162 



RESPIRATION 



even though the amount of CO 2 in the blood be not increased. 

 Again, if an animal be caused to breathe air containing the usual 

 amount of O and a large amount of CO 2 , it will suffer from dysp- 

 nea also. In either case the manifestations are practically the 

 same slow, deep and labored respiration. In cardiac disease, 

 hemorrhage, pulmonary diseases, etc., the dyspnea is from a 

 lack of O in the tissues, because of enfeebled action of the heart, 



FIG. 51. The heart in the first stage of asphyxia. 



The left cavities are seen to be distended; the left ventricle partly overlaps the 

 right; La, left auricle; l.v. left ventricle; a, aorta; p.a. pulmonary artery; p.v. pul- 

 monary vein; r.a. right auricle; r.v. right ventricle; v.c.d. descending vena cava; 

 v.c.a. ascending vena cava. (Kirkes after Sir George Johnson.) 



deficient quantity of blood, insufficient exposure of the blood in 

 the lungs, etc. 



Asphyxia may be looked upon as exaggerated dyspnea. The 

 labored breathing of dyspnea becomes convulsive, and finally 

 collapse ensues. Respiration becomes shallow, consciousness 

 is lost, the pupils are dilated, opisthotonus develops, the re- 

 flexes disappear, and at last the heart stops beating. The skin 

 and mucous membranes become blue from non-oxygenation of 

 the blood. Asphyxia from submersion is harder to overcome 

 than from simple deprivation of air outside the water. Resusci- 



