- Email: [email protected]
Cardiovascular changes after the three stages of nasotracheal intubation
British Journal of Anaesthesia 91 (5): 667±71 (2003)
DOI: 10.1093/bja/aeg240
Cardiovascular changes after the three stages of nasotracheal intubation S. Singh and J. E. Smith* Department of Anaesthesia, University Hospital Birmingham, Selly Oak Hospital, Birmingham B29 6JD, UK *Corresponding author. E-mail: [email protected]
Methods. Seventy-®ve ASA I or II patients, aged 16±65 yr, requiring nasotracheal intubation as part of their anaesthetic management, received a standardized general anaesthetic and were allocated randomly to receive either nasopharyngeal intubation or nasopharyngeal intubation plus direct laryngoscopy or full nasotracheal intubation. Results. There was a signi®cant hypertensive response, compared with pre-induction levels, in all three groups. The maximum mean (SD) mean arterial pressure in the nasotracheal intubation group was 113 (17.1) mm Hg, which was signi®cantly greater than that in the nasopharyngeal intubation (97 (13) mm Hg) (P<0.001) and in the nasopharyngeal intubation plus laryngoscopy (103 (10.3) mm Hg) (P=0.007) groups. There was no signi®cant difference between the nasopharyngeal intubation and nasopharyngeal intubation plus laryngoscopy groups (P=0.206). A similar pattern was seen for both systolic and diastolic arterial pressure. Nasotracheal intubation caused a signi®cant increase in maximum mean (SD) heart rate, compared with pre-induction values, whereas the other two groups caused signi®cant falls. The heart rate in the nasotracheal intubation group (92 (16.5) beats min±1) was signi®cantly greater than in the other two groups (74 (8.6) (P<0.001) and 76 (12) (P<0.001) beats min±1 respectively). There was no signi®cant difference in heart rates between the nasopharyngeal intubation and nasopharyngeal intubation plus laryngoscopy groups (P=0.420). Conclusions. Nasopharyngeal intubation causes a signi®cant pressor response. Stimulation of the larynx and trachea by the passage of the tracheal tube, but not direct laryngoscopy, causes a signi®cant increase in this response. Br J Anaesth 2003; 91: 667±71 Keywords: anaesthesia, general; intubation nasotracheal, complications Accepted for publication: June 9, 2003
Stimulation of the upper respiratory tract during tracheal intubation under general anaesthesia causes activation of the sympathoadrenal system and results in hypertension, tachycardia and also an increase in intracranial pressure.1 It has been shown that different phases of the intubation process cause different degrees of cardiovascular response,2 3 as indeed does mechanical stimulation of different sites lower down the airway.4 Orotracheal intubation comprises two distinct phases of airway stimulation.
First, direct laryngoscopy is carried out to identify the vocal cords, then the tracheal tube is advanced through the vocal cords into the trachea. Two studies2 3 have attempted to differentiate the contributions to the pressor response by laryngoscopy alone and laryngoscopy followed by intubation, but they have given con¯icting results. Shribman and colleagues2 concluded that the hypertensive effect of laryngoscopy alone appeared to be similar to that of laryngoscopy followed by intubation, whereas Shinji and
Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2003
Downloaded from http://bja.oxfordjournals.org/ at Purdue University Libraries ADMN on May 22, 2015
Background. Nasotracheal intubation typically comprises three distinct stages: (i) nasopharyngeal intubation; (ii) direct laryngoscopy to identify the vocal cords; and (iii) the passage of the tracheal tube into the trachea. The aim of this study was to identify and compare the cardiovascular responses associated with each of these stages.
