Pulmonary Infarction: Background, Pathophysiology, Etiology

Most pulmonary emboli derive from a free-floating thrombus. In rare situations, extension of an existing pulmonary thrombus may result in pulmonary infarction. Many materials and substances may form emboli and move to the pulmonary circulation; these include fat, tumor, septic emboli, air, amniotic fluid, and injected foreign material.

The size of a pulmonary embolism determines at which points in the pulmonary vasculature it lodges. After the embolus lodges, it occludes the vessel, reducing distal blood flow to the area directly supplied by the vessel. The degree of obstruction of the pulmonary circulation directly affects the resulting pathophysiology.

In all cases of pulmonary embolism, ventilation/perfusion (V/Q) mismatch occurs to some degree, in which continued ventilation of lung units without circulation is present. Oxygenation is usually not affected by the V/Q mismatch, in contrast with V/Q mismatch that arises from obstruction of airways and lung parenchyma. Impaired oxygenation in the context of suspected pulmonary embolism implies a massive obstruction.

An increase in effective alveolar dead space is a direct result of the V/Q mismatch. Ventilation (carbon dioxide removal) is usually compensated for by tachypnea.

In cases in which the pulmonary embolus is large, a sudden increase in pulmonary artery pressure may lead to right ventricular strain and right heart failure. A sudden rise in the right ventricular pressure may cause a leftward shift of the intraventricular septum, which may impair left ventricular filling and output (classic obstructive shock).

Reflex bronchoconstriction is often associated with pulmonary embolism. This increases the work of breathing and decreases pulmonary compliance. Pulmonary infarction is also associated with diminished surfactant levels, which may contribute to the increased work of breathing and diminished oxygenation.

Children with pulmonary emboli often have a serious underlying condition that predisposes them to embolus development and may worsen their clinical outcome. Some of the more common underlying conditions include the following:

• Sickle cell disease

• Nephrotic syndrome

• Cancer

• Chemotherapy

• Inherited hypercoagulable state

• Vasculitis

In sickle cell disease, an initial trigger (often infection) exacerbated by dehydration (eg, due to fever, tachypnea, or decreased intake) leads to sickling of RBCs within small blood vessels of the lung and other organs. This precipitates a cycle of relative deoxygenation that further exacerbates the sickling tendency, leading to small vessel occlusion and, ultimately, infarction of areas of the pulmonary parenchyma. Allied to this sequence is the tendency of many patients with sickle cell disease to have a component of reactive airways disease, which may further decrease oxygenation.