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The ventricular escape rhythm reveals the anatomic site of the block. Taquicardia paroxistica supraventricular pdf download. A ventricular septal defect vsd. La taquicardia ventricular es cuando el nódulo SA ya no controla el latido de los El aleteo o flúter auricular se produce cuando las aurículas laten muy rápido. Descriptor English: Ventricular Flutter. Descriptor Spanish: Aleteo Ventricular. Descriptor Portuguese: Flutter Ventricular. Synonyms English: Ventricular Flutters .

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Is it really that difficult to distinguish between atrial flutter and atrial fibrillation, or is it that electrophysiologists like to complicate the issue?. Strictly speaking, the approach taken in the study could be criticized on the basis of the bias inherent in the selection of the patients, since if patients were selected according to presentation of atrial fibrillation with an “organized electrical pattern” it is not surprising that the variation in the intervals between the electrograms was not indicative of atrial fibrillation in aoeteo group.

The study also lacks quantification of the incidence of such an organized pattern of atrial fibrillation in the right evntricular to allow assessment of the general applicability of the values of sensitivity and specificity calculated based on the study group. However, aside from methodologic questions, which can always be raised, the study addresses an underlying problem that is of major theoretical and practical interest and that can be summarized in the question expressed in the title of this editorial: Surprising as it may seem, there is no simple and accurate electrophysiologic definition of atrial fibrillation.

Atrial fibrillation is also defined in this way in many studies from the electrophysiology literature.

It is true that at least the latest guidelines draw attention to the fact that an irregular ventricular rate is not diagnostic of atrial fibrillation and that atrial flutter can generate this irregularity as a result of irregular atrioventricular conduction patterns.

But, in continuing to focus on the ECG pattern as the only diagnostic criterion of atrial fibrillation, have we not made any progress at all in 35 years?

And to what extent do we understand the underlying causes of this irregular ECG pattern?. Atrial fibrillation has always been considered a reflection of the fragmentation of atrial activation into multiple wavelets of varying width and spread. In the s, it was suggested that there was a focal origin for this activation during atrial fibrillation, implying that the fragmentation of activation would be due to the inability of the atrial myocardium to conduct regularly at very high frequencies 4 Figure 1.

Impulse conduction would encounter refractory and anisotropic regions that would produce functional blocks with a variable spatial distribution, leading to fragmentation of activation into multiple fronts or waves.

This is known as fibrillatory conduction. This hypothesis of the focal origin of atrial fibrillation was soon sidelined by the hypothesis of sustained reentry of multiple wavelets proposed by Moe et al 5 and confirmed in by Allessie et al 6 using advanced atrial endocardial mapping. According to this hypothesis, atrial fibrillation is a chaotic reentry complexly determined with multiple simultaneously active wavefronts Figure 1 that can be sustained indefinitely as long as the preparation or the fibrillating organ is sufficiently large, the refractory period is short and variable dispersion of refractorinessand the conduction velocity is slow.

Allessie et al found that the coexistence of at least 6 activation fronts was necessary in order for atrial fibrillation to be sustained indefinitely.

During mapping of atrial fibrillation, they occasionally observed new activation fronts that indicated the presence of foci, 6,7 but these apparent anomalies were explained as the result of 3-dimensional reentry. Schematic representation of the 3 mechanisms described for atrial fibrillation.

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The endocardial surface is shown through the mitral and tricuspid valves, revealing the openings of the inferior vena cava IVCthe coronary sinus CSand the left pulmonary veins PV. The surfaces colored in orange represent the activation fronts and the arrows indicate the direction in which the wavefront is propagated, with a lighter leading edge and a darker refractory wake.

The grey areas represent lines of functional block. The hatched regions represent anisotropic fiber bundles: A Activation through multiple wavelets, with no localized point of origin, maintained by the dynamics of the activation fronts themselves. B Focal mechanism in which irregular fibrillatory activation has its origin in a high frequency automatic focus yellow star in a pulmonary vein. C Rotor anchored in the region of the left inferior pulmonary vein that drives activation and also produces fibrillatory conduction.

Studies of atrial activation during atrial fibrillation in humans have revealed a notable complexity, making it difficult to arrive at a simple definition using endocardial recordings. Already inWells et al 9 published a study in patients with atrial fibrillation following heart surgery in which isolated atrial electrograms were recorded over periods of up to 15 minutes via electrodes sutured in an unspecified region of the “atrial epicardium.

However, in all cases, analysis of a large number of complexes over time revealed variation in the intervals between individual complexes of up to ms with changes from highly organized electrograms to a disorganized pattern and vice versa.

