Patient is informed of her husband's death: is it OMI or it stress cardiomyopathy?

Written by Willy Frick

Disclaimer at the outset: Some aspects of this case are not completely clear to me, and approach being unknowable. I've presented the case as best I understand it, but I can see good arguments for other interpretations.

A woman in her late 60s presented after a car crash. Her husband was driving and she was a passenger. They were hit at high speed. She sustained a large scalp hematoma along with several rib and vertebral fractures, but with CT scanning of chest/abdomen/pelvis/C-T-L-spine and head, no life threatening injuries were found. She complained of pain from her injuries. Her first ECG is shown.

Overall bland. Normal sinus rhythm with non-specific ST abnormality. After this ECG was obtained, the ER physician received word that the patient's husband had died in the crash. He told the patient this horrible news. Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Here is an image showing a few excerpted segments with time stamps:

If you wish to see the transition, I've included a video as I scroll through the telemetry. The changes start to become apparent about 25 seconds into the video.

Repeat ECG was obtained immediately, just 24 minutes after the prior ECG:

Given the context, my top differential diagnosis would be stress cardiomyopathy AKA takotsubo. But that is a diagnosis of exclusion, and OMI must obviously be ruled out with this dramatic ECG. If this were OMI, I would favor proximal RCA culprit (since that commonly produces inferolateral changes and occasionally produces anterior HATW from RV infarct), but LAD is also possible. The other point in favor of RCA is junctional rhythm. Bradycardia and heart block are very common in RCA OMI.

The emergency physician immediately activated the cath lab. In lab, patients are monitored on continuous abbreviated ECG with 5 electrodes. During ballooning, we often see immediate hyperacute T waves. After stent deployment, we often see improvement in the ST-T within seconds or minutes. The patient's ECG at the beginning of the case is shown below.

1:45, case start

To orient you to this screen, the top is obviously ECG waveforms. You can see the lead labels on the left, I, II, aVF, and V (a single precordial lead) in descending order. The bottom half of the screen shows the arterial pressure. Right now it is not hooked up, so it just shows a noisy waveform close to zero.

For a more detailed discussion of the this patient's angiography and angiography in general, please refer to my angiography guide. The patient's left sided arteries had only mild disease. The RCA film is shown below. You will see the following:

First, filling of the RCA and posterolateral system. Second, a freeze frame when the whole vessel is opacified, but no PDA is yet seen. Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. Fourth, the same clip repeated at normal speed.

This LAO cranial angiogram shows at least three findings, annotated below:

• An ostial lesion (red arrow), more on this below.

• A distal RCA lesion (blue arrow),

• Delayed brisk filling of an initially occluded PDA due to a thrombus dislodged during injection which embolized distally. The yellow arrow points to the stump of the PDA before the thrombus embolizes allowing contrast to fill the vessel.

Although the ostial lesion may not appear very impressive angiographically, there is reason to believe it is severe, due to an observation in the cath lab called "pressure damping." This requires a little explanation. The arterial pressure waveform is transduced using the coronary catheter. Normally, the diameter of the coronary artery ostium is much greater than the diameter of the catheter so that catheter engagement does not significantly impair antegrade coronary perfusion. But in the case of an ostial lesion, there is little or no space between the outside of the catheter and the wall of the coronary artery. This prevents antegrade flow into the coronary artery during catheter engagement, and as a result the transduced pressure drops significantly below systemic arterial pressure.

Here is the ECG and arterial waveform during RCA angiography. Note the pressure on the arterial line, estimated at 45/25 mm Hg.

1:51, diagnostic RCA angiography

At this point, the patient very clearly has a diagnosis of OMI, especially since we visualized embolism within the PDA. But is the coronary pathology enough to explain the persistent ECG changes? Here is the final angiogram following placement of a stent in the ostial RCA.

2:04 PM, post stent deployment

You can see that even after complete restoration of flow, the ECG still looks terrible, V most of all. It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! In my opinion, the more likely explanation is that the ST-T changes are primarily driven by stress cardiomyopathy.

At this point, with TIMI 3 flow in all vessels, the interventional cardiologist performed right heart catheterization. The patient's wedge pressure was 18 mm Hg with normal cardiac output and index by estimated Fick. After completing the right heart catheterization, the patient had worsening ST segments on EKG. The catheter was out of the body and the arteriotomy had been closed, so there is no pressure waveform.

2:34 PM, following right heart catheterization

She then went into atrial fibrillation with complete heart block and junctional escape rhythm prompting placement of transvenous pacemaker.

2:38, atrial fibrillation with complete heart block

Given her hemodynamic instability, the cardiologist placed an Impella and prepared to repeat angiography. In the midst of this, she went into VF. Several 200 J shocks did not terminate the VF, so a second defibrillator was applied for double sequential defibrillation with 400 J. The patient developed electrical storm with recurrent VF. During the resuscitation, she received amiodarone 450 mg IV, lidocaine 100 mg IV, and magnesium 6 g IV. She was defibrillated perhaps 25 times.

Angiography was technically challenging as the patient was receiving CPR, but the cardiologist suspected acute stent thrombosis and initiated cangrelor, although no repeat angiography was able to be obtained. Unfortunately, even with Impella in place and when the patient was in rate controlled AF, she remained pulseless.

3:07 PM, slow atrial fibrillation with electromechanical dissociation

At this time, the patient's family terminated resuscitation efforts and the patient was pronounced dead.

Case discussion:

This is a tragic case. The patient survived the car crash, but upon learning of her husband's death, she deteriorated. Despite almost immediate revascularization, she had persistent dramatic ST-T abnormalities. The cardiologist thought she had stent thrombosis which is possible, but I do not necessarily think is sufficient to explain her complete hemodynamic collapse.

Just a few weeks ago, I took care of a patient who had ostial RCA OMI (TIMI 0 at cath) and his only complaint was syncope! He had no chest pain, dyspnea, or any other anginal equivalent, and his vital signs were normal. 

