title: Acute hemodynamic effects of adjustable atrial septal defect closure in the lateral tunnel Fontan procedure.
abstract: OBJECTIVE
  This study evaluated the acute hemodynamic changes with atrial septal defect closure in the postoperative period in patients undergoing the Fontan procedure.
  
  
  BACKGROUND
  The adjustable atrial septal defect is a modification of the Fontan procedure designed to improve cardiac output and reduce systemic venous hypertension during the postoperative period. Limited information is available on the effects of inter-atrial shunting on the physiology of direct cavopulmonary connection.
  
  
  METHODS
  In 11 patients (aged 9 months to 14.5 years), the atrial septal defect was closed 8 h to 4.6 days (mean 1.7 days) postoperatively. Indications for closure included mean right atrial pressure < 15 mm Hg or arterial oxygen saturation < 80%, or both.
  
  
  RESULTS
  Data presented are mean values +/- 1 SD. Mean right atrial pressure was 13.4 +/- 3.0 mm Hg on admission to the intensive care unit, 10.0 +/- 2.0 mm Hg (p = 0.02) immediately before closure and 11.4 +/- 2.8 mm Hg (p = 0.02) after closure. There was a significant decrease in cardiac output, as calculated from arteriovenous oxygen saturation difference (26 +/- 9%, p = 0.003), Doppler aortic flow (19 +/- 9%, p = 0.0002) and ventricular volumes by two-dimensional echocardiography (20 +/- 8%, p = 0.0001). Arterial oxygen saturation increased from 82 +/- 5% to 94 +/- 4% (p = 0.0001), and arteriovenous oxygen saturation difference increased from 25 +/- 8% to 33 +/- 9% (p = 0.0001). Systemic oxygen delivery decreased from 727 +/- 354 to 655 +/- 325 ml/min per m2 (p = 0.02). One patient required reopening of the atrial septal defect.
  
  
  CONCLUSIONS
  These data demonstrate that a controlled right to left atrial shunt improves cardiac output and systemic oxygen delivery and facilitates the postoperative management of patients after the Fontan procedure. Atrial septal defect closure increases systemic saturation to normal values and prevents potential systemic embolization but significantly decreases oxygen delivery and might limit exercise tolerance.
authors.affiliation: Division of Pediatric Cardiology, University of California, Los Angeles School of Medicine.
authors.forename: B
authors.initials: B
authors.lastname: Harake
authors.forename: M A
authors.initials: MA
authors.lastname: Kuhn
authors.forename: J M
authors.initials: JM
authors.lastname: Jarmakani
authors.forename: H
authors.initials: H
authors.lastname: Laks
authors.forename: Y
authors.initials: Y
authors.lastname: al-Khatib
authors.forename: A
authors.initials: A
authors.lastname: Elami
authors.forename: R G
authors.initials: RG
authors.lastname: Williams
mesh_terms: D000293:Adolescent; D001158:Arteries; D002302:Cardiac Output / Q000502:physiology; D002675:Child, Preschool; D005260:Female; D006344:Heart Septal Defects, Atrial / Q000503:physiopathology* / Q000601:surgery*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007223:Infant; D008297:Male; D008722:Methods; D015588:Observer Variation; D010100:Oxygen / Q000097:blood; D011184:Postoperative Period
chemical_list: D010100:Oxygen