Supraventricular tachycardia

0 downloads 0 Views 1MB Size Report
London SW17 ORE, U.K. reference to the 12-lead surface ECG appearance and .... lead aVL has a sensitivity of 88% and a specificity of 79% of predicting right ...
European Heart Journal (1997) 18 (Supplement Q, C2-C11

Supraventricular tachycardia ECG diagnosis and anatomy O. A. Obel and A. J. Camm Department of Cardiological Sciences, St. Georges Hospital Medical School, London

This paper reviews the anatomical substrates responsible for the induction and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy of the supraventricular conducting system, particularly within the atria, is complex with conduction proceeding along preferential pathways, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an anterior fast pathway.

Supraventricular tachycardia presents as a narrow complex tachycardia unless pre-existing or rate-related bundle

Introduction Supraventricular tachycardia is a common clinical problem. Considerable progress has been made in the elucidation of the pathophysiology and treatment of supraventricular tachycardia. In this paper special

ECG features which can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (1) the presence of a 8 wave during sinus rhythm which is highly suggestive of atrioventricular re-entrant tachycardia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V,) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tachycardia when bundle branch block occurs ipsilateral to the accessory pathway and (4) the finding of QRS alternans during tachycardia which is suggestive of atrioventricular re-entrant tachycardia. 'Long RP' tachycardia may be caused by an atrial tachycardia due to an inferiorly situated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventricular re-entrant tachycardia with an accessory pathway conducting slowly from ventricle to atrium during tachycardia. (Eur Heart J 1997; 18 (Suppl C): C2-C11)

Key Words: Anisotropic, dual atrioventricular nodal pathways, crista terminalis, Eustachian ridge, wavelength, atrioventricular nodal re-entrant tachycardia, atrioventricular re-entrant tachycardia, orthodromic, antidromic.

reference to the 12-lead surface ECG appearance and anatomical substrates involved will be discussed.

Normal anatomy of the atrial and atrioventricular nodal conducting tissue

Correspondence: Prof A. John Camm, MD, FRCP, Cardiological Sciences, St. Georges Hospital Medical School, Cranmer Terrace, The conduction system comprises a network of modified cardiac muscle that initiates and transmits the cardiac London SW17 ORE, U.K. 0195-668X/97/OC0002+10 $18.00/0

1997 The European Society of Cardiology

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

It is sometimes possible to relate ECG findings directly to anatomical substrates; for example, in some cases of atrial tachycardia the site of the atrial focus (left or right, superior or inferior) can be determined by the polarity of the P wave. The anatomical substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagation and areas of slow conduction. In atrial flutter the crista terminalis, Eustachian valve, inferior vena cava, coronary sinus os, and tricuspid annulus have been identified as anatomical barriers to conduction around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atria] fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocardium and are responsible for the irregular 'fibrillation waves' on the ECG.

branch block is present. Less common causes for a broad complex tachycardia occurring in supraventricular tachycardia include an accessory atrioventricular or atriofascicular pathway conducting antegradely during tachycardia, or accessory pathway participation as a bystander during supraventricular tachycardia.

Supraventricular tachycardia: ECG and anatomy

determined by the influence of ultra-structure on functional properties, characterizes uniform anisotropy and forms the basis of preferential conduction in the atrium'61. Non-uniform anisotropy can result from separation of bundles by fibrous tissue septa which can result in uncoupling of side-to-side conduction, complex multiphasic waveforms, and differences in refractory periods between longitudinally and transversely conducting tissue. The compact atrioventricular node lies in the lower part of the right atrium within the triangle of Koch. The anatomical landmarks of the triangle of Koch are the tendon of Todaro (the fibrous extension of the valves of the inferior vena cava or Eustachian valve), the septal attachment of the septal leaflet of the tricuspid valve, and the orifice of the coronary sinus. The His bundle represents the direct continuation of the atrioventricular node, passing through the tissue of the central fibrous body into the postero-inferior portion of the membranous interventricular septum. The atrioventricular node is composed of three distinct histological cell types; atrionodal, nodal, and nodal-His cells'71. Although it is not always possible to correlate the physiological characteristics of the cells with their histological appearance, the longest delay of the impulse during both normal conduction and premature stimulation occurs within the compact region of the atrioventricular node containing the nodal cells. The anatomical correlates of dual atrioventricular nodal pathways are yet to be fully defined; however, a large body of evidence exists to suggest separate atrial connections for fast and slow atrioventricular nodal pathways.

ECG characteristics of supraventricular tachycardia The various supraventricular tachycardias usually exhibit a narrow complex. Notable exceptions in which supraventricular tachycardia presents as a broad complex tachycardia include situations in which there is: (1) the presence of pre-existing or rate-related bundle branch block (which occurs as a result of a high rate of depolarization, and may perpetuate due to concealed retrograde invasion of the impulse into the bundle branch)'81; (2) antidromic atrioventricular or atriofascicular re-entrant tachycardia, or (3) accessory pathway participation as a bystander in atrioventricular nodal re-entrant and atrial tachycardias, and in atrial fibrillation. Any of the tachycardias discussed below can present as a broad complex tachycardia due to one or more of the above mechanisms. With the exception of atrial fibrillation, most supraventricular tachycardias are regular, and, depending on the specific supraventricular tachycardia, P waves may or may not be visible. If visible, the P wave during tachycardia may exhibit a morphology similar to the P wave in sinus rhythm; however, more commonly the Eur Heart J, Vol. 18, Suppl C 1997

