12-Kanal-Elektrokardiogramm

The surface electrocardiogram (ECG) is an important diagnostic tool for the diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardias (SVT) are paroxysmal tachycardias as are sinus tachycardia, atrial tachycardia, AV nodal reentry tachycardia, and tachycardia due to accessory pathways. All SVT are characterized by a ventricular heart rate >100/min and small QRS complexes (QRS width <0.12 s) during tachycardia. It is important to analyze the relation between P wave and QRS complex to look for an electrical alternans as a leading finding for an accessory pathway. Wide QRS complex tachycardias (QRS width ≥ 0.12 s) occur in SVT with aberrant conduction and SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardias, AV dissociation, negative or positive concordant pattern in V₁–V₆, a notch in V₁ and QR complexes in V₆ in tachycardias with left bundle branch block morphologies are findings indicating VT. In addition, an R/S relation <1 in V₆ favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the right way with a systematic approach, the specificity and sensitivity of correctly identifying a SVT or VT can be raised by >95%. The 12-lead surface ECG allows the coronary culprit lesion to be located in 97% due to determination of the 12-lead ST segment deviation score.     

Differenzialdiagnostik und Therapie tachykarder Herzrhythmusstörungen

The 12-channel surface electrocardiogram (ECG) is an important diagnostic tool for diagnosis of arrhythmias and acute coronary syndrome. Supraventricular tachycardia (SVT) is a paroxysmal tachycardia as are sinus tachycardia, atrial tachycardia, atrioventricular (AV) nodal reentry tachycardia and tachycardia due to accessory pathways. All SVTs are characterized by a ventricular heart rate >?100 beats/min and small QRS complexes (QRS width <?0.12 s) during tachycardia. It is important to analyze the relation between p-wave and QRS complex, to look for an electric alternans as a main finding for an accessory pathway. Wide QRS complex tachycardia (QRS width ≥?0.12 s) occurs in SVT with aberrant conduction, SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardia, AV dissociation, negative or positive concordant patterns in V1–V6, a notch in V1 and qR complexes in V6 in tachycardia with left bundle branch block morphology, are findings indicating VT. In addition, an R/S relation <?1 in V6 favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the correct way with a systematic approach, the specificity and sensitivity of correctly identifying SVT or VT can be raised to >?95?%. Therapy of tachycardia is possible with few antiarrhythmic drugs (concept of the 5As), beta-blocking agents, cardioversion and defibrillation. Using these approaches termination of tachycardia is possible in the majority of cases with high success rates.     

Supraventricular tachycardia mechanisms and their age distribution in pediatric patients.

To better define the natural history of supraventricular tachycardia (SVT) in young patients, age distribution of SVT mechanisms was examined in 137 infants, children and adolescents. Patients with a history of cardiac surgery or neuromuscular diseases were excluded. An electrophysiologic study was performed in each patient: transesophageal (110 patients) or transvenous (14 patients) or both (13 patients). Mechanisms were classified as SVT using accessory atrioventricular (AV) connection (SVT using accessory connection, including orthodromic and antidromic reciprocating tachycardia), primary atrial tachycardia (including chaotic, automatic and reentrant atrial tachycardia), and tachycardia due to reentry within the AV node. SVT using accessory connection occurred in 100 of 137 patients (73%) and was the most prevalent mechanism. Primary atrial tachycardia and reentry within the AV node were present in 19 of 137 (14%) and 18 of 137 (13%) patients, respectively. Using a multinomial logit model, relative probabilities for tachycardia mechanisms for 5 age groups--prenatal, less than 1, 1 to 5, 6 to 10 and greater than 10 years--were determined. Primary atrial tachycardia (11 to 16%) and SVT using accessory connection (58 to 84%) appeared throughout infancy, childhood and adolescence. On the other hand, tachycardia due to reentry within the AV node (0 to 31%) rarely appeared before age 2 years. Mechanisms of SVT appear to have age-dependent distributions. SVT using accessory connection is the most common mechanism in young patients. We speculate that the propensity to tachycardia due to reentry within the AV node occurs during postnatal development.     

Wolff-Parkinson-White syndrome in children: electrophysiologic and pharmacologic characteristics.

