Why the sudden shock after a few days of malaise?

Written by Magnus Nossen - Edits by Grauer and Smith

The patient in today’s case is a woman in her 70s with a previous medical history of HTN and hyperlipidemia. She presented to an outside hospital after several days of malaise and feeling unwell. At the time of admission, her vital signs were normal. Heart rate was in the 80s. She had a very elevated troponin T at 12,335 ng/L at the time of presentation. (This is a value typical for a large subacute MI, normal value < 0-14ng/L.)  

Below is the presentation ECG.

The patient initially denied chest pain, but when questioned directly — did admit to vague "chest discomfort" in previous days. She was transferred to our facility for angiography. On arrival she was without distress. Due to acute renal failure and the duration of her symptoms over a number of days — it was decided to perform angiography the following day. Serial Troponin T values were decreasing, consistent with subacute completed MI. The ECG on admission showed sinus rhythm with a heart rate in the 80s — and was consistent with a subacute completed inferior, lateral and posterior transmural infarction, with Q waves and ST elevation in the inferiolateral leads — and ST depression in lead V2. The patient was put on telemetry while waiting for angiography the following day.

The patient awoke suddenly during the night — stating that she felt "strange". The ECG below was recorded at this time. What do you think?

This ECG is consistent with infero-postero-lateral infarction — with persistent inferior lead ST elevation and reciprocal high-lateral ST depression — ST depression in lead V2 — and some terminal T wave inversion in inferior and lateral chest leads. It is not significantly different from the admission ECG. Perhaps the most remarkable change — is the increase in heart rate, with this ECG now showing sinus tachycardia at 118/minute! Also of note is the still upright (not inverted) T waves. Persistent ST elevation with upright T waves >48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis (PIRP).

Sinus tachycardia has many potential causes. In my experience, for the patient at rest and not anxious — it often signifies severe illness. This is especially true for the elderly patient with sinus tachycardia. The patient in today’s case suddenly became tachycardic while sleeping. The heart rate almost doubled within a minute. What might account for the sudden rate change in this patient? See if you can identify the problem in the below parasternal view of the heart.

The above video file was recorded from a subcostal «window» and it shows the heart with all four chambers. Right atrium, right ventricle, left atrium and left ventricle viewed through the liver. What is the cause of the sudden tachycardia? 

Below is a still image from the above video. The heart chambers are annotated. From the subcostal "window" the heart is viewed through the liver and thus the liver parenchyma is closest to the transducer (top of the image). Below the liver is the heart with the right atrium (RA), right ventricle (RV), left atrium (LA) and left ventricle (LV) The red arrow points to a large opening in the basal region of the interventricular septum. This is a ventricular septal rupture (VSR). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. PIRP is strongly associated with myocardial rupture. This patient developed a rupture of the basal portion of the interventricular septum (VSR). The VSR is what is causing the cardiogenic shock!

A Short Comment on PIRP and T Waves: 

Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. PIRP was associated with persistent upright T waves. He found two types of atypical T wave development in PRIP

1) Persistently positive (upright) T waves beyond 48 hours in a patient with acute MI

2) Premature change from inverted T waves to pseudonormal T waves (within 48-72 hours) 

In our case, PIRP is a likely explanation for the continued positive T waves. Since serial ECGs are not available so either of the two patterns described above could be present (only serial ECG could differentiate). 

Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery. This does not fit with the clinical scenario in today's case. 

Below are two more video files. These images were obtained  from the parasternal short axis which transects the left and right ventricles. The VSR is located in inferior and basal portion of the ventricular septum and is readily visible. The second video file below shows the shunt by color doppler. 

Discussion: The patient in today’s case experienced a mechanical complication secondary to completed OMI. Troponin at presentation was very significantly elevated and T waves were still upright. She had atypical symptoms which made her postpone seeking medical attention. Mechanical complications secondary to myocardial infarction are infrequent due to most patients receiving revascularization quite rapidly. The patient in today’s case developed a large basal septal ventricular septal rupture (VSR) as a complication of an untreated OMI. Auscultation of a NEW harsh holosystolic murmur lead to rapid evaluation with echocardiography that confirmed the clinical suspicion. 

