PulmCrit Blogitorial - Use of ECGs for management of (sub)massive PE

(A blogitorial is like a tweetorial in blog form, so folks on different platforms can see it).

Our approach to risk stratification and management of (sub)massive PE tends to be dominated by CT scan and echocardiography (eye-candy modalities). And these are great. But I think there are situations where ECG can be really helpful – and it tends to get overlooked.

ECG has numerous advantages – especially at a referral center when managing PEs across a large geographic region (where echocardiography usually isn't immediately available). Advantages of ECG include:

Immediately available everywhere (the patient already has an ECG in the chart).
Easily scanned into computers, or photographed and sent via text-message from a remote location.
Can be done on anyone regardless of echocardiographic windows.
Often can be compared to prior ECGs.

Aside from PE diagnosis, the ECG can help with risk stratification. The best meta-analysis on this seems to be Qaddoura A et al. (28628222) These authors pooled numerous studies, to correlate various ECG findings with in-hospital mortality:

OR 4.7: qR in V1.
OR 4.3: STE in V1.
OR 3.9: Complete RBBB.
OR 3.4: SI-Q3-T3.
OR 3.2: Right axis deviation.
OR 3.1: STE in III.
OR 2.5: STD in V4-V6 (subendocardial ischemia).
OR 2.0: Atrial fibrillation.
OR 1.6: TWI in precordial/inferior leads. (28628222)

These odds ratios aren't huge, but they aren't terrible either. For comparison, a positive troponin often clocks in somewhere around an OR of ~4 (although this varies depending on different methodologies and cutoffs).

To render this discussion more concrete, here are four situations where I've found ECG to be helpful. As a super important disclaimer, the clinical management is always based on a consideration of all the data points (clinical story, vitals, CT scan, EKG, labs, vibes, etc.).

(#1) adjudication of RV dilation

A lot of PE management depends on whether the RV is dilated.
CT scan determines this in a binary fashion based on RV/LV ratio. In some situations the RV size is on the borderline, leading to a false dichotomy between “dilated” and “not dilated.”
When the CT is equivocal, I think ECG can be helpful. If the CT scan is equivocal and the ECG is stone-cold normal, it's dubious that there is clinically relevant RV strain going on.

(#2) troponin substitute

Our institutional approach to PE involves a decision tree that incorporates whether or not the troponin is elevated (as do many, I'm sure).
Occasionally we may encounter a patient who seems pretty worrisome – probably with a high-risk submassive PE. But the troponin hasn't been checked.
If the ECG shows ST elevation and/or ST depression, I think it may be reasonable to use the electrocardiographic current of injury as a surrogate for troponin elevation in this situation – allowing us to proceed immediately to treatment (rather than wait for the troponin to return).

(#3) diagnosis of PE in a patient too unstable to go to CT scan

We've all been in a situation where a patient probably has a PE, and they're crashing, and we are considering whether to proceed with thrombolysis.
ECG can be helpful here because the sicker the patient is, the more diagnostic the ECG will be. If the patient is dying in front of you from a massive PE, there really ought to be some ECG findings to support the PE diagnosis.
This is obviously a very challenging situation that needs to be managed on a case-by-case basis. POCUS is fundamental. But occasionally there will be cases where ECG can be helpful to argue for or against a PE diagnosis.

(4) diagnosis of RVH (right ventricular hypertrophy)

With an aging and multimorbid patient population, we are increasingly encountering patients with chronic pulmonary hypertension and right ventricular hypertrophy.
Chronic pulmonary hypertension is challenging because these patients will always have a dilated RV. So even if they have a small PE, it may look like they're having a submassive PE (the CT scan will be interpreted as showing “RV strain”).
EKG features of RVH (e.g., tall R-wave in V1) may help suggest an underlying diagnosis of RVH – which may be a sign that the patient isn't necessarily having an acute submassive PE. These patients represent a high-risk group, but if the clot burden is low and there are signs of chronicity (e.g., chronic RVH findings on old ECGs) – then the patient is less likely to benefit from tPA or immediate interventional therapy.

So I think we should pay more attention to ECGs in (sub)massive PE patients. In nearly all patients, ECG won't affect management. But, if we routinely look at ECGs and integrate them into our cognitive schema, then we may be more nimble in applying ECGs to rare situations where we cannot get all the echo and CT data that we want.

Bye for now, more on management of (sub)massive PE here.