title: Pulmonary and left ventricular decompression by artificial pulmonary valve incompetence during percutaneous cardiopulmonary bypass support in cardiac arrest.
abstract: 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.
  
  
  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.
authors.affiliation: Department of Cardiology, Georg-August University of Göttingen, Germany.
authors.forename: K H
authors.initials: KH
authors.lastname: Scholz
authors.forename: H R
authors.initials: HR
authors.lastname: Figulla
authors.forename: T
authors.initials: T
authors.lastname: Schröder
authors.forename: J P
authors.initials: JP
authors.lastname: Hering
authors.forename: H
authors.initials: H
authors.lastname: Bock
authors.forename: M
authors.initials: M
authors.lastname: Ferrari
authors.forename: H
authors.initials: H
authors.lastname: Kreuzer
authors.forename: G
authors.initials: G
authors.lastname: Hellige
mesh_terms: D000818:Animals; D002315:Cardiopulmonary Bypass / Q000295:instrumentation / Q000379:methods*; D004867:Equipment Design; D006323:Heart Arrest / Q000601:surgery*; D008168:Lung / Q000503:physiopathology*; D011312:Pressure; D011664:Pulmonary Valve / Q000503:physiopathology*; D012756:Sheep; D014693:Ventricular Fibrillation / Q000503:physiopathology; D016277:Ventricular Function, Left