In my opinion, the ECG changes and hemodynamic collapse seem out of proportion to the observed/suspected coronary pathology. Additionally, the timing is highly suggestive of stress induced etiology. Takotsubo characteristically occurs in women in their 60s. It is now well recognized that acute MI can precipitate takotsubo. Here is a case report and review of the literature. The authors describe a case with some features in common with our patient -- a stressful event followed by a stress cardiomyopathy/acute myocardial infarction overlap syndrome. No LVgram was done in this patient's case, but even that could be challenging to interpret if the patient had one of the recognized phenotypes other than classical apical ballooning (e.g. midventricular, basal, focal).

In my review of the literature, there are many articles which purport to demonstrate an acutely increased risk of plaque rupture from emotional stress, but I could not find any credible case reports that were not at least as likely to be takotsubo. Please message me on Bluesky or Twitter if you know of any such case reports. Here is some of what I found:

• A case report which describes stress induced acute MI but is much more likely to be takotsubo in my opinion (including characteristic ECG changes)
• A review article which asserts the role of emotional stress in plaque rupture, and cites the above case report as well as a few population studies that are hard to draw firm conclusions from
• Another review article with similar citations
• A case control study ostensibly showing increased risk of MI following death of a loved one, but without angiographic data and the authors even acknowledge that takotsubo could have been present
• An autopsy study claiming a role for stress in sudden cardiac death from coronary disease, but not clearly proving it
• These authors describe a case of takotsubo syndrome complicated by suspected LV thrombus and cardioembolic OMI

Ultimately, most of this discussion is clinically irrelevant. The patient certainly had OMI and received treatment for it. There is no specific treatment for stress cardiomyopathy, only supportive treatment. Was her outcome to be expected for ostial RCA OMI? Or was it out of proportion, perhaps worsened by the sympathetic surge? We will never know for certain.

In addition to profound acute heart failure, the patient suffered from electrical storm. After completing the ACS algorithm with amiodarone and lidocaine, there are diminishing returns on further treatments. If the patient can be temporized with VA ECMO, consider propranolol or stellate ganglion blockade. Both treat sympathetic surge which is a driver of electrical storm.

Learning points:

• Takotsubo and OMI can co-exist

• If max output on the defibrillator doesn't terminate VT, add another defibrillator

• If amiodarone, lidocaine, and magnesium are ineffective at suppressing VT/VF, consider VA ECMO or propranolol

References:

Angulo‐Llanos, R., Sanz‐Ruiz, R., Solis, J., & Fernández‐Avilés, F. (2013). Acute myocardial infarction: an uncommon complication of takotsubo cardiomyopathy. Catheterization and Cardiovascular Interventions, 82(6), 909–913. https://doi.org/10.1002/ccd.24846 

Bai, J., Xiang, W., Kong, L.-Y., Zhao, L.-T., Liu, F., Liu, L.-F., Tang, Z., & Zhang, P. (2022). Acute myocardial infarction complicated with takotsubo syndrome in an elderly patient: case report and literature review. Journal of Geriatric Cardiology, 19(6). https://doi.org/10.11909/j.issn.1671-5411.2022.06.007 

Bentzon, J. F., Otsuka, F., Virmani, R., & Falk, E. (2014). Mechanisms of plaque formation and rupture. Circulation Research, 114(12), 1852–1866. https://doi.org/10.1161/circresaha.114.302721 

Chatzidou, S., Kontogiannis, C., Tsilimigras, D. I., Georgiopoulos, G., Kosmopoulos, M., Papadopoulou, E., Vasilopoulos, G., & Rokas, S. (2018). Propranolol versus Metoprolol for treatment of electrical storm in patients with implantable cardioverter-defibrillator. Journal of the American College of Cardiology, 71(17), 1897–1906. https://doi.org/10.1016/j.jacc.2018.02.056 

Cheskes, S., Verbeek, P. R., Drennan, I. R., McLeod, S. L., Turner, L., Pinto, R., Feldman, M., Davis, M., Vaillancourt, C., Morrison, L. J., Dorian, P., & Scales, D. C. (2022). Defibrillation strategies for refractory ventricular fibrillation. New England Journal of Medicine, 387(21), 1947–1956. https://doi.org/10.1056/nejmoa2207304 

Falk, E., Shah, P. K., & Fuster, V. (1995). Coronary plaque disruption. Circulation, 92(3), 657–671. https://doi.org/10.1161/01.cir.92.3.657 

Gelernt, M. D., & Hochman, J. S. (1992). Acute myocardial infarction triggered by emotional stress. The American Journal of Cardiology, 69(17), 1512–1513. https://doi.org/10.1016/0002-9149(92)90918-o 

Ghadri, J.-R., Wittstein, I. S., Prasad, A., Sharkey, S., Dote, K., Akashi, Y. J., Cammann, V. L., Crea, F., Galiuto, L., Desmet, W., Yoshida, T., Manfredini, R., Eitel, I., Kosuge, M., Nef, H. M., Deshmukh, A., Lerman, A., Bossone, E., Citro, R., … Templin, C. (2018). International expert consensus document on takotsubo syndrome (part I): Clinical characteristics, diagnostic criteria, and pathophysiology. European Heart Journal, 39(22), 2032–2046. https://doi.org/10.1093/eurheartj/ehy076 

Jentzer, J. C., Noseworthy, P. A., Kashou, A. H., May, A. M., Chrispin, J., Kabra, R., Arps, K., Blumer, V., Tisdale, J. E., & Solomon, M. A. (2023). Multidisciplinary critical care management of electrical storm. Journal of the American College of Cardiology, 81(22), 2189–2206. https://doi.org/10.1016/j.jacc.2023.03.424 

Mostofsky, E., Maclure, M., Sherwood, J. B., Tofler, G. H., Muller, J. E., & Mittleman, M. A. (2012). Risk of acute myocardial infarction after the death of a significant person in one’s life. Circulation, 125(3), 491–496. https://doi.org/10.1161/circulationaha.111.061770 

Myers, A., & Dewar, H. A. (1975). Circumstances attending 100 sudden deaths from coronary artery disease with coroner’s necropsies. Heart, 37(11), 1133–1143. https://doi.org/10.1136/hrt.37.11.1133 

