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Atrial fibrillation (AF)
is the most common rhythm disorder. It is registered everywhere and occurs in almost all age groups, but the frequency of its occurrence increases with each decade of life.
If you consult a doctor in a timely manner, correctly selected treatment and the patient follows all the doctor’s orders, the prognosis for this disease is quite favorable and the patient’s quality of life does not suffer significantly.
This applies to patients of all age groups, including the elderly.
Normally, the human heart has a conducting system. It is similar to electrical wiring and its function is to conduct impulses from the sinus node located in the left atrium to the heart muscle, causing it to contract. With atrial fibrillation, the function of one “power source” (sinus node) is taken over by multiple arrhythmic foci in the atrium and the heart contracts chaotically. That is why this arrhythmia is also called delirium cordis (delirium of the heart).
These arrhythmic foci can be quite small and multiple, and then this form of AF is called atrial fibrillation
(from Latin fibrillatio - small contractions, trembling). With larger and more organized foci of arrhythmia, they speak of atrial flutter (reminiscent of the flutter of a bird or butterfly wing). Atrial fibrillation is always chaotic and absolutely arrhythmic contractions of the heart. Atrial flutter can be either regular or irregular in shape. In the first case, the rhythm is correct, but in the second, it is as chaotic as in atrial fibrillation. These forms of MA can be distinguished only by ECG. However, the methods of diagnosis and treatment, as well as prevention of these forms of the disease, are the same. Although with atrial flutter there is a greater effect from surgical treatment methods.
Like any disease, MA has its own course. It begins, as a rule, with a suddenly developing episode (paroxysm), which can end as suddenly as it began.
In this case, restoration of normal (sinus) rhythm can occur both spontaneously (on its own) and with the help of special medications - antiarrhythmic drugs.
The further course of this disease is completely unpredictable. After the first paroxysm, this ari often lasts for many years, and then it can appear at the most unexpected moment. Or, conversely, after the first episode, rhythm disturbances become more and more frequent. And, as a rule, with the increase in frequency and lengthening of paroxysms of MA, it gradually turns into a permanent form, that is, it settles in the patient’s heart forever.
In some cases, when paroxysms are repeated quite often and exhaust the patient, the transition of the arrhythmia to a permanent form brings him relief, because each episode of failure and recovery leads to complications.
In any case, you can live with this arrhythmia, you just need to master the basic principles of managing it. However, it should be understood that it is almost impossible to cure this disease once and for all, like many other diseases (bronchial asthma, diabetes mellitus, hypertension, coronary heart disease, etc.) - you can only coexist with MA, control its symptoms and prevent the development of complications.
A special cohort consists of patients with frequent relapses of AF. In this case, we are talking about either incorrect treatment (the patient does not take the medications, or takes them in an insufficient dose, and the problem can be solved with the help of an arrhythmologist). However, in some cases, an increase in paroxysmal AF is a natural course of the disease, indicating that the paroxysmal form of AF will soon become permanent. This process can be interrupted using surgical treatments.
Atrial fibrillation is usually divided into the following forms:
1.According to development mechanisms;
A. atrial fibrillation B. atrial flutter:
- correct form
- irregular shape
2.By heart rate (HR);
- tachysystolic (heart rate 90-100 per minute and above)
- bradysystolic (heart rate 60 per minute and below)
- normosystolic (heart rate 60-80 per minute)
3. According to the frequency of occurrence of arrhythmia;
- paroxysmal (occurring periodically, each such paroxysm (episode of arrhythmia) lasts no more than 7 days and often goes away on its own, sometimes requiring the use of special medications to restore the rhythm)
- persistent (lasts more than 7 days and requires active rhythm restoration)
- permanent (lasts more than a year and an attempt may be made to restore the rhythm)
- constant (lasts more than a year, rhythm restoration is not indicated due to its ineffectiveness)
Naturally, all these forms are combined with each other. For example, the diagnosis may indicate a paroxysmal tachysystolic form of atrial fibrillation, an increase in paroxysms.
How to treat atrial fibrillation
There are 2 generally accepted treatment strategies for patients with symptoms of atrial fibrillation. The first is the restoration and maintenance of normal sinus rhythm of the heart. The second is a decrease in the frequency of contractions of the ventricles of the heart, that is, atrial fibrillation remains, but becomes less intense (within 80–100 beats per minute), and the patient does not feel it.
