ECG Blog #382 — What Does the Holter Show?

I was sent the Holter monitor tracing in Figure-1 — but without the benefit of any clinical information.

QUESTIONS:

A total of 9 QRS complexes are seen in the 2 simultaneously-recorded monitoring leads.

• How would YOU interpret the rhythm in Figure-1?
• How many P waves do you see?
• Why do the QRS complexes of beats #4 and 5 in the bottom lead look different than the other 7 beats?
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• What do you suspect as the clinical diagnosis?

Figure-1: The initial 15-second rhythm strip in today’s case.

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NOTE: The recording system used in rhythm strips from today’s post may be different from what you are accustomed to. In Figure-2 — I've labeled some of these differences — and I highlight atrial activity.

• Note in Figure-2 — in the upper right corner of this rhythm strip (within the RED rectangle) — that the recording speed is 12.5 mm/second (instead of the 25 mm/sec. speed that many of us are used to) — BUT — that the width of each large box on the ECG grid paper has been reduced by 50% (so that each small rectangular box on this ECG grid paper still represents 200 msec. = 1/5 second — as shown by the RED arrow).
• As a result — the time to record 5 of these small rectangular boxes on each rhythm strip in today’s post is still 1.0 second (with each increment of 1.0 second separated by vertical dotted GRAY lines).
• The advantage of this system of recording is that QRS amplitude of each complex is maintained — while an easier-to-read longer rhythm strip can be displayed (ie, ECG Rhythm #1 displays a full 15 seconds of today’s rhythm! — instead of the usual 6-10 second rhythm strips many of us are used to).
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• Finally — Note that each R-R interval in Figure-2 has been precisely calculated for you. For example — the R-R interval between beats #1-2 = 1820 msec. ( = 1.82 second = 9.1 little boxes, as per the GREEN arrows ==> which corresponds to a heart rate of 300 ÷ 9.1 = 33 beats/minute). 
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• PEARL #1: This computer-determined calculation allows us to instantly appreciate small changes in heart rate (ie, The R-R interval before beat #4 = 1679 msec. — which is significantly shorter than the 1820 msec. R-R interval for the first few beats in this tracing). 

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How Many P-Waves are there in ECG Rhythm #1?

The benefit of having 2 simultaneously-recorded leads in a given rhythm strip — is that this allows us to see ECG findings that may only be visibile in one of the 2 leads being monitored.

• Sinus P waves with a constant PR interval are clearly seen to precede beats #4-thru-9 (RED arrows in the upper monitoring lead in Figure-2).
• P waves in the upper lead of Figure-2 are upright, albeit small in amplitude. These P waves that precede beats #4-thru-9 — are larger and biphasic in the lower monitoring lead.
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• The QRS complexes of beats #1,2,3 are wider — and look very different in both monitoring leads in Figure-2, than the QRS morphology of sinus beats #4-thru-9. These wider beats are not preceded by sinus P waves — which suggests they are ventricular escape beats! The R-R interval that separates these ventricular beats = 1820 msec. — which corresponds to a ventricular rate of ~33/minute (which fits perfectly within the usual range of an idioventricular escape rhythm).
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• PEARL #2: The fact that the R-R interval preceding return of the 1st sinus-conducted beat ( = beat #4) is shorter ( = 1679 msec.) than the 1820 msec. R-R interval of the 3 ventricular escape beats — suggests that the reason sinus rhythm resumes beginning with beat #4, is that the rate of sinus discharge sped up sufficiently to surpass the rate of idioventricular escape!
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• PEARL #3: Note that the R-R interval varies significantly between sinus-conducted beats #4-thru-9 (ie, from 1679 msec. to 1828 msec.) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This suggested to me from this initial rhythm strip — that additional rhythm strips from this patient's 24-hour Holter recording will probably show episodes of varying duration of ventricular escape when the rate of sinus bradycardia slows below the ventricular escape rate!
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• PEARL #4: In view of the etiology I suspected for the mechanism of explaining the rhythm change in Figure-2 — I looked closer at the lower monitoring lead for partially hidden atrial activity. Note tiny-but-real differences in QRS morphology for the first 3 beats in the lower lead (ie, a pseudo r' notch at the end of the QRS for beats #1 and 2 that is not seen at the end of beat #3 — and an extra initial positive deflection at the beginning of beat #3 that is not seen at the beginning of beats #1 and 2). This strongly suggests that sinus P waves are occurring throughout this rhythm strip — and are partially hidden under the PINK arrows!

Figure-2: I've labeled the initial rhythm strip in today’s case (See text).

Why Do Beats #4 and 5 Look Different?

