ECG Blog #453 — Is this Wellens' Syndrome?

The ECG in Figure-1 was obtained from a middle-aged man who presented with a 2 week history of progressively increasing CP (Chest Pain) with exertion. He had his most severe episode of CP the day before he was seen with this ECG. His CP was much less compared to the day before — but it had not yet completely resolved.

• An initial Troponin drawn less than 1 hour after the ECG in Figure-1 was recorded was over 10,000.

 

QUESTIONS:

• Given this history — How would YOU interpret this ECG?
• Is this Wellens’ Syndrome?

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

MY Thoughts on Today’s CASE:

The rhythm for the ECG in Figure-1 is sinus at ~85/minute. The PR and QRS intervals are normal; the QTc appears to be borderline prolonged (counting the terminal negative part of the T waves in V3,V4). There is no chamber enlargement. 

Regarding Q-R-S-T Wave Changes:

• Small q waves are seen in each of the inferior leads. The q wave in lead III is a bit wider than usual for a normal septal q wave — so I was uncertain if these inferior q waves might be of clinical significance.
• That said — there is a definite QS complex in lead V3 (See Figure-2). This QS complex takes on additional significance because there is loss of r wave from lead V2-to-V3. As a result of this QS in V3 — I interpreted the small Q wave in lead V4 as also significant.
• Small and narrow q waves of uncertain significance are seen in lateral chest leads V5 and V6.
• R Wave Progression is delayed because of the loss of anterior forces in leads V3 and V4.

Regarding ST-T Wave Changes:

• There is ST segment straightening with slight ST elevation in lead V2.
• The ST segment take-off in lead V3 is slightly elevated and coved in shape — with sharp descent into terminal T wave negativity (BLUE arrow in this lead in Figure-2).
• Similar ST segment straightening with terminal T wave negativity continues in lead V4, and to a lesser extent in lead V5 (Blue arrows in these leads).
• There is nonspecific ST-T wave flattening in lead V6 — and in the limb leads.

My Impression of ECG #1 given Today's History:

In this middle-aged man with a 2-week history of CP — with his most severe episode the day before ECG #1 was recorded — and with reduced (but not completely resolved) CP at the time this ECG was recorded — this tracing suggests there has been anterior infarction.

• My "eye" was immediately drawn to the 2 leads within the RED rectangles in Figure-2 — which highlight the QS complex in lead V3 and the Q in V4 that indicate infarction.
• NOTE: Preservation of the initial positive deflection (that is the r wave) in leads V1,V2 — suggest the septum is still intact.
• The initial Troponin of >10,000 confirms infarction has occurred — perhaps the day before ECG #1 was recorded, since CP was most severe at that time.
• The modest amount of residual ST elevation in anterior leads, in association with terminal T wave inversion in leads V3,V4,V5 and greatly reduced CP — suggest there has been some spontaneous reperfusion.

BOTTOM Line: Clinical correlation with today's ECG point to LAD (Left Anterior Descending) occlusion, now with reperfusion T waves (in association with the reduction of CP). 

• The above said, this is not Wellens' Syndrome — because a large infarction has already occurred! (See below for full explanation).
• P.S.: Cardiac cath was performed — and showed a distal LAD "culprit" lesion that was successfully stented. Echo revealed an ejection fraction of 35-40%.

Figure-2: I've labeled the initial ECG in today's case.

What is Wellens’ Syndrome?

When we talk about Wellens’ Syndrome — It is all about timing. As reviewed in ECG Blog #350 — the clinical significance of Wellens' Syndrome — is that its recognition tells you that the patient has a high-grade LAD narrowing with presumably "hot" thrombus having high propensity to propagate and/or totally occlude the LAD at any point in time (including immediately). 

