Friday, October 23, 2020

A 40-something male complains of worrisome chest pain and possible "fever"

This was sent by an EM colleague at Highland Hospital in Oakland.  His name is "Deep" 


A 40-something male complained of chest pain and SOB that began 2 hours prior at work and was becoming progressively worse.  He had additional nausea and vomiting and complained of fever.  The pain was constant, pressure-like, substernal, without radiation, and was 10/10 in intensity.  

He stated that his wife had been diagnosed with Covid 3 months prior and that he, too, had been tested but never received the results. 

BP was 213/128.  Apparently no temperature was recorded as the patient looked very uncomfortable.  Temp was not recorded until much later when it was 36.5.

Here was his triage ECG:

There is ST Elevation that meets STEMI criteria in V2 and V3
What do you think?










The initial 4th generation troponin I was less than 0.010 ng/mL (undetectable).

The ECG looks a lot like early repolarization because: 

1. There are asymmetric T-waves (slower upstroke, faster downstroke) 2. There is upward concavity in all of leads V2-V6 (in this case, even in V1) 3. There is no reciprocal ST depression 4. There is no terminal QRS distortion (there are S-waves in both V2 and V3) 5. There are no Q-waves 

However, there is lots of ST Elevation, and Upright T-wave, in V1:  (In our study, Upright T-wave in V1 was found in 46% of Normals and 73% of LAD occlusion.  T-wave in V1 larger than T-wave in V6 was found in 15% of Normals and 39% of LAD occlusion.  Both results were highly significant but did not add value to the multivariate logistic regression formula.

Because of V1, and also due to the patient's clinical presentation, Deep was pretty sure this was a STEMI, but because it also has a lot of features of benign ST Elevation (also frequently called "Early Repolarization") which also has STE in V2-V4, he used the relatively new 4-variable formula, which is used to differentiate subtle LAD occlusion (in that it looks normal) from normal variant ST Elevation.

See use of the formula here: 12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

WARNING: the formula is not perfect.  Beware of using it to reverse your prior opinion that the ECG represents LAD occlusion.  I recommend using it when you are worried that an ECG with apparent normal ST Elevation might be LAD occlusion.  Sensitivity is not perfect.

Using these values, he calculated the formula using these 4 variables: QTc-Bazett = 418, QRSV2 = 33, R-wave V4 = 12.5, STE (60 ms after J point) = 4.  Value = 17.65.  18.2 is the most accurate cutpoint.

In this external validation, "the published cut-point of 18.2 had a sensitivity, specificity, and diagnostic accuracy of 83.3%, 87.7%, and 85.9%, respectively."  A tale of two formulas: differentiation of subtle anterior MI from benign ST segment elevation.

Remember that it was only subtle LAD occlusion that was studied, so the sensitivity for all LAD occlusion is substantially higher.

In our Hennepin data, the sensitivity at a cutpoint of 17.0 was 97% (only 3% of LAD occlusions had a value less than 17.0).

Clinical Course

Deep realized that this was a false negative formula value, and he activated the cath lab.  A 100% LAD occlusion was found and opened and stented.

Here is the post PCI ECG:

Classic Wellens' Pattern A T-waves diagnostic of reperfusion.
Notably, there is not much R-wave amplitude, suggesting that there was substantial myocardial loss.

(Wellens' pattern A T-waves biphasic, with terminal T-wave inversion -- up-down).  
These will always evolve into Wellens' Pattern B over hours to day.  

Classic Evolution of Wellens' T-waves over 26 hours



Peak troponin was 19.9 ng/mL, which is typical of STEMI, but is at the low end of peak troponins in anterior STEMI.




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MY Comment by KEN GRAUER, MD (10/24/2020):

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TOUGH case today! — and one that I fully acknowledge that I was not at all certain about my answer after seeing the initial ECG. Reasons this case is so challenging include:

  • Reason #1: The initial ECG looks a lot like a repolarization variant (because of the 5 findings noted above by Dr. Smith).
  • Reason #2: There is at-the-least voltage for LVH (by Peguero Criteria) — and given how markedly increased this patient’s BP was in triage (ie, 213/128 mm Hg!) — there is most likely true chamber enlargement.

