Background
In 1912, Walter Garrey of Washington University in St. Louis published several of the basic concepts explaining why, 75 years later, the surgical Maze procedure was successful in ablating atrial fibrillation. This is the frontispiece of that article:
THE NATURE OF FIBRILLARY CONTRACTION OF THE
HEART.- ITS RELATION TO TISSUE
MASS AND FORM
BY WALTER E. GARREY
[From the Physiological Laboratory of Washington University, St. Louis.]
The main features of this work were reported to the St. Louis Medical Science Club, November 12, 1912, and a synopsis appears in the Proceedings of the Society, Interstate medical journal, December, 1912, xix, p. 1081.
Garrey’s seminal studies showed that although atrial fibrillation (AF) could be induced by rapid stimulation at a focal site, the fibrillation continued after the initiating stimulus (triggers) had stopped discharging electrical impulses. Therefore, some mechanism other than the triggering focus had to be sustaining the fibrillation. His studies also showed that when the focal triggering stimulus stopped, the maintenance of AF depended on the availability of a critical mass of myocardium to sustain the fibrillation. Interestingly, Garrey also demonstrated that “fibrillation was impossible in sufficiently narrow strips” and that if the strips of myocardium remained connected to each other by narrow bands of tissue, they would all contract synchronously in response to a regular stimulus.
Garrey’s experiments were contemporaneous with those of GR Mines, who first described reentry as a mechanism for cardiac arrhythmias in an article published posthumously in 1914. Sir Thomas Lewis subsequently used a string galvanometer to record electrical activity directly from the heart. He mapped both normal sinus rhythm and atrial flutter and was the first to show fibrillatory conduction in a dog with atrial flutter and irregular left atrial electrograms. Lewis believed that AF was caused by a single right atrial reentrant circuit with fibrillatory conduction and partial atrioventricular (AV) block. Some 50 years later, Gordon Moe suggested that AF was characterized by multiple and random wandering waves of electrical activity that he called the “multiple wavelet hypothesis” ( Fig. 5.1 ). He then developed a computer model of AF, and his multiple wavelet hypothesis became widely accepted as the electrophysiologic basis of AF. Allessie then published some of the early multi-electrode maps of AF showing the presence of multiple wavelets that he described as a “circus movement” pattern of atrial activation, thus seeming to confirm Moe’s multiple wavelet hypothesis as the mechanism by which AF is sustained.
Moe hypothesized that atrial fibrillation (AF) was caused by “multiple wavelets” propagating randomly throughout both atria, causing them to look like a “bag of worms.” His “multiple wavelet theory” was debunked years ago. It is important to understand that this theory is fundamentally different from the concept that multiple macro-reentrant circuits serve as the drivers of AF. Even some recognized authorities in electrophysiology still do not understand the difference.
(Reproduced from Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn. 1962;140:183–188.)
When we began to use multipoint computerized mapping systems for the study of human AF some 20 years later, it quickly became clear that large areas of the atria activated simultaneously during AF, which was being driven by macro-reentrant circuits in the atria. This finding was in direct contrast to Moe’s computer model that proposed a “random motion” of activation during AF. A fundamental flaw in Moe’s computer model of simulated AF was that specific effective refractory periods (ERPs) were randomly assigned to individual cells in the model. In reality, although the ERPs of cells can be inhomogeneous, they are not random because they do form patterns. Although Moe’s “multiple wavelet theory” has been challenged by numerous other studies, our finding of macro-reentrant drivers and large areas of the atrium being activated passively, simultaneously, and irregularly in human AF unequivocally refuted Moe’s hypothesis.
Although the random multiple wavelet theory has now been thoroughly debunked, confusion still exists some 60 years later regarding the difference between the random multiple wavelet hypothesis and the simultaneous presence of multiple macro-reentrant circuits in the atria that drive atrial flutter and AF. For example, a recent statement suggesting that reentrant circuits “almost never manifest what we call head-tail interaction or circus movement” directly contradicts overwhelming evidence to the contrary. The purveyors of such misconceptions are left with the unenviable task of trying to explain how the Maze procedure can be successful if AF is not sustained by multiple macro-reentrant circuits. Even these respected electrophysiologic experts seem to stumble into incoherent and erroneous preconceived notions such as the following:
“The original MAZE surgical procedure to cure AF was postulated on the basis… that if you made a whole bunch of incisions in the atria they would heal the fibrosis, and these multiple reentrant wavelets couldn’t conduct through the fibrosis so they would stop. When the MAZE procedure had some success [some?], they thought it was indirect confirmation of this theory.”
