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Published on: May 13, 2019
Heart-Rate-Dependent Right-to-Left Shunting Through a Patent Foramen Ovale in Severe Right Ventricular Dysfunction: A
Qianfeng Xiao1, Xin Wei1, Ying Xu1
1Department of Cardiology, West China Hospital, Sichuan University, 37 Guoxue Road, Chengdu 610041, China.
Abstract:
Background: Right-to-left shunting through a patent foramen ovale (PFO) is an underrecognized yet potentially reversible cause of refractory hypoxemia, particularly in patients with right ventricular dysfunction. This case report describes heart-rate-dependent right-to-left shunting through a PFO causing refractory hypoxemia in a patient with inflammatory cardiomyopathy and severe right ventricular dysfunction, presumably arising from biventricular output mismatch. Case Presentation: We report the case of a 41-year-old male with inflammatory cardiomyopathy and a recently implanted single-chamber pacemaker (VVI mode, lower rate limit 50 bpm), admitted for decompensated heart failure. After initial clinical improvement with guideline-directed therapy, the patient's intrinsic heart rate declined, and ventricular pacing at 50 bpm became the dominant rhythm. He subsequently developed refractory hypoxemia unresponsive to mechanical ventilation. Systematic hemodynamic assessment was performed using transthoracic echocardiography and thoracic electrical bioimpedance (TEB) monitoring at different pacing rates. Results: Echocardiographic evaluation revealed dynamic interatrial shunting through a PFO with the following characteristics: left-to-right at a pacing rate of 80 bpm and right-to-left at 50 bpm. Hemodynamic and echocardiographic data suggested that bradycardia induced biventricular output mismatch-left ventricular outflow tract velocity-time integral (VTI) increased by approximately 38% (from 17.5 cm to 24.1 cm), whereas right ventricular outflow tract VTI increased by only approximately 4% (13.3 cm vs. 13.8 cm). This mismatch likely resulted in relative elevation of right atrial pressure, thereby driving right-to-left shunting through the PFO. Increasing the pacing rate to 80 bpm reversed the shunt direction, normalized oxygenation, and facilitated successful extubation. Conclusions: This case suggests that in patients with severe right ventricular dysfunction, bradycardia may induce biventricular output mismatch with substantially greater left than right ventricular stroke volume augmentation, and presumably relative elevation of right atrial pressure, potentially leading to dynamic right-to-left shunting through a PFO. For such patients with unexplained hypoxemia, the possibility of dynamic PFO shunting should be considered. Appropriately increasing the pacing rate may help restore biventricular output matching, reverse shunt direction, and improve oxygenation; individualized heart rate management strategies warrant clinical consideration.
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