Tidal volume cardiac output and functional residual capacity determine end-tidal CO2 transient during standing up in humans

摘要

In man assuming the upright position, end-tidal PCO2 (PETCO2) decreases. With the rising interest in cerebral autoregulation during posture change, which is known to be affected by PETCO2, we sought to determine the factors leading to hypocapnia during standing up from the supine position. To study the contribution of an increase in tidal volume (VT) and breathing frequency, a decrease in stroke volume (SV), a ventilation–perfusion (V/Q) gradient and an increase in functional residual capacity (FRC) to hypocapnia in the standing position, we developed a mathematical model of the lung to follow breath-to-breath variations in PETCO2. A gravity-induced apical-to-basal V/Q gradient in the lung was modelled using nine lung segments. We tested the model using an eight-subject data set with measurements of VT, pulmonary O2 uptake and breath-to-breath lumped SV. On average, the PETCO2 decreased from 40 mmHg to 36 mmHg after 150 s standing. Results show that the model is able to track breath-to-breath PETCO2 variations (r²= 0.74, P < 0.05). Model parameter sensitivity analysis demonstrates that the decrease in PETCO₂ during standing is due primarily to increased V_T, and transiently to decreased SV and increased FRC; a slight gravity-induced V/Q mismatch also contributes to the hypocapnia. The influence of cardiac output on hypocapnia in the standing position was verified in experiments on human subjects, where first breathing alone, and then breathing, FRC and V/Q were controlled.