A short review of the heart's intrinsic electrical system is useful when considering pathogenesis and therapy of disorders of cardiac impulse formation and transmission. The functions of the conduction system are not only initiation and regulation of rat¸e of the heartbeat but also its coordinated transmission to the entire heart resulting in maximum mechanical efficiency.
Cardiac electrical activity is determined by transmembrane potential -the voltage difference between the intracellular and extracellular environments. This potential difference can only exist because of the selectively permeable cardiac cell membrane, composed of a lipid bilayer in which are situated specialized proteins that allow passage of selected ions at certain times between the intra- and extracellular spaces. Normally, the intracellular compartment has more negative than positive ions and is thus polarized to a negative potential relative to the extracellular space (about 85 to 90 mV for most cardiac cells). Changes in cell membrane potential are due to flow of positively charged ions that may occur directly to and from the extracellular space through specialized “channels” in the membrane or between adjoining cardiac cells through so-called gap junctions. These latter connections are critical for the normal rapid spread of electrical activity throughout the heart.
Each membrane channel is selective for its particular ion (na + , k + , ca 2+ ). How much of each ion passes through its own channel at any time (its current) depends on both voltage and chemical gradients. Resting membrane potential for most cells is determined by potassium current. Following depolarization, the resting potential is restored by an energy-dependent na + -k + exchange pump. Until a certain amount of this repolarization process has been completed (which requires 150 to 250 ms), the cell cannot depolarize again; it is said to be refractory to stimulation. The cell regains full capacity to depolarize once this refractory period is over.
The cellular action potential (AP) is the curve of voltage change over time during depolarization/repolarization of the cardiac cell (Fig. 25-1) . The sodium current is turned on and then off very quickly at the beginning of the action potential; na + thus mediates the rapid upstroke (phase 0) of the AP. Calcium influx occurs slightly later and lasts longer, accounting for the plateau (phase 2) of the AP, and mediates cardiac muscle contraction. These are followed by k + efflux from the cell, leading to repolarization (phase 3) back to the resting membrane potential (phase 4). Cells in which this type of “fast-response” AP is operative comprise most of the heart (atrium, ventricles, His-Purkinje system); other specialized cells (in the sinoatrial and atrioventricular nodes) have “slow-response” APs, in which na + is less important and ca 2+ more important in mediating phase 0.
The heartbeat normally originates in cells of the 5 × 15 mm teardrop-shaped sinoatrial, or sinus, node located in the high lateral right atrium where it adjoins the superior vena cava (embryonic sinus venosus region). Cells in the center of the sinus node have the ability to depolarize spontaneously (phase 4 depolarization), reaching a threshold voltage at which time the cell as a whole is electrically activated. Although cells in other portions of the conduction system are also capable of spontaneous depolarization, their discharge rates are typically slower than that of the sinus node, and thus the heart rate is controlled in most individuals by the sinus node. Impulses spread from the sinus node over the atria, from right to left, top to bottom, completing atrial depolarization in about 80 to 100 ms. This accounts for the morphology of the normal P wave on a standard ECG (upright in leads I, II, and III). Although “bundles” of atrial tissue exist to which some have ascribed enhanced conduction properties (Bachmann's bundle, Thorel's tract, etc.), there are really no specialized interatrial tracts. Rather, particular arrangements of atrial cells, such as those in the crista terminalis, facilitate impulse transmission along their long axis. Congenital defects in the region of the sinus node, such as a sinus venosus atrial septal defect, can be associated with an absence of sinus rhythm per se; instead, subsidiary pacemaker cells from other areas of the atrium control the heartbeat at a rate lower than would be expected in the presence of an intact sinus node. Blood supply to the sinus node is from the right coronary artery in 55 percent of cases and the circumflex branch of the left coronary artery in 45 percent; occlusion of the artery supplying the sinus node can result in significant bradycardia. The sinus node is richly innervated by both sympathetic and parasympathetic fibers and responds with acceleration or deceleration of its intrinsic discharge rate depending on the balance of autonomic tone.
