Cardiorespiratory responses to head-down tilt: An investigation of the arterial-end-tidal PCO₂ difference

Steep (50°) head down tilt (HDT) augments the ventilatory response to steady state hypercapnia although the mechanism is unclear. We hypothesised that changes in pulmonary blood flow distribution and ventilatory homogeneity during 50° HDT in hypercapnia would result in elevated arterial (PaCO2) with no concomitant change in end-tidal CO₂ (PETCO₂). We exposed 15 healthy participants (mean (SD) age 29 (10) years, 7 female, BMI 24.7 (5.5) kg/m2) to 50° HDT for eight minutes while breathing air or normoxic, hypercapnia (5% CO₂). Ventilation (Ve, pneumotachograph), end tidal O2 and CO2 concentration, and blood pressure (Finapres) were measured continuously. Arterialised capillary earlobe blood samples were obtained at baseline and during HDT to provide an estimate of PaCO₂. In a separate protocol, we measured carbon monoxide transfer factor (TLCO) during 50° HDT while breathing air in 6 healthy participants (mean (SD) age 34.7 (12.8) years, 2 female, BMI 23.7 (2.2) kg/m2). In protocol 1, ventilation increased significantly (mean (SD) 115 (24)%, p<0.05) compared to baseline during HDT in hypercapnia with a corresponding increase in PaCO₂ (42.9 ± 3.0 to 45.1 ± 3.5 mmHg; P=0.028) and no change in PETCO₂. The arterial to end-tidal PCO2 difference (P(a–ET)CO2) fell significantly from −4.0 ± 2.4 to −1.6 ± 2.2 mmHg; P=0.034). No changes were observed while breathing air. Mean (SD) TLCO increased significantly during 50° HDT from 28.4 (6.5) to 36.9 (7.3) mL/min/mmHg, p<0.0001). The augmented hypercapnic ventilatory response during 50⁰ HDT is consistent with alterations in lung ventilation perfusion matching.