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Background: 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., Methods and Results: 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., Conclusions: 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.

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.

We have examined in sheep the efficiency of the Hemopump during ventricular fibrillation. Circulatory arrest was induced by electrical stimulation and maintained for 30 min. Haemodynamic measurements were recorded continuously and blood samples were taken before, during and after fibrillation to determine total body and myocardial metabolic activity. All hearts were defibrillated successfully after 30 min of fibrillation. During fibrillation, the Hemopump sustained a mean arterial pressure of about 60 mm Hg with a blood flow rate of about 2.3 litre min-1. These perfusion conditions were sufficient for maintenance of aerobic myocardial metabolism, but with a borderline circulatory supply to the total organism.