title: Impact of afterload reduction strategies on regional tissue oxygenation after the Norwood procedure for hypoplastic left heart syndrome.
abstract: OBJECTIVE
  Low cerebral tissue oxygenation saturations have been observed by near-infrared spectroscopy (NIRS) after the Norwood procedure. Altered cerebral vascular resistance and pharmacological afterload reduction redirecting blood flow away from the cerebral circulation are possible mechanisms.
  
  
  METHODS
  Two different afterload reduction strategies were evaluated in patients with hypoplastic left heart syndrome or variants after the Norwood procedure. In patients of Group 1 (n=34), afterload reduction was controlled with sodium nitroprusside or with the α-blocker phentolamine. In addition, a phosphodiesterase-III inhibitor was administered. Patients of Group 2 (n=34) received a phosphodiesterase-III inhibitor only. Cerebral and somatic tissue oxygenation saturations and routine intensive care monitoring data were recorded for 24 h before and 48 h after the Norwood procedure. Mean values of the last 4 preoperative (baseline) and of the first and last 4 postoperative hours (early and late course) were calculated.
  
  
  RESULTS
  Baseline, early and late cerebral saturations were 58±7, 52±9 and 60±6% for Group 1 and 58±7, 52±12 and 61±7% for Group 2 and somatic saturations were 59±8, 76±10 and 67±9% and 58±9, 78±8 and 69±10%, respectively. Regional saturations were not different between groups. The postoperative cerebral tissue oxygen saturation was below 40% for 50 (0-1040) min in Group 1 and for 45 (0-720) min in Group 2 (P=1.00). Preoperative cerebral NIRS values (OR 0.85 [0.76-0.96], P=0.007), age at operation (OR 1.39 [1.02-1.88], P=0.034) and early postoperative diastolic blood pressure (OR 0.88 [0.78-0.99], P=0.038) were associated with cerebral tissue oxygen saturations below 40% for more than 60 min. Patients with a prolonged period of low cerebral tissue oxygen saturation had longer duration of mechanical ventilation (69 (37-192) vs 60 (33-238) h, P=0.039) and afterload reduction therapy was terminated later (95 (47-696) vs 74 (39-650) h, P=0.006). Early mortality was 9.4% (3 of 32) compared with 2.8% (1 of 36) in the remainder (P=0.336).
  
  
  CONCLUSIONS
  The postoperative decline of cerebral tissue oxygen saturation was observed with both afterload reduction strategies. The difference between cerebral and somatic NIRS values may indicate a mismatch between cerebral and splanchnic oxygenation. Other strategies to improve cerebral tissue oxygenation are warranted.
authors: Department of Congenital Heart Disease and Pediatric Cardiology, University Hospital Schleswig-Holstein, Kiel, Germany.
authors: Jan Hinnerk
authors: JH
authors: Hansen
authors: Jana
authors: J
authors: Schlangen
authors: Inga
authors: I
authors: Voges
authors: Olaf
authors: O
authors: Jung
authors: Anke
authors: A
authors: Wegmann
authors: Jens
authors: J
authors: Scheewe
authors: Hans-Heiner
authors: HH
authors: Kramer
mesh_terms: D002560:Cerebrovascular Circulation / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D018636:Hypoplastic Left Heart Syndrome / Q000097:blood / Q000503:physiopathology / Q000601:surgery*; D007223:Infant; D007231:Infant, Newborn; D058327:Norwood Procedures / Q000379:methods*; D010100:Oxygen / Q000097:blood*; D011184:Postoperative Period; D019265:Spectroscopy, Near-Infrared; D016896:Treatment Outcome
chemical_list: D010100:Oxygen
keywords: Cerebral oxygenation; Congenital heart disease; Hypoplastic left heart syndrome; Near-infrared spectroscopy; Neuroprotection