A VSR will lead to sudden left to right shunt and if large enough can lead to low output left sided failure. The RV acts as a conduit and does not necessarily become acutely dilated. Left ventricular afterload reduction is essential to decrease the trans-septal pressure gradient and thus decrease shunt volume, making a larger proportion of the blood flow from the left ventricle through the aortic valve.

For the patient in today's case nitroprusside (vasodilator) infusion was started to lower systemic vascular resistance (SVR), and an intra aortic balloon pump (IABP) was placed to further decrease afterload and better the hemodynamics. Surgical repair of the VSR was eventually done. The patient needed short term dialysis post surgery, but she eventually made a full recovery.

Mechanical complications are dreaded sequela of myocardia infarctions and can  come in the form of free wall rupture, ventricular septal rupture or papillary muscle rupture. The true incidence of the three mechanical complications may differ from reported incidence due to underreporting, miscoding, or variation in the populations studied. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. Among patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common. 

Mechanical complications occur acutely and significantly alter hemodynamics leading to compensatory mechanism which usually involve vasoconstriction and tachycardia, both hallmarks of cardiogenic shock. 

A VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking. It commonly occurs in the setting of a first myocardial infarction (MI) in the background of delayed or absent reperfusion therapy. Angiography usually reveals an absence of collateral circulation to the infarct zone. 

Because previous ischemia induces myocardial preconditioning, decreasing the likelihood of transmural myocardial necrosis and myocardial rupture, patients with evidence of diabetes mellitus, chronic angina or previous MI are less likely to experience a rupture. VSR may develop within 1-14 days post MI, however it’s incidence usually shows a bimodal peak which is within 24 hours and after 3-5  days post MI.

Survival after ventricular septal rupture may occur only after surgical repair. Thus, the diagnosis of ventricular septal rupture should prompt a heart team discussion of options. This discussion should take into account that, for some patients, surgery is futile as mortality approaches 100 percent. Older patients and those with poor right ventricular function often fall into this group. The timing of ventricular septal rupture repair is controversial.

Subacute AnteroSeptal STEMI, With Persistent ST elevation and Upright T-waves

Learning Points:

1. Sinus tachycardia (especially in the elderly) often signifies serious illness as it did in today’s case.
2. Mechanical complications of transmural infarction are rare and dreaded sequela and have high morbidity and mortality. 
3. Post infarction regional pericarditis (PIRP) can be suspected from the ECG and is associated with an increased risk of myocardial rupture.

Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis

Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction

Ventricular septal rupture

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

MY Comment, by KEN GRAUER, MD (9/5/2024):

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

As I emphasized in My Comment in the December 6, 2022 post and the August 19, 2023 post of Dr. Smith's ECG Blog — Not all patients with acute MI report chest pain. I thought the presentation of today's case makes it worthwhile to review the data regarding this issue.

• As per Dr. Nossen — today's patient concerns an older woman with a several day history of malaise and "not feeling well". Mention of vague "chest discomfort" over a period of recent days was only elicited when specifically requestioned. By history — providers were not expecting her initial ECG to show recent completed infarction with marked Troponin elevation.

The Framingham studies from many years ago taught us that the incidence of “Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

• The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
• But in the other half of this 30% (ie, in ~15% of all patients with MI) — although these patients found on follow-up ECG to have had infarction did not have chest pain — they did have "something else" thought to be associated with their MI.
• The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
• 
  
• BOTTOM Line: It's especially important for emergency providers to be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is often appreciated. Not all patients with acute (or recent) MI have chest pain with their event.

Application to Today's Case: Today's patient developed ventricular septal rupture the evening after she was admitted to the hospital. Her nonspecific symptoms that brought her to the hospital began a number of days before she finally sought medical assistance. 

• Awareness that this patient's malaise and her "not feeling well", as well as her vague chest discomfort might represent a cardiac problem — could have resulted in more timely initiation of treatment, that potentially might have averted the severe mechanical complication of her initially unrecognized extensive infarction.

  

Seizure in a 30 something

 Written by Magnus Nossen — with edits by Grauer.