Although QRS morphology for each of the sinus-conducted beats in the upper monitoring lead in Figure-2 look similar — beats #4 and 5 clearly look different than the other 7 beats in the lower monitoring lead!

• Beats #4 and 5 manifest a narrow biphasic (almost equal R wave and S wave) morphology in the lower lead. This is an intermediate morphology between the predominantly upright QRS of sinus-conducted beats #6-thru-9 — and the wider predominantly negative QRS of beats #1-thru-3, which are the ventricular escape beats.
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• PEARL #5: The most logical explanation for why the QRS complex of beats #4 and 5 in the lower monitoring lead look different and intermediate in morphology between QRS morphology of the initial 3 ventricular escape beats and the pure sinus-conducted beats that follow ( = beats #6-thru-9) — is that beats #4 and 5 must be Fusion beats! Identification of beats #4 and 5 as "fusion" beats (F) confirms a ventricular etiology for beats #1,2,3. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia, with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
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• NOTE: The rhythm strip in Figure-2 is a Holter tracing — so baseline artifact undulations that we see, in addition to some variation in QRS amplitude for sinus beats #6-thru-9 is not unexpected. That said — the difference in QRS morphology between beats #4,5 vs beats #6-thru-9 in the lower lead is clearly real, and most logically explained by interpreting beats #4 and 5 as fusion beats.

What Do YOU Suspect as the Clinical Diagnosis?

As mentioned above — I had no clinical information (not even the age of this patient) at the time I was sent this initial tracing. That said — Common things are Common.

• Although there are a number of ECG findings that characterize SSS (Sick Sinus Syndrome) — by far, the most common initial rhythm of this syndrome will be sinus bradycardia and arrhythmia. There is often a long subclinical period (of up to a decade or more!) — during which sinus bradycardia and arrhythmia may be seen as the only indication of SSS, albeit not yet to a degree that produces symptoms.

PEARL #6: As I discuss in my review of SSS (See ECG Blog #342 for details) — establishing a diagnosis that sinus bradycardia indicates SSS — will depend on the following:

• Finding out the age of the patient (ie, SSS is most common in older individuals) — and learning whether the patient has been symptomatic? (ie, with syncope-presyncope, fatigue, dyspnea, chest pain?).
• Checking the rest of the Holter to see if episodes of bradycardia primarily occur at night? (since sleep apnea is a readily treatable cause of nighttime bradycardia, as well as of other arrhythmias).
• Checking all medications that the patient is taking (including herbal products). You are looking for potential rate-slowing medication — that may be the cause of bradycardia (Not to forget inquiry about beta-blocker eye drops — which are partially absorbed, and which can be an easily overlooked as an iatrogenic cause of bradycardia). 
• Ruling out other potential causes of bradycardia (ie, recent ischemia-infarction; hypothyroidism).
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• BOTTOM Line: Although many questions remain to be answered regarding clinical correlation of today's case — I immediately considered SSS as being statistically the most common cause of a rhythm like the one we see in Figure-2.

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What Else did the 24-Hour Holter Show?

I was sent a number of additional 15-second rhythm strips from this patient's 24-hour Holter Monitor. In addition — I was provided with the Holter Summary Report. Pertinent ECG findings from this summary included the following:

• An overall average heart rate for the day of monitoring of between 45-50/minute. The rate did not drop below 30/minute — and it did not exceed 100/minute. Bradycardia was not limited to nighttime hours.
• No pause beyond 2.0 second.
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• Occasional PVCs throughout the day without sustained repetitive forms.
• 2 short runs of SVT (presumably atrial tachycardia).
• Periodic transition from wide-to-narrow QRS complexes (similar to that seen in Figure-2).

Below in ECG Rhythms #2-thru-6 — are selected additional rhythm strips I received. Do these tracings support my initial impression?

ECG Rhythm #2:

ECG Rhythm #3:

ECG Rhythm 4:

ECG Rhythm #5:

 ECG Rhythm #6:

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MY Thoughts on ECG Rhythms #2-thru-6:

Overall — these additional rhythm strips support my initial impression.

ECG Rhythm #2:

Amazingly — We see no less than 7 variations in QRS morphology for the 9 beats shown in ECG Rhythm #2. For clarity in Figure-3 — I've labeled P waves in this tracing (RED arrows in Figure-3).