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

impulse. The sinus node is a small ellipsoid structure situated subepicardially in the terminal groove formed by the lateral junction of the superior caval vein with the remainder of the right atrium. Histologically the sinus node consists of specialized conduction cells embedded in a dense matrix of collagenous tissue, the proportion of which increases with age. Its blood supply is from the right coronary artery in approximately 55% of cases and from the left circumflex artery in almost all of the remainder1'1. The sinus node is richly supplied with parasympathetic nerves and to a lesser degree by sympathetic fibres. The anatomical sinus node probably exhibits a multicentricity of pacemaker sites, but the exact mechanism of impulse formation and exit from the node has yet to be determined. Based on experiments on both canine and human atria, Boineau and co-workers have demonstrated variable sites of earliest impulse formation depending largely on the underlying heart rate and therefore relating in part to autonomic tone'2'31. This so-called 'pacemaker complex' incorporates an area extending from the right atrium-inferior vena cava junction in the posteroinferior aspect of the right atrium to the right atriumsuperior caval vein junction on the anterior aspect of the right atrium. Fast heart rates appear to originate from the superior parts of the complex, with a progressively inferior location being associated with progressively slower rates. The spread of activation and therefore P wave morphology depends to a large extent on the site of the initial impulse. To what degree these different sites of initial impulse formation operate under normal physiological conditions is not clear. The subject of whether there exist specialized tracts of conduction within atrial tissue between the sinus node and atrioventricular node has been debated for years. It is now widely accepted that there are no insulated tracts in the atria such as the proximal His Purkinje system in the ventricles. However, conduction does appear to be conducted preferentially via the major muscle bundles, notably along the crista terminalis (a distinct muscle bundle in the right atrium marking the junction between the smooth posterior wall and the trabeculated anterior wall) and the anterior lip of the oval fossa1'41. This preferential conduction is generally accepted to arise from the intrinsic anisotropic conduction properties of the atrial muscle bundles and the orientation of the muscle fibres. As a wavefront of depolarization propagates, current flows between cells through the gap junctions of the intercalated disks, the distribution of which have a profound influence on axial resistance and conduction'51. The atria and ventricles are composed of bundles of myocardial cells which are connected to each other through numerous intercellular connections with resultant uniform and synchronous activation of individual bundles. Connections between parallel bundles are relatively sparse, thus myocardium is better coupled and conduction is faster in the direction of the long axis of its myocytes and myofibrils than in their transverse direction. This smooth depolarization,

C3

C4

O. A. Obel and A. J. Camm

P wave during supraventricular tachycardia and that during sinus rhythm are different. The presence of atrioventricular block during the arrhythmia is of diagnostic importance and will be discussed later. If the onset of the tachycardia is observed on the ECG, for example during a Holter or telemetry recording, the mode of onset and termination of the tachycardia can yield useful diagnostic information. For instance, the tachycardia may be seen to 'warm up and cool down', as occurs in sinus tachycardia and in some forms of atrial tachycardia, or may terminate with evidence of a retrograde P wave which does not conduct to the ventricles in atrioventricular re-entrant tachycardia.

Tachycardias arising from the sinus node

Atrial tachycardia Atrial tachycardia may result from abnormal automaticity, or as a result of intra-atrial re-entry. Atrial tachycardia due to focal increased automaticity often occurs in the presence of cardiac or pulmonary disease'91. These supraventricular tachycardias may also 'warm up and cool down', however, P wave morphology during sustained tachycardia is different from that during sinus rhythm, reflecting the site of origin. The first or initiating beat often has a P wave morphology identical to that seen during tachycardia. Eur Heart J, Vol. 18, Suppl C 1997

Right atrial tachycardia

avL

Left atrial tachycardia

Figure 1 The 12-lead ECG may be useful in determining the site of an atrial focus. A positive P wave in V, has a sensitivity of 93% and a specificity of 88% in predicting a left atrial focus, whilst a positive or biphasic P wave in lead aVL has a sensitivity of 88% and a specificity of 79% of predicting right atrial foci. The example of focal left atrial tachycardia in this figure was taken from a 17-yearold female who presented with tachycardiomyopathy which completely resolved after successful radiofrequency ablation of her incessant left atrial focal tachycardia.

In a study in which atrial tachycardia due to abnormal automaticity was mapped for the purposes of radiofrequency catheter ablation, approximately equal proportions of the foci were found to be in the left and right atria'101. An attempt was made to correlate the P wave configuration on the surface ECG with the site of origin of the tachycardia as determined by earliest site of activation during intracardiac recording and by successful ablation of the focus. Analysis of leads aVL and V, provided a reasonable guide as to whether the tachycardia arose from the left or right atrium. A positive P wave in V, had a sensitivity of 93% and a specificity of 88% in predicting a left atrial focus. This is in keeping with the fact that the left atrium is a posterior midline structure and would be expected to produce a P wave vector that is positive in V,. Owing to their proximity to the left atrium, posterior right atrial foci also produced a positive P wave in V,. A positive or biphasic P wave in lead aVL had a sensitivity and specificity of 88% and 79%, respectively, for predicting a right atrial focus. Furthermore, examination of P wave polarity in the inferior leads was helpful in distinguishing a superior focus (positive P wave) from an inferior focus (negative P wave) in both right and left atria (Fig. 1). Supraventricular tachycardia due to intra-atrial re-entry is also frequently associated with organic heart disease. Tachycardia may be paroxysmal or incessant, although the latter is more often the case'"', the rate varies from approximately 140-240 beats . min" 1 . The PR interval is often shorter than the RP interval in this form of supraventricular tachycardia ('long RP tachycardia' see below), and thus the differential diagnosis includes fast/slow (uncommon) atrioventricular nodal re-entrant tachycardia, and orthodromic atrioventricular re-entrant tachycardia with an accessory pathway which conducts slowly in the retrograde direction. P wave morphology differs from that during sinus

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

Sinus tachycardia is usually a response to a physiological stress such as exercise or pyrexia, or may be as a result of an abnormally heightened sympathetic tone such as occurs in thryrotoxicosis. Many drugs, for example caffeine, aminophylline and alcohol, have a propensity to cause sinus tachycardia. Inappropriate sinus tachycardia in the absence of an obvious precipitant occurs as a mechanism of supraventricular tachycardia in some patients. The mechanism of tachycardia in some cases may be a hypersensitivity to catecholamines. Tachycardia in these patients can be recognised by the fact that they gradually 'warm up and cool down' and P wave morphology is identical to that during sinus rhythm. Sinus node re-entry tachycardia has an abrupt initiation and termination, although otherwise the ECG appearance is similar to inappropriate sinus tachycardia. Each QRS complex is preceded by a P wave of identical morphology to that in sinus rhythm. It should be noted that, at fast rates, the P wave may be buried in the preceding QRST complex, and thus may not be visible on the surface ECG. At the onset of sinus node re-entry tachycardia, the PR interval is often prolonged since the atrioventricular node has not adapted to the sudden rate increase'91.

