Suri Sarabjeet S, Pamboukian Salpy V
Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, AL, USA.
Ann Transl Med. 2021 Mar;9(6):517. doi: 10.21037/atm-20-4600.
Heart failure (HF) is one of the major causes of morbidity and mortality in the world. According to a 2019 American Heart Association report, about 6.2 million American adults had HF between 2013 and 2016, being responsible for almost 1 million admissions. As the population ages, the prevalence of HF is anticipated to increase, with 8 million Americans projected to have HF by 2030, posing a significant public health and financial burden. Acute decompensated HF (ADHF) is a syndrome characterized by volume overload and inadequate cardiac output associated with symptoms including some combination of exertional shortness of breath, orthopnea, paroxysmal nocturnal dyspnea (PND), fatigue, tissue congestion (e.g., peripheral edema) and decreased mentation. The pathology is characterized by hemodynamic abnormalities that result in autonomic imbalance with an increase in sympathetic activity, withdrawal of vagal activity and neurohormonal activation (NA) resulting in increased plasma volume in the setting of decreased sodium excretion, increased water retention and in turn an elevation of filling pressures. These neurohormonal changes are adaptive mechanisms which in the short term are associated with increased contractility of the left ventricular (LV) and improvement in cardiac output. But chronically, the failing heart is unable to overcome the excessive pressure and volume leading to worsening HF. The primary symptomatic management of ADHF includes intravenous (IV) diuresis to help with decongestion and return to euvolemic status. Even though diuretics have not been shown to provide any mortality benefit, they have been clinically proven to be of significant benefit in the acute decompensated phase, as well as in chronic management of HF. Loop diuretics remain the mainstay of therapy for symptomatic management of HF with use of thiazide diuretics for synergistic effect in the setting of diuretic resistance. Poor diuretic efficacy has been linked with higher mortality and increased rehospitalizations.
心力衰竭(HF)是全球发病和死亡的主要原因之一。根据美国心脏协会2019年的一份报告,2013年至2016年间,约620万美国成年人患有心力衰竭,导致近100万人住院。随着人口老龄化,预计心力衰竭的患病率将会增加,预计到2030年将有800万美国人患有心力衰竭,这将带来巨大的公共卫生和经济负担。急性失代偿性心力衰竭(ADHF)是一种综合征,其特征是容量超负荷和心输出量不足,伴有劳力性气短、端坐呼吸、阵发性夜间呼吸困难(PND)、疲劳、组织充血(如外周水肿)和意识障碍等症状的某种组合。其病理特征是血流动力学异常,导致自主神经失衡,交感神经活动增加、迷走神经活动减弱和神经激素激活(NA),从而在钠排泄减少、水潴留增加的情况下导致血浆容量增加,进而使充盈压升高。这些神经激素变化是适应性机制,短期内与左心室(LV)收缩力增加和心输出量改善有关。但长期来看,衰竭的心脏无法克服过高的压力和容量,导致心力衰竭恶化。ADHF的主要症状管理包括静脉注射(IV)利尿剂,以帮助消除充血并恢复血容量正常状态。尽管利尿剂尚未显示出任何降低死亡率的益处,但它们在临床上已被证明在急性失代偿期以及心力衰竭的慢性管理中具有显著益处。袢利尿剂仍然是心力衰竭症状管理的主要治疗药物,噻嗪类利尿剂用于在利尿剂抵抗的情况下发挥协同作用。利尿剂疗效不佳与较高的死亡率和再住院率增加有关。