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Ann Thorac Surg 2000;69:973-974
© 2000 The Society of Thoracic Surgeons
a Research Department, Kokura Memorial Hospital, Kitakyushu-City, Japan
b Department of Physiology, University of the Ryukyus School of Medicine, Okinawa, Japan
To the Editor
We read with great interest the timely and long overdue article by Parolari and colleagues, "Cardiopulmonary Bypass and Oxygen Consumption: Oxygen Delivery and Hemodynamics" [1]. The authors are to be congratulated for having clinically demonstrated beyond any doubt that O2 extraction is decreased during even mild to moderate hypothermic (28°C to 30°C) alpha-stat perfusion, which was attributed to redistribution of blood. They speculate that higher O2 delivery could possibly be obtained by manipulating the vascular resistance.
It seems that the very cause was missed. The problem probably lies in the impaired O2 delivery caused by the increased O2 affinity of hemoglobin during hypothermia, aggravated by alkalosis to the point of developing tissular hypoxia (Bohr effect), which may result in redistribution of blood flow through the microvascular beds. The body fails to extract, ie, become hypoxic, because hemoglobin does not release the O2. Alpha-stat strategies during hypothermic perfusion have been preferred for 25 to 30 years against physiologic principles that have proved to be effective for millions of years. Nature has adapted to temperature changes and prevented hypoxia through the evolutionary scale of the animal kingdom using hemoglobin as the pigment to carry O2 by increasing the O2 delivery capabilities and changing the paCO2 readily achieved by respiratory rate changes to maintain eucapnia, ie, pH-stat strategy.
Indeed better cardiovascular function (hemodynamics) could be preserved during surface-induced hypothermia (without pump) down to 20°C in dogs [2] and down to 29°C in rabbits [3] by maintaining eucapnia (monitoring expiratory CO2 concentration and adjusting ventilation to obtain 5%) or minimal hypercapnia (5.5%) below 32°C.
Alpha-stat results in alkalosis. Alkalinity further exacerbates the excessive CNS N-methyl D-aspartate (NMDA) receptor activation, or excitotoxicity induced by hypoxia, and sensitizes neurons to ischemic injury [4]. NMDA activation generates nitric oxide (NO) that may also cause neuronal injury [5].
The neuronal injury caused by Ca++ influx, glutamate neurotoxicity, and oxygen-glucose deprivation is diminished by mild acidosis in cortical cultures [6] as well as in hippocampal neurons [7] by reduction of NMDA receptor activation.
If O2 can not be delivered, extraction will decrease regardless of the vascular resistance manipulation, since in the mild to moderate hypothermia ranges, O2 delivery is still dependent on oxyhemoglobin rather than the physically dissolved O2. We concur with the authors on the need of improving O2 delivery during hypothermic perfusion, but suggest doing it by physiologic means. pH-stat strategies, obtained by maintaining the expiratory CO2 concentration eucapnic (5 to 5.5%, monitored at the gas outflow of the oxygenator, especially below 32°C by changing the O2 flow rate, which should also result in close to normoxia paO2 levels without increasing microbubbles) needs to be reappraised with studies, as careful as the one presented by the authors, to settle the long debated issue as to which strategy is better during hypothermic perfusion.
References
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