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 p rocedures, such as chest compressions and external defibrillation, on the r elease of creatine kinase (CK)-MB and cardiac troponin T (cTnT). Methods: I n 87 patients with out-of-hospital cardiac arrest and successful cardiopulm onary 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 even t. We also assessed whether the patient developed cardiogenic shock within 12 h, and if the patient had acute myocardial infarction (AMI), which was c onfirmed or eliminated by of typical ECG findings, thallium-201 myocardial scintigraphy, or autopsy within the hospital stay. A backward stepwise line ar regression model was applied to assess the association between the marke rs of myocardial injury (CK-MB and cTnT) and the above clinical variables. Results: CK-MB concentrations were independently associated with the presen ce of AMI [B 68.5 (SE 28.5, P = 0.018)], the duration of CPR las 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 c oncentrations were only associated with the presence of AMI [B 4.86 (SE 1.3 4, 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 mo del. Conclusion: The release of CK-MB appears to be influenced by the durat ion of resuscitation and the presence of cardiogenic shock. This has to be considered when interpreting serum CK-MB concentrations after CPR. The rele ase of cTnT seems to be only associated with acute myocardial infarction, b ut not with the duration of chest compressions, or with the number of defib rillations administered. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.