Biomedical subjects
Publications and source records attributed to N F Goldschlager.
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These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs Homer A. Boushey, Professor of Medicine, and David G. Warnock, Associate Professor of Medicine, under the direction of Dr Lloyd H. Smith, Jr, Professor of Medicine and Associate Dean in the School of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.
Many factors affect the threshold for myocardial stimulation in patients with cardiac pacemakers. The acute local tissue reaction at the electrode-myocardium interface accounts for early threshold rises and may be minimized by choice of specific electrodes (steroid-eluting or carbon-tip). Physiologic variations due to changes in autonomic tone (including eating, sleeping, and exercise) account for day-to-day fluctuations in pacing threshold. Electrolyte and metabolic abnormalities, especially hyperkalemia, alkalosis, acidosis, and hyperglycemia, increase the pacing threshold. Commonly used antiarrhythmic drugs (quinidine and procainamide) also increase pacing threshold. Patients with pacemakers who require antiarrhythmic agents or who have coincident metabolic or electrolyte disturbances should be observed closely for failure to capture. Management of failure to capture is directed at removing the inciting cause and attempting to lower the pacing threshold with isoproterenol, if the situation is urgent. Acute increases in pacing threshold immediately following pacing system implantation can be treated with corticosteroids. Increasing the energy output of programmable pacemakers, in specific circumstances, or insertion of a temporary pacemaker capable of delivering higher energy output than the implanted generator may also be successful.
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