Sepsis is life-threatening multi-organ dysfunction caused by a dysregulated immune response to an infectious cause. Sepsis and septic shock are major healthcare problems, affecting millions of people around the world. Early recognition and appropriate management in the initial phases of sepsis improve outcomes.

The difference between arterial carbon dioxide tension (PaCO2) and ETCO2 is shown to correlate with the physiologic dead space (VD/VT), which is normally 3–5 mmHg in healthy adults. Higher value of arterial to end tidal CO2 difference has been found to predict worse outcomes in trauma and respiratory distress patients. Sepsis can be associated with myocardial depression and changes in total peripheral vascular resistance , Acute respiratory distress syndrome (ARDS) and respiratory failure irrespective of aetiology of sepsis. Septic encephalopathy, with its associated reduction in respiratory drive, appears outcomes. Thus reduced cardiac output, diminished respiratory drive, impaired alveolar ventilation with arteriovenous shunting and/or sepsis related ARDS may act in isolation or together manifesting  as an increased arteriolar- end tidal CO₂  gap and thus predict

reduced survival and increased need for intensive care support in patients with sepsis. 

In this study we intend to evaluate arterial to end tidal carbon dioxide difference as predictor of mortality and morbidity in patients with suspected sepsis. We also extend our study to find the correlation between arteriolar - end tidal CO2 gap and already established prognostic markers of sepsis like Lactate level, capillary refill time and Sequential Organ Failure Assessment Score (SOFA).