The body of patient undergoing cardiopulmonary resuscitation after cardiac arrest experiences a process of ischemia, hypoxia, and reperfusion injury. This state of intense stress response is accompanied with hemodynamic instability, systemic hypoperfusion, and subsequent multiple organ dysfunction, and is life-threatening. Pulmonary vascular endothelial injury after cardiopulmonary resuscitation is a pathological manifestation of lung injury in multiple organ injury. Possible mechanisms include inflammatory response, neutrophil infiltration, microcirculatory disorder, tissue oxygen uptake and utilization disorder, etc. Neutrophils can directly damage or indirectly damage lung vascular endothelial cells through activation and migration activities. They also activate the body to produce large amounts of oxygen free radicals and release a series of damaging cytokines that further impaire the lung tissue.