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Pulmonary Embolism

  • Pulmonary Embolism (PE) occurs when thromboemboli lodge in the vessels of the pulmonary circulation. Because the vast majority of thromboemboli resulting in PEs are derived from Deep Venous Thromboses (DVTs), pulmonary embolic disease can simply be thought of as an extension of venous thrombosis. Consequently, the risk factors for the two diseases are precisely identical and are summarized by "Virchow's Triad" detailed in the thrombosis page. It should be pointed out that other types of emboli can result in pulmonary embolisms; however, these are very rare and not discussed further.
Clinical Consequences
  • Overview
    • PEs occur when DVTs dislodge from their site of origin and travel in the venous system, through the right heart, and ultimately deposit within the pulmonary circulation. The subsequent pathophysiological sequelae largely depend on what sized vessels the emboli deposit in and their number. It should be pointed out that in individuals with patent foramen ovale or atrial septal defect, thromboemboli may bypass pulmonary circulation and enter the systemic circulation, resulting in paradoxical systemic thromboemboli.
  • Small Emboli
    • Small pulmonary emboli are typically well-tolerated if few in number, resulting in little pathophysiological sequelae and minimal if any symptomology. However, repeated showers of small PEs can result in progressive increases in pulmonary vascular resistance, eventually yielding pulmonary hypertension.
  • Medium Emboli
    • Medium-sized emobli often result in pleuritic chest pain, dyspnea, and tachycardia. Although the pathophysiology is not well-understood, these emboli often result in hypoxemia, likely by generating ventilation-perfusion defects and right-left shunts of blood. Why right-left shunts of blood are created in scenarios of PE is counter-intuitive; however, it appears that PEs result in regions of atelectasis.
  • Large Emboli
    • Large emboli can obstruct the pulmonary artery or one of its major branches resulting in a near instantaneous rise in pulmonary vascular resistance. This can lead to acute right heart failure manifesting as a sudden rise in jugular venous pressure along with rapid declines in cardiac output yielding shock and potentially death.
  • Like the clinical consequences, the morphology of PEs depend on the size of the emboli. Because the lungs are also supplied by the bronchial circulation, PEs typically do not produce overt infarctions of pulmonary tissue unless the systemic circulation is also compromised. Although falling short of infarction, pulmonary tissue downstream of impacted thromboemboli will still display significant ischemia that can yield defects in the vascular barrier and thus pulmonary hemorrhages, especially from the functioning bronchial circulation. When systemic circulation is also compromised, as might occur in the context of a large pulmonary embolus, infarction of lung tissue will result and may take on a wedge-shape if a large branch of the pulmonary artery is occluded. Here, the apex of the pathological wedge lies near the hilum and the base lies at the pleural surface, indicating the geographic region of pulmonary tissue supplied by the pulmonary artery branch. Over time this area of lung will undergo coagulative necrosis followed by progressive healing and fibrosis.