Park, J., Choi, K. H., Lee, J. M., Kim, H. K., Hwang, D., Rhee, T., Kim, J., Park, T. K., Yang, J. H., Song, Y. B., Choi, J., Hahn, J., Choi, S., Koo, B., Chae, S. C., Cho, M. C., Kim, C. J., Kim, J. H., Jeong, M. H., … Kim, H. (2019). Prognostic implications of Door‐to‐balloon time and onset‐to‐door time on mortality in patients with st‐segment–elevation myocardial infarction treated with primary percutaneous coronary intervention. Journal of the American Heart Association, 8(9). https://doi.org/10.1161/jaha.119.012188 

Singh, T., Khan, H., Gamble, D. T., Scally, C., Newby, D. E., & Dawson, D. (2022). Takotsubo syndrome: Pathophysiology, emerging concepts, and clinical implications. Circulation, 145(13), 1002–1019. https://doi.org/10.1161/circulationaha.121.055854

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MY Comment, by KEN GRAUER, MD (3/8/2025):

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If you Google, “Broken Heart Syndrome” — you will immediately see reference to many pages of “Patient Education” news briefs and informationals, in which the questions addressed are, “Can You Really Die of a Broken Heart?” — and if so, “How Can this Happen?”.

• The answer is YES, you can die of "Broken Heart Syndrome" — as becomes tragically evident in today’s case presented by Dr. Frick.

The syndrome referred to was first identified in 1990 — and initially named "Takotsubo" CardioMyopathy (TCM) because of the heart's resemblance on a ventriculogram to the shape of the container used by Japanese fishermen to trap octopuses. 

• As shown in Figure-1 — the unusual round bottom and narrow neck design of takotsubo is similar to cath findings that manifest ballooning of the cardiac apex with hypercontraction of the base.
• Additional names for this syndrome followed — including "Stress" Cardiomyopathy (Stress CM) — "Apical Ballooning Syndrome" — and the lay press name of "Broken Heart" Syndrome.
• Many variations regarding the location of cardiac involvement have since been described. Instead of LV dysfunction localized to the apex — the dysfunction may be of the base = "Reverse" Takotsubo, in which case there will not be apical ballooning. Or, there could be mid-ventricular Takotsubo, in which there is poor function (and ballooning) of the mid-LV, with good function at both the base and the apex — and, still other anatomic possibilities (See the June 24, 2014 post — and My Comment in the July 21, 2022 post of Dr. Smith's ECG Blog regarding Takotsubo variant patterns).
• And, as often occurs with “newly described” clinical syndromes — once they appear in the medical literature, the syndrome becomes increasingly recognized (whereas it probably had been present all along at some undefined frequency). Thus, the entity of Stress CM is not "one size fits all" — but instead encompasses a range of anatomic (and therefore electrocardiographic) presentations.
• Although the precise mechanism for this entity remains unclear — the common denominator appears to be sympathetic overdrive (catecholamine excess), with a marked preponderance in post-menopausal women — in which the entity is often precipitated by strong emotional or physical stress. That said — many cases are not that simple, and I found myself both emotionally moved — as well as intellectually fascinated by the sequence of events in today's case.

Figure-1: Collection of actual "octobus traps" (takotsubo) — showing the round bottom and narrow neck that resembles the diagnostic picture seen on the cardiac cath ventriculogram (shown here during end-systole). Note characteristic “ballooning” of the apex and hypercontractility of the base during cardiac cath (Figure excerpted from Grauer K: ECG-2014- Expanded ePub, KG/EKG Press).

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MY Thoughts on Today’s CASE:

Although we do not know details of the relationship between today’s patient (a woman in her late 60s) and her husband — I found it easy to imagine a marriage of many decades duration, in which the patient, while she herself is being treated for severe but not life-threatening injuries — suddenly learns that her life-time partner has died in the auto crash.

• Given the immediate physiologic “chain reaction” of intense autonomic dysfunction that followed on learning of her husband's death (and which ultimately led to this patient’s demise) — I have to wonder WHEN (and How?) to best convey the terrible news that a loved one has just died in the accident that just occurred?
• Clearly — the physiologic “chain reaction” of autonomic dysfunction seen in today’s case does not commonly lead to death of the person learning this news. But if faced with a similar decision in the future — I wonder, if in the interest of the patient's medical condition — it might be better not to immediately convey the death of a loved one in the same accident until the patient was in a more capable state to process what happened. I do not know the answer to this.

With regard to the Physiologic “Chain Reaction” …

• As per Dr. Frick — We do not have all the answers. Cardiac cath apparently showed some ventricular dysfunction, though not the typical findings of Takotsubo CM (hard to do procedures while patients are receiving CPR ...).
• What is known — is that the repeat ECG in today’s case (shown in Figure-2) — suggests profound parasympathetic hyperactivity.

• Whereas the patient's initial ECG shows sinus rhythm and nonspecific ST-T wave abnormalities — just 24 minutes later, there is now profound bradycardia with a junctional escape rhythm (YELLOW arrows highlighting retrograde P waves) — and obvious findings of an acute inferior STEMI.
• Marked inferior lead ST elevation (greater in lead III than in lead II) — with equally marked reciprocal ST depression in lead aVL suggest an RCA "culprit" — though uncharacteristically flat ST segments in V1,V2 (competing RV and posterior wall involvement?) with ST elevation in V3-thru-V6 indicate a complicated picture.

The patient's condition deteriorated. As per Dr. Frick — the ongoing ECG changes in association with hemodynamic collapse seemed out of proportion to the apparent coronary pathology.

• There was indication of parasympathetic overdrive (the acute inferior STEMI with profound bradycardia and junctional escape).
• This was overtaken by a predominance of sympathetic surge (tachycardia, persistent ST elevation — development of electrical "storm" with failure to respond to recurrent defibrillation).
• Perhaps best summed up as a tragic case of extreme autonomic dysfunction precipitated by overwhelming psychologic stress that proved too much for the most intense efforts at treatment.

Figure-2: Comparison between the initial 12-lead ECG in today's case — with the repeat ECG done just 24 minutes later, after the patient learns that her husband has died.

