This is the follow-up and discussion for 85 year old female CC: Respiratory distress. As usual, thank you for all the insightful comments!
The case demonstrates some very important points not the least of which is that the differential diagnosis of shortness of breath can be difficult, even for emergency physicians who have access to chest x-rays and blood tests like the BNP / NT-proBNP.
It also shows why paramedics need to think more more clinicians and less like technicians! Some of us were taught that we “only treat symptoms” but there’s a big difference between treating the shortness of breath associated with asthma or COPD versus CHF versus a tension pneumothorax.
When a patient like this one has co-morbidities it’s not always straight-forward. As some of you mentioned in the comments, it’s entirely possible to have overlapping COPD and CHF. For this case, COPD certainly played a role (how could it not when it’s part of the patient’s history?) but the patient was also in severe acute pulmonary edema.
As some of you also mentioned, acute pulmonary edema can lead to reflex airway spasms that cause wheezing (so-called “cardiac asthma”). In this case, the paramedics placed the patient in high-Fowlers, gave SL NTG, placed the patient on CPAP, and gave an in-line nebulizer treatment. After several minutes the patient was moving enough air for them to appreciate crackles bilaterally in all lung fields.
Let’s take another look at the 12-lead ECG.
I’ve seen this computerized interpretation several times and I always find it a bit confusing because to me, this ECG meets all of the criteria for left bundle branch block (i.e., supraventricular rhythm with a QRS duration > 120 ms, rS complex in lead V1 and a monomorphic (but notched) R-wave in lead I) .
It would be interesting to know why the computer calls it left ventricular hypertrophy with QRS widening.
So what is the rhythm? Based on the appearance of flutter waves in lead V1 I would call this atrial flutter, although it’s entirely possible for a heart rhythm to switch back and forth between atrial flutter and atrial fibrillation. On the cardiac unit we used to call this “fib-flutter” and it’s pretty common.
In this image we can see flutter waves in lead V1 (blue arrows). rS complexes are present in lead V1 and the red dotted lines show where I am measuring the QRS duration.
Here we can see monomorphic R-waves in leads I and V6 (lead I shows an rR’ complex). To me this clinches the ECG diagnosis of left bundle branch block. Your mileage may vary.
So, we all know that new onset pulmonary edema is ACS until proven otherwise.
Could this ECG show acute STEMI in the presence of LBBB?
Lead V3 shows greater than 5 mm of discordant ST-elevation which is cause for concern. However, we don’t know if the ST-segments are excessively discordant when taking into account the depth of the S-wave because the S-waves are cut off by the bottom of the ECG paper.
Fortunately, the ECG was transferred over the LIFENET and that ECG does show the depth of the S-wave.
With calipers, the S-waves in lead V3 measure about 60 mm deep. Using a ST/QRS ratio of 0.2 as a cut-off, we would require at least 12 mm of ST-elevation in lead V3 to be significant for this patient!
She ruled-out for acute myocardial infarction.