Wednesday, November 30, 2022

Upon arrival to the emergency department, a senior emergency physician looked at the ECG and said "Nothing too exciting."

This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. 

This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chest pain. The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. 

A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chest pain. On medic arrival, she walked out of the house in no distress, but was diaphoretic. She described intermittent chest discomfort for a week, and went to the clinic one day prior where a 12-lead was recorded and reportedly "normal." Today's pain felt similar to previous episodes of "Reflux;" it radiated to her neck and jaw.

VS were: BP 188/72, HR 88 and 99% SPO2 on room air.

Our first 12 lead ECG was then recorded at 0926.

What do you think?

Here is Spencer's interpretation:

is a sinus rhythm with narrow QRS complexes and a normal axis. V1 has 0.5 mm of ST segment elevation, V2 and V3 have 1 mm of elevation, v4 has 2 mm of elevation and v5 around 1.5 mm of elevation. More notably there are hyperacute T waves in V3 through V5. These T waves are too large in proportion to their QRS complexes with broad bases, and they are symmetric or nearly symmetric in appearance.

There is also T wave inversion In aVL with a very small amount of ST segment depression. The T waves in the inferior leads appear to be turning hyperacute with broad bases and proportionally large size in comparison to their QRS complexes. The inferior T waves also appear to have a quick take off from the J point with a near symmetrical appearance.

These findings are suggestive of Occlusion of a wraparound LAD.

Smith: I would be more emphatic. These findings are diagnostic of an apical OMI as a result of LAD Occlusion.

Another ECG was recorded 5 minutes later just before arrival at the hospital:


The patient was transported to a nearby suburban hospital with PCI capabilities while my partner cared for her.

Upon arrival to the emergency department, a senior emergency physician looked at the ECG and said "Nothing too exciting."

Then she began complaining of severe dizziness and quickly went into ventricular fibrillation and resuscitation was initiated by hospital staff. She was defibrillated and resuscitated.

It is apparently fortunate that she had a cardiac arrest; otherwise, her ECG would have been ignored.

Smith: this ECG and clinical presentation is diagnostic of LAD Occlusion. I need to innoculate you against the subsequent opinions below. by making it clear to everyone that this is NOT an EKG that one sees with takotsubo cardiomyopathy. It is also NOT the clinical scenario of takotsubo (a week of intermittent chest pain). Takotsubo is a sudden event, not one with crescendo angina. An apical OMI has the same ultrasound findings as takotsubo, and thus mimics takotsubo.

Hospital Course

The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy.

Here is the cath report:

There is severe hypokinesis of entire LV apex and apical segment of all the walls.  
EF is 30-35%

The high sensitivity troponin I peaked at 9,324 ng/L 
(approximately equivalent to 9.32 ng/mL by 4th generation and older assays.)

This is important because troponin I elevations in takotsubo are not that high.  In a recent article (J Electrocardiol this year, see reference below), peak troponin I levels in takotsubo presenting with ST Elevation were median 1.02 ng/mL [IQR: 0.46, 2.35].  

Note 1: Levels were significantly lower in takotsubo that presented with T-wave inversion.
Note 2: This article fails to specify whether it was troponin I or T, but I contacted the institution and they used exclusively troponin I during that time period.

Reference on Troponins: Xenogiannis I, Vemmou E, Nikolakopoulos I, et al. The impact of ST-segment elevation on the prognosis of patients with Takotsubo cardiomyopathy. J Electrocardiol [Internet] 2022;Available from:

Cardiology opinion: 
Takotsubo Cardiomyopathy (EF 30-35%)
V Fib Cardiac arrest
Prolonged QTC
NSTEMI (Smith comment: is it NSTEMI or is it Takotsubo?  -- these are entirely different)
Moderate single-vessel CAD.

Then they did an MRI:

Patient underwent cardiac MRI on 10/4 that showed mildly reduced BiV systolic function. LVEF 51% and RVEF 49% with severe hypokinesis of distal septal, distal anterior, apical and distal inferior segments.  

Noted increased myocardial and pericardial fluid content. Delayed enhancement reveals small, subendocardial scar in the distal septal, apical and distal inferior segments consistent with scar in the LAD distribution. Findings consistent with infarct in LAD distribution (likely recent). 

Just to add more evidence, here is the post reperfusion ECG:
There is terminal T-wave inversion (identical to Wellens' Pattern A).
Although one sees diffuse symmetric T-wave inversion develop in takotsubo, with a long QT, one does NOT see Wellens' pattern A in takotsubo.

