Sunday, May 19, 2019

LVH with expected repolarization abnormalities, or acute OMI?

A patient with DM presented with acute chest pain.

Here was his ED ECG:
There is LVH in limb leads, with a 17 mm R-wave in aVL, and deep S-wave in inferior leads.
With this much voltage, one expects some repolarization abnormalities.
Indeed, there is a bit of ST depression in aVL (discordant to the tall R-wave) that does not appear to be out of proportion.
There is inferior ST Elevation, but the S-waves are also of high voltage.
Is this an inferior STEMI?  Or is the LVH with expected repolarization abnormalities? 

There is also some ST depression in V2.  Possible posterior involvement?









Comment

To me, the inferior ST Elevation is out of proportion to the S-wave.  This is however a subjective opinion, as I do not have any data-based rule.  If you measure it, the STE is 2.5-3.0 mm at the J-point, relative to the PQ junction.  With an S-wave amplitude of 17 mm, this is a ratio of 14.6 - 17.6 %.   Without any formal research data to support my opinion, I have advocated that, in LVH, a ratio greater than 15% is abnormal and highly suspicious for STEMI.  (The article by Armstrong  that advocates 25% in V1-V3 for anterior MI is severely flawed and should not be used -- see my comments at the bottom of the page and the associated post).

Here is a great example of limb lead LVH with inferior PseudoSTEMI.  (Thanks to Life in the Fast Lane for this one).
Notice the high voltage.  Notice that there is STE in III with reciprocal STD in aVL
The ratio in III is 1 mm divided by 17 mm. = 6%.  This is normal.


It is important to remember that these entities can have STE in III with reciprocal STD in aVL in the absence of acute MI:

LVH
LV Aneurysm
LBBB
WPW

For this reason, we excluded all these kinds of ECGs in our study showing the very high sensitivity and specificity for inferior MI of STE in III with reciprocal STD in aVL:  ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

Case continued:

In this case, there was an ECG that had been recorded the previous day when the patient had presented with hyperglycemia.
The baseline had zero STE in inferior leads.
This proves that the STE seen on the first ECG is indeed new and ischemic.



2nd ED ECG:
There appears to be less STE now.



The Cath lab was activated.

First troponin returned at 0.048 ng/mL (0.030 is URL), suggesting that this is a true positive.  previous troponins were less than 0.010 ng/mL (undetectable)

Cr was 3.0, with GFR quite low.  Because of this, the interventionalist was tempted to use medical therapy alone, in order not to further damage the kidneys.  Although the contrast used for CT scans probably causes little or no damage to kidneys with low GFR, angiography, especially with PCI, uses far more contrast and can indeed damage kidneys.

Results

Angiogram showed a narrowing of the RCA with TIMI III flow and probable ruptured plaque, but not certain.  The RCA has some posterolateral branches.  The best management strategy was far from clear.   There was a desire to not give too much contrast for fear of renal failure.  Medical management was considered.

Ultimately, intervention was undertaken and there was a complication: either dissection or thrombus formation at the stent, with a decrease to TIMI-1 flow.  Further intervention and use of eptifibatide (a GP IIb-IIIa inhibitor) was undertaken to fix this.

Here was the post stent ECG:
The inferior ST Segments really look ischemic here, with upward convexity (coving).  There is terminal T-wave inversion consistent with reperfusion.
The T-waves in V2 and V3 are far larger, indicating reperfusion of the posterior wall.

The Cr rose to 4.1 mg/dL.

Here is another ECG a bit later
Reperfusion T-waves (inverted) in II, III, aVF, with a reciprocally upright T-wave in aVL
There are now large T-waves in V2 and V3 -- these are clearly reperfusion T-waves of the posterior wall.

If you recorded the posterior wall, there would be negative posterior reperfusion T-waves.
But since it is recorded on the anterior wall, and ADDED to the upright anterior wall T-waves, the result is an extra large T-wave in anterior precordial leads.

Read this article on Posterior Reperfusion T-waves.

