Editor’s Note: Adequate sedation and its associated physical signs have been discussed in recent issues of the Newsletter, and the resulting letters to the editor have provoked much interest in the topic. This article provides a more detailed discussion of the issue.

In a conscious person, normal breathing takes place through the nose, because the soft palate directs the respired flow via the nose, and prevents flow through the mouth. (1) When normal subjects he in the supine position, nasal flow persists but the resistance of the upper airways is greater (2) and the retropalatal airway narrows (3) and the pharyngeal cross-sectional area is reduced. (4)

The upper airway, between the posterior nose and the larynx, is a flexible collapsible tube. The upper airway muscles act to maintain its patency, reducing its resistance and preventing collapse. The patency of the upper airway is normally maintained by activity of muscles such as genioglossus and sternohyoid, which act to dilate and thus decrease the resistance and collapsibility of the airway. (5-8) During normal sleep the resistance of the region of the soft palate increases considerably, and becomes exaggerated at greater flows, suggesting that collapse may be taking place. (9) Permutt and his colleagues suggest that this part of the airway is like a Starling resistor, in which collapse will occur if the resistance of the upstream segment of the airway is increased, so that flow is not related to the pressures downstream from this point. (10) If the resistance of the retropalatal airway increases, then collapse may occur in the downstream pharynx during inspiration.

In the awake state, the upper airway muscles act to maintain upper airway patency. They become active before the onset of inspiratory flow (11) and can be reflexly activated by decreases in airway pressure. (12) In the supine position, although airway dimensions are reduced, there is an increase in airway muscle activity (4,13) which is probably a response to the increase in airway resistance. A similar increase in activity is found when airway caliber is reduced by a decrease in end-expiratory lung volume. (14) Upper airway patency in sleeping humans is impaired by anaesthesia of the airway. (15,16)

Changes similar to those that occur during sleep are also seen after drug administration. Airway resistance, both in the nasopharynx and in the oropharynx, is increased in volunteers after alcohol ingestion (17) and airway resistance is increased after administration of midazolam. (18) Even very mild sedation with thiopentone, insufficient to abolish the nasal route of respiration, can impair the ability of humans to alter the route of respiration from nose to mouth if the nose is occluded. (19) Incremental doses of thiopentone cause a progressive reduction in airway muscle activity. (20) Although airway obstruction may result in reflex activation of the muscles, the increased activity is generally unable to overcome the obstruction. (20) Increasing doses of anesthetics appear to reduce activity of the upper airway nerves and muscles more profoundly than the diaphragm (21,22) and this action appears to be mediated by GABA. (23)

Consequently, agents such as the benzodiazepines would be expected to have profound effects on the airway, as indeed they do. (18) Evidence of the change of respiration from the nasal to the oral route, as shown by the movement of the relaxed lips [the ‘pouf’ sign suggested as indicating ‘adequate’ sedation], described by Dr. Shea (APSF Newsletter, Spring 1994), indicates that the soft palate has started to relax: airway resistance is likely to be greater. If resistance is increased, airway obstruction may occur through the Starling resistor phenomenon, with pharyngeal collapse. The problem may be exaggerated if the sedation is sufficient to result in the patient falling asleep, since this also increases airway resistance; and by the lips becoming drawn in on inspiration, since this yet again increases the airway resistance.

Drawing in of the lips during inspiration, and a puffing out on expiration, is a sign of excessive sedation, and a warning of impending episodes of airway obstruction as a result of loss of tissue/muscle tone and dynamic airway collapse. It is a “bad sign’ (for the patients safety).

Dr. Drummond is Senior Lecturer, Department of Anaesthetics, The University of Edinburgh, Edinburgh, Scotland.

References

1. Rodenstein DO, Stanescu DC. Soft palate and oronasal breathing in humans. journal of Applied Physiology 1984; 57:651-657.

2. Anch AM, Remmers JE, Bunce H. Supraglottic airway resistance in normal subjects and patients with occlusive sleep apnea. Journal of Applied Physiology 1982, 53: 1158-1163.

