Drugs used for bradycardia and heart block

Cardiologist

Sokolov

Denis Vladimirovich

16 years of experience

Cardiologist of the first category, candidate of medical sciences, member of the Asute Cardiovascular Care Association (ASSA)

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Bradycardia is a pathological decrease in heart rate observed in patients of various ages. Develops against the background of acute or chronic heart disease. The threshold value for diagnosis is 60 heart muscle contractions per minute. Patients suffer from weakness, systematic loss of consciousness, dizziness and changes in blood pressure. Severe sinus bradycardia (40 heart rate/min) can lead to the development of heart failure. To prevent this, a pacemaker is implanted in the patient.

General information

The pathology develops against the background of the inability of the sinus node to produce the number of electrical impulses necessary for a normal heart rate. Moderate sinus bradycardia may not lead to hemodynamic disturbances. A severe form of pathology provokes insufficient blood supply to tissues. Oxygen starvation of organs develops.

Professional athletes may experience physiological bradycardia, which is considered normal by cardiologists. At rest, trained people record 50-60 heart beats per minute. In a dream, this value drops by 25-30%.

Types of pathology

Cardiologists distinguish five forms based on etiology:

• extracardiac;
• organic;
• medicinal;
• toxic;
• sinus sports.

The extracardiac type develops under the influence of neurogenic factors, the organic type develops against the background of pathological lesions of the heart. Medicinal and toxic forms of the disease occur when the patient enters the body of toxins or medications in excessive dosages. Sinus bradycardia in athletes is the result of many years of training aimed at achieving maximum heart rate during physical activity.

Pathological types can occur in acute or chronic forms. In the first case, the cause of heart rate disturbances are heart attacks, myocarditis, and intoxication. Chronic bradycardia becomes the result of age-related sclerotic lesions of the heart muscle.

Bradycardia - symptoms and treatment

Since both cardiac and extracardiac diseases can lead to bradycardia, diagnosis is aimed at identifying not only heart diseases.

When talking with the patient, the doctor identifies symptoms that may be associated with bradycardia: fainting, presyncope, episodes of dizziness, shortness of breath and weakness on exercise. The doctor also finds out what medications the patient is taking and what diseases he has suffered.

Standard electrocardiography (ECG) at rest will allow you to evaluate the heart rhythm in the short time during which it is recorded. For clinically significant bradycardia, this is sufficient in situations where disorders accompanied by bradycardia (for example, atrioventricular block or decreased sinus node activity) are constantly recorded.

Another important diagnostic method for assessing heart rhythm throughout the day (and with the advent of multi-day recorders, even for several days) is Holter ECG monitoring. Its diagnostic qualities significantly exceed those of a standard ECG. When performing Holter ECG monitoring:

• estimate the average heart rate during the day, day, night;
• detect significant pauses in the heart rhythm, episodes of sinoatrial and atrioventricular blocks, as well as any cardiac arrhythmias that occur while wearing the ECG recorder;
• compare symptoms and episodes of bradycardia and arrhythmias.

The patient keeps a diary in which he indicates his symptoms and the time of their occurrence, and the doctor, looking at the ECG recording made at these moments, evaluates the connection between the described symptoms and the findings on the ECG. It is this approach that makes it possible to identify the so-called “symptomatic bradycardia,” which is one of the most important indications for installing an electrical pacemaker (pacemaker).

If symptoms presumably associated with bradycardia occur 1-2 times a month, then an external loop recorder is used. The principle of operation of the device is that the recorded data is deleted from memory over time, and the final recording is made only at the moment when the device automatically recognizes the presence of an arrhythmia or the patient himself activates the recording when symptoms occur.

A pharmacological test with atropine will allow one to assess the contribution of the autonomic nervous system to the development of bradycardia in a patient [5].

An electrophysiological study (EPS) in the diagnosis of bradycardia is of less importance, since spontaneously occurring episodes of bradycardia are often diagnosed using Holter ECG monitoring.

non-invasive - using a thin probe-electrode inserted into the esophagus through the nose, electrical stimulation of the heart is performed, and then the time for restoration of spontaneous activity of the sinus node is assessed. This method allows you to assess atrioventricular conduction disturbances.

