Facebook
Twitter
LinkedIn
Email
 |
Checking for direct PDF access through Ovid | |
Excerpt
Carbon dioxide plays a significant role in the normal physiological control of the cerebral blood flow (CBF). At normotension, there is a linear response of the CBF between a PaCO2 of 20 and 80 mmHg (the CBF changes about 2-4% for each 1 mmHg change in PaCO2). In general, doubling the PaCO2 from 40 to 80 mmHg doubles the CBF, and halving the PaCO2 from 40 to 20 mmHg halves the CBF.
Hypocapnia reduces cerebral blood volume (CBV), both through an effect on CBF and through a direct effect on cerebral veins which contain the major part of the blood volume. This hyperventilation, through its effect on CBV, can be life-saving for patients with critically raised intracranial pressure (ICP). Because of this observation, intraoperative hyperventilation is commonly employed to facilitate surgical exposure. This has been staunchly supported by neurosurgeons since the 1950s.
In both awake and anaesthetized human volunteers, PaCO2 below 25 mmHg is associated with EEG slowing and a significantly reduced SjvO2 and a widened arteriovenous oxygen gradient. However, afterwards, none of the volunteers was noted to exhibit clinical features suggestive of ischaemia although no sensitive psychometric testing was used. Similarly, animal studies of severe hypocapnia (<20 mmHg) have found increases in lactate and reductions in ATP and Pcr (Phosphocreatinine) indicating a failure of adequate cellular metabolism [1]. Nevertheless, intraoperative hyperventilation has not been evaluated rigorously, and the overall effect on patient outcome is unknown.
Today, propofol is commonly used to effect the hypnotic component of neuroanaesthesia. However, conflicting results have been obtained on the influence of hypocapnia on CBF during a propofol-based anaesthesia [2,3]. Therefore, we started a first study to investigate the effect of a propofol-based anaesthesia on the CBF response to hypocapnia and we did this study in neurosurgical patients with a brain tumour.
The main findings of this study: These can be summarized as follows. In the normocapnic patients during a propofol anaesthesia, CBF is already low, so that an additional decrease of the CBF during hypocapnia may not be important enough to reduce the cerebral blood volume importantly [4]. We wondered if this reduced CO2 responsiveness was the same in older and younger patients. Therefore, we conducted a prospective study to compare the responsiveness of the CBF to hypocapnia in neurosurgical patients younger and older than 50 years anaesthetized with propofol. The same anaesthesia technique was used as in the first study.
This study showed that, in anaesthetized patients with a brain tumour, absolute reactivity is decreased with advancing age and suggests that the age-related decrease in CO2 reactivity described by Yamaguchi and co-workers [5] is accentuated by propofol. We concluded from this study that the usefulness of hypocapnia as an ICP decreasing measure could be questioned in older patients [6].
These results were confirmed in the next study in which we compared isoflurane and propofol for their effect on CO2 responsiveness. The hypocapnic CBF reactivity was significantly reduced in patients older than 50 years in the propofol group compared with the propofol group younger than 50 years. In the isofluorane group older and younger than 50 years, CO2 reactivity was maintained [7].
As decreased or absent CO2 reactivity is considered as a major sign of decreased cerebral vascular reserve and has been considered as a strong predictor of temporary postoperative confusion [8], we compared also the influence of moderate hypocapnia on cerebral oxygenation in neurosurgical patients, anaesthetized consecutively with isoflurane and propofol. In the isoflurane group, SjvO2 and CBF decreased, while the AvDO2 increased in both groups.