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

NOTE: Among the criteria for ECG diagnosis of LVH that I favor — are Peguero Criteria, which state: LVH is present IF sum of deepest S in any chest lead + S in V4 ≥23 mm (female) or ≥28 mm (male). If the deepest S wave is in lead V4 — then double this value.

  • Applying Peguero Criteria to ECG #1 in today’s case (Figure-1 below) — the deepest S wave is ~21 mm in lead V2 + an S wave ~ 11 mm in lead V4 = 32 mm, which satisfies voltage criteria for LVH.
  • For those wanting review of “My Take” on a user-friendly approach to the ECG diagnosis of LVH  Please SEE My Comment at the bottom of the page in the June 20, 2020 post of Dr. Smith’s ECG Blog.

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


PEARL #1: Although the ED physician in this case knew to immediately activate the cath lab — You do not have to definitively decide on whether or not there is acute OMI on the basis of this single ECG!

  • We have shown numerous cases on Dr. Smith’s ECG Blog of acutely evolving OMIs in which a 2nd ECG done no more than a few minutes later showed obvious hyperacute changes or frank ST elevation. Therefore — Repeat the ECG ~5-15 minutes later (and if needed, frequently thereafter) — and, the chances are good that “the Answer” will soon become apparent.
  • Other modalities (ie, high-sensitivity troponin, stat Echo during chest pain, finding a prior ECG for comparison) may all help clarify if ongoing OMI is in progress.
  • That said, even without a definitive ECG diagnosis of OMI — persistence of chest pain + the ECG findings that we do see in ECG #1 are enough to justify prompt cath.



TAKE another LOOK at the initial ECG in today’s case (Figure-1).

  • HOW MANY LEADS show suspicious ECG findings? WHAT are the abnormalities?
  • HINT: Look at the leads in which there are horizontal RED or PINK dotted lines.


Figure-1: The initial ECG in this case (See text).



MY Thoughts on ECG #1:

When I first saw this case (before I read what happened) — I was aware of 3 types of “input” information that went into my decision-making process:

  • Input Type #1: Consideration of the History = which is of a 40-something man who presented to the ED with new-onset chest pain that began just 2 hours earlier. Chest pain was pressure-like and constant, with a 10/10 severity rating. Clearly, this presentation places this patient in a high-prevalence likelihood for OMI even before you look at his ECG!
  • Input Type #2: Consideration of objective ECG findings in the initial tracing that further increase concern. These include: i) ST elevation in lead V1 that looks disproportionate given modest depth of the S wave in this lead; ii) Somewhat more-than-expected ST elevation in the next 2 anterior leads (leads V2 and V3); iii)Unexpected ST flattening in leads I, V5 and V6 (short RED horizontal lines in these leads); iv) flattening of the ST segment before the inverted T wave in lead aVL (ie, Although the T wave in aVL may normally be inverted when the QRS complex in this lead is predominantly negative — the preceding ST segment in lead aVL is usually not as flat as seen here) — andv) The upright T wave in lead V1 is larger than the T wave in lead V6.
  • Input Type #3: Consideration of “stuff-that-I-feel” but am not able to put into objective terms. In view of the fact that this patient presented with new-onset worrisome chest pain + an initial ECG showing more-than-expected ST elevation in anterior lead V1 — if anything, it looked to me as if despite less deep S waves, the relative amount of J-point ST elevation in lead V3 is more than what is seen in lead V2. My “intuitive” sense of concern was heightened by this suspicion of abnormal anterior ST elevation (in leads V1, V2 and V3) — in the context of unusual and abnormal ST segment flattening in the 4 lateral leads (leads I, aVL; V5 and V6).


PEARL #2: An under-appreciated important clue to potential acute changes is the above noted finding of new upright T wave in lead V1 that is taller than the T wave in lead V6. When found in a patient with new chest pain who does not have LBBB (that normally produces tall, upright anterior T waves) — one should be suspicious of acute ischemia, if not impending OMI.

