves in association with hyperkalemia. Not commonly appreciated — is that sometimes, you may see deep, symmetric and pointed T wave inversion in a number of leads. This is usually not ischemic — but rather another ECG manifestaion of hyperkalemia.
  • Applying PEARLS #1,2,3 to today's case — and, knowing that the extra peaked deflections in ECG #1 are part of the ST-T wave (and do not represent "extra" atrial activity) — should suggest hyperkalemia from this initial ECG! 
  • I say this because: i) Today's clinical setting of metamphetamine toxicity leading to PEA arrest may predispose to hyperkalemia via mechanisms of rhabdomyolysis and acute renal failure (Gurel — Clinical Case Reports 4(3):226, 2016)andii) Parts of upright T waves that are seen in ECG #1 are tall, upright, peaked and pointed (RED arrows in ECG #1 — especially in lead V3) — whereas many leads show the mirror-image opposite picture of deep, negative T waves that are pointed with a narrow base (BLUE arrows in ECG #1). As per PEARL #3 — pointed T waves that are inverted instead of upright are an important ECG sign of hyperkalemia.

Returning to Figure-1: As per Dr. Smith — ECG #2 is pathognomonic of hyperkalemia because of the wide (and unusual-looking) QRS complex — with peaked T waves (that are tall and pointed, with a narrow base — similar in appearance to the Eiffel Tower).
  • That said — Note (as per PEARL #3) that 2 of the leads in ECG #2 show the mirror-image opposite picture of slender, pointed T waves that are inverted (BLUE arrows in ECG #2).

MY "Devil's AdvocateQUESTION:
  • Are we certain there is a sinoventricular rhythm in ECG #2

While I completely agree with Dr. Smith that ECG findings of hyperkalemia with QRS widening and tall, peaked, pointed T waves but without any P waves — is most often associated with a sinoventricular rhythm (in which sinus node activity continues with marked hyperkalemia despite the disappearance of P waves on ECG) — my "eye" in ECG #2 was captured by the tiny, seemingly negative deflections occurring at the end of the QRS in all inferior leads (BLUE lines in ECG #2). I thought these tiny negative deflections might represent retrograde P waves — in which case, the rhythm in ECG #2 might be ventricular escape instead of a sinoventricular rhythm. In support of this possibility:
  • Doesn't the QRS complex in ECG #2 look very different — compared to morphology of the fairly narrow QRS in ECG #1?
  • Why are almost all of the the pointed T waves with narrow base upright in ECG #2? — whereas T waves in ECG #1 were biphasic with a predominantly negative T wave?

  • PEARL #4: I do not think we can reliably distinguish between sinoventricular vs accelerated idioventricular rhythm in ECG #2. That said — PEARL #4 is that clinically (as I emphasize in the February 27, 2023 post) — Most of the time it does not matter what the rhythm disturbance is with hyperkalemia — because: i) Arrhythmias tend not to "obey the rules" when there is marked hyperkalemia; andii) Rhythm disturbances from hyperkalemia usually improve (or completely resolve) as soon as IV calcium is administered.

Saturday, April 27, 2024

Two prehospital ECGs of patients with chest pain.

Written by Pendell Meyers and Steve Smith

Here are two cases of middle-aged men with chest pain who had prehospital ECGs.

Patient 1, ECG 1:
What do you think?


Patient 2, ECG 2:

What do you think?

Queen of Hearts interpretation of ECG 1:

Queen of Hearts interpretation for ECG 2:

Interpretation of ECG 1 (OMI): Sinus rhythm, normal QRS, with easily diagnostic signs specific for inferior and posterior wall transmural ischemia, with the most likely etiology of course being acute coronary occlusion MI. Inferior T waves are hyperacute, with reciprocal negative hyperacute T waves in aVL. Posterior OMI is indicated by the inappropriate ST depression maximal in V2. However, I do not believe this case has sufficient STE to meet STEMI criteria.

Interpretation of ECG 2: (Not OMI):  There ﹥1 mm of ST elevation in consecutive inferior leads (meets STEMI criteria), with no reciprocal ST depression in aVL.  There is a slight T-wave inversion in aVL.  The upward concavity of the ST segments is pronounced.  The T-waves are NOT hyperacute; they do not have much "bulkiness" especially in proportion to the well-formed R-waves.  This is a NORMAL ECG.

