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

Phase 2RecruitingNCT06744361

Christian Hassager282 enrolled

Overview

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.

Study Type

INTERVENTIONAL

Allocation

RANDOMIZED

Purpose

TREATMENT

Masking

QUADRUPLE

Enrollment

282

Conditions

Out-of-hospital Cardiac Arrest (OHCA)

Interventions

Eligibility

Sex: ALLMin age: 18 Years

Medical Language ↔ Plain English

Inclusion Criteria: * Adults (age ≥18 years) AND * resuscitated OHCA of presumed cardiac cause with a shockable first recorded heart rhythm AND * mean arterial pressure (MAP) \>40 mmHg AND * a decision to perform prehospital intubation. Exclusion Criteria: * Advanced life support termination-of-resuscitation (TOR) criteria met * Systolic blood pressure \>190 mmHg * Known allergy to ketamine or propofol * Chronic diseases making 180-day survival unlikely * Body temperature \<30° C.

Outcomes

Primary Outcomes

Neuron-specific enolase (NSE) measured 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

Time frame: 48 hours after OHCA

Secondary Outcomes

Death from any cause

Death from any cause 180 days after cardiac arrest

Time frame: 180 days after cardiac arrest

Neurological outcome: modified Rankin Score (mRS)

Neurological outcome by and modified Rankin Score (mRS). Meassured from 0 to 6, where 0 is no symptoms.

Time frame: At 2 weeks (at discharge)

Neurological outcome: Cerebral Performance Categories (CPC)

Neurological outcome by Cerebral Performance Categories (CPC) meassured fra 1-5 (a score of 1 is normal/good cerebral function).

Time frame: At 2 weeks (at discharge)

Neurological outcome: modified Rankin Score (mRS)

Neurological outcome by and modified Rankin Score (mRS). Meassured from 0 to 6, where 0 is no symptoms.

Time frame: At 180 days after OHCA.

Neurological outcome: modified Rankin Score (mRS)

Neurological outcome by and modified Rankin Score (mRS). Meassured from 0 to 6, where 0 is no symptoms.

Time frame: At 240 days after OHCA.

Neurological outcome: Cerebral Performance Categories (CPC)

Neurological outcome by Cerebral Performance Categories (CPC) meassured fra 1-5 (a score of 1 is normal/good cerebral function).

Time frame: At 180 days after OHCA.

Neurological outcome: Cerebral Performance Categories (CPC)

Neurological outcome by Cerebral Performance Categories (CPC) meassured fra 1-5 (a score of 1 is normal/good cerebral function).

Time frame: At 240 days after OHCA.

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

Overview

Conditions

Interventions

Eligibility

Locations (2)

Outcomes

Primary Outcomes

Secondary Outcomes

Central Contacts