•BNP levels above 600 pg/mL indicate moderate heart failure.
•BNP levels above 900 pg/mL indicate severe heart failure.
Radiologic Findings
Chest Radiograph
•Bilateral fluffy opacities with a predominantly central position in the chest
•Dilated pulmonary arteries
•Left ventricular hypertrophy (cardiomegaly)
•Kerley A and B lines
•“Bat's wing” or “butterfly” pattern
•Pleural effusion (transudate)—see Chapter 24, Pleural Effusion and Empyema
Cardiogenic Pulmonary Edema
The radiographic findings associated with left heart failure are commonly described as follows:
•Mild left-sided heart failure: Pulmonary venous congestion with dilated pulmonary arteries is present.
•Moderate left-sided heart failure: Cardiomegaly, engorgement of the pulmonary arteries, and Kerley A and B lines are present. When cardiomegaly is present, the heart is greater than half the diameter of the thorax in a posteroanterior chest radiograph (Fig. 20.2). Because radiographic densities primarily reflect alveolar filling and not early interstitial edema, by the time abnormal findings are encountered, the pathologic changes associated with pulmonary edema are advanced. Chest x-ray films typically reveal dense, fluffy opacities that spread outward from the hilar areas to the peripheral borders of the lungs (Figs. 20.2 and 20.4).
FIGURE 20.2 Cardiomegaly (arrow), hilar prominence, and pulmonary edema in congestive heart failure. Note that the heart diameter is greater than half the diameter of the thorax.
• Kerley A lines, which represent deep interstitial edema, radiate out from the hilum into the central portions of the lungs. Kerley A lines do not reach the pleura and are most prevalent in the middle and upper lung regions. Kerley B lines are short, thin, horizontal lines of interstitial edema, usually less than 1 cm in length, that extend inward from the pleural surface. They appear peripherally in contact with the pleura and are parallel to one another at right angles to the pleura. Although they may be seen in any lung region, they are most commonly seen in the lung bases (Fig. 20.3).
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FIGURE 20.3 Kerley lines. Septal lines caused by pulmonary edema. Kerley B lines are short horizontal lines at the lung periphery (vertical arrows). Kerley A lines are lines radiating from the hila (oblique arrow). (From Hansell, D. M., Lynch, D. A.,
McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.]. Philadelphia, PA: Elsevier.)
• Severe left-sided heart failure: During this stage, the patient's chest radiograph shows cardiomegaly; pulmonary artery engorgement; interstitial pulmonary edema; fluffy, patchy areas of alveolar edema; and often the appearance of the “bat's wing pattern” (also called the butterfly pattern). The peripheral portion of the lungs often remains clear, and this produces what is described as a “butterfly” or “bat's wing” distribution (see Fig. 20.4). Pleural effusion also may be seen.
FIGURE 20.4 Bat's wing or butterfly pattern caused by pulmonary edema. This example is typical in that it is bilateral but not symmetric. The shadowing is maximal in the central (perihilar) portions of the lung, and the outer portions of the lungs are relatively clear. (From Hansell, D. M., Lynch, D. A., McAdams, H. P., et al. [2010]. Imaging of diseases of the chest [5th ed.].
Philadelphia, PA: Elsevier.)
Noncardiogenic Pulmonary Edema
In noncardiogenic pulmonary edema the chest radiograph commonly shows areas of fluffy densities that are usually more dense near the hilum. The infiltrates may be unilateral or bilateral. Pleural effusion is usually not present and (most important) the cardiac silhouette is not enlarged.
General Management of Pulmonary Edema
The treatment for pulmonary edema is based on the cause—that is, noncardiogenic versus cardiogenic pulmonary edema— and the severity.