They go on to hypothesize that the reason the Maze procedure works is simply because it includes pulmonary vein isolation (PVI) as a part of every procedure. This is precisely the type of misunderstanding of how AF is sustained that has resulted in the persistent practice of performing PVI alone in patients with long-standing persistent AF, the large majority of whom will not benefit from the procedure.
The only available experimental models of AF before 1980 consisted of Langendorf perfusion models with excised animal atria, simulated computer models, or the topical application of the irritant Aconitine to the atrium to make it fibrillate. We decided to develop a more clinically relevant animal model of AF in which under sterile operative conditions, a high-fidelity Millar pressure catheter and a Cope biopsy needle were passed into the left atrium through a pursestring suture placed in the extrapericardial portion of the left superior pulmonary vein ( Fig. 5.2 ). This extrapericardial approach specifically avoided the pericardial space in order to preclude the later formation of pericardial adhesions that could theoretically affect the characteristics of AF. In addition, it avoided the necessity of placing incisions in the atria for the same reason. The biopsy needle was used to transect the chordae tendineae of the mitral valve sequentially until the left atrial pressure increased from its normal levels of 2 to 3 mm Hg to above 20 mm Hg, and then both the Millar catheter and the biopsy device were removed. The dogs were allowed to recuperate from surgery, and over the ensuing 3 months to 3 years, the left atrium enlarged from the mitral regurgitation as expected. AF was then easily induced with a single premature beat, and it was usually sustained indefinitely thereafter.
Animal model of atrial fibrillation (AF). Mitral valve regurgitation was created by transecting the chordae tendineae until the left atrial pressure exceeded 20 mm Hg. The pericardium was not entered to preclude pericardial adhesions, and no scars were placed on or in the left atrium. After left atrial enlargement occurred at least 3 months later, AF could be easily induced by simple atrial pacing. This was a more clinically relevant model in which to study AF than previous animal models that used such artificial stimulants as topical aconitine and/or hyperstimulation of the vagus nerves.
Between 1980 and 1983, the atria could be mapped only with analogue systems that were inadequate to perform global mapping of the atria. However, in 1983, a computerized mapping system was developed by Frank Witkowski and Peter Corr ( Fig. 5.3 , upper panel ) that allowed multiple atrial electrodes to be recorded simultaneously. This provided a means of performing multipoint digital global mapping of both atrial flutter ( Fig. 5.4 ) and AF ( Fig. 5.5 ) for the first time in humans. It soon became possible to reconstruct the atria in three dimensions using gated magnetic resonance imaging (MRI) scans, a method developed specifically for this purpose by Michael Vanier at the Mallinckrodt Institute of Radiology at Washington University in St. Louis (see Fig. 5.3 ). John Boineau and Richard Schuessler ( Fig. 5.6 ), had already developed a three-dimensional (3D) electrode array with 256 bipolar electrodes for experimental 3D atrial mapping. Barry Branham (see Fig. 5.3 and Fig. 1.14 ), a computer scientist working in our laboratory, developed a computer program that allowed the 3D maps to be superimposed on the MRI-reconstructed 3D atrial anatomy that for the first time ever, provided anatomically accurate 3D maps of AF in animals ( Fig. 5.7 ) (Video 5.1). Boineau and Schuessler then developed electrode arrays with 156 bipolar electrodes that form fit the epicardial surfaces of the atria in patients undergoing surgery for Wolff-Parkinson-White (WPW) syndrome, 30% of whom had associated AF ( Fig. 5.8 ). Now, for the first time ever, human AF could be mapped in three dimensions.Over the ensuing years and with the cooperation of clinical electrophysiologists Michael Cain and Bruce Lindsay ( Fig. 5.9 ), AF was routinely mapped three dimensionally using the multi-point computerized mapping system in the operating room and studied extensively in hundreds of patients.
