Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias

The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS less than 0.12 s) adenosine (2.5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS greater than or equal to 0.12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses of over 2 s in 16% of patients, the longest pause being 6.1 s. Adenosine is of value in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence or arrhythmia.     

Acute treatment of paroxysmal tachycardia by adenosine

Background: Adenosine has proven efficacy in clinical trials and in the electrophysiological laboratory for the treatment of paroxysmal tachycardia.
Aims: To evaluate the efficacy and safety of adenosine administered in a clinical setting by non-consultant staff.
Methods: Incremental doses of adenosine were administered intravenously to five children and 32 adults during 39 episodes of paroxysmal tachycardia in a clinical setting. Structural heart disease was present in 43% of patients.
Results: Of 35 episodes of narrow complex tachycardia, adenosine terminated 26 of 28 episodes of supraventricular re-entrant tachycardia (SVRT), one episode of ectopic atrial tachycardia, and induced transient atrioventricular block to reveal atrial arrhythmias in four. Termination of SVRT occurred at a mean (SD) dose of 9.2 (4.0) mg in adults and 0.09 (0.04) mg/kg in children, but two patients had later spontaneous reinitiation of SVRT. Two patients with narrow complex tachycardia who failed to respond to adenosine were subsequently found to have ventricular tachycardia. Adenosine was therapeutic or diagnostic in three of four episodes of broad complex tachycardia. Overall, by intention to treat by the clinician, adenosine was therapeutic or diagnostic in 34 of 39 episodes (87%). Breathlessness (26%), chest tightness (18%) and flushing (18%) occurred transiently. There were no episodes of hypotension. Adenosine was given safely to 15 patients in whom verapamil was considered contraindicated.
Conclusions: Adenosine is a safe treatment for both narrow and broad complex tachycardias; usually effective for the former and diagnostic for the latter.     

Akuttherapie lebensbedrohlicher tachykarder Rhythmusstörungen

Life-threatening supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with rapid ventricular response and preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain one of the leading causes of death; these arrhythmias include monomorphic and polymorphic ventricular tachycardia, torsade de pointes tachycardia, ventricular fibrillation and ventricular flutter. In all patients with tachycardias, an attempt should be made to differentiate between narrow (QRS duration < 0.12 s) or wide QRS complex (QRS duration ≥ 0.12 s) tachycardias. In the assessment of patients (pts) with supraventricular/ventricular tachyarrhythmias, attention should be given to identify whether the tachycardia is associated with worsening angina or low cardiac output. In pts with narrow QRS complex tachycardias or pts with atrial fibrillation and preexcitation syndromes immediate synchronized cardioversion should be performed if signs or symptoms of instability (hypotension, evidence of end-organ dysfunction, worsening angina) exist. In pts with a stable hemodynamic situation, vagal maneuvers, adenosine or calcium channel blockers can be used. Management of atrial flutter usually centers on cardioversion or rapid atrial pacing to normal sinus rhythm. In the treatment of patients with deemed unstable ventricular tachycardia (VT), electrical cardioversion is the treatment of choice. In more stable patients, ajmaline is the preferred agent after myocardial infarction and lidocaine if myocardial ischemia is present. In pts with torsade de pointes tachycardias aggressive steps must be taken to prevent degeneration of this rhythm to ventricular fibrillation (VF). Magnesium sulfate has recently been demonstrated efficacious and is currently considered first-line drug therapy. Transcutaneous overdrive pacing should be attempted if magnesium is unsuccessful. The pt with pulseless VT or VF demands early electrical countershock.     

The therapeutic and diagnostic cardiac electrophysiological uses of adenosine

Summary Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A₁ purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.     

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.     

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.     

Enlarged effects of adenosine in a septic patient with multiple myeloma and atrial flutter

We report the history of a 60-year-old patient with a multiple myeloma and Staphylococcus aureus associated sepsis to whom adenosine in a dose of 6 mg was administered, when a regular, narrow QRS complex tachycardia at a heart rate of 120 beats/minute started. Adenosine led to a complete AV-block and revealed atrial flutter. Atrial flutter waves persisted for about 15 seconds and were followed by atrial and ventricular asystole for about 20 seconds. Repeated nonsustained polymorphic ventricular tachycardias followed and after about 90 seconds sinus rhythm was restored.     

