lobar pneumonia, when the pulse becomes rapid, when there is rapid and labored respiration, when the right heart dilates, when there is cold perspiration, and when the signs of impending death are plainly evident. The cyanosis of influenzal pneumonia seemed to be due to an entirely different cause or combination of conditions from those present in lobar or pneumococcic pneumonia. The cyanosis of influenzal pneumonia was, therefore, most confusing, and became all the more so when it was recognized that it did not yield to the respiratory and circulatory stimulants usually employed when cyanosis is present. The inhalation of oxygen was resorted to rather routinely early in the epidemic. It seemed to temporarily influence the cyanosis, but the results were not permanent, and the outcome of the cases did not seem to be different from those in which oxygen inhalations were not used. The blood pressure in those cases in which cyanosis was observed was invariably low. This seemed to be due to the infection, for in several private patients not belonging to this group of patients with previously known high blood pressures the blood pressure was observed as much lower throughout the course of the infection. _Leucopenia_ The peculiar behavior of the white blood corpuscles will be discussed more fully in another paper of this series. Our remarks will deal more particularly with the clinical observations and interpretations. The leucocytes fell below the normal from the very onset of the disease; they varied very little regardless of great changes in temperature; they did not always increase, or if they did increase at all it was comparatively little, even in an extensive invasion of the lungs or in severe complications. Concerning the leucopenia we have no explanation to suggest, save that it is a clinical characteristic of the disease. Our first thought was that the infection came on so suddenly and profoundly there was no time for a leucocyte reaction. But when we recall other diseases associated with a leucopenia, notably typhoid fever, which does not come on with such suddenness, our explanation for the leucopenia of influenza does not seem to hold. The leucopenia must be simply a peculiar toxic blood reaction characteristic of the Pfeiffer bacillus invasion. Such an explanation has long been accepted in the Eberth bacillus infection. _Asthenia_