Scholz K H, Figulla H R, Schröder T, Hering J P, Bock H, Ferrari M, Kreuzer H, Hellige G
Department of Cardiology, Georg-August University of Göttingen, Germany.
Circulation. 1995 May 15;91(10):2664-8. doi: 10.1161/01.cir.91.10.2664.
In cardiac arrest, use of percutaneous cardiopulmonary bypass support (PCPS) may lead to left ventricular loading, with deleterious effects on the myocardium, and is often accompanied by an increase in pulmonary artery pressure. The present study was designed to assess the potential of artificially induced pulmonary valve incompetency to retrogradely decompress the left ventricle during PCPS in ventricular fibrillation.
Studies were performed using a standardized experimental animal model in sheep (n = 12; body weight, 77 to 112 kg). When PCPS was used during fibrillation, an increase in left ventricular pressure (from 21.4 +/- 5.0 mm Hg after 1 minute to 28.4 +/- 9.5 mm Hg after 10 minutes of fibrillation) was observed in all animals, with a simultaneous increase in pulmonary artery pressure in 6 animals, from 15.5 +/- 3.8 to 24.3 +/- 5.4 mm Hg (group A). In these animals, artificial pulmonary valve incompetency, which was induced by a special "pulmonary valve spreading catheter," led to effective decompression of both the pulmonary circulation (decrease in pulmonary artery pressure from 24.3 to 11.3 mm Hg) and the left ventricle (decrease in left ventricular pressure from 30.5 to 17.7 mm Hg). We simultaneously measured a decrease in the myocardial release of lactate (increase in arterial coronaryvenous difference in lactate content from -0.01 to 0.14 mmol/L), demonstrating the myocardial protective effect of the procedure. In contrast, in 6 animals without an increase in pulmonary artery pressure during PCPS (group B), artificial pulmonary valve incompetency did not reduce left ventricular loading, which was probably because of competent mitral valves in these animals.
In case of increasing pulmonary artery pressure during PCPS in cardiac arrest, artificial pulmonary valve incompetency might be a useful tool for effective pulmonary and retrograde left ventricular decompression.
在心脏骤停时，使用经皮心肺旁路支持（PCPS）可能导致左心室负荷增加，对心肌产生有害影响，并且常常伴有肺动脉压力升高。本研究旨在评估在心室颤动时PCPS期间人为诱导肺动脉瓣关闭不全以逆向减压左心室的可能性。
使用标准化的绵羊实验动物模型（n = 12；体重77至112千克）进行研究。当在颤动期间使用PCPS时，在所有动物中均观察到左心室压力升高（从颤动1分钟后的21.4±5.0毫米汞柱升至颤动10分钟后的28.4±9.5毫米汞柱），6只动物的肺动脉压力同时升高，从15.5±3.8毫米汞柱升至24.3±5.4毫米汞柱（A组）。在这些动物中，由特殊的“肺动脉瓣扩张导管”诱导的人为肺动脉瓣关闭不全导致肺循环（肺动脉压力从24.3毫米汞柱降至11.3毫米汞柱）和左心室（左心室压力从30.5毫米汞柱降至17.7毫米汞柱）均有效减压。我们同时测量到心肌乳酸释放减少（动脉-冠状静脉乳酸含量差值从-0.01毫摩尔/升增加至0.14毫摩尔/升），证明了该操作对心肌的保护作用。相比之下，在6只PCPS期间肺动脉压力未升高的动物（B组）中，人为肺动脉瓣关闭不全并未降低左心室负荷，这可能是因为这些动物的二尖瓣功能正常。
在心脏骤停时PCPS期间肺动脉压力升高的情况下，人为肺动脉瓣关闭不全可能是有效进行肺和逆向左心室减压的有用工具。