The above said — Wellens' Syndrome remains a misunderstood and often misdiagnosed clinical entity. The following are the KEY clinical and ECG features that establish the diagnosis of Wellens' Syndrome:

• There should be a history of prior chest pain that has resolved at the time the defining ECG is obtained.
• There should be no more than minimal (if any) troponin elevation. 
• There are no new infarction Q (or QS) waves. R wave progression should be preserved (so there is not loss of anterior forces).
• There may be slight (but not marked) ST elevation in one or more of the chest leads.
• There is a characteristic biphasic T wave, with rapid T wave descent into terminal negativity in one or more of the chest leads (most often in lead V2 and/or V3 and/or V4).
• 
  
• CAVEAT: The diagnosis of Wellens' Syndrome should be made with caution (if at all) in a patient with marked LVH and ST-T wave changes of LV "strain". This is because the ECG finding of increased QRS amplitude that occurs in association with abrupt precordial transition from predominantly negative to predominantly positive QRS complexes — may result in an ST-T wave appearance identical to the biphasic T wave with terminal negativity characteristic of Wellens' changes (See ECG Blog #209 and Blog #254 and Blog #309 — for several examples of this "false positive" appearance).

Why Today's ECG does Not represent Wellens' Syndrome:

Appreciation of the pathophysiology of Wellens' Syndrome facilitates understanding why today's case does not qualify. 

• The characteristic biphasic T wave with rapid T wave descent into terminal T wave negativity — is indication that there has been brief total occlusion of the LAD, which has now spontaneously reperfused. This ECG finding is a "reperfusion T wave". It may look identical to the ST-T wave appearance seen after a STEMI with marked troponin elevation, that has now reperfused (be this reperfusion spontaneous — or by treatment with PCI or thrombolytics).
• The Chest Pain required for the definition of Wellens' Syndrome occurred at the time of coronary occlusion. The reason the patient is pain-free at the time the defining ECG is done — is that the "culprit" LAD lesion is now open. IF the "culprit" LAD lesion was still occluded — then rather than a warning of impending infarction (which is the purpose of promptly recognizing Wellens' Syndrome) — there would be ongoing acute infarction.
• The reason there is no more than minimal (if any) troponin elevation with Wellens' Syndrome — is because the duration of coronary occlusion was so brief that no more than minimal myocardial damage resulted. In contrast, if Troponin is significantly elevated — this implies significant myocardial damage has already occurred (which by definition means you are dealing with a completed infarction — and not with the "warning" of an impending large infarction).
• For this same reason — there should not be new infarction Q (or QS) waves, which would imply completed infarction.
• The reason there is no more than slight ST elevation — is because Wellens' Syndrome is not a STEMI (ie, it is not an "ST Elevation" MI).
• The clinical risk posed by Wellens' Syndrome — is that it is proof there has already been acute thrombotic occlusion of the LAD (albeit brief in duration and followed by spontaneous reopening of the vessel). BUT — What has spontaneously occluded and then spontaneously reopened — is at high-risk of another spontaneous reocclusion (with no guarantee that there will again be spontaneous reopening this next time that the vessel occludes).

Regarding Today's CASE: 

Reread the history in today's case (in the opening paragraph above) — and Take another LOOK at the ECG in Figure-2.

• Loss of r wave from lead V2-to-V3, so as to form the large QS complex in lead V3 (with Q wave also in lead V4) — indicates that significant anterior infarction has already occurred in today's patient, whose CP has not yet completely resolved — and whose initial Troponin value is already markedly increased (at over 10,000). This indicates completed infarction — and does not fit the definition of Wellens' Syndrome.

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Acknowledgment: My appreciation to Josep Serra Tarragon (from Tarragona, Spain) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #209 and ECG Blog #254 and ECG Blog #309 — Review cases of marked LVH that result in similar ST-T wave changes as may be seen with Wellens' Syndrome. 
• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).
• 
  
• ECG Blog #320 — Reviews acute OMI of the 1st or 2nd Diagonal (presenting as Wellens' Syndrome).
• 
  
• ECG Blog #326 — Reviews a case of Wellens' Syndrome that was missed.
• ECG Blog #350 — another case of Wellens' Syndrome.
• 
  
• ECG Blog #337 — for Review of a case illustrating step-by-step clinical correlation between serial ECGs with symptom severity.
• 
  
• See the October 15, 2022 post (including My Comment at the bottom of the page) — for review and illustration of the concept of "Precordial Swirl" (due to proximal LAD OMI).

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ADDENDUM (10/26/2024): I excerpted what follows below from My Comment in the August 12, 2022 post in Dr. Smith's ECG Blog).