avL

rrrr

Supraventricular tachycardia: ECG and anatomy

Atrial flutter and atrial fibrillation The terminology of atrial flutter has been inconsistent and the subject of disagreement. Hence terms such as 'usual', 'classic', 'orthodromic' and 'typical' atrial flutter have been used interchangeably resulting in confusion regarding definition and mechanism. It is recommended by some authors that atrial flutter be classified into the 'typical' and 'atypical' (which may also be termed 'type 1' and 'type 2' by other investigators)'131. Typical atrial flutter can further be sub-classified into a counterclockwise' type, which is the more commonly observed, and a rarer 'clockwise' type. It is beyond the scope of this article to describe in detail the electrophysiological mechanisms of the atrial arrhythmias and the considerable investigation that has explained them. However, a brief explanation will follow since their anatomical details and appearance of the surface ECG relate closely to their mechanisms. There is considerable evidence that typical (or type 1) atrial flutter results from a single re-entrant circuit in the right atrium. Lewis's original concept of a re-entrant circuit including the superior and inferior venae cavae as part of a central area of block'141 was taken further by Rosenblueth and Garcia-Ramos who created a crush lesion between the two cavae creating a single obstruction to conduction'151. Frame extended this lesion to the right atrial appendage thus creating a 'Y' shaped incision. It was noted that the arrhythmia became more stable and a re-entrant circuit around the tricuspid annulus was mapped'161. Boineau and coworkers ligated and compressed the crista terminalis, creating an area of slow conduction, and subsequently induced atrial repetitive activity similar to atrial flutter'17'. Waldo and co-workers developed the concept of

entrainment which was then used in studies of atrial flutter, confirming their re-entrant nature and providing evidence that an area of slow conduction existed in the region of the triangle of Koch between the inferior vena cava, coronary sinus os, and tricuspid annulus'181. Thus atrial flutter is caused by a macro re-entrant circuit with areas of anatomical and functional block (although the relative contribution of each in any particular patient is not clear). Recent observations in humans with typical atrial flutter using activation and entrainment mapping, guided by intracardiac echocardiography, have confirmed re-entry as being its mechanism and have enabled functional electrophysiological properties to be correlated to specific anatomic landmarks'191. In this study, catheters were placed along the crista terminalis, the inter-atrial septum, and into the coronary sinus. A roving catheter was also introduced and the sites chosen for measurement included the anterior and posterior Eustachian ridge, the anterior and posterior crista terminalis, and sites between the Eustachian ridge and tricuspid annulus. All catheter positions were confirmed with both fluoroscopy and intracardiac ultrasound. Activation maps of the re-entrant circuits were then obtained by measuring conduction times from the coronary sinus os to each recording site. Typical atrial flutter was seen to occur in a counter-clockwise rotation. Part of the flutter circuit was mapped, and it was noted that the free wall of the right atrium was activated from superior to inferior in the trabeculated area anterior to the crista terminalis. This direction of activation accounts for the fact that cases of typical (or type 1) atrial flutter of the counter-clockwise type exhibit 'F' waves on the surface ECG which are negative in the inferior leads. The impulse then travelled to a narrow isthmus of slowly conducting tissue between the Eustachian ridge and tricuspid annulus. The authors identified the crista terminalis and Eustachian ridge as being anatomical barriers (resulting in anisotropic uncoupling and discontinuous conduction) by finding split potentials in these areas and by observing that sites anterior to these structures were activated significantly earlier than sites posterior to them. The atrium in the region of the tricuspid ring contains two layers: one composed of radial fibres, and another of circumferentially arranged fibres'201. Atrial stretch or disease may result in thinning of the circumferential fibres. Thus longitudinal propagation through the corridor between the coronary sinus os and tricuspid ring might encounter radial fibres transverse to its direction, and linear conduction might be impaired resulting in slow conduction and ultimately re-entry'121. Areas of slow conduction, juxtaposed between barriers to conduction, constitute ideal circumstances for re-entry to occur and represent targets for successful catheter based ablative therapy'12'2'1. Some cases of atrial flutter may involve a re-entrant circuit involving the tricuspid annulus solely. The left atrium is activated secondarily in atrial flutter and does not usually appear to be a necessary component of the re-entrant circuit. Eur Heart J, Vol. 18, Suppl C 1997

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

rhythm and varies according to the site of intra-atrial re-entry. Lesh and co-workers noted in their report on radiofrequency catheter ablation of intra-atrial re-entry tachycardia, in which several cases had undergone prior atrial surgery, that scars produced by surgery served as anatomical barriers to conduction around which re-entrant excitation could circulate'121. Atrial tachycardia due to intra-atrial re-entry can be differentiated from that caused by an automatic focus by their initiation by atrial extra-stimuli, and the absence of a 'warm up' phenomenon. It should be stressed that the electrophysiological criteria used for differentiating tachycardias due to re-entry from those due to automatic foci (including initiation and termination by extra-stimuli, manifest and concealed entrainment, and the response to pharmacological intervention) are not uniform amongst investigators and do not always produce consistent results. It is likely, for example, that some cases of atrial tachycardia due to abnormal 'automatic foci' are in fact due to micro re-entry. The distinction between macro re-entrant atrial tachycardia and atypical atrial flutter (see below) is difficult, and is largely due to discrepancies in nomenclature.