The AV node is situated in the inferomedial right atrium and forms the entrance to the only normal electrical connection between atria and ventricles. Special cells transmit impulses very slowly, requiring 60 to 130 ms to traverse about 1 cm of compact node. The AV node's slowing of the impulse facilitates optimal filling of the ventricles afforded by atrial contraction (since it takes a small but finite amount of time for the blood to be propelled through the AV valves and distend the ventricular walls). This slowing also protects the ventricles to a variable extent from racing in response to rapid atrial arrhythmias (atrial fibrillation) by not allowing all impulses through; it also can fail to let any impulses through and is the most common location of heart block. The AV node is profoundly influenced by autonomic tone, having rich innervation from both the sympathetic and parasympathetic fibers; blood supply is from the right coronary artery in 90 percent of cases and the left circumflex in the rest. Under most clinical circumstances, AV nodal cells do not have the capacity to depolarize spontaneously; so-called nodal rhythms are in fact generated in the infranodal portion of the conduction system (His bundle).
Rapid spread of impulses through the ventricles is mediated by cells of the His-Purkinje system. The AV node terminates in the top of the His bundle, which then branches into a left and right bundle branch; the left bundle branch soon divides again into an anterior and posterior fascicle, and each fascicle further ramifies into the rest of the Purkinje network. This network is situated just beneath the endocardial surface. Conduction is especially rapid through these cells, activating the left side of the interventricular septum, then the apex, and finally the base, from endocardium to epicardium. In this way, ventricular contraction starts at the apex, and blood is propelled efficiently toward the semilunar valves. The entire mass of ventricular myocardium is depolarized in about 80 to 100 ms, the same as in the atria. Blood supply to the His and main bundle branches is almost entirely from the left anterior descending artery; the very proximal His bundle may have a variable right coronary arterial supply. Cells within the HPS are capable of spontaneous depolarization at rates from 30 to 50 beats per minute depending on autonomic tone; consequently, the pacemaker function of these cells is suppressed in the presence of a faster rhythm from the sinus node but may become manifest if extreme sinus bradycardia or AV block occurs.
An electrode catheter placed in the region of the AV node and His bundle can record the His deflection, or potential; the amount of time taken to traverse the AV node is approximated by the AH interval (local atrial deflection to His spike, normally 60 to 125 ms), and the duration of activation of the proximal HPS is reflected in the HV interval (from His spike to QRS onset, normally 40 to 55 ms) (Fig. 25-3) .
Additional atrioventricular connections (aside from the normal AV node-HPS) exist in about 1 to 3 in 1000 individuals. These are generally comprised of fibers of myocardium from 5 to 20 cells thick, histologically indistinguishable from normal atrial or ventricular cells, that traverse the AV groove extrinsic to the valve ring tissue. [4 ] , [5 ] These fibers, present from birth, typically have properties similar to normal myocardial tissue (i.e., rapid conduction) and connect directly between atrium and ventricle-not using the HPS. They can conduct anterogradely (atrium to ventricle), leading to the unusual and characteristic ECG appearance of WPW syndrome (the delta wave), since ventricular depolarization occurs (1) without the usual AV nodal delay and (2) without the rapid spread of impulses mediated by the HPS (Fig. 25-4) . These “bypass tracts” also can conduct retrogradely (ventricle to atrium) and participate in tachycardias (see below). Some bypass tracts cannot conduct anterogradely (from atrium to ventricle) but only in the retrograde direction; these are termed concealed bypass tracts, and although patients with this type of tract have normal PR intervals and QRS complexes in sinus rhythm rather than the characteristic ECG findings of WPW, they are still susceptible to supraventricular tachycardia (SVT) because only retrograde conduction in the bypass tract is necessary for this arrhythmia to occur.
