Morbidities Associated With Obstructive Sleep Apnea
Morbidities Associated With Obstructive Sleep Apnea
Obstructive sleep apnea (OSA)-induced biological changes include intermittent hypoxia, intermittent hypercapnia, intrathoracic pressure changes, sympathetic activation and sleep fragmentation. OSA can cause metabolic dysregulation, endothelial dysfunction, systemic inflammation, oxidative stress and hypercoagulation, and neurohumoral changes. There is evidence suggesting that OSA is independently associated with metabolic syndrome. OSA has been shown to increase the risk for systemic hypertension, pulmonary vascular disease, ischemic heart disease, cerebral vascular disease, congestive heart failure and arrhythmias. Although there are evidences accumulating that there may be a causal relationship between OSA and cardiovascular disorders, there is a need for more data from randomized controlled intervention trials to confirm this relationship. Many risk factors of OSA (age, male gender and obesity) are also known risk factors for cardiovascular disease. Severe OSA-hypopnea significantly increases the risk of fatal and nonfatal cardiovascular events in both men and women, and continuous positive airway pressure treatment reduces this risk in both. Neurocognitive consequences of OSA include daytime sleepiness, loss of alertness, memory deficit, reduced vigilance, impaired executive function, increased risk for automobile and occupational accidents, and decreased quality of life.
Man spends 85% of sleep time in the nonrapid eye movement stage in which there is a decrease in sympathetic nervous system activity, heart rate, blood pressure (BP), cardiac output, systemic vascular resistance and metabolic rate. However, there is an increase in parasympathetic activity during nonrapid eye-movement stage. Rapid eye-movement sleep constitutes 15% of sleep time, and during this period, there will be intermittent surges in sympathetic activity. The obstructive sleep apnea (OSA) is the repetitive interruption of ventilation during sleep caused by collapse of the pharyngeal airway and the central sleep apnea is the repetitive cessation of ventilation during sleep resulting from loss of ventilatory drive. OSA is defined as reduction in airflow associated with upper airway collapse or narrowing that occurs during the change from wakefulness to sleep. Apnea due to upper airway collapse is defined as nearly complete cessation of airflow associated with oxygen desaturation or an arousal from sleep, and hypopnea is due to partial collapse of upper airways. Apnea is defined as a cessation of airflow for ≥10 s, despite continuing ventilatory effort, with five or more such episodes per hour of sleep, and is usually associated with a ≥4% decrease in oxyhemoglobin saturation. Hypopnea is characterized by a reduction of ≥50% in airflow for >10 s associated with a ≥3% decrease in oxygen saturation and/or arousal. In upper airway resistance syndrome, there will be no significant decrease in airflow but snoring is usual, and can have 15 or more episodes of arousal per hour of sleep with no significant decrease in oxyhemoglobin saturation. It has been estimated that the OSA syndrome (OSAS) affects 2–4% of middle-aged adults. The apnea–hypopnea index (AHI) is used to characterize OSA. OSAS is defined as sleep-disordered breathing associated with daytime symptoms, most often excessive daytime sleepiness. A Wisconsin sleep study has identified baseline obesity, older age and presence of snoring as factors important in progression of disease. Chronic intermittent hypoxia is the cardinal feature of OSA. Risk factors for the development of OSA are classified into non-modifiable and modifiable factors. The non-modifiable risk factors are age, gender (male), ethnicity (being black, Hispanic), anatomical abnormalities of craniofacial regions and upper airway, a thick neck with circumference more than 17 inches, and genetic predisposition. The modifiable risk factors are excessive body weight, use of alcohol, sedatives or tranquilizers, narrowed airways due to enlarged tonsils or adenoids, smoking, chronic nasal congestion, myxedema and menopause.
Abstract and Introduction
Abstract
Obstructive sleep apnea (OSA)-induced biological changes include intermittent hypoxia, intermittent hypercapnia, intrathoracic pressure changes, sympathetic activation and sleep fragmentation. OSA can cause metabolic dysregulation, endothelial dysfunction, systemic inflammation, oxidative stress and hypercoagulation, and neurohumoral changes. There is evidence suggesting that OSA is independently associated with metabolic syndrome. OSA has been shown to increase the risk for systemic hypertension, pulmonary vascular disease, ischemic heart disease, cerebral vascular disease, congestive heart failure and arrhythmias. Although there are evidences accumulating that there may be a causal relationship between OSA and cardiovascular disorders, there is a need for more data from randomized controlled intervention trials to confirm this relationship. Many risk factors of OSA (age, male gender and obesity) are also known risk factors for cardiovascular disease. Severe OSA-hypopnea significantly increases the risk of fatal and nonfatal cardiovascular events in both men and women, and continuous positive airway pressure treatment reduces this risk in both. Neurocognitive consequences of OSA include daytime sleepiness, loss of alertness, memory deficit, reduced vigilance, impaired executive function, increased risk for automobile and occupational accidents, and decreased quality of life.
Introduction
Man spends 85% of sleep time in the nonrapid eye movement stage in which there is a decrease in sympathetic nervous system activity, heart rate, blood pressure (BP), cardiac output, systemic vascular resistance and metabolic rate. However, there is an increase in parasympathetic activity during nonrapid eye-movement stage. Rapid eye-movement sleep constitutes 15% of sleep time, and during this period, there will be intermittent surges in sympathetic activity. The obstructive sleep apnea (OSA) is the repetitive interruption of ventilation during sleep caused by collapse of the pharyngeal airway and the central sleep apnea is the repetitive cessation of ventilation during sleep resulting from loss of ventilatory drive. OSA is defined as reduction in airflow associated with upper airway collapse or narrowing that occurs during the change from wakefulness to sleep. Apnea due to upper airway collapse is defined as nearly complete cessation of airflow associated with oxygen desaturation or an arousal from sleep, and hypopnea is due to partial collapse of upper airways. Apnea is defined as a cessation of airflow for ≥10 s, despite continuing ventilatory effort, with five or more such episodes per hour of sleep, and is usually associated with a ≥4% decrease in oxyhemoglobin saturation. Hypopnea is characterized by a reduction of ≥50% in airflow for >10 s associated with a ≥3% decrease in oxygen saturation and/or arousal. In upper airway resistance syndrome, there will be no significant decrease in airflow but snoring is usual, and can have 15 or more episodes of arousal per hour of sleep with no significant decrease in oxyhemoglobin saturation. It has been estimated that the OSA syndrome (OSAS) affects 2–4% of middle-aged adults. The apnea–hypopnea index (AHI) is used to characterize OSA. OSAS is defined as sleep-disordered breathing associated with daytime symptoms, most often excessive daytime sleepiness. A Wisconsin sleep study has identified baseline obesity, older age and presence of snoring as factors important in progression of disease. Chronic intermittent hypoxia is the cardinal feature of OSA. Risk factors for the development of OSA are classified into non-modifiable and modifiable factors. The non-modifiable risk factors are age, gender (male), ethnicity (being black, Hispanic), anatomical abnormalities of craniofacial regions and upper airway, a thick neck with circumference more than 17 inches, and genetic predisposition. The modifiable risk factors are excessive body weight, use of alcohol, sedatives or tranquilizers, narrowed airways due to enlarged tonsils or adenoids, smoking, chronic nasal congestion, myxedema and menopause.