• Sleep Medicine and Psychophysiology
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• v.3 no.1
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• pp.38-46
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• 1996

The purpose of this study is to investigate the neurocognitive dysfunction and the degree of severity according to the oxygen desaturation in obstructive sleep apnea patients. We performed nocturnal polysomnographic recording and administered 3 Vienna Test System subtest of Reaction unit, Continuous attention and Cognitrone to 11 obstructive sleep patients and 13 controls. The result were as follows: 1) On Continous attentin and Cognitrone, patients with obstructive sleep apnea showed significant lower score on correct answer, higher score on missed answer and prolonged reaction time than control. But, there was no significant difference on Reaction unit between two groups. 2) Among 3 groups divided by degree of oxygen desaturation, there were no significant differences on Reaction unit. As the oxygen saturation decreased however, the obstructive sleep apnea group revealed significantly poor performance score on continuous attention and cognitrone. We suggested that obstructive sleep apnea patients showed disturbed neurocognitive function with complex cognitive process and the severity of neurocognitive dysfunction was also correlated with oxygen desaturation.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.129-139
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• 1997

The data collected to date indicate that sleep-related breathing disorders, including sleep-disordered breathing(sleep apnea) and underlying respiratory system diseases, are one of the important risk factors for cardiovascular dysfunction. Sleep-disordered breathing(sleep apnea) is now recognized as one of the leading causes of systemic hypertension, cardiac arrhythmias, coronary heart disease, pulmonary hypertension, right heart failure, and stroke. Sleep may exert a profound effect on breathing in patients with underlying respiratory system disease including bronchopumonary diseases, chest wall abnormalities, central alveolar hypoventilation syndromes or respiratory neuromuscular disorders. Chronic hypoxia and hypercapnia in these patients may accelerate the development of long term cardiovascular complications such as cardiac arrhythmias, pulmonary hypertension, and right heart failure(cor pulmonale). Several recent studies reported that sleep-related breathing disorders are associated with long-term cardiovascular morbidity and mortality. Careful assessment of respiratory and cardiovascular function in these patients is critical. Aggressive and highly effective treatment of sleep-related breathing disorders using tracheostomy, mechanical ventilation, nasal continuous positive airway pressure therapy(nCPAP), intercurrent oxygen therapy or other interventions can reduce the prevalence of cardiovascular dysfunction and the long-term mortality.

• Sleep Medicine and Psychophysiology
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• v.2 no.1
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• pp.55-64
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• 1995

During sleep, relatively major respiratory physiological changes occur in healthy subjects. The contributions and interactions of voluntary and metabolic breathing control systems during waking and sleep are quite different Alterations of ventilatory control occur in chemosensitivity, response to mechanical loads, and stability of ventilation. The activities of intercostal muscles and muscles involved in regulating upper airway size are decreased during sleep. These respiratory physiological changes during sleep compromise the nocturnal ventilatory function, and sleep is an important physiological cause of the nocturnal alveolar hypoventilation. There are several causes of chronic alveolar hypoventilation including cardiopulmonary, neuromuscular diseases. Obstructive sleep apnea syndrome (OSAS) is an important cause of nocturnal hypoventilation and hypoxia. Coexistent cardiopulmonary or neuromuscular disease in patients with OSAS contributes to the development of diurnal alveolar hypoventilation, diurnal hypoxia and hypercapnia. The existing data indicates that nocturnal recurrent hypoxia and fragmentation of sleep in patients with OSAS contributes to the development of systemic hypertension and cardiac bradytachyarrhythmia, and diurnal pulmonary hypertension and cor pulmonale in patients with OSAS is usually present in patients with coexisting cardiac or pulmonary disease. Recent studies reported that untreated patients with OSAS had high long-term mortality rates, cardiovascular complications of OSAS had a major effect on mortality, and effective management of OSAS significantly decreased mortality.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.153-168
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• 1998

Background: The existing data indicate that obstructive sleep apnea syndrome contributes to the development of cardiovascular dysfunction such as systemic hypertension and cardiac arrhythmias, and the cardiovascular dysfunction has a major effect on high long-term mortality rate in obstructive sleep apnea syndrome patients. To a large extent the various studies have helped to clarify the pathophysiology of obstructive sleep apnea, but many basic questions still remain unanswered. Methods: In this study, the influence of obstructive sleep apnea on systemic blood pressure, cardiac rhythm and urinary catecholamines concentration was evaluated. Over-night polysomnography, 24-hour ambulatory blood pressure and ECG monitoring, and measurement of urinary catecholamines, norepinephrine (UNE) and epinephrine (UEP), during waking and sleep were undertaken in obstructive sleep apnea syndrome patients group (OSAS, n=29) and control group (Control, n=25). Results: 1) In OSAS and Control, UNE and UEP concentrations during sleep were significantly lower than during waking (P<0.01). In UNE concentrations during sleep, OSAS showed higher levels compare to Control (P<0.05). 2) In OSAS, there was a increasing tendency of the number of non-dipper of nocturnal blood pressure compare to Control (P=0.089). 3) In both group (n=54), mean systolic blood pressure during waking and sleep showed significant correlation with polysomnographic data including apnea index (AI), apnea-hypopnea index (AHI), arterial oxygen saturation nadir ($SaO_2$ nadir) and degree of oxygen desaturation (DOD). And UNE concentrations during sleep were correlated with AI, AHI, $SaO_2$ nadir, DOD and mean diastolic blood pressure during sleep. 4) In OSAS with AI>20 (n==14), there was a significant difference of heart rates before, during and after apneic events (P<0.01), and these changes of heart rates were correlated with the duration of apnea (P<0.01). The difference of heart rates between apneic and postapneic period (${\Delta}HR$) was significantly correlated with the difference of arterial oxygen saturation between before and after apneic event (${\Delta}SaO_2$) (r=0.223, P<0.001). 5) There was no significant difference in the incidence of cardiac arrhythmias between OSAS and Control In Control, the incidence of ventricular ectopy during sleep was significantly lower than during waking. But in OSAS, there was no difference between during waking and sleep. Conclusion : These results suggested that recurrent hypoxia and arousals from sleep in patients with obstructive sleep apnea syndrome may increase sympathetic nervous system activity, and recurrent hypoxia and increased sympathetic nervous system activity could contribute to the development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac function.