Normal sinus rhythm is defined as a regular rhythm originating in the sinus node with a rate between 60 and 100 beats per minute. However, the use of normal must be interpreted within the context of patient activity. For instance, a heart rate of 70 would be normal for a middle-aged person reading a book but very abnormal in a teenager playing soccer. The maximum rate of discharge of the sinus node (i.e., maximum heart rate) decreases with age following this relation: maximum sinus heart rate = 225 - age in years. Sinus node dysfunction, manifested as inappropriate sinus bradycardia, is a major cause of fatigue, weakness, and syncope in the elderly due to the combination of suboptimal cardiac output and poor vascular compliance. Other manifestations of sinus node dysfunction include the “brady-tachy” syndrome, in which atrial fibrillation or flutter bombards the sinus node with impulses, suppressing its capacity for spontaneous depolarization; when the atrial arrhythmia ceases, the sinus node may be abnormally sluggish in recovering from this suppression and take several seconds to resume functioning. If there is no His bundle (“junctional”) escape beat to support the circulation, syncope can result. Medications that normally slow the sinus discharge rate (beta blockers, ca 2+ blockers) can have dramatically enhanced effects in susceptible individuals.
The cardiac impulse may fail to conduct from one point in the heart to another in one of three ways: delayed conduction (first-degree block), intermittent conduction (second-degree block), and no conduction (third-degree block). These are best illustrated in disorders of atrioventricular (AV) conduction, but the same principles apply to practically all other portions of the conduction system. These types of disordered conduction will first be considered within the AV conduction system and then generalized to other parts of the conduction apparatus.
This is the most common location for clinically important conduction disturbances and serves as a model for conduction abnormalities in other locations within the heart.
This is actually a misnomer, since there is really no “block”; all impulses do get to the ventricles, but with a longer-than-normal PR interval (>200 ms). Accordingly, it is sometimes called “1° AV delay.” The most common location for 1° AVB to occur is within the AV node, correlating with an increased AH interval on intracardiac recordings; in some cases, the HPS is responsible (yielding a long HV interval). Medications (particularly beta and Ca [2 ] + blockers) can slow AV nodal conduction enough to produce 1° AVB within the AV node. Figure 25-6 is an example of 1° AV delay due to prolongations in both the AH (AV node) and HV (HPS) intervals.
The hallmark of 2° AVB is an intermittent, sudden lapse of AV conduction. This takes two forms, named after Mobitz:
Mobitz type I 2° AVB . This is characterized by a gradual increase in the PR interval that eventually leads to a nonconducted P wave, after which conduction resumes for another cycle; most often a 3:2 or 4:3 ratio of P waves to QRS complexes is observed. An additional feature of this type of AVB is that the increment in the PR interval on successive beats gradually decreases, and if the PP interval remains constant, the resulting RR intervals decrease progressively. Usually known as Wenckebach block , this type of AVB is relatively common and is almost always localized to the AV node. Accordingly, it is less serious than block at a lower level, since if condution through the AV node fails entirely, the discharge rate of the subsidiary pacemaker (His bundle) is sufficient to prevent asystole and death.
Mobitz type II 2° AVB . This is manifested as 1:1 AV conduction with a constant PR interval until a P wave suddenly fails to conduct, after which P waves are once again conducted faithfully until another QRS is “dropped.” This type of AVB is less common than type I but more serious; the location of the block is in the HPS, and if conduction fails entirely, the rate of the escape focus (lower HPS) is less reliable and may not support the circulation.
In this disorder, also known as complete heart block (CHB), there is no electrical communication between atria and ventricles; each beats at its own rate (ventricles typically slower, driven by an escape focus in the HPS). The location of the block may be in either the AV node or the HPS. Symptoms are related to the decrease in cardiac output caused by the slow rate; some individuals have relatively rapid escape focus rates (55 to 65 beats per minute) and are largely asymptomatic, while others who have little or no escape rhythm may have syncope or die suddenly when CHB develops.
In addition to abnormal impulse formation, sinus node dysfunction may be manifested by abnormal transmission of the impulse from the sinus node to the surrounding atrium. First-degree sinus exit block cannot be diagnosed from the ECG; it is even difficult to make direct intracardiac recordings from the sinus node itself (in order to observe delayed conduction from it to the atrial muscle). However, 2° sinus exit block is occasionally observed on ECG strips, manifested as either type I 2° sinus exit block (a gradual decrease in the PP interval culminating in lack of a P wave) or type II 2° sinus exit block (constant PP interval followed by sudden absence of a P wave). Complete (3°) sinus exit block would appear as sinus arrest on the ECG, and intracardiac recordings would be necessary to confirm the presence of sinus nodal depolarization without spread to the surrounding atrium. It is important to note that abnormalities of conduction exiting the sinus node may exist independently of other conduction system disease.