Outcome of case with ECG 2: Inferior STEMI was diagnosed by the emergency physician and the patient needed to be flown by helicopter to a cath lab.  The arteries were clean.  There was no MI.  This was the patient's baseline ECG.   It was a false positive.  The patient ruled out for MI by serial troponins. Chest pain was non-cardiac.

 Register for access to Queen of Hearts here

Case 1 continued:

Time = 50 minutes, in the ED:

Now it meets STEMI criteria also. Although its not labelled, V5 and V6 are likely posterior leads.

Initial hs trop I: 56 ng/L

Time = 80 minutes


Acute 100% (TIMI 0) RCA occlusion, PCI performed


Next morning:

Independently diagnostic for inferoposterior reperfusion.
(deeply inverted inferior T-waves, and increased amplitude T-waves in V2, V3)

Smith: Why do the T-waves in V2 and V3 enlarge in reperfusion of the posterior wall?
If the recording was on the posterior wall, there would be T-wave inversion.  But T-wave inversion measure from the anterior wall (opposite) appears UPRIGHT!  Then add this upright deflection to the already upright T-waves of the anterior wall and you have extra large anterior T-waves!!

See our paper here: Driver BE, Shroff GR, Smith SW. Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall. Emerg Med J [Internet]. 2017;34:119–123. Available from: http://dx.doi.org/10.1136/emermed-2016-205852

High sensitivity Troponin Ts (ng/L): 56





EF 57%

Basal to mid inferolateral hypokinesis

Learning Points:

1. Expert or Queen of hearts interpretation makes the diagnosis of OMI 50 minutes sooner than STEMI criteria in this case. In our recent external validation, the average time savings compared to STEMI criteria was about 3 hours. Read for yourself here.

2. Hyperacute T waves are now endorsed by the ACC as a full STEMI equivalent finding (though they do not give any objective criteria for how to diagnose them). 

3. STEMI criteria are often met when there is no OMI (false positives).  In our prehospital study of 117 cases, STEMI criteria diagnosed only 70% of 48 true OMI and had 15 false positives.

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MY Comment, by KEN GRAUER, MD (4/27/2024):

Today's case by Dr. Meyers provides yet one more example of an acute OMI that failed on initial presentation to satisfy STEMI criteria.
  • As per Dr. Meyers' detailed description — today's initial ECG, in association with the history of new CP — is readily diagnostic of acute infero-postero OMI, with need for prompt cath with PCI.

From a qualitative perspective — I'll add the findings that allow ECG diagnosis from today's initial tracing within seconds. For clarity — I've labeled this initial ECG in Figure-1.
  • In a patient with new CP — the ST-T wave within the RED rectangle in lead III immediately "caught" my eye. Given tiny amplitude of the QRS in lead III — there is no way that the hypervoluminous T wave in this lead (that totally dwarfs the QRS) can can possibly be normal.
  • Given this certainty that the ST-T wave in lead III is hyperacute — there is no doubt that the ST-T waves within the BLUE rectangles of the other 2 inferior leads ( = leads II and aVF) — are also hyperacute (obviously disproportionate in lead aVF, being slightly taller than the R wave in this lead, as well as "fat"-at-its-peak and wide-at-its-base — with by extension, less marked but still disproportionate ST-T wave appearance in lead II).
  • Confirmation that these hyperacute inferior lead ST-T wave changes are truly hyperacute — is forthcoming from the "magic" mirror-image opposite ST-T wave appearance that we so often allude to between lead III and lead aVL — which is so characteristic of acute inferior OMI.

Although assessment of the Chest Leads is not essential to know that acute cath is indiated — it provides even more confirmation.
  • As we so often emphasize — normally, there is slight ST elevation with gentle upsloping in leads V2,V3. Loss of this normal appearance in a patient with new CP — suggests acute posterior OMI until you prove otherwise.
  • PEARL: Given common blood supply in most patients with acute inferior OMI from either RCA or LCx occlusion — I treasure the finding of abnormal ST-T waves in leads V2, V3 and/or V4 in a patient with suspected inferior OMI as strong support of true coronary occlusion.

