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GENERAL CONSIDERATION AND HISTORY

Pulmonary emboli (PE), along with deep vein thrombi (DVT), comprise the spectrum of diagnoses referred to as venous thromboembolism (VTE). PE are associated with significant morbidity and mortality: their prevention and treatment are important as they are one of the principal causes of sudden cardiovascular death, third in line after strokes and heart attacks.1 This high rate of mortality makes PE the most important short-term complication of a DVT. Thus, prevention of a PE is critical, and DVT treatment guidelines are aimed at achieving this goal.2

Patients with PE may not display any signs or symptoms that would suggest a PE; this can happen in up to 75% of the patients.3 One of the explanations for this high incidence of asymptomatic PE is based on the dual blood supply of the lung through the bronchial and pulmonary arteries along with the small size of the majority of PE. However, the higher the thrombus load and greater the number of affected locations, the greater the clinical severity of the PE. The Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED II) study documented that most patients with symptomatic PE will present with sudden onset dyspnea, pleuritic chest pain, cough, orthopnea, calf/thigh pain with associated swelling suggestive of DVT, or signs compatible with thrombophlebitis (redness and tenderness to palpation of erythematous superficial veins in the legs).4

The American Heart Association (AHA) has proposed three categories to stratify patients with PE: nonmassive, submassive, and massive.5 The reason for stratifying patients into these categories is to aid in mortality risk assessment and to assist in determining the best treatment strategies. A nonmassive PE, also referred to as a low-risk PE, includes those patients who have experienced a PE yet have normal blood pressure, normal levels of cardiac biomarkers, and normal right heart (specifically, right ventricle) function on imaging. Normal blood pressure includes a systolic blood pressure ranging from 90 mmHg to 120 mmHg and a diastolic blood pressure ranging from 60 to 80 mmHg. Cardiac biomarkers used to assess PE stress include troponins and natriuretic peptides. Imaging modalities used to assess the right ventricle include an echocardiogram (“echo”) and CT scan. Additionally, an electrocardiogram (“EKG”) is used to identify patients at risk of adverse outcomes in acute PE.

A submassive PE is defined as an acute PE with a normal systolic blood pressure (≥90 mmHg) but with right ventricular (RV) dysfunction or the presence of ischemic heart muscle (myocardial necrosis). RV dysfunction is determined by dilation of the RV on imaging, abnormal findings on an EKG, or elevation of cardiac biomarkers (described above). Myocardial necrosis is defined by the elevation of troponins (a type of cardiac biomarker). A massive PE refers to those patients in whom an acute PE has occurred with a resulting systolic blood pressure of <90 mmHg for more than 15 minutes or requiring intravenous ...

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