Department of Anaesthesiology, Chiba University School of Medicine, Chiba, Japan**Corresponding author
LMA® is the property of Intavent Limited.
Accepted for publication: June 28, 2001
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Abstract |
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Br J Anaesth 2001; 87: 70610
Keywords: anaesthetic techniques, inhalation; ventilation, occlusion pressure; ventilation, pattern; surgery, minor
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Introduction |
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Methods |
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Experimental procedure
When the breathing pattern was unchanged, the ventilatory variables were measured before the operation while maintaining a constant anaesthetic level (1 MAC). After the steady-state breathing measurements, the occlusion pressure (P0.1) was obtained during an inspiratory effort against the airway occluded at end expiration for one breath. Then, vecuronium 810 mg, was given and a cuffed tracheal tube (ID 7.0 mm for females and 8.0 mm for males) was inserted after removal of the LMA and the polyethylene catheter. During surgery, anaesthesia was maintained with isoflurane (13%) or sevoflurane (13%) with nitrous oxide (66%), and vecuronium intermittently as necessary.
After surgery, the tracheal tube was removed and the LMA and subglottic catheter were inserted again. Residual muscle paralysis was reversed by i.v. administration of atropine 1.0 mg and neostigmine 2.0 mg, and the patients were allowed to breathe spontaneously. Adequate reversal of neuromuscular block was confirmed by the presence of stable ventilation and by observing a normal train-of-four responses to the ulnar nerve stimulation.
When the breathing pattern was stable, the same ventilatory measurements as in the period immediately before the operation were repeated while maintaining the same anaesthetic level (1 MAC).
Data analyses
Using the software (ANADAT 5.1 and 5.2; RHT-Infodat Inc., Montreal, Quebec, Canada), durations of inspiration (TI) and expiration (TE), duty ratio (TI/Ttot: TI divided by TI+TE), respiratory frequency (RR), tidal volume (VT), and minute volume (MV) were determined from the flow signal. To analyse the respiratory waveform in detail, TE was divided into the duration of active expiration (TE-active; period with the presence of expiratory airflow) and the duration of end-expiratory pause (TE-pause; period of no airflow before onset of inspiration) as evaluated by Byrick and Janssen.12
As the presence of LMA contributes to the Pdelta, we estimated the resistive pressure decrease caused by the LMA. By measuring the pressure difference across the LMA passing 100% oxygen at a range of flow rates, we found that the resistance of the LMA (RLMA) varies with size and flow (V·), and can be fitted by the following Rohrers equations for each LMA size; LMA of #4: RLMA=0.077+0.093*V· (kPa litre1 s), LMA of #3: RLMA=0.074+0.085*V· (kPa litre1 s). Trans-laryngeal pressure (Plarynx) was, therefore, calculated by subtracting the RLMA*V· from the Pdelta for each flow rate. We calculated laryngeal resistance (Rlarynx) at a constant flow rate of 0.15 litre s1 (Rlarynx-0.15) during inspiration and expiration in addition to Rlarynx at maximum inspiratory and expiratory flow rates (Rlarynx-max).
Statistical analysis
All values are given as median (1090th percentiles). Comparison between the pre- and postoperative variables for each group and comparison between Rlarynx on inspiration and expiration were performed using the Wilcoxon Signed Rank test. Statistical differences were considered significant when P<0.05.
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Results |
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Breathing patterns
Ventilatory variables and the values of PE'CO2 obtained from each group before and after operation are shown in Table 2. In the ISO group, TI was longer (P=0.008) and TE shorter (P=0.016) after surgery while RR did not change. In the SEVO group, TI did not change after surgery while TE was significantly less than before surgery (P=0.008), resulting in a slight, but significant increase in RR (P=0.016). In addition to these changes, P0.1 significantly increased after the surgery in SEVO group (P=0.016). In both groups, TE was less because TE-pause was less (P=0.008) (Fig. 1). TI/Ttot increased after surgery in both groups (P=0.008). No difference was observed in VT, MV, and PE'CO2 before and after the surgery.