  • NOTE: This Pearl #2 is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “strain”. Instead, it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly much taller than the T wave in lead V6 to be an insightful clue (as it was for me in today’s case) of impending acute anterior OMI.


BOTTOM Line: It’s not common that anterior OMI is seen on an ECG that satisfies criteria for LVH. Today’s case provides one such example.

  • ECG findings suggesting OMI on the initial ECG are extremely subtle. Nevertheless — suspicious ECG findings are seen in 7/12 leads. I’d bet that a repeat ECG done no more than a short while later would have been more definitive.






Wednesday, October 21, 2020

What happens if you do not recognize this ECG instantly?

Written by Pendell Meyers


A young man in his 20s with history of end stage renal disease and dialysis presented for acute chest pain. His last dialysis was 4 days ago. He was very hypertensive and short of breath, but oxygen saturation was normal.


Triage ECG:

What do you think?









Pathognomonic for severe, life threatening hyperkalemia. QRS widening, PR interval prolongation (I believe those are P waves best seen in V1 and V2, but it matters not), and peaked T waves are apparent.  There is also a large R-wave in aVR, which is typical of severe hyperkalemia.


Prior ECG on file from 12 days ago:

Baseline LVH with repolarization abnormalities.


It is unclear if hyperkalemia was immediately diagnosed from the triage ECG. 

15 minutes later there was a change in the cardiac monitor and the patient became lethargic:

What is the rhythm here?



I believe it is ventricular tachycardia (with sine wave appearance and extreme QRS widening due to hyperkalemia) for the first two thirds, then the VT breaks and we glimpse one or two beats of normal conduction (widened by the hyperkalemia), followed by likely VT from a different focus than before (different morphology compared to the prior run of VT).

The patient was still alert, and so he was sedated given etomidate and cardioverted, simultaneously with calcium, insulin, dextrose, and albuterol.

After these therapies, this ECG was recorded:

Dramatic improvement, with QRS narrowing and reorganization of rhythm.



The serum potassium level returned at 9.3 mEq/L.


The patient was taken immediately to dialysis and did well.



Learning Points:

Severe hyperkalemia must be recognized instantly on ECG.

Hyperkalemic deaths are sometimes characterized by bradycardia/PEA/asystole, and other times with ventricular tachycardia.

There is no maximum dose of calcium in a patient like this. Titrate to a narrow QRS and be prepared to redose.



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MY Comment by KEN GRAUER, MD (10/21/2020):

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

As we have emphasized on numerous posts in Dr. Smith’s ECG Blog — Hyperkalemia must be recognized promptly! If it isn’t — the disorder may progress to life-threatening VT, as occurred in today’s case.

  • The “good news” — is that rapidly-acting, highly effect treatment is available (as per the Calcium, Insulin & Dextrose, and Albuterol administered in today’s case that saved this patient).

NOTE: In the hope of supplementing the clinical points brought out in the above discussion by Dr. Meyers — I focus my comments below on a number of Advanced Points. My GOAL is to enhance appreciation and facilitate rapid recognition (and long-term care) of patients who develop life-threatening hyperkalemia.

  • I have previously reviewed the “Textbook” Sequence of ECG Findings expected with progressive severity of Hyperkalemia (For Review — Please SEE My Comment that appears at the bottom of the page in the January 26, 2020 post of Dr. Smith’s ECG Blog).

Regarding today’s case — Dr. Meyers highlighted pathognomonic ECG features of life-threatening Hyperkalemia that were seen in the 1st tracing shown above. These included:

  • QRS widening.
  • Tall, peaked T waves.
  • A rhythm disturbance ...

That said — there is MORE to discuss regarding the 1st tracing in today’s case. Please TAKE another LOOK at ECG #1 — which I’ve reproduced in Figure-1.

  • In addition to QRS widening and peaked T waves — WHAT else do you see in ECG #1?
  • What is the RHYTHM in this tracing?


Figure-1: The initial ECG in today’s case (See text).



