Monday, June 17, 2024

Another deadly triage ECG missed, and the waiting patient leaves before being seen. What is this nearly pathognomonic ECG?

Written by Bobby Nicholson, MD

67 year old male with history of hypertension and hyperlipidemia presented to the Emergency Department via ambulance with midsternal nonradiating chest pain and dyspnea on exertion. Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage.

What do you think?

If this EKG were handed to you to screen from triage without any clinical information, what would you think?  (for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context)

The ECG was read simply as "No STEMI." Unfortunately, there was a long wait and the patient left before being seen by a provider. However his EKG was overread as "abnormal" the following day and he was asked to return to the Emergency Department for evaluation.

Upon presenting to the Emergency Department the next day, the patient reported chest pain for approximately 10 days with associated shortness of breath and diaphoresis. He also reported an episode of syncope which occurred earlier in the morning.

VS on arrival: HR 95, BP 131/83, RR 14, SpO2 98%, Temp 36.7 C

Examination notable for diaphoresis, 1+ bilateral lower extremity edema, regular heart rate and rhythm, and no signs of respiratory distress with normal breath sounds.

EKG obtained on arrival to the Emergency Department:

Has your differential diagnosis changed since the original presentation?

Labs obtained and notable for an elevated troponin I to 0.10 ng/mL, BNP 2790, and lactate 3.7. Repeat troponin I obtained ~5h after the first results as 0.14 ng/mL.

While waiting in the Emergency Department, the patient attempted to ambulate to the restroom and developed recurrence of his chest tightness which was associated with shortness of breath and diaphoresis after walking approximately 10-15 feet.

Do you appreciate any dynamic changes compared to the patient’s prior EKG?

Given his exertional chest pain and elevated troponin, the patient was admitted to the hospital for "NSTEMI" with a plan for left heart catheterization the next day. He was started on a heparin drip and CTA of the chest was ordered to rule out pulmonary embolism.

Upon admission, CTA of the chest revealed pulmonary emboli with large clot burden extending from the main pulmonary artery to the lobar, segmental, and subsegmental arteries affecting all 5 lobes with infrahepatic contrast reflux and evidence of heart strain.

Echocardiogram showed severe RV dilation with McConnell’s sign and an elevated RVSP. The patient was upgraded to the ICU for closer monitoring.

This is a case like many others posted (see list below) and the EKG from the patient’s original presentation can be quickly recognized as diagnostic for pulmonary embolism. In fact, Kosuge et al. showed that among patients with either acute coronary syndrome or acute pulmonary embolism and negative T waves in the precordial leads (V1-V4), that inverted T waves in leads III and V1 were present in only 1% of patients with acute coronary syndrome and 88% of patients with pulmonary embolism. “The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of APE were 88%, 99%, 97%, and 95%, respectively.”

1. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect. Accessed May 28, 2024.

Smith comments

The ECG at the top was texted to me and, without clinical info, I said "It looks like PE."  It is nearly pathognomonic for PE.  Why?  There is T-wave inversion in V1-V4 AND T-wave inversion in lead III (see above).  Moreover, the T-wave inversion morphology in V1-V3 is typical of PE.  One characteristic of that morphology is this, in V1-V3: a small R-wave and relatively deep S-wave.   

See this very instructive post:

A crashing patient with an abnormal ECG that you must recognize

More PE ECGs with that typical morphology from the above post:
Contrast with Wellens' T-wave inversions below [Both Pattern A, biphasic terminal T-wave inversion in panels A and B, and Pattern B, deep symmetric in panel C).  There are well preserved R-waves in Wellens waves.

Pendell: See our other acute right heart strain / pulmonary embolism cases:

A man in his 50s with shortness of breath

A man in his 40s with RUQ abdominal pain

A woman in her 50s with shortness of breath

A crashing patient with an abnormal ECG that you must recognize

A man in his 40s with a highly specific ECG

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something with 8 hours of chest pain and an elevated troponin

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

What do you suspect from this ECG in this 40-something with SOB and Chest pain?

