ECG Criteria to Distinguish Between Aberrantly Conducted Supraventricular Tachycardia and Ventricular Tachycardia:Practical Aspects for the Immediate Care Setting

To reevaluate ECG criteria for distinguishing Supraventricular tachycardia (SVT) with aberrant conduction from ventricular tachycardia (VT), 133 wide QRS tachycardias were recorded in patients undergoing invasive electrophysiological (EP) study. Surface ECG leads (standard 12-lead and MCL leads) were compared to EP recordings to provide a standard for correct diagnosis. Criteria from six studies were pooled to select QRS morphology agreed to be highly specific for SVT or VT (specificity > 90%). Some morphological criteria were modified to simplify analysis for the immediate care setting. Results : Although the 12-lead ECG was useful in distinguishing aberrancy from VT, 13 tachycardias (10%) were misdiagnosed or could not be diagnosed. The MCL₁ lead recorded clearly different QRS morphology than lead V₁ in 40% of VT cases and was diagnostically inferior to V₁^.Most established criteria were highly specific for a diagnosis, but not very sensitive as individual criteria. Neither a QRS width of > 0.14 seconds nor a monophasic R wave pattern in lead V₁ were valuable in diagnosing VT. Conclusions : In distinguishing SVT with aberrant conduction from VT: (1) Although the 12-lead ECG is valuable, about 1 in 10 wide QRS tachycardias defy differentiation; (2) tachycardias > 190 beats/mm often do not exhibit unequivocal criteria with which to make a certain diagnosis; (3) multiple leads are required for accurate assessment of QRS width, presence of AV dissociation or VA block, QRS axis, and morphological criteria; and (4) the MCL₁ lead cannot be substituted for V₁ in the use of morphological criteria for VT.     

Electrocardiographic and clinical features of tricyclic antidepressant intoxication. A survey of 88 cases and outlines of therapy

The data of 88 consecutive patients with intoxication due to tricyclic antidepressant drugs were retrospectively surveyed. Apart from sinus tachycardia, temporary electrocardiographic changes developed in 48 patients (55%). These included, in order of their frequency, QTc prolongation (85%), T-wave abnormality (82%), PQ prolongation (19%), widening of QRS with or without bundle branch block pattern (19%), and supraventricular or indefinable tachycardia with wide QRS complexes (8%). The clinical course was more severe in patients with electrocardiographic changes. They were more frequently unconscious and more often required assisted ventilation than those without electrocardiographic changes (p less than 0.001). Hypotension developed in 6 patients within the first hours of poisoning; all had repolarization abnormalities and 3 developed paroxysmal supraventricular tachycardia with aberrant ventricular conduction. All 88 subjects made a good recovery and no haemodynamic problems occurred after the first 12 hours of intoxication. Second and third degree atrio-ventricular block, bradyarrthythmias and asystole were not seen in any of the patients. A prophylactic cardiac pacemaker was inserted in 13 patients with wide QRS complexes and/or prolonged PQ interval, but was never needed for bradyarrhythmias or overdrive pacing.     

Late Potentials in a Porcine Model of Anterior Wall Myocardial Infarction and Their Relation to Inducible Ventricular Tachycardia

In this study, normal values for signal averaged electrocardiographic parameters were assessed in healthy pigs (n = 100) and the development of late potentials after myocardial infarction (n - 41) in relation to inducible ventricular tachycardia was investigated. Normal values are: filtered QHS duration (QRS) ± 78 msec; root mean square voltage of the averaged QRS complex (V_tot) ± 51 μV, and duration of terminal activity below 30 μV (D₃₀) ± 37 msec. The distribution of the root mean square voitage in the last 30 msec (V₃₀) was biphasic. Two weeks after myocardial infarction, QRS was prolonged from 55 ± 10 to 66 ± 19 msec (P < 0.002), D₃₀ was prolonged from 19 ± 6 msec to 28 ± 13 (P < 0.002). V₃₀ was decreased from 107 ± 135 μV to 45 ± 77 (P < 0.02). The total voltage (V_tot) was decreased from 195 ± 78 to 123 ± 61 μV (P < 0.002). In four pigs (19%) late potentials developed. Sustained ventricular tachycardia was inducible in 11 pigs (52%), ventricular fibrillation in two pigs (10%) and eight pigs (38%) were noninducible. Three of 11 inducible pigs and one of the noninducible pigs had a late potential. The incidence of late potentials and their relation to inducibie sustained ventricular tachycardia is comparable to the situation in man. Therefore, this pig model is an attractive alternative to the commonly used dog models.     