I could have told you this (and did tell you this) without an MRI.  This entire case is not consistent with takotsubo.  Just because you don't see hemodynamically significant CAD on angiogram does not mean it is not OMI.  To prove there is no plaque rupture, you need to do intravascular ultrasound (IVUS).  An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!  It can only be seen by IVUS.

Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries).  MINOCA has many etiologies. One of the most common is rupture of a non-obstructive plaque, with thrombus formation and OMI that spontaneously lyses and leaves a wide open artery.  We can tell from the history and ECG that this case is MINOCA that was a result of transient LAD Occlusion with thrombus that subsequently lysed.  One need not have obstructive coronary disease to have occlusive thrombus!  In fact, the majority of acute MI occur in coronary arteries that do not have hemodynamically significant stenoses (see New England Journal Review below)

Here is a quote from a review article in NEJM:

Pathogenesis of Acute Coronary Syndromes

Findings from clinical and pathological studies have challenged these commonly held notions of the pathophysiological features of coronary atherosclerosis and its treatment.1-4 Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Angiographic monitoring of responses to thrombolytic therapy has shown that after lysis of the offending thrombus, the underlying stenosis is often not the cause of the critical stenosis of the artery. In a prospective angiographic study involving patients undergoing percutaneous intervention for coronary artery disease, only half the subsequent events arose from lesions with sufficient stenosis to have warranted intervention at the time of revascularization.5 Computed tomographic (CT) angiography, which permits evaluation of the arterial wall (not just the lumen), has shown that the characteristics of plaque associated with acute coronary syndromes include low attenuation (i.e., little or no calcification) and outward expansion of the artery wall, a process that tends to accommodate the growth of plaque while minimizing luminal encroachment.6-8 Intravascular ultrasonography has shown that in acute coronary syndromes, the culprits often lie proximal to the sites of maximal stenosis — the traditional targets of revascularization therapies.9 This dissociation between the degree of stenosis and the propensity to provoke an acute coronary syndrome helps to explain why myocardial infarction often occurs without being heralded by the demand-induced symptoms of angina that would result from a high-grade stenosis.

Learning Points:
1. Learn to Recognize Hyperacute T-waves
2. Many paramedics are far better than any physician (Emergency or Cardiology) at diagnosing OM
3. Do not let your consultants diagnose takotsubo when it is clearly OMI.

I do not have the bandwidth here to write a review of MINOCA.

But a few items: 

The definition of MINOCA is predicated on the patient fulfilling all three main diagnostic criteria, namely: 
1) the Universal Definition of Acute MI (which requires ischemia); 
2) the presence of non-obstructive coronary artery on angiography (defined as no coronary artery stenosis ≥50%) in any potential infarct-related artery; and 
3) the absence of another specific, clinically overt cause for the acute presentation. 

MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli, and coronary dissection; myocardial disorders, including myocarditis, takotsubo cardiomyopathy, and other cardiomyopathies.

We know that most type 1 acute MI due to plaque rupture and thrombosis occurs in lesions that are less than 50% (see Libby reference).  This is in spite of the known proclivity of tighter stenoses to thrombose.  The reason for this is population-based: there are many more moderate stenoses out in the population than there are tight stenoses, and so more MIs are generated from these moderate ones.  

Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event.  However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram.  Coronary thrombosis with complete lysis is clearly possible, but its contribution to MINOCA is really not known because adequate investigation is rarely undertaken.  The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram.

Furthermore, the clinical presentation of sudden chest pain, typical ECG findings of occlusion (hyperacute T-waves in this case), ECG findings in a coronary distribution, rise and fall of troponin with peak in the typical range for STEMI/OMI, and new wall motion abnormality in the area indicated by the ECG, must be considered to be due to coronary thrombosis.   The degree of stenosis is not a great predictor of thrombosis, and culprits may not be visible.  Even if there is a tight stenosis, it is not proof of culprit, as many individuals have tight fixed stenoses at baseline.  There may be a chronic tight stenosis and a non-obstructed lesion that thrombosed.  

Contemporary research studies of MINOCA have evaluated the prognosis of these patients, reporting a 12-month all-cause mortality of 4.7% (95% confidence interval, 2.6–6.9),3 with comparative studies consistently demonstrating a better prognosis than for those who experience AMI associated with obstructive coronary artery disease.

Lindahl et al. associated typical Myocardial Infarction therapies such as statins and ACE inhibitors with significantly decreased 1 year mortality in MINOCA patients, which suggests that they do indeed have a similar pathophysiology to MI patients with obstructive coronary disease.