Singh and Smith
Methods After local ethics committee approval, 75 ASA group I or II patients, aged between 16 and 65 yr, undergoing elective maxillofacial surgery under general anaesthesia, requiring nasotracheal intubation as part of their anaesthetic management and giving informed written consent, participated in the study. Patients with cardiovascular disease, morbid obesity, oesophageal re¯ux, bleeding diatheses, diabetes mellitus, taking vasoactive drugs or with a history of nasal obstruction were excluded. Thirty minutes before the induction of anaesthesia, two sprays of xylometazoline were applied to the nasal mucosa of each nostril as the patient inhaled. 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, 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 oxygen 100%. Anaesthesia was induced with fentanyl 1 mg kg±1 and propofol 2.5 mg kg±1 followed by atracurium 0.5 mg kg±1, and the patient's lungs were ventilated with oxygen 30%, nitrous oxide 70% and iso¯urane by means of a face mask attached to a circle system. Ventilator settings were adjusted to maintain the end-expired carbon dioxide concentration at 4.5±5% and the iso¯urane vaporizer was adjusted to maintain the end-tidal iso¯urane concentration
at 0.6%. Indirect arterial pressure measurements were taken at 1 min intervals. After 4 min ventilation, patients were allocated to one of two groups using block randomization. Patients in Group 1 underwent nasopharyngeal intubation only. Patients in Group 2 were alternately allocated to one of two subgroups: in Subgroup 2a they underwent nasopharyngeal intubation followed by direct laryngoscopy, and in Subgroup 2b they underwent full nasotracheal intubation. In these two subgroups, it was important to ensure that the direct laryngoscopy times were identical, as the duration of laryngoscopy may have affected the pressor response.8 Therefore, the ®rst patient randomized to Group 2 underwent nasotracheal intubation and the laryngoscopy time was recorded. Then the next patient randomized to group 2 had nasopharyngeal intubation and direct laryngoscopy, and the laryngoscopy time used was the same as that during the previous nasotracheal intubation, and so on. After group allocation, the oscillotonometer was switched to standby mode and the appropriate procedures were carried out. Preformed, cuffed RAEÔ nasal tubes were used for all the intubations, size 6 mm for females and size 7 mm for males. In the two groups having nasopharyngeal intubations, the tubes were shortened to 5 cm for females and to 6 cm for males. The nostril used for the ®rst attempt at intubation was selected randomly. If undue resistance was encountered in this nostril, the other nostril was used instead. The ease of navigability through the nostril used was assessed as no signi®cant resistance, minor resistance or moderate resistance. After the completion of the intubation procedures, and the re-establishment of ventilation, the oscillotonometer was switched to automatic mode and four further arterial pressure determinations were made at 1 min intervals. The lungs were ventilated by means of the tracheal tube in the nasotracheal intubation group or with a face mask in the other two groups. The intubation time was taken as the interval between the start of the insertion of the tube through the nostril and the removal of the laryngoscope from the mouth, and the laryngoscopy time was taken as the interval between inserting the laryngoscope through the mouth and the removal of the laryngoscope from the mouth. If any dif®culty was encountered in performing mask ventilation after the induction of anaesthesia or if signi®cant epistaxis occurred after any intubation, the patient was withdrawn from the study and treated appropriately. After completing the cardiovascular recordings, the shortened tubes used in Groups 1 and 2a were removed and the trachea was intubated normally with the aid of a Macintosh laryngoscope. Between group data were analysed using ANOVA and t-tests with the Student±Newman±Keuls method. Within group data were analysed using Friedman's repeated measures ANOVA on ranks, with multiple comparisons vs control using Dunnett's method. A power analysis indicated that if the minimum clinically important difference in mean arterial pressure was deemed to be 12 mm Hg, then a sample
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colleagues3 reported that laryngoscopy followed by intubation produced signi®cantly greater hypertension than did laryngoscopy alone. Nasotracheal intubation is often necessary in elective or emergency maxillofacial surgery and previous work5±7 has suggested that the increase in blood pressure after this procedure is signi®cantly greater than that after orotracheal intubation. Nasotracheal intubation typically comprises three stages: (i) the tracheal tube is advanced through the nose and into the pharynx; (ii) direct laryngoscopy is carried out to identify the vocal cords; and (iii) the tube is passed through the glottis and into the trachea. It is possible that the stimulation of nose and nasopharynx, which does not occur during orotracheal intubation, is responsible for the greater hypertensive response to nasotracheal intubation. However, no attempt has been made to differentiate the contributions made by the three stages of nasotracheal intubation, so there is no information about the relative signi®cance of the nasal/ nasopharyngeal response in comparison with nasotracheal intubation. There is also no information about whether the combination of nasal/nasopharyngeal stimulation plus the more prolonged direct laryngoscopy required for nasal intubation6 produces a similar cardiovascular response to nasotracheal intubation, or less. The objective of this study, therefore, was to identify and compare the haemodynamic responses after the three stages of nasotracheal intubation.
Responses to the three stages of nasal intubation Table 1 Patient characteristics and baseline systolic, mean and diastolic arterial pressures and heart rate. Data are presented as mean (SD or range) or number Nasopharyngeal intubation
Age (yr) Weight (kg) Sex (F/M) Smoking history (yes/no) Pre-induction values Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate Pre-procedure values Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate
Nasopharyngeal intubation plus direct laryngoscopy
28.5 (17±50) 71.2 (14.8) 14/11 10/15 122 87 69 74
29.6 (18±54) 70.1 (13.1) 15/10 9/16
(12.5) (11.1) (13.3) (13.3)
123 87 70 77
103 (12.8) 70 (10.5) 53 (10.4) 73 (9.4)
(14.5) (9.1) (10.5) (15.4)
101 (9.8) 71 (6.5) 57 (6.3) 75 (11)
Nasotracheal intubation
29.6 (17±50) 69.7 (15) 16/9 9/16 126 90 72 77
(12.7) (13.9) (12.3) (9.4)
100 (14.8) 68 (11.8) 52 (10.9) 73 (9.7)
Nasopharyngeal intubation
One/two nostrils entered Resistance to navigability (none/minor/moderate) Laryngoscopy time (s) Intubation time Maximum values after procedure Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate Maximum increases (compared with pre-procedure values) Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate
Nasopharyngeal intubation plus direct laryngoscopy
17/8 9/11/5
Nasotracheal intubation
16/9 8/10/7
19/6 12/9/4
14.8 (6.8)
14.8 (6.8) 26.8 (7.9)
130 97 80 74
(17.7)² (13)² (12)² (8.6)
136 103 86 76
(13.2)² (10.3)² (11.2)² (12)
151 113 93 92
(24.4)²* (17.1)²* (16.1)²* (16.5)²*
27 27 27 1
(12.9) (11.9) (13) (6.1)
35 31 29 1
(12.4) (10.9) (12.2) (6.9)
51 45 41 19
(20)* (13.5)* (14.4)* (12.3)*
size of 25 patients in each group would be required when a is 0.05 and b is 0.2. Statistical analysis was performed using SigmaStat (v2).