The Role of Parasympathetic Modulation of the Reentrant Arrhythmic Substrate in the Genesis of Sustained Ventricular Tachycardia

The influence of parasympathetic activity on the reentrant arrhythmic substrate in the genesis of sustained ventricular tachycardia remains unclear. To assess this influence, we studied the heart rate variability in 59 patients referred for invasive electrophysiological testing. In addition, the presence of late potentials and high grade ventricular ectopy, and the left ventricular ejection fraction was determined. The 28 patients with inducible sustained ventricular tachycardia were found to have lower heart rate variability by time- and frequency-domain measurements over 24 hours when compared to the 31 subjects who were noninducible. PNN50 was 4% in the inducible patients, whereas it was 9% in the subjects who were noninducible (P = 0.03). Similarly, HFP24H was 9 and 14 msec, respectively (P = 0.02). MAXHFP1H also differed (20 vs 27 msec [P = 0.04]) but not MINHFP1H (5 vs 6 msec). There was no association between heart rate variability and late potentials, degree of ventricular ectopy, or left ventricular ejection fraction. Thus, vagal tone does not appear to correlate with the presence of late potentials, ventricular ectopy, or left ventricular dysfunction. Low mean as well as maximal vagal tone, in contrast to minimal vagal tone, predicts inducibility of sustained ventricular tachycardia. Our data suggest that the inability to modulate parasympathetic tone appears to be an important determinant in the genesis of reentrant sustained ventricular tachycardia.     

Do Steroid-Eluting Electrodes Really Have Better Performance Than Other State-of-the-Art Designs?

A multicenter study evaluated the performance of atrial and ventricular unipolar leads with porous steroid-eluting and platinized grooved electrodes. A total of 563 leads were implanted in 451 patients. These included 311 ventricular and 97 atrial steroid-eluting electrodes; and 112 ventricular and 43 atrial leads with platinized electrodes. Mean follow-up was ± 1 year. At implant there were no significant differences in threshold parameters in either chamber. Chronically, however, the steroid eluting lead consistently had significantly lower pacing thresholds in both chambers. For example, after 360 days implant, steroid-eluting electrodes had 0.23 ± 0.10 msec ventricular thresholds at 0.8 V compared to 0.45 ± 0.3 msec in the platinized group (P < 0.0001). In the atrium, the steroid-eluting lead's 6-month thresholds at 0.8 V were 0.15 ± 0.06 msec compared to 0.9 ± 0.8 msec for the platinized electrode (P < 0.01). The chronic ventricular QRS amplitudes were significantly greater for the steroideluting electrode (P < 0.0005). There were no significant differences in atrial sensing and no incidence of atrial undersensing in the study. The low and consistent thresholds of the steroid-eluting electrodes would have permitted pacing in the ventricle at ± 2.5 V without compromising safety factor in 99.4% of the patients. The other 0.6% required 5 V temporarily. In the atrium, 100% of the patients could have been paced safely at reduced output. In spite of this, 63% of the implanters lacked the confidence to use reduced outputs.     

ECG Leads I and II to Evaluate Diuresis of Patients with Congestive Heart Failure Admitted to the Hospital via the Emergency Department

Background: Attenuation of electrocardiogram (ECG) QRS complexes is observed in patients with a variety of illnesses and peripheral edema (PERED), and augmentation with alleviation of PERED. Serial ECGs in stable individuals display variation in the amplitude of QRS complexes in leads V1–V6, stemming from careless placement of recording electrodes on the chestwall. Electrocardiographs record only leads I and II, and mathematically derive the other four limb leads in real time. This study evaluated the sum of the amplitudes of ECG leads I and II, along with other sets of ECG leads in the monitoring of diuresis in patients with congestive heart failure (CHF).
Methods: Twenty patients with CHF had ECGs and weights recorded on admission and at discharge. The amplitude of the QRS complexes in all ECG leads were measured and sums of I and II, all limb leads, V1–V6, and all 12 leads were calculated.
Results: There was a good correlation between the weight loss and the increase in the sums of the amplitudes of the QRS complexes from leads I and II (r = 0.55, P = 0.012), and the six limb leads (r = 0.68, P = 0.001), but a poor correlation with the V1–V6 leads (r = 0.04, P = 0.85) and all 12 leads (r = 0.1, P = 0.40).
Conclusions: Sums of the amplitudes of the ECG QRS complexes from leads I and II constitute a reliable, easily obtainable, ubiquitously available, bedside clinical index, which can be employed in the diagnosis, monitoring of management, and follow-up of patients with CHF.     

