ECG Blog #532 — A Surprise Diagnosis ...

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ECG Blog #532 — A Surprise Diagnosis ... 

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The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with a 1-week history of intermittent "burning chest pain" — with some "shortness of breath".

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?
•   — Should you do anything else at the bedside?

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

MY Thoughts:

The ECG in Figure-1 was sent to me with the above history. I wrote back that my initial interpretation of this tracing was the following:

• This is a very worrisome ECG!
• There is sinus tachycardia — which of itself is a worrisome sign, since sinus tach tends to be an uncommon finding with acute MI — unless "something else" is going on (ie, heart failure, shock, etc.).
• There are inferior Q waves in a "qRS" pattern — which in the inferior leads usually means that an inferior MI has occurred at some point in time.
• At the least — there is DSI (Diffuse Subendocardial Ischemia) — as indicated by ST elevation in lead aVR, with ST depression in the other 5 limb leads (as well as in the lateral chest leads).
• I suspect there is a Precordial "Swirl" pattern — with clearly abnormal ST elevation and T wave inversion in lead V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in lead V6 (A "Swirl" pattern is typically seen with acute or recent proximal LAD occlusion — and the loss of R wave from V2-to-V3 suggests anterior infarction).

The difficult question is what is "new" vs "old" — and, if "new" (as I suspect) — How "new" given the 1 week history of intermittent CP?

• I asked the following: i) Any prior history of heart disease in this patient? — and, ii) Any prior ECGs available?
• I suggested that, "The patient needs prompt cath" — with my suspicion of an LAD "culprit" artery.

QUESTION:

• BUT — What did I not mention in my above comments? 

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CASE Follow-Up:

• The patient was admitted to the Intensive Care Unit with a diagnosis of acute ACS (Acute Coronary Syndrome).
• While contemplating the best approach to management — bedside Echo was done. Surprisingly — bedside Echo showed a markedly dilated RV with a "D-shaped" septum.
• CTPA (CT Scan Pulmonary Angioram) was then performed — which confirmed the diagnosis of massive acute PE (Pulmnary Embolism).
• The patient was treated with injection of low molecular weight heparin (Enoxaparin) — and rapidly improved.

PEARL #1: Bedside Echo is a non-invasive, amazingly helpful diagnostic tool in emergency medicine — that with training, can be performed within minutes (and without which — the correct diagnosis in this otherwise puzzling case would have been delayed for hours!).

• Bedside Echo can be extremely helpful in confirming acute MI when ECGs are equivocal — IF — Echo shows a localized wall motion defect.
• The caveat is that if the patient is no longer having CP (Chest Pain) at the time that Echo is done — then nothing is ruled out if the Echo is normal. But if CP persists and the Echo shows perfectly normal LV function — this makes an acute MI much less likely.
• Bedside Echo may suggest Takotsubo Cardiomyopathy if there is "apical ballooning" due to apical akinesis or hypokinesis with preserved or hypercontractile basal segments (Izumo and Akashi — Cardiovasc Diagn Ther 8(1):90-100, 2018).

BOTTOM Line: Bedside Echo can provide invaluable assistance for strongly suggesting acute PE as the cause of your patient's symptoms — and it does so in a matter of minutes! 

• In today's case — Echo was the KEY Clue that led providers away from the diagnosis of ACS (Acute Coronary Syndrome) — and to the correct clue of massive acute PE! (See ECG Blog #443 — for a case in which I review the findings of Bedside Echo and CTPA in a patient with a large acute PE). 

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What Did We Miss?

In cases like this one — I find it helpful to "soul-search" and GO BACK to try and learn from any clinical clues that may have been missed.

• "Some shortness of breath" was mentioned in the brief history we were given. It's hard to know how significant the symptom of dyspnea was in today's case from words on the printed page. Sometimes — "Ya just gotta be there!" ( = at the bedside!).
• PEARL #2: In my experience — by far, the most commonly overlooked vital sign is the respiratory rate! Much of the time — the clinician at the bedside simply does not take the time to COUNT the respiratory rate. 
• Nurses also (in my experience) do not always count the respiratory rate. Instead — they sometimes just put down 12 or 15/minute if the patient "seems OK".
• Clinical Reality: Unless you spend a conscious moment in which you truly LOOK at the patient — it is all-too-easy to miss a patient taking small but rapid breaths — unless you actually COUNT the breaths per minute. And if the patient was breathing 25-30/minute at rest ==> that's tachypnea, which should serve as an important clue that an acute pulmonary problem may be the cause!

