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J Thorac Cardiovasc Surg 1997;114:872-873
© 1997 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Anesthesiology
Children's Hospital of Philadelphia
34th St. and Civic Center Blvd.
Philadelphia, PA 19104
Reply to the Editor:
We appreciate the interest of Nollert and colleagues in our article "Cerebral Oxygenation During Cardiopulmonary Bypass in Children."
1 In their letter, several comments were directed toward the conclusions in our paper and the physiology of tissue oxygen transport, to which we are happy to respond.
The purpose of our study was to determine the effect of temperature, pump flow, and hematocrit value on cerebral oxygen saturation (SCO 2) as measured by near-infrared spectroscopy (NIRS) in children. As background, we had observed distinct changes in SCO 2 in children during deep hypothermic cardiopulmonary bypass (CPB) and circulatory arrest.2, 3 These changes included an increase in SCO 2 during CPB cooling, a curvilinear decrease during circulatory arrest, and a return to preoperative levels during CPB reperfusion and rewarming. We wished to determine which factors influenced SCO 2 during CPB cooling because children with neurologic sequelae did not experience the typical increase in SCO 2. 3 In our study, we concluded that brain hypothermia was the main factor increasing SCO 2 during CPB cooling, although a certain CPB pump flow and hematocrit value were required to effect this increase. 1
Nollert and colleagues propose an alternative conclusion that is inconsistent with the data. They correctly point out that arterial carbon dioxide tension (PCO 2) influences cortical oxygen extraction during CPB cooling. 4 They also correctly point out that we had used alpha-stat management during CPB and that temperature-corrected arterial PCO 2 would have decreased during hypothermic CPB. However, they incorrectly conclude that this decrease in PCO 2 would have increased SCO 2 during CPB cooling, because hypocapnia decreases SCO 2, just as hypocapnia decreases cerebral blood flow and increases cortical oxygen extraction. Thus hypothermia is associated with an increased SCO 2, in contradistinction to the reduction that would be predicted on the basis of diminished PCO 2.
Nollert and associates also misstated our conclusions (i.e., hypothermia increased cerebral oxygenation). Although not well defined, cerebral oxygenation includes cellular energetics as well as cerebral saturation. We did not measure cellular energetics. As mentioned in our study, the critical SCO 2 necessary to maintain cellular energetics is approximately 30% at normothermia, although it may be higher during hypothermia or anemia. 1 Our belief, therefore, is that cerebral oxygenation was maintained during full-flow normothermic CPB and full-flow hypothermic CPB because SCO 2 remained well above the critical level.
Nollert and coworkers voice the concern that the increased oxyhemoglobin binding affinity at deep hypothermia may prevent hemoglobin from unloading oxygen to the cell, resulting in cellular hypoxia despite the increased SCO 2. Several observations should partially allay this concern. Oxygen flux is driven mainly by the steep oxygen tension (PO 2) gradient from capillary to mitochondria. When hemoglobin does not unload oxygen sufficiently to support cellular respiration, then tissue PO 2 decreases until it reaches a critical value, at which point further decreases in PO 2 result in decreased cerebral oxygen metabolic rate, brain high-energy phosphates, and eventually cellular energy failure and brain damage. During CPB cooling, there is no convincing evidence of brain hypoxia from the inability of oxyhemoglobin to unload. In fact, several studies have documented stability of brain tissue PO 2 and high-energy phosphates during deep hypothermic CPB. 4-6 Hemoglobin can clearly unload oxygen to support intracellular respiration at deep hypothermia because, during low-flow CPB, cerebral oxygen extraction increases to sustain cerebral metabolic rate and brain high-energy phosphates. 7-9 At deep hypothermia, the low-flow CPB threshold at which cerebral energetics begin to decrease remains uncertain. NIRS may be useful in defining the low-flow threshold in a given patient at a certain temperature and hematocrit value.
Nollert and coauthors allude to the debate about brain oxygenation during hypothermic CPB generated from NIRS measurement of cytochrome aa3 redox state. In particular, cytochrome aa3 oxidation as measured by NIRS is often inconsistent with hemoglobin oxygenation, tissue PO 2, and high-energy phosphates. More than 10 years ago, there was also debate about cerebral oxygenation and the inconsistent behavior of cytochrome aa3 measured by NIRS. In considering this issue, one should keep in mind that at the present time, cytochrome aa3 redox state cannot be measured reliably by NIRS when hemoglobin is present. 10-12 Of relevance to hypothermic CPB, the NIRS cytochrome signal has been found to decrease spuriously during hemodilution. 12 Therefore great caution should be exercised in interpreting brain oxygenation during hypothermic CPB from the NIRS cytochrome aa3 redox signal.
In summary, NIRS is a developing technology with considerable promise in congenital heart surgery. However, before it can be used to treat patients or define the adequacy of cerebral oxygenation, work is needed to identify the critical levels of brain oxygen saturation and to reliably measure cytochrome aa3 redox state.
12/8/84299
References
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