– Sudden blockage of a pulmonary artery by foreign matter, which impedes the blood flow to the lung tissue.
Causes and Incidence
The most common cause is a thrombus, which typically forms in the leg or pelvic vein but may be seen in other locations. Other causes include fat, amniotic fluid, air, and gas. Common risk factors are thrombophlebitis, major surgery, pregnancy and childbirth, fractures, myocardial infarction, congestive heart failure, venous insufficiency, polycythemia vera, prolonged immobility, and chronic illness. It is estimated that up to 5% of hospital deaths are attributable to pulmonary emboli.
Emboli in whatever form travel through the bloodstream and lodge in one or more pulmonary arteries. The area of the lung supplied by the affected artery becomes underperfused but is still ventilated. This results in physiologic dead space or wasted ventilation and contributes to hyperventilation. Histamine release from the embolus produces reflex bronchoconstriction, leading to further hyperventilation. Depletion of alveolar surfactant results in diminished lung volume and compliance. If the clot is large enough and interferes greatly with pulmonary perfusion, it may result in pulmonary hypertension.
The manifestations of a pulmonary embolus (PE) are nonspecific and vary in degree and intensity, depending on the size of the embolus, the extent of occlusion, the amount of collateral circulation, and preexisting cardiopulmonary function. Small emboli may be asymptomatic. The chief manifestation is breathlessness. Other symptoms include anxiety, restlessness, tachypnea, sweating, cough, hemoptysis, chest pain, fever, and rales. Cyanosis may be present with a massive embolus.
Cardiac arrhythmias, cor pulmonale, atelectasis, shock, hepatic congestion, and necrosis are complications. Pulmonary infarction is an uncommon complication of PE that results in hemorrhagic consolidation and tissue necrosis distal to the occlusion. Death following a PE usually occurs within 1 to 2 hours of the initial event. Those with underlying cardiovascular or pulmonary disease and those with a large embolus are at greater risk of dying. Untreated individuals risk recurrent emboli and about a 50% chance of death.
The diagnosis is suggested by the presenting clinical picture and confirmed by the following procedures.
Visualization of intraarterial filling defects
Lung perfusion scan
To detect perfusion defects
To detect altered ventilation patterns
Arterial hypoxemia (decreased PaO2 and PaCO2)
To rule out myocardial infarction; PE is characterized by tall, peaked P waves, depressed ST segments, T-wave inversions, and supraventricular tachyarrhythmias
Unilateral elevation of the diaphragm, enlarged pulmonary artery, and pleural effusion 2 hours or longer after the event
Embolectomy for large emboli unresponsive to treatment; umbrella filter in inferior vena cava to trap multiple emboli before they reach the lung; interruption of blood flow through the inferior vena cava by ligation for multiple emboli.
Anticoagulants to halt clot propagation (heparin is used in the acute phase and is replaced by coumadin, which may be administered for 6 months to life; medications should overlap for 5 to 7 days to achieve effective blood levels of coumadin); fibrinolytic enzymes may be used in place of anticoagulants for clot lysis, particularly of large clots; analgesics for pain; vasopressors, dopamine to treat hypotension.
Oxygen therapy; bed rest in acute phase, followed by progressive mobilization; hemodynamic and cardiac monitoring; facilitation of breathing; intake and output measurements to monitor renal function; observation for bleeding as a side effect of anticoagulants, and safety measures to prevent bleeding; information about long-term anticoagulant therapy; antiembolism hose and instruction in preventing pooled blood in the lower extremities.