Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary, Edinburgh EH3 9YW, UK 1Present address: Department of Anaesthetics, Royal Brisbane Hospital, Herston, Queensland 4029, Australia*Corresponding author
Presented to the Anaesthetic Research Society. Abstract published in Br J Anaesth 2001; 86: 325P6P.
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Accepted for publication: November 8, 2001
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Abstract |
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Methods. We studied 14 patients undergoing laparoscopy for minor gynaecological procedures, anaesthetized with isoflurane in nitrous oxide, and breathing spontaneously through a laryngeal mask airway. We made direct recordings of intra-abdominal pressure and respiratory flow before and after giving fentanyl 25 µg i.v.
Results. Satisfactory records were obtained in 11 patients. Before fentanyl, the abdominal pressure changes were small and had an inconsistent pattern, increasing in inspiration in seven patients and during expiration in five. After fentanyl, an increase in pressure during inspiration was seen in only two patients, and the intra-abdominal pressure during expiration was increased. The mean value of maximum abdominal pressure (which always occurred during expiration) increased from 17 (SD 5) cm H2O before to 25 (9) cm H2O after fentanyl (P<0.01).
Conclusions. Direct measurements support previous findings that opioids stimulate active phasic expiratory activity and can cause large increases in abdominal pressure.
Br J Anaesth 2002; 88: 3848
Keywords: analgesics, opioid, fentanyl; muscles, respiratory
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Introduction |
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Materials and methods |
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When the breathing pattern and inspired and expired gas compositions were stable, abdominal pressure and respiratory flow waveforms were recorded for 30 s. Fentanyl, 25 µg in 5 ml normal saline, was given rapidly intravenously, followed by 5 ml normal saline. Pressure and flow were recorded for a further 2 min. At the end of this time measurements were stopped, abdominal gas was released, the cannulae were removed and clinical management was continued. We took readings of inspired and end-tidal values from the gas analyser just before and 2 min after administration of fentanyl. Recordings were also made in two patients in whom only the saline flush was administered.
Pressure and flow signals were converted into text files and analysed using a spreadsheet program on a personal computer. The pressure transducer was calibrated using a water manometer.
We analysed three complete respiratory cycles, immediately before and 100 s after giving fentanyl. We displayed these data graphically and measured the following values in each cycle: the minimum intra-abdominal pressure during inspiration; the intra-abdominal pressure at onset of expiration; the maximum intra-abdominal pressure during expiration; and the intra-abdominal pressure at the end of expiration. We also measured the time from the start of each respiratory cycle to each chosen value. We took means of the measurements from the three cycles and constructed an average respiratory pressure cycle for each patient, before and after fentanyl.
Statistics
Group results are expressed as mean and SD and data were analysed by paired t test (Minitab v 12.1, Minitab Ltd, Coventry). Statistical significance was assumed if P<0.05.
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Results |
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Discussion |
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In some of the patients we studied, abdominal pressure increased during inspiration, caused by contraction of the diaphragm. In normal conscious subjects, this is the major influence on abdominal pressure. However, in our subjects this pressure change was small, and in some patients no increase in pressure during inspiration was detected, suggesting that either the diaphragm was contracting poorly or that this pressure change was concealed by the actions of other muscles. For example, relaxation of the abdominal muscles or, less likely, inspiratory activity of the rib-cage muscles could reduce the increase in abdominal pressure during inspiration and conceal any pressure change generated by contraction of the diaphragm.
Pressure changes consistent with some expiratory activity of the abdominal muscles were noted before opioid administration but these changes increased markedly and consistently after fentanyl. The close temporal relationship of these changes to the injection, and the characteristics of fentanyl, make other causes very unlikely. There were no changes in breathing pattern, gas measurements, or pressure after saline administration. We made measurements of the effects after 100 s because this would reliably give three breaths to analyse before the recording stopped at 120 s. We did not have ethical permission to prolong the recording further, and it is possible that the pressure changes were not maximal when we made our measurements. However, because ventilation is reduced, other confounding factors such as carbon dioxide tension, anaesthetic depth, and perhaps cerebral blood flow, will be changing too. Early measurements allow these factors to have less impact, and interpretation of changes noted after prolonged observations would have to be limited. Other studies have shown that the effects of fentanyl in the conscious subject take considerably longer to cause rigidity,9 and some even suggest that loss of consciousness may be a necessary condition for the feature to develop.10 Such observations are consistent with the cerebral kinetics of fentanyl,11 but animal studies suggest that the rigidity may be mediated by brainstem structures and it is evident that the respiratory effects of fentanyl are equally prompt.
Although these effects of opioids have been noted before, our study shows that a modest dose can cause a considerable increase in abdominal pressure change during expiration, to well above the limits usually set for gas insufflation during laparoscopy. However, the pressures generated by maximum expulsive efforts can be at least 10 times the values we noted.12 Distension of the abdomen by gas insufflation during laparoscopy would increase the length of the abdominal muscle fibres and might augment the tension the fibres could generate and the pressure changes produced. However, animal experiments suggest that the abdominal muscles, in contrast to the diaphragm, normally work over a limited range of fibre length.13
The effects of opioids on the abdominal muscles may be increased during anaesthesia. In healthy conscious volunteers, morphine 2 mg kg1, caused abdominal muscle activity in expiration and this activity was greatly increased by 70% nitrous oxide, which caused board-like rigidity and prevented mechanical ventilation.3 Abdominal muscle activity of this degree is potentially harmful, reducing the lung volume at end expiration, which could impair gas exchange by causing airway closure.14 During laparoscopy, abdominal muscle contraction will reduce the volume of gas that can be introduced before the pressure limit of the insufflator is reached and this could impair surgical access. During pelvic floor surgery, increased venous pressure caused by increased abdominal pressure may cause excessive bleeding. Abdominal muscle action can cause abnormal patterns of respiratory movement, which could be difficult for the inexperienced anaesthetist to distinguish from movements seen when airway obstruction is present, and lead to misdiagnosis and mismanagement of the airway.
There are several agents that could potentially reduce this effect. Although µ opioid effects are responsible for increased muscle tone, the effects are reduced by 1 or
1 opioid agonists.15 Opioids increase muscle activity by action at several central sites, including the peri-aqueductal grey matter and the locus coeruleus. Lesions in the latter site reduce the ability of opioids to increase muscle tone16 and it is possible that other agents that act at this site, such as
2 adrenergic agonists, could modulate this process. The control of muscle tone from the locus coeruleus is by
1-adrenergic and glutaminergic pathways, probably arranged in series.17 The
1 antagonist prazosin antagonizes the central effects of opioids whereas the spinal
2 blocker yohimbine does not.18
In summary, respiration is active in both expiration and inspiration but in the normal conscious subject expiratory activity in the abdominal muscles is small. Both anaesthesia and opioids can increase this activity. Even a small dose of opioid during anaesthesia increases abdominal pressure during expiration. In our patients, the expiratory pressure changes dominated the pressure waveform, suggesting a radical change in the mechanics of breathing in the anaesthetized patient given an opioid. During anaesthesia with spontaneous breathing, anaesthetists should be aware of the marked changes in abdominal pressure that can be brought about by even small doses of fentanyl.
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References |
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