阿托品试验诱发急性心肌缺血一例

临床资料　患者女性,19岁。主因间断胸骨后疼痛4年,呕血3口于1998年5月28日入院。既往常感头晕,曾有1次晕厥,数分钟缓解。无药物过敏史。入院后经心电图检查示窦性心动过缓。24h动态心电图示,最慢心率34bpm,最快心率137bpm,平均心率49bpm。超声心动图正常。食管起搏示窦房结恢复时间1720s,窦房传导时间14s。于6月23日行阿托品试验,应用前查心电图仍为窦性心动过缓,窦性心律不齐,40bpm。给予阿托品1.5mg静脉推注后,患者即感剧烈心前区疼痛,伴大汗,烦躁不安。即刻做心电图示窦性心动过速,最快心率140bpm,频发多源室性早搏,二联律,、、aVF、V…     

伞状起搏电极三尖瓣腱索嵌顿一例

患者男性、62岁,因发作性头晕伴一过性意识丧失三个月入院。入院后体表心电图示重度窦性心动过缓伴窦性停搏,24h动态心电图显示最快心率66bpm、最慢心率为22bpm、平均心率42bpm、最长RR间隔为3.0s,有时伴交界区逸搏。阿托品试验:静脉注射阿托品2mg,心率最快为80bpm。入院诊断为病窦综合征,于入院后1周行永久起搏器安置术。选用西门子公司产2040K起搏器,先采用右头静脉途径送入J型电极至右心耳行AAI起搏,因电极难以固定在右心耳,撤出J型电极,再沿原途径插入伞状心室起搏电极(型号Pacesetter1400K)行VVI起搏。在送入伞状电极过程中,先在…     

一度Ⅰ型房室阻滞偶伴房性早搏未下传1例

1病例介绍患者男,71岁,因"前列腺增生、急性尿潴留"入我院。术前常规心电图发现偶发房性早搏,24h动态心电图示全天平均心率92bpm;夜间每小时平均心率84-99bpm;房性早搏13次;SDNN:59ms。图1-6为动态心电图记录第二天凌晨片段图,图7为动态心电图开始记录当天白天片段图。图1中基础节律为窦性心律,R7后见提前的P’波落于T波升支未下传,其前后窦性PP间期基本恒定,PR间期存在变化,PR1~PR7由360ms变至350ms,R6-R7间期大于R1-R2间期,PR8~PR9由200ms变至240ms,PR9~PR13恒定不变,均为240ms,R9-R10间期小于R8-R9间期(详见梯形图);似不典型文氏现象。     

窦性心动过速对心率变异的影响

目的 进一步认识心率变异,探讨心脏自主神经系统功能.方法 对58例心电图诊断正常者与心电图诊断窦性心动过速患者进行24h动态心电图观察,检测出最快心率、最慢心率、平均心率,再采用时域法、频域法进行心率变异分析,了解自主神经系统对窦房结的支配有无改变.结果 心电图诊断正常组与心电图诊断窦性心动过速组相比较,窦性心动过速组24h的最快心率、最慢心率、平均心率增高,心率变异的RR间期标准差(SDNN)、RR间期平均值标准差(SDANN)、相邻RR间期差值均方根(RMSSD)、相邻RR间期差值＞50 ms所占百分比(PNN50)、三角指数(HRVI)等时域指标有所降低,频域指标低频域值(LF)增高,高频域值(HF)降低.结论 心率变异是评价心脏自主神经系统功能的指标.交感神经兴奋,迷走神经功能相对降低,可减弱对窦房结的支配.     

aVR导联成功鉴别宽QRS波心动过速1例

<正>患者男、44岁,因反复心悸不适就诊,超声心动图检查未见心脏结构及功能异常,动态心电图检查为窦性心律(图1),最低心率58bpm,最高心率164bpm,平均心率82bpm,可见房早、房速,阵发房颤,同时伴有阵发性室速(图2)。     

起搏-室早-夺获三联律1例

患者女性,64岁。自觉头晕、胸闷3月,加重1周入院。动态心电图为窦性心动过缓。白天心率平均45～50bpm,夜间最慢心率28bpm,频发室性早搏,临床诊断:病态窦房结综合征,植入V VI起搏器。此图为植入起搏器术后1天记录。窦性心动过缓,频率为48～50bpm,延迟出现的QR S波群前有钉样起搏     

