Another MUST know ECG, and why its notoriety annoys Dr. Smith

Written by Magnus Nossen

The ECG below was obtained from 50-something male with a history of hypertension and tobacco use. The patient contacted the ambulance service after he experienced sudden onset chest pain and diaphoresis that had started 20 minutes prior. The ECG below ECG was recorded on the scene.

What is the cause of the ECG changes here? How will you manage this patient?

ECG #1

The ECG shows sinus rhythm with a narrow QRS complex. The frontal plane axis is about 0 degrees. Heart rate is 85 beats per minute. There are significant and widespread ST-segment and T wave changes. The ST-segment in lead V1 has upward convexity. Throughout the precordium (V2-V6) there is ST depression followed by bulky, hyperacute T waves. 

• This ECG pattern was described by de Winter et. al in 2008, and is eponymously named after the main author. The de Winter ECG pattern (sometimes referred to as de Winter's T-wave pattern) consists of an ST-segment upsloping depression at the J point of 1 to 3 mm in leads V1 to V6, associated with tall, bulky or "hyperacute" T waves. 

The de Winter electrocardiogram pattern is an infrequent presentation, reported to occur in 2% to 3.4% of patients with anterior myocardial infarction (1). Below I have marked the J-point on the limb leads and the precordial leads showing the upsloping ST depression in leads V2-V6. There is a de Winter T- wave pattern also in lead I.

This ECG is diagnostic of a proximal LAD occlusion. This ECG pattern is my favorite example of how the STEMI criteria are fundamentally flawed. I was handed this ECG while caring for another OMI patient, and I immediately recognized this ECG pattern and activated the cath lab. If you have seen this pattern once — the diagnosis is obvious to you. The ECG-to-balloon time was short, only 35minutes. At cath there was a 100% proximal LAD occlusion, which was opened and stented.

• This patient received optimal care. Troponin T peaked at 9378 ng/L. Echocardiography showed septal and apical hypokinesis, with a left ventricular ejection fraction of 35-40%. 
• The hypokinesis was transient. Echocardiography 3 months following the infarct showed a normal ejection fraction of 55% without apparent hypokinesis! 
• Due to the rapid treatment — much myocardium was saved, and the initial hypokinesis was due to myocardial stunning (see below). Peak troponin may be very high following rapid reperfusion. 

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Smith: This is a classic case and well managed, as it should be.  However, I get annoyed by the attention devoted to de Winter's T-waves because they are a TINY minority of subtle hyperacute T-waves that result from LAD Occlusion (LAD OMI).  They are the most recognizable of all the hyperacute T-waves because of the depressed ST takeoff.  This means that the less recognizable HATW are not recognized and so many patients get ignored!  Moreover, de Winter stated that the morphology was "persisent."  First, de Winter T-waves are NOT always persistent (in fact, frequently are not), but, more importantly, the same can be said for standard hyperacute T-waves: they very frequently do not evolve to ST Elevation.  We have a series of 20 TIMI-0 LAD Occlusions that do meet STEMI criteria.  17 have HATW.  None evolved to ST Elevation.  Under Review.

See all the other manifestations of HATW in LAD Occlusion: Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

In addition, these hyperacute T-waves with a depressed ST takeoff were first described by Soo in 1995, but he gets little credit for that.  De Winter did not reference Soo.  I have referenced Soo 3 times.

Soo CS. Tall precordial T waves with depressed ST take-off: an early sign of acute myocardial infarction? Singapore Med J 1995;36(2):236–7.

 CS Soo, Lecturer and Cardiologist, Department of Medicine, Universiti Malaya, Malaysia
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Myocardial stunning is a state of cardiac dysfunction that can occurs in a portion of myocardium without necrosis after a brief interruption in perfusion. This typically occurs in the setting of a rapidly reperfused coronary artery following a myocardial infarction. In this situation, even after the ischemia is relieved and myocardial blood flow is restored — myocardial contractile function remains impaired for a variable period of time (usually days to a few weeks).

