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Atrial Tachycardia by Dr Aziz
 

Atrial Tachycardia by Dr Aziz

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    Atrial Tachycardia by Dr Aziz Atrial Tachycardia by Dr Aziz Presentation Transcript

    • AtriAl tAchycArdiA Dr Mohamed Salih Aziz King Abdualaziz Medical City Riyadh
    • definition Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for initiation and maintenance of the tachycardia
    • The ECG typically shows a narrow QRS complex tachycardia (unless bundle branch block aberration occurs Heart rates during atrial tachycardia are highly variable, with a range of 100-250 beats per minute The atrial rhythm is usually regular The conducted ventricular rhythm is also usually regular but may become irregular, often at higher atrial rates because of variable conduction through the AV node, thus producing conduction patterns such as 2:1, 3:1, and Wenckebach AV block.
    • The P wave morphology may give clues to the site of origin and mechanism of the atrial tachycardia. In the case of a focal tachycardia, the P wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the case of macroreentrant circuits, the P wave morphology and axis depend on activation patterns.
    • Types of Atrial Tachycardia A-Based on endocardial activation: 2) focal atrial tachycardia arises from a localized area in the atria such as the crista terminalis, pulmonary veins, ostium of the coronary sinus, or atrial septum. Focal atrial tachycardia that originates from the pulmonary veins may trigger atrial fibrillation 2) reentrant atrial tachycardias . most commonly occur in persons with structural heart disease, complex heart disease, and particularly after surgery involving incisions or scarring in the atria. these atrial tachycardias are similar to the typical atrial flutters
    • 3)Sinoatrial reentrant tachycardia 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 are similar to those of sinus tachycardia
    • MAT is a unique type of atrial tachycardia in which atrial activation originates from multiple atrial foci. MAT often occurs in patients experiencing an exacerbation of chronic obstructive pulmonary disease, a pulmonary thromboembolism, an exacerbation of congestive heart failure, or severe illness especially under critical care with inotropic infusion. It is often associated with hypoxia and sympathetic stimulation. Digitalis toxicity also may be present in persons with MAT, with triggered activity as the mechanism
    • Pat hophysi ol ogi c mechani sms Several pathophysiologic mechanisms have been ascribed to atrial tachycardia. These mechanisms can be differentiated based on the pattern of onset and termination and response to drugs and atrial pacing.
    • Automatic atrial tachycardia (enhanced automaticity) is observed both in patients with normal heart structure and in those with organic heart disease. The tachycardia typically exhibits a warm-up phenomenon, during which the atrial rate gradually accelerates after its initiation and slows prior to its termination. It is rarely initiated or terminated by single atrial stimulation or rapid atrial pacing, but it may be transiently suppressed by overdrive pacing. Carotid sinus massage and adenosine do not terminate the tachycardia even if they produce a transient AV nodal block. Electrical cardioversion is ineffective (being equivalent to attempting electrical cardioversion in a sinus tachycardia
    • Triggered activity is due to delayed after-depolarizations occurs in patients with digitalis intoxication or conditions associated with excess catecholamines. the arrhythmia can be initiated, accelerated, and terminated by rapid atrial pacing. It may be sensitive to physiologic and pharmacologic maneuvers such as adenosine, verapamil, and beta-blockers, which all can terminate the tachycardia. Occasionally, this atrial tachycardia may arise from multiple different sites in the atria, producing a multifocal or multiform atrial tachycardia. This may be recognized by varying P wave morphology and irregularity in the atrial rhythm.
    • Reentrant tachycardia Intra-atrial reentry tachycardias may have either a macroreentrant or a microreentrant circuit. Macroreentry is the usual mechanism in atrial flutter and in scar- and incision-related (postsurgical) atrial tachycardia. Microreentry can arise in a small focal area such as in sinus node reentrant tachycardia. Typically, reentrant atrial tachycardia arises suddenly, terminates suddenly, and is paroxysmal. Carotid sinus massage and adenosine are ineffective in terminating the tachycardia even if they produce a transient AV nodal block. On electrophysiologic study, it can be induced and terminated by programmed extrastimulation. As is typical in other reentry tachycardias, electrical cardioversion terminates this type of atrial tachycardia.
    • History Typically, atrial tachycardia manifests as a sudden onset of palpitations. If atrial tachycardia is due to enhanced automaticity, it may be nonsustained but repetitive or continuous or sustained, as in reentrant forms of atrial tachycardia. Patients may present with a tachycardia that gradually speeds up soon after its onset (warm-up phenomenon). The patient may be unaware of this. This finding during ECG monitoring, as with a Holter, is suggestive that the supraventricular tachycardia is atrial tachycardia.
    • •If accompanied by palpitations, patients also may report dyspnea, dizziness, lightheadedness, fatigue, or chest pressure. One should recognize the early manifestations of tachycardia-induced cardiomyopathy, ie, a decline in effort tolerance and symptoms of heart failure, in patients with frequent or incessant tachycardias. * Lightheadedness may result from relative hypotension, depending on the heart rate and other factors such as the state of hydration and particularly the presence of structural heart disease. The faster the heart rate, the more likely a patient is to feel lightheaded. If the patient has a rapid rate and severe hypotension, syncope may occur.
    • Physical The primary abnormality noted upon physical examination is a rapid pulse rate. In most atrial tachycardias this is regular. However, in rapid atrial tachycardias with variable AV conduction and in multifocal atrial tachycardia (MAT), the pulse may be irregular. Blood pressure may be low in those patients with fatigue, lightheadedness, or presyncope. The cardiovascular examination should be aimed at excluding underlying structural heart diseases such as valvular abnormalities and evidence of heart failure. Abnormal thyroid function should also be in the differential diagnosis
    • Atrial Tachycardia With 3:2 and 2:1 AV Block-KH The ectopic atrial rate is 150 bpm. Some of the ectopic P waves are easily seen and indicated by the arrows. Other P waves are burried in the T waves and not so easily identified. Atrial tachycardia with AV block is often a sign of digitalis intoxication. 3:2 and 2:1 AV block is seen in this example.
    • The ectopic P waves, easily seen in this example, occur in groups, separated by short pauses. This is likely due to an exit block just distal to the atrial pacemaker. Because not all of the P waves make it to the ventricles, there is also 2nd degree AV block. Therefore, two levels of block are present: one in the atria and one at the level of the AV junction.
    • Very Subtle Atrial Tachycardia With 2:1 Block-KH Frank Yanowitz Copyright 1996 Although at first glance this looks like normal sinus rhythm at 95 bpm. On closer look, there are 2 'P' waves for every QRS; the atrial rate is 190 bpm. Note the hidden 'P' in the T waves. This rhythm is likely due to digitalis intoxication, as are the GI symptoms.
    • Atrial tachycardia With 3:2 AV Block
    • Thanks