EFFECTS OF SEDATION PRODUCED BY THIOPENTONE ON RESPONSES TO NASAL OCCLUSION IN FEMALE ADULTS

Transcription

1 British Journal of Anaesthesia 1993; 71: EFFECTS OF SEDATION PRODUCED BY THIOPENTONE ON RESPONSES TO NASAL OCCLUSION IN FEMALE ADULTS T. NISHINO AND T. KOCHI SUMMARY To test the hypothesis that full wakefulness is an important factor in the control of the route of breathing in adult humans, we have studied the responses to nasal occlusion before and during sedation with thiopentone in 14 female subjects. A tightly fitting partitioned face mask separated the nasal and oral breathing routes. Nasal and oral breathing were identified from changes in carbon dioxide concentration and airway pressure in the different compartments of the face mask. Arterial oxygen saturation (Sp 0 J was monitored simultaneously. Eleven of 14 subjects breathed only through the nose (nasal breathers) both before and during sedation. In these subjects, the time required to initiate oral breathing in response to nasal occlusion during sedation was significantly longer than that before sedation (mean 37.7 (SD 15.5) s vs 3.2 (1.3) s(? < O.O1)). Also, there was a significant difference (? < 0.01) in the smallest values of Sp 02 attained during nasal occlusion before (98.0 (0.8) %) and after (89.3 (4.3) %) sedation. In adult humans the ability to maintain adequate ventilation by switching from the nasal to the oral route in response to nasal occlusion is greatly impaired during sedation, probably because of the impairment of conscious influence on the control of the palatal muscles. (Br. J. Anaesth. 1993; 71: ) KEY WORDS Airway: obstruction. Ventilation: obstruction. Ability to change from the nasal route of airflow to the oral route during nasal obstruction is crucial for maintenance of adequate ventilation. Although the physiological mechanisms underlying the change from nasal to oral passage are not entirely clear, the change of breathing route would depend, not only on reflexes, but also on voluntary control of the palatal muscles. It is generally believed that airway obstruction during sedation and anaesthesia occurs at the pharynx and larynx, because of depression of the upper airway dilating muscles [1]. However, it is possible also that, even in the presence of a patent upper airway, alterations in consciousness caused by sedation or anaesthesia may diminish or abolish the ability to change the breathing route and lead to airway obstruction during nasal occlusion. The recent study by Wood and Harding [2] showed, in neonatal and mature sheep, that sedating doses of pentobarbitone and diazepam depressed the effectiveness of oral breathing when the nose was blocked. It is not clear if nasal occlusion leads to prompt alterations of breathing route from the nose to the mouth in sedated humans. Consequently, we have examined the responses of adult humans to acute nasal obstruction during wakefulness and after sedation with thiopentone. PATIENTS AND METHODS We studied 14 female patients aged yr (mean 37.8 yr) undergoing elective surgery (hysterectomy, nine patients; mastectomy, five patients) under general anaesthesia. All subjects were devoid of respiratory, cardiovascular, laryngeal or neuromuscular disorders. None had a history or clinical evidence of partial nasal occlusion, nasal pathology or nasal trauma. The average heights and weights were (SD 2.8) cm (range cm) and 54.4 (2.8) kg (range kg), respectively. The study was approved by the Ethics Committee of our institution, and each subject gave informed consent. The patients received atropine 0.5 mg i.m. 1 h before the study, which was carried out in a quiet, warm operating room. Each patient rested in the supine position for 10 min with the head resting on a ring support in a comfortably neutral position and an air-tight custom-made, partitioned face mask (Senkousha, Japan) was fitted. A hard rubber septum inside the mask separated nasal and oral chambers, each with its own opening port (i.d. 9 mm, length 40 mm) having a side-arm outlet (i.d. 3.5 mm). The rubber septum was positioned under the upper lip and on the outer gum of the patient so that the mouth and lips were kept slightly apart. Each mask chamber was tested separately for air leaks by pressurizing to +10 cm H 2 O and ensuring that the pressure was constant for 10 s. Deadspace for nasal and mouth chambers were 90 and 120 ml, respectively. Nasal TAKASHI NISHINO, M.D.; TETSUO KOCHI, M.D.; Department of Anaesthesia, National Cancer Centre Hospital East, Kashiwanoha 6-5-1, Kashiwa-shi, Chiba 277, Japan. Accepted for Publication: March 25, Correspondence to T.N.

