Atrial Fibrillation: irregular heartbeat in afib, symptoms, causes, treatment

Medically reviewed: 15, February 2024

Atrial Fibrillation: shortness of breath

Atrial fibrillation is a heart rhythm disorder in which there is no mechanical atrial systole and chaotic electrical activity of the myocardium occurs; the condition is accompanied by irregular contractions of the ventricles and hemodynamic disorders.

• Signs of atrial fibrillation on an ECG:

• the absence of clearly defined P waves with their replacement by fibrillation waves (ff) with varying amplitudes and frequencies from 350 to 700 per minute. The changes are most clearly recorded in chest lead 1 (V1);
• irregular R-R intervals.

The prevalence of atrial fibrillation in the general population is 1 to 2%.

In most cases, the development of fibrillation is associated with organic pathology of the organs of the cardiovascular system, which creates a substrate for the preservation of fibrillation, however, the appearance of this symptom complex does not always fit into any nosological category; in such a situation they speak of isolated atrial fibrillation.

Among the diseases associated with this pathology are:

• hypertension;
• damage and malformations of the valvular apparatus of the heart;
• congenital heart defects;
• coronary heart disease and previous myocardial infarction;
• severe cardiovascular insufficiency (II-IV functional class);
• various types of cardiomyopathy and cardiomyodystrophy (including toxic and alcoholic);
• hyper- and hypothyroidism;
• carbohydrate metabolism disorders and diabetes mellitus types 1 and 2;
• obesity;
• Pickwick’s syndrome (sleep apnea);
• chronic kidney disease.

Lifestyle factors that contribute to atrial fibrillation

Some medications, narcotic substances, tobacco smoking, neuropsychic stress, heart surgery, electric shock, and HIV infection can also provoke the occurrence of atrial fibrillation.

• Irregular heartbeat can lead to the development of chronic heart failure.

Inconsistent contraction of the heart chambers can significantly affect hemodynamics. Lack of coordinated atrial contraction can reduce cardiac output by approximately 10%. This reduction is usually well tolerated except in cases of increased ventricular rate, when the rhythm becomes too rapid (eg, greater than 140 beats/minute) or when patients have borderline or reduced cardiac output at baseline. In such cases, heart failure may develop.

• Development of acute cerebrovascular accident.

The risk of developing ischemic stroke is 1.5% in people 50-59 years old and 23.5% in people 80-89 years old. Particularly dangerous is paroxysmal atrial fibrillation with frequent disruptions of sinus rhythm. The risk of developing thrombosis of cerebral vessels especially increases during the period of disruption and restoration of sinus rhythm. There is a so-called atherothrombotic subtype of acute ischemic cerebrovascular accident.

Atrial Fibrillation symptoms

With atrial fibrillation, there is no effective mechanical systole. In this case, the ventricles are filled predominantly passively due to the pressure gradient between the cavities of the heart during diastole. Under conditions of increased heart rate, the ventricles do not fill sufficiently, which leads to hemodynamic disorders of varying severity.

Patients complain of palpitations, a feeling of interruption in the rhythm of the heart, decreased performance, increased fatigue, shortness of breath and palpitations during previously habitual exercise. In addition, symptoms of existing cardiovascular diseases may worsen.

Chronic diseases of the cardiovascular system, as well as conditions characterized by increased activity of the RAAS, cause structural remodeling of the walls of the atria and ventricles – proliferation and differentiation of fibroblasts into myofibroblasts, synthesis of connective tissue fibers and the development of fibrosis. The processes of remodeling of the heart chambers lead to heterogeneity in the conduction of the action potential and to the dissociation of contraction of muscle bundles. In this case, the mechanical systole of the atria is disrupted and conditions are created for the persistence of this pathological condition.

The ventricles produce non-rhythmic contractions, as a result, blood is retained in the atria, their volume increases. Decreased ventricular filling, frequent contraction, and lack of effective atrial contraction can lead to decreased cardiac output and severe hemodynamic disturbances.

