The passage of air through the nasal cavity generates rhythmic oscillations transmitted by the olfactory bulb to the brain, which induces cerebral activation in functional areas and is associated with better cognitive performance compared to oral breathing. Consequently, the abolition of nasal ventilation in patients intubated via the orotracheal route could have deleterious effects on brain activity. Besides the loss of olfaction, the abolition of nasal ventilation could affect brain activity and respiratory control, consequently altering regional pulmonary ventilation.
The hypothesis of the study is that nasal ventilation through the passage of humidified nasal airflow in patients intubated via the orotracheal route would be associated with modulation of cerebral electrical activity and tissue oxygenation and a modification of regional pulmonary ventilation.
Age ≥ 18 years old
Hypoxemic acute respiratory failure
Intubation and mechanical ventilation since less than 4 days
PaO2/FiO2 ratio less than 200
Central nervous system diseases (stroke, MS, epilepsy)
Psychiatric illnesses (psychosis, depression) (indicated on patient's medical record)
Hemodynamic instability (noradrenalin>2mg/h)
Patient on AME
The study population will be adult patients with acute respiratory failure who are orally intubated and sedated. These patients should be free of neurological and psychiatric diseases prior to ICU admission. The choice of this particular population is justified by its exposure to mechanical ventilation and continuous sedation, which are recognized risk factors for brain damage.
Cohort
Prospective
EEG activity measurement
DeviceThe nasal ventilation device (placed as part of the research) (AIRVO 2; Fisher and Paykel Healthcare, Auckland, New Zealand) will be positioned via nasal cannulas adapted to the patient's anatomy. The FiO2 will be set at 21% and the flow rate will be fixed at 0 L/min at the inclusion visit. The temperature of the humidified nasal oxygenator will be set at 31°C. Six 30-minute experimental conditions will be performed successively: 1) 0 L/min flow, FiO2 21%, 2) 30 L/min flow, FiO2 21%, 3) 30 L/min flow, FiO2 100%, 4) 60 L/min flow, FiO2 21%, 5) 60 L/min flow, FiO2 100%, 6) Negative control. At the end of each condition, a 10-minute thoracic electrical impedance tomography recording, a 10-minute EEG recording, a 10-minute cerebral NIRS recording and an instantaneous temporal Doppler velocity measurement will be performed. A blood gas (1.5 mL) will also be taken at the end of each condition.
Study the effects of nasal ventilation on brain electrical activity using electroencephalogram recording (EEG) in sedated orotracheally intubated patients.
EEG spectral density spectrum of gamma frequency.
Study the effects of nasal ventilation on cerebral perfusion
This outcome will be assessed by the evaluation of the Index of Pulsatility (IP) (IP=(Vs-Vd)/Vm: Vs: Systolic velocity; Vd: Diastolic Velocity; Vm: Mean Velocity)
Study the effects of nasal ventilation on cerebral tissue oxygenation
Cerebral tissue oxygenation (% of O2) measured by NIRS (Near Infrared Spectroscopy) electrodes
Study the effects of nasal ventilation on gas exchange
Ratio of PaO2 (partial pressure of O2) /FiO2 (inspired oxygen fraction)
Study the effects of nasal ventilation on gas exchange
Evaluation of PaCO2 (partial pressure of CO2) (mmHG)
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