C63-42 Chronic Hypoxic Respiratory Failure Secondary to Right-To-Left Shunting Through a Patent Foramen Ovale

Abstract Introduction Chronic hypoxic respiratory failure usually results from pulmonary diseases. However, cardiac abnormalities like patent foramen ovale (PFO) can cause refractory hypoxemia. This etiology is often overlooked in patients with chronic respiratory conditions, delaying appropriate management. Case Presentation A 75-year-old male with a history of asthma, resolved hypersensitivity pneumonitis, obstructive sleep apnea on CPAP with oxygen bleed-in, chronic hypoxic respiratory failure on 3-5 L/min O2, morbid obesity, and chronic lymphocytic leukemia presented to the pulmonary clinic with two weeks of progressive dyspnea and increased oxygen requirement. Prior pulmonary function tests showed reduced FEV1 and FVC with a preserved ratio and diffusion capacity, and chest imaging revealed no COPD. At baseline, he required 3 L/min at rest and 5 L/min with exertion but recently needed 6 L/min with persistent desaturations to the 70s. He denied cough, fever, or edema. In clinic, SpO2 was 85-87% on 6 L/min, improving to 92% on 10 L/min, prompting emergency department referral. Laboratory evaluation and imaging were unremarkable. Despite bronchodilators, corticosteroids, and antibiotics, hypoxemia persisted. Transthoracic echocardiography showed severe right ventricular enlargement with moderate to severe systolic dysfunction. Right and left heart catheterization demonstrated normal right atrial (6 mmHg), mean pulmonary artery (15 mmHg), and wedge pressures (10 mmHg), with a Qp/Qs ratio of 1.04. A bubble contrast study identified a significant right-to-left shunt, confirmed by transesophageal echocardiography showing a large PFO with bidirectional flow. The patient underwent successful percutaneous closure with a 37 mm Gore ASD device. Post-procedure echocardiogram showed no residual shunt, and oxygen requirement improved from 6 L/min to room air-1 L/min at discharge. Discussion Right-to-left shunting through a PFO is an uncommon but reversible cause of chronic hypoxemia. PFOs are present in about 25-30% of adults and are typically asymptomatic. Hypoxemia occurs when anatomic variations redirect venous blood toward the defect, allowing deoxygenated blood to bypass pulmonary circulation. Because the mechanism is intracardiac shunting rather than ventilation-perfusion mismatch, conventional therapies often fail to correct hypoxemia. Clinical clues such as platypnea-orthodeoxia and lack of response to hyperoxia should raise suspicion for an interatrial shunt. Diagnosis is best made by transthoracic echocardiography with agitated saline contrast, with transesophageal echocardiography confirming the finding. Percutaneous closure can markedly improve oxygenation, exercise tolerance, and quality of life. Therefore, PFO-mediated shunting should be considered in chronic hypoxic respiratory failure unresponsive to standard therapy. This abstract is funded by: NONE