Delay or block of the cardiac electrical impulse also can occur in the HPS distal to the His bundle itself. The clinical significance of these disturbances (bundle branch or fascicular blocks) is generally much less than that of block in the AV node or His bundle. Most of the conduction disturbances within this group can be viewed as complete (3°); although delayed conduction can occur in a bundle branch or fascicle, it is very difficult to diagnose and of minimal clinical significance if found. The different types of bundle branch and fascicular blocks are as follows:
This abnormality is characterized by a prolongation of the overall QRS duration to approximately 0.12 s with a tall R wave forming the terminal portion of the QRS in lead V 1 . Other features, such as a prominent terminal S wave in leads I and V 6 , are corroborative. Since ventricular activation during the initial portion of the QRS complex is mediated by the left bundle branch, disturbances of conduction in the RBB have minimal influence on the initial QRS deflection. RBBB is seen in 1.7 percent of standard ECG recordings and of itself has little prognostic importance. (If a terminal small R wave is present in V 1 but the QRS duration is 0.10 to 0.12 s, an incomplete RBBB is diagnosed.)
This type of block is manifested by a prolongation of the overall QRS duration to approximately 0.12 s with a deep S wave forming the terminal portion of the QRS in lead V 1 . Additional helpful features are lack of a Q wave in leads I and V 6 , as well as a delay in the intrinsicoid deflection (initial R-wave development) in V 5 and V 6 ; this occurs because of the dependence of normal initial ventricular activation on impulse propagation in the LBB. Observed in 1.2 percent of routine ECGs, LBBB likewise has a poor correlation with the subsequent development of heart block due to disturbances in other portions of the conducting system.
This relatively uncommon abnormality is diagnosed when the QRS complex is prolonged to approximately 0.12 s, but specific criteria for both LBBB and RBBB are absent. This generally suggests the presence of disordered intramyocardial conduction rather than disease of the main bundle branches. There does not appear to be a significantly increased risk of development of CHB with this disorder.
Also known as left anterior hemiblock , this abnormality consists of interruption of conduction in one of the two branches of the LBB. Because of this, the anterolateral portion of the left ventricular free wall is activated slightly later than normal; the QRS duration, however, is rarely prolonged to a measurable extent. The diagnosis is made largely on the basis of a frontal plane axis of -60 to -90 degrees (marked left axis deviation); additional criteria are presence of a small Q wave in leads I and V 6 , RS waves in leads II, III, and aV F , and the inscription of the peak of the R wave in lead aVL prior to that of lead aVR (corresponding to a counterclockwise direction of the loop inscribed in a vectorcardiogram). This abnormality is observed in an isolated form in up to 1.5 percent of routine ECGs and, like other disorders in this group, has little prognostic value.
This disorder, also known as left posterior hemiblock , is diagnosed based on a frontal plane axis of +120 to +170 degrees (marked right axis deviation) and the presence of a small R wave in lead I with small Q waves in leads II, III, and aVF. The diagnosis is difficult to make because a variety of other disorders can cause a similar degree of right axis deviation (right ventricular hypertrophy, posterior wall infarction); it is likewise rare, occurring in only about 0.3 percent of routine ECGs as an isolated abnormality.
The fascicular blocks can occur in combination with another form of conduction block; for instance, a commonly occurring abnormality is the presence of RBBB plus LAFB. It would seem that in situations like this (with only a single fascicle still conducting), complete heart block would develop in many patients. While there is a slight increase in incidence of CHB in such individuals, it is not high enough to warrant prophylactic implantation of permanent pacemakers. [6 ]
Twenty years ago, only two mechanisms of arrhythmia were recognized: automaticity , in which a cell or group of cells autonomously discharge at an inappropriately rapid rate, and reentry , in which an impulse travels within a circuit in a continuously repetitive fashion. Of these, automaticity was felt to be the predominant cause of clinical arrhythmias; within this construct, an entire group of arrhythmias now recognized as distinct entities was termed paroxysmal atrial tachycardia , with the implication that an automatic focus was responsible for the rapid firing. Subsequent studies in basic science laboratories, as well as in animal models and in humans, have led to the description of subtypes of both these mechanisms of arrhythmia as well as others. These additional mechanisms include triggered activity (two subtypes), postrepolarization refractoriness, boundary currents, and others. This chapter will deal only with the more clinically relevant mechanisms, according to our current understanding.