Drs. Frank Witkowski (top left) and Peter Corr (top right) built the first multipoint computerized mapping system for humans that originally recorded data from 58 individual bipolar electrodes simultaneously and stored on a digital tape recorder. The system was later expanded to 256 channels. Dr. Michael Vanier (bottom left) developed the first three-dimensional (3D) reconstructions of the atria using “stacked” electrocardiography-gated magnetic resonance imaging scans. Barry Branham (bottom right) developed computer programs that allowed the recorded 3D electrical maps to be superimposed on the 3D atrial anatomy of the specific animal being mapped so that the first accurate anatomic-electrophysiologic maps of atrial fibrillation could be studied in animals.
Human atrial flutter. This is the first multipoint computerized activation-time map of human atrial flutter ever constructed. A total of 156 bipolar electrodes were imbedded into three silastic electrode plaques designed to form fit on the epicardial surfaces of both atria. The map shows a large macro-reentrant circuit in the right atrium rotating around a linear area of functional conduction block in the crista terminalis (gray zone). The cycle length of this macro-reentrant driver (“flutter wave”) is precisely 200 ms, meaning that electrical activity spins around the circuit five times per second (1000 ms) or 300 times per minute. Thus the atrial rate during atrial flutter is 300 beats/min (beats/min). (See text for further discussion.) SVC, Superior vena cava.
Human atrial fibrillation (AF). This is the first multipoint computerized activation-time map of human AF ever constructed. The posterior and anterior surfaces of the atria are displayed as if the atria had been opened in the midsagittal plane and the anterior surface had been reflected upwards. A total of 156 bipolar electrodes were imbedded into three electrode plaques designed to form fit on the epicardial surfaces of both atria (see Fig. 5.10 ). The map shows the presence of multiple macro-reentrant circuits involving both atria (red arrows). No atrial septal data were available because there were no septal electrodes in place. However, septal activity can be deduced from the pattern and timing of wavefront activation in the other areas of the atria. LAA
LAA, Left atrial appendage; M, mitral Valve; PV, pulmonary vein; RAA, right atrial appendage; T, tricuspid valve.
Drs. John Boineau (left) and Richard Schuessler (right) were the first to map experimental atrial fibrillation (AF) in three dimensions. They developed special “target” bipolar electrode arrays for the study of anatomically accurate three-dimensional (3D) video maps of AF. Each bipolar electrode was constructed like a target with the anode in the center surrounded by the cathode. This eliminated any effect on the local bipolar electrogram that might be caused by the direction of the wavefront being recorded. They then studied the 3D video maps of AF and documented that AF is “driven” by at least two macro-reentrant circuits in the atria simultaneously.
Left panel: Silastic endocardial electrode arrays developed by Boineau and Schuessler that form fit inside canine atria during atrial fibrillation (AF). Right panel: Multiple snapshots from a three-dimensional video of canine AF recorded in early 1987. The ability to visualize such video maps of AF left no doubt that the underlying mechanism of AF was macro-reentry. IVC, Inferior vena cava; LAA, left atrial appendage; LPV, left pulmonary vein; MV, mitral valve; RAA, right atrial appendage; RPV, right pulmonary vein; SVC, superior vena cava; TV, tricuspid valve.
Silastic epicardial electrode arrays also developed by Boineau and Schuessler for mapping human atrial fibrillation (left upper panel). The form-fitting electrode arrays were positioned on the exposed epicardial surfaces of both atria as illustrated. IVC, Inferior vena cava; LAA, left atrial appendage; LSPV, left superior pulmonary vein; PA, pulmonary artery; PV, pulmonary vein; RAA, right atrial appendage; SVC, superior vena cava.
Drs. Michael Cain (left) and Bruce Lindsay (right) were the first clinical electrophysiologists to map human atrial fibrillation (AF) using a digital computer system developed by Witkowski, Corr, and Branham and using epicardial electrode arrays developed by Boineau and Schuessler. With Barnes Hospital institutional review board approval, patients undergoing surgery for Wolff-Parkinson-White syndrome who also had a history of AF (∼30%) were the subjects for mapping. The three silastic electrode arrays shown in Fig. 5.8 were sutured to the exposed epicardial surfaces of both atria, and AF was induced by atrial pacing. Several seconds of AF were recorded for later analysis.
