Effects of high oxygen tension on healthy volunteer microcirculation.

INTRODUCTION: Previous studies have highlighted hyperoxia-induced microcirculation modifications, but few have focused on hyperbaric oxygen (HBO) effects. Our primary objective was to explore hyperbaric hyperoxia effects on the microcirculation of healthy volunteers and investigate whether these modifications are adaptative or not. METHODS: This single centre, open-label study included 15 healthy volunteers. Measurements were performed under five conditions: T0) baseline value (normobaric normoxia); T1) hyperbaric normoxia; T2) hyperbaric hyperoxia; T3) normobaric hyperoxia; T4) return to normobaric normoxia. Microcirculatory data were gathered via laser Doppler, near-infrared spectroscopy and transcutaneous oximetry (PtcO2). Vascular-occlusion tests were performed at each step. We used transthoracic echocardiography and standard monitoring for haemodynamic investigation. RESULTS: Maximal alterations were observed under hyperbaric hyperoxia which led, in comparison with baseline, to arterial hypertension (mean arterial pressure 105 (SD 12) mmHg vs 95 (11), P < 0.001) and bradycardia (55 (7) beats·min⁻¹ vs 66 (8), P < 0.001) while cardiac output remained unchanged. Hyperbaric hyperoxia also led to microcirculatory vasoconstriction (rest flow 63 (74) vs 143 (73) perfusion units, P < 0.05) in response to increased PtcO2 (104.0 (45.9) kPa vs 6.3 (2.4), P < 0.0001); and a decrease in laser Doppler parameters indicating vascular reserve (peak flow 125 (89) vs 233 (79) perfusion units, P < 0.05). Microvascular reactivity was preserved in every condition. CONCLUSIONS: Hyperoxia significantly modifies healthy volunteer microcirculation especially during HBO exposure. The rise in PtcO2 promotes an adaptative vasoconstrictive response to protect cellular integrity. Microvascular reactivity remains unaltered and vascular reserve is mobilised in proportion to the extent of the ischaemic stimulus.

Hyperbaric hyperoxemia as a risk factor for ventilator-acquired pneumonia?

OBJECTIVES: Ventilator-acquired pneumonia (VAP) is the leading cause of serious associated infections in Intensive Care Units (ICU) and is associated with significant morbidity. The use of hyperbaric oxygen therapy (HBOT) in patients on mechanical ventilation may increase exposure to certain risk factors such as hyperoxemia and the need for multiple transfers. The aim of our study was to assess the relationship between HBOT and VAP. METHOD: This retrospective observational study was performed from March 2017 to March 2018 in a 10-bed ICU using HBOT. All patients receiving mechanical ventilation (MV) for more than 48 hours were eligible. VAP was defined using clinical and radiological criteria. Data collection was carried out via digital medical records. Risk factors for VAP were determined by univariate and multivariate analysis. RESULTS: Forty-two (23%) of the 182 patients enrolled developed at least one episode of VAP. One hundred and twenty-four (68%) patients received HBOT. The incidence rate of VAP was 34 per 1000 ventilator days. The occurrence of VAP was significantly associated with immunosuppression (p<0.029), MV duration (5 [3-7] vs 8 [5-11.5] days, p<0.0001), length of stay (8 [5-13] vs 19.5 [13-32] days, p<0.0001), reintubation (p<0.0001), intra-hospital transport (p = 0.001), use of paralytic agents (p = 0.013), tracheotomy (p = 0.003) and prone position (p = 0.003). The use of HBOT was not associated with the occurrence of VAP. Multivariate analysis identified reintubation (OR: 8.3 [2.6-26.6]; p<0.0001), intra-hospital transport (OR: 3.5 [1.3-9.2]; p = 0.011) and the use of paralytic agents (OR: 3.3 [1.3-8.4]; p = 0.014) as independent risk factors for VAP. CONCLUSION: Known risk factors for VAP are to be found within our ICU population. HBOT, however, is not an extra risk factor for VAP within this group. Further experimental and clinical investigations are needed to understand the impact of HBOT on the occurrence of VAP and on physiological microbiome.

Evaluation of pressure in water-filled endotracheal tube cuffs in intubated patients undergoing hyperbaric oxygen treatment.

INTRODUCTION: Inflating endotracheal tube cuffs using water instead of air before hyperbaric oxygen treatment (HBOT) is common. The objective of this study was to assess cuff pressure (Pcuff), when the cuff was inflated using water, in normobaric conditions and during HBOT. METHODS: This was a prospective, observational study taking place in hyperbaric centre and intensive care unit of the University Hospital of Lille. Every patient who required tracheal intubation and HBOT at 253.3 kPa (2.5 atmospheres absolute [atm abs]) was included. Pcuff was measured using a pressure transductor connected to the cuff inflating port. Measurements were performed at 'normobaria' (1 atm abs) and during HBOT at 2.5 atm abs. RESULTS: Thirty patients were included between February and April 2016. Recordings were analysable in 27 patients. Mean Pcuff at normobaria was 60.8 (SD 42) cmH2O. Nineteen (70%) of patients had an excessive Pcuff (higher than 30 cmH2O). Coefficient of variation was 69%. Mean Pcuff at 2.5 atm abs was 51.6 (40.7) cmH2O, significantly lower than at normobaria (P < 0.0001). Coefficient of variation was 79%. In only five (18%) patients was Pcuff < 20 cmH2O at 2.5 atm abs. CONCLUSIONS: In normobaric conditions, when the cuff was inflated using water and not specifically controlled Pcuff was not predictable. The cuff was typically over-inflated exceeding safe pressure. During HBOT Pcuff decreased slightly.