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

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Standard

Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage. / Olsen, Markus Harboe; Capion, Tenna; Riberholt, Christian Gunge; Bache, Søren; Ebdrup, Søren Røddik; Rasmussen, Rune; Mathiesen, Tiit; Berg, Ronan M. G.; Møller, Kirsten.

I: Acta Anaesthesiologica Scandinavica, Bind 67, Nr. 8, 2023, s. 1054-1060.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Olsen, MH, Capion, T, Riberholt, CG, Bache, S, Ebdrup, SR, Rasmussen, R, Mathiesen, T, Berg, RMG & Møller, K 2023, 'Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage', Acta Anaesthesiologica Scandinavica, bind 67, nr. 8, s. 1054-1060. https://doi.org/10.1111/aas.14277

APA

Olsen, M. H., Capion, T., Riberholt, C. G., Bache, S., Ebdrup, S. R., Rasmussen, R., Mathiesen, T., Berg, R. M. G., & Møller, K. (2023). Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage. Acta Anaesthesiologica Scandinavica, 67(8), 1054-1060. https://doi.org/10.1111/aas.14277

Vancouver

Olsen MH, Capion T, Riberholt CG, Bache S, Ebdrup SR, Rasmussen R o.a. Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage. Acta Anaesthesiologica Scandinavica. 2023;67(8):1054-1060. https://doi.org/10.1111/aas.14277

Author

Olsen, Markus Harboe ; Capion, Tenna ; Riberholt, Christian Gunge ; Bache, Søren ; Ebdrup, Søren Røddik ; Rasmussen, Rune ; Mathiesen, Tiit ; Berg, Ronan M. G. ; Møller, Kirsten. / Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage. I: Acta Anaesthesiologica Scandinavica. 2023 ; Bind 67, Nr. 8. s. 1054-1060.

Bibtex

@article{539dee3370b34fe6a69cefd5b0e16181,
title = "Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage",
abstract = "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 (PbtO2), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction. 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 PbtO2 increased significantly (baseline, median: 24, 95%CI: 19–31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24–33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged. Conclusion: In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO2 increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD. Trial registration: clinicaltrials.gov (NCT03987139; 14 June 2019).",
keywords = "blood pressure, brain tissue oxygenation, cerebral blood flow, subarachnoid haemorrhage",
author = "Olsen, {Markus Harboe} and Tenna Capion and Riberholt, {Christian Gunge} and S{\o}ren Bache and Ebdrup, {S{\o}ren R{\o}ddik} and Rune Rasmussen and Tiit Mathiesen and Berg, {Ronan M. G.} and Kirsten M{\o}ller",
note = "Publisher Copyright: {\textcopyright} 2023 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.",
year = "2023",
doi = "10.1111/aas.14277",
language = "English",
volume = "67",
pages = "1054--1060",
journal = "Acta Anaesthesiologica Scandinavica",
issn = "0001-5172",
publisher = "Wiley-Blackwell",
number = "8",

}

RIS

TY - JOUR

T1 - Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage

AU - Olsen, Markus Harboe

AU - Capion, Tenna

AU - Riberholt, Christian Gunge

AU - Bache, Søren

AU - Ebdrup, Søren Røddik

AU - Rasmussen, Rune

AU - Mathiesen, Tiit

AU - Berg, Ronan M. G.

AU - Møller, Kirsten

N1 - Publisher Copyright: © 2023 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.

PY - 2023

Y1 - 2023

N2 - 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 (PbtO2), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction. 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 PbtO2 increased significantly (baseline, median: 24, 95%CI: 19–31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24–33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged. Conclusion: In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO2 increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD. Trial registration: clinicaltrials.gov (NCT03987139; 14 June 2019).

AB - 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 (PbtO2), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction. 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 PbtO2 increased significantly (baseline, median: 24, 95%CI: 19–31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24–33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged. Conclusion: In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO2 increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD. Trial registration: clinicaltrials.gov (NCT03987139; 14 June 2019).

KW - blood pressure

KW - brain tissue oxygenation

KW - cerebral blood flow

KW - subarachnoid haemorrhage

U2 - 10.1111/aas.14277

DO - 10.1111/aas.14277

M3 - Journal article

C2 - 37192754

AN - SCOPUS:85159366820

VL - 67

SP - 1054

EP - 1060

JO - Acta Anaesthesiologica Scandinavica

JF - Acta Anaesthesiologica Scandinavica

SN - 0001-5172

IS - 8

ER -

ID: 347748671