Electrocardiographic manifestations: aberrant ventricular conduction

Aberrant ventricular conduction is a common electrocardiographic (EKG) manifestation that occurs when the supraventricular electrical impulse is conducted abnormally through the ventricular conducting system. This results in a wide QRS complex that may be confused with a ventricular ectopic beat. This differentiation is important because the treatment and prognosis is quite different. Hemodynamically unstable patients with a wide-complex tachycardia should be promptly cardioverted. Although up to 10% of cases will defy differentiation, ventricular tachycardia and aberrant conduction can be distinguished utilizing history, physical examination, and EKG criteria. The mechanisms of aberrant ventricular conduction are discussed.     

Prominent R wave in lead V1: electrocardiographic differential diagnosis

Tall lead V1 (tall RV1), defined as an R/S ratio equal to or greater than 1, is not an infrequent occurrence in emergency department patients. This electrocardiographic finding exists as a normal variant in only 1% of patients. Physicians should therefore be familiar with the differential diagnosis for this important QRS configuration. The electrocardiographic entities which can present with this finding include right bundle branch block, left ventricular ectopy, right ventricular hypertrophy, acute right ventricular dilation (acute right heart strain), type a Wolff-Parkinson-White syndrome, posterior myocardial infarction, hypertrophic cardiomyopathy, progressive muscular dystrophy, dextrocardia, misplaced precordial leads, and normal variant. Various cases are presented to highlight the different causes of the tall RV1.     

Ventricular Tachycardia in Neonates

Infant VT can be a devastating arrhythmia, with high mortality for those presenting with myocarditis, long QT syndrome, or cardiovascular collapse with rapid VT due to tumors. While management of these patients can be challenging and discouraging, other infants with wide QRS rhythms tend to follow a more benign course. These latter patients have accelerated idio-pathic ventricular rhythm or aberrant forms of infant supraventricular tachycardia. Distinguishing these forms of wide QRS tachycardia from the more lethal forms is paramount to institution of appropriate therapies.     

Electrocardiographic manifestations: wide complex tachycardia due to accessory pathway

Tachycardia with a wide QRS complex is usually due to ventricular tachycardia (VT), supraventricular tachycardia (SVT) with aberrant intraventricular conduction, or an accessory pathway-mediated dysrhythmia. The most common type of accessory pathway causing a wide complex tachycardia is the atrioventricular bypass tract. Distinguishing the accessory pathway-mediated tachycardia from VT or SVT with aberrancy is often difficult, but has important clinical consequences. This article will review the diagnosis of wide complex tachycardia due to an accessory pathway and its related management in the emergent setting.     

偏心或对称型室间隔缺损封堵器对介入封堵术后心电生理的影响

目的通过对心电监护、心电图及动态心电图分析,评价应用偏心或对称型室间隔缺损封堵器治疗先天性膜周部室间隔缺损后对早期心电生理的影响。方法123例膜周部室间隔缺损患者,偏心封堵器治疗56例,对称封堵器治疗67例。患者术前、术后行心电图及动态心电图检查,术中、术后行心电监护,对数据进行统计分析。结果（1）心导管资料及介入治疗结果：手术成功率,平均肺动脉压（mmHg）,Qp／Qs,室间隔缺损直径（cm）,距主动脉瓣距离（cm）,封堵器直径（cm）,手术时间（min）,X线曝光时间（min）两组比较未见明显差异。（2）心电图及Holter结果：两组内经连续变量配对t检验后,术后室性早博数目增加有显著性差异（P=0．03）,室上性早博增加不显著（P=0．05）,PR间期、QRS宽度、QTc术前术后无显著性差异;两组间经χ^2检验,平均心率（Ha）,豫间期,QRS波宽度,校正QT间期（QTc）,房室交界区早搏（AVE）,室性早搏（vr）,非阵发性交界性心动过速（NPJT）,非阵发性室性心动过速（NpVT）,房室传导阻滞（AVB）和束支传导阻滞（BBB）均未见显著差异;独立变量与室性早博的线性回归分析提示年龄与室性早博数目的增加相关（P=0．02）,而体重、性别、室缺大小、封堵器直径与室性早搏无关。结论经导管堵闭膜周部室间隔缺损术后,室性早搏数目明显增加并出现加速性交界性和室性自主心律;但更应防止术后高度房室传导阻滞的发生及其带来的危害,加强患者的术后心电监护。     

Frequency and Output-Dependent Change in Conduction Over Slow Pathways in a Patient with Sustained Ventricular Tachycardia Unrelated to Coronary Artery Disease

