Broad Complex Tachycardia Research Articles

A family with abnormal electrocardiograms: part I

A 40-year-old woman (Patient 1) had a broad complex tachycardia with left bundle branch block morphology and right axis compatible with ventricular tachycardia. Her electrocardiogram (ECG) was abnormal ( Figure 1 ). An echocardiogram revealed a moderate depressed left ventricular function, especially wall motion disturbances in the inferoposterolateral part with an ejection fraction of 40%. The right …

Wide complex tachycardia in a healthy young man

We describe a case of a young man referred with a broad complex tachycardia for evaluation and ablation. Electrophysiological study was performed and revealed a left lateral accessory pathway with antegrade decremental conduction causing antidromic reciprocating re-entrant tachycardia. Ablation was successfully performed. Left lateral accessory pathways with decremental conduction are rarely encountered.

Infraatrial Supraventricular Tachycardias: Mechanisms, Diagnosis, and Management

Tachycardias are traditionally classified as either ventricular tachycardia (VT) or supraventricular tachycardia (SVT). VT can be defined as a tachycardia which requires only ventricular structures for perpetuation. SVT is defined in terms of exclusion of VT and hence is any tachycardia which requires participation of at least one supraventricular structure for perpetuation. Certain SVTs require only participation of the atrioventricular node (AVN) and the His bundle (HB) but not the atrial myocardium or any of the great thoracic veins for perpetuation and hence can be described as "infraatrial." The three main mechanisms of infraatrial SVTs are: (1) intranodal atrioventricular reentrant tachycardia; (2) junctional ectopic tachycardia; and (3) nodoventricular reentrant tachycardia. The clinical significance of infraatrial SVTs is that they are compatible with any A:V ratio and even atrioventricular (AV) dissociation. Infraatrial SVTs are often suspected when a narrow complex tachycardia presents with apparent AV dissociation and a counterintuitive A:V ratio of < 1:1. However, if the same tachycardia is conducted with aberrant conduction or preexcitation, a broad complex tachycardia with an A:V ratio of < 1:1 will arise and that can be easily mistaken for VT. The possible patterns of electrical association and dissociation between different cardiac structures are examined, and how individual types of infraatrial SVT can be diagnosed and managed are reviewed.

Broad Complex Tachycardia: A Broad Differential

Journal of Cardiovascular ElectrophysiologyVolume 19, Issue 2 p. 217-218 Broad Complex Tachycardia: A Broad Differential MATTHEW WRIGHT M.B.B.S., Ph.D., MATTHEW WRIGHT M.B.B.S., Ph.D. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorMARK D. O'NEILL M.B.B.Ch., D.Phil., MARK D. O'NEILL M.B.B.Ch., D.Phil. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorIAN WRIGHT B.Sc., IAN WRIGHT B.Sc. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorNICHOLAS S. PETERS M.D., F.R.C.P., NICHOLAS S. PETERS M.D., F.R.C.P. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorD. WYN DAVIES M.D., F.R.C.P., D. WYN DAVIES M.D., F.R.C.P. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorPRAPA KANAGARATNAM M.B.B.S., Ph.D., PRAPA KANAGARATNAM M.B.B.S., Ph.D. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this author MATTHEW WRIGHT M.B.B.S., Ph.D., MATTHEW WRIGHT M.B.B.S., Ph.D. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorMARK D. O'NEILL M.B.B.Ch., D.Phil., MARK D. O'NEILL M.B.B.Ch., D.Phil. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorIAN WRIGHT B.Sc., IAN WRIGHT B.Sc. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorNICHOLAS S. PETERS M.D., F.R.C.P., NICHOLAS S. PETERS M.D., F.R.C.P. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorD. WYN DAVIES M.D., F.R.C.P., D. WYN DAVIES M.D., F.R.C.P. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this authorPRAPA KANAGARATNAM M.B.B.S., Ph.D., PRAPA KANAGARATNAM M.B.B.S., Ph.D. Department of Cardiology, Imperial College, St. Mary's Hospital, London, UKSearch for more papers by this author First published: 25 October 2007 https://doi.org/10.1111/j.1540-8167.2007.00980.xCitations: 1 Address for correspondence: Matthew Wright, M.B.B.S., Ph.D., Department of Cardiology, St. Mary's Hospital, Praed St., London W2 1NY, UK. Fax: +44-207-886-6239; E-mail: [email protected] J Cardiovasc Electrophysiol, Vol. 19, pp. 217-218, February 2008. Section Editor: George J. Klein, M.D. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume19, Issue2February 2008Pages 217-218 RelatedInformation