• I find it difficult to determine which (if any) of the 9 beats in Rhythm #2 are purely sinus-conducted.
• Although the QRS complex of beat #8 occurs earlier-than-expected and looks similar to the QRS of sinus-conducted beats in Figure-2 — this beat is biphasic in the lower monitoring lead, and we previously determined that biphasic beats #4 and 5 in the lower lead of Figure-2 were fusion beats (F).
• For this reason — I suspect beat #2 in Figure-3 is also a fusion beat (because beat #2 is also biphasic in the lower lead).
• Beats #3-thru-7 in Figure-3 represent various degrees of ventricular etiology, with-or-without some component of fusion. Note that the PR interval for beats like #3,4,5 is clearly too short for normal conduction (therefore predisposing to a certain amount of fusion). 
• Beat #9 is different — and shows us a different shape (V) for this wide beat in both the upper and lower monitoring lead (compared to the shape of previous ventricular escape beats in these 2 leads). Therefore — There appear to be at least 2 different ventricular sites for the ventricular escape rhythm!
• Finally — I put a question mark (?) above beat #1 — because I can't figure out what this beat represents (ie, Ventricular escape, possibly with fusion from perhaps yet another ventricular site?).

PEARL #7: The specific etiology of each beat in these selected tracings is not important. Instead — What counts is the "theme" of the overall rhythm disturbance in today's Holter report.

• The overall "theme" of these rhythm strips — is that there is an underlying marked sinus arrhythmia and bradycardia, with frequent escape rhythms arising from one or more ventricular sites. This results in a variety of fusion beats between sinus-conducted beats and ventricular escape rhythms.

Figure-3: I've labeled P waves (RED arrows) and selected beats in ECG Rhythm #2. Note that the PR interval is clearly too short to conduct normally for a number of beats (that therefore must represent fusion between sinus and ventricular beats).

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ECG Rhythm #3:

The overall "theme" of today's Holter monitor recording continues. For clarity in Figure-4 — I've labeled P waves in this tracing (RED arrows in Figure-4).

• None of the P waves in Figure-4 come before the QRS. Therefore — there are no sinus-conducted beats in ECG Rhythm #3. Instead — all beats in Figure-4 must be of a ventricular etiology!
• Beat #3 clearly manifests an intermediate QRS morphology (Best appreciated in the lower monitoring lead — where beat #3 is intermediate in shape to the wide positive QRS of beats #1,2,4 — and the wide negative QRS of beats #7 and 8). Therefore — Beat 4 represents a fusion beat between 2 different ventricular escape foci!
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• Negative but narrow beats #5 and 6 are also clearly intermediate in QRS morphology between the wide upright QRS of beats #1,2,4 — and the wide negative QRS of beats #7 and 8. Therefore — beats #5 and 6 also represent fusion between 2 different ventricular escape foci!

Figure-4: I've labeled ECG Rhythm #3.

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ECG Rhythms #4, 5 and 6:

The "theme" of today's Holter monitor continues with these last 3 rhythm strips.

• There is marked bradycardia throughout — with frequent ventricular escape from different ventricular foci — often for extended periods without return of sinus rhythm.

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Putting It All Together:

I have subsequently found out that the patient in today's case is a woman in her 80s — so the likelihood of Sick Sinus Syndrome increases! I previously mentioned that the Holter Summary showed the following:

• An overall average heart rate for the day of monitoring of between 45-50/minute. The rate did not drop below 30/minute — and it did not exceed 100/minute. Bradycardia was not limited to nighttime hours.
• No pause beyond 2.0 second.
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• Occasional PVCs throughout the day without sustained repetitive forms.
• 2 short runs of SVT (presumably atrial tachycardia).

Clinically — the degree of persistent marked bradycardia is worrisome, even if prolonged pauses (of >2.5-to-3.0 second) are not yet seen — and even if this patient is not yet reporting "symptomatic bradycardia".

• Failure of the heart rate to go over 100/minute during the course of a day suggests there may be chronotropic incompetence — another concerning sign of SSS.
• The short runs of SVT are consistent with possible "Tachy-Brady" Syndrome — in which many patients with SSS alternate between marked bradycardia and various tachyarrhythmias.
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• Follow-Up: Our interpretation of this Holter was passed on to the patient's primary physician. I would bet that this patient will soon receive a permanent pacemaker.

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Acknowledgment: My appreciation to Andreas Röschl (from Neumarkt, Germany) for the case and this tracing.

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ADDENDUM (June 3, 2023): 

• The Audio PEARL (2:45 minutes) below reviews the ECG findings of SSS.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
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• ECG Blog #342 — reviews the ECG diagnosis of SSS (Sick Sinus Syndrome)
• ECG Blog #256 — Reviews another case of SSS.
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• ECG Blog #128 — ECG Blog #129 — and ECG Blog #133 — for review on Fusion Beats (that also show AV dissociation).
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• ECG Blog #295 — Reviews the concept of bradycardic-induced BBB ( = Phase 4 block). This is discussed near the bottom of the page (ie, in Pearl #5 — that appears just under Figure-6).
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• The July 5, 2018 post in Dr. Smith's ECG Blog — (Please see My Comment at the bottom of the page for Review on the ECG diagnosis of Sick Sinus Syndrome).

