1. A simple method for arterial puncture is given which does no permanent injury to the artery. Arterial and venous punctures have been done on 33 cases of pneumonia and five normal subjects, and the blood thus obtained has been studied with reference to the oxygen capacity and arterial and venous unsaturation.

2. In five normal subjects the mean arterial unsaturation was 5 per cent of the total oxygen capacity; the mean venous unsaturation was 26.8 per cent.

3. In the pneumonia cases the arterial oxygen unsaturation varied over a wide range. The arterial unsaturation varied from 0.0 to 68.2 per cent, the venous from 14.4 to 85.5 per cent. In the fatal cases as opposed to the non-fatal cases of pneumonia, the mean arterial oxygen unsaturation was 32 per cent as against 13.9 per cent. As a rule, an arterial unsaturation of over 20 per cent was associated with a fatal outcome. Similarly, the mean venous oxygen unsaturation was 57 per cent in the fatal cases and 36.3 per cent in the non-fatal cases.

4. In five cases in which no cyanosis was observed at any time the mean arterial oxygen unsaturation was 5.4 per cent, the mean venous oxygen unsaturation 31.5 per cent. In cases which showed cyanosis of varying degree during the course of the illness, the mean arterial unsaturation was 24.7 per cent, and the mean venous unsaturation 44.5 per cent. Cases without cyanosis have an arterial unsaturation close to the normal.

5. There is a definite relation between the degree of cyanosis and the per cent of arterial unsaturation. With increasing cyanosis the arterial unsaturation becomes greater. The venous unsaturation varies similarly.

6. In individual cases with marked cyanosis associated with high arterial unsaturation, the clinical improvement of the patient and the diminution of the cyanosis are accompanied by a similar diminution in the arterial and venous unsaturation. Conversely, an increase of cyanosis is accompanied by an increase in arterial unsaturation.

It is evident that the cyanosis of pneumonia patients is due to the incomplete saturation of venous blood with oxygen in the lungs, and that the various shades of blue observed in the distal parts are caused by an admixture of reduced hemoglobin and oxyhemoglobin in the superficial capillaries.

7. No unusually low total oxygen capacities were observed, even in fatal cases with intense cyanosis. On the contrary, in these cases the total oxygen capacity was unusually high, pointing toward a concentration of the blood. Again in only one case was there any marked fall in the oxygen capacity during the illness. Therefore, methemoglobin formation, in these cases, can hardly have occurred to such an extent as to be an important factor in the production of cyanosis. Of the 33 cases studied, however, only seven were lobar pneumonia, the rest being of types ordinarily unusual, which have accompanied the recent influenza epidemic; and of the seven, not all were in all respects typically lobar. The possibility still remains, therefore, that in typical lobar pneumonia caused by the pneumococcus methemoglobin may play a part in the cyanosis.

8. The oxygen consumption, i.e. difference between arterial and venous contents, was within normal limits, indicating that the cardiac output was not diminished in the cases (chiefly post influenza) of pneumonia studied.

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