Abstract Introduction Pulmonary arteriovenous malformations (AVMs) are rare vascular anomalies that create direct connections between pulmonary arteries and veins, resulting in right-to-left shunting and hypoxemia. While often associated with hereditary hemorrhagic telangiectasia (HHT), sporadic cases also occur. Patients with coexisting cardiac anomalies, such as patent foramen ovale (PFO) or valvular heart disease, may present with overlapping symptoms, complicating the identification of the primary cause of hypoxia. We present a case in which pulmonary AVMs were determined to be the main contributor to hypoxemia in a patient with a PFO, illustrating the diagnostic and management challenges in such complex presentations. Case Presentation A 40-year-old male with a history of Hodgkin’s lymphoma s/p thoracic radiation, Barrett’s esophagitis, intravenous drug use, and mixed aortic valve disease was hospitalized for pneumonia and Streptococcus mutans bacteremia. He was discharged on amoxicillin, as TEE performed during that admission did not show vegetations, though aortic valve endocarditis could not be completely excluded. Two days later, he presented with syncope and persistent hypoxia. Prior TEE had shown a PFO with left-to-right shunt, raising concern for embolic stroke or septic emboli; however, negative blood cultures made septic embolization less likely. Brain MRI demonstrated a small subacute lacunar infarct. Chest CT revealed multiple pulmonary AVMs, also seen on imaging one month prior but absent on earlier studies. Echocardiography had previously suggested moderate-to-severe AS, prompting left and right heart catheterization, which confirmed moderate AS with normal right heart pressures. A shunt study demonstrated oxygen saturations of 72.2% in the right atrium, 70.8% in the pulmonary artery, and 94.9% in the aorta, supporting minimal contribution from the PFO. Pulmonology determined that persistent hypoxia was primarily driven by pulmonary AVMs. The patient was transferred to Johns Hopkins, where interventional radiology embolized three large pulmonary AVMs, resulting in rapid improvement from 5 L nasal cannula to room air. Evaluation for HHT was negative. Discussion This case highlights the diagnostic challenge of hypoxia in patients with multiple potential contributors. While PFOs can facilitate paradoxical embolic events and AS can cause syncope, neither accounted for the patient’s hypoxemia. Pulmonary AVMs were identified as the primary driver, and embolization led to prompt resolution of hypoxia, emphasizing the importance of thorough imaging, hemodynamic assessment, and interdisciplinary collaboration. Clinicians should maintain a high index of suspicion for pulmonary AVMs in patients with unexplained hypoxia, even in the presence of concurrent cardiac anomalies, and prioritize targeted interventions to address these lesions. This abstract is funded by: None
Shah et al. (Fri,) studied this question.