C5

C6

O. A. Obel and A. J. Camm

Eur Heart J, Vol. 18, Suppl C 1997

be due to a focal mechanism. Haissaguerre and colleagues have described cases of atrial fibrillation with localised primary mechanisms (one was a focal atrial tachycardia which reproducibly degenerated into atrial fibrillation) and where thus amenable to radiofrequency catheter ablation'281. The more wavelets present, the more likely it is that atrial fibrillation will self-perpetuate. The size of the wavelength determines the number of waves that can circulate through the atrial myocardium with the smallest wavelengths producing the largest number of waves and hence greater stability of the arrhythmia. Tissue mass is an important determinant of the space available for wavelets to circulate, hence larger tissue masses can support more wavelets and, therefore, favour the induction and sustainability of atrial fibrillation'291. Atrial size has been shown to correlate with increased vulnerability to atrial fibrillation in humans'30', and it is well recognized that an enlarged left atrium is a consistent predictor of failure of cardioversion to sinus rhythm. Alterations in microstructure and anisotropic properties of the atrial myocardium can cause inhomogeneous and discontinuous propagation of the impulse. Extensive degenerative changes have been shown to be present in the atria of patients with atrial fibrillation'311, and increasing age is known to be associated with the development of collagenous septa and electrical uncoupling of side-to-side fibre connections'321. There have been several studies in humans examining the electrophysiological substrates responsible which result in atrial vulnerability to atrial fibrillation. Shortening of atrial refractoriness'331, inhomegeneity in atrial refractory periods and slow conduction have been shown to be more common in patients with atrial fibrillation'341. Heterogeneity in both anatomical and electrophysiological properties of the atrium are likely to contribute to the initiation and perpetuation of atrial fibrillation; however, it is not possible to determine which factor is the most influential in any particular patient. Examination of the surface ECG in atrial fibrillation reveals an absence of distinct P wave activity. The baseline consists of largely 'random' low amplitude and variable deflections occurring at a rate of greater than 350 beats. min ~'. The ventricular rate varies according to the conduction properties of the atrioventricular node, with the RR intervals showing no ordered pattern. However, at higher rates the ventricular response may appear to be regular. The QRS complexes are narrow unless bundle branch block, (either rate-related or preexistent) is present. Likewise, if atrial fibrillation is pre-excited, QRS complexes are broad, and of bizarre morphology, the ventricles being stimulated via an antegradely conducting accessory atrioventricular pathway. Recognition of pre-excited atrial fibrillation is of particular importance since if the refractory period of the accessory pathway is sufficiently short, atrial fibrillation may conduct with an extremely rapid ventricular response.

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

Typical atrial flutter can also occur (either spontaneously or as an induced phenomenon) in a clockwise direction with a cycle length and re-entrant circuit similar to that seen in the counter-clockwise rotation. The crista terminalis, Eustachian ridge, and tricuspid annulus act similarly as anatomical barriers to conduction. Most cases of atrial flutter are 'typical' and the re-entrant circuit conducts in a counter-clockwise direction. This pattern is the arrhythmia that most physicians associate with the term 'atrial flutter'. Broad sawtoothed F waves are most often visible as negative deflections in the inferior leads and as positive deflections in lead V, with atrial rates of 240-340 beats. min~1[221. The ventricular response rate varies with the refractory properties of the atrioventricular conducting system, often conducting with 2:1 or 4:1 block; however, the block may vary resulting in an irregular ventricular rate. When the atrial rhythm conducts with 2:1 block, F waves may be obscured by the preceding QRS complex, in which case vagal manoeuvres or the administration of an atrioventricular nodal blocking agent, such as adenosine, will reveal underlying F waves. When the re-entrant circuit conducts in a clockwise direction, the F waves are positive in the inferior leads, and negative in lead V,. Atypical (type 2) atrial flutter occurs at rates of approximately 340-430 beats. min~', and appears as positive deflections in the inferior leads. The mechanism of this type of atrial flutter may be 'leading circle' re-entry'231 in which barriers to conduction tend to be functional rather than fixed anatomical structures. Atrial fibrillation is known to occur frequently in patients with atrial flutter. Alternation of fibrillation and flutter during a 24-h period was documented in 35% of postoperative patients using ambulatory ECG monitoring1241. In the early 1960s, Moe and co-workers1251 developed the so-called 'multiple wavelet hypothesis' using a computer-derived mathematical model. In this model fibrillation is maintained by the presence of a number of wavelets that wander randomly through the atrial myocardium around islets or strands of refractory tissue; the number of wavelets present determine whether 'fine' atrial fibrillation (numerous wavelets) or 'coarse' atrial fibrillation (small number of wavelets) develops. The more wavelets present, the less the likelihood of their simultaneous extinction and, therefore, the less likely that atrial fibrillation will terminate. Allesie and coworkers mapped the spread of excitation during atrial fibrillation in isolated blood-perfused canine atria'261 and confirmed the presence of multiple wandering wavelets. These findings were then validated using high-density epicardial mapping of the free wall of the right atrium in patients with Wolff-Parkinson-White syndrome undergoing surgery for interruption of their accessory pathway, in whom atrial fibrillation was induced using rapid atrial pacing'271. The mechanism of some cases of atrial fibrillation may not be completely random wavelets, but may involve a 'mother' wavelet which gives rise to 'daughter' wavelets. Some cases of atrial fibrillation may

Supraventricular tachycardia: ECG and anatomy

Atrioventricular and atrioventricular nodal re-entrant tachycardia

ttrfrp AVNRT

Sinus rhythm St George's

data

Pseudo r '

No Pseudo s Pseudo r ' (ID (vi)

AVNRT AVRT AT

32 2 0

68 98 100

24 0 0

No Pseudo s (ID 76 100 100

Figure 2 Atrioventricular nodal re-entrant tachycardia: pseudo r' wave. Note that a pseudo r' or pseudo s wave is highly suggestive of atrioventricular nodal re-entrant tachycardia. Comparing the ECG in V, during sinus rhythm and during tachycardia reveals a terminal positive deflection in the QRS complex which easily could be interpreted as an r' wave but is in fact a retrogradely conducted P wave in this case of typical atrioventricular nodal re-entrant tachycardia.

