Inhaled nitric oxide in mechanically ventilated patients with COVID-19

Death from the novel coronavirus disease (COVID-19) predominantly occurs by refractory hypoxemia [1]. Some Authors have suggested that this type of respiratory failure differs from typical Acute Respiratory Distress Syndrome (ARDS) [2]. Patients with COVID-19 can present with (i) higher respiratory system compliance, and (ii) lower amount of non-ventilated lung tissue than expected given the severity of hypoxemia. These two elements may suggest a different primary cause of gas exchange impairment in COVID-19 compared to ARDS of another origin: excessive perfusion of small non-normally ventilated lung regions rather than a large anatomical shunt [3]. In line with this model, a recent series has revealed the presence of diffuse pulmonary endothelial injury and microthrombosis in COVID-19 lung pathology [4]. Given the novelty of COVID-19, its treatment is currently grounded on our knowledge of ARDS. Modern supportive therapy of ARDS generally consists of endotracheal intubation and mechanical ventilation with supplemental oxygen and Positive End Expiratory Pressure (PEEP), along with muscle paralysis, prone positioning, and ExtraCorporeal Membrane Oxygenation (ECMO) for the most severe cases [5,6]. Inhaled nitric oxide (iNO) can be considered as rescue therapy for hypoxemia due to its potent vasodilator effect on the pulmonary circulation [7]. International guidelines [5], and experts in the field [6,[8], [9], [10]], all suggest considering iNO even for refractory hypoxemia due to COVID-19. However, there are no strong clinical data to support this indication. Herein we describe the response to iNO in a small group of mechanically ventilated patients with severe COVID admitted to our Intensive Care Unit.