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The History of Wellens' Syndrome:

It's hard to believe that the original manuscript describing Wellens' Syndrome was published over 40 years ago! I thought it insightful to return to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):

• The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
• I've reproduced (and adapted) in Figure-3 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
• Most patients also showed characteristic changes in lead V4.
• Most patients showed some (but less) ST-T wave change in lead V1.
• In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.
• 
  
• Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after hospital admission.
• Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated

ECG Patterns of Wellens' Syndrome:

The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-3:

• Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
• Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep.

Figure-3: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:

I've reproduced (and adapted) in Figure-4 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.

• The patient whose ECGs are shown in Figure-4 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
•  
• Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-3 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).
• 
  
• Not shown in Figure-4 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-4). During this time — this patient remained asymptomatic and was gradually increasing his activity level.
• 
  
• Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-4: Representative sequential ECGs from one of the patients in the original 1982 article. 
— Panel A: The initial ECG on admission to the hospital; 
— Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing). 
— Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

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Relevant Findings from the 1982 Article:

The ECG pattern known as Wellens' Syndrome was described over 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.

• One of the 2 ECG Patterns shown in Figure-3, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
• Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remained normal, or were no more than minimally elevated.
• Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.

• We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.
• The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).
• BUT: What spontaneously occludes, and then spontaneously reopens — may continue with this cycle of occlusion — reopening — reocclusion — reopening — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).
• 
  
• Clinically: We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example — resolution of chest pain in association with reduction of ST elevation suggests that the "culprit" vessel has spontaneously reopened. And, if this is followed by return of chest pain in association with renewed ST elevation — the "culprit" artery has probably reclosed.
• The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
• Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
• It is not "Wellens' Syndrome" — IF the patient is having CP (Chest Pain) at the time one of the ECG patterns in Figure-3 are seen. Active CP suggests that the "culprit" artery is still occluded.
• Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.
• Finally, a word about the 2 ECG Patterns in Figure-3. As suggested from data in the original 1982 manuscript, Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
• Unlike the example in Figure-3 — Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. Deep, symmetric T wave inversion per se is seen in a number of other conditions, and is much less specific for Wellens' Syndrome.

In Conclusion: The 145 patients studied by de Zwaan, Bär & Wellens in 1982 continue to this day to provide clinical insight into the nature of Wellens' Syndrome.

 

ECG Blog #452 — Is this Wide QRS Rhythm VT?

The patient whose ECG is shown in Figure-1 — presented with acute dyspnea and hypotension.

QUESTION:

• In Figure-1 — Is the rhythm VT?
•   — How certain are you of your answer?

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

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MY Thoughts on the ECG in Figure-1:

Although at first glance, the ECG in Figure-1 appears to be wide — this is a false initial impression! Closer inspection suggests that the QRS complex is actually narrow — and that the reason the QRS appears to be wide, is that the dramatic picture of "Shark Fin" ST Elevation is present!

• I have previously reviewed a number of cases of "Shark Fin" morphology (See ECG Blog #364 — Blog #410 — Blog #265 — among others).

Consider the following in Figure-2 — in which I've labeled today's ECG:

• Look closely in all 12 leads — to see if there are one or more leads that allow you to precisely define the limits of the QRS complex. I've drawn vertical RED lines to highlight these leads. Everything to the right of these RED lines marks the beginning of the ST segment (BLUE arrows in Figure-2) — which shows marked ST elevation in multiple leads!
• Following these RED lines upward — suggests there is ST depression in leads aVL; aVR; V1,V2.
• Sinus P waves are best seen in lead V1. Note that the 4th QRS complex in lead V1 is wider, and preceded by an on-time sinus P wave with a shorter PR interval (PINK arrow P wave in lead V1). The fact that this PR interval is shorter than all other PR intervals in this lead — means that this 4th QRS complex in lead V1 must be a PVC (albeit possibly with some fusion) — because there is not adequate time for this PINK arrow P wave to conduct all the way through the ventricles. This proves that the other 5 beats in lead V1 (that are each preceded by an on-time RED arrow P wave) — are sinus-conducted beats.
• Isn't it easier to appreciate that the 5th colored arrow in lead V1 is a sinus P wave — because of the slightly longer R-R interval that precedes it? (made possible because the 4th QRS complex in this lead is a PVC that occurs before the next sinus-conducted beat would have occurred).
• We call this 4th QRS complex in lead V1 a "late-cycle" PVC (Premature Ventricular Contraction) — because it occurs at a fairly late point in the R-R interval.
• Late-cycle PVCs are also seen in lead II and in lead aVL. In each of these leads — we see an on-time sinus P wave preceding a wider and different-looking QRS complex with a PR interval that is too short to conduct normally — thereby proving that the QRS complexes seen right after these PINK arrow P waves in leads II and aVL are PVCs (albeit possibly with some fusion).
• There is another PVC that occurs immediately after the lead change in lead aVL — but the lead change (vertical black line) blocks our view of the P wave before this beat.