1. Camm AJ, Kirchhof P., Gregory YH at al. ACC/AHA/ESC 2010 guidelines for the management of patients with atrial fibrillation-executive summary // Eur. Heart J. – 2010. – Vol. 31. – P. 2369-2429.
Numerous clinical studies have shown that the strategic goal of maintaining sinus rhythm does not provide advantages over a hands-off approach during AF other than attempts to limit (control) the ventricular rate of the heart. Tighter heart rate control also had no additional effect.
It turns out that with proper treatment, diet and proper physical training with the symptoms of atrial fibrillation, you can live happily ever after? This is almost true, if not for the high risk of stroke.
2. Hylek EM, Go AS, Chang Y., et al. Effect of intensity of oral anticoagulation on stroke severity and mortality in atrial fibrillation. N Engl J Med 2003; 349:1019–1026.
Research results indicate that only antithrombotic therapy (one of the most optimal methods of blood thinning) causes a decrease in mortality associated with atrial fibrillation.
What to drink to thin your blood?
To prevent stroke, anticoagulant blood thinners are prescribed. They are indicated for almost 90% of patients with signs of atrial fibrillation, regardless of the stage of the disease. However, anticoagulants should be taken with caution: if used incorrectly, they can reduce blood clotting and provoke bleeding. Anticoagulant therapy should be accompanied by careful monitoring of the blood coagulation system using INR determination. This stops many people from taking anticoagulants for a long time.
Rice. 1. Insufficient frequency of warfarin prescription
As an additional therapy, in addition to medications, in the early stages of the disease or with mild symptoms, on the recommendation of a doctor, treatment of atrial fibrillation with folk remedies can be used, which helps thin the blood and strengthens the heart. Basically, folk treatment is herbal medicine: a decoction of hawthorn or viburnum berries, an infusion of yarrow, a decoction of dill seeds.
So what do you need to thin your blood?
“The study results demonstrated that when treating atrial fibrillation, antithrombotic therapy alone was associated with a reduction in mortality.”
The decision on the advisability of eliminating atrial fibrillation should be made by the attending physician. This largely depends on the form of the arrhythmia, the cause of its occurrence, the disease against which it arose and on the effectiveness of the previously prescribed drug treatment for atrial fibrillation.
Figure 1. Warfarin reduces the risk of stroke in atrial fibrillation (based on Hart et al., 2007)
Despite the fact that the paroxysmal form of atrial fibrillation most often goes away on its own within a few hours or days, it is usually sought to be eliminated with the help of antiarrhythmic drugs.
If the paroxysmal form of atrial fibrillation lasts more than 2 days, before eliminating it, it is necessary to carry out prophylaxis with drugs that reduce blood clotting. This is necessary to prevent the occurrence of thromboembolism at the time of restoration of normal sinus rhythm or in the first hours after elimination of the arrhythmia.
With a permanent form of atrial fibrillation, the attending physician can choose both tactics for eliminating atrial fibrillation and tactics for preserving it. In any case, this can only be done after long-term (3-4 weeks) use of drugs that reduce blood clotting. In addition, these drugs should be taken for at least 1 month after the permanent form of atrial fibrillation has been eliminated.
The main reasons for the development of MA are:
1. diseases of the cardiovascular system:
- hypertonic disease
- heart defects
- previous heart attacks
- previous myocarditis (inflammatory heart disease)
- toxic (alcoholic) cardiomyopathy
2. diseases of the bronchopulmonary system:
- bronchial asthma
- chronic obstructive pulmonary disease
- pneumonia
3. diseases of the gastrointestinal tract:
- peptic ulcer
- erosive gastroduodenitis
- HP infection (Helicobacter pylori gastroduodenitis)
- cholelithiasis
- chronic pancreatitis
- inflammatory bowel diseases
4.endocrine disorders:
- thyroid disease (thyrotoxicosis)
- diabetes
5. infections (ARVI, influenza, sepsis)
6. bad habits:
- alcohol abuse
- drug use
- heavy smoking
7.violation of the work and rest regime (work without days off and holidays, frequent business trips)
8.exacerbation of any concomitant pathology
9.oncological diseases, especially after courses of radiation and chemotherapy
10. combination of factors
AF can be detected when recording an electrocardiogram, when measuring blood pressure (the “arrhythmia” icon flashes on the tonometer screen), or the patient himself feels an unusual heartbeat.