 

What is this rhythm? And why rhythm problems are easier for the Emergency Physician than acute coronary occlusion (OMI).

Written by Pendell Meyers

Don't miss Ken Grauer's excellent assessment at the bottom.

With no context, what do you think this rhythm is?

Smith comments: Wide complex tachycardia.  The differential diagnosis of WCT is:  

1) Sinus tachycardia with "aberrancy" (in this case RBBB and LAFB), but there are no P-waves and the QRS morphology is not typical of simple RBBB/LAFB.  If you are wondering if there are P-waves that you just can't see, you can use Lewis Leads to magnify the P-waves (or not, if they are not there).  Also, if the rate is constant, not wavering up and down, it is highly unlikely to be sinus tachycardia.  Sinus tach is often misinterpreted as a dysrhythmia.  See this case, for example: A Relatively Narrow Complex Tachycardia at a Rate of 180.  

2) PSVT with "aberrancy" (atypical RBBB+LAFB).  Possible but, again, the QRS morphology is atypical

3) Atrial Flutter with 2:1 conduction and "aberrancy".  I do not see flutter wave baseline, and again the QRS morphology is not typical for a supraventricular rhythm.

4) Antidromic ARVT, which is supported by the slow onset of the QRS. But the superior axis with positive QRS in V1 is difficult to reconcile with an accessory pathway.  Slow onset of QRS is probably the best hallmark of VT.

5) Ventricular Tachycardia: by far most likely, but what kind?

Fortunately, you don't need to make a definite diagnosis.  It is not sinus tachycardia, so you can electrically cardiovert, whether the patient is stable or unstable.

Why are rhythms easier to recognize and manage than OMI for the Emergency Physician?  

First, When you have a rhythm problem, you know you have a problem because the rate is either fast, slow, or irregular.  With OMI, all you know is that your patient has some nonspecific chest pain, SOB, shoulder pain etc. which is probably NOT due to acute MI.  So if you don't recognize the OMI on the ECG immediately, then myocardium is irreversibly lost.  And if you wait for troponin, much myocardium is lost by the time you make the diagnosis. Second, when you have a rhythm problem, you are likely to be able to fix the problem with electricity (cardioversion, defibrillation, pacing).  Third, while you are making a decision about a rhythm, myocardium is not rapidly dying.  Fourth, you can get help from a cardiology colleague; they are very good at this even though they may not be so good at recognizing OMI on the ECG.  Fifth, potential management actions are in your hands; you do not need to request a coronary interventionalist or cath lab team.

Making a specific ECG Diagnosis (less important in the ED)

Without reading the below, I suspected posterior fascicular VT.  There are no P-waves, there is an RBBB + LAFB morphology, with rate slightly over 150, QRS duration is wide but not VERY wide.  This type of VT is often diagnosed in younger patients without any baseline cardiac disease.  They often have good ejection fraction and tolerate the dysrhythmia quite well.  So if the patient is stable, has good LV function on bedside echo, and is relatively young with no history of heart failure or cardiomyopathy, then posterior fascicular VT is likely.  In any case, I would electrically cardiovert.  See Ken's excellent analysis at the end.

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Case continued: Here is the clinical context and all ECGs in order:

An elderly comorbid woman presented with acute respiratory distress. She was critically ill and required noninvasive positive pressure ventilation and ICU admission for suspected infectious respiratory illness.

Smith: now that I know she is "elderly," and in respiratory distress, I am much less confident in that diagnosis.  It would be good to know more about her cardiac history and her ejection fraction on bedside echo.

Case continued

Bedside echo showed a significantly reduced LV ejection fraction (prior echo on file had EF 45%). Here were her first two ECGs:

I believe these two rhythms are supraventricular with LBBB morphology. I think the first one is likely sinus, and the second one is less certain to me, could be sinus or flutter.

Then her rhythm abruptly changed to this:

Regular, monomorphic, just a bit over 120 msec in my estimation. The QRS morphology is completely different than before, and now could be called similar to RBBB and LAFB morphology.

Overall, it would be best to assume VT until proven otherwise. It might not be "classic" VT, but instead Posterior Papillary Muscle VT, or Posterior Fascicle VT. Both of these types of VT access the left posterior fascicle, thereby creating VT with RBBB/LAFB morphology and thus QRS duration shorter than "classic" VT.

Smith: Now that we see the preceding ECGs and the clinical story, Posterior Fascicular VT is far less likely than standard monomorphic VT arising from a sick left ventricle, though Pendell's assessment may be correct

Case Continued

Thanks to several colleagues for this interpretation, including Pierre Taboulet and Nanashi and Willy Frick.

Amiodarone was chosen as an "antidysrhythmic", and it was later attributed temporally to cessation of the rhythm.

(Ever since Dr. Nils Johnson told me that he calls them "rhythm modifying drugs", I also prefer this term, as we all know that any of these medications in general can be both "anti-dysrhythmic" and "pro-dysrhythmic.")

Later in her hospital course, here is another ECG:

Sinus rhythm with bigeminal PVCs. In my opinion, the PVCs match the likely VT from the prior ECG. This increases the confidence that the prior rhythm was VT.  I believe this makes Posterior Papillary Muscle VT more likely, but these cases are still a bit rare and esoteric to me, especially when they are likely caused by (and resolve with) a critical illness. There is no evidence that this elderly patient has suffered from VT or other primary dysrhythmias in the past.

Unfortunately, the patient continued to worsen, was intubated and admitted to the ICU, where she ultimately expired days later, with an overall impression of multifactorial respiratory failure.

Here is an article about PPM VT

Here are some other relevant cases:

A 12 year old with Wide Complex Tachycardia

Incessant Regular Wide Complex Tachycardia

Wide complex tachycardia in a 36 year old

Also see my prior post with EM-focused teaching on Fascicular VTs:

Idiopathic Ventricular Tachycardias for the EM Physician

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MY Comment, by KEN GRAUER, MD (3/6/2025):

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Among the greatest challenges faced by emergency care providers — is assessment of the regular WCT (Wide-Complex Tachycardia). Today's case presented by Dr. Meyers amplifies this challenge by presenting us with not one, but 3 serial WCT rhythms. 