Noncardiogenic Pulmonary Edema
The treatment for noncardiogenic pulmonary edema is largely supportive and aimed at ensuring adequate ventilation and oxygenation. Unfortunately, there are no specific treatments to correct an underlying alveolar-capillary membrane permeability problem or to control the pulmonary inflammatory events that ensue once they are triggered—for example, by inhaled toxic agents or a drug overdose—beyond mechanical ventilation and supportive care. Occasionally, the specific cause of the noncardiogenic pulmonary edema can be identified and treated. For example, noncardiogenic pulmonary edema caused by a severe infection, such as sepsis, is treated with antibiotics, and high altitude pulmonary edema (HAPE) by returning the patient to a lower elevation or by supplemental oxygen and positive-pressure ventilation.
Cardiogenic Pulmonary Edema
For cardiogenic pulmonary edema, the initial management is directed at the use of digitalis (if indicated), supplemental oxygen, assisted ventilation if necessary, and a loop diuretics for volume overload.
The therapeutic intervention to address the patient's circulatory systems has the following three main goals: (1) reduction of pulmonary venous return (preload reduction), (2) reduction of systemic vascular resistance (afterload reduction), and (3) inotropic support (treatment of reduced cardiac contractility).
Reduction of the preload decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli. Reduction of afterload increases cardiac output and improves renal perfusion, which in turn allows for diuresis in the patient with fluid overload. Inotropic agents are used to treat hypotension or signs of organ hypoperfusion. While the patient's circulatory problem(s) is/are treated, intubation and mechanical ventilation may be
necessary to achieve adequate ventilation, oxygenation, and airway management. Common medications used to treat cardiogenic pulmonary edema are discussed as follows.
Preload Reducers
Reduced pulmonary venous return decreases pulmonary capillary hydrostatic pressure and reduces fluid transudation into the pulmonary interstitium and alveoli. Preload reducers include:
•Nitroglycerin (Nitro-Bid, Minitran, Nitrostat): A very effective, predictable, and rapid-acting medication for preload.
•Loop diuretics (e.g., furosemide): Considered a cornerstone in the treatment of cardiogenic pulmonary edema. Loop diuretics are presumed to decrease preload through diuresis and direct vasodilation.
•Morphine sulfate: May be used in some cases to reduce preload. However, the adverse effects (e.g., nausea and vomiting or respiratory depression) may outweigh the potential benefit, especially with the availability of nitroglycerin, which is a more effective preload reducing agent.
Afterload Reducers
Reduced systemic vascular resistance increases cardiac output and improves renal perfusion, allowing for diuresis. Afterload reducers include:
•Captopril: Prevents the conversion of angiotensin I to angiotensin II. It is a potent vasodilator. Afterload and cardiac output usually improve in 10 to 15 minutes.
•Enalapril (Vasotec): Is a competitive angiotensin-converting enzyme (ACE) inhibitor and reduces angiotensin II levels.
•Nitroprusside (Nitropress): Is a potent, direct smooth muscle-relaxing agent that primarily reduces afterload. It can also mildly reduce preload.
Positive Inotropic Agents
These agents are used for their vasodilation effects and to increase myocardial contraction and cardiac output. Positive inotropic agents include the following:
• Dobutamine: Is a synthetic catecholamine that mainly has beta1-receptor activity but also has some beta2-receptor and alpha-receptor activity. Commonly used for patients with mild hypotension (e.g., systolic blood pressure 90 to 100 mm Hg).
•Dopamine: Is a naturally occurring catecholamine that acts as a precursor to norepinephrine. Dopamine hemodynamic effect is dose dependent. A low dose is associated with dilation in the renal and splanchnic vasculature, enhancing diuresis. A moderate dose enhances cardiac contractility and heart rate. A high dose increases afterload because of peripheral vasoconstriction and must be used with care in patients with normal blood pressure (i.e., normotensive). Dopamine is generally reserved for patients with moderate hypotension (e.g., systolic blood pressure 70 to 90 mm Hg).
•Norepinephrine: Is a naturally occurring catecholamine with potent alpha-receptor and mild beat-receptor activity. It simulates beta1-adrenergic and alpha-adrenergic receptors,
increasing myocardial contractility, heart rate, and vasoconstriction. Norepinephrine increases blood pressure and afterload. Norepinephrine is generally reserved for patients with severe hypotension (e.g., systolic blood pressure less than 70 mm Hg).
