Pulmonary embolism overview: Difference between revisions

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Revision as of 02:38, 15 July 2014

Editor(s)-In-Chief: The APEX Trial Investigators, C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2]

Overview

Pulmonary embolism (PE) is an acute obstruction of the pulmonary artery (or one of its branches). The obstruction in the pulmonary artery that causes a PE can be due to thrombus, air, tumor, or fat. Most often, this is due to a venous thrombosis (blood clot from a vein), which has been dislodged from its site of formation in the lower extremities. It has then embolized to the arterial blood supply of one of the lungs. This process is termed thromboembolism. PE is a potentially lethal condition. The patient can present with a range of signs and symptoms, including dyspnea, chest pain while breathing, and in more severe cases collapse, shock, and cardiac arrest. PE treatment requires rapid and accurate risk stratification before the development of hemodynamic collapse and cardiogenic shock. Treatment consists of an anticoagulant medication, such as heparin or warfarin, and in severe cases, thrombolysis or surgery. Pulmonary embolism can be classified based on the time course of symptom presentation (acute and chronic) and the overall severity of disease (stratified based upon three levels of risk: massive, submassive, and low-risk).

Historical Perspective

Throughout history, many renowned researchers and health care professionals have contributed to the understanding, definition, and treatment of pulmonary embolism. Though the first documented case of pulmonary embolism occurred in 1837, historical record of thrombotic disease dates as far back as the 7th century BCE.^[1]

Classification

Pulmonary embolism (PE) can be classified based on the time course of symptom presentation (acute and chronic) and the overall severity of disease (stratified based upon three levels of risk: massive, submassive, and low-risk). Massive PE is characterised by the presence of either sustained hypotension, or pulselessness, or bradycardia. Submassive PE is characterized by the presence of either right ventricular dysfunction or myocardial necrosis in the absence of hypotension. In low risk PE, there is absence of hypotension, shock, right ventricular dysfunction and myocardial necrosis.^[2]

Pathophysiology

Pulmonary embolism (PE) occurs when there is an acute obstruction of the pulmonary artery or one of its branches. It is commonly caused by a venous thrombus that has dislodged from its site of formation and embolized to the arterial blood supply of one of the lungs. The process of clot formation and embolization is termed thromboembolism. PE results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. When pulmonary vascular resistance occurs following an acute PE, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure.^[3]^[4]

Causes

Pulmonary embolism (PE) is the acute obstruction of the pulmonary artery or one of its branches by a thrombus, air, tumor, or fat. Most often, PE is due to a venous thrombus which has been dislodged from its site of formation in the deep veins of the lower extremities, a process referred to as venous thromboembolism.

Differentiation of Pulmonary Embolism from other Diseases

Pulmonary embolism must be distinguished from other life-threatening causes of chest pain including acute myocardial infarction, aortic dissection, and pericardial tamponade, as well as a large list of non-life-threatening causes of chest discomfort and shortness of breath.

Epidemiology and Demographics

The precise number of people affected by venous thromboembolism (VTE), that is either deep vein thrombosis, pulmonary embolism (PE), or both, is unknown, but estimates range from 300,000 to 600,000 (1 to 2 per 1,000, and in those over 80 years of age, as high as 1 in 100) each year in the United States. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited thrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.^[5]^[6]

Risk Factors

The most common sources of pulmonary embolism (PE) are proximal leg deep venous thromboses (DVTs) or pelvic vein thromboses; therefore, any risk factor for DVT also increases the risk of PE. Approximately 15% of patients with a DVT will develop a PE. In these chapters on venous thromboembolism (VTE), the word risk factors refers to those epidemiologic and genetic variables that expose someone to a higher risk of developing venous thrombosis. The word triggers refer to those factors in the patients immediate history or environment that may have lead to the occurrence of the venous thrombosis. The risk factors for VTE are a constellation of predisposing conditions which stem from the three principles of Virchow's triad: stasis of the blood flow, damage to the vascular endothelial cells, and hypercoagulability. Approximately 5 to 8% of the U.S. population has one of several genetic risk factors, also known as inherited thrombophilias in which a genetic defect can be identified that increases the risk for thrombosis.^[7]^[6] The risk factors for VTE can be classified as temporary, modifiable and non-modifiable. It is suggested that venous thrombosis also shares risk factors with arterial thrombosis, such as obesity, hypertension, smoking, and diabetes mellitus.^[8]

Triggers

The triggers of VTE include injury to a deep vein from surgery, a fracture, or other trauma, especially a paralytic spinal cord injury.^[9] Another trigger for VTE is prolonged immobilization that causes stasis in the deep veins which may occur after surgery, prolonged bed-rest, or prolonged seating during travel.

Natural History, Complications and Prognosis

Pulmonary embolism (PE) can be acutely complicated by the development of cardiogenic shock, pulseless electrical activity and sudden cardiac death and chronically by the development of pulmonary hypertension. The medical management of PE often requires the administration of potent parenteral anticoagulants and fibrinolytics and massive bleeding can be a complication of their administration. If left untreated almost one-third of patients with PE die, typically from recurrent PE. However, with prompt diagnosis and treatment, the mortality rate is approximately 2–8%. The true mortality associated with PE may be underestimated as two-thirds of all PE cases are diagnosed by autopsy. Estimates suggest that 60,000-100,000 Americans die of VTE, 10 to 30% of which will die within one month of diagnosis. Sudden death is the first symptom in about one-quarter (25%) of people who have a PE. One-third (about 33%) of people with VTE will have a recurrence within 10 years.^[10]^[6]

Diagnosis

Diagnostic Algorithm

When a patient presents with the cardinal symptoms of pulmonary embolism (PE), such as sudden onset of dyspnea, pleuritic chest pain, tachypnea, and/or tachycardia, the initial step is to stratify the patient into high risk or non-high risk depending on their hemodynamic status. Patients who are suspected to have PE and who are hemodynamically unstable should be administered anticoagulation and should undergo a CT scan or echocardiography if CT scan is unavailable. Among patients who are hemodynamically stable, the pretest probability of PE should be estimated using one of the available scoring systems, the most used of which is the Wells score. Patients who have a low or intermediate pretest probability of PE should undergo D-dimer testing as the initial test, whereas those who have a high pretest probability of PE should undergo a CT scan without a D-dimer test. Patients at intermediate or high pretest probability of PE should be administered anticoagulation therapy before the completion of the diagnotic testing.