Taking Another Look at Today's ECG ...

In addition to the history of CP (described as a "burning" chest pain in today's case) — the ST elevation in the anterior leads in the initial ECG (in Figure-1) led me to suspect an acute cardiac event as my primary diagnosis.

• PEARL #3: Instead of the anterior ST depression or T wave inversion of RV "strain" — anterior lead ST elevation may sometimes be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2,V3 in today's initial ECG).

What I also found confusing about the initial ECG in today's case — was the question of whether there is (or is not) ST depression in multiple leads.

• The answer to this question depends on how you define the ST segment baseline — which sometimes is not an easy task.
• As review — I include below in Figure-2 my approach for determining the ST segment baseline in any given tracing.

   

Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub).

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With PEARL #3 and Figure-2 in mind — I'll add Figure-3 below, which is my summarizing chart of the ECG Findings associated with acute PE — which I then reapply to today's initial ECG in Figure-4.

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Figure-3: ECG Findings associated with acute PE (updated since ECG Blog #443).

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Figure-4: Another Look at Today's Initial ECG ...

 

Figure-4: I've labeled today's initial ECG.

KEY Point: With the above information in mind — Today's ECG (that I've labeled in Figure-4) — could be consistent with the diagnosis of acute PE, albeit without the typical appearance of RV "strain", in which T wave inversion is seen in anterior and/or inferior leads. Among the ECG findings in Figure-4 potentially consistent with acute PE are the following:

• Sinus tachycardia (Here at a rate of ~115/minute).
• S waves in multiple leads (ie, Leads I,II,III; aVF; V4,5,6).
• ST elevation in lead aVR.
• RV "strain" (Here in the form of ST depression in the inferior leads — assuming one uses the TP baseline for judging if there is ST elevation or depression).
• Anterior lead ST elevation — which as noted in PEARL #3, can be a sign of acute PE.
• ST depression in the remaining chest leads (V4,V5,V6) — again assuming one uses the TP baseline for judging if there is ST depression.

PEARL #4: ECG findings in Figure-4 against acute PE are: i) Q waves in each of the inferior leads (YELLOW arrows in leads II,III,aVF); — and, ii) Loss of r wave between lead V2-to-V3, with a QS wave in lead V3.

• In this patient who presented with a 1-week history of "burning" CP and some "shortness of breath" — this ECG leaves us with trying to distinguish between acute LAD occlusion vs acute PE (with the additional possibility of Takotsubo Cardiomyopathy — given diffuse ST-T wave abnormalities, and what appears to be a prolonged QT interval).
• KEY Point: Until bedside Echo was done in today's case — I strongly suspected acute proximal LAD occlusion as the diagnosis.

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"Take Home" Message:

On occasion — acute PE may present with a "pseudo-infarction pattern, as it did in today's case.

• Bedside Echo made the diagnosis in a matter of minutes.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
• ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
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• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 
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• ECG Blog #380 — Reviews the concept of Precordial "Swirl".
• ECG Blog #483 — Reviews the concept of DSI (Diffuse Subendocardial Ischemia) in Pearl #1 of this blog post.

ECG Blog #531 — WCT: What to Do?

I was sent the ECG in Figure-1 — with the question, "VT or SVT"?

• The sender wanted to know, "Adenosine or Amiodarone"?
• The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded, so although synchronized cardioversion could be perfectly appropriate — it would seem reasonable to try medical therapy.

QUESTION:

• How would YOU interpret the ECG in Figure-1?

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

My Thoughts:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~135/minute, without clear sign of sinus P waves.

• As always when confronted with a regular WCT without clear sign of sinus P waves — the principal differential is between VT (Ventricular Tachycardia) — vs some form of SVT (SupraVentricular Tachycardia) with QRS widening from either preexisting bundle branch block or rate-related aberrant conduction.

