Diaphragmatic function during sevoflurane anaesthesia in dogs

The effect of increasing the concentration of sevoflurane anaesthesia on diaphragmatic function was investigated in six mechanically ventilated dogs. Diaphragmatic function was assessed by measuring the transdiaphragmatic pressure (Pdi) generated during bilateral supramaximal stimulation of the cervical phrenic nerves at frequencies of 0.5, 10, 20, 50, and 100 Hz under quasi-isometric conditions. Measurements were performed at 1, 1.5 and 2 MAC concentrations after maintaining stable conditions for one hour. The Pdi-stimulus frequency relationship was compared at each anaesthetic concentration. The sequence of changing anaesthetic depth was altered in random fashion among animals. The Pdi amplitude generated by single twitch (0.5 Hz) was unchanged at the three concentrations. In addition, no change in Pdi during 10, 20, 50 Hz stimulation was noted at any of the three levels of anaesthesia. By contrast, Pdi with 100 Hz stimulation during 2 MAC sevoflurane exposure (28.1 +/- 5.0 cmH2O) decreased below Pdi levels seen at 1 and 1.5 MAC (35.3 +/- 4.3 cmH2O and 31.5 +/- 4.3 cmH2O, respectively) (P less than 0.05). From these results, we conclude that sevoflurane impairs diaphragmatic function in deep anaesthesia.     

Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET

Background: Arterial carbon dioxide tension (PaCO₂) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia‐induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H₂¹⁵O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO₂ was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.     

Influence of aortic blood flow velocity on changes of middle cerebral artery blood flow velocity during isoflurane and sevoflurane anaesthesia

BACKGROUND AND OBJECTIVE: We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia. METHODS: Forty patients (age: isoflurane 24-62 years; sevoflurane 24-61 years; ASA I-III) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50-60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspiratory and end-expiratory concentrations of 0.75, 1.00, and 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvI). CSvI of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity. RESULTS: Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvI decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 +/- 25%/81 +/- 23%, 1.0 MAC: 79 +/- 19%/74 +/- 16%, 1.25 MAC: 71 +/- 16%/79 +/- 21%; [mean +/- SD] P = 0.0001). CONCLUSIONS: The reduction of the CSvI vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.     

Correlation of EEG spectral entropy with regional cerebral blood flow during sevoflurane and propofol anaesthesia

ENTROPY index monitoring, based on spectral entropy of the electroencephalogram, is a promising new method to measure the depth of anaesthesia. We examined the association between spectral entropy and regional cerebral blood flow in healthy subjects anaesthetised with 2%, 3% and 4% end-expiratory concentrations of sevoflurane and 7.6, 12.5 and 19.0 microg.ml(-1) plasma drug concentrations of propofol. Spectral entropy from the frequency band 0.8-32 Hz was calculated and cerebral blood flow assessed using positron emission tomography and [(15)O]-labelled water at baseline and at each anaesthesia level. Both drugs induced significant reductions in spectral entropy and cortical and global cerebral blood flow. Midfrontal-central spectral entropy was associated with individual frontal and whole brain blood flow values across all conditions, suggesting that this novel measure of anaesthetic depth can depict global changes in neuronal activity induced by the drugs. The cortical areas of the most significant associations were remarkably similar for both drugs.     

Leucocyte distribution during sevoflurane anaesthesia

We have examined if sevoflurane anaesthesia per se modified the number of circulating leucocytes in humans. Fifty-nine patients undergoing elective surgery were anaesthetized with sevoflurane in oxygen. The inhaled concentration was increased gradually to 5% and maintained for 20 min. Arterial blood samples were obtained before induction of anaesthesia and at 20 min. While the total number of leucocytes remained constant, circulating neutrophils decreased (mean 3370 (SD 1030) mm-3 to 3170 (940) mm-3; P < 0.01) and lymphocytes increased (1870 (520) mm-3 to 2040 (580) mm-3; P < 0.01). We conclude that high concentrations of sevoflurane modified the distribution of leucocytes in anaesthetized patients.      

