Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage.


Journal

Acta anaesthesiologica Scandinavica
ISSN: 1399-6576
Titre abrégé: Acta Anaesthesiol Scand
Pays: England
ID NLM: 0370270

Informations de publication

Date de publication:
09 2023
Historique:
revised: 24 03 2023
received: 30 12 2022
accepted: 01 05 2023
medline: 21 8 2023
pubmed: 17 5 2023
entrez: 16 5 2023
Statut: ppublish

Résumé

Patients with aneurysmal subarachnoid haemorrhage (SAH) might have impaired cerebral autoregulation, that is, CBF - and thereby oxygen delivery - passively increase with an increase in CPP. This physiological study aimed to investigate the cerebral haemodynamic effects of controlled blood pressure increase in the early phase after SAH before any signs of delayed cerebral ischaemia (DCI) occurred. The study was carried out within 5 days after ictus. Data were recorded at baseline and after 20 min of noradrenaline infusion to increase mean arterial blood pressure (MAP) by a maximum of 30 mmHg and to an absolute level of no more than 130 mmHg. The primary outcome was the difference in middle cerebral artery blood flow velocity (MCAv) measured by transcranial Doppler (TCD), while differences in intracranial pressure (ICP), brain tissue oxygen tension (PbtO Thirty-six participants underwent the intervention 4 (median, IQR: 3-4.75) days after ictus. MAP was increased from 82 (IQR: 76-85) to 95 (IQR: 88-98) mmHg (p-value: <.001). MCAv remained stable (baseline, median 57, IQR: 46-70 cm/s; controlled blood pressure increase, median: 55, IQR: 48-71 cm/s; p-value: .054), whereas PbtO In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO clinicaltrials.gov (NCT03987139; 14 June 2019).

Sections du résumé

BACKGROUND
Patients with aneurysmal subarachnoid haemorrhage (SAH) might have impaired cerebral autoregulation, that is, CBF - and thereby oxygen delivery - passively increase with an increase in CPP. This physiological study aimed to investigate the cerebral haemodynamic effects of controlled blood pressure increase in the early phase after SAH before any signs of delayed cerebral ischaemia (DCI) occurred.
METHODS
The study was carried out within 5 days after ictus. Data were recorded at baseline and after 20 min of noradrenaline infusion to increase mean arterial blood pressure (MAP) by a maximum of 30 mmHg and to an absolute level of no more than 130 mmHg. The primary outcome was the difference in middle cerebral artery blood flow velocity (MCAv) measured by transcranial Doppler (TCD), while differences in intracranial pressure (ICP), brain tissue oxygen tension (PbtO
RESULTS
Thirty-six participants underwent the intervention 4 (median, IQR: 3-4.75) days after ictus. MAP was increased from 82 (IQR: 76-85) to 95 (IQR: 88-98) mmHg (p-value: <.001). MCAv remained stable (baseline, median 57, IQR: 46-70 cm/s; controlled blood pressure increase, median: 55, IQR: 48-71 cm/s; p-value: .054), whereas PbtO
CONCLUSION
In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO
TRIAL REGISTRATION
clinicaltrials.gov (NCT03987139; 14 June 2019).

Identifiants

pubmed: 37192754
doi: 10.1111/aas.14277
doi:

Substances chimiques

Oxygen S88TT14065

Banques de données

ClinicalTrials.gov
['NCT03987139']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1054-1060

Subventions

Organisme : Grosserer Jakob Ehrenreich og Hustru Grete Ehrenreichs Fond
Organisme : TrygFonden

Informations de copyright

© 2023 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.

Références

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Auteurs

Markus Harboe Olsen (MH)

Department of Neuroanaesthesiology, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Tenna Capion (T)

Department of Neurosurgery, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Christian Gunge Riberholt (CG)

Department of Neuroanaesthesiology, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.
Department of Brain and Spinal Cord Injury, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Søren Bache (S)

Department of Neuroanaesthesiology, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Søren Røddik Ebdrup (SR)

Department of Neuroanaesthesiology, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Rune Rasmussen (R)

Department of Neurosurgery, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Tiit Mathiesen (T)

Department of Neurosurgery, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.

Ronan M G Berg (RMG)

Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital, Denmark.
Centre for Physical Activity Research, Copenhagen University Hospital, Rigshospitalet, Denmark.
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.
Neurovascular Research Laboratory, Faculty of Life Sciences and Education, University of South Wales, Pontypridd, UK.

Kirsten Møller (K)

Department of Neuroanaesthesiology, The Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark.
Institute of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.

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