CJA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by STOYKA, W. W.
Right arrow Articles by GARVEY, M. B.
Right arrow Search for Related Content
PubMed
Right arrow Articles by STOYKA, W. W.
Right arrow Articles by GARVEY, M. B.

Canadian Journal of Anesthesia, Vol 21, 325-334, Copyright © 1974 by Canadian Anesthesiologists' Society

Haematological and Cardiorespiratory Responses to Induced Hyperpyrexia

W. W. STOYKA B.SC, M.D., F.R.C.P.(C)1 and M. B. GARVEY B.SC, M.D., F.R.C.P.(C)2

1 Department of Anaesthesia, University of Toronto, St. Michael's Hospital
2 Department of Medicine, University of Toronto, St. Michael's Hospital

Induced hyperpyrexia was compared to malignant hyperpyrexia and heat stroke to determine whether similar abnormalities in haematological function were present. Induced hyperpyrexia showed no evidence of red blood cell haemolysis, no abnormalities in individual clotting factor assay or specific diagnostic clotting tests, no evidence of fibrinolysis or intravascular coagulation and no abnormal platelet count or clot lysis times. These findings are contrary to documented reports on heat stroke and malignant hyperpyrexia and emphasize the fact that induced hyperpyrexia is haematologically dissimilar to heat stroke and malignant hyperpyrexia. The physiological consequences of induced hyperpyrexia were hown as changes due to haemoconcentration and increased oxygen demand. Cardiac function responses were primarily the result of haemoconcentration and decreased blood volume. Acid-base disturbances occurred terminally when temperatures exceeded 43° C (107° F) due to metabolic demands exceeding metabolic stores and preferential organ perfusion causing ischaemia in previously perfused tissues. Associated with these changes was significant hyperkalaemia which proved to be the cause of death in several experimental animals.

The documented results in this study enable one to conclude that induced hyperpyrexia is relatively harmless haematologically and that it can be readily treated with adequate fluid replacement, buffer infusion as required and a method of cooling to quickly return body temperatures to normal. The results also indicate the necessity for temperature monitoring as the most effective therapeutic tool.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1974 by the Canadian Anesthesiologists' Society.