Epicardial ablation of an arrhythmogenic left ventricular micro-aneurysm guided by fusion of electro-anatomical activation maps and computed tomography images

A 32-year-old male patient presented with palpitations and near loss of consciousness during exercise because of a broad complex tachycardia of 230 bpm terminating spontaneously. A 12-lead ECG showed sinus rhythm, small Q-waves in the inferolateral leads, an incomplete right bundle branch block (RBBB), and VPBs with an RBBB morphology and a north-west axis. Echocardiogram and coronarography were normal. The left ventriculography showed a small aneurysm (14 mm×10 mm) in the inferolateral wall. This was confirmed …

A case of a borderline-broad complex tachycardia

Prompt and correct treatment of broad complex tachycardias in the emergency department can often be life-saving to the patient and satisfying for the emergency physician. They, however, are often a diagnostic challenge. Here, we present a case of posterior fascicular ventricular tachycardia, an idiopathic form of ventricular tachycardia that occurs in patients without coronary artery disease and verapamil sensitive. The differential diagnoses of posterior fascicular ventricular tachycardia and supraventricular tachycardia with aberrancy will also be discussed.

Characterization and incidence of inducible monomorphic ventricular tachycardia in a postinfarction rabbit model

Objective Ventricular tachycardia (VT), occurring late after myocardial infarction, is an important cause of sudden death. Animal models are useful for the investigation of this arrhythmia. The aim of this study is to develop and characterize a model of late postinfarction monomorphic VT in the rabbit. Methods and Results Myocardial infarction was created by ligation of the left circumflex artery. Cardiac electrophysiologic studies were performed 10 to 17 days postinfarction in 39 rabbits, in 10 sham-operated rabbits, and 6 control rabbits. Ventricular tachycardia was defined as a broad-complex tachycardia with a cycle length of more than 100 milliseconds, a duration of more than 10 seconds, and monomorphic QRS complexes. Using programmed stimulation, we induced VT in 9 rabbits (23%) in the infarct group but in none of the sham or control animals. The mean infarct size was 23% ± 9% (mean ± SD) of the left ventricle. Conclusion Coronary ligation in the rabbit creates a substrate, which allows the induction of sustained monomorphic VT with programmed stimulation. Monomorphic VT is not inducible in rabbits without myocardial infarction. This model might allow the testing of interventions that reduce the incidence of VT late after myocardial infarction.

Abstracts for the British Congenital Cardiac Association Annual Meeting: The Barbican, London, 24–25 November 2005: Poster Presentations: ECMO support for lifethreatening arrhythmia in infancy permits successful radiofrequency treatment

