The Pathophysiological Etiology and Rationale for a Pulmonary Embolism

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The Pathophysiological Etiology and Rationale for a Pulmonary Embolism

Pulmonary embolism is the occlusion of thrombi to the pulmonary artery, typically originating from pelvis and large veins in the legs.  In pulmonary embolism etiology, embolization risk is higher when thrombi proximal are in the calf veins. Thromboemboli can also originate from central veins in the chest or arm veins which can be as a result of thoracic outlet syndromes or caused by central venous catheters (Blann, 2009). Risk factors for pulmonary embolism and deep venous thrombosis are similar both in adults and children. These risk factors include, conditions that cause endothelial dysfunction or injury, conditions impairing venous return including confinement without walking and bed rest. Another risk factor is underlying thrombophilic (hypercoagulable) disorders.

In its pathophysiology, after the development of deep venous thrombosis, clots may dislodge and travel through the right side of the heart and the venous system, and lodge in pulmonary arteries, where they completely or partially occlude one or more vessels. The consequences depend on the number and size of the emboli, the functioning of the right ventricle, lungs underlying conditions, and intrinsic thrombolytic ability to dissolve the clot (Blann, 2009). If the right ventricle fails, death may occur. Small embolic may begin to lyse immediately and may have no acute physiologic effects and should resolve within days or hours. Large emboli can cause hypoxemia due to perfusion/ventilation (V/Q) mismatch, low mixed venous oxygen content resulting from low cardiac output, a reflex increase in ventilation (tachypnea), atelectasis due to abnormalities in surfactant and alveolar hypocapnia, and increased pulmonary vascular resistance caused by vasoconstriction and mechanical obstruction. Most emboli are reduced by endogenous lysis, with the physiological alterations decreasing within hours or days with some emboli resisting lysis and sometimes persisting (Bordow, Ries, & Morris, 2005).

According to Bordow, Ries, and Morris (2005), in 3-4% of cases, the chronic obstruction residue leads to chronic thromboembolic pulmonary hypertension, which evolves over months to years resulting in chronic heart failure. During large emboli occlusion in major pulmonary arteries, right ventricle pressure increases and can lead to its failure, shock, or death. The death risk depends on the rate and degree of rise of right-sided pressures and underlying cardiopulmonary status of the patient. Pulmonary infarction which is often wedge-shaped, Hampton hump and other modalities of imaging occur in 10% of pulmonary embolism patients. The low rate is attributed by the dual blood supply in the lungs. Normally, pulmonary infarction is caused by small emboli that are lodged in many distal pulmonary arteries.

In preventing extensive clot formation, further embolization and new clot formation, initial coagulation should be followed by maintenance anticoagulation. This therapy should start after pulmonary embolism is suspected (Bordow, Ries, & Morris, 2005). Elimination of clots by dissolution with IV or embolectomy or catheter-based thrombolytic therapy should be reflected on patients associated with hyponesion.

References

Blann, A. (2009). Deep vein thrombosis and pulmonary embolism. Keswick: M & K Update.

Bordow, R., Ries, A., & Morris, T. (2005). Manual of clinical problems in pulmonary medicine. Philadelphia: Lippincott Williams & Williams.