Reproduced from a prior post:

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 


MY Comment, by KEN GRAUER, MD (6/17/2024):

Today's case by Drs. Nicholson and Meyers provides an important reminder of a potentially life-threatening entity that still gets overlooked — namely, acute PE (Pulmonary Embolism).
  • We've come a long way since the days of my residency training — in which hypoxemia on ABGs (Arterial Blood Gases) served as a KEY test for initial suggestion of acute PE (albeit pain-induced hyperventilation induced by this bedside procedure often obscured results).
  • In 2024 — once the diagnosis of acute is contemplated, point of care Echo and/or CTPA (Computed Tomography Pulmonary Angiography) enable expedited confirmation. 

  • That said — as shown again by today's case, the diagnosis must be thought of. And, as is also shown again by today's case — recognition of the ECG signs of acute PE often provide a KEY clue to massive (and often submassive) acute PE — IF we are listening ...

An Often Forgotten Clinical NOTE:
Initial assessment of the patient for possible acute PE begins by counting the respiratory rate. During my decades of working with residents when hospital Attending — by far, the most commonly overlooked vital sign was respiratory rate. 
  • KEY Point: The respiratory rate that is written on the chart does not count! I cannot tell you how many times such "written" documentation was off, due to the tendency to inscribe a normal number instead of counting for 30 seconds because "the patient looked like they were breathing normally".
  • Patients may "look" like they are breathing normally — when in fact they are tachypneic if you simply take the time to watch them and count. All it takes is a few seconds of concentration for you to determine how fast the patient is breathing. And IF the patient's respiratory rate is increased and their initial ECG looks like the initial ECG in today's case — You have made the diagnosis of acute PE until proven otherwise!
  • The RR (Respiratory Rate) in today's case is recorded as 14/minute at the time the patient presented to the ED on the day after their initial presentation. I maintain that this written RR may or may not be accurate. The only way to know for certain would be for YOU to count.
  • No RR was noted on the 1st day that the patient was seen at triage. Given the appearance of the initial ECG in today's case (which was recorded at that first triage visit) — this represents an opportunity lost ...

Today's Initial ECG:
As per Drs. Nicholson and Meyers — Given the history of this 67-year old man with chest pain and shortness of breath over the days prior to presenting to the ED — this patient's initial ECG (that I've reproduced and labeled in Figure-1) — is diagnostic of acute PE until proven otherwise.
  • Drs. Nicholson and Meyers provide numerous links at the end of their discussion to insightful related cases of acute PE that we've presented in Dr. Smith's ECG Blog. I refer to My Comment in the March 4, 2023 post — in which I included a Table with ECG Findings of Acute PE. I have amended this Table to the one that I show below in Figure-2 — with a note that emphasizes the key clinical point highlighted in their Primer on the ECG in PE.
  • As per their Primer — When T waves are inverted in precordial leads — IF they are also inverted in leads III and V1 — then acute PE is far more likely than ACS.

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

Today's initial ECG shows the following:
  • Sinus rhythm at ~85/minute.
  • Normal intervals and axis — although the S wave in lead I is deeper than is usually seen in this left-sided lead. I thought this was a subtle harbinger of the increasing right axis deviation that evolved over the next 2 tracings in today's case.
  • No chamber enlargement.
  • Slightly delayed transition — with the R wave becoming taller than the S wave is deep between leads V4-to-V5 (with the taller, then shorter R wave in lead V2 compared to V3 probably the result of slight chest electrode lead misplacement).
  • Another subtle sign of PE is persistence of precordial S waves that are seen through to lead V6 (YELLOW arrows in Figure-1 — with there typically not being S waves this far over in lateral chest leads).

  • KEY ECG Findings in Figure-1 that suggest acute PE until proven other are: i) S1Q3T3; — ii) Deep, symmetric T wave inversion in leads V1-thru-V4 (BLUE arrows in these leads = RV "strain"); — iii) In the presence of chest lead T wave inversion — there is prominent T wave inversion in both lead V1 and in lead III; — andiv) Not only do we see RV "strain" in the chest leads — but the T wave inversion in leads III and aVF suggest RV "strain" also in the limb leads.

  • To Emphasize: We do not see all of the ECG signs of acute PE in today's case. Most of the time — we will not see all of these ECG indicators that I list in Figure-2 (and which I discussed in My Comment in the March 4, 2023 post). That said — the pattern of T wave inversion in ECG #1 that is absolutely diagnostic of acute RV "strain", in association with the clinical history — makes the diagnosis in today's case until proven otherwise.

Figure-2: ECG Findings associated with acute PE.

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