title: Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency.
abstract: OBJECTIVE
  To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency.
  
  
  METHODS
  Six anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers.
  
  
  RESULTS
  RV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05).
  
  
  CONCLUSIONS
  In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency.
authors.affiliation: Hemodynamics Research Laboratory (HemoLiege), University of Liege, Liege, Belgium. b.lambertmont@chu.ulg.ac.be
authors.forename: Bernard
authors.initials: B
authors.lastname: Lambermont
authors.forename: Alexandre
authors.initials: A
authors.lastname: Ghuysen
authors.forename: Philippe
authors.initials: P
authors.lastname: Kolh
authors.forename: Vincent
authors.initials: V
authors.lastname: Tchana-Sato
authors.forename: Patrick
authors.initials: P
authors.lastname: Segers
authors.forename: Paul
authors.initials: P
authors.lastname: Gérard
authors.forename: Philippe
authors.initials: P
authors.lastname: Morimont
authors.forename: David
authors.initials: D
authors.lastname: Magis
authors.forename: Jean-Michel
authors.initials: JM
authors.lastname: Dogné
authors.forename: Bernard
authors.initials: B
authors.lastname: Masereel
authors.forename: Vincent
authors.initials: V
authors.lastname: D'Orio
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006328:Cardiac Catheterization; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D006339:Heart Rate; D008297:Male; D011651:Pulmonary Artery / Q000503:physiopathology; D011897:Random Allocation; D012772:Shock, Septic / Q000503:physiopathology*; D013552:Swine; D013599:Systole; D018497:Ventricular Dysfunction, Right / Q000209:etiology* / Q000503:physiopathology
chemical_list: D004731:Endotoxins