Due to the fact that blood flow in the atria slows down due to a violation of their mechanical systole, as well as due to turbulent mixing of blood, blood clots form, mainly in the left atrial appendage.

Depending on the presence of an artificial valve and lesions of the valvular apparatus, valvular and non-valvular forms of atrial fibrillation are distinguished.

Clinically, there are several forms of atrial fibrillation, depending on which the patient’s management tactics are determined:

Forms of atrial fibrillation

Form of Atrial Fibrillation	Description
Newly Diagnosed Atrial Fibrillation	Any new episode of fibrillation, regardless of its cause and duration
Paroxysmal Form	Periodic episodes lasting up to 7 days with spontaneous cessation
Persistent Form	Episodes lasting more than 7 days without spontaneous cessation
Long-Persistent Form	Episodes lasting more than 1 year
Permanent Form	Always present

The last two forms are essentially the same, since in both cases episodes of fibrillation persist for more than a year. They differ precisely in management tactics: if the patient and the doctor decided to control the rhythm, then we will be talking about a long-persistent form, and if not, then about a permanent form. If management tactics change towards rhythm control, then we will talk about a long-persistent form.

Why is atrial fibrillation dangerous?

Development of chronic heart failure. Inconsistent contraction of the heart chambers affects the movement of blood in the vascular bed. Lack of coordinated atrial contraction can reduce cardiac output by approximately 10%. This reduction is usually well tolerated except in cases of increased ventricular rate, when the rhythm becomes too rapid (eg, greater than 140 beats/minute) or when patients have borderline or reduced cardiac output at baseline. In such cases, a serious complication of atrial fibrillation may develop – heart failure.

Development of acute cerebrovascular accident. The risk of developing ischemic stroke is 1.5% in people 50-59 years old and 23.5% in people 80-89 years old. Particularly dangerous is paroxysmal atrial fibrillation with frequent disruptions of sinus rhythm. The risk of developing thrombosis of cerebral vessels especially increases during the period of disruption and restoration of sinus rhythm.

Thus, there is a close connection between atrial fibrillation and stroke and heart failure.

Diagnostics of Atrial Fibrillation

The mandatory minimum diagnostics includes:

• UAC;
• OAM;
• general clinical biochemical blood test;
• determination of total cholesterol and LDL;
• determination of APTT, PT and coagulation to assess the readiness of whole blood for thrombus formation;
• INR during warfarin therapy;
• ECG;
• Holter ECG monitoring, especially if paroxysmal atrial fibrillation is suspected;
• conducting ECHO-CS to assess the functional and anatomical state of the heart;
• chest x-ray;
• scheduled consultation with a cardiologist.

Holter ECG monitoring

Additional examination methods may be used:

• transesophageal ECHO-CS;
• stress echocardiography with dobutamine stimulation;
• coronary angiography;
• duplex ultrasound of neck vessels;
• ultrasound duplex scanning of arteries and veins of the lower extremities;
• intracardiac electrophysiological study;
• determination of free T4 and TSH;
• CT and MRI examination of the chest organs, etc., depending on the clinical situation;
• Ultrasound scanning of arteries and veins of the legs.

Emergency care for patients with an acute attack of atrial fibrillation

For the first episode of atrial fibrillation, each patient is indicated for hospitalization in a 24-hour hospital. Hospitalization is also indicated for patients with an attack lasting more than 24 hours.

Atrial Fibrillation: heart arrhythmia treatment

How to deal with an episode of arrhythmia and live with atrial fibrillation? If shortness of breath, dizziness, loss of consciousness, or pressing pain behind the sternum during an attack occur, the patient or an accompanying person must call an emergency team.

The goals of treatment for atrial fibrillation are:

• prevention of thrombovascular complications;
• improved clinical prognosis;
• reducing symptoms of the disease and improving the patient’s quality of life;
• reduction in the frequency of hospitalizations.

