Hyperoxia Before and After Cardiac Arrest and Myocardial Damage

University Hospital Bispebjerg and Frederiksberg163 enrolled

Overview

Several studies show how patients with hyperoxia after cardiac arrest has increased mortality, but the association of hyperoxia before cardiac arrest and myocardial damage has never been investigated. Neither has the association between hyperoxia after cardiac arrest and myocardial injury. Our research hypothesis is that hyperoxia before cardiac arrest aggravates myocardial damage, secondly we wish to analyze the association between hyperoxia after cardiac arrest and myocardial injury. The exposure variables is oxygenation within 48 hours before and 48 hours after cardiac arrest, our primary outcome is myocardial damage and will be measured as peak troponin within 30 days after cardiac arrest.

Study Type

OBSERVATIONAL

Enrollment

163

Conditions

Cardiac Arrest

Interventions

OxygenationOTHER

Oxygenation measured as oxygen supply and saturation before cardiac arrest, and oxygenation measured as PaO2 after cardiac arrest.

Eligibility

Medical Language ↔ Plain English

Inclusion Criteria: * 18 years or older * With a record of ICD-10 diagnosis of cardiac arrest in 2014, admitted to a hospital in the Capital Region of Denmark. * First recorded cardiac arrest in 2014 * Admitted to ICU * Serum troponin measured within 7 days after cardiac arrest Exclusion Criteria: * Out of hospital cardiac arrest, OHCA * In of hospital cardiac arrest, IHCA, but with no registered saturation before cardiac arrest.

Outcomes

Primary Outcomes

Peak troponin within 30 days after cardiac arrest

Troponin measurements on patients after cardiac arrest.

Time frame: 30 days

Secondary Outcomes

30-day and 1-year mortality

Time frame: Up to 1 year.

Troponin area under the curve within 3 days after cardiac arrest

Time frame: 3 days

Length of ICU stay after cardiac arrest

Time frame: through study completion,on average of 4-8 weeks.

Length of hospital stay after cardiac arrest