Vital bedrohliche brady- und tachykarde Herzrhythmusstörungen

Bradycardic (heart rate <50/min) and tachycardic heart rhythm disturbances (100/min) require rapid therapeutic strategies. Supraventricular tachycardias (SVT) are sinus tachycardia, atrial tachycardia, AV-nodal reentrant tachycardia and tachycardia due to accessory pathways. Mostly SVT are characterized by small QRS complexes (QRS width <0,12 ms). It is essential to evaluate the arrhythmia history, to perform a good physical examination and to exactly analyze the 12-lead electrocardiogram. An exact diagnosis is then possible in >90% of SVT patients. Ventricular tachycardias have a broad QRS complex (≥ 0,12 s), ventricular flutter and ventricular fibrillation are associated with chaotic electrophysiologic findings. For acute therapy, we will present the new concept of the “5A” that includes adenosine, adrenaline, ajmaline, amiodarone and atropine. Additional “B, C and D strategies” include betablocking agents, cardioversion as well as defibrillation. The “5A” concept allows a safe and effective antiarrhythmic treatment of all bradycardic and tachycardic arrhythmias as well as asystolia.     

Intravenous adenosine triphosphate during wide QRS complex tachycardia: safety, therapeutic efficacy, and diagnostic utility

PURPOSE: Inappropriate administration of intravenous verapamil to patients with wide QRS complex tachycardia due to ventricular tachycardia or atrial fibrillation with Wolff-Parkinson-White syndrome occurs frequently because of misdiagnosis, and may precipitate a cardiac arrest. We evaluated the safety and the diagnostic and therapeutic utility of adenosine triphosphate administered to a consecutive series of 34 patients during wide QRS complex tachycardia due to a variety of mechanisms. PATIENTS AND METHODS: Patients who had a hemodynamically and electrically stable, monomorphic, wide (greater than 120 msec) QRS complex tachycardia induced during an invasive cardiac electrophysiologic test were studied. Hemodynamic stability was defined by a systolic blood pressure greater than 80 mm Hg and no clinical evidence of cerebral or myocardial ischemia. Adenosine triphosphate, 20 mg, was administered as a rapid intravenous bolus via a peripheral vein during wide QRS complex tachycardia. Five surface electrocardiogram leads, at least three intracardiac electrograms, and blood pressure were monitored. RESULTS: Ventricular tachycardia was present in 14 patients (mean age 50.6 +/- 19 years, cycle length 326 +/- 67 msec) and adenosine triphosphate terminated the arrhythmia in one case. Ventricular tachycardia cycle length did not change. Among 10 patients with supraventricular tachycardia with mechanisms not involving the AV node (average ventricular cycle length 346 +/- 82 msec), one case of ectopic atrial tachycardia was terminated. The ventricular rate was transiently increased in patients with Wolff-Parkinson-White syndrome and atrial fibrillation (average R-R interval 351 +/- 84 msec in control and 317 +/- 82 msec after adenosine triphosphate, p less than 0.001). Reentrant tachycardias involving the AV node (cycle length 302 +/- 52 msec) terminated in seven of 10 patients. The drug was well tolerated, and no patient developed hemodynamic compromise necessitating cardioversion as a result of adenosine triphosphate. CONCLUSION: In the setting of electrophysiology testing, adenosine triphosphate is a safe agent, even when administered inappropriately during arrhythmias for which it is relatively ineffective, such as ventricular tachycardia, and Wolff-Parkinson-White syndrome with atrial fibrillation. It is an effective agent in terminating supraventricular tachycardia involving the AV node. Tachycardia termination following adenosine triphosphate, when used as a diagnostic test to indicate obligatory participation of the AV node, had a sensitivity of 70%, specificity of 92%, and a positive predictive accuracy of 85%. Thus, adenosine triphosphate also has diagnostic utility, but should be used after the appropriate arrhythmia diagnosis has been made based on the clinical history and analysis of the 12-lead electrocardiogram.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children.