Troponin Profile



Echocardiogram:
The wall motion abnormality involves the inferior wall and some of the inferoseptal region, c/w with an infarct in the PDA territory of the RCA.  One view suggests some inferolateral hypokinesis as well but this is less convincing.


Here is another very interesting case of inferior MI in LVH, in which the interventionalist blamed the ST elevation on LVH

ST changes due to limb lead LVH?



Here is a very detailed post on the topic of LVH pseudoSTEMI vs. STEMI, with a great case.

LVH with anterior ST Elevation. When is it anterior STEMI?


Here is part of the discussion in this post:

Is there a “Smith-modified-Sgarbossa” rule for ST elevation in LVH?
Similar to the anterior STE seen with LBBB, the degree of STE in leads V1-V3 of patients with LVH is generally proportional to the depth of the proceeding S wave. In the case of LBBB, it has been shown that STE that exceeds 25% of the proceeding S-wave depth is disproportionately high, and identifies ACO with excellent specificity.9 Could this also work in LVH?

One retrospective analysis by Armstrong et al. suggested that, with LVH, STE in V1-V3 that exceeds 25% of the preceding QRS complex could be an accurate means for ruling out ACO, and fairly sensitive for identifying ACO. 

Smith comment: The Armstrong paper did not have appropriate methods to study this.  The appropriate methods would be to take consecutive ECGs with high voltage and ST elevation in the leads with ST elevation, separate them into those with and without LAD occlusion, and see what are the differences in ST/S ratio.  I have inserted at the bottom of this post some examples from Armstrong's paper.  You will see that they are not cases that you would have difficulty with.  I have tried to study this topic twice and failed because there are very few cases of high voltage in V1-V4 and LAD occlusion.   In fact, even this case does not fit, as the voltage in the affected leads does not meet LVH criteria!


Most importantly, since STE in LVH rarely exceeds 4 mm in height, the 25% criterion is likely far too insensitive. For example, in a patient with an S-wave 30 mm in depth, the STE would have to exceed almost 7 mm.  


