Haraldsen Pernille, Lindstedt Sandra, Metzsch Carsten, Algotsson Lars, Ingemansson Richard
Department of Cardiothoracic Surgery, Anaesthesia and Intensive Care, Skåne University Hospital, Lund University, Lund, Sweden.
Interact Cardiovasc Thorac Surg. 2014 Jan;18(1):43-8. doi: 10.1093/icvts/ivt418. Epub 2013 Oct 2.
To establish an experimental model for acute ischaemic isolated right ventricular dysfunction and the subsequent haemodynamic changes.
An open-chest porcine model with ischaemic dysfunction of the right ventricle induced by ligation of the three main branches supporting the right ventricular free wall. Invasive monitoring of mean arterial blood pressure (MAP), central venous pressure (CVP), left atrial pressure (LAP) and right ventricular pressure (RVP); ultrasonic measurement of cardiac output (CO) and calculation of haemodynamic parameters such as stroke volume (SV), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and right ventricular stroke work (RVSW) using standard formulae.
The ischaemic challenge to the right ventricle resulted in a significant (≥30%) reduction in RVSW associated with an increase (6-25%) in CVP and reduction (8-18%) in pulmonary artery pressure (PAP) despite unchanged PVR, all reflecting the failing right ventricle. There was also a significant drop in CO (14-22%) despite unchanged LAP indicating lessened transpulmonary delivery of left ventricular preload due to the failing right ventricle causing the haemodynamic compromise rather than left ventricular failure. Supraventricular and ventricular arrhythmias occurred in three and two out of seven pigs, respectively-all of which except one were successfully resuscitated with cardioversion and/or defibrillation.
This novel open-chest porcine model of induced ischaemia of the right ventricular free wall resulted in significant haemodynamic compromise confirmed using standard haemodynamic measurements making it useful for further research on acute, ischaemic isolated right ventricular failure.
建立急性缺血性孤立右心室功能障碍及后续血流动力学变化的实验模型。
采用开胸猪模型,通过结扎支持右心室游离壁的三个主要分支诱导右心室缺血性功能障碍。有创监测平均动脉压(MAP)、中心静脉压(CVP)、左心房压(LAP)和右心室压(RVP);超声测量心输出量(CO),并使用标准公式计算诸如每搏输出量(SV)、体循环血管阻力(SVR)、肺血管阻力(PVR)和右心室每搏功(RVSW)等血流动力学参数。
尽管PVR不变,但右心室的缺血性刺激导致RVSW显著降低(≥30%),同时CVP升高(6 - 25%),肺动脉压(PAP)降低(8 - 18%),所有这些都反映了右心室功能衰竭。尽管LAP不变,但CO也显著下降(14 - 22%),这表明由于右心室功能衰竭导致左心室前负荷经肺输送减少,从而引起血流动力学损害,而非左心室衰竭。7头猪中有3头和2头分别发生室上性和室性心律失常,除1头外,其余均通过心脏复律和/或除颤成功复苏。
这种新型的开胸猪右心室游离壁缺血模型导致了显著的血流动力学损害,通过标准血流动力学测量得到证实,使其可用于急性缺血性孤立右心室衰竭的进一步研究。