经食管信号平均心电图记录窦房结电图的研究(英文)

目的探讨无创性经食管信号平均技术直接记录窦房结电位（SNP）的方法。方法采用自制三导心电微电位检测仪对256例窦房结功能正常者进行检测,其中男142例,女114例,年龄10～74（44.2±12.4）岁。将食管导联的信号放大（增益达到100μV/cm）、滤波（0.1～50）Hz,16位模/数（A/D）转换,系统采样频率2kHz,对食管SNP进行信号平均,并通过同步信号平均对人食管和心内膜所记录的SNP,犬食管和心外膜所记录的SNP进行分析研究。结果记录到食管SNP189例（74%）,所测信号平均食管SNP为P波前的低幅、低频波,可见有2种形态:园顶型（60%）和上斜型（40%）;窦房传导时间为（83.3±26.7）ms,分布范围为（23～118）ms;波幅为（3.5～27.7）μV;dv/dt为（0.43～1.93）mV/s。结论在适当滤波、高增益和抗基线漂移技术条件下,利用经食管信号平均技术,大多数窦房结功能正常的患者可直接记录到食管SNP。     

经食管信号平均心电图记录窦房结电图的临床研究

探讨无创性经食管信号叠加直接记录窦房结电位 (SNP)的技术 ,对 2 5 6例食管电生理检查窦房结传导时间(SACT)和窦房结恢复时间 (SNRT)均在正常范围的患者 ,其中男 14 2例、女 114例 ,年龄 4 4 .2± 12 .4 (10～ 74 )岁进行检测。采用自制三导心电微电位检测仪将食管导联的信号放大 (增益达到 10 0 μV/cm)、滤波 (0 .1～ 5 0Hz) ,16位模 /数 (A/D)转换 ,系统采样频率 2kHz,对信号进行叠加 ,189例 (74 % )记录到食管SNP。所测信号叠加食管SNP为P波前的低幅、低频波 ,可见有两种形态 :园顶型 (6 0 % )和上斜型 (4 0 % )。所测窦房传导时间为 83.3± 2 6 .7ms ,分布范围为 2 3～ 118ms;波幅为 3.5～ 2 7.7μV ;dv/dt为 0 .4 3～ 1.93mV/s。笔者认为在适当的滤波、高增益和抗基线漂移技术条件下 ,利用经食管信号叠加技术 ,大多数窦房结功能正常的患者可直接记录到食管SNP。     

循环系统疾病

8吕20了01宾房结电田的再论证/郑爬…刀中华心血管病杂志·诗功8了,注8(6)、一298一299 于7条犬同步记录心表窦房结电图(5 NE),造成矛条犬的窦性心律失常模型,:当静脉内推注异搏定后班窦房结电位即消失,证实在心表可录到窦房结电位。吞例于电极部位取材,电镜观察其超微结构符合P;细胸特征,于7例先心患者测心表5 NE,窦房传导吐间郁土2旦.7二。,于7例窦性心律失常患者,记录,今内s孤E,“旦记录电极向心室方向移动,窦房结电位即俏失,、在犬实验时,心表、心内与食管5 NE同步对那结果一致,个体心内与食管5 NE同步对照也一致。食管5 NE的窦房…     

用QRS波触发的讯号叠加法:人体希氏-浦顷野系统电活动的非侵入性记录

本文旨在:(1)研究心电讯号经过滤波器变换后的形态;(2)研究叠加处理对希氏束电位记录的影响;(3)比较心房起搏波触发和病人QRS波触发两种不同触发方式叠加讯号的心前区记录。方法:图一为仪器的方框图。选择具有高讯/噪比的高增益放大器(前置放大器A)来记录讯号,增益为1 x 10~5,带通滤波器置于30～300赫兹。另用同一类型的放大器作为第二前置放大器(前置放大器B)以提供QRS触发讯号,此放大器的带通滤波器置于10～30赫兹,增益1～5x10~3。双极导联的心电讯号在5000赫兹的采样频率进行数字化,贮入暂存讯号记录器,经QRS触发记忆的数字转输入1024字18位的叠加仪,叠加次数为128或256次心动周期,叠加后的图形在示波屏上显示并摄影。     

食管心电图诊断宽QRS心动过速1例

患者男性,40岁。体表心电图示阵发性宽QRS心动过速。为明确心动过速时心房与心室激动的关系记录食管导联心电图。在患者咽部喷散1％丁卡因,表面麻醉后从鼻孔插入食管电极约35cm,根据食管内单极心电图略微调整电极深度,使食管内心电图的P波振幅最大。采用双极食管电极导管,电极间距为2cm。将2个电极接日本Kohden RM-6000型8道生理记录仪生物电放大器,时间常数选择为3ms,滤波选择为30Hz,该导联为食管内双极导联(ESO-DP);以食管电极导管的近端电极接体表心电     