The patient in today’s case is a 30-something female. She has no known previous medical history. Her husband called EMS when the patient experienced new onset seizures accompanied by micturition. The ECG below was recorded by EMS. What is your assessment? 

ECG #1

Interpretation: ECG #1 shows sinus rhythm at a heart rate of 77 bpm. The QRS is narrow with a normal PR interval. QRS axis is normal. There is some baseline wander. At first glance, the ECG does not look too abnormal.  However, cardiac syncope is always a differential diagnosis when someone presents with first time seizures.  In my experience, the pathologic finding in the above ECG is the easiest one to overlook — especially if you are in a rush and do not do a systematic review.

There are a number of things to look for in an ECG that can hint at arrhythmia as the cause of an apparent seizure. Below are some of the conditions to be aware of:

1. Preexcitation
2. Brugada syndrome.
3. Arrhythmogenic cardiomyopathy
4. Long QT syndrome 
5. Hypertrophic cardiomyopathy.

I find it is easier to measure the QTc when the paper speed is 50mm/s, as it is in the image above. I measure the RR interval at 795ms and the QT interval at 475ms. The QTc comes out at 533ms, dangerously prolonged.

En route to the hospital the patient experienced multiple short-lasting episodes, with cramping and loss of consciousness. She quickly regained consciousness — and was alert in between episodes. One episode was of longer duration. The ECGs below were captured on continuous 12-lead monitoring during transport! 

ECG #2

Interpretation of ECG #2: 

Underlying sinus rhythm. The sinus beats have a very prolonged QT-interval that seems even longer than in the first ECG. There is a run of polymorphic ventricular tachycardia — which given the QT prolongation, qualifies as Torsades de Pointes (TdP). This run of TdP is initiated by a PVC — but it then self-terminates. 

ECG #3

Interpretation of ECG #3: 

This rhythm begins as Torsades de Pointes — that then becomes V-Fib. This episode self terminated before defibrillation was possible.

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

Discussion: The patient in today’s case presented with "seizures". This case illustrates why all patients with seizures should have an ECG done. This patient was having recurrent episodes of polymorphic ventricular tachycardia with an underlying long QT interval ( = Torsades de Pointes). In the stabilizing area she received 10mmol magnesium sulfate IV, followed by a mantenance drip. Potassium chloride drip was also started. Potassium on admission was 3.5mmol/L (Ref 3.6-4.6) and magnesium 0.88 mmol/L (Ref 0.71-0.94). She stabilized after electrolyte administration with no further episodes of TdP.

• Following more detailed questioning — it turned out the patient had started taking 9 different herbal remedies to ease lethargy and unspecific neurological symptoms. It is unknown exactly what specific herbal medicine and what doses that had been ingested.

Below is a follow up ECG after discontinuation of the herbal remedies. The QTc is significantly shorter. It is very likely that the herbal remedies caused a lengthening of the QT-interval and led to Torsades de Pointes. 

In today's case — the QTc shortened after discontinuation of herbal remedies. It is important to be aware that this does not rule out congenital long QT syndrome (LQTS). The QT interval can be normal in patients with LQTS, and sometimes only manifests after a trigger such as hypokalemia or certain drugs.

• The patient did not have a positive family history of epilepsy, sudden cardiac death (SCD) or recurrent syncope. 
• Results from genetic testing for LQTS are pending — and the patient has been referred for evaluation of ICD placement.

Learning Points:

• LQTS can have normal QTc.
• All patients with seizures needs an ECG.
• Herbal remedies can potentially be life threatening

See this case for another example of ventricular arrhythmia secondary to herbal medicine.

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

MY Comment, by KEN GRAUER, MD (9/2/2024):

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

Today's case by Dr. Nossen is fascinating in its complexity — as the patient is a previously healthy young adult woman, whose presentation was with a new-onset Seizure.