• While fully agreeing with the key concepts conveyed above by Dr. Meyers — I'll offer an additional perspective to these 3 serial rhythms.
• For those wanting Quick Review of my approach to the regular WCT — Please See my May 5, 2020 post in Dr. Smith's ECG Blog.

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— ECG #1 — (The initial ECG shown by Dr. Meyers):

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From an educational standpoint — I thought Dr. Meyers' choice was excellent, to begin today's case by first showing the 3rd ECG that was recorded (even though this ECG that I have labeled in Figure-1 — was recorded after ECG #2 and ECG #3 that appear in Figure-2 below). 

Emergency providers need to attain high confidence that ECG #1 is all-but-certain to represent VT.

• We are told that the rhythm in Figure-1 is from an acutely ill elderly woman with underlying comorbid conditions. This rhythm is a regular WCT at ~160/minute, without clear sign of atrial activity. Knowing this — before we even begin to look at specific features in this ECG, we need to remember that statistical likelihood  that this rhythm is VT approach 90%. As a result — our mindset is not to determine if this rhythm "might be" VT — but rather that we need to assume VT (and treat accordingly) unless we can conclusively prove otherwise.
• Although it may be tempting to interpret the small negative deflections marked by BLUE arrows in the long lead V5 rhythm strip as P waves — these are not P waves. As shown by the double RED arrows — the QRS complex in each of the limb leads begins with subtle slurring. Thus, the parallel BLUE time lines show this initial negative deflection in lead V5 to be part of the QRS. 
• KEY Point: When you see deflections that "look" like sinus P waves in one or 2 leads, but you do not see anything resembling a sinus P wave in either lead II or lead V1 — then those deflections you are seeing in those other leads (like the negative deflections here in lead V5) are not sinus P waves!
• "12 leads are better than one" — and skillful use of simultaneously recorded leads can be invaluable. For example — the parallel GREEN timeline tells us that a similar small negative deflection also appears at the onset of the QRS complex in leads V4 and V6. This negative deflection is a Q wave — and it is surprisingly wide for its tiny size, and followed by a notched (fragmented) r'rS wave in lead V6. In my experience, seeing surprisingly wide, successive Q waves in a series of chest leads (as we do in leads V4,V5,V6) — is a "tip-off" that the rhythm is almost certain to be VT.
• Returning to the limb leads in Figure-1 — there is extreme frontal plane axis deviation during this WCT (which we easily recognize by the finding of all negative QRS complexes in each of the inferior leads). This is another "tip-off" to 98+% likelihood that the rhythm is VT (barring the rare exception of a markedly distorted baseline tracing with identical morphology). 
• To Emphasize: The criterion of "extreme" frontal plane axis deviation during a WCT is not valid unless the QRS is entirely negative in either lead I or lead aVF. But especially given the initial slurred descent of the inferior lead QS complexes in Figure-1 — the "picture" that we see here is almost never seen with supraventricular rhythms.
• Is there relative “delay” in the initial QRS deflection? SVT rhythms tend to manifest more rapid initial depolarization vectors — because supraventricular depolarization generally begins its path toward the ventricles by travel over established conduction pathways. A notable exception to this generality is when there is an AP (accessory pathway) that bypasses the AV node (ie, in a patient with WPW). That said — “relative delay” in the initial portion of the QRS complex in multiple leads favors VT. And — in no lead in Figure-1 is there rapid initial depolarization of the QRS complex, thus one more feature pointing to VT. (Remember this criterion! — as we will apply momentarily when we take another look below at Figure-2).

But before moving on to Figure-2 — Consider this last criterion: Is there resemblance to any known form of conduction block?

• In ECG #1 — it might initially seem that the QRS complex in lead V1 resembles RBBB morphology. But does it? As highlighted within the dotted GREEN oval — QRS morphology in lead V1 is that of an rsR'R'' — or, a truly bizarre morphology not anything like the typical triphasic rSR' that characterizes RBBB conduction. And while patients with underlying heart disease often manifest variations on that typical triphasic scheme — this is a truly bizarre QRS morphology that we see in lead V1.
• If anything — the limb leads resemble lbbb conduction (and not rbbb conduction). Therefore — QRS morphology in Figure-1 does not come close to resembling any known form of conduction defect.

BOTTOM Line: I have reviewed the above features of ECG #1 in "slow motion". That said, with practice in applying these features — a conclusion of 98+% likelihood of VT should be arrived at for this tracing within seconds!

Figure-1: This is the 1st ECG shown by Dr. Meyers in today's case. How certain were YOU that this is VT?

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— ECG #2 and ECG #3 — (The first 2 ECGs recorded in Today's Case):

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I agree with Dr. Meyers that ECG #2 and ECG #3 (that I have reproduced in Figure-2) — most likely both represent supraventricular rhythms with LBBB-like morphology.

• That said — I also agree with Dr. Meyers that a definitive diagnosis of the specific type of SVT rhythm is difficult (if not impossible) to make on the sole basis of these 2 ECGs.

Again — the clinical history is helpful. While admittedly not certain of the specific etiology of ECG #2 ( = the 1st ECG recorded in the ED in today's case) — Several features immediately suggest a supraventricular etiology to me:

• The rate of the rhythm is fast (a bit over 120/minute) — but not as fast as the VT in Figure-1. We often need to begin treatment of our patient before we know for certain what the rhythm is. So, given that this patient presents with an acute infectious respiratory illness — IF she is hemodynamically stable, it would be reasonable to continue to treat her acute pulmonary illness as we look further at this ECG.
• Sinus P waves in lead V1 with tachycardia often manifest as subtle negative deflections. While admittedly not certain — I suspect that the vertical RED lines in lead V1 of ECG #2 represent sinus P waves.
• Clearly, baseline artifact in the limb leads prevents identification of atrial activity. That said — some extra "width" to the terminal T wave peak in lead II (RED arrow) could represent a hidden sinus P wave with similar PR interval as for the RED arrow I drew in lead V1. Admittedly — I am not at all certain about these suppositions from this difficult-to-interpret tracing — but I suspect (like Dr. Meyers) that ECG #2 represents sinus tachycardia.
• QRS morphology in ECG #2 is consistent with LBBB conduction (wide, all upright QRS in lateral leads I and aVL — with minimal positivity and very rapidly descending S waves in leads V1,V2,V3 — transitioning to predominant positivity by lead V6).
• And — there is a very narrow initial deflection of the QRS in leads V1-thru-V5 (within the dotted BLUE ovals in these leads). This is in marked contrast to the wide initial QRS deflections seen in Figure-1 with VT.
• BOTTOM Line: While I am in no way certain that ECG #1 represents sinus tach with LBBB accounting for QRS widening — as long as this patient was hemodynamically stable, I'd continue for the moment with treatment of her acute pulmonary condition.