用模拟窦房结电活动信号寻找记录窦房结电图的部位

窦房结(SN)电活动信号比较微弱,在犬心脏窦房结部位的心外膜上检测到窦房结电位(SNP)的幅度仅50—230μV,而众多因素可干扰SNP的检测。尤其是一些干扰信号的特征类似于窦房结电图(SNE),增加了记录的困难,容易发生误认。国内文献对无创性的检测方法,如食管内和体表记录SNE以及有创性的心内检测提出了不少疑问。为此,我们采用电子计算机模拟产生SN电活动信号,将信号输入犬心脏,观察机体各部位对其衰减情况,力图从另外一个角度探索比较可靠的记录SNE的部位和方法。     

体表希氏束电图检测新方法

希氏束电图(HBE)是描记心内传导系统电位变化的曲线,其电信号极其微弱,只有1～10μV左右,通常的放大方法无法记录到。我们采用数字滤波加模式识别的新方法,联合研制出TZXJ-1型体表逐搏希氏束检测仪,对7只杂种犬进行了动物实验,取得了满意的图形。现将研究结果报告如下:1.逐搏体表希氏束检测仪是一个在微机下根据USB接口的三导联测量系统来进行体表希氏束电位的逐拍检测,由硬件和软件两部分组成。(1)硬件。系统中有,一路心电放大器和两路希氏束(心内和体表)放大器。放大器总增益均为2000,滤波范围为0.1～200Hz。均采用差动放大电路,由于…     

自制针电极记录急性缺血和再灌注犬希氏-浦肯野系统的电冲动

探讨针电极记录犬在体心脏希氏 浦肯野系统 (HPS)电冲动的可行性 ,观察其图形特点、规律与影响因素。以注射针头和不锈钢丝自制针电极 ,2 5只犬开胸后沿HPS的解剖行程探查电冲动。结扎冠状动脉前降支 ,观察缺血和再灌注时心脏电图与电生理参数的变化。结果 :HPS电冲动为高频、持续时间短暂的电位 ,HPS近心房插入端 ,电位隐含于心房电图尾部 ;中段游离于房室肌间 ,电位独立于房、室电图之间 ;远端插入心内、外膜下层心室肌 ,电位隐含于心室电图的内部。高通滤波衰减低频高幅电位 ,显露基线稳定的高频低幅电位。双极电极与HPS走行平行排列所记HPS电位的幅度最大。缺血区HPS电位迟于心肌电位消失 ,再灌注HPS电位最先恢复。结论 :以针电极记录HPS电冲动稳定可靠 ,其图形与记录部位HPS的解剖和电生理特性有关外并受记录技术的影响。     

双极食管导联记录右心房电位探讨

目的　探讨双极食管导联记录右心房电位的方法及其临床意义。　方法　心内电生理检查时同步记录高位右心房、希氏束、冠状静脉窦和双极食管导联心电图 ,分析食管导联中右心房电位和左心房电位的关系。　结果　双极食管导联记录到的窦性 P波由圆钝直立的右心房电位和尖锐高大的左心房电位组成。 2 8例右心房、左心房传导时间分别为 (4 2 .86± 8.81) ms和 (6 4.2 8± 6 .78) ms,右心房/左心房 =0 .10± 0 .0 3。在窦性心律 ,右心房、左心房和右心室起搏时 ,食管导联的右心房电位和心腔内高位右心房导联的 A波一致 ,左心房电位与冠状静脉窦导联的 A波基本一致。　结论　双极食管导联记录方法能够可靠记录到右心房电位 ,并且分别反映出右心房和左心房激动顺序 ,对了解心房间传导功能 ,分析房性心律失常 ,初步判断隐匿性房室旁路部位等方面 ,有一定的实用价值     

右心房上部心律的确诊

为探讨右心房上部心律的诊断方法，通过动物实验自身对照，同步记录１５只犬心电图Ⅱ、ａＶＲ导联、心腔内窦房结电图、高位右心房电图。结果发现在窦房结局部注入维拉帕米、石碳酸及电刺激右侧颈迷走神经情况下，窦房结功能被抑制后出现房性逸搏心律时，心电图有时仍为窦性心律（ＰⅡ直立、ＰａＶＲ倒置）；而窦房结电图上则记录不到窦房结电位，心率亦有明显降低（ｔ＝２．４２０，Ｐ〈０．０５）。提示窦房结附近的右心房上部心律     

