SEPSIS-INDUCED VASOPARALYSIS DOES NOT INVOLVE THE CEREBRAL VASCULATURE - INDIRECT EVIDENCE FROM AUTOREGULATION AND CARBON-DIOXIDE REACTIVITY STUDIES

We have studied cerebral autoregulation and vasoreactivity to carbon d ioxide in 10 patients with the sepsis syndrome receiving intensive the rapy. All patients were sedated with infusions of midazolam and fentan yl, and their lungs were ventilated mechanically with oxygen-air to ma intain normoxia and normocapnia. Inotropic support and antibiotics wer e administered as necessary. During a period of constant level of seda tion and stable haemodynamics, cerebral autoregulation was tested by i ncreasing mean arterial pressure (MAP) by 23 (SD 2) mm Hg from baselin e with an infusion of phenylephrine and simultaneously recording middl e cerebral artery blood flow velocity (vmca) using transcranial Dopple r ultrasonography. Carbon dioxide reactivity was tested by varying Pa- CO2 between 3.0 and 7.0 kPa and simultaneously recording vmca. There w as no significant change in vmca (57 (22) and 59 (23) cm s(-1)) during the increase in MAP (75 (11) to 98 (10) mm Hg). The mean index of aut oregulation (IOR) was 0.92 (SEM 0.03), which was not significantly dif ferent from 1, indicating near perfect autoregulation. Although absolu te carbon dioxide reactivity was lower than reported previously in awa ke subjects, relative carbon dioxide reactivity was within normal limi ts for all patients (11.6 (SEM 0.8) cm s(-1) and 20.3 (3) % kPa(-1), r espectively). We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remained intact in patients with the sepsis sy ndrome, providing indirect evidence that at least in the early stages of the syndrome, the widespread sepsis-induced vasoparalysis does not involve the cerebral vasculature.