Case Presentation

A 55-year-old woman with a medical history of hereditary hemorrhagic telangiectasia (HHT) complicated by recurrent nosebleeds, severe blood loss anemia, hepatic arterial-venous malformation (AVM), pulmonary hypertension, and severe tricuspid regurgitation presented to the HHT specialty clinic with acute hypoxic respiratory failure (new 3-L O₂ requirement), weight gain, and volume overload. She was directly admitted to the pulmonary hypertension unit of our hospital. She had two recent admissions for similar symptoms thought to be due to worsening pulmonary arterial hypertension. In prior admissions, she had undergone right heart catheterization demonstrating mild pulmonary hypertension (pulmonary arterial pressure, 29 mm Hg, cardiac output by Fick 5.76, and cardiac index 3.22, mildly elevated pulmonary vascular resistance to 5.5 woods units). She would undergo diuresis with symptomatic improvement; however, after discharge she would rapidly develop recurrent heart failure symptoms. She reported compliance with guideline-directed medications, diuretics, and dietary restrictions and was still suffering severe symptoms. Notably she had previously elevated liver enzymes concerning for cirrhosis and had begun a workup to evaluate for causes of cirrhosis; she had a history of mild alcohol use, negative hepatitis viral serology, and no known history of liver disease.

中文翻译：

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高输出心力衰竭一例

案例展示

一名 55 岁女性，有遗传性出血性毛细血管扩张症 (HHT) 病史，并伴有反复流鼻血、严重失血性贫血、肝动静脉畸形 (AVM)、肺动脉高压和严重三尖瓣反流，就诊于 HHT 专科诊所急性缺氧性呼吸衰竭（新 3-LO ₂要求）、体重增加和容量超负荷。直接住进我院肺动脉高压病房。她最近两次因类似症状入院，被认为是由于肺动脉高压恶化所致。在之前入院时，她接受了右心导管检查，显示有轻度肺动脉高压（肺动脉压 29 mmHg，Fick 心输出量 5.76，心指数 3.22，肺血管阻力轻度升高至 5.5 伍兹单位）。她将接受利尿，症状有所改善；然而，出院后，她会迅速出现反复发作的心力衰竭症状。她报告遵守了指南指导的药物、利尿剂和饮食限制，但仍有严重症状。值得注意的是，她之前曾升高与肝硬化有关的肝酶，并开始进行检查以评估肝硬化的原因；她有轻度饮酒史，肝炎病毒血清学阴性，并且没有已知的肝病史。