The pulmonary vascular bed mechanically retains the solid particles in physiological conditions enter the venous system. When they are oversized or very heavy, there is a known pathological vascular occlusion stroke. The materials can be embolized clots of venous thrombosis detached fragments of bone marrow that enter the blood in fractures of long bones, cells and debris of amniotic fluid, and so on. Being the most frequent thrombotic embolism, which is discussed below.
Venous thrombosis is favored by three factors that were identified by Virchow in the last century:
1. venous stasis: produced by congestive heart failure, venous insufficiency, limb immobilization, bed rest, obesity, pregnancy;
2. intimal damage from trauma, burns, local surgery, infections;
3. increased coagulability: postpartum period, major surgery, cancer, contraceptive use, polycythemia vera, hypercoagulability syndromes (deficiency of protein C and S, and antithrombin III, resistance to activated protein C, antiphospholipid syndrome and hyperhomocysteinemia).
Pathophysiology
The effects of pulmonary embolism are primarily respiratory and hemodynamic.
Respiratory effects. The main consequences of acute respiratory embolism are fourfold increase in alveolar dead space, bronchoconstriction, tachypnea and hypoxemia. More lately may have regional loss of surfactant and pulmonary infarction.
The immediate consequence of arterial occlusion is an increase in alveolar dead space as continuously ventilated alveoli without perfusion. If the occlusion is not complete, there will be insufficient perfusion for the degree of ventilation, creating an area in which the relationship V / Q is high. Neither alterations cause hypoxemia. Another constant is change very tachypnea, with a slight increase in tidal volume, probably due to stimulation of J receptors altered land, producing hyperventilation, with mild or moderate fall in PaCO2.
It is common but not constant, the presence of hypoxia, which is attributed to several mechanisms:
1. excess alveolar perfusion territories unaffected by shunting of blood from occluded areas. This mechanism determines the appearance of areas with V / Q low and becomes more significant if the lung was not damaged by the stroke has damaged;
2. reduced cardiac output due to right heart failure, which increases peripheral oxygen extraction decreases the O2 content of venous blood returning to the lung and magnifies the effect of areas with V / Q low;
3. intra-or extrapulmonary shunt frequently observed and due to edema, alveolar collapse or opening of the foramen ovale, by increased right atrial pressure, with anatomic shunt from right to left. This latter phenomenon is only active when there is high pulmonary hypertension.
Hemodynamic effects. The mechanical reduction of mild to moderate vascular bed does not significantly modify the resistance of the pulmonary circuit, but when it exceeds 50% there is a sudden increase in resistance and pressure. When mechanical plunger factor plus vasoconstrictor effect of amines released by the platelet thrombus. If the blockage exceeds 60 to 75% of the pulmonary circulation, pulmonary heart elicits a sharp, sudden decrease in cardiac output. In this case the pulmonary circuit pressure longer reflects the magnitude of the embolic event, because the fall in cardiac output is accompanied by a reduction in pulmonary artery pressure. The increased afterload of the right ventricle increases its requirement of O2, which is critically dependent on coronary perfusion. Therefore, if spending is reduced systemic right ventricular ischemia may occur, the greater drop in spending and arrhythmias.
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