- Poster presentation
- Open Access
Heart dysfunction evaluated by troponin, stroke work analysis and QT dispersion can predict outcome in patients with septic shock
© BioMed Central Ltd 2006
- Published: 21 March 2006
- Septic Shock
- Pulmonary Artery Catheterization
- Myocardial Depression
- Heart Dysfunction
- High Cardiac Output
Sepsis is the leading cause of mortality in ICUs. The mortality rate approaches 29%. As far as the heart is concerned, adequately volume-resuscitated patients in septic shock present a hyperdynamic circulatory state with high cardiac output and reduced systemic vascular resistance, and this profile seems to persist throughout the septic event regardless of the outcome. Myocardial depression in patients with septic shock is characterized by biventricular dilatation and decreased systolic contractile function, all in the presence of an overall hyperdynamic circulation. In addition, sepsis and septic shock is characterized by an impaired sympathetic modulation of the heart, suggesting that a central autonomic regulatory impairment contributes to the circulatory failure that is seen. The purpose of this study was to analyze echocardiographic, ultrasonographic, hemodynamic and serum cardiac markers in patients with septic shock and to evaluate their relationship to the outcome.
Prospective study on a six-bed ICU of a university hospital and a five-bed medical ICU of a tertiary care hospital. Data were collected over a period of 2 years. We studied 68 septic patients that met the ACCP/SCCM consensus criteria for sepsis and septic shock. All patients had continuous monitoring of blood pressure (BP) and heart rate (HR). Blood samples were collected on the first day of the septic shock and on days 3, 5, 7, and 10, and were analyzed for troponin, CPK, CK-MB, SGOT, SGPT, and LDH. Pulmonary artery catheterization was performed in all patients and the results were recorded for the days in question. Cardiac ultrasonography and echocardiography was also performed on the aforementioned days. Measurements of the patients' QT intervals on a 12-lead electrocardiogram (ECG) were also made. The QT interval was corrected (QTc) using the heart rate according to the Bazett's formula. The QT dispersion (QT-d) was defined as the difference between the maximum and the minimum value of the QTc in different leads. QT-d was measured and recorded for all the aforementioned days.
The patients were divided into survivors and nonsurvivors. We had 28 patients in the nonsurvivor group and 40 patients that recovered from their septic shock. The mortality rate was approximately 41%. The APACHE II scores for both groups were similar with no significant difference during the study. A hyperdynamic circulatory state with high cardiac output and low vascular resistance was observed throughout the study, and no significant difference was shown in any of the patients in either group. All the serum cardiac markers except troponin showed no significant difference. Troponin and stroke work analysis, however, showed a significant difference between the two groups. Troponin levels showed a significant difference from day 1 of the study and continued to the end, whereas the stroke work analysis difference became evident from day 5 and onwards. The QT-d measured from the ECG on days 1 and 3 were significantly increased especially in the nonsurvivor group (49 ± 20 ms vs 34 ± 11 ms). QT-d measurements of the following days had similar patterns to day 3 in either group.
Heart dysfunction was evident by the troponin serum values, by the QT-d and by the hemodynamic stroke work analysis. All these variables presented a significant difference between survivors and nonsurvivors during the study. The establishment of heart dysfunction seems to correlate to patient outcome.