Assessment of Clinical Probability and Risk Scores

The diagnosis of pulmonary embolism (PE) is based primarily on the clinical assessment of the pretest probability of PE combined with diagnostic modalities such as spiral CT, V/Q scan, use of the D-dimer, and lower extremity ultrasound. Clinical prediction rules for PE include: the Wells score, the Geneva score and the PE rule-out criteria (PERC).

Assessment of the Probability of Subsequent PE ad Risk Scores

Venous thromboembolism (VTE) consists of deep vein thrombosis (DVT), pulmonary embolism (PE), or both. VTE is a disease associated with morbidity and mortality; therefore, VTE prophylaxis is indicated among specific categories of patients at elevated risk for VTE. Several scores have been developed for the assessment of risk of subsequent VTE such as the Padua prediction score and the IMPROVE score among hospitalized medically ill patients, and Roger's score and Caprini score among surgical patients.

History and Symptoms

A proper history and physical exam is crucial to establish an accurate diagnosis of pulmonary embolism (PE). The symptoms of pulmonary embolism (PE) depend on the severity of the disease, ranging from mild dyspnea, chest pain, and cough, to sustained hypotension and shock.^[11]^[12] A PE may also be an incidental finding in so far as many patients are asymptomatic.^[12]^[13] Sudden death can be the initial presentation of PE. One of the first steps in the management of PE is the determination of the Wells score for PE, whose criteria can be ascertained solely on the basis of history and physical exam. Symptoms of DVT of the lower extremity may be present.

Physical Examination

Pulmonary embolism (PE) is associated with the presence of tachycardia and tachypnea. Signs of right ventricular failure include jugular venous distension, a right sided S3, and a parasternal lift. These signs are often present in cases of massive and submassive pulmonary emboli, also known as intermediate-risk and high-risk respectively.^[11]^[14] Since PE most commonly occurs as a complication of deep vein thrombosis (DVT), the physical examination should include an assessment of the lower extremities for erythema, tenderness, and/or swelling.

Laboratory Findings

The results of routine laboratory tests including arterial blood gas analysis are non-specific in making the diagnosis of pulmonary embolism (PE). These laboratory studies can be obtained to rule-out other cause of chest discomfort and tachypnea. In patients with acute PE, non-specific lab findings include: leukocytosis, elevated ESR with an elevated serum LDH and serum transaminase (especially AST or SGOT). A negative D-dimer in a patient with low to intermediate probability of PE strongly suggests PE is not present.

Arterial Blood Gas Analysis

Hypoxemia, hypocapnia, increased alveolar-arterial gradient, and respiratory alkalosis are the typical findings that may be observed in patients with pulmonary embolism (PE). The absence of the typical results of the arterial blood gas (ABG) analysis, however, does not exclude PE.^[15] ABG analysis results do not contribute reliably to tailoring the management of the patients among whom PE is suspected.^[16]

D-dimer

D-dimer is used in the diagnosis of deep vein thrombosis and pulmonary embolism among patients with low or unlikely probability of venous thromboembolism.^[17]^[18] While 500 ng/mL has long been the most commonly used cut off value for abnormal D-dimer concentration, recent studies suggest the use of an age adjusted cut-off concentration of D-dimer. The age adjusted cut-off value of D-dimer is 500 ng/mL for subjects whose age is less than 50 years, and the age multiplied by 10 for subjects older than 50 years.^[19]^[20]^[21]

Biomarkers

Although the usefulness of brain natriuretic peptide (BNP) concentrations to diagnose pulmonary embolism (PE) is limited,^[22] elevated BNP and pro-BNP levels are associated with right ventricular dysfunction and increased mortality, and are therefore useful prognostic markers.^[12] The evaluation of troponin concentration also serves as a useful prognostic marker to identify myocardial necrosis^[23]^[24] and mortality associated with acute PE.^[25]

Electrocardiogram

The electrocardiogram (ECG) in the cases of pulmonary embolism (PE) is often abnormal; however, the ECG abnormalities are neither sensitive nor specific.^[26]^[27] Some of the most common ECG abnormalities in PE include T wave inversion in the anterior leads and sinus tachycardia.^[28]^[29]^[27] The ECG abnormalities reported in PE are also present in a variety of other conditions rendering the utility of ECG for the diagnosis of PE limited. Nevertheless, an ECG is routinely performed in all patients with suspected PE in order to rule out other differential diagnoses such as myocardial infarction.

Chest X Ray

A chest X ray is often obtained in patients with shortness of breath to diagnose pneumonia, congestive heart failure, and rib fracture. Although the chest X ray in the setting of a pulmonary embolism is often abnormal, the findings are non-specific and are not diagnostic of a pulmonary embolus.^[30]

Ventilation/Perfusion Scan

A ventilation/perfusion scan (otherwise known as V/Q scan or lung scintigraphy) is a study which shows whether an area of the lung is being ventilated with oxygen and perfused with blood. In the setting of a PE, perfusion can be obstructed due to the formation of a clot. The V/Q scan is less commonly used due to the more widespread availability of CT technology, however it may be useful in patients who have an allergy to iodinated contrast. It may also be useful in pregnant patients in an attempt to minimize radiation exposure.

Echocardiography

Approximately 40% of patients with pulmonary embolism have evidence of right heart strain on echocardiography. When RV dysfunction or RV thrombus are identified on echocardiography, this finding provides further risk stratification. Routine echocardiography in patients with suspected pulmonary embolism is not required. However if elevations in the cardiac troponins or brain natriuretic peptide are present, then acute right ventricular strain may be present and echocardiography may be warranted.^[31]

Compression Ultrasonography

Compression Ultrasonography, also known as a Doppler study of the legs, or lower extremity noninvasive studies (LENIS) is used to evaluate a patient for the presence of deep venous thrombosis (DVT) in the lower extremities, which can lead to the development of a pulmonary embolism. The presence of a DVT shown by ultrasonography is enough to warrant anticoagulation without a V/Q or spiral CT scans. The decision to anticoagulant patient with a positive compression ultrasound is due to the strong association between deep vein thrombosis and subsequent pulmonary embolism. Compression ultrasonography is also a preferred method of evaluation during pregnancy, a time during which the other modalities would increase the risk of birth defects due to radiation exposure. A negative compression ultrasound does not rule out a pulmonary embolism, and an additional low-radiation dose scanning may be required in a pregnant patient to further rule out pulmonary embolism.

