At the height of infection the resulting disturbance of the circulation is clinically characterized by softness of the pulse and diminution of the blood pressure, not necessarily connected with feebleness of the heart's action. These changes are to be separated from those which develop in the further course, the defervescence of, and convalescence from, the febrile disease, when the heart may be dilated, abnormally rapid or slow, occasionally irregular.
No characteristic anatomical changes are necessarily connected with the first kind of disturbance. In many cases, especially in diphtheria and typhoid fever, there are, it is true, important parenchymatous changes in the heart's muscle fibers; in other infections, with acute clinical symptoms, such changes are entirely absent. It is quite generally accepted that an acute infectious myocarditis—Romberg—accompanies the symptoms of cardiac weakness characteristic of convalescence from many acute infectious diseases.
Experiments bearing on the nature of the mechanism of the circulatory