A43-28 Reversible Hypoxemia in Idiopathic Pulmonary Fibrosis

Abstract An 83-year-old woman with IPF on home oxygen (2 L/min at rest, 3 L/min with exertion) and a history of kidney transplantation presented with progressive dyspnea and increasing oxygen needs up to 6 L/min over several weeks, despite stable imaging and pulmonary function tests. Echocardiography revealed preserved left ventricular function with hyperdynamic circulation and elevated cardiac output. Right heart catheterization showed high mixed venous oxygen saturation without pulmonary hypertension. Doppler ultrasound identified a patent left upper-extremity AV fistula with flow exceeding 2.5 L/min. The AVF was surgically ligated. Within days, she experienced marked improvement in exertional tolerance and returned to her baseline oxygen requirement of 2 L/min at rest with stable saturations on exertion. Follow-up evaluation showed normalization of heart rate and improved oxygenation, consistent with resolution of high-output physiology. This case illustrates a reversible form of hypoxemia in fibrotic lung disease mediated by systemic shunting. High-output AVF can cause hypoxemia by three mechanisms: transient pulmonary edema, worse VQ mismatch, and incomplete oxygen diffusion across the A-a membrane. The AVF diverted cardiac output through low-resistance systemic channels, increasing venous return and cardiac workload. In the setting of IPF-related vascular remodeling, this high-flow state likely worsened ventilation-perfusion mismatch and diffusion limitation. Ligation restored balanced circulatory distribution and improved effective pulmonary perfusion. High flow through a surgically constructed peripheral arteriovenous fistula can cause high-output heart failure, this diagnosis must be considered in appropriate patients who present with symptoms and signs of pulmonary or systemic venous congestion, and the treatment is directed at reducing flow through the fistula. This abstract is funded by: No external funding