Intracardiac electrophysiologic studies were performed on 28 infants and children, ages 1 month to 18 years, with the Wolff-Parkinson-White syndrome to try to determine 1) the electrophysiologic characteristics of the accessory connection and 2) the mechanisms of associated supraventricular dysrhythmias. Although the antegrade refractory periods of the normal conduction system were shorter than those found in adults, those of the accessory connection were slightly longer. Reciprocating supraventricular tachycardia (SVT), which had been a clinical problem in 26 of 28, could be induced in the laboratory in all 26 subjects. The mechanism involved reentry with antegrade conduction through the atrioventricular (AV) node and retrograde through the accessory connection in 22. Eleven of these 22 had a wide QRS during tachycardia due to a bundle branch block. Three other subjects had wide QRS tachycardia, but the mechanism involved antegrade conduction through the accessory connection and retrograde through the AV node. The other patient had AV node reentry tachycardia. Two patients did not have clinical SVT, and in these two, SVT could not be induced. Neither patient had retrograde conduction through the accessory connection. The site of the accessory connection could be identified in 26 subjects by the sequence of retrograde activation of the atrium during SVT or ventricular pacing. Digitalis shortened the refractory period of the accessory connection in five of the eight patients studied.     

Regelm??ige Tachykardien mit breitem Kammerkomplex

Differential diagnosis of regular tachycardia with broad QRS complex can be challenging in daily practice. There are four different arrhythmias that have to be taken into account when being confronted with a broad QRS complex tachycardia: (1) ventricular tachycardia (VT); (2) supraventricular tachycardia (SVT) with bundle branch block (BBB); (3) SVT with AV conduction over an accessory AV pathway; (4) paced ventricular rhythm. Due to potentially fatal consequences, the correct diagnosis is important in view of both the acute treatment and the long-term therapy. Since SVT with accessory conduction is rare and a paced ventricular rhythm can be identified easily by stimulation artifacts, in most cases, a VT has to be differentiated from an SVT with BBB. Several ECG criteria can be helpful: (1) QRS complex duration > 140 ms in right BBB tachycardia or > 160 ms in left BBB tachycardia; (2) ventricular fusion beats; (3)“Northwest” QRS axis; (4) ventriculoatrial dissociation; (5) absence of an RS complex or RS interval > 100 ms in leads V₁-V₆; (6) a positive or negative concordant R wave progression pattern in leads V₁-V₆; (7) absence of an initial R wave or an S wave in lead V₁ in right BBB tachycardia; (8) absence of an R wave or an R/S ratio < 1 in lead V₆ in right BBB tachycardia; (9) absence or delay of the initial negative forces in lead V₁ in left BBB pattern (R wave duration > 30 ms in V₁; interval between onset of R wave and Nadir of S wave > 60 ms in V₁); (10) presence of Q wave. Any of these variables favor VT. However, none of the criteria has both a sufficient sensitivity and specificity when utilized on its own. Therefore, various diagnostic algorithms have been proposed using a number of the above criteria consecutively. By doing so, the specificity and sensitivity of correctly identifying a VT or an SVT with BBB can be raised to > 95%.     

Treatment of supraventricular and paroxysmal ventricular tachycardia with bepridil

Bepridil is a molecule which, apart from its anti-anginal properties, also has antiarrhythmic effects due to its calcium antagonist action which depresses antero and retrograde AV conduction in the physiological pathways. Conduction in accessory AV pathways is also depressed to a lesser and more variable extent. It also has an anti-ventricular arrhythmic action probably due to an associated membrane-stabilising effect. This drug was used intravenously to treat attacks of reciprocating supra-ventricular tachycardia (SVT) (60 p. 100 conversion to sinus rhythm: 6 out of 10 cases of intra-nodal reentry, 6 out of 10 cases of reentry via an accessory pathway) and also in ventricular tachycardia (VT) (7 conversions in 15 patients within 2 to 9 minutes). It was impossible to induce attacks of SVT after administering the drug in about a third of patients; better results were obtained in intra-nodal SVT (5 cases of effective prevention out of 10) than in SVT involving an accessory pathway (1 case out of 10). It was not possible to reinitiate VT after treatment in 3 out of 6 cases (very aggressive pacing methods, a long QT interval and accelerated idio-ventricular rhythm were responsible for the failures). Oral therapy (400 to 800 mg, usually 600 mg daily in 3 doses) prevented any recurrence of SVT in over half the patients (prevention of intranodal SVT: 80 p. 100; prevention of SVT involving an accessory pathway: 13 p. 100) and in 4 out of 6 patients with VT. Provocative pacing studies after intravenous or oral bepridil provide a good indication of long-term efficacy. The drug is generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical Experience with Orthocor II Antitachycardia Pacing System for Recurrent Tachyarrhythmia Termination

