134 CLINICAL VETERINARY MEDICINE AND SURGERY. 



Nevertheless the animal had been able to regularly perform trotting^ 

 work up to the day of its death. Although the mitral changes were of 

 old standing, they had been compensated. The increased functional 

 acti\ity of the left auricle had proved sufficient to overcome the obstacle 

 resulting from the valvular lesion, and to prevent the appearance of 

 symptoms which would have betrayed the altered conditions. 



As a rule, this phase of mitral insufficiency, where regurgitation of 

 blood is confined to the left auricle, is not of long duration. The 

 pulmonary veins soon become engorged and dilated ; stasis gradually 

 extends to the pulmonary capillaries, the main arterial trunks of 

 the pulmonic circulation, and the right ventricle. In turn the right 

 ventricle becomes distended, with or without its walls hypertro- 

 ph5^ing ; then, on account of the tricuspid insufficiency which follows, 

 the right auricle undergoes similar changes. These disturbances 

 extend to the veins of the greater circulation, to the portal system, 

 to the systemic capillaries and to the whole arterial system. The 

 increased tension in the latter is finally felt in the left ventricle, 

 which, being overworked, becomes dilated and to a certain extent 

 hypertrophied. 



Such is the cycle of troubles produced by mitral insufficiency. 

 The heart is their point of origin, and the object on which in the last 

 instance they react. But very rareh' indeed are they alloN\ed to 

 develop in their entirety in working animals, the patient being almost 

 always destroyed when incapable of further work, that is, as soon as 

 blood-stasis in the pulmonary capillaries produces grave respiratory 

 disease. 



Let us now consider the changes which occur, first in the lung 

 and then in the other viscera, under the influence of blood-stasis. 



The effects produced by dilatation of the pulmonar}- vessels and 

 retardation of the blood-current through them grow rapidly in im- 

 portance. The capillaries become varicose, their walls thinned, and 

 the nutrition of the cells composing them suffers. Congestion of the 

 bronchial mucous membrane follows distension of the pulmonary 

 capillaries, and b}- diminishing the calibre of the air conduits tends 

 to produce dyspnoea. Blood-plasma filters through the thin vessel 

 walls and becomes extravasated, partly into the alveoli, parti}' into the 

 pulmonary tissue itself. In time pulmonar)- oedema increases : in 

 places induration may occur, and disseminated centres of interstitial 

 pneumonia appear. The respirator}- surface is thus considerably 

 diminished, oxygenation of the blood becomes very imperfect, and 

 dyspnoea follows. 



As soon as general venous stasis occurs internal organs become 



