I received this ECG from someone who wishes to remain anonymous.
“Last night we had a Stage 4 Lymphoma Cancer Patient presenting with this ECG above. Wife advised that he just woke up from a nap and was being assisted on a walk when he became dizzy and had a syncopal episode. Patient was A&O when EMS arrived. Patient seemed confused. Patient had shortness of breath when EMS got to him. Initial vitals as follows:”
“Patient was cool to touch and dry, Lung sounds clear.”
“Patient denied any other complaint other than SOB. SpO2 improved to 97% on 15lpm on a non rebreather.”
“The ECG notes sinus Tach with RBBB and LPFB. What was throwing me off was the ST Elevation in aVR and lead III with the depression in the lateral leads. Is this rate related or possible occlusion?”
|What do you think?
I read this on my phone and responded:
“This is a classic fake-out.”
“All of what appears to be ST elevation and ST depression is really part of the QRS, which is very wide.”
“Take another close look.”
“This is probably a pulmonary embolism.”
Had I not been on the run and looking on my phone, I would have said: “This is almost certainly a pulmonary embolism.”
Clinical: In a cancer patient with sudden SOB with clear lungs, low saturations, increased respiratory rate, sinus tachycardia, and low end tidal CO2, the top 3 diagnoses on the differential are pulmonary embolism.
ECG: There is sinus tachycardia at a rate of 138, with RBBB. There is right axis deviation which may be LPFB. If you realize that the QRS is 140 ms, then you realize that what appears to be ST elevation in leads III and aVR, and reciprocal ST depression in leads I and aVL, is really just part of the QRS. The only ST segment shift is in leads V2 and V3, in which ST depression discordant to the positive R’-wave is normal. Thus this ECG shows no convincing ischemia.
This ECG is classic for acute PE.
If the ECG did show subendocardial ischemia (diffuse ST depression), I would still say that pulmonary embolism is the most likely diagnosis: tachycardia and hypoxia can lead to myocardial ischemia.
Even if the ECG showed ischemic ST elevation, pulmonary embolism would be high on the differential. Acute MI only causes hypoxia by resulting in pulmonary edema. Clinically, there were clear lungs, and thus no evidence of pulmonary edema. On the other hand, acute PE can cause such severe ischemia that there is ST elevation.
Follow up came the next day:
Found out that the guy passed away later that evening from a pulmonary embolism.
Comment by KEN GRAUER, MD (7/26/2018):
Insightful case by Dr. Smith, to which I will add the following points:
- As per Dr. Smith — the clinical presentation should strongly suggest Acute PE (Pulmonary Embolism) until proven otherwise. The concern by the anonymous contributor of this case was the question about possible ST elevation in leads III and aVR with possible reciprocal ST depression in lateral leads. The KEY to assessment lies with use of simultaneously-obtained leads. Although ideally there would also be a simultaneously-obtained long lead II rhythm strip underneath the 12-lead tracing — we can still clarify the question about QRS width vs ST segment deviation, by starting with the anterior leads (V1, V2, V3), in which we can clearly see the limits of the QRS complex (Figure-1).
|Figure-1: Use of simultaneously-obtained leads to determine QRS width — and the presence (or absence) of ST segment deviations. For clarity, we have enlarged leads V1, V2, V3 (See text).
Although significant angulation and folding of the tracing in Figure-1 is present — I have done my best to draw in RED lines that are parallel to heavy ECG grid lines in each of the 12-leads. I’ve placed these RED lines at what I believe represents the beginning and end of the QRS complex in each of the 12 leads.
- Assessment of QRS width is best accomplished in leads V1, V2, V3 — and suggests the QRS is at least 0.13 second in duration. As per Dr. Smith — knowing the width of the QRS (from V1,V2,V3) — tells us the width of the QRS in the remaining 9 leads.
- It is always insightful to see how some leads (especially lead aVF in this tracing!) look deceptively narrow — because part of the QRS lies on the baseline.
- The RED lines I have drawn in apply this principle in all leads — and clearly demonstrate Dr. Smith’s point that there is NO ST elevation in leads III and aVR — and no reciprocal ST depression in leads I and aVL.
My “Take” on this case was that while this ECG is certainly consistent with acute PE — of itself, it is not diagnostic. Sinus tachycardia and RBBB are clearly common ECG findings with acute PE — but they are not specific for this diagnosis. Without availability of a prior tracing — we have no idea if the RBBB is new or old. Assessing for an S1Q3T3 pattern is problematic when there is RBBB, which by definition produces a wide terminal S wave in lead I.
- PEARL: There is suggestion of abnormal anterior ST depression. While with RBBB, the rSR’ (or other RBBB-equivalent pattern) in lead V1 is expected to be accompanied by ST-T wave depression in this lead — the amount of J-point ST depression should not increase as one moves from lead V1-to V2-to V3 if this ST-T wave depression is solely the result of the RBBB. A look at the RED arrows in Figure-1 clearly shows the opposite is occurring — namely, that the relative amount of J-point ST depression is increasing as we move from V1-to V2-to V3 — which strongly suggests something other than RBBB as the cause. Abnormal anterior ST depression provides one more point in support of our strong clinical impression that acute PE is the cause of this patient’s symptoms.
COMMENT: In my experience, the concept of using simultaneously-obtained leads remains underused, if not at times completely ignored. This case provides a wonderful illustration of how this concept quickly resolved the question about whether or not there was ST elevation with reciprocal ST depression in the limb leads in Figure-1. And, as I note above — if the only lead being monitored was aVF — one would mistakenly conclude that the QRS is narrow.
- Many is the time during hospital teaching rounds that I would be asked to interpret a problematic rhythm strip from a single monitoring lead. My standard reply was to ask for the patient’s chart in search of a recent 12-lead ECG — that very often would immediately clarify questions about QRS width, atrial activity and QRS morphology that were not answerable from the single lead monitoring strip. Regular use of simultaneously-obtained leads is a concept worth remembering.