Noah Morris

The Indirect Determination of the pH of the Blood in Children.

It has long been known that the tension of CO, in arterial blood is approximately the same as that of the alveolar air. Thus, by obtaining samples of alveolar air, one can readily calculate the CO2 tension in the blood and, by usinig Bohrs coefficient, arrive at the figure for the free CO, content (H2CO ,). The total CO2 contenlt less this figure will then represent the combined CO2 (BHCO3) of the blood.

Observations on the Chloride Metabolism in Congenital Pyloric Stenosis

A fall in the chloriine content of the blood in cases of high intestiiial obstruction is a well-recognized biochemical finding. The opinion is genierally held that the diminution in the level of the blood chlorine is due primarily to the loss of chlorine by the vomitus. Accompanying this decrease in chlorine there is ani increase in the CO2 content, resulting in a non-gaseouis alkalosis ww ith a diminution in the respiratory exchange. This increase in CO2 Mould appear to be the result of the bodys effort to maintain the ionic concentration of the blood at the normal level, and simultaneously, to compensate the deficienicy in the acid radicle. Very strong experimental proof has been brought forward by Gamblel and others in favour of the truth of this hypothesis. In a previous communication2 we have shown that the blood chlorine tends to be low in congenital pyloric stenosis, the diminution being roughly related to the severity of the vomiting. But we have seen cases in which there was present a typical picture of alkalosis, as indicated by the raised blood CO2 content and the depressed breathing, either duiring a period in which no vomiiitinig occurred or, as in one instance, when there u-as a complete absenlce of vomiting. In Table 1 examples are given in which the depressed breathing was a feature despite the comparatively normal valuie for the blood chlorine. lIncidenitally, it shows that there is iiot necessarily a correlation betweeni the

The role of acidosis and phosphate retention in the pathogenesis of rickets and rachitic tetany of infants.

There is no evidence that acidosis is either a causal or associated factor in infantile rickets. There is an increased urinary output of ammonia but the fact that it is associated with a diminution in the titratable acidity of the urine renders it unlikely that there is a condition of acidosis present. This conclusion is further strengthened by the fact that healing of rickets as evidenced by increased retention of minerals and X‐ray signs, may take place during prolonged administration of an acid‐producing substance.