Upon successfully completing this continuing education course, you should be able to:
In the recent past, sleep’s implications for the physiology and pathogenesis of disease have been ignored. With the evolution of sleep laboratories, an awareness of the relationship between sleep and various gastrointestinal phenomena has been rapidly emerging. Most notable has been burgeoning interest in the relationship between sleep-related gastroesophageal reflux (GER) and the development of esophageal and aerodigestive complications such as esophagitis, chronic cough, exacerbation of bronchial asthma, and pulmonary aspiration. Work examining the relationship between sleep and GER has captured the attention of gastroenterologists and primary care physicians involved in the treatment of this common, perplexing problem. Sleep results in a significant alteration in basic physiology that can profoundly affect responses to GER.
Sleep is experienced by all mammalian species and is associated with remarkable behavioral and physiological changes. Sleep is a ubiquitous biological need for which the ultimate function, other than restoring behavioral alertness, remains unknown. Accordingly, attempts to understand the basic pathophysiology of GER and its consequences require an understanding and examination of sleep-related reflux events, acid clearance, and arousal responses.
Sleep itself can be divided into five separate stages determined by the simultaneous monitoring of the electroencephalogram, electrooculogram, and electromyogram, according to internationally accepted criteria. The basic criteria of sleep staging and the fundamental physiology of sleep are outlined elsewhere.1
Sleep is not merely a passive process; the activation of a variety of brain mechanisms is needed to initiate the onset of sleep. Stage 1 sleep is generally regarded as the transition between waking and sleep. Stages 2, 3, and 4 are generally combined into one entity referred to as non–rapid-eye-movement (NREM) sleep. REM or dreaming sleep occurs at intervals of approximately 90 minutes during a normal night of sleep. The occurrence of REM sleep is controlled and regulated by specific brainstem nuclei that include the locus ceruleus and several nuclei located in the pontine tegmentum.1,2
Physiologically, NREM sleep is characterized by the general slowing of autonomic function, with diminution of heart rate, blood pressure, and metabolic rate. In contrast to NREM, REM sleep is characterized by marked and unique physiological changes. For example, regulation of normal core body temperature is suspended in warm-blooded animals, rendering them poikilothermic.1 The mechanisms that normally control and regulate blood oxygen, carbon dioxide, and pH are essentially suspended during REM sleep. Furthermore, a complete skeletal-muscle paralysis exists during REM sleep and is generally thought to preclude physically acting out a dream.1 Thus, the physiological changes associated with sleep may influence nocturnal GER and esophageal acid clearance