Monthly Archive March 2019

ECG for atrial tachycardia

The source of atrial tachycardia can serve as foci located both in the right atrium (PP) and in the left atrium (LP), resulting in the formation of discrete teeth P of a modified form, following in an accelerated correct rhythm.

The exception is multifocal atrial tachycardia, which is characterized by an irregular atrial rhythm with P teeth of different morphology. Causes are myocardial damage, respiratory diseases and damage to the valvular apparatus of the heart.

Often, atrial tachycardia is idiopathic. As with atrial flutter (AV), in some cases the AV node may conduct all atrial impulses on the ventricles, but AV-blockade is often observed to varying degrees. Antiarrhythmic drugs may be effective. In difficult cases, an RFA catheter is required.

The source of atrial tachycardia can serve as foci, located in the PP, and in the LP. It can be stable or paroxysmal. In practical terms, the difference between atrial tachycardia and TP is that in the first case the frequency of atrial contractions is lower (120-240 beats / min). As with TP, in some cases, the AV node can conduct all atrial impulses to the ventricles, but AV-blockade of varying degrees is often observed.

The frequency of atrial contractions is lower than in TP, and there is no sawtooth change in the isoline. In the absence of a preexisting blockade of the bundle of the His or aberrant intraventricular conduction, ventricular complexes will be narrow. As with TP, atrial activity is usually best seen in lead V1.

Atrial tachycardia with 1: 1 AV conduction may occur. Massage of the carotid sinus is useful in the diagnosis. Adenosine can also be used for diagnosis, but in some cases the drug suppresses atrial tachycardia without causing transient AV blockade.

At AV-conduction 1: 1 it is difficult to distinguish atrial tachycardia from sinus. In sinus tachycardia, the PR interval is usually short, since catecholamines, which increase the activity of the sinus node, increase the rate of AV conduction.

Thus, an extended PR interval is more likely to indicate the presence of atrial, rather than sinus tachycardia. A positive P wave in lead V1 or a negative P wave in leads I or aVL indicate that the source of tachycardia is in the LP, while a positive tooth P in the lead aVL indicates the origin of the tachycardia from PP.

In the presence of a high AV block, due to the fact that the ventricular rate is relatively low, an erroneous conclusion can be made that there is a complete heart block. As a consequence, it is likely that there is an unreasonable question about the advisability of performing an ECS if the high incidence of atrial contractions is not properly assessed! Atrial tachycardia is usually paroxysmal. However, with a long continuous course, it can lead to the development of heart failure.

Causes of atrial tachycardia

Etiological factors of atrial tachycardia include cardiomyopathy, left ventricular (LV) dysfunction of ischemic origin, rheumatic heart disease, cardiac surgery for valvular or congenital heart disease, chronic obstructive pulmonary disease and SSS. It is often idiopathic. In case of left atrial tachycardia, the place of its occurrence is often the transition zone between the atrium and the pulmonary vein: these tachycardias have the same mechanism as paroxysmal AF and may be its precursor. Sometimes an arrhythmia occurs after successful ablation of a slow conductive path performed on AVURT, and its source is localized in close proximity to the point of application of radio frequency exposure. Atrial tachycardia with AV block may be due to digitalis intoxication. Such an arrhythmia is called “paroxysmal atrial tachycardia with blockade”. The term “paroxysmal” is misplaced because tachycardia is usually stable.

Frequent Atrial Stimulation

Atrial stimulation (within 30 s) with a frequency that is approximately 25% higher than the natural frequency of atrial contractions often leads to the restoration of sinus rhythm. It may take several attempts at such stimulation to stop TP. Sometimes this may cause AF, but usually within a few hours (and often within a few minutes) there is a recovery in sinus rhythm.

It is important to ensure that the applied stimuli ensure the capture of the atrial rhythm. Signs of such seizure are usually an increase or decrease in the frequency of ventricular contractions depending on the state of AV conduction.

The advantage of the method is that it does not require general anesthesia and substantial sedative preparation. If atrial flutter develops during cardiac surgery and electrodes for temporary atrial stimulation have not yet been extracted, they can be used to relieve arrhythmia.

Systemic embolism in atrial flutter (TP)

Like AF, TP can cause systemic embolism. The limited data available suggests that their risk is lower than with AF. Perhaps this is due to the fact that with TP some mechanical activity of the atria is preserved, and therefore the likelihood of thrombus formation in the atrium is reduced.

However, according to current guidelines, the need for prescribing anticoagulants to patients with TA should be assessed using the same stroke risk scale used for AF. Perhaps in some cases, systemic emboli in patients with atrial flutter (TP) are due to episodes of paroxysmal AF.

Reception of warfarin can be stopped after 6 weeks. after successful ablation for atrial flutter (TP), but on condition that no evidence of paroxysmal AF is obtained (outpatient ECG monitoring reduces the likelihood that AF will be skipped).