• Milrinone: Is a positive inotropic agent and vasodilator. It reduces afterload and preload and increases cardiac output.
Other Agents
•Antidysrhythmic agents: Such as drugs to control bradycardia (e.g., atropine) or tachycardia (e.g., digitalis, procainamide or metoprolol) may be administered.
•Albumin: Is sometimes administered to increase the patient's oncotic pressure in an effort to offset the increased hydrostatic forces of cardiogenic pulmonary edema, if the patient's osmotic pressure is extremely low.
Respiratory Care Treatment Protocols
Oxygen Therapy Protocol
Oxygen therapy is used to treat hypoxemia, decrease the work of breathing, and decrease myocardial work. The hypoxemia that develops in pulmonary edema is most commonly caused by the interstitial and alveolar fluid, atelectasis, and capillary shunting associated with the disorder. Hypoxemia caused by capillary shunting is at least partially refractory to oxygen therapy (see Oxygen Therapy Protocol, Protocol 10.1).
Lung Expansion Therapy Protocol
Lung expansion therapy is commonly used to offset the fluid accumulation and atelectasis associated with cardiogenic pulmonary edema. High-flow mask continuous positive airway pressure (CPAP) has been shown to produce a significant and rapid improvement in oxygenation and ventilatory status in patients with pulmonary edema. Mask continuous positive airway pressure improves decreased lung compliance, reduces the work of breathing, enhances gas exchange, and decreases vascular congestion in patients with pulmonary edema. In fact, mask CPAP is initially prescribed (at least for a trial period) for patients with pulmonary edema who have arterial blood gas (ABG) values that indicate impending ventilatory failure or acute ventilatory failure—the hallmark clinical manifestations for mechanical ventilation. Often, mask CPAP dramatically improves oxygenation and ventilatory status in these patients and eliminates the need for mechanical
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ventilation (see Lung Expansion Therapy Protocol, Protocol 10.3).
Mechanical Ventilation Protocol
Mechanical ventilation may be necessary to provide and support alveolar gas exchange and eventually return the patient to spontaneous breathing. Because acute ventilatory failure is occasionally seen in patients with severe cardiogenic and noncardiogenic pulmonary edema, continuous mechanical ventilation may be required. Continuous mechanical ventilation is justified when the acute ventilatory failure is thought to be reversible (see Ventilator Initiation and Management Protocol, Protocol 11.1, and Ventilator Weaning Protocol, Protocol 11.2).
Case Study Pulmonary Edema
Admitting History and Physical Examination
This 76-year-old man was admitted to the emergency department (ED) in obvious respiratory distress. His wife reported that her husband had gone to bed feeling well. He woke up with chest pain at about 2:30 a.m., very short of breath. She became concerned and called an ambulance. Neither the patient nor the wife was a good historian, but they did report that the patient had been under a physician's care for some time for “heart trouble” and that he was taking “little white pills” on a daily basis. For the previous 3 days, he had not taken any medication.
On admission to the ED, the patient was mildly disoriented and slightly cyanotic. He repeatedly tried to take the oxygen mask from his face. He complained of a feeling of suffocation. His neck veins were distended, and the skin of his extremities was mottled. On auscultation, there were coarse crackles in both lower lung fields and some crackles in the middle and upper lung fields.
His cough was productive of pinkish, frothy sputum. His vital signs were blood pressure 105/50, heart rate 124 beats/min, and respiratory rate 28 breaths/min. He was afebrile. An electrocardiogram (ECG) showed evidence of an old myocardial infarct, sinus tachycardia, and an occasional premature ventricular contraction. Chest x-ray films taken in the ED with the patient in a sitting position revealed bilateral fluffy infiltrates, more marked in the lower lung fields. The heart was enlarged. All other laboratory findings were within normal limits. Blood gases on an FIO2 of 0.30 were pH 7.11, PaCO2
72 mm Hg, 
22 mEq/L, PaO2 56 mm Hg, and SaO2 75%.
