Cerebral autoregulation and CO2 reactivity in anterior and posterior cerebral circulation during sevoflurane anesthesia.

The purpose of the study was to compare cerebral autoregulation (CA) and CO2 reactivity (CO2R) between the anterior and posterior circulation under sevoflurane anesthesia. We studied 9 adult ASA physical status I patients (22-47 yr) scheduled for elective orthopedic surgery. Blood flow velocity in the middle cerebral artery (Vmca) and in the basilar artery (Vba) were measured using transcranial Doppler ultrasonography. For CA testing, arterial blood pressure was increased using phenylephrine infusion. CA was quantified with the autoregulatory index (ARI). CO2R was investigated at PaCO2 of 30 +/- 2.8 mm Hg, 39.4 +/- 2.6 mm Hg, and 48.7 +/- 2.8 mm Hg. Linear regression analysis was used for CO2R. We found ARI was preserved in both arteries: ARImca (middle cerebral artery) = 0.72 +/- 0.2; ARIba (basilar artery) = 0.66 +/- 0.2; P = 0.5. With regard to CO2R, Vmca increased with slope of 1.7 cm/s/mm Hg PaCO2, Vba increased with slope of 1.5 cm/s/mm Hg PaCO2; P = 0.83. Absolute Vmca was higher compared with Vba; P < 0.05. We conclude that in healthy individuals under 0.5 MAC of sevoflurane and small-dose remifentanil: 1) mean flow velocities of BA are less than those of MCA; 2) autoregulation and CO2R are preserved in the basilar artery and are similar to those of MCA.

Cerebral autoregulation in pediatric traumatic brain injury.

OBJECTIVE: The aims of this study were to document the incidence of impaired cerebral autoregulation in children with traumatic brain injury using transcranial Doppler ultrasonography and to examine the relationship between autoregulatory capacity and outcome in children following traumatic brain injury. DESIGN: Prospective cohort study. SETTING: Harborview Medical Center (level I pediatric trauma center) in Washington state. PATIENTS: Thirty-six children <15 yrs old with traumatic brain injury: Glasgow Coma Scale score <9 (n = 12, group 1), Glasgow Coma Scale score 9-12 (n = 12, group 2), and Glasgow Coma Scale score 13-15 (n = 12, group 3). INTERVENTIONS: Cerebral autoregulation testing was conducted during extracranial surgery. Mean middle cerebral artery flow velocities were measured using transcranial Doppler as mean arterial pressure was increased to whichever variable was greater: 20% above baseline or a set value (80 mm Hg for <9 yrs and 90 mm Hg for 9-14 yrs). Autoregulatory capacity was quantified by the Autoregulatory Index. Autoregulatory Index <0.4 was considered impaired cerebral autoregulation. Discharge outcome using the Glasgow Outcome Scale score was considered good if the Glasgow Outcome Scale score was > or =4. MEASUREMENTS AND MAIN RESULTS: Twenty-four (67%) of 36 children had an Autoregulatory Index > or =0.4. The incidence of impaired cerebral autoregulation was 42% (five of 12) in group 1, 42% (five of 12) in group 2, and 17% (two of 12) in group 3. Ten (42%) of the 24 children with intact cerebral autoregulation had a good outcome compared with only one of 12 (8%) children with impaired cerebral autoregulation (p =.04). Six of 12 (50%) children with impaired cerebral autoregulation had hyperemia compared with one of 24 (4%) children with intact cerebral autoregulation (p <.01). Hyperemia was associated with poor outcome (p =.01). CONCLUSIONS: The incidence of impaired cerebral autoregulation was greatest following moderate to severe traumatic brain injury. Impaired cerebral autoregulation was associated with poor outcome. Hyperemia was associated with impaired cerebral autoregulation and poor outcome.

Ophthalmic artery blood flow velocity increases during hypocapnia.