===================================
Comment by KEN GRAUER, MD (5/19/2019):
===================================
I found this a difficult case — that to me illustrates how challenging it may be to try to assess serial tracings for subtle signs of acute ischemia in patients with both LVH and slight variability from tracing-to-tracing in QRST morphology.
  • I limit My Comments to the first 3 tracings shown for this patient — which for clarity, I have put together in Figure-1.
  • The KEY to comparison of serial tracings — is to appreciate any differences that might exist in QRS and ST-T wave morphology between one tracing and the next — and then to try to determine whether or not such differences are due to an acute change — or, whether they might be due to other factors (ie, frontal plane axis shift; lead position variation; or other non-ischemic hard-to-define-and-quantify differences). As per Dr. Smith — some of this assessment is admittedly subjective without firm reference to data-based rule.
  • My Preference when assessing serial tracings on a patient — is to begin by complete, systematic interpretation of any one of the tracings in the group. I then make a lead-by-lead comparison with each of the remaining tracings in the group.
Figure-1: The first 3 tracings that are shown for the patient in this case (See text).
=================
MThoughts on ECG #1:
  • I think it most logical in this case to begin with the initial ECG done in the Eon this diabetic patient with new-onset chest pain. There is a fairly regular sinus rhythm at ~80-85/minute. All intervals (PR, QRS, QTc) appear to be of normal duration.
  • Axis  The frontal plane axis in ECG #1 is significantly leftward (about -40 degrees) — consistent with LAHB.
  • Chamber Enlargement  There is a deep negative component to the P wave in lead V1 This may be consistent with LAA (Left Atrial Abnormality)QRS amplitude is dramatically increased in ECG #1 — satisfying voltage criteria for LVH by: ilead aVL findings (R ≥12mm in aVL)ii) by Cornell Criteria (Sum of R in aVL + S in V3 ≥20mm [female] or ≥28mm [male] — andiiiby Peguero Criteria (deepest S in any chest lead + S in V4 ≥23mm [female] or 28mm [male] ). ST-T wave appearance in lead aVL is consistent with at-the-least strain equivalent” pattern. (For details on “My Take” for assessing LVH by ECG — CLICK HERE and HERE).
Q-R-S-T Changes in ECG #1:
  • Waves  A small and narrow septal q wave is seen in lead aVL.
  • Wave Progression  Lead aVL looks “out-of-place”. It’s very unusual for an all-negative complex in lead V1 — to be immediately followed by an almost-all-positive complex by lead V2 — only to return to a predominantly negative QRS complex by lead V3. I suspect some technical misadventure (perhaps lead misplacementto account for this unusual sequence of R wave progression.
  • ST-Waves  There clearly is ~2mm of J-point ST elevation in each of the 3 inferior leads — albeit this is associated with an upward-concavity ( = “smiley”-configuration) to the ST segment. Elsewhere, the ST-T wave appears flat in leads aVL and V2. The T wave inversion in lead V1 is not necessarily abnormal — and ST-T waves in leads V3-thru-V6 do not appear abnormal given the increased QRS amplitude.
COMMENT — As a single initial tracing in this patient with new-onset chest pain — I was not at all certain about the clinical significance of the ECG findings I have justed noted for ECG #1
  • I thought there was a technical problem with the tracing (ie, Lead V2 looks out-of-place) — and this could clearly affect assessment of chest lead appearance. 
  • There is a dramatic increase in QRS amplitude (~30 mm S wave in V3 + lots of overlap with the S in V4 and the R in V5) — and, ST-T wave appearance in lead aVL is consistent with a “strain-equivalent” pattern — so this patient has marked LVH
  • did see the 2mm of J-point ST elevation in each of the inferior leads — but I thought ( = my opinion) that the shape of inferior ST-T waves was not necessarily abnormal given the marked LVH — and, the lack of clear evidence for acute posterior involvement (or for that matter, clear evidence for involvement in any of the other 9 leads) made me uncertain as to whether ECG #1 reflected anything more than marked LVH + LAHB. I didn’t feel able to make a call ...
=================
MThoughts on ECG #2:
  • I found ECG #2 (recorded the previous day when the patient had presented with hyperglycemia) — to be confusing rather than illuminating ( = my opinion).
  • QRS morphology in the limb leads is virtually identical (ie, marked left axis with LAHB). However, there are some changes in chest lead appearance: iTransition is delayed in ECG #2 (doesn’t occur until between leads V5-to-V6 — whereas the R wave became predominantly positive between leads V4-to-V5 in ECG #1); andiiQRS amplitude still satisfies voltage criteria for LVH in ECG #2 — but not as dramatically as it did in ECG #1. Attention to potential differences in QRS morphology between tracings being compared is important — because significant shift in frontal plane axis and/or alteration in chest lead positioning can sometimes make it very difficult to know whether ST-T wave differences reflect acute change vs positional change. I did not think QRS morphology differences between ECG #1 and ECG #2 were enough to alter my assessment of ST-T wave changes.
  • ST-Wave Differences between ECG #vs ECG #— The inferior lead ST elevation seen in ECG #1 is clearly new compared to ECG #2 done a day earlier. That said — ST segments are clearly coved in lead II of ECG #2; coved and slightly elevated in lead V2 — and present a straight ST segment takeoff in leads V3-thru-V6 in ECG #2 that to me looks more acute than the more benignly-shaped upward concavity seen in these same leads in ECG #1. So in some ways — ST-T wave appearance in ECG #2 (done a day earlier) looked more worrisome to me than did ECG #1 ( = my opinion).
=================
MThoughts on ECG #3:
  • Comparison of QRS morphology in ECG #1 compared to ECG #3 looked quite similar (no more than minimal chest lead differences). Looking at all 12 leads in both tracings — I was not convinced that there were significant acute ST-T wave changes between the 2 tracings ( = my opinion).
=================
FINAL Comment: The 4th and 5th tracings on this patient (shown above) — clearly confirm evolution of an acute event. The purpose of my discussion was merely to highlight how challenging assessment of serial tracings can be — especially when there is LVH and other slight variations from one tracing to the next. Our THANKS to Dr. Smith for presenting this challenging case!
  • P.S.It turns out that all 3 of the tracings in Figure-1 showed a highly unusual appearance for the QRS complex in lead V2. Of note — R wave progression across the chest leads looked very different (and normal!) in the 4th ECG on this patient ( = the post-stent ECG) — and different still in the 5th (final) ECG. Therefore — I wonder what the true R wave progression would look like in this patient IF an ECG was to be done with validated chest lead electrode placement ...

