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The English term “embolus” derives from the Greek word meaning “plug” or “stopper.” A pulmonary embolus consists of material that gains entry towards the venous program and then towards the pulmonary circulation. Eventually, it reaches a vessel whose caliber is too small to permit free passage, and there it forms a plug, occluding the lumen and obstructing perfusion.

There are lots of kinds of pulmonary emboli. The most typical is pulmonary thromboembolism, which happens when venous thrombi, chiefly from the reduce extremities, migrate to the pulmonary flow A normal function from the pulmonary microcirculation is to get rid of venous emboli. The lungs possess each excess functional capability along with a redundant vascular supply, producing them a superb filter for preventing little thrombi and platelet aggregates from attaining access to the systemic flow.

Nevertheless, large thromboemboli, or an accumulation of smaller types, can trigger substantial impairment of cardiac and respiratory function and death. Pulmonary thromboemboli are common and cause significant morbidity. They’re found at autopsy in 25-50% of hospitalized patients and are regarded a main contributing trigger of death inside a third of those. However, the diagnosis is made antemortem in only 10-20% of instances.

Etiology & Epidemiology:

Pulmonary embolism and deep venous thrombosis represent a continuum of a single disease that has been coined venous thromboembolic disease, or VTE. Thromboemboli almost never originate in the pulmonary circulation; they arrive there by traveling through the venous flow. More than 95% of pulmonary thromboemboli arise from thrombi in the deep veins of the lower extremity:

the popliteal, femoral, and iliac veins. Venous thrombosis below the popliteal veins or occurring in the superficial veins of the leg is clinically typical but not a risk factor for pulmonary thromboembolism because thrombi in these locations rarely migrate towards the pulmonary circulation without first extending above the knee.

Since fewer than 20% of calf thrombi will extend into the popliteal veins, isolated calf thrombi may be observed with serial tests to exclude extension into the deep system and do not necessarily require anticoagulation. Venous thromboses occasionally occur in the upper extremities or in the right side of the heart; this happens most commonly in the presence of intravenous catheters or cardiac pacing wires and may be of increasing clinical importance as the use of long-term intravenous catheters increases.

Risk factors for pulmonary thromboembolism are, therefore, the risk factors for the development of venous thrombosis in the deep veins from the legs (deep venous thrombosis). The German pathologist Rudolf Virchow stated these risk factors in 1856: venous stasis, injury towards the vascular wall, and increased activation from the clotting program. His observations are still valid today.

Probably the most prevalent risk factor in hospitalized patients is stasis from immobilization, especially in those undergoing surgical procedures. The incidence of calf vein thrombosis in patients who do not receive heparin prophylaxis after total knee replacement is reported to be as high as 84%; it is more than 50% after hip surgery or prostatectomy.

The risk of fatal pulmonary thromboembolism in these patients may be as high as 5%. Physicians caring for these patients must, therefore, be aware of the magnitude from the risk and institute appropriate prophylactic therapy. Malignancy and tissue damage at surgery are the two most common causes of increased activation from the coagulation system.

Abnormalities in the vessel wall contribute small to venous as opposed to arterial thrombosis. Nevertheless, prior thrombosis can damage venous valves and lead to venous incompetence, which promotes stasis. Advances now permit identification of genetic disorders in up to one third of unselected individuals with venous thrombosis and in more than half of individuals with familial thrombosis. It is now clear that these genetic variants may interact with other factors (eg, oral contraceptive use, dietary deficiencies) to increase thrombosis risk.

Pathophysiology:

Venous thrombi are composed of a friable mass of fibrin, with numerous erythrocytes along with a few leukocytes and platelets randomly enmeshed in the matrix. When a venous thrombus travels towards the pulmonary flow, it causes a broad array of pathophysiologic changes.

Hemodynamic Changes:

Every patient with a pulmonary embolus has some degree of mechanical obstruction. The effect of mechanical obstruction depends on the proportion of the pulmonary flow obstructed and the presence or absence of preexisting cardiopulmonary disease.

