The effect of hypercapnia on static cerebral autoregulation

Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure ( BP ); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ±  SD : age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady‐state elevations in mean arterial BP ( MAP ), induced via lower body positive pressure ( LBPP ). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO 2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity ( MCA v), BP , partial pressure of end‐tidal carbon dioxide ( P ET CO 2 ) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCA v was apparent between eupcapnic baseline and LBPP s (grouped mean 65 ± 11 cm·s −1 , all P  >   0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P  <   0.001 vs. baseline). Conversely, MCA v during the hypercapnic +40 mm Hg stage (Δ31 ± 13 cm·s −1 ) was greater than hypercapnia alone (Δ25 ± 11 cm·s −1 , P  =   0.026), due to an increased MAP (Δ14 ± 7 mm Hg, P  <   0.001 vs. hypercapnia alone and P  =   0.026 vs. hypercapnia +20 mm Hg). As cardiac output and P ET CO 2 were similar across all hypercapnic stages (all P  >   0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation.