Alteration of pacemaker threshold by drug and physiological factors.

Abstract

In order to accurately measure changes in cardiac electrical threshold, as evoked by pharmacological or physiological interventions, it is necessary to define clearly the term threshold and the method of measuring it. Electrical threshold at any given time is the minimum electrical impulse necessary to stimulate the heart for the specific electrical system being used at that time. Determinants of threshold for any pacemaker system are many, and can be thought of as comprising extrinsic and intrinsic factors. Extrinsic factors, which are determined by engineering design, include electrode composition, electrode surface area, electrode impedance, and the waveform, voltage, current, and duration of the stimulus. Since the biological impedance of the heart and other body tissues is nonlinear, threshold may vary with different stimulus-voltage or current levels, and changes in stimulus duration also produce changes in threshold. Intrinsic threshold factors, more the domain of the biological scientist, include the position of the electrode on or inside the heart, the electrochemical interface between the electrode and surrounding tissue, and the intrinsic excitability of the tissue. The electrode-tissue interface is partly extrinsic and partly intrinsic, but probably cannot be altered by external interventions after complete implantation of a pacemaker system. Similarly, with the exception of repositioning a catheter, electrode position is also fixed after permanent implantation. We are therefore usually left with only one factor that can be altered after permanent implantation of a pacemaker system, i.e., excitability of cardiac tissue. Exit block is a term that we believe may be justifiably applied to the clinical condition in which a normal pacemaker stimulus fails to excite the heart because of an abnormally high threshold. It is apparent that any total system, employing any type of pulse generator, electrodes, and electrode position in a heart, will deliver a maximal stimulus distributed through the heart in a pattern specific for that system. It is equally apparent that if the tissue which is most easily excited by that system has an excitability threshold exceeding that of the implanted system, excitation of the heart will not result. Since the range of threshold varies greatly from patient to patient and from implant to implant for any given patient,'B2 a system in which the output is great enough that exit block is never seen is probably wasteful of energy in the majority of cases. In addition, the stimulus-to-threshold ratio may be dangerously high in such a design. Because fibrillation threshold is in the range of only 10-20 times excitation threshold, proper pacemaker design may occasionally encounter a high threshold and clinical exit block, unless the output of the power unit is so high that it always exceeds any threshold encountered. Several situations arise in which it is clinically helpful to be able to alter the excitability of the heart relative to the output of the implanted pacemaker system. Since tissue excitability is the only factor that usually can be manipulated in totally implanted systems, alteration of threshold by drug and physiological factors is of clinical importance. Measurement of threshold changes after inter-