BOTTOM Line:

• Today's patient presented in shock (presumably cardiogenic) — with acute dyspnea, hypotension, and the ECG that is shown in Figure-2.
• This ECG shows marked sinus tachycardia with end-cycle (late-diastolic) PVCs — and with Shark Fin ST elevation in multiple leads. Given the diffuse nature of ST-T wave changes — this ECG picture presumably is the result of acute LAD occlusion (or possibly even LMain occlusion).

Figure-2: I've labeled the initial ECG in today's case.

CASE Follow-Up: 

Unfortunately, my follow-up of today's case is limited. The "good news" — is that this patient did survive!

• Optimal treatment of the patient in today's case would entail recognizing there is sinus tachycardia with marked and diffuse Shark Fin ST elevation — with need for prompt cath and almost certain need for coronary reperfusion with PCI (Percutaneous Coronary Intervention).

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Acknowledgment: My appreciation to Haseeb Raza Naqvi (from Multan, Pakistan) for the case and this tracing.

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ADDENDUM (10/19/2024):

• The Audio Pearl below reviews the concept of "shark fin" ST elevation. 

—  — 

ECG Media PEARL #73 (5:40 minutes Audio) — Reviews the concept of "Shark Fin" ST elevation and depression as a sign of extensive acute infarction.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #364 — Blog #410 — Blog #265 — for more examples of Shark Fin Morphology.

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ECG Blog #451 — Premature Closure ...

I was sent the ECG shown in Figure-1 — told only that the patient was a middle-aged man with septicemia.

QUESTIONS: 

• Is this rhythm too fast to be sinus tachycardia?
• Are flutter waves hidden within the QRS and T waves?
• Are we seeing the retrograde P waves of AVNRT?
• Is this ATach (Atrial Tachycardia)?

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

MY Thoughts on Today’s CASE:

In my opinion — none of the above answers are optimal to describe the rhythm in Figure-1. I say this for the simple reason that to pick any of the above 4 choices — is to imply with 100% certainty that you know the answer (or, as is implied in the title of today’s Blog post — this would be premature closure).

• Instead, I feel it preferable to openly acknowledge that — We do not know for certain what the rhythm is. 

The above said — I did have a good idea what this rhythm was most likely to be. However, until such time that we know for certain — I think it best to simply describe what we see:

• PEARL #1: Realize that for any tachycardia — there are 6 Parameters that need to be assessed. The 1st Parameter — is to ensure that the patient is hemodynamically stable. This is because IF your patient is not stable — then it no longer matters what the rhythm is (because immediate cardioversion will be needed — regardless of whether the rhythm is VT or an SVT).
• Next (assuming your patient is hemodynamically stable) — Assess the rhythm for the remaining 5 KEY Parameters — that are most easily remembered by the saying, “Watch your Ps, Qs — and the 3Rs”. With practice — it should literally take no more than seconds to assess these 5 Parameters (See ECG Blog #185 — for more on the Ps,Qs,3R Approach to rhythm interpretation).

