Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury

Abstract

Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with imparied CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

Effects of Midazolam on Cerebral Hemodynamics and Cerebral Vasomotor Responsiveness to Carbon Dioxide

“…This responsiveness is impaired by many factors, such as atherosclerosis with aging (Yamaguchi et aI., 1979; Yamamoto et aI., 1980), severe head trauma, and subarachnoid hemorrhage (Enevoldsen and Jensen, 1978;Mendelow et aI., 1981) Pharmacologi cal agents have also been demonstrated to influence cerebral vasomotor reactivity to CO2, Propranolol decreased the vasodilatory effect of hypercarbia without affecting cerebrovasoconstriction induced by hypocarbia (Aoyagi et al, 1976). The influence of anesthetic agents seems to depend on the condi tions of the experiments.…”

Cerebral autoregulation following minor head injury

“…[6,9,21,22,25,26] Muizelaar and colleagues [21,22] evaluated autoregulation in head-injured patients by obtaining CBF values and either raising or lowering MABP to a new steady state and repeating the CBF measurement. They defined intact autoregulation as the •% CPP/ %• CVR ¾ 2 following the change in MABP, where CVR = CPP/CBF.…”

“…[14,26] Cerebral autoregulation can be impaired or absent following severe closed head injury. [4][5][6]8,9,21,22,25,26] Impairments in autoregulation may contribute by several mechanisms to secondary neuronal injury following head injury. Lowered cerebral perfusion pressure (CPP) caused by arterial hypotension or increased intracranial pressure (ICP) can occur and may cause critical reductions in cerebral blood flow (CBF) to ischemic levels more easily in head-injured patients who have poorly functioning or absent autoregulation.…”

Intracranial pressure pulse amplitude during changes in head elevation: a new parameter for determining optimum cerebral perfusion pressure?

“…Impairment of autoregulation is found in a variety of diseases, such as head injury, ischemic stroke, and SAH [35]. In circumstances where autoregulation is impaired, changes in CPP or MAP may aggravate secondary brain injury, and this was found to be associated with poor outcome [15,25,36]. Up to now, it is still unclear whether disturbances in autoregulation are generalized, regional, or perifocal.…”