Inhaled nitric oxide in acute severe pulmonary hypertension and severe acute respiratory distress syndrome secondary to COVID-19 pneumonia: a case report
Palabras clave : 
Área de Medicina Clínica y Epidemiología
Cardiac output, low
COVID-19
Familial primary pulmonary hypertension
Hypoxia
Nitric oxide
Tricuspid valve insufficiency
Fecha de publicación : 
2022
ISSN : 
1941-5923
Nota: 
This work is licensed under Creative Common AttributionNonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
Cita: 
Vives-Santacana, M. (Marc); Gasco, I.; Pla, G.; et al. "nhaled nitric oxide in acute severe pulmonary hypertension and severe acute respiratory distress syndrome secondary to COVID-19 pneumonia: a case report". The American Journal Of Case Reports. 23, 2022, e937147
Resumen
Objective: Rare diseaseBackground: Inhaled nitric oxide (iNO) is used as a treatment for pulmonary arterial hypertension (PAH). Severe hypoxia with hypoxic vasoconstriction caused by severe acute respiratory distress syndrome (ARDS) can induce pul-monary hypertension with hemodynamic implications, mainly secondary to right ventricle (RV) systolic func-tion impairment. We report the case of the use of iNO in a critically ill patient with bilateral SARS-CoV-2 pneumonia and severe ARDS and hypoxemia leading to acute severe PAH, causing a ventilation/perfusion mismatch, RV pressure over-load, and RV systolic dysfunction.Case Report: A 36-year-old woman was admitted to the Intensive Care Unit with a severe ARDS associated with SARS-CoV-2 pneumonia requiring invasive mechanical ventilation. Severe hypoxia and hypoxic vasoconstriction developed, leading to an acute increase in pulmonary vascular resistance, severe to moderate tricuspid regurgitation, RV pressure overload, RV systolic function impairment, and RV dilatation. Following 24 h of treatment with iNO at 15 ppm, significant oxygenation and hemodynamic improvement were noted, allowing vasopressors to be stopped. After 24 h of iNO treatment, echocardiography showed very mild tricuspid regurgitation, a non -dilat-ed RV, no impairment of transverse free wall contractility, and no paradoxical septal motion. iNO was main-tained for 7 days. The dose of iNO was progressively decreased with no adverse effects and maintaining an improvement of oxygenation and hemodynamic status, allowing respiratory weaning. Conclusions: Sustained acute hypoxia in ARDS secondary to SARS-CoV-2 pneumonia can lead to PAH, causing a ventila-tion/perfusion mismatch and RV systolic impairment. iNO can be considered in patients with significant PAH causing hypoxemia and RV dysfunction.

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