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(Circulation. 1995;91:2664-2668.)
© 1995 American Heart Association, Inc.

Articles

Pulmonary and Left Ventricular Decompression by Artificial Pulmonary Valve Incompetence During Percutaneous Cardiopulmonary Bypass Support in Cardiac Arrest

Karl H. Scholz, MD; Hans R. Figulla, MD; Thomas Schröder, MD; Jens P. Hering, MD; Herbert Bock; Marcus Ferrari, MD; Heinrich Kreuzer, MD; Gerhard Hellige, MD

From the Department of Cardiology (K.H.S., H.R.F., H.K.), Department of Anesthesiology (T.S., J.P.H., M.F., G.H.), and Department of Cardiothoracic Surgery (H.B.), Georg-August University of Göttingen, Germany.

Correspondence to Karl Heinrich Scholz, MD, Department of Cardiology, Center for Internal Medicine, Georg-August University of Göttingen, Robert-Koch Str 40, 37075 Göttingen, Federal Republic of Germany.

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 coronary-venous 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.

Key Words: cardiopulmonary bypass • extracorporeal circulation • myocardium • hemodynamics • heart-assist device