Happy Fri-yay, Christy Soran presented a cool case of a patient with unexplained hypoxemia, after the fact thought to be a combo of microatelectasis and OHS.
Obesity and Pulmonary function
This paper is a nice overview of the different effects of obesity on pulmonary function. Patients w/ BMI>40 generally have a widened a-a gradient at baseline, though rarely have frank hypoxemia on pulse oximetry, also have reduced expiratory reserve volume, and probably have both reduced chest wall and lung compliance. Diffusion capacity is generally reserved, but they also tend to have more resting VQ mismatch (hence the a-a gradient) at baseline, where the bases are slightly more overperfused than usual.
The hypothesis in this gentleman, who had a low prob VQ scan (contrast allergy), relatively normal chest CT, but was requiring 100% FiO2 on HFNC to maintain sats in the low 90’s after an uncomplicated surgical procedure, was a combination of OHS and “microatelectasis” not detected on imaging, which improved with more aggressive pulmonary toilet and alveolar recruitment maneuvers. Dr. James Frank also mentioned a study showing reduced aspiration pneumonia in post-op patients who get CPAP when they have increasing O2 requirements post-operatively. This gentleman improved with BiPAP but was also empirically anti-coagulated, so hard to say. Take away points: obese patients have wider a-a gradients at baseline, reduced chest wall and lung compliance, and more VQ mismatch, and are thus maybe more prone to hypoxemia from relatively smaller insults.
Also, as we’ve discussed before, in general HFNC is preferred to NIPPV in hypoxemic respiratory failure given risks of barotrauma from uncontrolled tidal volumes in BiPAP.