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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.

Introduction: Little is known about cerebral autoregulation in children. The aim of this study was to examine cerebral autoregulation in children., Methods: Cerebral autoregulation testing was performed during less than 1 MAC sevoflurane anaesthesia in children (from 6 months to 14 yr) and in adults (18-41 yr). Mean middle cerebral artery flow velocities (V(MCA)) were measured using transcranial Doppler ultrasonography. Mean arterial pressure (MAP) was increased to whichever was greater: 20% above baseline or (i) 80 mm Hg for less than 9 yr, (ii) 90 mm Hg for 9-14 yr, and (iii) 100 mm Hg for adults. Cerebral autoregulation was considered intact if the autoregulatory index was > or =0.4., Results: There were 13 subjects less than 2 yr old (Group 1), 13 subjects 2-5 yr (Group II), 14 subjects 6-9 yr (Group III), 12 subjects 10-14 yr (Group IV), and 12 adults (Group V; control group). All subjects had an autoregulatory index > or =0.4. There was no difference in autoregulatory index between children in Groups I-IV or between children and adults., Discussion: We found no age-related differences in autoregulatory capacity during low-dose sevoflurane anaesthesia. We report no differences in autoregulatory capacity between children and adults.

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.

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.

Background: Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia., Methods: Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation., Results: The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg., Conclusions: Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.

Transcranial Doppler (TCD) ultrasonography has been used in a variety of clinical contexts to assess cerebrovascular reserve by measuring carbon dioxide reactivity. Reproducibility with time and altered position of the patient is examined in the present study. Carbon dioxide reactivity was determined in 10 healthy volunteers using TCD. Hypocarbia was produced by voluntary hyperventilation, and hypercarbia was produced by rebreathing from a circuit primed with 7% carbon dioxide. Each patient was studied in the supine position twice (1 week apart) and once in the seated position. Carbon dioxide reactivity was determined from linear regression analysis of paired middle cerebral artery flow velocity and end-tidal carbon dioxide values. Analysis of covariance for repeated measures was used for statistical analysis. Both the absolute slope and the relative slope (absolute slope expressed as a percentage of flow velocity at 40 mm Hg) were compared. In the supine position, flow velocity, absolute and relative slopes, and mean arterial pressure were similar from one week to the next at all carbon dioxide levels. In contrast, flow velocity, mean arterial pressure (adjusted for hydrostatic gradient), and absolute slope were decreased in the seated position (p < 0.05). No difference was observed when the relative slope was used for comparison. We conclude that absolute carbon dioxide reactivity is reproducible over time but may be influenced by position. Relative reactivity (relative slope), however, was both time and position independent.