I looked more closely at the rhythm in Figure-1:

• KEY Point #1: Statistically — at least 80-90% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT (with this figure increasing to over 90% if the patient is "older" and has underlying heart disease). This of course means that sometimes (ie, 10-20% of the time) — the WCT rhythm in front of you will be supraventricular. But it especially means that we should assume VT until proven otherwise (especially if your patient is "older" and known to have underlying heart disease). — (See ECG Blog #361 — for more on assessment of the regular WCT).
• 
  
• KEY Point #2: QRS morphology in Figure-1 is perfectly consistent with LBBB conduction (ie, Monophasic upright QRS complex in left-sided leads I and V6 — and predominantly negative QRS in lead V1, as well as in other anterior leads that all manifest a very steep S wave downslope). So, although we still need to assume VT until proven otherwise — this perfectly consistent QRS morphology for LBBB conduction clearly reduces the likelihood of VT (See ECG Blog #204 — for more on the QRS morphology of LBBB conduction).
• 
  
• KEY Point #3: There does appear to be sign of some form of atrial activity — as the narrow, pointed peak to the T waves in lead aVF looks too pointed for a naturally occurring T wave — which makes me suspicious that an underlying P wave is peaking the T wave (RED arrows in Figure-2). And if these RED arrows are P waves — they are upright, and therefore not the negative P waves of retrograde conduction that are seen with reentry SVT rhythms. Instead — these upright P waves would have a surprisingly long PR interval for this tachycardia rhythm, which suggests the Bix Rule discussed in ECG Blog #227, in which when a P wave is seen near the middle of the R-R interval, tihs often means there is 2:1 AV conduction.
• 
  
• KEY Point #4: The most commonly overlooked arrhythmia (by far!) — is AFlutter (Atrial Flutter) with 2:1 AV conduction — especially when the ventricular rate is close to 150/minute (range between 130-160/minute). As a result, the BEST way to avoid overlooking AFlutter — is to always think AFlutter until proven otherwise whenever you have a regular SVT without clear sign of sinus P waves, when the ventricular rate falls within the above rate range (See ECG Blog #287 — for review of why AFlutter is so commonly overlooked) — (And for another Step-by-Step example of my "Thought Process" for uncovering AFlutter — See my discussion in the November 12, 2019 post in Dr. Smith's ECG Blog).

Figure-2: In today's case — the lead that most made me suspect underlying atrial activity was lead aVF (RED arrows).

KEY Point #5: My "Go-To" leads when I am trying to identify subtle (partially hidden) atrial activity — are leads II, III, aVF; lead aVR; and lead V1. IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.

• KEY Point #6: The BEST way to quickly find partially hidden atrial activity is to use calipers. Calipers instantly make you smarter! (and in my experience those clinicians who do not use calipers will commonly miss the diagnosis of complex rhythms).
• Since the most common conduction ratio of untreated AFlutter is 2:1 — the way in which I look for hidden flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT rhythm.

I illustrate this approach in Figure-3 — in which I've added colored arrows to 4 additional leads:

• PINK arrows in lead II highlight where I strongly suspect flutter waves are hiding.
• YELLOW arrows in leads III and aVR ( = 2 more of my "Go-To" leads) highlight even more subtle atrial activity (ie, I suspect the tiny upright deflection at the beginning of some QRS complexes in lead III is the beginning of a flutter wave — as I suspect the slow upslope of the last part of the QRS in lead aVR reveals where the 2nd negative flutter wave in this lead is hiding).
• To Emphasize: Flutter waves are very subtle in leads III and aVR — but it is the perfect regularity of 2:1 AFlutter in lead aVF with the strong suggestion of supraventricular LBBB conduction that makes me all-but-certain that the underlying rhythm in Figure-3 is 2:1 AFlutter.
• P.S.: I fully admit that I do not see flutter waves in lead I — but the YELLOW arrows clearly show where 2:1 flutter waves might be hiding.

Figure-3: It is the RED arrows in lead aVF that convinced me the underlying rhythm in today's case is AFutter with 2:1 AV conduction. Less obvious in leads II,III,aVF — I strongly suspect the colored arrows in those leads highlight where flutter waves are hiding.

 

= = = = = = = = = = = = = = 

Final Point #7: A deceptively easy but all-too-commonly-forgotten way to demonstrate hidden atrial activity is to use a Lewis Lead. Once familiar with the technique (that is described in Figure-4) — it should take no more than seconds to apply a Lewis Lead for assistance with the problematic arrhythmia you are working with.

Figure-4: How to record a Lewis Lead.

