Severe hypoxemia in some patients with coronavirus disease (COVID-19) has been related to loss of hypoxic pulmonary vasoconstriction (1, 2). A 77-year-old male with 6 days of mild respiratory symptoms and no comorbidities was admitted with signs of respiratory failure (Pa O 2 /FI O 2 : 61 mm Hg/0.36 mm Hg = 169.4 mm Hg; reference values [RVs] of 400-500 mm Hg). Chest computed tomography (CT) showed extensive ground-glass opacities (50-75% right-lung involvement and 25-50% left-lung involvement). Laboratory findings showed a D-dimer concentration of 652 ng/ml (RV , 500 ng/ml) and a C-reactive-protein concentration of 93.5 mg/dl (RV , 0.1 mg/dl). Nasopharyngeal swab test (RT-PCR) results confirmed COVID-19. The standard institutional protocol was initiated with a nasal oxygen catheter (4.0 L/min), antibiotics, dexamethasone, and enoxaparin. The patient required invasive ventilation on the 10th day and died on the 35th day of hospitalization. Lung-perfusion single-photon-emission CT/CT using 99m Tc-labeled macroaggregated albumin (3) and positron emission tomography/CT using 18 F-fluorodeoxyglucose (4) were sequentially performed on the third day of hospitalization during the same visit to the Nuclear Medicine Service to simultaneously assess pulmonary perfusion and inflammation. Normal or increased lung perfusion was detected in most of the hypermetabolic areas evidenced by positron emission tomography/CT images (Figure 1). Image quantification was conducted using free, opensource image-processing software (5, 6). Quantification results showed 59% of the total pulmonary perfusion occurring in inflamed lung tissue, which corresponded to 39% of the total anatomic lung volume (Figure 1D). This suggested a high right-to-left shunt fraction in the inflamed areas, which was probably related to loss of hypoxic vasoconstriction, as has been proposed before to occur in COVID-19 pneumopathy (1, 2). The vasoconstriction reflex seemed preserved in a few areas of 18 F-fluorodeoxyglucose uptake. Inflammation and loss of hypoxic pulmonary vasoconstriction can be assessed and quantified using the described methodology.Further studies are needed to evaluate its possible clinical uses. nAuthor disclosures are available with the text of this article at www.atsjournals.org.