Effect of sevoflurane on systemic and cerebral circulation, cerebral autoregulation and CO2 reactivity

Background: Sevoflurane is one of the most frequently used inhaled anesthetics for general anesthesia. Previously it has been reported that at clinically used doses of sevoflurane, cerebral vasoreactivity is maintained. However, there are no data how sevoflurane influences systemic and cerebral circulation in parallel. The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during sevoflurane anesthesia. Methods: Twenty nine patients undergoing general anesthesia were enrolled. Anesthesia was maintained with 1 MAC sevoflurane in 40% oxygen. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35 and 30 mmHg EtCO2 for 5 min respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded. Results: Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure and augmentation index as markers of arterial stiffness significantly increased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained at 1 MAC sevoflurane. Discussion: Cerebral autoregulation and CO2-reactivity is preserved at 1 MAC sevoflurane. Cerebrovascular effects of anesthetic compounds have to be assessed together with systemic circulatory effects. Trial registration: The study was registered at http://www.clinicaltrials.gov, identifier: NCT02054143, retrospectively registered. Date of registration: February 4, 2014. Keywords: Sevoflurane, Cerebral blood flow, cerebral autoregulation, CO2-reactivity, applanation tonometry, Transcranial DopplerL

Desflurane results in higher cerebral blood flow than sevoflurane or isoflurane at hypocapnia in pigs.

Background: In clinical neuroanaesthesia, the increase in cerebral blood flow (CBF) and intracranial pressure caused by the cerebral vasodilative effects of an inhalational anaesthetic agent is counteracted by the cerebral vasoconstriction induced by hypocapnia. Desflurane and sevoflurane may have advantages over the more traditionally used isoflurane in neuroanaesthesia but their dose-dependent vasodilative effects at hypocapnia have not been compared in the same model using truly equipotent minimal alveolar concentrations (MACs). Method: Desflurane, sevoflurane and isoflurane were administered in a randomized order to six pigs at 0.5 and 1.0 MAC. The intra-arterial xenon clearance technique was used to calculate CBF. Blood pressure was invasively monitored. Cerebral and systemic physiological variables were recorded first at normocapnia (PaCO2 5.6 kPa) and then at hypocapnia (PaCO2 3.5 kPa). Electroencephalographic (EEG) activity was continuously recorded. Results: None of the three agents abolished cerebrovascular reactivity to hyperventilation, and at 0.5 MAC all had similar effects on CBF at hypocapnia. Desflurane at 1.0 MAC was associated with 16% higher CBF (P = 0.027) at hypocapnia than isoflurane, and with 24% higher CBF (P = 0.020) than sevoflurane. There was no seizure activity in the EEG. Conclusion: More cerebral vasodilation at hypocapnia with high doses of desflurane than with sevoflurane or isoflurane indicates that desflurane might be less suitable for neuroanaesthesia than sevoflurane and isoflurane

The effects of dexmedetomidine on cerebral glucose metabolism, systemic cytokine release and cerebral autoregulation: Studies on healthy volunteers and aneurysmal subarachnoid haemorrhage patients

Dexmedetomidine is a very selective α2-agonist that has become a popular sedative in the intensive care unit. It has characteristics that make it appealing especially for neurologically compromised patients. Aneurysmal subarachnoid haemorrhage (aSAH) is a complicated disease where cerebral physiology and the regulation of cerebral blood flow, i.e., autoregulation, are often disturbed. It is important that the used anaesthetic and sedative drugs do not cause further damage. The aim of this study was to explore how dexmedetomidine affects cerebral glucose metabolism, systemic cytokine response, and cerebral autoregulation. The first two studies included healthy male volunteers. The first study investigated the effects of dexmedetomidine on cerebral glucose metabolism along with three other anaesthetic drugs (propofol, sevoflurane, S-ketamine) and a placebo group. The second study investigated the effects of dexmedetomidine and propofol on the release of cytokines, chemokines, and growth factors. The third study included 10 aSAH patients. We examined the effects of dexmedetomidine on cerebral autoregulation with three increasing doses after the baseline sedation with propofol and/or midazolam was suspended. In the volunteer studies, we found that the cerebral glucose metabolism was lowest with dexmedetomidine. In addition, we found that dexmedetomidine induced an anti-inflammatory cytokine response, whereas propofol induced a partly pro-inflammatory and slightly anti-inflammatory cytokine response. In aSAH patients, dexmedetomidine did not alter the static cerebral autoregulation compared to baseline. However, after the dose of 1.0 µg/kg/h, we observed a minor but statistically significant decrease in dynamic cerebral autoregulation which may suggest that in aSAH patients sedated with dexmedetomidine, sudden decreases in mean arterial pressure should be avoided

Brain perfusion, part 2: anesthesia and brain perfusion in small animals

Sedatives and anesthetics can influence cerebral metabolism and respiratory and cardiovascular dynamics, which results in changes in cerebral perfusion. This is of major importance when functional brain imaging techniques are used to measure cerebral blood flow or to evaluate neurotransmitter systems, and also during neurosurgery. In the present review, the influences on brain perfusion of different sedatives including opioids and anesthetics commonly used in veterinary medicine are summarized

Cerebral haemodynamic changes during propofol-remifentanil or sevoflurane anaesthesia: transcranial Doppler study under bispectral index monitoring.