年轻健康男性动态心电图检测心律失常的分析

目的研究年轻健康男性受检者的心律、心率、心律失常、心率变异性等。方法记录和分析177例年轻健康男性动态心电图资料,分析24h心律和心率,进行资料分析;并分析92例健康男性的心率变异性。结果177例健康男性均为窦性心律,24h平均心率为68bpm,心率范围33～183bpm。心律失常检出率达100%:100%检出窦性心动过缓;12%有窦性静止、房室阻滞,但缓慢型心律失常均发生在夜间;57%检出房性早搏;室性早搏检出率16%。结论正常年轻健康男性经动态心电图可检出有不同程度的心律失常。     

心房颤动致DDD起搏器介导的心动过速一例

<正> 患者男性,58岁。因头晕、黑矇7个月,晕厥3次入院。心电图示:窦性心率40bpm。食管心房调搏:窦房结恢复时间2700ms同时出现继发性窦性停搏达4700ms,文氏阻滞点<120bpm,未诱发出快速心律失常及心房颤动(简称房颤)。提示:窦房结功能衰竭,房室传导不良。临床拟诊:冠心病,病态窦房结综合征,阿-斯综合征。于1991年11月27日安装CPI公司Delta TRS 937 DDD起搏器,术中安置心房电极时,由于反复机械刺激心房而诱发房颤,待起搏器植入体内,心电图示:心室起搏频率过速(120～125ppm)。此时起搏器为DDD工作方式,其有关参数:起搏频率65ppm,最大频率(MTR)125ppm,房室延迟150ms,心房感知度0.75mV,心室搏动后的心房不应期(PVARP)250ms,疑为起搏器介导的心动过速(PMT)。采用程控器程控为VVI型,心动过     

吞咽性心房颤动一例

患者男性,49岁,进餐、进水时反复发作心悸半年,近日加重。体检:血压140/75mmHg(1mmHg=0.133kPa),心界不大,心率86bpm,心律齐,未闻及杂音,甲状腺不大。心脏X线胸片、心肌酶谱、心肌ECT、静息时超声心动图、食管吞钡X线检查等各项检查结果提示患者无器质性食管或心脏性疾病。　　静息心电图正常,心电图监测示患者吞咽伴心悸时发生了阵发性心房颤图1　A　静息时体表心电图,窦性心律,心率80bpm。B　吞咽食物时心率逐渐增加到105bpm后,房性早搏诱发短阵心房颤动,心率160bpm动(房颤),最快时心室率约180bpm左右,吞咽后房颤可自行终止,恢复窦性…     

触发性房性心动过速

临床心电学杂志心电快递专栏编辑:近时我遇到一位心动过速的女性患者,56岁,因阵发性心悸20天住院,超声心动图检查提示患者左房、左室扩大,左室侧壁运动节段性减弱。入院后心电图:①窦性心律伴完全性右束支阻滞,心率68bpm,PR间期0.20,QRS波宽0.18,心电轴120°(图1)。②心动过速反复发作,平均心率160bpm,心动过速时12导联QRS波的形态与窦律一致(图2)。③心动过速发作的频率高低不等,心率从115bpm(520ms)到215bpm(280ms)不等,心动过速心电图中偶见容易确认的P波,是否还有其他P'波,是否P'波与T波重叠而使辨认困难(图3)。④为明确心动过速的…     

