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General Health & Fitness
Health & Wellness
Diagnosis and Management of Obstructive Sleep Apnea
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<blockquote data-quote="madman" data-source="post: 235252" data-attributes="member: 13851"><p><strong>Figure 3. Putative Causal Mechanisms of Obstructive Sleep Apnea–Related Cardiovascular and Metabolic Disease</strong></p><p><strong>[ATTACH=full]26162[/ATTACH]</strong> <strong>Obstructive sleep apnea results in 3 proximate pathophysiological events: <u>intermittent hypoxemia, sleep fragmentation, and large swings in intrathoracic pressure</u>. These events initiate a cascade of interacting processes that contribute to adverse health outcomes. Intermittent hypoxemia, particularly in the presence of hypercapnia, causes elevation of sympathetic nervous system activity that persists during wakefulness. Arousal from sleep, due to the increased respiratory effort against an obstructed airway and to hypoxemia and hypercapnia, also contributes to sympathetic activity and activation of the hypothalamic-pituitary-adrenal axis. Intermittent hypoxemia and reoxygenation result in the production of reactive oxygen species. Both sympathetic activity and oxidative stress contribute to blood pressure elevation, metabolic dysregulation, systemic inflammation, and endothelial dysfunction. These abnormalities are likely precursors of clinical hypertension, type 2 diabetes, and coronary and cerebrovascular disease. Large intrathoracic pressure swings, which result from respiratory efforts against an obstructed upper airway, increase cardiac preload and afterload that, together with the effects of sympathetic activity, oxidative stress, inflammation, and gas exchange abnormalities, may contribute to heart failure and cardiac rhythm disturbances.</strong></p></blockquote><p></p>
[QUOTE="madman, post: 235252, member: 13851"] [B]Figure 3. Putative Causal Mechanisms of Obstructive Sleep Apnea–Related Cardiovascular and Metabolic Disease [ATTACH type="full"]26162[/ATTACH][/B] [B]Obstructive sleep apnea results in 3 proximate pathophysiological events: [U]intermittent hypoxemia, sleep fragmentation, and large swings in intrathoracic pressure[/U]. These events initiate a cascade of interacting processes that contribute to adverse health outcomes. Intermittent hypoxemia, particularly in the presence of hypercapnia, causes elevation of sympathetic nervous system activity that persists during wakefulness. Arousal from sleep, due to the increased respiratory effort against an obstructed airway and to hypoxemia and hypercapnia, also contributes to sympathetic activity and activation of the hypothalamic-pituitary-adrenal axis. Intermittent hypoxemia and reoxygenation result in the production of reactive oxygen species. Both sympathetic activity and oxidative stress contribute to blood pressure elevation, metabolic dysregulation, systemic inflammation, and endothelial dysfunction. These abnormalities are likely precursors of clinical hypertension, type 2 diabetes, and coronary and cerebrovascular disease. Large intrathoracic pressure swings, which result from respiratory efforts against an obstructed upper airway, increase cardiac preload and afterload that, together with the effects of sympathetic activity, oxidative stress, inflammation, and gas exchange abnormalities, may contribute to heart failure and cardiac rhythm disturbances.[/B] [/QUOTE]
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General Health & Fitness
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Diagnosis and Management of Obstructive Sleep Apnea
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