The majority of arrhythmias presenting in infancy cardiovert readily or rapidly respond to conventional medical therapy. A small number prove highly refractory to anti-arrhythmic medications. Myocardial performance may be severely compromised by the combination of fast heart rate and negatively inotropic drugs. Some babies die. We have recently supported 2 babies with refractory arrhythmias on ECMO, both to pursue drug therapy and eventually, to support the circulation during radiofrequency ablation, with very successful results. The first patient was a 2.5 kg neonate presenting with collapse secondary to atrial ectopic tachycardia with a rate of 300/minute. Myocardial function was severely impaired. The arrhythmia was adenosine resistant and after iv amiodarone loading had no effect, esmolol infusion was started. This produced profound hypotension and the arrhythmia rapidly recommenced after DC cardioversion. In the face of such severe haemodynamic disturbance, VA ECMO was instituted. Further anti-arrhythmics were tried on-circulatory support, but the arrhythmia was incessant despite multiple DC cardioversions. Therefore radiofrequency ablation of the atrial ectopic focus was attempted on ECMO support. This was achieved uneventfully and the myocardial function rapidly improved, with decannulation 24 hours later. Unfortunately the arrhythmia recurred 2 weeks later, but was successfully treated by further ablation without ECMO. The child remains well with normal development on no medication. An 11-month-old baby presented to the GP with acute onset of lethargy and poor feeding and a heart rate of 350 bpm was noted! This was a broad complex tachycardia with independent p wave activity (confirmed with adenosine); ie ventricular tachycardia. Although initially well tolerated, the tachycardia resisted DC “cardioversion” even up to 60 J. Progressive and severe myocardial dysfunction and hypotension ensued, exacerbated by any attempts at drug therapy. The patient was therefore placed on VA ECMO. Some slowing of the ventricular rhythm was achieved with amiodarone and flecainide. The patient was then decannulated but the rapid arrhythmia recurred and ECMO was reinstituted. Electro-physiological mapping was then undertaken on ECMO support. NAVEX mapping identified a right ventricular outflow tract focus. This was resistant to conventional RF energy but was eventually successfully ablated with a “Cool-tip” catheter. Myocardial function improved rapidly, the patient was decannulated after 48 hours observation and there has been no recurrence of the arrhythmia since discharge. Although viewed as a very invasive technique, VA ECMO support here has prevented two otherwise unavoidable deaths in babies with conditions readily treated by radio-frequency techniques in older children. Not only did ECMO permit institution of aggressive drug therapy but also safely supported catheter interventions in very small patients. ECMO support should be considered early for small patients with refractory arrhythmias, before irreversible neurological compromise ensues. It could also be used electively to permit radiofrequency ablation in children whose size causes concern for safe catheter manipulation.

Alternating R‐R Intervals During Broad‐Complex Tachycardia: What Is the Mechanism?

Alternating R‐R Intervals During Broad‐Complex Tachycardia: What Is the Mechanism?

Congenital and surgically acquired Wolff-Parkinson-White syndrome in patients with tricuspid atresia

There are reports associating an increased incidence of Wolff-Parkinson-White syndrome with tricuspid atresia. Here we report on electrophysiologic studies in patients with tricuspid atresia and Wolff-Parkinson-White syndrome after the Fontan operation. In these patients the atrial arrhythmia often seen in patients undergoing the Fontan operation triggered atrioventricular re-entrant tachycardia or caused life-threatening arrhythmias. Five patients with tricuspid atresia after palliation with a modified Fontan operation (atrioinfundibular connections) and Wolff-Parkinson-White syndrome are presented. Four of these patients had symptomatic paroxysmal orthodromic atrioventricular re-entrant tachycardia and a history of syncope; one of them additionally had atrial flutter with 2:1 conduction to the ventricle. A fifth patient presented with a life-threatening broad-complex tachycardia. In electrophysiologic studies an accessory pathway was localized in the right septal area in 3 patients. In 2 patients the accessory atrioventricular pathways were created by means of surgical intervention, connecting the right atrial appendage to the right ventricular outflow tract. All patients could be managed successfully by means of catheter ablation. In patients with tricuspid atresia, there are congenital and surgically acquired accessory pathways responsible for the increased rate of Wolff-Parkinson-White syndrome. Both types of accessory pathways can and should be treated by means of catheter ablation because atrial arrhythmia often seen in patients undergoing the Fontan operation can trigger atrioventricular re-entrant tachycardia or cause life-threatening tachycardia. Congenital accessory pathways should be excluded carefully before surgical intervention for total cavopulmonary anastomosis in patients with tricuspid atresia.

Broad complex tachycardia during treatment of atrial fibrillation with a 1c antiarrhythmic drug: Ventricular or supraventricular proarrhythmia?

