PASSIVi: NYI'EKEMIA 313 



Pathological active hyperemia is seldom of long enough duration 

 to lead to any alterations in the tissues in which it oceurs. The blood 

 itself remains unehanged, except that the venous blood going from the 

 part contains nuich less CO, and more oxygen tliaii usual, because 

 more oxj-gen is brought to the tissues than can be used.- 



PASSIVE HYPEREMIA 



Passive hyperemia is almost equally unassociated with chemical 

 changes, especially in its etiology, which depends almost solely upon 

 mechanical factors. Some chemical alterations result, however, from 

 the changes in the stagnating blood, which may, if the obstruction 

 to outflow is severe, become of venous character in the capillaries of 

 the congested area. Oxidation in the tissues is, therefore, impaired, 

 and some fatty changes may result, e. g., in the center of congested 

 liver lobules. Waste products accumulate, and possibly noxious 

 products of metabolism are formed under lack of oxidation ; either 

 from these causes or solely from pressure and lack of nutrition there 

 is a tendency to atrophy of the more specialized parenchymatous cells, 

 and a proliferation of connective tissues. The atrophy of parenchyma 

 is seen particularly in the liver, the increase of connective tissue in the 

 spleen.^ In the kidney neither atrophy nor stroma proliferations 

 are pronounced, but the renal function is greatly impaired, since it 

 depends upon the amount and quality of the blood brought to the 

 kidney.* Whether connective-tissue proliferation in hyperemia de- 

 pends upon overnutrition or upon irritation by waste-products, or is 

 compensatory to parenchymatous atrophy, may be looked upon as 

 still an open question. Probably only the first two factors apply to 

 the connective-tissue growth observed in the congested spleen, the 

 clubbing of the fingers in congenital heart disease, or the thickening 

 of the subcutaneous tissues in passive congestion of the lower ex- 

 tremities. 



Changes in the Blood. — Venous blood differs from arterial, not 

 only in its increased load of COo and other waste products, but also 

 in other ways. Venous blood generally clots less readily than arterial 

 blood.^ It contains more diffusible alkali because the CO, combines 

 with and tears away part of the bases that are held by the proteins, 

 especially in the corpuscles, and so alkaline carbonates are formed 



2 Polycythemia {Vaquez-Osler disease) is accompanied by an increase in tlie 

 total nitrocren of the blood, in proportion to the number of erythrocytes; but the 

 nitrogen content of the individual erythrocyte is decreased, (v. .Jaksch, Zent. inn. 

 Med., 1912 (33), 397). 



3 See Christian, Jour. Amer. Med. Assoc, 1905 (45), 1615. 



4 See Ro^yntree and Geraghty, Arch. Int. Med., 1913 (11), 121; Xonnenljruch, 

 Deut. Arch. klin. Med., 191,3 (110), 162. 



sVierordt (Arch. f. Heilk., 1878 (19), 193) found coagulation faster in the 

 blood in passive congestion than in normal venous blood; but Hascbrock (Zeit. f. 

 Biol., 1882 (18), 41) found that if the stasis is protracted, the coagulation be- 

 comes delayed because of the excess of CO;. 