Watch your Ps, Qs — and the 3Rs:

Regarding today's initial rhythm — I see the following:

• There is significant artifact, especially in leads V1,V2 (See Figure-2). This makes assessment of P waves impossible in these 2 chest leads. 
• That said — I thought sinus P waves might be present in the inferior leads. However, I could not with certainty distinguish between what might be a P wave? — vs a T wave? — vs a P wave hiding within the preceding T wave (ie, under the ?'s that I placed in the inferior leads).
• On the other hand — Doesn't it look like there might be 2:1 atrial activity in lateral leads V5,V6 (slanted RED lines in these leads)? As a result — I was not certain about the presence and/or nature of atrial activity.
• NOTE: My "Go-To" Leads when looking for extra atrial activity are leads II,III,aVF; aVR; and V1 — which is why I was not convinced on the basis of the RED lines I drew in Figure-2 that this truly represented 2:1 atrial activity.

Continuing with the 5 Parameters:

• The rhythm in Figure-2 is Regular — at a Rate of ~160/minute (ie, with an R-R interval slightly less than 2 large boxes in duration).
• The QRS complex is narrow in all 12 leads (ie, Not more than half a large box in any of the 12 leads).
• The last of the 5 Parameters — is whether P waves are Related to the QRS complex. But since we are not certain if there even is atrial activity? (and if so — whether such atrial activity represents sinus P waves, flutter waves, or something else?) — we can not yet address this 5th Parameter.
• 
  
• BOTTOM Line: Today's initial rhythm is a regular SVT (SupraVentricular Tachycardia) at ~160/minute, but without clear indication of the presence and nature of atrial activity.

PEARL #2: Recognition that the rhythm in Figure-1 is a regular SVT — but with uncertainty regarding atrial activity — should prompt consideration of the followling differential diagnosis LIST (See ECG Blog #240):

• i) Sinus Tachycardia (if sinus P waves are hidden below the ?'s in Figure-2 ). 
• ii) A reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an accessory pathway outside the AV node is involved); 
• iii) Atrial Tachycardia (ATach);
• iv) Atrial Flutter (AFlutter) with 2:1 AV conduction.

KEY Point: Although other entities may also produce a regular SVT (ie, sinoatrial node reentry tachycardia, junctional tachycardia) — they are far less common in practice. Therefore, remembering to think of the 4 entities in the above LIST whenever you encounter a regular SVT rhythm without clear indication of atrial activity — will greatly facilitate determining the correct diagnosis.

PEARL #3: Consider the History:

• Is the patient on any antiarrhythmic medication? (This is important to consider — as it may affect the rate and conduction properties of the SVT).
• Any known history of similar rhythms?
• What is the clinical situation? (ie, In today's case the patient has septicemia — therefore seemingly susceptible to sinus tachycardia!).

PEARL #4: Consider the Rate of the SVT:

• In adults — Sinus Tachycardia usually does not exceed 160-170/minute in a "horizontal" patient (ie, in a patient you are examining, who has not just been running). This is not to say that sinus tachycardia will never go faster than 170/minute — but rather to suggest that when the rate of the regular SVT rhythm you are assessing is well over this rate range — then the rhythm is less likely to be sinus tachycardia. NOTE: All bets are off in children — in whom sinus tachycardia over 200/minute is not that uncommon.
• With AFlutter — the most common ventricular response in the patient who is not being treated with an antiarrhythmic medication is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range ~250-350/minute) — and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. As a result — IF the ventricular rate of the regular SVT rhythm you are assessing is over ~170-180/minute (but under ~250/minute) — then AFlutter is less likely (because this rate would be faster-than-expected for 2:1 AV conduction, and too slow for 1:1 AV conduction). 
• NOTE: This ~140-160/min. range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial rate (and therefore slower ventricular response) for AFlutter.
• It is well to remember that ATach is less common as a cause for a strictly regular SVT, especially in an otherwise healthy young-to-middle-aged adult. ATach is more likely to be seen in patients referred for EP (ElectroPhysiologic testing) — and in older adults with SSS (Sick Sinus Syndrome). I include ATach in the above differential diagnosis LIST for completeness — but take into account that it won't be seen as often as AFlutter and the reentry SVTs.
• Therefore — IF the rate of a regular SVT without clear sign of sinus P waves is substantially faster than 160-170/minute — then a reentry SVT rhythm (ie, AVNRT or AVRT) becomes the most likely diagnosis. 
• But — IF the rate of the regular SVT is close to 150/minute (as it is with today's initial rhythm at ~160/minute) — then any of the 4 diagnostic entities in the above LIST could be present!

