Slowing of the pulse rate during the course and convalescence of certain acute infectious diseases has been a clinical observation for many years. Osler's classical description of post-typhoidal bradycardia was made in 1898; he was the first to record pulse rates as low as 30 a minute following this disease.1 Morison2 noted the slow pulse rate in certain types of pneumonia. In 1922, Cowan and Ritchie3 were among the first to describe its development following influenzal infections.
During a recent study of postinfluenzal disturbances of the heart4 and postinfluenzal heart block,5 a rather definite type of bradycardia was discovered with certain associated irregularities of rhythm; this type, though apparently common, has not been discussed in the available literature. The rather frequent occurrence of bradycardia during the recent outbreak of influenza and the apprehension aroused by its detection prompted a closer investigation of these bradycardial irregularities. What constitutes pathologic bradycardia, so