Results The three groups were similar with respect to age, weight and sex distribution (Table 1). The numbers of smokers and non-smokers in each group were similar (Table 1). Six patients were withdrawn from the trial because satisfactory mask ventilation could not be maintained without a Guedel airway after the induction of anaesthesia. On direct laryngoscopy, 41 patients were found to have minor nosebleeds, either with small amounts of blood present on the posterior pharyngeal wall or with blood visible only on the tube. No patient had signi®cant epistaxis and no patient was withdrawn from the study because of this complication. The number of times the second nostril was used, after
undue resistance had been encountered in the ®rst nostril, was similar in each group (Table 2). The mean intubation time in the nasotracheal intubation group and the mean laryngoscopy times in the nasotracheal intubation group and the nasopharyngeal intubation plus laryngoscopy group are shown in Table 2. Before the induction of anaesthesia (pre-induction) and immediately before the test procedure was carried out (preprocedure), there was no signi®cant difference in mean arterial pressure (MAP) between the three groups. After induction of anaesthesia, MAP decreased signi®cantly in all three groups (Fig. 1). One minute after the test procedure had been completed, MAP was signi®cantly higher than both the pre-procedure and the pre-induction levels in all three groups. At 1 min after the procedure, there was a signi®cant difference in MAP between the nasotracheal intubation group and both the nasopharyngeal intubation group and the nasopharyngeal intubation plus laryngoscopy
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Table 2 Ease of navigability through nostril, laryngoscopy and intubation times and systolic, mean and diastolic arterial pressures and heart rate responses. Data are presented as mean (SD). ²P<0.05 compared with pre-induction values. *P<0.05 compared with other two groups
Singh and Smith
group. However, there was no signi®cant difference between the nasopharyngeal intubation and the nasopharyngeal intubation plus laryngoscopy group. A similar pattern was seen for both systolic and diastolic arterial pressure (Tables 1 and 2). At pre-induction and pre-procedure, there were no signi®cant differences in heart rates between the three groups. After induction of anaesthesia, there were no signi®cant changes in heart rate (Fig. 2). After the test procedure had been carried out, the heart rate in the nasopharyngeal intubation and nasopharyngeal plus laryngoscopy groups fell and at 4 min post-procedure, the heart rate was signi®cantly lower than pre-induction heart rates in these two groups. After nasotracheal intubation, the heart rate increased, and at 2 min after procedure, was signi®cantly greater than pre-induction level. At 2 min after procedure, the heart rate in the nasotracheal intubation group was signi®cantly greater than in the other two groups. There was no signi®cant difference in heart rates between the nasopharyngeal intubation and the nasopharyngeal intubation and laryngoscopy group.
Discussion This investigation has shown that the nasopharyngeal intubation stage of nasotracheal intubation produces a signi®cant hypertensive response. Applying direct laryngoscopy for a clinically appropriate time immediately after passing the tube into the pharynx does not add signi®cantly to this response. Advancing the tube from the pharynx into the larynx and trachea adds substantially to the hypertensive response generated by the ®rst two stages of nasotracheal intubation. These changes were observed even after the
Fig 2 Heart rate (mean, SEM) changes in nasopharyngeal intubation, nasopharyngeal intubation plus direct laryngoscopy and nasotracheal intubation groups before induction (Pre-ind), before test procedure (Preproc), and 1, 2, 3, and 4 min after test procedure (Post-proc). *P<0.05 between groups.
