Risk Factors, Diagnosis, Pathophysiology and Management of Pulmonary Embolism
Abstract:
Pulmonary embolism is a relatively common acute cardiovascular disorder with high early mortality rates. Prolonged immobility, advanced age, postoperative period, post-infarction period, heart failure, obesity and pregnancy are common risk factors for thromboembolic disease via venous stasis. The pathophysiology and clinical manifestations of pulmonary embolism based upon four main factors such as a) the extent of occlusion of the vascular tree and the size of the emboli; b) the patient’s pre-existing cardiopulmonary condition; c) chemical vasoconstriction due to the secretion of serotonin and thromboxane from platelets that adhere to the embolus, as well as to fibropeptide B, which is a product of fibrinogen breakdown; and d) the reflex vasoconstriction that is likely to occur as a consequence of pulmonary artery dilatation. The cornerstone therapy for pulmonary embolism is prevention of new embolic episodes with anticoagulant treatment or a filter in the inferior vena cava, since it has been resulted that the majority of patients do not die from the embolism that leads to diagnosis, but to the continuing deterioration of their condition due to new emboli. Anticoagulant therapy can be classified into two overlapping phases. The first is treatment of the presenting episode of pulmonary embolism, which takes about three months. The second, which is optional, is extended therapy designed to inhibit new episodes of venous thromboembolism. Standard primary therapy is with subcutaneous low molecular weight heparin, fondaparinux, or unfractionated heparin, or intravenous unfractionated heparin.
