Extracardiac recordings of His-Purkinje activity during conduction disorders and junctional rhythms.
Previous investigations have demonstrated a surface recording technique using signal averaging to detect electrical activity during the "isoelectric" P-R segment. Various physiological and pharmacological interventions suggest that the source of these potentials isthe His-Purkinje system (HPS). In order to assess the sensitivity of averaged recordings to changes in HPS activation, i.e., conduction defects in the HPS recordings were made directly from the heart surface using a bipolar, anterior-posterior epicardial lead in 15  dogs which underwent thoractomy. The signal was amplified, filtered and averaged using a digital computer for purposes of signal enhancement. The epicardial averaged lead (EAL) contained activity coincident with HPS depolarization and similar to those recorded by leads on the body surface of intact dogs from previous studies. The standard ECG and His bundle electrogram from an electrode catheter served as references in localizing and assessing several conduction disorders experimentally produced by traumatic and ischemic injury. Among the disorders produced were: 1) atrioventricular (A-V) nodal block which resulted in loss of recorded activity in the EAL following the P wave. 2) First and second degree intra-His bundle block produced by anterior septal artery ligation showed split His potentials in the HBE (1 degree) and 2:1 conduction with block in the His bundle (2 degrees). In the blocked beats the EAL showed a reproducible portion of the activity coincident with proximal His bundle activity of the split His potentials in both cases. 3) In four cases of proximal right bundle branch block produced by anterior septal artery ligation the relatively proximal portions of HPS activity in the EAL showed marked diminution. 4) Two cases of distal His bundle or bilateral bundle branch delay were seen as prolonged H-V time and a normal QRS pattern. The early and late portions of the HPS activity in the EAL were not markedly changed while the middle portion was prolonged and fractionated. 5) Junctional rhythms produced by crushing the SA node resulted in no atrial activity occurring prior to HPS depolarization in the EAL. However, the QRS was preceded by HPS activity whose onset was coincident with the H recorded in the His bundle electrogram. The EAL showed consistent and reproducible morphology and timing of HPS activity at different heart rates during normal conduction and consistent alterations of the HPS activity during abnormal conduction.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000503:physiopathology; D002036:Bundle of His / Q000503:physiopathology*; D002037:Bundle-Branch Block / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels; D004285:Dogs; D004562:Electrocardiography; D005557:Formaldehyde; D006325:Heart Atria / Q000503:physiopathology; D006327:Heart Block / Q000139:chemically induced / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate; D008026:Ligation; D010138:Pacemaker, Artificial; D011690:Purkinje Fibers / Q000503:physiopathology*
D005557:Formaldehyde