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Pulmonary Embolism

Pulmonary embolism (PE) refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart. Most commonly, PE is due to a blood clot or thrombus. However, there are other types of emboli: air, fat, amniotic fluid, and septic (from bacterial invasion of the thrombus).

Although most thrombi originate in the deep veins of the legs, other sites include the pelvic veins and the right atrium of the heart. A venous thrombosis can result from slowing of blood flow (stasis), secondary to damage to the blood vessel wall (particularly the endothelial lining) or changes in the blood coagulation mechanism. Atrial fibrillation is also a cause of pulmonary embolism. An enlarged right atrium in fibrillation causes blood to stagnate and form clots in this area. These clots are prone to travel into the pulmonary circulation.

Clinical Manifestations

The symptoms of PE depend on the size of the thrombus and the area of the pulmonary artery occluded by the thrombus; they may be nonspecific. Dyspnea is the most frequent symptom; tachypnea (very rapid respiratory rate) is the most frequent sign (Goldhaber, 1998). The duration and intensity of the dyspnea depend on the extent of embolization. Chest pain is common and is usually sud- den and pleuritic. It may be substernal and mimic angina pectoris or a myocardial infarction. Other symptoms include anxiety, fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, and syncope. 

A massive embolism is best defined by the degree of hemodynamic instability rather than the percentage of pulmonary vasculature occlusion. It is described as an occlusion of the outflow tract of the main pulmonary artery or the bifurcation of the pulmonary arteries that produces pronounced dyspnea, sudden substernal pain, rapid and weak pulse, shock, syncope, and sudden death. Multiple small emboli can lodge in the terminal pulmonary arterioles, producing multiple small infarctions of the lungs. A pulmonary infarction causes ischemic necrosis of an area of the lung and occurs in less than 10% of cases of PE (Arroliga, Matthay & Matthay, 2000). The clinical picture may mimic that of broncho-pneumonia or heart failure. In atypical instances, the disease causes few signs and symptoms, whereas in other instances it mimics various other cardiopulmonary disorders.

Assessment and Diagnostic Findings

Death from PE commonly occurs within 1 hour of symptoms; thus, early recognition and diagnosis are priorities. Because the symptoms of PE can vary from few to severe, a diagnostic workup is performed to rule out other diseases. Deep venous thrombosis is closely associated with the development of PE. Typically, patients report sudden onset of pain and/or swelling and warmth of the proximal or distal extremity, skin discoloration, and superficial vein distention. The pain is usually relieved with elevation. The diagnostic workup includes a ventilation–perfusion scan, pulmonary angiography, chest x-ray, ECG, peripheral vascular studies, impedance plethysmography, and arterial blood gas analysis.

The chest x-ray is usually normal but may show infiltrates, atelectasis, elevation of the diaphragm on the affected side, or a pleural effusion. The chest x-ray is most helpful in excluding other possible causes. The ECG usually shows sinus tachycardia, PR interval depression, and nonspecific T-wave changes. Peripheral vascular studies may include impedance plethysmography, Doppler ultrasonography, or venography. Test results confirm or exclude the diagnosis of PE. Arterial blood gas analysis may show hypoxemia and hypocapnia (from tachypnea); however, arterial blood gas measurements are normal in up to 20% of patients with PE. 

A ventilation–perfusion scan is the test of choice in patients with suspected PE. The perfusion portion of the scan may indicate areas of diminished or absent blood flow and is the most useful test to rule out clinically important PE. A ventilation scan may show whether there is also a ventilation abnormality present. A normal perfusion scan rules out the diagnosis of PE. If there is a ventilation–perfusion mismatch, the probability of PE is high.

Spiral CT of the chest may also assist in the diagnosis. If lung scan results are not definitive, pulmonary angiography, considered the gold standard for the diagnosis of PE, can be used. This test is invasive and is performed in the interventional radiology department. A contrast agent is injected into the pulmonary arterial system, allowing visualization of obstructions to blood flow and abnormalities.