MY Thoughts on ECG #1:

  • Often overlooked when assessing an ECG for Hyperkalemia — is that T waves may be inverted. When this happens — these negative T waves also tend to be peaked, thus forming a mirror-image of the slender, symmetric positive T wave peaking familiar to us all. ECG #1 goes one step further in showing us a number of biphasic T waves — which feature both negative and positive peaked components to the T waves in leads V4, V5 and V6. Please recognize that these pointed negative T wave components in these lateral chest leads are an ECG finding consistent with marked hyperkalemia.
  • QRS morphology with significant Hyperkalemia may be varied. One may see any form of bundle branch block or hemiblock — or — there may be a very unusual QRS morphology that does not resemble any known conduction defect. This latter possibility is what we see in Figure-1 — in which a number of features similar to sodium channel blockade are seen. These include marked QRS widening (I measure a QRS duration of ~0.20 second in lead V3!) — an indeterminate frontal plane axis (nearly isoelectric complexes in 5/6 limb leads) — a prominent terminal R’ in lead aVR — and — marked QTc prolongation.
  • The marked QTc prolongation seen in ECG #1 raises the possibility of associated hypocalcemia (which often accompanies hyperkalemia in patients with renal failure). Information regarding the serum Ca++ level wasn’t available in today’s case.


WHAT is the Rhythm in ECG #1?

It is often extremely difficult to determine the rhythm in patients with marked hyperkalemia. I found this true in ECG #1. Some of the reasons why rhythm determination may be so difficult with marked hyperkalemia are listed in Figure-2.

  • I did not think P waves were visible in ECG #1. Instead of P waves in leads V1 and V2 — I thought the small biphasic deflections in the middle of the R-R interval in these leads were T waves — because their timing corresponds to the peak of the tall T waves in simultaneously-recorded leads V3 and the long lead II. I suspected a sinoventricular rhythm.
  • Given other signs in ECG #1 that suggested marked hyperkalemia — if P waves were present, I would have expected them to be of smaller amplitude than the mid-interval deflections we see in leads V1 and V2.
  • I did not see an upright P wave in lead II. (If the slight slurring we see on the downslope of the T wave in lead II is from a hidden P wave — the amplitude of such a P wave would be larger than I would expect in a patient with marked hyperkalemia).
  • THE ABOVE SAID — I fully acknowledge that I could be wrong about a lack of visible atrial activity in ECG #1 (for all of the reasons I state in Figure-2).


Figure-2: Reasons for difficulty determining the rhythm in a patient with marked hyperkalemia (See text).



WHAT Can We Learn from the Prior ECG on this Patient?

There is a lot we can learn about Hyperkalemia in today’s case from retrospective review of ECG #1  in comparison to ECG #2, which is a prior ECG obtained on this patient 12 days before ECG #1 (Figure-3).

  • Awareness of a brief History on today’s patient is invaluable for optimal clinical interpretation of the ECGs in this case: We are told that the patient is a young man in his 20s with end-stage renal disease, whose last dialysis treatment was 4 days ago. This patient presented with acute chest pain and dyspnea (with a normal O2 saturation) — with marked hypertension at the time he was seen.
  • GIVEN this History — even before looking at ECG #1i) Marked hyperkalemia may be anticipated, given that this patient is at least 1-2 days late for dialysis; ii) This patient is almost certain to have marked LVH — given end-stage renal disease and greatly elevated BP at the time he was seen; andiii) It is likely that a non-cardiac cause of this patient’s acute chest pain will be found.


QUESTIONS: 

  • Do YOU think serum K+ was normal at the time this patient’s prior ECG ( = ECG #2) was done?
  • WHAT other observations would you make from comparison of ECG #2 with ECG #1?


Figure-3: Comparison of ECG #1 — with a prior ECG on this patient done 12 days earlier (See text).



ANSWERS (My Thoughts on ECG #2):

We were not told what the serum K+ value was at the time ECG #2 was obtained — only that ECG #2 was a prior ECG obtained 12 days before ECG #1.

