Treating Obstructive Sleep Apnea With Positive Pressure Therapy

2011 ◽  
Vol 13 (5) ◽  
pp. 458-472
Author(s):  
Ninon Pachikara ◽  
Reena Mehra
2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Kartikeya Rajdev ◽  
Pretty Sara Idiculla ◽  
Shubham Sharma ◽  
Susanna G. Von Essen ◽  
Peter J. Murphy ◽  
...  

Pulmonary barotrauma such as pneumothorax (PTX) is a known complication of invasive mechanical ventilation. However, it is uncommonly reported with the use of noninvasive positive pressure ventilation (NPPV) and CPAP (continuous positive airway pressure) therapy. We present a case of a 66-year-old female who presented with chronic dyspnea on exertion secondary to right-sided diaphragmatic hernia. The patient also underwent a home sleep study which suggested obstructive sleep apnea (OSA) for which she was initiated on CPAP. She then underwent surgical repair of her right diaphragmatic hernia. The patient developed pneumothorax three times over the course of the following several months, once on the right side and twice on the left side. The patient’s incidences of PTX had a temporal association with the CPAP initiation. Her CPAP therapy was discontinued permanently after the third occurrence of PTX. With this case report, we highlight the risk of barotrauma with the use of CPAP for OSA. There are very few reported cases of PTX in association with NPPV therapy for OSA. The lung-protective ventilation strategies and limiting the positive airway pressures can help reduce the risk of pulmonary barotrauma with CPAP.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Aviv D. Goldbart ◽  
Meital Gannot ◽  
Hen Haddad ◽  
Jacob Gopas

AbstractObstructive sleep apnea syndrome (OSA) is associated with cardiovascular morbidity in adults and children. NFκB activity is enhanced in circulating monocytes of adults with OSA, that decreases following positive pressure therapy. OSA children’s serum activates NFκB in a cell line. We hypothesized that OSA children’s serum can activate NFκB in cardiomyocytes (CM) and effect their viability. In order to explore the role played by NFκB in OSA cardiovascular pathophysiology, rat, mouse and human immortalized CM were exposed to human serum drawn from OSA children and matched controls. Increased expression of NFκB classical subunits p65/p50 as well as major morphological changes occurred in cardiomyocytes following OSA’s serum exposure. OSA children’s serum induced NFκB activity as measured by p65 nuclear translocation in immortalized human CM and rat cardiomyocytes as well as dense immunostaining of the nucleus. Trypan blue and XTT assays showed that OSA sera induced CM apoptosis. We conclude that NFκB is systemically activated in cardiomyocytes, who also demonstrate decreased viability and contractility following exposure to OSA serum. It supports the hypothesis NFκB plays a role in the evolution of cardiovascular morbidity in OSA. It may support the search for new therapeutic interventions controlling NFκB activation in OSA.


2021 ◽  
Vol 22 (5) ◽  
pp. 2300
Author(s):  
Ronni Baran ◽  
Daniela Grimm ◽  
Manfred Infanger ◽  
Markus Wehland

Obstructive sleep apnea (OSA) is a common disease, with approximately 3–7% of men and 2–5% of women worldwide suffering from symptomatic OSA. If OSA is left untreated, hypoxia, microarousals and increased chemoreceptor stimulation can lead to complications like hypertension (HT). Continuous positive airway pressure (CPAP) is the most common treatment for OSA, and it works by generating airway patency, which will counteract the apnea or hypopnea. More than one billion people in the world suffer from HT, and the usual treatment is pharmacological with antihypertensive medication (AHM). The focus of this review will be to investigate whether the CPAP therapy for OSA affects HT.


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