"Anterior" ST Depression: Which Lesion is the Culprit?

Written by Hans Helseth

Hans is an EKG tech who is applying to medical school. EKG interpretation skills have little to do with one's level of education. In fact, much of what passes for EKG education can actually harm one's interpretation skills.

A 62 year old man with hyperlipidemia presented to a rural emergency department with 7 hours of 3/10 chest pain. Here is his triage EKG:

With ST depression maximal in V2-V4 and resolved by V5-V6, this is diagnostic of posterior OMI, as shown by Meyers et al. (https://www.ahajournals.org/doi/10.1161/JAHA.121.022866)

_________

Smith: Although many writers state that the tall R-wave is essential to the diagnosis of posterior OMI, that is a false statement: we showed in the above study that the R-wave is irrelevant. A large R-wave is analogous to a Q-wave and only shows that the infarct has progressed to involve a large territory. ACUTE posterior OMI does not have a large R-wave. (We also showed that an upright T-wave is not required, and that many have a negative or biphasic T-wave). The pain has been present for 7 hours, which corresponds to a long duration of infarction and the presence of "Q" waves (in this case tall R-waves)

_________

With inferior ST depression and possible ST segment straightening in aVL there is also suggestion of high lateral involvement, meaning the likely culprit artery is the left circumflex or one of its branches.

Here is the QoH interpretation:

The ED provider described the T waves in V2 and V3 as “hyperacute”. It is not clear by her note what she meant by this (whether or not she recognized this EKG as diagnostic of transmural ischemia, and if so, of what territory) but emergent reperfusion therapy was not pursued.

At 1022, a troponin I (ref range <0.034 ng/mL) resulted at 4.437 ng/mL. This was the only troponin measured during this case. The patient was diagnosed with NSTEMI and placed on a heparin drip.

[Smith: this high initial troponin confirms that this is a subacute OMI and that one should expect Q-waves (tall R-waves)].

Another EKG was recorded after almost two hours. The status of the patient’s pain at this time is unknown:

It remains mostly unchanged. 

At 1210, the case was discussed with a cardiologist at a PCI capable facility, who accepted the patient for transfer, noting the ST depression in anterior leads as “consistent with ischemia” but “not a STEMI”. The patient arrived to the ED of the PCI facility where this EKG was recorded:

The ST depressions have almost completely resolved, which suggests reperfusion of the posterior wall, although again, the patient’s pain status at this time is unknown.

At 1547 the patient was taken for angiography:

The cath report by the interventionist describes:

• 80% Ostial LAD (green arrows)

• 95% Mid LAD (blue arrows)

• 100% First Obtuse Marginal (red arrows)

Some may prefer to call the occluded vessel the second obtuse marginal, as a small branch with the same course can be seen originating proximally to it (see Terminology and Semantics of Willy Frick’s cardiac cath guide).

Based on the EKGs, which lesion is most likely the culprit?

In this case, the interventionist called the mid LAD lesion the likely culprit. The proximal and mid LAD stenoses were stented and the OM 2 was left alone. It is unclear by the note whether or not the OM lesion was interpreted as CTO, but it was not touched.

An EKG was recorded after cath:

The ST depression has worsened. There is no restoration of flow through the likely true culprit lesion in the second obtuse marginal, so the EKG continues to show transmural ischemia of the posterior and high lateral walls.

Another EKG was recorded the day after PCI:

The ST depression has worsened further. There is still no restoration of flow past the lesion.

An Echo performed the day after PCI showed an EF of 51% and hypokinesis in the mid posterior, mid lateral, and basal lateral segments. This distribution of wall motion abnormality is more consistent with a culprit in the obtuse marginal rather than the mid LAD. Had more troponins been measured, it is likely they would have continued to climb as the patient’s artery remained occluded.

The patient was discharged the day after PCI. There is no follow up.

It is still widely believed that ST depression localized to a certain territory on the EKG is indicative of subendocardial ischemia of that territory. In this case, it is possible that the physicians interpreted the ST depression in anterior leads as subendocardial ischemia of the anterior wall, and the mid LAD stenosis as the culprit of that ischemia.

Subendocardial ischemia does not localize. It manifests with an ST elevation vector towards lead aVR, causing ST depression maximal in apical leads (II, V5-V6). See this exemplified many times on this blog. Localized ST depression, as in this case, is indicative of transmural ischemia of the opposite territory. Anterior ST depression = posterior ST elevation. 