Image reproduced from Kloner, R.A. (2020) 

If you are a regular reader of this blog — this diagnosis will be easy for you, and you will manage this type of patient correctly with immediate revascularization. Unfortunately, for providers not familiar with this type of LAD OMI presentation — the diagnosis will likely be delayed, as will appropriate treatment.

Learning to recognize ECG findings consistent with OMI takes time and practice. Artificial intelligence can assist providers in detecting patients in need of emergent revascularization. The Queen of Hearts was not used in the management of today's patient. Had the AI model been used it would have identified the ECG as OMI with high confidence. Below you can see the QoH interpretation of the initial ECG in today’s case. 

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Two Additional Examples: ECG interpretation is pattern recognition — and pattern recognition takes practice both for humans and AI models. Below I have added ECGs from two other patients. Both cases below show a textbook de Winter ECG pattern. Originally recorded with a paper speed 50mm/sec ECGs — below these ECGs are compressed by 50% on the X-axis to "look" like they where recorded at 25mm/sec.

The above ECG is from man in his 80s with crushing chest pain. This patient suffered V-fib arrest soon after this ECG was recorded. Sadly, he could not be resuscitated. This ECG and patient outcome is a reminder of why it is so important to recognize this ECG pattern. 

• Below is the Queen of heart explainability chart. The overall interpretation was OMI with high confidence.

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This 2nd Example shows the ECG from a 50-year old male with sudden onset typical chest pain. This is another example of the de Winter ECG pattern. At cath there was a subtotally thrombotic occlusion of a proximal LAD with TIMI 2 flow. Peak troponin T 5933 ng/L.

Again I have added the QoH explainability feature below. Overall interpretation was OMI high confidence. 

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Discussion: The de Winter ECG pattern is seen in about two percent of patients with LAD OMI. The pattern is mostly described with LAD OMI, but has been reported in other coronary distributions as well. This ECG pattern is seen in the acute phase of OMI and it these patients need to be taken immediately to the cath lab or, if primary PCI is not available they should be given thrombolytic therapy as a conventional STEMI. 

It was previously thought that the de Winter ECG pattern represents ECG changes when there is a minimal trickle of blood reaching the downstream myocardium. However, many patients with de Winter ECG pattern have TIMI 0 at angiography and the ECG pattern does not necessarily progress to STEMI.

See this page for more ECG cases involving de Winters pattern

Learning points:

• The de Winter ECG pattern may remain unchanged never developing to STEMI. 
• Time is myocardium and prompt revascularization improves patient outcomes.
• Transient ischemia may lead to "stunning". Stunned myocardium will regain its function after a period of days to weeks.

References: 

Kloner, R. A. (2020). Stunned and hibernating myocardium: Where are we nearly 4 decades later? Journal of the American Heart Association

Vilela, E. M., & Braga, J. P. (2024, January 31). The de Winter ECG Pattern. StatPearls - NCBI Bookshelf

De Winter, R. J., Verouden, N. J. W., Wellens, H. J. J., & Wilde, A. a. M. (2008). A new ECG sign of proximal LAD occlusion. New England Journal of Medicine.. 

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MY Comment, by KEN GRAUER, MD (1/26/2025):

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"Some patients read the textbook. Others don't". I offer this quote as my reflection on today's case. The 50-something year old man presented by Dr. Nossen certainly "read the textbook" regarding deWinter T waves in the initial ECG from today's case.

From the original description by deWinter et al (N Engl J Med 359:2071-2073, 2008) — There is a “new ECG pattern” without ST elevation that signifies acute occlusion of the proximal LAD (Left Anterior Descending) coronary artery.

• The authors recognized this pattern in ~2% of patients with acute anterior MI (ie, in 30/1532 patients studied). Cardiac cath confirmed LAD occlusion in all cases — with ~50% of patients having a "wraparound" LAD. Left mainstem occlusion was not present.
• This was the authors’ original description of the new ECG pattern: “Instead of the signature ST-segment elevation — the ST segment showed 1-3 mm of upsloping ST depression at the J point in leads V1-to-V6 — that continued into tall, positive symmetrical T waves”.
• The QRS complex was usually not widened (or no more than minimally widened).
• Most patients also manifested 1-2 mm of ST elevation in lead aVR. 

