1. Pulmonary Embolism Chapter 28
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2. Pulmonary Embolism
Blockage of pulmonary arteries by thrombus, fat or air embolus, or tumor tissue
Obstructs alveolar perfusion
Most commonly affects lower lobes
Pulmonary embolism (PE) is the blockage of pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue. The word embolus derives from a Greek word meaning “plug” or “stopper.” Emboli are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system.
A pulmonary embolus consists of material that gains access to the venous system and then to the pulmonary circulation. The embolus travels with the blood flow through ever-smaller blood vessels until it lodges and obstructs perfusion of the alveoli.
Because of higher blood flow, the lower lobes of the lung are commonly affected.
Approximately 10% of patients with PE die within the first hour. An additional 30% die from recurrent embolism.
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3. Pulmonary Embolism From: Brooks, M.L., Exploring
Medical Language – A Student-Directed
Approach, Mosby Elsevier, 2012
Describe the figures—the one on the left demonstrates decreased perfusion beyond the embolus location as the pulmonary embolus blocks blood flow. The lung is ventilated, but gas exchange is decreased as there is no blood supply to the ventilated alveoli.
The picture on the right depicts a large pulmonary embolus located within a pulmonary vessel.
From: Brooks, M.L., Exploring
Medical Language – A Student-Directed
Approach, Mosby Elsevier, 2005
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4. Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

5. Case Study
D.F. is a 74-year old female who arrives in the E.D. with complaints of chest pain and shortness of breath.
D.F. was recently discharged from rehab after undergoing bilateral knee replacements.
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6. Case Study She is 5 ft 2 in. tall and weighs 178 lb.
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She is 5 ft 2 in. tall and weighs 178 lb.
Her past medical history is negative except for mitral regurgitation and heart failure.
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7. Case Study
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What risk factors does D.F. have for the development of pulmonary embolism?
Obesity, orthopedic surgery, immobility, dehydration, heart failure
(See next slide for discussion of all risk factors.)
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8. Risk Factors Deep vein thrombosis (90%) Immobility or reduced mobility
Surgery
History of DVT
Malignancy
Obesity
Oral contraceptives/ hormones
Smoking
Heart failure
Pregnancy/delivery
Clotting disorders
Atrial fibrillation
Central venous catheters
Fractured long bones
More than 90% of pulmonary emboli arise from deep vein thrombosis (DVT) in the deep veins of the legs.
Risk factors for PE include immobility or reduced mobility, surgery within the last 3 months (especially pelvic and lower extremity surgery), history of DVT, malignancy, obesity, oral contraceptives and hormone therapy, heavy cigarette smoking, prolonged air travel, heart failure, pregnancy, and clotting disorders.
Other sites of origin of PE include the right side of the heart (especially with atrial fibrillation), the upper extremities (rare), and the pelvic veins (especially after surgery or childbirth). Upper extremity DVT occasionally occurs in the presence of central venous catheters or cardiac pacing wires. These cases may resolve with the removal of the catheter.
Less common causes of PE include fat emboli (from fractured long bones), air emboli (from improperly administered IV therapy), bacterial vegetations, amniotic fluid, and tumors.
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9. Case Study You perform a focused assessment on D.F.
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You perform a focused assessment on D.F.
Her vital signs are BP 100/64, HR 110, Respirations 24, Temp 37.
She has bibasilar crackles.
Her breathing appears labored.
She is somewhat restless and in obvious distress.
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10. Case Study
What clinical manifestations of pulmonary embolism does D.F. demonstrate?
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Chest pain, dyspnea, tachycardia, tachypnea, restlessness, crackles
(See next slide for discussion of all clinical manifestations.)
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11. Clinical Manifestations
Variable
Dyspnea most common
Tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, change in LOC
Dependent on size and extent of emboli
The signs and symptoms in PE are varied and nonspecific, making diagnosis difficult. Symptoms may begin slowly or suddenly.
Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE.
A mild to moderate hypoxemia with a low PaCO2 is a common finding.
Other manifestations are tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, and sudden change in mental status as a result of hypoxemia. Can also cause accentuation of pulmonic heart sound.
