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Atrial fibrillation (atrial fibrillation): causes, symptoms, diagnosis, treatment

Medical expert of the article

Cardiologist, heart surgeon
, medical expert
Last reviewed: 11.04.2020

Atrial fibrillation (atrial fibrillation) is a frequent, irregular atrial rhythm. Symptoms include palpitations, sometimes weakness, dyspnea and presyncopal conditions. Clots are often formed in the atria, which creates a high risk of ischemic stroke. Diagnosis is carried out according to the ECG. Treatment includes pharmacological control of heart rate, prevention of thromboembolic complications with the help of anticoagulants and sometimes restoration of sinus rhythm by drugs or cardioversion.

Atrial fibrillation (atrial fibrillation) arises from a large number of small impulses with a chaotic re-entry in the atria. At the same time, in many cases, the appearance of ectopic foci at the sites of venous trunks in the atria (usually in the pulmonary veins) can provoke development and probably support atrial fibrillation (ciliary arrhythmia). Atrial fibrillation does not contract atrial fibrillation, and the atrioventricular (AB) conduction system is stimulated by a large number of electrical impulses, which leads to erratic random conduction of pulses and irregular ventricular rhythm, often with a high frequency (tachycardic type).

Atrial fibrillation (atrial fibrillation) is one of the most common arrhythmias, in the US it suffers from 2.3 million adults. More often atrial fibrillation occurs in men of the European race than in women and people of the Negroid race. The frequency increases with age. Almost 10% of people over the age of 80 suffer from atrial fibrillation (ciliary arrhythmia). More often, atrial fibrillation (atrial fibrillation) occurs in people with heart disease, sometimes leading to heart failure, since cardiac output is impaired in the absence of atrial contraction. The absence of atrial contractions also suggests the formation of thrombi, the annual risk of cerebrovascular embolic complications is about 7%. The risk of stroke is higher in patients with rheumatic valve disease, hyperthyroidism, arterial hypertension, diabetes mellitus, left ventricular systolic dysfunction, or previous embolic complications. Systemic embolism can also lead to necrosis of other organs (eg, heart, kidney, GIT, eye) or limbs.

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The causes of atrial fibrillation (atrial fibrillation)

The most frequent causes of atrial fibrillation are arterial hypertension, cardiomyopathy, defects of the mitral or tricuspid valve, hyperthyroidism, alcohol abuse (the "Sunday heart"). Rarely, the causes may be pulmonary embolism, defect of the septa and other congenital heart defects, COPD, myocarditis and pericarditis. Atrial fibrillation without an accurate cause in people younger than 60 years of age is called isolated atrial fibrillation.

  • Acute atrial fibrillation - arose paroxysm of atrial fibrillation, lasting less than 48 h.
  • Paroxysmal atrial fibrillation is a recurring atrial fibrillation that lasts usually less than 48 hours and spontaneously recovers into the sinus rhythm.
  • Persistent atrial fibrillation lasts more than 1 week and requires treatment to restore sinus rhythm.
  • Constant atrial fibrillation can not be restored to sinus rhythm. The longer atrial fibrillation exists, the less likely its spontaneous recovery and the more difficult becomes cardioversion due to atrial remodeling.

Symptoms of atrial fibrillation

Atrial fibrillation often occurs asymptomatically, but many patients experience palpitations, chest discomfort or signs of heart failure (eg, weakness, dizziness, dyspnea), especially if the frequency of ventricular contractions is very high (often 140-160 per minute). Patients may also have symptoms of acute stroke or injury to other organs due to systemic embolism.

The pulse is irregular, with a lost a-wave (when examining the pulse on the jugular veins). Heart rate deficit (heart rate on the apex of the heart is greater than on the wrist) may be present because the left ventricular stroke volume is not always sufficient to create a peripheral venous wave with frequent ventricular rhythm.

Diagnosis of atrial fibrillation

The diagnosis is made according to ECG data. The changes include the absence of R waves, waves (fibrillation) between QRS complexes (irregular in time, different in shape, oscillations at the isoline at a frequency of more than 300 per minute are not always visible in all leads) and unequal intervals. Other irregular rhythms may mimic atrial fibrillation on an electrocardiogram, but they can be distinguished by the presence of a clear prong or flutter waves, which can sometimes be better seen when conducting vagal samples. Muscle tremors or external electrical effects may be similar to R waves, but in this case the rhythm is correct. In AF, a phenomenon simulating ventricular extrasystole and ventricular tachycardia (Ashman phenomenon) is also possible. This phenomenon usually occurs when a short interval follows a long RR interval . A longer interval increases the refractory period of the conducting system below the bundle, and the resulting QRS complex is aberrant, usually changing in the manner of a disruption in the right arm of the bundle.

In the initial study, it is important to perform echocardiography and to investigate the functions of the thyroid gland. Echocardiography is performed to identify the structural pathology of the heart (for example, enlargement of the left atrium, movement of the left ventricular wall, evidence of transferred or existing ischemia, valve defects, cardiomyopathy) and additional risk factors for stroke (eg, atrial stasis or thrombus, atherosclerotic lesion aorta). Atrial thrombi are more often found in the ear of the atria, where it is easier to identify them using transoesophageal, rather than transthoracic echocardiography.

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What do need to examine?

Treatment of atrial fibrillation

If you suspect a significant etiological cause of the patient with the first occurrence of atrial fibrillation, you need to be hospitalized, but patients with recurrent episodes do not need mandatory hospitalization (in the absence of severe symptoms). The treatment tactic consists of monitoring the frequency of ventricular contractions, controlling heart rhythm and preventing thromboembolic complications.