Anticoagulant therapy for Atrial Fibrillation: Preventing the risk of blood clots

The primary goal of treatment for atrial fibrillation is the prevention of thrombovascular complications.

If there is pathology in the venous system of the lower extremities, the patient should be consulted by a vascular surgeon.

To reduce the readiness of blood clots to form, direct and indirect anticoagulants are used.

Indications for anticoagulant therapy and the choice of drug are determined by the risk of thromboembolism, which is calculated using the CHADS2 scale. If the total score on the CHADS2 scale is ≥ 2, then long-term therapy with oral anticoagulants is indicated in the absence of contraindications. However, anticoagulant therapy is dangerous due to bleeding. To assess the risk of this complication, the HAS-BLED scale was developed. A score ≥ 3 indicates a high risk of bleeding, and the use of any antithrombotic drug requires extreme caution.

Indirect anticoagulants include the vitamin K antagonist warfarin. The drug belongs to the group of antimetabolites and disrupts the synthesis of coagulation factor X in the liver.

Direct anticoagulants include heparin and low molecular weight heparin preparations (fraxiparin, enoxaparin, etc.). Transferring patients from an indirect to a direct anticoagulant is recommended if surgical treatment is necessary due to the convenience of adjusting the therapeutic dose range.

New indirect anticoagulants include drugs such as direct thrombin inhibitors (dabigatran) and coagulation factor Xa inhibitors (drugs from the xaban group – apixaban, rivaroxaban, edoxaban). The drugs have an effectiveness comparable to taking warfarin with a minimum of hemorrhagic complications. The evidence base for drugs currently exists only for the problem of non-valvular atrial fibrillation.

The effectiveness of drugs against valvular atrial fibrillation is currently the subject of clinical trials. Therefore, in the presence of congenital and acquired pathology of the valvular apparatus and the presence of an artificial heart valve, the only drug from the group of anticoagulants is still warfarin.

To restore or not to restore sinus rhythm?

The choice of management strategy is carried out individually. The patient’s age, severity of symptoms of atrial fibrillation, the presence of structural myocardial pathology, and physical activity are taken into account.
Maintaining a stable heart rate

Long-term therapy for atrial fibrillation involves choosing a strategy – maintaining sinus rhythm or controlling the heart rate.

• In case of paroxysmal fibrillation, it is possible to consider the tactics of maintaining sinus rhythm.
• In case of persistent and constant form, elderly age, low physical activity and satisfactory subjective tolerance of fibrillation, most specialists are inclined to the tactics of heart rate control, since the restoration of sinus rhythm and its subsequent disruption are accompanied by changes in the rheological properties of the blood and an increased risk of intravascular thrombus formation, and the tactics of maintaining sinus rhythm does not improve the long-term prognosis of patients.

Atrial Fibrillation supportive therapy

The heart rate control strategy involves regular use of frequency-lowering drugs from the group of cardiac glycosides, beta-blockers, Ca++ channel blockers and class III antiarrhythmics (amiodarone, dronedarone), and their combinations are also used.

When selecting medications, it is important to know whether the patient has atrial flutter. This disorder is often combined with fibrillation. If the doctor does not take this combination into account when selecting therapy, the drugs will only affect fibrillation, and flutter will persist. This is fraught with the development of heart failure: flutter leads to it faster than fibrillation.

Today there is no exact answer to the question of the target heart rate level for atrial fibrillation. Clinical and methodological recommendations are based on the opinion of experts in the field of cardiology.

Initially, it is recommended to reduce the ventricular rate to less than 110 beats at rest and during exercise. If a decrease in the frequency of ventricular contractions does not lead to the disappearance of restrictions on physical activity, then it is advisable to reduce the frequency of their contractions to 60-80 at rest and 90-115 per minute during physical activity.

Cardiac glycosides are in most cases prescribed to elderly patients with low physical activity, with a tendency to arterial hypotension. The most common drug is digoxin, which is taken daily at a dose of 1/2 – 1/4 TB. per day.

