Acta Anaesthesiol Scand 1992: 36: 1-4

Attenuating the hypertensive response to laryngoscopy and endotracheal intubation using awake fibreoptic intubation S. J. HAWKYARD, A. MORRISON, L. A. DOYLE, R. S. CROTON and P. N. WAKE Departments of Surgery and Anaesthesia, Warrington District General Hospital, Cheshire, U K

Blood pressure and pulse rate measurements were recorded in 35 patients undergoing endotracheal intubation during general anaesthesia (Group A), and 35 patients who had an awake fibreoptic intubation under local anaesthesia (Group B). The mean arterial pressure in Group A rose by a mean of 35 mmHg immediately after intubation, compared with a mean fall of 9 mmHg in Group B. The mean pulse rate in Group A rose by 24 beats per minute (b.p.m.) immediately after intubation, compared with a rise of 3 b.p.m. in Group B. Both these differences were statistically significant (P< 0.0001 and P< 0.001 respectively, Mann Whitney U test). Postoperative discomfort was assessed 24 h later by means of linear analogue scales. There was a statistically higher mean score in relation to nose discomfort in Group B (P<0.002) . Awake fibreoptic intubation successfully reduces the pressor response to endotracheal intubation in normotensive adults. It'is suitable for use in those patients who are at risk from the pressor response.

Received 30 November 1990, accepted f o r publication 30 April 1991

Key words: Endotracheal intubation; fibreoptic intubation; pressor response.

There is often a well-recognised rise in blood pressure and pulse rate during laryngoscopy and endotracheal intubation ( l ) , which is most marked in the hyperten- sive patient (2) . This is an important cause of peri- operative morbidity in patients with compromised myocardial function or cerebrovascular disease (2-4). Several pharmacological manipulations, e.g. beta- blockers ( 5 , 6) and opiates (7-1 1) have been tried, in order to reduce the pressor response.

The hypertensive response is mainly a sympathetic one, associated with raised noradrenaline levels ( 12). Local anaesthesia of the air passages has been shown to be of benefit, however ( 1 3), as it diminishes the strength of the afferent pathway of the reflex arc.

Awake fibreoptic intubation is an established tech- nique (14, 15). It has been shown to be safe and to reduce the hypertensive response in an uncontrolled study of 200 patients (16). We set out to prove its efficiency in a randomised prospective study.

PATIENTS AND METHODS The study was given approval by the \.$Jarrington Area Health Auth- ority Ethical Committee.

Written informed consent was obtained from each patient. Seventy consecutive normotensive adults who wcre undergoing elective surgi- cal procedures which required endotracheal intubation were random- ised by sealed envelope into one of two groups. Group A received a general anaesthetic including oral intubation, and Group B under-

went awake fibreoptic nasal intubation. Patients on warfarin therapy, those in whom intubation was known to be dillicult, and patients unable to give informed consent were excluded from the trial.

All patients received premedication with diazepam 10 mg orally 2 h before surgery. O n arrival in the anaesthetic room, an intravenous infusion of Hartmann's solution was commenced via a 16-gauge cannula. The pressure cuff of a Dinamap recording machine (Criti- kon, Tampa, Florida, U S A . ) was applied to the right arm of the patient, and subsequent readings were taken every 60 s.

Anaesthesia in the Group A patients was induced using thipentone (4-5 mg kg-') and maintained with nitrous oxide (66%), oxygen (33%) and halothane 0.5%. Suxamethonium (1.5 mg kg-') was then given and respiration assisted. Ninety seconds later, the patient was intubated orally, and intermittent positive pressure ventilation was continued with the same gaseous mixture. When the suxamethonium wore off, the patient was allowed to breathe spontaneously. Patients in Group B were sedated with incremental doses of midazolam (up to 7.5 mg) and fentanyl (50-100 pg) so that they remained co- operative. One nostril and the nasopharynx were anaesthetised using cocaine 5% on cotton swab-sticks. The pretracheal skin was infil- trated with lidocaine and two 2-ml aliquots of lidocaine 4% were injected into the trachea through the cricothyroid membrane using a 19-gauge needle. The nostril was then calibrated using successive Bard nasal airways and a prewarmed nasotracheal tube was intro- duced into the nasopharynx. A fibreoptic bronchoscope (Keymed, Southend-On-Sea, England) was then passed through the nasotra- cheal tube as far as the carina and the endotracheal tube advanced over the bronchoscope. During this procedure supplementary oxygen was delivered close to the patient's mouth. A gaseous induction with nitrous oxide (66%), oxygen (33%) and halothane 0.5% was then given.

