Action of driving stimuli from intrinsic and extrinsic sources on in situ cardiac pacemaker tissues.

• It is common knowledge that the heart possesses subsidiary pacemaker tissues capable of initiating effective heart action in the absence of normal sinoatrial node function.' When sinoatrial node pacemaker action is stopped by crushing or by quick inactivation, a heart beat originates in the atrioventricular conducting system or from another region of the myocardium but only after some delay, as though "latent" or subsidiary pacemakers are normally somewhat depressed. Furthermore, these subsidiary pacemakers do not immediately attain their maximum rate of action after inactivation of the sinoatrial node. Termination of imposed drive may likewise result in a period of asystole followed by slow acceleration of pacemaker action. As early as 1884, Gaskell found that intrinsic pacemaker activity tended to be inhibited by a series of rapidly applied stimuli. Among the problems which have been encountered by those who deal with failure of intrinsic pacemakers and with the use of artificial cardiac pacemakersare subnormality of function related to pacemaker placement, the consequences of various rates of drive, and the abnormality of cardiac activity subsequent to drive termination. In studies of isolated tissues it has been found that after imposed drive there is a period of depressed activity followed by a late acceleration of pacemaker action." In the work to be re-