CASE Conclusion:

To return to the 2nd question I was asked by the sender of today's case:

• Since today's patient was hemodynamically stable — I thought an initial attempt at medical treatment was reasonable.
• For the reasons discussed above — I was virtually certain the rhythm in today's ECG was AFlutter with 2:1 AV conduction (If uncertain about the rhythm — a vagal maneuver could be tried to bring out flutter waves or a Lewis Lead may have made flutter waves more visible).
• While Adenosine could have been used — this drug is not effective for cardioverting AFlutter (Instead — IV Adenosine would act as a "chemical Valsalva" to slow the ventricular response, which most likely would have revealed underlying flutter waves).
• I would have instead favored IV Amiodarone — which may be effective for both VT and SVT rhythms.

Providers treated this patient with IV Amiodarone. The patient remained hemodynamically stable — and within 2 hours sinus rhythm was restored. The diagnosis of AFlutter was confirmed.

• Unfortunately — the patient was an older man with significant underlying comorbidities. He did not survive the hospitalization.

= = = = = = = = = = = = = = 

Extra Credit:

Return for a moment to the ECG in Figure-3. Did you notice the markedly coved, hyperacute-appearing ST-T waves in leads V4,V5?

• My initial concern on seeing the ST-T wave appearance in leads V4,V5 — was that whatever the etiology of the regular WCT rhythm, the "cause" of this rhythm might be an ongoing acute MI.
• That said — both QRS widening and tachycardia are notorious for affecting ST-T wave appearance (ie, In today's case — underlying flutter waves might be superimposed, thereby producing the "picture" we see in Figure-3).
• I did not think the markedly peaked ST-T waves in leads V1,V2,V3 of Figure-3 looked abnormal — as they appeared to be "proportional" given how deep the anterior S waves are. But the shape of the ST-T waves in leads V4,V5 clearly suggested the possibility of an underlying ongoing MI.
• 
  
• Bottom Line: First priority in today's patient was to determine the etiology and treat the WCT rhythm — and then repeat the ECG once converted to sinus rhythm to rule out the possibility of an ongoing infarction. This was done — and by Troponins and follow-up tracings an acute MI was ruled out (and the peaked ST coving in leads V4,V5 resolved once sinus rhythm at a controlled rate was restored). An acute infarction was not the reason for this patient's unfortunate demise. 

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Acknowledgment: My appreciation for the anonymous contribution of this case.

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Relevant ECG Blog Posts to Today’s Post: 

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).
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• ECG Blog #287 — Working through the diagnosis of AFlutter (with Audio Pearls, PDF, Lewis Lead).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

ECG Blog #530 — New or Old or Wellens?

I was sent the ECG in Figure-1 — but without the benefit of any history. I was asked for my opinion as to whether this tracing represented an acute STEMI? 

QUESTIONS:

• How should I answer? 
• Is this "new" or "old" Wellens?

Figure-1: The initial ECG in today's case — which was sent to me without the benefit of any history. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Answer:

Even without knowing the history — the ECG in Figure-1 is clearly of concern:

• PEARL #1: Although there is often a tendency to skip the basics, and go straight to the obvious findings (which are seen here in the inferior leads!) — I prefer to always take a brief look first at the rhythm. (For this — I favor the Ps,Qs,3R Approach for systematic rhythm interpretation = ECG Blog #185).
• To Emphasize: There is no need to spend more than a couple of seconds with this initial glance at the rhythm — and there is no need to come up with a definitive rhythm diagnosis at this point in time!
• Instead — You simply want to find out: i) What is the approximate Rate of the rhythm? (ie, Is the patient likely to be hemodynamically stable at this heart rate?); — and, ii) Is the rhythm sinus or something else?).

Is the Rhythm Sinus?