The following beta blockers are used:

• Metoprolol succinate with modified release in an average therapeutic dose of 100-200 mg once a day;
• Bisoprolol 2.5-10 mg once a day;
• Carvedilol 3.125-25 mg. 2 times a day;
• Atenolol 25-100 mg. once a day.

Among non-dihydroperidine Ca++ antagonists, the following are prescribed:

• Verapamil daily distribution (Isoptin SR) 240 mg. 2 times a day at intervals of 12 hours;
• Diltiazem 60 mg. 3 times a day.

Class III antiarrhythmics are used:

• Amiodarone (Cordarone) 100-200 mg. once a day;
• Dronedarone (Multac) 400 mg. 2 times a day.

There is clinical data on the effectiveness of omega-3 polyunsaturated fatty acids in the complex therapy of atrial fibrillation, in particular eicosapentaenoic acid and docosahexaenoic acid. According to the multicenter placebo-controlled clinical studies FORWARD and OPERA, the effect of omega-3 polyunsaturated fatty acids on reducing the risk of sudden death and overall mortality in patients with chronic heart failure and patients who have suffered acute myocardial infarction has been proven.

According to the GISSI-Prevenzione study, the administration of omega-3 polyunsaturated fatty acids can reduce relapses of atrial fibrillation within 3 weeks from the start of therapy. The maximum effect is observed after a year of continuous use of the drug.

The sinus rhythm control strategy does not exclude the heart rate control strategy. Reducing the ventricular rate to the target level makes it possible to reduce the clinical symptoms of atrial fibrillation during inevitable disruptions of the atrial rhythm.

Rhythm control tactics do not have a significant advantage over heart rate control tactics in terms of predicting cardiovascular mortality, but they significantly reduce the severity of clinical symptoms that occur with this disease.
Drugs to restore sinus rhythm

To maintain sinus rhythm during atrial fibrillation, the following medications are recommended:

• Amiodarone (cordarone);
• Dronenador (multak);
• Disopyramide (rhythmodan);
• Ethacizin;
• Allapinin;
• Moracizin (Ethmozin);
• Propaphenone (Propanorm, Ritmonorm);
• Sotalol (Sotalex);
• Flecainide.

When a paroxysm of atrial fibrillation develops, sinus rhythm is restored spontaneously on its own within several hours or days (up to 7 days).

In case of severe clinical symptoms of the disease, as well as if a strategy to maintain sinus rhythm is chosen in the future, drug cardioversion is necessary.

To prevent thrombovascular complications, the patient is offered to take 500 mg. acetylsalicylic acid or 2 tb. (150 mg) clopidogrel.

• In patients with severe organic heart disease (ischemic heart disease, CHF, severe LVH, etc.), drug cardioversion is recommended to be performed with intravenous drip administration of amiodarone.
• Novocainamide 500-1000 mg. (5-10 ampoules) IV slowly at 20 ml. isotonic solution or intravenous drip or intravenous drip – 500–600 mg. (5-6 ampoules) per 200 ml. saline solution for 30 minutes. Due to the possibility of lowering blood pressure, it should be administered in a horizontal position of the patient, having a prepared syringe with 0.3-0.5 ml of a 1% solution of phenylephrine (mesatone) nearby.
• It is possible to take procainamide orally for self-help in stopping paroxysm of atrial fibrillation, provided that the safety of this method has been previously tested in a hospital: 1–1.5 g (4–6 tb) once. After 1 hour (if there is no effect), another 0.5 g (2 tb.) and then every 2 hours, 0.5–1 g (until the paroxysm stops). The maximum daily dose is 3 g (12 tablets).
• Propanorm or rhythmonorm is administered intravenously at 2 mg/kg (4-6 ampoules) per 10-15 ml. saline solution for 5 minutes. Can be taken in tablet form – 2 TB. 300 mg each.