2 SHIFT OF BREATHING ROUTE DURING SEDATION 389 Pna (kpa) 0.3 r n<- - Pmo (kpa) 0.1 r ol Awake Sedation Spo,(%) ioor Cnaco (%) "1AAMAAJ JV\MJ\ J1MAAJU FIG. 1. Experimental records of respiratory responses to nasal occlusion during the awake state and sedation. Pna = Nasal pressure; Pmo = mouth pressure; Sp 02 = arterial oxygen saturation; Cna CO! = carbon dioxide concentration at the nose; Cmo COj = carbon dioxide concentration at the mouth. Horizontal bars indicate periods of nasal occlusion; arrow indicates start of oral breathing. 10 s pressure (Pna) and mouth pressure (Pmo) were measured using pressure transducers (Statham P231D) at the opening ports. Carbon dioxide concentrations in the nasal chamber (Cna CO2 ) and the mouth chamber (Cmo CO]! ) were monitored with Datex infra-red carbon dioxide analysers. In this way, nasal breathing was reflected in the values of Pna and Cna COi!, whereas oral breathing was reflected in Pmo and Cmo CO2. Arterial oxygen saturation (5po 2 ) was monitored continuously using a pulse oximeter (Nihon Kohden, Japan). All variables were recorded on a Nihon Kohden 8 channel recorder (RJG-4128). The patient was asked to close the eyes and breathe as normally as possible for 3-5 min without instruction as to the breathing route, while listening to music through headphones. During this period, the patients who breathed only through the nose were designated "nasal breathers". The patients who breathed through both the nose and mouth were designated "oronasal breathers". To determine the ability to change the breathing route in response to nasal occlusion, in nasal breathers the opening of the nasal chamber was occluded suddenly during one expiration in such a manner that the subject was unable to detect the onset of application of occlusion. Nasal occlusion was continued until three consecutive oral breaths ensued, after which time the occlusion was released. Three nasal occlusions were performed in each patient and the response time required to start oral breathing after nasal occlusion was measured in each trial period. Each trial period was separated by 1 min'; three results were averaged for each patient. Immediately thereafter, each patient received a sedative dose of thiopentone 1.5mgkg~ l i.v. Two minutes after administration of thiopentone, the level of consciousness in each patient was determined by physical stimulation and verbal commands; the anterior chest wall of the patient was tapped gently and the patient asked to open the eyes and squeeze the hands. When the patient was capable of rational responses, nasal occlusion was performed in those patients who continued to breathe only through the nose after administration of thiopentone. The response time required to start oral breathing after nasal occlusion was measured and this value was compared with those obtained in awake state. Statistical analysis was performed using the Wilcoxon test. P < 0.05 was considered significant. RESULTS In the awake state, only one patient of 14 was an oronasal breather; the others were nasal breathers. After administration of thiopentone, all the patients became drowsy, but responded to physical stimulation and verbal commands while maintaining airway patency (conscious sedation). During this sedated state, 11 of 13 patients who had been designated nasal breathers in the awake breathers continued to breathe only through the nasal route, while two nasal breathers started to breathe through both the nasal and oral routes. The patient designated as an oronasal breather in the awake state continued this pattern after sedation. Figure 1 shows the responses to nasal occlusion observed in one of the nasal breathers. In this particular patient, during full wakefulness (fig. 1) nasal occlusion caused immediate cessation of airflow, as shown by the nasal and oral carbon dioxide tracings. Oral breathing was initiated some 4 s after occlusion of the nasal passage, and there was almost no change in Sp Oi. After the release of nasal occlusion, exclusive nasal breathing was resumed promptly. After sedation (fig. 1) with thiopentone, there was a progressive increase in inspiratory efforts during nasal occlusion, but the onset of oral breathing was greatly delayed, leading to a progressive decrease in Sp Oj. In two nasal breathers, nasal occlusion failed to initiate oral breathing within 60 s after occlusion (fig. 2), after which time they became hypoxic and the nasal occlusion was released. In these patients the response time was recorded as 60 s, although it was actually longer.