3. Yildirim N, Fitzpatrick MF, Whyte KF, Jalleh R, Wightman AJA, Douglas NJ. The effect of posture on upper airway dimensions in normal subjects and in patients with the sleep apnea/hypopnea syndrome. Am Rev Respir Dis 1991 ; 144: 845-847.

4. Fouke JM, Strohl KP. Effect of position and lung volume on upper airway geometry. Journal of Applied Physiology 1987; 63:375-380.

5. van Lunteren E, Haxhiu MA, Cherniack NS. Relationship between upper airway volume and hyoid muscle length. journal of Applied Physiology 1987,63:1443-1449.

6. Brouillette RT, Thach BT. A neuromuscular mechanism maintaining extrathoracic airway patency. Journal of Applied Physiology 1979; 46: 772-779.

7. Fouke JM, Teeter JP, Strohl KP. Pressure-volume behavior of the upper airway. Journal of Applied Physiology 1986; 61: 912-918.

8. Odeh M, Schnall R, Gavriely N, Oliven A. Effect of upper airway muscle contraction on supraglottic resistance and stability. Respir Physiol 1993,92:139-150.

9. Hudgel DW, Hendricks C. Palate and Hypopharynx-sites of inspiratory narrowing of the upper airway during sleep. Am Rev Respir Dis 1988; 138:1542-1547.

10. Smith PL, Wise RA, Gold AR, Schwartz a Permutt S. Upper airway pressure-flow relationships in obstructive sleep apnea. Journal of Applied Physiology 1988; 64:789-795.

11. Strohl KP, Hensley MS, Hallett M, Saunders NA, Ingram RJ. Activation of upper airway muscles before onset of inspiration in normal humans. journal of Applied Physiology 1980; 49: 638-642.

12. Mathew OP. Upper airway negative pressure effects on inspiratory activity of upper airway muscles. journal of Applied Physiology 1984,56:500-505.

13. Douglas NJ, Jan MA, Yildirim N, Warren PM, Drummond GB. Effect of posture and breathing route on genioglossal electromyogram activity in normal subjects and in patients with the sleep apnea/hypopnea syndrome. American Review of Respiratory Disease 1993; 148:1341-1345.

14. Aronson RM, Carley DW, Onal E, Wilborn J, Lopata M. Upper airway muscle-activity and the thoracic volume dependence of upper airway-resistance. Journal of Applied Physiology 1991; 70:430-438.

15. McNicholas WT, Coffey M, McDonnell T, O’Regan R, Fitzgerald MX. Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. Am Rev Respir Dis 1987; 135:1316-1319.

16. DeWeese EL, Sullivan TY. Effects of upper airway anesthesia on upper airway patency during sleep. Journal of Applied Physiology 1988; 64:1346-1353.

17. Robinson RW, White DP, Zwilhch CW. Moderate alcohol ingestion increases upper airway resistance in normal subjects. Am Rev Respir Dis 1985; 132:1238-1241.

18. Montravers P, Diureuil B, Desmonts JM. Effects of I.V. midazolam on upper airway resistance. British Journal of Anaesthesia 1992; 68:27-31.

19. Nishino T, Kochi T. Effects of sedation produced by thiopentone on responses to nasal occlusion in female adults. British journal of Anaesthesia 1993; 71: 38&392.

20. Drummond GB. Influence of thiopentone on upper airway muscles. British journal of Anaesthesia 1989; 63: 12-21.

21. Hwang J, St.john WM, Bartlett D. Respiratory related hypoglossal nerve activity: influence of anesthetics. Journal of Applied Physiology 1983 55:785-792.

22. Ochiai R, Guthrie RD, Motoyama EK. Differential sensitivity to halothane anesthesia of the genioglossus, intercostals, and diaphragm in kittens. Anesthesia and Analgesia 1992; 74: 338-344.

23. Haxhiu MA, Mitra J, van Lunteren E, Prabhakar N, Bruce EN, Cherniack NS. Responses of hypoglossal and phrenic nerves to decreased respiratory drive in cats. Respiration 1986; 50:130-138.