tachycardia), and a 'fast' pathway which is anteriorly situated, possibly in the anterior inter-atrial septum, and which usually has a relatively long refractory period. Whether or not there is a lower common pathway, and whether this pathway exists entirely within the compact atrioventricular node, is still unknown. The surface ECG during atrioventricular nodal re-entrant tachycardia is narrow complex unless bundle branch block is present or there is bystander participation by an accessory pathway. The ventricular myocardium is not part of the re-entrant circuit, and therefore, in contrast to some cases of atrioventricular re-entrant tachycardia, coexistent bundle branch block does not result in a lengthening of the tachycardia cycle length. The heart rate in atrioventricular nodal reentrant tachycardia ranges from 100-250 beats, min" 1 with a mean of approximately 170 beats . min ~'. In its usual form, the re-entrant circuit in atrioventricular nodal re-entrant tachycardia conducts antegradely down the slow pathway and retrogradely up the fast pathway, causing near-simultaneous activation of atria and ventricles (slow/fast atrioventricular nodal re-entrant tachycardia). As a result, the retrograde P wave is partially or fully A recent post-mortem report describes a patient with atrioventricular nodal re-entrant tachycardia who concealed within the QRS complex during tachycardia, (pseudo s in lead died of unrelated causes 5 months after successful slow and when visible appears as a distortion [39] 381 II wave or pseudo r' wave in V,) of the terminal portion pathway ablation' . Histological examination revealed a right atrial lesion 1 • 15 cm from the compact atrioven- of the QRS complex (Fig. 2). De novo slow/fast atrioventricular node which was not damaged by the procedure, tricular nodal re-entrant tachycardia is usually initiated and was separated from the lesion by intervening normal by an atrial premature beat which blocks in the fast pathway and is thus accompanied by a prolongation of atrial tissue. the PR interval. Most investigators would agree that there are at least dual inputs to the atrioventricular node; a posteriIn its uncommon form, atrioventricular nodal orly situated 'slow' pathway, which in most cases has a re-entrant tachycardia circulates in the opposite direcrelatively short refractory period and which may consist tion, i.e. fast/slow atrioventricular nodal re-entrant of insulated fibres entering the region of the atrioven- tachycardia. This occurs when the refractory period of tricular node between the coronary sinus ostium and the the fast pathway has a shorter refractory period than tricuspid annulus (the site usually chosen for catheter the slow pathway; unidirectional block occurs in the ablation of slow/fast atrioventricular nodal re-entrant slow pathway but continues to activate orthodromically Eur Heart J, Vol. 18, Suppl C 1997

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

Atrioventricular nodal re-entrant tachycardia accounts for more than 70% of cases of paroxysmal supraventricular tachycardia. There are three different forms of atrioventricular nodal re-entrant tachycardia; 'slow/fast', 'fast/slow', and 'slow/slow', all requiring dual atrioventricular nodal pathways with different functional properties. The concept of duality of atrioventricular nodal pathways has been questioned by some, since alternative explanations for re-entrant arrhythmias arising from the region of the atrioventricular node exist. For example, Jaliffe has shown that if conduction occurs electronically along an area of block, re-entry can occur in a linear structure'351. Another theoretical mechanism for the presence of re-entry in the absence of atrioventricular nodal duality is non-uniform anisotropy within the complex anatomical structure of the atrioventricular node, which could result in longitudinal dissociation and re-entry. Evidence, such as double responses (2:1) to atrial or ventricular stimuli1361 and the ability to advance atrial echo beats by ventricular extrastimuli delivered simultaneously with slow pathway conduction during 'slow/fast' supraventricular tachycardia'371, strongly suggest that dual pathways displaying distinct electrophysiological properties form the substrate for atrioventricular nodal re-entrant tachycardia. The anatomical details of such a circuit have long been the subject of investigation, and in the age of curative intervention using radiofrequency catheter ablation, the elucidation of these details is of fundamental importance for the optimal management of patients with such arrhythmias. Debate about whether the pathway for atrioventricular nodal re-entrant tachycardia exists entirely within the atrioventricular node or whether the atrium participates in the circuit arises partly from disagreement on the boundaries of the true atrioventricular node. Evidence for an atrial component in the re-entrant circuit includes penetration of an excitable gap during slow/fast atrioventricular nodal re-entrant tachycardia from a site remote from the compact atrioventricular node.

C7

C8

O. A. Obel and A. J. Camm

The location of the accessory pathway determines polarity of the 6 wave. For example left-sided accessory pathways activate the left ventricle early and conduction spreads through the ventricular myocardium, activating the right ventricle aberrantly and producing the initial appearance of right bundle branch block with a broad, slurred upstroke in V,. Several authors have created algorithms for the localization of these pathways using intra-operative and electrophysioEur Heart J, Vol. 18, Suppl C 1997