administration of fentanyl, a drug that is known to reduce the pressor response to intubation. Fentanyl was used in this investigation in order that the anaesthetic induction would re¯ect a technique that is widely used in clinical practice. The brisk pressor response to nasopharyngeal intubation has not been reported previously and may have important clinical consequences. It could have an adverse effect in patients with poorly controlled hypertension, critical myocardial ischaemia or those with raised intracranial pressure. In particular, the Advanced Life Support guidelines9 recommend the use of a nasopharyngeal airway as an adjunct in maintaining a compromised airway in patients with a depressed conscious level, whether attributable to anaesthesia, intracranial pathology or metabolic abnormalities. Resuscitators should, however, be aware of the possibility that the pressor response to the insertion of a nasopharyngeal airway may be associated with an increase in intracranial pressure, which could result in signi®cant morbidity or even mortality in patients with head injury or other intracranial pathology. It is possible that the application of lidocaine to the nasal mucosa, by means of a spray or drops, before nasopharyngeal intubation might attenuate cardiovascular responses,4 but there is no evidence to con®rm this at the present time. It is not clear why the extra stimulus of direct laryngoscopy, applied in patients of Group 2a, did not add signi®cantly to the hypertensive response to nasopharyngeal intubation. Laryngoscopy alone is known to be a potent airway stimulus that produces signi®cant hypertension and, in addition, in the technically more dif®cult nasotracheal intubations, the mean laryngoscopy time probably exceeded that normally associated with orotracheal intubation.6 It is
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Fig 1 Mean arterial pressure (mean, SEM) changes in nasopharyngeal intubation, nasopharyngeal intubation plus direct laryngoscopy and nasotracheal intubation groups before induction (Pre-ind), before test procedure (Pre-proc), and 1, 2, 3, and 4 min after test procedure (Postproc). *P<0.05 between groups.
Responses to the three stages of nasal intubation
and nasopharyngeal intubation plus laryngoscopy. It might be hypothesized that the nasocardiac re¯ex10 11 accounted for increased vagal activity in the ®rst two stages of nasotracheal intubation.
References
671
1 Burney RG, Winn R. Increased cerebrospinal ¯uid pressure during laryngoscopy and intubation for induction of anesthesia. Anesth Analg 1975; 54: 687±90 2 Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamines responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987; 59: 295±9 3 Shinji T, Taro M, Masayuki M, Hidenori T. Hemodynamic responses to tracheal intubation with laryngoscope versus lightwand intubating device (Trachlightâ) in adults with normal airway. Anesth Analg 2002; 95: 480±4 4 Yoshihiro H, Shuji D. Differences in cardiovascular response to airway stimulation at different sites and blockade of the responses by lidocaine. Anesthesiology 2000; 93: 95±103 5 Fassoulaki A, Andreopoulou K, Saleh M, Kitharatzi D. Metabolic and cardiovascular responses following oral and nasal intubation of the trachea. Acta Anaesth Belgica 1990; 41: 381±6 6 Smith JE, Grewal MS. Cardiovascular effects of nasotracheal intubation. Anaesthesia 1991; 46: 683±6 7 Smith JE, Grewal MS. Cardiovascular effects of nasotracheal intubationÐa reply. Anaesthesia 1992; 47: 278 8 Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation: in¯uence of duration of laryngoscopy with or without prior lidocaine. Anesthesiology 1977; 47: 381±4 9 Resuscitation Council UK. Advanced Life Support Course Provider Manual, 4th Edn. London: Resuscitation Council, 2000 10 Baxandall ML, Thorn JL. The nasocardiac re¯ex. Anaesthesia 1988; 43: 480±1 11 Bailey PL. Sinus arrest induced by trivial nasal stimulation during alfentanil-nitrous oxide anaesthesia. Br J Anaesth 1990; 65: 718±20
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possible that there may be a ceiling effect associated with this response, a ceiling that is not breached even when the stimulus of laryngoscopy is added to the stimulus of nasopharyngeal intubation. Tracheal intubation, however, produced a marked hypertensive response, signi®cantly greater than the response to the ®rst two stages. This ®nding concurs with the results of Shinji and colleagues,3 in their orotracheal intubation studies, and contrasts with those of Shribman and colleagues2 who found that oral intubation did not add signi®cantly to the hypertensive response of laryngoscopy. It is dif®cult to explain the discrepancy between these two publications, but Shribman and colleagues did, in fact, ®nd that the response to