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66th Annual Meeting of the German Society of Neurosurgery (DGNC)
Friendship Meeting with the Italian Society of Neurosurgery (SINch)

German Society of Neurosurgery (DGNC)

7 - 10 June 2015, Karlsruhe

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Hypercapnia for therapy of subarachnoid hemorrhage (SAH) – dose optimization trial

Meeting Abstract

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  • Thomas Westermaier - Neurochirurgische Klinik und Poliklinik und
  • Ekkehard Kunze - Neurochirurgische Klinik und Poliklinik und
  • Nadine Willner - Neurochirurgische Klinik und Poliklinik und
  • Franziska Weidner - Neurochirurgische Klinik und Poliklinik und
  • Judith Weiland - Neurochirurgische Klinik und Poliklinik und
  • Christian Kilgenstein - Klinik für Anästhesie und Intensivmedizin, Universitätsklinikum Würzburg
  • Ralf-Ingo Ernestus - Neurochirurgische Klinik und Poliklinik und
  • Norbert Roewer - Klinik für Anästhesie und Intensivmedizin, Universitätsklinikum Würzburg
  • Ralf Michael Muellenbach - Klinik für Anästhesie und Intensivmedizin, Universitätsklinikum Würzburg
  • Christian Stetter - Neurochirurgische Klinik und Poliklinik und

Deutsche Gesellschaft für Neurochirurgie. 66. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Karlsruhe, 07.-10.06.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocMO.09.07

doi: 10.3205/15dgnc044, urn:nbn:de:0183-15dgnc0442

Published: June 2, 2015

© 2015 Westermaier et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Temporary hypercapnia leads to a reproducible increase of cerebral blood flow (CBF). The aim of this study was to measure the course of PaCO2-reactivity after prolonged SAH, and to evaluate the therapeutic effect of graded hypercapnia.

Method: Eight patients with SAH (Hunt / Hess grade 3-5, Fisher grade 3) were supplied with an external ventricular drainage. Between day 4 and 14 they underwent a trial intervention in which the respiratory minute volume was reduced in order to maintain a target PaCO2 of 55 mmHg for 2 hours. Arterial blood gas analysis (ABG) and transcranial Doppler sonography (TCD) were performed in 15-minute intervals. ICP, CPP, and cardiovascular parameters were monitored continuously. Intracerebral CBF-measurement and transcutaneous measurement of brain tissue oxygen saturation (StiO2) were the primary and secondary endpoints.

Results: Following an elevation of PaCO2 from a baseline of 38.8 ± 1.13 mmHg to 54.57 ± 0.91 mmHg, CBF and StiO2 significantly increased in all patients. MABP remained stable. ICP remained unchanged under a continuous CSF-drainage. StiO2 started to decline after 60 minutes, CBF 90 minutes after the onset of hypercapnia under a stable cardiac output.

Conclusions: Hypercapnia causes a highly reproducible increase of CBF and StiO2 in high-grade SAH patients. Under continuous CSF-drainage, no elevation of ICP could be recorded. The ideal duration of hypercapnia is likely to be between 60 and 90 minutes. Thereafter, adaptation to increased PaCO2 and decreased CSF pH, most likely by the activation of buffer mechanisms, occurs and starts to reverse the CBF-enhancing effect.