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Chapter: Medical Surgical Nursing: Management of Patients With Chest and Lower Respiratory Tract Disorders

Pulmonary Embolism

Pulmonary embolism (PE) refers to the obstruction of the pul-monary 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.

Pulmonary Embolism


Pulmonary embolism (PE) refers to the obstruction of the pul-monary 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 throm-bus. However, there are other types of emboli: air, fat, amniotic fluid, and septic (from bacterial invasion of the thrombus). It is es-timated that more than half a million people develop PE yearly, resulting in more than 50,000 deaths. PE is a common disorder and often is associated with trauma, surgery (orthopedic, major abdominal, pelvic, gynecologic), pregnancy, heart failure, age older than 50 years, hypercoagulable states, and prolonged immobility. It also may occur in an apparently healthy person. Risk factors for developing PE are identified in Chart 23-8.


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 mech-anism. 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.



When a thrombus completely or partially obstructs a pulmonary artery or its branches, the alveolar dead space is increased. The area, although continuing to be ventilated, receives little or no blood flow. Thus, gas exchange is impaired or absent in this area. In addition, various substances are released from the clot and sur-rounding area, causing regional blood vessels and bronchioles to constrict. This causes an increase in pulmonary vascular resis-tance. This reaction compounds the ventilation–perfusion imbalance.


The hemodynamic consequences are increased pulmonary vascular resistance from the regional vasoconstriction and re-duced size of the pulmonary vascular bed. This results in an in-crease in pulmonary arterial pressure and, in turn, an increase in right ventricular work to maintain pulmonary blood flow. When the work requirements of the right ventricle exceed its capacity, right ventricular failure occurs, leading to a decrease in cardiac output followed by a decrease in systemic blood pressure and the development of shock.


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 sudden 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 hemody-namic instability rather than the percentage of pulmonary vascu-lature occlusion. It is described as an occlusion of the outflow tract of the main pulmonary artery or the bifurcation of the pul-monary arteries that produces pronounced dyspnea, sudden sub-sternal pain, rapid and weak pulse, shock, syncope, and sudden death. Multiple small emboli can lodge in the terminal pul-monary 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 bronchopneumonia 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, pa-tients report sudden onset of pain and/or swelling and warmth of the proximal or distal extremity, skin discoloration, and super-ficial 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, at-electasis, 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 con-firm or exclude the diagnosis of PE. Arterial blood gas analysis may show hypoxemia and hypocapnia (from tachypnea); however, ar-terial 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 indi-cate areas of diminished or absent blood flow and is the most use-ful 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 radiol-ogy 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. Additional strategies for prevention are listed in the checklist in Chart 23-9..

Patients who are older than 40, whose hemostasis is adequate, and who are undergoing major elective abdominal or thoracic surgery may receive anticoagulant therapy. Low doses of heparin may be given before surgery to reduce the risk of postoperative deep venous thrombus and PE. Heparin should be administered subcutaneously 2 hours before surgery and continued every 8 to 12 hours until the patient is discharged. Low-dose heparin is thought to enhance the activity of antithrombin III, a major plasma inhibitor of clotting factor X. This regimen is not recom-mended for patients with an active thrombotic process or for those undergoing major orthopedic surgery, open prostatectomy, or surgery on the eye or brain. Low-molecular-weight heparin (eg, enoxaparin [Lovenox]) is an alternative therapy. It has a longer half-life, enhanced subcutaneous absorption, a reduced in-cidence of thrombocytopenia, and reduced interaction with platelets as compared to unfractionated heparin (Ansell, Hickey, Kleinschmidt et al., 2000).


The intermittent pneumatic leg compression device is useful in preventing thromboembolism. The device inflates a bag that in-termittently compresses the leg from the calf to the thigh, thereby improving venous return. It may be applied before surgery and continued until the patient is ambulatory. The device is particu-larly useful for patients who are not candidates for anticoagulant therapy (Clagett, Anderson, Geerts et al., 1998).


