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Jerome S. Litvinoff, MD
Chula Vista, Calif

JAMA. 1989;261(12):1729.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Field and colleagues¹ are to be congratulated for their clear exposition of the neurophysiological derangements seen in brain death. I agree with their statement that brain death results in loss of medullary vagal activity while the spinal sympathetic nuclei survive. I do take issue, however, with their statement that after brain death cardiac activity is determined by the sympathetic system alone. The spinal sympathetic nuclei are driven by the sympathetic cells in the hypothalamus, and these hypothalamic nuclei are just as vulnerable as the medullary vagal nuclei in brain death. Thus, both sympathetic and vagal (parasympathetic) systems become severely deranged and eventually nonfunctional. These derangements tend to balance each other out. It is not surprising, therefore, that tachycardia was noted in less than half of the brain dead patients. It does not seem necessary to invoke "additional influences" such as hypothermia or myocardial ischemia to account . . . [Full Text PDF of this Article]

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