Noninvasive His bundle electrogram: Value of three vector lead recordings

Studies were conducted in 45 patients to determine whether the reliability of the measurement of the His bundle potential from the body surface was increased by signal averaging of three simultaneously recorded electrocardiographic potentials from horizontal (X), frontal (Y) and sagittal (Z) axes as opposed to recording of any of these. Potentials from the X, Y and Z leads were amplified by 250,000, filtered between 80 hertz (12 dB/octave) and 200 hertz (24 dB/octave) and signal averaging of 1,000 beats was performed. The His bundle potential could be clearly defined in 25 of the 45 patients in the X, Y or Z lead. His bundle potentials were evident in the X lead in 17 (68 percent) of these 25 patients, in the Y lead in 19 (77 percent) and in the Z lead in 11 (44 percent). No single lead gave satisfactory His bundle electrographic potentials in all patients. In 20 patients the His bundle electrogram could not be recorded because terminal atrial activity overlapped activity of the His bundle potential. The three lead system defined the His bundle potential in a significantly greater number of patients than did the best single lead because it (1) displayed the vectorial lead with the largest His bundle potential, (2) permitted validation of the His bundle potential in more than one lead, and (3) displayed the vectorial lead with the most isoelectric terminal P wave. It is concluded that reliable His bundle potential measurements are obtained in a significantly greater number of patients with use of the simultaneous three lead system than with use of any single lead.     

A Case of Widely Split Double P Waves with Marked Intra-Atrial Conduction Delay

Widely Split Double P Wave. We report a 78-year-old man as the first documented case of double P waves separated by 400 msec on 12-lead ECG. These P waves had different polarities on lead V₁. The first P wave represented activation of the lateral wall of the right atrium, and the latter P wave represented activation of the nudial right atrium and the left atrium. Widely spaced double potentials were recorded craniocaudally along the line, presumably corresponding to the crista terminalis during sinus rhythm. For this to occur, conduction disturbance has to be present both in the upper and lower right atrium. Conduction disturbance in the upper right atrium would interrupt excitation from the sinus node to the medial wall, and conduction disturbance in the lower right atrium would interrupt excitation spreading from the lower lateral right atrium to the isthmus area where fragmented potentials were recorded. These multiple discrete lesions appear to constitute a unique electrical atriopathy in this patient.     

The effects of elevated intracranial pressure on the canine electrocardiogram

Striking electrocardiographic abnormalities have been noted in some patients with central nervous system injury. To study the relationship between the electrocardiogram and intracranial pressure, intracranial pressure was elevated in 14 open chest pentobarbital-anesthetized dogs. The right vagus was stimulated to produce sinus slowing and the right atrium was paced at a constant cycle length fast enough to prevent arrhythmias and maintain heart rate constant (750 msec in 11 dogs and 600 msec in three dogs). In nine dogs, intracranial pressure was sequentially elevated to 100, 150, and 200 mmHg. Systolic arterial blood pressure consistently rose to exceed intracranial pressure (P less than 0.005). At a pressure of 150 and 200 mmHg, mean QT intervals shortened significantly in recorded leads II, X, Y, and Z from 0.01). T wave changes were also noted that consisted of increasing positivity in leads II, X, and Y and increasing negativity in lead Z. To delinate the role of the sympathetic nervous system, an additional five dogs were subjected to an intracranial pressure of 200 mmHg before and after bilateral stellate ganglionectomy and timolol (0.1 mg/kg IV). Elimination of sympathetic influences did not significantly alter the electrocardiographic effects of elevated intracranial pressure. Thus, intracranial hypertension results in significant QT shortening and T wave changes that are not entirely mediated by the sympathetic nervous system.     

A Noninvasive Transesophageal Signal Averaging Technique for Detection of Sinus Node Electrogram

We have developed a noninvasive transesophageal signal averaging technique for direct recording of sinus node electrogram. In this study, sinus node electrograms were recorded from 106 of 138 patients (77%), comparable to that (46%) recorded by conventional transesophageal technique, 59 were male and 47 were female ranging in age from 10–74 years (mean 44.2±12.4 years). The signals from lead I, surface averaged lead and esophagus averaged lead were amplified (up to 100V/cm), filtered (0.1–50Hz), AD converted to 16-bit accuracy at a sampling rate of 2KHz and averaged by using the three channel low-noise amplifier. The signal averaged esophageal sinus node potentials are deflections of low-amplitude and low-frequency preceding the P wave. Two morphologies, the domed wave (64 of 106 patients, 60%) and the smooth upstroke slope (42 of 106 patients, 40%), can be seen. The directly recorded sinoatrial conduction time was 82.3 ±18.6msec (mean±2 SD), ranged from 23–112msec, amplitude was 3.8–27.7V and dv/dt was 0.42–1.92mV/sec. The sinoatrial conduction time recorded by the transesophageal catheter technique was comparable to that (80.4±18.1msec) recorded by the transvenous catheter method perfectly. We think that signal averaged sinus node electrogram could be recorded in sinus rhythm in most patients with normal sinus node function and proper filter settings, high amplification and anti-drift technique are important in recording signal averaged esophageal sinus node electrogram.     

