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J Thorac Cardiovasc Surg 1999;117:1228-1229
© 1999 Mosby, Inc.

LETTERS TO THE EDITOR

Regional cerebral blood flow and regional glucose use during rewarmingafter hypothermic cardiopulmonary bypass

Research Department
Kokura Memorial Hospital
Kitakyushu, Japan

Koho-J. Miyamoto MD, PhD

Assistant Professor
Department of Physiology
University of theRyukius School of Medicine
Okinawa, Japan

To the Editor:

We read with great interest the article titled "Regional CerebralBlood Flow During Rewarming of Cardiopulmonary Bypass Correlates With PosthypothermicRegional Glucose Use" (J Thorac Cardiovasc Surg 1998;116:503-10). Theauthors are to be congratulated on the timely demonstration of the potentiallydeleterious derangements caused by a period of hypothermic perfusion followedby rewarming.

Because cerebral blood flow and metabolism remained coupled during hypothermic(20°C) perfusion for 60 minutes, but apparently not during or after rewarming,particularly in the parietal cortex, rewarming was considered to be the culprit.However, the 60-minute period of hypothermic perfusion used in their protocol2 might not have been long enough to assess the effects of hypothermia perse, since reducing the temperature to only 29.5°C can provide protectionfor 60 minutes of total blood flow cessation in a rabbit model of spinal cordischemia with pH-stat ventilation. ¹ Metabolic derangements may result from inadequate oxygen deliverycaused by the leftward shift of the oxyhemoglobin curve and alkalosis inducedby hypothermia. Given the relatively short hypothermic period with continuousperfusion, these derangements may have been present before rewarming, butmay have been too subtle even for the sophisticated methods used by the authors.Those metabolic derangements could not recover fast enough during the rewarmingtime and indeed were exaggerated by the increased metabolic rate. Thus theybecame apparent only after body temperature was returned to normal. If metabolismwas impaired and oxygen could not be consumed, there was no need for flow;consequently, decreased flows were observed.

Unfortunately, the authors studied only animals with alpha-stat strategiesfor pH management during hypothermia. Alpha-stat strategies have been consideredas the standard for many years to avoid the so-called "luxury perfusion"of pH-stat management and consequent increased chances of microembolization.Such "luxury perfusion" may actually not be a "luxury"but a necessary compensatory mechanism for the leftward shift of the oxyhemoglobindissociation curve induced by hypothermia. A recent report ² indicated better neurologic outcome of pH-stat overalpha-stat strategies for deep hypothermic cardiopulmonary bypass in infants,an observation that could have been anticipated and should not be surprising.Whether this improved outcome was due to better blood flow ³ or better oxygen delivery and use is irrelevant. However,it is in line with the physiologic principles of the remarkable constancyof the expiratory carbon dioxide concentration remaining close to that observedin normothermic conditions in hibernating animals, regardless of the bodytemperature, by ventilatory rate adjustment, which is the nature-providedpH-stat management. This is most obvious in poikilothermic animals,

The authors have the modern methods to resolve the controversial issueof whether alpha-stat is better than pH-stat management or vice versa. Webelieve the neurologic injury coincidental to hypothermic perfusion is theresult of the algebraic sum of both factors, positive metabolic factors andnegative microembolization. The relative role of each one is variable foreach individual depending on various factors—the duration of the hypothermicperfusion period, the rate of cooling and rewarming, the hemodynamic statusbefore and after cardiopulmonary bypass, the type of oxygenator, and the lackof pulsatility. The metabolic component is maximized by pH-stat strategy ofthe ventilation, which restores oxygen delivery to the tissues. However, ifthe supposedly positive metabolic influences of hypothermia are less thanideal because of the impaired oxygen delivery caused by alpha-stat management,which would be equivalent to hypoxic perfusion, the negative influence ofmicroembolization will become relatively more significant. If sustained forlong enough, it would be detrimental by itself, thus resulting in overt neurologicimpairment.

Hemodynamic superiority of pH-stat over alpha-stat strategies in dogsduring surface-induced hypothermia was reported years before the term of pH-statmanagement was coined. ³ Itwould not be surprising if the reported hypotension during the hypothermicstate and the flow-metabolism derangements would be at least abated, if notcompletely prevented, provided that expiratory carbon dioxide concentrationsof the oxygenator are maintained constant close to 5% to 6%. pH-Stat strategiesare used by controlling the oxygen/blood flow ratio of cardiopulmonary bypass(or gasses, by adding carbon dioxide, if necessary), not only during coolingbut during rewarming as well.

12/8/97600

[Response declined]

References

1. Miyamoto TA, Miyamoto KJ, Ohno N. Objectiveassessment of CNS function within 6 hours of spinal cord ischemia in rabbits.J Anesth 1998;12:189-94.
   
2. du Plessis AJ, Jonas RA, Wypij D, HickeyPR, Riviello J, Wessel DL, et al. Perioperative effects of alpha-stat versuspH-stat strategies for deep hypothermic cardiopulmonary bypass in infants.J Thorac Cardiovasc Surg 1997;114:991-1001.[Abstract/Free Full Text]
   
3. Miyamoto TA, Hosoi N, Chiba T, ShibataS, Saito H, Wakusawa R. The effects of the "ideal PCO₂" on the hemodynamics during surface inducedhypothermia (in Japanese). Nihon Kyobu-Geka Gakkaishi (J Jpn Assoc ThoracSurg) 1970;18:45-6.
   

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				K. Ueno, S. Takamoto, T. Miyairi, T. Morota, K. Shibata, A. Murakami, and Y. Kotsuka Arterial blood gas management in retrograde cerebral perfusion: the importance of carbon dioxide Eur. J. Cardiothorac. Surg., November 1, 2001; 20(5): 979 - 985. [Abstract] [Full Text] [PDF]

				T.-A. Miyamoto and K.-J. Miyamoto Is alpha-stat management still justified for deep hypothermic circulatory arrest in adults? J. Thorac. Cardiovasc. Surg., September 1, 1999; 118(3): 569 - 570. [Full Text] [PDF]

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