Our experimental and clinical studies confirmed by direct measurement that after initiation , AF maintenance depends on the presence of two or more active macro-reentrant circuits (drivers) in the atria simultaneously ( Fig. 5.10 ). , The Maze procedure was conceived in 1987 on the basis that in order for macro-reentrant circuits to develop, a relatively large area of the atrium must be available to support the macro-reentrant circuit and that there was a relationship between the local conduction velocity, refractory period, and area of atrium available to participate in the macro-reentry. That concept was documented again in 2005 ( Fig. 5.11 ), and the relationship between the area of atrium available and the local atrial refractory period was further confirmed in 2013 ( Fig. 5.12 ). These fundamental anatomic-electrophysiologic characteristics of AF are not only consistent with the reentry concept of atrial arrhythmias described in Chapter 4 , but they also confirm that once initiated, AF is sustained by macro-reentrant drivers, not by focal triggers.
Every map recorded of either experimental or human atrial fibrillation using the computerized three-dimensional mapping system showed the presence of two or more macro-reentrant circuits in the atria (red circles). The macro-reentrant circuits typically rotated around anatomic structures where there was no electrical activity (anatomic orifices of the pulmonary veins or vena cavae or around areas of functional conduction block such as along the crista terminalis; see Fig. 5.4).
(Reproduced from Schuessler RB, Grayson TM, Bromberg BI, Cox JL, Boineau JP. Cholinergically mediated tachyarrhythmias induced by a single extrastimulus in the isolated canine right atrium. Circ Res . 1992;71;1254–1267.)
Upper Panel: Under experimental conditions, atrial fibrillation (AF) was induced by atrial pacing in isolated canine atria. The area of each isolated segment was measured as was the effective refractory period (ERP) of the local myocardium in each segment. The atrium was then divided into sequentially smaller isolated segments and the area and ERP were measured after each segmentation. Lower Panel: Eventually, the relationship between the atrial segment size and its local ERP would no longer support AF. The graph shows that shorter ERPs promote the development of AF.
(Reproduced from Byrd GD, Prasad SM, Ripplinger CM, et al. Importance of geometry and refractory period in sustaining atrial fibrillation: testing the critical mass hypothesis. Circulation. 2005;112(9):I-7–I-13.)
The relationship between the local effective refractory period (ERP), the area of atrium available to support atrial fibrillation (AF), and the probability of developing AF. Both short ERPs and large areas of available atrium promote the maintenance of AF. These anatomic-electrophysiologic data document that although episodes of AF are usually induced by focal atrial triggers, they are not sustained by focal atrial triggers.
(Reproduced from Byrd GD, Prasad SM, Ripplinger CM, et al. Importance of geometry and refractory period in sustaining atrial fibrillation: testing the critical mass hypothesis. Circulation. 2005;112(9):I-7–I-13.)
It was at this point that we realized we needed to crystallize our understanding of the relationship between the electrophysiology and atrial anatomy pertinent to AF. We leaned on the wisdom of one of our pediatric cardiology predecessors, Dr. Helen Tausig, to do so by turning to her experience during the development of congenital heart surgery.
Clarification and Simplification of the Anatomic-Electrophysiologic Relationships in Atrial Fibrillation
In the 1950s, the renowned pediatric cardiologist at Johns Hopkins University Dr. Helen Taussig developed an elegant and simple method to explain the various congenital heart anomalies so that their basic anatomy and pathophysiology could be better understood. She sketched the abnormal anatomy of each congenital heart anomaly and then superimposed the disrupted physiology of each anomaly onto the anatomic diagram. We used similar simplistic anatomic diagrams to represent the anatomy of the atria and then superimposed the observed electrophysiology on that schematic anatomy. We started with a simple box as a two-dimensional representation of the atria, arbitrarily designating one side of the box as the right atrium and the other as the left atrium with the atrial septum lying between the two ( Fig. 5.13 ). “Atrial appendages” were added to both the right and left atrium, and the large “holes” in the right atrium caused by the superior vena cava (SVC) and inferior vena cava (IVC) orifices were illustrated as well. The four pulmonary veins were represented as a contiguous box within the left atrium. At the “top” of the atrial septum was the sinoatrial (SA) node, and at its bottom was the AV node, which tapered into the bundle of His, the bundle branches, and the ventricular myocardium.
