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British Journal of Anaesthesia, Vol 82, Issue 2 271-273, Copyright © 1999 by The Board of Management and Trustees of the British Journal of Anaesthesia

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Dissociation of pituitary-adrenal and catecholamine activation after induced cardiac arrest and defibrillation

M. J. O'Leary, A. C. Timmins, J. N. Appleby, S. Medbak, A. B. Grossman, A. W. Nathan and C. J. Hinds
Department of Intensive Care, Department of Endocrinology and Department of Cardiology, St Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK

To avoid factors which confound attempts to characterize the neuroendocrine response to cardiac arrest, we studied the pituitary- adrenocortical and catecholamine responses to induced ventricular fibrillation (VF) and direct current cardioversion in 10 patients undergoing testing of 'implanted cardioverter defibrillator' devices under sedation. Plasma concentrations of epinephrine were increased 5 min after VF (from a mean basal of 0.39 (S.E.M. 0.09) to a peak of 0.632 (0.212) nmol litre-1; P < 0.05) but were unchanged at other times. Plasma concentrations of norepinephrine did not change at any time. Plasma concentrations of cortisol increased significantly at 10 min (from a mean of 367 (SEM 62) to 539 (64) nmol litre-1; P < 0.001) and remained increased 30 min after VF (470 (74) nmol litre-1; P < 0.05) but had returned towards baseline at 60 min, whereas plasma prolactin concentrations were increased at 5 min (from a mean of 224 (SEM 54) to 320 (63) micrograms litre-1; P < 0.01) and remained increased until the end of the sampling period at 60 min (288 (65) micrograms litre-1; P < 0.05). Concentrations of adrenocorticotrophic hormone (ACTH) (n = 5) tended to increase but this was not statistically significant. We conclude that a short period of cardiac arrest in lightly sedated humans activated the pituitary-adrenocortical axis but did not appear to stimulate catecholamine secretion. These findings raise questions about the nature and mechanisms of the neuroendocrine response to cardiac arrest.
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