ECG Blog #381 — Why was the Troponin Normal?

The ECG in Figure-1 was obtained from a 60-ish year old man with a history of coronary disease (including prior CABG) — who presented to the ED (Emergency Department) with new CP (Chest Pain) of 3 hours duration, diaphoresis and nausea/vomiting. 

• The patient was hypotensive at the time his initial ECG in Figure-1 was obtained.

The decision was made not to immediately perform cardiac cath — because there is no ST elevation in Figure-1 — and because the initial troponin was negative.

• Do YOU agree with the decision not to cath at this time?
• How would you interpret ECG #1? 

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

MY Initial Thoughts on Today's CASE:

The clinical scenario presented in today's case is extremely concerning:

• The patient has a known history of coronary disease.
• His symptoms of CP are new! These symptoms are associated with diaphoresis, naursea/vomiting — and of special concern, hypotension! Even before looking at the initial ECG — the clinical scenario suggests probable need for prompt cath until proven otherwise!

Interpretation of ECG #1:

Normal sinus rhythm at ~80-85/minute is seen in Figure-1. The PR interval is normal — but the QRS is wide, with QRS morphology consistent with RBBB (Right Bundle Branch Block) and LAHB (Left Anterior HemiBlock). There is no chamber enlargement. 

Regarding Q-R-S-T Changes:

• There is a Q wave in leads aVL that is "significant" — given its width relative to the R wave in this lead. This may represent high-lateral infarction at some point in time. No other Q waves are present (ie, There is a tiny initial r wave in lead V1).
• R wave progression — is irrelevant, given the RBBB. 

Regarding ST-T wave Changes:

• The most "eye-catching" abnormalities are in leads V3 and V4 — both of which show definitely abnormal ST depression. The QRS complex is tiny (as well as fragmented) in lead V3 — with disproportionate J-point ST depression, followed by a coved, downsloping ST segment with an abnormally biphasic terminal T wave. The shelf-like ST depression in lead V4 is never normal, nor is the terminal T wave positivity seen in this lead. The S wave in lead V4 is also fragmented (ie, a sign of prior "scar" and/or infarction).
• Abnormal ST depression continues in leads V5 and V6, each with prominent (? hyperacute) T waves. The QRST appearance of these 2 lateral chest leads looks very similar to the QRST appearance in each of the inferior leads (albeit there is less J-point depression in the inferior leads).
• There is ST segment coving and T wave inversion in lead aVL.
• There is significant ST elevation in lead aVR.
• Finally, in lead V1 — the ST-T wave depression is expected with RBBB — but the subtle-but-real ST elevation in this lead is not expected with simple RBBB.

Putting It All Together:

Missing from this presentation at this time — is a prior (baseline) ECG on this patient who has a known history of significant coronary disease. As a result — I was not initially sure what was "new" vs "old". That said:

• There is bifascicular block (RBBB/LAHB) — which if new, would be an extremely worrisome sign.
• Multiple leads show abnormal ST segment straightening, with ST depression. This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI (Occlusion-based Myocardial Infarction) — most probably with multi-vessel disease (ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1).
• This patient has new CP — and — he is hypotensive.
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• BOTTOM Line: The normal initial troponin — and lack of ST elevation are not reasons for not performing cardiac catheterization. Acute posterior OMI results in ST depression, not ST elevation (with this ST depression typically maximal in leads V2-to-V4). Troponin rise is sometimes delayed. Even if acute coronary occlusion is not present in today's case — the findings of diffuse subendocardial ischemia in a patient with bifascicular block and known coronary disease — who presents with new CP and hypotension — constitute clear indication for immediate cath lab activation at this point in the case.

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The CASE Continues:

Another ECG was obtained 54 minutes after ECG #1. Unfortunately — I do not have information on the patient's symptoms and hemodynamics at the time ECG #2 was recorded.

For ease of comparison in Figure-2 — I've put these 2 ECGs together.

• How would you interpret ECG #2 in light of the initial tracing done 54 minutes earlier?

Figure-2: Comparison between the initial and repeat ECGs.

MY Thoughts on the Repeat ECG:

QRS morphology in the repeat ECG is virtually the same as in the initial tracing — which means that lead-by-lead comparison for subtle differences in ST-T wave morphology will be valid.

• There are now Q waves in leads V1 and V2 of ECG #2 — that were not previously present.
• There is more ST elevation in leads aVR and V1.
• There is more ST depression in virtually all leads compared to what was present in ECG #1.
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• Impression: ECG signs of diffuse subendocardial ischemia have clearly increased. Coronary reperfusion is urgently needed.