Wednesday, May 15, 2019

Potassium and Magnesium: how low is too low?

A 30-something woman with h/o HTN on losartan presented for vomiting, diarrhea, and cough for 2-3 days.

K returned at 2.4 mEq/L (3.5 - 5.0 is normal) and Mg returned at 0.7 mg/dL (1.6-2.6 is normal)

An ECG was recorded:
What do you think?


Here is her ECG a couple years prior with a K of 3.7 mEq/L:














Analysis

The QT is long at about 470 ms, with a QTc that is longer (that number depends on the correction formula used).   The heart rate is 81 beats per minutes (RR interval = 0.74 sec, or 740 ms).   Our computer calculated the QTc at 505 ms.  I believe it uses the Hodges formula.

There are very minimal (normal) U-waves.

(The previous QT was normal.)

Other formulas:

The QTc-Bazett is 546 ms
The QTc-Fridericia is 519 ms
The QTc-Framingham is 510 ms.

How acutely dangerous is a QTc greater than 500 ms?

That is uncertain.  We will shortly be publishing a review of this and of QT correction methods in the Western Journal of Emergency Medicine, but I will not (yet) give details of that.

But we do know that hypokalemia with an abnormal ECG (long QT or prominent U-waves) is dangerous.  

We just published an abstract on hypokalemia, and it is being presented at SAEM:   https://onlinelibrary.wiley.com/doi/epdf/10.1111/acem.13756, abstract 253.

The Incidence of Serious Adverse Events After Emergency Department Treatment for Hypokalemia
Brian Driver1, Jacob Helmer, Ashley Nelsen, Joseph Pasquarella, Maros Cunderlik, Lauren R. Klein1, Rajesh Satpathy1, Michael A. Puskarich2, and Stephen W. Smith.  Hennepin County Medical Center/University of Minnesota

Conclusion: Adverse events in patients with hypoK were rare and not directly related to the K level.  



But just one case of death is enough to affect patient management.

Case continued:

The patient felt better after treatment, including K supplementation, and wanted to go home.  She was told that this was a very bad idea and that she could die.

Shortly thereafter, she became unresponsive and was found to be in ventricular fibrillation.

She was defibrillated.

All serial troponins were negative.


Learning Point:

Hypokalemia with associated ECG abnormalities is very dangerous.


Here is a previous case of ventricular fibrillation from hypokalemia:

Prehospital Ventricular Fibrillation in a Young Woman. What is the Diagnosis?



Here is a detailed post on hypokalemia:



===================================
Comment by KEN GRAUER, MD (5/15/2019):
===================================
I found this case extremely interesting — because had I not been told at the outset what serum K+ and Mg++ values were — I never would have guessed they were critically low from looking at the initial ECG.
  • For clarity — I have put both tracings together in Figure-1.
Figure-1: The 2 ECGs that are shown in this case (See text).
=================
MThoughts on ECG #1:
  • There is a regular sinus rhythm at ~80/minute. The PR and QRS intervals are of normal duration — but the QTc is clearly prolonged. I estimated a corrected QTc ~510 ms (similar to values calculated by Dr. Smith).
  • Other descriptive analysis findings on this tracing included — a normal frontal plane axis (about +35 degrees) — no chamber enlargement — and peaked waves in multiple leads.
  • COMMENT — Had I not been aware of this patient’s severe electrolyte imbalance — my clinical impression of this tracing would have centered on 2 ECG findings: ithe prolonged QTcandiipeaked T waves in multiple leads. I would not have suspected critically low values of serum K+ and serum Mg++ — because these electrolyte abnormalities are most commonly associated with ST-T wave flattening (sometimes with ST depression) — U waves — and, a long QT (QU) interval — but not with the overly tall and peaked T waves that we see in ECG #1. If anything — I would have considered hyperkalemia from the T wave appearance in ECG #1 (albeit the base of peaked T waves with pure hyperkalemia tends to be narrower than that seen here). NOTE: Combined hyperkalemia + hypocalcemia (as is sometimes seen with renal failure) — may produce a picture of peaked T waves + a prolonged QTc.
Regarding the Prolonged QTc:
In a patient with a normal-duration QRS (ie, no BBB or IVCDand no sign of ischemia/infarction — the finding of a Prolonged QTc should suggest: iDrug Effect (from one or more of any number of medications that may prolong the QTc— iiElectrolyte Disturbance (low K+/low Mg++/low Ca++ — or some combination of these— and/oriiiCNS Catastrophe (ie, stroke, seizure, CNS bleed, trauma, coma, tumor — may all produce marked ST-T wave abnormalities, together with marked prolongation of the QT interval).
  • Clinical correlation is needed to discern between which one or more of the above common causes of QTc prolongation is operative in the case at hand. From the brief history given in this case — it sounds like the principal cause of the long QTc was the severe electrolyte disturbance.
=================
MThoughts on ECG #2:
  • There is sinus tachycardia at ~110/minute. The PR and QRS intervals are both normal. The frontal plane axis is normal — and there is no chamber enlargement.
  • Assessment of the QT interval is more difficult when the heart rate is rapid (especially when >100/minute). Considering the rapid rate in ECG #2 — I thought the QTc here was borderline prolonged. That said — the QTc has clearly become longer in ECG #1 than it was in this baseline tracing.
  • T waves were prominent in the prior ECG (ie, in ECG #2). Especially in leads V3, V4 and V5 (and to a lesser extent in leads II and V6) — these T waves are tall, peaked if not pointed, symmetric in ascent and descent, and manifest a narrow base. This appearance could clearly be consistent with hyperkalemia.
COMMENT — It should be remembered that the overwhelming majority of body K+ (and body Mg++) is intracellular — so a single serum (extracellular) K+ value in the lower normal range = 3.7 mEq/L does not necessarily reflect “adequate” body stores of this cation. The serum Mg++ value of 0.7 mg/dL in ECG #1 was critically low — and we do not know serum Mg++ at the time ECG #2 was obtained — so it’s difficult to know how to compare relative ST-T wave changes in these 2 tracings on the basis of serum K+ values alone.
  • T wave peaking can be seen transiently in normal subjects during exercise (I saw numerous examples of this in many ETTs I did over the years in otherwise healthy young adults). Then again, this young adult woman at seemingly low risk of acute ischemic heart disease did develop VFib, and only did so after a period of electrolyte replacement …
  • Speculation  I would have loved to see a true baseline ECG on this patient obtained at a time when we knew body electrolyte stores were normal — and, when heart rate was normal. Only then would we know with certainty IF this patient’s baseline tracing had prominent T wave peaking — or — if perhaps both the long QTc and the prominent T waves with wide base in ECG #1 might be an acute response to something in addition to acute electrolyte disturbance (ie, acute ischemia …).
=================
FINAL Thoughts: It proved lifesaving that the clinicians in this case were able to convince this patient not to go home after partial electrolyte replacement!
  • Severe hypokalemia and hypomagnesemia do not always manifest the ECG findings expected with these 2 electrolyte disorders. If anything — ECG #1 should prompt consideration of hyperkalemia rather than hypokalemia …
  • Recognition of the prolonged QTc in ECG #1 (which is clearly longer than on the prior ECG of this patient) — proved critical to appreciating high risk for adverse event in this patient!
Our THANKS to Dr. Smith for presenting this insightful case!