心房颤动伴长R-R间期的临床意义

目的 探讨心房颤动伴长R-R间期的临床意义.方法 记录204例心房颤动患者环肺静脉隔离术（CPVA）前后的动态心电图,根据患者术后恢复窦性心律后的动态心电图有无二度房室传导阻滞分为：无二度房室传导阻滞组（A组）及二度房室传导阻滞组（B组）,分析两组平均心率、长R-R间期及逸搏心律的平均次数及R-R间期、逸搏心律的分布规律.结果 204例（A组193例,B组11例）心房颤动患者CPVA术后均成功转为窦性心律,两组R-R间期＞2.0s、R-R间期＞2.7s及逸搏心律平均次数比较,差异均有统计学意义（均P＜0.05）.A组中R-R间期＞2.0s及逸搏心律的分布与睡眠或休息有关,而B组中则日夜均可见.结论 不能单纯根据长R-R间期诊断心房颤动伴二度房室传导阻滞,只有R-R间期＞2.0s明显增多并出现R-R间期＞2.7s且心室率＜35 次 / min的逸搏心律（与睡眠或休息无关或伴有器质性心脏病）时,心房颤动伴二度房室传导阻滞的诊断才可能成立.     

Circadian variations in the electrical properties of the human heart assessed by sequential bedside electrophysiologic testing

To assess the variability of the currently used electrophysiologic parameters and their possible circadian rhythm, sequential bedside electrophysiologic testing was performed during a 24-hour period, at intervals of 1 to 2 hours, in 12 patients who had normal atrioventricular (AV) conduction times and normal sinus node function. The coefficients of variation during the 24-hour period were: +/- 10.4% for the R-R interval, +/- 10.6% for the sinus node recovery time (SRT) at atrial pacing of 100 bpm, +/- 32.5% for the corrected SRT, +/- 15.1% for the ventriculoatrial (VA) effective refractory period (ERP), +/- 8.3% for the AV nodal ERP, +/- 5.7% for the AH interval, +/- 5.2% for the HV interval, +/- 5.5% for the atrial ERP, +/- 3.3% for the right ventricular ERP, +/- 2.8% for the QT interval, +/- 4% for the VA interval, and +/- 3.4% for the retrograde Kent bundle ERP. Between 12:00 midnight and 7:00 AM, there was significant lengthening of: the sinus node rate (p less than 0.0005), the SRT at atrial paced rates of 100 and 120 bpm (p less than 0.025), the QT interval duration (p less than 0.025), and the ERP of the atria (p less than 0.025), AV node (p less than 0.01), and right ventricle (p less than 0.05). Thus conventional electrophysiologic parameters are subject to daily variability and, like sinus node function, AV nodal and myocardial refractoriness follow a circadian rhythm with an acrophase between 12:00 midnight and 7:00 AM. In addition, prolonged bedside recording of the His bundle potential can be reliably obtained.     

The QT interval in atrial fibrillation.

The electrocardiogram was recorded for 100 seconds in 50 patients with atrial fibrillation to determine the relations between QT intervals and both the mean and instantaneous ventricular rates. The mean ventricular rate was 94 beats per minute with a mean QT interval of 357 ms. The mean QTc, corrected beat by beat with Bazett's formula, was 444 ms--longer than reported for sinus rhythm. Between subjects, the mean QT interval was linearly related to the mean RR interval, with a slope of +21%. Within all 50 recordings there was a statistically significant correlation between QT intervals and immediately preceding RR intervals, with an average slope of +7%. This within subject QT/RR interval slope was greater at faster mean ventricular rates. In atrial fibrillation, as in sinus rhythm, the QT interval is a function of both the mean ventricular rate and the instantaneous ventricular rate, with the mean ventricular rate predominating; a simple correction of QT intervals for heart rate is therefore inadequate. Comparison of uncorrected QT intervals with those of earlier published series of people in sinus rhythm, however, suggested that atrial fibrillation is associated with prolongation of the mean QT interval.     

Active vs passive rhythms as an explanation of bigeminal rhythm with similar P waves.

We describe the criteria for differential diagnosis between 3:2 sinoatrial block from atrial bigeminy due to an ectopic focus in the sinus or parasinus zone. In the 3:2 sinoatrial block the RR interval of the basic rhythm is similar to the short R-R interval of the paired rhythm. In atrial bigeminy, the R-R interval of the basic rhythm is similar to the long R-R interval of the paired rhythm.     