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The Baseline ECG was Found:

A prior ECG on today's patient, done ~9 months earlier — was found. For ease of comparison in Figure-3 — I've put this baseline tracing together with the initial ECG in today's case. 

• What do we learn from the baseline ECG? 

Figure-3: Comparison between the initial ECG in today's case — with a prior tracing recorded ~9 months earlier. What does this baseline ECG tell us?

MY Thoughts on the Baseline ECG:

Although I lack information regarding when the baseline ECG was obtained with respect to this patient's bypass surgery — 9 months earlier, the QRS was narrow without evidence of any conduction defect. With the exception of minimal, nonspecific inferior lead ST-T wave flattening — ECG #3 is essentially a normal tracing!

• Impression: The baseline tracing confirms that all of the above-described findings in ECG #1 are acute!

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CASE Conclusion:

A final 12-lead ECG was obtained on today's patient — which for ease of comparison in Figure-4, I have put together with ECG #2.

• Unfortunately — I do not have information on the sequence of treatment interventions, nor on correlation between patient symptoms, hemodynamics and specific timing with each of these serial ECGs.
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• At some point ~1-2 hours after the initial ECG — the patient developed runs of VT, leading to cardiac arrest. He could not be resuscitated.

There are lessons to be learned from this case. I include the final 12-lead that was done in Figure-4 — as I found it instructive to compare this last tracing with ECG #2 done 52 minutes earlier.

• How would you interpret ECG #4?

Figure-4: Comparison between the last ECG and ECG #2.

MY Thoughts on the Final ECG:

I am not certain what the rhythm in ECG #4 is.

• We see runs of rapid beats that I initially thought represented an irregular VT. However, the long lead II rhythm strip at the bottom of the tracing shows these runs to be punctuated by a number of pauses (ie, between beats #3-4; 5-6; 7-8; and 15-16) — and that an upright sinus P wave is clearly seen to be present at the end of each pause before beats #1, 4, 6, 8 and 16.
• Looking at each of the 18 beats in this long lead rhythm strip — the QRS morphology of sinus beats #1,4,6,8,16 is similar to QRS morphology of the rapid, irregular beats that follow these sinus-conducted beats in virtually each of the simultaneously-recorded leads of the 12-lead tracing (with possible exception of beats #14,15) — which makes me wonder if the rhythm in the long lead II is sinus with multiple successive PACs (perhaps a short run of AFib from beats #9-thru-15?) — vs — sinus rhythm with very frequent PVCs manifesting a QRS morphology very similar to the morphology of sinus beats.
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• What is certain — is the continued marked ST depression in the mid-chest leads, consistent with an ongoing, extensive infarction in this patient with severe symptoms and hypotension.

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Acknowledgment: My appreciation to 張三毛 = JJ (from Taiwan) 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.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
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• ECG Blog #271 — Reviews the concept of diffuse Subendocardial Ischemia.
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• ECG Blog #316 — The patient died. Was the LMain coronary artery the "culprit"?

Additional Relevant ECG Blog Posts

• ECG Blog #193 — Reviews a case with a dominant LCx as the "culprit" artery (with ECG AUDIO Pearl on the concept of "OMI" and on Predicting the "Culprit" Artery).
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• ECG Blog #184 — That magical inverse relationship between leads III and aVL.
• ECG Blog #167 — More on that "magical" lead III-aVL relationship.
• ECG Blog #183 — deWinter-like T waves.
• ECG Blog #374 — Acute LMain Occlusion.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
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• ECG Blog #56 — Posterior MI; Mirror Test.
• ECG Blog #80 — What's the Culprit Artery (and the Mirror Test).
• ECG Blog #82 — What’s the Culprit Artery?
• ECG Blog #162 — What’s the Culprit Artery?
• ECG Blog #193 — What's the Culprit Artery? 
• ECG Blog #222 — What's the Culprit Artery? 
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• ECG Blog #367 — for another example of acute LCx OMI. 
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• ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
• ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
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• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
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• ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes
• ECG Blog #230 — How to compare serial ECGs.
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• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
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• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.

ECG Blog #380 — What is "Swirl"?

The ECG in Figure-1 — was obtained from an older woman with persistent CP (Chest Pain) over the previous day. Her symptoms lessened after Nitroglycerin — so the decision was made not to activate the cath lab. Do YOU agree with this decision?

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

MY Thoughts on the ECG in Figure-1:

In a patient with CP that had been persistent over the previous day (until Nitroglycerin was given) — the initial ECG shown in Figure-1 is extremely worrisome. 

