significant prolongations in TRCont and NTR

Cont withlower circulatory arrest temperatures even in the neuro-logically normal patients. This result can be explainedeither by brain injury occurring as a result of the lowtemperatures or by the fact that it takes longer to rewarma colder brain (with brain temperature being cooler thanthe nasopharyngeal temperature [7]). The fact that therecovery of the N20-P22 has been shown to be morehighly affected by the transient effects of circulatoryarrest, but is not affected by the circulatory arrest tem-perature, argues against the first possibility. It can there-fore be argued that the circulatory arrest temperaturechosen by the appearance of ECS is consistent frompatient to patient [1] and is neither “too low” or “toohigh.”

References

1. Stecker MM, Cheung AT, Kent GP, et al. Deep hypothermiccirculatory arrest: I. Effects of cooling on EEG and evokedpotentials. Ann Thorac Surg 2001;71:14–21.

2. Salerno TA, Lince DP, White DN, Lynn RB, Charrette EJP.Monitoring of electroencephalogram during open-heart sur-gery. J Thorac Cardiovasc Surg 1978;76:97–100.

3. Witoszka MM, Tamura H, Indeglia R, Hopkins RW, SimeoneFA. Electroencephalographic changes and cerebral complica-tions in open-heart surgery. J Thorac Cardiovasc Surg 1973;66:855–64.

4. Mezrow CK, Midulla PS, Sadeghi AM, et al. Quantitativeelectroencephalography: a method to assess cerebral injuryafter hypothermic: circulatory arrest. J Thorac CardiovascSurg 1995;109:925–34.

5. Stecker MM, Cheung AT, Patterson T, et al. Detection ofstroke during cardiac operations with somatosensory evokedresponses. J Thorac Cardiovasc Surg 1996;112:962–72.

6. Coles JG, Taylor MJ, Pearce JM, et al. Cerebral monitoring ofsomatosensory evoked potentials during profoundly hypo-thermic circulatory arrest. Circulation 1984;70(Suppl 3 Part2):I96–102.

7. Stone JG, Young WL, Smith CR, et al. Do standard monitoringsites reflect true brain temperature when profound hypother-mia is rapidly induced and reversed? Anesthesiology 1995;82:344–51.

8. Markand ON, Warren C, Mallik GS, et al. Temperaturedependent hysteresis in somatosensory and auditory evokedpotentials. Electroencephalogr Clin Neurophysiol 1990;77:425–35.

9. Guerit JM, Verhelst R, Rubay J, et al. The use of somatosen-sory evoked potentials to determine the optimal degree ofhypothermia during circulatory arrest. J Card Surg 1994;9:596–603.

INVITED COMMENTARY

Stecker and coauthors have presented an elegant de-scription of the natural history of brain cooling, assessedby a variety of neurophysiologic parameters infrequentlyapplied in a clinical setting. In Part I, the variability ofcooling to achieve electrocerebral silence (ECS) is strik-ing. In Part II, the “hysteresis” of warming and coolingseen in neural tissue is beautifully illustrated by thedisappearance of sensory evoked potentials (SEP) priorto ECS during cooling, with reappearance of SEP whileECS persists during warming. An interesting subanalysissuggests that retrograde cerebral perfusion produces amore rapid rate of rewarming, when comparing resultsfrom this series to previous published experience. Notsurprisingly, the duration of circulatory arrest appears tocorrelate with the rate of SEP recovery, and a lowertemperature during circulatory arrest is associated with atrend toward later return of neurologic function.

No doubt the authors hoped to connect observation topractice by linking conduct of circulatory arrest to out-come. This is something of a Holy Grail in the treatmentof conditions requiring circulatory arrest. Specifically, isthere a “best temperature” for circulatory arrest? Theconventional answer to this question would be 16° to18°C, clouded by uncertainty about the relationship be-tween brain temperature and the temperature recordedat various peripheral monitoring sites. One implication ofthis pair of articles is that a significant number of patientsarrested at 18°C will not have achieved ECS. Does thismean that EEG monitoring, to allow confirmation of ECS,is essential for safe conduct of circulatory arrest? Alter-natively, should all patients be cooled to 12°C, or cooledfor 50 minutes? The authors are careful to warn against

leaping to these conclusions, which their data do notsupport. They can only conclude that “appearance ofECS is consistent from patient to patient and is neither‘too low’ or ‘too high’.”

The difficulty linking observation to practice lies inisolating the variables. “Best temperature” variables suchas ECS are dwarfed by other clinical variables. Whereneurologic outcome is concerned, the most striking find-ing in this series is that mean circulatory arrest time was36.6 6 12 minutes in neurologically normal patients,versus 51.6 6 21 minutes in patients with postoperativeneurologic impairment ( p 5 0.006). Therefore, durationof circulatory arrest is the most important predictor ofoutcome. Assuming reasonable technical facility, dura-tion of circulatory arrest is determined by the complexityof the surgical pathology, not by the management ofwarming and cooling. The authors make no claims tohave assessed the relationship between surgical com-plexity and outcome, which is difficult to accomplish, andwas not the goal of this study. As a result, the findings fallshort of a mandate for a change in practice, while stillcontributing to our understanding of warming andcooling.

Craig R. Smith, MD

Division of Cardiothoracic SurgeryCollege of Physicians & Surgeons of Columbia University177 Ft Washington AveSuite 7-435New York, NY 10032

28 STECKER ET AL Ann Thorac SurgEEG AND EP DURING REWARMING 2001;71:22–8

© 2001 by The Society of Thoracic Surgeons 0003-4975/01/$20.00Published by Elsevier Science Inc PII S0003-4975(00)02169-X