Hyperventilation-induced reductions in cerebral blood flow velocity outlive the reduction in intracranial pressure in head-injured patients

Objective

In healthy volunteers, cerebral blood flow (CBF) recovers to baseline within a few hours of continued hyperventilation due to normalization of perivascular pH. The same mechanism is thought to be responsible for the brevity of intracranial pressure (ICP) control in head-injured patients. We measured recovery of middle cerebral artery mean flow velocity (FVm) in head-injured patients during continued hyperventilation and investigated the relationship between the time-course of changes in FVm and ICP.

Methods

Twenty-eight head-injured patients were investigated. After recording baseline data (cerebral perfusion pressure, ICP, averaged bilateral FVm, PaCO₂) for 20 min, the respirator settings were changed to achieve an acute 20–25% increase in minute volume. This was followed by a 10-min stabilization period and 50 min of continued hyperventilation at constant arterial CO₂ levels.

Results

In 64% of the patients FVm did not recover during hyperventilation. The time-course of ICP changes was significantly different from that of FVm, with ICP reaching its lowest value earlier (23 ± 12 vs 37 ± 20 min; P = 0.001) and returning more rapidly towards baseline than FVm (0.23 ± 0.22 vs -0.04 ± 0.14%/min; P = 0.00001) (Fig. 1).

Figure 1

Conclusions

The impaired FVm recovery and the discordance between ICP and FVm recovery patterns suggest that cerebrovascular responses to hyperventilation are altered after head injury. Reductions in ICP and reductions in FVm may involve different microvascular compartments. Potentially harmful reductions in CBF persist beyond the duration of useful ICP reduction.