Low voltage electrical activity preceding right atrial depolarisation in man.

Electrical recordings were made in the high right atrium in 28 patients undergoing cardiac catheterisation and in 3 healthy volunteers. After filtering and amplification by 3 to 10 million times, the signals were passed through a signal averaging process in a digital computer. Of the 28 subjects who had technically satisfactory recordings, 23 showed low voltage electrical activity preceding the conventionally-recorded atrial depolarisation. The low voltage activity started 50 to 200 ms before the atrial deflection and was variable in shape. These early signals may be the result of activity in the region of the sinus node.     

Low voltage electrical activity preceding right atrial depolarisation in man.

Electrical recordings were made in the high right atrium in 28 patients undergoing cardiac catheterisation and in 3 healthy volunteers. After filtering and amplification by 3 to 10 million times, the signals were passed through a signal averaging process in a digital computer. Of the 28 subjects who had technically satisfactory recordings, 23 showed low voltage electrical activity preceding the conventionally-recorded atrial depolarisation. The low voltage activity started 50 to 200 ms before the atrial deflection and was variable in shape. These early signals may be the result of activity in the region of the sinus node.     

Demonstration of a widely distributed atrial pacemaker complex in the human heart

Atrial depolarization was analyzed in 14 patients with the Wolff-Parkinson-White syndrome undergoing surgery to ablate accessory atrioventricular pathways associated with tachyarrhythmias. Bipolar potentials were recorded simultaneously from 156 atrial epicardial electrodes arranged in three templates to fit the anterior and posterior aspects of both atria. Spontaneous or sinus rhythms were recorded, as were atrial escape rhythms after overdrive pacing at rates of 150 and 200 beats/min. Atrial activation maps revealed different patterns of impulse initiation varying from typical unifocal sinus node impulse origin, unifocal extranodal impulse origin, and multicentric impulse origin from two to four widely distributed atrial pacemaker sites. In subjects demonstrating only unifocal impulse origin during control or sinus rhythm, other widely divergent pacemaker sites were recorded in other maps during subsequent rhythms. In addition to sites located at the upper superior vena cava-right atrium junction, pacemakers also dominated at sites anterior and inferior to the sinus node region during both control and escape depolarizations. Most of the subjects were found to have two or more pacemaker sites when maps of all control and postpacing conditions were analyzed. The right atrial pacemaker region encompassed a zone of 7.5 X 1.5 cm centered about the long axis of the sulcus terminalis posteriorly and the precaval band anteriorly. An unexpected finding was the participation of left atrial escape pacemakers. The functional behavior of both the control and escape pacemakers, as assessed by sinus node recovery time, was normal, indicating physiologic operation of the extranodal sites as part of an overall system of distributed pacemakers involved in the control of rate. Although functional assessment was limited in these initial patient studies, correspondence with similar observations in extensive previous canine studies supports the concept of a widely distributed atrial pacemaker complex in man.     

The sequence of retrograde atrial activation in the canine heart. Correlation with positive and negative retrograde P waves.

The relationship of P-wave polarity and morphology in leads II, III, and aVF to the sequence of atrial activation was studied in the canine heart when the atria were paced from the region of the sinus node or the posterior-inferior left atrium and when retrograde activation of the atria occurred with right ventricular epicardial pacing. Deeply negative P waves in leads II, III, and aVF which occurred when the posterior-inferior left atrium was paced were associated with true retrograde activation of the atria. Positive P waves recorded in leads II, III, and aVF during retrograde atrial capture with right ventricular pacing were associated with rapid retrograde spread of the impulse in the interatrial septum to the region of Bachmann's bundle from which site the impulse spread to depolarize significant portions of both atria in a manner similar to that demonstrated during pacing from the region of the sinus node. When the atria were paced from a site just anterior to the coronary sinus ostium, positive P waves recorded in leads II, III, and aVF were associated with early activation in the vicinity of Bachmann's bundle and later activation of the posterior-inferior left atrium. When the atria were paced from a site just posterior to the coronary sinus ostium, negative P waves in leads II, III, and aVF were associated with early activation of the posterior-inferior left atrium and later activation in the vicinity of Bachmann's bundle. It was concluded that the time of arrival of the impulse at Bachmann's bundle relative to that at the posterior left atrium and the direction of spread of the impulse from and within Bachmann's bundle are critical in determining P-wave polarity and morphology.