When we went through our hardware and software upgrade last August, one of the changes we made was to stop reporting the FEF25%-75% (AKA MMEF, MMFR, MMF). The pulmonary physicians had long since stopped using this value when assessing spirometry results and we had kept it on our reports as long as we did only for inter-laboratory compatibility. Along with other changes we made at that time we decided it was time to drop the FEF25%-75% off our reports.
FEF25%-75% has been used to assess “small airways disease” but more than one of our pulmonary physicians has said that they don’t believe there is such a thing. I’m not a clinician but I’ve always felt that tests and results need to be clinically useful in order to be performed or reported and more than one study has shown little correlation between anatomical findings and FEF25%-75%.
Regardless of whether or not small airways disease is an actual entity my first objection to the FEF25%-75% has to do with the concept that it measures flow in small airways when for most patients it lies within their FEV1. For this reason it has never been clear to me what the FEF25%-75% is measuring that the FEV1 isn’t. More importantly, I have significant concerns about the limitations involved in measuring the FEF25%-75% in the first place.
A report of a patient’s complete set of PFTS came across my desk yesterday. There were a lot of inconsistencies in the report and I ended up looking at the raw data for every single test. When I looked at the spirometry results I was surprised to see which effort the technician had selected to report the FEV1.
The patient’s spirometry efforts were highly variable and not terribly reproducible. The FEV1 that had been selected came from an effort with an expiratory pause that occurred before the first second and with a number of cough artifacts. There was another spirometry effort effort however, that did not have a pause and had a larger FEV1. The reason the other effort had not been selected was that it did not meet ATS-ERS criteria for back-extrapolation whereas the first effort did.
Patients are advised not to smoke prior to DLCO testing, primarily because it increases carboxyhemoglobin. The effect of COHb on DLCO has been well studied, but COHb is not often measured before DLCO testing. Alveolar carbon monoxide (PACO) can be measured however, and there is a good correlation between PACO and COHb.
The single-breath DLCO calculation assumes that PACO is zero. At first glance this is a reasonably good approximation since a non-smoker will normally have a PACO of less than 5 ppm. This is no more than 0.17 percent of the 0.3% CO concentration (3000 ppm) used for testing which is negligible. Even so, smokers can have significantly elevated COHb levels and COHb increases during testing.
Elevated PACO and COHb levels will decrease DLCO. PACO back-pressure is estimated to be responsible for about 40% of the decrease and the anemia effect of COHb about 60%. Since PACO and COHb are usually in equilibrium in the lung, the effects are combined and DLCO is corrected according to COHb.
I was recently contacted by a physician looking for an illustration or diagram to help make gas exchange and DLCO more understandable. We’ve all seen the diagram of the alveoli with a capillary stretched around it and with oxygen and carbon dioxide exchanging across the membrane. I think I first saw it in Comroe’s ‘The Lung” published in the 1960’s, but it may well be older than that. It’s hard to improve on this and dozens of versions have been made of it.
He said something that got me thinking “for instance in a preoperative setting … all we know is a number on a seedy print out and all we use is a DLco % to tell us what to do!”. When I review reports I can access all of the raw data from all of a patient’s efforts so there’s a lot I can see about test quality that doesn’t show up on the final report. So what is a reduced DLCO test trying to tell you when all you have are numbers to look at?