Sustained moderate reductions in arterial CO2 after brain trauma Time-course of cerebral blood flow velocity and intracranial pressure

Abstract

Objective: In healthy volunteers cerebral blood flow starts to recover towards baseline within a few minutes of continued hyperventilation due to normalisation of perivascular pH. We investigated the timecourse of changes in middle cerebral artery mean flow velocity (FVm) and intracranial pressure (ICP) in head-injured patients during sustained moderate reductions in arterial partial pressure of CO 2 (PaCO 2 ). Design: Observational study. Patients: Twenty-seven sedated, mechanically ventilated patients with severe head injury. Interventions: Measurements were made during and after routine determination of CO 2 -reactivity: an acute 20% increase in respiratory minute volume was followed by a 10-min stabilisation period and 50 min of continued moderate hyperventilation at a constant PaCO 2 (>3.5 kPa). Measurements and results: FVm was monitored with transcranial Doppler, ICP was monitored with intraparenchymal probes. During the 50-min period with stable PaCO 2 FVm increased in 36% of patients. All other patients showed a decline in FVm over the same time period. Overall FVm recovery was 0.03€0.14%·min -1 . The time-course of ICP changes was significantly different from that of FVm, with ICP reaching its lowest value earlier than FVm (23€12 vs 37€20 min; P = 0.001) and returning more rapidly towards baseline than FVm (0.23€0.23 vs 0.

Dynamic optic nerve sheath diameter responses to short-term hyperventilation measured with sonography in patients under general anesthesia

“…CO 2 is known as a major factor affecting the ICP, even in patients with moderate to severe head injury [19]. ICP monitoring in association with CO 2 can be effective in appropriate management of mechanically ventilated patients in intensive care unit, as well as intraoperative period.…”

Post-cardiac arrest syndrome: Epidemiology, pathophysiology, treatment, and prognostication: A Scientific Statement from the International Liaison Committee on Resuscitation; the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; the Council on Stroke (Part 1)

“…There are no data to support the targeting of a specific PaCO 2 after resuscitation from cardiac arrest; however, extrapolation of data from studies of other cohorts suggest ventilation to nor-mocarbia is appropriate. Studies in brain-injured patients have shown that the cerebral vasoconstriction caused by hyperventilation may produce potentially harmful cerebral ischaemia (Muizelaar et al, 1991;Steiner et al, 2004;Coles et al, 2007). Hyperventilation also increases intratho-racic pressure, which will decrease cardiac output both during and after CPR (Aufderheide et al, 2004;Aufderheide and Lurie, 2004).…”

Monitoring of head injured patients

“…An important recent finding of Steiner et al [27 ], who measured CBF velocity in 27 head injured patients during sustained moderate hyperventilation, was that following onset of hyperventilation, reduction in CBF continues for longer in patients with head injury than in healthy volunteers. Moreover, ICP values return to baseline sooner than flow velocity, suggesting that potentially harmful reductions in CBF may persist beyond the useful period of ICP reduction.…”