CT

Contrast pulmonary angiography is the gold standard when diagnosing a PE. The disadvantages of using pulmonary angiography are its invasiveness, high costs, limited availability, and the need of an expert radiologist. This chapter deals with the advantages of multidetector CT over CTPA.

CT Pulmonary Angiography

Computed tomography with radiocontrast is the imaging modality of choice in the diagnosis of pulmonary embolism.

MRI

Magnetic resonance pulmonary angiography should be considered in the setting of a pulmonary embolism only at centers that routinely perform it well and only for patients for whom standard tests are contraindicated. MRA has a sensitivity and specificity of 78% and 99% respectively.^[32]

Other Imaging Findings

Pulmonary angiography is the gold standard for diagnosing a pulmonary embolism (PE). The Pulmonary angiogram has a sensitivity and specificity of >95% in diagnosing a PE. The estimated false-negative rate is 0.5% – 1.7%. Pulmonary angiography is presently used less frequently in the diagnosis of pulmonary embolism due to wider acceptance of CT scans, which are non-invasive. CT pulmonary angiography is the recommended first line diagnostic imaging test in most people. A negative CT pulmonary angiogram excludes a clinically important pulmonary embolism.^[33] Multi-Detector Computed Tomography (MDCTA) has rapidly replaced the use of pulmonary angiography in the clinical setting because MDCT is less invasive and easier to perform. Therefore, pulmonary angiography should only be performed first if MDCTA is unavailable or contraindicated.

Treatment

Treatment Algorithm

Prompt recognition, diagnosis and treatment of pulmonary embolism is critical. Anticoagulant therapy is the mainstay of treatment for patients who are hemodynamically stable. If hemodynamic compromise is present, then fibrinolytic therapy is recommended.

Surgery

Surgical management of acute pulmonary embolism (pulmonary thrombectomy) is uncommon and has largely been abandoned because of poor long-term outcomes. However, recently, it has gone through a resurgence with the revision of the surgical technique and is thought to benefit selected patients.^[34] Chronic pulmonary embolism leading to pulmonary hypertension (known as chronic thromboembolic hypertension) is treated with a surgical procedure known as a pulmonary thromboendarterectomy.

References

↑ Wood KE (2009). "A history of pulmonary embolism and deep venous thrombosis". Crit Care Clin. 25 (1): 115–31, viii. doi:10.1016/j.ccc.2008.12.014. PMID 19268798.
↑ Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ; et al. (2011). "Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association". Circulation. 123 (16): 1788–830. doi:10.1161/CIR.0b013e318214914f. PMID 21422387.
↑ Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.
↑ Lualdi JC, Goldhaber SZ (1995). "Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications". Am Heart J. 130 (6): 1276–82. PMID 7484782.
↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
↑ ^6.0 ^6.1 ^6.2 Beckman MG, Hooper WC, Critchley SE, Ortel TL (2010). "Venous thromboembolism: a public health concern". Am J Prev Med. 38 (4 Suppl): S495–501. doi:10.1016/j.amepre.2009.12.017. PMID 20331949.
↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
↑ Goldhaber SZ (2010). "Risk factors for venous thromboembolism". J Am Coll Cardiol. 56 (1): 1–7. doi:10.1016/j.jacc.2010.01.057. PMID 20620709.
↑ Anderson FA, Spencer FA (2003). "Risk factors for venous thromboembolism". Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980. Unknown parameter |month= ignored (help)
↑ CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein
↑ ^11.0 ^11.1 Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK (2007). "Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II". The American Journal of Medicine. 120 (10): 871–9. doi:10.1016/j.amjmed.2007.03.024. PMC 2071924. PMID 17904458. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
↑ ^12.0 ^12.1 ^12.2 Agnelli G, Becattini C (2010). "Acute pulmonary embolism". The New England Journal of Medicine. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
↑ Stein PD, Matta F, Musani MH, Diaczok B (2010). "Silent pulmonary embolism in patients with deep venous thrombosis: a systematic review". The American Journal of Medicine. 123 (5): 426–31. doi:10.1016/j.amjmed.2009.09.037. PMID 20399319. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)
↑ Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). "Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)". Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.
↑ Stein PD, Goldhaber SZ, Henry JW, Miller AC (1996). "Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism". Chest. 109 (1): 78–81. PMID 8549223.
↑ Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS (2000). "Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism". American Journal of Respiratory and Critical Care Medicine. 162 (6): 2105–8. PMID 11112122. Retrieved 2012-04-30. Unknown parameter |month= ignored (help)
↑ Wells PS, Owen C, Doucette S, Fergusson D, Tran H (2006). "Does this patient have deep vein thrombosis?". JAMA. 295 (2): 199–207. doi:10.1001/jama.295.2.199. PMID 16403932. Review in: Evid Based Med. 2006 Aug;11(4):119 Review in: ACP J Club. 2006 Jul-Aug;145(1):24
↑ Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D; et al. (2001). "Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer". Ann Intern Med. 135 (2): 98–107. PMID 11453709.
↑ Douma RA, Tan M, Schutgens RE, Bates SM, Perrier A, Legnani C; et al. (2012). "Using an age-dependent D-dimer cut-off value increases the number of older patients in whom deep vein thrombosis can be safely excluded". Haematologica. 97 (10): 1507–13. doi:10.3324/haematol.2011.060657. PMC 3487551. PMID 22511491.
↑ Schouten HJ, Geersing GJ, Koek HL, Zuithoff NP, Janssen KJ, Douma RA; et al. (2013). "Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis". BMJ. 346: f2492. doi:10.1136/bmj.f2492. PMC 3643284. PMID 23645857.
↑ Righini M, Van Es J, Den Exter PL, et al. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study. JAMA. 2014;311(11):1117-1124. doi:10.1001/jama.2014.2135.
↑ Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR (2006). "Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism". Journal of Thrombosis and Haemostasis : JTH. 4 (3): 552–6. doi:10.1111/j.1538-7836.2005.01752.x. PMID 16405522. Retrieved 2012-05-01. Unknown parameter |month= ignored (help)
↑ Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB (2000). "Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction". Journal of the American College of Cardiology. 36 (5): 1632–6. PMID 11079669. Retrieved 2012-05-02. Unknown parameter |month= ignored (help)
↑ Horlander KT, Leeper KV (2003). "Troponin levels as a guide to treatment of pulmonary embolism". Current Opinion in Pulmonary Medicine. 9 (5): 374–7. PMID 12904706. Retrieved 2012-05-02. Unknown parameter |month= ignored (help)
↑ Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S; et al. (2008). "Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism". Eur Respir J. 31 (4): 847–53. doi:10.1183/09031936.00113307. PMID 18094010.
↑ Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV (2005). "Prognostic value of the ECG on admission in patients with acute major pulmonary embolism". Eur Respir J. 25 (5): 843–8. doi:10.1183/09031936.05.00119704. PMID 15863641.
↑ ^27.0 ^27.1 Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P; et al. (2000). "Diagnostic value of the electrocardiogram in suspected pulmonary embolism". Am J Cardiol. 86 (7): 807–9, A10. PMID 11018210.
↑ Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M (1997). "The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports". Chest. 111 (3): 537–43. PMID 9118684.
↑ Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). "The electrocardiogram in acute pulmonary embolism". Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.
↑ Worsley D, Alavi A, Aronchick J, Chen J, Greenspan R, Ravin C (1993). "Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study". Radiology. 189 (1): 133–6. PMID 8372182.
↑ Kucher N, Goldhaber SZ (2003). "Cardiac biomarkers for risk stratification of patients with acute pulmonary embolism". Circulation. 108 (18): 2191–4. doi:10.1161/01.CIR.0000100687.99687.CE. PMID 14597581.
↑ Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR (1997). "Diagnosis of pulmonary embolism with magnetic resonance angiography". N. Engl. J. Med. 336 (20): 1422–7. doi:10.1056/NEJM199705153362004. PMID 9145679. Retrieved 2011-12-14. Unknown parameter |month= ignored (help)
↑ Stein PD, Henry JW, Gottschalk A (1999). "Reassessment of pulmonary angiography for the diagnosis of pulmonary embolism: relation of interpreter agreement to the order of the involved pulmonary arterial branch". Radiology. 210 (3): 689–91. PMID 10207468.
↑ Augustinos P, Ouriel K (2004). "Invasive approaches to treatment of venous thromboembolism". Circulation. 110 (9 Suppl 1): I27–34. PMID 15339878.

