Johnston, Jessica I.

AbstractAimWe investigated whether a commercial bi‐level positive airway pressure (BPAP) device, would improve peripheral oxygen saturation (SpO2) during recreational aviation up to 12,500 feet without supplemental oxygen. Ten adults with recreational flight experience (age:47 ± 14; female = 5) completed a standardized flight profile in an unpressurised aircraft, involving randomized crossover design at 8,000 feet and 12,500 feet with BPAP or control. SpO2, middle cerebral artery velocity (MCAv), heart rate (HR), respiratory rate (RR), and relative tidal volume (TV) index were measured continuously. Psychomotor vigilance test (3‐min) assessed reaction time halfway through taxi and altitude stages. Altitude significantly (p < 0.05) decreased mean SpO2, MCAv, and RR, and increased TV index and HR. There was no effect of altitude (p > 0.05) on reaction time. BPAP increased mean SpO2 at 8,000 feet [Control: 92 ± 1%; BPAP: 94 ± 2%; mean difference (MD) = 2 ± 2%; p = 0.002] and 12,500 feet [Control: 86 ± 4%; BPAP: 89 ± 4%; MD = 2 ± 3%; p = 0.013]. BPAP lowered MCAv at 8,000 feet [Control: 53 ± 10 cm/s; BPAP: 50 ± 9 cm/s; MD = ‐3 ± 2 cm/s; p = 0.001] and 12,500 feet [Control: 52 ± 10 cm/s; BPAP: 50 ± 8 cm/s; MD = ‐2 ± 3 cm/s; p = 0.041]. BPAP increased TV index at 8,000 feet (Control: 6.6 ± 1.3; BPAP:8.1 ± 1.8; MD = 1.9 ± 0.8; p < 0.001) but not 12,500 feet, without effect on RR or reaction time. This study provides preliminary results that BPAP may improve mean SpO2 for recreational aviators up to 12,500 feet without supplemental oxygen.

Introduction: Patients with coronary artery disease (CAD) are at increased risk of cognitive decline. A proposed mechanism is cerebral hypoperfusion related to vascular dysfunction and impaired cerebral blood flow regulation Hypothesis: Patients with CAD will have lower cerebrovascular function than age- and sex-matched controls, assessed as reactivity to a vasodilatory carbon dioxide (CO 2 ) stimulus. Methods: Adults 40-70years old with CAD were recruited on enrollment to a cardiac rehabilitation program following a cardiac event or hospitalization. Age and sex-matched adults without known disease or cardiovascular risk factors were recruited as healthy controls. Cognitive function was assessed by the Fluid Composite of the NIH Cognition Toolbox. Following a familiarization visit, participants underwent a stepped CO 2 protocol (room air, 2% CO 2 , 4% CO 2 , 6% CO 2 ) while continuously measuring middle cerebral artery velocity (MCAv) using transcranial doppler ultrasound, mean arterial pressure (MAP), ventilation (VE), and end-tidal CO 2 . Cerebrovascular conductance (CVCi) was calculated as MCAv/MAP. Cerebrovascular reactivity was calculated as the linear regression slope of CVCi against the change in end-tidal CO 2 . The reactivity of MAP and VE (or chemosensitivity) were also calculated. Results: 19 patients with CAD and 10 healthy controls were recruited ( Table 1 ). Compared with controls, patients with CAD had a 2-fold lower cerebrovascular reactivity (p=0.003), higher MAP reactivity (p<0.05), and a trend towards higher chemosensitivity (p<0.1) ( Table 2 ). There were no group differences in resting CVCi or cognition ( Table 2 ). After adjustment for age and sex, lower cerebrovascular reactivity was associated with lower peak oxygen uptake, diabetes, and smoking history ( Table 3 ). Conclusions: Compared with healthy controls, we report that patients with CAD have significantly lower cerebrovascular function, with no differences in cognitive function.