One hundred and seventeen episodes of supraventricular tachycardia in 50 children, including 28 infants, were treated with intravenous adenosine. Adenosine was prepared in a sterile solution of 0.9% saline (1 mg/ml) and given in incremental doses of 0.05 mg/kg every two minutes to a maximum of 0.25 mg/kg. Ninety of the 117 episodes were terminated. This included 88 of the 102 episodes of junctional tachycardia (79 of the 92 episodes of atrioventricular reentry tachycardia, seven of the eight episodes of atrioventricular nodal reentry tachycardia, and both of the episodes of long R-P' tachycardia). Only one of four episodes of His bundle tachycardia and one of the eight episodes of ectopic atrial tachycardia were terminated. None of the three episodes of atrial flutter were terminated. Side effects were frequent but mild and included transient complete atrioventricular block (less than 6 s), sinus bradycardia (less than 40 s), ventricular extrasystoles, flushing, nausea, headache, and respiratory disturbance. Reinitiation (within 5 s) of supraventricular tachycardia occurred in 13 of the terminated episodes. Although reinitiation limited its clinical efficacy in some patients, intravenous adenosine offered a safe and efficient method of rapid termination of most episodes of supraventricular tachycardia and in some cases facilitated diagnosis of the mechanism.     

Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children

One hundred and seventeen episodes of supraventricular tachycardia in 50 children, including 28 infants, were treated with intravenous adenosine. Adenosine was prepared in a sterile solution of 0.9% saline (1 mg/ml) and given in incremental doses of 0.05 mg/kg every two minutes to a maximum of 0.25 mg/kg. Ninety of the 117 episodes were terminated. This included 88 of the 102 episodes of junctional tachycardia (79 of the 92 episodes of atrioventricular reentry tachycardia, seven of the eight episodes of atrioventricular nodal reentry tachycardia, and both of the episodes of long R-P' tachycardia). Only one of four episodes of His bundle tachycardia and one of the eight episodes of ectopic atrial tachycardia were terminated. None of the three episodes of atrial flutter were terminated. Side effects were frequent but mild and included transient complete atrioventricular block (less than 6 s), sinus bradycardia (less than 40 s), ventricular extrasystoles, flushing, nausea, headache, and respiratory disturbance. Reinitiation (within 5 s) of supraventricular tachycardia occurred in 13 of the terminated episodes. Although reinitiation limited its clinical efficacy in some patients, intravenous adenosine offered a safe and efficient method of rapid termination of most episodes of supraventricular tachycardia and in some cases facilitated diagnosis of the mechanism.     

Administration of adenosine for termination of atrioventricular nodal reentry tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway and unmasking of concomitant Wolff-Parkinson-White syndrome

The antiarrhythmic properties of adenosine, its ultra-short half-life and the absence of frequent serious side effects make it a front-line agent in arrhythmia management, especially in the treatment of atrioventricular nodal reentrant tachycardia. Due to a shortening of atrial refractoriness, adenosine can facilitate the induction of atrial fibrillation. Life threatening tachycardias may result from a potential rapid conduction of atrial fibrillation over an accessory pathway especially if the latter one has a short antegrade refractory period. We report a case of a 59 year old female patient in which intravenous administration of adenosine during typical atrioventricular nodal reentrant tachycardia was followed by atrial fibrillation with rapid conduction over a hitherto unknown accessory pathway. After intravenous administration of adenosine the tachycardia was terminated successfully within 38 s. After a short period of asystole, spontaneous atrial fibrillation developed unmasking an antegrade preexcitation with subsequent rapid ventricular response (210 b/min). The three-lead ECG showed a narrow QRS complex tachycardia. Because of spontaneous conversion to sinus rhythm and the absence of hemodynamic compromise there was no need for external cardioversion. During electrophysiological study an antidromic atrioventricular reentrant tachycardia was recorded over a left posteroseptal accessory pathway including antegrade conduction properties only. Because of its ultrashort half-life, serious side effects after adenosine administration are rare. The possibility of life threatening proarrhythmias after intravenous adenosine administration should be taken into consideration if the etiology of a paroxysmal supraventricular tachycardia is not clear and a concomitant Wolff-Parkinson-White syndrome cannot be excluded. As with application of all intravenous antiarrhythmic agents, the administration of adenosine should only be performed if continuous ECG monitoring and cardioversion facilities are available and possible.     