From UpToDate:

Acute thrombosis at the site of non-obstructive eccentric plaque thrombosis — Many atherosclerotic plaques expand outward rather than encroaching on the arterial lumen. These ”positively-remodelled” plaques are often lipid rich and have a thin fibrous cap; they are vulnerable to rupture into the lumen [1,9,10]. Transient and partial thrombosis at the site of a non-obstructive plaque with subsequent spontaneous fibrinolysis and distal embolization may be one of the mechanisms responsible for the occurrence of MINOCA. Similarly, coronary erosion with loss of surface endothelium, possibly due to hyaluronan and neutrophil accumulation, can also cause MINOCA [1,11]. (See "Mechanisms of acute coronary syndromes related to atherosclerosis".)

The reason for these cases to be labeled as MINOCA is that angiography is of limited utility for the purpose of elucidating plaque-related thrombosis as a cause of thrombosis due to its low resolution as well as the fact that it does not interrogate the lumen of the vessel. Thus, intracoronary imaging modalities are crucial in this setting. Plaque rupture or erosion has been diagnosed by intravascular ultrasound in about 40 percent of women with MINOCA [12]. Optical coherence tomography, due to its high resolution, may provide additional information [10,13].

As MINOCA is associated with a risk of recurrent cardiovascular events over time, comparable with that of patients with acute coronary syndromes (ACS) and obstructive atherosclerosis [5,14,15], these patients require dual antiplatelet treatment for 12 months and statins. In particular, long-term lipid-lowering therapy with statins after MI is associated with a significant increase of the fibrous-cap thickness, paralleling the reduction of the lipid content of the plaque [16]. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

From Gue at al.


STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. In patients presenting with non-ST-segment elevation MI (NSTEMI), the infarct is subendocardial. This pathophysiological difference also seems to be present within the MINOCA cohort. Registry data indicate that 6–11% of patients with acute MI have nonobstructive coronary arteries.  Within the literature, MINOCA tends to present more commonly as NSTEMI than STEMI: the incidence of MINOCA reported in patients presenting with NSTEMI is about 8–10% and in STEMI cohorts it is 2.8–4.4%. This has resulted in an under-representation of STEMI MINOCA patients in the literature. Most studies examine undifferentiated ACS cohorts, with only a handful providing separate data. These studies indicate that the 1-year mortality of MINOCA presenting as STEMI is 4.5%, in contrast to the mortality of unselected MINOCA ACS patients who have a mortality of 4.7%. The underlying aetiology of MINOCA is similar among those presenting with STEMI and in all-comer MINOCA patients with ACS, with non-coronary aetiology responsible for presentation in 60–70% of individuals with STEMI and in 76% of unselected ACS patients. 


1.  Lindahl B, Baron T, Erlinge D, et al. Medical Therapy for Secondary Prevention and Long-Term Outcome in Patients With Myocardial Infarction With Nonobstructive Coronary Artery Disease. Circulation [Internet] 2017;135(16):1481–9. Available from:

2. Pasupathy S, Tavella R, Beltrame JF. Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA): The Past, Present, and Future Management [Internet]. Circulation. 2017;135(16):1490–3. Available from:

3. Gue YX, Kanji R, Gati S, Gorog DA. MI with Non-obstructive Coronary Artery Presenting with STEMI: A Review of Incidence, Aetiology, Assessment and Treatment. Eur Cardiol [Internet] 2020;15:e20. Available from:

4. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med [Internet] 2013;368(21):2004–13. Available from:

My Comment by KEN GRAUER, MD (11/30/2022):
Today's case is one to remember — as it shatters previous misconceptions regarding the patient who despite non-occlusive disease on cath — may nevertheless have just completed having an extensive acute infarction. As per the brilliant discussion above by Dr. Smith — all-too-many clinicians remain unaware of this possibility. 
  • My focus today is on brief additional commentary regarding the ECGs in this case — and — some thoughts about MINOCA (MI with Non-Obstructive Coronary Arteries).

The ECGs in Today's Case:
Superb interpretation by Spencer Schwartz of the initial ECG in today's case! ( = ECG #1 in Figure-1). To this — I would add the following points.
  • Even more leads than were mentioned show acute changes in today's case! While this point is not essential for initial management (ie, Spencer emphasized his suspicion for acute OMI — with need for transport to a facility with PCI capability) — there are plenty of cases in which recognition of how many leads actually show acute changes is important for accurate diagnosis.
  • As per Spencer — the most notable changes in ECG #1 — are the hyperacute ST-T waves in anterior leads V3-thru-V5.

