阻塞性睡眠呼吸暂停作为静脉淤血、心肾功能障碍和心脏传导疾病的驱动因素：一项综合性综述。

文献信息

中文摘要

引言： 阻塞性睡眠呼吸暂停（OSA）是重要的全身性疾病之一，具有显著的心血管和肾脏后果。除了OSA与高血压和代谢紊乱的众所周知联系外，越来越多的数据表明，OSA通过多种机制与液体再分布、静脉淤血、心力衰竭、肾脏问题和心律失常之间存在关联。
方法： 为进行本叙述性综述，使用PubMed、Scopus和Google Scholar进行检索，查找2000年1月至2026年1月期间发表的英文论文，以获取关于阻塞性睡眠呼吸暂停（OSA）、间歇性缺氧、静脉淤血、心肾功能障碍、交感神经激活、氧化应激、炎症、心律失常和持续气道正压通气（CPAP）等的文章。对临床研究、科学声明、系统综述和机制相关的实验研究进行了叙述性综合。
结果： 上气道反复发生的阻塞性事件导致低氧血症、觉醒时的交感反应以及显著的胸腔内负压。这些生理变化可触发交感神经和肾素-血管紧张素-醛固酮系统的激活，从而导致钠潴留、液体转移和心脏负荷增加。间歇性缺氧还触发氧化炎症反应，甚至在动物模型中通过NLRP3炎症小体依赖性途径。
讨论： 交感神经系统激活、间歇性低氧血症、炎症和压力增加继发的机械应力，是可能将OSA与静脉淤血以及心肾和电生理功能障碍联系起来的复杂机制网络的一些组成部分。然而，许多分子途径尚未被证明具有临床相关性。
结论： 在考虑静脉淤血的可能原因时，除了心肾疾病和心律失常外，还需要考虑阻塞性睡眠呼吸暂停（OSA）的存在。识别和治疗可以改善心血管结局，但需要更多研究来理解其临床意义。

英文摘要

INTRODUCTION: Obstructive sleep apnea (OSA) represents one of the significant systemic diseases with considerable cardiovascular and renal consequences. Along with the wellknown links of OSA with hypertension and metabolic disorders, growing data have been found that indicate the connection between OSA and redistribution of fluids, venous congestion, heart failure, kidney problems, and cardiac arrhythmias via several mechanisms.
METHODS: For this narrative review, a search was performed using PubMed, Scopus, and Google Scholar to find English-language papers published between January 2000 and January 2026 to obtain articles on obstructive sleep apnea (OSA), intermittent hypoxia, venous congestion, cardiorenal dysfunction, sympathetic activation, oxidative stress, inflammation, arrhythmias, and continuous positive airway pressure (CPAP), among others. Clinical studies, scientific statements, systematic reviews, and mechanistically relevant experimental studies were narratively synthesized.
RESULTS: Obstructive episodes occurring recurrently in the upper airway cause hypoxemia, sympathetic responses on arousals, and marked negative intrathoracic pressure. Such physiologic changes can trigger the activation of the sympathetic and renin-angiotensin-aldosterone systems, thus causing sodium retention, fluid shift, and an increased workload for the heart. Intermittent hypoxia also triggers an oxidative-inflammatory response, even through NLRP3 inflammasomedependent pathways in animal models.
DISCUSSION: Activation of the sympathetic nervous system, intermittent hypoxemia, inflammation, and mechanical stress secondary to increased pressure are some of the components of a complex network of mechanisms that could potentially link OSA to venous congestion, as well as cardiorenal and electrophysiological dysfunction. However, many molecular pathways have not yet been shown to have clinical relevance.
CONCLUSION: The existence of obstructive sleep apnea (OSA) needs to be taken into consideration when thinking about possible causes of venous congestion, in addition to cardiorenal disease and dysrhythmias. Recognition and treatment can lead to improved cardiovascular outcomes, but more research is needed to understand the clinical implications.