NEED FOR ACTIVE LEFT-VENTRICULAR DECOMPRESSION DURING PERCUTANEOUS CARDIOPULMONARY SUPPORT IN CARDIAC-ARREST

During ventricular fibrillation, myocardial hemodynamic and metabolic effects of percutaneous cardiopulmonary support (PCPS) were analyzed i n 11 adult sheep (body weight 77-112 kg). During supported fibrillatio n, 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 cor onary 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 PCP S-supported fibrillation (mean flow rate 4.5 +/- 0.7 liters/min). Simu ltaneously, myocardial perfusion pressures decreased from an average o f 32.4 +/- 11.7 to 22.3 +/- 9.4 mm Hg and myocardial lactate release w as observed. Additional transapical LV venting using a 9-Fr catheter l ed 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 d ecreased myocardial oxygen consumption (from 5.3 +/- 1.4 to 4.8 +/- 0. 9 ml/min.100 g), and reduced myocardial lactate release, which indicat es myocardial protection. Protective effects were most pronounced usin g 12-Fr-, and 21-Fr-venting cannulas (with 21 Fr: decrease in myocardi al oxygen consumption to 2.7 +/- 0.6 ml/min.100 g, and reversal of myo cardial lactate release to lactate uptake during fibrillation). Conclu sions. Hemodynamic and metabolic data clearly demonstrate the deleteri ous effects of PCPS to the unvented left ventricle during cardiac arre st. The results emphasize the need for active left-ventricular decompr ession during PCPS in ventricular fibrillation.