Objective: To define the changes in middle cerebral artery flow velocity (Vmca) and the electroencephalogram (EEG) during rapid reduction in arterial carbon dioxide (PCO2) from acute hypercapnia. Design: Human volunteer study. Setting: University-affiliated hospital experimental laboratory. Participants: Nine healthy volunteers aged 25-35 years. Interventions: Subjects rebreathed exhaled gas from a bag pre-filled with 5% carbon dioxide (CO2) in oxygen, up to an end-tidal CO2 of 10% or to the limit of discomfort, when they were disconnected. Measurements and results: Middle cerebral artery blood flow velocity was continuously measured by transcranial Doppler ultrasound, quantitative EEG was recorded and hemodynamics were monitored non-invasively. Vmca closely correlated with end-tidal CO2 changes (r=0.65, p<0.001). When rebreathing ceased, there was a rapid decline in end-tidal CO2 and in Vmca to baseline within 42±14 s, followed by a rapid further decline in both variables to below baseline. End-tidal CO2 reached a nadir of 4.4±1.1% at 146±79 s, with Vmca decreasing to 37±10 cm/s at 104±65 s (a 40% reduction and 31% below basal values). Electroencephalogram alpha activity significantly decreased and delta activity increased during hypercapnia. During subsequent hypocapnia, delta activity decreased back to baseline, while alpha activity increased, but remained below baseline. Conclusions: These findings demonstrate the rapid changes occurring in cerebral blood flow during rapid declines in arterial CO2 and the consequent potential for producing brain ischemia and hemodynamic alterations if inadvertent hyperventilation occurs following institution of mechanical ventilation for acute hypercapnia.
- Carbon dioxide
- Middle cerebral artery