> Sepsis is life threatening organ dysfunction caused by a dysregulated host response as a consequence of an infection.Sepsis followed by septic shock is a leading cause of mortality in intensive care unit . Despite recent advances in the management, mortality has remained high.

>Myocardial dysfunction was shown to be common in patients of sepsis and septic shock. The use of cardiac biomarkers is not included in the decision making of sepsis.

>Cardiac dysfunction, referred to as Sepsis Induced Myocardial dysfunction (SIMD), is a loosely defined syndrome and presents in various ways , such as myocardial injury with cardiac biomarker elevation, myocardial dysfunction on echocardiography and haemodynamic instability. SIMD is a common complication (40-60%) which could possibly be result of increased circulating catecholamine and cytokine levels in severe sepsis and septic shock and its presence worsens the outcome significantly.[6]

>SIMD may involve either the left ventricle , right ventricle or both .This may manifest as systolic dysfunction,LV diastolic dysfunction , RV dysfunction , global hypokinesia or regional wall motion abnormalities. Early recognition , aggressive supportive therapy  and appropriate catecholamine regimen are mandatory in order to improve survival.

>The Cardiac Troponin complex – consisting of troponin C, troponin T and troponin I is involved in the regulation of cardiac muscle contraction.The regulatory role of cardiac troponin I consists of inhibition of adenosine 5’-triphosphatase(ATPase) activity of the actomyosin complex and modulation of cross-bridge formation and cardiac muscle contraction.

>Troponin I is exclusively of cardiac origin. It is sensitive and specific biomarker of myocardial damage and is related to prognosis in non – acute coronary syndromes such as pulmonary embolism , trauma , stroke and subarachnoid haemorrhage .  Recent studies have demonstrated that cardiac troponin release in sepsis is associated with poor outcomes , including higher mortality and longer length of stay in ICU. Theories for troponin elevation in septic shock include inflammation , increased myocardial stress by volume overload, toxicity by medications and kidney dysfunction.

  >New generation of  High sensitivity Troponin I assays has been recently been developed that allow the detection of concentrations 10 times lower than those measurable with conventional assays.

>We will estimate the High Sensitivity Troponin I assay values occurring due to effect  of sepsis on myocardium and correlate these with SOFA score to evaluate the predictive value of this assay in outcome of sepsis.

Hypothesis Testing

 Null Hypothesis : There is no correlation between HS-Troponin I values and severity of sepsis.

 Alternate Hypothesis : There is positive correlation between HS-Troponin I values and severity of sepsis.