C63-45 A Case of Platypnea-orthodeoxia Syndrome Secondary to Aortic Dilation and Patent Foramen Ovale

Abstract Platypnea-orthodeoxia syndrome (POS) is a rare cause of refractory hypoxemia characterized by dyspnea (platypnea) and desaturation (orthodeoxia) when upright, which improves when supine. The syndrome requires two components: an interatrial communication, typically a patent foramen ovale (PFO), and a functional or anatomical factor that directs systemic venous return across the shunt in the upright position. This is a case of a 76-year-old man with history of ascending thoracic aortic aneurysm presented with one week of progressive shortness of breath, found to have normal cardiopulmonary exam and unremarkable labs, including troponin and ProBNP. Notably saturations improved in the supine position but consistently fell to the mid-80s when upright. An arterial blood gas confirmed hypoxemia with an elevated A-a gradient. CT angiography ruled out pulmonary embolism. Given the concern for an extra-pulmonary shunt, a transthoracic echocardiogram (TTE) with a bubble study was performed, revealing a large right-to-left (R-L) shunt. A subsequent transesophageal echocardiogram (TEE) confirmed a large PFO with an interatrial septal aneurysm. The TEE provided the definitive mechanism: the dilated aortic root was found to compress and distort the right atrium, redirecting inferior vena cava (IVC) flow directly toward the fossa ovalis. This R-L shunt was shown to significantly increase when the patient was moved to an upright (90-degree) position. Right-sided pressures were normal. The patient underwent successful percutaneous PFO closure with a 35mm Amplatzer Talisman device under TEE guidance. Post-procedure echo showed no residual shunt. The patient’s hypoxemia resolved immediately, and he was discharged on dual antiplatelet therapy. POS is an often-missed diagnosis for refractory hypoxemia. This case highlights the classic pathophysiology, where an anatomical defect (PFO) becomes hemodynamically significant due to a functional trigger (aortic root ectasia). The aortic dilation distorted the atrial geometry, shunting deoxygenated blood from the IVC to the left atrium when the patient was upright. Diagnosis relies on high clinical suspicion for positional desaturation and confirmation with positional contrast echocardiography. As demonstrated, transcatheter PFO closure is a safe and curative therapy, providing immediate resolution of profound hypoxemia. This abstract is funded by: None