Seminars in respiratory and critical care medicine最新文献

Comorbid insomnia and sleep apnea (COMISA) represents a highly prevalent and clinically significant overlap between the two most common sleep disorders: insomnia and obstructive sleep apnea (OSA). COMISA is associated with greater impairment in sleep, daytime functioning, and physical and mental health compared with insomnia or OSA alone. Despite its prevalence, COMISA has historically been underrecognized, partially due to the conflicting symptoms of insomnia (e.g., hyperarousal and sleeplessness) and OSA (e.g., sleep fragmentation and excessive daytime sleepiness). Recent research highlights that COMISA is not merely the coexistence of insomnia and OSA but may involve unique pathophysiological interactions and clinical phenotypes. This review explores the epidemiology, mechanisms, and clinical manifestations of COMISA. We examine insomnia as a potential extension of OSA, where repeated apneic events lead to conditioned hyperarousal, as well as OSA as an extension of chronic insomnia through mechanisms such as autonomic dysregulation and respiratory instability. Furthermore, we consider COMISA as a distinct entity, characterized by bidirectional interactions between the two conditions that exacerbate their clinical and physiological burden. Key challenges in diagnosing COMISA are discussed, including overlapping symptoms and limitations in current assessment tools. Emerging evidence suggests that COMISA is associated with increased cardiovascular and metabolic risks, greater mental health burden, and reduced treatment adherence to positive airway pressure (PAP) therapy. Advances in tailored therapeutic approaches, including combined cognitive-behavioral therapy for insomnia and OSA management strategies, are highlighted as promising avenues to improve outcomes. Understanding COMISA as a multidimensional condition with diverse phenotypes and mechanisms underscores the need for integrated diagnostic frameworks and personalized treatment strategies to optimize patient care. Further research into its unique features and long-term consequences is critical to advancing clinical practice in sleep and respiratory medicine.

World Health Organization (WHO) estimates reveal that over 777 million people were reportedly infected by SARS-CoV-2, with approximately 7 million deaths and 770 million surviving the disease up to April 2025. Beyond the immediate social and economic impact, an additional challenge arises as a large percentage of COVID-19 survivors report a wide range of symptoms after the acute phase, including fatigue, shortness of breath, cognitive difficulties, joint and muscle pain, chest pain, heart palpitations, loss of taste or smell, headaches, depression, anxiety, and sleep and circadian alterations. In this chapter, we will specifically address the sleep- and circadian rhythm-related alterations within this context. First, we will focus on sleep-related changes following the acute phase of the disease, detailing their manifestations, prevalence, and associated factors. We will then discuss the potential impact of these sleep-related aspects on the risk of SARS-CoV-2 infection, the severity of COVID-19, and the presence of post-COVID-19 conditions. A similar approach will be applied to address the circadian-related alterations. Finally, we will provide a comprehensive discussion on the overall limitations of available knowledge and its applicability, highlighting the relevance of these findings for the present and future.

Sleep is recognized as a foundational pillar of health, essential for maintaining nearly all vital processes, and a crucial component of cardiovascular function. In recent years, there has been a paradigm shift to conceptualize sleep health as a combination of multiple domains, including duration, timing, quality, variability/regularity, habits/behaviors, and disordered sleep. This review provides a comprehensive overview of the current evidence linking the multifaceted elements that contribute to healthy sleep with cardiovascular and blood pressure-related outcomes. The reviewed literature indicates a strong relationship between sleep and cardiovascular health. However, the specific pathophysiological mechanisms that bridge the various dimensions of sleep with cardiovascular outcomes remain elusive. Given the global burden of cardiovascular disease, understanding the interplay between sleep and cardiovascular health has important implications for both individual and population health. Sustained efforts to move beyond a focus on discrete domains of sleep are essential to fully understand this complex and potentially bidirectional relationship. Promoting healthy sleep patterns and optimizing the management and treatment of sleep disorders are key steps toward developing more comprehensive strategies for reducing cardiovascular risk. Integrating sleep health into routine clinical care is identified as a critical opportunity to enhance cardiovascular disease prevention and management, particularly among vulnerable and high-risk populations.

Pulmonary embolism (PE) and obstructive sleep apnea (OSA) remain a major health issue worldwide with potential overlapping pathophysiological mechanisms. PE, the most severe form of venous thromboembolism, is associated with high morbidity and mortality, presenting challenges in management and prevention, especially in high-risk populations. OSA is a prevalent condition characterized by repeated episodes of upper airway closure resulting in intermittent hypoxia and sleep fragmentation. Although the understanding of epidemiological and pathogenic relationships between OSA and PE is still limited, current data suggest that interactions between these two conditions appear to be relevant. OSA is emerging as a novel risk factor for PE, potentially affecting all components of Virchow's triad: hypercoagulability, endothelial dysfunction, and venous stasis. Epidemiological studies indicate a high prevalence of undiagnosed OSA in acute PE patients. Moderate-to-severe OSA has been linked to worse clinical presentations and outcomes. Furthermore, OSA has been associated with increased risks of PE recurrence and mortality. Future research directions should include clarifying the bidirectional relationship between these conditions and evaluating the effectiveness and safety of continuous positive airway pressure therapy in improving outcomes in patients with concurrent acute PE and OSA.

