Monthly Archive February 2019

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).

Pharmacological cardioversion for atrial fibrillation

Means for intravenous administration. With recent atrial fibrillation (AF) (ejection fraction (AF) up to 7 days old), sinus rhythm can be restored with the help of intravenous administration of flekine, propafenone, sotalol or amiodarone. In patients with heart failure or drastically reduced pumping function of the ventricles, only amiodarone must be used for this purpose: other drugs may worsen myocardial contractility and cause ventricular arrhythmias. Sinus rhythm recovery is possible in no more than 2/3 of cases. The relief effect of amiodarone may require waiting up to 24 hours.

Flankaine and propafenone in some cases do not restore sinus rhythm, but reduce the frequency of atrial activity and, thus, transform AF in TP or atrial tachycardia. Paradoxically, the lower frequency of atrial activity can lead to a noticeable increase in the frequency of ventricular contractions due to the fact that the AV node is able to conduct most or all of the atrial impulses on the ventricles, which sometimes makes it necessary to perform emergency electrical cardioversion.

Dofetilide and ibutilide are newer drugs with class III antiarrhythmic drugs. They are moderately effective as a means of stopping a newly emerging AF (there are more chances for success with TA). However, when they are used, there is a significant risk of developing tirade de pointes. In the UK, these drugs are currently unavailable.

One of the means of a new group of drugs that have a selective effect on the electrophysiological properties of atrial myocardium is vernacalant. It has been shown that with recent AF, intravenous administration of the drug restores sinus rhythm within a few minutes in about 50% of patients.

It should be borne in mind that almost half of the episodes of recent atrial fibrillation (AF) for 8 hours spontaneously stop. Therefore, strictly speaking, the introduction of antiarrhythmic drugs is not necessary in order to restore sinus rhythm in each case!

Ineffective drugs. Digoxin is ineffective as a means of restoring sinus rhythm, and there is evidence that it can actually contribute to the preservation of arrhythmia by shortening the refractory period of atrial myocardium. BAB and calcium channel blockers, although they have the ability to effectively reduce the frequency of ventricular contractions in AF, do not restore sinus rhythm.

Drugs for oral administration. Flekainid and propafenone have moderate efficacy in preventing recurrences of AF and have the same contraindications for use as with intravenous administration. They should not be prescribed to patients with myocardial dysfunction or ischemic heart disease, and if TP occurs, which can lead to a significant increase in the frequency of ventricular contractions, ideally should be combined with BAB or calcium channel blockers. The author of these lines gives preference to flekainid and, with normal ventricular function, recommends it as a first-line agent.

BAB rarely prevent atrial fibrillation (AF), but if the medical history suggests that arrhythmia is provoked by exercise or due to hyperthyroidism, they are the drugs of choice. Some (but not all) studies have shown that sothalol, a class III antiarrhythmic drug, is more effective in preventing AF, compared with other BABs, but should be avoided in patients with a prolonged QT interval.

The most effective means of preventing recurrence of atrial fibrillation (AF) is amiodarone, but due to the high incidence of undesirable effects, the drug should only be used as a backup for treating patients with severe symptoms if the other drugs listed above have been ineffective or cannot be prescribed. Amiodarone is the drug of choice in treating patients with heart failure.

Dronedarone, a derivative of amiodarone, due to reports of a large number of cardiac and extracardiac adverse effects, is currently recommended only as a second-line drug for maintaining sinus rhythm in adult clinically stable patients with paroxysmal AF or persistent AF after successful cardioversion.

For the prevention of paroxysmal atrial fibrillation for many years used quinidine. However, a meta-analysis of research data showed that taking the drug is associated with a significant increase in mortality (presumably due to its proarrhythmic action), so it is no longer used to prevent recurrence of AF.

Digoxin shortens the refractory period of the atrial myocardium and thus increases the susceptibility to AF. There is no evidence that it prevents arrhythmia.

