Nocturnal oxygen attenuates sleep desaturations among stable patients, without increases in PaCO 2 of clinical concern. Nocturnal polysomnographic monitoring in COPD is usually performed when coexistence of sleep apnea (“overlap syndrome”) is suspected, while in most other cases nocturnal oximetry may be enough. Conversely, it is generally accepted that occurrence of sleep apneas in COPD is associated with a worse evolution of the disease. Effects of the “desaturator” condition on pulmonary hemodynamics, evolution of diurnal blood gases, and life expectancy are also controversial. The role of nocturnal hypoxemia as a determinant of alterations in sleep structure observed in COPD is dubious. Subjects with diurnal PaO 2 of 60–70 mmHg are distinguished in “desaturators” and “nondesaturators” according to nocturnal oxyhemoglobin saturation behavior. The severity of gas exchanges alterations is proportional to the degree of impairment of diurnal pulmonary function tests, particularly of partial pressure of oxygen (PaO 2) and of carbon dioxide (PaCO 2) in arterial blood, but correlations between diurnal and nocturnal blood gas levels are rather loose. This is mainly due to hypoventilation, while a deterioration of ventilation/perfusion mismatch plays a minor role. Right-to-left shunt was found on lateral imaging of the brain during a ventilation-perfusion scan.įurther evaluation of the aneurysmal atrial septum on transesophageal echocardiogram with anĪgitated saline bubby study demonstrated a patent foramen ovale with a right-to-left shunt.Patients with COPD may show slow, progressive deteriorations in arterial blood gases during the night, particularly during rapid eye movement (REM) sleep. Prior transthoracic echocardiogram had demonstrated an atrial septalĪneurysm without communication between the atrial chambers. Restrictive defect on pulmonary function testing, and a normal chest computed tomography Showed normal resting oxygen saturation, no desaturation on a six-minute walk test, mild He was referred to pulmonology for further evaluation that Than 5 events per hour but demonstrated hypoxemia with 49.7% of total sleep time spentīelow an oxygen saturation of 90%. He frequently reported shortness of breath duringĭuring a polysomnogram, the patient was found to have a total apnea-hypopnea index of fewer The patient was a never smoker without evidence of malignancy or renal disease leading to suspicion that his polycythemia was due to hypoxemia despite normal oxygen saturations during point of care evaluations. Further evaluation suggested secondary polycythemia after serum erythropoietin and JAK2 mutation testing were negative. Over the span of six years, he had multiple cryptogenic strokes and VTEs in the setting of polycythemia and normal hypercoagulability labs. Report of Cases: A 60-year-old male with history of recurrent venous thromboembolic events (VTE), secondary polycythemia, and cryptogenic strokes was referred for a polysomnogram during the evaluation of polycythemia. In this case, prior workup of cryptogenic stroke failed to identify a PFO that was diagnosed after further investigation of polycythemia which revealed nocturnal hypoxemia on polysomnogram. Patent foramen ovale (PFO) in adults often remains asymptomatic until clinical manifestations such as cryptogenic stroke, migraine headache, air embolism, hypoxemia, or platypnea-orthodeoxia syndrome occur.
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