In a patient with sustained ventricular tachycardia, we obtained two different paced QRS morphologies from a single pacing site. In one QRS morphology the stimulus to the QRS complex was long, 150 msec, and in the other it was 100 msec. At the paced cycle length of 600 msec and the stimulus output of 4 V, one QRS morphology with the stimulus to the onset of QRS activation (St-QRS) interval of 150 msec was observed. At the paced cycle length of 400 msec, the other QRS morphology with a St-QRS interval of 100 msec was observed alternatively with the former. At the paced cycle length of 353 msec or 316 msec, the latter with a shorter St-QRS interval was exclusively observed. When the stimulus output was increased from 4 to 10 V, keeping with the paced cycle length at 400 msec, the St-QRS interval was shortened from 100 to 80 msec. For the two QRS morphologies with two St-QRS intervals, two slowly conducting pathways would be responsible. The site of the block in the faster pathway must be located at the proximity of the pacing site and the conduction at a shorter paced cycle length would be explained by "supernormal conduction."     

Correlation of the Endocardial Fragmented Electrogram with Body Surface Signal-Averaged Electrocardiographic Mapping

We compared signal-averaged electrocardiography (SAE), SAE mapping, and left ventricular catheter mapping in 60 patients with ischemic heart disease. Using the data obtained in patients with no fragmented electrograms (EE) in the left ventricle, the late potential was defined by SAE as a filtered QRS duration > 131 msec or a root mean square voltage < 16 μV for the last 40 msec of the QRS complex. SAE mapping was performed by recording the signal-averaged electrocardiogram at 48 sites on the body surface. With SAE mapping, the filtered QRS duration and the area in the last 20 msec of the QRS complex were significantly different between the patients with and without EEs. The late potential was defined by SAE mapping as a filtered QRS duration > 136 msec or an area < 28 μV.msec for the last 20 msec of the QRS complex. The sensitivity and specificity of detecting FEs were 46% and 88%, respectively, by the SAE filtered QRS criterion, while they were 66% and 88% by the root mean square criterion. In contrast, SAE mapping gave values of 66% and 92% by the filtered QRS criterion, as well as values of 100% and 92% by the area criterion. Thus, SAE mapping provided better detection of the EE and was more closely correlated with the results of catheter mapping, suggesting its potential for clinical application.     

Ashman's phenomenon--a source of nonsustained wide-complex tachycardia: case report and discussion.

The refractory period of the right bundle branch is increased when the R-R interval between the prior two conducted impulses is long. Thus, an impulse that arrives soon after the second of two impulses separated by a long R-R interval may be aberrantly conducted with a right bundle branch block morphology on electrocardiogram. This aberrant conduction is termed "Ashman's phenomenon" and is often responsible for isolated wide QRS complexes in the presence of underlying atrial fibrillation. This process may also produce runs of wide QRS complexes that must be distinguished from nonsustained ventricular tachycardia. A case of such multibeat Ashman's phenomena is presented, and the characteristics used to identify this phenomenon are discussed. A brief review of several recent studies on the differentiation of sustained ventricular tachycardia from supraventricular tachycardia with aberrancy in the setting of a regular underlying rhythm is given as well.     

Broad QRS tachycardia: Electrocardiographic diagnosis and management

The diagnostic difficulties between supraventricular tachyarrhythmias with intraventricular conduction delay and ventricular tachycardia have challenged the physician since the first recording of a ventricular tachycardia by Lewis in 1909. The examples selected emphasize some of the diagnostic and therapeutic dilemmas of "broad QRS tachycardias" and their major differential features from abberrancy. Multiple simultaneous surface ECG leads are valuable in showing the direction of the initial activation forces of the QRS complexes, the frontal QRS axis and the configuration of the QRS in lead V1. Vagal maneuvers and intra-atrial or esophageal leads are very useful in demonstrating the underlying atrial rhythm and atrioventricular dissociation when present. In life-threatening situations, urgent therapy or D.C. cardioversion may be required before a definitive diagnosis has been established. In recent years electrode catheter techniques for the diagnosis, for arrhythmia induction and for the selection and assessment of the effectiveness of the antiarrhythmic drug therapy have been carried out in the management of recurrent broad QRS tachycardia. In view of the inherent risks with the use of this invasive technique, it should be restricted to a carefully selected number of patients with recurrent life-threatening dysrhythmias as suggested by Scheinman.     

Wide QRS complex tachycardia: ECG differential diagnosis.