The respiratory therapist working in the ED during the night shift recorded the following SOAP note.
Respiratory Assessment and Plan
S Patient states “a feeling of suffocation.”
O Cyanosis, disorientation. Distended neck veins and mottled extremities. BP 105/50, HR 124, RR 28. ECG: Sinus tachycardia and occasional PVCs. Coarse crackles bilaterally. Frothy pink sputum. CXR: Bilateral fluffy infiltrates and an enlarged heart. ABGs: pH 7.11, PaCO2 72,
22, PaO2 56, and SaO2 75% (FIO2 0.30).
A
•Myocardial infarction (old)
•Acute pulmonary edema (CXR)
•Acute ventilatory failure with moderate hypoxemia (ABG)
•Lactic acidosis likely
•Large and small airway secretions (coarse crackles)
P Oxygen Therapy Protocol: Increase FIO2 to 0.60 via continuous CPAP mask at 25 cm H2O per
Lung Expansion Therapy Protocol. Remain on standby for emergency endotracheal intubation and ventilator support. Continue ECG and oximetry monitoring, and repeat ABG in 30 minutes.
The patient was admitted on the cardiology service with a diagnosis of pulmonary edema–cardiogenic congestive heart failure (CHF). ECG monitoring and continuous oximetry were followed. Treatment consisted of intravenous furosemide, dopamine, nitroprusside, and mask CPAP at 25 cm H2O pressure with an FIO2 of 0.60. A Foley catheter was placed.
Two hours later, the patient's condition was very much improved and he was no longer cyanotic. Vital signs were blood pressure 126/70, heart rate 96 beats/min, and respiratory rate 18 breaths/min. The ECG revealed no ectopic beats. Auscultation showed considerable improvement. There were still some basilar crackles, but the upper lung fields were clear. Cough was much reduced and no longer productive. Repeat chest x-ray examination at the bedside showed considerable improvement. Urine output was in excess of 600 mL/h. The patient was calm and rational, stating that he was
less short of breath and had no pain. Repeat ABGs revealed pH 7.35, PaCO2 46 mm Hg, |
24 mEq/L, PaO2 |
120 mm Hg, SaO2 97% on an FIO2 of 0.60 and CPAP of 25 cm H2O. His LVEF was 47%. The following respiratory therapy SOAP note was made at the time.
Respiratory Assessment and Plan
S Patient states, “I'm less short of breath. No pain.”
O Not cyanotic. BP 126/70, HR 96, RR 18. ECG: Mild sinus tachycardia without ectopic beats.
Fewer crackles; no sputum production; CXR: Improved. ABGs: pH 7.35, PaCO2 46, 
24, PaO2 120, and SaO2 97% (FIO2 0.60 and CPAP of 25 cm H2O).
A
•Decreased pulmonary edema (overall impression from the data)
•No longer in acute ventilatory failure (ABG)
•Acceptable acid-base status with mild overcorrected hypoxemia (ABG)
•Secretions controlled (no sputum and fewer crackles)
•Congestive heart failure with resolving pulmonary edema
P Reduce O2 per Oxygen Therapy Protocol to 2 L/min by nasal cannula. Discontinue CPAP per Lung Expansion Therapy Protocol. Continue ECG and oximetry monitoring. Repeat ABG in 60
minutes.
Discussion
Acute pulmonary edema is a classic finding in severe CHF. Several clinical manifestations associated with increased alveolar-capillary membrane thickness (see Fig. 10.9) were present in this case. For example, the patient's decreased lung compliance was manifested in his tachycardia and tachypnea, whereas his hypoxemia reflected diffusion blockade and intrapulmonary shunting associated with classic pulmonary edema. His lung compliance was so reduced that he had progressed to acute ventilatory failure—that is, the severe stage of pulmonary edema. Frank pulmonary edema caused by left ventricular failure typically improves markedly when treated with CPAP. Some atelectasis (see Fig. 10.7) was doubtless also present and provided further rationale for CPAP therapy.
