Wednesday, August 7, 2019

A young woman with altered mental status and hypotension

Written by Pendell Meyers

I texted this Prehospital ECG with no clinical information to Dr. Smith.

What do you think?

Dr. Smith texted back "Pulmonary Embolism" within seconds.

Here is the clinical information:

A woman in her 30s with no known past medical history presented by ambulance for altered mental status and syncope. She was delirious, ill-appearing, hypotensive, tachycardic, afebrile, satting 99% on 2L/min masal cannula.

Sinus tachycardia
Acute RV strain pattern evidenced by the morphology of the QRS and T-wave in V1-V3, including small-moderate R-wave followed by deep S-wave, then concave ST segment into whole T-wave inversion. The fact that lead V3 does not have a deep S-wave like the other examples you will find in the link below is simply due to it being the transition lead in this case, where the QRS progresses from mostly negative to mostly positive. There is TWI in lead III as well, completing the "inferior and anterior T-wave inversion" characteristic sometimes seen in acute right heart strain.

See this post for many side-by-side examples of this exact morphology

Based on this ECG we had high suspicion of PE.

We performed bedside echo which showed a large RV, with "D sign" of the RV impinging on the LV septum. The IVC was plethoric with minimal respiratory variation. We looked at the legs briefly and were unable to find an obvious DVT.

Here is the initial ED ECG:
This is much less convincing, as only V1-V2 still have the morphology described above. This could be due to lead placement, but it is not possible to say for sure.

Despite the fact that the initial ED ECG was not as convincing of acute right heart strain, the EMS ECG was nearly diagnostic and we proceeded with massive PE as our working diagnosis, despite the absence of any hypoxia.

She was hypotensive requiring 5-10 mcg/min of norepinephrine prior to CT scan.

She was quite altered, so we elected not to begin anticoagulation before obtaining head CT scan to exclude intracranial hemorrhage as a cause of her altered mental status (her mental status did not improve significantly despite her mean arterial pressure being raised to 65-70 mmg Hg with norepinephrine).

We rushed her to CT scan which revealed no intracranial hemorrhage and bilateral mainstem pulmonary emboli.

We diagnosed massive PE and gave alteplase. There are many different ways to give alteplase in this scenario, but we elected to give 10 mg over 2 minutes, followed by 10 mg over the next 10 minutes, followed by 80 mg over the next 2 hours (total dose 100 mg).

Over the next hour, her vitals normalized and pressors were discontinued. Her mental status returned to normal as her vitals normalized.

We discovered that her sister also had a massive PE last week! Her formal DVT ultrasound showed nonocclusive DVT throughout her left leg. She had a recent flight to Italy.

We started heparin drip several hours after alteplase was given.

Her formal echo hours later could only detect "mild RV strain" at that time.

She was admitted to the ICU.

Hypercoagulability workup has thus far been unrevealing.

Case 2

Here are 2 ECGs recorded from one patient with pulmonary embolism just this week.  The patient had sudden chest pain and SOB:
Notice again the T-wave inversion in V1-V3 AND lead III.
The T-wave inversion is domed, which is different from Wellens'
This ECG is deceptive because there is no tachycardia, which is unusual in a patient who is not on beta blockers

Here is a followup ECG:

The patient had an initial troponin of 0.100 ng/mL, which could easily have been mistaken for acute coronary syndrome, but a D dimer was measured and was 2000.  CTPA confirmed pulmonary emboli.  The patient was NOT on a beta blocker.

Learning Points:

Learn the morphology of acute right heart strain vs. Wellens' T-wave inversions here:
See this post for many examples.

Use point of care ultrasound to confirm ECG findings of PE, OMI, etc.


  1. excellent , Pendell. thank you.

    when I first saw the ecg, I wondered if this might be Arrythmogenic right ventricular cardiomyopathy with the deep T waves anteriorly, and what I thought was an epsilon wave in V1.

    but of course I was wrong. but then I wondered : is the effect similar; i.e., a stressed, "ill" , unhappy right ventricle (stretched, strained , ischemic in the case of a pulmonary embolus. diseased myocardium in the right ventricle in ARVC.
    and is that why the pattern of the ECG's are similar in these two very different diseases.
    or am i completely off base?



  2. Is long QT part of this typical ST change pattern?

    1. I would guess, but have no data.

    2. I also realize a long QT in EKG. I thought that was a cause of syncope. But I was wrong.


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