[Identification and diagnosis of myocardial damage and acute myocardial infarction during cardiopulmonary resuscitation].

OBJECTIVE: To observe the change in contents of creatine kinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI) in peripheral blood, the elevation of ST in electrocardiogram, and the result of coronary arteriography, to identify myocardial damage and acute myocardial infarction during cardiopulmonary resuscitation (CPR).

METHODS: Twenty-six patients with sudden cardiac arrest received CPR, and those patients who had blood circulation maintained for over 24 hours were included. The expression of CK-MB and cTnI activation in peripheral blood were determined at 0, 4, 8, 12, 16 and 20 hours after CPR in all patients. Electrocardiogram was checked every 2 hours in all patients. If CK-MB, cTnI and ST segment of electrocardiogram was higher than usual, or myocardial infarct with suspicious elevation of ST (STEMI), coronary arteriography and interventional therapy were carried out immediately. Patients were divided into three groups. The patients who were not found to have coronary artery block were classified as group A (15 cases), those who were found to have coronary artery block were group B (6 cases), and the remaining patients in whom ST segment of electrocardiogram did not elevate, and coronary arteriography and interventional therapy were not consider were classified as group C (5 cases). Control group consisted of 15 healthy people (group D). The change in CK-MB and cTnI in peripheral blood and the elevation of electrocardiogram ST segment were analyzed.

RESULTS: In group A, CK-MB level began to elevate at CPR 4 hours, and it peaked at CPR 12 hours. cTnI began to raise at CPR 4 hours, peaking at CPR 16 hours, then decreased gradually. Elevation of ST was seen in more than two leads in electrocardiogram at the beginning of restoration of spontaneous circulation (ROSC), then lowered quickly, and the decrease exceeded 50% of the elevation at ROSC 2 hours. In group B, the levels of CK-MB and cTnI began to increase at CPR 4 hours, and remained elevated at CPR 20 hours. ST segment was elevated in more than two leads in electrocardiogram at the beginning of ROSC, and remained elevated after ROSC 2 hours. In group C, the CK-MB and cTnI concentrations were increased 4 hours after successful CPR, and reached peak at CPR 12, 16 hours respectively, then they decreased. ST segment of electrocardiogram was not elevated. In group D, the CK-MB and cTnI concentration was in the normal range. ST segment of electrocardiogram was not elevated.

CONCLUSION: All patients manifested myocardial damage after CPR. Some patients showed STEMI after CPR. CK-MB and cTnI concentrations increased gradually after successful CPR without specificity for earlier identification of myocardial damage and STEMI. It is necessary to find a new reliable marker to check for myocardial damage. Relatively speaking, elevation of the ST segment in electrocardiogram has more predictive value. A decrease exceeds 50% of the elevation of ST segment in electrocardiogram at ROSC 2 hours, or the peak of contents of CK-MB and cTnI appear at CPR 12 hours or 16 hours indicates myocardial damage. If the elevation of ST segment does not descend after ROSC 2 hours, or the levels of CK-MB and cTnI remain elevated at CPR 20 hours, STEMI should be suspected, and it is necessary to undertake interventional therapy or thrombolysis therapy.