Berbari E J, Lazzara R, El-Sherif N, Scherlag B J
Circulation. 1975 May;51(5):802-10. doi: 10.1161/01.cir.51.5.802.
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.
先前的研究已经证明了一种表面记录技术,该技术使用信号平均法来检测“等电位”P-R段期间的电活动。各种生理和药理学干预表明,这些电位的来源是希氏-浦肯野系统(HPS)。为了评估平均记录对HPS激活变化的敏感性,即HPS中的传导缺陷,在15只接受开胸手术的犬中,使用双极前后心外膜导联直接从心脏表面进行HPS记录。信号经过放大、滤波,并使用数字计算机进行平均以增强信号。心外膜平均导联(EAL)包含与HPS去极化同时发生的活动,并且与先前研究中完整犬体表导联记录的活动相似。来自电极导管的标准心电图和希氏束电图用作定位和评估由创伤和缺血性损伤实验性产生的几种传导障碍的参考。所产生的障碍包括:1)房室(A-V)结阻滞,导致P波后EAL中记录的活动丧失。2)前间隔动脉结扎产生的一度和二度希氏束内阻滞在希氏束电图(1度)中显示希氏电位分裂,在希氏束中出现2:1传导阻滞(2度)。在阻滞搏动中,两种情况下EAL均显示与分裂希氏电位的近端希氏束活动同时发生的可重复活动部分。3)在前间隔动脉结扎产生的四例近端右束支阻滞中,EAL中HPS活动的相对近端部分显示明显减弱。4)两例远端希氏束或双侧束支延迟表现为H-V时间延长和QRS波型正常。EAL中HPS活动的早期和晚期部分没有明显变化,而中间部分延长并分裂。5)挤压窦房结产生的交界性心律导致EAL中HPS去极化之前无心房活动发生。然而,QRS波之前有HPS活动,其起始与希氏束电图中记录的H波一致。EAL在正常传导期间不同心率下显示HPS活动一致且可重复形态和时间,在异常传导期间显示HPS活动一致改变。