Case Presentation: An 89-year-old woman with hypertension, dementia, and vertebral fracture was admitted to another hospital because of hip pain after fall. Since she was also found to have oxygen desaturation, the patient was referred to our hospital for further workup. She denied dyspnea, cough, sputum, chest pain, palpitation, episode of aspiration, or fever. On physical examination, oxygen saturation was 70% on room air, while the remainder of the vital signs was normal. She had clear lungs and no murmurs or cardiac gallop sounds. A contrast-enhanced CT of the chest showed no evidence of pulmonary embolism or anatomical intrapulmonary shunt. A compression ultrasonography of the lower extremity revealed a deep venous thrombosis of the right calf. Under a tentative diagnosis of distal type pulmonary embolism, she received anticoagulant therapy. However, hypoxia did not resolve and we noticed intermittent oxygen desaturation. Close observation with pulse oximetry revealed that oxygen saturation decreased in sitting positions (i.e. brushing teeth, eating foods) but it increased in recumbent positions. Transesophageal echocardiogram with agitated saline showed right-to-left shunt (R-L shunt) through patent foramen ovale (PFO) and the compressed right atrium by the aorta. There was no evidence suggestive of pulmonary hypertension. By reviewing the chest CT, we found that the elongated aorta compressed and distorted the right atrium. The etiology of hypoxia was considered to derived from R-L shunt through PFO, which was probably exaggerated by the aortic compression against the right atrium. She and her family decided not to undergo any further treatments by considering age, comorbidity and their preference. Eventually, she was referred to palliative care.

Discussion: In this patient, aortic elongation, as a consequence of atherosclerosis related to aging, contributed to R-L shunt through PFO. The patient showed “platypnea-orthodeoxia syndrome,” characterized by dyspnea and hypoxia in upright posture and its relief in recumbent position. One of the major etiologies of this syndrome is intracardiac shunt such as PFO, atrial septal defect, or atrial septal aneurysm. Elevation in right-sided intracardiac pressure, typically caused by pulmonary hypertension, is usually required to cause R-L shunt, but previous studies reported cases with normal right-sided pressure. A possible mechanism for the shunt in our case is that a deformation of the atrial septum resulting from anatomically acquired changes might have altered the direction of blood flow and exaggerated R-L shunting. As these changes about the aorta typically occur in elderly patients, most of the patients reported as such were indeed elderly.

Conclusions: R-L shunt is an important etiology of refractory hypoxia. Close observation can reveal the specific physical finding for R-L shunting, platypnea-orthodeoxia. Generally, congenital heart defects may cause R-L shunt in an earlier stage of life, but we should keep in mind that acquired anatomical abnormalities by aging also can cause it in the elderly.