logical data'40"43'. Pathway location using electrophysiological testing at the time of radiofrequency catheter ablation reveals that 50-60% of pathways are situated in the left free wall, 10-20% occur in the right free wall, 20-30% in a posteroseptal location, and 5-10% in an anteroseptal location'44'451. During orthodromic atrioventricular re-entrant tachycardia the 12-lead ECG usually reveals a narrow QRS complex unless bundle branch block is present. If this is the case, and the bundle branch block is ipsilateral to the accessory pathway, the cycle length of the tachycardia will be longer compared to that during normal ventricular conduction. The P wave occurs after the inscription of the QRS complex, usually within the ST-T segment. However, if the pathway is slowly conducting, the retrograde P wave may occur well after the T wave, close to the ensuing QRS complex. If bundle branch block is present, the P wave may be obscured. The P wave polarity during tachycardia may give some idea of pathway location. For example, a negative P wave in lead I suggests a left atrial insertion of an accessory pathway'46', and positive P waves in the inferior leads during orthodromic tachycardia suggest a posteroseptal accessory pathway. The finding of electrical alternans of the QRS complex during sustained narrow complex tachycardia is almost diagnostic of orthodromic atrioventricular re-entrant tachycardia'471. However, this finding is also present in a small proportion of cases of rapid atrioventricular nodal re-entrant tachycardia. Since QRS alternans occurs at a slower rate during atrioventricular re-entrant tachycardia than during atrioventricular nodal re-entrant tachycardia, QRS alternans at rates less than 210 beats . min ~' is highly suggestive of atrioventricular re-entrant tachycardia. Atrioventricular reentrant tachycardia can never be associated with second or third degree atrioventricular block since continued conduction within the entire atrioventricular nodal complex and His-Purkinje system is required for perpetuation of the arrhythmia (Fig. 3). If observed on an ECG, tachycardia onset will be seen to be sudden, and termination (either spontaneous, vagally mediated, or after administration of an atrioventricular blocking agent such as adenosine) is associated with the presence of a retrograde P wave that is not conducted antegradely via the atrioventricular node to the ventricles. Antidromic atrioventricular re-entrant tachycardia occurs when the ventricle is activated totally by the accessory pathway. Multiple accessory pathways are common in this condition. Retrograde atrial activation may occur via the His-Purkinje and atrioventricular nodal systems or by a second accessory pathway. Antidromic atrioventricular re-entrant tachycardia is facilitated by a large distance between the accessory pathway and the atrioventricular node-His bundle (usually of at least 4 cm)'481, and is therefore rare in association with septal accessory pathways. The QRS complexes are broad but the morphology is not typical of left or right bundle branch block. Atrio-fascicular accessory pathways usually conduct only in an antegrade direction, and are therefore

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

down the fast pathway without an accompanying proloHgation of the PR interval. Retrograde atrial activation conduction via the slow pathway occurs later than ventricular activation with a resultant inverted P wave visible after the QRS complex ('long RP' supraventricular tachycardia). Atrioventricular nodal reentrant tachycardia may be present in the presence of atrioventricular block in either a 2:1 or a Wenckebach fashion. Slow/slow atrioventricular nodal re-entrant tachycardia appears to be rare. Atrioventricular re-entrant tachycardia occurs as a result of propagation through an accessory atrioventricular pathway. Other possibilities include atrio-His, nodo-ventricular, and fasciculo-ventricular pathways. The most common form of tachycardia associated with an accessory atrioventricular pathway is orthodromic atrioventricular re-entrant tachycardia, in which antegrade conduction occurs through the atrioventricular node and His-Purkinje system and retrograde conduction propagates through the accessory ventriculoatrial connection. Less commonly, the direction of conduction is reversed producing antidromic atrioventricular reentrant tachycardia. Most patients with atrioventricular re-entrant tachycardia have no evidence of structural heart disease other than the accessory connections which are thought to be composed of atrial tissue, and which can bridge the atrioventricular groove at any location along the mitral and tricuspid annulus except for the region where the mitral annulus is contiguous with the aorta. The surface ECG appearances during sinus rhythm depend on the location of the pathway, whether it conducts antegradely, in which case the pathway is termed 'manifest', or if it only conducts in a retrograde direction, in which case there will be no evidence of the accessory pathway on the surface ECG during sinus rhythm and it is termed a 'concealed' accessory pathway. Antegradely conducting pathways produce the classical appearance of the Wolff-Parkinson-White syndrome with a short PR interval due to rapid conduction over the bypass tract and a ventricular delta wave due to early and eccentric ventricular activation. The length of the PR interval and degree of pre-excitation depend on the conduction properties of the bypass tract and its site of insertion into the ventricular myocardium. Rapidly conducting pathways activate the ventricles well before depolarisation via the atrioventricular node and HisPurkinje system and hence a greater proportion of the ventricular myocardium will be pre-excited resulting in a short PR (fast conduction) and prominent 6 (delta) wave.

Supraventricular tachycardia: ECG and anatomy

m

70 60 50 40 30 20 10 0

>210 120-150 151-180 181-210 Tachycardia rate (beats.min"1)

Figure 3 Narrow QRS alternans after the first 10 A of tachycardia. S shows the percentage with atrioventricular re-entrant tachycardia (57 pts) and • the percentage with atrioventricular nodal re-entrant tachycardia (89 pts). Note the alternating height of QRS complexes. The finding of QRS alternans is suggestive of atrioventricular re-entrant tachycardia particularly if the heart rate is less than 210 beats . min|471.

Figure 4 Long RP' tachycardia may be caused by (1) atrial tachycardia due to either intra-atrial re-entry or an automatic focus; (2) atypical ('fast-slow') atrioventricular nodal re-entrant tachycardia or (3) atrioventricular reentrant tachycardia with slow retrograde accessory pathway conduction as occurs, for example, in this case of the permanant form of junctional reciprocating tachycardia.

demonstrated multiple accessory pathways in their report on five cases of the permanent form of junctional reciprocating tachycardia15'1. Slow retrograde conduction results in a retrograde P wave that occurs long after the QRS complex. Thus along with focal atrial tachycardia, intra-atrial re-entry, and fast/slow atrioventricular nodal re-entrant tachycardia, the permanent form of junctional reciprocating tachycardia must be considered in the differential diagnosis of 'long RP' tachycardia (Fig. 4).

Conclusions In the era of curative treatment for supraventricular tachycardia, anatomical details of the various substrates which support supraventricular arrhythmias are no longer of pure academic interest, but are fundamental to the optimal management of patients. Many ECG phenomena relate directly to the anatomical pathophysiological substrates which support the supraventricular tachycardias. An understanding of these mechanisms will help physicians to diagnose these arrhythmias correctly and to devise new and effective methods of treatment.

