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Cerebral energy failure following experimental cardiac arrest: Hypothermia treatment reduces secondary lactate/pyruvate-ratio increase
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Anaesthesiology and Intensive Care.
2009 (English)In: Resuscitation, ISSN 0300-9572, E-ISSN 1873-1570, Vol. 80, no 5, 573-579 p.Article in journal (Refereed) Published
Abstract [en]

AIM: This was an experimental study performed to investigate cerebral metabolism during hypothermia treatment and rewarming after resuscitation from cardiac arrest (CA). MATERIALS AND METHODS: Sixteen pigs underwent CA followed by cardiopulmonary resuscitation (CPR). After randomisation into one hypothermic (n=8) and one normothermic group (n=8) the animals received infusion of 4 or 38 degrees C saline, respectively. Following restoration of spontaneous circulation (ROSC) both groups were observed for 360min. The hypothermic group was cooled for 180 min and then rewarmed. Temperature was not modulated in the normothermic group. Cerebral microdialysis was conducted and lactate/pyruvate (L/P)-ratio and glutamate were analysed. Intracranial pressure probe was inserted. Oxygen saturation in venous jugular bulb blood (SjO2) was analysed. RESULTS: All animals initially had increased L/P-ratio (>30). A total of nine animals developed secondary increase. In the hypothermic group this was observed in 2/7 animals and in the normothermic group in 7/8 (p=0.04). Glutamate increased initially in all animals with secondary increases in two animals in each group. No differences in L/P-ratio or glutamate were detected during the rewarming phase compared to the hypothermic phase. The hypothermic group had higher SjO(2) (p=0.04). In both groups intracranial pressure increased after ROSC. CONCLUSION: After resuscitation from CA there was a risk of cerebral secondary energy failure (reflected as an increased L/P-ratio) but hypothermia treatment seemed to counteract this effect. Cerebral oxygen extraction, measured by SjO(2,) was increased in the hypothermic group probably due to reduced metabolism. Rewarming did not reveal any obvious harmful events.

Place, publisher, year, edition, pages
2009. Vol. 80, no 5, 573-579 p.
Keyword [en]
Cardiac arrest, Cardiopulmonary resuscitation, Hypothermia, Rewarming, Brain ischaemia, Microdialysis, Lactate, Glutamate
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-98092DOI: 10.1016/j.resuscitation.2009.02.003ISI: 000266670300014PubMedID: 19328618OAI: oai:DiVA.org:uu-98092DiVA: diva2:173272
Available from: 2009-02-12 Created: 2009-02-12 Last updated: 2013-08-16Bibliographically approved
In thesis
1. Aspects of Induced Hypothermia following Cardiopulmonary Resuscitation: Cerebral and Cardiovascular Effects
Open this publication in new window or tab >>Aspects of Induced Hypothermia following Cardiopulmonary Resuscitation: Cerebral and Cardiovascular Effects
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Hypothermia treatment with cooling to a body temperature of 32-34°C has been shown to be an effective way of improving neurological outcome and survival in unconscious patients successfully resuscitated after cardiac arrest (CA). The method is used clinically but there are still many questions on the biological mechanisms and on how the treatment is best performed. This thesis focuses on cerebral and haemodynamic effects of hypothermia and rewarming.

A porcine model of CA was used. To shorten time to reach target temperature, induction of hypothermia, by means of infusion of 4°C cold fluid, was started already during ongoing cardiopulmonary resuscitation. The temperature was satisfactorily reduced without obvious haemodynamic disturbances.

Cerebral effects of hypothermia and rewarming were studied. Microdialysis monitoring showed signs of cerebral energy failure (increased lactate/pyruvate-ratio) and excitotoxicity (increased glutamate) immediately after CA. There was a risk of secondary energy failure that was reduced by hypothermia. Intracranial pressure (ICP) increased gradually after CA irrespectively of if hypothermia was used or not. There were no indications of increasing cerebral disturbances during rewarming.

Haemodynamic effects of hypothermia treatment and rewarming were examined in a study of patients successfully resuscitated after CA. Hypothermia was induced by means of cold intravenous infusion. No negative effects on the cardiovascular system were revealed. There were indications of decreased intravascular volume in spite of a positive fluid balance.

Cerebral microdialysis and ICP recording were performed in four patients. All patients had signs of energy failure and excitotoxicity following CA. ICP was only exceptionally above 20 mmHg. In contrast to the experimental study indications of increasing ischemia were seen during rewarming. Glycerol had a biphasic pattern, perhaps due to an overspill of metabolites from the general circulation. As most patients become extensively anti-coagulated following CA, intracranial monitoring is not suitable to be used in routine care.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2009. 81 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 422
National Category
Anesthesiology and Intensive Care
urn:nbn:se:uu:diva-9562 (URN)978-91-554-7419-5 (ISBN)
Public defence
2009-03-28, Skoogsalen, Akademiska sjukhuset ing. 78/79, Uppsala, 09:15 (English)
Available from: 2009-02-25 Created: 2009-02-12 Last updated: 2009-02-25Bibliographically approved

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