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
M. Mullner et al., 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, RESUSCITAT, 38(2), 1998, pp. 99-105
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.