• The rhythm is sinus. Intervals (PR, QRS and the QTc) and the frontal plane axis are normal.
• Voltage for LVH is satisfied — at least by Peguero Criteria (Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73).

Regarding Q-R-S-T Wave Changes: 

• Q Waves — None are seen. 
• R Wave Progression — Transition (where the R wave becomes taller than the S wave is deep) is slightly delayed, occurring between leads V4-to-V5. That said — R wave amplitude is of reasonable size in all anterior leads (with slight reduction in R wave size from V2-to-V3 probably the result of lead placement).

The most significant abnormalities relate to ST-T Wave Changes:

• In the Limb Leads — There is nonspecific ST-T wave flattening, with slight ST depression in multiple leads (ie, in leads I,II,III,aVF).
• In the Chest Leads — Assessment for ST elevation in the anterior leads is especially challenging in ECG #1. This is because there is normally a small amount of upward-sloping ST elevation in leads V2 and V3. That said — in a patient with CP, the amount of ST elevation in leads V2 and V3 looks excessive to me, in association with ST-T waves that look potentially hyperacute. Thus, despite satisfying voltage criteria for LVH — considering the depth of the S waves in leads V2,V3 — the ST-T waves in these leads still look a little bit taller, fatter-at-their-peak and wider-at-their-base than I would expect them to be.
• Support that the ST-T waves in leads V2,V3 are likely to be abnormal — is forthcoming from the appearance of the ST-T wave in lead V1. In the absence of a deep S wave in lead V1 — it is uncommon to see ST elevation in this lead. It is simply not normal to see a full 1 mm of ST elevation in lead V1 (as we do in Figure-1) — especially in view of the ST segment straightening that is present in this lead.
• 
  
• PEARL #1: The above noted findings in leads V1,V2,V3 are subtle! It is for this reason that I'll emphasize that the one lead in ECG #1 that indisputably manifests an abnormal ST-T wave is lead V6. In a patient with new and persistent CP — it is never normal to see the amount of flat ST depression that is present in lead V6. Abnormal ST segment flattening and depression is also seen in neighboring lead V5, but not nearly as marked as in lead V6. 
• KEY Point: It is the fact that I know the flat ST depression in lead V6 is abnormal in a patient with persistent CP — that tells me the ST-T waves in leads V1,2,3 also have to be assumed abnormal until proven otherwise!

BOTTOM Line: The patient in today's case is an older woman who presents with a 1-day history of new and persistent CP. Her initial ECG should be interpreted as highly suggestive of acute proximal LAD occlusion until proven otherwise.

• NEW Concept: In a patient with CP — the ECG findings of anterior lead ST elevation, in association with lateral chest lead ST depression — is consistent with the pattern of Precordial "Swirl" (that I discuss below).

Continuation of Today's CASE:

A prior ECG on today's patient (done ~5 years earlier) was found — and is shown in comparison with the initial ECG in Figure-2. 

• Does this previous tracing strengthen our impression about this patient's initial ECG? 

Figure-2: Comparison of the initial ECG in today's case — with a prior ECG done ~5 years earlier. What do we learn from reviewing this previous ECG?

Comparison of ECG #1 and ECG #2:

IF there was any doubt about whether the ECG findings in today's tracing (ie, in ECG #1) are acute — it should have vanished the moment the prior ECG in Figure-2 was found!

• NOTE: It's important to correlate ongoing circumstances at the time that a prior tracing was done (ie, Was the patient stable and asymptomatic — or were they having chest pain, an exacerbation of heart failure, or some other ongoing process at the time the prior ECG was recorded?). This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. In addition — there were more prominent anteroseptal forces on this earlier tracing (ie, in the form of an R wave = S wave in lead V1, with similar-looking equiphasic QRS complexes in leads V2-thru-V5).
• The above said — there previously was no indication of any ST elevation, or of any potentially hyperacute ST-T waves in the anterior leads of ECG #2 — nor was the distinct, flat ST depression in lead V6 present in this prior ECG! These differences between the 2 tracings in Figure-1 strongly support our suspicion that the ST-T wave changes in ECG #1 have to be interpreted as acute until proven otherwise!

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What is Precordial Swirl?

In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers introduce the colorfully descriptive term known as Precordial Swirl — as an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.

PEARL #2: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in leads V1 and aVR — and — reciprocal ST depression in leads V5 and V6.

• When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
• Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal!). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!
• 
  
• NOTE: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.

In Figure-3 — I've selected 6 sets of V1,V2 leads from the series of tracings shown by Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl.

