Both epidural and paravertebral blocks are effective in controlling post-thoracotomy pain, but comparison of preoperative and balanced techniques, measuring pulmonary function and stress responses, has not been undertaken previously. We studied 100 adult patients, premedicated with morphine and diclofenac, allocated randomly to receive thoracic epidural bupivacaine or thoracic paravertebral bupivacaine as preoperative bolus doses followed by continuous infusions. All patients also received diclofenac and patient-controlled morphine. Significantly lower visual analogue pain scores at rest and on coughing were found in the paravertebral group and patient-controlled morphine requirements were less. Pulmonary function was significantly better preserved in the paravertebral group who had higher oxygen saturations and less postoperative respiratory morbidity. There was a significant increase in plasma concentrations of cortisol from baseline in both the epidural and paravertebral groups and in plasma glucose concentrations in the epidural group, but no significant change from baseline in plasma glucose in the paravertebral group. Areas under the plasma concentration vs time curves for cortisol and glucose were significantly lower in the paravertebral groups. Side effects, especially nausea, vomiting and hypotension, were troublesome only in the epidural group. We conclude that with these regimens, paravertebral block was superior to epidural bupivacaine.
The predominant gas exchange impairment in BPD is a reduced V(A):Q, described by the right shift of the Spo(2) versus PIo(2) relationship. This provides a simpler method for defining BPD, which can grade disease severity.
The effect of increasing end-tidal enflurane concentration on the auditory evoked response was studied in six patients. After a standard induction, anesthesia was maintained with 70% nitrous oxide in oxygen and the end-tidal enflurane concentration was increased gradually from 0 to 1% over a period of 30 min. The averaged auditory evoked response was derived from the electroencephalogram and measurements were made of the latencies and amplitudes of waves I, III, V, Pa and Nb within the auditory evoked response. The latencies of all waves and the interpeak latencies I to V and III to V showed significant linear increases and the amplitudes of Pa and Nb showed significant linear decreases with increasing end-tidal enflurane concentration. These results could not be explained by changes in deep body temperature or end-tidal carbon dioxide concentration. The study demonstrated a dose-related direct effect of enflurane on the brainstem and early cortical components of the auditory evoked response.
We have examined the effects of isoflurane (0.6-2.9% end-tidal) on the auditory evoked response (AER) in six patients before elective surgery. Isoflurane produced significant dose-related changes in the AER: reductions in amplitude and increases in latency of the cortical waves Pa and Nb, and increases in the latency of the brainstem waves III and V. When isoflurane was compared with halothane and enflurane using an MAC-based comparison, we found no differences in the effect of the three agents on the amplitude of the early cortical waves, although the latencies showed significant differences. The consistent dose-related effect on the amplitudes of the cortical waves implies that the AER could be a promising index of the depth of anaesthesia.
The effects of increasing concentrations of halothane and enflurane on selected components of the auditory evoked response were studied in 12 patients; six received halothane and six enflurane. After the induction of anaesthesia with thiopentone, anaesthesia was maintained with 70% nitrous oxide in oxygen. Ventilation was controlled. The inspired concentration of the inhalation agent was increased incrementally, halothane in steps of 0.5% up to 2.5%, and enflurane in steps of 1% up to 5%. With both agents, linear dose-related increases were seen in the latencies of waves III, V, Pa and Nb and the interpeak intervals I-V and III-V, with decreases in the amplitudes of Pa and Nb. In five of the patients the inhalation agent was discontinued at the end of the test period, resulting in reversal of the changes in some or all of these waves. End-tidal carbon dioxide tension was controlled and variations of temperature and arterial pressure were insufficient to produce the observed changes. The results show that halothane and enflurane delay neural transmission along the brainstem and cortical sections of the auditory pathway and that the effects of these agents are approximately related to their known anaesthetic potencies.
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