Abstract 4353187: Platypnea-Orthodeoxia Syndrome Triggered by Acute Lung Injury and Mechanical Ventilation in a Patient with Known Patent Foramen Ovale: A Case of Pulseless Electrical Activity Arrest from Dynamic Shunting

Introduction: Patent foramen ovale (PFO) is present in ~25% of adults and is typically asymptomatic. Two indications for PFO closure include cryptogenic stroke and platypnea-orthodeoxia syndrome (POS), a rare condition marked by dyspnea and desaturation in the upright position due to posture-dependent right-to-left shunting. POS usually involves anatomic vulnerability, intrathoracic pressure (ITP) changes, and dynamic physiological triggers. We present a complex case illustrating this uncommon but life-threatening scenario. Case Vignette: A 66-year-old man with HIV non-adherent to antiretroviral therapy, emphysema, and a known small PFO presented with fever, hypoxia, leukopenia, and left lower lobe consolidation. Labs showed elevated procalcitonin, and he was treated for bacterial pneumonia based on CT findings. During hospitalization, when transitioning from bed to standing, he suffered sudden pulseless electrical activity (PEA) arrest. He was resuscitated and mechanically ventilated. He remained in the ICU for 10 days, requiring multiple extubations and reintubations for recurrent hypoxia. After each extubation, he showed marked positional desaturation (SpO 2 93% supine → 70% upright) despite radiographic improvement of consolidation. CT chest revealed no PE, but significant right lung hyperinflation, likely from barotrauma and air trapping compounded by underlying emphysema. Bubble contrast echo showed a large right-to-left shunt with immediate LA/LV opacification in one cardiac cycle. TEE confirmed an enlarged PFO with interval growth compared to prior imaging and a 1 cm anterior rim. Right heart catheterization showed no signs of Eisenmenger’s physiology, and patient underwent successful transcatheter closure with resolution of hypoxemia and successful extubation. Discussion: This case illustrates how a silent PFO can become clinically significant with multiple converging triggers. The patient’s non-compliant HIV status increased susceptibility to pulmonary infection. Combined with mechanical ventilation and right lung hyperinflation, there was increased right-sided intrathoracic pressure, worsening the right-to-left shunting and enlarging the PFO. These changes led to POS, likely causing the initial PEA arrest. Clinicians should suspect POS in cases of unexplained positional hypoxia or PEA arrest. Early recognition is key, as closure can be curative as illustrated in our challenging clinical case.