PRESSOR AND CATECHOLAMINE RESPONSE TO NASAL INTUBATION OF THE TRACHEA

PRESSOR AND CATECHOLAMINE RESPONSE TO NASAL INTUBATION OF THE TRACHEA

Br. J. Anaesth. (1989), 63, 283-286 PRESSOR AND CATECHOLAMINE RESPONSE TO NASAL INTUBATION OF THE TRACHEA B. H. MEIKLEJOHN AND S. COLEY BOYD H . MEI...

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Br. J. Anaesth. (1989), 63, 283-286

PRESSOR AND CATECHOLAMINE RESPONSE TO NASAL INTUBATION OF THE TRACHEA B. H. MEIKLEJOHN AND S. COLEY

BOYD H . MEIKLEJOHN, B.SC, M.B., CH.B., F.F.A.R.C.S. J SUSAN COLBY, M.B., B.S., F.F.A.R.C.S. ; Department of Anaesthesia,

Leicester Royal Infirmary, Leicester LEI 5WW. Accepted for Publication: January 26, 1989.

SUMMARY The catecholamine and cardiovascular responses to nasal intubation of the trachea with and without laryngoscopy have been compared in 23 patients allocated randomly to each treatment. Arterial pressure, heart rate and plasma concentrations of adrenaline and noradrenaline were measured before and after induction and at 1, 3 and 5 min after intubation of the trachea. There were significant increases in systolic and diastolic pressures after trachea/ intubation in both groups. The values at 1 min after intubation were significantly higher in the group undergoing laryngoscopy and intubation compared with the group undergoing blind nasal intubation.

PATIENTS AND METHODS

We studied 28 adult patients (ASA I or II) presenting as in-patients for extraction of 3rd molar teeth under general anaesthesia. The study was approved by the local Ethics Committee, and informed consent was obtained from all patients. Patients were premedicated with diazepam 10 mg orally, 1 h before operation. In the anaesthetic room, systemic arterial pressure and heart rate were measured using a COPAL semiautomated sphygmomanometer with printer (UA 251) with the cuff on the left arm. An 18-gauge cannula was placed in a vein in the right antecubital fossa to permit blood sampling for catecholamine assay. Ten millilitre of venous blood was withdrawn for baseline catecholamine assay before a 20-gauge cannula was inserted in the dorsum of the left hand for administration of drugs. Anaesthesia was induced with thiopentone 3-4 mg kg"1 i.v., followed by suxamethonium 1.5 mg kg"1 i.v. to facilitate tracheal intubation. Anaesthesia was maintained with 67 % nitrous oxide

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It has been known since 1951 that intubation and laryngoscopy are associated with hypertension and tachycardia [1]. More recently , it has been demonstrated that an increase in plasma concentrations of adrenaline and noradrenaline occurs also in response to this stimulus [2, 3]. These changes may produce arrhythmias, myocardial ischaemia, cardiac failure and intracranial haemorrhage [4, 5]; thus most interest has centred on methods designed to attenuate these responses. In a comparison of the stress response to laryngoscopy with and without intubation, Shribman and colleagues [6] found that laryngoscopy produced the major contribution to the stress response, and tracheal intubation per se contributed little additional effect. Althought this suggests that tracheal intubation without laryngoscopy may cause little sympathoadrenal stimulation, Smith [7] found that fibreoptic-assisted tracheal intubation produced greater cardiovascular stimulation than that following tracheal intubation using a laryngoscope. Blind nasal intubation was reported by PrysRoberts to produce no significant cardiovascular changes [4]. However, a subsequent study by Hartigan and colleagues [8] found that significant increases in arterial pressure occurred after nasal intubation without laryngoscopy. In view of these conflicting findings, we have reexamined the cardiovascular responses to laryngoscopy and nasal intubation and compared the data with the changes associated with blind nasal intubation, in an attempt to assess the contribution produced by laryngoscopy per se. In addition, we have measured changes in plasma catecholamine concentrations as a further guide to changes in sympathoadrenal activity.

