Hypertonic lactate infusion reduces vasopressor requirement and biomarkers of brain and cardiac injury after experimental cardiac arrest

Introduction Prognosis after resuscitated cardiac arrest (CA) remains poor with high morbidity and mortality due to extensive cardiac and brain injuries and the lack of effective treatments. Hypertonic sodium lactate (HSL) could be beneficial after CA by buffering severe metabolic acidosis, increasing brain perfusion and cardiac performance, reducing cerebral swelling, and serving as alternative energetic cellular substrate. The aim of this study was therefore to test the effects of HSL infusion on brain and cardiac injury in an experimental model of CA. Methods After a 10-min electrically induced CA followed by 5 min of cardiopulmonary resuscitation maneuvers, adult swine (n=35) were randomly assigned to receive either balanced crystalloids (controls, n=11) or HSL infusion, either starting during cardiopulmonary resuscitation (CPR, Intra-arrest, n=12) or after return of spontaneous circulation (Post-ROSC, n=11) for the following 12 hours. In all animals, extensive multimodal neurological and cardiovascular monitoring was implemented. All animals were treated with target temperature management at 34°C. Results 34 out of 35 (97.1%) animals achieved ROSC and one animal in the Intra-arrest group deceased before completing the observation period. Arterial pH, lactate, sodium concentrations and plasma osmolarity were higher in treated animals then in controls (p<0.001), while potassium concentrations were lower (p=0.004). HSL infusion either Intra-arrest or Post-ROSC improved hemodynamic compared to controls, as shown by reduced vasopressors need to maintain mean arterial pressure target above 65 mmHg (p=0.005 for interaction; p=0.01 for groups). Moreover, plasmatic troponin-I levels and glial fibrillary acid protein (GFAP) concentrations were lower in treated groups at several time-points than in controls. Conclusions In this experimental CA model, HSL infusion was associated with reduced vasopressor requirements and decreased plasmatic levels of biomarkers of cardiac and cerebral injury.