Cardiac troponins are specific biomarkers of myocardial injury. Elevated cardiac troponin has long been considered to be a specific hallmark of myocardial infarction. Increasing evidence of myocardial injury in the absence of coronary artery disease has led to the need to review the classification of myocardial injury and infarction, as nonischemic causes have been clearly observed as being able to raise cardiac troponin levels as well. Cardiac troponin elevation is a frequent finding in patients with respiratory diseases such as pneumonia, acute respiratory distress syndrome, sepsis, acute exacerbation of chronic obstructive pulmonary disease, pulmonary hypertension and pulmonary embolism. Several different mechanisms have been proposed to explain this phenomenon including an oxygen supply and demand mismatch, inflammation - induced coronary plaque rupture and subsequent myocardial necrosis, right ventricular dysfunction, subendocardial ventricular ischemia, direct myocarditis as well as previously undiagnosed coronary artery disease. However, regardless of the underlying etiology, elevated cardiac troponin in respiratory disease is associated with increased disease severity, risk of complicated hospital stay, need for cardiac interventional procedures, as well as increased fatal outcome. The measurement of cardiac troponin poses significant usefulness in the management of severe respiratory disease and therefore should be considered as routine for patients admitted on account of acute respiratory disease. This would help in early identification of myocardial injury and categorization of more at-risk patients, in order to allow for more aggressive and targeted therapy and by doing so, improve outcomes.