laryngoscopy and intubation was greater than the response to laryngoscopy alone, but the increase did not achieve statistical signi®cance. The explanation may therefore be that a type 2 error occurred in their study, which involved 12 patients in each group. This investigation has shown that the heart rate after nasotracheal intubation was signi®cantly greater than that after either nasopharyngeal intubation or nasopharyngeal intubation plus laryngoscopy. Similarly, both Shribman and colleagues2 and Shinji and colleagues3 found that heart rate after laryngoscopy plus intubation was signi®cantly greater than laryngoscopy alone when studying orotracheal intubation. Shribman and colleagues hypothesized that laryngoscopy produced balanced stimulation of vagal and cardiac accelerator ®bres, whereas intubation produced less vagal stimulation. This explanation could also account for some of the ®ndings in our study. However, in the orotracheal intubation studies, there were increases in the heart rate after laryngoscopy alone whereas in this investigation there were decreases in heart rate after both nasopharyngeal intubation
DOI: 10.1093/bja/aeg240
Cardiovascular changes after the three stages of nasotracheal intubation S. Singh and J. E. Smith* Department of Anaesthesia, University Hospital Birmingham, Selly Oak Hospital, Birmingham B29 6JD, UK *Corresponding author. E-mail: [email protected]
Methods. Seventy-®ve ASA I or II patients, aged 16±65 yr, requiring nasotracheal intubation as part of their anaesthetic management, received a standardized general anaesthetic and were allocated randomly to receive either nasopharyngeal intubation or nasopharyngeal intubation plus direct laryngoscopy or full nasotracheal intubation. Results. There was a signi®cant hypertensive response, compared with pre-induction levels, in all three groups. The maximum mean (SD) mean arterial pressure in the nasotracheal intubation group was 113 (17.1) mm Hg, which was signi®cantly greater than that in the nasopharyngeal intubation (97 (13) mm Hg) (P<0.001) and in the nasopharyngeal intubation plus laryngoscopy (103 (10.3) mm Hg) (P=0.007) groups. There was no signi®cant difference between the nasopharyngeal intubation and nasopharyngeal intubation plus laryngoscopy groups (P=0.206). A similar pattern was seen for both systolic and diastolic arterial pressure. Nasotracheal intubation caused a signi®cant increase in maximum mean (SD) heart rate, compared with pre-induction values, whereas the other two groups caused signi®cant falls. The heart rate in the nasotracheal intubation group (92 (16.5) beats min±1) was signi®cantly greater than in the other two groups (74 (8.6) (P<0.001) and 76 (12) (P<0.001) beats min±1 respectively). There was no signi®cant difference in heart rates between the nasopharyngeal intubation and nasopharyngeal intubation plus laryngoscopy groups (P=0.420). Conclusions. Nasopharyngeal intubation causes a signi®cant pressor response. Stimulation of the larynx and trachea by the passage of the tracheal tube, but not direct laryngoscopy, causes a signi®cant increase in this response. Br J Anaesth 2003; 91: 667±71 Keywords: anaesthesia, general; intubation nasotracheal, complications Accepted for publication: June 9, 2003
Stimulation of the upper respiratory tract during tracheal intubation under general anaesthesia causes activation of the sympathoadrenal system and results in hypertension, tachycardia and also an increase in intracranial pressure.1 It has been shown that different phases of the intubation process cause different degrees of cardiovascular response,2 3 as indeed does mechanical stimulation of different sites lower down the airway.4 Orotracheal intubation comprises two distinct phases of airway stimulation.
First, direct laryngoscopy is carried out to identify the vocal cords, then the tracheal tube is advanced through the vocal cords into the trachea. Two studies2 3 have attempted to differentiate the contributions to the pressor response by laryngoscopy alone and laryngoscopy followed by intubation, but they have given con¯icting results. Shribman and colleagues2 concluded that the hypertensive effect of laryngoscopy alone appeared to be similar to that of laryngoscopy followed by intubation, whereas Shinji and
Ó The Board of Management and Trustees of the British Journal of Anaesthesia 2003
Downloaded from http://bja.oxfordjournals.org/ at Purdue University Libraries ADMN on May 22, 2015
Background. Nasotracheal intubation typically comprises three distinct stages: (i) nasopharyngeal intubation; (ii) direct laryngoscopy to identify the vocal cords; and (iii) the passage of the tracheal tube into the trachea. The aim of this study was to identify and compare the cardiovascular responses associated with each of these stages.