A 60-year old woman was known with lone paroxysmal atrial fibrillation. She used for several years metoprolol slow release 50 mg once daily and propafenone 300 mg three times daily. During an arrhythmia recurrence, she presented with an atrial flutter with slow ventricular response (Fig. 1A). After performing slight exercise, i.e. walking in the hospital, she showed a broad complex tachycardia with hemodynamic consequences (Fig. 1B). Adenosine was given intravenously, which resulted in a slightly slower tachycardia with small QRS (Fig.

Radiofrequency catheter ablation of two accessory pathways with different unidirectional conduction properties

Simultaneous occurrence of narrow and broad QRS complex tachycardias in patients with WPW syndrome usually indicates a macroreentry in an orthodromic atrioventricular reentry-tachycardia using the AV node as antegrade and the accessory pathway as retrograde conduction and vice versa in an antidromic circuit. We report on a 32-year-old woman with WPW syndrome presenting with both a narrow and a broad QRS complex tachycardia using two accessory pathways with different unidirectional conduction properties in combination of an exclusively antegrade conducting AV node. This case report describes conventional mapping techniques and ablation of this unusual entity of a WPW syndrome.

Cardiac Arrhythmias – Part II:Broad Complex Tachycardia . . .

The acute management of the patient presenting with a broad complex tachycardia is a daunting clinical challenge. A broad complex tachycardia may be ventricular or supraventricular in origin and the ability to interpret correctly the 12-lead electrocardiogram is of critical importance in this differentiation. Broad complex tachycardia should be assumed to be ventricular in origin unless there is compelling clinical and electrocardiographic evidence to the contrary. This article focuses on the immediate diagnosis and management of broad complex tachycardia. In view of the broadening indications for implantation of cardioverterdefibrillator devices (ICD) in the management of ventricular arrhythmias, an approach to the ICD patient presenting to the accident and emergency department with recurrent device discharges is discussed.

Editorial

As ward round ‘faux-pas’ go, this week’s was a bad one. The patient was a middle aged man with pneumonia – nothing out of the ordinary. Turning to the somewhat hirsute ‘adolescent’ sitting in the chair next to him I asked the question: ‘Are you his son?’, to which the indignant response: ‘No, I’m his wife!’ came as something of a shock. Things went from bad to worse when the house officer helpfully suggested that it was a sign of getting older when you can no longer distinguish the sex of the ‘younger generation’. Not that I needed reminding: I recently reached an interesting milestone, when I realised that that I had once babysat for one of our third year medical students (while she was still in nappies). Having said that, getting older has its compensations – it is now several years since any patient told be I look too young to be a doctor; what’s more, it won’t be long before I have an answer for those sceptics who ask if I will still be doing my job when I am fifty… The first edition of 2005 brings another varied series of review articles. Mark O’Neill follows up his previous paper on bradycardia with a comprehensive account of the management of broad complex tachycardia. Guy Thwaites gives a practical approach to the assessment and treatment of PUO, while Lloyd and Garfield’s review of Non-invasive ventilation helps to demystify this complex subject. For many readers, ‘query urinary tract infection’ will probably stand alongside off legs’ and ‘collapse query cause’ in the ranking of ‘heartsink’ referrals on the medical take. However, if ‘prescribe trimethoprim’ would have been the only two words you would have been able to write on the subject I would commend to you Dr Chaudhuri’s comprehensive account of this topic. A couple of new features appear in this edition. A picture quiz section provides a variation on the case-report theme – no prizes, I am afraid, but you can find the answers on p36. Future submissions of this type, in addition to the standard case report format, are encouraged. Practices in medical admissions units vary widely, and it is important that we share each others’ experiences, both positive and otherwise. To this end I am keen to encourage readers to submit papers describing their activity along the ‘How we do it here…’ theme. To launch this series, Dr Vincent Connolly, winner of the Hospital Doctor Acute Medicine Team of the Year award describes the evolution of his innovative unit in Middlesborough. Finally, the more observant of you may have noticed a subtle change to the title of the journal, with the removal of the CPD Journal prefix to Acute Medicine. Although the educational themes of the journal remain unchanged, it is hoped that this will broaden its appeal beyond consultants and other ‘Points collectors’. I hope this does not detract from your enjoyment of the current and future editions, the reading of which can, as ever, be counted towards your ‘personal’ CPD.