This was likely a case of wrong-vessel PCI. This is surprisingly common. Heitner et al found that in 14% of patients with NSTEMI, a blinded interventional cardiologist interpreting coronary angiograms identified a different culprit artery than CMR (https://www.ahajournals.org/doi/10.1161/CIRCINTERVENTIONS.118.007305). This is a case which demonstrates the importance of OMI findings on the EKG in the job of the interventionist. 

Learning Points:

• ST depression maximal in V1-V4 is posterior OMI, not anterior ischemia, not subendocardial ischemia

• This should have undergone emergent angiograph and PCI of the correct vessel

• Wrong-vessel PCI is not uncommon in “NSTEMI”

• Serial troponins and EKGs can be a useful tool for confirming the success of PCI.

Smith: here is a post with many ECGs which compares and contrasts the ST depression of posterior OMI from that of deWinter's T-waves:

De Winter's T-waves are Not a Stable ECG condition. Upright T-waves in Posterior OMI are Distinct from de Winter's waves.

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MY Comment, by KEN GRAUER, MD (3/10/2025):

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I wrote the following in My Comment in the September 21, 2020 post of Dr. Smith's ECG Blog: 

"I wish those cardiologists who continue to strictly adhere to STEMI millimeter criteria would read Dr. Smith’s ECG Blog. IF they don’t — they will continue to overlook obvious OMIs that deserve to undergo prompt cardiac catheterization for optimal care." 

5 years later (now in 2025) — the problem remains.

• The posterior wall of the LV is not directly viewed by any of the 12 leads on a standard ECG. As a result — ST elevation will not be seen in any of the standard 12 leads in an isolated posterior OMI.
• Posterior leads (ie, leads V7, V8, V9) — have been suggested as a way to enhance ECG visualization of the posterior wall. With acute posterior MI — these posterior leads will sometimes manifest ST elevation not seen on the standard 12 leads.
• That said, as we have often emphasized in Dr. Smith's ECG Blog — the amount of ST elevation you are likely to see with posterior leads in acute posterior MI is limited. As a result, the diagnostic utility of posterior leads is limited (See My Comment in the September 21, 2022 post).
• Most of the time when there is acute posterior OMI — there will be associated acute inferior and/or lateral MI. But when the OMI is isolated to the posterior wall — there simply won't be any ST elevation in any of the standard leads.

Among the problems in today's case were the following:

• Cardiac cath was delayed for nearly 6 hours — because none of the ECGs that were done showed ST elevation. 
• Meanwhile — acute coronary occlusion causing an isolated posterior OMI was not recognized by several providers, including the consulting cardiologist. This, despite the diagnostic initial ECG that was done at the time the patient first arrivd in the ED.
• The initial Troponin came back markedly elevated — but because there was no ST elevation, the infarction was labeled a NSTEMI. This outdated (useless) term ignores the clinical reality that many acute coronary occlusions do not manifest ST elevation.
• And, because the concept that acute coronary occlusion causing isolated posterior OMI is readily recognized by ST depression that is maximal in leads V2,V3,V4 — when cath was finally done, it was performed on the wrong coronary artery (whereas ECG recognition of isolated posterior OMI on the initial ECG immediately pointed to the LCx system as the "culprit" artery — as is shown below in Figure-3).

As I lamented in 2020 — Rather than taking the extra time to obtain another ECG with posterior leads (that at best — provides limited information) — I favor GETTING GOOD at using the Mirror Test as an aid for recognizing acute posterior MI.

• The Mirror Test is a simple visual aid: It helps the clinician recognize acute posterior infarction. It is based on the premise that the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the “mirror-image” of leads V1, V2, V3 (See Figure-2 below).
• I’ve previously discussed application of the Mirror Test on many occasions (in My Comment at the bottom of the September 13, 2020 post and the February 16, 2019 post, among others).
• In Figure-1 — I apply the Mirror Test to leads V2,V3 in today's initial ECG. As shown in the mirror-image RED insert — Isn't it now obvious that there is acute coronary occlusion causing isolated posterior OMI?

Figure-1: Application of the Mirror Test to leads V2,V3 in today's initial ECG.

Figure-2: Illustration of the rational for the Mirror Test (Figure excerpted from Grauer K: ECG-2014 Pocket Brain ePub).

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In Figure-3 — We see the rationale for anatomic localization of the "culprit" artery to either a non-dominant LCx or an Obtuse Marginal branch of the LCx — when there is isolated posterior OMI.

Figure-3: KEY points in the recognition of isolated posterior MI (adapted from my ECG-2014-ePub — with addition of Figure from Vince DiGiulio).

 

 

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.