2012, Number 2
Pulmonary embolism
Gutiérrez-Romero A
Full text
Language: Spanish
References: 17
Page: 93-99
PDF size: 83.33 Kb.
ABSTRACT
Venous thromboembolism (VTE) includes both deep venous thrombosis (DVT) and pulmonary embolism (PE). PE is the third most common cardiovascular disease, after heart disease and stroke. It is especially common in hospitalized patients and may constitute the greatest mortality risk to some inpatient population. The pathophysiology of PE includes the formation of a DVT, embolization through the right heart chambers, and the effects of the thrombotic material within the pulmonary arteries. The obstruction of blood flow through the pulmonary arteries has several physiologic consequences, including ventilation/perfusion mismatching and ischemia of the lung parenchyma. The most important clinical effects are the acute obstruction of blood flow and increase in pulmonary vascular resistance, which increase the demand on the right ventricle and may lower cardiac output. These effects can cause right ventricular strain, cardiogenic shock, cardiac arrest, and death. The risk factors for PE and DVT can be categorized according to the triad of pathogenic conditions first identified by Rudolf Virchow in 1860: venous stasis, vascular (endothelial) damage, and hypercoagulability. Hypercoagulability may be associated with clinical conditions (cancer or trauma) or with medications (estrogen in doses used for birth control or even those used for hormone replacement therapy). Thrombi can be induced by circulating procoagulant substances (the lupus anticoagulant or mediators released by adenocarcinoma of the lung, breast, and viscera) or from genetic deficiencies in such anticoagulant enzymes as protein C, its cofactor protein S, and antithrombin III. These conditions usually require high-dose anticoagulation. Although patients with PE may present with the classic symptoms of dyspnea, chest pain, hemoptysis, or syncope, the presentation is often more subtle. Clinical rules have been developed and verified to help establish the diagnosis of DVT or PE; the best-known predictive model is the Wells criteria. If the hemodynamic and gas-exchange effects of PE are not severe, it can be treated with the same regimens used for proximal vein DVT; unfractionated heparin, LMWH, and fondaparinux are all safe and effective. Hemodynamic instability from PE is a result of the acutely elevated pulmonary arterial resistance, which may lead to right ventricular strain, ischemia, and catastrophic cardiac dysfunction. Cardiopulmonary support may be indicated in patients with PE, including administration of oxygen in those with arterial hypoxemia. Careful fluid loading may increase right atrial and right ventricular end-diastolic pressure, thereby worsening right ventricular function. Systemic vasoconstrictive agents, such as norepinephrine, may raise the mean arterial pressure during PE-associated shock. Many patients die of PE in the first 2 weeks after presentation. During this time, almost 5% of DVTs reembolize, even when treated. The mortality rate from PE increases greatly in patients who develop hypotension and shock and require cardiopulmonary resuscitation; the acute beneficial hemodynamic benefits of thrombolytic therapy may have a much greater benefit for these patients. Thrombolytic therapy should likely be reserved for management of patients with persistent hypotension due to PE who have no contraindications. Embolectomy can be lifesaving in patients with confirmed massive embolism who fail to respond to medical therapy. During the first 5 or so days of therapy for PE, heparin, LMWH, or fondaparinoux is necessary because these drugs prevent propagation of thromboemboli; warfarin is used to prevent recurrence. Therapy should usually be continued for at least 3 months. Patients with unresolved risk factors for thromboembolism and who are therefore at high risk of recurrence may require prolonged anticoagulation. Patients with unprovoked VTE have high rates of recurrence and may require long-term anticoagulation.REFERENCES
Chairperson AT, Perrier A, Konstantinides S, Agnelli G, Galié N, Pruszczyk P, et al. 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 2008; 29: 2276-315.
Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, De Simone G, et al; on behalf of American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics: 2010 update: a report from the American Heart Association. Circulation 2010; 121: e46-e215 [published correction appears in Circulation 2010; 121: e260].