Clinical,electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined In 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia.In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.     

Narrow QRS Tachycardia with Ventriculoatrial Dissociation Mediated by a Left Fasciculoventricular Fiber

A 30-year-old man presented with narrow QRS tachycardia. The intracardiac electrocardiogram showed an atrial-HIS (AH) interval of 75 msec and a HIS-ventricular (HV) interval of 44 msec during baseline. Atrial incremental pacing revealed HV shortening, with apparent incomplete right bundle branch block (RBBB) morphology without QRS complex axis deviation. The induced tachycardia exhibited several QRS morphologies: a narrow QRS, complete RBBB and complete left bundle branch block (LBBB) morphology. Spontaneous conversion of the QRS pattern from wide to narrow was observed. The cycle length of the tachycardia was significantly shortened (from 316 to 272 ms) from LBBB morphology to narrow QRS complex. The atrial activation was dissociated from the ventricular activation during all tachycardias. Each QRS complex during tachycardia was preceded by a HIS deflection and HV interval was 35 ms, which was shorter than that of sinus rhythm. HIS deflection was earlier than right bundle potential during all kinds of tachycardia. This tachycardia is most likely mediated by a left fasciculoventricular fiber which connects the HIS bundle below the atrioventricular node to the myocardial tissue of the left ventricle. The HIS-Purkinje system is used as an antegrade conduction limb and the fasciculoventricular fiber as a retrograde limb in the tachycardia circuit.     

Spectrum of regular tachycardias with wide QRS complexes in patients with accessory atrioventricular pathways

Reciprocating tachycardia and atrial flutter or fibrillation are the rhythm disorders most frequently documented in patients with accessory atrioventricular (A-V) pathways. Reciprocating tachycardia typically results in a regular tachycardia (140 to 250/min) with a normal QRS pattern, although on occasion bundle branch block aberration occurs. Atrial flutter or fibrillation may result in an irregular ventricular response, with the QRS configuration being normal or exhibiting bundle branch block or various degrees of ventricular preexcitation, or both. Although much less common than either reciprocating tachycardia or atrial flutter/fibrillation, regular tachycardias with a wide QRS complex suggestive of ventricular preexcitation are observed in patients with accessory pathways. Excluding functional or preexisting bundle branch block, several arrhythmias may cause these electrocardiographic findings which may mimic those of ventricular tachycardia.In the present study a variety of arrhythmias that resulted in tachycardias with a wide QRS complex were examined in 163 patients with accessory pathways who underwent clinical electrophysiologic study for evaluation of recurrent tachyarrhythmias. Twenty-six patients (15 percent) manifested a regular tachycardia with a wide QRS complex suggesting ventricular preexcitation. Atrial flutter with 1:1 anterograde conduction over an accessory pathway (15 of 26 patients, 58 percent) was the most frequent arrhythmia and was usually associated with a heart rate of 240/min or greater (12 of 15 patients). Reciprocating tachycardia with conduction in the anterograde direction over an accessory pathway (antidromic reciprocating tachycardia) occurred in 7 of 26 patients (27 percent), and resulted in a slower ventricular rate than atrial flutter (217 ± 22 versus 262 ± 42, P < 0.01). Other arrhythmias included reciprocating tachycardia with reentry utilizing a fasciculoventricular or nodoventricular connection (two patients, 8 percent), reciprocating tachycardia with reentry in the atrium or A-V node and anterograde accessory pathway conduction (one patient, 4 percent) and ventricular tachycardia (one patient, 4 percent).In this study the clinical electrophysiologic diagnostic features of several arrhythmias which cause tachycardias with a wide QRS compex suggesting ventricular preexcitation are outlined. It is apparent that definitive arrhythmia diagnosis during these tachycardias is often complex and usually requires careful study using intracardiac electrode catheter techniques.     

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.     

