Wednesday, September 12, 2018

Comatose after opiate overdose, with tachycardia and hypotension

I was texted this ECG with the info that a female patient in her 20s was found down with probable opiate overdose:
What do you think?















Here was my response: "It looks like a pulmonary embolism EKG.  But if she was hypoxic for a variety of reasons, that could result in pulmonary hypoxic vasoconstriction, with resulting elevated pulmonary artery pressure and right heart strain on the EKG, mimicking PE."

Why did I say that?  There is sinus tachycardia with T-wave inversions in V1-V3 and in lead III (also with an S1Q3T3, which is a less specific finding).  This is a classic ECG for right heart strain.

Here is the whole story:

A young woman was not waking up the morning after reportedly encountering drugs with her boyfriend.  When paramedics arrived, she was unresponsive, with agonal breathing.  Initial BP was in the 70s.  2 mg of naloxone was administered without improvement in level of consciousness.

On arrival she was unresponsive.  Pulse was 137 and BP was variable with systolics from 50-117 and diastolics from 32 to 77.  SpO2 on oxygen was 100%.

She was intubated.

A POCUS of the heart was done:


This shows a dilated right ventricle and a small, empty, and hyperdynamic left ventricle.  This is typical of pulmonary embolism.  There was also a reportedly flat IVC, indicating volume depletion (if this is PE, the IVC should be dilated unless there is profound volume depletion).

It seems that the interpreters mostly saw the good LVF and volume depletion, but not the large RV, and they gave IV fluids.

Sats were 100% after intubation.  BP rose to 140/80 after fluids.  She was taken to head CT which was negative.

There was a lactic acidosis, WBC count of 18,000, and Creatinine of 3.5.

A troponin I, which is automatically ordered on critical cases, returned at 7.979 ng/mL (very high).  A repeat 12-lead was unchanged.

An ED Transesophageal echo (TEE), which we do on most intubated patients in shock (and all in cardiac arrest), was done:



Orientation: The probe is directly behind the left atrium.
The left ventricle is on the right.
The right atrium is upper left.
The RV is at the bottom of the image.
Interpretation:  This again shows a hyperdynamic LV and enlarged RV.  Note also the small left atrium.

Bedside lower extremity venous ultrasound showed no DVT.  This was confirmed with a radiology ultrasound.  Thus, PE was not definitively diagnosed.

Therefore, in spite of elevated Cr, a CT pulmonary angiogram was done and showed with filling defect in the distal right main pulmonary artery extending into the segmental pulmonary arteries of the right lower lobe and right upper lobe. There is associated right heart strain. Probable small infarct associated with a subsegmental embolism in the posterior right lower lobe.  

The patient was put on heparin.  She recovered.


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Comment by KEN GRAUER, MD (9/12/2018):
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Great read by Dr. Smith on this ECG, taken from a woman in her 20s, who was found down with an opiate overdose. Insightful illustration of how associated point-of-care Echos can be so helpful (!) — showing key findings of Acute PE in this case. I limit my comments to the ECG.
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  • Dr. Smith instantly recognized a number of ECG findings on the ECG in this case that suggest “Acute PE until proven otherwise!” He notes sinus tachycardia and, symmetric T wave inversion in lead III, and in the anterior leads — which when combined with the clinical setting clearly suggest acute right heart strain.
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QUESTIONS:
  • There are several additional ECG findings consistent with the diagnosis of acute RV strain. What are they?
  • Technically — Is there an S1Q3T3? Clinically — Does the answer to this question matter?
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ANSWERS:
  • Acute RV “strain” may be seen in 2 lead areas on ECG. These are the anterior leads (ie, V1, V2, V3— and, the inferior leads (leads II, III, aVF). It is not always seen in both of these lead areas — but when it is, in the “right” clinical setting — the likelihood of acute PE increases dramatically. Although less marked than the fairly deep T wave inversion that we see here in lead III — there also is ST-T wave depression in both leads II and aVF.
  • There is an IRBBB (incomplete RBBB) pattern — in the form of an rSr’ in V1 that occurs in association with narrow terminal s waves in leads I and V6. Both complete and incomplete RBBB are potential indicators of acute RV strain.
  • Although not meeting the ECG definition of IRBBB — I have always interpreted a clear rSR’ pattern in lead III (as we see hereas an IRBBB “equivalent”, with similar clinical implications as IRBBB. So, in this case — I assess the rSR’ in lead III as providing further support of acute RV strain.
  • Technically then, we don’t have an S1Q3T3 pattern in this ECG — because there is no Q wave in lead III. Instead, there is a small-but-definitely-present initial positive deflection (r wave) in this lead. That said — there are so many other ECG findings pointing to the diagnosis of acute RV strain, that lack of an S1Q3T3 pattern is irrelevant to our assessment.
  • There is suggestion of RAA (Right Atrial Abnormality— even though strict ECG criteria (ie, P wave amplitude in an inferior lead of ≥2.5mm) are not met. That’s because the P wave in lead II is abnormally peaked (pointed) — and, because we also see a pointed (albeit small) P wave in lead V2. It is unusual for either of these findings to be seen in a normal ECG. I’ll emphasize that as isolated findings — I would not call RAA. But in the context of everything else that we see on this tracing — the most logical reason for a much-more-pointed-than-usual P wave in both leads II and V2 is RAA in a patient with acute RV strain.
  • Finally — there is marked ST elevation in lead aVR. A very limited number of conditions produce ST elevation that is most marked in lead aVR — but minimal or nonexistent elsewhere (except perhaps in V1). One of these conditions is acute PE (ie, another manifestation of acute RV strain).
FINAL Thought: The ECG diagnosis of RVH is often challenging. That’s because there is no one single finding that is diagnostic. Instead, a combination of findings is generally needed. So it is with the ECG diagnosis of acute PE. No single finding is diagnostic — but rather a combination of findings occurring in the “right clinical context” is needed to suggest the diagnosis. Our thanks to Dr. Smith for this case — which superbly illustrates application of these principles.
  • NOTE: For those wanting review of the ECG findings of RVH, and how to use this information to suspect acute PE — CLICK HERE).



2 comments:

  1. As always a very informative and enlightening case on this blog. My question is about the QT interval in the first ECG . Isn't the QT prolonged ??

    ReplyDelete
    Replies
    1. I measure a QT of 280 ms, with RR interval of 420 ms. Using Fridericia (the best correction method), that gives a QT of 353 which is, in fact, short.

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