Cardiac arrest is associated with a very high rate of mortality, in part due to inadequate tissue perfusion during attempts at
resuscitation. Parameters such as mean arterial pressure and end-tidal
carbon dioxide may not accurately reflect adequacy of tissue perfusion during cardiac
resuscitation. We hypothesised that quantitative measurements of tissue
oxygen tension would more accurately reflect adequacy of tissue perfusion during experimental
cardiac arrest. Using
oxygen-dependent quenching of phosphorescence, we made measurements of
oxygen in the microcirculation and in the interstitial space of the brain and muscle in a porcine model of
ventricular fibrillation and
cardiopulmonary resuscitation. Measurements were performed at baseline, during untreated
ventricular fibrillation, during
resuscitation and after return of spontaneous circulation. After achieving stable baseline brain tissue
oxygen tension, as measured using an Oxyphor G4-based phosphorescent microsensor,
ventricular fibrillation resulted in an immediate reduction in all measured parameters. During
cardiopulmonary resuscitation, brain
oxygen tension remained unchanged. After the return of spontaneous circulation, all measured parameters including brain
oxygen tension recovered to baseline levels. Muscle tissue
oxygen tension followed a similar trend as the brain, but with slower response times. We conclude that measurements of brain tissue
oxygen tension, which more accurately reflect adequacy of tissue perfusion during
cardiac arrest and
resuscitation, may contribute to the development of new strategies to optimise perfusion during cardiac
resuscitation and improve patient outcomes after
cardiac arrest.