EXTRA COPY — ECG Blog #533: A Wide Tachycardia — EXTRA COPY

The ECG in Figure-1 was obtained from a previously healthy 60-something year old man — who sought medical care for the abrupt onset of a “fast heart rate”. The patient was hemdynamically stable at the time this ECG was recorded.

QUESTIONS:

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

Figure-1: The initial ECG in today's case — obtained from 60-something year old patient. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

The “good news” — is that the patient is hemodynamically stable at the time this ECG was recorded. As a result — We have at least a moment in time to assess the tracing before we would need to begin treatment. 

• As always, I like to start with assessment of the rhythm — for which I favor the P’s,Q’s,3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3R Approach).
• The ECG in Figure-1 lacks a long lead rhythm strip. That said, we can still interpret the rhythm — beginning with whichever of the 5 KEY parameters is easiest to assess.
• The rhythm in today’s ECG is Regular. 
• The Rate is fast, at about 170/minute.
• The QRS is wide (ie, clearly more than half a large box in duration — and probably ~0.12 second in duration).
• With regard to P waves — there is no clearly upright P wave deflection in lead II — and in general, the fast rate and large ST-T waves seem capable of “hiding” atrial activity within them. 

My Impression from the Ps,Qs,3Rs: 

In this 60-something year old man (about whom we do not yet know anything about his medical history) — The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, but without clear sign of sinus P waves.

The differential diagnosis includes the following:

• i) VT (Ventricular Tachycardia) — which always needs to be assumed for any regular WCT rhythm without sinus P waves until proven otherwise.
• ii) Sinus Tachycardia (with sinus P waves being hidden within the giant T waves that precede each QRS complex).
• iii) An SVT (SupraVentricular Tachycardia) reentry rhythm (ie, most commonly AVNRT or AVRT). 
• iv) AFlutter (Atrial Flutter).
• v) ATach (Atrial Tachycardia).

PEARL #1: To emphasize that although I've described my above assessment in “slow motion” — With practice, all that I’ve written above should be noted and considered within less than 1 minute!

• Because this patient is hemodynamically stable — We can take a few extra moments to see what additional clues might be present to help us narrow down our differential diagnosis.
• Statistically — in an unselected adult population of a "certain age" — at least 80% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT. 
• That said — 80% is not 100%. Therefore, if your patient is hemodynamically stable — this means that we still have a moment to look for additional clues to the etiology of the rhythm. Two of my “favorite potential clues” to look for are: 
• i) Is there any sign of atrial activity? — and, 
• ii) QRS morphology.

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Is there any sign of Atrial Activity?

Take another LOOK at the ECG in Figure-1.

• Keep in mind that sinus P waves should be upright in lead II — whereas retrograde P waves are almost always negative in one or more of the inferior leads.
• 
  
• What do YOU see? 

ANSWER:

It turns out that there is atrial activity in today's ECG — in the form of 1:1 V-A (retrograde) conduction (YELLOW arrows in Figure-2).

• Although this retrograde atrial activity is only seen in one of the inferior leads — it's hard to imagine what else this slender spike that occurs toward the end of the QRS in lead II could be other than a retrograde P wave.
• As suggested by the parallel RED timeline — these retrograde P waves clearly fall within the QRS complex, which explains why retrograde P waves might not be seen in other leads.
• P.S.: We now have an answer to the 5th parameter of the Ps,Qs,3Rs — which is the 3rd "R" = Related. So there is atrial activity, in the form of retrograde P waves that manifest a constant relationship ( = Related by a fixed RP' interval) to neighboring QRS complexes = 1:1 retrograde conduction.

PEARL #2: It's important to appreciate that the finding of 1:1 VA conduction does not distinguish between VT vs an SVT rhythm. This is because both reentry SVTs and VT may manifest 1:1 retrograde conduction.

• But IF today's rhythm is supraventricular — then it is almost certain to represent AVNRT (AV Nodal Reentrant Tachycardia) because:
• These P waves are not upright in lead II — so assuming no lead reversal, the rhythm cannot be sinus tachycardia.
• There is no sign of 2:1 AV conduction — so this is not AFlutter.
• It seems unlikely that ATach would manifest a negative P wave in only lead II with such a long RP interval.
• The other form of reentry SVT, which is AVRT ( = AtrioVentricular Reciprocating Tachycardia) generally has a longer RP' interval — with the retrograde P wave occurring later in the ST segment because of the greater amount of time needed to complete a reentry circuit that includes an AP (Accessory Pathway) that lies outside the AV Node (as I illustrate and discuss in ECG Blog #240).

Figure-2: I've labeled the retrograde P waves in today's ECG.

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Does QRS Morphology provide any Clue?

Practically speaking — aberrant conduction is most likely to take the form of some type of bundle branch block and/or hemiblock pattern. As discussed in ECG Blog #211 — although RBBB (Right Bundle Branch Block) aberration is the most common form — you can also see rate-related aberrant conduction that manifests LBBB and/or either hemiblock (with or without RBBB).

• As emphasized in ECG Blog #204 — the 3 KEY leads for the ECG diagnosis of the bundle branch blocks are right-sided lead V1 — and left-sided leads I and V6.
• Assessment of these 3 KEY leads during the WCT rhythm in today's case is consistent with LBBB morphology — because we do see an all upright QRS in lateral leads I and V6 — and the QRS is predominantly negative in right-sided lead V1, with a steep S wave downslope in the anterior leads (as discussed in ECG Blog #346).