References [1] Anderson RH, Yen Ho S, Becker AE. The surgical anatomy of the conduction system. Thorax 1983; 38: 408-20. [2] Boineau JP, Canava TE, Scheussler RB. Demonstration of a widely distributed atrial pacemaker complex in the human heart. Circulation 1988; 77: 1221. [3] Boineau JP, Schuesler RB, Mooney CR et al. Mutlicentric origin of the atrial depolarisation wave: the pacemaker complex. Circulation 1978; 58: 1036. [4] Anderson RH, Becker AE. Cardiac morphology. In: Julian DG, Camm AJ, Fox KM, Hall RJC, Poole-Wilson PA, eds. Diseases of the Heart. London: W. B. Saunders 1996: 1-18. [5] Spach MS, Miller WT, Geselowitz DB. The discontinuous nature of propagation in normal cardiac muscle: evidence for Eur Heart J, Vol. 18, Suppl C 1997

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

only associated with antidromic circus movement tachycardia. These pathways may also participate as bystanders in other forms of supraventricular tachycardia. The atrial insertion in some of these pathways is close to the tricuspid annulus, either laterally or antero-laterally in the right free wall, and the ventricular insertion site appears to be into the right bundle branch'491. Unlike most atrioventricular accessory pathways, these pathways exhibit decremental properties similar to those of the atrioventricular node, and thus the atrioventricular conduction interval increases with faster or more premature pacing. Nodo-ventricular accessory pathways appear to exist but are thought to be rare. The permanent form of junctional reciprocating tachycardia is a form of orthodromic atrioventricular re-entrant tachycardia with a slowly conducting accessory pathway. These supraventricular tachycardias are almost completely incessant and occur at slower rates than other forms of atrioventricular re-entrant tachycardia, hence patients often do not present with a history of sudden onset of rapid tachycardia. Patients with the arrhythmia are at risk of developing a tachycardiainduced cardiomyopathy and thus may present with a history of exertional dyspnoea or orthopnoea. These arrhythmias have been shown to be caused by retrogradely conducting accessory pathways that characteristically conduct slowly. Critelli and co-workers demonstrated that these pathways are likely to occur in the posterior septal area[50], although they have been described elsewhere. This accounts for the consistent finding that retrograde P wave polarity is negative in the inferior leads during tachycardia. Furthermore, postmortem on a patient with the permanent form of junctional reciprocating tachycardia revealed an anomalous posteroseptal atrioventricular connection that pursued a tortuous path which might explain why these pathways conduct slowly. Shih and co-workers

C9

CIO O. A. Obel and A. J. Camm

Eur Heart J, Vol. 18, Suppl C 1997

of atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology and arrhythmias. Orlando, Florida: Grune & Stratton, 1985: 265-75. [27] Konings K, Kirchhof CJHJ, Smeets JRLM, Wellens HJJ, Penn OC, Allessie MA. High-density mapping of electrically induced atrial fibrillation in humans. Circulation 1994; 89: 1665-80. [28] Haissaguerre M, Marcus FI, Fischer B, Clementy J. Radiofrequency catheter ablation in unusual mechanisms of atrial fibrillation. J Cardiol Electrophys 1994; 5: 743-50. [29] Allessie MA, Rensma PL, Brugada J, Smeets JLRM, Penn O, Kirchhof CJHJ. Pathophysiology of atrial fibrillation. In: Zipes DP, Jalife J. eds. Cardiac electrophysiology: from cell to bedside. Philadelphia: W. B. Saunders 1990: 548-59. [30] Henry WL, Morganroth J, Pearlman AS et al. Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 1976; 53: 273-9. [31] Davies MJ, Pomerance A. Pathology of atrial fibrillation in man. Br Heart J 1972; 34: 520-5. [32] Spach MS, Dolber P. Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic level in human muscle: evidence for electrical uncoupling of side to side fiber connections with increasing age. Circulation Research 1987; 60: 206-19. [33] Michelucci A, Padeletti L, Fradella GA. Atrial refractoriness and spontaneous or induced atrial fibrillation. Acta Cardiologica 1982; 5: 333^4. [34] Cosio FG, Palacios J, Vidal JM, Cocina EG, Gomez-Sanchez MA, Tamargo L. Electrophysiologic studies in atrial fibrillation. Slow conduction of premature impulses: a possible manifestation of the background for reentry. Am J Cardiol 1983; 51: 122-30. [35] Jaliffe J. The sucrose gap preparation as a model of AV nodal transmission: Are dual pathways necessary for reciprocation and AV nodal 'echoes'? PACE 1983; 6: 1106. [36] Lin FC, Yeh SJ, Wu D. Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways. J Am Coll Cardiol 1985; 5: 168. [37] Wu D, Denes P, Wyndham C, Amat-y-Leon F, Dhingra RC, Rosen KM. Demonstration of dual atrioventricular nodal pathways utilising a ventricular extrastimulus in patients with atrioventricular nodal reentrant paroxysmal tachycardia. Circulation 1975; 52: 789. [38] Olgin JE, Ursell P, Kao AK, Lesh MD. Pathological findings following slow pathway ablation for AV nodal reentrant tachycardia. J Cardiovasc Electrophysiol 1996; 7: 625-31. [39] Kalbfleisch SJ. el-Atassi R. Calkins H. Langberg JJ. Morady F. Differentiation of paroxysmal narrow complex tachycardias using the 12-lead electrocardiogram. J Am Coll Cardiol 1993; 21: 85-9. [40] Tonkin AM, Wagner GS, Gallagher JJ, Cope GD, Kasell J, Wallace AG. Initial forces of ventricular depolarization in the Wolf-Parkinson-White Syndrome. Analysis based upon localization of the accessory pathway by epicardial mapping. Circulation 1975; 52: 1030-6. [41] Gallagher JJ, Pritchett EL, Sealy WC, Kasell J, Wallace AG. The preexcitation syndromes. [Review] Prog Cardiovas Dis 1978; 20: 285-327. [42] Milstein S, Sharma AD, Guiraudon GM, Klein GJ. An algorithm for the electrocardiographic localization of accessory pathways in the Wolff-Parkinson-White syndrome. PACE 1987; 10: 555-63. [43] Fitzpatrick AP. Gonzales RP. Lesh MD. Modin GW. Lee RJ. Scheinman MM. New algorithm for the localization of accessory atrioventricular connections using a baseline electrocardiogram. J Am Coll Cardiol 1994; 23: 107-16. [44] Jackman WM, Wang XZ, Friday KJ et al. Catheter ablation of accessory atrioventricular pathways (Wolff-ParkinsonWhite syndrome) by radiofrequency current. N Engl J Med 1991; 324: 1605-11. [45] Lesh MD, Van Hare GF, Schamp DJ et al. Curative percutaneous catheter ablation using radiofrequency energy for

