Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado, Aurora, CO, USA.
Division of Pulmonary, Critical Care and Sleep Medicine, National Jewish Health, Denver, CO, USA.
J Physiol. 2024 Nov;602(21):5523-5537. doi: 10.1113/JP284943. Epub 2024 Feb 26.
Acute hypoxia increases pulmonary arterial (PA) pressures, though its effect on right ventricular (RV) function is controversial. The objective of this study was to characterize exertional RV performance during acute hypoxia. Ten healthy participants (34 ± 10 years, 7 males) completed three visits: visits 1 and 2 included non-invasive normoxic (fraction of inspired oxygen ( ) = 0.21) and isobaric hypoxic ( = 0.12) cardiopulmonary exercise testing (CPET) to determine normoxic/hypoxic maximal oxygen uptake ( ). Visit 3 involved invasive haemodynamic assessments where participants were randomized 1:1 to either Swan-Ganz or conductance catheterization to quantify RV performance via pressure-volume analysis. Arterial oxygen saturation was determined by blood gas analysis from radial arterial catheterization. During visit 3, participants completed invasive submaximal CPET testing at 50% normoxic and again at 50% hypoxic ( = 0.12). Median (interquartile range) values for non-invasive values during normoxic and hypoxic testing were 2.98 (2.43, 3.66) l/min and 1.84 (1.62, 2.25) l/min, respectively (P < 0.0001). Mean PA pressure increased significantly when transitioning from rest to submaximal exercise during normoxic and hypoxic conditions (P = 0.0014). Metrics of RV contractility including preload recruitable stroke work, dP/dt, and end-systolic pressure increased significantly during the transition from rest to exercise under normoxic and hypoxic conditions. Ventricular-arterial coupling was maintained during normoxic exercise at 50% . During submaximal exercise at 50% of hypoxic , ventricular-arterial coupling declined but remained within normal limits. In conclusion, resting and exertional RV functions are preserved in response to acute exposure to hypoxia at an = 0.12 and the associated increase in PA pressures. KEY POINTS: The healthy right ventricle augments contractility, lusitropy and energetics during periods of increased metabolic demand (e.g. exercise) in acute hypoxic conditions. During submaximal exercise, ventricular-arterial coupling decreases but remains within normal limits, ensuring that cardiac output and systemic perfusion are maintained. These data describe right ventricular physiological responses during submaximal exercise under conditions of acute hypoxia, such as occurs during exposure to high altitude and/or acute hypoxic respiratory failure.
急性缺氧会增加肺动脉（PA）压力，但其对右心室（RV）功能的影响存在争议。本研究的目的是描述急性缺氧时的运动性 RV 功能。10 名健康参与者（34±10 岁，7 名男性）完成了 3 次访问：第 1 次和第 2 次访问包括非侵入性常氧（吸入氧分数（ ）=0.21）和等压缺氧（ ）=0.12）心肺运动测试（CPET），以确定常氧/缺氧最大摄氧量（ ）。第 3 次访问涉及侵入性血流动力学评估，其中参与者随机 1:1 接受 Swan-Ganz 或传导导管插入术，通过压力-容积分析量化 RV 功能。动脉血氧饱和度通过桡动脉导管化的血气分析确定。在第 3 次访问期间，参与者以 50%常氧（ ）和 50%低氧（ ）再次进行侵入性亚最大 CPET 测试（ ）=0.12）。常氧和低氧测试期间非侵入性 值的中位数（四分位距）分别为 2.98（2.43，3.66）l/min 和 1.84（1.62，2.25）l/min（P<0.0001）。当从休息过渡到常氧和低氧条件下的亚最大运动时，平均 PA 压力显着增加（P=0.0014）。在常氧和低氧条件下，从休息过渡到运动时 RV 收缩性的指标（包括前负荷可募集的冲程工作、dP/dt 和收缩末期压力）显着增加。在常氧运动时，心室-动脉偶联在 50% 时得以维持。在 50%低氧 时的亚最大运动期间，心室-动脉偶联下降，但仍在正常范围内。总之，在吸入氧分数为 0.12 的急性缺氧暴露和相关的 PA 压力增加时，静息和运动性 RV 功能得到维持。关键点：在急性低氧条件下，健康的右心室在代谢需求增加（例如运动）期间增强收缩性、松弛性和能量学。在亚最大运动期间，心室-动脉偶联降低，但仍在正常范围内，确保心输出量和全身灌注得以维持。这些数据描述了急性低氧条件下亚最大运动时右心室的生理反应，例如在暴露于高海拔和/或急性低氧性呼吸衰竭时发生的情况。
