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Abstract The cardiopulmonary bypass machine supports the respiratory and circulatory functions of the body while surgery is being performed upon the heart. The basic cardiopulmonary bypass circuit consists of oxygenator, pump and reservoir which are connected by tubes for the purpose of converting the patient’s low pressure, venous blood into “arterialized” blood and returning it to the arterial system of the patient. It has been recognized that CPB is associated with a systemic inflammatory response, and occasionally leads to major organ dysfunction. This has been termed post-pump syndrome, however; the exact mechanisms involved in PD following CPB have not yet been fully clarified. Recent researches have underlined importance of some of the humoral and cellular mechanisms involved. Neutrophils, monocytes, and macrophages undergo activation resulting in local and systemic secretion of humoral inflammatory mediators. On the humoral level activation of complement, secretion of cytokines, and the production of surface adhesion molecules result in activation of neutrophils and macrophages which in turn resulting in further secretion of enzymes such as proteases and oxygen free radicals which induce direct lung injury. When endothelial cells are activated by cytokines, complement and ischemia-reperfusion, they begin to produce surface adhesion molecules which help further adhesion and activation of neutrophils. This pathophysiological process leads to disruption of endothelial and epithelial integrity, and allows albumin, plasma and activated neutrophils to enter the interstitial and alveolar space causing tissue edema and reducing pulmonary compliance and blood oxygenation. Physiological disturbance in the lungs can be categorized grossly into abnormal gas exchange and poor lung mechanics. Histological changes on the microscopic level include injury of alveolar epithelium, and pulmonary endothelium with extravasation of fluid rich in protein, neutrophils and other cellular elements resulting in interstitial pulmonary edema. There are also a various biochemical changes reflecting the presence of lung injury after CPB. A number of different strategies have been employed during the last few years in attempt to minimize the impact of lung injury on the outcome of cardiac surgical patients. Technical modification in CPB machine itself such as the usage of heparin coated circuits, leucocyte depletion, ultrafiltration, usage of new membrane oxygenators hypothermia and strict fluid mangment. Mechanical ventilation during CPB used to ensure adequate gas exchange, using lower tidal volume, higher level of PEEP and high frequency oscillatory ventilation. Inhaled therapies were used as direct therapy to avoid systemic side effects like NO, prostacyclin and exogenous surfactant. Role of genetic study and immunophenotyping of individuals represent the promising future to patients with ALI. |