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BRITISH JOURNAL OF ANAESTHESIA period, a throat pack was inserted and surgery proceeded after administration of an opioid i.v. The 10-ml blood samples were collected into heparinized tubes, and centrifuged as soon as possible. The separated plasma was frozen at — 70 °C until analysis for adrenaline and noradrenaline concentrations using a high pressure liquid chromatographic technique as described in previous studies from this department [3]. Data were analysed using analysis of variance followed by paired or unpaired Student's t test when appropriate; P < 0.05 was considered to be significant. RESULTS

Twenty-eight patients were entered to the study, but one patient was withdrawn from the laryngoscopy group because of unexpected difficulties with intubation requiring bougies and repeated doses of neuromuscular blocker. Two patients in the blind nasal group were withdrawn during intubation because of difficulties requiring laryngoscopy and a further two patients in this group were withdrawn because of doubts regarding the location of the tube. Laryngoscopy was performed, and in one patient, the tube was resited in the trachea. All these patients were excluded from the study, and therefore data were analysed for a total of 23 patients, 12 in the blind nasal group, and 11 in the laryngoscopy group. There were no significant differences between the two groups in age, weight and sex (table I). At 1 min after intubation, the systolic pressure increased to values significantly greater in both groups (P < 0.001) than the pre-induction values. In the laryngoscopy group, this value was also significantly greater (P<0.01) than the value after induction (table II). At 1 and 5 min after intubation, the systolic pressure in the laryngoscopy group was significantly greater (P < 0.05) than the blind nasal group (table II). Similarly, the diastolic pressure at 1 min after intubation

TABLE I. Demographic data (Mean (SEAT))

Blind nasal intubation Laryngoscopy and nasotracheal intubation

Sex

n

Age (yr)

Weight (kg)

(M:F)

12

27.4(1.4)

61.2 (2.8)

3:9

11

26.0 (2.5)

64.1 (3.02)

3:8

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and 1—1.5% enflurane in oxygen via a face mask attached to a Magill breathing system, with a fresh gas flow of 6 litre min"1 while the patients breathed spontaneously and 12 litre min"1 during artificial ventilation of the lungs. When the fasciculations caused by the suxamethonium had stopped, arterial pressure was measured, and a sample of blood taken for catecholamine assay. The patients were allocated randomly to undergo tracheal intubation either by the "blind" nasal method, or by nasal intubation using a Macintosh laryngoscope and a Magill forceps when required. Blind nasal intubation was carried out in the following manner: a size 7.0 mm red rubber uncuffed nasotracheal tube, lubricated with K-Y jelly was introduced through the right nostril into the nasopharynx and then into the oropharynx. With the patient's neck well flexed, the head was extended on the neck and the nasotracheal tube advanced through the cords. This was achieved usually on the first two attempts. Correct placement was confirmed by observing symmetrical chest expansion, and by auscultation by a second experienced anaesthetist over both lung fields, and over the epigastrium. If any doubt existed regarding the location of the tube, a laryngoscope was used and the patient was excluded from the study. Patients in the laryngoscopy group underwent tracheal intubation in a similar fashion, except that a laryngoscope was used in all, and Magill forceps when required. All tracheal intubations were carried out by the same anaesthestist (B.M.). Manual ventilation of the lungs was continued until spontaneous ventilation had resumed, when the fresh gas flow was reduced to 6 litre min"1. Capnography was used in the last two patients studied and this confirmed that the end-expired carbon dioxide was maintained at approximately 5-5.5 % during the study period in these patients. Venous samples were obtained, and arterial pressure and heart rate measured, at 1, 3 and 5 min after intubation. At the end of the study

SYMPATHOADRENAL RESPONSES TO NASAL INTUBATION

285

TABLE II. Cardiovascular variables and catecholamine concentrations (mean (SEM)). Significant differences: * P < 0.05 between groups; ***P < 0.001 compared with pre-induction values Time after intubation (min) Control Systolic AP (mm Hg) Blind

Diastolic AP (mm Hg) Blind Laryngoscopy Heart rate (beat min"1) Blind Laryngoscopy Adrenaline concn (pmol ml"1) Blind Laryngoscopy Noradrenaline concn (pmol ml"1) Blind Laryngoscopy

1

3

5

121.3 (4.8)

128.1 (5.0)

138.8*** (4.9)

120.0 (4.3)

127.5 (3.9)

128.7 (4.7)

154.4*** (4.5)

131.8 (4.6)

107.5 (3.8) * 122.3 (5.1)

72.2 (2.4)

85.8 (2.4)

79.3 (2.9)

69.6 (2.6)

77.3 (2.9)

91.4 (4.2)

91.0*** (3.2) * 103.1*** (3.9)

84.3 (4.5)

78.3 (4.3)

101.6 (3.6) 103.3 (3.6)

91.9 (3.8) 100.7 (3.6)

79.8 (4.1) 80.4 (5.6)

112.3*** (4.7) 99.8*** (6.1)

107.0 (3.7) 101.8 (5.7)

0.82 (0.14) 0.94 (0.2)

0.96 (0.17) 1.07 (0.16)