Between June 1986 and December 1988, eight patients were treated with an Orthocor II 284 A antitachycardia pacemaker (Cordis Corp., Miami, FL, USA) forsupraventricular tachycardia (SVT) and ventricular tachycardia (VT) termination. Four patients had intra-AV nodal reentrant tachycardias; 1 patient had AV reentrant tachycardia with an atrio-nodal accessory bypass tract; 2 patients had AV reentrant tachycardias with concealed Kent bundle, and 1 patient had ventricular tachycardia. All patients had been treated with three or more drugs and were considered to be drug refractory. The programmed antitachycardia mechanism used for patients with SVT were: automatic overdrive in five patients and burst scanning in two patients. In the patient with VT, a critically timed double extrastimulus with fixed coupling interval was programmed. Follow-up ranged from 2 to 30 months. The pacemaker proved to be effective in terminating tachycardias in all cases with SVT; in the patient with VT, the programmed antitachycardia mechanism was effective for a long time, but after an episode of sustained VT not interrupted by the pacemaker, the patient underwent automatic cardioverter/defibrillator (AICD) implantation. Additional antiarrhythmic therapy was required in 3 patients to control their maximum sinus rate, in 1 patient to reduce tachycardia episodes and to enable termination, and in 2 patients to prevent spontaneous atrial fibrillation. It is concluded that Orthocor II is a flexible and versatile antitachycardia pacemaker providing a safe and effective control of recurrent tachycardia in selected patients.     

The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty-three patients with paroxysmal Supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.     

Transvenous catheter ablation of the His bundle in ventricular tachycardia

The usefulness of transvenous catheter ablation of the His bundle in three patients with recurrent ventricular tachycardia (VT), in which the initiating mechanism was recognized during a rapid atrial rhythm, is reported. Tachycardia was refractory to conventional treatment and required transthoracic direct-current shocks in all patients. In patient No. 1 double tachycardia (atrial flutter and VT) was documented and VT was easily induced by rapid atrial pacing. In patients Nos. 2 and 3 initiation of VT during junctional reciprocating and atrial tachycardia, respectively, was observed. Interruption of the His bundle was performed by means of fulguration. Stable atrioventricular (AV) block was observed in patient No. 1 after the ablative procedure; patient No. 2 showed anterograde conduction over a posterior septal accessory pathway with no evidence of conduction over the normal conduction system in both the anterograde and retrograde directions. In patient No. 3, transient AV block was observed; AV conduction resumed 2 days later and the cardiac rhythm showed persistent ectopic atrial tachycardia with second-degree AV block. Patients Nos. 1 and 2 underwent pacemaker implantation, but patient No. 2 was not pacemaker dependent. After the procedure, VT no longer occurred in any of the patients (follow-up: 2 years, 5 months, and 6 months).     

Value of esophageal pacing in evaluation of supraventricular tachycardia

Esophageal stimulation was performed in 40 patients who had spontaneous paroxysmal supraventricular tachycardias (SVTs). The purpose of this study was to look for the most sensitive stimulation protocol and criteria that would help to define the mechanism of reentry. In 20 patients (group I) atrial pacing up to second-degree atrioventricular block was performed under control conditions and isoproterenol, and SVT was induced in 14 patients (70%), 11 in the control state and 3 while receiving isoproterenol. In 20 patients (group II) atrial pacing and programmed atrial stimulation using 1 and 2 extrastimuli delivered at 2 cycle lengths (600 and 500 ms) was performed in the control state and while receiving isoproterenol. SVT was induced in all patients, in 13 patients in the control state and in 7 while receiving isoproterenol. Programmed stimulation always induced SVT and was the only method capable of tachycardia induction in 14 patients. The mechanism of SVT could be established in 91%. The measurement of the ventriculoatrial interval was the most useful sign to define the site of reentry. Occurrence of a bundle branch block helped to delineate the mechanism in 4 patients. When a positive P wave in V1 preceded the esophageal atrial electrocardiogram, it suggested that there was reentry through a left-sided accessory atrioventricular connection in 6 patients. SVT could always be induced by programmed atrial stimulation in the control state and under isoproterenol. The location of the P wave in V1 compared to the ventriculogram and the esophageal electrocardiogram helped to define the mechanism of tachycardia.     