Two-dimensional schematic representation of atrial anatomy that is pertinent to understanding the mechanisms of atrial flutter and atrial fibrillation. (See text for further discussion.) AV, Atrioventricular; IVC, inferior vena cava; LAA, left atrial appendage; PV, pulmonary vein; RAA, right atrial appendage; SA, sinoatrial.
(Reproduced from Cox JL, Schuessler RB, D’Agostino HJ Jr, et al. The surgical treatment of atrial fibrillation: III. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg. 1991;101:569–583.)
Normal Sinus Rhythm
The SA node and perinodal right atrial tissue is the “driver” for normal sinus rhythm because this is where each electrical impulse usually originates ( Fig. 5.14 ). The SA node, normally fires regularly and the impulse is conducted away from the SA node passively to the rest of the atrial myocardium. If the driver fires once per second (i.e., every 1000 ms), the atrial heart rate will be 60 beats/min. After the SA node driver fires, both atria are subsequently activated by passive conduction of the sinus impulse away from the SA node across both atria. Conduction from the SA node, located near the top of the right atrium, to the top of the left atrium occurs quickly because of rapid conduction across Bachmann’s bundle (see Chapter 3 ). The wavefront propagates passively across both atria and down the atrial septum until it reaches the AV groove, where it is blocked everywhere except at the site of the AV node–His bundle complex. This coordinated activation of the atria gives rise to a normal “p-wave” on the standard electrocardiogram (ECG). The impulse is normally delayed approximately 100 ms (0.1 s) in the AV node and is then conducted rapidly down the His bundle, bundle branches, and Purkinje system to the ventricular myocardium. Assuming that the conduction through the AV node is stable, a ventricular response will follow each sinus beat. Activation of the ventricle results in a regular QRS complex after each P wave on the standard ECG. Thus the ventricular rate (“heart rate”) depends on the rate at which the SA node driver is firing.
Electrical activation of the atria during normal sinus rhythm (NSR) is superimposed on the two-dimensional anatomic diagram of the atria. NSR is driven by an impulse that arises spontaneously in the sinoatrial (SA) node and is passively conducted to the rest of the atrial myocardium. The impulse is then delayed 100 ms in the atrioventricular node and passes into the ventricles, which are also passively activated. The regularity of impulse generation in the SA node, in this case at a rate of 60 beats/min (cycle length of 1000 ms, or 1 s), results in a regular p-wave and QRS complex on the standard electrocardiogram. AV, Atrioventricular; LAA, left atrial appendage; RAA, right atrial appendage.
(Modified and reproduced from Cox JL, Schuessler RB, D’Agostino HJ Jr, et al. The surgical treatment of atrial fibrillation: III. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg. 1991;101:569–583.)
Atrial Flutter
The anatomic-electrophysiologic basis of atrial flutter can also be described by superimposing its observed electrophysiology on the same anatomic diagram of the atria ( Fig. 5.15 ). However, the driver during atrial flutter is not the SA node; rather, it is a single large macro-reentrant circuit (the so-called “flutter wave”) that resides in the right atrium (see Fig. 5.4 ). This is a large macro-reentrant circuit because the refractory periods in the right atrium are relatively long (see Chapter 4 ). In fact, a normal right atrium is capable of harboring only this single macro-reentrant circuit because of the long refractory periods and the area of the right atrium available to participate in the reentrant circuit. The flutter wave is particularly stable because it has a large excitable gap, so changes in the ERP caused by variations in the autonomic tone do not affect the anatomic circuit or the time it takes to travel around it (see Chapter 4 ). The flutter wave (of which there are three possible locations) always uses the cavotricuspid isthmus (CTI) between the orifice of the IVC and the tricuspid valve, which explains why a CTI lesion is so successful for the treatment of atrial flutter.