Medical Management


Because PE is often a medical emergency, emergency management is of primary concern. After emergency measures have been taken and the patient’s condition stabilizes, the treatment goal is to dis-solve (lyse) the existing emboli and prevent new ones from form-ing. The treatment of PE may include a variety of modalities:


              General measures to improve respiratory and vascular status


·         Anticoagulation therapy


·         Thrombolytic therapy


·         Surgical intervention




Massive PE is a life-threatening emergency. The immediate ob-jective is to stabilize the cardiopulmonary system. A sudden rise in pulmonary resistance increases the work of the right ventricle, which can cause acute right-sided heart failure with cardiogenic shock. Most patients who die of massive PE do so in the first 1 to 2 hours after the embolic event. Emergency management consists of the following:


·        Nasal oxygen is administered immediately to relieve hy-poxemia, respiratory distress, and central cyanosis.


·        Intravenous infusion lines are started to establish routes for medications or fluids that will be needed.


·        A perfusion scan, hemodynamic measurements, and arte-rial blood gas determinations are performed. Spiral (heli-cal) CT or pulmonary angiography may be performed. Spiral CT is more advanced and quicker than routine to-mography. With spiral CT, the patient continuously moves as the x-ray tube rotates. With this type of CT, im-ages can be reconstructed at select levels and locations for diagnostic purposes.


·       Hypotension is treated by a slow infusion of dobutamine (Dobutrex) (which has a dilating effect on the pulmonary vessels and bronchi) or dopamine (Intropin).


·        The ECG is monitored continuously for dysrhythmias and right ventricular failure, which may occur suddenly.


·       Digitalis glycosides, intravenous diuretics, and antiarrhyth-mic agents are administered when appropriate.


·      Blood is drawn for serum electrolytes, complete blood count, and hematocrit.


·      If clinical assessment and arterial blood gas analysis indicate the need, the patient is intubated and placed on a mechanical ventilator.


·      If the patient has suffered massive embolism and is hypo-tensive, an indwelling urinary catheter is inserted to moni-tor urinary output.


·       Small doses of intravenous morphine or sedatives are ad-ministered to relieve the patient’s anxiety, to alleviate chest discomfort, to improve tolerance of the endotracheal tube, and to ease adaptation to the mechanical ventilator.




Measures are initiated to improve the patient’s respiratory and vascular status. Oxygen therapy is administered to correct the hy-poxemia, relieve the pulmonary vascular vasoconstriction, and re-duce the pulmonary hypertension. Using elastic compression stockings or intermittent pneumatic leg compression devices re-duces venous stasis. These measures compress the superficial veins and increase the velocity of blood in the deep veins by redirect-ing the blood through the deep veins. Elevating the leg (above the level of the heart) also increases venous flow.




Anticoagulation Therapy. 

Anticoagulant therapy (heparin, war-farin sodium) has traditionally been the primary method for managing acute deep vein thrombosis and PE (Goldhaber, 1998). Heparin is used to prevent recurrence of emboli but has no effect on emboli that are already present. It is administered as an intravenous bolus of 5,000 to 10,000 units, followed by a con-tinuous infusion initiated at a dose of 18 U/kg per hour, not to exceed 1,600 U/hour in otherwise healthy patients (Goldhaber, 1998). The rate is reduced in patients with a high risk of bleed-ing. The goal is to keep the partial thromboplastin time 1.5 to 2.5 times normal (or 46 to 70 seconds). Heparin is usually admin-istered for 5 to 7 days. Low-molecular-weight heparin (eg, enoxa-parin [Lovenox]) may also be used.


Warfarin sodium (Coumadin) administration is begun within 24 hours after the start of heparin therapy because its onset of action is 4 to 5 days. Warfarin is usually continued for 3 to 6 months. The prothrombin time is maintained at 1.5 to 2.5 times normal (or an INR [international normalized ratio] of 2.0 to 3.0). Anticoagulation therapy is contraindicated in patients who are at risk for bleeding (eg, those with gastro-intestinal conditions or with postoperative or postpartum bleeding).


Thrombolytic Therapy. 

