ECG for atrial tachycardia

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).

Cardioversion for Atrial Flutter

Stable atrial flutter (TP) can almost always be stopped by a low-amplitude electrical discharge (50 J). It is generally accepted that, whenever possible, cardioversion should be preceded by anticoagulant therapy, as with AF. The need for anticoagulation is higher in patients with episodes of AF in the past.

In half the cases, sooner or later, atrial flutter (TP) may recur, although, according to the author, recurrences of arrhythmia are less common if it developed in the early postoperative period after cardiac surgery.

Recurrence of atrial flutter (TP) after cardioversion requires consideration of the issue of RFA. If the intervals between the recurrences of the arrhythmia are long enough, then as an alternative, you can choose to repeat cardioversion.

Antiarrhythmic drugs for atrial flutter (TP)

Atrial flutter (TP) can be stopped with sotalol, flecainide and propafenone. However, it should be borne in mind that in case of failure, these drugs can increase the frequency of ventricular contractions by reducing the frequency of atrial contractions, which leads to a decrease in AV-conduction rate and a “paradoxical” increase in the frequency of ventricular contractions.

The use of ibutilide (available only for intravenous administration) and dofetilide can be effectively used to stop recent atrial flutter (TP). Both drugs increase the duration of the QT interval, which may be the cause of tachycardia of the “pirouette” type.

Drugs that can prevent AF can also be effective in preventing recurrence of TA. Amiodarone can successfully maintain sinus rhythm when other drugs have proven ineffective. Even if the TA has a persistent flow, the drug, reducing the frequency of atrial contractions and suppressing AV-conduction, contributes to a significant reduction in the frequency of ventricular contractions.

Controlling the frequency of ventricular contractions Intravenous administration of verapamil or diltiazem will help to quickly reduce the frequency of ventricular contractions in TP. However, it is often not possible to control the frequency of ventricular contractions when taking these drugs orally. Amiodarone is more effective.

Treatment of Atrial Flutter (TP)

In atrial flutter (AT), attempts to reduce the frequency of ventricular contractions with medications often fail, so if possible, treatment should be aimed at restoring and maintaining sinus rhythm. Atrial flutter catheter ablation

In typical atrial flutter (TP), catheter ablation can be used to interrupt the re-Entry circuit in the right atrium (PP) in order to stop and prevent arrhythmia. Radiofrequency energy is directed to the narrowest part of the re-Entry chain – to the caval-tricuspid isthmus (isthmus), which is located between the back of the three-fold valve and the inferior vena cava.

The percentage of successful interventions is very high, which makes the method more preferable compared to antiarrhythmic therapy and cardioversion: the frequency of recurrences of arrhythmia is lower, and the need for re-hospitalization arises less frequently. Thus, RFA is a first-line treatment for atrial flutter (TP).

Before ablation for atrial flutter (TP), it is necessary to begin anticoagulant therapy, which is crucial, especially if the patient has a high risk of systemic embolism in accordance with the CHADS2 scale. In some cases, AF may develop AF. On the other hand, in some patients, in addition to atrial flutter (TL), episodes of AF are observed, while ablation performed for atrial flutter (TF) is sometimes able to eliminate AF.

Causes of Atrial Flutter

Atrial flutter (TP) has the same causes as AF, and sometimes can be caused by antiarrhythmic drugs when prescribed for the treatment of AF. It can also be due to atrial scarring after surgery (for example, after the atrial septal defect is removed).

It is now known that atrial flutter (TP) can often be idiopathic. There are reports of a higher prevalence of TA among people whose sports are associated with prolonged heavy physical exertion.

Atypical atrial flutter (TP), the source of which is located in the LP, sometimes appears after the ablation procedure of the LP, performed on AF. Prevalence. Atrial flutter (TP) is less common than AF. According to recent observational studies, the frequency of annual detection is 88 cases per 100,000 population. As with AF, TP is more common in the elderly, but it can also occur in young people.

ECG for atrial flutter

Typical atrial flutter (TP) is a common arrhythmia caused by the movement of the excitation wave along the re-entry circuit (re-entree) within the PT (usually counterclockwise). TP can be paroxysmal or stable. Atrial activity is represented on the ECG by regular F waves, following with a frequency of about 300 beats / min.

