Biomedical subjects
Publications and source records attributed to D H Singer.
Pseudo first- and second-degree atrioventricular (AV) block can occur due to depressive effects of concealed junctional discharges on AV conduction of sinus impulses. Pseudo AV block is not indicative of a primary impairment of AV conduction and is reversible by interventions that suppress ectopy.
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Artifacts mimicking a variety of dysrhythmias occur relatively frequently in ambulatory ECG (Holter) monitoring records. Proper interpretation is imperative if serious therapeutic errors are to be avoided. Two-channel recording systems may facilitate recognition of some, but not all, of these artifacts. Pseudodysrhythmias may mimic paroxysmal supraventricular tachycardia and atrial fibrillation, atrial dissociation, extrasystoles, and sinus pauses. There are several causes of pseudodysrhythmias. Failure to recognize these patterns may result in serious errors in patient management.
Glass microelectrode studies on posterior papillary muscle (PPM) slice preparations from 20 pentobarbital-anesthetized dogs (15 subjected to prior circumflex coronary artery ligation, 5 to sham ligation) have resulted in the definition of an electrophysiological marker of irreversible ischemic injury, namely, findings of areas composed of cells unable to generate a significant resting potential (less than -25) mV), designated "electrically inactive areas." Electrically inactive areas were essentially confined to PPM from dogs with circumflex coronary ligation; the incidence and distribution of the areas was related to duration of ischemia. Correlative phase- and light-microscopic studies demonstrated close correspondence between such areas and morphological evidence of irreversible ischemic injury. Analysis of frequency and distribution of electrically inactive areas permits quantitative assessment of the extent and spatial distribution of irreversible injury. This method has been used to quantitate injury in PPM from dogs that had been subjected to ligation for varying time periods. The potential utility of this method for evaluation of interventions designed to protect against ischemic injury and to assess electrical properties of surviving cells is considered.
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Ventricular pacing may mimic or obscure the Q waves of myocardial infarcton. Although ST-T changes may occur for other reasons, their presence should alert the physician to the possibility of acute infarction. QRS complexes may be evaluated for infarction if supraventricular beats without left bundle-branch block occur prematurely, as part of a supraventricular tachycardia or as escape beats after inhibition of the articifial pacemaker.
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The case of a 22-year-old white male without known heart disease who presented with activity related lightheadedness at age 19 and dizziness and fatigue at age 21 is described. Standard electrocardiograms (ECG's) revealed intermittent complete trifascicular block. Rapid progression of symptoms over the succeeding eight months resulted in increasing incapacity. Holter monitoring demonstrated that symptoms were related to development of second and higher degrees of A-V block. Normal A-H interval and markedly prolonged H-Q interval on His bundle electrograms indicated that block was infranodal and localized to bundle branch system. Conduction problems aside, clinical and laboratory evaluation, including echocardiograms and cardiac catheterization, were unremarkable. Progression of bilateral bundle branch disease in a young patient without other demonstrable heart lesions and a negative family background conforms with criteria for Lenegre's disease. To our knowledge, this represents the youngest reported patient with this entity. Possible electrophysiologic basis of block and of exercise induced improvement in A-V conduction also are considered.
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