• As noted above — the patient had cardiac syncope following a series of episodes of TdP (Torsades de Pointes) — raising the question of whether TdP caused her 1st Seizure — or — if it was the seizure itself that precipitated her malignant arrhythmia? (See Costagliola et al — Ann Clin Transl Neurol 8(7): 1557-1568, 2021 — for more on the complex "Brain-Heart Interaction" in Epilepsy).
• Today's case is further complicated by what I suspect represents body (therefore myocardial) K+ and Mg++ depletion — given the at best "borderline" serum (ECF) levels of these cations reported above in today's case (ie, 3.5 mEq/L for K+ and 1.76 mEq/L for Mg++) — given that ECF levels of these cations comprise only ~1-2% of total body stores (Jahnen-Dechent and Ketteler — Clin Kidney J 5(Suppl 1):i3-i14, 2012 — and — Udensi and Tchounwou — Int J Clin Exp Physiol 4(3): 111-122, 2017).
• Added to this is the fact that today's patient had been taking multiple herbal products for an unknown period of time, with it not known which herbal products were being taken, thereby also being unknown the potential for interactions by possible herbal combinations (See Déléaval et al — HeartRhythm Case Rep 8(5), 2022 — and — Kawatani et al — Oxford Med Case Rep 2023(9), 2023 — for more on potential proarrhythmic effects, including QTc prolongation of herbal products).

For clarity in Figure-1 — I've reproduced the initial ECG in today's case. As per Dr. Nossen — it would be all-too-easy to brush over this ECG as being "unremarkable" — IF one was not routinely systematic in the interpretation of all ECGs they encounter.

• For review of how Systematic 12-Lead ECG Interpretation not only increases accuracy, but also speeds you up — Please check out ECG Podcast #1, with outline and link to my talk on this subject in the July 24, 2024 post in Dr. Smith's ECG Blog.

Regarding my Systematic assessment of ECG #1:

• There is significant baseline artifact, as well as baseline wander. Keep in mind that your interpretation of the ECGs of your patients is part of the medical record. I therefore feel it relevant to document (in your dictation/on the medical chart) when significant artifact potentially impairs the accuracy of your interpretation. Given the importance of accurate measurement of the QT interval in this case — noting there is artifact in ECG #1 is relevant!
• The rhythm in ECG #1 is sinus at ~75/minute.
• Intervals: The PR interval is slightly prolonged (I measure ~0.22 second). The QRS complex is normal (ie, not more than 0.10 second). The QT interval looks to be prolonged (SEE below for details).
• The frontal plane axis is normal (about +70 degrees).
• There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There appears to be a Q wave in lead aVL (vs an rSr' ) — which as an isolated finding is of uncertain (if any) significance.
• R wave progression is appropriate — with Transition (where the R wave becomes taller than the S wave is deep) occurring normally by lead V4.
• Assessment of ST-T Waves — is challenging, because of the baseline wander and artifact (resulting in changing morphology from 1 beat-to-the-next) — and — because of the nonspecific ST-T wave flattening in multiple leads. However, as shown within the BLUE rectangle in Figure-1 — the end limit of the T wave is clearly seen in leads V4,V5,V6 (the vertical BLUE line in these leads).

KEY Point: The QT interval should be measured in THAT lead in which you most clearly see the end of the QT interval, and, in which lead the QT is longest.

• As shown in Figure-1 — By my calculation, the measured QT = 450 msec. To determine the QTc — We need to correct this 450 msec. value for the patient's heart rate of ~75/minute.
• There are many ways to estimate the QTc (ie, I illustrate a user-friendly method I developed and have used for decades in the October 25, 2023 post).
• PEARL #1: Alternatively — MD CALC is a handy link that provides near instant correction of the measured QT according to heart rate — allowing you to calculate the QTc by any of the 5 most commonly used corrective formulas ( = Bazett — Fridericia — Framingham — Hodges — Rautaharju). Plugging in the above numbers into MD CALC for a heart rate of 75/minute yields results between 476-to-503 msec. for the QTc (depending on which of these 5 formulas you choose). All of these values are clearly over the ~450 msec. that I favor as a "ballpark" upper normal QTc level.
• 
  