3 390 BRITISH JOURNAL OF ANAESTHESIA Pna (kpa) 0.3 r Pmo (kpa) 0.1 r ol - Sp Ol<%) IOO 80 Cn acoi (%) (%) t 10 s FIG. 2. Prolonged airway obstruction in response to nasal occlusion during sedation. Note that no initiation of oral breathing occurred during nasal occlusion. See figure 1 for abbreviations. TABLE I. Ventilatory frequency (f), end-tidal Pco 2 (P^COz ), and Sp Ot during the conscious state and sedation {mean (SD) {range]). ** P < 0.01 compared with conscious state and with before nasal occlusion /(b.p.m.) Before nasal occlusion During nasal occlusion Awake state 14.5(1.9) [ ] 5.3 (0.52) [ ] 98.2 (0.6) [96-99] 98.0 (0.8) [97-99] Sedation 15.4(2.3) [ ] (n = 14) 5.6 (0.51) [ ] (» = 14) 97.3 (0.9) [96-99] («= 11) 89.3 (4.3)** [82-95] The mean response time in the conscious state obtained from 13 nasal breathers was 3.0 (1.2) s (range s). In 11 nasal breathers who continued to breathe through the nose after administration of thiopentone, the response time during sedation (mean 37.7 (15.5) s; range s) was significantly longer than that in the awake state (mean 3.2 (1.3) s; range s) (P < 0.01). Also, there was a significant difference in the smallest values of Sp Ot attained during nasal occlusion between the awake and sedated states (table I). DISCUSSION Confirming observations made elsewhere [3-5], we have demonstrated that the majority of awake patients were nasal breathers during quiet breathing. Although the mechanisms and factors responsible for a marked preference of breathing via the nose are not entirely clear, both physiological and anatomical factors may influence the choice of breathing route. Rodenstein and Stanescu [3] demonstrated that, when the mouth is open, the airflow depends on the position and function of the soft palate. Thus when the soft palate lies downward against the base of the tongue, flow is entirely nasal. In contrast, when the soft palate extends horizontally from hard palate to posterior pharyngeal wall and closes the nasopharynx, air flows through mouth only. When the soft palate lies midway between tongue and posterior pharyngeal wall, airflows through both the nose and mouth. Two major muscles responsible for the active movement of the soft palate are the palatoglossus muscle, which directs the soft palate caudally and ventrally, and the levator veli palatini, which pulls the soft palate cephalad and in a dorsal direction. The major finding in the present study was that, in nasal breathers, the ability to switch from nasal breathing to oral breathing in response to nasal occlusion was greatly obtunded during sedation with thiopentone. This finding is in good agreement with that of Wood and Harding [2], who showed, in lambs and ewes, that sedation with pentobarbitone and diazepam delayed the onset of oral breathing and led to a greater degree of asphyxia during nasal obstruction. However, considerable differences exist between sheep and humans in responses to nasal occlusion. For example, the time required to initiate oral breathing after nasal occlusion in awake humans obtained in this study (3.0 (1.2) s) is much shorter than that reported in awake ewes (59.7 (8.7) s) [2]. Also, a considerable decrease in Spo 2 was observed before initiation of oral breathing in awake ewes, whereas hypoxaemia was never observed in awake humans. These differences in responses to nasal occlusion between human and sheep may be explained by the difference in voluntary control of breathing route. Presumably, in humans the contribution of behavioural control may play a more important role in the change of breathing route than in sheep. Most subjects in this study reported that they were aware of nasal occlusion during wakefulness and might respond consciously to the occlusion. The finding that sedation caused delayed onset of oral breathing after nasal occlusion supports our hypothesis that, in humans, wakefulness is the most

4 SHIFT OF BREATHING ROUTE DURING SEDATION 391 important factor in control of the change in breathing route. This view is also compatible with the observation of Rodenstein, Perlmutter and Stanescu [6] that in human infants the time required to initiate oral breathing after nasal occlusion is related to age, conscious state, or both; that is, infants who are older or awake, or both, respond faster than those who are younger or sleeping, or both. Similarly, Kuna and Smickley [7] observed in normal sleeping adults that, during non-rem sleep, oral breathing occurred only in association with arousal. Other factors which may affect the control of the route of breathing are chemoreceptor and mechanoreceptor inputs. Although there is