  • Regarding the chest leads: By the concept of "neighboring leads" — the T waves in leads V2 and V6 are also hyperacute. By this I mean that in isolation — the T waves in leads V2 and V6 might not seem abnormal. But both of these leads do show a T wave that is "fatter"-at-its-peak and wider-at-its-base than it should be — so in the context of obviously hyperacute ST-T waves in leads V3-V5 — I interpreted the range of acute ST-T wave changes as encompassing leads V2-thru-V6.

  • In addition — the deep and wide Q waves in leads V1,V2 (with no more than the tiniest of initial r wave in lead V3) — suggests significant myocardial injury has already occurred in the anterior myocardium.

  • Regarding the limb leads: More than just "turning" hyperacute — the ST-T waves in each of the inferior leads are hyperacute for the very reasons that Spencer mentions ( = these inferior T waves are too large in proportion to their QRS complexes — with broad bases) — as well as also being "fatter"-than-they-should-be at their peak. My point being simply that while I might not be certain from the inferior lead ST-T wave appearance alone that there are acute changes — I know that there are acute inferior lead changes in the context of the obviously hyperacute chest lead changes (supported as per Spencer — by reciprocal T wave inversion in lead aVL).

  • Spencer correctly identified key abnormalities while expediting transport to a PCI-capable facility. But as per Dr. Smith — it is worth emphasizing that in a patient who presents with new chest pain (as in today's case) — the findings in ECG #1 are truly diagnostic of acute LAD OMI until you prove otherwise
  • To Emphasize: The reason definitive diagnosis is important in today's case — is that the senior ED physician interpreted ECG #1 as "nothing too exciting". It is essential to impress upon that physician that we are not dealing with a "maybe" — but rather with an ECG that provides definitive diagnosis of acute LAD OMI in need of immediate cath until proven otherwise.

  • Beyond-The-Core: As discussed in the November 13, 2022 post by Emre Aslanger in Dr. Smith's ECG Blog — ST elevation in both anterior and inferior leads does not necessarily indicate an LAD "wraparound" lesion, as used to be thought (Bozbeyoğlu, Yildirimtürk, Aslanger et al — Anatol J Cardiol 21:253-8, 2019).

The Post-Reperfusion ECG:
Today's case illustrates the confusion that may arise in diagnosis of acute chest pain patients who do not manifest coronary occlusion (or a likely "culprit" artery) at the time of acute cath.
  • As per Dr. Smith — the cardiology opinion following evaluative testing on today's patient was contradictory — because "NSTEMI" is a very different entity from Takotsubo Cardiomyopathy.

  • PEARL #1: As we have often emphasized on Dr. Smith's ECG Blog — Because of the common (albeit still not well appreciated) phenomenon of spontaneous reperfusion of the "culprit" coronary artery (which may sometimes reopen and reocclude multiple times) — more than a single ECG is often needed to identify a recent OMI that shows a relatively normal initial tracing as a result of the "pseudonormalization" that may be seen when acute chest pain resolves because the "culprit" artery has spontaneously reperfused. In order to fully appreciate the sequence of events — serial timed ECGs that are all correlated to serial timed troponin assays and chest pain severity scores may be needed.

  • As per Dr. Smith — the post-reperfusion ECG seen in Figure-1 is not consistent with the expected findings of Takotsubo Cardiomyopathy(For review of ECG findings expected with Takotsubo Cardiomyopathy — Please see My Comment at the bottom of the page in the March 25, 2020 post in Dr. Smith's ECG Blog). Instead — We see typical reperfusion T waves in the diffuse distribution of what was hyperacute ST-T wave changes on the initial tracing.
  • The "good news" — is that anterior R wave progression has improved since the initial tracing (ie, There are now definite initial R waves in leads V2 and V3 of ECG #3 — without loss of R wave amplitude in other leads)

Figure-1: Comparison of the initial ECG in today's case — with the post-reperfusion ECG(To improve visualization — I've digitized the original ECG using PMcardio).

The Unappreciated Entity of MINOCA:
Dr. Smith reviews the all-too-often ignored entity known as MINOCA. For clarity in Figure-2 — I've adapted the Table from the article by Sykes et al that reviews the diagnostic entities to consider in the patient with an acute MI despite non-obstructive coronary arteries.
  • As per Dr. Smith — Perhaps the most common etiology of MINOCA is plaque rupture with thrombus formation and OMI that spontaneously lyses, resulting in a patent "culprit" artery at the time of cardiac catheterization.

