Abstract

This study investigated the effects of different cooling strategies on cerebral metabolic response to circulatory arrest. In particular, it examined the impact of blood gas management and degree of cooling on cerebral metabolism before and after deep hypothermic circulatory arrest. Sixty-nine 1-week-old piglets (2 to 3 kg) were placed on cardiopulmonary bypass (37°C) at 100 ml/kg per minute. Animals were cooled to 18°or 14°C as follows: alpha-stat strategy to 18°C ( n = 9) or 14°C ( n = 6), pH-stat strategy to 18°C ( n = 9) or 14°C ( n = 7), or pH-stat strategy for 18 minutes followed by a switch to alpha-stat strategy for the last 5 minutes of cooling to 18°C ( n = 12) or 14°C ( n = 10). Animals underwent 60 minutes of circulatory arrest followed by rewarming with alpha-stat strategy to 36°C. Control animals were cooled with alpha-stat strategy to 18°C ( n = 10) or 14°C ( n = 3) and then maintained on cold cardiopulmonary bypass (100 ml/kg per minute) for 60 minutes. Three animals were excluded (see text). With the use of xenon 133 clearance methods, cerebral blood flow was measured at the following points: point I, cardiopulmonary bypass (37°C); point II, cardiopulmonary bypass before circulatory arrest or control flow (18° or 14°C); and point III, cardiopulmonary bypass after rewarming (36°C). Cerebral metabolic rate of oxygen consumption was calculated for each point. At point II, cerebral metabolism was more suppressed at 14°C compared with that at 18°C. At any given temperature (18° or 14°C), pH-stat strategy provided the greatest suppression of cerebral metabolism. In control animals, cerebral metabolic oxygen consumption at point III returned to baseline values after 60 minutes of cold bypass. Sixty minutes of circulatory arrest resulted in a significant reduction in cerebral metabolic oxygen consumption at point III compared with that at point I regardless of cooling temperature or blood gas strategy. The amount of cerebral metabolic recovery was significantly reduced in the pH-stat 14°C group compared with that in the pH-stat 18°C group at point III. The use of pH-stat strategy followed by a switch to alpha-stat at 14°C provided better cerebral metabolic recovery compared with either strategy used alone. The use of pH-stat strategy during initial cooling may provide the animal with maximal cerebral metabolic suppression. The cerebral acidosis produced with pH-stat cooling may worsen cerebral metabolic injury from circulatory arrest, but this effect is eliminated with the use of alpha-stat just before the period of circulatory arrest. (J T HORAC C ARDIOVASC S URG 1995;110:1649-57)

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