INTRODUCTION: Transcranial Doppler (TCD) can detect the cerebral circulation arrest (CCA) in brain death. TCD is highly specific, but less sensitive because of false-negatives accounting for up to 10%. The aim of the study was to explore the diagnostic accuracy of TCD and to determine whether it can be augmented by strategies such as the insonation of the extracranial internal carotid artery (ICA) and sequential examinations. METHODS: Data of 184 patients, who met clinical criteria of brain death, observed from 1998 through 2006, were retrospectively reviewed. The study of cerebral arteries was performed through the transtemporal approach, suboccipital insonation of the vertebro-basilar system, transorbital insonation of the ICA and ophthalmic artery, and transcervical insonation of the extracranial ICA. Repeated exams were performed in cases of persistent diastolic flow. RESULTS: The specificity of the testing was 100%, no false-positive cases were recorded. The sensitivity of conventional TCD examination was 82.1%. The insonation of the extracranial ICA increased sensitivity to 88% allowing the detection of CCA in those patients lacking temporal windows; serial examinations further increased sensitivity to 95.6%. CONCLUSIONS: The addition of insonation of the cervical ICA and of the siphon increased sensitivity of TCD. Nevertheless, a CCA flow patterns may appear later on those segments. Serial examinations, may be needed in those cases

Cerebrovascular carbon dioxide reactivity in sheep: Effect of propofol or isoflurane anaesthesia

Publisher's copy made available with the permission of the publisher © Australian Society of AnaesthetistsPropofol and isoflurane are commonly used in neuroanaesthesia. Some published data suggest that the use of these agents is associated with impaired cerebral blood flow/carbon dioxide (CO₂) reactivity. Cerebrovascular CO₂ reactivity was therefore measured in three cohorts of adult merino sheep: awake (n=6), anaesthetized with steady-state propofol (15 mg/min; n=6) and anaesthetized with 2% isoflurane (n=6). Changes in cerebral blood flow were measured continuously from changes in velocities of blood in the sagittal sinus via a Doppler probe. Alterations in the partial pressure of carbon dioxide in arterial blood (PaCO₂) over the range 18-63 mmHg were achieved by altering either the inspired CO₂ concentration or the rate of mechanical ventilation. Cerebral blood flow/CO₂ relationships were determined by linear regression analysis, with changes in cerebral blood flow expressed as a percentage of the value for a PaCO₂ of 35 mmHg. Propofol decreased cerebral blood flow by 55% relative to pre-anaesthesia values (P=0.0001), while isoflurane did not significantly alter cerebral blood flow (88.45% of baseline, P=0.39). Significant linear relationships between cerebral blood flow and CO₂ tension were determined in all individual studies (r2 ranged from 0.72 to 0.99). The slopes of the lines were highly variable between individuals for the awake cohort (mean 4.73, 1.42-7.12, 95% CI). The slopes for the propofol (mean 2.67, 2.06-3.28, 95% CI) and isoflurane (mean 2.82, 2.19-3.45, 95% CI) cohorts were more predictable. However, there was no significant difference between these anaesthetic agents with respect to the CO₂ reactivity of cerebral blood flow.J. A. Myburgh, R. N. Upton, G. L. Ludbrook, A. Martinez, C. Granthttp://www.aaic.net.au/Article.asp?D=200137

High salt diet impairs cerebral blood flow regulation via salt‐induced angiotensin II suppression

ObjectivesThis study sought to determine whether salt‐induced ANG II suppression contributes to impaired CBF autoregulation.MethodsCerebral autoregulation was evaluated with LDF during graded reductions of blood pressure. Autoregulatory responses in rats fed HS (4% NaCl) diet vs LS (0.4% NaCl) diet were analyzed using linear regression analysis, model‐free analysis, and a mechanistic theoretical model of blood flow through cerebral arterioles.ResultsAutoregulation was intact in LS‐fed animals as MAP was reduced via graded hemorrhage to approximately 50 mm Hg. Short‐term (3 days) and chronic (4 weeks) HS diet impaired CBF autoregulation, as evidenced by progressive reductions of laser Doppler flux with arterial pressure reduction. Chronic low dose ANG II infusion (5 mg/kg/min, i.v.) restored CBF autoregulation between the pre‐hemorrhage MAP and 50 mm Hg in rats fed short‐term HS diet. Mechanistic‐based model analysis showed a reduced myogenic response and reduced baseline VSM tone with short‐term HS diet, which was restored by ANG II infusion.ConclusionsShort‐term and chronic HS diet lead to impaired autoregulation in the cerebral circulation, with salt‐induced ANG II suppression as a major factor in the initiation of impaired CBF regulation.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149286/1/micc12518_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149286/2/micc12518.pd