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J Thorac Cardiovasc Surg 2001;121:816-817
© 2001 The American Association for Thoracic Surgery
Letters to the Editor |
aResearch Department Kokura Memorial Hospital 1-1 Kifune-cho Kokura-kitaku Kitakyushu-shi 802-8555, Japan
bAssistant Professor II Department of Physiology University of Ryukyus School of Medicine Okinawa Japan
To the Editor:
Li and associates
1 attributed the increase in oxygen consumption (VO2) after surgery with hypothermic cardiopulmonary bypass in children to the increase in central temperature. We believe metabolic recovery leading to normalization of oxygen extraction was manifested as increases in both VO2 and central temperature. Although not specified in the article, we assume alpha-stat hypothermic perfusion was used.
Development of central nervous system (CNS) hypoxia during induction of alpha-stat cooling before arrest was recognized by the redox state of cytochrome despite increased hemoglobin oxygenation, but was disregarded. 2 Both phenomena can be explained by the increased hemoglobinoxygen affinity and consequent tissue hypoxia (or Bohr effect) caused by hypothermia, which is exacerbated by alkalotic alpha-stat strategies. The circulatory arrest worsens the hypoxia.
The increase in VO2 most likely represents repayment of the oxygen debt incurred by organs with high metabolic rates and large blood flows (CNS, heart, kidneys, intraperitoneal organs) during hypoxia, rather than the increase in central temperature caused by rewarming of the muscular and subcutaneous fatty mass. In the latter case, the temperature gradient should have favored the peripheral site, but it did not. The peak central temperature increase correlated with peak VO2 increase, which supports the view that metabolic recovery is the heat-generating cause. Resting or paralyzed muscles and subcutaneous fat are tissues with low metabolism and VO2 compared with major organs, and they are unlikely to generate enough heat to increase central temperature.
The mild lactatemia in the absence of hemodynamic compromise with uneventful clinical courses indicates that the hypoxic anaerobic metabolism was not severe enough to preclude recovery.
Pesonen and associates 3 reported increased concentrations of xanthine and hypoxanthine with relatively high oxygen saturations in the cerebral venous blood during the first 2 to 4 hours after alpha-stat hypothermic arrest in children. Their observation suggests anaerobic metabolism (persisting breakdown of adenosine triphosphate or failure to resynthesize adenosine triphosphate), although interpreted otherwise, because of decreased oxygen delivery or CNS inability to extract oxygen. This theory agrees with the impaired glucose use after alpha-stat hypothermic (20°C) perfusion for 60 minutes reported by Miyano and colleagues, 4 which is likely to represent the metabolic derangement caused by the Bohr effect hypoxia, for circulatory arrest was not induced in their study.
The alkalosis of alpha-stat strategies will increase Na+ and Ca++ influx during reperfusion after a period of ischemia, 5-7 interfering with the metabolic recovery of the highly oxygen-consuming mechanisms involved in maintaining normal transmembrane Na+/Ca++ gradients. Thus, the metabolic recovery cannot be completed during pump rewarming, but requires several hours postoperatively. When aerobic metabolism is restored, glucose use is normalized, lactate, xanthine, and hypoxanthine are no longer produced, oxygen is extracted, and VO2 increases.
Although the authors' study is not neurologic, clinically pH-stat management of hypothermic cardiopulmonary bypass in infants has resulted in better neurologic outcomes than alpha-stat strategies. 8
The relative roles played by alpha-stat management during the induction of hypothermia, circulatory arrest, and reperfusion are unknown, but the alkalosis certainly must have been detrimental at each level. Prevention of the Bohr effect with pH-stat strategies preserves the metabolic machinery, resulting in decreased generation of free radicals or better ability to cope with free radicals and to use glucose adequately. The result might be normal postoperative VO2 and normal lactatemia.
12/8/112524doi:10.1067/mtc.2001.112524
References
This article has been cited by other articles:
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  M. J. Scallan Cerebral injury during paediatric heart surgery: perfusion issues Perfusion, July 1, 2004; 19(4): 221 - 228. [Abstract] [PDF]
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