Template:WH Template:WS

[pmid19268798-1] Wood KE (2009). "A history of pulmonary embolism and deep venous thrombosis". Crit Care Clin. 25 (1): 115–31, viii. doi:10.1016/j.ccc.2008.12.014. PMID 19268798.

[pmid21422387-2] Jaff MR, McMurtry MS, Archer SL, Cushman M, Goldenberg N, Goldhaber SZ; et al. (2011). "Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association". Circulation. 123 (16): 1788–830. doi:10.1161/CIR.0b013e318214914f. PMID 21422387.

[pmid3916797-3] Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.

[pmid7484782-4] Lualdi JC, Goldhaber SZ (1995). "Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications". Am Heart J. 130 (6): 1276–82. PMID 7484782.

[CDC-5] CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein

[pmid20331949-6] 6.0 ^6.1 ^6.2 Beckman MG, Hooper WC, Critchley SE, Ortel TL (2010). "Venous thromboembolism: a public health concern". Am J Prev Med. 38 (4 Suppl): S495–501. doi:10.1016/j.amepre.2009.12.017. PMID 20331949.

[7] CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein

[pmid20620709-8] Goldhaber SZ (2010). "Risk factors for venous thromboembolism". J Am Coll Cardiol. 56 (1): 1–7. doi:10.1016/j.jacc.2010.01.057. PMID 20620709.

[pmid12814980-9] Anderson FA, Spencer FA (2003). "Risk factors for venous thromboembolism". Circulation. 107 (23 Suppl 1): I9–16. doi:10.1161/01.CIR.0000078469.07362.E6. PMID 12814980. Unknown parameter |month= ignored (help)

[10] CDC- Deep Vein Thrombosis (DVT) / Pulmonary Embolism (PE) — Blood Clot Forming in a Vein

[pmid17904458-11] 11.0 ^11.1 Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK (2007). "Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II". The American Journal of Medicine. 120 (10): 871–9. doi:10.1016/j.amjmed.2007.03.024. PMC 2071924. PMID 17904458. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)

[pmid20592294-12] 12.0 ^12.1 ^12.2 Agnelli G, Becattini C (2010). "Acute pulmonary embolism". The New England Journal of Medicine. 363 (3): 266–74. doi:10.1056/NEJMra0907731. PMID 20592294. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)

[pmid20399319-13] Stein PD, Matta F, Musani MH, Diaczok B (2010). "Silent pulmonary embolism in patients with deep venous thrombosis: a systematic review". The American Journal of Medicine. 123 (5): 426–31. doi:10.1016/j.amjmed.2009.09.037. PMID 20399319. Retrieved 2012-04-26. Unknown parameter |month= ignored (help)

[pmid18757870-14] Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P; et al. (2008). "Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC)". Eur Heart J. 29 (18): 2276–315. doi:10.1093/eurheartj/ehn310. PMID 18757870.

[pmid8549223-15] Stein PD, Goldhaber SZ, Henry JW, Miller AC (1996). "Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism". Chest. 109 (1): 78–81. PMID 8549223.

[pmid11112122-16] Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS (2000). "Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism". American Journal of Respiratory and Critical Care Medicine. 162 (6): 2105–8. PMID 11112122. Retrieved 2012-04-30. Unknown parameter |month= ignored (help)

[pmid16403932-17] Wells PS, Owen C, Doucette S, Fergusson D, Tran H (2006). "Does this patient have deep vein thrombosis?". JAMA. 295 (2): 199–207. doi:10.1001/jama.295.2.199. PMID 16403932. Review in: Evid Based Med. 2006 Aug;11(4):119 Review in: ACP J Club. 2006 Jul-Aug;145(1):24

[pmid11453709-18] Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D; et al. (2001). "Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer". Ann Intern Med. 135 (2): 98–107. PMID 11453709.

