Department of Anaesthesia, University Hospital Birmingham, Selly Oak Hospital, Birmingham B29 6JD, UK
* Corresponding author. E-mail: j.e.smith{at}bham.ac.uk
Accepted for publication April 28, 2004.
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Abstract |
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Methods. Twenty-four ASA I or II patients aged 1665 yr, requiring nasotracheal intubation as part of their anaesthetic management, received a standardized general anaesthetic and were randomly allocated to receive either a nasopharyngeal or an oropharyngeal airway.
Results. The two groups were similar with respect to age, weight and gender. There was a significant decrease in systolic pressure following the induction of anaesthesia in both groups. Following nasopharyngeal airway insertion, there was a significant rise in systolic pressure above pre-insertion levels (P0.001), though not above pre-induction levels (P=0.808). There was no significant change in the oropharyngeal airway insertion group (P=0.619). At 1 min post-insertion, the mean (SD) systolic pressure in the nasopharyngeal insertion group, 122 (21.6) mm Hg, was significantly greater than that in the oropharyngeal insertion group, 103 (15.3) mm Hg (P=0.017). Diastolic pressure followed a similar pattern. In both groups, heart rate fell after induction and fell further after insertion, and at 4 min post-insertion was significantly lower than pre-induction and pre-insertion levels. There was no significant difference in heart rates between the two groups (P=0.372).
Conclusions. The pressor response following the insertion of nasopharyngeal airways in anaesthetized patients is significantly greater than that following the insertion of oropharyngeal airways. However, the mean rise in arterial pressure does not exceed pre-induction level, and thus the response is less severe than that likely to be associated with orotracheal or nasotracheal intubation.
Keywords: anaesthesia, general ; complications, intubation nasal
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Introduction |
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The cardiovascular responses following the insertion of oropharyngeal airways in anaesthetized patients has been found to be of little clinical significance,5 but the pressor responses to the insertion of nasopharyngeal airways have not been studied. When investigating the pressor responses to the three stages of nasotracheal intubation, Singh and Smith6 recently found that the nasal insertion of stiff plastic tubes, derived from RAETM tracheal tubes, caused a significant rise in arterial pressure compared with pre-induction values. There is no information about whether soft pliable dedicated nasopharyngeal airways used in normal clinical practice would have similar effects.
Although transient increases in arterial pressures are of little consequence in healthy patients, any increase in oxygen demand in patients with ischaemic heart disease may lead to further ischaemia which could depress myocardial function and possibly cause infarction. Therefore this study aimed to compare the cardiovascular responses to the insertion of standard oropharyngeal and nasopharyngeal airways in anaesthetized patients.
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Methods |
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Thirty minutes before the induction of anaesthesia, the vasoconstrictor xylometazoline hydrochloride 0.1% was applied to the nasal mucosa. As the patient leaned forward slightly, the nozzle of the xylometazoline spray was inserted into a nostril and the patient was asked to sniff as the bottle was squeezed. Two sprays (0.09 mg per spray) were applied to each nostril. Electrocardiogram, indirect arterial pressure, arterial oxygen saturation and carbon dioxide concentrations were monitored in the anaesthetic room. All patients were investigated with the same calibrated and checked indirect arterial pressure machine (AgilentTM CMS2001) and an appropriately sized cuff was selected for each individual. After a stabilization period of at least 5 min, baseline recordings were made and the patient was given 100% oxygen. Anaesthesia was induced with fentanyl 1 µg kg1 and propofol 2.5 mg kg1 followed by atracurium 0.5 mg kg1, and the patient's lungs were ventilated with oxygen 30%, nitrous oxide 70% and isoflurane by means of a face mask attached to a circle system. Ventilator settings were adjusted to maintain the end expired carbon dioxide concentration at 4.55% and the isoflurane vaporizer was adjusted to maintain the end tidal isoflurane concentration at 0.6%. Indirect arterial pressure measurements were taken at 1 min intervals.
After 4 min of ventilation, patients were allocated to receive either an oropharyngeal airway (oropharyngeal airway group) or a nasopharyngeal airway (nasopharyngeal airway group) using block randomisation stratified for gender. After group allocation, the oscillotonometer was switched to standby mode and the appropriate airways were inserted. Plastic Guedel airways (size 3 for males and size 2 for females) or nasopharyngeal (PortexTM) airways (size 7 mm for males and 6 mm for females) were used. The nasopharyngeal airways were not softened by warming but were lubricated with a water-soluble gel. After completion of the insertion procedure, ventilation was resumed, the oscillotonometer was switched to automatic mode and four further arterial pressure determinations were made at 1 min intervals. If any difficulty was encountered in performing mask ventilation after the induction of anaesthesia or if significant epistaxis occurred after any insertion, the patient was withdrawn from the study and treated appropriately. After completing the cardiovascular recordings, the pharyngeal airways were removed and nasotracheal intubation was performed using a Macintosh laryngoscope.
Within-group data were analysed using repeated measures ANOVA with multiple comparisons versus control using Dunnett's method. Between-group data were analysed using t-tests. Power analysis indicated that if the minimum clinically important difference in peak systolic arterial pressures was deemed to be 18 mm Hg, then a sample size of 12 patients in each group would be required when =0.05 and ß=0.2. Statistical analysis was performed using SigmaStat 2·03 (SPSS Inc., Chicago, IL).
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Results |
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Discussion |
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It appears unlikely that the modest pressor response following the insertion of standard nasopharyngeal airways would result in deleterious effects in most anaesthetized patients. However, it should be borne in mind that, although indirect non-invasive arterial pressure monitors have been shown to be reasonably accurate79 and have been widely used in the assessment of the pressor response to intubation, they provide only intermittent reports and typically take 2025 s to make a determination. It is thus possible that the peak arterial pressure was missed and that the true peak pressure could be higher than that observed in this investigation. Direct intra-arterial pressure measurement would have been more precise and continuous, but the use of this technique would not be ethically justifiable in patients presenting mainly for extraction of wisdom teeth.
It should also be borne in mind that in this work we studied only anaesthetized patients, in whom cardiovascular responses may have been partially attenuated by the anaesthetic agents used (particularly fentanyl, propofol and isoflurane). Therefore anaesthetists should be aware that the study does not exclude the possibility that the pressor response may be exaggerated, and thus potentially harmful, in other situations where nasopharyngeal airways may be used, for example in lightly anaesthetized patients, awake or comatose maxillofacial patients or patients with head injury or other intracranial pathology.10
All the patients in this clinical trial received two sprays of xylometazoline to each nostril at least 30 min before the induction of anaesthesia. The local application of vasoconstrictors to reduce the incidence of epistaxis before nasotracheal or nasopharyngeal intubation is standard practice in anaesthesia for maxillofacial surgery. It is unlikely that this treatment had any affect on the results. It was applied to every patient before randomization. The mean arterial pressure of the 24 patients before the induction of anaesthesia was 122/71 mm Hg and the mean heart rate was 76 beats min1. No patients had arrhythmias or any other ECG changes. These findings concur with those of previous studies6 1113 involving nasal pre-treatment with vasoconstrictors.
The pressor response to the insertion of nasopharyngeal airways should be added to the other recognized complications of the device, which include failure of insertion, epistaxis (due to mucosal tears or avulsion of turbinates), laryngospasm (if the tube is too long), submucosal tunnelling and pressure sores. Contraindications include nasal airway occlusion, nasal fractures, coagulopathy (because of the risk of epistaxis), cerebrospinal fluid rhinorrhoea (resulting from base of skull fracture) and adenoid hypertrophy (in paediatric patients).
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References |
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