Pulmonary embolism : A pulmonary embolism is a blockage in the pulmonary artery, which is the blood vessel that carries blood from the heart to the lungs. Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities; however, they rarely also originate in the pelvic, renal, or upper extremity veins or the right heart chambers. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis.
Drug therapy choices include Unfractionated heparin, Low-molecular-weight heparin, Factor Xa Inhibitors, Fondaparinux, Warfarin, Alteplase, Reteplase, Urokinase and Streptokinase.
Venous Thrombo Embolism : DEFINITION
Thrombosis – process of pathological clot (thrombus) formation.
Embolism – process whereby the clot or a piece of it breaks off and travels through the circulation until progress is obstructed by vessels of smaller diameter.
• Venous thrombi – “red clots” predominantly red cells in a fibrin mesh.
• Arterial thrombi - “white clots” in which platelets and fibrin are major features.
PATHOPHYSIOLOGY
The intact endothelial lining of the blood vessels normally repels platelets and inhibits clot formation through secretion of numerous inhibitory substances. Damage to this endothelium leads to exposure of circulating blood to substances, and this results in complex series of events, including platelet adhesion, activation ,and aggregation, followed by activation of clotting cascade. These events result in formation of fibrin clot. After endothelial damage, blood exposes to sub endothelial collagen and phospholipids, resulting in platelet adhesion to the surface. VonWillebrand factor serves as the binding ligand for platelet adhesion,via the glycoprotein I receptor on the platelet surface. Adhered platelets become activated and release numerous compounds,including adenosine diphosphate and thrombaxane A2 which stimulate platelet aggregation. Fibrinogen serves as binding ligand for platelet aggregation,viatheGPIIb/IIIa receptor on the platelet surface. Once stimulated, both the extrinsic and intrinsic pathways activate the common pathway of clotting cascade via factor10. Activated forms of factor 5 and 8 serve independently to accelrate this process. The final step includes, conversion of factor 2 to factor 2a with eventual formation of a stable fibrin clot. Naturally occuring inhibitors of clotting factors play a role in localizing fibrin formation to the sites of injury and in maitaining the fluidity of circulating blood .In addition, the fibrinolytic system is involved in degradation of fibrin clots. The actions of both clotting inhibitors and the fibrinolytic system prevent excessive coagulation.thus the process of clot formation is dynamic and involves various factors tht can stimulate ,inhibit, and dissolve a fibrin clot.
Pathologic thrombi some times are classified according to location and composition. They are:
1) Arterial thrombi(in artery):is called white thrombus consist mainly of platelets and leucocytes in fibrin mesh usually associated with atherosclerosis. Intercepts blood flow causing ischemia/death beyond.
2) Venous thrombi(in vein):is called red thrombus and consist of small white head and a large jelly like red tail similar to blood clot ,which streams away in the flow. Thrombus can break away, forming an embolus. This may lodge in lungs or, if it comes from the left heart/carotid artery, in brain or other organ, causing death/other disaster.
?Increased coagulability of blood can be inherited and referred as thrombofilia