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Transient influence of end-tidal carbon dioxide tension on the postural restraint in cerebral perfusion

Departments of ¹Anesthesiology and ²Internal Medicine, Laboratory for Clinical Cardiovascular Physiology, and ³AMC Center for Heart Failure Research, Academic Medical Center, University of Amsterdam, Amsterdam; and ⁴Department of Anesthesiology and ⁵The Copenhagen Muscle Research Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

Submitted 8 September 2008 ; accepted in final form 30 June 2009

In the upright position, cerebral blood flow is reduced, maybe because arterial carbon dioxide partial pressure (Pa_CO2) decreases. We evaluated the time-dependent influence of a reduction in Pa_CO2, as indicated by the end-tidal PCO₂ tension (PET_CO2), on cerebral perfusion during head-up tilt. Mean arterial pressure, cardiac output, middle cerebral artery mean flow velocity (MCA V_mean), and dynamic cerebral autoregulation at supine rest and 70° head-up tilt were determined during free breathing and with PET_CO2 clamped to the supine level. The postural changes in central hemodynamic variables were equivalent, and the cerebrovascular autoregulatory capacity was not significantly affected by tilt or by clamping PET_CO2. In the first minute of tilt, the decline in MCA V_mean (10 ± 4 vs. 3 ± 4 cm/s; mean ± SE; P < 0.05) and PET_CO2 (6.8 ± 4.3 vs. 1.7 ± 1.6 Torr; P < 0.05) was larger during spontaneous breathing than during isocapnic tilt. However, after 2 min in the head-up position, the reduction in MCA V_mean was similar (7 ± 5 vs. 6 ± 3 cm/s), although the spontaneous decline in PET_CO2 was maintained (P < 0.05 vs. isocapnic tilt). These results suggest that the potential contribution of Pa_CO2 to the postural reduction in MCA V_mean is transient, leaving the mechanisms for the sustained restrain in MCA V_mean to be identified.

blood pressure; cardiac output; cerebral blood velocity

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