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Updated: Sep 22, 2026

Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
Obstructive Sleep Apnea as a Driver of Venous Congestion, Cardio-Renal Dysfunction, and Cardiac Conduction Disease: A
Sidhartha Gautam Senapati1, Satya Priya Paritala1, Srija Sirineni2
1Department of Internal Medicine, Texas Tech University Health Sciences Center, El Paso, Texas, USA.
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.
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