  • There is no way that the shape of the ST-T wave in lead V3 of Figure-1 is "normal" in a patient with new CP (with the RED rectangle in this lead) — because the ST segment in this lead is flat and there is no ST elevation.
  • Knowing that the ST-T wave in lead V3 is definitely abnormal in a patient with new CP — I immediately direct my attention to the ST-T waves in neighboring leads V2 and V4  — which show within the BLUE rectangles that there is ST straightening with shallow-but-abnormal T inversion in lead V2 — and, in the context of definitely abnormal lead V3 — abnormal ST segment flattening in lead V4.

BOTTOM Line: The above qualitative approach should allow the informed clinician to attain near certainty for the diagnosis of acute postero-infero OMI within seconds!
  • The "trained eye" should within less than 5 seconds know that in a patient with new CP — that the ST-T waves within the RED rectangles in Figure-1 almost certainly indicate acute infero-postero OMI.
  • Knowing this — it should take no more than 15 additional seconds for the "trained eye" to take in the ST-T waves within the BLUE rectangles — and know that your ECG diagnosis of acute infero-postero OMI has been confirmed. You have within seconds — confirmed the need for prompt cath with PCI.

Figure-1: I’ve labeled the initial ECG in today's case. 

Wednesday, April 24, 2024

Take the OMI Quiz and Test yourself against the Queen of Hearts

The PM Cardio Queen of Hearts AI model for ECG interpretation from Powerful Medical is still in its early days. 

Do you think you can outperform the toddler version of the AI model? 

Version 2.0 will soon be available with four times the training data.

The QoH groups ECGs into OMI and NOT OMI. Each category is subdivided into three levels of confidence. 

Thus you can get a reading of NOT OMI (low, mid or high). Or you can get sa reading of OMI (low, mid or high). 

In other words there are six outputs with NOT OMI high confidence on one end and OMI high confidence on the other end.

Take the Quiz below. It is not easy. Good luck! 

Get Queen of Hearts here for free: 

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:


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.


Monday, April 22, 2024

Chest pain, resolved. Does it need emergent cath lab activation (some controversy here)? And much much more.

50-something male with hypertension and 20- to 40-year smoking history presented with 1 week of stuttering chest pain that is worse with exertion, which takes many minutes to resolve after resting and never occurs at rest.  It is associated with mild dyspnea on exertion.  At times the pain does go to his left neck.  It was present on arrival at triage but then resolved before bed placement in the ED.

EKG from triage:

Queen of Hearts Interpretation:

Here is his previous ECG:

Normal ST Elevation

Queen of Hearts Interpretation:

Resident's interpretation: Reperfusion pattern/Wellens' with biphasic T waves in V2 and V3, and in comparison to an EKG in 2020 this is new.  

Course: Aspirin 325mg, chemistry, CBC, troponin panel all ordered.  Bedside ultrasound with no apparent wall motion abnormalities, no pericardial effusion, no right heart strain. Aorta briefly viewed, appears normal caliber and diameter. 

Repeat EKG:

Resident interpretation: ST elevation in V2 significantly different than his previous EKG.  Patient still not having chest pain however this is more concerning for OMI/STEMI.  He was transferred to the stabilization room for cath lab activation.  Labs ordered but not yet drawn.  Aspirin given.

Smith: I don't think that there is really any change in ST Elevation.  This change is due to a change in lead placement: in the first ECG (top), leads V1 and V2 were placed too high (P-wave inverted).  This leads to recording less ST elevation in lead V2.  In the later, 2nd, ECG, the leads are correctly placed and the ST Elevation appears to be greater.

This is a stable ECG.  Patient is pain free and clearly has Wellens' syndrome: 1) pain free episode following an episode of angina, typical Pattern A (biphasic, terminal T-wave inversion with an initial upsloping ST Segment) findings, preserved R-waves.  Pattern B is has deep symmetric T-wave inversion without the initial upwardly sloping ST Elevation.  Pattern A evolves into Pattern B.

This is a great series of ECGs demonstrating the evolution:

Classic Evolution of Wellens' T-waves over 26 hours


Does Wellens' syndrome require emergent cath lab activation??  Or is antiplatelent and antithrombotic therapy adequate to prevent re-occlusion before delayed intervention?

Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI).  

