A 59-year-old man with hypothyroidism and obesity was transferred from an outside hospital to our medical intensive care unit for management of acute hypoxemic respiratory failure due to coronavirus disease 2019 (COVID-19). One day prior to transfer, the patient required endotracheal intubation and mechanical ventilation, heavy sedation with neuromuscular blockade, and norepinephrine for hemodynamic support. His cardiac exam showed a regular rate and rhythm with 1+ peripheral pulses in all extremities and a capillary refill time of 2 to 3 s. Breath sounds were diminished bilaterally. Laboratory studies were notable for acute kidney injury (creatinine, 1.91 mg/dl [reference interval, 0.40 to 1.20 mg/dl]; blood urea nitrogen [BUN], 117 mg/dl [reference interval, 7 to 20 mg/dl]) and leukocytosis (white blood cells, 16.76 k/μl [reference interval, 4.3 to 11.3 k/μl]). A chest radiograph demonstrated diffuse bilateral patchy airspace opacities without focal consolidation (Fig. 1A). The patient was given one dose each of ceftriaxone and azithromycin for community-acquired pneumonia the day before transfer, but these were discontinued due to a low suspicion for a secondary bacterial pneumonia. Treatment for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia included dexamethasone and remdesivir. Due to clinical improvement, paralysis was stopped and sedation lifted, and the patient remained stable on his ventilator settings with improvement in his oxygenation and hemodynamics. Ventilator settings were weaned over several days and he no longer required norepinephrine.