Pulmonary Infarction

Mechanism of development and role of thromboembolism

Pulmonary infarction is closely related to the size of the thromboembolus and the caliber of the affected vessel. Morphological and clinical manifestations depend on the level of occlusion:

• Small size of the embolus. Occlusion of small branches of the pulmonary artery occurs. It is this variant that leads to the formation of a classic hemorrhagic pulmonary infarction.
• Massive embolism. If the thrombus blocks large branches, the infarction does not have time to develop. An acute drop in blood pressure (collapse) and severe bronchospasm occur, which can be the direct cause of death.

Pulmonary infarctions, along with pneumonia, pleurisy, and bronchitis, are serious pulmonary complications. The condition itself often acts as a consequence of systemic thromboembolic syndrome.

Sources of emboli

Thromboembolic syndrome is characterized by multiple embolisms. Pathologically altered heart structures most frequently serve as sources of thrombotic masses. These include:

1. Leaflets of the mitral and aortic valves.
2. Left heart chambers.

The main causes for the formation of such thrombi are bacterial endocarditis, myocardial infarction, and chronic cardiac aneurysm. Detached pieces of thrombi migrate through the bloodstream, causing infarctions not only in the lungs, but also in the spleen, kidneys, intestines, brain, and even the myocardium.

Bacterial infective endocarditis as the primary cause

Bacterial infective endocarditis is an independent nosology rather than a complication of rheumatic fever (which is proven by the presence of primary forms of the disease). Its pathogenesis is based on a perverted immune system response and the formation of circulating immune complexes (CIC).

The course of the disease is determined by the severity of allergic reactions and is divided into:

• Acute form (about 2 weeks, extremely rare).
• Subacute form (up to 3 months).
• Chronic (protracted) form (lasts months and years, synonym — sepsis lenta).

The disease is characterized by a tetrad of lesions: valvular endocarditis, vasculitis, kidney and spleen damage, as well as changes due to thromboembolic syndrome. Most commonly, the mitral (40%) and aortic (30%) valves are affected, less frequently the tricuspid (10%), or combined lesions are observed (20%).

Pathological anatomy of the local lesion

To understand where pulmonary emboli come from, it is necessary to examine the local changes on the valve leaflets in infective endocarditis. The septic lesion exhibits:

• Microorganism colonies and foci of necrosis with rapid ulceration.
• Tissue infiltration by macrophages and lymphohistiocytic elements (meanwhile, neutrophilic leukocytes are absent).
• Massive polypoid thrombotic deposits form on the ulcerative defects.

These polypoid masses easily crumble, detach, and become emboli. In addition, progressive destruction of the valve can lead to the formation of aneurysms, perforation, or complete detachment of the leaflet, causing acute heart failure. When embolized by infected masses in organs (e.g., in the myocardium), small abscesses may additionally develop.

Class and exam questions

What else to study on this topic

• Pathogenesis of circulating immune complex (CIC) formation
• Morphological differences between infective and rheumatic endocarditis
• Manifestations of hypersensitivity: Osler's nodes and glomerulonephritis
• Productive interstitial myocarditis in endocarditis
• Outcomes of local changes on valves (aneurysms, perforations, valve defects)

Other topics in the section "Pathology of the Cardiovascular System"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.