  • Putting Today's Case Together: The history of intermittent chest discomfort over the course of 1 week — together with the initial and post-reperfusion ECG findings — is most consistent with acute apical OMI. This impression was confirmed on cardiac MRI.

  • PEARL #2: The fact that the initial ECG in today's case showed hyperacute changes in at least 9 leads in the infero-antero-lateral distribution is consistent with acute apical OMI. As per Dr. Smith — it's important to appreciate that Echo findings of an extensive apical OMI may mimic those of Takotsubo Cardiomyopathy!

  • PEARL #3: The importance of Figure-2 — is that it highlights the need to open ourselves to a series of diagnostic entities when confronted with a patient showing positive troponins and an ECG suggestive of acute MI despite the finding of non-obstructive coronary disease on cath.

Figure-2: Classification of Underlying Diagnoses in Patients with MINOCA (Adapted from Table-1 in Sykes et al: Interventional Cardiology Review: 16:e10, 2021)NOTE: As per Sykes et al — The entities listed under "Other Etiology" may be diagnosed following further investigation and should be considered separately (because they are typically associated with myocardial injury but not considered an MI by the 4th universal definition of MI). This is an important indication for cardiac MRI in patients suspected of MINOCA.

Monday, November 28, 2022

A woman in her 20s with syncope

Written by Destiny Folk MD, with edits by Meyers, peer reviewed by Smith and Grauer

A woman in her late 20s with a past medical history of cervical cancer status post chemotherapy and radiation therapy presented to the emergency department for shortness of breath, chest tightness, and two episodes of syncope.

Her initial vital signs revealed a temp of 97.7F, HR 125, RR 20, BP 115/90, and an oxygen saturation of 95% on room air. Upon arrival, she did not appear in acute distress. She was noted to be tachycardic and her heart sounds were distant on physical exam. She had a normal respiratory effort, and her lungs were clear to auscultation bilaterally.

Given her reported chest pain, shortness of breath, and syncope, an ECG was quickly obtained:
What do you think?

The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). The beat-to-beat variation in QRS amplitude and morphology is electrical alternans.

A bedside cardiac ultrasound was performed with a parasternal long axis view demonstrated below:

There is a large pericardial effusion with collapse of the right ventricle during systole. It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia. However, if you freeze the ultrasound clip and scroll forwards and backwards to find a time during the clip where the patient’s mitral valve is open, you know the heart is filling, and is therefore in diastole.

Still image with blue arrow indicating the right ventricular collapse during diastole

This photo shows the heart in diastole and at the arrow you can see caving in of the right ventricle. Some say this looks like someone jumping on a trampoline. Diastolic collapse of the right ventricle is one of the defining features of cardiac tamponade. To diagnose pericardial tamponade, you need to have a pericardial effusion (the size of the effusion doesn’t necessarily matter) + right atrial diastolic collapse OR right ventricular diastolic collapse. Right atrial diastolic collapse is the earliest sign, but the patient needs to have right atrial collapse for at least 1/3 of the cardiac cycle which can be difficult to identify with ultrasound. So, we usually diagnose tamponade with right ventricular diastolic collapse.

This patient’s pericardial effusion may likely be subacute given the size and echogenicity of the effusion (new blood is anechoic and this looks more isoechoic).

Given her tachycardia and episodes of syncope, the patient was judged to be in compensated obstructive shock with very high risk of imminent decompensation. Cardiology emergently came down to see the patient and took her immediately to the cath lab for a pericardiocentesis (if the cardiologist and cath lab had not been immediately available, then the EM team would have needed to perform pericardiocentesis). A pericardiocentesis was performed by the subxiphoid approach with fluoroscopy. 780 cc of bloody fluid was removed from the pericardial cavity. For reference, a normal heart has about 25-50 cc in the pericardial space. Fluid samples were sent for culture and cytology and results showed malignant cells. A repeat POCUS showed resolution of her pericardial effusion. She was discharged after a short hospitalization with oncology and cardiology follow-up.

As emergency physicians, we see various etiologies of pericardial effusions. The table below shows common causes of tamponade in medical patients. Approximately 40% of tamponade cases in medical patients are due to metastatic malignancy. The second most common cause of medical cardiac tamponade is acute idiopathic pericarditis. Less common etiologies include uremia, bacterial or tubercular pericarditis, chronic idiopathic pericarditis, hemorrhage, and other causes such as autoimmune diseases, radiation, myxedema, etc.