Monday, May 13, 2019

Acute chest pain in a patient with cardiomyopathy and a paced rhythm.

A 70-something with h/o cardiomyopathy, ICD, LVH was awoken with sharp chest pain, 8/10, non-radiating.   It worsened through the morning and she was eventually brought to the hospital.

An ECG was recorded:
What do you think?


Here is one from 3 years prior:








There is a paced rhythm in all 12 leads.  The new ECG has new ST Elevation that meets the Smith modified Sgarbossa criteria in leads I, aVL, and V2.  (ST elevation at the J-point is at least 25% of the depth of the preceding S-wave).  Meeting the criteria in just one lead is very specific for OMI in paced rhythm.

She was given aspirin, ticagrelor, and heparin, and the cath lab was activated.

The initial troponin was 0.138 ng/mL.  Previous values were approximately 0.030 ng/mL (chronic myocardial injury from cardiomyopathy).

Angiogram results:
"No evidence of plaque rupture, coronary occlusion or severe epicardial noted to explain chest pain, anterior ST segment changes in the setting of LBBB and troponin elevation."

"Patent mid-RCA stent and otherwise mild, diffuse CAD."

"Consider cardio-embolism, resolved thrombus with medical therapy or non-cardiac etiology for myocardial injury."


After angiogram:
The findings are still present.
This suggests that whatever caused this new ST elevation is still present, so it is hard to attribute this to transient thrombosis or lysed embolism.

Troponin profile:
baseline was about 0.030 ng/mL


Echo next day:


Enlarged left ventricular size with severe systolic dysfunction.
The estimated left ventricular ejection fraction is 18 %.
There is no left ventricular wall motion abnormality identified.
Asynchronous interventricular septal motion from right ventricular pacing .

The patient then developed supraventricular tachycardias and did not have another ECG with a paced rhythm for a about a week.

There was one in LBBB:
Sinus tachycardia with LBBB.
No evidence of ischemia.
No concordance or excessive discordance

Then a few days later, he had another ECG while being paced:
It is back to baseline.
What happened?  

It is a conundrum:
Why did she present with chest pain and a paced rhythm with excessively discordant ST elevation (OMI on ECG), and an elevated and dynamic troponin, both BEFORE and AFTER an angiogram showing good flow in the coronaries.  And no wall motion abnormality on echo?  

I have no good explanation.

However, I do know that if the same situation comes up in the future (chest pain and a positive modified Sgarbossa in paced rhythm), I will activate the cath lab.


