Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

Abstract

This study examined the effect of high, normal, and uncontrolled end-tidal Pco(2) (Pet(CO(2))) on the ventilatory, peak cerebral blood flow velocity (V(p)), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal Po(2) was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (Pet(CO(2)) +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure V(p) in the middle cerebral artery. The slopes of the linear regressions of ventilation, V(p), and MAP with arterial O(2) saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia (P < 0.05). Strong, significant correlations were observed between ventilation, V(p), and MAP with each Pet(CO(2)) condition. These data suggest that 1). a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2). in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of Pet(CO(2)) and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in V(p) and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high V(p) and MAP responses to hypoxia.