British journal of anaesthesia
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Randomized Controlled Trial Clinical Trial
Effect of apparatus on functional residual capacity.
As the route of breathing and use of airway apparatus such as mask, mouthpiece and noseclip can alter breathing pattern, this study has used the helium dilution method to estimate the effects of mouthpiece and mask breathing on functional residual capacity (FRC) in the supine position, and the change in FRC that occurs between the sitting and supine positions while breathing by mouthpiece. In 13 normal subjects, breathing by mouthpiece, FRC was smaller, by a median of 1.07 litre (interquartile values 0.73-1.43 litre) in the supine compared with the sitting position (P < 0.01), but residual volume (RV) did not change significantly. FRC measured in the supine position was significantly greater when breathing by mask than by mouthpiece (0.25, 0.04-0.38 litre) and RV was greater by similar amounts (0.20, -0.02 to 0.49 litre). This difference may result from increased inspiratory activity while breathing via the mask.
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We have examined the effects of sedation with midazolam 0.1 mg kg-1 and reversal with flumazenil 0.5 mg on beat-to-beat heart rate (HR) variability (HRV), systolic arterial pressure (SAP), finger photoplethysmograph amplitude (PLA) and impedence pneumography in eight volunteers. With the onset of sedation there was a small decrease in SAP and increase in HR (ns). ⋯ These were thought to be secondary to activity of coupled cardiorespiratory neurones within the brain stem and the ventilatory periodicity appeared similar to that observed during the early stages of sleep. The diminished high frequency and increased low frequency oscillations induced by midazolam sedation were reversed by administration of flumazenil.
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Propofol is used widely during general anaesthesia but there has been concern that it may be implicated in provoking seizure activity. We have investigated the effects of low-dose propofol on the electrocorticogram of anaesthetized patients undergoing surgery for medically intractable epilepsy. During continuous peroperative recording of the electrocorticogram, propofol was administered in 25 mg increments until burst suppression occurred. ⋯ There was an increase in mean spike frequency in 16, extension of spike distribution in 15 and polyphasia in 13 patients. The mean dose of propofol required to cause burst suppression was 88.2 (range 25-175) mg. We conclude that at low doses, propofol caused activation of the electrocorticogram in epileptic patients but at higher doses burst suppression was induced.