Invasive EPI involves recording the spontaneous electrical activity of the heart in its various parts and electrical stimulation of the heart through electrodes inserted into the chambers of the heart (atria and ventricles). To do this, you have to pierce the femoral artery or vein and pass the electrode to the heart. However, the diagnosis of bradycardia in most cases does not require invasive EPS. The method is used only when non-invasive methods are not informative and to clarify the issue of implantation of a pacemaker.

In cases where there is reason to believe that blockades develop during physical activity, or there is chronotropic insufficiency of the sinus node (heart rate does not increase with exercise), a stress test under ECG control can be used: the patient walks on a moving treadmill, or pedals a bicycle ergometer, and in parallel, an ECG is recorded, blood pressure is recorded and symptoms are assessed.

Echocardiography is usually performed as part of the examination of almost all cardiac patients and allows one to assess the size of the heart cavities, wall thickness, the condition of the valves and myocardial contractility, and to identify a number of diseases that can lead to bradycardia.

Causes of heart rhythm disturbances

The organic type manifests itself against the background of several pathologies:

• myocardial infarction;
• myocardial dystrophy;
• myocarditis;
• cardiosclerosis.

The listed diseases provoke degenerative changes in the sinus node and conduction disturbances in the myocardium.

The extracardiac form of bradycardia is the result of neuroses, increased intracranial pressure or compression of the carotid sinus by clothing.

Toxic lesions develop when a person comes into contact with hazardous chemicals. Bradycardia of this type often develops against the background of the patient’s professional activity.

Drug-induced bradycardia occurs when a person violates the prescribed dosage of a drug or long-term use of medications with a pronounced effect on the heart rate.

Causes of bradycardia

There are two groups of reasons: factors not related to heart disease (extracardiac) and factors directly related to pathologies of the cardiovascular system (cardiac).

Extracardiac factors

• persistent lack of thyroid hormones (hypothyroidism);
• stomach and duodenal ulcers;
• cerebral hemorrhage;
• head injuries (bruises and swelling);
• rheumatic fever and other systemic connective tissue diseases;
• toxoplasmosis, diphtheria and other infectious diseases;
• prolonged abstinence from food;
• neurocircular dystonia;
• neuroses accompanied by autonomic dysfunction;
• general hypothermia;
• lead poisoning, nicotine;
• reduced body temperature.

Cardiac causes

• myocarditis (inflammation of the myocardium);
• congenital anomalies of the cardiac conduction system;
• cardiosclerosis;
• myocardial dystrophy;
• IBS.

Separately, bradycardia caused by taking medications is distinguished:

• beta blockers;
• cardiac glycosides;
• antiarrhythmic drugs;
• ivabradine.

Symptoms of the disease

Moderate course is rarely accompanied by obvious clinical symptoms. A severe form of pathology provokes:

• dizziness;
• weakness;
• fainting conditions;
• decreased muscle tone;
• blood pressure surges;
• profuse sweating.

Patients may experience difficulty breathing and severe chest pain. Representatives of the older age group are faced with impaired concentration, short-term memory loss, and episodic visual impairment.

Violation of myocardial contractile function leads to cerebral hypoxia. In the background, attacks of convulsions lasting up to 60 seconds may develop. This condition is considered by cardiologists as the most dangerous with confirmed bradycardia. The patient needs urgent help, since prolonged attacks of convulsions provoke cessation of respiratory activity.

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Diagnostic procedures

Diagnosis and treatment of bradycardia is performed by a cardiologist. The doctor examines the child or adult and collects data for the medical history. Close attention is paid to the patient's pulse, the sonority of heart sounds and the frequency of respiratory movements. If there are appropriate indications, the cardiologist can refer the patient to a neurologist, neurosurgeon, or infectious disease specialist.

The organic form requires an ultrasound of the heart. Ultrasound examination allows one to evaluate changes in the size of the heart muscle and identify foci of degenerative lesions. Load bicycle ergometry is aimed at determining the increase in heart rate under various volumes of physical activity.