evidence [8, 9] that both mechanical and chemical sensory mechanisms are involved in the reflex initiation of oral breathing after nasal obstruction in experimental animals, the relative contribution of each of these factors to the control of oral breathing was not explored systematically in this study. However, an immediate initiation of oral breathing after nasal occlusion in the awake state suggests that at least chemical inputs play little or no role in control of breathing route in awake nasal breathers. In a previous study [10], we showed that, in awake subjects, topical lignocaine in the nasal passages delayed the onset of oral breathing in response to nasal occlusion (before lignocaine 4.4 (2.7) s; after lignocaine 10.8 (7.8) s), suggesting that sensory information arising from upper airway receptors may play an important role in controlling the change in breathing route. The greater differences found between full wakefulness and sedation in our study, compared with before and after topical upper airway anaesthesia, emphasize the importance of behavioural factors. Whatever the mechanisms may be, some form of centrally co-ordinated series of motions such as opening the mouth, contracting the muscles of the tongue and elevation of the soft palate is necessary to open the oral passage and initiate oral breathing. In our study, because the mouth was kept open, contraction of the muscles of the tongue and elevation of the soft palate may have been two major factors necessary to create the oral airway. As adequate airway patency was maintained before nasal occlusion, even during sedation, it is possible that the delay in creating an oral airway during sedation might be caused mainly by preferential depression of activity in the genioglossus and levator veli palatini, leaving other airway-maintained muscles unaffected. It should be noted that we studied only young female patients, and our findings may not be applicable to males or more elderly patients. However, as the control of the upper airway in males and elderly subjects is more capricious [11], it is possible that impairment of the ability to change the breathing route during sedation may be particularly pronounced in these populations. Our findings may be relevant to the clinical problem of airway obstruction during sedation. Nasal obstruction could occur as a result of increased nasal secretory activity, increased mucosal congestion or the presence of a nasogastric tube. Under such circumstances, impairment of the ability to initiate oral breathing could cause airway obstruction, despite apparent oral airway patency. It has been reported that, in sedated human adults, nasal packing for control of epistaxis causes hypoxaemia [12, 13]. Similar considerations may apply to patients with sleep apnoea. Indeed, several reports [14-16] suggest that nasal obstruction is an important predisposing factor in sleep apnoea. Release of airway obstruction during sleep in sleep apnoea patients often coincides with central arousal [17]. Although this release of oropharyngeal occlusion is considered to be the likely mechanism during central arousal, release of airway obstruction may result partly from change in breathing route from the nose to the mouth. ACKNOWLEDGEMENT The authors are grateful to Professor G. Sant'Ambrogio for constructive criticism of the manuscript. REFERENCES 1. Iscoe SD. Central control of the upper airway. In: Mathew OP, Sant'Ambrogio G, eds. Respiratory Function of the Upper Airway. New York; Dekker, 1988; Wood GA, Harding R. The effects of pentobarbitone, diazepam and alcohol on oral breathing in neonatal and mature sheep. Respiration Physiology 1989; 75: Rodenstein DO, Stanescu DC. Soft palate and oronasal breathing in humans. 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Effects of topical anaesthesia of the nasal passage on the shift of breathing route in human adults. Lancet 1992; 339: Block AJ, Wynne JW, Boysen PG. Sleep apnea, hypopnea, and oxygen desaruration in normal subjects: a strong male predominance. New England Journal of Medicine 1979; 300: Cassisi NJ, Biller HF, Ogura JH. Changes in arterial oxygen tension and pulmonary mechanics with the use of posterior packing in epistaxis: a preliminary report. Laryngoscope 1971; 81: Cook TA, Komorn RM. Statistical analysis of the alterations of blood gases produced by nasal packing. Laryngoscope 1973; 83: Simmons FB, Guilleminault C, Dement WC, Ilkan AG. Surgical management of airway obstructions during sleep. Laryngoscope 1977; 87: Zwillich CW, Pickett CK, Hanson FN, Weil JV. Disturbed

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