Disorders of impulse conduction and impulse formation caused by hyperkalemia in man.
In eight patients we have demonstrated manifold types of impairment of impulse conduction produced by hyperkalemia. These abnormalities of impulse conduction occurred either simultaneously or in sequence, and were located in the atria, in the A-V junction, in the fascicular distribution of the ventricular conduction system, or in the free ventricular walls. In association with the abnormalities of conduction, abnormal impulse formation was also frequently observed as manifested by acceleration of normal pacemakers or the emergence of ectopic pacemakers. In one patient hyperkalemia produced alteration in sinus and A-V junctional impulse formation which overshadowed conduction disorders. In all of the eight cases the hyperkalemia was considered to be noniatrogenic. Hyperkalemia appears to potentiate subclinical conduction abnormalities, especially in the His-Purkinje system. However, the presence of pre-existent intraventricular conduction defects such as a bifascicular block does not exclude the possibility that the site of an A-V conduction delay during hyperkalemia can be in the A-V node, as demonstrated by His bundle recording in one instance after development of second-degree (type I) A-V block.
D000293:Adolescent; D000328:Adult; D000368:Aged; D002036:Bundle of His / Q000503:physiopathology; D002037:Bundle-Branch Block / Q000209:etiology; D004562:Electrocardiography; D005260:Female; D006327:Heart Block / Q000209:etiology*; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D006947:Hyperkalemia / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D013610:Tachycardia / Q000209:etiology