In their original 2008 manuscript — deWinter et al went on to describe the following additional features:

• “Although tall, symmetrical T waves have been recognized as a transient early feature that changes into overt ST elevation in the precordial leads — in this group of patients, this new pattern was static, persisting from time of the 1st ECG until the pre-cath ECG.”
• Hyperkalemia was not a contributing factor to this ECG pattern (ie, Serum K+ levels on admission were normal for these patients).   

 

NOTE: Technically speaking — the deWinter T wave pattern as described in 2008 by deWinter et al differs from the finding of simple "hyperacute" anterior T waves — because ECG findings with a strict deWinter T wave pattern persist for an hour or more until the "culprit" LAD vessel has been reperfused.

• As suggested from the 8 example ECGs taken from the deWinter manuscript (labeled A-thru-H, as shown in Figure-1) — there should be involvement in all 6 chest leads with the strict deWinter pattern, with most leads showing several mm of upsloping J-point ST depression and giant T waves.

Figure-1: Comparison of ECG findings in today's case (LEFT panel) — with the deWinter T Wave Pattern, as first described by Robbert J. de Winter et al (N Engl J Med 359:2071-2073, 2008). ECGs for the 8 patients shown here from the original deWinter manuscript (labeled A-thru-H ) — were obtained between 26 and 141 minutes after the onset of symptoms.
=  =  =  =  =
NOTE: I have corrected in Figure-1 for an error that I believe was made by the authors in their original manuscript ( = Leads I and aVL were switched in Patient C in the original manuscript from what I show above. That original mounting of those 2 leads would make for an impossible frontal plane axis and unlikely ST-T wave picture. I believe what shows above in my Figure-1 is now correct).

Today's Patient "Read" the Textbook ... 

• The initial ECG from today's patient clearly manifests the "Can't Miss!" typical deWinter T wave picture of marked, upsloping J-point ST depression — that continues into tall, positive symmetric T waves (seen here in 5/6 chest leads — with coved ST elevation in the remaining chest lead V1). 
• And, as if to say, "Don't dare delay my PCI!" — there is also the "Can't Miss" picture of marked reciprocal ST depression in the inferior leads.

Is Inferior Lead ST Depression a Part of deWinter T Waves?

For as many cases as I have seen of this entity — I had to go back and look at the representative figure from the original manuscript to answer this question.

• The ANSWER: As shown in Figure-1 — 6/8 of the representative ECGs from the original manuscript manifest inferior lead reciprocal ST depression in association with the deWinter T wave pattern in the chest leads.
• The 2 representative ECGs that did not manifest reciprocal ST depression are from Patient B and Patient E. On the contrary — T waves in the ECGs from these 2 patients were prominently upright (perhaps with the slightest amount of ST depression in a couple of leads).
• Bottom Line: While common to see inferior lead reciprocal ST depression with deWinter T waves — this is not an invariable finding.

Additional Observations from Figure-1:

• The original manuscript notes that most patients in their study of deWinter T waves had ST elevation in lead aVR. This is seen in all 8 representative ECGs in Figure-1.
• Finally — I found the variable ST-T wave picture in lead aVL highly interesting. One of my "Go To" leads when assessing for the likelihood of proximal LAD occlusion — is to look for ST elevation in lead aVL. Yet among the 8 representative ECGs in Figure-1 — the ST-T wave picture in lead aVL ranged from hyperacute ST elevation (in A and C) — to a flat ST-T wave (in E) — to T wave inversion (in B and H).
• Bottom Line: Even among these 8 "representative" tracings (from the 30 patients identified as manifesting deWinter T waves) — there is variability in the ECG picture of this entity.

New Observations regarding deWinter T Waves:

The "good news" — deWinter T waves are now accepted as a "STEMI Equivalent", even when there is no ST elevation (Ricci, Smith, et al — Ann Emerg Med, 2025 in Press). Emergency angiography is needed and indicated for this ECG pattern.

