Wessels Jeroen N, Celant Lucas R, de Man Frances S, Vonk Noordegraaf Anton
PHEniX Laboratory, Department of Pulmonary Medicine, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Amsterdam Cardiovascular Sciences, Pulmonary Hypertension and Thrombosis, Amsterdam, The Netherlands.
Semin Respir Crit Care Med. 2023 Dec;44(6):738-745. doi: 10.1055/s-0043-1770117. Epub 2023 Jul 24.
The right ventricle plays a pivotal role in patients with pulmonary hypertension (PH). Its adaptation to pressure overload determines a patient's functional status as well as survival. In a healthy situation, the right ventricle is part of a low pressure, high compliance system. It is built to accommodate changes in preload, but not very well suited for dealing with pressure overload. In PH, right ventricular (RV) contractility must increase to maintain cardiac output. In other words, the balance between the degree of RV contractility and afterload determines stroke volume. Hypertrophy is one of the major hallmarks of RV adaptation, but it may cause stiffening of the ventricle in addition to intrinsic changes to the RV myocardium. Ventricular filling becomes more difficult for which the right atrium tries to compensate through increased stroke work. Interaction of RV diastolic stiffness and right atrial (RA) function determines RV filling, but also causes vena cava backflow. Assessment of RV and RA function is critical in the evaluation of patient status. In recent guidelines, this is acknowledged by incorporating additional RV parameters in the risk stratification in PH. Several conventional parameters of RV and RA function have been part of risk stratification for many years. Understanding the pathophysiology of RV failure and the interactions with the pulmonary circulation and right atrium requires consideration of the unique RV anatomy. This review will therefore describe normal RV structure and function and changes that occur during adaptation to increased afterload. Consequences of a failing right ventricle and its implications for RA function will be discussed. Subsequently, we will describe RV and RA assessment in clinical practice.
右心室在肺动脉高压（PH）患者中起着关键作用。其对压力超负荷的适应决定了患者的功能状态以及生存率。在健康状态下，右心室是低压、高顺应性系统的一部分。它的构造是为了适应前负荷的变化，但不太适合应对压力超负荷。在肺动脉高压中，右心室（RV）收缩力必须增加以维持心输出量。换句话说，右心室收缩力程度与后负荷之间的平衡决定了每搏输出量。肥厚是右心室适应的主要特征之一，但除了右心室心肌的内在变化外，它还可能导致心室僵硬。心室充盈变得更加困难，为此右心房试图通过增加搏功来进行代偿。右心室舒张期僵硬与右心房（RA）功能的相互作用决定了右心室充盈，但也会导致腔静脉反流。评估右心室和右心房功能在评估患者状态时至关重要。在最近的指南中，通过在肺动脉高压的风险分层中纳入额外的右心室参数，这一点得到了认可。多年来，右心室和右心房功能的几个传统参数一直是风险分层的一部分。了解右心室衰竭的病理生理学以及与肺循环和右心房的相互作用需要考虑右心室独特的解剖结构。因此，本综述将描述正常右心室的结构和功能以及在适应增加的后负荷过程中发生的变化。将讨论右心室衰竭的后果及其对右心房功能的影响。随后，我们将描述临床实践中的右心室和右心房评估。