In individuals without preexisting cardio-pulmonary disease, pulmonary arterial pressure increases in proportion to the fraction from the pulmonary circulation occluded by emboli. If that fraction is greater than about one third, pulmonary artery pressures will rise out of the normal range and trigger right ventricular strain.

The pulmonary circulation can adapt to increased flow, but this depends on (1) recruitment of underperfused capillaries, which may not be available because of obstruction, and (2) relaxation of central vessels, which does not occur instantaneously. In patients with preexisting cardiopulmonary disease, increases in pulmonary artery pressures do not correlate with extent of embolization.

In these studies, there were relatively few individuals with both preexisting cardiopulmonary disease and extensive arterial occlusion. A correlation may be obscured by the possibility that massive emboli may either kill patients with preexisting cardiopulmonary disease or perhaps make them too unstable for angiography.

The most devastating and feared complication of acute pulmonary thromboembolism is sudden occlusion from the pulmonary outflow tract, reducing cardiac output to zero and causing immediate cardiovascular collapse and death. Large emboli that do not completely occlude vessels, particularly in patients with compromised cardiac function, may trigger an acute increase in pulmonary vascular resistance.

This leads to acute right ventricular strain along with a fatal fall in cardiac output. Such dramatic presentations occur in less than 5% of cases and are essentially untreatable. They serve to highlight the importance of primary prevention of venous thrombosis.

Changes in Ventilation/Perfusion Relationships:

Pulmonary thromboembolism reduces or eliminates perfusion distal to the site of the occlusion. The immediate effect would be to increase the proportion of lung segments with high / ratios. If there is complete obstruction to flow, then the / ratio reaches infinity.

This represents alveolar dead space. An increase in dead space ventilation impairs the excretion of carbon dioxide. This tendency is generally compensated by hyperventilation. After several hours, hypoperfusion interferes with production of surfactant by alveolar type II cells. Surfactant is depleted, resulting in alveolar edema, alveolar collapse, and areas of atelectasis.

Edema and collapse may result in lung units with small or no ventilation. If there is perfusion to these segments, there will be an increase in lung units with low / ratios or areas of true shunting, both of which will contribute to arterial hypoxemia.

Hypoxemia:

Mild to moderate hypoxemia having a low PaCO2 is probably the most typical finding in acute pulmonary thromboembolism. Mild hypoxemia may be obscured by the tendency to rely on oximetry alone, because more than half of patients will have oxygen saturations (SaO2) above 90%.

Historically, the A-a PO2 was thought to be a more sensitive indicator of pulmonary embolism because it compensates for the presence of hypocapnia and the amount of inspired FiO2. Nevertheless, the recent Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) study has called this thinking into question.

An A-a PO2 less than 20, which is normal or near typical depending on patient age, was discovered in one third of patients with an acute PE identified by CT scanning.There is no one mechanism that will fully account for hypoxemia. Two causes have been mentioned previously. An increase in lung units with low / ratios impairs oxygen delivery.

In patients whose underlying disease makes them unable to increase their minute ventilation, an increase in lung units with high / ratios can also result in hypoxemia. In some individuals with preexisting impaired cardiac function or with big emboli that trigger acute right ventricular strain, cardiac output may fall, with a resultant fall in the mixed venous oxygen concentration.

This is an important cause of hypoxemia in seriously ill individuals. Finally, there may be true right-to-left shunts. Such shunts have been described in a small percentage of patients with severe hypoxemia in the setting of an acute pulmonary thromboembolism. It is presumed that these represent pulmonary artery to pulmonary venous shunting, or perhaps opening of a foramen ovale, but their exact location is unknown.

Obstruction of little pulmonary arterial branches that act as end arteries leads to pulmonary infarction in about 10% of instances. It is generally associated with some concomitant abnormality from the bronchial circulation such as is seen in individuals with left ventricular failure and chronically elevated left atrial pressures.

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Source by Francesco Zinzaro

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