This contrasted with the exquisite organization and regularity of the recordings obtained by the same group ventricuoar episodes of atrial flutter in the same clinical context. One limitation of that study was the short analysis time of 12 seconds actually very similar to that used in the study of Iza et al 1. A longer period of recording would probably increase the possibility of detecting greater variation in the local intervals.

Aleteo ventricular pdf file

The organization of electrical activity in the right atrium can be a,eteo in cases of atrial fibrillation with defective interatrial conduction. InSchuessler et al 19 demonstrated in dogs that localized reentry could provoke irregular fibrillatory activation of the atria that was indistinguishable from atrial fibrillation unless very detailed mapping of the origin of the activation was performed.

Later, the group led by Jalife demonstrated using optical venhricular in sheep that a stable rotor could sustain atrial fibrillation 20 Figure 1. These rotors were mainly located in the left atrium, while the right atrium tended to be passively and irregularly activated through the appearance of lines or regions in venntricular high frequency activation was blocked.

Local ablation of the anchor point of the rotor can prevent induction of atrial fibrillation in some experimental models 21 ; however, other models of functional reentry in the atrium have confirmed that rotors can migrate from one zone to another in both atria, 22 making the proposed “focal” ablation of these anchor points highly debatable.

Returning to the diagnosis of atrial fibrillation, we find that endocardial recordings in patients with irregular atrial activation and a changeable configuration in the ECG can exhibit highly variable patterns. It is easy to record electrograms from multiple points in the right atrium with multielectrode catheters, but the activity of the left atrium is usually only recorded from the coronary sinus.

In some cases relatively organized ventrichlar is recorded in both the right atrium and the coronary sinus, but with continuously changing sequences Figure 2 ; however, in other cases with highly fragmented activity throughout the right atrium and in the recordings from the coronary sinus, a highly regular and very rapid activity can be recorded in a highly localized point, perhaps indicating the presence of a microreentrant circuit rotor with fibrillatory conduction to both atria Figure 3.

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Moving from top to bottom, the figure shows leads II, III, and V1, which record low voltage disorganized atrial waves, followed by bipolar recordings from the right atrium RA that cover the anterior wall from the roof Ant Roof to the most inferior portion A4 centimeter by centimeter, and the septal wall from the most inferior portion S4 to the most superior Post Roofcentimeter by centimeter.

The lower part of the figure shows the recordings in the coronary sinus from the ostium CSo to the distal coronary sinus CS4centimeter by centimeter.

Ventricular Flutter • LITFL • ECG Library Diagnosis

The numbers indicate the intervals between the complexes. The arrows indicate changes in the direction of activation. It can be seen that although there are wide isoelectric intervals between the complexes, the intervals and sequences change continually. In the upper part of the figure, leads II and V1 show disorganized atrial activity. All of the recordings from the right atrium RA and coronary sinus CS display complete disorganization, with multiple deflections and a nonexi stent baseline at numerous points.

Antiarrhythmia drugs would tend to increase the organization of the atrial fibrillation, either by prolonging the refractory period or by widening the radius of the pivot point for the reentrant wavefront, 23 with a reduction in the number of small rotors.

The drugs can also increase the block at the crista terminals, 24 an effect that would accentuate even further the organization of activation. In fact, the appearance of flutter in patients with atrial fibrillation treated with antiarrhythmic drugs is no more than a consequence of this organization of reentry.

What can we use then to establish a differential diagnosis between atrial fibrillation and flutter, to allow us to obtain an automatic diagnosis?

When using individual electrograms, the answer lies in the recording time. The use of a long detection period is perfectly possible in this situation, since these arrhythmias are rarely life threatening; in addition, it would avoid unnecessary and potentially arrhythmogenic interventions in episodes of self-limiting tachycardia.

Sufficient time for recording and examination is also central to differential diagnosis of atrial flutter and atrial fibrillation, where transitions between one arrhythmia and the other are also possible and the use of various recording points over an extended period will sooner or later reveal the irregularity and changes in sequence associated with atrial fibrillation. Similarly, detailed analysis of the pattern of atrial waveforms in the ECG allows recognition of their irregularity and changing morphology during atrial fibrillation in cases where their relative organization suggests a possible diagnosis of atrial flutter.

Finally, how do we refer to a rhythm that generates organized activity in one atrium and disorganized activity in the other? Should we develop terms like “localized flutter with fibrillatory conduction” or “atrial fibrillation with a localized source?

If fibrillatory conduction is an indicator of diffuse defects in atrial conduction, the distinction between this and multiple reentry would be of little practical use, because both would indicate profound electrophysiologic dysfunction. Hospital Universitario de Getafe. Calls from Spain 88 87 40 9 to 18 hours. Images subject to Copyright.

February Next article. Iberoamerican Cardiovascular Journals Editors’ Network.