Bradycardia. Real danger?

Bradycardia is a slowing of the heart rate (HR) due to decreased sinus node function. With bradycardia, the cells of the first order pacemaker, the sinus node, are affected.

The causes of bradycardia may be an imbalance with increased activity of the parasympathetic autonomic nervous system and organic irreversible damage to the heart.

The pacemaker cells of the sinus node produce 60–80 impulses per minute. The lower limit of the normal frequency of sinus rhythm is considered to be 60 per minute. Nearly 25% of healthy young men have a resting heart rate between 50 and 60 bpm. A decrease in heart rate to values ​​less than 15% serves as another criterion for bradycardia.

Bradycardia is divided according to clinical and pathogenetic principles.

Classification of bradycardia:

• neurogenic (vagal);
• endocrine;
• toxic;
• medicinal;
• myogenic (organic);
• constitutional-family.

The neurogenic (vagal) form is represented by various variants and accompanies: neuroses with vagotonia, vagoinsular crises, increased intracranial pressure, subarachnoid bleeding, labyrinthitis, peptic ulcer, sliding hiatal-diaphragmatic hernia, renal, hepatic, intestinal colic, acute diffuse glomerulonephritis, acute period of lower myocardial infarction (Bezold-Jarisch reflex), convalescence after severe infectious diseases.

Vagal bradycardia is often combined with severe sinus arrhythmia.

Endocrine bradycardia is most often associated with decreased function of the thyroid gland and adrenal cortex.

Toxic (endogenous or exogenous) bradycardia accompanies severe states of intoxication (uremia, liver failure). This group includes bradycardia against the background of severe hyperkalemia or hypercalcemia.

Drug-induced bradycardia occurs with the use of beta-blockers, non-dihydropyridine calcium antagonists (verapamil, diltiazem), centrally acting antihypertensives (clonidine, moxonidine), antiarrhythmics (amiodarone), cardiac glycosides, and opiates.

Particular difficulties arise when assessing bradycardia in athletes. In trained athletes (runners, swimmers, skiers), the resting heart rate can slow down to 30–35 per minute. Bradycardia of athletes reflects the optimal level of neurovegetative regulation of the heart outside the period of exercise, a relative decrease in sympathetic tone with an increase in the tone of the vagus nerve. Detection of bradycardia in people involved in sports requires the exclusion of organic heart pathology.

Constitutional familial bradycardia is inherited in an autosomal dominant manner. It is distinguished by the stability of autonomic imbalance with a predominance of vagus nerve tone.

The myogenic (organic) form of bradycardia is associated with cardiac diseases such as hypertrophic cardiomyopathy and primary pulmonary hypertension [1]. Bradycardia can serve as the first manifestation of such a life-threatening disease as sick sinus syndrome (SSNS, sinus node dysfunction).

SSSS is based on degenerative changes, the development of which depends on genetic predisposition, neurovegetative changes, and sensitivity to various damaging factors.

In most cases, sinus bradycardia and SSSS reflect different degrees of severity of disturbances in pacemaker activity and are different stages of a single pathological process. Bradycardia in SSSS can be detected incidentally or during examination for fainting. Without treatment, the disease progresses and dysfunction of the sinus node increases.

SSSS is a clinical electrocardiographic syndrome that reflects structural damage to the sinoatrial node as the first-order pacemaker of the heart, ensuring the regular conduction of automatic impulses to the atria. SSSU include:

• severe sinus bradycardia <40 beats per minute;
• minimum heart rate during the day < 40 per minute, determined by ECG monitoring, and its increase during physical activity, not exceeding 90 minutes;
• bradysystolic variant of atrial fibrillation;
• atrial pacemaker migration;
• stopping the sinus node and replacing it with other ectopic rhythms;
• sinoauricular block;
• pauses > 2.5 s resulting from sinus node arrest, sinoauricular block, or rare escape rhythms;
• tachy-brady syndrome (alternating periods of tachycardia and bradycardia);
• slow and unstable restoration of sinus node function after extrasystoles, paroxysms of tachycardia and fibrillation, as well as at the moment of termination of stimulation during an electrophysiological study of the heart > 1600 ms;
• inadequate reduction in rhythm when using small doses of beta-blockers. Presence of bradycardia during the administration of atropine and exercise testing.