Iatrogenic hyperkalaemia

A 75-year-old Asian woman was admitted following a sudden collapse at home. She had a short history of feeling generally unwell with nausea and vomiting. On arrival she was clammy with a heart rate of 200 bpm, systolic blood pressure 100 mm Hg. An ECG showed broad complex tachycardia. This spontaneously reverted to “atrial fibrillation” and she was transferred to the coronary care unit for observation. She had a past history of hypertension treated with enalapril 5 mg daily, and took omeprazole 20 mg daily.

The reliable electrocardiographic diagnosis of regular broad complex tachycardia: a holy grail that will forever elude the clinician's grasp?

The reliable and accurate diagnosis of regular broad complex tachycardia (BCT) by the ECG is a goal that has eluded clinicians and electrophysiologists alike for years. This article explores the reason for this by first giving an historical account on the development of the subject. Next, the electrophysiological mechanisms of ventricular tachycardia, supraventricular tachycardia with aberrant conduction, and preexcited tachycardia, the three main differential diagnoses for regular BCT, according to the latest knowledge from cellular and clinical electrophysiology study will be reviewed, together with considerations on how such understanding may help account for the manifestations of these tachycardias on the ECG and the difficulty in distinguishing between them. Finally, the use of electrophysiological study as the criterion standard for diagnosing regular BCT, as has been the case in most studies on the subject, will be critiqued in terms of the potential for misdiagnosis by the method and the use of any ECG diagnostic algorithms developed with its aid in the acute medical care setting.

Management of peri‐arrest arrhythmia

104 Arrhythmias, potentially serious electrical abnormalities of the heart, cause most sudden cardiac death (SCD). Cardiac arrhythmias are a wellrecognised complication of myocardial infarction but can also be precipitated by metabolic or endocrine abnormalities or drugs (Table 1). They may precede ventricular fibrillation (VF) or follow successful defibrillation. Emergency cardiovascular care no longer focuses just on the patient in established cardiac arrest. Advanced life support (ALS) providers must be able to recognise promptly and effectively treat patients ‘on their way to a cardiac arrest’ and those recovering in the immediate post-resuscitation period. There are peri-arrest arrhythmia algorithms for: (i) broad complex tachycardia; (ii) narrow complex tachycardia; (iii) atrial fibrillation; and (iv) bradycardia. These algorithms, provided by the European Resuscitation Council (ERC) and adopted by the Resuscitation Council (UK), aim to facilitate the safe, effective and timely initial treatment of arrhythmias by the non-specialist ALS provider. They universally recommend seeking expert help expeditiously at various stages whilst assessment and life-saving first-line emergency treatment is undertaken. They also clearly re-assure the non-specialist and outline recommendations in case of non-life-threatening arrhythmias.

Calcium channel blockers as first line treatment for broad complex tachycardia with right bundle branch block: ingenuity or folly?

Objective: To study the response of regular broad-complex tachycardia (BCT) demonstrating right bundle branch block (RBBB) to treatment in the Emergency department (ED). Methods: Retrospective chart review of management of patients with BCT, RBBB without a history of ischaemic heart disease. A diagnosis of ventricular tachycardia (VT) was made if the ECG showed features such as atrioventricular dissociation, capture or fusion beats or if VT was demonstrated during electrophysiological studies (EPS). Results: A total of 25 patients were eligible. Nineteen patients were given intravenous (IV) calcium channel blockers (either verapamil or diltiazem), as first line treatment. Of these, 18 converted to sinus rhythm and the other one patient subsequently converted with amiodarone. The remaining six patients were given IV adenosine ( n=3), lignocaine ( n=2) or amiodarone ( n=1) as first line treatment but none of them were converted. Of these, four of them converted with IV calcium channel blockers eventually. Of the other two patients, who were both given lignocaine initially, one deteriorated haemodynamically with the use of verapamil and required synchronised cardioversion to convert. The other patient did not respond to amiodarone and synchronised cardioversion but was subsequently converted with verapamil. The difference between the success rate of calcium channel blockers and other anti-arrhythmics is statistically significant ( P<0.01 by Fischer's exact method). Fourteen cases had diagnoses of VT, including the two patients given lignocaine. Five cases were found to have supraventricular tachycardia with aberrant conduction. Six cases did not have confirmed diagnoses. Conclusion: In patients presenting with BCT and RBBB but without underlying ischaemic heart disease, there is evidence to suggest that calcium channel blockers could effectively be used as the treatment of choice.