Often, the first-line management of pulmonary edema consists only of improving myocardial efficiency, decreasing the cardiovascular afterload, decreasing the hypervolemia, providing CPAP, and improving oxygenation. Furosemide (Lasix) is a potent loop diuretic, dopamine has direct inotropic effects, and nitroprusside is a potent peripheral vasodilator. In this case, the combination of all these therapies resulted in a marked improvement of the patient's condition.
In short, this patient had an acute respiratory problem but the basic cause was cardiac. After the cardiac condition was treated, the respiratory symptoms rapidly disappeared. CPAP and an increased FIO2 were adequate, and this patient was
spared the trauma and risk associated with intubation and mechanical ventilation. No evidence of acute myocardial infarction was found. He was discharged after 48 hours, with his condition much improved. He was instructed to take his cardiac medication and diuretics without fail and to return to his family physician in 3 days.
Self-Assessment Questions
1.Which of the following is an afterload reducer?
a.Procainamide
b.Dopamine
c.Furosemide
d.Nitroprusside
2.What is the normal hydrostatic pressure in the pulmonary capillaries?
a.5 to 10 mm Hg
b.10 to 15 mm Hg
c.15 to 20 mm Hg
d.20 to 25 mm Hg
3.What is the normal oncotic pressure of the blood?
a.10 to 15 mm Hg
b.15 to 20 mm Hg
c.20 to 25 mm Hg
d.25 to 30 mm Hg
4.Which of the following are causes of cardiogenic pulmonary edema? 1. Excessive fluid administration
2.Right ventricular failure
3.Mitral valve disease
4.Pulmonary embolus
a.1 and 2 only
b.1, 2, and 3 only
c.2, 3, and 4 only
d.1, 3, and 4 only
5.As a result of pulmonary edema, the patient's:
1.RV is decreased
2.FRC is increased
3.VC is increased
4.TLC is increased
a.1 only
b.1 and 4 only
c.2 and 3 only
d.3 and 4 only
6.The left ventricular ejection fraction:
1.Normally is greater than 75%
2.Is a good measure of alveolar ventilation
3.Correlates well with the brain natriuretic peptide values
4.Provides a noninvasive measurement of cardiac contractility
a.1 and 2 only
b.2 and 4 only
c.3 and 4 only
d.2, 3, and 4 only
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C H A P T E R 2 1
Pulmonary Vascular Disease
Pulmonary Embolism and Pulmonary Hypertension
CHAPTER OUTLINE
Pulmonary Embolism
Anatomic Alterations of the Lungs
Etiology and Epidemiology
Diagnosis and Screening
Common Tests for Suspected Pulmonary Embolism
Overview of the Cardiopulmonary Clinical Manifestations Associated With Pulmonary Embolism
General Management of Pulmonary Embolism
Thrombolytic Agents
Preventive Measures
Respiratory Care Treatment Protocols
Pulmonary Hypertension
Diagnosis
Management of Pulmonary Hypertension
The Emerging Role of the Respiratory Therapist in Pulmonary Vascular Disorders
Case Study: Pulmonary Embolism
Self-Assessment Questions
CHAPTER OBJECTIVES
After reading this chapter, you will be able to:
•List the anatomic alterations of the lungs associated with pulmonary embolism.
•Describe the causes of pulmonary embolism.
•List the cardiopulmonary clinical manifestations associated with pulmonary embolism.
•Describe the general management of pulmonary embolism.
•Define pulmonary hypertension.
•Differentiate the five clinical classifications of pulmonary hypertension.
•Identify the common signs and symptoms associated with pulmonary hypertension.
•Describe the tests and procedures used to diagnose pulmonary hypertension.
•Describe the pulmonary hypertension severity rating.
•Differentiate the signs and symptoms between right-sided heart failure and left-sided heart failure.
•Describe the role of the respiratory therapist in pulmonary vascular disorders.
•Discuss the treatment selections used to manage acute pulmonary embolism, pulmonary infarction, and pulmonary hypertension.