PEARL #5: Other potentially helpful considerations:  

• Look for Atrial Activity! — which we've already addressed for today's rhythm (See above). Using calipers can facilitate your search for atrial activity.
• Look for a “Break” (or subtle change) in the Rhythm! — Even a slight pause in the SVT rhythm, may be all that is needed to reveal underlying atrial activity that had been hidden by the regular tachycardia. There is no "break" in the rhythm in Figure-2. That said, it may be helpful to search Telemetry — as there may have been some change in the rhythm a little earlier in the patient's course.
• Look for the “Onset” (and/or Termination) of the Rhythm! — The KEY clue to the etiology of an SVT often lies with capturing either the beginning and/or the end of the SVT. 
• ATach often begins gradually, with progressive acceleration of the ectopic focus (ie, “warm-up” phenomenon). Then, there may be gradual slowing (ie, “cool-down”) of the rhythm as it ends. 
• In contrast — SVT reentry rhythms often start with 1 or more PACs that block conduction down one of the AV nodal pathways, which serves to set up the reentry circuit as the impulse starts down the other pathway. As a result — the onset of a reentry SVT is often abrupt (ie, accounting for the previous term used to designate this rhythm = PSVT = Paroxysmal SVT). The termination of reentry SVT rhythms is also usually quick (though this may occur over several beats).
• Finally, when Sinus Tachycardia is suspected clinically (as it is in today's case) — awareness that over time the rate of sinus tachycardia will often change (become slower or faster) as the patient's condition becomes better or worse.

 

PEARL #6: While our goal is to arrive at as precise of a rhythm diagnosis as possible — the "good news" is that for practical purposes — initial diagnostic and/or treatment measures in the field or in the ED for an undifferentiated regular SVT rhythm are similar (ie, consideration of a vagal maneuver — and/or use of an AV nodal blocking agent such as Verapamil/Diltiazem; a ß-Blocker, and possibly Adenosine).

• P.S.: If you suspect that the regular SVT rhythm is likely to be sinus tachycardia — then rather than antiarrhythmic medication, simply treating the underlying disorder may be all that is needed.

Figure-2: I've labeled the initial ECG in today's case.

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Today's CASE Continues:

The patient was treated for sepsis. A very lose dose of IV Metoprolol was given. The repeat ECG is shown below in Figure-3.

• What has happened?

Figure-3: The ECG was repeated after beginning treatment for sepsis.

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ANSWER — and CASE Conclusion: 

To facilitate comparison in Figure-4 — I've put together both ECGs in today's case.

• Following treatment for sepsis — the patient improved clinically. As a result — the heart rate in ECG #2 has now slowed just enough to allow clear distinction of sinus P waves (RED arrows in lead II of the repeat ECG).
• Clear distinction of sinus P waves is now also seen in each of my "Go-To" Leads (BLUE arrows in these leads), as well as in virtually all leads on this tracing.
• Comparing ECG #2 with the initial tracing — We can see that sinus P waves were present the entire time! Because of the very fast rate in ECG #1 — the sinus P waves were simply hidden within the terminal part of preceding T waves.
• Otherwise, on the repeat ECG — there are some nonspecific ST-T wave abnormalities (potentially rate-related) — and the possibility of large U waves (hard to tell — given the still rapid heart rate of 140-150/minute). Serum K+ and Mg++ levels need to be verified.

Figure-4: Comparison of the repeat ECG with the initial ECG (after treatment of sepsis).

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Acknowledgment: My appreciation to Sam Ghali @EM_RESUS (from Jacksonville, Florida — USA) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.
• 
  
• ECG Blog #240 — The regular SVT ...
• ECG Blog #229 — Why is AFlutter so commonly overlooked?
• ECG Blog #138 — AFlutter vs Atrial Tachycardia. 
• ECG Blog #40 — Another regular SVT that turned out to be AFlutter.

Other sites where I've discussed similar cases:

• The March 6, 2020 post in Dr. Smith's ECG Blog.
• The October 16, 2019 post in Dr. Smith's ECG Blog. 
• Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter).