In second-degree AV block, some P waves conduct while others do not. This type is subdivided into Mobitz I (Wenckebach), Mobitz II, mal mo La Lm Fig Bloqueo AV de 2o grado Mobitz. Se observa Bloqueo AV de 2ogrado Mobitz II no hay enlenteciBloqueo AV 1– P-R —-9 is. Fig . AV nodal blocks do not carry the risk of direct progression to a Mobitz II block or a complete heart block ; however, if there is an underlying.
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Bradyarrhythmias are a common clinical finding and comprise a number of rhythm disorders including sinus node dysfunction and atrioventricular conduction disturbances. Clinical presentation varies from asymptomatic electrocardiogram findings eg, during a routine examination to a wide range of symptoms such as heart failure symptoms, near syncope or syncope, central nervous symptoms, or nonspecific and chronic symptoms such as dizziness or fatigue.
Conditions resulting in bradyarrhythmic disorders are divided into intrinsic and extrinsic conditions causing damage to the conduction system. Furthermore bradyarrhythmias can be a normal physiologic reaction under certain circumstances. A proper diagnosis including a symptom-rhythm correlation is extremely important and is generally established by noninvasive diagnostic studies lead electrocardiogram, Holter electrocardiogram, exercise testing, event recorder, implantable bloqqueo recorder.
Invasive electrophysiologic testing is rarely required.
In this article of the current series on arrhythmias we will review the pathophysiology, diagnosis and treatment options of bradyarrhythmias, especially sinus blouqeo dysfunction and atrioventricular conduction blocks. Bradyarrhythmias and conduction blocks are a common clinical finding and may be a physiologic reaction mobbitz example in healthy, athletic persons as well as a pathologic condition.
Arbitrarily, bradyarrhythmias are defined as a heart rate below 60 beats per minute bpm. These af be further categorized on the basis of the level of disturbances in the hierarchy of the normal cardiac conduction system.
In this article, we will review the mobitzz, diagnosis, prognosis, and treatment options of these rhythm disorders. Further information can be obtained from the recently published book, Clinical Arrhythmology, by Antonio Bayes de Luna. Clinical presentation of bradyarrhythmias varies from asymptomatic electrocardiographic findings to a broad bloqqueo of symptoms which most bradycardias have in common Table 1.
A can be either permanent or intermittent and unpredictable, as with SND. The physiologic conduction system consists of the sinus node, the AV node, and the bundle of His including the right and left bundle branch as well as the Purkinje system. The conduction system can be considered as a hierarchy of pacemakers with the sinus node being the primary pacemaker of the heart. The sinus node was first identified as the region responsible for the primary activation of the heart by Mobbitz and Flack in Although the sinus node qv often depicted as a small, localized area in medical textbooks, this is not consi stent with electrophysiologic findings.
It has long been believed that impulses from the sinus node are conducted to the AV node via 3 intraatrial pathways the anterior, middle and posterior internodal tractbut more recent studies suggest that atrial fiber orientation may account for preferred ways of conduction.
Apart from patients with accessory pathways the AV node is the sole connection between the atria and the ventricles. Impulses from the atria to the ventricle are modulated by the AV node. One of the main functions of the AV node is to delay and to limit the number of atrial impulses reaching the ventricle. Furthermore, the inferior nodal extensions of the AV node can act as a subsidiary pacemaker in cases of AV block.
Impulses are then conducted from the His bundle to the right and left bundle. The proximal part of the AV node is supplied by the AV nodal artery, whereas the distal part has a dual blood supply which makes it less vulnerable to ischemia.
Second Degree Atrioventricular Block
The cardiac conduction system is innervated by a rich supply of both, the sympathetic and parasympathetic nervous system. Stimulation of the sympathetic nervous system increases automaticity, enhances conduction, and shortens refractory periods.
The parasympathetic influence has the opposite effect. The conduction in the His bundle, though, is neither influenced by sympathetic nor by vagal stimulation. SND also called sick sinus syndrome in symptomatic patients comprises a variety of disturbances affecting sinus node impulse generation and transmission within the atria and may lead a bradyarrhythmias but also tachycardias.
Possible electrocardiographic manifestations are:. Atrial tachycardia including atrial fibrillation or atrial flutterand thus. SND is estimated to occur in to patients per million people. By convention, sinus bradycardia is defined by a heart rate below 60 bpm with the sinus moitz being the primary pacemaker. In the majority of cases sinus bradycardia is rather a physiologic reaction than a pathologic condition.
Sinus bradycardia is a common, often transient finding and is predominantly caused by increased vagal tone. It is therefore seen in trained athletes and in healthy young adults at rest and at night heart rate may fall below 30 bpm at night. Sinus arrest or pauses imply failure of an expected atrial activation. Though there are currently no cut-off values, pauses of 3s or more are uncommon and warrant implantation of a pacemaker in symptomatic patients.
Pauses frequently occur in bradycardia-tachycardia syndrome Figure 1 when an atrial tachyarrhythmia spontaneously terminates and sinus node recovery time is prolonged. This is the time during which no secondary or tertiary pacemaking center takes over until the sinus node resumes its activity. Reproducibility of such pauses by high-rate atrial pacing is relatively low.
Suppression of sinus node activity may be aggravated by antiarrhythmic drugs. An example of a patient with typical bradycardia-tachycardia syndrome: Chronotropic incompetence is defined as the inability of the heart to adjust its rate adequately in response to increased physical activity or changing metabolic demands.
Atrial tachyarrhythmias have been the subject of this series on arrhythmias and will therefore not be discussed here. The reader is referred to previous chapters addressing atrial tachycardia and atrial flutter 28 and atrial fibrillation SND can result from various conditions, which cause depression of the automaticity in and electrical conduction from the sinus node, perinodal and atrial tissue.
The most common cause of SND is idiopathic degenerative fibrosis of nodal tissue which is associated with aging. Although SND is as mentioned above often associated with underlying heart disease and is primarily a disease of the elderly, it is also known to occur in fetuses, infants, children, and young adults without obvious heart disease or other contributing factors. Due to the predominantly intermittent and often unpredictable nature of SND this can be very difficult.
In patients with symptoms occurring more than once a month an external event recorder which can be kept for a maximum of 30 days is often sufficient. An implantable loop recorder may be used in patients with infrequent and transient symptoms in whom none of the aforementioned electrocardiographic recordings could achieve diagnostic information.
Electrophysiologic studies are usually not required in patients with symptomatic bradyarrhythmias such as high grade or complete AV block or SND because the information given by the surface ECG is most often sufficient. However, electrophysiologic studies can be useful in patients with symptoms highly suspicious of AV conduction abnormalities or SND in whom a documentation on surface ECG or ambulatory Holter monitoring was not successful or in persi stentasymptomatic 2: Treatment should be restricted to those patients in whom a strong symptom-rhythm correlation has been documented.
The first step is to rule out or treat reversible extrinsic causes of SND Table 2 and to exclude physiologic sinus bradycardia. Pharmacologic therapy is not effective in SND. If there are no reversible conditions causing SND, cardiac pacing should be implemented to relieve symptoms Table 3.
Taking into account that atrial tachyarrhythmias, particularly atrial fibrillation, are common in patients with SND and thrombembolism is the most important cause of mortality in SND, 23 oral anticoagulation should be considered in each patient with SND and a history of intermittent tachycardias. Oral anticoagulation should be implemented according to the latest ESC guidelines for the management of atrial fibrillation. The natural course of SND can be highly variable and is often unpredictable.
However, patients with a history of syncope due to SND are likely to have recurrent syncope. AV conduction block is a disorder in which atrial impulses are conducted with a delay or are not at all conducted to the ventricles at a time when the AV conduction pathway is not physiologically refractory.
