Dr. Johnson. On Asphyxia and the 



5, 



last stage of asphyxia, while the right cavities are in a state of 

 extreme distension, the left are, as a rule, flaccid and comparatively 

 empty, the lungs themselves, us before mentioned, being extremely 

 anamiic and collapsed. The condition of the heart's cavities in t In- 

 successive btagcs of asphyxia was clearly shown by an experimei 

 which Dr. Rutherford performed in my presence in 1873. Tl 

 details of this experiment are given in my paper (see diagram with 

 tracing). 



The true explanation of these facts appears to be that, daring the 

 latter stages of asphyxia, the pulmonary arterioles contract, and 

 cause the extreme distension of the right cavities with anaemia of the 

 pulmonary capillaries, and a corresponding defective supply to the 

 left cavities of the heart. 



The continued increase of pressure in the pulmonary vein, obsc-r . <! 

 by Air. Martin, may perhaps be accounted for by the fact that in tho 

 last stage of asphyxia the suction power of the left auricle is im- 

 paired, partly by anaemia of the cardiac tissue, consequent on the 

 contraction of the arterioles both pulmonary and systemic, tl 

 coronary included and partly by the fact that the small amount 

 blood with which it is supplied is more or less completely dt 

 oxidised. 



[I venture further to suggest the following explanation of tt 

 increased blood pressure which has been observed to occur in the 

 pulmonary veins during the successive stages of asphyxia. During 

 the first stage, when the left cavities of the heart are over-distended, 

 as seen in Dr. Rutherford's experiment, there would be a backward 

 pressure extending through the pulmonary veins and capillaries, 

 even, perhaps, to the branches of the pulmonary artery ; but this 

 backward pressure from the left side of the heart must obviously 

 cease when, in the last stage of asphyxia, those cavities are nearly 

 empty of blood. When, however, portions of the ribs are removed 

 in order to introduce a manometer into one of the pulmonary veins, 

 new and artificial cause of obstruction to the pulmonary veiioi 

 circulation is introduced. 



The collapse of the lung, which results from the breach in the che 

 wall, compresses the thin-walled pulmonary veins more than 

 corresponding arteries, and so increases the intra-venous pulmonf 

 pressure. It is an acknowledged fact that the comparatively slight 

 compression of the pulmonary veins which occurs towards the end of 

 a normal expiration lessens the flow of blood into the left side of tl 

 heart.* It is obvious, however, that the pulmonary venous obstruc- 

 tion thus caused must be very much less than that occasioned by the 

 extreme collapse of the lung which results from an opening in the 

 wall of the chest. March 3, 1891.] 



* See Dr. M. Foster's ' Phjsiology,' 5th edition, p. 61S. 