Singh and Smith
Methods After local ethics committee approval, 75 ASA group I or II patients, aged between 16 and 65 yr, undergoing elective maxillofacial surgery under general anaesthesia, requiring nasotracheal intubation as part of their anaesthetic management and giving informed written consent, participated in the study. Patients with cardiovascular disease, morbid obesity, oesophageal re¯ux, bleeding diatheses, diabetes mellitus, taking vasoactive drugs or with a history of nasal obstruction were excluded. Thirty minutes before the induction of anaesthesia, two sprays of xylometazoline were applied to the nasal mucosa of each nostril as the patient inhaled. 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, 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 oxygen 100%. Anaesthesia was induced with fentanyl 1 mg kg±1 and propofol 2.5 mg kg±1 followed by atracurium 0.5 mg kg±1, and the patient's lungs were ventilated with oxygen 30%, nitrous oxide 70% and iso¯urane by means of a face mask attached to a circle system. Ventilator settings were adjusted to maintain the end-expired carbon dioxide concentration at 4.5±5% and the iso¯urane vaporizer was adjusted to maintain the end-tidal iso¯urane concentration
at 0.6%. Indirect arterial pressure measurements were taken at 1 min intervals. After 4 min ventilation, patients were allocated to one of two groups using block randomization. Patients in Group 1 underwent nasopharyngeal intubation only. Patients in Group 2 were alternately allocated to one of two subgroups: in Subgroup 2a they underwent nasopharyngeal intubation followed by direct laryngoscopy, and in Subgroup 2b they underwent full nasotracheal intubation. In these two subgroups, it was important to ensure that the direct laryngoscopy times were identical, as the duration of laryngoscopy may have affected the pressor response.8 Therefore, the ®rst patient randomized to Group 2 underwent nasotracheal intubation and the laryngoscopy time was recorded. Then the next patient randomized to group 2 had nasopharyngeal intubation and direct laryngoscopy, and the laryngoscopy time used was the same as that during the previous nasotracheal intubation, and so on. After group allocation, the oscillotonometer was switched to standby mode and the appropriate procedures were carried out. Preformed, cuffed RAEÔ nasal tubes were used for all the intubations, size 6 mm for females and size 7 mm for males. In the two groups having nasopharyngeal intubations, the tubes were shortened to 5 cm for females and to 6 cm for males. The nostril used for the ®rst attempt at intubation was selected randomly. If undue resistance was encountered in this nostril, the other nostril was used instead. The ease of navigability through the nostril used was assessed as no signi®cant resistance, minor resistance or moderate resistance. After the completion of the intubation procedures, and the re-establishment of ventilation, the oscillotonometer was switched to automatic mode and four further arterial pressure determinations were made at 1 min intervals. The lungs were ventilated by means of the tracheal tube in the nasotracheal intubation group or with a face mask in the other two groups. The intubation time was taken as the interval between the start of the insertion of the tube through the nostril and the removal of the laryngoscope from the mouth, and the laryngoscopy time was taken as the interval between inserting the laryngoscope through the mouth and the removal of the laryngoscope from the mouth. If any dif®culty was encountered in performing mask ventilation after the induction of anaesthesia or if signi®cant epistaxis occurred after any intubation, the patient was withdrawn from the study and treated appropriately. After completing the cardiovascular recordings, the shortened tubes used in Groups 1 and 2a were removed and the trachea was intubated normally with the aid of a Macintosh laryngoscope. Between group data were analysed using ANOVA and t-tests with the Student±Newman±Keuls method. Within group data were analysed using Friedman's repeated measures ANOVA on ranks, with multiple comparisons vs control using Dunnett's method. A power analysis indicated that if the minimum clinically important difference in mean arterial pressure was deemed to be 12 mm Hg, then a sample
668
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colleagues3 reported that laryngoscopy followed by intubation produced signi®cantly greater hypertension than did laryngoscopy alone. Nasotracheal intubation is often necessary in elective or emergency maxillofacial surgery and previous work5±7 has suggested that the increase in blood pressure after this procedure is signi®cantly greater than that after orotracheal intubation. Nasotracheal intubation typically comprises three stages: (i) the tracheal tube is advanced through the nose and into the pharynx; (ii) direct laryngoscopy is carried out to identify the vocal cords; and (iii) the tube is passed through the glottis and into the trachea. It is possible that the stimulation of nose and nasopharynx, which does not occur during orotracheal intubation, is responsible for the greater hypertensive response to nasotracheal intubation. However, no attempt has been made to differentiate the contributions made by the three stages of nasotracheal intubation, so there is no information about the relative signi®cance of the nasal/ nasopharyngeal response in comparison with nasotracheal intubation. There is also no information about whether the combination of nasal/nasopharyngeal stimulation plus the more prolonged direct laryngoscopy required for nasal intubation6 produces a similar cardiovascular response to nasotracheal intubation, or less. The objective of this study, therefore, was to identify and compare the haemodynamic responses after the three stages of nasotracheal intubation.
Responses to the three stages of nasal intubation Table 1 Patient characteristics and baseline systolic, mean and diastolic arterial pressures and heart rate. Data are presented as mean (SD or range) or number Nasopharyngeal intubation
Age (yr) Weight (kg) Sex (F/M) Smoking history (yes/no) Pre-induction values Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate Pre-procedure values Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate
Nasopharyngeal intubation plus direct laryngoscopy
28.5 (17±50) 71.2 (14.8) 14/11 10/15 122 87 69 74
29.6 (18±54) 70.1 (13.1) 15/10 9/16
(12.5) (11.1) (13.3) (13.3)
123 87 70 77
103 (12.8) 70 (10.5) 53 (10.4) 73 (9.4)
(14.5) (9.1) (10.5) (15.4)
101 (9.8) 71 (6.5) 57 (6.3) 75 (11)
Nasotracheal intubation
29.6 (17±50) 69.7 (15) 16/9 9/16 126 90 72 77
(12.7) (13.9) (12.3) (9.4)
100 (14.8) 68 (11.8) 52 (10.9) 73 (9.7)
Nasopharyngeal intubation
One/two nostrils entered Resistance to navigability (none/minor/moderate) Laryngoscopy time (s) Intubation time Maximum values after procedure Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate Maximum increases (compared with pre-procedure values) Systolic arterial pressure Mean arterial pressure Diastolic arterial pressure Heart rate
Nasopharyngeal intubation plus direct laryngoscopy
17/8 9/11/5
Nasotracheal intubation
16/9 8/10/7
19/6 12/9/4
14.8 (6.8)
14.8 (6.8) 26.8 (7.9)
130 97 80 74
(17.7)² (13)² (12)² (8.6)
136 103 86 76
(13.2)² (10.3)² (11.2)² (12)
151 113 93 92
(24.4)²* (17.1)²* (16.1)²* (16.5)²*
27 27 27 1
(12.9) (11.9) (13) (6.1)
35 31 29 1
(12.4) (10.9) (12.2) (6.9)
51 45 41 19
(20)* (13.5)* (14.4)* (12.3)*
size of 25 patients in each group would be required when a is 0.05 and b is 0.2. Statistical analysis was performed using SigmaStat (v2).