1.27 (0.31) 1.30 (0.28)

0.78 (0.14) 1.24 (0.26)

0.78 (0.78) 1.08 (0.23)

2.44 (0.42) 2.65 (0.26)

2.22 (0.28) 2.66 (0.32)

3.38 (0.56) 3.06 (0.5)

2.98 (0.43) 2.70 (0.45)

2.77 (0.48) 2.70 (0.41)

increased to values significantly greater (P < 0.001) than pre-induction values. These were significantly greater (P < 0.05) in the laryngoscopy group compared with the blind nasal group (table II). In both groups, heart rate increased significantly following induction (P < 0.01) and this difference persisted throughout the study period; at no time were there significant inter-group differences (table II). Increases in plasma catecholamine concentrations were observed in both groups, but there were no significant changes within or between groups (table II).

significant increase in systolic and diastolic pressures. In addition, our data demonstrate that these changes in cardiovascular variables were significantly less than those produced when intubation was assisted by laryngoscopy. Increases in plasma catecholamine concentrations were seen also in both groups, although there were no significant differences between the two. Shribman, Smith and Achola [6] investigated the sympathoadrenal responses to laryngoscopy alone and concluded that laryngoscopy contributed the major component to orotracheal intubation with laryngoscopy. Although our data do not suggest that laryngoscopy is the more potent stimulus, our study involved stimulation of the nose and nasopharynx by passage of a nasotracheal DISCUSSION tube and, in addition, there were differences in Our results confirm the findings of the only patient selection and study design which make it previous study of this subject [8], notably that difficult to compare directly the results of the blind nasal intubation was associated with a present study with those of Shribman [6].

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Laryngoscopy

After intubation

286

REFERENCES 1. King BD, Harris, LC, Greifenstein FE, Elder JD, Dripps RD. Reflex circulatory response to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiology 1951; 12: 556-566.

2. Russell WJ, Morris RG, Frewin DB, Drew SE. Changes in plasma catecholamine concentrations during endotracheal intubation. British Journal of Anaesthesia 1981; 53: 837-839. 3. Derbyshire DR, Chmielewski A, Fell D, Vater M, Achola K, Smith G. Plasma catecholamine responses to tracheal intubation. British Journal of Anaesthesia 1983; 55: 855-860. 4. Prys-Roberts C, Greene LT, Meloche R, Foex P. Studies of anaesthesia in relation to hypertension. II: Haemodynamic consequences of induction and endotracheal intubation. British Journal of Anaesthesia 1971; 43: 531-546. 5. Fox EJ, Sklar GS, Hill CH, Villanueva R, King BD. Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977; 47: 524-525. 6. Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. British Journal of Anaesthesia 1987; 59: 295-299. 7. Smith JE. Heart rate and arterial pressure changes during fibreoptic tracheal intubation under general anaesthesia. British Journal of Anaesthesia 1988; 43: 629-632. 8. Hartigan ML, Cleary JL, Gross JB, Schaffer DW. A comparison of pretreatment regimens for minimizing the haemodynamic response to blind nasal intubation. Canadian Anaesthetists Society Journal 1984; 31: 497-502. 9. Derbyshire DR, Smith G. Sympathoadrenal responses to anaesthesia and surgery. British Journal of Anaesthesia 1984; 56: 725-739. 10. Derbyshire DR, Achola KJ, Smith, G. Effects of topical lignocaine on the sympathoadrenal responses to tracheal intubation. British Journal of Anaesthesia 1987; 59: 300-304. 11. Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation: influence of duration of laryngoscopy with or without prior lignocaine. Anesthesiology 1977; 47: 381-384.

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Several manoeuvres have been advocated to attenuate the pressor response to laryngoscopy and intubation [9]. It has been suggested that the pressor response to blind nasal intubation may be attenuated by the prior use of topical local anaesthesia to the airway [8]. This manoeuvre was not used in the present study, which was designed to investigate the unmodified responses to blind nasal intubation. However, previous studies of orotracheal intubation have suggested that application of local anaesthetic to the upper airway shortly before orotracheal intubation causes little attenuation of the pressor response [10, 11]. Avoidance of laryngoscopy by use of a fibreoptic laryngoscope has been advocated, but this was shown to be associated with a greater increase in arterial pressure than that observed with the use of a conventional laryngoscope [7]. Blind nasal intubation is another technique which avoids the use of a laryngoscope. However, the present study indicates that, although the accompanying pressor response is significantly less than that produced with concomitant laryngoscopy, manoeuvres designed to obviate laryngoscopy cannot prevent sympathoadrenal responses.

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