This case was contributed by Vince DiGiulio.
A 63 year old woman who was otherwise healthy had a syncopal episode. She had no CP, no SOB, but did have dyspnea on exertion. Her BP was 106/56 with a pulse of 95. Here is her ECG:
The ECG differential includes Wellens' syndrome and pulmonary embolism.
Here is her previous ECG from 2 months prior:
|There is sinus rhythm at a normal rate (75). There is abnormal T-wave inversion in lead V2 only now, but the S1Q3T3 (the finding which suggests PE) is here also.|
So is this just baseline T-wave inversion? Wellens'? Pulmonary embolism? First, the increased heart rate should always sway you towards PE. Wellens' syndrome implies open arteries, perfusion of the myocardium, and the patient uncommonly has tachycardia. Baseline T-wave inversion is an unlikely explanation because there is extension out to V5. PE is very likely with this ECG.
An EMT student who has never had any ultrasound training, who like this blog, likes EKGs, and likes to experiment with ultrasound was working in this ED where the attending emergency physicians do not use ultrasound frequently. He had learned ultrasound from online sources only, including our own hqmeded, and related sites.
|The thick white arrow shows the right ventricle, which is dilated. The thin red arrow shows the left ventricle, which should not be smaller than the RV, as it is here.|
This self-trained EMT rolled the ultrasound into the patient's room and found this very large RV. The patient underwent immediate CTPA, had a submassive saddle embolus, and underwent immediate catheter directed thrombolysis.
My colleague Dave Plummer points out that:
To be clear, the bedside ultrasound shows indirect evidence of PE by RV dilation only in cases of acute cor pulmonale. This will manifest as:
1) dilated RV
)2 hypo kinetic RV and
3) thin walled RV.
This is common to any acute RV outflow obstructions, including valvular. As you point out, it can be discerned with minimal training
The ECG in PE:
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 angiograms in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE. Today, however, that number would be lower because we diagnose more of the submassive PEs that have minimal symptoms.
This is a paper worth reading: Marchik 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. What is it? 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.
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 there are T-wave inversions in the right precordial leads and in lead III, 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.