On the basis of intracardiac electrophysiological recordings, supra- intra- or infra-Hisian block can be differentiated. Many of these patients are particularly symptomatic during exercise because the PR interval does not shorten appropriately as the R-R interval decreases.
An example of a patient with asymptomatic first-degree atrioventricular block with marked prolongation of the PR interval PR 0. Every P wave is conducted with a constant PR interval. The amplitude of the P wave is higher than normal 0.
The term second-degree AV block is applied when intermittent failure of AV conduction occurs. This classification should not be used to describe the anatomical site of the block because the terms type I and type II only refer to a certain ECG conduction pattern. To avoid mistakes and pitfalls often associated with the diagnosis of second-degree AV block, it is important to adhere mobutz a correct definition.
The classic Mobitz type I bloqjeo AV block is characterized by a progressive PR interval prolongation prior to the nonconducted P wave Wenckebach behavior.
The first conducted P wave after the nonconducted P wave has the shortest PR interval of such a cycle and so the pause between the QRS complexes encompassing the nonconducted P wave will be less than twice the P-P interval. R ratio in classic type I ratios of 3: However, many type I second-degree AV block sequences are atypical and do not show the classical progressive prolongation of the PR interval 5961 Figure Atypical second-degree Mobitz type I Wenckebach atrioventricular block with a 6: The sequence in this patient does not follow the mathematical structure proposed by Wenckebach.
The mkbitz to fourth PR intervals are prolonged but bolqueo and it is the fifth, but not the second PR interval showing the greatest increment.
The first conducted P wave after the nonconducted P wave has the shortest PR interval ms. According to the statements of bloqyeo World Health Organization and the American College of Cardiology a more appropriate definition of type I second-degree AV block is occurrence of a single nonconducted P wave associated with inconstant PR intervals before and after the blocked impulse as long as there are at least 2 consecutive conducted P waves ie, 3: Type Bloquoe second-degree AV block typically occurs in conjunction with intraventricular block.
Second-degree Mobitz type II atrioventricular block with intermittent left bundle branch block: The QRS complex of the first conducted P wave is narrow and recurs in a similar pattern. The following Bloquueo complexes are wider 0. Mobitz type II pattern in the setting of left bundle branch block indicates block below the His bundle. With only one PR interval before the blocked P wave a 2: Considering that second-degree AV block type II is a class I indication for permanent pacing it is of huge therapeutic importance to make the exact diagnosis.
Recording a long surface ECG strip, carotid sinus pressure test as well as giving atropine or exercise can reveal the correct type of second-degree AV block. If Wenckebach cycles are observed during long-term Monitz recording or sometimes during longer recordings of the standard ECG of a patient with 2: A year-old patient with second-degree atrioventricular block and intermittent third-degree atrioventricular block not shown during invasive electrophysiologic study lead ECG, high right atrium, His and right ventricular apex catheter.
The basic rhythm is a relatively stable sinus rhythm, but only every second P wave is conducted to the ventricle with a narrow QRS complex. Third-degree or complete AV block is characterized by the failure of each P wave or each atrial impulse to conduct to the ventricle resulting in complete AV dissociation with atrial rates higher than the ventricular ones Figure 6Figure 7. It can be congenital bloquso acquired and can be localized to the AV node, the His bundle, or the ramifications of the right and left bundles.
The ventricular escape rhythm reveals the anatomic site of the block: Intermittent third-degree atrioventricular block with asystole in a patient who was admitted due to recurrent syncopes.
The upper panel initially shows sudden onset of a third-degree atrioventricular block with no ventricular escape rhythm followed by an atrioventricular junctional escape rhythm with narrow QRS complexes in the lower panel first 4 beats as well as two conducted P waves at the end of the lower panel. Acquired AV block can be caused by a number of extrinsic and intrinsic conditions which were already discussed with SND Table 2. Idiopathic progressive degeneration of the cardiac conduction system, referred to as Lenegre 63 or Lev disease, 64 accounts for approximately one half of cases of AV block.