The 2020 pandemic of the coronavirus (SARS-CoV2) has lead to an increase in ARDS cases requiring invasive mechanical ventilation in the ICU (Intensive Care Unit). The investigators hypothesize that airway pressure release ventilation (APRV) could be beneficial in patients with ARDS secondary to SARS-COV2 viral pneumonia.
Lung protective mechanical ventilation is the cornerstone of ARDS management, reducing the
work of respiratory muscles and optimizing gas exchange. However, it can be the source of
deleterious effects, grouped under the terms of ventilator induced lung injury (VILI) and
ventilator induced diaphragm dysfunction.
The protective ventilatory strategy has led to a significant improvement in the prognosis of
ARDS patients, by reducing the volume of the air and oxygen mixture (lower tidal volume)
delivered to the lungs and thus reducing the pulmonary stress and strain. However, this
protective ventilation usually requires deep sedation and neuromuscular blockade to avoid
deleterious patient-ventilator asynchrony.
Airway Pressure Release Ventilation (APRV) has been proposed to reduce patient-ventilator
asynchrony and reduce the VILI. The operating principles of APRV are based on the presence of
two pressure levels that are kept constant. Spontaneous breathing is possible at any time at
both pressure levels if the patient is not deeply sedated or under neuromuscular blockade.
The investigators hypothesize that APRV mode could be beneficial on oxygenation and
respiratory work in patients with ARDS secondary to SARS-COV2 viral pneumonia.
Other: Airway pressure release ventilation
Ventilator management strategy
Inclusion Criteria:
- Patients treated in Nancy University Hospital between 01/04/2020 and 31/06/2020 for
COVID-19 ARDS, requiring invasive ventilation
- Trial of airway pressure release ventilation during the ICU stay
Exclusion Criteria:
- Patients requiring veno-venous ECMO
- Patients unable to complete the 6-hour APRV trial due to poor tolerance : SpO2
decrease < 90% on FiO2 70%, haemodynamic instability (MAP < 65mmhg without
vasopressors, or 0.5 mg/h increase in norepinephrine, ventilator asynchrony
(respiratory rate >35), hypercapnia (pH < 7,25 or PaCO2 >60mmHg)
Centre Hospitalier Régional Universitaire de Nancy
Nancy, France
Matthieu Koszutski, MD, Principal Investigator
CHRU de NANCY, Médecine Intensive et Réanimation Brabois