Use of inhaled nitric oxide as an adjuvant therapy in C-ARDS

Introduction: COVID-29 related ARDS (C-ARDS) has specific pathophysiologic features that include a relatively higher compliance as non C-ARDS of similar severity and a pulmonary vascular thrombosis diathesis together with a severe early hypoxemia Given these features inhaled nitric oxide (iNO) could have a potential adjuvant role in the ventilatory management of C-ARDS Objectives: To study the effects of iNO on the relative change in pulmonary perfusion and on gas exchange in C-ARDS Methods: Retrospective analysis C-ARDS patients with severe ARDS treated with iNO delivered via the SoKINOXTM device (Air Liquide) The relative distribution of pulmonary blood flow before and after the administration of iNO was determined by EIT (Enlight, 1800 Timpel) Perfusion data were obtained by means of a bolus infusion of 10 ml of hypertonic (7 6%) Saline solution during a brief apnea period maintaining the same PEEP level(1) Ventilator settings before and after iNO were maintained unchanged so that no changes in the regional distribution of ventilation were expected At least one blood gas before and after iNO, although at different time periods in relation to the start of iNO therapy, were obtained Due to the low number of patients and measurments no statistical analysis was performed in this descriptive study Results: A total of 8 patients were included in the analysis After a few dose response trials performed in the first patients average lowest iNO dose resulting in the maximum change in perfusion was 15 ppm Changes in the relative distribution of ventilation were < 1% for all studied regions The response to iNO was very variable both in terms of the distribution of perfusion and gas exchange with no clear defined pattern Only four patients responded according to oxygenation with an average increase in PaO2/FiO2 of 40 5 ± 17 7% When analyzing the changes in the distribution of perfusion in vertical gravitational axis, iNO predominantly shifted perfusion to the ventral (non-dependent) lung half in 3 patients (13 ± 6 95% shift) and to the dorsal (dependent) lung half in 5 patients (8 4 ± 4 1% shift) This corresponded to a decrease of 5 5 ± 4 4% in PaO2/FiO2 and an increase of 13 7 ± 17 7% in PaCO2 and an increase of 29 9 ± 28 3% in PaO2/FiO2 and a decrease of 2 3 ± 14 5% in PaCO2 in those predominantly shifting perfusion to ventral and to dorsal regions respectively Conclusion: The response to iNO in C-ARDS patients was highly variable and required higher than usual doses In responding patients iNO caused a redistribution of pulmonary blood flow to dorsal nondependent regions