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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Nils Kristian Skjærvold, NTNU: Norwegian University of Science and Technology
- Second opponent: Associate Professor Mattias Günther, Karolinska Institutet, Sweden
- Third member and chair of the evaluation committee: Associate Professor Maja Elstad, University of Oslo
Chair of the Defence
Professor II Knut Jørgen Labori, University of Oslo
Principal Supervisor
Researcher Lars Øivind Høiseth, University of Oslo
Summary
Blood loss is a leading cause of potentially preventable deaths in trauma patients, with many dying before reaching hospital care. Investigating the hemodynamic response to blood loss in such patients presents challenges. In the thesis Systemic and cerebral hemodynamics in simulated blood loss induced by lower body negative pressure in healthy volunteers, Sole Lindvåg Lie and colleagues simulated blood loss using lower body negative pressure (LBNP) in healthy volunteers to study the systemic and cerebral hemodynamic responses. The aim was to study how key systemic hemodynamic variables interact to regulate cerebral blood flow (CBF).
Healthy volunteers were exposed to progressive LBNP to reduce cardiac output, combined with isometric handgrip exercise to increase mean arterial pressure (MAP) and systemic vascular resistance (SVR). Stroke volume was measured by suprasternal ultrasound and pulse wave analysis (PWA). In a separate randomized, controlled crossover trial, LBNP was combined with supplemental oxygen therapy. CBF was estimated by measuring blood velocity in the Middle Cerebral Artery using transcranial Doppler ultrasound, with mixed linear regression used to estimate effects.
Stroke volume measured by suprasternal ultrasound was more reliable than stroke volume estimated by PWA during increased SVR, emphasizing a cautious approach when using PWA. During changes in MAP and cardiac output, both variables had independent effects on CBF. Supplemental oxygen therapy did not adversely influence the systemic or cerebral hemodynamic response to LBNP.
These findings highlight the importance of exploring new measurement techniques and suggest that CBF regulation may be more pressure-passive and cardiac output-dependent than traditionally described. While cardiac output appears to play a role in CBF regulation, the use of supplemental oxygen did not seem to have an adverse effect on the systemic or cerebral response to blood loss.
Additional information
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