Lyhne Mads Dam, Schultz Jacob Gammelgaard, Kramer Anders, Mortensen Christian Schmidt, Nielsen-Kudsk Jens Erik, Andersen Asger
Department of Cardiology and Department of Clinical Medicine, Aarhus University Hospital, Denmark.
Eur Heart J Acute Cardiovasc Care. 2021 May 11;10(3):243–249. doi: 10.1177/2048872620925253. Epub 2020 May 21.
The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0-12 hours after acute pulmonary embolism in an in-vivo porcine model.
Pigs were randomly allocated to pulmonary embolism ( = 6) or sham ( = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure-volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses.
Mean pulmonary arterial pressure increased ( < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo-arterial coupling was reduced ( < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( < 0.01) suggesting right ventricular failure.
In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo-arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.
急性中度风险肺栓塞后的血流动力学反应尚未得到充分描述。我们旨在描述在体内猪模型中急性肺栓塞后最初关键的0至12小时内的心血管变化。
将猪随机分为肺栓塞组（n = 6）或假手术组（n = 6）。通过注入自体血凝块（20×1 cm）造成肺栓塞，直至平均肺动脉压翻倍或平均肺动脉压大于34 mmHg。假手术组动物接受生理盐水。干预后12小时内，通过双心室压力-容积环记录、有创压力测量、动脉和中心静脉血气分析评估心肺变化。
与假手术组相比，肺栓塞组平均肺动脉压升高（P < 0.0001）并在12小时内持续升高。与假手术组相比，肺栓塞后最初11小时和6小时，肺血管阻力和右心室动脉弹性（右心室后负荷）分别增加（两者均P < 0.01）。与假手术组相比，肺栓塞组右心室射血分数降低8小时（P < 0.01），而右心室每搏输出量在4小时内出现接近显著的降低（P = 0.06）。尽管肺栓塞组右心室机械功增加（P < 0.01），提示右心室衰竭，但急性肺栓塞后6小时右心室室动脉耦联降低（P < 0.05）。
在中度风险肺栓塞的猪模型中，右心室后负荷增加导致最初的右心室室动脉解耦联和功能障碍。大约6小时后，尽管肺动脉压持续升高，但右心室后负荷恢复到肺栓塞前的值，右心室功能改善。这些结果表明急性肺栓塞在血流动力学适应之前存在一个最初的关键且易损阶段。
