Ewalts Michiel, Dawkins Tony, Boulet Lindsey M, Thijssen Dick, Stembridge Mike
Cardiff School of Sport and Health Sciences, Cardiff Metropolitan University, Cardiff, UK.
Department of Physiology, Radboudumc, Nijmegen, The Netherlands.
Exp Physiol. 2021 Apr;106(4):925-937. doi: 10.1113/EP088657. Epub 2021 Jan 8.
What is the central question of this study? Right ventricular dyssynchrony is a marker of function that is elevated in healthy individuals exposed to acute hypoxia, but does it remain elevated during sustained exposure to high altitude hypoxia, and can it be normalised by augmenting venous return? What is the main finding and its importance? For the first time it is demonstrated that (i) increasing venous return in acute hypoxia restores the synchrony of right ventricular contraction and (ii) dyssynchrony is evident after acclimatisation to high altitude, and remains sensitive to changes in venous return. Therefore, the interpretation of right ventricular dyssynchrony requires consideration the prevailing haemodynamic state.
Regional heterogeneity in timing of right ventricular (RV) contraction (RV dyssynchrony; RVD) occurs when pulmonary artery systolic pressure (PASP) is increased during acute hypoxia. Interestingly, RVD is not observed during exercise, a stimulus that increases both PASP and venous return. Therefore, we hypothesised that RVD in healthy humans is sensitive to changes in venous return, and examined whether (i) increasing venous return in acute hypoxia lowers RVD and (ii) if RVD is further exaggerated in sustained hypoxia, given increased PASP is accompanied by decreased ventricular filling at high altitude. RVD, PASP and right ventricular end-diastolic area (RVEDA) were assessed using transthoracic two-dimensional and speckle-tracking echocardiography during acute normobaric hypoxia ( = 0.12) and sustained exposure (5-10 days) to hypobaric hypoxia (3800 m). Venous return was augmented with lower body positive pressure at sea level (LBPP; +10 mmHg) and saline infusion at high altitude. PASP was increased in acute hypoxia (20 ± 6 vs. 28 ± 7, P < 0.001) concomitant to an increase in RVD (18 ± 7 vs. 38 ± 10, P < 0.001); however, the addition of LBPP during hypoxia decreased RVD (38 ± 0 vs. 26 ± 10, P < 0.001). Sustained hypoxia increased PASP (20 ± 4 vs. 26 ± 5, P = 0.008) and decreased RVEDA (24 ± 4 vs. 21 ± 2, P = 0.042), with RVD augmented (14 ± 5 vs. 31 ± 12, P = 0.001). Saline infusion increased RVEDA (21 ± 2 vs. 23 ± 3, P = 0.008) and reduced RVD (31 ± 12 vs. 20 ± 9, P = 0.001). In summary, an increase in PASP secondary to acute and sustained exposure to hypoxia augments RVD, which can be at least partly reduced via increased venous return.
本研究的核心问题是什么？右心室不同步是一种功能标志物，在暴露于急性低氧的健康个体中会升高，但在持续暴露于高原低氧期间它是否仍保持升高，并且能否通过增加静脉回流使其恢复正常？主要发现及其重要性是什么？首次证明：（i）在急性低氧时增加静脉回流可恢复右心室收缩的同步性；（ii）在适应高原环境后不同步明显，并且对静脉回流的变化仍敏感。因此，对右心室不同步的解读需要考虑当前的血流动力学状态。
当急性低氧期间肺动脉收缩压（PASP）升高时，右心室（RV）收缩时间出现区域异质性（右心室不同步；RVD）。有趣的是，在运动期间未观察到RVD，运动是一种使PASP和静脉回流均增加的刺激因素。因此，我们假设健康人RVD对静脉回流变化敏感，并研究了：（i）急性低氧时增加静脉回流是否会降低RVD；（ii）鉴于高原时PASP升高伴随心室充盈减少，持续低氧时RVD是否会进一步加剧。在急性常压低氧（海平面， = 0.12）和持续暴露（5 - 10天）于低压低氧（3800米）期间，使用经胸二维和斑点追踪超声心动图评估RVD、PASP和右心室舒张末期面积（RVEDA）。在海平面通过下体正压（LBPP； + 10 mmHg）增加静脉回流，在高原通过输注生理盐水增加静脉回流。急性低氧时PASP升高（20 ± 6 vs. 28 ± 7，P < 0.001），同时RVD增加（18 ± 7 vs. 38 ± 10，P < 0.001）；然而，低氧期间添加LBPP可降低RVD（38 ± 0 vs. 26 ± 10，P < 0.001）。持续低氧使PASP升高（20 ± 4 vs. 26 ± 5，P = 0.008）并使RVEDA降低（24 ± 4 vs. 21 ± 2，P = 0.042），RVD加剧（14 ± 5 vs. 31 ± 12，P = 0.001）。输注生理盐水使RVEDA增加（21 ± 2 vs. 23 ± 3，P = 0.008）并降低RVD（31 ± 12 vs. 20 ± 9，P = 0.001）。总之，急性和持续暴露于低氧继发的PASP升高会加剧RVD，这至少可通过增加静脉回流部分减轻。