The classic presentation of pericardial tamponade is Beck’s Triad which is hypotension, JVD, and muffled heart sounds. Pericardial tamponade is also associated with pulsus paradoxus which is an abnormally large drop in systolic blood pressure greater than 10 mmHg during inspiration. Beck’s triad only happens all 3 together in approximately 1/3rd of patients. This patient was reported to have distant heart sounds but was not hypotensive and did not have JVD according to documentation.

Smith comment: First, IV fluids are indicated to improve preload.  Even in tamponade, one can improve RV output and LV filling with an IV fluid bolus -- it increases filling pressures and thus filling volumes.   At our hospital, I think all of our docs would want to place a pigtail catheter in the ED, under ultrasound guidance and not wait for cardiology to take the patient to the cath lab.  This patient is only pseudo-stable.  She has already had syncope.  Her pulse is 125.  See how unstable these patients can be by reading this: 
A young woman in her early 20s with syncope

My colleague, Denise Fraga MD, summarizes the sonographic features of cardiac tamponade:

Sonographic tamponade features

IVC plethoric (greater than 2cm with less than 50% variation with respiration) (caveat: IVC might not be dilated in hypovolemic patient)

Respiratory change in MV inflow velocity greater than 30% and TV inflow velocity greater than 60% (seen on AP4 view using PWD) (caveat: not specific for tamponade when COPD, A fib, acute RV failure present)

Pericardial effusion

Collapse/inversion of RA chamber (late diastole/early systole. seen on AP4 or SX view) = high sens, low spec

Collapse/inversion of RA greater than 1/3 of cardiac cycle (increases specificity)

Early diastolic inversion of RV free wall (can use M-mode in PSLA or PSSA to see this) = most specific. High Spec, Lower sensitivity (caveat: elevated RV pressure w/ pHTN, severe TR can prevent RV inversion)


Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, Hung J, Garcia MJ, Kronzon I, Oh JK, Rodriguez ER, Schaff HV, Schoenhagen P, Tan CD, White RD. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr. 2013 Sep;26(9):965-1012.e15. doi: 10.1016/j.echo.2013.06.023. PMID: 23998693. 

Appleton C, Gillam L, Koulogiannis K. Cardiac Tamponade. Cardiol Clin. 2017 Nov;35(4):525-537. doi: 10.1016/j.ccl.2017.07.006. PMID: 29025544.

Learning Points

Echocardiographically, pericardial tamponade features a pericardial effusion + right ventricular diastolic collapse.

The beat-to-beat variation in the QRS complexes (electrical alternans) is a classic ECG finding of a large pericardial effusion or pericardial tamponade.

Beck’s Triad is only seen in approximately 1/3rd of patients with pericardial tamponade but consists of hypotension, JVD, and muffled heart sounds.

Comment by KEN GRAUER, MD (11/28/2022):
Today's case is remarkable for the presence of 2 important ECG findings: i) Low Voltage; and, ii) Electrical Alternans. As per Drs. Meyers and Folk — this unfortunate young woman with cervical cancer presented to the ED with syncope, chest tightness and acute dyspnea.
  • For clarity in Figure-1 — I've reproduced her initial ECG.

Figure-1: The initial ECG in today's case.

MY Thoughts on the ECG in Figure-1:
The rhythm in ECG #1 — is sinus tachycardia at ~125/minute. The QRS complex is narrow in all 12 leads. Further assessment of ECG findings is challenging — because the baseline wanders, and every-other-beat shows a changing QRS morphology.
  • This is not a bigeminal rhythm in the usual sense — because both the PR interval and R-R interval remain constant throughout the tracing. There are no premature beats. Instead (as per Drs. Meyers and Folk) — this is electrical alternans!
  • Note that the frontal plane axis shifts with each beat (ie, from being isoelectric in lead I — to being markedly negative in this lead).
  • In lead V1 — every-other-beat shows a tiny QRS with an incomplete RBBB pattern.
  • Overall QRS amplitude is markedly reduced — especially every-other-beat. Thus, there is diffuse low voltage.
  • There appears to be some ST elevation in leads II and aVF, as well as to a lesser extent in the lateral chest leads.

  • IMPRESSION: The overall appearance of this ECG is not suggestive of either acute PE or an acute cardiac event. Instead — the KEY for determining the etiology of ECG findings in Figure-1 rests with the history and the diagnostic Echo (that confirms a large pericardial effusion).

We have reviewed many of the causes of low voltage on ECG in previous posts of Dr. Smith's ECG Blog. The differential diagnosis for "low voltage" that is most frequently put forth by many providers tends to begin-and-end with pericardial effusion. But a look at Figure-2 reminds us that there is a long list of additional entities to consider!
  • The above said — The history in today's case, in association with the dramatic appearance of electrical alternans (with beat-to-beat shift in the baseline over the course of the long lead rhythm strip in Figure-1) — immediately points to a large pericardial effusion as the most likely cause.