All intubations were performed by a single consultant anaesthetist (AM). In both groups a Bain's circiut was used to maintain normo- capnia throughout, at a free gas flow of 70 ml kg-'. Pulse and

2 S. J. HAWKYARD E T AL.

Table I Prcopcrtive r>atii.nt data.

Table 2 Postoperative discomfort.

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Group A Group B

No. of patients 35 35 Mean age (years) 56 (19) 59 (19) Wc~mrii 6 17 Systolic pressure (mniHg) 135 (19) 142 (19) Diastolic pressure (mmHg) 79 (9) 80 (12)

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( ) =standard deviation.

blood pressure recordings were taken every minute for 5 min after intubation, during which the patient remained in the anaesthetic room undisturbed. The time taken from arrival in the anaesthetic room until the positioning of the endotracheal tube was recorded by the Dinainap recorder.

Twenty-four hours after surgery all the patients indicated on an ungraduated linear analogue scale 10 cm long, their discomfort in thr nos”, throat and on $wallowing. They were also asked about any iecall of events during anaesthesia.

Results were analyscd using the Mann-Whitney U test, and the Wilcoxon’s rank tcst with the tied modification.

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Fig. I . ’l‘he mean artcrial pressure (MAP) on arrival in the anaes- thetic room and immediately after endotracheal intubation. The “standard” general anaesthetic group is Group A and the awake “libreoptic” group is Group B. Mean values are marked by the bar lines. P<O.O001, Mann-Whitney U test.

Group A Group B Significance ~ ~~

Sore throat 12 (23) 13 ( 1 7 ) N.S. Swallowing discomfort 5 (13) 8 (16) N.S. Sore nose 0 (0) 10 (22) P<0.002*

Mean linear analogue scores. ( ) =standard deviation. *Wilroxon’s rank test.

RESULTS One patient was withdrawn, because of technical fail- ure of the Dinamap recorder. The two groups were well matched for age and preoperative blood pressure. There was a preponderance of males in Group A (Table 1 ) .

The mean arterial pressure (MAP) rose in Group A by 35 mmHg immediately after intubation, com- pared to a mean fall of 9 mmHg in Group B. This difference was statistically significant, P < 0.000 1 (Fig. 1). The difference persisted for at least 4 min (Fig. 2) . The pulsr rate in Group B remained constant through- out intubation, showing a mean rise of only 3 b.p.m. immediately after intubation. This comparrd with a mean rise of 24 b.p.m. in Group A, again statistically significant, P< 0.001 (Fig. 3) . During the anaesthetic procedure in Group B the mean MAP fluctuated (Fig. 4) . The minimum value was 85 mmHg and occurred after the sedation of the patient with fentanyl and midazolam, i.e. a fall of 22 mmHg from the base line (a fall of 12 mmHg in the mean MAP occurred alter the thiopentone in Group A). Intratracheal injection of lignocaine was associated with a short episode of coughing and the mean MAP reached a maximum of 105 mmHg, i.e. almost rcturncd to base-line levels.

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Fig. 2. The MAPS during the 4 min Ibllowing criclutradirnl intu- bation. P<O.OOOl, Mann-Whitney U test.

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Fig. 3. Pulse rates on arrival in the anaesthetic room and immediately after endotracheal intubation. P< 0.001, Mann-Whitney U test.

