• Sleep Medicine and Psychophysiology
• /
• v.4 no.2
• /
• pp.140-146
• /
• 1997

Sleep-related breathing disorders, especially sleep apnea syndrome are complicated by neuropsychiatric dysfunction such as excessive daytime sleepiness, cognitive dysfunction, and depression. As the determinants of daytime sleepiness, sleep fragmentation is more influential than nocturnal hypoxia. Daytime sleepiness can be improved by continuous positive airway pressure (CPAP) or surgery in up to 95% of the treated subjects. Both sleepiness and nocturnal hypoxia would cause cognitive dysfunction. While impairments in attention and verbal memory are more related with sleepiness and prominent in mild to moderate sleep apnea syndrome (SAS), impairments in general intellectual function and executive function are more related with nocturnal hypoxia and prominent in severe SAS. Several cognitive deficits related with nocturnal hypoxia may be irreversible despite CPAP or surgical treatments. So, early detection and early appropriate treatment of SAS would prevent sleepiness and cognitive deterioration.

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

• Journal of Oral Medicine and Pain
• /
• v.40 no.2
• /
• pp.63-71
• /
• 2015

Purpose: To investigate the relationship between headache and sleep by evaluating sleep quality, daytime sleepiness, and specific features related to sleep-disordered breathing (SDB). Methods: One hundred one subjects with headache and 118 healthy controls were enrolled. To collect various information on headache attacks, headache group completed self-reported questionnaire about the characteristics of headache attacks and the migraine disability assessment (MIDAS) questionnaire. The subjective quality of sleep was evaluated in all of the subjects using the Pittsburgh sleep quality index (PSQI) and Epworth sleepiness scale (ESS). In addition, the following specific features of sleep were evaluated in 28 subjects selected randomly from each group: apnea-hypopnea index (AHI), prevalence of SDB, nocturnal oxygen saturation (SaO2), and oxygen desaturation index (ODI) as measured using a portable monitoring device. Results: The global PSQI and the prevalence of poor sleeping (global PSQI >5), ESS scores and the prevalence of daytime sleepiness (ESS score >10) were significantly higher in the headache group (both p<0.0001, respectively). The mean scores on the numerical rating scale and the MIDAS were significantly higher in the poor-sleeper group than in the good-sleeper group (p=0.0347 and p=0.0016, respectively). The global PQSI and prevalence of daytime sleepiness were significantly higher in the chronic-headache group than in the acute-headache group (p=0.0003 and p=0.0312, respectively). Conclusions: There is a significant association between headache and sleep. Especially, severity and chronicity of headache were significantly associated with sleep quality and daytime sleepiness.

• Sleep Medicine and Psychophysiology
• /
• v.6 no.1
• /
• pp.19-25
• /
• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.

• Korean Circulation Journal
• /
• v.53 no.7
• /
• pp.425-451
• /
• 2023

Most patients with heart failure (HF) have multiple comorbidities, which impact their quality of life, aggravate HF, and increase mortality. Cardiovascular comorbidities include systemic and pulmonary hypertension, ischemic and valvular heart diseases, and atrial fibrillation. Non-cardiovascular comorbidities include diabetes mellitus (DM), chronic kidney and pulmonary diseases, iron deficiency and anemia, and sleep apnea. In patients with HF with hypertension and left ventricular hypertrophy, renin-angiotensin system inhibitors combined with calcium channel blockers and/or diuretics is an effective treatment regimen. Measurement of pulmonary vascular resistance via right heart catheterization is recommended for patients with HF considered suitable for implantation of mechanical circulatory support devices or as heart transplantation candidates. Coronary angiography remains the gold standard for the diagnosis and reperfusion in patients with HF and angina pectoris refractory to antianginal medications. In patients with HF and atrial fibrillation, longterm anticoagulants are recommended according to the CHA₂DS₂-VASc scores. Valvular heart diseases should be treated medically and/or surgically. In patients with HF and DM, metformin is relatively safer; thiazolidinediones cause fluid retention and should be avoided in patients with HF and dyspnea. In renal insufficiency, both volume status and cardiac performance are important for therapy guidance. In patients with HF and pulmonary disease, beta-blockers are underused, which may be related to increased mortality. In patients with HF and anemia, iron supplementation can help improve symptoms. In obstructive sleep apnea, continuous positive airway pressure therapy helps avoid severe nocturnal hypoxia. Appropriate management of comorbidities is important for improving clinical outcomes in patients with HF.

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