Continuous monitoring of carbon dioxide reactivity in traumatic brain injury

Introduction

The objective is to study the relationship between end-tidal carbon dioxide (EtCO₂) and cerebrovascular pressure reactivity in traumatic brain injury (TBI). Cerebrovascular pressure reactivity is the ability of cerebral vessels to respond to changes in transmural pressure. A cerebrovascular pressure reactivity index (PRx) can be determined as the moving correlation coefficient between the mean intracranial pressure (ICP) and mean arterial blood pressure. A negative or zero value reflects a normally reactive vascular bed whereas positive values reflect passive, non-reactive vessels. This index correlates significantly with outcome after TBI [1]. Carbon dioxide affects the cerebral vascular response. Our aim is to identify the optimal EtCO₂, at which PRx reaches its lowest value.

Methods

A prospective observational study of 20 patients with TBI at the Royal London Hospital. All patients were managed according to the local guidelines for the management of TBI. PRx was determined by ICM+ (Cambridge University) software by calculating the correlation coefficient between ICP and arterial blood pressure. A total of 965 hours of data were recorded including the mean arterial pressure, ICP, cerebral parfusion pressure, PRx and EtCO₂.

Results

We plotted EtCO₂ against PRx to identify the optimal EtCO₂ and the range of carbon dioxide reactivity. The graph of PRx compared with EtCO₂ indicated a U-shaped curve, suggesting that too low or too high ETCO₂ was associated with a disturbance in pressure reactivity (Figure 1). We found this pattern in 66% of the patients. In the other patients (34%) there was no such correlation, so it was not possible to identify optimal EtCO₂, probably indicating loss of carbon dioxide reactivity.

Figure 1

abstract

Conclusion

PRx allows the determination of the carbon dioxide level at which cerebrovascular pressure reactivity reaches its optimal value in individual patients. That would allow a dynamic approach to the carbon dioxide target in TBI.