• Although admittedly subtle — the ST segment coving with slight but disproportionate ST elevation in lead V1 of A, B and C in Figure-3 is clearly an abnormal appearance for the ST segment in lead V1. In association with neighboring chest leads suggestive of acute LAD OMI — this picture should raise suspicion of Precordial Swirl.
• Example F in Figure-3 is more subtle — because the S wave in lead V1 is deeper. That said — this coved shape of ST elevation in lead V1 of F should still raise suspicion in a patient with new symptoms.
• The ST-T wave segment in lead V1 of example D — closely resembles the "shape" of LV strain in an anterior lead from a patient with LVH. However, the S wave in example D — is not at all deep in either lead V1 or V2 — which in a patient with chest pain should strongly suggest the possibility of Precordial Swirl.
• The ST-T wave shape in lead V1 of example E also appears to be subtly abnormal. Support that this finding is real — is forthcoming from our impression that the T wave in neighboring lead V2 looks more peaked than expected — which in a patient with new symptoms, should strengthen our suspicion of a disproportionately positive T wave in lead V1.

Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

NOTE: It's EASY to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves) will suggest LVH rather than Precordial Swirl (See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog).

• For additional examples that illustrate this concept of "proportionality" (regarding relative size of ST-T wave deviations compared to QRS amplitude in the respective lead) — Check out the additional examples of LVH that mimic Precordial Swirl which are provided in the October 15, 2022 post in Dr. Smith's ECG Blog.

Precordial Swirl Appearance in Lead V6:

The final component for diagnosing Precordial Swirl — is to see reciprocal ST depression at least in lead V6 (if not also in lead V5):

• Once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6.
• 
  
• I've reviewed my approach to the ECG diagnosis of LVH often (See ECG Blog #245 — among many other posts). In Figure-4 — I've reproduced from the above cited June 20, 2020 post my schematic illustration of the ST-T wave appearance that may be seen in one or more lateral leads for demonstrating LV "strain".

PEARL #3: In general, the shape of ST-T wave depression in lead V6 with Precordial Swirl does not look like either C or D in Figure-4. Instead — the depressed ST segment tends to be flatter. Therefore — THINK Precordial Swirl in a patient with new symptoms IF you see: 

• Other signs suggestive of acute LAD OMI.
• The ST-T wave in lead V1 looking "different-than-expected". 
• A relatively flattened appearance to the depressed ST segment in at least lead V6 (if not also in lead V5).

Figure-4: Schematic illustration and description of LV "strain" on ECG.

CASE Follow-Up:

Cardiac cath was performed on today's patient — and complete proximal LAD occlusion was found.

• In Figure-5 — I compare the post-PCI ECG with the initial tracing in today's case.

FINAL QUESTION:

• How would YOU interpret the post-PCI tracing? 
• Based on the ECGs in Figure-5 — Did PCI succeed in opening the "culprit" artery?

Figure-5: Comparison of the initial ECG in today's case — with a post-PCI tracing. Was PCI successful?

Interpretation of the Post-PCI ECG:

There is significant baseline artifact in the limb leads of ECG #3. Despite this artifact — this tracing is still interpretable.

• The frontal plane axis in both of the ECGs in Figure-5 is similar — which means that lead-to-lead comparison will be valid. There are no acute changes in Limb Lead ST-T wave appearance.

In contrast — the Chest Leads show that there has been marked evolution of this patient’s anterior MI:

• There has been significant loss of anterior R wave forces in ECG #3 since the initial ECG. Specifically — the R wave in lead V2 is now smaller — with further loss of R wave from V2-to-V3 — and disappearance of the initial R wave in lead V4 (to form a QS complex in this lead). This loss of anterior forces is consistent with myocardial injury from the large infarction.
• 
  
• PEARL #4: Note change (deepening) of the S waves in leads V3,V4 of ECG #3. This is not indicative of LVH — but instead results from the loss of anterior forces, that now leaves posterior forces “unopposed” (with resultant deeper anterior S waves). 
• KEY POINT: It’s good to be aware that QRS amplitudes may undergo hard-to-predict amplitude changes over the course of acute MI evolution.

Chest Leads also show marked changes in ST-T wave appearance:

• Compared to ECG #1 — there is clearly more ST elevation in leads V2,V3 of ECG #3 — with new ST elevation now present in lead V4. 
• That said — an even more striking change in ST-T wave appearance — is the very steep decline of the descending limb of the T wave in leads V2,V3,V4!
• 
  
• PEARL #5: It's important to appreciate that although this steep T wave decline appearance looks like the anterior T waves seen in Wellens' Syndrome — this is not Wellens' Syndrome, because infarction has already taken place (whereas Wellens' Syndrome occurs in the absence of CP — and serves as an ECG warning sign that appears before a large infarction with QS waves has taken place — as discussed in ECG Blog #254).
• 
  
• Finally — The ST-T wave appearance in leads V5,V6 of the post-PCI tracing ( = ECG #3) — is very different than it was in the initial ECG. Instead of ST segment flattening and depression (that was seen in ECG #1 ) — there is now ST segment coving in lead V5 (a continuation of the ST coving seen in neighboring lead V4, albeit without any ST elevation) — and, there is no longer ST depression in lead V6.