• My Impression of ECG #1: Sinus rhythm at ~75/minute — with nonspecific ST-T wave changes and a prolonged QTc. Because of the baseline artifact and marked variability in ST-T wave morphology from 1 beat-to-the-next — I found it hard to determine if there were (or were not) U waves in ECG #1. That said — in a patient who develops TdP — the overall ECG appearance of this initial ECG is consistent with low K+ and/or low Mg++ (See My Comment in the May 9, 2020 post — for more on the ECG diagnosis of hypokalemia and hypomagnesemia).
• 
  
• PEARL #2: The principal abnormal finding on this ECG is QT prolongation, here with generalized nonspecific ST-T wave abnormalities. Over the years, I have found recall of a short LIST of Causes of QT Prolongation to be of invaluable assistance. As per My Comment in the March 19, 2019 post of Dr. Smith’s ECG Blog — Assuming there is no bundle branch block, ischemia or infarction (as these entities can prolong the QT) — THINK OF: i) DRUGS (many drugs [including herbal preparations] may prolong the QT interval — and combinations of drugs can result in marked prolongation); ii) LYTES (ie, Think of low K+, low Mg++, low Ca++); and/or, iii) a CNS Catastrophe (ie, stroke, bleed, coma, seizure, trauma, brain tumor).
• 
  
• Application of the above LIST to Today's Case: All 3 of the categories in the above LIST may be contributing to the QTc prolongation we see in ECG #1: i) Drugs (This patient was taking a number of herbal medications); — ii) Lytes (Probable body depletion of K+ and Mg++ — given low normal serum levels of these cations and generalized nonspecific ST-T wave abnormalities with QTc [or QT-U] prolongation on ECG); — and, iii) CNS (Seizure activity).
• 
  
• P.S.: For another clinical example of how EASY-it-is to overlook a long QTc if one is not systematic in approach — Please check out the May 3, 2020 post in Dr. Smith's ECG Blog.

Figure-1: I labeled the initial ECG in today's case.

The Follow-Up ECG in Figure-2:

The patient in today's case stopped her herbal remedies. Some time after doing so — the ECG shown in Figure-2 was obtained (this being the 4th ECG that was shown above in Dr. Nossen's discussion).

QUESTION:

Dr. Nossen interpreted ECG #4 as showing significant reduction of the QTc after the patient stopped her herbal preparations.

• Instead of a decrease in the QTc — Doesn't return of the T wave to the baseline in lead V3 (at the point just over the RED arrow in this lead) suggest that the QTc is increasing?

Figure-2: The follow-up 12-lead ECG after the patient discontinued all herbal remedies. Has the QTc decreased? — or is there an increase in the QTc (as suggested by the RED arrow in lead V3)?

ANSWER:

Rather than highlighting the end of the T wave in lead V3 — I believe the RED arrow in this lead marks the end of a fairly large U wave. Surprisingly — a distinct U wave is not seen in any other lead, which makes it hard to determine what (if any) meaning this single U wave in lead V3 has.

• Determination of the QTc is made by measurement of the longest QT interval that you can clearly see in any of the 12 leads. In Figure-2 — we can clearly delineate the end point of the T wave in most leads. I once again used the last 3 chest leads (within the BLUE rectangle) — with the vertical BLUE line illustrating my measured QT = 370 msec.
• Correcting this measured QT value for a heart rate of ~85/minute — and plugging in these values into MD CALC results between 414-to-440 msec. for the QTc (depending on which of the 5 formulas in MD CALC that you choose). 
• 
  
• CASE Conclusion: The QTc in follow-up ECG #4 shows return of the QTc to normal (as per Dr. Nossen's assessment). Electrolyte replacement — cessation of seizure activity — and stopping herbal preparations all contributed to normalization of this patient's QTc, with improvement of ST-T wave appearance in most leads.
• As per Dr. Nossen — results of genetic testing for LQTS are pending.
• Perhaps this patient may not need ICD placement? — since what appears to be a major causative factor (simultaneous ingestion of 9 herbal preparations) is no longer operative. Further evaluation should help provide an answer.

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

P.S. — for "Purists": As a longterm "student of French" — I have wondered for decades what the "correct" spelling for TdP is. French grammar is beautiful and challenging — and I have seen numerous versions in anglo texts regarding the spelling of this fascinating arrhythmia.