Figure-2: Causes of Low Voltage on ECG (Figure reproduced from My Comment at the bottom of the page in the November 12, 2020 post in Dr. Smith's ECG Blog).


The fascinating phenomenon of electrical alternans — is a relatively uncommon clinical entity that is frequently misunderstood. It is often overlooked when it does occur. A look at Figure-3 explains why: This ECG sign can be subtle indeed.
  • Electrical alternans is a general term that encompasses a number of different pathophysiologic mechanisms. Its occurrence is not limited to pericardial tamponade — but instead has been associated with an expanding array of clinical conditions. 
  • Distinction should be made between electrical and mechanical alternans. The term "alternans" itself — merely indicates that there is phasic fluctuation in some cardiac signal from one beat to the next within the cardiac cycle. This may be in the strength of the pulse (or the blood pressure recorded) — or it may be in one or more waveforms in the ECG recording.

NOTE: It may be helpful to first define other alternans phenomena that may sometimes be confused with the various ECG manifestations (especially since these other forms of alternans phenomena may also be seen with cardiac tamponade).
  • Pulsus alternans — is a mechanical form of alternans. The rhythm is regular — but cardiac output varies from beat-to-beat. It is seen with severe systolic dysfunction. Pulsus alternans should be distinguished from a bigeminal pulse — in which a weaker beat follows the stronger beat by a shorter time interval (as occurs when the alternating beat is a PVC, which understandably generates less cardiac output).
  • Pulsus alternans should also be distinguished from pulsus paradoxus — in which there is a palpable decrease in pulse amplitude (or a measured drop of >10 mm in blood pressure) during quiet inspiration. While pulsus alternans and paradoxus may both be seen with pericardial tamponade — they are different phenomena than the various types of electrical alternans.

Regarding FIGURE-3:
Electrical alternans is easy to recognize when the alternating difference in QRST complexes is obvious — as it is when looked for within the 3 RED rectangles in Figure-3
  • That said — Did YOU also See the much more subtle beat-to-beat variation in R wave amplitude in the long lead II rhythm strip in Figure-3

  • While not definitive (See below) — the finding of electrical alternans in an SVT rhythm strongly suggests reentry as the mechanism.

Figure-3: I’ve enclosed within a RED rectangle the 3 leads in this tracing in which there is clear evidence of electrical alternans. (Figure reproduced from My Comment at the bottom of the page in the September 7, 2020 post in Dr. Smith's ECG Blog).

Electrical Alternans: Definition/Features/Mechanisms
Electrical alternans — is a beat-to-beat variation in any one or more parts of the ECG recording. It may occur with every-other-beat — or with some other recurring ratio (3:1; 4:1; etc.). Amplitude or direction of the P wave, QRS complex, ST segment and/or T wave may all be affected (although P wave alternans is rare). Alternating interval duration (of PR, QRS or QT intervals) may also be seen.
  • Electrical alternans — was first observed in the laboratory by Herring in 1909. It was reported clinically by Sir Thomas Lewis a year later, who characterized the phenomena as occurring, “either when the heart muscle is normal but the heart rate is very fast or when there is serious heart disease and the rate is normal”. This 1910 description by Lewis serves well to this day to remind us of the 2 principal clinical situations in which electrical alternans is most often encountered: i) Supraventricular reentry tachycardias; and ii) Pericardial tamponade.

  • Returning to Figure-1: The principal variation that we see in this tracing relates to a repetitive pattern of alternate beat change in QRS morphology. Interval duration does not vary. There may be slight variation in some leads in P wave and ST-T wave morphology — but I thought this to be minimal compared to the much more obvious change in QRS morphology.