Antidromic tachycardia utilizing decremental,latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia

Objectives. We studied two patients with latent, decremental atrioventricular (AV) fibers in whom pre-excitation could be demonstrated only during wide complex tachycardia.Background. The presence of decremental AV fibers participating in antidromic AV reentrant tachycardia is usually suspected by the presence of pre-excitation either in sinus rhythm or during atrial pacing.Methods. Two patients were referred for evaluation and treatment of wide complex tachycardia whose configuration suggested ventricular tachycardia that could be terminated with adenosine infusion. They underwent standard electrophysiologic studies.Results. Baseline AH and HV intervals were normal. No pre-excitation was noted with atrial overdrive at multiple sites or during atrial extrastimulation. Retrograde conduction was present with a sequence compatible with AV node conduction. Sustained wide complex tachycardia was induced with ventricular overdrive pacing. Late atrial premature depolarizations during tachycardia pre-excited the subsequent ventricular activation. Earlier atrial premature depolarizations delayed the subsequent ventricular activation. In one patient, early atrial premature depolarizations terminated the tachycardia without activating the ventricle. In the other patient, spontaneous tachycardia termination was accompanied by ventriculoatrial block. The earliest ventricular activation was at the annulus in the posteroseptal region in one patient and at the left posterior region in the other. Atrioventricular node reentry and atrial tachycardia with by-stander AV fibers were also excluded. These findings establish the diagnosis of antidromic AV reentrant tachycardia utilizing a slow, decrementally conducting AV pathway.Conclusions. This is the first report describing the presence of latent, decremental accessory AV pathways in which conduction was manifest only during antidromic AV reentrant tachycardia. To differentiate these wide complex tachycardias from adenosine-sensitive ventricular tachycardia, we recommend that atrial premature depolarizations be applied during tachycardia to rule out the presence of a latent, decremental AV fiber even in patients who do not otherwise have pre-excitation with atrial pacing techniques.     

Supraventricular paroxysmal tachycardias with normal electrocardiogram in sinus rhythm

Paroxysmal supraventricular tachycardia (SVT) was studied in 46 patients with normal electrocardiogram (ECG) during sinus rhythm (SR), All of them had had at least one SVT crisis. They all complained of palpitations starting and ending abruptly, and of more than one hour duration. There were never seen ECG alterations suggesting ventricular preexcitation during SR. An electrophysiologic study using atrial and ventricular programmed stimulation and intracardiac electrograms, was used to establish the diagnosis. There was no significant difference in sex or age distribution according to the ethiologic diagnosis. It was found that 67.4% had a concealed accessory bundle, responsible of the SVT, 32.6% had A-V nodal reentry (p less than 0.01). Of all concealed accessory bundles, 67.7% were left lateral Kent (45.6% of all patients). It is discussed the possibility of antegrade conduction through concealed bundles during SR and that this may be seen by means of a M-mode echocardiography. We conclude that neither sex nor age help to suspect ethiologic diagnosis; the most common accessory bundle is the left lateral Kent and that in some cases it can be detected by M-mode echocardiography. This accessory bundle is the most usual cause of SVT in patients with normal ECG during SR.     

Acute blood pressure effects at the onset of supraventricular and ventricular tachycardia

This study was designed to assess the effects of tachycardia origin, the significance of atrial contribution, and the effects of left ventricular ejection fraction on hemodynamically tolerated ventricular tachycardia (VT) and supraventricular tachycardia (SVT). Forty-one subjects with inducible hemodynamically tolerated VT (n = 24) or SVT (n = 17) with mean ages of 60 ± 13 and 40 ± 16 years and mean ejection fractions of 32 ± 15% and 59 ± 5%, respectively, were studied. VT and SVT were induced by standard techniques, and femoral arterial blood pressure (BP) was recorded for 30 seconds. After tachycardia termination, with ≥3 minutes between conditions, ventricular overdrive pacing was performed from the right ventricular (RV) apex and then the RV outflow tract, followed by atrioventricular (AV) pacing at the tachycardia cycle length. Mean BP was measured every 5 seconds. Linear regression methods were used to model BP response for the 2 groups. There was a significant increase in BP over the 20-second interval after the induction of VT and SVT (0.55 ± 0.21 and 1.0 ± 0.20 mm Hg/s, respectively, p <0.05). In patients with hemodynamically tolerated VT, RV apex and RV outflow tract pacing at the tachycardia cycle length decreased BP by 6.7 ± 2.0 (p <0.002) and 4.7 ± 2.5 mm Hg (p = 0.06), respectively. AV pacing at the tachycardia cycle length did not improve BP compared with RV pacing alone. In patients with SVT, RV apex and RV outflow pacing at the tachycardia cycle length decreased BP by 5.6 ± 2.9 (p = 0.05) and 4.1 ± 2.7 mm Hg (p = 0.12), respectively. However, AV pacing at the tachycardia cycle length was associated with improved BP response over RV pacing alone. Increased age and lower ejection fraction adversely influenced BP response in the VT group and longer cycle length, and higher preinduction BP favorably influenced BP response in the SVT group. The determinants of BP response after tachycardia onset are complex and differ in patients with SVT and VT.     