•Describe the clinical strategies and rationales of the SOAPs presented in the case study.
•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.
KEY TERMS
Alteplase
Biventricular Failure
Calcium Channel Blockers
Chronic Thromboembolic Pulmonary Hypertension
Computed Tomography Pulmonary Angiogram (CTPA)
Cor pulmonale
D-Dimer Blood Test
Deep Venous Thrombosis (DVT)
Echocardiography
Embolus/Embolism
High-Molecular-Weight Heparins
Inferior Vena Cava Vein Filter (Greenfield Filter)
Inhaled Nitric Oxide (iNO) Therapy
Left-Sided Heart Failure
Low-Molecular-Weight Heparins
Phosphodiesterase-5 Inhibitors
Physiologic Dead Space (Wasted Ventilation)
P-Pulmonale (ECG Finding)
Prostanoids
Pulmonary Angiogram
Pulmonary Artery Pressure
Pulmonary Embolectomy
Pulmonary Embolism (PE)
Pulmonary Hypertension (PH)
Pulmonary Infarction
Pulmonary Veno-occlusive Disease
Reteplase
Right-Sided Heart Failure
Saddle Embolus
Streptokinase
Thrombolytic Agents
Thrombus
Ultrasonography
Urokinase
Venous Thrombosis
Ventilation-Perfusion Lung Scan (V/Q Scan)
Virchow's Triad
Warfarin (Coumadin)
Wells Clinical Prediction Rule for Deep Venous Thrombosis
Westermark Sign
Pulmonary Embolism
Anatomic Alterations of the Lungs
A blood clot that forms and remains in a vein is called a thrombus. A blood clot that becomes dislodged and travels to another part of the body is called an embolus (embolism). In some cases, when the embolus significantly disrupts pulmonary arterial blood flow, pulmonary infarction may develop, which in turn may cause alveolar atelectasis, consolidation, and tissue necrosis. Bronchial smooth muscle constriction occasionally accompanies pulmonary embolism. Although the precise mechanism is not known, it is believed that the embolism causes the release of cellular mediators such as serotonin, histamine, and prostaglandins from platelets, which in turn leads to bronchoconstriction. Local areas of alveolar hypocapnia and hypoxemia may also contribute to the bronchoconstriction associated with pulmonary embolism.
An embolus may originate from one large thrombus or occur as a shower of small thrombi and may or may not interfere with the right ventricle's ability to perfuse the lungs adequately. When a large embolus detaches from a thrombus and passes through the right side of the heart, it may lodge in the bifurcation of the pulmonary artery, where it forms what is known as a saddle embolus. A large saddle embolus is often quickly fatal, because it can significantly block pulmonary blood from returning to the left ventricle and being pumped out to the systemic circulation (partially shown in Fig. 21.1A).
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FIGURE 21.1 (A) Pulmonary embolism (PE). (B) Bronchial smooth muscle constriction; (C) atelectasis; and (D) alveolar consolidation are common secondary anatomic alterations of the lungs.
The major pathologic or structural changes of the lungs and heart associated with pulmonary embolism are as follows:
•Blockage of the pulmonary vascular system
•Pulmonary hypertension
•Right-heart failure (cor pulmonale)
•Pulmonary infarction (when severe)
•Alveolar atelectasis
•Alveolar consolidation
•Bronchial smooth muscle constriction (bronchospasm)
Etiology and Epidemiology
Deep vein thrombosis (DVT) and pulmonary embolism (PE) are often clinically insidious disorders. If the pulmonary embolus is relatively small, the early signs and symptoms of its presence are often vague and nonspecific. By contrast, sudden death is often the first symptom in about 25% of people who have a large pulmonary embolus. A massive pulmonary embolism is one of the most common causes of sudden and unexpected death in all age groups. Many cases of pulmonary emboli are undiagnosed and therefore untreated. In fact, because of the subtle and misleading clinical manifestations associated with a pulmonary embolus, the possibility of a blood clot lodged in the lung is often not considered until autopsy in about 70% to 80% of cases.