Wide QRS complex tachycardias (WCT) present significant diagnostic and therapeutic challenges to the emergency physician. WCT may represent a supraventricular tachycardia with aberrant ventricular conduction; alternatively, such a rhythm presentation may be caused by ventricular tachycardia. Other clinical syndromes may also demonstrate WCT, such as tricyclic antidepressant toxicity and hyperkalemia. Patient age and history may assist in rhythm diagnosis, especially when coupled with electrocardiographic (ECG) evidence. Numerous ECG features have been suggested as potential clues to origin of the WCT, including ventricular rate, frontal axis, QRS complex width, and QRS morphology, as well as the presence of other characteristics such as atrioventricular dissociation and fusion/capture beats. Differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction frequently is difficult despite this clinical and electrocardiographic information, particularly in the early stages of evaluation with an unstable patient. When the rhythm diagnosis is in question, resuscitative therapy should be directed toward ventricular tachycardia.     

Prognostic Implications of Loss of Late Potentials Following Acute Myocardial Infarction

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during seriai testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G-week follow-up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 ± 11 msec at discharge to 104 ± 11 msec (P < 0.01), terminal QRS voltage rose from 15 ± 4 μV to 31 ± 9 μV (P = 0.001), and late potential duration fell from 42 ± 6 msec to 28 ± 6 msec (P = 0.001) at the 6-week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non-Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6-week assessment, 11 additional arrhythmic events occurred during median follow-up of31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P - NS) but significantly greater than palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal-averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal-averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.     

T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction

OBJECTIVES: Reperfusion therapy for acute myocardial infarction (AMI) is indicated in the presence of ST elevation (STE) and ischemic symptoms. Previous MI may present with persistent STE or "left ventricular aneurysm" (LVA) morphology that mimics AMI. Hypothesis A high ratio of T amplitude to QRS amplitude best distinguishes AMI from LVA. METHODS: This was a retrospective cohort analysis. Patients with anatomical LVA by echocardiography were identified and those who presented to the ED with ischemic symptoms and STE of at least 1 mm in 2 consecutive leads and ruled out for acute left anterior descending coronary artery (LAD) occlusion were selected. Electrocardiograms (ECGs) were compared with a control group of 37 consecutive anterior AMI (aAMI) with proven acute LAD occlusion. Bundle-branch block was excluded. Various ECG measurements and ratios were compared. RESULTS: Twenty patients with LVA met the inclusion criteria. The best discriminator was T amplitude sum to QRS amplitude sum ratio V1-V4, misclassifying only 4 (6.8%) of 59 cases at a cutoff of >0.22 for AMI. For aAMI and LVA, respectively, mean (+/-95% CI) ratio of the sum of T amplitudes in V 1 to V 4 to the sum of QRS amplitude in V1-V4 was 0.54+/-0.085 and 0.16+/-0.021 (P<.00012). Thirty-five of 37 aAMI had a ratio>0.22; the false negatives (ratio<0.22) had 11.5 and 6 hours of symptoms before the ECG. Twenty of 22 LVA had a ratio相似文献   

Atrial Flutter With 1:1 AV Conduction and Aberrant Ventricular Conduction

Atrial flutter with 1:1 atrioventricular response may be spontaneous or drug-induced and may occur in persons with or without known organic heart disease. The response is often caused by sympathetic discharge associated with exertion or excitement. The presence of wide QRS complexes due to aberrant ventricular conduction complicates the diagnosis.     

The influence of intracardiac asynchronism on the clinical course of chronic cardiac insufficiency

Intracardiac asynchronism presents systolic and/or diastolic dyscoordination in different myocardial areas within one and/or between different cardiac chambers. QRS complex widening is the marker of electric asynchronism. In 1/3 of patients with chronic cardiac insufficiency (CCI), the width of QRS complex is more than 120 msec. sixty-five CCI patients (56 men aged 63.7 +/- 7.3 years and 9 women aged 66.8 +/- 8.2 years) were divided into two groups: the group with a wide QRS (more than 120 msec) and the group with a narrow QRS (less than 120 msec), 30 and 35 patients, respectively. In the group with a wide QRS, 96.6% of patients suffered from clinically significant CCI (functional class III to IV); in the other group it was observed in 65.7% of patients. The patients were observed during three years. CCI dynamics was evaluated, quality of life was assessed using the Russian version of SF questionnaire, and three-year survival rate was assessed by Kaplan-Meyer method. The presence of electric asynchronism in a form of a wide QRS complex promotes CCI progression, accompanied by CCI functional class deterioration as well as clinical worsening and decreased physical exercise tolerance according to 6-min walking test. The frequency of seeking medical aid was significantly higher among patients with a wide QRS complex.