  • Sinus rhythm at ~90/minute is present in ECG #2. Of note — the P wave is upright in lead II, and the P wave appears to be negative in lead V1. But P wave amplitude is small in leads V1 and V2 of ECG #2 — which supports my suspicion that those biphasic deflections in leads V1 and V2 of ECG #1 were too large to be P waves (especially since the initial serum K+ value = 9.3 mEq/L at the time ECG #1 was obtained — and P waves get smaller when K+ is markedly elevated).
  • As expected — the prior ECG confirms marked LVH. For clarity regarding assessing the size of overlapping complexes in the chest leads of ECG #2 — I’ve colored in the S wave in lead V3 (which measures ~30 mmand the R wave in lead V5 (which is ~31 mm— which documents dramatically increased QRS amplitudes.
  • Further supporting the ECG diagnosis of marked LVH in ECG #2 are: i) The History (the patient has end-stage renal disease with marked hypertension on admission)andii) That there are ST-T wave abnormalities in the lateral chest leads (ie, leads V5,V6) consistent with LV “Strain”. Taken together — these 2 factors dramatically increase specificity for true LV chamber enlargement.
  • In addition to resolution of QRS widening — NOTE how different QRS morphology is between ECG #1 and ECG #2. Specifically: i) There is a marked difference in frontal plane axis between the 2 tracings (ie, The axis is indeterminate in ECG #1 — whereas the frontal plane axis was +45 degrees in the prior ECG); ii) The terminal R’ in lead aVR of ECG #1 was not seen in the prior ECG; andiii) Amplitude of the QRS complex is very different in a number of leads (ie, LVH was not evident in ECG #1). BOTTOM Line: I found it interesting how dramatically (and how unpredictably) QRS morphology can change when serum K+ is extremely elevated.


WHAT do YOU Think Serum K+ was in ECG #2:

Review of this patient’s file provided us with a prior ECG on this patient obtained from 12 days earlier. But we are not told the circumstances under which ECG #2 was obtained — and we are not told the serum K+ level at that time. That said — I strongly suspect serum K+ was at least slightly elevated at the time ECG #2 was obtained! I say this because:

  • Although modest in height — the T wave in lead V3 of ECG #2 is uncharacteristically pointed! This is not the normal appearance of an anterior lead T wave.
  • The lowest point of the shallow inverted T waves in leads V5 and V6 is pointed. ST-T wave abnormalities due solely to LV “strain” do not do this.
  • I would normally expect in a patient with marked LVH (to the extent that is obvious in ECG #2) — that there would be comparable ST-T wave changes of LV “strain” (ie, with a downsloping depressed ST segment — rather than the ST segment coving we see in leads V5 and V6 of ECG #2). I suspect the reason for this unexpected “strain” appearance in these lateral chest leads of ECG #2 — is that the downsloping ST depression that probably would have been seen if serum K+ was normal, has been attenuated by T wave changes from a serum K+ level that was at least slightly elevated at the time this prior ECG was done.

PEARL #1: Remember that the ST-T wave appearance seen on ECG in association with marked hyperkalemia is the net result of ST-T wave changes caused by increased serum K+ — superimposed on whatever the ST-T waves looked like before serum K+ became elevated!

  • As a result — it is impossible to assess the ST-T wave changes for ischemia in ECG #1, because this tracing was obtained at a time when serum K+ = 9.3 mEq/L. In my experience — you never know what ST-T waves will look like until serum K+ is completely corrected and the ECG is repeated.


PEARL #2: The relevance of Pearl #1, is that even though the “textbook” sequence of ECG findings with increasing serum K+ levels is not strictly followed in all patients — in any given patient, the sequence for development of the ECG findings I illustrate in our January 26, 2020 post tends to be surprisingly consistent (in my experience) over the course of that patient’s hospital stay.

  • I suspect the patient in today’s case is a frequent ED user. I say this because this young man has end-stage renal disease with dramatic LVH — he presented with life-threatening hyperkalemia (presumably the result of being late for his last dialysis treatment) — and, his prior ECG from just 12 days earlier also shows subtle-but-real signs of hyperkalemia at that time.
  • I speak from my experience of reading all ECGs from 35 medical providers over a 30-year period, including frequent hospital Attending stints. As such — I got to know many of our clinic patients by their ECGs. As a result — I could sometimes immediately know for certain patients from their ECG (without need to first draw labif their serum K+ level was in the process of going up again. 
  • TAKE HOME Message  IF I was a medical provider charged with caring for today’s patient — awareness of what the serum K+ level was at the time ECG #2 was done would be insightful. Knowing this would help me with earlier recognition on return visits about when hyperkalemia was returning.