The uptake of sevoflurane during anaesthesia

The rate of uptake of sevoflurane during clinical anaesthesia (1.3 MAC) was measured by computer-controlled injection of liquid anaesthetic into a closed breathing system. The cumulative uptake of sevoflurane was 4.8 ml, 7.4 ml. 9.5 ml and 11.5 ml at 30, 60, 90 and 120 min, respectively. The ratio of inspired to end-expired sevoflurane was greater than similar measurements we have made for desflurane in the past, but the absolute rate of sevoflurane uptake was less than the rate of uptake of desflurane in these cases. The rate of uptake was equivalent to 0.59e^{−0.32 t}  + 0.039e^{−0.036 t}  + 0.105e^{−0.0034 t}  mlmin⁻¹ liquid sevoflurane. Plasma urea and creatinine measured on the first postoperative day were not significantly different from pre-operative values.     

Low flow desflurane and sevoflurane anaesthesia in children

BACKGROUND AND OBJECTIVE: Low flow desflurane and sevoflurane anaesthesia were administered to children and compared for haemodynamic response, renal and hepatic function, recovery time and postoperative nausea and vomiting. METHODS: Eighty ASA I-II patients aged 5-15 yr were included in the study. Midazolam was given for premedication. Anaesthesia induction was performed with fentanyl, propofol and atracurium. After intubation, the first group received desflurane, oxygen and nitrous oxide at 6 L min(-1) and the second sevoflurane, oxygen and nitrous oxide at 6L min(-1). Ten minutes after induction the flow was decreased to 1 L min(-1) in both groups. Haemodynamic parameters, preoperative and postoperative renal and hepatic function, the times of operation and anaesthesia, and early recovery data were recorded. Modified Aldrete scores were noted at the 10th and 30th minutes postoperatively and postoperative nausea, and vomiting were assessed. RESULTS: There were no significant differences in haemodynamic parameters, renal and hepatic functions, postoperative recovery and postoperative nausea and vomiting between groups. The recovery time was shorter in the desflurane group compared to the sevoflurane group. CONCLUSION: Low flow desflurane and sevoflurane anaesthesia do not adversely affect haemodynamic parameters, hepatic and renal function in children. Desflurane may be preferred when early recovery from anaesthesia is warranted.     

Excitation phenomena during sevoflurane anaesthesia in children

The advantages of rapid induction of and emergence from sevoflurane anaesthesia may be more than offset by the frequent occurrence of agitation during induction and recovery, and a possible epileptogenic effect. The mechanisms and possible strategies to prevent these drawbacks are reviewed, on the basis of the most recent literature.     

Cerebral autoregulation in children during sevoflurane anaesthesia

Introduction. Little is known about cerebral autoregulationin children. The aim of this study was to examine cerebral autoregulationin children. Methods. Cerebral autoregulation testing was performed duringless than 1 MAC sevoflurane anaesthesia in children (from 6months to 14 yr) and in adults (18–41 yr). Mean middlecerebral artery flow velocities (V_MCA) were measured using transcranialDoppler ultrasonography. Mean arterial pressure (MAP) was increasedto whichever was greater: 20% above baseline or (i) 80 mm Hgfor less than 9 yr, (ii) 90 mm Hg for 9–14 yr, and (iii)100 mm Hg for adults. Cerebral autoregulation was consideredintact if the autoregulatory index was     

Glucose intolerance during prolonged sevoflurane anaesthesia

Purpose

The effects of prolonged sevoflurane anaesthesia on insulin sensitivity were investigated by two successive intravenous glucose tolerance tests (IVGTT) in eight patients who underwent prolonged surgery.

Methods

The first IVGTT was administered (25 g glucose as 20% dextrose in water iv) over two minutes 35 min after initiation of surgery. Arterial blood samples were obtained at 0, 5, 10, 30, 60, and 120 min after glucose administration for blood glucose and plasma insulin determination. A second IVGTT was performed six hours following the initiation of surgery.

Results

The disappearance rate of glucose (k-value) for the first IVGTT was 0.887 ± 0.436 (mean ± SD) % · min^?1, and 0.784 ± 0.289 for the second IVGTT. Both k-values are lower than the normal value. The maximum insulin response to glucose (ΔIRI · ΔBS^?1) of the second IVGTT was lower than the first IVGTT (0.124 ± 0.092 vs 0.071 ± 0.056, P < 0.05). The total insulin output of the first IVGTT was higher than the second IVGTT (1,161 ± 830 vs 568 ± 389 μU · min · ml^?1, P < 0.05).

Conclusion

Glucose intolerance is enhanced by diminished insulin output in response to blood glucose elevation during prolonged anaesthesia and surgery.     