For those at risk, the most effective approach to preventing PE is to prevent deep venous thrombosis. Active leg exercises to avoid venous stasis, early ambulation, and use of elastic compression stockings are general preventive measures.

Nursing Management:


A key role of the nurse is to identify patients at high risk for PE and to minimize the risk of PE in all patients. The nurse must have a high degree of suspicion for PE in any patient, but particularly in those with conditions predisposing to a slowing of venous return.


Preventing thrombus formation is a major nursing responsibility.

The nurse encourages ambulation and active and passive leg exercises to prevent venous stasis in patients on bed rest. The nurse instructs the patient to move the legs in a “pumping” exercise so that the leg muscles can help increase venous flow. The nurse also advises the patient not to sit or lie in bed for prolonged periods, not to cross the legs, and not to wear constricting clothing. Legs should not be dangled or feet placed in a dependent position while the patient sits on the edge of the bed; instead, the patient’s feet should rest on the floor or on a chair. In addition, intravenous catheters (for parenteral therapy or measurements of central venous pressure) should not be left in place for prolonged periods.


The nurse examines patients who are at risk for developing PE for a positive Homans’ sign, which may or may not indicate impending thrombosis of the leg veins. To test for Homans’ sign, the patient assumes a supine position, lifts the leg, and dorsiflexes the foot. The nurse asks the patient to report whether calf pain occurs during this maneuver. The occurrence of pain—a positive Homans’ sign—may indicate deep venous thrombosis.


The nurse is responsible for monitoring thrombolytic and anticoagulant therapy. Thrombolytic therapy (streptokinase, urokinase, tissue plasminogen activator) causes lysis of deep vein thrombi and pulmonary emboli, which helps dissolve the clots. During thrombolytic infusion, the patient remains on bed rest, vital signs are assessed every 2 hours, and invasive procedures are limited. Tests to determine prothrombin time or partial thromboplastin time are performed 3 to 4 hours after the thrombolytic infusion is started to confirm that the fibrinolytic systems have been activated. Because of the prolonged clotting time, only essential arterial punctures or venipunctures are performed, and manual pressure is applied to any puncture site for at least 30 minutes. Pulse oximetry is used to monitor changes in oxygenation. The nurse immediately discontinues the infusion if uncontrolled bleeding occurs.


Chest pain, if present, is usually pleuritic rather than cardiac in origin. A semi-Fowler’s position provides a more comfortable position for breathing. However, it is important to continue to turn the patient frequently and reposition the patient to improve the ventilation–perfusion ratio in the lung. The nurse administers opioid analgesics as prescribed for severe pain.


Careful attention is given to the proper use of oxygen. It is important to ensure that the patient understands the need for continuous oxygen therapy. The nurse assesses the patient frequently for signs of hypoxemia and monitors the pulse oximetry values to evaluate the effectiveness of the oxygen therapy. Deep breathing and incentive spirometry are indicated for all patients to minimize or prevent atelectasis and improve ventilation. Nebulizer therapy or percussion and postural drainage may be used for management of secretions.


The nurse encourages the stabilized patient to talk about any fears or concerns related to this frightening episode, answers the patient’s and family’s questions concisely and accurately, explains the therapy, and describes how to recognize untoward effects early.


When caring for a patient who has had PE, the nurse must be alert for the potential complication of cardiogenic shock or right ventricular failure subsequent to the effect of PE on the cardiovascular system.


After surgery, the nurse measures the patient’s pulmonary arterial pressure and urinary output. The nurse assesses the insertion site of the arterial catheter for hematoma formation and infection. It is important to maintain the blood pressure at a level that supports perfusion of vital organs. To prevent peripheral venous stasis and edema of the lower extremities, the nurse elevates the foot of the bed and encourages isometric exercises, use of elastic compression stockings, and walking when the patient is permitted out of bed. Sitting is discouraged because hip flexion compresses the large veins in the legs.


Teaching Patients Self-Care. Before hospital discharge and at follow-up visits to the clinic or during home visits, the nurse instructs the patient about how to prevent recurrence and what signs and symptoms to report immediately.