Galsulfase (Naglazyme)- Multum

Мне Galsulfase (Naglazyme)- Multum идея

Certain atrial tissues, such as Galsulfase (Naglazyme)- Multum crista terminalis and pulmonary veins, are common sites for automaticity or triggered activity. Additionally, disease processes or age-related degeneration of the atria may give rise to the arrhythmogenic substrate.

These mechanisms can be differentiated on the basis of the pattern of onset and termination and the response to drugs and atrial pacing. Automatic atrial tachycardia arises due to enhanced tissue automaticity and is observed in patients with structurally normal hearts and nacl mr those with organic heart disease. The Galsulfase (Naglazyme)- Multum typically exhibits a warm-up phenomenon, during which the atrial rate gradually accelerates after its initiation and slows prior to its termination.

Automatic atrial tachycardia is rarely initiated or terminated by a single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed Galsulfase (Naglazyme)- Multum overdrive pacing. It almost always requires isoproterenol infusion to facilitate induction and is predictably terminated by propranolol. Galsulfase (Naglazyme)- Multum cardioversion is ineffective (being equivalent to attempting electrical cardioversion in a sinus tachycardia).

Atrial tachycardia caused by triggered activity is due to delayed after-depolarizations, which are low-amplitude oscillations occurring at the end of the action potential. If these oscillations are of sufficient amplitude to reach the threshold potential, depolarization Galsulfase (Naglazyme)- Multum again and a spontaneous action potential is generated.

If single, this is recognized as an atrial ectopic beat (an extra or premature beat). If it recurs and spontaneous depolarization continues, a sustained tachycardia may result. Characteristically, the arrhythmia can be initiated, accelerated, and terminated by rapid atrial pacing. It may be Galsulfase (Naglazyme)- Multum to physiologic maneuvers and drugs such as adenosine, verapamil, and beta-blockers, all of which can terminate the tachycardia.

Occasionally, this atrial tachycardia may arise from multiple sites in the atria, producing a multifocal or multiform atrial tachycardia. This may be recognized by varying P wave morphology and irregularity Galsulfase (Naglazyme)- Multum the atrial rhythm. Pulmonary vein tachycardias originate from the os of the pulmonary vein or even deeper localized atrial fibers.

These strands of atrial tissue are generally believed to gain electrical independence, since they are partially isolated from the atrial myocardium. These tachycardias are typically very rapid (heart rate of 200-220 bpm or more)Although pulmonary vein tachycardias frequently trigger episodes of atrial fibrillation, the associated atrial tachycardias may be the clinically dominant or exclusive manifestation. Galsulfase (Naglazyme)- Multum latter typically involves only a single pulmonary vein as opposed to the multiple pulmonary vein involvement seen in atrial fibrillation.

Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit. Macroreentry is the usual Galsulfase (Naglazyme)- Multum in atrial flutter and in scar- and incision-related (postsurgical) Galsulfase (Naglazyme)- Multum tachycardia. The more common and recognized form of atrial tachycardia, seen as a Galsulfase (Naglazyme)- Multum of the advent of pulmonary vein isolation and linear ablation procedures, is left atrial tachycardia.

In this situation, gaps in the ablation lines allow for slow conduction, providing the requisite anatomic substrate for reentry. These tachycardias may be self-limiting but if they persist, mapping and a repeat ablative procedure should be considered. Microreentry can arise in Galsulfase (Naglazyme)- Multum small focal area, such as in sinus node reentrant tachycardia. Typically, episodes of reentrant atrial tachycardia Galsulfase (Naglazyme)- Multum suddenly, terminate suddenly, and are paroxysmal.

Carotid sinus massage and adenosine are ineffective in terminating macroreentrant tachycardias, even if they produce a transient AV nodal wheel. During electrophysiologic study, it can be induced and terminated by programmed extrastimulation.

As is typical of other reentry tachycardias, electrical cardioversion terminates this type of Galsulfase (Naglazyme)- Multum tachycardia. Based on endocardial activation, atrial tachycardia may be divided into two groups: focal and reentrant. Focal atrial tachycardia arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or intra-atrial septum. If it originates from the pulmonary veins, it Galsulfase (Naglazyme)- Multum trigger atrial fibrillation and often forms a continuum of arrhythmias.

Reentrant (usually Galsulfase (Naglazyme)- Multum atrial tachycardias most commonly occur in persons with structural heart disease or complex congenital heart disease, particularly after surgery involving incisions or scarring in the Galsulfase (Naglazyme)- Multum. Electrophysiologically, these atrial tachycardias are similar to atrial flutters, typical or atypical.

Often, the distinction is semantic, typically based on arbitrary cutoffs of atrial rate. Some tachycardias cannot be easily classified. Reentrant sinoatrial tachycardia (or sinus node reentry) is a subset of focal atrial tachycardia due to reentry arising within the sinus node situated at the superior aspect of the crista terminalis. The P wave morphology and atrial activation sequence Galsulfase (Naglazyme)- Multum identical or very similar to those of sinus tachycardia.

Atrial tachycardia can occur in individuals with structurally normal hearts or in patients with organic heart disease. When it Galsulfase (Naglazyme)- Multum in patients with congenital heart disease who have undergone corrective or palliative cardiac surgery, such as a Fontan procedure, an atrial tachycardia can have potentially life-threatening consequences. Digitalis intoxication is an important cause of atrial tachycardia, with triggered activity being the underlying mechanism.

Reentrant atrial tachycardia tends to occur in patients crab structural heart disease, including ischemic, congenital, postoperative, and valvular disorders.



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