Variability in the manifestation of pre-excited atrial fibrillation: its quantification, theoretical origin, and diagnostic potential.

Irregular broad complex tachycardia (BCT) may be due to atrial fibrillation (AF) occurring in the presence of ventricular pre-excitation (pre-excited AF) or bundle branch block (BBB-AF). While irregularity is a defining characteristic of AF, it is a common subjective impression that greater variability in manifestation exists for pre-excited AF than BBB-AF. This difference can potentially be exploited for distinguishing the two conditions if some means can be found to quantify it. For each of 75 ECGs showing irregular BCT (41 pre-excited AF and 34 BBB-AF), a random sample of 10 distinct QRS complexes were selected for quantitative measurement of variability in manifestation, which included the standard deviation (SD) of the width, the SD of the axis, and the coefficient of variation (CV) of the amplitude of the QRS complex. Pre-excited AF showed statistically significantly greater values than BBB-AF with respect to these measures, and receiver-operating characteristic curves showed that these differences could be useful for their discrimination. For the SD of QRS width, a cut-off value of 8 ms appeared optimal (sensitivity 1.00 and specificity 0.79). For the SD of QRS axis, a cut-off value of 2.5 degrees appeared optimal (sensitivity 0.84 and specificity 0.56). For the CV of QRS amplitude, a cut-off value of 0.10 appeared optimal (sensitivity 0.82 and specificity 0.76). Pre-excited AF demonstrated greater variability than BBB-AF in manifestation. The measures of variability developed can potentially be useful for diagnosing irregular BCT in practice, especially in the context of automated computer-aided diagnosis.

Electrocardiographic criteria for diagnosis of irregular broad complex tachycardia with a high sensitivity for preexcited atrial fibrillation.

AF may appear as an irregular broad complex tachycardia (BCT) if atrioventricular conduction occurs via an accessory pathway (preexcited AF) or if bundle branch block (BBB), preexistent or rate related, exists in the His-Purkinje system (BBB-AF). While BBB-AF is relatively benign, preexcited AF may herald sudden cardiac death. Hence it is important that the two conditions can be reliably distinguished. Yet, there is no preexistent algorithms for this purpose. Griffith et al. previously proposed a simple algorithm for a similar problem, that of distinguishing the two differential diagnoses for regular BCT: VT and SVT with BBB, on the basis that unless the QRS morphologies in V1 and V6 are absolutely typical of BBB, VT will be diagnosed. The authors propose an extrapolation of this principle to irregular BCT by stating that, unless the QRS morphologies in V1 and V6 are absolutely typical of BBB, preexcited AF will be diagnosed. Seventy-five ECGs showing irregular BCT (41 preexcited AF and 34 BBB-AF) were shown to two fellows in electrophysiology who were given no other information and were instructed to diagnose preexcited AF unless the QRS morphology pattern was typical of BBB. Observer 1 achieved a sensitivity of 100% (41/41) and a specificity of 79% (27/34), while observer 2 achieved a sensitivity of 100% and a specificity of 85% (29/34). By QRS morphology pattern, an average sensitivity of 100% and specificity of 82% were achieved for the diagnosis of irregular BCT. The algorithm is simple and easy to implement and recommended for clinical use.