• First described by the French physician, François Dessertenne in 1966 — the French version of Wikipedia allows for 2 potential spellings: i) Torsades de Pointes; and, ii) Torsades de Pointe.
• The English version of Wikipedia adds: iii) Torsade de Pointes and, iv) Torsades des Pointes.

It does gets confusing ... So I contacted Dr. Pierre Taboulet (French cardiologist with special expertise in the intricacies of ECG interpretation — and creator of the wonderful e-cardiogram ECG Blog — that I highly recommend for French-speaking clinicians).

• Dr. Taboulet acknowledges that even French-speaking clinicians use different terms for TdP. That said, in his words — it really is much simpler than it may seem because — "Il y a une "torsade de(s) pointes", ce qui est le phénomène de base — mais quand il y en a plusieurs (ce qui en est presque toujours le cas), il y a des "torsades de pointes"!  
• 
  
• Loosely TRANSLATED — The basic phenomenon regarding TdP is that there is one episode of a "twist" (around the baseline) of the QRS tip (or point) — but if a given patient has several runs of TdP (which is almost always the case) — then there will be multiple episodes with "twist(s)" (around the baseline) of the points (the ups & downs of the QRS).
• 
  
• My sincere THANKS to Dr. Taboulet for explaining this concept that I've wondered about for decades. His explanation strengthens my preference to continue uniformly using "Torsades de Pointes" as the written form of TdP. But the reality is that clinicians around the world (and in the literature) will continue to use multiple other spellings.

Epigastric and Right Upper Quadrant pain after eating spicy food

A 60-something woman with no cardiac history presented with epigastric and right upper quadrant pain after eating spicy food.

She had an ECG recorded at triage:

What do you think?

This was sent to me without any info while I was out and about, and I looked at it on my phone.  I responded: "That is a tough one.  V2 is very worrisome.  But no other leads are.   I probably would call it OMI.  What was the outcome?"

More analysis while looking at it on a computer screen: There is an intraventricular conduction delay with appropriately discordant ST segments and T-waves.  But there is also concordant STE in V2.  The STE in V1 is out of proportion to the S-wave, so V1 is also very worrisome (something I did not see on my phone).

It turns out that the conventional algorithm was also worried, and because of that, the patient was brought to the critical care area.  

Here is that interpretation of the conventional computer algorithm:

SINUS RHYTHM
INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
LEFT VENTRICULAR HYPERTROPHY AND ST-T CHANGE  [VOLTAGE CRITERIA PLUS ST/T ABNORMALITY]
POSSIBLE SEPTAL MYOCARDIAL INFARCTION , PROBABLY RECENT [30 ms Q WAVE IN V1/V2]
LATERAL MYOCARDIAL INFARCTION , PROBABLY RECENT [40+ ms Q WAVE AND/OR ST/T ABNORMALITY IN I/aVL/V5/V6]
***ACUTE MI*** 

Later, there was an overread by a Cardiologist, who removed the ***Acute MI***

SINUS RHYTHM. No Previous ECGs Available.

INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
LEFT VENTRICULAR HYPERTROPHY AND ST-T CHANGE  
ABN R PROGRESSION, ASMI OR LEAD PLACEMENT

The providers ran the ECG through the Queen of Hearts:

If it is OMI, she does not see it.  

But she does label V2 as "OMI High Confidence" and V1 as "OMI Low confidence"

Like good physicians, they recorded another ECG at 10 min:

What do you think?

Now there is S-wave shortening in multiple precordial leads, rendering the T-waves hyperacute!  The T-waves have barely changed, but the S-waves have shortened and thus the T/QRS ratio is much larger (that is both T-wave amplitude and T-wave area under the curve).

Now it is diagnostic of OMI.

Here is the conventional algorithm:

SINUS RHYTHM

INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
ABNORMAL ECG 

And the Cardiology overread:

SINUS RHYTHM
INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
ABN R PROGRESSION, ASMI OR LEAD PLACEMENT
Comparison Summary: NO SIGNIFICANT CHANGE.
Compared with: 8/18/2024 6:08 AM 

This time neither see acute MI.