This mechanism, defined as the spontaneous (unstimulated) discharge of cells once threshold potential has been reached, is responsible for sinus rhythm as well as a variety of rhythm disturbances. At least three subtypes of automaticity exist: normal, enhanced normal, and abnormal ( Fig. 25-7 ). Sinus rhythm is based on normal automaticity; the cells of the sinus node are capable of spontaneous depolarization, which occurs because of progressive decay of the polarized resting membrane potential toward a threshold value (a process known as phase 4 depolarization ). Once this threshold has been reached, a rapid depolarization of the cell can occur, followed by spread of the impulse to adjacent cells and beyond. Enhanced normal automaticity occurs generally when some extrinsic agent modifies the resting membrane potential, the rate of phase 4 depolarization, or both. An example of this is adrenergic stimulation. The final subset, abnormal automaticity, occurs in partially depolarized cells and appears to be a calcium-dependent phenomenon. [7 ] Ischemic myocardial cells may exhibit this mechanism on occasion, but it is likely that clinical arrhythmias related to it are rare.
Supraventricular arrhythmias due to automaticity include ectopic atrial tachycardias and junctional ectopic tachycardia, occasionally observed after valve surgery. Ventricular arrhythmias due to automaticity are rare but probably include some cases of idioventricular rhythm following myocardial infarction and some ventricular tachycardias (VTs) occurring in normal hearts (such as those originating in the right ventricular outflow tract).
Research over the last two decades-much of which was conducted in the operating room-has produced an overwhelming body of information showing reentry to be the most frequent mechanism of arrhythmias in humans, whether supraventricular or ventricular. [8 ] It is thus worthwhile to consider in some detail the essential elements of reentrant arrhythmias in general, which are (1) the presence of a closed loop of electrically excitable tissue, (2) heterogeneity of electrophysiologic properties (conduction velocity and refractoriness), and (3) an initiator to begin the reentrant process. Occasionally, additional factors such as increased adrenergic effect (neural or humoral) are required to facilitate the development of reentry. The prototype for all reentrant arrhythmias is the WPW syndrome ( Fig. 25-8 ). In this condition, an additional strand of normal working myocardium connects atrium to ventricle on the epicardial surface of the AV valve rings. As noted above, the PR interval is short because there is little or no delay of conduction as the electrical impulse traverses the bypass tract (as would normally be encountered in the AV node). The initial portion of the QRS complex, mediated by conduction over the bypass tract, is abnormally wide (the delta wave) because of relatively slow muscle-muscle spread of impulses once activation of the ventricular myocardium begins.
In the absence of a bypass tract (i.e., a normal individual), an impulse beginning in the sinus node spreads through atrial myocardium and penetrates the AV node. Conduction of the impulse slows, allowing the mechanical distension of the ventricles following the atrial contraction, and then rapid spread of the impulse occurs over the HPS starting near the apex and ending at the base. At this point the impulse stops, since there is normally no additional excitable tissue to electrically activate. The presence of the bypass tract provides a complete circuit of electrically excitable tissue, incorporating the atrium, AV node, His bundle, ventricle, and bypass tract. The mere presence of this complete loop does not suffice for reentry to take place, however. One of the other features that also must be present is a disparity between the refractory periods, or duration of inexcitability between two successive beats, of two portions of the circuit. In WPW, this typically takes the form of a longer refractory period in the bypass tract than in the AV node, such that a premature beat in the atrium fails to conduct over the bypass tract but still finds the AV node ready to transmit the impulse (see Fig. 25-8 ). This still does not suffice for reentry to occur; an additional necessary factor is slow conduction, which in this case occurs in the AV node and allows enough time for recovery of excitability in the bypass tract that had been found refractory initially. If the impulse then approaches the bypass tract from the ventricular aspect and the bypass tract can conduct (recovered excitability), the atrium can be activated retrogradely; at this point, the impulse has returned to its point of origin, and a single cycle of reentry has occurred. Assuming the AV node and all other parts of the circuit can again conduct the impulse, a sustained tachycardia (“orthodromic”) can ensue.
