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Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
Published on: September 24, 2020
Effects of Sevoflurane Inhalation on Pulmonary Hemodynamics in Moderate to Severe Acute Respiratory Distress Syndrome
Giovanni Bousquet1,2, Gabriel Parzy1, Damien Barrau1,2
1Service de Médecine Intensive Réanimation, Hôpital Nord, Assistance Publique-Hôpitaux de Marseille, Marseille, France.
Objectives:
Our study aimed to investigate the effects of sevoflurane inhalation on mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistances (PVRs) in acute respiratory distress syndrome (ARDS) patients during lung protective ventilation.
Design:
Prospective cohort study.
Setting:
Medical ICU of a university teaching hospital.
Patients:
Deeply sedated, intubated adult patients with moderate to severe ARDS with Pa o2 /F io2 less than 150 mm Hg, with a positive end-expiratory pressure of greater than or equal to 5 cm H 2 O and septic shock monitored with a pulmonary arterial catheter.
Interventions:
Sedation was switched from IV midazolam to sevoflurane inhalation.
Measurements And Main Results:
Main objective was the change in mPAP between before (T0) and 1 hour (H + 1) after sevoflurane inhalation. Main secondary outcomes were mPAP 12-18 hours (H + 12-18) after inclusion, PVR indexed (PVRI), cardiac index, Pa o2 /F io2 , pulmonary shunt at H + 1, and H + 12-18 after inclusion. The H + 12-18 measurements were performed either in supine position (SP) or in prone position (PP), if Pa o2 /F io2 ratio was less than 150 mm Hg at H + 1. Fifteen patients were included in interim analysis. mPAP was 24 ± 4 mm Hg at inclusion and remained unchanged after 1 hour (24 ± 5 mm Hg) and 12-18 hours (23 ± 6 mm Hg) of sevoflurane inhalation. The mean expired fraction of sevoflurane was 0.75% ± 0.25% at H + 1 and 0.71% ± 0.25% at H + 12-18. No significant variations in PVRI, cardiac index, mean arterial pressure, pulmonary shunt were observed at H + 1 and H + 12-18. An improvement of Pa o2 /F io2 was observed at H + 12-18 in patients who remained in SP (from 158 ± 49 to 249 ± 86 mm Hg; p = 0.015) and in those turned prone (from 134 ± 36 to 241 ± 109 mm Hg; p = 0.018).
Conclusions:
In mechanically ventilated moderate to severe ARDS patients receiving lung protective ventilation, sevoflurane inhalation was not associated with decreases in mPAPs and PVRs. However, the smaller than planned sample size does not allow definitive conclusions.
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