Control of the frequency of ventricular contractions

Patients with atrial fibrillation of any length need to control the frequency of contractions of the ventricles (usually less than 80 per minute at rest) to prevent the development of symptoms and tachycardia-induced cardiomyopathy.

In acute paroxysms with high frequency (for example, 140-160 per minute) intravenous blockers of the AV-node are used.

ATTENTION! Blockers conducting through the AV-node can not be used in the Wolff-Parkinson-White syndrome, when an additional beam participates in the conduct (manifested by the prolongation of the QRS complex); these drugs increase the frequency of conductions along the bypass, which can lead to ventricular fibrillation.

Beta-blockers (such as metoprolol, esmolol) are considered preferable if a high content of catecholamines in the blood is assumed (for example, in thyroid pathology, in cases caused by excessive physical exertion), non-hydroperidine calcium channel blockers (verapamil, diltiazem) are also effective. Digoxin is the least effective, but may be preferred in heart failure. These drugs can be taken for a long time inward to monitor heart rate. If Beta-adrenoblockers, non-hydroperidinic calcium channel blockers and digoxin (as monotherapy and in combination) are ineffective, amiodarone may be prescribed.

Patients who do not respond to such treatment or who can not take medications that monitor heart rate can be subjected to RF ablation of the AV node in order to cause a complete AV blockade. After this, implantation of a permanent pacemaker is necessary. Ablation of only one route for AB-connection (AV-modification) allows reducing the number of atrial pulses reaching the ventricles and avoiding the need for implantation of ECS, but this intervention is considered less effective than complete ablation.

Control of rhythm

Patients with heart failure or other hemodynamic disorders directly associated with atrial fibrillation, the restoration of a normal sinus rhythm is necessary to increase cardiac output. In some cases, conversion to normal sinus rhythm is optimal, but antiarrhythmic drugs that can provide such conversion (la, lc, III classes), have a risk of side effects and may increase mortality. Restoration of sinus rhythm does not exclude the need for permanent anticoagulant therapy.

For an emergency recovery of the rhythm, you can use synchronized cardioversion or drugs. Before the beginning of the restoration of the rhythm, it is necessary to achieve a heart rate of <120 per minute, and if atrial fibrillation is present for more than 48 hours, the patient should be prescribed anticoagulants (regardless of the conversion method, it increases the risk of thromboembolism). Anticoagulant therapy with warfarin is performed for at least 3 weeks (until the rhythm is restored), and if possible, continue for a long time, as atrial fibrillation may repeat. Alternatively, heparin sodium treatment is possible. Transesophageal echocardiography is also shown; if an atrial thrombus is not detected, cardioversion can be performed immediately.

Synchronized cardioversion (100 J, followed by 200 J and 360 J if necessary) converts ciliary arrhythmia to a normal sinus rhythm in 75-90% of patients, although the risk of repeated attacks is great. The effectiveness of retention of the sinus rhythm after the procedure increases with the appointment of drugs la, lc or III class for 24-48 h before cardioversion. This procedure is more effective in patients with a short duration of atrial fibrillation, isolated atrial fibrillation or atrial fibrillation due to reversible causes. Cardioversion is less effective with an increase in the left atrium (more than 5 cm), a decrease in flow in the ears of the atria, or the presence of pronounced structural changes in the heart.

Drugs used to restore the sinus rhythm include la (procainamide, quinidine, disopyramide), lc (flecainide, propafenone) and III classes (amiodarone, dofetilide, ibutilide, sotalol) antiarrhythmic drugs. All of them are effective in approximately 50-60% of patients, but they have different side effects. These drugs should not be used until heart rate can be controlled with b-blockers and non-hydroperidine calcium channel blockers. These drugs, restoring the rhythm, are also used to maintain a sinus rhythm (with or without previous cardioversion). The choice depends on the patient's tolerance. At the same time, with paroxysmal atrial fibrillation that occurs only or mostly during rest or in sleep, when there is a high tone of the vagus nerve, drugs with a vagolytic effect (for example, dizopyramide) may be particularly effective, and the induced atrial fibrillation may be more is sensitive to beta-blockers.

ACE inhibitors and angiotensin II receptor blockers can reduce myocardial fibrosis, which creates a substrate for atrial fibrillation in patients with heart failure, but the role of these drugs in the routine management of atrial fibrillation has not yet been established.

Prevention of thromboembolism

Preventive maintenance of a thromboembolism is necessary at carrying out of a cardioversion and during long treatment at the majority of patients.

The dose of warfarin is gradually increased to achieve MHO from 2 to 3. It must be taken at least 3 weeks before electrical cardioversion in the case of isolated atrial fibrillation, which lasts more than 48 hours, and within 4 weeks after effective cardioversion. Treatment with anticoagulants should be continued in patients with repeated paroxysmal, persistent or atrial fibrillation in the presence of risk factors for thromboembolism. Healthy patients with a single episode of atrial fibrillation receive anticoagulants for 4 weeks.

Acetylsalicylic acid is less effective than warfarin, but it is prescribed to patients with risk factors for thromboembolism, which is contraindicated in warfarin. Ximelagatran (36 mg twice daily), a direct thrombin inhibitor that does not require monitoring of MHO, has an equivalent warfarin action in terms of preventing stroke in high-risk patients, but before it is recommended instead of warfarin, further research. In the presence of absolute contraindications to the appointment of warfarin or antiplatelet drugs, surgical ligation of the atrial auricles or closure by catheter methods is possible.


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