The influence of chest compressions and external defibrillation on the release of creatine kinase-MB and cardiac troponin T in patients resuscitated from out-of-hospital cardiac arrest.

OBJECTIVES

This study sought to determine the influence of resuscitative procedures, such as chest compressions and external defibrillation, on the release of creatine kinase (CK)-MB and cardiac troponin T (cTnT).

METHODS

In 87 patients with out-of-hospital cardiac arrest and successful cardiopulmonary resuscitation (CPR), the initial ECG rhythm, the duration of cardiac arrest and CPR, and the number of defibrillations were assessed on arrival in the hospital. The serum CK-MB and cTnT were measured 12 h after the event. We also assessed whether the patient developed cardiogenic shock within 12 h, and if the patient had acute myocardial infarction (AMI), which was confirmed or eliminated by of typical ECG findings, thallium-201 myocardial scintigraphy, or autopsy within the hospital stay. A backward stepwise linear regression model was applied to assess the association between the markers of myocardial injury (CK-MB and cTnT) and the above clinical variables.

RESULTS

CK-MB concentrations were independently associated with the presence of AMI [B 68.5 (SE 28.5, P = 0.018)], the duration of CPR (as a measure of trauma to the chest by means of chest compressions) [B 2.07 (SE 1.01, P = 0.045)] and cardiogenic shock [B 52.3 (SE 23.4, P = 0.03)]. The remaining clinical variables listed were excluded by the model. Cardiac troponin T concentrations were only associated with the presence of AMI [B 4.86 (SE 1.34, P = 0.0005)]. There was a non-significant association between increasing serum cTnT concentrations and the presence of cardiogenic shock [B 2.51 (SE 1.46, P = 0.09)]. The remaining clinical variables were excluded by the model.

CONCLUSION

The release of CK-MB appears to be influenced by the duration of resuscitation and the presence of cardiogenic shock. This has to be considered when interpreting serum CK-MB concentrations after CPR. The release of cTnT seems to be only associated with acute myocardial infarction, but not with the duration of chest compressions, or with the number of defibrillations administered.