TY - CHAP M1 - Book, Section TI - Pulmonary Embolism A1 - Tapson, Victor F. A2 - Fuster, Valentin A2 - Narula, Jagat A2 - Vaishnava, Prashant A2 - Leon, Martin B. A2 - Callans, David J. A2 - Rumsfeld, John S. A2 - Poppas, Athena PY - 2022 T2 - Fuster and Hurst's The Heart, 15e AB - Chapter SummaryThis chapter discusses the pathogenesis, diagnosis, and management of acute pulmonary embolism (PE). Approximately one-third of patients die from PE within the first hours of presentation, often before the diagnosis can be confirmed and therapy initiated, or because the diagnosis was simply missed. When acute PE is suspected, if the bleeding risk is deemed acceptable, anticoagulation should be initiated because this is the one approach that has proven to reduce mortality. Once PE is diagnosed, risk stratification is critical and should involve consideration of clot burden, heart rate, respiratory rate, blood pressure, oxygenation, right ventricular size and function, and biomarkers. The risk-stratification terminology has evolved (see Fuster and Hurst’s Central Illustration) and the term “high-risk” (rather than “massive”) is suggested, while “intermediate-risk” is now used more commonly than “submassive.” Carefully selected low-risk patients can be considered for outpatient anticoagulation therapy. Therapy more aggressive than anticoagulation alone is indicated when patients are hemodynamically compromised—hypotension caused by PE is the clearest indication. Various potential aggressive therapeutic options are available, including systemic thrombolysis, catheter-directed therapy, surgical embolectomy, and extracorporeal membrane oxygenation (ECMO). Following an acute PE episode, resolution may be incomplete despite optimal anticoagulant therapy, which in approximately 1% of cases may lead to chronic thromboembolic pulmonary hypertension. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/29 UR - accesscardiology.mhmedical.com/content.aspx?aid=1202456414 ER -