BLOOD-GAS MANAGEMENT AND DEGREE OF COOLING - EFFECTS ON CEREBRAL METABOLISM BEFORE AND AFTER CIRCULATORY ARREST

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 c erebral metabolism before and after deep hypothermic circulatory arres t, Sixty-nine 1-week-old piglets (2 to 3 kg) were placed on cardiopulm onary bypass (37 degrees C) at 100 ml/kg per minute, Animals were cool ed to 18 degrees or 14 degrees C as follows: alpha-stat strategy to 18 degrees C (n = 9) or 14 degrees C (n = 6), pH-stat strategy to 18 deg rees C (n = 9) or 14 degrees C (n = 7), or pH-stat strategy for 18 min utes followed by a switch to alpha-stat strategy for the last 5 minute s of cooling to 18 degrees C (n = 12) or 14 degrees C (n = 10), Animal s underwent 60 minutes of circulatory arrest followed by rewarming wit h alpha-stat strategy to 36 degrees C, Control animals were cooled wit h alpha-stat strategy to 18 degrees C (n = 10) or 14 degrees C (n = 3) and then maintained on cold cardiopulmonary bypass (100 ml/kg per min ute) for 60 minutes, Three animals were excluded (see text), With the use of xenon 133 clearance methods, cerebral blood flow was measured a t the following points: point I, cardiopulmonary bypass (37 degrees C) ; point II, cardiopulmonary bypass before circulatory arrest or contro l flow (18 degrees or 14 degrees C); and point III, cardiopulmonary by pass after rewarming (36 degrees C), Cerebral metabolic rate of oxygen consumption was calculated for each point, At point II, cerebral meta bolism was more suppressed at 14 degrees C compared with that at 18 de grees C. At any given temperature (18 degrees or 14 degrees C), pH-sta t strategy provided the greatest suppression of cerebral metabolism. I n control animals, cerebral metabolic oxygen consumption at point III returned to baseline values after 60 minutes of cold bypass, Sixty min utes of circulatory arrest resulted in a significant reduction in cere bral metabolic oxygen consumption at point III compared with that at p oint I regardless of cooling temperature or blood gas strategy. The am ount of cerebral metabolic recovery was significantly reduced in the p H-stat 14 degrees C group compared with that in the pH-stat 18 degrees C group at point III. The use of pH-stat strategy followed by a switc h to alpha-stat at 14 degrees C provided better cerebral metabolic rec overy compared with either strategy used alone. The use of pa-stat str ategy during initial cooling may provide the animal with maximal cereb ral 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.