Ketamine Sedation As Neuroprotective Agent Following Out-of-hospital Cardiac Arrest

Condition(s) studied

Investigational drug(s) / intervention(s)

esketamine hydrochloride: Prehospital intravenous or intraosseous bolus administration at a minimum of 0.5 mg/kg of esketamine

propofol: Prehospital intravenous or intraosseous bolus administration at a minimum dose of 0.25 mg/kg propofol

Study summary

OHCA is a critical medical emergency with significant mortality and morbidity primarily due to hypoxic-ischemic brain injury (HIBI). Despite advances in resuscitation techniques, the neurological outcomes for survivors remain poor. Current post-resuscitation practices lack specific neuroprotective strategies. Ketamine, an N-Methyl-D-Aspartate (NMDA) receptor antagonist, has shown potential neuroprotective properties in preclinical and clinical studies due to its ability to inhibit excitotoxicity and reduce neuronal apoptosis. This trial hypothesizes that ketamine, when used for sedation in OHCA patients, may offer superior neuroprotective benefits compared to the commonly used sedative propofol. By comparing the effects of ketamine and propofol on neuronal damage markers and long-term neurological outcomes, this study aims to identify a potentially effective intervention to improve the prognosis of OHCA patients.

Eligibility

Primary outcome measure(s)

• Neuron-specific enolase (NSE) measured 48 hours after OHCA — 48 hours after OHCA
  To determine the neuroprotective efficacy of ketamine compared with propofol administered as part of sedation for intubation after initial resuscitation from OHCA

Trial sites (2)

More Christian Hassager trials in Denmark