Increased blood volume locally in a particular tissue

active process
increased tissue inflow of blood due to arteriolar dilation
affected tissue is redder due to engorgement with oxygenated blood
Usually short-lasting
E.g.
Physiological- Exercise
Pathological - Inflammation

a passive process
results from impaired Outflow from a tissue
affected tissue is of bluish-red color (cyanosis) due to de-oxygenated blood accumulation
May show chronicity
E.g.
Systemic - cardiac failure
local - isolated venous obstruction
DVT(deep venous thrombosis)
TOO Syndrome
Chronic Passive Hyperemia/ Congestion
A long-standing congestion where the stasis of poorly oxygenated blood causes chronic local hypoxia resulting in parenchymal cell degeneration or death
Break down of RBCs and the debris onbeing phagocytosed give rise to hemosiderin laden macrophages
A small foci of hemorrhage may arise at the site of chr. Congestion due to capillary rupture
Micrscopic appearences
Acute pulmonary congestion
alveolar capillaries engorged with blood
associated alveolar septal edema may be present with or without focal minute intra-alveolar hemorrhage
Pasive pulmonary congestion
Alveolar septa – thickened and fibrotic
Numerous hemosiderin laden macrophages referred to as heart failure cells in alveoli
Ac. Pul. Congestion
Chr. Pul. Congestion with heart failure cells

Hemosiderin laden heart failure cells

Acute hepatic congestion
central vein and sinusoids distended with blood
Centrilobular degeneration as the hepatocytes at the periphery receive better oxygenated blood because of their proximity to hepatic arterioles
Chronic passive congestion of the liver
Grossly ‘nut-meg’ liver on cut section
Microscopically –
centrilobular necrosis, hepatocyte drop-out and hemorrhage with hemosiderin laden macrophages
Cardiac Cirrhosis – Hepatic fibrosis in chronic severe passive congestion of liver due to rt. Sided heart failure
Nutmeg liver

Centrilobular necrosis

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