Nocturnal hypoxemia is a prevalent feature of various respiratory diseases, significantly impacting patient outcomes and therapeutic strategies. Oximetry, a noninvasive and widely accessible tool, enables the measurement of nocturnal hypoxemia through oxyhemoglobin saturation (SpO₂)-derived metrics such as the oxygen desaturation index, percentage of sleep time with SpO₂ below 90%, mean SpO₂, and measures of the area under the desaturation curve (e.g., sleep apnea-specific hypoxic burden). While these metrics are well established in obstructive sleep apnea (OSA), their application in other respiratory conditions, including chronic obstructive pulmonary disease, pulmonary hypertension, obesity hypoventilation syndrome, heart failure, neuromuscular disorders, pregnancy, and high-altitude residents, remains an area of active investigation. This review explores the pathophysiology of hypoxemia in these conditions and evaluates the role of SpO₂-derived metrics in risk stratification beyond OSA. We also discuss the challenges of interpreting SpO₂ data, particularly the difficulty differentiating disease-related hypoxemia from comorbid OSA. Additionally, we examine the limitations of oximetry, including sensor inaccuracies, motion artifacts, and skin pigmentation. Finally, we emphasize the need for further research to standardize these metrics across diverse conditions and advocate for their integration into clinical practice to enhance patient management and outcomes.

Obesity hypoventilation syndrome (OHS) is defined by the combination of obesity (body mass index [BMI] ≥30 kg/m²), sleep-disordered breathing, and daytime hypercapnia (arterial carbon dioxide tension [PaCO₂] ≥45 mm Hg at sea level) during wakefulness occurring in the absence of an alternative neuromuscular, mechanical, or metabolic explanation for hypoventilation. Patients with OHS can be classified by phenotypes depending on whether or not they have obstructive respiratory events: hypoventilation and no or not significant obstructive sleep apnea (OSA) and hypoventilation and significant OSA; we also add a third phenotype, which is the hospitalized patient with acute-on-chronic respiratory failure. We describe the mid- and long-term outcomes with and without positive airway pressure (PAP) by these three phenotypes.

Sleep and circadian disruptions are frequently reported in studies of critically ill patients. Less is known about sleep and circadian disruptions after an intensive care unit (ICU) admission. It is recognized now that survivors of critical illness may develop what is termed post-intensive care syndrome (PICS) which is a constellation of symptoms of which two of the most prominent features are fatigue and sleep complaints. Clinicians and researchers are now recognizing the importance of examining symptoms in survivors which impact their quality of life. Although current data are limited this review addresses what is now known about sleep and circadian disruptions post-ICU. Current ongoing research and future studies should continue to inform our understanding of how critical illness and the ICU environment both influence long-term outcomes in critically ill patients.

The interrelationship between asthma, obesity, and obstructive sleep apnea (OSA) presents a critical area of investigation within sleep medicine, given the rising prevalence of these conditions globally. This article explores the multifactorial interactions among these three disorders that contribute to significant morbidity. Asthma, a chronic inflammatory condition of the airways, is one of the most common chronic respiratory conditions globally. Asthma in people with obesity is associated with poor asthma control, increased asthma severity, and an increased frequency of exacerbations. Obesity, characterized by excessive fat accumulation, is a well-established risk factor for the development of OSA. This sleep-related breathing disorder disrupts airflow during sleep due to pharyngeal collapse. Conversely, OSA may worsen asthma symptoms through intermittent hypoxia and sleep fragmentation, further complicating asthma management. This review analyzes existing literature to illustrate the bidirectional relationships among these conditions. It discusses the role of systemic inflammation, hormone dysregulation, and lifestyle factors, such as diet and physical inactivity, in the development and persistence of asthma and OSA in obese patients. Furthermore, it highlights the importance of comprehensive management strategies that address these overlapping disorders. Clinical implications are examined, with consideration given to the potential for targeted therapies and lifestyle interventions that could mitigate symptoms and improve the quality of life for affected individuals. Understanding these complex interactions is essential for healthcare practitioners in optimizing the management of patients with asthma, obesity, and OSA. By recognizing the interconnectedness of these conditions, clinicians can adopt a more holistic approach to treatment, leading to improved outcomes and a better understanding of the patient's overall health trajectory. Future research directions are suggested to investigate potential therapeutic interventions and the influence of socioeconomic factors on these chronic conditions.

Sleep disorders that involve circadian rhythm disruption and sleep-disordered breathing (SDB) such as obstructive sleep apnea (OSA) are closely linked to respiratory infections. SDB leads to a proinflammatory state due to intermittent hypoxia, sleep fragmentation, increased oxidative stress, and elevation of inflammatory mediators such as tumor necrosis factor (TNF), interleukin-6 (IL-6), and C-reactive protein (CRP). Furthermore, inflammatory mediator levels correlate with SDB severity, especially in people with OSA. Nocturnal microaspiration, gastroesophageal reflux, and associated comorbidities (e.g., obesity) increase the risk of community-acquired pneumonia, viral infections such as SARS-CoV-2, respiratory complications, and death. OSA has been associated with post-COVID syndrome. It also increases the risk of postoperative complications in both adults and children. Circadian rhythm disorders such as insomnia predispose to immune disorders and increase the risk of infection. Chronic conditions such as bronchiectasis, with or without concomitant cystic fibrosis, can lead to structural sleep changes and increase the risk of OSA due to chronic cough, arousals, aspirations, hypoxia, upper airway edema, and overexpression of proinflammatory cytokines. The protective effect of treatment for sleep disorders against respiratory infection is currently unknown. However, in people presenting with respiratory infection, it is important to test for SDB to prevent complications.