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Ann Thorac Surg 2000;70:1447-1448
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, 1-1 Kifune-cho, Kokura-kitaku, Kitakyushu-shi Fukuoka 802-8555, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa, Japan
To the Editor
We read with great interest the article by Pesonen and colleagues [1]. The authors are to be congratulated for having demonstrated the lasting effects of the deleterious metabolic derangements caused by alpha-stat hypothermia followed by a period of circulatory arrest and rewarming.
In their discussion, the authors attribute to reduced cerebral oxygen utilization the decrease of cytochrome c oxidase despite high cerebral oxygen saturation of hemoglobin. During hypothermia, the latter is the manifestation of hypothermia—induced increased O2 affinity of hemoglobin, further aggravated by the alkalosis of alpha-stat strategies to the point of causing hypoxia (Bohr effect) at the tissue level which is translated as decrease of cytochrome c oxidase, representing O2 delivery failure rather than reduced O2 utilization [2, 3]. After rewarming, the implications are different.
Regarding the development of late cerebral venous hemoglobin O2 desaturation, the following is our explanation. The impaired glucose utilization following rewarming posthypothermic perfusion (20°C, alpha-stat) for 60 minutes even without circulatory arrest [4] will cause failure of adenosine triphosphate synthesis. The increased hypoxanthine and xanthine during the early postoperative period indicates adenosine triphosphate breakdown still prevailing as a consequence of that impaired glucose utilization; the brain fails to extract O2 in spite of being delivered, resulting in relatively high venous O2 saturation values. When metabolic recovery takes place, the O2 is now extracted maximally to repay the O2 debt and manifested as desaturation. The time required for this desaturation to appear indicates the time required to recover from the metabolic insult. The relatively high O2 saturation values during the early postoperative period is actually the abnormal state rather than the late desaturation.
Although Miyano and colleagues [4] attributed impairment of glucose utilization to rewarming, we believe it was caused by hypoxia (Bohr effect) incurred during the hypothermic state induced by alpha-stat management that was made apparent by the increased metabolic rate of rewarming.
The alkalosis of alpha-stat strategies, as opposed to the mild acidosis of pH-stat strategies, will increase Na+ and Ca++ influx after reperfusion following a period of circulatory arrest and obligatory ischemia [5]. Mechanisms involved in maintaining the normal trans-membrane gradient of Na+ and Ca++, which are highly O2 consuming, only attain efficiency when metabolic recovery takes place, several hours postoperatively, thus desaturation becomes greatest late. Miyano and associates [4] reported decreased blood flow with the inability to utilize glucose, and if flows were to be measured, post-rewarming would be greatest when desaturation is greatest.
pH-stat strategies should prevent the Bohr effect from occurring; the metabolic machinery not being affected might result in adequate glucose utilization and O2 consumption postoperatively with consequent normal venous O2 saturation. Clinically, pH-stat management of hypothermic cardiopulmonary bypass in infants has resulted in better neurologic outcome than alpha-stat strategies [6]. Using eucapnic ventilation (equivalent to pH-stat cardiopulmonary bypass) and surface-induced hypothermia, 60 minutes of spinal cord ischemia in rabbits could be consistently protected at 29.5°C [7].
References
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