Department of Clinical Medicine, Aarhus University, Palle Juul Jensens Boulevard 82, Aarhus N, 8200, Denmark.
Department of Anaesthesiology and Intensive Care, Aarhus University Hospital, Palle Juul Jensens Boulevard 99, Aarhus N, DK-8200, Denmark.
BMC Pulm Med. 2024 May 14;24(1):233. doi: 10.1186/s12890-024-03006-9.
Acute pulmonary embolism (PE) induces ventilation-perfusion mismatch and hypoxia and increases pulmonary pressure and right ventricular (RV) afterload, entailing potentially fatal RV failure within a short timeframe. Cardiopulmonary factors may respond differently to increased clot burden. We aimed to elucidate immediate cardiopulmonary responses during successive PE episodes in a porcine model.
This was a randomized, controlled, blinded study of repeated measurements. Twelve pigs were randomly assigned to receive sham procedures or consecutive PEs every 15 min until doubling of mean pulmonary pressure. Cardiopulmonary assessments were conducted at 1, 2, 5, and 13 min after each PE using pressure-volume loops, invasive pressures, and arterial and mixed venous blood gas analyses. ANOVA and mixed-model statistical analyses were applied.
Pulmonary pressures increased after the initial PE administration (p < 0.0001), with a higher pulmonary pressure change compared to pressure change observed after the following PEs. Conversely, RV arterial elastance and pulmonary vascular resistance was not increased after the first PE, but after three PEs an increase was observed (p = 0.0103 and p = 0.0015, respectively). RV dilatation occurred following initial PEs, while RV ejection fraction declined after the third PE (p = 0.004). RV coupling exhibited a decreasing trend from the first PE (p = 0.095), despite increased mechanical work (p = 0.003). Ventilatory variables displayed more incremental changes with successive PEs.
In an experimental model of consecutive PE, RV afterload elevation and dysfunction manifested after the third PE, in contrast to pulmonary pressure that increased after the first PE. Ventilatory variables exhibited a more direct association with clot burden.
急性肺栓塞（PE）可导致通气-灌注不匹配和缺氧，增加肺动脉压和右心室（RV）后负荷，在短时间内导致潜在致命的 RV 衰竭。心肺因素对血栓负荷的增加可能有不同的反应。我们旨在阐明在猪模型中连续 PE 发作期间的即时心肺反应。
这是一项随机、对照、双盲的重复测量研究。12 头猪被随机分为假手术组或连续 PE 组，每组每隔 15 分钟进行一次 PE，直到平均肺动脉压增加一倍。在每次 PE 后 1、2、5 和 13 分钟，使用压力-容积环、有创压力和动脉及混合静脉血气分析进行心肺评估。应用方差分析和混合模型统计分析。
初始 PE 给药后肺动脉压升高（p<0.0001），与后续 PE 后观察到的压力变化相比，变化更大。相反，RV 动脉弹性和肺血管阻力在第一次 PE 后没有增加，但在第三次 PE 后增加（p=0.0103 和 p=0.0015）。RV 扩张发生在初始 PE 后，而 RV 射血分数在第三次 PE 后下降（p=0.004）。尽管机械功增加（p=0.003），但 RV 耦合呈下降趋势，从第一次 PE 开始（p=0.095）。随着连续的 PE，通气变量显示出更渐进的变化。
在连续 PE 的实验模型中，与第一次 PE 后升高的肺动脉压相比，RV 后负荷增加和功能障碍在第三次 PE 后表现出来。通气变量与血栓负荷有更直接的关系。