[pmid22511491-19] Douma RA, Tan M, Schutgens RE, Bates SM, Perrier A, Legnani C; et al. (2012). "Using an age-dependent D-dimer cut-off value increases the number of older patients in whom deep vein thrombosis can be safely excluded". Haematologica. 97 (10): 1507–13. doi:10.3324/haematol.2011.060657. PMC 3487551. PMID 22511491.

[pmid23645857-20] Schouten HJ, Geersing GJ, Koek HL, Zuithoff NP, Janssen KJ, Douma RA; et al. (2013). "Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis". BMJ. 346: f2492. doi:10.1136/bmj.f2492. PMC 3643284. PMID 23645857.

[JAMA_2014-21] Righini M, Van Es J, Den Exter PL, et al. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study. JAMA. 2014;311(11):1117-1124. doi:10.1001/jama.2014.2135.

[pmid16405522-22] Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR (2006). "Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism". Journal of Thrombosis and Haemostasis : JTH. 4 (3): 552–6. doi:10.1111/j.1538-7836.2005.01752.x. PMID 16405522. Retrieved 2012-05-01. Unknown parameter |month= ignored (help)

[pmid11079669-23] Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB (2000). "Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction". Journal of the American College of Cardiology. 36 (5): 1632–6. PMID 11079669. Retrieved 2012-05-02. Unknown parameter |month= ignored (help)

[pmid12904706-24] Horlander KT, Leeper KV (2003). "Troponin levels as a guide to treatment of pulmonary embolism". Current Opinion in Pulmonary Medicine. 9 (5): 374–7. PMID 12904706. Retrieved 2012-05-02. Unknown parameter |month= ignored (help)

[pmid18094010-25] Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S; et al. (2008). "Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism". Eur Respir J. 31 (4): 847–53. doi:10.1183/09031936.00113307. PMID 18094010.

[pmid15863641-26] Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV (2005). "Prognostic value of the ECG on admission in patients with acute major pulmonary embolism". Eur Respir J. 25 (5): 843–8. doi:10.1183/09031936.05.00119704. PMID 15863641.

[pmid11018210-27] 27.0 ^27.1 Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P; et al. (2000). "Diagnostic value of the electrocardiogram in suspected pulmonary embolism". Am J Cardiol. 86 (7): 807–9, A10. PMID 11018210.

[pmid9118684-28] Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M (1997). "The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports". Chest. 111 (3): 537–43. PMID 9118684.

[pmid123074-29] Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). "The electrocardiogram in acute pulmonary embolism". Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.

[30] Worsley D, Alavi A, Aronchick J, Chen J, Greenspan R, Ravin C (1993). "Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study". Radiology. 189 (1): 133–6. PMID 8372182.

[31] Kucher N, Goldhaber SZ (2003). "Cardiac biomarkers for risk stratification of patients with acute pulmonary embolism". Circulation. 108 (18): 2191–4. doi:10.1161/01.CIR.0000100687.99687.CE. PMID 14597581.

[pmid9145679-32] Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR (1997). "Diagnosis of pulmonary embolism with magnetic resonance angiography". N. Engl. J. Med. 336 (20): 1422–7. doi:10.1056/NEJM199705153362004. PMID 9145679. Retrieved 2011-12-14. Unknown parameter |month= ignored (help)

[pmid10207468-33] Stein PD, Henry JW, Gottschalk A (1999). "Reassessment of pulmonary angiography for the diagnosis of pulmonary embolism: relation of interpreter agreement to the order of the involved pulmonary arterial branch". Radiology. 210 (3): 689–91. PMID 10207468.

[34] Augustinos P, Ouriel K (2004). "Invasive approaches to treatment of venous thromboembolism". Circulation. 110 (9 Suppl 1): I27–34. PMID 15339878.