If AF is detected, the patient should immediately contact an arrhythmologist or cardiologist. He will be offered an outpatient examination or, if necessary, hospitalization.
The optimal time to seek medical help is within 48 hours from the moment of the development of MA, since in this case it is possible to restore the rhythm as quickly, effectively and safely as possible.
In the latter case, artificial restoration of sinus rhythm with the help of drugs is called drug cardioversion. In the case when the heart rhythm is restored using an electric current (defibrillator), we talk about electrical cardioversion
One way or another, any form of this disease needs treatment. The global cardiological community has long developed a strategy for the management of such patients and identified the main goals of treating patients with atrial fibrillation.
Sotahexal
Monitoring of patients taking the drug should include monitoring heart rate and blood pressure (at the beginning of treatment - daily, then once every 3-4 months), ECG, blood glucose concentration in patients with diabetes (once every 4-5 months) . In elderly patients, it is recommended to monitor renal function (once every 4-5 months). Due to the presence of class III antiarrhythmic properties in the drug, the possibility of prolongation of the QT interval should be monitored and, if necessary, individual dosage selection should be carried out.
For stable angina pectoris, exercise tolerance, the number of angina attacks per day, and the number of nitroglycerin tablets to relieve an angina attack are assessed. The dose of the drug is adequate if the heart rate at rest decreases to 55-60/min, and during exercise - no more than 110/min. It is recommended to use the paired stress test method.
The patient should be taught how to calculate heart rate and instructed about the need for medical consultation if the heart rate is less than 50/min.
Beta blockers are less effective in smokers.
Patients using contact lenses should take into account that during treatment the production of tear fluid may decrease.
Patients with pheochromocytoma are prescribed only after taking an alpha-blocker.
IV administration is possible in the presence of life-threatening tachyarrhythmic heart rhythm disturbances.
IV injections should be carried out slowly under constant monitoring of ECG parameters, respiratory function and blood pressure. If there is a pronounced decrease in blood pressure or a decrease in heart rate, the daily dose should be reduced. Patients with renal failure require dosage adjustment.
In case of thyrotoxicosis, the use of the drug can mask certain clinical signs of thyrotoxicosis (for example, tachycardia). Abrupt withdrawal in patients with thyrotoxicosis is contraindicated because it can increase symptoms.
When prescribing beta-blockers to patients receiving hypoglycemic drugs, caution should be exercised, since hypoglycemia may develop during long breaks in food intake. Moreover, its symptoms such as tachycardia or tremor will be masked due to the action of the drug. Patients should be instructed that the main symptom of hypoglycemia during treatment with beta-blockers is increased sweating.
When taking clonidine concomitantly, it can be discontinued only a few days after discontinuation of the drug.
It is possible that the severity of the hypersensitivity reaction may increase and the absence of effect from usual doses of epinephrine against the background of a burdened allergic history.
A few days before general anesthesia with chloroform or ether, you must stop taking the drug. If the patient took the drug before surgery, he should select a drug for general anesthesia with minimal negative inotropic effect.
Reciprocal activation of the n.vagus can be eliminated by intravenous administration of atropine (1-2 mg).
Drugs that reduce catecholamine reserves (for example, reserpine) can enhance the effect of beta-blockers, so patients taking such combinations of drugs should be under constant medical supervision to detect arterial hypotension or bradycardia.
Use with caution in combination with psychoactive drugs, such as MAO inhibitors, when taking them on a course for more than 2 weeks.
If elderly patients develop increasing bradycardia (less than 50/min), arterial hypotension (systolic blood pressure below 100 mm Hg), AV block, bronchospasm, ventricular arrhythmias, severe liver and kidney dysfunction, it is necessary to reduce the dose or stop treatment . It is recommended to discontinue therapy if depression caused by taking beta-blockers develops.
Treatment should not be abruptly interrupted due to the risk of developing severe arrhythmias and myocardial infarction. Cancellation is carried out gradually, reducing the dose over 2 weeks or more (reduce the dose by 25% in 3-4 days).
Use during pregnancy and lactation is possible if the benefit to the mother outweighs the risk of side effects in the fetus and child. The drug should be discontinued 48-72 hours before the expected due date.
Avoid ethanol intake during treatment.