Functional Bundle Branch Block as a Delayed Manifestation of Retrograde Concealment in the His-Purkinje System

Delayed Manifestation of Retrograde HPS Concealment. Introduction: The mechanism of functional bundle branch block induced at the onset of supraventricular tachycardia (SVT) is well established. However, no data exist to address the underlying mechanism of functional bundle branch block occurring in the second beat of SVT, when the first beat is conducted with a narrow QRS morphology and preceded by ventricular stimulation. Methods and Results: Two patients showing such a phenomenon form the basis of this report. Patient 1 with AV nodal reentrant tachycardia of the common variety persistently demonstrated functional right bundle branch block in the second SVT complex when a short train of ventricular pacing was introduced during SVT. This occurred without any discernible change in the SVT cycle length. Patient 2 bad a manifest posteroseptal accessory pathway and inducible orthodromic reentrant tachycardia. Functional bundle branch block during propagation of the second SVT complex invariably occurred either in the left bundle when SVT was induced by a bundle branch reentrant complex during premature ventricular stimulation, or in the right bundle when SVT was induced with a short train of ventricular pacing. The development of functional bundle branch block was preceded by minimal or no cycle length variations in the His-bundle inputs. Conclusion: These observations suggest that the type of functional bundle branch block occurring in the second SVT complex as a de novo phenomenon may be related to the relative timing of the retrograde penetration of the right versus left bundle during ventricular pacing or bundle branch reentrant complex. Therefore, due to its longest cycle length of activation and refractoriness, the earliest site of retrograde penetration is the most likely site of functional block during propagation of the second SVT complex. This delayed manifestation of retrograde concealment may provide new information regarding the electrophysiologic behavior of the His-Purkinje system.     

Injectable and oral propafenone in nodal reentry and pathways of ventricular preexcitation

Propafenone, an antiarrhythmic drug of IC type, was applied to 10 patients with supraventricular tachycardia (SVT) produced by intranodal reentry (group I) and in 14 patients with reentry by an accessory atrioventricular (AV) pathway (group II), 10 of them suffering from orthodromic SVT. Propafenone given intravenously depresses or blocks the antegrade or retrograde conduction in the AV node and in the accessory AV pathway. The same effect is observed with orally given propafenone: 66% of antegrade blocking and 54% of retrograde blocking of the accessory conduction pathway. Intravenously given propafenone reduces within 2 to 3 min by antegrade or retrograde blocking 70% of SVT produced by intranodal reentry and by 85% of SVT produced by reentry by the accessory pathway. After injection it becomes impossible to induce intranodal SVT in 60% of cases and SVT by the accessory pathway reentry in 28% of cases. With oral treatment (600 mg/day) reinduction of intranodal SVT becomes impossible in 66% of cases and of SVT produced by reentry by the accessory pathway in 42% of cases. Long-term oral administration (17 +/- 3.7 months) of the same dose prevents 88% of SVT produced by internodal reentry and 80% of spontaneous SVT produced by reentry by the accessory pathway. Cardiologic tolerance is satisfactory: one case of atrioventricular and intraventricular dysrhythmia is observed. The same holds true for general tolerance: in 2 cases drug administration is discontinued and 11 patients present neurologic and digestive troubles improving after lowering the dosage or increasing the fractionation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.     