Atrial flutter is driven by a large macro-reentrant circuit in the right atrium called the “flutter wave.” It takes 200 ms for the electrical impulse to complete one cycle around this macro-reentrant circuit (“cycle length”), meaning that the impulse completes 5 cycles per second (1000 ms/200 ms) or 300 cycles per minute (5 cycles/second × 60 seconds). The electrical impulse exits the cycle with each circumvention and is conducted passively to the rest of the atrial myocardium, resulting in a regular atrial rate of 300 beats/min. Each of the 300 passively conducted atrial impulses enters the atrioventricular (AV) node, which is incapable of conducting activity at that high rate. Thus every other atrial impulse (rate, 300 beats/min) is blocked in the AV node, allowing 150 impulses to reach the ventricles. This electrophysiology results in a peripheral electrocardiogram that shows a regular p-wave at 300 beats/min and a regular QRS complex at 150 beats/min. LAA, Left atrial appendage; RAA, right atrial appendage.
Electrical activity during atrial flutter typically completes one trip around the circumference of this flutter wave every 200 ms, which is called the “cycle length” of the macro-reentrant circuit. One complete cycle every 200 ms is 5 cycles per second or 300 cycles per minute. With each trip around the macro-reentrant flutter-wave circuit, electrical activity exits the main circuit to activate the remainder of the atrium passively (see Chapter 4 ). Therefore, the atria are activated 300 times per minute during atrial flutter by this single macro-reentrant driver in the right atrium. Activation of the atrial myocardium outside the driver occurs by passive atrial conduction just as it does during sinus rhythm. Each coordinated activation of the atria causes a p-wave on the ECG, so the classic ECG characteristic of atrial flutter is a clear and discernible p-wave that occurs regularly at 300 times per minute.
The AV node is normally incapable of conducting 300 impulses per minute, so when the passive wavefront reaches the AV node 300 times per minute, every second impulse is blocked, resulting in only 150 impulses reaching the ventricles per minute. Because the passive atrial wavefronts are reaching the AV node on a regular basis of 300 beats/min and because the 2:1 AV nodal block is stable, the ventricular response to atrial flutter is regular at a ventricular rate of 150 beats/min. Thus the ECG during classic atrial flutter shows a regular p-wave at 300 beats/min and a regular ventricular rate of 150 beats/min.
Atrial Fibrillation
The electrophysiologic events that take place during AF are more complex but can be understood using the same anatomic-electrophysiologic framework as described for normal sinus rhythm and atrial flutter. Although there is general agreement that individual episodes of AF are induced by triggers in the atria, usually in or around the pulmonary vein orifices (see below), there is considerable controversy over what sustains AF after it has been induced. However, our studies clearly show that the drivers that sustain AF are the self-sustaining macro-reentrant circuits themselves. Just as atrial flutter is sustained by a single self-perpetuating macro-reentrant circuit in the right atrium (see Figs. 5.4 and 5.15 ), AF is sustained by multiple self-sustaining macro-reentrant circuits that are usually, but not always, located in the left atrium ( Fig. 5.16 ).
Atrial fibrillation (AF) is typically driven by multiple macro-reentrant circuits, most of which are in the left atrium. Each of these macro-reentrant circuits acts as an individual driver because of natural “exit sites” in each circuit. All other electrical activity in the atria is passive. The passive atrial conduction of each of these impulses results in the inability to activate the atria in a regular, uniform fashion because of colliding wavefronts coming from each of the macro-reentrant circuits and the persistence of the circuits themselves. Although activation of the atria during AF at times appears to be chaotic, it is simply a case of the local atrial myocardium responding normally by passively conducting the repeated electrical impulses generated by the macro-reentrant circuits.
