J Thorac Cardiovasc Surg 2002;123:394-395
© 2002 The American Association for Thoracic Surgery
Alkalosis induced by alpha-stat management: Cause of neuronal injury after deep hypothermic circulatory arrest?
Carl Wong, MA, MB, BChir, FRCS, FRCSEd
Department of Cardiothoracic Surgery
Freeman Hospital
Newcastle upon Tyne, United Kingdom
To the Editor:
Miyamoto and Miyamoto's comments
1 on the excellent article by Kurth and associates 2 raise interesting issues that require further discussion.
Alpha-stat cardiopulmonary bypass is known to produce arterial alkalosis. The letter by Miyamoto and Miyamoto asserted that the cerebral injury found by Kurth and associates was caused by the detrimental effects of alkalosis on cerebral metabolism and well-being by the Bohr effect shifting the oxygen–hemoglobin dissociation curve to the left and exposing the brain to excitotoxic injury.
However, blood gas samples measured in standard blood gas machines are heated to 37°C. This alters the pH, PO2, and PCO2 because energy is added to the sample, but correction to a specific temperature can be performed by the use of internationally recognized formulas. 3 Kurth and colleagues reported that the blood gas values were measured at 37°C with no temperature correction (Table 1 legend). The physiologic arterial blood pH range is more alkalotic in pigs than in human beings (7.4–7.53). 4 Therefore, the pH values reported by Kurth's group during cooling and rewarming cardiopulmonary bypass (mean 7.46 ± 0.1 and 7.41 ± 0.11, respectively) are not alkalotic for a pig. 2 Even if the appropriate temperature corrections are applied according to the standard formulas, there is alkalosis only at deep hypothermia and this is mild(Table 1).
Miyamoto and Miyamoto extrapolated their experimental results on rabbit spinal cord to the human brain, suggesting that at least 2 hours of cerebral protection could be obtained and, therefore, cerebral injury must be due to the alkalosis of alpha-stat pH management.
There are a number of problems with this hypothesis. First, in human beings brain temperature does not correlate well with esophageal temperature. Many institutions in cardiac surgery use esophageal temperature as a marker of body temperature and use nasopharyngeal temperature as a surrogate of cerebral temperature. Studies have shown that the latter has a better correlation. 5,6
Second, their linear extrapolation is dangerous because no data exist to support this assumption either from their own studies or from the literature. On the contrary, data do suggest that a nonlinear relationship exists. Busto and associates 7 have shown that mild hypothermia has a disproportionate effect on cerebral protection and that this alone can explain the dramatic impact of cerebral protective agents in middle cerebral artery occlusion studies. Michenfelder and Milde 8 have shown that metabolic suppression is nonlinear, being greater in the earlier cooling period.
Arterial blood samples do not reflect cerebral tissue pH. The metabolic debt induced by any hypoxic insult, including circulatory arrest, will lower the pH in the tissues by the generation of the products of glycolysis such as lactic acid. Therefore, the temperature-corrected cerebral venous pH is probably a better indication of actual cerebral pH.
The Bohr effect is only one of the many factors acting on the oxygen-hemoglobin dissociation curve during profound hypothermic cardiopulmonary bypass. The hypothermia has the most important effect such that the p50 may fall into the ischemic PO2 range.
12/8/121154
doi:10.1067/mtc.2002.121154
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