In the United States, about 100,000 individuals die each year from a pulmonary embolism. Pulmonary embolism is slightly more common in males than females, and the incidence increases with age. The experienced health care practitioner actively works to confirm the diagnosis of a pulmonary embolism as soon as the suspicion arises. This is especially true as the origin of the signs and symptoms of pulmonary embolic disease often cannot be readily identified.
Although there are many possible sources of pulmonary emboli (e.g., fat, air, amniotic fluid, bone marrow, tumor fragments), blood clots are by far the most common. Most pulmonary blood clots originate—or break away from—sites of deep venous thrombosis in the lower part of the body (i.e., the leg and pelvic veins and the inferior vena cava). When a thrombus or a piece of a thrombus breaks loose in a deep vein, the blood clot (now called an embolus) is carried through the venous system to the right atrium and ventricle of the heart and ultimately lodges in the pulmonary arteries or arterioles. There are three primary factors (known as the Virchow triad) associated with the formation of DVT. The Virchow triad includes (1) venous stasis (i.e., slowing or stagnation of blood flow through the veins), (2) hypercoagulability (i.e., the increased tendency of blood to form clots), and (3) injury to the endothelial cells that line the vessels. Box 21.1 provides common risk factors for pulmonary embolism.
Box 21.1
Risk Factors Associated With Pulmonary Embolism
Venous Stasis
•Inactivity
•Prolonged bed rest and/or immobilization
•Prolonged sitting (e.g., car or plane travel)
•Congestive heart failure
•Varicose veins
•Thrombophlebitis
Surgical Procedures
•Hip surgery
•Pelvic surgery
•Knee surgery
•Certain obstetric or gynecologic procedures
Trauma
• Bone fractures (especially of the pelvis and the long bones of the lower extremities)
•Extensive injury to soft tissue
•Postoperative or postpartum states
•Extensive hip or abdominal operations
•Phlegmasia alba dolens puerperium (“milk-leg” of pregnancy)
Hypercoagulation Disorders
•Oral contraceptives
•Polycythemia
•Multiple myeloma
Others
•Obesity
•Pacemakers or venous catheters
•Pregnancy and childbirth
•Supplemental estrogen (estrogen in birth control formulations can increase clotting factors)
•Family history of venous thromboembolism
•Smoking
•Malignant neoplasms
•Burns
Diagnosis and Screening
The diagnosis of a pulmonary embolism is primarily based on the clinical manifestations that support the possibility of pulmonary embolism, followed by the results of a variety of possible blood tests, venous ultrasonography, and one or more lung imaging techniques to secure a definitive diagnosis. Depending on how much of the lung is involved, the size of the embolism, and the overall health of the patient, the signs and symptoms of a pulmonary embolism can vary greatly. Box 21.2 provides common signs and symptoms associated with a suspected pulmonary embolism. As shown in Table 21.1, when a pulmonary embolism is possible, the most commonly used tool to predict its clinical probability is the modified Wells Scoring System. Table 21.2 provides the Wells Clinical Prediction Rule for Deep Venous Thrombosis.
Box 21.2
Signs and Symptoms Commonly Associated With Pulmonary Embolism
•Sudden shortness of breath
•Cardiac arrhythmias
•Sinus tachycardia
•Atrial arrhythmias
•Atrial tachycardia
•Atrial flutter
•Atrial fibrillation
•Acute right ventricular strain pattern and right bundle branch block
•P pulmonale (peaked P waves)
•Weak pulse
•Lightheadedness or fainting
•Anxiety
•Excessive sweating
•Cyanosis
•Cool or clammy skin to the touch
•Chest pain that resembles a heart attack—that is, chest pain that may radiate to the shoulder, arm, neck, or jaw. The pain is often described as sharp, stabbing, aching, or dull. The pain often intensifies when the patient inhales deeply, coughs, eats, or bends over. The pain often intensifies during exertion but may not go completely away during rest.
