UPPER AIRWAY OBSTRUCTION DURING SEDATION

Abstract

The upper airway has a framework of bone and cartilage with attached soft tissue structures, beginning at the nose and lips and ending at the larynx. Where not supported by bone or cartilage, the upper airway may collapse, because muscle tone provides rigidity and this tone can change, as with sleep or anesthesia. These state-related changes and the influence of dynamic factors are related to airflow through narrow, potentially collapsible, segments that limit the ability to predict possible collapse during sleep or anesthesia from examination of the airway in the awake state. Principal causes of Airway Obstruction may be nasopharyngeal, oropharyngeal and hypopharyngeal, supraglottic, glottis, subglottic, tracheobronchial or psychogenic, and any of these could be either congenital, inflammatory, traumatic or neoplastic. Obstructive sleep apnea is a common condition with substantial associated morbidity. The patient with disordered breathing during sleep is likely to also have disturbed breathing when sedated. This effect is compounded by sedation-related compromise of arousal, the mechanism that protects the sleeping patient from life threatening consequences of a breathing disturbance. Furthermore, the upper airway abnormalities that predispose to breathing obstruction during sleep may also make tracheal intubation difficult. The severity of the clinical complaint is an indication for treatment, even when the apnea index or apnea–hypopnea index are ‘low’. Many pathological processes are predictably associated with difficult airway maintenance or intubation, such as epiglottitis and tumors of the larynx or pharynx. Not all difficult airways are associated with major pathology, but result from more subtle anatomical predisposition, modulated by neuromuscular forces. Such difficulties may only become manifest with the state-related decreases in neuromuscular activation that accompany sleep and anesthesia. Examination of the awake patient may not reveal these influences or the dynamic effect of airflow across potentially vulnerable segments, reducing the capacity to identify airways at risk. The effects of standardized levels of anesthetic and sedative agents on upper airway patency are an important step in advancing safety for non-intubated, sedated patients. Sleep apnea researchers have extensively investigated a myriad of factors that affect upper airway collapsibility. In comparison, upper airway studies during sedation or general anesthesia are in their infancy, and we should follow their lead. The risk of upper airway obstruction during sedation is greatest when caring for patients already medically compromised. It is reassuring that significant unpleasant events can generally be prevented by careful preoperative assessment, along with attentive intraoperative monitoring and postoperative care. Nevertheless, we must be prepared to manage unpleasant events which may occur.