Electrical cardioversion

Direct current electrical cardioversion quickly and effectively converts atrial fibrillation into sinus rhythm. Preference for this type of sinus rhythm restoration is given in case of unstable hemodynamics (increasing symptoms of chronic heart failure) and the appearance of myocardial ischemia according to ECG/ECHO-CS.

Radiofrequency catheter ablation

Radiofrequency ablation is an effective method of restoring and maintaining sinus rhythm. The effectiveness of this treatment method for atrial fibrillation is up to 74% [10]. The therapeutic effect is achieved through targeted impact on arrhythmogenic zones of the heart with high frequency current (radiofrequency energy) with a temperature of 40-55 degrees.

Data on the use of radiofrequency ablation in first-line therapy in patients with atrial fibrillation remain controversial, while in patients with recurrent fibrillation this procedure is most justified and effective.

Unfavorable factors have been identified that increase the frequency of relapses after this procedure: dilatation of the left atrium, age over 65 years, duration of the disease, number of previous procedures, as well as insufficiency of the aortic and mitral valves.

Types of surgery procedure for atrial fibrillation

For atrial fibrillation, surgical treatment methods are used. One option is a Cox maze operation.

The essence of the operation is to isolate the posterior wall of the left atrium, cavatricuspid and cavacaval isthmus and exclude the left atrium orifice from the bloodstream. Thus, the operation creates an electrical labyrinth of passages for the propagation of excitation, through which the impulse from the sinoatrial node finds its way to the atrioventricular node, preventing the formation of “re-entry” waves.

Cox maze procedures have primarily been used in patients undergoing other open heart surgery. Performing such combined operations for atrial fibrillation leads to a reduction in relapses of fibrillation, atrial flutter and atrial tachycardia, but does not affect overall mortality. The selection of patients for such methods of surgical treatment should be carried out by a multidisciplinary council of specialists.

Surgical isolation of the left atrial appendage has been performed by cardiothoracic surgeons for several decades, but prospective randomized studies of the effect on the incidence of ischemic stroke in patients after surgical treatment are currently lacking.

Paroxysmal and persistent forms of atrial fibrillation may be a reason for release from work with the issuance of a certificate of incapacity for work. The approximate period for release from work in order to relieve an attack is 7-10 days; selection of anti-relapse therapy requires an average of 7 to 18 days. The criteria for closing a temporary disability certificate are:

• normalization of sinus rhythm or achievement of a target heart rate of 80 or 110 per minute if a heart rate control strategy is selected (depending on the presence of symptoms);
• achieving the target INR level during treatment with a vitamin K antagonist (2-3, optimally 2.5);
• absence of cardiac decompensation;
• absence of thromboembolic complications;
• absence of complications in the form of bleeding while taking indirect anticoagulants;
• improvement in quality of life indicators according to the SF-36 questionnaire and the EHRA scale.

Literature used:

• Camm AJ, Kirchhof P, Lip GY, et al. (October 2010). “Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC)”. Eur. Heart J 31(19):2369–429
• Nodari S., Manerba A., Madureri A., et al. Effects of polyunsaturated fatty acids n-3 in the prophylaxis of atrial fibrillation relapses after external electric cardioversion. Eur. Heart J., 2006; 27, 887
• GISSI-Prevenzione Investigators Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E aftermyocardial infarction: results of the GISSI-Prevenzione trial. Lancet 1999; 354 (9177): 447-455
• Rodionov V.A., Antonchenko I.V., Egai Yu.V., Popov S.V. The effect of Omega-3 polyunsaturated fatty acids on atrial electrophysiology in patients with atrial fibrillation – cardiovascular therapy and prevention. Moscow, 2008
• Arboix A. Cardiovascular risk factors in patients aged 85 or older with ischemic stroke. // Clin neurol neurosurg, 2006. – Vol. 108. – P. 638–643.
• Radiofrequency Ablation for Atrial Fibrillation. A Guide for Adults // Eisenberg Center at Oregon Health & Science University, 2009.