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Hyperoxia Before and After Cardiac Arrest and Myocardial Damage

2019-07-10 20:05:50 | BioPortfolio

Summary

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 Design

Conditions

Cardiac Arrest

Intervention

Oxygenation

Location

Bispebjerg Hospital
Copenhagen
Denmark
2400

Status

Recruiting

Source

University Hospital Bispebjerg and Frederiksberg

Results (where available)

View Results

Links

Published on BioPortfolio: 2019-07-10T20:05:50-0400

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Medical and Biotech [MESH] Definitions

Occurrence of heart arrest in an individual when there is no immediate access to medical personnel or equipment.

The omission of atrial activation that is caused by transient cessation of impulse generation at the SINOATRIAL NODE. It is characterized by a prolonged pause without P wave in an ELECTROCARDIOGRAM. Sinus arrest has been associated with sleep apnea (REM SLEEP-RELATED SINUS ARREST).

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The artificial substitution of heart and lung action as indicated for HEART ARREST resulting from electric shock, DROWNING, respiratory arrest, or other causes. The two major components of cardiopulmonary resuscitation are artificial ventilation (RESPIRATION, ARTIFICIAL) and closed-chest CARDIAC MASSAGE.

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