This is a demonstration of how Wellens' is transient OMI:

First ED ECG is Wellens' (pain free). What do you think the prehospital ECG showed (with pain)?

There are more examples here: https://hqmeded-ecg.blogspot.com/search?q=wellens+prehospital

And this is literature from Wellens' himself showing how Wellens waves occur after reperfusion with thrombolytics. (first authors are Wehrens and Doevendans, respectively)

Wehrens XH, Doevendans PA, Ophuis TJ, Wellens HJ. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J. 2000;139:430–436.

Doevendans PA, Gorgels AP, van der Zee R, Partouns J, Bar FW, Wellens HJJ. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol. 1995;75:1206–1210.

As far as I can tell, there is only one randomized trial of immediate vs. delayed intervention for transient STEMI.  

(There is no randomized trial, or even observational trial, of immediate vs. delayed intervention for Wellens' syndrome.)

Lemkes JS, et al. Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial. Eur Heart J [Internet]. 2019;40:283–291. Available from: http://dx.doi.org/10.1093/eurheartj/ehy651.  

In this study, the major outcomes were the same for both groups, but of 70 patients in the delayed group, 4 required emergent intervention for sudden re-occlusion.  You can make your own conclusions.  

I think I would want to intervene before there is risk of re-occlusion.

However, one could make a reasonable argument for delaying, especially if you would need to awaken your cath team in the middle of the night.  It requires full antiplatelent and antithrombotic therapy, and, in my opinion, if you delay, you should institute continuous 12-lead ECG monitoring.  

This is why:

1. Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome


Case Continued

The Cath lab was activated 70 minutes after ED arrival.

First hs troponin I returned 108 minutes after ED arrival and was normal: (12 ng/L)


No "upstream"  P2Y12 were given in the ED ("upstream" means "before the angiogram "defines" the coronary anatomy).  Upstream P2Y12 is often given, but my reading of the literature is that the benefit is limited, especially since intravenous Cangrelor can be given at the time of angiography, after the coronary anatomy is defined. This way, if there is need for CABG, surgery need not be delayed due to risk of bleeding from persistent P2Y12 inhibition.

Paper on upstream P2Y12: https://www.nejm.org/doi/full/10.1056/nejmoa1407024

Thus, in this case, no ticagrelor was given.  


--Culprit for the patient's unstable angina/Wellen syndrome is a ruptured plaque in the mid LAD.

--As suggested by the EKG, there is TIMI-3 flow on initial angiography

--LAD is a large-caliber vessel that extends to the apex

--There is an 80 to 90% stenosis in the mid LAD with TIMI-3 flow beyond on initial angiography

--This lesion has angiographic characteristics of plaque rupture and is likely the culprit for the patient's Wellens syndrome/unstable angina

Cangrelor given after coronary anatomy defined

The lesion was stented

Peak troponin was 108 ng/L.  Total coronary occlusion, if very brief, may have minimal infarction and yet be very dangerous.

Formal Echo:

Normal left ventricular cavity size, and normal LV systolic function.

Normal estimated left ventricular ejection fraction; 54%.

Regional wall motion abnormality-apical septum and apex, hypokinetic.

Increase in LV wall thickness, asymmetric (see below).

Normal right ventricular size and function.


 Thus, even with this very small infarct, there was myocardial stunning (wall motion abnormality in the absence of significant infarct.  This is common and the wall will almost always recover some time before about 6 weeks.

Here are other very interesting posts:

Wellens' syndrome: to stent or not? IVUS negative, Symptoms persist, Stress Testing, Instantaneous Wave Free Ratio, and Fractional Flow Reserve.

Wellens' has mimics and some are extremely difficult, as in this post:

Is it Wellens' Syndrome?

Here are many examples of a very common mimic, which we call "Benign T-wave Inversion" and is a variant of Early Repol:


MY Comment, by KEN GRAUER, MD (4/22/2024):

When we talk about Wellens’ Syndrome — It is all about timing. Despite description of Wellens’ Syndrome over 40 years ago — this syndrome remains misunderstood by all-to-many clinicians (See My Comment at the bottom of the page in the August 12, 2022 post in Dr. Smith’s ECG Blog).