Thrombolytic therapy (urokinase, strepto-kinase, alteplase, anistreplase, reteplase) also may be used in treating PE, particularly in patients who are severely com-promised (eg, those who are hypotensive and have significant hypoxemia despite oxygen supplementation). Thrombolytic therapy resolves the thrombi or emboli more quickly and re-stores more normal hemodynamic functioning of the pul-monary circulation, thereby reducing pulmonary hypertension and improving perfusion, oxygenation, and cardiac output. Bleeding, however, is a significant side effect. Contraindications to thrombolytic therapy include a cerebrovascular accident within the past 2 months, other active intracranial processes, ac-tive bleeding, surgery within the past 10 days of the thrombotic event, recent labor and delivery, trauma, or severe hypertension. Consequently, thrombolytic agents are advocated only for PE affecting a significant area of blood flow to the lung and caus-ing hemodynamic instability.


Before thrombolytic therapy is started, prothrombin time, partial thromboplastin time, hematocrit values, and platelet counts are obtained. Heparin is stopped prior to administration of a thrombolytic agent. During therapy, all but essential invasive procedures are avoided because of potential bleeding. If necessary, fresh whole blood, packed red cells, cryoprecipitate, or frozen plasma is administered to replace blood loss and reverse the bleed-ing tendency. After the thrombolytic infusion is completed (which varies in duration according to the agent used and the condition being treated), the patient is given anticoagulants.




A surgical embolectomy is rarely performed but may be indicated if the patient has a massive PE or hemodynamic instability or if there are contraindications to thrombolytic therapy. Pulmonary embolectomy requires a thoracotomy with cardiopulmonary by-pass technique. Transvenous catheter embolectomy is a technique in which a vacuum-cupped catheter is introduced transvenously into the affected pulmonary artery. Suction is applied to the end of the embolus and the embolus is aspirated into the cup. The sur-geon maintains suction to hold the embolus within the cup, and the entire catheter is withdrawn through the right side of the heart and out the femoral vein. Catheters are available that pulverize the clot with high-velocity jets of normal saline solution (Goldhaber, 1998). An inferior caval filter is usually inserted at the time of surgery to protect against a recurrence.


Interrupting the inferior vena cava is another surgical tech-nique used when PE recurs or when the patient is intolerant of anticoagulant therapy. This approach prevents dislodged thrombi from being swept into the lungs while allowing ade-quate blood flow. The preferred approach is the application of Teflon clips to the inferior vena cava to divide the lumen into small channels without occluding caval blood flow. Also, the use of transvenous devices that occlude or filter the blood through the inferior vena cava is a fairly safe way to prevent re-current PE. One such technique involves inserting a filter (eg, Greenfield filter) through the internal jugular vein or common femoral vein (Fig. 23-7). This filter is advanced into the infe-rior vena cava, where it is opened. The perforated umbrella per-mits the passage of blood but prevents the passage of large thrombi. It is recommended that anticoagulation be continued in patients with a caval filter, if there are no contraindications to its use.


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 partic-ularly in those with conditions predisposing to a slowing of ve-nous return (see Chart 23-8).



Preventing thrombus formation is a major nursing responsibility. The nurse encourages ambulation and active and passive leg ex-ercises 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, intra-venous catheters (for parenteral therapy or measurements of cen-tral 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 im-pending 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 antico-agulant therapy. Thrombolytic therapy (streptokinase, urokinase, tissue plasminogen activator) causes lysis of deep vein thrombi and pulmonary emboli, which helps dissolve the clots. During throm-bolytic infusion, the patient remains on bed rest, vital signs are as-sessed 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. Be-cause of the prolonged clotting time, only essential arterial punc-tures or venipunctures are performed, and manual pressure is applied to any puncture site for at least 30 minutes. Pulse oxime-try is used to monitor changes in oxygenation. The nurse imme-diately 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 po-sition 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 administersopioid analgesics as prescribed for severe pain.




Careful attention is given to the proper use of oxygen. It is im-portant to ensure that the patient understands the need for con-tinuous 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 mini-mize 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 cardio-vascular 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 sup-ports perfusion of vital organs. To prevent peripheral venous sta-sis and edema of the lower extremities, the nurse elevates the foot of the bed and encourages isometric exercises, use of elastic com-pression 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 atfollow-up visits to the clinic or during home visits, the nurse in-structs the patient about how to prevent recurrence and what signs and symptoms to report immediately. Patient instructions, as presented in Chart 23-9, are intended to help prevent recur-rences and side effects of treatment.


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