Abstract
We did not observe high values of cardiac markers and changes in central hemodynamic parameters in patients with acute gastrointestinal bleeding (AGIB) and a correlation between them, this led to the decision to conduct a study. Clinical materials of 457 patients diagnosed with GIB were analyzed. Cardiac pathology was detected in 150 patients. Dynamic changes in cardiac biomarkers and central hemodynamic indicators in patients were studied in 3 stages. Phase I, period included in ICU; Stage II - 24 hours after admission to the ICU; the third stage covers the next 48 hours. The concentration troponin, BNP, myoglobin and CK-Mb was studied in the patients and it was found that although the concentration of these biomarkers was high in the first stage, these concentrations decreased and reached normal levels in the later stages of the dynamics against the background of the treatment. Dynamic changes of central hemodynamic indicators (CHI): stroke volume, cardiac minute volume, peripheral vascular resistance and myocardial oxygen demand were studied in 3 stages. It was found that although SV was low, it dynamically increased in the later stages and did not reach the normal level. This is a clear example of continued hypovolemia. Peripheral vascular resistance (PVR) from blood loss from the gastrointestinal tract was greater than normal in all three phases. PVR remained high and was statistically honest because the volume of circulating blood was not fully corrected despite the treatments. Also, the correlation between central hemodynamic indicators and cardiac markers was studied, showing that in stage I, there is a strong contrast between CMV and CK-MB; Strong straight between PVR and BNP; In stage II, strong contrast between CMV and BNP; Strongly flat between PVR and CK-MB; In stage III, the average level is between CMV and myoglobin; We proved that there is a moderate inverse correlation between PVR and cTn and it is statistically honest. Thus, although CHI was slightly less than the norm in the initial period, it normalized in the later stages, but PVR remained high in all stages. This caused a sharp increase in PVR as a compensatory response to the decrease in circulating blood volume during acute GIB. Among the cardiac markers, we associate the rise of troponin during the bleeding period with damage to postanemic, hypoxic myocardial muscles. Among the cardiac markers, a sharp increase in BNP is an indicator of the development of left ventricular failure and is associated with a sharp increase in PVR, and we also proved that there is a strong direct relationship between them.
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