Scholz K H, Schröder T, Hering J P, Ferrari M, Figulla H R, Chemnitius J M, Kreuzer H, Hellige G
Department of Cardiology, Georg-August University of Göttingen, FRG.
Cardiology. 1994;84(3):222-30. doi: 10.1159/000176402.
During ventricular fibrillation, myocardial hemodynamic and metabolic effects of percutaneous cardiopulmonary support (PCPS) were analyzed in 11 adult sheep (body weight 77-112 kg). During supported fibrillation, an abrupt increase in left-ventricular pressures with alignment to aortic pressures was observed in 2 animals, which was probably due to spontaneous aortic regurgitation, and resulted in deterioration of coronary perfusion. In 9 animals, left-ventricular pressures rose from 22.9 +/- 4.9 to 31.2 +/- 7.9 mm Hg elevating left ventricular wall stress from 16,750 +/- 8,745 to 28,835 +/- 8,892 dyn/cm2 after 10 min of PCPS-supported fibrillation (mean flow rate 4.5 +/- 0.7 liters/min). Simultaneously, myocardial perfusion pressures decreased from an average of 32.4 +/- 11.7 to 22.3 +/- 9.4 mm Hg and myocardial lactate release was observed. Additional transapical LV venting using a 9-Fr catheter led to a decrease in both LV pressure (to 25.7 +/- 5.3 mm Hg) and wall stress (to 20,612 +/- 7,499 dyn/cm2). Left-ventricular decompression decreased myocardial oxygen consumption (from 5.3 +/- 1.4 to 4.8 +/- 0.9 ml/min.100 g), and reduced myocardial lactate release, which indicates myocardial protection. Protective effects were most pronounced using 12-Fr-, and 21-Fr-venting cannulas (with 21 Fr: decrease in myocardial oxygen consumption to 2.7 +/- 0.6 ml/min.100 g, and reversal of myocardial lactate release to lactate uptake during fibrillation). Conclusions. Hemodynamic and metabolic data clearly demonstrate the deleterious effects of PCPS to the unvented left ventricle during cardiac arrest. The results emphasize the need for active left-ventricular decompression during PCPS in ventricular fibrillation.
在11只成年绵羊（体重77 - 112千克）身上分析了心室颤动期间经皮心肺支持（PCPS）对心肌血液动力学和代谢的影响。在支持性颤动期间，2只动物出现左心室压力突然升高并与主动脉压力对齐的情况，这可能是由于自发性主动脉反流，导致冠状动脉灌注恶化。在9只动物中，在PCPS支持的颤动10分钟后（平均流速4.5±0.7升/分钟），左心室压力从22.9±4.9毫米汞柱升至31.2±7.9毫米汞柱，左心室壁应力从16,750±8,745达因/平方厘米升至28,835±8,892达因/平方厘米。同时，心肌灌注压力从平均32.4±11.7毫米汞柱降至22.3±9.4毫米汞柱，并观察到心肌乳酸释放。使用9Fr导管进行额外的经心尖左心室排气导致左心室压力（降至25.7±5.3毫米汞柱）和壁应力（降至20,612±7,499达因/平方厘米）均降低。左心室减压降低了心肌耗氧量（从5.3±1.4降至4.8±0.9毫升/分钟·100克），并减少了心肌乳酸释放，这表明具有心肌保护作用。使用12Fr和21Fr排气套管时保护作用最为明显（对于21Fr套管：心肌耗氧量降至2.7±0.6毫升/分钟·100克，并且在颤动期间心肌乳酸释放逆转为乳酸摄取）。结论。血液动力学和代谢数据清楚地证明了心脏骤停期间PCPS对未排气的左心室的有害影响。结果强调了心室颤动时PCPS期间积极进行左心室减压的必要性。
