Myocardial cell injury in septic shock
© BioMed Central Ltd 2003
Published: 3 March 2003
To determine the presence of otherwise undetected myocardial cell injury in patients with septic shock using daily eletrocardiographics, and bidimensional echocardiography, serum troponin I (cTN I) and serum C-reactive protein (when electrocardiographic evidence of acute myocardial infarction).
Prospective observational study.
Intensive care unit (ICU) of a tertiary institution.
Twenty-eight consecutive patients with sepsis or septic shock.
Daily collection of blood for the measurement of cTN I serum levels. Cineangiography when necessary. Illness severity assessment and collection of demographic data.
Measurements and main results
Twenty-eight patients were studied for a mean period in the ICU of 17.2 days (range, 3–37 days). All 10 patients who died in the intensive care unit had elevated levels of cTN I, mean 21.9 ng/ml (range, 2.9–94.1). Survivors tended to lower levels of cTN I than nonsurvivors in septic shock, mean 12.4 ng/ml (range 0.5–57.0). All five patients who had abnormal cineangiography had elevated levels of cTN I, mean 38.4 ng/ml (range, 5.4–94.1), while normal cineangiography had cTN I mean 9.1 ng/ml (range, 0.5–27.8). The difference between serum C-reactive protein and cTN I or mortality failed to reach statistical significance. No patient had electrocardiographic evidence of acute myocardial infarction, although, on admission, five patients had left bundle branch patterns, two patients had right bundle branch patterns and two had evidence of an atrial fibrillation. Seventeen cardiac catheterizations were done and five were abnormal correlating to abnormalities of the ecochardiogram. Three patients used intraaortic baloon pumping in a period of time up to 6 days (mean 3 days).
Myocardial cell injury (cardiac dysfunction) appears to be common in patients with septic shock but does not correlate with coronary artery disease. It seems to be an imbalance between oxygen delivery and consumption.