Monday, October 19, 2020

Acute coronary occlusion seen in paced *and* non-paced ECGs

This was written by Brooks Walsh @BrooksWalsh, an emergency physician in Connecticut.

A paced ECG

The family of a very elderly person called EMS when they became short of breath. The patient had a number of comorbidities, including a pacemaker.

EMS obtained a number of ECGs, including this one:


Could a cath lab activation be justified with this ECG?

Well, yes, it should be!

The classic- and modified-Sgarbossa criteria for determining acute MI in the context of a paced rhythm are likely already well appreciated by readers of this blog. This ECG is a great illustration of those rules, particularly the criterion that ST elevation that exceeds 20-25% of the depth of the S wave (“excessive discordance”) suggests acute coronary occlusion.

We see this in lead V3, where the ST segment  in the first QRS complex is about 3.6 mm high, and the S wave 13.7 mm deep - this gives a ratio of 0.26. There is some unfortunate baseline wander, but the proportion holds for the 3rd complex as well. (The second complex is uninterpretable, as the S wave runs off the paper).


Lead III shows similar excessive discordance, with the third beat giving a ratio of 3.5/11.7, or 0.29. The fourth beat (3.5/10.4 = 0.33) is distorted but diagnostic.


Additionally, the ST segment in V2 suggests > 1 mm of concordant STE (in beats #2 and #3), but the baseline wander here makes this less certain.

 So, did these rules correctly predict a coronary occlusion?

Although angiography was not performed in this case, there is enough evidence to reasonably “prove” acute coronary occlusion. First of all, the paramedics had obtained another ECG about 10 minutes earlier:

This non-paced ECG shows ST elevations in the inferior and anterolateral leads, as well as ST depression in aVL, suggesting a “wrap-around” LAD lesion.
 

The non-paced ECG subsequently obtained in the ED was similar:



This was markedly different from an ECG obtained 1 year prior:

 

After evaluation by the emergency physician and the interventionist, and a discussion with the patient and family, neither angiography nor chemical fibrinolysis were pursued (the patient was quite old and debilitated).

Although angiography was not performed, acute occlusion of the LAD was supported by other tests. The initial troponin was 2.3 ng/ml (< 0.01), rising to 4 ng/ml about 10 hours later. The patient became hypotensive and showed signs of CHF. An echocardiogram showed severe systolic dysfunction, with akinesis of the apex, mid anterior, mid anterolateral, mid inferoseptal, mid anteroseptal, and mid inferolateral segments (Prior echo had been normal for age).

Apical 4 chamber in systole


Lastly, an ECG obtained the next day showed evolving lateral T waves, further supporting an acute occlusion.



The PERFECT Study [From the Paced ECG Requiring Fast Emergent Coronary Therapy (PERFECT) Study Group]

The PERFECT trial will show that acute coronary occlusion can be reliably predicted from paced ECGs, despite the prevailing belief that paced ECGs are “uninterpretable.” That trial used angiographic data, so this case (despite good circumstantial evidence) would not have met inclusion criteria. Hopefully the rigorous methodology can change the out-dated perspectives of emergency physicians and cardiologists!

The study is now under revision for Annals of Emergency Medicine.

Below is the Results and Conclusion portion of the abstract, which was published in AEM and presented at SAEM in 2018.  Annals is requesting that we also look at patients with AMI but without occlusion (Non-OMI).  We don't think that is terribly relevant, but do believe it will only reinforce the results.  We are almost done with that analysis and then will re-submit.

We presented the study at SAEM 2018.  Here are the results in modified form.  I am not publishing the entire abstract, as it will hopefully be published in the future.

Electrocardiographic Diagnosis of Acute Coronary Occlusion in Ventricular Paced Rhythm Using the Smith Modified Sgarbossa Criteria.     