Splanchnic blood flow during halothane-relaxant anaesthesia in elderly patients

We have previously found that halothane-relaxant anaesthesia in elderly patients causes a change towards a hyperkinetic circulation, with a decrease in the arterial-mixed venous oxygen content difference. This could be attributed to vasodilation. In the present study the splanchnic contribution to these changes was investigated. Nine patients were studied during halothane-relaxant anaesthesia prior to surgery. During anaesthesia splanchnic blood flow was markedly reduced, while splanchnic oxygen uptake decreased only moderately compared with the awake level. This resulted in an increase in splanchnic oxygen extraction. It is concluded that the splanchnic vascular bed does not contribute to the "hyperkinetic" circulation during halothane anaesthesia.     

Peripheral blood flow in the elderly during inhalational anaesthesia

We investigated whether aging altered the peripheral vascular effects of inhaled anaesthetic agents. Forearm blood flow (FBF) was measured in 20 young (18–34 yrs) and 21 healthy elderly (60–79 yrs) patients receiving isoflurane or halothane with 66% nitrous oxide (N₂O) in oxygen (O₂). After etomidate 0.3 mg/kg and vecuronium 0.1 mg/kg, the trachea was intubatcd and controlled ventilation instituted with 66% N₂O in O₂. Halothane or isoflurane were administered to achieve end-tidal concentrations of 0.5% halothane or 0.9% isoflurane after 20 min. FBF was measured by venous occlusion plethysraography during the 20 min study period. Induction of anaesthesia with etomidate decreased FBF below baseline (awake) values in both elderly and young; intubation returned FBF to baseline values in the young but not in the elderly. FBF decreased below baseline values in young and elderly patients receiving halothane and in elderly patients receiving isoflurane but not in young patients receiving isoflurane. FBF was significantly greater in young patients receiving isoflurane than halothane after 20 min administration.
We conclude that perfusion of forearm muscle and skin is maintained in the young but not in the elderly during anaesthesia with isoflurane/N₂O. Perfusion of forearm muscle and skin decreases in both young and elderly patients during anaesthesia with halothane/N₂O. The cardiovascular effects of isoflurane/N₂O and halothane/ N₂O did not differ significantly in healthy elderly patients.     

Degradation products of sevoflurane during low-flow anaesthesia

Low-flow (1 litre min^–1) sevoflurane anaesthesia was usedin 16 patients undergoing laparoscopic cholecystectomy (groupLSC, n = 8) or tympano-plasty (group TP, n = 8), and concentrationsof sevoflurane degradation products were measured. Degradationproducts in the circuit were measured hourly, and end-tidalcarbon dioxide concentration, inspired and end-tidal sevofluraneconcentrations, and carbon dioxide elimination were monitored.The only degradation product detected was CF₂=C(CF₃)-O-CH₂F(compound A). The mean maximum concentrations of compound Awere 21.6 (SEM 1.6) ppm and 1 9.6 (0.8) ppm in the LSC and TPgroups, respectively (ns). The maximum temperatures of sodalime were 46.4 (0.5) °C, and 44.8 (0.5) °C, respectively(P < 0.05). Hourly end-tidal sevoflurane concentrations andconcentrations of sevoflurane degradation products were thesame for both groups. Carbon dioxide elimination was the samefor both groups 1 h after the start of anaesthesia, but washigher in group LSC after 2 h (P < 0.05). Intraperitonealcarbon dioxide insufflation associated with laparoscopic cholecystectomyhad no effect on the concentration of sevoflurane degradationproducts.     

Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and TIVA

BACKGROUND: Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and total intravenous anesthesia (TIVA) is unclear. We examined the cerebral circulation autoregulation during anesthesia by sevoflurane or TIVA. METHODS: We measured mean blood pressure (MBP) and blood flow velocity of the middle cerebral artery by a transcranial Doppler ultrasonography before and during anesthesia using sevoflurane (volatile induction and maintenance of anesthesia (VIMA) group) and using propofol and fentanyl (TIVA group), and the relationship between changes in MBP and cerebral blood flow velocity was evaluated using the method of transfer function analysis. We calculated transfer gain and coherence by cross-spectrum from autospectra of MBP and cerebral blood flow velocity. RESULTS: Transfer gain during anesthesia by TIVA in the low frequency range and high frequency range was near 1 cm.sec-1.mmHg-1. It was about equal to the value of transfer gain before anesthesia. But transfer gain during anesthesia by VIMA was above 2 cm.sec-1.mmHg-1. CONCLUSION: These results suggest that TIVA by propofol and fentanyl maintains the dynamic autoregulation of cerebral blood flow, but sevoflurane impairs the autoregulation.     

