Part II - Disorders
A complication of patients in the health care facility, pulmonary embolism is an obstruction of the pulmonary arterial bed by a dislodged thrombus, heart valve vegetation, or foreign substance. It strikes about 6 million adults each year in the United States, resulting in 100,000 deaths.
· Dislodged thrombi, originating in the leg veins (most common)
· Other sites where thrombi may originate:
§ Pelvic veins
§ Renal veins
§ Hepatic vein
§ Right side of the heart
§ Upper extremities
· Long-term immobility
· Chronic pulmonary disease
· Heart failure or atrial fibrillation
· Deep vein thrombosis (DVT)
· Polycythemia vera or thrombocytosis
· Autoimmune hemolytic anemia or sickle cell disease
· Varicose veins
· Recent surgery or lower-extremity fractures
· Advanced age
· Vascular injury
· I.V. drug abuse
· Hormonal contraceptives
A triad of DVT formation is stasis, endothelial injury, and hypercoagulability. Risk factors include long car or plane trips, cancer, pregnancy, hypercoagulability, and prior DVT or pulmonary emboli.
Thrombus formation results directly from vascular wall damage, venostasis, or hypercoagulability of the blood. Trauma, clot dissolution, sudden muscle spasm, intravascular pressure changes, or a change in peripheral blood flow can cause the thrombus to loosen or fragmentize. Then the thrombus—now called an embolus—floats to the heart's right side and enters the lung through the pulmonary artery. There, the embolus may dissolve, continue to fragmentize, or grow.
If the embolus occludes the pulmonary artery, it prevents alveoli from producing enough surfactant to maintain alveolar integrity. As a result, alveoli collapse and atelectasis develops. If the embolus enlarges, it may clog most or all of the pulmonary vessels and cause death.
Rarely, the emboli contain air, fat, bacteria, amniotic fluid, talc, or tumor cells.
Signs and symptoms
Total occlusion of the main pulmonary artery is rapidly fatal; smaller or fragmented emboli produce symptoms that vary with the size, number, and location, as follows:
· pleuritic chest pain
· productive cough (sputum may be blood-tinged)
· low-grade fever
· pleural effusion.
Less common signs include:
· massive hemoptysis
· splinting of the chest
· leg edema and pain
· cyanosis, syncope, and distended jugular veins
· pleural friction rub
· signs of circulatory collapse (weak, rapid pulse and hypotension)
· signs of hypoxia (restlessness and anxiety).
· right ventricular S3 gallop and increased intensity of a pulmonic component of S2
· crackles and a pleural rub may be heard at the embolism site.
Diagnostic test results
· Chest X-ray may show areas of atelectasis, elevated diaphragm and pleural effusion, prominent pulmonary artery and, occasionally, the characteristic wedge-shaped infiltrate suggestive of pulmonary infarction
· Lung scan shows perfusion defects in areas beyond occluded vessels.
· Pulmonary angiography reveals the location of the emboli.
· Electrocardiography may show right axis deviation (extensive embolism); tall, peaked P waves (right bundle-branch block); depression of ST segments and T-wave inversions (indicative of right-sided heart strain); and supraventricular tachyarrhythmias. A pattern sometimes observed is S1, Q3, and T3 (S wave in lead I, Q wave in lead III, and inverted T wave in lead III).
· Arterial blood gas measurements may show decreased partial pressure of arterial oxygen and partial pressure of arterial carbon dioxide.
· If pleural effusion is present, thoracentesis may rule out empyema, which indicates pneumonia.
Treatment is designed to maintain adequate cardiovascular and pulmonary function during resolution of the obstruction and to prevent recurrence of embolic episodes. Because most emboli resolve within 10 to 14 days, treatment may consist of:
· oxygen therapy and fibrinolytic therapy
· anticoagulation with heparin
· vasopressors and antibiotics
· vena caval ligation, plication, or insertion of a device to filter blood returning to the heart and lungs, to prevent future pulmonary emboli.