Results The three groups were similar with respect to age, weight and sex distribution (Table 1). The numbers of smokers and non-smokers in each group were similar (Table 1). Six patients were withdrawn from the trial because satisfactory mask ventilation could not be maintained without a Guedel airway after the induction of anaesthesia. On direct laryngoscopy, 41 patients were found to have minor nosebleeds, either with small amounts of blood present on the posterior pharyngeal wall or with blood visible only on the tube. No patient had signi®cant epistaxis and no patient was withdrawn from the study because of this complication. The number of times the second nostril was used, after
undue resistance had been encountered in the ®rst nostril, was similar in each group (Table 2). The mean intubation time in the nasotracheal intubation group and the mean laryngoscopy times in the nasotracheal intubation group and the nasopharyngeal intubation plus laryngoscopy group are shown in Table 2. Before the induction of anaesthesia (pre-induction) and immediately before the test procedure was carried out (preprocedure), there was no signi®cant difference in mean arterial pressure (MAP) between the three groups. After induction of anaesthesia, MAP decreased signi®cantly in all three groups (Fig. 1). One minute after the test procedure had been completed, MAP was signi®cantly higher than both the pre-procedure and the pre-induction levels in all three groups. At 1 min after the procedure, there was a signi®cant difference in MAP between the nasotracheal intubation group and both the nasopharyngeal intubation group and the nasopharyngeal intubation plus laryngoscopy
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Table 2 Ease of navigability through nostril, laryngoscopy and intubation times and systolic, mean and diastolic arterial pressures and heart rate responses. Data are presented as mean (SD). ²P<0.05 compared with pre-induction values. *P<0.05 compared with other two groups
Singh and Smith
group. However, there was no signi®cant difference between the nasopharyngeal intubation and the nasopharyngeal intubation plus laryngoscopy group. A similar pattern was seen for both systolic and diastolic arterial pressure (Tables 1 and 2). At pre-induction and pre-procedure, there were no signi®cant differences in heart rates between the three groups. After induction of anaesthesia, there were no signi®cant changes in heart rate (Fig. 2). After the test procedure had been carried out, the heart rate in the nasopharyngeal intubation and nasopharyngeal plus laryngoscopy groups fell and at 4 min post-procedure, the heart rate was signi®cantly lower than pre-induction heart rates in these two groups. After nasotracheal intubation, the heart rate increased, and at 2 min after procedure, was signi®cantly greater than pre-induction level. At 2 min after procedure, the heart rate in the nasotracheal intubation group was signi®cantly greater than in the other two groups. There was no signi®cant difference in heart rates between the nasopharyngeal intubation and the nasopharyngeal intubation and laryngoscopy group.
Discussion This investigation has shown that the nasopharyngeal intubation stage of nasotracheal intubation produces a signi®cant hypertensive response. Applying direct laryngoscopy for a clinically appropriate time immediately after passing the tube into the pharynx does not add signi®cantly to this response. Advancing the tube from the pharynx into the larynx and trachea adds substantially to the hypertensive response generated by the ®rst two stages of nasotracheal intubation. These changes were observed even after the
Fig 2 Heart rate (mean, SEM) changes in nasopharyngeal intubation, nasopharyngeal intubation plus direct laryngoscopy and nasotracheal intubation groups before induction (Pre-ind), before test procedure (Preproc), and 1, 2, 3, and 4 min after test procedure (Post-proc). *P<0.05 between groups.