Clinical manifestations are dependent on the size and extent of emboli. Massive emboli may produce abrupt hypotension and shock. The mortality rate for massive PE is 30-60%, with most deaths occurring within 1-2 hours of onset.
Conversely, small emboli may go undetected or produce vague, transient symptoms. The exception to this is the patient with underlying cardiopulmonary disease. In these patients, even small or medium-sized emboli may result in severe cardiopulmonary compromise.
Repeated pulmonary emboli gradually cause a reduction in the capillary bed and eventual pulmonary hypertension. Right ventricular hypertrophy can develop secondary to pulmonary hypertension.
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12. Complications Pulmonary infarction Pulmonary hypertension
Alveolar necrosis and hemorrhage
Abscess
Pleural effusion
Pulmonary hypertension
Results from hypoxemia associated with massive or recurrent emboli
Right ventricular hypertrophy
Pulmonary infarction (death of lung tissue) is most likely when the following factors are present: (1) occlusion of a large or medium-sized pulmonary vessel (>2 mm in diameter), (2) insufficient collateral blood flow from the bronchial circulation, or (3) preexisting lung disease.
Infarction results in alveolar necrosis and hemorrhage.
Occasionally the necrotic tissue becomes infected, and an abscess may develop.
Concomitant pleural effusion is frequent.
Pulmonary hypertension results from hypoxemia or from involvement of more than 50% of the area of the normal pulmonary bed. As a single event, an embolus does not cause pulmonary hypertension unless it is massive.
Recurrent emboli may result in chronic pulmonary hypertension.
Pulmonary hypertension eventually results in dilation and hypertrophy of the right ventricle.
Depending on the degree of pulmonary hypertension and its rate of development, outcomes can vary, with some patients dying within months of the diagnosis and others living for decades.
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13. Case Study What diagnostic tests would you expect to teach D.F. about?
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What diagnostic tests would you expect to teach D.F. about?
Serum d-dimer levels, spiral CT scan, chest x-ray, ECG, troponin, b-natriuretic peptide. If can’t have contrast media for spiral CT scan, then would expect patient to have a ventilation-perfusion (V/Q) scan.
(See next slide for further discussion.)
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14. Diagnostic Studies Arterial blood gases Chest x-ray Electrocardiogram
Troponin levels
B-type natriuretic peptide
ABG analysis is important, but not diagnostic. The PaO2 is low because of inadequate oxygenation secondary to an occluded pulmonary vasculature preventing matching of perfusion to ventilation. The pH remains normal unless respiratory alkalosis develops as a result of prolonged hyperventilation or to compensate for lactic acidosis caused by shock.
Abnormal findings are usually reported on the chest x-ray (atelectasis, pleural effusion) and the ECG (ST segment and T wave changes), but they are not diagnostic for PE.
Serum troponin levels and b-type natriuretic peptide (BNP) levels are frequently elevated. Although not diagnostic, elevated levels of these markers are associated with increased mortality in patients with PE.
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15. Diagnostic Studies D-Dimer Spiral (helical) CT scan
Elevated with any clot degradation
False negatives with small PE
Spiral (helical) CT scan
Most frequently used dx test
Requires IV contrast media
D-dimer is a laboratory test that measures the amount of cross-linked fibrin fragments. These fragments are the result of clot degradation and are rarely found in healthy individuals. The disadvantage of D-dimer is that it is neither specific (other conditions cause elevation) nor sensitive as up to 50% of patients with small pulmonary emboli have normal results. Patients with suspected PE and an elevated D-dimer level but normal venous ultrasound may need a spiral CT or lung scan.
A spiral (helical) CT scan (also known as CT angiography or CTA) is the most frequently used test to diagnose PE. An IV injection of contrast media is required to view the blood vessels. The scanner continuously rotates while obtaining slices and does not start and stop between each slice. This allows visualization of all anatomic regions of the lungs. The computer reconstructs the data to provide a three-dimensional picture and assist in emboli visualization.