If I were charged with treating the patient in today’s case — I’d immediately go to the bedside to determine a brief history, and verify that this patient was hemodynamically stable with the rhythm shown in Figure-1. Since I was not yet provided with this information — I assumed the patient was stable enough for me to proceed with my interpretation of today’s initial ECG:

• PEARL #2: The rhythm is not sinus — because the P wave in lead II is not upright! ( = YELLOW arrows in the inferior leads in Figure-2). Assuming there is no lead reversal — the finding of a negative P wave in lead II indicates either a junctional or low atrial rhythm.
• Note that these negative P waves in lead II of Figure-2 do manifest a constant PR interval, such that they are conducting (because these P waves are Related by a fixed PR interval to neighboring QRS complexes).
• Note also that no P waves are seen throughout the long lead V1 rhythm strip at the bottom of the tracing. However, there is a negative P wave seen in simultaneously-recorded lead V3 (YELLOW arrow in that lead). Thus the reason no P wave is seen in lead V1 — is that morphology of the retrograde P wave in lead V1 must be isoelectric to the baseline.

Otherwise ... 

• The QRS complex is narrow ( = not more than half a large box in duration) — so the rhythm is supraventricular.
• The ventricular rhythm is Regular — at a Rate of ~50/minute (ie, R-R interval a tiny bit over 6 large boxes in duration).
• Bottom Line: Given lack of a visible P wave in lead V1 + the narrow QRS + the slow ventricular rate of ~50/minute — this appears to be a junctional escape rhythm.

Figure-2: Negative P waves in the inferior leads indicate this is a non-sinus rhythm. The narrow QRS, slow rate and lack of visible atrial activity in lead V1 suggest this is a junctional escape rhythm.

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The Rest of the ECG ...

In addition to the slow junctional escape rhythm — Figure-3 highlights KEY findings in the leads of most concern:

• Extremely large Q waves are seen in leads III and aVF. This is associated with a hyperacute appearance of the ST segment that manifests considerable J-point elevation with a straightened ascending ST segment takeoff. There is fairly deep terminal T wave inversion.
• The 3rd inferior lead ( = lead II) — manifests a bizarre, fragmented QRS, with similar looking but less marked ST-T wave changes.
• Reciprocal ST-T wave changes are seen in lead aVL (within the BLUE rectangle) — in the form of a straightened and depressed ST segment (that manifests gradual downsloping, but which finishes with terminal T wave positivity).
• Lead V3 is uninterpretable due to artifact ...
• Less marked but still concerning ST-T wave findings are present in 3 additional leads. These include: i) Lead I (which is similar in shape, but with less prominent reciprocal changes compared to aVL); ii) Lead V2 (which manifests ST segment straightening with loss of the normal slight ST elevation usually seen in this lead); — and, iii) Lead V6 (with a QRS and ST-T wave similar to that seen in lead II).

Putting It All Together:

I had more questions than answers after reviewing this ECG: 

• The extremely large Q waves in leads III and aVF indicate that the patient has had an inferior infarction at some point in time.
• The hyperacute-looking ST segments with ST elevation, in association with reciprocal ST depression in lead aVL — suggest an inferior MI that may be recent (or ongoing) — with the findings in leads V2 and V6 suggesting associated posterior and lateral involvement.
• The above said — the terminal T wave inversion in the inferior leads and in lead V6 + terminal T wave positivity in leads I,aVL and V2 could all represent evolving reperfusion changes of completed infarction.
• 
  
• BOTTOM Line: We need some history to proceed further with our interpretation. Along the way — finding a previous ECG for comparison should prove invaluable for determining what is "new" vs "old".

Figure-3: I've labeled the leads of most concern. 

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The CASE Continues:

I was finally able to learn a bit more about this case.

• This ECG is from a middle-aged woman with known coronary disease, having undergone stent placement following an MI about 1 year earlier.
• She presented this time with ongoing severe CP (Chest Pain) that began ~2 hours prior to the time that ECG #1 was recorded. 
• Despite the slow junctional escape rhythm — she was hemodynamically stable.

My Thoughts:

• Although with this past and present history I was still uncertain as to what was "new" vs "old" vs "new superimposed on old" — given the presence of hyperacute-looking ST-T wave changes with ST elevation and ongoing severe CP — prompt cath is needed to define the anatomy!
• 
  
• PEARL #3: The slow junctional escape rhythm in Figure-3 is an additional feature that suggests a recent and/or ongoing OMI (Occlusion-associated Myocardial Infarction) may be present ==> Prompt cath is needed!

A Previous ECG is Found ...

On searching the patient's chart — a previous ECG was found. To facilitate comparison — I've placed both tracings together in Figure-4.

QUESTIONS: 

• What do you learn from seeing this previous ECG? 
• What is the "problem" with this previous ECG?