What happens in ECG #3?

• The heart rate has significantly increased in ECG #3 (now ~150/minute). I no longer see the negative deflection that I had perceived as a probable sinus P wave in lead V1 of ECG #2.
• As per Dr. Meyers — at the rate of ~150/minute, we need to consider AFlutter with 2:1 AV conduction. But despite careful caliper review (Something impossible for providers at the bedside to do! ) — I can not get 2:1 atrial activity to march out, so I do not believe this is AFlutter. 
• On the contrary — vertical GREEN lines in the inferior leads suggest possible retrograde conduction — but I clearly would not be expecting sudden onset of a reentry SVT given the clinical situation.
• BUT — LBBB-like morphology persists (wide, upright QRS in lateral leads I,aVL — minimal positivity in anterior leads with very narrow initial upright deflections followed by steeply descending S waves — transitioning to predominant positivity by lead V6).
• BOTTOM Line: While I am again in no way certain — I agree with Dr. Meyers that ECG #3 most probably still represents a supraventricular rhythm. Clinically — this means that as long as the patient remains hemodynamically stable — We can continue with treatment of her acute pulmonary condition.

NOTE: At this point in the case, the VT rhythm shown in Figure-1 abruptly developed. This patient was apparently treated with Amiodarone — and some time thereafter, the rhythm shown in Figure-1 stopped.

• My Thought: Abrupt change in the rhythm from what we see in ECG #3 — to the virtually certain VT that we saw in Figure-1 would have prompted me to use synchronized cardioversion. 

Figure-2: The 2 ECGs shown above were recorded before the ECG shown in Figure-1. Did YOU think one or both of these ECGs were VT?

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— ECG #4 — (An ECG obtained later in this patient's hospital course):

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I wanted to review the final tracing in today's case — because I believe it resolves any doubt that may have existed about the etiology of ECG #1.

• As noted — ECG #4 was obtained later in this patient's hospital course. It shows ventricular bigeminy ( = sinus rhythm, with every-other-beat a PVC).
• We know with 100% certainty that all odd-numbered beats in Figure-3 are PVCs — because the subtle, variable distortion of the T wave of each PVC walks out perfectly for demonstrating an underlying regular sinus rhythm at ~80/minute (PINK arrows in the long lead II of Figure-3). This means that the wide, very different-looking QRS complex of beats #1,3,5,7,9,11,13 has to be coming from below the AV node ==> PVCs.
• A PEARL for retrospective confirmation of VT after conversion to sinus rhythm — is if you can demonstrate the same QRS morphology for post-conversion PVCs as was seen for the QRS during the WCT rhythm. While not all QRS complexes during ECG #1 are exactly the same — the all-negative QS complexes in each of the inferior leads with initial slurred descent of the S wave (within the dotted RED rectangles in ECG #4) look identical to QRS morphology in the inferior leads during ECG #1 — and QRS morphology in the other 9 leads looks close enough to confirm that ECG #1 was indeed VT.

Figure-3: Comparison of QRS morphology of the WCT rhythm in ECG #1 with the PVCs in the post-conversion tracing.

 

Pulmonary edema, with tachycardia and OMI on the ECG -- what is going on?

This was written by Hans Helseth.

A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chest pain and shortness of breath. She awoke in the morning with sharp chest pain which worsened throughout the morning. As her pain worsened, so did her dyspnea. She was found by paramedics with an oxygen saturation of 64%, but could not tolerate BiPAP during transport due to claustrophobia. She arrived to the ED with a nonrebreather mask. Her blood pressure on arrival was 153/69. An EKG was immediately recorded. The status of the patient’s chest pain at this time is unknown:

EKG 1, 1300:

There is sinus tachycardia and artifact of low and high frequency. The high frequency artifact may be caused by the patient shivering or tensing her muscles. A patient in acute distress may not be able to relax during the recording of their EKG, causing high frequency artifacts that give the waveform a fuzzy look. The low frequency artifact is caused by respiration which shifts the isoelectric baseline up and down with inspiration and expiration. It is best seen in V1 and V5 in this EKG. In fact, the patient’s respiratory rate can be calculated by measuring the time from peak to peak of the baseline in V5 at around 37 respirations per minute.

This EKG is also diagnostic of acute inferior OMI. There is tachycardia, but beneath the artifact, the ST segments in leads III and aVF are elevated, and the T waves are concave and terminally inverted, suggesting the possibility of reperfusion Leads I and aVL show ST depression with a terminally upright T wave, a morphology typically reciprocal to inferior ST elevation representing transmural ischemia of the inferior wall.

Smith: I would say this STE with T-wave inversion (suggesting reperfusion) is "between" active and reperfused inferior OMI, and with persistent symptoms or instability, it is active and acute until proven otherwise. There are no Q-waves to suggest old inferior MI, or inferior aneurysm as the etiology of the ST Elevation. However, there is also significant tachycardia, with heart rate of 116, and known hypoxia. Whenever there is tachycardia, I am skeptical of OMI unless it has led to severely compromised ejection fracction with cardiogenic shock. Or I suspect that there is OMI simultaneous with another pathology. We certainly know that there is hypoxia. I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. What other pathology is possible? Anything that causes pulmonary edema: poor LV function, fluid overload, previous heart failure (HFrEF or HFpEF), valvular disease. Summary: it is hard to say whether this ST Elevation was initiated by 1) something which led to pulmonary edema, then hypoxia, then supply-demand mismatch, or 2) whether ACS with OMI combined with some other pre-existing condition led to a decrease in LV function and pulmonary edema. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). See reference and discussion below. Also see these posts of Type II STEMI. Management?: stabilize the patient and repeat the ECG.

