Public Defence: Mikkel Torp Steinberg

Cand.med. Mikkel Torp Steinberg at Institute of Clinical Medicine will be defending the thesis "The impact of chest compressions on defibrillation success during out-of-hospital cardiac arrest and haemodynamics in an experimental animal model" for the degree of PhD.

Photo: Jon Olav Nesvold

Trial Lecture - time and place

See Trial Lecture.

Adjudication committee

  • 1st opponent: Professor Stig Steen, Lunds universitet
  • 2nd opponent: Associate Professor Kristina Hermann Haugaa, University of Oslo
  • Committee Chair: Professor Theis Tønnessen, University of Oslo

Chair of the Defence

Adjunct Professor Pål Aksel Næss,

Principal Supervisor

Senior Researcher Lars Wik

Summary

Patients suffering out-of-hospital cardiac arrest needs early cardiopulmonary resuscitation
(CPR) and defibrillation in order to prevent ischemic organ damage and death. Longer chest
compression pauses during resuscitation are associated with lower survival rates.

In this thesis Steinberg et al studied the connection between chest compressions and defibrillation with focus on minimizing chest compression pauses, optimizing defibrillation outcome during mechanical chest compressions, and the combination of mechanical CPR and active decompression (AD). Electronic defibrillator data from an RCT comparing manual and mechanical CPR were retrospectively studied in paper I and II, and paper III was based on an experimental RCT on pigs with cardiac arrest.

When a cardiac rhythm was confirmed shockable early in the CPR cycle, it stayed shockable after a period of chest compressions in the great majority of instances, but some patients regained spontaneous circulation. If one were to not reverify a shockable rhythm before defibrillation one poses the risk of shocking a beating heart back to cardiac arrest.

When mechanical CPR and defibrillation occurred at the same time, defibrillation success was lower when the shock was delivered in the compression phase of the mechanical chest compression cycle compared to shocks delivered in a chest compression pause. This might be explained by how chest compressions distort the intrathoracic anatomy. Defibrillation should not be delivered in the compression phase of mechanical chest compressions.

When AD CPR to 2 cm above anatomical chest level was delivered by a modified mechanical chest compression device, both cardiac output, carotid artery blood flow and brain blood flow increased compared to regular mechanical chest compressions in a porcine model of Cardiac arrest. AD produced a high number of injuries, some of which can be explained by pig anatomy and some by the attachment of the mechanical chest compression device.

Additional information

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Published Dec. 7, 2018 12:13 PM - Last modified Dec. 7, 2018 12:13 PM