Several subtypes of reentry have been described. These are (1) anatomic reentry , in which the impulse circulates around a fixed, anatomically determined path, (2) functional reentry , in which the impulse circulates within a circuit whose size is determined by refractory periods of the participating cells, [9 ] (3) anisotropic reentry , in which both anatomic and functional properties participate in determining the path taken by the circulating wavefront, [10 ] and (4) reflected reentry , in which the impulse retraces its steps along a linear path to return to or reflect on its point of origin. [11 ]
Clinical supraventricular arrhythmias due to reentry include
Orthodromic tachycardia in patients with bypass tracts (mentioned above)
Antidromic reentry in WPW (conduction in the opposite direction using the same circuit, leading to a very wide QRS complex and retrogate conduction over the AV node)
AV nodal reentry (intranodal circuit with “slow” and “fast” pathways)
Some cases of atrial tachycardia
Atrial flutter
Atrial fibrillation (multiple small circuits with changing locations)
Clinically important ventricular arrhythmias due to reentry include
Uniform-morphology VT (each beat looking the same as others) in the setting of prior myocardial infarction, [12 ] cardiomyopathy, arrhythmogenic RV dysplasia, [13 ] or after tetralogy of Fallot repair, [14 ] as well as others
Some cases of polymorphic VT (constantly changing QRS complex)
Ventricular fibrillation (multiple small circuits with changing locations)
This arrhythmia mechanism was well-characterized in laboratory preparations long before evidence of its clinical occurrence was discovered. The important features of this cause of arrhythmia are that a cell or group of cells depolarize normally but during or after the repolarization process, small-amplitude disturbances in the membrane potential are observed (in the direction of depolarization). Since these depolarizations occur following the normal period of cellular depolarization, they are called afterdepolarizations . Two types of afterdepolarizations exist ( Fig. 25-9 ): early (EADs, occurring during repolarization) and delayed (DADs, following complete repolarization). Both EADs and DADs appear to be caused by abnormalities of cellular calcium homeostasis. Evidence indicates that EADs are observed in cells of patients with polymorphic VT associated with a long QT interval (very often as an idiosyncratic consequence of treatment with type IA antiarrhythmic drugs), [15 ] whereas DAD-related arrhythmias appear to include digitalis-toxic atrial, junctional, and ventricular tachycardias, [16 ] as well as perhaps some cases of VT originating in the right ventricular outflow tract in individuals without structural heart disease.
To summarize, reentry, although requiring a complex set of conditions for its initiation and perpetuation, accounts for the majority of arrhythmias observed in humans. Automaticity accounts for a small but important group of tachycardias, and triggered activity in one of its forms is most likely responsible for a scattered variety of arrhythmias. The distinction is of considerable importance in that both automatic and triggered arrhythmias behave as though there is a point source of the abnormal impulses from which all electrical activation originates; the remainder of the heart is merely passively activated. Locating this very small “focus” is essential to successfully eradicate the arrhythmia during surgical or catheter ablation. On the other hand, in a reentrant arrhythmia, large areas of the heart may participate in the circuit, making removal of the entire circuit impractical. Instead, one must locate smaller areas of tissue that are absolutely critical to the maintenance of reentry and target these for ablation. In the case of WPW reentry, for example, complete excision of the circuit would involve removing half the heart, whereas eradicating the bypass tract will cure the arrhythmia but leave the rest of the heart intact. (In principle, dividing the AV node or His bundle also will cure the arrhythmia but will leave the patient pacemaker-dependent and is thus not a satisfactory option.)
Although it is not possible to undertake a detailed review of even the most commonly encountered clinical arrhythmias, important features of some typical varieties are discussed below ( Fig. 25-10 ).
In this disorder, as noted above, a reentrant circuit is present; during the most common form of clinical arrhythmia in these patients (orthodromic SVT), the impulse travels in the normal fashion over the AV node-His bundle, through the ventricles, and then retrogradely over the bypass tract, through the atria, and back to the AV node for another cycle. Impulses less commonly circulate in the opposite (antidromic) direction: down the bypass tract, through the ventricles, up the AV node-His bundle, through the atria, and back to the bypass tract. Patients may have multiple bypass tracts that may participate in various combinations (anterogradely or retrogradely) during SVT episodes.