 

Results: There were 59 OMI subjects and 102 controls (mean age 73 years; male 103 [64%]). The sensitivity and specificity of the MSC versus OSC for OMI were 81% (95% CI 69-90) versus 56% (95% CI 42-69; P<.001) and 96% (95% CI 90-99) versus 97% (95% CI 92-99). Adding concordant ST-depression in V4-V6 to the MSC yielded 86% (95% CI 75-94) sensitivity. For the excessive discordance component, the ratio identified 17 OMI patients vs. 2 for absolute ST Elevation of 5mm. 

Conclusions: For the diagnosis of OMI in the presence VPR, the MSC were more sensitive than the OSC; specificity was equivalent. 


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MY Comment by KEN GRAUER, MD (10/19/2020):

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

Important case by Dr. Walsh that adds to our growing collection of cases in which OMI is evident despite the presence of a pacemaker (Most recently — See our October 5, 2020 post in Dr. Smith’s ECG Blog).

  • I limit my comments in today’s case to the two 12-lead tracings obtained by the EMS team. I wanted to begin (as did Dr. Walsh) — by focusing on the 1st ECG shown above (which I have reproduced in Figure-1). Dr. Walsh asked the KEY question about this ECG = “Could cath lab activation be justified from ECG #1?"


Figure-1: The 1st ECG shown above in today’s case. For clarity — I’ve numbered the beats (See text).


MY THOUGHTS ON ECG #1:

As per Dr. Walsh, given the presence of new symptoms (ie, acute dyspnea) in this elderly patient — ECG findings in ECG #1 at the least justify strong consideration of cath lab activation. I’d add the following thoughts to the points highlighted in Dr. Walsh’s excellent discussion:

  • POINT #1: As emphasized in “Pearl #1” in My Comment to the October 11, 2020 post in Dr. Smith’s ECG Blog — as many as 30% of all patients with acute MI do NOT have chest pain. Among these patients with Silent MI” — the most common non-chest pain symptom associated with acute MI (especially among elderly patients) — is shortness of breath (which is the reason the elderly patient in today’s case came to the ED).


POINT #2: Although it is often more difficult to identify OMI in the presence of cardiac pacing — it is not always impossible to do so “just because the patient has a pacemaker”. And sometimes, acute OMI may be obvious despite the presence of a pacemaker. (SEE the links below — among other examples on Dr. Smith’s ECG Blog).

  • KEY: In many more cases than is commonly appreciated — modified Smith-Sgarbossa criteria provide an objective means for identifying acute MI despite the presence of cardiac pacing. As per Dr. Walsh — these modified Smith-Sgarbossa criteria are strongly suggestive of OMI in ECG #1.


Among many Other Examples of Acute OMI despite Cardiac Pacing:


POINT #3: In addition to modified Smith-Sgarbossa criteria — ECG #1 also shows suggestive Qualitative Criteria for acute OMI. By “qualitative” criteria, I mean that one focuses on ST-T wave shape — and the presence of ST-T wave deviations that simply should not be there in association with a given conduction defect (like LBBBor with a given paced QRS morphology.

  • Becoming comfortable with assessment of qualitative ST-T wave changes in shape provides another way to strongly suspect acute OMI — even when millimeter-determined criteria are not necessarily satisfied.


CAVEAT: The most challenging aspect of assessing ST-T wave morphology in ECG #1 — is the presence of baseline wander with artifact. Specifically — ST-T wave morphology varies significantly from one beat to-the-next in many leads. This makes it difficult to know which one(s) of the 2, 3 or 4 QRST complexes that we see in each of the 12 leads is the one(s) that we should be assessing for potential acute ischemia.

  • POINT #4: There is no perfect “rule” for addressing the above caveat. As a result, I favor a “Gestalt” ( = overall) approach — in which one “steps back” and mentally averages ST-T wave appearance for all complexes in each of the leads in a given lead area — all done in context to the overall findings on the 12-lead, with special attention to those leads expected to show reciprocal changes.
  • MY DISCLAIMER: Concrete measurable criteria for this “Gestalt Approach” do not exist. Instead, this is that indescribable “sense” that the experienced clinician gets within moments of seeing a patient as to what the diagnosis is likely to be.