An EKG from a year prior was available for comparison:

The ED physician noted “Initial EKG here read by the computer as a STEMI, however, there is a very poor baseline and a lot of artifact. She was quite tremulous and short of breath when this EKG was obtained.”

Truly, the Marquette 12 SL algorithm correctly identifies this “STEMI”. Of course, the Queen of Hearts also recognizes it:

While this EKG did not convince the attending physician, a repeat EKG was obtained an hour later once the patient’s respiratory status improved:

EKG 2, 1415:

Now the ST elevation is decreased. The inferior leads have T wave inversion, consistent with reperfusion. There is still ST depression in leads I and aVL, and in the lateral leads.

Now the Marquette 12 SL algorithm does not identify “STEMI”, but the Queen of Hearts can see past the lack of ST elevation. She still calls this a “STEMI equivalent” in need of emergent reperfusion:

This version of the Queen of Hearts will call a reperfused OMI "OMI."  She does not distinguish.  PMCardio will correct that in the future.

The ED physician noted “Once her respiratory status improved, her EKG looks much improved with no evidence of STEMI”.

Two high sensitivity troponin T values returned:

1307- 138 ng/L

1511- 120 ng/L

A chest X-Ray showed pulmonary edema. A CT scan showed no PE but showed bilateral pleural effusions and aortitis. She was started on lasix. Cardiology services were consulted at a PCI capable hospital. They recommended transfer for admission, but did not recommend emergent angiography. The patient was started on heparin “for possible NSTEMI vs demand ischemia”.

More troponin values were measured at the cardiac center:

2327- 267 ng/L

0821- 355 ng/L

1108- 305 ng/L

An echocardiogram on day three of the patient’s admission showed an ejection fraction of 46% with abnormal basal inferior and basal lateral segments, and severe aortic stenosis. (Smith: "decompensation" of aortic stenosis might have initiated this entire cascade. What "initiates" the aortic stenosis cascade? --increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.)

The patient was finally weaned to room air on day 4 and taken for a CT scan to evaluate the possibility of aortic valve replacement. The scan showed a bicuspid aortic valve with severe stenosis and coronary artery disease. A lesion in the mid LAD was described as moderate, and a mid RCA stenosis was described as “probably severe”.

No more EKGs were recorded during the patient’s admission. The final impression was that the troponin elevation represented type 2 MI with a fixed RCA and LAD stenosis after the respiratory distress caused by acute pulmonary edema. The EKGs from the ED presentation were felt by cardiology to represent "subendocardial ischemia."

Smith: these ECGs do NOT show subendocardial ischemia. They show transmural injury (OMI). Now, it is conceivable to have ST Elevation due to type 2 MI (supply demand mismatch), but it is VERY unusual. I studied this over 10 years ago and published this abstract. In our data, only 4% of Type 2 MI had new ST Elevation. The vast majority of ischemia from supply demand mismatch is diffuse ST depression, with ST Elevation in aVR. The top ECG is diagnostic of thrombotic type 1 OMI until proven otherwise.

Case Continued

The patient was discharged from the hospital with a plan for a scheduled coronary angiogram to assess the coronary arteries and the possibility of aortic valve replacement.

A month later, she presented again to the emergency department with a few hours of chest pain that resolved before ED presentation. An EKG was recorded in the ED:

EKG 3, a month later:

This EKG represents reperfusion of the inferior wall with terminal T wave negativity. But there are new Q-waves, indicating intervening infarction -- uncertain when. There is still slight ST depression in leads I and aVL.

A troponin T resulted at 24 ng/L.

This EKG was interpreted as showing no signs of ischemia, the troponin was interpreted as having “improved from previous” (meaning improved from the 305 ng/L value a month prior) and the patient was no longer in pain. She was discharged again from the emergency department without a second EKG or troponin. 

Another week and a half later (about 6 weeks after her original presentation for chest pain and shortness of breath) the patient presented to the hospital for her scheduled angiogram:

There is total occlusion of the middle segment of the RCA (Picture A, annotated in D). The RAO views above show the LAD and LCx arteries (pictures B and C, annotated in pictures E and F respectively). The green line in picture F shows contrast filling the PDA, representing left to right collateral circulation.

The full key to the annotations made by Willy Frick on these cath images can be found in his great guide to coronary angiography.

The RCA lesion was treated as a CTO and not intervened upon. The angiographer also noted all other vessels to have "mild disease".

Smith: I'm confused as to why it was called "CTO" (chronic total occlusion) if just a month prior it was only "severe stenosis."

The patient was again sent home with a plan for surgical aortic valve replacement and coronary artery bypass grafting to the PDA. Two months later, she had her surgery, which was successful. An EKG was recorded after her surgery:

Since the baseline EKG at the beginning of the post, the Q waves in lead III have increased in size. There are also inferior and lateral T wave inversions, but this could be an effect of the surgery.

Learning points:

• While OMI rarely presents with tachycardia, inferior OMI complicated by another cardiopulmonary pathology like pulmonary edema and aortic stenosis can show tachycardia.
• Acute coronary occlusion and acute pulmonary edema can coexist. Pulmonary edema caused by acute MI is especially worrisome.
• Chest pain patients should not be discharged without serial troponin measurements, especially if their EKG shows T wave inversion. In a patient with OMI, the first troponin value may be low or normal.
• A low troponin value should not be compared with an elevated troponin value a month old.
• EKGs obscured by artifact should be promptly repeated in critical patients, especially if the provider feels that the artifact is impeding the interpretation of an EKG in a patient with new chest pain.