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

recurrent discontinuities of intracellular resistance that affect membrane currents. Circ Res 1981; 48: 39^45. [6] Spach MS, Miller WT Jr, Dolber PC et al. The functional role of structural complexities in the propagation of depolarization in the atrium of the dog. Cardiac conduction disturbances due to discontinuities of effective axial resistivity. Circ Res 1982; 50: 175-91. [7] Billette J, Shrier A. Atrioventricular nodal activation and functional properties. In: Zipes DF, Jalife J, eds. Cardiac electrophysiology — from cell to bedside. London: W. B. Saunders 1995: 216-28. [8] Wellens HJJ, Durrer D. Supraventricular tachycardia with left aberrant conduction due to invasion into the left bundle. Circulation 1968; 38: 474-81. [9] Ward DE, Camm AJ. Atrial Tachycardias. In: Ward DE, Camm AJ, eds. Clinical Electrophysiology of the heart. London: Edward Arnold 1987: 150-72. [10] Tang CW, Scheinman MM, Van Hare GF et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol 1995; 26: 1315-24. [11] Wellens HJJ, Brugada P. Mechanisms of supraventricular tachycardia. Am J Cardiol 1988; 62: 10D-15D. [12] Lesh MD, Van Hare GF, Epstein LM et al. Radiofrequency catheter ablation of atrial arrhythmias — results and mechanisms. Circulation 1994; 89: 1074-89. [13] Lesh MD, Kalman JM. To 'fumble flutter' or tackle tach'? Toward updated classifiers for atrial tachyarrhythmias. J Cardiovasc Electrophysiol 1996; 7: 460-6. [14] Lewis T, Feil HS, Stroud WD. Observations upon flutter and fibrillation. II Nature of auricular flutter. Heart 1920; 7: 191. [15] Rosenblueth A, Garcia Ramos J. Studies on flutter and fibrillation. II The influence of obstacles on experimental auricular flutter. Am Heart J 1947; 33: 677. [16] Frame LH, Page RL, Hoffman BF. Atrial reentry around an anatomic barrier with a partially refractory exitable gap-a canine model of atrial flutter. Circ Res 1986; 58: 495-511. [17] Boineau JP, Wylds AC, Autry LJ, Schuessler RB, Miller CB. Mechanisms of atrial flutter as determined from spontaneous and experimental models. In: Josephson ME, Wellens HJJ, eds. Tachycardias: mechanisms, diagnosis, treatment. Philadelphia: Lea & Febiger 1984: 91-111. [18] Waldo AL, Henthorn RW, Plumb VJ. Atrialflutter-recentobservations in man. In: Josephson ME, Wellens HJJ, eds. Tachycardias: mechanisms, diagnosis, treatment. Philadelphia: Lea & Febiger, 1984: 113-135. [19] Olgin JE, Kalman JM, Fitzpatrick AP, Lesh MD. Role of right atrial endocardial structures as barriers to conduction during human type I atrial flutter. Circulation 1995; 92: 1839-48. [20] Racker DK, Ursell PC, Hoffman BF. Anatomy of the tricuspid annulus: circumferential muscle fibres as structural basis for atrial flutter in a canine model. Circulation 1991; 84: 841-51. [21] Feld GK, Fleck RP, Chen P et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation 1992; 86: 123340. [22] Wells JLJ, Maclean WAH, James TN, Waldo AL. Characterization of atrial flutter. Studies in man after open heart surgery usingfixedatrial electrodes. Circulation 1979; 60: 665-73. [23] Cosio FG, Goicolea A, Lopez Gil M, Arribas F, Barroso JL, Chicote R. Atrial endocardial mapping in the rare form of atrial flutter. Am J Cardiol 1990; 66: 715-20. [24] Tunick PA, McElhinney L, Mitchell T, Kronzon I. The alternation between atrial flutter and atrial fibrillation. Chest 1992; 101: 34-6. [25] Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn Ther 1962; 140: 183-8. [26] Allessie MA, Lammers WJEP, Bonke FIM, Hollen JM. Experimental evaluation of Moe's multiple wavelet hypothesis

Supraventricular tachycardia: ECG and anatomy

accessory pathways in all locations: results in 100 consecutive patients. J Am Coll Cardiol 1992; 19: 1303-9. [46] Puech P, Grolleau R, Cinca J. Reciprocating tachycardia using a latent left sided accessory pathway. Diagnostic approach by conventional ECG. In: Kulbertus HE, ed. Reentrant arrhythmias. Mechanisms and treatment. Baltimore: University Park Press, 1976. [47] Green M, Heddle B, Dassen W et al. Value of QRS alteration determining the site of origin of narrow QRS supraventricular tachycardia. Circulation 1983; 68: 368-73. [48] Bardy GH, Packer DL, German LD et al. Pre-excited reciprocating tachycardias in patients with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation 1984; 70: 377-91.

Cll

[49] Grogin HR, Lee RJ, Kwasman M et al. Radiofrequency catheter ablation of atriofascicular and nodoventricular mahaim tracts. Circulation 1994; 90: 272-81. [50] Critelli J, Gallagher JJ, Monda V, Coltorti F, Scherillo M, Rossi L. Anatomic and electrophysiological substrate of the permanent form of junctional reciprocating tachycardia. J Am Coll Cardiol 1984; 4: 601-10. [5]] shih H, Miles WM, Klein SK, Hubbard JE. Zipes DP. Multip i e accessory pathways in the permanent form of junctional reciprocating tachycardia. Am J Cardiol 1994; 73: 361-7.

Downloaded from eurheartj.oxfordjournals.org by guest on July 21, 2011

Eur Heart J, Vol. 18, Suppl C 1997