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 === History and Symptoms ===
-The symptoms of pulmonary embolism (PE) depends on the severity of the disease. A Pulmonary embolism may be an incidental finding in so far as many patients are asymptomatic.<ref name="pmid20399319">{{cite journal |author=Stein PD, Matta F, Musani MH, Diaczok B |title=Silent pulmonary embolism in patients with deep venous thrombosis: a systematic review |journal=[[The American Journal of Medicine]] |volume=123 |issue=5 |pages=426–31 |year=2010 |month=May |pmid=20399319 |doi=10.1016/j.amjmed.2009.09.037 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(09)01111-5 |accessdate=2012-04-26}}</ref><ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294 |doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-04-26}}</ref> The common symptoms of PE range from mild [[dyspnea]], [[chest pain]], and [[tachypnea]], to sustained [[hypotension]] and [[shock]].<ref name="pmid17904458">{{cite journal |author=Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK |title=Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II |journal=[[The American Journal of Medicine]] |volume=120 |issue=10 |pages=871–9 |year=2007 |month=October |pmid=17904458 |pmc=2071924 |doi=10.1016/j.amjmed.2007.03.024 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(07)00463-9 |accessdate=2012-04-26}}</ref><ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294 |doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-04-26}}</ref> The absence of these symptoms may be associated with a reduced clinical probability of pulmonary embolism, however it does not exclude the diagnosis of pulmonary embolism. The [[Deep vein thrombosis history and symptoms|symptoms]] of lower extremity [[Deep vein thrombosis|deep venous thrombosis]] may also be present.
+A proper history and physical exam is crucial to establish an accurate diagnosis of pulmonary embolism (PE).  The symptoms of pulmonary embolism (PE) depend on the severity of the disease, ranging from mild [[dyspnea]], [[chest pain]], and [[cough]], to sustained [[hypotension]] and [[shock]].<ref name="pmid17904458">{{cite journal |author=Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK |title=Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II |journal=[[The American Journal of Medicine]] |volume=120 |issue=10 |pages=871–9 |year=2007 |month=October |pmid=17904458 |pmc=2071924 |doi=10.1016/j.amjmed.2007.03.024 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(07)00463-9 |accessdate=2012-04-26}}</ref><ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294 |doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-04-26}}</ref>  A PE may also be an incidental finding in so far as many patients are asymptomatic.<ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294 |doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-04-26}}</ref><ref name="pmid20399319">{{cite journal |author=Stein PD, Matta F, Musani MH, Diaczok B |title=Silent pulmonary embolism in patients with deep venous thrombosis: a systematic review |journal=[[The American Journal of Medicine]] |volume=123 |issue=5 |pages=426–31 |year=2010 |month=May |pmid=20399319 |doi=10.1016/j.amjmed.2009.09.037 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(09)01111-5 |accessdate=2012-04-26}}</ref>  [[Sudden death]] can be the initial presentation of PE. One of the first steps in the management of PE is the determination of the [[Wells score for PE]], whose criteria can be ascertained solely on the basis of history and physical exam.  [[Deep vein thrombosis history and symptoms|Symptoms of DVT]] of the lower extremity may be present.
 === Physical Examination ===
-Pulmonary emboli are associated with the presence of [[tachycardia]] and [[tachypnea]]. Signs of [[right ventricular failure]] include [[jugular venous distension]], a [[Heart sounds#Third heart sound S3|right sided S3]], and a [[Parasternal heave|parasternal lift]].  These signs are often present in cases of massive pulmonary emboli.<ref name="pmid17904458">{{cite journal |author=Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK |title=Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II |journal=[[The American Journal of Medicine]] |volume=120 |issue=10 |pages=871–9 |year=2007 |month=October |pmid=17904458 |pmc=2071924 |doi=10.1016/j.amjmed.2007.03.024 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(07)00463-9 |accessdate=2012-04-29}}</ref>
+Pulmonary embolism (PE) is associated with the presence of [[tachycardia]] and [[tachypnea]].  Signs of [[right ventricular failure]] include [[jugular venous distension]], a [[Heart sounds#Third heart sound S3|right sided S3]], and a [[Parasternal heave|parasternal lift]].  These signs are often present in cases of massive and submassive pulmonary emboli, also known as intermediate-risk and high-risk respectively.<ref name="pmid17904458">{{cite journal |author=Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK |title=Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II |journal=[[The American Journal of Medicine]] |volume=120 |issue=10 |pages=871–9 |year=2007 |month=October |pmid=17904458 |pmc=2071924 |doi=10.1016/j.amjmed.2007.03.024 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(07)00463-9 |accessdate=2012-04-29}}</ref><ref name="pmid18757870">{{cite journal| author=Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P et al.| title=Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). | journal=Eur Heart J | year= 2008 | volume= 29 | issue= 18 | pages= 2276-315 | pmid=18757870 | doi=10.1093/eurheartj/ehn310 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18757870  }} </ref>  Since PE most commonly occurs as a complication of [[deep vein thrombosis]] (DVT), the physical examination should include an assessment of the lower extremities for [[erythema]], [[tenderness]], and/or [[swelling]].
 === Laboratory Findings ===
-The results of routine laboratory tests including [[ABG|arterial blood gas]] analysis are non-specific in making the diagnosis of pulmonary embolism.  These laboratory studies can be obtained to rule-out other cause of chest discomfort and tachypnea.  In patients with acute pulmonary embolism, non-specific lab findings include: [[leukocytosis]], [[erythrocyte sedimentation rate|elevated ESR]] with an elevated [[LDH|serum LDH]] and [[transaminases|serum transaminase]] (especially [[Aspartate transaminase|AST or SGOT]]).
+The results of routine laboratory tests including [[ABG|arterial blood gas]] analysis are non-specific in making the diagnosis of pulmonary embolism (PE).  These laboratory studies can be obtained to rule-out other cause of [[chest discomfort]] and [[tachypnea]].  In patients with acute PE, non-specific lab findings include: [[leukocytosis]], [[erythrocyte sedimentation rate|elevated ESR]] with an elevated [[LDH|serum LDH]] and [[transaminases|serum transaminase]] (especially [[Aspartate transaminase|AST or SGOT]]).  A negative [[D-dimer]] in a patient with low to intermediate probability of PE strongly suggests PE is not present.
 === Arterial Blood Gas Analysis ===
