title: Mechanisms of right ventricular dysfunction after pulmonary resection.
abstract: BACKGROUND
  Significant right ventricular (RV) dysfunction as measured by increased end-diastolic volume and reduced ejection fraction has been documented in the postoperative period after pulmonary resection. We hypothesized that changes in RV contractile state or afterload may contribute to this RV pump dysfunction.
  
  
  METHODS
  In part one of the study, RV preload was altered on postoperative day 2 (n = 6) by rapid infusion of Hespan to a total of 250, 500, and 1,000 mL. The relationship between RV stroke work and end-diastolic volume was plotted using linear regression. This preload recruitable stroke work relation had been previously validated as a load-insensitive index of RV contractility. The slopes of the preoperative relation (n = 35) and postoperative relation were compared. In part two of the study, RV afterload was reduced by continuous infusion of prostaglandin E1 (n = 6) through postoperative day 2 and RV pump function was assessed.
  
  
  RESULTS
  Comparison of the slopes of the preload recruitable stroke work relation plotted preoperatively and on postoperative day 2 revealed no significant difference, indicating no change in RV contractile state. Infusion of prostaglandin E1 in the postoperative period (n = 6) significantly reduced pulmonary vascular resistance (3.67 +/- 0.19 versus baseline 5.72 +/- 0.19 dyne . s . cm-5/ m2; p < 0.05). However, RV ejection fraction remained significantly reduced (0.34 +/- 0.01 versus baseline 0.42 +/- 0.01; p < 0.05) and end-diastolic volume significantly increased (105 +/- 5 versus baseline 93 +/- 2 mL/m2; p < 0.05). Heart rate was increased compared with baseline throughout the postoperative period.
  
  
  CONCLUSIONS
  The present study suggests that RV dysfunction after pulmonary resection is not caused by primary alterations in contractility or immediate changes in afterload. Better control of heart rate with minimal effect on inotropy may enhance RV pump function.
authors.affiliation: Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425, USA.
authors.forename: C E
authors.initials: CE
authors.lastname: Reed
authors.forename: B H
authors.initials: BH
authors.lastname: Dorman
authors.forename: F G
authors.initials: FG
authors.lastname: Spinale
mesh_terms: D000527:Alprostadil / Q000627:therapeutic use; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use; D008175:Lung Neoplasms / Q000601:surgery; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D011013:Pneumonectomy; D011183:Postoperative Complications / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology; D013815:Thermodilution; D018497:Ventricular Dysfunction, Right / Q000209:etiology* / Q000503:physiopathology
chemical_list: D006895:Hydroxyethyl Starch Derivatives; D000527:Alprostadil