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Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome

BACKGROUND: Most patients with sepsis develop potentially irreversible cerebral dysfunctions. It is yet not clear whether cerebral haemodynamics are altered in these sepsis patients at all, and to what extent. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaire...

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Autores principales: Thees, Christof, Kaiser, Markus, Scholz, Martin, Semmler, Alexander, Heneka, Michael T, Baumgarten, Georg, Hoeft, Andreas, Putensen, Christian
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246217/
https://www.ncbi.nlm.nih.gov/pubmed/18045492
http://dx.doi.org/10.1186/cc6185
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author Thees, Christof
Kaiser, Markus
Scholz, Martin
Semmler, Alexander
Heneka, Michael T
Baumgarten, Georg
Hoeft, Andreas
Putensen, Christian
author_facet Thees, Christof
Kaiser, Markus
Scholz, Martin
Semmler, Alexander
Heneka, Michael T
Baumgarten, Georg
Hoeft, Andreas
Putensen, Christian
author_sort Thees, Christof
collection PubMed
description BACKGROUND: Most patients with sepsis develop potentially irreversible cerebral dysfunctions. It is yet not clear whether cerebral haemodynamics are altered in these sepsis patients at all, and to what extent. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns. METHODS: After approval of the institutional ethics committee, 10 mechanically ventilated patients with sepsis syndrome and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure by 0.93 ± 0.7 kPa iu by ypervent ilation. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A t test for matched pairs was used for statistical analysis (P < 0.05). RESULTS: During stable mean arterial pressure and cardiac index, reduction of the arterial carbon dioxide partial pressure led to a significant increase of the capillary closing pressure from 25 ± 11 mmHg to 39 ± 15 mmHg (P < 0.001), with a consecutive decrease of blood flow velocity in the middle cerebral artery of 21.8 ± 4.8%/kPa (P < 0.001), of cerebral blood flow from 64 ± 29 ml/100 g/min to 39 ± 15 ml/100 g/min (P < 0.001) and of jugular venous oxygen saturation from 75 ± 8% to 67 ± 14% (P < 0.01). CONCLUSION: In contrast to other experimental and clinical data, we observed no pathological findings in the investigated parameters of cerebral perfusion and oxygenation.
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spelling pubmed-22462172008-02-20 Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome Thees, Christof Kaiser, Markus Scholz, Martin Semmler, Alexander Heneka, Michael T Baumgarten, Georg Hoeft, Andreas Putensen, Christian Crit Care Research BACKGROUND: Most patients with sepsis develop potentially irreversible cerebral dysfunctions. It is yet not clear whether cerebral haemodynamics are altered in these sepsis patients at all, and to what extent. We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns. METHODS: After approval of the institutional ethics committee, 10 mechanically ventilated patients with sepsis syndrome and pathological electroencephalogram patterns underwent measurements of cerebral blood flow and jugular venous oxygen saturation before and after reduction of the arterial carbon dioxide partial pressure by 0.93 ± 0.7 kPa iu by ypervent ilation. The cerebral capillary closing pressure was determined from transcranial Doppler measurements of the arterial blood flow of the middle cerebral artery and the arterial pressure curve. A t test for matched pairs was used for statistical analysis (P < 0.05). RESULTS: During stable mean arterial pressure and cardiac index, reduction of the arterial carbon dioxide partial pressure led to a significant increase of the capillary closing pressure from 25 ± 11 mmHg to 39 ± 15 mmHg (P < 0.001), with a consecutive decrease of blood flow velocity in the middle cerebral artery of 21.8 ± 4.8%/kPa (P < 0.001), of cerebral blood flow from 64 ± 29 ml/100 g/min to 39 ± 15 ml/100 g/min (P < 0.001) and of jugular venous oxygen saturation from 75 ± 8% to 67 ± 14% (P < 0.01). CONCLUSION: In contrast to other experimental and clinical data, we observed no pathological findings in the investigated parameters of cerebral perfusion and oxygenation. BioMed Central 2007 2007-11-28 /pmc/articles/PMC2246217/ /pubmed/18045492 http://dx.doi.org/10.1186/cc6185 Text en Copyright © 2007 Thees et al, licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Thees, Christof
Kaiser, Markus
Scholz, Martin
Semmler, Alexander
Heneka, Michael T
Baumgarten, Georg
Hoeft, Andreas
Putensen, Christian
Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title_full Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title_fullStr Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title_full_unstemmed Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title_short Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
title_sort cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246217/
https://www.ncbi.nlm.nih.gov/pubmed/18045492
http://dx.doi.org/10.1186/cc6185
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