**2. Epidemiology and prevalence**

Venous thromboembolism is the third most common acute cardiovascular disease after myocardial infarction and stroke (Giuntini 1995). The incidence of venous thromboembolism is estimated to be 100-300 per 100,000 individuals but is age dependent increasing from 5 per 100,000 in childhood to 500-600 per 100,000 in those over 75 years of age (Douma 2010). Based upon the International Cooperative Pulmonary Embolism Registry (ICOPER), 4.2% of PE are classified as massive and are associated with systemic hypotension and cardiogenic shock (Stein 2003). In the Emergency Medicine Pulmonary Embolism in the Real World Registry (EMPEROR), 58 of 1875 patients (3.1%) presented with massive PE and their 30-day mortality was 14% (Lin 2012). The mortality rate for individuals with hemodynamically stable acute PE is 2-8% (Goldhaber 1999, Nijkeuter 2007) and the main cause of death is RV failure (Schoefp 2004, Kasper 1997, Wood 2002). However, in the first 3 months after acute PE, the case fatality rate increases to 15-18% (Goldhaber 1999).

© 2013 Elwing and Panos; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 Elwing and Panos; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

#### **2.1. Clinical presentation**

Risk factors for PE are summarized in table 1 (Stein and Matta Curr Probl Cardiol 2010). Conditions predisposing to the development of deep venous thrombosis (DVT) include malignancy (especially pancreatic and brain cancers), chronic obstructive pulmonary disease, stroke, pregnancy, obesity, and immobilization, especially after lower extremity trauma or after surgery (hip and knee replacement). Hypercoagulable states may be acquired or inher‐ ited. Deficiencies in antithrombin, protein C, or protein S, factor V Leiden mutation, pro‐ thrombin gene 20210 mutation, and antiphospholipid antibodies predispose individuals to the development of venous thrombosis and subsequent PE.

syndrome of pulmonary hemorrhage or infarction with pleuritic chest pain or hemoptysis; 2) syndrome of isolated dyspnea, breathlessness with no accompanying chest discomfort, hemoptysis, or hemodynamic alteration; and 3) syndrome of circulatory collapse with loss of

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Alterations in vital signs occur frequently in patients with PE. Respiratory and heart rates are often increased; elevated temperatures occur less frequently. Blood pressure is reduced in hemodynamically significant PE. Physical examination findings are often not specific and are usually detected in only a minority of patients. Cardiac examination may reveal tachycardia, elevated jugular venous pressure, right ventricular lift, and increased sound of pulmonic valve closure. Pulmonary auscultation may identify crackles, rales, wheezes, diminished breath sounds, or rarely a pleural friction rub. Lower extremity swelling, edema, or tenderness is

Because the clinical presentation and manifestations of PE are not specific, further diagnostic testing is required to establish the diagnosis definitively. Patients are usually categorized by the clinical probability, either high or intermediate/low, based upon the clinician's suspicion for the presence of PE. Several evaluation systems have been developed to assess the clinical probability for the presence of PE and the most widely used algorithms are the Wells score and the revised Geneva score (Wells 2000, LeGal 2006). If the suspicion for PE is intermediate or low, a D-dimer assay is performed. D-dimer is formed during the degradation of crosslinked fibrin and its presence is very sensitive for intravascular thrombosis due to either venous thrombosis or PE. The threshold value for D-dimer testing depends upon the assay but a value below the threshold indicates a very low risk for the presence of thrombosis. However, a value above the threshold is not specific for thrombosis and further evaluation is required. Com‐ pression ultrasonography is the currently preferred evaluation for suspected DVT and chest

computed tomographic pulmonary angiography (CTPA) is used to diagnose PE.

Troponin I and T and brain natriuretic peptide (BNP) are cardiac biomarkers that are released into the circulation when cardiac myocytes are stretched or injured as may occur during right ventricular dysfunction after an acute pulmonary embolism (Samama 2006). Elevation of these biomarkers identifies patients who are normotensive but have an increased risk of mortality (Pruszcyk 2003). Neither biomarker is a sensitive assay for the diagnosis of pulmonary

Measurement of PaO2 and PaCO2 are routinely performed in patients presenting with breath‐ lessness or pleurisy. In patients suspected to have PE, the sensitivity and specificity of a PaCO2<36 mmHg are 45% and 60%, respectively, and a PaO2<80 mmHg are 57% and 53%,

consciousness, hypotension, or cardiogenic shock (Ouellette 2012).

detected infrequently.

**3. Diagnostic studies**

**3.1. Laboratory abnormalities**

embolism (Meyer 2003).

respectively (Rodger 2000).


**Table 1.** Predisposing conditions in patients with PE (based upon data from PIOPED I and II; (adapted from Stein and Matta 2010)

#### **2.2. Clinical manifestations**

The clinical manifestations and presentation of acute PE are not specific and range from mild breathlessness to hemodynamic collapse. Dyspnea either at rest or with exertion occurs in approximately three quarters of patients diagnosed with PE (Stein 2010). Pleuritic or non‐ pleuritic chest discomfort occurs less frequently. Hemoptysis occurs in 5-15% of patients with PE. Approximately one third of patients with DVT have clinically asymptomatic PE (Stein 2010). The clinical presentation of PE has been classified recently into three categories: 1) syndrome of pulmonary hemorrhage or infarction with pleuritic chest pain or hemoptysis; 2) syndrome of isolated dyspnea, breathlessness with no accompanying chest discomfort, hemoptysis, or hemodynamic alteration; and 3) syndrome of circulatory collapse with loss of consciousness, hypotension, or cardiogenic shock (Ouellette 2012).

Alterations in vital signs occur frequently in patients with PE. Respiratory and heart rates are often increased; elevated temperatures occur less frequently. Blood pressure is reduced in hemodynamically significant PE. Physical examination findings are often not specific and are usually detected in only a minority of patients. Cardiac examination may reveal tachycardia, elevated jugular venous pressure, right ventricular lift, and increased sound of pulmonic valve closure. Pulmonary auscultation may identify crackles, rales, wheezes, diminished breath sounds, or rarely a pleural friction rub. Lower extremity swelling, edema, or tenderness is detected infrequently.
