Impact of afterload reduction strategies on regional tissue oxygenation after the Norwood procedure for hypoplastic left heart syndrome.

OBJECTIVES: 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.