Two ECG patterns were described by the original investigators in 1982 as being consistent with a Wellens’ Syndrome prediction of high-grade LAD stenosis.
  • Pattern B — was the more common form in the original Wellens’ report. In my experience — this ECG pattern is less specific for high-grade LAD stenosis, because other entities (including non-cardiac CNS conditions) may also be associated with symmetric T wave inversion. 
  • In contrast, Pattern A — was much less common in the original Wellens’ report. That said, when the history is “right” for Wellens’ Syndrome — the steep T wave descent from the T wave peak that Pattern A features is more specific for Wellens’ Syndrome in my experience, than the symmetric T wave inversion of Pattern B.

  • In the initial ECG from today’s case — the ST-T wave appearance within the light BLUE rectangles in Figure-1 is consistent with the more specific ECG Pattern A. This is especially true for the ST-T wave in lead V3 — in which descent of the T wave from the peak of the coved and slightly elevated ST segment, is extremely steep ( = another example of an ECG condition in which a picture is “worth 1,000 words” — because the shape of this steep T wave descent is unique).

Misunderstood Features of Wellens:
  • For Wellens’ Syndrome to be present — the Hx must be of prior CP (Chest Pain) that has now resolved at the time the ECG is recorded. If CP is still present — then this is not Wellens’ Syndrome. Instead, persistent CP may indicate ongoing infarction and/or reperfusion T waves that develop after a completed event.
  • It is the pathophysiology of a true "Wellens' Syndrome" that is commonly misunderstood — in that there has been transient coronary occlusion — that then spontaneously resolves, with resultant resolution of CP (and no more than minimal myocardial damage).
  • The above pathophysiology is the reason Dr. Smith's recognition that the repeat ECG in today's case was not evolving is important. This is because by the above rationale — recognition of Wellens' Syndrome implies a temporarily "stable" situation after there has been spontaneous reperfusion of the "culprit" LAD lesion.
  • As per Dr. Smith’s above review of current literature on this issue — it would seem that prompt cath with PCI of a patient with Wellens' Syndrome is preferable to close monitoring while you wait and hope that you don't have to do emergency cath IF the "culprit vessel" reoccludes. And, given that such reocclusion of the "culprit" vessel might occur at almost any time after spontaneous reperfusion (ie, hours or even days later) — What IF the spontaneous reocclusion only occurs after the patient has been sent home because "nothing happened" during the 1-2 days that the patient was monitored in the hospital?

Figure-1: I've labeled the initial ECG in today's case.

Additional Take-Home Points:
I thought the KEY clinical point underscored by Dr. Smith's insightful presentation of today's case is how quickly the diagnosis of Wellens' Syndrome can be made.
  • Clearly — comparison of ECG #1 with the previous ECG on today's patient confirmed that the steep T wave downsloping, in association with anterior T wave inversion was a new finding. BUT — prior tracings are not always available — and even IF this prior ECG would not have been found — the diagnosis of Wellens' Syndrome was already confirmed by brief history that the patient's CP had resolved at the time the uniquely steep anterior T wave downsloping was seen on the initial ECG.
  • Sobering Note: The need for prompt cath in today's case was only appreciated after the 2nd ECG was done — in which a change in lead placement led to the team mistakenly concluding that there was increased ST elevation. (See My Comment in the April 17, 2022 post of Dr. Smith's ECG Blog for review on how to recognize too-high placement of the V1,V2 electrodes).

Final Thoughts:
  • The diagnosis of Wellens' Syndrome in today's case was made more difficult because this 50-something man with hypertension has LVH on ECG (by Peguero Criteria — as sum of the 25 mm S in V3 + the 13 mm S in V4 >28 mm — as per LVH Criteria that I detail in my Figure-3 of the April 17, 2022 post).
  • That said —  LV "strain" should never look like the steep T wave descent that we see in lead V3 of Figure-1, in which there is no indication of LV "strain" in the lateral chest leads.

  • BOTTOM Line: The history in today's case of new CP that had resolved by the time the initial ECG showing the unique steep T wave downsloping with anterior T wave inversion was done — should allow immediate recognition of Wellens' Syndrome. From what we know about the pathophysiology of Wellens' Syndrome — it would seem that the sooner prompt cath with PCI can be arranged, the better the chance for optimal outcome.

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