Public defence: Hilde Karlsen

Cand.med. Hilde Karlsen at Institute of Clinical Medicine will be defending the thesis “New insights in cardiac arrest management aimed to improve cardiac and cerebral perfusion during and after resuscitation” for the degree of PhD (Philosophiae Doctor).

Bildet kan inneholde: person, hår, hake, kinn, øyenbryn.

Photo: Åsne Rambøl Hillestad, UiO

Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.

Trial Lecture – time and place

See Trial Lecture.

Adjudication committee

  • First opponent: Professor Asger Granfeldt, Aarhus University
  • Second opponent: Professor Erik Waage Nielsen, Nord University
  • Third member and chair of the evaluation committee: Professor Ida Gjervold Lunde, University of Oslo

Chair of the Defence

Associate Professor Jon Ramm-Pettersen, University of Oslo

Principal Supervisor

Professor II Theresa Mariero Olasveengen, University of Oslo

Summary

Sudden cardiac arrest abruptly stops of blood flow, threatening the heart, brain, and other vital organs. Even after successful resuscitation, patients remain at high risk of serious complications that can trigger new life-threatening events. Advancing knowledge to support the heart and brain during and after resuscitation is crucial.

In the thesis New insights in cardiac arrest management aimed to improve cardiac and cerebral perfusion during and after resuscitation, Hilde Karlsen and colleagues used experimental animal models to explore novel treatments.

The first study tested whether esmolol before adrenaline could protect cardiac function after resuscitation but found no benefit.

The second compared two mean arterial blood pressure targets of 60 vs. 90 mmHg with and without cooling to 33°C; the higher target improved cerebral perfusion and preserved autoregulation, but did not clearly reduce biochemical markers of ischemia.

The third examined controlled hypercapnia, again with and without cooling. Increased carbon dioxide enhanced cerebral blood flow, but in normothermia the accompanying rise in intracranial pressure reduced perfusion pressure. Metabolic findings nevertheless suggested less ischaemic injury.

Together, these investigations provide new insight into how targeted cardiovascular and ventilatory strategies may protect the heart and brain after cardiac arrest.

Additional information

Contact the research support staff.

Published Oct. 31, 2025 11:27 AM - Last modified Nov. 12, 2025 2:26 PM