Pulmonary Embolism

The process starts in the deep veins, usually without any warning until a serious event happens.

Venous Thromboembolism Connection

The vast majority of pulmonary embolisms originate as deep vein thrombosis, typically in the lower extremity deep veins, such as the popliteal, femoral, or iliac veins. A thrombus forms due to stasis of blood, endothelial injury, or hypercoagulability. When a portion of this clot breaks loose, it becomes an embolus. This embolus travels through the venous system, passes through the right atrium and right ventricle of the heart, and is pumped into the pulmonary arteries. Because the pulmonary arteries branch into progressively smaller vessels, the embolus eventually becomes lodged, occluding blood flow. This occlusion creates a dead space where air enters the alveoli but cannot participate in gas exchange due to the lack of blood flow, leading to hypoxia.

Hemodynamic Consequences

The immediate impact of a pulmonary embolism is hemodynamic instability. The obstruction increases pulmonary vascular resistance, forcing the right ventricle to generate higher pressures to maintain forward flow. If the obstruction is significant, as seen in a massive pulmonary embolism or a saddle pulmonary embolism, the right ventricle may fail acutely. This right ventricular failure leads to decreased cardiac output, hypotension, and potential shock. The interventricular septum may bow toward the left ventricle, impairing its filling and further reducing systemic perfusion. This chain of physiological events explains why prompt diagnosis and treatment are critical to survival.