Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.

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dc.citation.issue6
dc.citation.volume43
dc.contributor.authorPerry BG
dc.contributor.authorKorad S
dc.contributor.authorMündel T
dc.coverage.spatialEngland
dc.date.accessioned2024-06-17T01:49:41Z
dc.date.available2024-06-17T01:49:41Z
dc.date.issued2023-06-18
dc.description.abstractBACKGROUND: During hyperthermia, the perturbations in mean arterial blood pressure (MAP) produced by the Valsalva manoeuvre (VM) are more severe. However, whether these more severe VM-induced changes in MAP are translated to the cerebral circulation during hyperthermia is unclear. METHODS: Healthy participants (n = 12, 1 female, mean ± SD: age 24 ± 3 years) completed a 30 mmHg (mouth pressure) VM for 15 s whilst supine during normothermia and mild hyperthermia. Hyperthermia was induced passively using a liquid conditioning garment with core temperature measured via ingested temperature sensor. Middle cerebral artery blood velocity (MCAv) and MAP were recorded continuously during and post-VM. Tieck's autoregulatory index was calculated from the VM responses, with pulsatility index, an index of pulse velocity (pulse time) and mean MCAv (MCAvmean ) also calculated. RESULTS: Passive heating significantly raised core temperature from baseline (37.9 ± 0.2 vs. 37.1 ± 0.1°C at rest, p < 0.01). MAP during phases I through III of the VM was lower during hyperthermia (interaction effect p < 0.01). Although an interaction effect was observed for MCAvmean (p = 0.02), post-hoc differences indicated only phase IIa was lower during hyperthermia (55 ± 12 vs. 49.3 ± 8 cm s- 1 for normothermia and hyperthermia, respectively, p = 0.03). Pulsatility index was increased 1-min post-VM in both conditions (0.71 ± 0.11 vs. 0.76 ± 0.11 for pre- and post-VM during normothermia, respectively, p = 0.02, and 0.86 ± 0.11 vs. 0.99 ± 0.09 for hyperthermia p < 0.01), although for pulse time only main effects of time (p < 0.01), and condition (p < 0.01) were apparent. CONCLUSION: These data indicate that the cerebrovascular response to the VM is largely unchanged by mild hyperthermia.
dc.description.confidentialfalse
dc.edition.editionNov 2023
dc.format.pagination463-471
dc.identifier.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/37332243
dc.identifier.citationPerry BG, Korad S, Mündel T. (2023). Cerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.. Clin Physiol Funct Imaging. 43. 6. (pp. 463-471).
dc.identifier.doi10.1111/cpf.12843
dc.identifier.eissn1475-097X
dc.identifier.elements-typejournal-article
dc.identifier.issn1475-0961
dc.identifier.urihttps://mro.massey.ac.nz/handle/10179/69861
dc.languageeng
dc.publisherJohn Wiley & Sons Ltd on behalf of Scandinavian Society of Clinical Physiology and Nuclear Medicine
dc.publisher.urihttps://onlinelibrary.wiley.com/doi/10.1111/cpf.12843
dc.relation.isPartOfClin Physiol Funct Imaging
dc.rights(c) 2023 The Author/s
dc.rightsCC BY 4.0
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectblood pressure
dc.subjectcerebral autoregulation
dc.subjectcerebral blood flow
dc.subjectheat stress
dc.subjectmiddle cerebral artery blood velocity
dc.subjectHumans
dc.subjectFemale
dc.subjectYoung Adult
dc.subjectAdult
dc.subjectValsalva Maneuver
dc.subjectMiddle Cerebral Artery
dc.subjectHomeostasis
dc.subjectCerebrovascular Circulation
dc.subjectHyperthermia, Induced
dc.subjectBlood Flow Velocity
dc.subjectBlood Pressure
dc.titleCerebrovascular and cardiovascular responses to the Valsalva manoeuvre during hyperthermia.
dc.typeJournal article
pubs.elements-id462215
pubs.organisational-groupCollege of Health
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