Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis.

Abstract

This New Frontiers article reviews the epidemiology, pathophysiology, diagnosis, treatment, and prevention of pulmonary embolism (PE) in 2 parts. In this first section we summarize the mechanisms of right ventricular dysfunction, arterial hypoxemia, and other abnormalities of gas exchange. For diagnosis, we streamline and expedite the work-up. For the second part we provide a contemporary approach to risk stratification to determine which patients may warrant intervention beyond use of heparin and warfarin alone. We conclude with an overview of contemporary concepts in optimizing prophylaxis. PE is a common cardiovascular and cardiopulmonary illness with an incidence in the United States that exceeds 1 per 1000 and a mortality rate 15% in the first 3 months after diagnosis. 1 This makes PE possibly as deadly an illness as acute myocardial infarction. Nevertheless, the lay public has not been well educated about PE. Consequently, early detection and prompt presentation for medical evaluation have lagged far behind the public awareness of acute coronary syndromes and stroke. Although discussion of the etiology of PE has classically focused on acquired and inherited causes of hypercoagulability, there is also an association between atherosclerotic disease and spontaneous venous thrombosis.2 The most common reversible risk factor for PE is obesity, an increasing pandemic in our society. Other common reversible risk factors include cigarette smoking and hypertension. Nevertheless, public fascination with PE has centered on long-haul air travel, a rare cause of venous thromboembolism. 3 PE also occurs in the context of illness attributable to surgery, trauma, immobilization, cancer,4 oral contraceptives,5 pregnancy, and postmenopausal hormone replacement therapy, 6 as well as medical conditions such as pneumonia and congestive heart failure. Genetic predisposition to venous thrombosis is being increasingly recognized, 7 and twin studies have demonstrated the important contribution of an inherited prothrombotic state. 8 Increased levels of clotting factors and activation peptides contribute to the risk of PE. Deficiencies of anticoagulant factors also increase thrombotic risk.9 Pathophysiology