Pulmonary Changes: Brown Induration
In venous congestion, erythrocytes extravasate (diapedesis) and break down. The pigment hemosiderin is formed and phagocytosed by macrophages. These cells, termed hemosiderophages, can be found in the patient's sputum and are clinically referred to as "heart failure cells".
Macroscopically, the lungs become firm and acquire a brown color (induratio fusca pulmonum). Prussian blue staining is used to precisely identify iron within the pigment.
Chronic congestion triggers diffuse connective tissue proliferation in the interalveolar septa and around bronchovascular bundles. Two factors contribute to the progression of sclerosis:
- Lymphatic system insufficiency (progresses through resorption and mechanical stages when capillaries become blocked by siderophages).
- Action of SH-ferritin (a component of hemosiderin). It exerts a sclerogenic effect and induces vascular paralysis, further increasing hyperemia.
Hepatic Changes: "Nutmeg Liver"
Venous blood accumulates in the central regions of the hepatic lobules. Its movement toward the periphery is hindered by the high pressure within the hepatic arterial system. As a result, the organ enlarges, becomes firm, and its edges become rounded.
On cross-section, the liver acquires a mottled appearance resembling a nutmeg:
- Centrilobular zone: dark red due to marked congestion, hemorrhages, and hepatocyte necrosis.
- Perilobular zone: yellowish-brown due to the development of cellular fatty degeneration.
Chronic hypoxia leads to connective tissue proliferation along the sinusoids, resulting in capillarization of the sinusoids. This creates a capillary-parenchymal block. Ultimately, nutmeg fibrosis or cardiac micronodular cirrhosis of the liver develops.
Renal Changes: Cyanotic Induration
During congestion, the kidneys enlarge, become firm, and turn cyanotic. The pathological process is driven by a combination of venous congestion and lymphedema. The most prominent changes are localized in the renal medulla, which is associated with blood shunting through juxtamedullary shunts.
The mechanism of damage in chronic heart failure is as follows:
- Cardiac output decreases, and renal blood flow drops.
- Tissue hypoxia worsens, stimulating the renin-angiotensin-aldosterone system (RAAS).
- RAAS activation causes spasm of intrarenal arteries.
- Result: accelerated dystrophy of the renal tubular epithelium and activation of stromal sclerosis.
Splenic Changes: Cyanotic Induration
Congestive splenomegaly develops—the organ significantly increases in size and becomes firm. A specific macroscopic sign: on cross-section, the pulp cannot be scraped off the surface.
Microscopic examination reveals that lymphoid follicles are atrophic, while the red pulp is markedly congested and sclerotic. Clinically, these morphological changes are most prominently manifested in portal hypertension syndrome.