The strategy of “frequency control” in the treatment of atrial fibrillation

A number of drugs slow down AV conduction (the so-called negative dromotropic effect) and thereby reduce heart rate with persistent AF.

1. Calcium channel blockers in atrial fibrillation Intravenous verapamil quickly and effectively suppresses AV conduction, and thus within a few minutes helps to reduce the frequency of ventricular contractions against the background of persistent AF. At the same time, however, it is unlikely that the sinus rhythm will be restored. In fact, there is good reason to believe that verapamil may contribute to the persistence of arrhythmias. Ingestion of verapamil (120-240 mg / day) usually also allows for effective control of the frequency of ventricular contractions in the background of AF both at rest and during exercise. Diltiazem (but not dihydropyridine calcium channel blockers nifedipine and amlodipine) has a verapamil-like effect. Inside the drug is prescribed in a long-acting dosage form at a dose of 200-300 mg / day. Patients with heart failure are advised to avoid prescribing these drugs or use them with caution.

2. Beta-blockers in atrial fibrillation BAB have an effect similar to that of calcium channel blockers.

3. Digoxin in atrial fibrillation The administration of digoxin orally is widely used to control the frequency of ventricular contractions in the background of atrial fibrillation (AF). Its advantages are the long duration of action and the presence of a positive inotropic effect. However, digoxin often does not allow for adequate control of heart rate at rest and rarely provides rhythm control during physical activity, despite adequate plasma concentration. Side effects are often observed. Old age, renal or electrolyte disorders, the appointment of other drugs can contribute to the development of digitalis intoxication in patients taking the drug in an adequate therapeutic dose. Intravenous administration of digoxin is usually ineffective in rapidly reducing the frequency of ventricular contractions during atrial fibrillation (AF). As indicated below, digoxin does not allow to stop or prevent AF. Due to the many restrictions on the use of the drug and the possibility of reducing the frequency of ventricular contractions with AF, using calcium channel blockers or BAB, digoxin may no longer be used for this purpose.

4. Assessment of the adequacy of rhythm frequency control It is important to remember that although monitoring the frequency of ventricular contractions may seem satisfactory at rest, it is often possible to inadequately increase the heart rate during exercise. To ensure that adequate heart rate control is achieved against the background of FP, outpatient ECG monitoring should ideally be used. Standard, although arbitrarily chosen values, indicating effective control of heart rate, are 60-80 beats / min at rest and 90-115 beats / min during moderate exercise. A “soft frequency control” strategy, aimed at maintaining the ventricular rate at less than 110 beats / min at rest, has recently been compared with the standard “strict frequency control” strategy. It was shown that the first of the mentioned strategies is not inferior to the latter. Although asymptomatic patients “mild frequency control” may be considered acceptable, in patients with severe symptoms (such as shortness of breath and palpitations), as well as in individuals with significantly reduced ventricular pumping function, it is important to achieve good control over the frequency of their contractions.

5. High and low frequency of ventricular contractions during atrial fibrillation Some patients with atrial fibrillation (AF) have both very high and low frequency of ventricular contractions during daytime (with AF, a low frequency during sleep is considered normal). In some cases, to suppress high frequencies with the help of drugs that block AV-conduction, the ventricular ECM may be required. In some patients with atrial fibrillation (AF), probably due to impaired AV conduction, there is no adequate increase in heart rate in response to exercise (chronotropic insufficiency). To improve tolerance to a physical load will allow EX- with function of frequency adaptation.

6. Heart failure in atrial fibrillation. Particular attention should be given to patients with heart failure and atrial fibrillation (AF). Persistently high frequency of ventricular contractions may worsen the course of heart failure or be its true cause. As mentioned above, in some patients, due to a violation of AV conduction (both spontaneous and medically caused by drugs, such as BAB), chronotropic insufficiency can be observed. Therefore, it is important to ensure that the patient’s tolerance to physical exertion is not limited by the inability of the heart to adequately increase heart rate during its implementation.