But the Queen of Hearts now sees it:

Notice that the dark blue in this explainability map tells you that she also is seeing the short S-wave and the hyperacute T-wave!

Click here to sign up for Queen of Hearts Access

Unfortunately, the team did not see it and they did not use the Queen on the 2nd ECG.  So it was not until 68 minutes that they recorded another ECG:

Now it is obvious with massive relative hyperacute T-waves in lead V4

The conventional algorithm diagnosed it:

SINUS RHYTHM
INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
LEFT VENTRICULAR HYPERTROPHY AND ST-T CHANGE  [VOLTAGE CRITERIA PLUS ST/T ABNORMALITY]
ANTEROLATERAL MYOCARDIAL INFARCTION , PROBABLY RECENT [40+ ms Q WAVE IN I/aVL/V3-V6]
***ACUTE MI*** 

And the Cardiology overread see the evolution but is not convinced:

SINUS RHYTHM
INTRAVENTRICULAR CONDUCTION DELAY  [130+ ms QRS DURATION]
LEFT VENTRICULAR HYPERTROPHY AND ST-T CHANGE  [VOLTAGE CRITERIA PLUS ST/T ABNORMALITY]
ANTERIOR AND LATERAL ST CHANGES
ABN R PROGRESSION, ASMI OR LEAD PLACEMENT.
Comparison Summary: ANTEROLATERAL ST CHANGES ARE NOW MORE PRONOUNCED, RATE DEPENDENT VS ISCHEMIC CHANGES 

Here is the Queen's diagnosis:

The cath lab was activated:

Culprit Lesion (s): Thrombotic 99% mid LAD stenosis with TIMI II flow 

Peak troponin not measured, unfortunately.  So we don't have a good idea how large the final infarct size was.

Echocardiography:

Normal left ventricular size with mild to moderately reduced LV systolic function; estimated LVEF is 44 %.

There is akinesis of the distal septum, anterior, apex, and distal inferior wall consistent with LAD territory ischemia or infarction.

How large is the infarct?

It is impossible to conclude from this that the infarct was VERY large, though it likely was very large since the time to intervention was long.  The area of insult was indeed large, but whether that area is all irreversibly infarcted or not would require MRI or a 6 week followup ("convalescent") echocardiogram, to see how much myocardium recovers (was only "stunned", not infarcted)

Post PCI EKG:

There is loss of anterior forces (Q-waves) which was not there before.  Probably significant infarction. 

Learning Points:

Serial ECGs are critical.  

Apply the Queen of Hearts to all serial ECGs.  

Occasionally, the conventional algorithm will beat the Queen

Cardiology overreads are not sensitive for OMI.

 

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

MY Comment, by KEN GRAUER, MD (8/26/2024):

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

I saw ECG #1 knowing only that, "a 60-something woman with no cardiac history presented with RUQ pain after eating spicy food."

• Although clearly a history of abdominal pain suggesting cholecystitis — an ECG was appropriately done. This is an important reminder of the many ways other than chest pain, that acute coronary syndromes may present (See Talakic et al — Cardiovasc Med, 2023 and Tsipouras — Austral Fam Phys 37(8), 2008, among many other sources). 

I've highlighted the KEY leads in the initial ECG that immediately drew my attention:

• As per Dr. Smith — there is no way that the QRST complex in lead V2 can be normal (within the RED rectangle in Figure-1). There is abnormal ST segment coving — and — considering how small QRS amplitude is in this lead, there is marked ST elevation.
• There is also a fragmented and a markedly widened initial Q wave in lead V2.
• Finally — there is an "orphan" (ie, predominantly tall) R wave in lead V2 — which is distinctly different from all other chest leads (See below).

Are there Other Abnormal Leads in ECG #1?

The importance of recognizing that there can be no way lead V2 in ECG #1 is "normal" — is that it necessitates closer scrutiny of the remaining 11 leads.