PEARL #3: While I was in no way certain of the diagnosis — as soon as I appreciated that QRS morphology in Figure-2 was perfectly consistent with LBBB conduction — I suspected that this regular WCT rhythm might be supraventricular!

• KEY Point: We often need to begin treatment of the patient in front of us before we are 100% certain of the etiology of the rhythm. So although I could not rule out the possibility of VT on the basis of this single ECG, since the patient was hemodynamically stable — I would have tried Adenosine as a diagnostic-therapeutic trial (Adenosine should successfully convert the rhythm if this is AVNRT or AVRT) — with providers ready to cardiovert if at any time the patient became unstable.
• 
  
• PEARL #4: The most common form of VT that manifests LBBB-like conduction in the chest leads is RVOT VT (Right Ventricular Outflow Track VT) — but against RVOT VT in Figure-2 is the lack of an inferior frontal plane axis (See ECG Blog #525 — for review of RVOT VT).

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CASE Follow-Up:

I subsequently learned the history of today's patient:

• XXXXXX

ARMAN REPLY:

More background- the pt had an SVT ablation 5 years ago but developed palpitations again. Was evaluated outpatient and admitted for an elective ablation. Baseline ECG had no aberrancy. He developed this tachycardia in our ward, a day before his scheduled ablation. Good thing about a telemetry unit is that we could go back in time and see that it initiated with a PAC( I curse myself for not saving that strip). The tachycardia was terminated with 6 of adenosine.

EP results- concealed left lateral accessory pathway with no inducible tachycardia. Slow- Fast AVNRT induced and ablated. Rate related LBBB. 

Could this have been orthodromic AVRT? I dont think so, as I said, it initiated with a PAC.

However, I still don’t understand why LBB was refractory instead of the RBB, it’s usually the other way around.

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Acknowledgment: My appreciation to @PrecordialSwirl for submission of today's case with these tracings.

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EXTRA COPY — ECG Blog #531: WCT: What to Do? — EXTRA COPY

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 used to technique described in Figure-4 — it should take no more than seconds to apply a Lewis Lead.

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.

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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.
• 
  
• ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).
• 
  
• 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.

EXTRA COPY — ECG Blog #530: Old or New Wellens? — EXTRA COPY

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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EXTRA COPY — ECG Blog #532: A Surprise Diagnosis — EXTRA COPY

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Please NOTE: 

• After today — No new ECG Blog posts for ~4 weeks ...
•     — I will also not be prompt in replying to emails ... 

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• 
  
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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). 

==================================

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).

==================================

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).

================================== 

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.

================================== 

"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.

XXXXXXX 

XXXXXXX 

==================================

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

==================================

 

=======================

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).
• 
  
• 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”. 
• 
  
• 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 #443 

https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html

==================

The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.

QUESTIONS:

• In view of the above history — How would YOU interpret the ECG in Figure-1?
• Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?

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

MY Thoughts on this CASE:

Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1. I see the following:

• There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
• Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
• There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).

Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2). 

• PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7, -8, -9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".

• Sinus Tachycardia and RAD — as already noted above.
• PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.
• 
  
• Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).
• 
  
• S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE. 
• 
  
• PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
• As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).
• 
  
• PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can 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 in Figure-2).

PEARL #5: The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history. 

• Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis. 
• Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).
• 
  
• ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; and, ii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).

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

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QUESTION: 

Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.

• What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?

ANSWER:

• A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
• The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).

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The ECHO on Today's Patient:

In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?

Figure-3: Still picture of the Echo 4-chamber view.

Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.

Figures-3 and -4 on Today's Echo:

For orientation — the 4 chambers are shown in Figure-3:

• The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".
• 
  
• PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE. 
• 
  
• A McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber); and, ii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."
• 
  
• References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.

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Diagnostic CTPA on Today's Patient:

Final confirmation of acute PE in today's case was obtained by CTPA ( = Pulmonary Angiography in Figure-5). 

• Excellent review of diagnostic testing for acute PE (Moore et al — Cardiovasc Diagn Ther 8(3):225-243, 2018).
• For a 10-minute video review on reading Pulmonary CT Scan — WATCH_this_VIDEO by Dr. Jake Gibbons.

Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries.

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CASE Follow-Up:

The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.

• PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.

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Repeat ECG After Thrombolytic Therapy:

I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).

• Sinus tachycardia has resolved.
• Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
• RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
• Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
• S waves no longer persist through to lead V6.

Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy.

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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

==================================

 

=======================

Related ECG Blog Posts to Today’s Case: 

• ECG Blog #313 and ECG Blog #435 — Review 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).
• 
  
• 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”. 

==================================

ADDENDUM #1 (8/16/2024): 

I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".

Figure-7: ECG Findings associated with acute PE (from ECG Blog #435).

==============================

PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).

==============================

Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub).

Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

 

ADDENDUM #2 (8/17/2024): 

My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.

• The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
• Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?

Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case). 

ANSWER:

The ECG in Figure-10 shows the following findings in favor of acute PE:

• Sinus tachycardia.
• S1Q3T3.
• Persistent precordial S waves (through to lead V6).
• Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.