小儿室上性心动过速的食管心电生理分型及演变

目的 :探讨小儿室上性心动过速 (SVT)的类型及其电生理特征 ,以及食管起搏对小儿SVT的干预作用。方法 :对 4 7例 8个月～ 15岁有SVT发作史的患儿进行了食管心电生理研究。结果 :4 7例SVT经食管心房调搏 (TEAP)确定分型 4 2例 (89.4 % ) ,其中旁路折返 2 8例 (6 6 .7% ) ,房室结内折返 10例 (2 3.8% ) ,心房内折返l例 ,窦房结折返l例 ,心房自律性增高 2例 ;不能定型 5例 (10 .6 % )。结论 :小儿SVT近 95 %为折返机制所致 ,以旁路折返最常见 ,其次为房室结内折返 ,与成人报道不同 ,可能与小儿传导系统发育规律以及旁路电生理特性发生演变有关     

Usefulness of the pre-excitation index to determine the mechanism of supraventricular paroxysmal tachycardia and the location of the anomalous pathway

To evaluate the preexcitation index in determinate the mechanism of paroxysmal supraventricular tachycardia and localize accessory pathway, fifty nine patients with clinical and electrocardiographic supraventricular tachycardia were analyzed. There were thirty eight patients (64.4%) with orthodromic AV reentry using an accessory pathway for retrograde conduction and 21 patients (35.6%) with typical AV nodal reentrant tachycardia. Preexcitation of the atrium during tachycardia by premature ventricular complex at a time when anterograde His bundle activation was present in 30 o 38 (79%) patients with AV reentry while only 8 of 21 (38%) patients with AV nodal reentry demonstrated preexcitation during tachycardia. There was no significant difference between left and right accessory pathways and in mean tachycardia cycle length between the two groups. However, atrioventricular reentry demonstrated atrial preexcitation during tachycardia more frequently than AV nodal reentry. In conclusion, our findings show that the preexcitation index is a useful method for determinate the mechanism of supraventricular tachycardia and to localize accessory pathways.     

Wide complex tachycardias. Differential diagnosis and management.

The majority of wide complex tachycardias are secondary to VT. The differential diagnosis of wide complex tachycardia also includes SVT with aberrancy or underlying bundle branch block and antegrade SVT conduction over an accessory pathway (antidromic SVT). VT is usually the result of reentry and most commonly arises in an area of diseased myocardium in the setting of previous myocardial infarction or cardiomyopathy. VT, however, can also occur in patients with structurally normal hearts. Criteria useful in diagnosis of wide complex tachycardia include clinical criteria (presence of structural heart disease or a history of previous myocardial infarction) and electrocardiographic criteria (the presence of capture or fusion beats, relation of atrial or ventricular activity, QRS duration and axis, and morphology). The acute management of wide complex tachycardia includes cardioversion and intravenous pharmacologic therapy. Almost all patients with VT require chronic therapy, although in rare patients treatment of acute precipitating factors may be sufficient. While pharmacologic therapy has been the mainstay of treatment for these patients, there have been many exciting advances using surgical, device, and ablative therapies.     

12-Kanal-Elektrokardiogramm bei Kindern und Jugendlichen

The surface electrocardiogram (ECG) is an important diagnostic tool in general medicine, for children, adolescents and adults. Although technical aspects of ECG recordings are similar in young and old patients, there are some age-specific differences between children and adults. The QRS axis shifts from right to left at several stages during childhood. The heart rate decreases from 140/min (newborns) to 130/min (young children) to 75/min (adolescents). First and second degree atrioventricular (AV) blocks (I and II type Wenckebach) are frequent in children. Duration of the QRS is age-dependent as is the R peak amplitude. The ST-segment elevation is relatively frequent in children and is normal up to 0.1 mV. Negative T waves diminish with age and QTc times are also age-dependent. Supraventricular tachycardia (SVT) is characterized by small QRS complexes (QRS width <?0.12 s) during tachycardia. It is important to analyze the relationship between the p wave and QRS complex and to look for electrical alternans as a leading finding for an accessory pathway. Wide QRS complex tachycardia (QRS width ≥?0.12 s) occurs in SVT with aberrant conduction, SVT with bundle branch block or ventricular tachycardia (VT). In broad complex tachycardia, AV dissociation, negative or positive concordant pattern in V₁–V₆, a notch in V₁ and qR complexes in V₆ in tachycardia with left bundle branch block morphologies are findings indicating VT. In addition, an R/S relationship in V₆ favors VT when right bundle branch block tachycardia morphologies are present. By analyzing the surface ECG in the correct way with a systematic approach, a specificity and sensitivity of correctly identifying SVT or VT of over 95?% can be achieved.