Usually, F waves are alternately carried out on the ventricles (alternating AV-conduction), as a result of which their frequency of contraction is about 150 bpm. In many ECG leads, the isoelectric line between F waves is absent, which gives rise to a characteristic sawtooth curve, which is best manifested in leads II, III and aVF.

At the same time, in the lead V1, atrial activity is recorded, as a rule, in the form of discrete waves. The etiological factors of TP are similar to the causes of AF. Often observed idiopathic TP. Antiarrhythmic drugs are often ineffective and in some cases can cause an increase in the frequency of ventricular contractions. First-line treatment methods are cardioversion and catheter ablation. The risk of systemic emboli should be monitored in the same way as with AF.

Arrhythmia is caused by the repeated circulation of an electrical impulse in the right atrium (PP). Usually the impulse moves upwards along the interatrial septum and returns down the side wall of the PT. LP is activated by pulses arising in the PP. TP can be paroxysmal or stable.

In the typical form of atrial flutter, the frequency of regular electrical activity of the atria is approximately 300 bpm. In many leads between the waves of atrial activation, called F waves, there is no isoelectric line, which leads to the formation of a characteristic saw-like curve, which is best manifested in leads II, III and aVF. However, in some leads, especially in lead V1, atrial activity is manifested by discrete waves.

In the typical form of atrial flutter (TP), the impulse circulates within the PC, as a rule, in the counterclockwise direction, and therefore the F waves in leads II, III and aVF are mostly negative, in lead I – very low amplitude, and in lead V1 – positive. Less commonly, the impulse circulates in a clockwise direction; in this case, the F waves will be positive in the lower leads and negative in the V1 lead.

Atypical flutter. In atypical atrial flutter (TF), the frequency of atrial contractions is higher (350-450 beats / min). It cannot be eliminated by ablation of the isthmus (see below) and is not stopped by frequent atrial stimulation.

Atrioventricular conduction during atrial flutter (TP). As with AF, the ventricular response to atrial flutter (TP) is determined by the conductive ability of the AV junction. Often, waves F are carried out alternately on the ventricles (i.e., alternating conduction with blockade or AV-conduction ratio of 2: 1 is observed), as a result of which the frequency of their contractions approaches 150 beats / min.

Drugs that block the AV node, dysfunction of the AV node, or increase the tone of the vagus nerve at night can lead to an increase in the degree of AV block. A high level of sympathetic nervous system activity, which can be observed during physical exertion, on the contrary, can cause an increase in AV conduction to a level of 1: 1, which is accompanied by an increase in the frequency of ventricular contractions up to 300 beats / min.

Treatment of refractory (resistant) atrial fibrillation

1. Amiodarone in refractory atrial fibrillation. Amiodarone is a powerful drug that often allows you to maintain sinus rhythm or at least control the frequency of ventricular contractions in the presence of persistent AF, when other means are ineffective.

However, due to its many undesirable effects, amiodarone should be prescribed only to patients for whom other drugs have been ineffective, or those at risk of side effects in the long term is not the main criterion for the choice of treatment due to poor prognosis, i.e. the elderly and / or those with severe organic myocardial damage.

2. Catheter ablation in refractory atrial fibrillation. To prevent recurrence of paroxysmal AF, as well as in some cases, persistent AF, transvenous catheter ablation is increasingly being used by applying radio frequency energy to various areas of myocardial LP.

This method of treatment is described in a separate article on the site (we recommend using the search form on the main page of the site). Sometimes ablation is performed surgically, usually simultaneously with another surgery.

In the presence of severe clinical symptoms in case of ineffectiveness or intolerance to antiarrhythmic drugs, another method of treatment is the RFA of the AV compound. The procedure involves the simultaneous implantation of a permanent EX and continued use of anticoagulants, but it allows you to very effectively control the symptoms and, as was shown in a number of studies, improves the quality of life of patients and eliminates the need to continue antiarrhythmic therapy.