Because the multiple drivers cause disorganized passive atrial conduction in both atria, the ECG records a p-wave that, if present at all, is irregularly irregular and has a varying morphology. As a result of the irregular manner in which the passive wavefronts strike the AV node, the conduction through the AV node to the ventricles is also irregularly irregular ( Fig. 5.17 ). The maximum rate at which these irregular impulses can be conducted through a normal AV node is approximately 150 per minute. Thus the ECG will show an irregular p-wave of varying morphology and an irregularly irregular QRS complex, the classic ECG findings of AF. It seems apparent that AF is an arrhythmia that is most commonly sustained by atrial macro-reentrant drivers that result in multiple wavefronts that are conducted passively to the rest of the atrium. Because 70% of these macro-reentrant drivers are located in the left atrium, the right atrium is usually activated passively in a random fashion. Theoretically, such random activation of the right atrium can induce a stable right atrial flutter wave so that the left atrium is fibrillating and the right atrium is in a regular atrial flutter that can be induced in the right atrium by the AF in the left atrium ( Fig. 5.18 ). In the latter case, the right atrial flutter wave remains passive and is not a “driver” of AF. Obviously, if the AF is being “driven” by multiple left atrial macro-reentrant circuits, it would be essential to ablate or interrupt those circuits to cure AF. There are other instances in which the primary problem may be right atrial flutter that can induce left atrial macro-reentry circuits so that the latter are passive. If the right atrial flutter wave were the primary “driver” of the AF, an exceedingly rare event, simple interruption of the right atrial flutter wave would eliminate the AF.
Atrial fibrillation. Because of the competing macro-reentrant drivers, the atrial myocardium is activated non-synchronously in an irregularly irregular fashion. This results in an irregular or imperceptible p-wave and an irregularly irregular QRS complex on the electrocardiogram, and the atria are correctly diagnosed to be fibrillating. AV, Atrioventricular; LAA, left atrial appendage; RAA, right atrial appendage.
In instances when the right atrium is completely normal, the disorganized impulses coming from left atrial reentrant circuits may be more organized when it reaches the right atrium. This can result in the development of a stable macro-reentrant circuit in the right atrium (“flutter wave”). The electrocardiogram will still show atrial fibrillation (AF) because there will be an irregular p-wave and QRS complex, but viewed by a surgeon in the operating room, one can see atrial flutter in the right atrium and AF in the left atrium. AV, Atrioventricular; LAA, left atrial appendage; RAA, right atrial appendage.
The Spectrum From Atrial Flutter to Atrial Fibrillation
It is important to recognize that the terms “atrial flutter” and “atrial fibrillation” describe arrhythmias that cause certain abnormalities on the standard ECG. They are descriptive names that have been applied to clinical events that in no way elucidate the electrophysiology that underlies either of them. When these arrhythmias could be mapped in detail, the underlying electrophysiologic events responsible for the ECG abnormalities could be delineated. Thus, it is now possible to understand the electrophysiological events that initiate and sustain the clinical arrhythmias that occupy the spectrum from simple atrial flutter to complex AF.
Classic Atrial Flutter
As explained earlier, there are three components of normal sinus rhythm, atrial flutter and AF: (1) the “driver(s)” of the arrhythmia, (2) passive atrial conduction that occurs as a result of the driver(s), and (3) conduction through the AV node ( Fig. 5.19 ). Slight variations in one or more of these three components result in the clinical arrhythmias that cover the spectrum between simple atrial flutter and complex AF. Classic atrial flutter is caused by a single, stable flutter wave in the right atrium. Unless the left atrium is severely abnormal, the passive atrial conduction that results from a stable right atrial flutter wave will be regular. The stable atrial flutter wave (driver) combined with stable passive atrial conduction to the right and left atria results in a regular p-wave on the standard ECG. Because the flutter wave is also driving impulses into the AV node on a regular basis, if the AV node is normal, it will block every second beat resulting in a regular ventricular response. Thus the ECG will show a regular p-wave (at 300 beats/min) with a 2:1 block resulting in a regular QRS complex (at 150 beats/min), and classic atrial flutter is the correct clinical diagnosis.
Classic atrial flutter. There are three electrophysiologic components of each of the clinical arrhythmias that make up the spectrum from atrial flutter to complex atrial fibrillation: (1) atrial macro-reentrant driver(s), (2) passive atrial conduction, and (3) atrioventricular (AV) node conduction. When the atrial macro-reentrant driver is a single stable circuit in the right atrium (“flutter wave”) and the passive atrial conduction to the right and left atria is stable, atrial activation will be regular, and a regular p-wave will appear on the electrocardiogram (ECG). If AV node conduction is also stable, then the QRS complex on the ECG will occur at half the rate of the p-wave, and the patient will have typical atrial flutter diagnosed on the ECG.
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