Ablation of cardiac tissues by an electrode catheter technique for treatment of ectopic supraventricular tachycardia in adults

Five patients with chronic or recurrent ectopic supraventricular tachycardias unresponsive to drugs underwent programmed stimulation, endocardial mapping, and attempted catheter ablation of the arrhythmia focus. For attempted ablation, an intracardiac electrode catheter was positioned near the exit point of the tachycardia and served as the cathode while a chest wall patch served as the anode. In two patients with tachycardia originating near the coronary sinus, discharges of 200 or 400 J each were delivered to two electrodes at the earliest area of endocardial activation. These two patients with incessant tachycardia remain free of tachycardia for 17 and 11 months, respectively. In one patient with tachycardia originating from the right atrial appendage, both catheter and surgical ablation proved unsuccessful in that a new focus of atrial tachycardia supervened. This patient subsequently underwent successful catheter ablation of the atrioventricular junction. Two patients with junctional tachycardia underwent catheter ablation of the atrioventricular junction. Complete atrioventricular block followed atrioventricular junctional ablation and these patients required permanent cardiac pacing. The junctional tachycardia was replaced by sinus rhythm with episodes of unsustained atrial tachycardia. However, after 13 +/- 5 months follow-up, neither of the patients require antiarrhythmic drugs. Catheter ablation can be effective for atrial foci near the coronary sinus os, and can be performed with preservation of atrioventricular conduction. Arrhythmia ablation is possible in those with atrioventricular junctional tachycardia but requires the sacrifice of atrioventricular conduction. After ablation, other automatic atrial foci may become operative and complicate use of dual-chamber pacemakers.     

Differentiation of Narrow QRS Complex Tachycardia Types Using the 12‐Lead Electrocardiogram

Background: Previous studies have shown that only 80% of narrow QRS supraventricular tachycardia (SVT) types can be differentiated by standard 12‐lead electrocardiographic (ECG) criteria. This study was designed to determine the value of some new ECG criteria in differentiating narrow QRS SVT. Methods and Results : 120 ECGs demonstrating paroxysmal narrow QRS complex tachycardia (QRS s 0.11 ms and rate > 120 beats/min) were analyzed. Forty atrioventricular reciprocating tachycardia (AVRT), 70 atrioventricular nodal reentrant tachycardia (AVNRT), and 10 atrial tachycardia defined with electrophysiologic study (EPS) consisted the study group. Eight surface ECG criteria were found to be significantly different between tachycardia types by univariate analysis. P waves separate from the QRS complex were observed more frequently in AVRT (70%) and atrial tachycardia (80%). Pseudo r’deflection in lead V¹, pseudo S wave in inferior leads, and cycle length alternans were more common in AVNRT (55, 20, and 6%, respectively). QRS alternans was also present during AVRT (28%). ST‐segment depression (≧ 2 mm) or T‐wave inversion, or both, were present more often in AVRT (60%) than in AVNRT (27%). During sinus rhythm, manifest preexcitation was observed more often in patients with AVRT (42%). When a P wave was present, RP/PR interval ratio > 1 was more common in atrial tachycardia (90%). By multivariate analysis, presence of a P wave separate from the QRS complex, pseudo r’deflection in lead V¹, QRS alternans, preexcitation during sinus rhythm, ST‐segment depression > 2 mm or T‐wave inversion, or both, were independent predictors of tachycardia type. Conclusions: Several new ECG criteria may be useful in differentiation of SVT types. Prediction of mechanism prior to EPS may provide additional benefits concerning the fluoroscopic exposure time and cardiac catheterization procedure. A.N.E. 2002;7(2):120–126     

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections

BACKGROUND. Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. METHODS AND RESULTS. We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261 +/- 41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 +/- 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 +/- 44 msec to 224 +/- 35 msec, p less than 0.01) after adenosine, but no change in average RR interval was observed (360 +/- 59 msec to 357 +/- 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 +/- 21 msec to 360 +/- 49 msec, p less than 0.05) due to shortening of flutter cycle length (207 +/- 10 msec to 180 +/- 24 msec, p less than 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. CONCLUSIONS. Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by beta-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.