22.25: Pulmonary Embolism I: Introduction

Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.

Etiology

PE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include fat emboli from fractured long bones, air emboli from improperly administered intravenous therapy, bacterial vegetation on heart valves, and amniotic fluid emboli. Risk factors for PE encompass prolonged immobility, recent pelvic or lower extremity surgery, a history of venous thromboembolism (VTE), cancer, obesity, use of oral contraceptives or hormone therapy (estrogen-containing therapy), smoking, prolonged air travel or during long flights (typically over 4 hours), heart failure, and pregnancy.

Pathophysiology

When a thrombus dislodges, it travels through the venous system, passing through the right atrium and ventricle before lodging in the pulmonary arteries. This results in a mechanical obstruction, which increases pulmonary vascular resistance and elevates pressures in the pulmonary arteries and right ventricle. The increased strain on the right ventricle can lead to right ventricular dysfunction and failure. The obstruction also causes a ventilation-perfusion (V/Q) mismatch, where affected lung areas receive ventilation but lack perfusion, impairing gas exchange and leading to hypoxemia. Furthermore, the embolic event triggers an inflammatory response, releasing cytokines and other mediators that cause local vasoconstriction and exacerbate pulmonary hypertension. This pathophysiological cascade can lead to hemodynamic instability, respiratory compromise, and potential cardiovascular collapse.

Clinical Manifestations

Clinical manifestations of PE can begin gradually or appear suddenly. Small emboli may cause vague and transient symptoms such as dyspnea, mild to moderate hypoxemia, tachypnea, cough, chest pain, hemoptysis, wheezing or crackles, fever, tachycardia, accentuation of the pulmonic heart sound, and syncope. In contrast, massive PE may result in sudden changes in mental status, feelings of impending doom, hypotension, and cardiorespiratory arrest. The rationale behind these manifestations lies in the degree of pulmonary arterial blockage, which dictates the severity of hemodynamic and respiratory compromise. Prompt recognition and intervention are critical to manage PE effectively and mitigate the risk of severe outcomes.