• This Ricci, Smith et al manuscript add that deWinter T waves, "are in fact just a small but more easily recognized subset of hyperacute T waves" — and that most such patients with hyperacute T waves do not manifest the originally described deWinter T wave feature of a depressed ST segment takeoff.
• Finally, Ricci, Smith et al acknowledge that while deWinter T waves were initially described as indication of acute coronary occlusion in the LAD distribution — that the deWinter T wave pattern may occur in any coronary distribution!
• 
  
• Grauer Note: Having now observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms — many (if not most) of these cases do not fit the strict original definition of "deWinter T waves" — in that fewer than all 6 chest leads are often involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, the number of leads that manifest giant T waves is limited.
• In addition — ECG changes in many of the cases I have observed are not “static” until reperfusion (as had been initially reported in 2008 by deWinter et al.). Neveretheless, cath follow-up has routinely confirmed LAD occlusion in almost all cases.
• My Impression: In large part, the ECG findings seen depend greatly on when during the ongoing process of acute coronary occlusion the ECG is taken. 
• Finally — hyperacute T waves with similar clinical implications as strictly defined deWinter T waves — appear to be a much more frequent occurence among patients with acute anterior OMI, than the 2% incidence initially cited by the deWinter group authors in their original manuscript.
• 
  
• Sobering Closing Note: Although the word is spreading that the deWinter T wave pattern is a STEMI-equivalent that merits prompt cath with PCI — all-too-many interventionists still deny (and delay) this initial treatment "because STEMI-criteria are not met". This needs to change. 

A 34 yo Man with chest pain and Zero ST Elevation

Written by Hans Helseth

A 34 year old man with no known medical history presented to the ED after an hour of chest pain. He described the pain as a mid sternal "burning sensation" and rated it 8.5 out of 10 at onset, but on presentation to the ED, reported that the pain had improved to 4.5. His first EKG is shown below, with a lead II rhythm strip:

EKG 1, 1645

A provisder who is looking for STEMI would not see much in this EKG. 

Despite zero ST elevation, however, the T waves in the inferior leads are symmetrical and large in proportion to their QRS complexes. This is the classic morphology of hyperacute T waves. This EKG coupled with the patient's story is highly suggestive if not diagnostic of inferior OMI.

I interpret this as manifesting active inferior OMI, although the patient's improving pain suggests at least some reperfusion. It is possible that the T waves in this EKG are of an intermediate morphology between full-blown STEMI and inferior reperfusion. It is also possible for hyperacute T waves to remain somewhat stable during either a sustained period of occlusion or partial reperfusion.

Here is the interpretation of the PMCardio Queen of Hearts AI Model:

Smith: The Queen does not know if the patient has active pain, resolving pain, or pain completely gone.  Although to me this is diagnostic of Acute ACTIVE Inferior OMI, I think the Queen says "reperfused" OMI because she thinks that there are reperfusion T-waves in aVL, with reciprocally hyperacute upright inferior T-waves.

Nevertheless, as you can see, she recommends cath lab activation if there are ongoing symptoms.  Patient has 4.5/10 chest pain.  So he needs the cath lab.

Case Continued

This EKG was interpreted as normal by the clinicians overseeing this patient's care.

A high sensitivity troponin I resulted at 336 ng/L (Upper limit: 76) after which the clinical suspicion changed from reflux/gastritis to "NSTEMI". The patient was given nitroglycerin, but his blood pressure dropped to 70 systolic, he became dizzy, and he still had chest pain. An EKG was repeated about an hour after the first:

EKG 2, 1745

The inferior T waves have inflated tremendously. 

A small amount ST elevation has developed, although still not enough to meet STEMI criteria. There is also diagnostic evidence of posterior OMI in V2 and lateral OMI in V6.

Cardiology was consulted at a PCI-capable hospital. The cardiologist agreed to accept the patient for transfer, but did not accept the patient for direct admission to the cath lab because the EKG was not felt to represent "STEMI".

Smith: This was a cardiologist who made this statement!!!  Hans has not even been to medical school.  

One's training has NOTHING to do with one's OMI ECG interpretation skills.