-[[Hypoxemia]], [[hypocapnia]], increased [[alveolar-arterial gradient]], and [[respiratory alkalosis]] are common findings that may be observed in patients with pulmonary embolism. In patients with suspected PE, Rodger et al, demonstrated that [[ABG]] analysis did not have sufficient [[negative predictive value]], [[specificity]], or likelihood ratios to be considered useful in the management these patients.<ref name="pmid11112122">{{cite journal |author=Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS |title=Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism |journal=[[American Journal of Respiratory and Critical Care Medicine]] |volume=162 |issue=6 |pages=2105–8 |year=2000 |month=December |pmid=11112122 |doi= |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=11112122 |accessdate=2012-04-30}}</ref> Similar findings were observed by the PIOPED II investigators.<ref name="pmid17145249">{{cite journal |author=Stein PD, Woodard PK, Weg JG, Wakefield TW, Tapson VF, Sostman HD, Sos TA, Quinn DA, Leeper KV, Hull RD, Hales CA, Gottschalk A, Goodman LR, Fowler SE, Buckley JD |title=Diagnostic pathways in acute pulmonary embolism: recommendations of the PIOPED II investigators |journal=[[The American Journal of Medicine]] |volume=119 |issue=12 |pages=1048–55 |year=2006 |month=December |pmid=17145249 |doi=10.1016/j.amjmed.2006.05.060 |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9343(06)00779-0 |accessdate=2012-04-30}}</ref>
+[[Hypoxemia]], [[hypocapnia]], increased [[alveolar-arterial gradient]], and [[respiratory alkalosis]] are the typical findings that may be observed in patients with pulmonary embolism (PE).  The absence of the typical results of the arterial blood gas (ABG) analysis, however, does not exclude PE.<ref name="pmid8549223">{{cite journal| author=Stein PD, Goldhaber SZ, Henry JW, Miller AC| title=Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism. | journal=Chest | year= 1996 | volume= 109 | issue= 1 | pages= 78-81 | pmid=8549223 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8549223  }} </ref>  ABG analysis results do not contribute reliably to tailoring the management of the patients among whom PE is suspected.<ref name="pmid11112122">{{cite journal |author=Rodger MA, Carrier M, Jones GN, Rasuli P, Raymond F, Djunaedi H, Wells PS |title=Diagnostic value of arterial blood gas measurement in suspected pulmonary embolism |journal=[[American Journal of Respiratory and Critical Care Medicine]] |volume=162 |issue=6 |pages=2105–8 |year=2000 |month=December |pmid=11112122 |doi= |url=http://ajrccm.atsjournals.org/cgi/pmidlookup?view=long&pmid=11112122 |accessdate=2012-04-30}}</ref>
 === D-dimer ===
-[[D-dimer]] is a [[fibrin degradation product]]. D-dimer levels are elevated in the plasma after the acute formation of a blood clot. The majority of patients with pulmonary embolism have some degree of endogenous [[fibrinolysis]] with  an elevation in [[D-dimer]] levels, therefore there is a high [[negative predictive value]] in ruling out a pulmonary embolism when D-dimer levels are low. However a wide range of diseases are associated with mild degree of [[fibrinolysis]] which elevate [[D-dimer]] levels and contribute towards a reduced [[specificity]] and a poor [[positive predictive value]] of a high D-dimer level. This means that it is more likely that one can rule out a PE with a low D-dimer level, but cannot necessarily confirm the diagnosis of a PE based on a high D-dimer level. Other disease states  that can also have a high d-dimer level include [[pneumonia]], [[Congestive heart failure|congestive heart failure (CHF)]], [[Myocardial infarction|myocardial infarction (MI)]] and [[malignancy]]. [[False-negative]] values may occur in patients with prolonged symptoms of [[venous thromboembolism]] (≥14 days), patients on therapeutic [[heparin|heparin therapy]], and patients with suspected [[deep venous thrombosis]] on oral anticoagulation, as these patients have will have low D-dimer levels in the presence of a PE.<ref name="pmid19712840">{{cite journal| author=Bruinstroop E, van de Ree MA, Huisman MV| title=The use of D-dimer in specific clinical conditions: a narrative review. | journal=Eur J Intern Med | year= 2009 | volume= 20 | issue= 5 | pages= 441-6 | pmid=19712840 | doi=10.1016/j.ejim.2008.12.004 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19712840  }} </ref><ref name="pmid20592294">{{cite journal| author=Agnelli G, Becattini C| title=Acute pulmonary embolism. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 3 | pages= 266-74 | pmid=20592294 | doi=10.1056/NEJMra0907731 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20592294  }} </ref>
+D-dimer is used in the diagnosis of [[deep vein thrombosis]] and [[pulmonary embolism]] among patients with low or unlikely probability of [[venous thromboembolism]].<ref name="pmid16403932">{{cite journal| author=Wells PS, Owen C, Doucette S, Fergusson D, Tran H| title=Does this patient have deep vein thrombosis? | journal=JAMA | year= 2006 | volume= 295 | issue= 2 | pages= 199-207 | pmid=16403932 | doi=10.1001/jama.295.2.199 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16403932  }}  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17213132 Review in: Evid Based Med. 2006 Aug;11(4):119]  [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16813372 Review in: ACP J Club. 2006 Jul-Aug;145(1):24] </ref><ref name="pmid11453709">{{cite journal| author=Wells PS, Anderson DR, Rodger M, Stiell I, Dreyer JF, Barnes D et al.| title=Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. | journal=Ann Intern Med | year= 2001 | volume= 135 | issue= 2 | pages= 98-107 | pmid=11453709 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11453709  }} </ref>  While 500 ng/mL has long been the most commonly used cut off value for abnormal D-dimer concentration, recent studies suggest the use of an age adjusted cut-off concentration of D-dimer.  The age adjusted cut-off value of D-dimer is 500 ng/mL for subjects whose age is less than 50 years, and the age multiplied by 10 for subjects older than 50 years.<ref name="pmid22511491">{{cite journal| author=Douma RA, Tan M, Schutgens RE, Bates SM, Perrier A, Legnani C et al.| title=Using an age-dependent D-dimer cut-off value increases the number of older patients in whom deep vein thrombosis can be safely excluded. | journal=Haematologica | year= 2012 | volume= 97 | issue= 10 | pages= 1507-13 | pmid=22511491 | doi=10.3324/haematol.2011.060657 | pmc=PMC3487551 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22511491  }} </ref><ref name="pmid23645857">{{cite journal| author=Schouten HJ, Geersing GJ, Koek HL, Zuithoff NP, Janssen KJ, Douma RA et al.| title=Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis. | journal=BMJ | year= 2013 | volume= 346 | issue=  | pages= f2492 | pmid=23645857 | doi=10.1136/bmj.f2492 | pmc=PMC3643284 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23645857  }} </ref><ref name="JAMA 2014"> Righini M, Van Es J, Den Exter PL, et al. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study. JAMA. 2014;311(11):1117-1124. doi:10.1001/jama.2014.2135. </ref>
 === Biomarkers ===