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16. Diagnostic Studies Ventilation-perfusion (V/Q) scan
Used if patient cannot have contrast
Two components
Perfusion scanning
Ventilation scanning
Pulmonary angiography
Most sensitive but invasive
Arterial blood gases (ABGs)
If a patient cannot have contrast media, a ventilation-perfusion (V/Q) scan is done. The V/Q scan has two components and is most accurate when both are performed:
Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation.
Ventilation scanning involves inhalation of a radioactive gas such as xenon. Scanning reflects the distribution of gas through the lung. The ventilation component requires the cooperation of the patient and may be impossible to perform in the critically ill patient, particularly if the patient is intubated.
Pulmonary angiography is the most sensitive and specific test for PE. However, it is an expensive and invasive procedure that involves the insertion of a catheter through the antecubital or femoral vein, advancement to the pulmonary artery, and injection of contrast medium. The reliability of the spiral CT has greatly diminished the need for pulmonary angiography.
ABG analysis is important, but not diagnostic. The PaO2 is low because of inadequate oxygenation secondary to an occluded pulmonary vasculature preventing matching of perfusion to ventilation. The pH remains normal unless respiratory alkalosis develops as a result of prolonged hyperventilation or to compensate for lactic acidosis caused by shock. Abnormal findings are usually reported on the chest x-ray (atelectasis, pleural effusion) and the ECG (ST segment and T wave changes), but they are not diagnostic for PE. Serum troponin levels and b-type natriuretic peptide (BNP) levels are frequently elevated. Although not diagnostic, elevated levels of these markers are associated with increased mortality in patients with PE.
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17. Case Study D.F.’s D-Dimer is positive.
Spiral CT scan confirms the diagnosis of pulmonary emboli.
What collaborative treatment measures would you expect to implement for D.F.?
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Anticoagulation therapy (either LMWH or unfractionated heparin), thrombolytics if severe, oxygen therapy.
Vasopressors and fluids if becomes hypotensive.
Inferior vena cava filter if patient has multiple lower extremity DVT – to prevent embolization to lungs.
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18. Collaborative Care Prevention—the key! Sequential compression devices
Early ambulation
Prophylactic anticoagulation
Prevention of PE begins with prevention of DVT. DVT prophylaxis includes the use of sequential compression devices, early ambulation, and prophylactic use of anticoagulant medications.
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19. Collaborative Care Goals of treatment Supportive care variable
Prevent further thrombi
Prevent further embolization to pulmonary system
Provide cardiopulmonary support
Supportive care variable
Oxygen → mechanical ventilation
Pulmonary toilet
Fluids, diuretics, analgesics
To reduce mortality risk, treatment is begun as soon as PE is suspected.
The objectives are to (1) prevent further growth or multiplication of thrombi in the lower extremities, (2) prevent embolization from the upper or lower extremities to the pulmonary vascular system, and (3) provide cardiopulmonary support if indicated.
Supportive therapy for the patient’s cardiopulmonary status varies according to the severity of the PE. O2 can be given via mask or cannula, and the concentration is determined by ABG analysis. In some situations, endotracheal intubation and mechanical ventilation are necessary to maintain adequate oxygenation.
Respiratory measures such as turning, coughing, deep breathing, and incentive spirometry are important to help prevent or treat atelectasis.
If manifestations of shock are present, IV fluids are administered followed by vasopressor agents as needed to support perfusion.
If heart failure is present, diuretics are used.
Pain resulting from pleural irritation or reduced coronary blood flow is treated with opioids (usually morphine).
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20. Drug Therapy Anticoagulation Fibrinolytic agents
Low-molecular-weight heparin (LHWH)
Unfractionated IV heparin
Warfarin (Coumadin)
Fibrinolytic agents
Tissue plasminogen activator (tPA)
Alteplase (Activase)
Immediate anticoagulation is required for patients with PE.
Subcutaneous administration of low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox]) has been found to be safer and more effective than unfractionated heparin.
It is the recommended choice of treatment for patients with nonmassive PE. Unfractionated intravenous heparin can be as effective but is more difficult to titrate to therapeutic levels. Monitoring the aPTT is not necessary or useful when using LMWH.
Warfarin (Coumadin) should be initiated within the first 3 days of heparinization and is typically administered for 3 to 6 months.