administration of fentanyl, a drug that is known to reduce the pressor response to intubation. Fentanyl was used in this investigation in order that the anaesthetic induction would re¯ect a technique that is widely used in clinical practice. The brisk pressor response to nasopharyngeal intubation has not been reported previously and may have important clinical consequences. It could have an adverse effect in patients with poorly controlled hypertension, critical myocardial ischaemia or those with raised intracranial pressure. In particular, the Advanced Life Support guidelines9 recommend the use of a nasopharyngeal airway as an adjunct in maintaining a compromised airway in patients with a depressed conscious level, whether attributable to anaesthesia, intracranial pathology or metabolic abnormalities. Resuscitators should, however, be aware of the possibility that the pressor response to the insertion of a nasopharyngeal airway may be associated with an increase in intracranial pressure, which could result in signi®cant morbidity or even mortality in patients with head injury or other intracranial pathology. It is possible that the application of lidocaine to the nasal mucosa, by means of a spray or drops, before nasopharyngeal intubation might attenuate cardiovascular responses,4 but there is no evidence to con®rm this at the present time. It is not clear why the extra stimulus of direct laryngoscopy, applied in patients of Group 2a, did not add signi®cantly to the hypertensive response to nasopharyngeal intubation. Laryngoscopy alone is known to be a potent airway stimulus that produces signi®cant hypertension and, in addition, in the technically more dif®cult nasotracheal intubations, the mean laryngoscopy time probably exceeded that normally associated with orotracheal intubation.6 It is
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Fig 1 Mean arterial pressure (mean, SEM) changes in nasopharyngeal intubation, nasopharyngeal intubation plus direct laryngoscopy and nasotracheal intubation groups before induction (Pre-ind), before test procedure (Pre-proc), and 1, 2, 3, and 4 min after test procedure (Postproc). *P<0.05 between groups.
Responses to the three stages of nasal intubation
and nasopharyngeal intubation plus laryngoscopy. It might be hypothesized that the nasocardiac re¯ex10 11 accounted for increased vagal activity in the ®rst two stages of nasotracheal intubation.
References
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1 Burney RG, Winn R. Increased cerebrospinal ¯uid pressure during laryngoscopy and intubation for induction of anesthesia. Anesth Analg 1975; 54: 687±90 2 Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamines responses to laryngoscopy with and without tracheal intubation. Br J Anaesth 1987; 59: 295±9 3 Shinji T, Taro M, Masayuki M, Hidenori T. Hemodynamic responses to tracheal intubation with laryngoscope versus lightwand intubating device (Trachlightâ) in adults with normal airway. Anesth Analg 2002; 95: 480±4 4 Yoshihiro H, Shuji D. Differences in cardiovascular response to airway stimulation at different sites and blockade of the responses by lidocaine. Anesthesiology 2000; 93: 95±103 5 Fassoulaki A, Andreopoulou K, Saleh M, Kitharatzi D. Metabolic and cardiovascular responses following oral and nasal intubation of the trachea. Acta Anaesth Belgica 1990; 41: 381±6 6 Smith JE, Grewal MS. Cardiovascular effects of nasotracheal intubation. Anaesthesia 1991; 46: 683±6 7 Smith JE, Grewal MS. Cardiovascular effects of nasotracheal intubationÐa reply. Anaesthesia 1992; 47: 278 8 Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation: in¯uence of duration of laryngoscopy with or without prior lidocaine. Anesthesiology 1977; 47: 381±4 9 Resuscitation Council UK. Advanced Life Support Course Provider Manual, 4th Edn. London: Resuscitation Council, 2000 10 Baxandall ML, Thorn JL. The nasocardiac re¯ex. Anaesthesia 1988; 43: 480±1 11 Bailey PL. Sinus arrest induced by trivial nasal stimulation during alfentanil-nitrous oxide anaesthesia. Br J Anaesth 1990; 65: 718±20
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possible that there may be a ceiling effect associated with this response, a ceiling that is not breached even when the stimulus of laryngoscopy is added to the stimulus of nasopharyngeal intubation. Tracheal intubation, however, produced a marked hypertensive response, signi®cantly greater than the response to the ®rst two stages. This ®nding concurs with the results of Shinji and colleagues,3 in their orotracheal intubation studies, and contrasts with those of Shribman and colleagues2 who found that oral intubation did not add signi®cantly to the hypertensive response of laryngoscopy. It is dif®cult to explain the discrepancy between these two publications, but Shribman and colleagues did, in fact, ®nd that the response to laryngoscopy and intubation was greater than the response to laryngoscopy alone, but the increase did not achieve statistical signi®cance. The explanation may therefore be that a type 2 error occurred in their study, which involved 12 patients in each group. This investigation has shown that the heart rate after nasotracheal intubation was signi®cantly greater than that after either nasopharyngeal intubation or nasopharyngeal intubation plus laryngoscopy. Similarly, both Shribman and colleagues2 and Shinji and colleagues3 found that heart rate after laryngoscopy plus intubation was signi®cantly greater than laryngoscopy alone when studying orotracheal intubation. Shribman and colleagues hypothesized that laryngoscopy produced balanced stimulation of vagal and cardiac accelerator ®bres, whereas intubation produced less vagal stimulation. This explanation could also account for some of the ®ndings in our study. However, in the orotracheal intubation studies, there were increases in the heart rate after laryngoscopy alone whereas in this investigation there were decreases in heart rate after both nasopharyngeal intubation