The average time for completion of intubation in Group A was 7.5 min compared with 2 1 min in Group B.

The mean analogue scores were similar in both groups in relation to throat and swallowing discomfort. However, there was a significantly higher incidence of nasal discomfort in Group B, P<0.002 (Table 2). Although the patients in Group B remained awake and co-operative throughout intubation, no patient had recall of events beyond the insertion of the intra- venous cannula.

DISCUSSION The pressor response to endotracheal intubation has only been appreciated since continuous pressure moni- toring has been available. Ever since its recognition ( l ) , efforts have been made to prevent it (5-11, 13, 16). The blood pressure and heart rate responses are associated with detrimental physiological effects ( 1 7-19), especially in patients with compromised cere- brovascular or myocardial circulations (2-4).

Pharmacological manipulations have had some suc-

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ARRIVAL POST POST POST SEDATION LIGNOCAINE INTUBATION

Fig. 4. The lowest MAPs following sedation with midazolam and fentanyl and the highest MAPs following the intratracheal injection of lidocaine in Group B patients. Bar lines mark the mean values.

cess. Beta-blockers have significantly reduced the rise in blood pressure (5, 6). Prys-Roberts and co-workers (6) used intravenous practolol prior to oral intubation in a group of hypertensives. This group showed a mean rise in systolic pressure of 24 mmHg, compared with a rise of 60 mmHg in an untreated group of hyperten- sives. The success of beta-blockers is at least in part due to the fact that the pressor response is a sym- pathetic one. Russel et al. (12) have shown that nor- adrenaline levels rise in parallel with the heart rate and blood pressure. The reflex arc is triggered by stimulation of the oropharynx and trachea with the laryngoscope and endotracheal tube. Steps to reduce these stimuli have also reduced the magnitude of the pressor response (1 1, 13, 16, 20). In Venus's study (13), aerosoled lidocaine prior to induction and oral endotracheal intubation prevented any rise in the blood pressure, compared with a mean rise of 13 mmHg in the control group. These are encouraging results, despite the small numbers of patients (nine in each group). Kautto ( l l ) , in a slightly larger study and with the addition of fentanyl (2 pg kg-') in the study group, showed a similar ablation of the response.

Ovassapian (16), using awake fibreoptic intubation in 200 consecutive patients which included treated hypertensives, demonstrated a mean MAP rise of only 10 mmHg following endotracheal intubation. Our ran- domised controlled study has shown the efficacy of this method. The controls, Group A, did not receive the

4 S. J. HAWKYARD ET AL.

fentanyl and midazolam that was given to the patients in Group B. For this reason the contribution of the small doses of fentanyl (2 pg kg-’) in relation to the overall prevention of the pressor response cannot be assessed. However, Dahlgren’s group (8) used fentanyl at a dose of 5 pg kg-I, and there was still a mean rise in MAP of 20 mmHg in the study group. Although opioids undoubtedly reduce the hypertensive response, it is unlikely that they account for the complete abol- ition that was seen in our study.

The method has proved acceptable to the patients, with minimal postoperative discomfort and no un- pleasant memories of the procedure. Despite greater nasal discomfort in the study group, no patient said that in retrospect it would have altered their decision about entry into the trial.

The advantage of awake fibreoptic intubation in reducing the hypertensive response is additional to its acknowledged benefit in patients who are difficult to intubate (15). We feel that this study justifies its in- creased use.

ACKNOWLEDGEMENTS Thr authors wish to express their sincere thanks to Dr. Jennie Hunter, Senior Lecturer in the Department of Anaesthesia, Royal Liverpool Hospital, for her constructive criticisms and assistance with the docu- ment, as well as her encouragement. Also to the theatre staff and nursing staff on wards 31 and 32, Warrington General Hospital, for their co-operation, and understanding.

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Address: S. H a w b a r d Department of Surgery Edinburgh University Medical School Buildings Teviot Place Edinburgh EH8 9AG Scotland, U.K.