SSSU is divided into primary or secondary.

Primary SSSS includes dysfunction caused by organic lesions of the sinoauricular zone with: coronary heart disease, hypertension, hypertrophic cardiomyopathy, heart defects, myocarditis, hypothyroidism, dystrophy of the musculoskeletal system, amyloidosis, sarcoidosis, etc.

Secondary SSSS occurs when the sinus node is exposed to external factors: hyperkalemia, hypercalcemia, treatment with β-blockers, amiodarone, verapamil, digoxin, etc.

Among the causes of bradycardia are autonomic sinus node dysfunction (ASD), which is observed with hyperactivation of the vagus nerve [2]. The diagnostic criteria for SSSU and VDSU are presented in Table.

The clinical manifestation of SSSS can be different. In the early stages, the course of the disease may be asymptomatic even if there are pauses of more than 4 s.

Patients with mild symptoms may complain of feeling tired, irritability, emotional lability and forgetfulness. As the disease progresses and blood circulation is further impaired, cerebral symptoms become more pronounced (the appearance or intensification of dizziness, momentary memory loss, paresis, “swallowing” of words, insomnia, memory loss).

As the disease progresses, symptoms associated with bradycardia are noted. The most common complaints include a feeling of dizziness, severe weakness, even fainting (Morgagni-Adams-Stokes syndrome). Fainting of a cardiac nature is characterized by the absence of an aura and convulsions.

Based on the characteristics of clinical manifestations, the following forms of SSSU are distinguished:

1. Latent form - absence of clinical and ECG manifestations.

Sinus node dysfunction is determined by electrophysiological study. There are no work restrictions. Implantation of an electrical pacemaker (pacemaker) is not indicated.

2. Compensated form: mild clinical manifestations, complaints of dizziness and weakness, there are changes on the ECG:

a) bradysystolic variant, pacemaker implantation is not indicated; b) brady/tachysystolic variant, pacemaker implantation is indicated in cases of CVS decompensation under the influence of antiarrhythmic therapy.

3. Decompensated form:

a) bradysystolic variant - persistently pronounced sinus bradycardia is determined, manifested by impaired cerebral blood flow (dizziness, fainting, transient paresis), heart failure. Significant limitation of ability to work. Indications for implantation are asystole and VVFSU more than 3000 ms; b) brady/tachysystolic variant - paroxysmal tachyarrhythmias (supraventricular tachycardia, atrial fibrillation) are added to the symptoms of the bradysystolic variant of the decompensated form. The patients are completely disabled. The indications for pacemaker implantation are the same [3, 4].

At the beginning of SSS therapy, all drugs that may affect the function of the sinus node are discontinued. In the future, it is possible to use metabolic therapy with unproven effectiveness, prescribed long-term for 3-6 months in continuous sequential courses:

• antioxidant and cardioprotective effects (Mexidol, coenzyme Q10, etc.);
• improving energy metabolism in the myocardium (creatine phosphate, Actovegin, Mildronate, L-Carnitine, trimetazidine, etc.);
• nootropic action (piracetam, gamma-aminobutyric acid, hopantenic acid, pyritinol, etc.);
• vitamin complexes.

With the progression of sinus node disorders, it may be necessary to install a pacemaker, which improves the quality of life, but does not increase its duration, which is determined by the nature and severity of concomitant organic heart disease [5].

Absolute indications for pacemaker implantation:

• history of Morgagni–Adams–Stokes attacks (at least once);
• severe bradycardia (less than 40 bpm and/or pauses of more than 3 s;
• VVFSU more than 3500 ms, corrected VVFSU - more than 2300 ms;
• the presence of dizziness caused by bradycardia, presyncope, coronary insufficiency, heart failure, high systolic arterial hypertension, regardless of heart rate;
• SSSU with rhythm disturbances requiring the prescription of antiarrhythmic drugs.