-Although the success of [[brain natriuretic peptide]] levels to diagnose  pulmonary embolism is limited due to the reduced sensitivity of the test,<ref name="pmid16405522">{{cite journal |author=Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR |title=Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism |journal=[[Journal of Thrombosis and Haemostasis : JTH]] |volume=4 |issue=3 |pages=552–6 |year=2006|month=March |pmid=16405522 |doi=10.1111/j.1538-7836.2005.01752.x |url=http://dx.doi.org/10.1111/j.1538-7836.2005.01752.x|accessdate=2012-05-01}}</ref> elevated [[BNP]] and [[BNP|pro-BNP]] levels accurately predict [[right ventricular dysfunction]] and associated mortality, and are therefore useful prognostic markers. <ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294|doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-05-01}}</ref> The evaluation of [[troponin]] levels also serves as a  useful prognostic marker to identify  right ventricular myocardial injury<ref name="pmid11079669">{{cite journal |author=Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB |title=Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction |journal=[[Journal of the American College of Cardiology]]|volume=36 |issue=5 |pages=1632–6 |year=2000 |month=November |pmid=11079669 |doi=|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(00)00905-0 |accessdate=2012-05-02}}</ref><ref name="pmid12904706">{{cite journal |author=Horlander KT, Leeper KV |title=Troponin levels as a guide to treatment of pulmonary embolism |journal=[[Current Opinion in Pulmonary Medicine]] |volume=9 |issue=5 |pages=374–7 |year=2003|month=September |pmid=12904706 |doi=|url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1070-5287&volume=9&issue=5&spage=374 |accessdate=2012-05-02}}</ref> and mortality associated with acute pulmonary embolism.<ref name="pmid18094010">{{cite journal| author=Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S et al.| title=Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism. | journal=Eur Respir J | year= 2008 | volume= 31 | issue= 4 | pages= 847-53 | pmid=18094010 | doi=10.1183/09031936.00113307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18094010  }} </ref>
+Although the usefulness of [[brain natriuretic peptide]] (BNP) concentrations to diagnose  pulmonary embolism (PE) is limited,<ref name="pmid16405522">{{cite journal |author=Söhne M, Ten Wolde M, Boomsma F, Reitsma JB, Douketis JD, Büller HR |title=Brain natriuretic peptide in hemodynamically stable acute pulmonary embolism |journal=[[Journal of Thrombosis and Haemostasis : JTH]] |volume=4 |issue=3 |pages=552–6 |year=2006|month=March |pmid=16405522 |doi=10.1111/j.1538-7836.2005.01752.x |url=http://dx.doi.org/10.1111/j.1538-7836.2005.01752.x|accessdate=2012-05-01}}</ref> elevated [[BNP]] and [[BNP|pro-BNP]] levels are associated with [[right ventricular dysfunction]] and increased mortality, and are therefore useful prognostic markers.<ref name="pmid20592294">{{cite journal |author=Agnelli G, Becattini C |title=Acute pulmonary embolism |journal=[[The New England Journal of Medicine]] |volume=363 |issue=3 |pages=266–74 |year=2010 |month=July |pmid=20592294|doi=10.1056/NEJMra0907731 |url=http://www.nejm.org/doi/abs/10.1056/NEJMra0907731?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-05-01}}</ref> The evaluation of [[troponin]] concentration also serves as a useful prognostic marker to identify [[myocardial]] necrosis<ref name="pmid11079669">{{cite journal |author=Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB |title=Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction |journal=[[Journal of the American College of Cardiology]]|volume=36 |issue=5 |pages=1632–6 |year=2000 |month=November |pmid=11079669 |doi=|url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(00)00905-0 |accessdate=2012-05-02}}</ref><ref name="pmid12904706">{{cite journal |author=Horlander KT, Leeper KV |title=Troponin levels as a guide to treatment of pulmonary embolism |journal=[[Current Opinion in Pulmonary Medicine]] |volume=9 |issue=5 |pages=374–7 |year=2003|month=September |pmid=12904706 |doi=|url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1070-5287&volume=9&issue=5&spage=374 |accessdate=2012-05-02}}</ref> and mortality associated with acute PE.<ref name="pmid18094010">{{cite journal| author=Jiménez D, Díaz G, Molina J, Martí D, Del Rey J, García-Rull S et al.| title=Troponin I and risk stratification of patients with acute nonmassive pulmonary embolism. | journal=Eur Respir J | year= 2008 | volume= 31 | issue= 4 | pages= 847-53 | pmid=18094010 | doi=10.1183/09031936.00113307 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18094010  }} </ref>
 === Electrocardiogram ===
-EKG abnormalities in the setting of pulmonary emolism are non-specific.<ref name="pmid15863641">{{cite journal| author=Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV| title=Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. | journal=Eur Respir J | year= 2005 | volume= 25 | issue= 5 | pages= 843-8 | pmid=15863641 |doi=10.1183/09031936.05.00119704| pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15863641  }} </ref><ref name="pmid11018210">{{cite journal| author=Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P et al.| title=Diagnostic value of the electrocardiogram in suspected pulmonary embolism. |journal=Am J Cardiol | year= 2000 | volume= 86 | issue= 7 | pages= 807-9, A10 |pmid=11018210 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018210  }}</ref> The EKG may also lack sensitivity as the EKG may be normal in the setting of a pulmonary embolus.  In a prospective study EKG abnormalities were present in 70% of patients with documented acute pulmonary embolism.  The most common EKG abnormality was [[nonspecific ST-segment and T-wave changes]].<ref name="pmid1746481">{{cite journal| author=Stein PD, Saltzman HA, Weg JG| title=Clinical characteristics of patients with acute pulmonary embolism. | journal=Am J Cardiol | year= 1991 | volume= 68 | issue= 17 | pages= 1723-4 | pmid=1746481 | doi= |pmc= | url= }} </ref>  An electrocardiogram (ECG) is routinely performed in all patients with [[chest pain]] to assess for a [[myocardial infarction]], but the diagnosis of a [[pulmonary embolism]] should be kept in mind as well.
+The [[electrocardiogram]] ([[ECG]]) in the cases of pulmonary embolism (PE) is often abnormal; however, the ECG abnormalities are neither sensitive nor specific.<ref name="pmid15863641">{{cite journal| author=Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV| title=Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. | journal=Eur Respir J | year= 2005 | volume= 25 | issue= 5 | pages= 843-8 | pmid=15863641 |doi=10.1183/09031936.05.00119704| pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15863641  }} </ref><ref name="pmid11018210">{{cite journal| author=Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P et al.| title=Diagnostic value of the electrocardiogram in suspected pulmonary embolism. |journal=Am J Cardiol | year= 2000 | volume= 86 | issue= 7 | pages= 807-9, A10 |pmid=11018210 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018210  }}</ref>  Some of the most common [[ECG]] abnormalities in PE include [[T wave inversion]] in the anterior leads and [[sinus tachycardia]].<ref name="pmid9118684">{{cite journal| author=Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, Baudouy M| title=The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports. | journal=Chest | year= 1997 | volume= 111 | issue= 3 | pages= 537-43 | pmid=9118684 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9118684  }} </ref><ref name="pmid123074">{{cite journal| author=Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW| title=The electrocardiogram in acute pulmonary embolism. | journal=Prog Cardiovasc Dis | year= 1975 | volume= 17 | issue= 4 | pages= 247-57 | pmid=123074 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=123074  }} </ref><ref name="pmid11018210">{{cite journal| author=Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P et al.| title=Diagnostic value of the electrocardiogram in suspected pulmonary embolism. | journal=Am J Cardiol | year= 2000 | volume= 86 | issue= 7 | pages= 807-9, A10 | pmid=11018210 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11018210  }} </ref>  The ECG abnormalities reported in [[PE]] are also present in a variety of other conditions rendering the utility of [[ECG]] for the diagnosis of PE limited.  Nevertheless, an [[ECG]] is routinely performed in all patients with suspected PE in order to rule out other differential diagnoses such as [[myocardial infarction]].
 === Chest X Ray ===