•Cough
•Blood-streaked sputum
•Wheezing
•Leg swelling
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TABLE 21.1
Wells Clinical Prediction Rule for Pulmonary Embolism
Clinical Feature |
Points |
Clinical symptoms of DVT |
3 |
Other diagnosis less likely than PE |
3 |
Heart rate greater than 100 beats per minute |
1.5 |
Immobilization or surgery within past 4 weeks |
1.5 |
Previous deep vein thrombosis or pulmonary embolism |
1.5 |
Hemoptysis |
1 |
Malignancy |
1 |
Total points |
|
Clinical Probability of Pulmonary Embolism |
|
• High: >6 points |
|
• Moderate: 2–6 |
|
• Low: <2 |
|
Modified from Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon C, Weitz J, D'Ovidio R, Cogo A, Prandoni P, Lancet. 1995;345(8961):1326.
TABLE 21.2
Wells Clinical Prediction Rule for Deep Venous Thrombosis
Clinical Feature |
Points |
Active cancer (treatment within 6 months, or palliation) |
1 |
Paralysis, paresis, or immobilization of lower extremity |
1 |
Bedridden for more than 3 days because of surgery (within 4 weeks) |
1 |
Localized tenderness along distribution of deep veins |
1 |
Entire leg swollen |
1 |
Unilateral calf swelling of greater than 3 cm (below tibial tuberosity) |
1 |
Unilateral pitting edema |
1 |
Collateral superficial veins |
1 |
Alternative diagnosis as likely as or more likely than deep vein thrombosis |
–2 |
Total points |
|
Clinical Probability of Deep Venous Thrombosis |
|
• High: >3 |
|
• Moderate: 1–2 |
|
• Low: <1 |
|
Modified from Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, Kearon C, Weitz J, D'Ovidio R, Cogo A, Prandoni P, Lancet. 1995;345(8961):1326.
Common Tests for Suspected Pulmonary Embolism
Blood Tests
Once it has been established that there is a likely probability of a pulmonary embolism, an array of blood tests may be performed to exclude important secondary causes of pulmonary embolism, including a full blood count, clotting status evaluation, and some screening tests (e.g., erythrocyte sedimentation rate, renal function, liver enzymes, electrolytes). Should any of these tests be abnormal, further investigation is justified.
In individuals who (1) have a family history of blood clots, (2) have had more than one episode of blood clots, or (3) have experienced blood clots for no known reason, the doctor may prescribe a series of blood tests to determine if there are any inherited abnormalities in the blood-clotting system. When genetic abnormalities (e.g., factor V [Leiden] deficiency) are found or there is a history of blood clots, the physician may recommend a lifelong course of anticoagulant therapy. The physician also may recommend that other members of the family receive a screening series of blood tests and other pertinent evaluations.
d-Dimer Blood Test
The D-dimer blood test (also called the fibrinogen test) is used to check for an increased level of the protein fibrinogen, an integral component of the blood-clotting process. The test is relatively simple and fast; it entails drawing a blood sample, and the results can be available in less than 1 hour. D-Dimer values higher than 500 ng/mL are considered positive, which may suggest the possibility of blood clots. However, it should be emphasized that there are many conditions that can increase an individual's D-dimer level, including recent surgery. Thus an elevated D-dimer value is usually used to supplement other clinical information. A normal D-dimer level essentially rules out the possibility of blood clots.
Ultrasonography
An ultrasonography test uses high-frequency sound waves to detect blood clots in the thigh veins. The test is noninvasive and takes only 30 minutes or less to perform. A wand-shaped transducer is used to direct the sound waves to the thigh veins being tested. The sound waves are then reflected back to the transducer and converted to a moving image on a computer screen. The test is very accurate for the diagnosis of blood clots behind the knee or thigh. Although it is relatively sensitive in detecting DVT above the knee, it is insensitive in detecting DVT below the knee
Chest X-Ray
Although the chest x-ray result is often normal in the patient with a pulmonary embolism, it can be used to rule out conditions that mimic a pulmonary embolism, such as pneumonia and pneumothorax. In addition, infiltrates or atelectasis
