Abstract Background High-output heart failure (HOHF) is characterized by elevated cardiac output, reduced systemic vascular resistance, and increased metabolic demand with low oxygen content. Common etiologies include peripheral vasodilation, hypermetabolic states, and shunt physiology such as transjugular intrahepatic portosystemic shunts (TIPS) and arteriovenous fistulas (AVF). Both TIPS and AVF independently increase preload and decrease systemic resistance, potentially precipitating HOHF. When present concurrently, their combined hemodynamic burden can overwhelm compensatory mechanisms, though such cases are scarcely documented. Case Presentation A 59-year-old man with atrial fibrillation, hypertension, end-stage renal disease on hemodialysis through an AVF, and non-cirrhotic portal hypertension underwent TIPS for refractory ascites. The procedure reduced his portosystemic gradient from 17 mmHg to 4 mmHg, with right atrial pressure rising to 24 mmHg. He subsequently developed refractory shock requiring vasopressors and mechanical ventilation. Pulmonary artery catheterization revealed cardiac output of 20 L/min with low systemic vascular resistance, consistent with HOHF. Echocardiography showed hyperdynamic LV Ejection Fraction (EF 70-75%), and AVF Doppler demonstrated high flow (3-3.5 L/min). Despite fluid removal, he remained in shock. AVF ligation reduced output to 15 L/min with partial improvement. Persistent overload prompted TIPS occlusion, which decreased output to 10.6 L/min and lowered right atrial pressure to normal. His course was complicated by gastrointestinal bleeding, arrhythmia, and progressive shock. He ultimately opted for comfort measures and died three months later. Discussion This case illustrates concurrent AVF- and TIPS-induced HOHF, producing profound circulatory overload and shock. While AVF and TIPS are recognized as independent causes of HOHF, their coexistence is seldom described. Recognition relies on invasive hemodynamic monitoring showing high cardiac output with low systemic resistance despite preserved EF. Interventions such as shunt revision or occlusion can reverse physiology, though outcomes may remain poor if diagnosis is delayed. Screening for pre-existing cardiac dysfunction and consideration of cumulative shunt burden are essential prior to AVF or TIPS creation. Conclusion Concurrent AVF and TIPS can precipitate severe HOHF and refractory shock. Early recognition and targeted intervention, including shunt ligation or occlusion, are critical to mitigating hemodynamic collapse. This abstract is funded by: None
Mukhopadhyay et al. (Fri,) studied this question.