Catecholamines, normetanephrine and vanillylmandelic acid should be discontinued before blood and urine tests; antinuclear antibody titers.
During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions (individual selection of doses is required for persons whose profession requires these qualities).
These include:
1. Rhythm control/pulse rate control
If rhythm disturbances occur more than once or twice a year, constant use of antiarrhythmic drugs is necessary.
Tactics to actively restore and maintain normal (sinus) rhythm using AAP are called rhythm control tactics. It is preferable in those patients with paroxysmal, permanent and persistent forms of the disease who lead an active lifestyle and do not have solid concomitant pathology. With fairly frequent, prolonged episodes of AF, ongoing planned antiarrhythmic therapy is also mandatory. Often, an increase in paroxysms is a natural course of the disease. But in some cases, this form of MA is caused by improper treatment, when the patient takes medications in insufficient doses or is not treated at all. It is the arrhythmologist who is called upon to select the treatment regimen that will help the patient cope with the disease. If it is unsuccessful, the patient may be recommended to consult a cardiac surgeon - arrhythmologist for surgical treatment of AF.
If this arrhythmia becomes permanent, active rhythm restoration is not indicated due to ineffectiveness. Under the influence of a long-term arrhythmia, the structure and function of the heart change and it “gets used” to living with it; it is no longer possible. In such patients, pulse control tactics are used, that is, with the help of medications, a heart rate that is comfortable for the patient is achieved. But no active attempts are made to restore the rhythm.
The following are currently used as antiarrhythmic drugs:
- beta blockers (metoprolol, bisoprolol, carvedilol)
- propafenone
- amiodarone
- sotahexal
- allapinin
- digoxin
- drug combination
2.Prevention of complications:
prevention of stroke and thromboembolism
With AF, there is no single, coordinated ejection of blood from the heart; some of the blood stagnates in its chambers and, in the form of blood clots, can enter the vessels. Most often, the blood vessels of the brain are affected and a stroke develops.
In order to prevent it, drugs that affect blood clotting are prescribed - warfarin, rivaroxaban, dabigatran, apixaban, which reliably (more than 90%) protect against stroke.
While taking these drugs, the patient should monitor for bleeding and monitor the complete blood count and creatinine quarterly. (when taking rivaroxaban, dabigatran and apixaban)., or test the INR (international normalized ratio) at least once a month when taking warfarin. This is necessary in order to correctly calculate the dose of the drug and monitor its safety.
Acetylsalicylic acid (aspirin, cardiomagnyl, thromboass) is not routinely used for the prevention of thromboembolism, since the degree of protection against venous thrombosis when used is only 25%.
prevention of heart failure
Heart failure (HF)
– a complication of many heart diseases, including AF. This condition is caused by the lack of full pumping function of the heart, as a result of which the liquid part of the blood stagnates in the tissues and organs, which is manifested by shortness of breath and edema.
For the prevention and treatment of heart failure, ACE inhibitors (enalapril, lisinopril, perindopril, etc.), veroshpiron (eplerenone), and diuretics (torasemide, furosemide, hypothiazide) are used.
3. Surgical treatment is used if there is no effect from medications and is carried out in specialized cardiac surgery clinics.
Types of surgical treatment of MA:
- implantation of a pacemaker for bradyform MA
- radiofrequency ablation of the pulmonary veins and other arrhythmogenic areas
- with paroxysmal tachyform of atrial fibrillation and flutter
Surgery for arrhythmias in general and AF in particular is the “last cartridge” used when drug therapy is unsuccessful.
After surgical treatment, in order to prevent recurrence of arrhythmia, patients are prescribed planned antiarrhythmic therapy.
Thus, treatment of atrial fibrillation is a way of life that involves the patient “working on himself.” And an arrhythmologist helps him with this.
A patient with MA should avoid colds, lead a healthy lifestyle, get rid of bad habits and avoid factors leading to its development, and strictly follow all the recommendations of his doctor. The doctor will help you choose an individual treatment regimen and recommend what to do if a recurrence of arrhythmia develops, and will also promptly refer you to a cardiac surgeon - arrhythmologist, if indicated.
It is important to understand that the selection of antiarrhythmic therapy takes some time, requires repeated examinations by a doctor and a number of dynamic studies (general clinical tests, study of thyroid hormone levels, cardiac ultrasound and Holter ECG monitoring, electrocardiogram registration) and this should be treated with understanding. In some cases, it is necessary to replace one drug with another.