Once again, a reentrant circuit is present, in this case comprised largely (or, in some cases, wholly) of AV nodal tissue. Patients with this disorder most often manifest the phenomenon of dual AV nodal pathways , denoted by a discontinuity in the curve of AH intervals resulting from delivery of progressively premature atrial extrastimuli. During the common variety of this arrhythmia, impulses proceed toward the His bundle over a very slowly conducting AV nodal pathway (the “slow pathway”) and retrogradely via a faster pathway (that may be intra- or extranodal). It happens that in most cases the time it takes for the impulse to traverse the lower portion of the node and His bundle is very nearly the same as the “fast-pathway” conduction time, such that the P wave during AV nodal reentrant SVT often occurs in the middle of the QRS complex and cannot be seen distinctly on the ECG. As in WPW, the AV nodal circuit can in some patients be reversed, with anterograde conduction proceeding via a “fast pathway” and retrograde conduction proceeding over a “slow pathway.”
Reentry is again the operative mechanism; in the most common variety of atrial flutter, the wavefront appears to circulate in a relatively large circuit comprised of the region of the coronary sinus os (inferior and posteromedial right atrium), the posteromedial right atrial free wall, the right atrium near the junction with the superior vena cava, the posterolateral right atrial wall, and finally, the isthmus of atrial muscle between the tricuspid annulus and the inferior vena caval (IVC) orifice. Some cases may involve revolution of the wavefront around the atrial rim of the tricuspid annulus itself; in either case, the isthmus of atrium between the annulus and the IVC appears to be of critical importance for perpetuation of the arrhythmia. As was the case in other reentrant arrhythmias, the same circuit can be traversed in the opposite direction (“atypical” flutter).
In this example of an automatic arrhythmia, an autonomous focus of perhaps just a few atrial cells discharges independently; although any region of the atria can be responsible, foci of atrial tachycardia seem to be concentrated in several confined areas. These include the pulmonary vein orifices, the mouths of the left and right atrial appendages, and the crista terminalis in the right atrium. These arrhythmias cannot be initiated with pacing or premature impulses, as can reentrant arrhythmias; thus studying them in the electrophysiology (EP) laboratory can be somewhat haphazard, depending on the presence of the arrhythmia at the time of the study. In many cases, however, catecholamine infusion (such as isoproterenol) can facilitate spontaneous tachycardia onset.
Reentry is again responsible for this important arrhythmia, [8 ] which occurs in from 2 to 10 percent of survivors of large myocardial infarctions. The circuit appears to be comprised of surviving sub-endocardial cells at the periphery of the main infarct zone, probably also including some deeper tissues in many cases. [17 ] The length of the circuit is likely 4 to 8 cm in most instances, with the impulse taking a meandering course in many. Although ultimately due to an ischemic basis (postinfarct scar interspersed among residual living fibers), this form of VT does not depend on active ischemia either for its onset or for perpetuation; i.e., periods of ischemia (such as on a stress test or during anxiety) rarely provoke VT episodes, whereas pacing and premature beats reliably do so. Most patients with this type of arrhythmia manifest more than one ECG morphology of VT [18 ] ; whether these different morphologies represent distinct circuits or (as has been noted before) different directions of wavefront propagation within the same circuit is not certain.
A special variety of VT has been described that involves the HPS; this disorder is observed most commonly in patients with dilated cardiomyopathy. In this reentrant arrhythmia, significant disease of the conduction system enables an impulse to travel anterogradely down the RBB, cross the interventricular septum, and travel retrogradely up the LBB and back down the RBB. [19 ] VT in these cases has a LBBB pattern on the ECG, and intracardiac recordings typically show His potentials inscribed prior to each QRS complex. Another hallmark is an HV interval during VT the same or slightly longer than in sinus rhythm. As with most other reentrant arrhythmias, it is possible in rare cases for the wavefront to traverse the same circuit in the opposite direction.