*Pathophysiology
Thrombosis usually originates as a platelet nidus on valves in the veins of the lower extremities.
Large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi occlude smaller vessels in the lung periphery that lead pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Lower lobes are involved more commonly than the upper lobes.
+Respiratory consequences: Acute respiratory consequences of pulmonary embolism include increased alveolar dead space, pneumoconstriction, hypoxemia, and hyperventilation. Later, 2 additional consequences may occur: regional loss of surfactant and pulmonary infarction. The mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt via a patent foramen ovale. Pulmonary infarction is an uncommon consequence because of the bronchial arterial collateral circulation
+Hemodynamic consequences: pulmonary embolism reduces the cross-sectional area of the pulmonary vascular bed, resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right ventricular afterload => right ventricular failure. Prior poor cardiopulmonary status of the patient is an important factor leading to hemodynamic collapse.
*Frequency
Pulmonary embolism is present in 60-80% of patients with deep venous thrombosis & 60% of patients who died in the hospital had pulmonary embolism, and the diagnosis was missed in up to 70% of the cases.
Race: The incidence of pulmonary embolism appears to be significantly higher in blacks than in whites (>50%)
Sex: The risk of pulmonary embolism is increased in pregnancy and during the postpartum period.
Age: In hospitalized elderly patients, pulmonary embolism is commonly missed and often is the cause of death.