A comparison of propofol and sevoflurane anaesthesia: effects on aortic blood flow velocity and middle cerebral artery blood flow velocity

We compared systemic (aortic) blood flow and cerebral blood flow velocity in 30 patients randomly allocated to receive either propofol or sevoflurane anaesthesia. Cerebral blood flow velocity (CBFv) was measured in the middle cerebral artery using transcranial Doppler. Systemic blood flow velocity (SBFv) was measured in the aorta using transthoracic Doppler sonography at the level of the aortic valve. Bispectral index (BIS) was used to measure the depth of anaesthesia. Measurements were made in the awake patient and repeated during propofol or sevoflurane anaesthesia, with BIS measurements of 40-50. The effects of SBFv on CBFv were estimated by calculating the cerebral/systemic blood flow velocity-index (CsvI). A CsvI value of 100 indicating a 1 : 1 relationship between CBFv and SBFv. The results demonstrated that propofol anaesthesia produced a significantly greater reduction in CsvI than did sevoflurane anaesthesia [propofol: 60 (19); sevoflurane: 83 (16), p = 0.009, t-test]. This suggests a direct reduction in CBFv independent of SBFv during propofol anaesthesia. The greater reduction of CBFv occurring during propofol anaesthesia may be due to lower cerebral metabolic demand compared with sevoflurane anaesthesia at comparable depths of anaesthesia.     

Cerebral blood flow and cerebral blood flow velocity during angiotensin-induced arterial hypertension in dogs

Pressure-passive perfusion beyond the upper limit of cerebral blood flow (CBF) autoregulation may be deleterious in patients with intracranial pathology. Therefore, monitoring of changes in CBF would be of clinical relevance in situations where clinical evaluation of adequate cerebral perfusion is impossible. Noninvasive monitoring of cerebral blood flow velocity using transcranial Doppler sonography (TCD) may reflect relative changes in CBF. This study correlates the effects of angiotensininduced arterial hypertension on CBF and cerebral blood flow velocity in dogs. Heart rate (HR) was recorded using standard ECG. Catheters were placed in both femoral arteries and veins for measurements of mean arterial blood pressure (MAP), blood sampling and drug administration. A left ventricular catheter was placed for injection of microspheres. Cerebral blood flow velocity was measured in the basilar artery through a cranial window using a pulsed 8 MHz transcranial Doppler ultrasound system. CBF was measured using colour-labelled microspheres. Intracranial pressure (ICP) was measured using an epidural probe. Arterial blood gases, arterial pH and body temperature were maintained constant over time. Two baseline measures of HR, MAP, CBF, cerebral blood flow velocity and ICP were made in all dogs (n = 10) using etomidate infusion (1.5 mg · kg^?1 · hr^?1) and 70% N₂O in O₂ as background anaesthesia. Following baseline measurements, a bolus of 1.25 mg angiotensin was injected iv and all variables were recorded five minutes after the injection. Mean arterial blood pressure was increased by 76%. Heart rate and ICP did not change. Changes in MAP were associated with increases in cortical CBF (78%), brainstem CBF (87%) and cerebellum CBF(64%). Systolic flow velocity increased by 27% and Vmean increased by 31% during hypertension (P < 0.05). Relative changes in CBF and blood flow velocity were correlated (CBF cortex — Vsyst: r = 0.94, CBF cortex — Vmean: r = 0.77; P < 0.001; CBF brainstem — Vsyst: r = 0.82, CBF brainstem — Vmean: r = 0.69; P < 0.05). Our results show that increases in arterial blood pressure beyond the upper limit of cerebral autoregulation increase CBF in dogs during etomidate and N₂O anaesthesia. The changes in CBF are correlated with increases in basilar artery blood flow velocity. These data suggest that TCD indicates the upper limit of the cerebral autoregulatory response during arterial hypertension. However, the amount of CBF change may be underestimated with the TCD technique.     

Convulsions associated with epidural analgesia during sevoflurane anaesthesia

A three-year-old girl who underwent an operation for adrenal neuroblastoma was anaesthetized with sevoflurane and epidural analgesia. In the immediate recovery period she had convulsions. The convulsions were successfully treated with thiopentone and sevoflurane, there were no neurological sequelae. The convulsions were considered to be a manifestation of mepivacaine toxicity because of a high plasma mepivacaine concentration. Complications of paediatric regional analgesia and manifestations of mepivacaine toxicity under sevoflurane anaesthesia are discussed.