===================================
Comment by KEN GRAUER, MD (5/13/2019):
==================================
This is a highly interesting case of a 70-ish year-old woman with a history of cardiomyopathy + an ICD, who presented to the ED for severe new-onset chest pain of several hours duration.
  • I limit my Comments to 2 of the 5 ECGs presented in this case. For clarity — I’ve reproduced in Figure-1 the initial ECG obtained in the ED — and the 4th ECG obtained some time after cardiac cath (ie, a few days later?).
  • The tracings in this case are complex. The patient has a biventricular pacer — and at least in the 2nd and 5th tracings presented (neither of which appear in Figure-1) — there was evidence of atrial pacing.
  • COMMENT: Not knowing the specific parameters that the ICD was set at — I fully acknowledge not understanding aspects of the rhythm in the long lead V1 rhythm strip shown at the bottom of the 5th tracing. Pacemakers are amazing devices — and, most of the time they perform as programmed. Awareness of this programming usually provides reasons for virtually all events that are seen. Input from readers of this blog who have pacemaker expertise is welcome!
Figure-1: The 1st and 4th ECGs shown in this case (See text).
=================
MThoughts on ECG #1:
  • Interpretation of paced tracings for potential acute ischemic changes is challenging! Use of Smith-modified-Sgarbossa criteria helps by providing a user-friendly calculation with predictive value. As per Dr. Smith — these criteria are clearly positive for ECG #1 (TOP tracing in Figure-1).
  • COMMENT — There is great variation in QRS morphology for paced tracings — especially when there is biventricular pacing. This may make comparison of ST-T wave changes between serial tracings (as well as with prior ECGs on a given patient) difficult. This challenge is clearly evident in this case — since scrutiny of QRS morphology in each of the 12 leads for each of the 4 paced tracings ( = ECGs #1, 2, 3 and 5) reveals that QRS morphology of paced complexes in certain leads is not the same in all tracings! That said — I completely agree with the general conclusions described in detail by Dr. Smith for these 4 paced tracings. BOTTOM Line: Judgment is needed when comparing ST-T wave changes in serial tracings (and when comparing to prior ECGs on the patient) when QRS morphology differs in some of the leads.
  • In addition to consideration of Smith-modified-Sgarbossa criteria — I also routinely use a qualitative approach. Realizing that conduction defects (LBBB, RBBB, IVCD) and ventricular pacing may each alter expected ST-T wave appearance — I look for those leads that clearly show ST-wave findings that should not bthere. Thus, ECG #1 shows marked J-point ST elevation with sharp angulation (highlighted by GREEN arrowsin leads I, aVL and V2. Of the remaining leads — the PURPLE arrow in lead III shows equally sharp angulation of the J-point ST-depression in this lead. Thus, the “magic” reciprocal relationship between leads III and aVL is present (ie, the sharp-angled ST elevation in aVL is the mirror image of the sharp-angled ST depression in lead III) — and this reciprocal relationship when present in leads III and aVL, suggests an acute STEMI until proven otherwise. This shape for the ST-T waves in these 4 leads should not be there ...
  • Finally, despite a minimal amount of ST depression in lead V1 — the PURPLE arrow in V1 highlights a flat shelf for this ST depression that just shouldn’t be there
  • Regardless of the fact that numeric criteria for Smith-modified-Sgarbossa are met in ECG #1 — it is the shape of the above abnormal ST-T waves in these 5 leads that tells me this patient with new-onset chest pain merits prompt cardiac cath.
=================
MThoughts on ECG #4:  As per Dr. Smith — Following cardiac cath, this patient developed a series of SVT (supraventricular tachycardia) rhythms — one of which is shown in the 4th ECG of this case (BOTTOM tracing in Figure-1).
  • I suspect that the regular WCT (= Wide-ComplexTachycardiathat is shown in ECG#4 is not sinus tachycardia. Assessment for atrial activity in all 12 leads suggests there are regularly-occurring P waves at a rate of ~210/minute in a number of leads (RED arrows).
  • Atrial activity is BEST seen in lead V1. Reasons that I believe this is real 2:1 atrial activity are: iRED arrows march out perfectly with precise caliper measurement — and the spike of the P wave in V1 produces an identical-slope spike at the end of the QRS in this lead V1; iiI can see similar 2:1 precise atrial activity in lead V2; iiiRegular atrial activity continues in simultaneously-obtained leads I, II and III despite the “break” (PVC) in the rhythm (RED arrows in these 3 leads); ivP wave amplitude is very small in lead II (much smaller than the atrial activity seen in lead I) — and that is unusual with sinus rhythm; andvWhenever what is initially thought of as a sinus P wave in a tachycardia rhythm manifests a “longish” PR interval — there is an excellent chance that rather than “sinus tachycardia”, there is really 2:1 atrial activity (ie, if anything, the PR interval usually shortens a bit with sinus tachycardia).
  • I suspect the rhythm in ECG #4 was Atrial Tachycardia with 2:1 Block.
Final Thought: Our THANKS to Dr. Smith for presenting this case! I completely agree with his ending comments = I have no explanation for the negative cath findings given the initial ECG in this case. That said, given recurrence of the same scenario — I would also once again activate the cath lab for the ECG findings we see in ECG #1. Isn't this a fascinating case study ...



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