Hypothermic cardiopulmonary bypass during aortocoronary grafting preserves water and energy metabolism but induces metabolic acidosis and intracellular alterations likely due to hypothermia-induced tissue hypoxia.
Metabolic acidosis and intracellular pH shifts may occur after hypothermic CPB; single-case data leave open their clinical relevance.
The main parameters of muscle acid-base, water and energy metabolism were studied in ten patients undergoing low-flux (1.5 l/min/m2), low-pressure (40 to 60 mmHg) hypothermic (26 degrees C) cardiopulmonary bypass (CPB) for aortocoronary grafting; absolute gas exchange and haemodynamic data were also measured throughout the entire CPB period. At the end of CPB a substantial preservation of water and energy metabolic indexes was found; a condition of extracellular metabolic acidosis was apparently sustained by muscle cell anaerobic glycolysis enhancement with a consequent increase of both muscle and plasma lactate content. Subnormal cell phosphocreatine levels as well as reduced bicarbonate buffer stores and decreased intracellular pH, were detected. Direct limiting effects of hypothermia on tissue O2 delivery and muscle oxidative metabolism as well as vasoconstriction and arteriovenous shunting associated with CPB procedures are likely to be involved in the above mentioned alterations of cell metabolism.
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Canale et al. (1988) studied this question.
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