Low postoperative hematocrit increases cerebrovascular damage after hypothermic circulatory arrest

The objective of this study was to evaluate the systemic and cerebral effects of different postoperative hematocrit management following cardiopulmonary bypass and deep hypothermic circulatory arrest.

Animal case study.

Laboratory.

Four-week-old Yorkshire piglets.

Twelve piglets were subjected to cardiopulmonary bypass (hematocrit = 25%) and 100 mins of deep hypothermic circulatory arrest (15 degrees C). After weaning cardiopulmonary bypass, they were randomized to either group L or H, in which the postoperative hematocrit was maintained approximately 20% vs. approximately 30%, respectively, and survived for 6 hrs.

Changes in body weight, bioimpedance, and colloid oncotic pressure were assessed. Near-infrared spectroscopy and immunohistochemical assays for cerebral transforming growth factor-beta(1) and caspase-3 were performed. Postoperative weight gain (kg) and decreases in bioimpedance (ohms) were significantly less in group H (1.5 +/- 0.2 [H] vs. 2.4 +/- 0.6 [L], p = .01; 39.3 +/- 15.5 [H] vs. 89.1 +/- 29.6 [L], p = .01). Mean colloid oncotic pressure (mm Hg) was significantly higher in group H (10.8 +/- 1.6 [H] vs. 8.2 +/- 0.8 [L], p = .01) at 6 hrs postoperatively. Oxyhemoglobin, oxidized cytochrome aa(3) (muM x differential path-length factor), and tissue oxygenation index (%) were significantly better in group H (65.7 +/- 31.8 [H] vs. -104.7 +/- 55.2 [L], p = .0001; 0.52 +/- 4.1 [H] vs. -12.8 +/- 6.1 [L], p = .0001, and 55.7 +/- 4.6% [H] vs. 45.3 +/- 6.4% [L], p = .004, respectively). Cerebral transforming growth factor-beta(1) and caspase-3 scores were significantly better in group H (3.0 +/- 0.6 [H] vs. 1.9 +/- 0.9 [L], p = .04 and 1.8 +/- 0.5 [H] vs. 3.2 +/- 0.8 [L], p = .02, respectively). Mean arterial pressure (mm Hg) was consistently higher with group H (94.7 +/- 13.0 [H] vs. 78.3 +/- 11.5 [L], p = .003) despite comparable central venous pressure ( approximately 11 mm Hg).

Lower postoperative hematocrit was associated with increased fluid retention, lower perfusion pressure, and worse cerebrovascular injury following deep hypothermic circulatory arrest. Postoperative hematocrit management may have profound systemic and cerebral effects after deep hypothermic circulatory arrest and merits further investigation.