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Discussion |
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Postoperative breathing pattern
Breathing abnormality, such as rapid shallow breathing with increase in central respiratory drive, has been reported to occur after upper abdominal and thoracic surgery.2 3 9 13 14 Postoperative pain relief did not normalize the breathing pattern after lower abdominal surgery.15 Tulla and colleagues found that minor surgery had a minimal effect on the breathing pattern.16 Postoperative breathing pattern may thus depend on the magnitude of the surgical stress, unrelated to pain. We observed no significant changes in VT, MV, and PE'CO2 in our patients, but, this does not necessarily mean that minor surgery does not affect the breathing pattern at all. Detailed analysis of breathing pattern from a consistent shortening of TE and increase in TI/Ttot after surgery in both the ISO and SEVO groups. The differences in TI and P0.1 suggest that minor surgery may have different effects on respiratory control, depending on the different anaesthetic agents. The effects we found could also be caused by a time effect as the design of our study does not allow us to be sure that the changes found were related specifically to the effects of minor surgery. The respiratory depression caused by volatile anaesthetics decreases with time despite the same end-tidal concentration of volatile anaesthetics, and the degree of recovery from respiratory depression is different between different volatile anaesthetics.17
There was a considerable difference in the values of P0.1 obtained before the surgery between the ISO and SEVO groups. Although the underlying mechanisms are unclear, the difference might be primarily a result of the different effects of the two agents on the central respiratory neural network, secondary to the difference in the shape of occlusion pressure waveform between the two groups. Thus, we should be cautious about comparing the P0.1 values of the two groups.
Role of the larynx
We examined the breathing pattern without bypassing the larynx, which is an internal variable resistance that may control respiratory timing.5 Respiratory timing is determined by interaction between central modulation and peripheral mechanics, and postoperative changes in respiratory timing may be affected by the laryngeal airflow regulation. Kuna, Insalaco and Woodson18 measured laryngeal adductor muscle activity in awake and sleeping human adults, and demonstrated that while awake, the level of phasic expiratory activity was directly related to TE and expiratory Rlarynx, but the activity was absent in NREM sleep. We know of no study on laryngeal modulation of the respiratory timing in anaesthetized humans. Although we did not measure laryngeal muscle action, we found no difference in resistance between inspiration and expiration, unlike the awake condition.19 Laryngeal regulation of respiratory airflow under general anaesthesia is probably less than in conscious state and the larynx may not have had an important role in the modulation of respiratory timing in our quietly breathing anaesthetized subjects. We did find that laryngeal resistance had increased after the surgery, probably from changes such as laryngeal swelling produced by the endotracheal intubation.
The influence of increased laryngeal resistance on the postoperative breathing pattern
It is reasonable to consider that an increase in laryngeal resistance could affect breathing pattern after minor surgery. Flow limitation by increased laryngeal resistance could prolong both TI and TE, reduce RR, and decrease MV. However, we did not find any reduction of RR, and MV was well preserved. Compensatory mechanisms may be active. Although TI increased in the ISO group, this prolongation did not accompany changes in P0.1. This could mainain VT in the face of increased laryngeal resistance. In contrast, P0.1 increased without changes in TI in SEVO group, suggesting that augmentation of neural drive has occurred. The compensatory mechanisms in response to a small increase in laryngeal inspiratory resistance during isoflurane anaesthesia seem to differ from those during sevoflurane anaesthesia, although we have no explanation for the difference between the two anaesthetic agents.
TI/Ttot consistently increased in both the SEVO and ISO groups after minor surgery in this study and this increase was mainly a result of significant shortening of TE. The increase in TI/Ttot was ascribed from shortening of TE-pause and that the duration of active expiration did not alter after the surgery. It is likely that these changes are caused by the effects of minor surgery on respiratory control and for the shortneing of TE-pause may be compensation for the increase in expiratory flow resistance.
Minor surgery changes breathing pattern, affecting respiratory timing. This change in breathing pattern may result from an increase in laryngeal resistance caused by endotracheal intubation. There was also a slight difference in postoperative breathing pattern between sevoflurane and isoflurane, presumably because the central nervous system has different responses to different anaesthetics.
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Acknowledgements |
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References |
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