Fibrinolytic agents, such as tissue plasminogen activator (tPA) or alteplase (Activase), dissolve the pulmonary embolus and the source of the thrombus in the pelvis or deep leg veins, thereby decreasing the likelihood of recurrent emboli. Indications for thrombolytic therapy in PE include hemodynamic instability and right ventricular dysfunction.
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21. Surgical Therapy Pulmonary embolectomy for massive PE
Inferior vena cava (IVC) filter
Prevents migration of clots in pulmonary system
Hemodynamically unstable patients with massive PE with contraindications for fibrinolytic therapy are candidates for immediate pulmonary embolectomy. This can be achieved via a vascular (catheter) or surgical approach. Pulmonary embolectomy has a high mortality rate and is thus not recommended for patients who can be successfully treated otherwise.
To prevent further emboli, an inferior vena cava (IVC) filter may be the treatment of choice in patients who remain at high risk and for patients for whom anticoagulation is contraindicated. This device is percutaneously placed at the level of the diaphragm in the inferior vena cava via the femoral vein. It prevents migration of large clots into the pulmonary system. The complications associated with this device are rare and include misplacement, migration, and perforation.
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22. Inferior Vena Cava Filters
These pictures depict some of the different types of inferior vena cava filters. A = Greenfield filter; B = Bird’s nest filter; D = Vena Tech LP filter
From: Pretorius, E.C. & Solomon,
J.A., Radiology Secrets Plus, 3e,
Mosby, 2011.
Copyright © 2014 by Mosby, an imprint of Elsevier Inc.

23. Case Study
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D.F. is started on a continuous IV drip of unfractionated heparin at units/hour.
Drip will be titrated to therapeutic level using aPTT levels drawn every 6 hours.
What nursing interventions would be appropriate in the care of D.F.?
Semi-Fowler’s position, maintain IV access, titrate oxygen therapy to maintain adequate oxygen saturation, frequent assessment of patient’s respiratory and cardiovascular status, monitor aPTT laboratory results and titrate heparin as needed, provide emotional support and reassurance, provide patient education retreatments and long-term anticoagulation.
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24. Nursing Management Semi-Fowler’s position IV access Oxygen therapy
Frequent assessments
Monitor laboratory results.
Emotional support and reassurance
The prognosis of a patient with PE is good if therapy is promptly instituted.
Keep the patient on bed rest in a semi-Fowler’s position to facilitate breathing.
Maintain an IV line for medications and fluid therapy.
Administer oxygen therapy as ordered.
Assess the patient’s cardiopulmonary status with careful monitoring of vital signs, cardiac rhythm, pulse oximetry, ABGs, and lung sounds.
Monitor laboratory results to ensure therapeutic ranges of INR (for warfarin) and aPTT (for intravenous heparin).
Monitor the patient for complications of anticoagulant and fibrinolytic therapy (e.g., bleeding, hematomas, bruising).
Provide appropriate interventions related to immobility and fall precautions.
The patient is usually anxious because of pain, a sense of doom, inability to breathe, and fear of death. Carefully explain the situation and provide emotional support and reassurance to help relieve the patient’s anxiety.
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25. Patient Teaching Regarding long-term anticoagulant therapy
Measures to prevent DVT
Importance of follow-up exams
Patient teaching regarding long-term anticoagulant therapy is critical. Anticoagulant therapy continues for at least 3 to 6 months. Patients with recurrent emboli are treated indefinitely. INR levels are drawn at intervals, and warfarin dosage is adjusted. Some patients are monitored by nurses in an anticoagulation clinic.
Discharge planning is aimed at limiting progression of the condition and preventing complications and recurrence. Teach the patient measures to prevent DVT.
Reinforce the need for the patient to return to the health care provider for regular follow-up examinations.
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26. Evaluation Expected Outcomes
Adequate tissue perfusion and respiratory function
Adequate cardiac output
Increased level of comfort
No recurrence of PE
The expected outcomes are that the patient who has a PE will have
Adequate tissue perfusion and respiratory function
Adequate cardiac output
Increased level of comfort
No recurrence of PE
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