PURPOSE: The effects of anesthetic management on blood flow to the optic nerve have not been well-studied. The ophthalmic artery provides the majority of the blood supply to the optic nerve via several smaller branches. Retinal blood flow has been shown to react to carbon dioxide (CO(2)) similar to intracranial vessels, but insufficient data exist for the ophthalmic artery. The purpose of this study is to examine the CO(2)-reactivity of the ophthalmic artery. METHODS: Eight healthy awake subjects aged 28 to 50 yr were tested for CO(2)-reactivity in the ophthalmic artery using transcranial Doppler (TCD) insonation of blood flow velocity (V(op)), while simultaneously recording the V(op) of the middle cerebral artery (V(mca)) as an internal control. V(op) and V(mca) recordings were made under hypocapnic, normocapnic and hypercapnic conditions. RESULTS: The CO(2)-reactivity slope of V(mca) was 3.27% per mmHg PaCO(2). From normocapnia to hypercapnia, V(op) did not change significantly (mean +/- SD, 18 +/- 4 cm*sec(-1) to 18 +/- 6 cm*sec(-1)), (end-tidal CO(2), etCO(2), = 43 +/- 5 mmHg to 53 +/- 4 mmHg, respectively). In contrast, V(op) increased significantly under hypocapnic conditions (etCO(2) = 26 +/- 4 mmHg) to 25 +/- 5 cm*sec(-1) (P < 0.05). The CO(2)-reactivity slope of V(op) from normocapnia to hypocapnia was 2.57% per mmHg. CONCLUSIONS: This study demonstrates that V(op) increases with hypocapnia, but is unaffected by hypercapnia. The anastomoses of the ophthalmic artery with the external carotid artery, which displays a relatively fixed resistance, may account for these findings.

Propofol: relation between brain concentrations, electroencephalogram, middle cerebral artery blood flow velocity, and cerebral oxygen extraction during induction of anesthesia.

BACKGROUND: The potential benefit of propofol dose regimens that use physiologic pharmacokinetic modeling to target the brain has been demonstrated in animals, but no data are available on the rate of propofol distribution to the brain in humans. This study measured the brain uptake of propofol in humans and the simultaneous effects on electroencephalography, cerebral blood flow velocity (V(mca)), and cerebral oxygen extraction. METHODS: Seven subjects had arterial and jugular bulb catheters placed before induction. Electroencephalography and V(mca) were recorded during induction with propofol while blood samples were taken from both catheters for later propofol analysis. Brain uptake of propofol was calculated using mass balance principles, with effect compartment modeling used to quantitate the rate of uptake. RESULTS: Bispectral index (electroencephalogram) values decreased to a minimum value of approximately 4 at around 7 min from the onset of propofol administration and then slowly recovered. This was accompanied by decreases in V(mca), reaching a minimum value of approximately 40% of baseline. Cerebral oxygen extraction did not change, suggesting parallel changes in cerebral metabolism. There was slow equilibrium of propofol between the blood and the brain (t(1/2keo) of 6.5 min), with a close relation between brain concentrations and bispectral index, although with considerable interpatient variability. The majority of the decreases in V(mca), and presumably cerebral metabolism, corresponded with bispectral index values reaching 40-50 and the onset of burst suppression. CONCLUSION: Description of brain distribution of propofol will allow development of physiologic pharmacokinetic models for propofol and evaluation of dose regimens that target the brain.

Chronic cocaine exposure alters carbon dioxide reactivity but does not affect cerebral blood flow autoregulation in anesthetized dogs.

BACKGROUND: Cocaine use is common in trauma victims. Consequently, understanding how cocaine alters normal physiology is important to providing appropriate medical care for these patients. This study was designed to identify how chronic cocaine exposure alters cerebrovascular physiology. METHODS: Ten dogs (seven experimental, three control) were studied. Transcranial Doppler was used to measure CO2 reactivity and autoregulation of cerebral blood flow velocity (CBFvel). Measurements were made in anesthetized animals (0.6% or 1.8% isoflurane in oxygen and intravenous fentanyl) at baseline before cocaine exposure and then at weekly intervals for 4 weeks. During the 4-week study period, cocaine was administered intravenously four times per day. RESULTS: Cocaine did not alter autoregulation of CBFvel in response to changes in mean arterial pressure. However, cocaine markedly impaired CO2 reactivity in three of the seven animals. In this subset of animals, increasing Paco2 decreased CBFvel, which is consistent with vasoconstriction rather than vasodilation. CONCLUSION: Chronic cocaine exposure does not alter autoregulation of CBFvel but does alter CO2 reactivity in a subset of susceptible animals. If confirmed in humans, these findings have implications for traumatic brain injury patients who are chronic cocaine users. Specifically, the findings suggest that hyperventilation could exacerbate intracranial hypertension in a subset of these patients.