PEARL #6: One of the KEY learning points of today’s case — is the importance of correlating ECG findings with the clinical situation. The more serial tracings recorded (and the better the notation of whether each serial tracing was associated with chest pain — and if so, relative severity of that CP) — the easier it becomes to correlate clinical events.

• For example — We would not normally expect to see more ST elevation after PCI (as we do in ECG #3) — unless reperfusion of the "culprit" artery with the procedure was not successful — or — unless additional ECGs done prior to PCI showed additional ST elevation occurred before angioplasty opened the occluded vessel. In today's case — presumably this latter possibility is what occurred — in which case (assuming no CP after PCI) — the steep T wave descent with deepening T wave inversion in the anterior chest leads of ECG #3 presumably reflects coronary reperfusion. 

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Acknowledgment: My appreciation to Kim Jiwon (from Seoul, Korea) 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.
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery — as well as the importance of the term, "OMI" ( = Occlusion-based MI) as an improvement from the outdated STEMI paradigm.
• ECG Blog #367 — for another example of acute LCx OMI. 
• 
  
• ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
• ECG Blog #194 — AIVR as a sign that the "culprit" artery has reperfused.
• 
  
• ECG Blog #260 and ECG Blog #292 — Reviews when a T wave is hyperacute — and the concept of "dynamic" ST-T wave changes.
• ECG Blog #230 — How to compare serial ECGs. 
• 
  
• ECG Blog #254 — What Wellens' Syndrome is and is not ...
• 
  
• ECG Blog #337 — an OMI misdiagnosed as an NSTEMI ...
• 
  
• ECG Blog #285 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #246 — for another example of acute Posterior MI (with positive Mirror Test).
• ECG Blog #80 — reviews prediction of the "culprit" artery (with another case to illustrate the Mirror Test for diagnosis of acute Posterior MI).
• 
  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #167 — another case of the "magical" mirror-image opposite relationship between lead III and lead aVL that confirmed acute OMI.
• 
  
• ECG Blog #350 — regarding T Wave Imbalance in the Chest Leads.
• 
  
• ECG Blog #271 — Reviews determination of the ST segment baseline (with discussion of the entity of diffuse Subendocardial Ischemia).
• 
  
• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• 
  
• The importance of the new OMI (vs the old STEMI) Paradigm — See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog.
• 
  
• 20 Cases of Precordial Swirl (or "Look-Alikes" ) — Reviewed in the October 15, 2022 post of Dr. Smith's ECG Blog (including My Comment at the bottom of the page).

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ADDENDUM (5/24/2023):

Josep Serra Tarragon wrote me asking whether inverted U waves were present in the lateral chest leads of ECG #1. On taking another look — I have to agree with him that they are! (BLUE arrows in leads V4,V5,V6 — in Figure-6).

• There are 2 QRS complexes in simultaneously-recorded leads V4,V5,V6, in which we see the ST-T wave. I do not see inverted U waves clearly in the first QRS complex — but BLUE arrows that I have drawn into Figure-6 are certainly consistent with inverted U waves for the 2nd QRS complex.
• Inverted U waves are an uncommon, usually ignored phenomenon. That said — when present in the right clinical situation, they are an indicator of significant ischemia (Correale et al — Clin. Cardiol 27:674-677, 2004).
• Attention to negative U waves was first pointed out to me by Dr. Barney Marriott in the mid 1980s. Thereafter — I looked for negative U waves over a period of many years, but very rarely found them. Much of the time, there was simply too much "noise" on the tracing to be certain of their presence — or the heart rate was such that it was difficult to distinguish what was "real" inverted U wave vs terminal ST-T wave, baseline movement, or the next P wave. 
• The mechanism for U wave inversion remains uncertain. Best theory is delayed repolarization of the His-Purkinje system.
• 
  
• Bottom Line: The clinical setting in this Blog #380 is certainly consistent with ischemia. I believe Dr. Tarragon is correct that this is highlighted by the BLUE arrows in Figure-6.
• 
  
• My THANKS to Dr. Tarragon for pointing this out! 

Figure-6: I've added BLUE arrows to leads V4,V5,V6 of ECG #1 — to indicate inverted U waves.