Anticoagulants before and after cardioversion of atrial fibrillation

Cardioversion can lead to immediate systemic embolism due to fragmentation of a blood clot that already exists in L. P. In addition, new blood clots can form after cardioversion, since recovery of the mechanical function of the atria often does not complete until 3 weeks. after the procedure, and also because cardioversion itself can cause hypercoagulation.

Thus, thromboembolic complications can occur within a few weeks after cardioversion. Therefore, it is important that planned cardioversion in patients with AF, which lasts more than 24-48 hours, is preceded by taking warfarin with retention of an MHO value of 2.5 for at least 3 weeks. and that the use of anticoagulants lasts for at least 4 weeks. after restoring rhythm. The deterioration of the mechanical function of the atria (denoted by the term “stunning”) is also noted after pharmacological cardioversion.

If emergency cardioversion is required, a transesophageal echocardiography can be performed to rule out thrombosis or blood stasis in the LP. If cardioversion is performed on an emergency basis, it should be preceded by the appointment of heparin, followed by the continuation of its introduction and the appointment of warfarin. It was shown that dabigatran is as effective as warfarin in preventing stroke associated with cardioversion.

Electrical Cardioversion Atrial Fibrillation

In most patients with atrial fibrillation (AF), sinus rhythm can be restored with the help of electrical cardioversion, but arrhythmia often recurs. The factors that increase the likelihood of recurrence are the long duration of AF, the presence of heart failure, a significant expansion of the LP and age. One year after cardioversion, a normal rhythm is maintained in no more than a quarter of patients.

The frequency of recurrence of atrial fibrillation (AF) after cardioversion is reduced by antiarrhythmic agents such as flecainide, sotalol, propafenone, and especially amiodarone. These drugs may have undesirable effects, and in many patients their prescription should be reserved for re-cardioversion, when restoring sinus rhythm seems reasonable and dictates the need for further restoration and maintenance of sinus rhythm. Digoxin may increase the frequency of recurrences of arrhythmias.

In the long term, after cardioversion, sinus rhythm is maintained in only a small number of patients. Therefore, the question of restoring rhythm should be primarily considered in the treatment of patients with relatively recently existing arrhythmias (less than 12 months), in whom no apparent causes of its occurrence were identified or if the identified cause was resolved or resolved independently.

In case of recurrence of atrial fibrillation (AF), the next cardioversion attempt should be undertaken after initiation of antiarrhythmic therapy in patients with severe symptoms caused by arrhythmia.

There are reports of successful recovery and retention of sinus rhythm after cardioversion in one third of patients with AF, in whom the arrhythmia had a continuous course for 12-24 months. and more. In patients with difficult-to-treat AF (even long-term), cardioversion should also be considered, since there is still a small chance of restoring and maintaining sinus rhythm.

A proven effective method of restoring normal rhythm is currently the transvenous cardioversion. A higher incidence of successful treatment was reported than with transthoracic cardioversion, especially when treating large patients. In most patients, cardioversion is performed as planned, but sometimes emergency cardioversion is required for hemodynamically unstable patients.

Upstream Therapy (Pathogenetic Atrial Fibrillation Therapy)

It is known that taking angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, omega-3 fatty acids and eating fatty fish reduce the incidence of AF. Recently, it has been shown that the administration of colchicine in the postoperative period significantly reduces the incidence of AF after cardiac surgery.

The “tablet in your pocket” approach. To avoid daily medication, some patients with infrequent episodes of paroxysmal atrial fibrillation (AF) may use the “pill in pocket” approach. According to this method, when a heartbeat occurs, the patient should take flekainid (200 mg) or propafenone (600 mg). If successful within 2-3 hours, we can expect a recovery of sinus rhythm. This strategy is rational for patients with rare but long-term episodes of AF, since it avoids the need for hospitalization.

However, in some patients with paroxysmal atrial fibrillation (AF), experiencing serious symptoms that violate the capacity, the use of the “pill in pocket” approach in the event of arrhythmia cannot be considered adequate. In addition, patients with coronary artery disease or with reduced ventricular contractility should not use these drugs, and since, due to their action, there is a high likelihood of atrial flutter or atrial tachycardia with a very high frequency of ventricular contractions, it is preferable to combine these drugs with drugs that block AV conduction (i.e. with BAB or calcium channel blockers).