Effect of flecainide on atrial and ventricular refractoriness and conduction in patients with normal left ventricle: Implications for possible antiarrhythmic and proarrhythmic mechanisms

We studied the effects of intravenous fiecainide (2 mg.kg^–1)on atrial and ventricular refractoriness and conduction duringsinus rhythm, induced atrial fibrillation and atrial pacingat rates of 100, 120 and 150 ppm, in 14 patients with normalleft ventricle. Flecainide caused a significant increase inQRS duration during sinus rhythm (mean ± SD: 87.2 ±8.4 ms vs 102.8 ± 9.1 ms, P<0.001) atrial fibrillation(87.8 ± 10.0 ms vs 108.8 ± 13.7 ms, P<0.001)and at all paced rates. The duration of the atrial electrogramwas significantly increased during sinus rhythm (54.9 ±13.2 ms vs 64.8 ± 16.6 ms, P=0.003) and at all pacingrates. The PA interval was also signficantly prolonged, as wasthe pacing stimulus-to-atrial-electrogram interval at all pacingrates. There was increased QRS duration and atrial electrogramprolongation at higher pacing rates. Atrial refractoriness wasprolonged during sinus rhythm (216.4 ± 28.2 vs 228.6± 36.1, P=0.02), but not during atrial pacing at anyrate. The QT interval, but not the JT interval or ventricularrefractoriness, was significantly prolonged during sinus rhythmand at all pacing rates. Flecainide slows atrial conductionin a use-dependent manner and increases atrial refractorinessduring sinus rhythm but not during faster atrial pacing, thusnot displaying a use-dependent effect. QRS duration is prolongedin a use-dependent manner without a commensurate increase inventricular refractoriness. In the presence of rapidly conductedatrial fibrillation, which was not found to be slowed by flecainide,this effect may constitute a proarrhythmic mechanism even inpatients with no apparent myocardial abnormality.     

Mechanism of closure of the mitral prosthetic valve and the role of atrial systole. Phonocardiographic and cinefluorographic study

Phonocardiographic and Cinefluorographic methods were used to study the mechanism of closure of the Starr-Edwards mitral prosthetic valve (model 6320) in 41 patients with a normal QRS interval. Atrial fibrillation was present in 23 patients and normal sinus rhythm in 18. The following intervals were measured: QRS to mitral closing click (Q-Mc), QRS to onset of closure (Q-Oc) and QRS to completion of closure (Q-Cc) of the prosthetic valve. Ball travel time was measured as Q-Cc minus Q-Oc. Mean Q-Oc was shorter in the group with normal sinus rhythm. In 8 patients in this group, Q-Oc occurred before ventricular systole and, in 2, completion of closure occurred before the QRS interval. Early closure in the group with normal rhythm was related to a prolonged P-R interval. In this group, values for Q-Mc and Q-Cc intervals did not differ significantly. Q-Cc in the groups with atrial fibrillation and normal sinus rhythm were not significantly different. Ball travel time was significantly longer in the latter group. Long R-R intervals in the group with atrial fibrillation may be associated with partial and occasionally complete premature closure of the valve. Q-Mc was inversely related to the R-R interval in this group.This study indicates 3 mechanisms for closure of the mitral prosthetic valve. Atrial or ventricular contraction alone may close the valve. The contribution of each is dependent on the time interval separating the contraction of these chambers. Spontaneous partial or complete closure may occur before ventricular systole during a prolonged R-R interval.     

Physiological importance of different atrioventricular intervals to improved exercise performance in patients with dual chamber pacemakers.

To determine the importance of different atrioventricular intervals during exercise in patients with dual chamber pacemakers, seven patients with complete heart block and sinus rhythm were exercised in different pacing modes and atrioventricular intervals: (a) ventricular inhibited (VVI) pacing with no synchronous atrial augmentation or rate responsiveness; (b) atrial synchronous ventricular or DDD pacing with a short mean (SD) atrioventricular interval of 66 (4) ms; and (c) DDD pacing with a long atrioventricular interval of 168 (12) ms. Pacing with a short or long atrioventricular interval gave similar maximum heart rates, oxygen uptake at the anaerobic threshold, end tidal pressure of carbon dioxide or oxygen pulse (a measure of stroke volume). Pacing with either a short or long atrioventricular interval produced a significantly higher oxygen consumption and anaerobic threshold and less lactate production than VVI pacing. During exercise a short atrioventricular interval does not provide a better cardiopulmonary performance than a long atrioventricular interval.     

