General pathology · Hemodynamic disorders
Hyperemia and congestion (the nutmeg liver, heart-failure cells) !
- Lesion
In both, an organ holds more blood. In hyperemia more flows in (active and red); in congestion it cannot get out (passive and bluish).
Updated 2026-11-01
What it is
Hyperemia is an active increase in flow from arteriolar dilation, as in exercise or inflammation: the tissue looks red and warm. Congestion is passive: venous blood does not drain well, because of heart failure or venous obstruction, and the tissue looks blue-red. Chronic congestion leaves typical marks in the lung and the liver that the pathologist recognises.
Structure
- Acute lung: engorged alveolar capillaries, septal edema and sometimes small hemorrhages.
- Chronic lung: thickened, fibrotic septa; alveoli with brown-pigmented macrophages; the lung looks brown and firm (brown induration).
- Acute liver: distended central vein and sinusoids; central hepatocytes may die.
- Chronic liver: cut surface mottled red and yellow, like a cut nutmeg; the better-oxygenated periportal hepatocytes survive or turn fatty.
Step by step
- A ventricle fails or a vein is blocked and blood backs up upstream.
- Veins and capillaries distend; poorly oxygenated blood gives the bluish tone.
- High capillary pressure pushes out fluid: edema.
- Capillaries rupture; macrophages eat the red cells and store the iron as hemosiderin.
- Chronic hypoxia damages the cells farthest from the arterial supply (the centrilobular zone of the liver).
- Over months or years fibrosis appears: brown induration of the lung, cardiac liver fibrosis.
Clinical notes
- A tender enlarged liver and hepatojugular reflux in right heart failure.
- Budd-Chiari syndrome (hepatic vein obstruction) gives a similar congested liver.
- Portal hypertension congests the spleen (congestive splenomegaly) and causes varices.
In the lab
- Biopsy or autopsy: Perls’ stain to show hemosiderin in alveolar macrophages.
- In severe acute hepatic congestion the aminotransferases can rise sharply.
Test yourself
Think of the answer, then tap the question to see it.
What are heart-failure cells?
Alveolar macrophages loaded with hemosiderin, after eating red cells that leaked from congested capillaries.
Which ventricular failure produces the nutmeg liver?
Right: blood backs up into the vena cava and hepatic veins and congests the centrilobular zone.
Why does the centrilobular zone of the liver suffer first?
Because it lies at the end of the sinusoidal path, gets the least oxygenated blood and sits next to the congested central vein.
Is the hyperemia of inflammation active or passive?
Active: it comes from arteriolar dilation that increases flow, which is why the tissue is red and warm.
Related
- Edema and effusions: the four mechanisms
- Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss does
- Pigments in tissue: lipofuscin, hemosiderin, melanin, bilirubin, carbon
- Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate
- Watershed areas and the organs most sensitive to ischemia
Related conditions
- Heart failure
- Mitral stenosis
- Budd-Chiari syndrome
- Portal hypertension
- Pulmonary hypertension and cor pulmonale
- Chronic venous insufficiency
Elsewhere in DurgiPedia
- Heart failure physiology
- Central venous pressure and the jugular pulse
- Liver: lobule, acinus, hepatocytes, sinusoids, Kupffer cells
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Heart failure: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Hepatic Cirrhosis (StatPearls (NCBI Bookshelf), 2025); Edema (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.