Returning to MY Thoughts on ECG #1:

Knowing that today’s case came from an elderly patient with new dyspnea but no chest pain — the following were my thoughts on seeing the paced tracing shown in Figure-1.

  • The rhythm in ECG #1 appears to be 100% paced. Regular pacing spikes are seen in many (not all) leads — with 100% capture showing a wide QRS at a regular rate of ~100/minute.
  • Looking first at the 6 limb leads in ECG #1 — Assessment of ST-T wave appearance in lead I is not helpful. There is just too much beat-to-beat variation in ST-T wave morphology.
  • There is also much beat-to-beat variation in ST-T wave morphology for each of the 4 QRST complexes in eachof the inferior leads. That said — Don’t YOU get a “sense” of disproportionate (ie, more-than-there-should-be) J-point ST elevation in each of these 3 inferior leads (given the modest depth of S waves in these inferior leads)?
  • Admittedly — the ST-T wave shapes of beat #1 in lead III — and of beats #5 and 7 in lead aVF do not look abnormal for paced beats. However, even though ST-T wave appearance of other complexes in these inferior leads all differ from one another — I thought they looked suspicious.
  • IF the J-point ST depression in beat #6 of lead aVL was real — this would indicate “tell-tale” reciprocal ST depression. The other 3 beats in lead aVL also suggest inappropriate J-point depression — although modest R wave amplitude makes this more difficult to assess.
  • I found assessment of chest leads even more challenging. We get at least a glimpse of 5 elevated ST segments in lead V3 (of beats #9-13) — and each of the 5 looks suspicious.
  • Each of the 3 ST segments in lead V4 look abnormal — with the amount of J-point ST elevation in beats #14 and 16 seemingly disproportionate to the modest S wave depth in this lead.
  • Regarding the other chest leads — lead V1 is of no help — the ST segments of beats #10 and 11 in lead V2 look suspiciously coved, though not overly elevated — and ST segment shape in leads V5 and V6 is clearly abnormal for beat #15, but unimpressive for beats #14 and 16.
  • BOTTOM Line: I would not be certain from ECG #1 that this elderly patient with new dyspnea (but no chest pain) was having an acute OMI — but I definitely would be suspicious. I’d want to repeat the ECG (hopefully with less beat-to-beat variation).



As per Dr. Walsh — it turned out the EMS team obtained multiple tracings on this patient. The one they obtained ~10 minutes before ECG #1 was absolutely diagnostic (Figure-2).


Figure-2: Comparison of ECG #1 in today’s case — with a non-paced tracing obtained in the field ~10 minutes earlier (See text).


POINT #5: Serial tracings are often diagnostic. This was especially true in today’s case — in which severe dyspnea resulted in beat-to-beat artifactual variation in ST-T wave morphology.

  • Ten minutes earlier — the patient had a spontaneous (non-paced) rhythm. Although hard to appreciate P waves due to the baseline artifact in ECG #2 — subsequent ED tracings showed an underlying sinus mechanism.
  • Although there is diffuse low voltage in ECG #2 — each of the inferior leads show subtle-but-real ST elevation. Lead aVL suggests even more subtle reciprocal ST depression.
  • Obvious hyperacute ST elevation is seen in leads V4 and V5 of ECG #2. Looking closely — ST elevation appears to begin in leads V2 and V3 — and extend through to lead V6.
  • ECG #2 is diagnostic of acute infero-antero-lateral OMI from acute LAD occlusion with “wraparound”.


FINAL Point: Take ANOTHER LOOK at both tracings in Figure-2.

  • It’s insightful to compare lead-to-lead paced ST-T wave appearance (in ECG #1) — with what ST-T waves look like in these same leads when there is no ventricular pacing (in ECG #2). My hope is that doing so will help to better appreciate what qualitative ST-T wave findings to look for the next time you encounter a paced tracing in a patient with new symptoms.

Our THANKS to Dr. Brooks Walsh for presenting this highly insightful case!



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