Physiological importance of different atrioventricular intervals to improved exercise performance in patients with dual chamber pacemakers

To determine the importance of different atrioventricular intervals during exercise in patients with dual chamber pacemakers, seven patients with complete heart block and sinus rhythm were exercised in different pacing modes and atrioventricular intervals: (a) ventricular inhibited (VVI) pacing with no synchronous atrial augmentation or rate responsiveness; (b) atrial synchronous ventricular or DDD pacing with a short mean (SD) atrioventricular interval of 66 (4) ms; and (c) DDD pacing with a long atrioventricular interval of 168 (12) ms. Pacing with a short or long atrioventricular interval gave similar maximum heart rates, oxygen uptake at the anaerobic threshold, end tidal pressure of carbon dioxide or oxygen pulse (a measure of stroke volume). Pacing with either a short or long atrioventricular interval produced a significantly higher oxygen consumption and anaerobic threshold and less lactate production than VVI pacing. During exercise a short atrioventricular interval does not provide a better cardiopulmonary performance than a long atrioventricular interval.     

Characterization of left ventricular mechanical function during arrhythmias with two dimensional echocardiography: I. premature ventricular contractions

Two dimensional echocardiography was applied experimentally in the closed chest dog to quantitate left ventricular function during and immediately after single premature ventricular contractions induced through threshold stimulation at the apex. Coupling intervals were varied over a range from 35 to 85 percent of the R-R interval during normal sinus rhythm (920 to 980 ms). The quality of tomographic echocardiographic images during premature as well as postextrasystolic beats was found to be satisfactory for quantitating short axis section areas at end-diastole and end-systole. A systolic fractional area change was computed from two dimensional echocardiographic measurements to characterize mid ventricular cardiac function, which correlated significantly with peak left ventricular pressure and maximal first derivative of left ventricular pressure (dP/dt). Marked shortening of coupling intervals reduced fractional shortening during premature systole and enhanced the degree of potentiation during the postextrasystolic beat. By contrast, premature beats with relatively long coupling intervals caused less reduction in contraction and only minor postextrasystolic potentiation.Systolic shortening of left ventricular length as well as transverse diameters were studied in a two dimensional echocardiographic long axis cross section. During long coupling intervals contraction was normal except for distinct regional systolic outward “bulging” in the apical region. In contrast, short coupling intervals were associated with a more significant generalized derangement of ventricular wall motion during systole. It is concluded that the two dimensional echocardiographic method can be used to portray and quantitate global as well as regional left ventricular function during disturbances of cardiac rhythm.     

Fragmenting of the His potential after atrial stimulation

Splitting of the His potential (H) in sinus rhythm is generally considered to be pathological but its significance during programmed atrial stimulation is not clear. This phenomenon was observed in 10 out of 53 patients aged between 19 and 45 years (average 31.8 years) not suspected of having paroxysmal intranodal block (asymptomatic, sinus rhythm without bundle branch block). Under basal conditions the H and the HV interval (35 to 50 ms; average 41 ms) were normal. Split H was observed with pacing periods of 680 to 885 ms (average 754 ms) and H1 H2 intervals of 325 to 450 ms (average 395 ms). The maximal interval between the split potentials ranged from 80 to 130 ms (average 100 ms). Splitting disappeared at the shortest periods when variable pacing cycles were used. The response to regular atrial pacing up to 150 bpm (10 cases) and to Ajmaline (1 mg/Kg) (4 cases) was normal. All patients but one were followed up to 10 to 41 months (average 21.4 months); the clinical and ECG parameters remained stable during this period. The presence of fragmented potentials between the atrial and ventricular complexes during programmed atrial stimulation may pose a difficult diagnosis problem, especially with respect to delayed atrial potentials. Splitting of the H is generally attributed to dispersion of the depolarisation wave front in the His bundle due to the persistence of the functional refractory state. Other mechanisms, especially longitudinal dissociation of the His bundle, may be discussed. From a prognostic point of view, this finding does not seem to carry more serious implications than simple lengthening of the HV interval or intranodal conduction delay, phenomena usually considered to be non-pathological.