British journal of anaesthesia
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Comparative Study
Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane.
The cerebral effects of sevoflurane were compared in dogs with those of enflurane and isoflurane. Initially, the minimum alveolar concentrations (MAC) of sevoflurane and enflurane were determined and the electroencephalographic (EEG) responses to increasing doses of sevoflurane (1.5, 2.0 and 2.5 MAC) or enflurane (1.5 and 2.0 MAC) in unparalysed animals were examined. Administration of sevoflurane was not associated with seizure activity at any concentration either during normocapnia (PaCO2 5.3 kPa) or hypocapnia (PaCO2 2.7 kPa), even in the presence of intense auditory stimuli. ⋯ In a separate group of dogs, the effects of increasing concentrations of sevoflurane and isoflurane (0.5, 1.5 and 2.15 MAC) were compared directly on arterial pressure, cardiac output and heart rate, cerebral blood flow and the cerebral metabolic rate for oxygen (CMRO2) using the venous outflow technique. Sevoflurane, in common with isoflurane, had minimal effects on cerebral blood flow at the concentrations studied, but significantly reduced the CMRO2 at end-tidal concentrations sufficient to produce a burst suppression pattern on the EEG (approximately 2.15 MAC). Both sevoflurane and isoflurane significantly decreased arterial pressure in a dose-dependent manner, but neither drug significantly altered cardiac output.
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The efficiency of a foam cuffed tracheal tube has been studied in protecting the pulmonary tree from aspiration of oropharyngeal and gastric contents. Following instillation of methylene blue dye above the cuff, subsequent fibreoptic bronchoscopy revealed no instance of dye staining of the tracheal mucosa. A "bench" study was undertaken subsequently to estimate the likely pressure that the cuff would exert on the tracheal mucosa as a result of elastic recoil properties of the foam. The results suggested that, under normal clinical conditions, the pressure is not likely to exceed a value at which impairment of the mucosal blood supply would occur.
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We have examined the effects on the cardiovascular system and on regional blood flow of propofol and thiopentone when administered with IPPV (FIO2 0.4). A longitudinal study design was used in which 16 studies were performed in eight sheep for 30 min before, during the last 30 min of 70 min anaesthesia, and for 6 h after anaesthesia. During anaesthesia with propofol and thiopentone, mean total body oxygen consumption decreased, respectively, by 47% (P less than 0.001) and 24% (P less than 0.01) of pre-anaesthesia baseline values, mean heart rate increased by approximately 50% (P less than 0.05) with both agents, mean arterial pressures increased by approximately 50% (P less than 0.05) with both agents and the mean cardiac output was unaltered with propofol anaesthesia but was decreased by 20% (P less than 0.05) with thiopentone anaesthesia. ⋯ Mean hepatic blood flow decreased consistently by a mean of 17% (P less than 0.01) during propofol anaesthesia, and inconsistently during thiopentone anaesthesia so that it was not significantly different from baseline values. Mean renal blood flow decreased during propofol anaesthesia by 7% (P less than 0.05) and by 27% (P less than 0.001) during thiopentone anaesthesia. Whereas most variables returned to baseline values within 2 h after propofol anaesthesia, this took 5 h after thiopentone anaesthesia.
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A case of prolonged neuromuscular block following the administration of suxamethonium is reported. Three hours after administration of suxamethonium, a well defined, recovering phase II block was demonstrated with a T4:T1 ratio of 0.25, and neostigmine was administered. Although the T4:T1 ratio was improved to 0.9, T1 remained at 25% of control, and significant paralysis persisted which responded to administration of cholinesterase. It is concluded that neuromuscular monitoring cannot reliably predict reversibility in such cases and that, even after 3 h, antagonism of prolonged suxamethonium block should commence with cholinesterase, followed by neostigmine if necessary.
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We have investigated the value of lower oesophageal contractility (LOC) in detecting awareness during anaesthesia in 20 human volunteer patients. LOC was measured either with subjects awake or after induction with propofol, during induction with propofol, and then as consciousness returned. Statistically significant changes were observed in the frequency of spontaneous contractions, peak and mean amplitude of spontaneous and provoked contractions, and the oesophageal contractility index as subjects lost consciousness and also as it was regained. The differences in LOC which occurred when subjects were conscious and unconscious support the view that LOC is related to the depth of anaesthesia, but its unreliability at the interface between consciousness and unconsciousness prevents selective detection of awareness, although the response in the presence of painful stimuli has not been tested.