The QoH now correctly sees active OMI:

A CT scan to rule out aortic dissection was performed (Smith: why???) before transferring the patient to the cath facility. It was without evidence of dissection. When the patient finally arrived to the PCI-capable hospital, his pain had reportedly improved, but not resolved. Another EKG, shown with a V1 rhythm strip, was recorded in the emergency department:

EKG 3, 1930

There appears again to be some reperfusion since the last EKG, as the T waves in inferior leads have deflated slightly. The Q waves in the inferior leads have deepened. 

This EKG was interpreted as showing "T wave inversion in aVL, otherwise no significant ST elevation or depression." 

The patient waited another three hours in the ED until the cath lab was ready to accept him.

6 hours after his initial presentation, he went to the cath lab:

There is a filling defect consistent with thrombus in the distal RCA. There was TIMI 2 flow distal to the thrombotic occlusion. The thrombus was aspirated and the distal RCA was stented. 

The rest of the patient's hospital stay was uneventful. A formal echo the next day showed an estimated EF of 55-60% with no definite regional WMA.

Learning Points:

• Hyperacute T waves can be present for a long period of time, especially if serial EKGs are not recorded frequently enough to observe their evolution.
• Hyperacute T-waves frequently NEVER progress to diagnostic ST Elevation
• Patients with ACS and pain refractory to anti-ischemic therapy should be sent emergently for catheterization, regardless of the ECG.
• Some OMI have zero ST elevation
• OMI can happen in young patients with no known medical history

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MY Comment, by KEN GRAUER, MD (1/28/2025):  

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There is a lot to be learned from today's post. In Figure-1 — I facilitate comparison of the 3 ECGs in today's case by putting them together.

• Although tempting to seek false reassurance from the relatively young age (34yo) of today's previously healthy patient — the history of new CP (Chest Pain) lasting an hour of sufficient severity to prompt an ED visit does place this patient in a higher risk category, pending other factors.

As per Hans Helseth — the initial ECG is clearly worrisome:

• My "eye" was immediately drawn to the inferior leads (within the RED rectangles) — each of which show disproportionately enlarged T waves that exceed R wave amplitude in the same lead (The huge T wave in lead aVF literally dwarfs the tiny QRS in this lead). In a patient with cardiac-sounding CP — T waves that are clearly taller-than-they-should-be — "fatter"-at-their-peak and wider-at-their-base than expected — have to be interpreted as hyperacute T waves until proven otherwise.
• Removal of any doubt that these inferior lead ST-T wave changes are significant — is forthcoming from the abnormal ST segment coving and surprisingly deep T wave inversion in lead aVL ( = reciprocal ST-T wave change). 
• NOTE: The T wave in lead aVL may at times be normally inverted. The physiologic reason for this finding — is that the T wave axis in the limb leads generally follows the QRS axis. As a result: i) The QRS complex will typically be predominantly negative in lead aVL when T wave inversion is benign; — ii) The ST segment in this lead should not be coved; — and, iii) The appearance of the inverted T wave should not be nearly as "bulky" as it appears to be in Figure-1.
• Impression: In this patient with new CP — ST-T wave findings in these 4 limb leads are diagnostic of acute inferior OMI until proven otherwise. 

Other findings in ECG #1 are more subtle. 

• There appears to be an IRBBB (Incomplete Right Bundle Branch Block) pattern in the form of an rsr' in lead V1 with terminal S waves in lateral leads I and V6. That said — typical IRBBB should not manifest ST segment coving with slight ST elevation in lead V1 (BLUE arrow in lead V1). Instead — there should be slight ST depression in association with IRBBB. In this patient with suspected inferior OMI — this raises suspicion of acute RV involvement.
• The ST-T wave in leads V2 and V3 normally manifest gently upsloping, slight ST elevation in leads V2,V3. Although the ST-T wave in lead V3 looks unremarkable in ECG #1 — the ST segment in lead V2 is isoelectric with a suggestion of ST segment flattening. In addition, the R wave in lead V2 is significantly taller-than-expected (given the tiny r wave in neighboring lead V1) — which in a patient with suspected inferior OMI — raises suspicion of associated posterior OMI.
• Finally, while not taller than the R wave in the same lead — the peak of the T wave in lead V6 appears "fatter"-than-expected — which in this patient with suspected inferior OMI, suggests this is a hyperacute T wave.
• 
  