There are 3 basic types of electrical alternans phenomena — each relating to a different pathophysiologic mechanism: i) Repolarization alternans; ii) Conduction and Refractoriness alternans; and, iii) Alternans due to abnormal cardiac motion. A common cellular mechanism may underlie each of these processes relating to abnormal calcium release or reuptake within the sarcoplasmic reticulum.
  • Repolarization Alternans  entails beat-to-beat variation in the ST segment and/or T wave. Alternation in ST segment appearance (or in the amount of ST elevation or depression) — is often linked to ischemia. In contrast — T wave alternation is more often associated with changes in heart rate or in QT duration (especially when the QT is prolonged). In patients with a long QT — T wave alternans may forebode impending Torsades de Pointes. Both ST segment and T wave alternans have been known to precede malignant ventricular arrhythmias. Thus, this type of electrical alternans may convey important adverse prognostic implications when seen in certain situations. That said — a variety of clinical conditions have been associated with repolarization alternans, such that adverse prognostic implications do not always follow. Among these clinical conditions are congenital long QT syndrome — severe electrolyte disturbance (hypocalcemia; hypokalemia; hypomagnesemia) — alcoholic or hypertrophic cardiomyopathy — acute pulmonary embolus — subarachnoid hemorrhage — cardiac arrest and the post-resuscitation period — and various forms of ischemia (spontaneous or induced by treadmill testing or other stimulus).
  • Conduction and Refractoriness Alternans  entails variance of impulse propagation along some part of the conduction system. This may result from fluctuations in heart rate or in nervous system activity or from pharmacologic treatment. ECG manifestations from this form of alternans may include alternating appearance of the P waveQRS complex or alternating difference in P-R or R-R interval duration. In particular — QRS alternans during narrow SVT rhythms has been associated with reentry tachycardias. While identification of QRS alternans during a regular SVT often indicates retrograde conduction over an AP (Accessory Pathway) — this phenomenon has also been seen in patients with simple PSVT/AVNRT that exclusively limits its reentry pathway to the AV Node. Therefore — identification of QRS alternans during a regular SVT does not prove the existence of an accessory pathway. Conduction and refractoriness alternans may be seen with WPW-related as well as AV Nodal-dependent reentry tachycardias — atrial fibrillation — acute pulmonary embolus — myocardial contusion — and severe LV dysfunction. NOTE: On occasion — Alternans may be seen with monomorphic VT (Maury and Metzger).
  • Cardiac Motion Alternans  is the result of cardiac movement rather than electrical alternation. The most important clinical entity associated with motion alternans is large pericardial effusion — though motion alternans has also been observed in some cases of hypertrophic cardiomyopathy. It is important to appreciate that not all pericardial effusions produce electrical alternans. Development of total electrical alternans (of P wave, QRS complex and T wave) — is likely to be a harbinger of impending tamponade. Unfortunately — the sensitivity of total electrical alternans is poor for predicting tamponade (ie, most patients who develop tamponade do not manifest preceding electrical alternans). Therefore — it may be helpful if you see total electrical alternans in a patient with a large pericardial effusion — but failure to see this ECG sign in no way rules out the possibility that tamponade is occurring. Echo studies in patients with documented cardiac tamponade confirm that electrical alternans is synchronous with and a direct result of the pendulous movement of the heart within the enlarged, fluid-filled pericardial sac of a patient with large pericardial effusion.

Electrical Alternans: KEY Clinical Points
In summary, electrical alternans is not common — but it does occur. You will see it — as evidenced by the unfortunate patient in today's case. 
  • In practice — It appears that electrical alternans is most often seen in association with regular SVT rhythms (as seen in Figure-3). Seeing it in this context suggests (but does not prove) the existence of an AP (Accessory Pathway). Regardless of whether the mechanism of the regular SVT is AVNRT or AVRT — it is likely that reentry is involved. This conclusion may prove useful in contemplating potential investigative and therapeutic interventions.
  • In a patient with pericarditis — OR — a large heart on chest X-ray — OR — simply unexplained dyspnea (as in today's case) — recognition of electrical alternans should suggest the possibility of a significant pericardial effusion that may be associated with tamponade. 
  • The above said — Electrical alternans is a nonspecific ECG sign that may also indicate myocardial ischemia, LV dysfunction and/or possibility of any of a number of other precipitating factors. BOTTOM Line: If you see electrical alternans — Look for an underlying clinical condition that may be responsible for this ECG sign. 
  • Development of electrical alternans per se — conveys no adverse prognostic implications beyond those associated with severity of the underlying disorder. Two exceptions to this general rule are: i) In a patient with QT prolongation or severe ischemia — recognition of electrical alternans may portend deterioration to Torsades or VT/VFib; and, ii) In a patient with a large pericardial effusion — development of total electrical alternans (of P wave, QRS complex and T wave) suggests there may now be tamponade.

  • FINAL Thought: Keep in mind that not all cases of pericardial effusion will manifest low voltage and electric alternans. The pathophysiology behind electrical alternans with a large pericardial effusion — is a "swinging heart" within the pericardial sac. Thus, alternans is unlikely to be seen with smaller effusions — and even with larger effusions, not all cases manifest alternans. 

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