Pathophysiology of Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) is a common sleep disorder that is characterized by recurrent episodes of upper airway obstruction and is associated with reductions in ventilation, resulting in recurrent arousals and episodic oxyhemoglobin desaturations dur
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Kivanc Gunhan
Keywords
Obstructive sleep apnea • Physiology of sleep • Pathophysiology • Wakefulness • Upper airway patency • Pharyngeal collapsibility • Neuromuscular • Neuroventilatory
Core Messages
• Obstructive sleep apnea (OSA) is a common sleep disorder affecting 4 % of men and 2 % of women and is characterized by recurrent episodes of upper airway obstruction and is associated with reductions in ventilation, resulting in recurrent arousals and episodic oxyhemoglobin desaturations during sleep. • Significant clinical consequences of the disorder cover a wide spectrum including daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease (hypertension, stroke, myocardial infarction, heart failure), metabolic dysfunction, respiratory failure, and cor pulmonale.
K. Gunhan, MD, PhD Department of Otorhinolaryngology and Head-Neck Surgery, Celal Bayar University, Mimar Sinam Bulv. No: 10, CBU Uncubozkoy Kampusu, Manisa, 45020, Turkey e-mail: [email protected]
• The major risk factors for the disorder include obesity, male gender, hormones, age, anatomical factors, genetic factors, posture, and gravity. • Wakefulness provides compensatory neuronal activation of dilator muscles in an anatomically compromised collapsible pharynx supporting ventilator control. Accordingly, when this activation is lost at sleep onset, the airway narrows and/or collapses. • The mechanical determinants of airway patency are similar to those regulating caliber of any collapsible tube. There is a critical closing pressure (Pcrit) of the passive airway, which is defined as the pressure inside the airway at which the airway collapses. With increasing Pcrit, as the differential between Pupstream and Pcrit decreases, inspiratory airflow limitation will eventually develop and complete airway occlusion occurs. • Neuromuscular controls of upper airway dynamics during sleep influence the pharyngeal muscle tone and upper airway collapsibility. A variety of defective
T.M. Önerci (ed.), Nasal Physiology and Pathophysiology of Nasal Disorders, DOI 10.1007/978-3-642-37250-6_24, © Springer-Verlag Berlin Heidelberg 2013
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respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal upper airway protective reflexes. • Tonic and phasic EMG activity of pharyngeal airway dilator muscles (genioglossus and tensor palatine) is progressively reduced from wakefulness to NREM to REM sleep. Changes in proprioceptive and chemoreceptor feedback play a significant role in the dynamics of upper airway caliber. Chemoreceptor influences also have substantial effects on upper airway muscle recruitment, and in the case of CO2, upper airway motor neurons relative to phrenic motor neurons have a substantially higher threshold for inhibition (via hypocapnia) and activation (via hypercapnia).
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Pathophysiology of Obstructive Sleep Apnea
Hypnos was the god of Sleep. He resided in Erebos, the land of eternal darkness, beyond the gates of the risi
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