Burn shock results from the interplay of direct tissue injury, hypovolemia, and the release of multiple mediators of inflammation, with effects on both the microcirculation and the function of large vessels, heart and lungs. Subsequently, burn shock continues as a significant pathophysiologic state, even if hypovolemia is corrected. Increases in pulmonary and systemic vascular resistance (SVR) and myocardial depression occur despite adequate preload and volume support.8–12 Such cardiovascular dysfunctions can further exacerbate the whole body inflammatory response into a vicious cycle of accelerating organ dysfunction.7,8,13 Hemorrhagic hypovolemia with severe mechanical trauma can provoke a similar form of shock.