Living with atrial fibrillation is not an easy process and it is very important that the patient feels supported and helped by the doctor. We are happy to help you with this and are ready to offer follow-up programs for a cardiologist, arrhythmologist and cardiac surgeon in our clinic.
SotaHEXAL
Withdrawal of the drug
Increased sensitivity to catecholamines is observed in patients after discontinuation of beta-blockers. After abrupt cessation of therapy, isolated cases of exacerbation of angina pectoris, the occurrence of arrhythmia, and, in some cases, the development of myocardial infarction have been reported. Therefore, careful monitoring of the patient is recommended, especially with coronary heart disease, if it is necessary to abruptly discontinue long-term therapy with Sotahexal. If possible, the dose should be reduced gradually over one or two weeks. If necessary, it is recommended to initiate replacement therapy. Abrupt cessation of drug use can provoke “hidden” coronary insufficiency, as well as the development of arterial hypertension.
Proarrhythmia
The most dangerous side effect of antiarrhythmic drugs is the exacerbation of existing arrhythmias or the provocation of new arrhythmias. Drugs that prolong the QT interval can cause torsade de pointes (TdP), or torsade de pointes (TdP).
The occurrence of such arrhythmias is associated with a prolongation of the QT interval, a decrease in heart rate, a decrease in serum potassium and magnesium, with high plasma concentrations of sotalol, as well as the simultaneous use of other drugs that prolong the QT interval. In women, these complications occur more often. Torsade de pointes tachycardia usually occurs early after the start of therapy or when the dose is increased, and stops spontaneously in most patients. At the same time, dose titration reduces the risk of proarrhythmia. Rarely, torsade de pointes tachycardia can progress to ventricular fibrillation.
Other risk factors for torsade de pointes include significant prolongation of the QT interval with cardiomegaly or congestive heart failure.
Patients with sustained ventricular tachycardia and congestive heart failure have the highest risk of serious proarrhythmias (7%). The drug Sotahexal should be used with extreme caution when the QT interval lasts more than 480 msec, or the dose of the drug must be reduced; therapy should be discontinued when the QT interval exceeds 550 msec.
Electrolyte abnormalities
The drug Sotahexal should not be used in patients with uncorrected hypokalemia or hypomagnesemia, because Possible prolongation of the QT interval, as well as an increase in the potential for tachycardia of the “pirouette” type. Particular attention should be paid to the water-electrolyte ratio and acid-base balance in patients with prolonged diarrhea or patients receiving magnesium and/or drugs that remove potassium from the body (diuretics).
Congestive heart
failure
Beta-adrenergic blockade may further reduce myocardial contractility and cause progression of symptoms
heart failure.
Therapy with Sotahexal should be started with caution and at a low dose in patients with impaired contractility.
left ventricular myocardium, controlled therapy
ACE inhibitors, diuretics, cardiac glycosides, etc. Myocardial infarction
Positive ratio
the benefit/risk of using sotalol in patients after myocardial infarction with impaired left ventricular function has not been proven. Careful patient monitoring and dose titration are critical during initiation and continuation of therapy. Sotalol should not be used in patients with a left ventricular ejection fraction <40% without serious ventricular arrhythmias.
ECG changes
Excessive prolongation of the QT interval, greater than 550 msec, may be a sign of drug toxicity. Anaphactoid reactions
In patients using beta-blockers with
history of anaphylactic reactions to various allergens; repeated contact with the antigen may result in more serious allergic reactions. Such patients may not respond to the usual doses of epinephrine used to treat an allergic reaction.
Diabetes
Sotahexal should be used with caution in patients with diabetes mellitus or with a history of episodes of spontaneous hypoglycemia, since the use of beta-blockers may mask signs of the onset of acute hypoglycemia, such as tachycardia.
Thyrotoxicosis
The use of beta blockers may mask some clinical signs of hyperthyroidism (eg, tachycardia). Patients with suspected thyrotoxicosis should be carefully monitored to avoid the development of thyrotoxicosis, including thyroid storm, when the drug is discontinued.
Renal dysfunction
Since sotalol is primarily excreted by the kidneys, dose adjustment is required in patients with impaired renal function.
Psoriasis
The use of beta blockers may worsen the symptoms of psoriasis.
