Abstract

Autoregulation and CO2-reactivity can be impaired independently of each other in many brain insults, the so-called 'dissociated vasoparalysis'. The theoretical combination of preserved CO2-reactivity and impaired or abolished autoregulation can have many clinical implications in the daily management of brain injured patients. To optimize their treatment, a bedside assessment of autoregulation and CO2-reactivity is desirable. When cerebral metabolic rate of oxygen is constant, changes in arterio-jugular differences of oxygen (AVDO2) reflect changes in CBF. In these situations relative changes in AVDO2 can be viewed as inverse changes in CBF and used as an evaluation method of CO2-reactivity and autoregulation. In 39 consecutive severe head injury patients with a mean age of 28 +/- 17 years and a diffuse brain injury, cerebrovascular response to changes in pCO2 was tested in the acute phase after injury (18 +/- 8 hours). In 28 of those cases autoregulation was also assessed. A relative CBF value (1/AVDO2) was calculated from baseline AVDO2 and was expressed as 100%. Changes in 1/AVDO2 after inducing pCO2 changes give a good estimate of changes in global CBF. Two different indexes were calculated for CO2-reactivity: 1) absolute CO2-reactivity (CO2RABS) and 2) percentage reactivity (CO2R%). CO2R% was used to separate patients with impaired/abolished CO2-reactivity from those with preserved CO2-reactivity. Patients with CO2R% above 1% were considered in the intact CO2-reactivity group and patients in whom CO2R% was below or equal to 1% were included in the impaired/abolished CO2-reactivity group. Only five cases (12.8%) presented an impaired/abolished CO2-reactivity. AVDO2 response to induced hypertension was studied in a subset of 28 patients. Phenylephrine was used to increase MABP about 25%. All AVDO2 values were corrected for changes in pCO2. Patients with changes in 1/AVDO2 less than or equal to 20% were included in the intact autoregulation group. Patients with estimated CBF changes above 20% were classified as having an impaired autoregulation (impaired/abolished). In 12 patients (43%) autoregulation was intact. In the remaining 16 patients (57%) autoregulation was imparied. Of the 28 cases, CO2-reactivity was impaired in only five cases. All patients with an impaired CO2-reactivity also had an impaired autoregulation. Monitoring relative changes in AVDO2 permits a reliable study of CO2-reactivity and autoregulation at the bedside. Introducing these variables into the day-to-day management should be considered in treatment protocols.

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