• The limb leads in ECG #1 show sinus rhythm with QRS widening and marked LAD (Left Axis Deviation). Although the frontal plane axis of -60 degrees is negative enough to be consistent with LAHB (Left Anterior HemiBlock) — with "pure" LAHB, the initial r waves in the inferior leads are generally not as wide as seen here — so a "nonspecific" conduction delay with marked LAD might be a better description of findings. That said — ST-T wave findings in the limb leads are non-diagnostic! Both LVH (which may be present here) and LAHB may be associated with the ST-T depression seen here in leads I and aVL.
• 
  
• BUT — Other Chest Leads in ECG #1 are not normal — especially the neighboring leads to lead V2. As per Dr. Smith — the relative amount of ST elevation in lead V1 is disproportionate to the tiny S wave depth in this lead (BLUE arrow in lead V1).
• As we often emphasize — there normally will often be slight, gently upsloping ST elevation in lead V3 — but no J-point elevation is seen here in this lead (BLUE arrow in V3). The reason that I found this subtle finding in lead V3 important — is the subtle-but-real "extra" amount of ST elevation that is present here in lead V4, which makes for concerning findings in the first 4 chest leads. I would not normally expect this much ST elevation in lead V4 given the lack of any ST elevation in lead V3.
• 
  
• In Summary: I was not certain about there being an acute OMI from my initial assessment of ECG #1. That said — I thought the chest lead findings in leads V1-thru-V4 suspicious enough that I was glad a repeat ECG was obtained within the next 10 minutes!

What Can Be Learned from the Repeat ECG?

There are 2 important things to be learned from the repeat ECG:

• #1 — There is no longer any question about acute LAD OMI! Today's case provides yet another example of how quickly definitive ECG changes can evolve — with directive to us, that we have a low threshold for repeating the ECG when concerned about a less-than-diagnostic initial ECG within the next 10-to-20 minutes. Continue repeating serial ECGs until such time that definitive management plans are made (sometimes meaning until you can convince the on-call interventionist to take the patient to the cath lab!).
• 
  
• #2 — The BEST way to get good at detecting early acute signs of OMI — is to routinely GO BACK to the initial tracing after ST-T wave changes have evolved. Doing so in Figure-1 facilitates recognizing how the subtle abnormalities I highlighted above in leads V1, V3 and V4 have evolved to obvious diagnostic findings.

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

An "Orphan" Tall R Wave in Lead V2?

Malposition of chest lead electrodes is common in general practice (Rehman and Rehman — Cureus 12(7):e9040, 2020). Because of placement issues with respect to breast tissue — optimal chest lead electrode placement is especially problematic in women — which leads to inconsistent, and all-too-often, technician dependent variations (Kligfield et al — AHA/ACC/HRS Scientific Statement, 2007).

• While possible that electrode lead placement of lead V2 in today's case is correct — given that the most remarkably abnormal lead in today's initial ECG is lead V2 (as the only chest lead with a predominant R wave) — ensuring accurate electrode lead placement would seem essential for accurate diagnosis. BEST practice when suspecting potential lead misplacement of a critical lead in your assessment — is to verify lead placement, and immediately repeat the ECG.

PEARL: The isolated ECG finding of a surprisingly tall R wave in lead V2 that was seen in today's case — may not always be due to lead misplacement. Chugh et al report on this uncommon ECG curiosity as a potential manifestation of acute coronary occlusion (Cureus 9(4):e1200, 2017).

• The mechanism proposed for the isolated finding of a tall R wave in lead V2 in a patient with acute chest pain is complex and not fully elucidated. It is thought to result from abnormal depolarization of an acutely ischemic area that leads to dispersion of repolarization times — such that unopposed positive forces facing an area of acute ischemia produce the isolated tall R wave in lead V2 (ie, repolarization dispersion during acute ischemia may lead to transient obliteration of the S wave — therefore leaving an unopposed R wave).
• In the case study by Chugh et al — the tall R in V2 was transient, resolving after acute ischemia was controlled. In today's case — the tall R in V2 resolved after successful PCI.
• 
  
• Editorial Note: I have seen this ECG finding before — but did not previously realize that rather than lead misplacent, this might be an indication of acute OMI. I will as of now be "on the lookout" for more examples, that I'll be correlating with clinical events to see if this finding portends acute LAD occlusion.

Figure-1: Comparison between the first 2 ECGs in today's case.