• To Emphasize: These findings in leads V1,V2 and V6 of ECG #1 are subtle — and in isolation would be nondiagnostic. But in the setting of a patient with new CP and suspected acute inferior OMI — these findings add concern for an acute evolving event. The cath lab should be activated.
• At the least — ECG #1 should be repeated within 15-20 minutes after the initial tracing.
• Failing that — return of the initial significantly elevated Troponin value given new CP and this abnormal ECG should have sufficed for activation the cath lab.

NOTE: This patient's BP dropped to 70 systolic on receiving NTG. He continued to have CP.

• In a patient with suspected inferior OMI — a marked hypotensive response to NTG strongly suggests acute RV involvement.
• Right-sided chest leads should be obtained to assess for acute RV MI, especially given suggestion of ST segment coving with slight elevation in lead V1.

The repeat ECG is the MIDDLE tracing in Figure-1:

• As per Hans Helseth — the inferior T waves in ECG #2 appear even more hypervoluminous than they were ECG #1. In addition — there are now Q waves in leads III and aVF — whereas there previously was an rSRs complex in ECG #1 in these leads.
• Support that the increase in inferior lead T wave hyperacuity is real — is forthcoming from the deeper T wave inversion in lead aVL of ECG #2, along with subtle-but-new ST depression in lead I. 
• There has been little change in the chest leads.
• KEY Point: It would be easy to miss these subtle-but-real changes in limb lead ST-T wave appearance in the repeat ECG if these 2 tracings were looked at separately. This highlights the importance of putting both tracings you are looking at together — and comparing both tracings lead-by-lead.
• The fact that this patient still has ongoing CP — and now demonstrates "dynamic" ST-T wave changes compared to the initial ECG is but one more indication of the need for prompt cath.

As noted by Hans Helseth — the patient was finally transferred to a PCI-capable facility.

• Cardiac cath was delayed a number of additional hours because, "the ECG did not show a STEMI". This unfortunately is faulty reasoning. As per Dr. Smith (See his comments in the January 24, 2025 post, among many other cases on Dr. Smith's ECG Blog): i) Up to 40% of OMIs do not meet STEMI criteria despite TIMI-0 flow. Delay in reperfusion of such patients by as little as 1-2 hours may reduce potential benefit from myocardial salvage by as much as 50%; — and, ii) The findings of new and now ongoing CP in association with localized hyperacute T waves — and now with "dynamic" ST-T wave changes is diagnostic of an acute ongoing cardiac event — especially in association with already significant Troponin elevation.

The 3rd ECG in today's case was obtained on arrival at the PCI center — and is the BOTTOM tracing in Figure-1. 

• Although there is not a lot of ST-T wave change since ECG #2 — what is new (and what once again is BEST noticed by comparing serial tracings when put next to each other) — is a significat increase in heart rate. While not quite "tachycardia" (ie, the rate in ECG #3 is ~90/minute) — in association with evidence of ongoing CP and acute infero-postero-lateral OMI, possibly with RV involvement — a significant increase in heart rate should prompt reassessment to ensure that the patient is not developing shock.

Figure-1: Comparison of the 3 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

 

Challenging Rhythms in an 80-something Man

 

Written by Magnus Nossen and Ken Grauer

You are shown the ECG that appears in Figure-1 — obtained from an 80-something year old man. Other than sinus rhythm — What else do you see in this tracing?

• Note: The ECG in Figure-1 was initially recorded using the Cabrera Format (See Comment by Dr. Grauer at the bottom of the page in the October 26, 2020 post for review of the Cabrera Format). The image was recorded with a paper speed of 50mm/sec; below it was been "compressed" to 25mm/sec.

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

Figure-1: While at first glance the rhythm in Figure-1 might be mistaken for sinus tachycardia in fact, this is not the rhythm. Instead there is 2:1 atrial activity that is best seen in lead V1 (See Figure-2).