The sinus node is a complexly organized multifunctional system. Sinus bradycardia can serve as the first symptom of a progressive degenerative process in the heart muscle. Timely examination makes it possible to identify patients at risk for the development of progressive dysfunction of the sinus node for timely installation of pacemaker.

Literature

1. Strutynsky A.V. Tachyarrhythmias and bradyarrhythmias: diagnosis and treatment. M.: MEDpress-inform, 2013. 288 p.
2. Ardashev A.V., Dzhandzhgava A.O., Zhelyakov E.G., Kuznetsov Yu.V., Voloshko S.V. Clinical effectiveness of permanent cardiac pacing in patients with bradysystolic forms of cardiac arrhythmia and conduction disorders // Cardiology. 2008. No. 1. P. 51–56.
3. Sayfutdinov R. G., Pak E. V., Garipova A. F., Gilyazova A. R., Gabitov S. Z., Rubanova E. F., Nasybullina R. S. Sick sinus syndrome in the practice of a cardiologist // Bulletin modern clinical medicine. 2010. T. 3, issue. 2. pp. 55–63.
4. Janashia P. Kh., Shevchenko N. M., Janashia N. D. Sick sinus syndrome // Heart. 2009. T. 1, No. 2. P. 97–99.
5. Bokeria L. A., Revishvili A. Sh., Golitsyn S. P., Egorov D. F., Sulimov V. A. Clinical recommendations for electrophysiological studies, catheter ablation and the use of implantable antiarrhythmic devices. GEOTAR-Media, 2013. 596 p.

G. I. Nechaeva1, Doctor of Medical Sciences, Professor T. V. Tkachenko, Candidate of Medical Sciences S. F. Gunter

State Budgetary Educational Institution of Higher Professional Education Omsk State Medical Academy of the Ministry of Health of the Russian Federation, Omsk

1 Contact information

Treatment of pathology

A moderate course of the disease without pronounced clinical manifestations does not require therapy. Organic, toxic and extracardiac forms of bradycardia require mandatory treatment of the underlying pathology. Patients with a drug-induced disease are prescribed reduced dosages of drugs that slow the heart rate.

In case of severe bradycardia with seizures, surgical intervention is performed. The patient is implanted with an electrical pacemaker, which serves as a replacement for the pacemaker. The frequency of impulses generated by the implant corresponds to the age norm of the patient. A stable heart rhythm leads to normalization of hemodynamics and elimination of oxygen starvation of organs.

Diagnostics

Patients with detected bradycardia are recommended to consult a cardiologist.

An electrocardiographic study for bradycardia allows you to record a rare heart rate, the presence of sinoatrial or atrioventricular block. If, at the time of ECG registration, episodes of bradycardia are not detected, 24-hour ECG monitoring is resorted to.

For the organic form of bradycardia, an ultrasound of the heart is performed. Ultrasound echocardiography determines a decrease in ejection fraction of less than 45%, an increase in heart size, sclerotic and degenerative changes in the myocardium. Using load bicycle ergometry, the increase in heart rate in connection with a given physical load is assessed.

Questions and answers

What preventive measures can prevent the development of bradycardia?

Sustained heart rhythm disturbances can be avoided by promptly seeking medical help due to intoxication or deterioration in health while taking medications. Patients with a family history are recommended to undergo annual examinations with a cardiologist.

At what age can a person experience symptoms of bradycardia?

Disturbances in the functioning of the heart rhythm driver are possible at any age. The likelihood of developing a stable form increases significantly when a person reaches 65 years of age.

Treatment of bradycardia

The selection of therapy depends on the reasons that led to this condition. If bradycardia occurs while taking medications, the doctor will recommend stopping or replacing medications that reduce heart rate.

If the cause relates to extracardiac factors, the cardiologist may schedule a consultation with a related specialist who is responsible for the treatment of the pathology that caused the bradycardia.

In some cases, for strict medical reasons, a surgical operation is prescribed, during which a pacemaker is installed.