Figure-4: Comparison of the initial ECG with a previous ECG.

ANSWERS: 

Before addressing the question as to what we learn from Figure-4 — Consider this "problem" with the previous ECG: 

• PEARL #4: All-too-often when I'm sent cases in which a previous ECG is provided for comparison — there is no indication as to what the clinical situation was at the time the prior tracing was recorded.
• For example, in Figure-4 — there are obvious marked abnormalities in the previous tracing. As a result, our approach as to how to interpret this comparison tracing that is now provided to us in Figure-4 may vary greatly depending on whether ECG #2 was recorded:
• During the acute phase of a previous OMI? 
• Immediately after this patient received her stent ~1 year earlier? 
• OR — At a routine follow-up visit after the patient had been pain-free for months?

On further review of this patient's chart — it was learned that this previous ECG was recorded around the time of her stent placement (probably shortly after stent placement in the "culprit" RCA).

• Presumably the deep Q waves in leads II,III,aVF of ECG #2 are the result of the patient's inferior MI — in which some residual ST elevation remains. In addition — there is deep symmetric T wave inversion in the inferior and lateral chest leads of this previous ECG that suggest reperfusion changes that most probably developed following stent placement.
• The overly tall T wave in lead V2 of ECG #2 — is also most probably a reperfusion change from associated posterior OMI.

KEY Point: Despite obvious abnormalities in the previous ECG — We are still able to advance our diagnosis in today's case given the clinical context that today’s patient is now presenting to the ED for acute severe CP beginning just 2 hours prior to the recording of ECG #1. My thoughts regarding Figure-4 were the following:

• The rhythm in today’s initial ECG is no longer sinus. Instead — there is a slow junctional escape rhythm at ~50/minute.
• Although the inferior Q waves are similar to those that were present in the previous ECG — there is now more ST elevation with a hyperacute appearance in each of the inferior leads (in the form of an upsloping, straightened ST segment takeoff).
• Reciprocal ST segment depression in high-lateral leads I, and especially aVL now clearly appears to be hyperacute (with ST segment straightening, prominent terminal T wave positivity, and a gently downsloping ST segment in lead aVL that reflects the mirror-image opposite picture to the ST-T wave in lead III).
• Lateral infarction is suggested by the acute ST elevation in lead V6.
• Finally — the reperfusion changes seen in the chest leads in ECG #2 have virtually resolved (ie, reduced T wave positivity in lead V2 — and resolution of T wave inversion in leads V4,V5).

Bottom Line: 

Given the presentation of new severe CP — comparison of today's initial ECG with the previous tracing suggests there is now acute reocclusion of the RCA — with need for prompt cath!

On reflection of this case — several points deserve emphasis: 

• As helpful as finding the previous tracing was in today's case — the need for prompt cath was already established by: i) The known history of coronary disease; — ii) The presentation of new severe CP just 2 hours before ECG #1 was recorded; — and, iii) The slow junctional escape rhythm in association with limb lead changes in ECG #1 that so clearly look to be hyperacute.
• An elevated Troponin would strengthen the need for prompt cath — but an increased Troponin is not needed to know that prompt cath is indicated (Remember that the initial Troponin may be normal despite acute coronary occlusion — and waiting until Troponin eventually elevated would only incur loss of more myocardium).
• An Echo at the bedside showing a localized inferior wall motion defect would strengthen the need for prompt cath — but this too is not needed to know that prompt cath is indicated (ie, We know this patient had a previous MI — so we would not be able to know if any wall motion abnormality was new or old).
• Although Wellens' Syndrome most commonly presents with ST-T wave abnormalities in the anterior chest leads (from high-grade narrowing of the LAD) — you can see the ST-T wave abnormalities of Wellens Syndrome in any coronary distribution. That said — today's patient presents with new CP — deep Q waves and hyperacute ST elevation — all of which tell us this is not Wellens' Syndrome. 
• Instead — Wellens' Syndrome manifests ST-T wave findings of reperfusion after brief coronary occlusion and before major damage occcurs — with the patient pain-free because the briefly occluded coronary vessel has now spontaneously reopened! 
• (See ECG Blog #350 and ECG Blog #453 — for review of the criteria and findings with Wellens' Syndrome).

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Acknowledgment: My appreciation for the anonymous submission of today's case with these tracings. 

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