 

There are several clues that suggest today's initial rhythm is not sinus in origin.

• The rate of ~100/minute would be fast for an 80-something year old adult — unless something acute is going on (infection, shock etc.). 
• If the upright deflection in lead V1 was a single sinus P wave — then the PR interval would be longer-than-expected for this to be sinus tachycardia.
• Whenever the PR interval looks longer-than-it-should-be for a supraventricular rhythm — there may be another P wave hidden within the QRS complex! (This is the "Bix Rule" — See Pearl #1 in Dr. Grauer Comment in the July 16, 2024 post).
• There is no distinct, upright P wave in lead II — as there should be if the rhythm was sinus. Also, sinus P waves are usually not all positive in lead V1 like in today's ECG (unless there is RAA).
• The presence of a pseudo-r' deflection in lead V1 is common as a "hiding place" for either extra or retrograde P waves.

Grauer: My “Go To” Leads when looking for less obvious atrial activity in a supraventricular rhythm — are leads II and V1 (as the best leads to look at first) — but also leads III, aVF and aVR, each of which may be surprisingly helpful for finding retrograde P waves or flutter waves.

Interpretation: The rhythm in the initial ECG in today's case is supraventricular with 2:1 AV conduction. The ventricular rate is ~100/minute. Since there are 2 P waves within each R-R interval, the atrial rate must be twice the ventricular rate, or ~200/minute. The differential diagnosis is between ATach (Atrial Tachycardia) vs AFlutter (Atrial Flutter). Although a subtle "sawtooth" pattern may be present in the inferior leads — an atrial rate of ~200/minute would be slow for untreated AFlutter.

Figure-2: Colored arrows highlight flutter waves, with 2:1 AV conduction.

Patient history: It turns out that today’s patient is an 80-something year old man with longstanding hypertension and paroxysmal atrial fibrillation. The AFib had been well controlled on Flecainide for many years. He presents now with an episode of syncope at rest. 

On questioning the patient reported intermittent palpitations in recent months. The initial ECG was wrongly interpreted as showing sinus rhythm. He was admitted to the hospital with a suspected diagnosis of Sick Sinus Syndrome (Paroxysmal AFib accounting for palpitations — and bradycardic spells accounting for the syncope). 

Nossen: I initially saw the ECG in Figure-1 — knowing only that the patient was an elderly man on Flecainide, who presented to the ED for syncope. I was told that an episode of a WCT (Wide Complex Tachycardia) was captured on telemetry. However, having noticed the 2:1 atrial activity in lead V1 — I was not at all convinced that the episode was VT.

In Figure-3 — is the wide tachycardia rhythm that was captured on telemetry:  

Figure-3: Rhythm captured on telemetry. (Recording speed = 25 mm/second.)

Figure-3: The ECG in Figure-3 shows a regular WCT with a heart rate of 180/minute. There is overlap of the 5 chest leads that we see, and we have lost most of the lead V6 recording. Within approximately 3 minutes telemetry recorded spontaneous conversion of the rhythm, as shown in Figure-4 below.

Figure-4: Spontaneous conversion of the WCT in Figure-3. (Recording speed = 25 mm/second.)

What do you make of the clinical scenario in today's case up to now?

• Do you agree that the WCT rhythm is VT?
•     What other possible explanations might there be?
•         Will you recommend ICD placement for this patient?

Nossen: I was suspicious that the underlying rhythm was AFlutter throughout the above clinical scenario. Use of Flecainide could account for the slower-than-expected flutter rate of ~200/minute that we saw in Figure-2. And, perhaps once the flutter rate dropped below 200/minute — 1:1 AV conduction of AFlutter became possible (with the marked increase in QRS widening that we see in Figure-4 being attributed to Flecainide toxicity). Therefore — No VT, but instead 1:1 AFlutter with Flecainide-induced QRS widening!

• Nossen Note: I went back as best I could, trying to correlate Flecainide dosing with the atrial rate of flutter during the patient's hospital stay. Prior to admission — the patient was on 150 mg bid of Flecainide (300 mg/day), which is a high dose of drug. On this dose — the atrial rate varied between ~180-200/minute during the 24 hours after admission. Ultimately, Flecainide was withdrawn — with resultant increase in the flutter rate to ~250-300/minute.