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MY Comment, by KEN GRAUER, MD (3/3/2025):

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Today's case reminds me of a selected number of cases I have had during my career in which the patient teaches the doctor. Fortunately, over the ensuing weeks after she was first seen — this patient survived despite a recurrence of her initial presentation. 

• The "good news" — is that this patient ultimately underwent successful surgical aortic valve replacement and coronary artery bypass grafting (albeit this wasn't until 3+ months after her initial presentation — with several providers not appreciating that rather than a "NSTEMI" or a "Type II MI", this patient's first ECG was clearly diagnostic of an acute coronary occlusion MI).
• For clarity in Figure-1 — I've reproduced and labeled that initial ECG. I focus my comments on assessment during that first hospital admission.

The Initial ECG in Today's CASE:

As per Hans Helseth — ECG #1 is diagnostic of acute inferior OMI.

• The history immediately places this patient at extremely high risk for OMI. She is older (69yo) — and she woke up with new chest pain that continually worsened throughout the morning. As a result — any potentially acute abnormality on ECG has to be taken as an acute OMI until proven otherwise.
• In addition — the patient was markedly dyspneic and tachypneic (RR >35/minute) — hypoxemic (O2 sat = 64%) — and tachycardic (~110-115/minute). This presentation clearly indicates more than simple ACS (Acute Coronary Syndrome).
• It is true that sinus tachycardia sometimes results in ST elevation from the tachycardia (with return to normal of ST segments once heart rate slows). That said — there is no mistaking the J-point elevation with ST segment coving in lead III and lead aVF (within the RED rectangles). Terminal T wave inversion in leads III and aVF (RED arrows) not only supports the legitimacy of ST elevation in these leads — but suggests that there may already be some element of spontaneous reperfusion (especially since by history, at least several hours have passed since onset of CP).
• Although true that there is much artifact on this initial tracing — this same obviously abnormal ST elevation is seen in all 7 complexes in leads III and aVF. This uniformity of ST elevation in every beat in these 2 leads does not happen if "artifact" is the cause.
• Any doubt about the legitimacy of this ST elevation in leads III and aVF should be instantly eliminated on seeing shelf-like reciprocal ST depression in all 7 complexes in high-lateral leads I and aVL.
• Further confirmation of the legitimacy of the diagnosis of acute OMI is forthcoming from lack of the normally expected, slight gently upsloping ST elevation in lead V2. Because of respiratory motion artifact (due to this patient's distress and tachypnea) — none of the 4 ST segments in lead V2 look the same. But the fact that all 4 of these ST segments lack the normal, slight gently upsloping ST elevation in lead V2 tells us this is a real effect indicative of associated posterior OMI (and not the result of artifact).
• I'll note that assessment of ST-T waves in lead V3 is more difficult to ascertain — but in the context of clear inferior OMI in the limb leads — lead V2 alone is diagnostic of associated posterior OMI.
• Perhaps part of the reason for the subtlety of ST-T wave changes in leads V2,V3 and the flattened ST-T wave in lead V1 — is that this patient with probable acute RCA occlusion may have associated RV involvement that attenuates the amount of ST depression usually expected with posterior OMI. Right-sided leads should be obtained.
• Finally — there is abnormal ST-T wave flattening in leads V4,V5,V6, as well as in lead II. I interpreted this ST-T wave flattening in these 4 leads as suggestive of multi-vessel coronary disease in the context of acute infero-postero OMI.

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

Respiratory Motion Artifact:

As per Hans Helseth — Today's ECG provides unique insight regarding how we know this patient's respiratory rate is so fast. Note the uniform 8.2 large box interval between the respiratory motion peaks that we see in beats #3,6,9,12,15 and 18.

• The easy way to determine heart rate is to divide 300 by the number of large boxes for the R-R interval — and, 300 ÷ 8.2 = 37 breaths/minute (as noted by Hans Helseth).
• PEARL: Obviously we do not need this insight in today's case, because we are told about this patient's dyspnea and tachypnea. But many of us are charged with overseeing the ECGs of patients that we do not have in front of us — and being able (with ECGs such as today's 1st tracing) to tell how very fast a patient is breathing could be a clue to how sick that patient is likely to be.

Insight's from Today's CASE:

• The artifact in today's initial ECG should not prevent a diagnosis of acute OMI in this older woman with sudden onset new, severe CP.
• If ever in doubt about the validity of ECG findings in a patient with new CP and artifact — Don't wait! Immediately repeat that ECG.
• When the patient presents with new, severe CP and is high risk for acute MI (as today's patient clearly was on this initial admission) — the initial ECG should be repeated within no more than 15-30 minutes.
• The diagnosis of acute OMI was confirmed in today's case in multiple ways (the abnormal initial ECG — evolutionary changes suggesting reperfusion on the repeat ECG — obvious ECG changes compared to the prior tracing from a year earlier — positive troponins — tachycardia, tachypnea, hypoxemia and pulmonary edema). Cardiac cath should have promptly been done.
• NOTE: When you don't cath the patient in a timely manner — then you will miss identifying the "culprit" artery a certain percentage of the time. When you wait 6 weeks after the event to do the cath (as was done in today's case) — then you will not know what things looked like 6 weeks earlier.

KEY Point: Today's patient had severe AS (Aortic Stenosis) complicating all of the above. From what we are told — the severity of her AS was not known prior to her initial hospitalization, especially given her apparent history of hypertension. And, especially in a patient with acute pulmonary edema — a bedside diagnosis of severe AS may be extremely difficult to pick up on auscultation. But at least on Day #3 — Echo did identify severe AS.

• Severe AS markedly complicates management and portends poorer longterm outcome when associated with acute MI (Abraham et al — Cath Cardiovasc Interv 102(1): 159-165, 2023 — Paquin et al — Open Heart 9(1):e002046, 2022 ).
• Critical AS complicates hemodynamics of the coronary circulation — including hemodynamics of collateral flow (Wiegerinck et al — Circ: Cardiovasc Interven 8(8): e002443, 2015). 
• 
  
• Looking at the case (admittedly in retrospect, and in the comfort of my desk chair) — One has to wonder about the time until cath was done, and about the time until surgery.