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Chapter: Medical Physiology: Hemostasis and Blood Coagulation

Thromboembolic Conditions in the Human Being

Thrombi and Emboli. An abnormal clot that develops ina blood vessel is called a thrombus.

Thromboembolic Conditions in the Human Being

Thrombi and Emboli. An abnormal clot that develops ina blood vessel is called a thrombus. Once a clot has developed, continued flow of blood past the clot is likely to break it away from its attachment and cause the clot to flow with the blood; such freely flowing clots are known as emboli. Also, emboli that originate in large arteries or in the left side of the heart can flow peripherally and plug arteries or arterioles in the brain, kidneys, or elsewhere. Emboli that originate in the venous system or in the right side of the heart gen-erally flow into the lungs to cause pulmonary arterial embolism.

Cause of Thromboembolic Conditions. The causes of throm-boembolic conditions in the human being are usually twofold: (1) Anyroughened endothelial surface of avessel—as may be caused by arteriosclerosis, infection,or trauma—is likely to initiate the clotting process. (2) Blood often clots when it flows very slowly through blood vessels, where small quantities of thrombin and other procoagulants are always being formed.

Use of t-PA in Treating Intravascular Clots. Geneticallyengineered t-PA (tissue plasminogen activator) is available. When delivered directly to a thrombosed area through a catheter, it is effective in activating plasminogen to plasmin, which in turn can dissolve some intravascular clots. For instance, if used within the first hour or so after thrombotic occlusion of a coronary artery, the heart is often spared serious damage.

Femoral Venous Thrombosis and Massive Pulmonary Embolism

Because clotting almost always occurs when blood flow is blocked for many hours in any vessel of the body, the immobility of patients confined to bed plus the practice of propping the knees with pillows often causes intravascular clotting because of blood stasis in one or more of the leg veins for hours at a time. Then the clot grows, mainly in the direction of the slowly moving venous blood, sometimes growing the entire length of the leg veins and occasionally even up into the common iliac vein and inferior vena cava. Then, about 1 time out of every 10, a large part of the clot disengages from its attachments to the vessel wall and flows freely with the venous blood through the right side of the heart and into the pulmonary arteries to cause massive blockage of the pulmonary arteries, called massive pulmonary embolism. If the clot is large enough to occlude both of the pulmonary arteries at the same time, immediate death ensues. If only one pulmonary artery is blocked, death may not occur, or the embolism may lead to death a few hours to several days later because of further growth of the clot within the pulmonary vessels. But, again, t-PA therapy can be a lifesaver.

Disseminated Intravascular Coagulation

Occasionally the clotting mechanism becomes acti-vated in widespread areas of the circulation, giving rise to the condition calleddisseminated intravascularcoagulation. This often results from the presence oflarge amounts of traumatized or dying tissue in the body that releases great quantities of tissue factor into the blood. Frequently, the clots are small but numer-ous, and they plug a large share of the small periph-eral blood vessels. This occurs especially in patients with widespread septicemia, in which either circulat-ing bacteria or bacterial toxins—especially endotox-ins—activate the clotting mechanisms. Plugging ofsmall peripheral vessels greatly diminishes delivery of oxygen and other nutrients to the tissues—a situation that leads to or exacerbates circulatory shock. It is partly for this reason that septicemic shock is lethal in 85 per cent or more of patients.

A peculiar effect of disseminated intravascular coagulation is that the patient on occasion begins to bleed. The reason for this is that so many of the clotting factors are removed by the widespread clot-ting that too few procoagulants remain to allow normal hemostasis of the remaining blood.

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