To further explore the possibility of underlying AFlutter persisting throughout this patient's hospital admission — I reviewed all telemetry recordings, 2 of which are shown below in Figure-5 and Figure-6. 

Figure-5: Additional telemetry tracing (atrial activity labeled).

Figure-6: Additional telemetry tracing. RED arrows highlight 2:1 AFlutter (with peaking of each T wave in lead V1 resulting from hidden flutter waves).

Nossen: Figures-5 and -6 clearly show an underlying atrial tachyarrhythmia at ~180/minute. I went through all the telemetry recordings and found that the patient had a number of short WCT episodes. Before each of these WCT episodes — the atrial rate decreased. Whenever the atrial rate remained over 190/minute — there was always 2:1 or 3:2 conduction of atrial flutter. 

Why is the R-R interval sometimes irregular in parts of Figure-5?

Grauer: It is common for AFlutter to manifest periods of group beating due to dual-level Wenckebach conduction out of the AV node. Despite consecutively non-conducted flutter waves — this is not a conduction "block" — but rather an expected reduced conduction by an AV node presented with too many rapid flutter impulses to be able to conduct them all.

The intricate relationships prevalent with dual-level AV conduction are easiest to appreciate by means of a laddergram — which I show in Figure-7. Many combinations of Wenckebach conduction out of 2 or more levels within the AV node are possible (ie, the relationships illustrated in my Figure-7 laddergram do not represent the only possibility).

The "good news" — is that Wenckebach conduction out of the AV node is usually not a fixed (ie, pathologic) conduction defect. Instead — the chances are excellent that normal AV conduction will resume once sinus rhythm is restored!

Figure-7: Proposed laddergram for the lead V1 rhythm strip in Figure-5.

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Regarding Flecainide: Flecainide toxicity is a relatively uncommon, but extremely important condition to recognize. Among the potential manifestations of Flecainide Toxicity are the following:

• QRS widening, which may be marked, often with bizarre QRS morphology that does not resemble any known form of conduction block.  
• Slowing of conduction in atrial and ventricular tissue, as well as in the His-Purkinje system.
• VT as a proarrhythmic effect. 
• Facilitating conversion of AFib to AFlutter as another proarrhythmic effect. 
• Because of Flecainide’s adverse effect on conduction through atrial, ventricular and His-Purkinje tissue — the usual diagnostic and therapeutic effects of antiarrhythmic agents may be much less effective (if they are effective at all). This probably accounts for the refractoriness of Flecainide-induced proarrhythmia to antiarrhythmic treatment.

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Conclusion: The WCT rhythm in today's case was the result of intermittent 1:1 AV conduction of AFlutter (and not the result of VT). This patient had been on longterm Flecainide, but was not receiving a ß-blocker! This facilitated episodes of AFlutter with 1:1 AV conduction.

• Marked QRS widening with an unusual QRS morphology (that resembles VT) was the result of Flecainide toxicity.
• Flecainide was discontinued. A ß-blocker was started. After withdrawing Flecainide, the rate of AFlutter increased, approaching a rate of 300/minute.
• Despite ß-blocker treatment — 2:1 AV conduction persisted, with a ventricular response of ~150/minute. The decision was then made to electrically cardiovert the patient — and to then refer him for ablation of his AFlutter.

Learning Points:

• Diagnosis of AFlutter may be challenging — especially when flutter waves are not readily visible in the usual leads. 
• Flutter waves may simulate the sinus P waves of sinus tachycardia. Always consider 2:1 AFlutter when sinus tachycardia does not fit the clinical picture.
• Be aware of the signs of Flecainide toxicity — especially of the tendency to slow the atrial rate of AFlutter (and in patients who are not on an AV nodal blocker — to precipitate 1:1 AV conduction).
• Regardless of how bizarre QRS morphology during a WCT rhythm may be — Consider 1:1 AV conduction of AFlutter (and not VT) if the patient is taking Flecainide.