Apnea is defined as the absence of airflow at the nose and mouth for longer than 10 seconds. Sleep apnea syndrome (SAS) is described as the occurrence of more than 30 apnea episodes over a seven-hour period of nocturnal sleep. The majority of sleep apnea cases are obstructive as opposed to central. The upper airway becomes impeded while respiratory effort and diaphragmatic contraction still occur. In the absence of formal sleep studies, the diagnosis can be made clinically by interviewing patients and their sleeping partners. Clinical signs include loud snoring, observed apneic episodes, and excessive daytime somnolence.
Physiologic studies have demonstrated that patients with SAS have narrowed upper airways to start with, so they are more susceptible than other patients to drugs or anesthetics that suppress pharyngeal muscle tone. In normal, awake patients, there is a phasic activity of the pharyngeal muscles that contracts them immediately before respiration, helping to resist the negative pressure generated by the diaphragm and keeping the airway from collapsing. This phasic pharyngeal contraction is markedly reduced both by REM sleep and by narcotic pain administration. Patients with sleep apnea appear to be much more sensitive than normal individuals, even to minimal levels of sedation. The increased sensitivity of their hypoglossal nerves to low doses of anesthesia has been well described.
Literature review suggests that the traditional nursing measurement of respiratory rate is ineffective in SAS patients for a number of reasons. Critical hypoxemia occurred during sporadic episodes of obstruction with continued respiratory effort that could be difficult to differentiate from effective respiration. These episodes were only rarely associated with slow respiratory rates (fewer than 10 breaths per minute), making rate alone an insensitive indicator of compromise. One solution would be to use audible pulse oximeter monitoring on the ward. Although this is not currently the standard of care, the apparent high incidence of respiratory obstruction in SAS patients should make this a strong consideration, especially if narcotic analgesics are to be used.
Sleep apnea should be suspected in patients with the classical body habitus of obesity with a short, thick neck. A history of loud snoring as reported by the sleeping partner is a cardinal sign mentioned in almost all case reviews. One study suggests that snoring be considered significant if obstruction was noted by the sleeping partner, including episodes of gasping and choking while asleep, the noise obliged the couple to sleep in different rooms or the snoring was associated with excessive daytime somnolence. Although these signs are noted in a number of studies, these are not questions routinely asked by anesthesiologists. Perhaps not all patients exhibiting these symptoms will have sleep apnea if evaluated by formal sleep studies, but it might be safer to treat them as if they did until proven otherwise.
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