Bradycardia - causes, symptoms, diagnosis and treatment

Bradycardia is a type of arrhythmia with a heart rate of less than 60 beats per minute. It occurs as a variant of the norm in trained athletes, but more often accompanies various cardiac pathology. It is manifested by weakness, semi-fainting states and short-term loss of consciousness, cold sweat, pain in the heart, dizziness, instability of blood pressure. With severe bradycardia (heart rate less than 40 beats per minute), leading to the development of heart failure, an operation may be required to implant an electrocardiostimulator.

General information

Bradycardia is a type of arrhythmia with a heart rate of less than 60 beats per minute. It occurs as a variant of the norm in trained athletes, but more often accompanies various cardiac pathology. It is manifested by weakness, semi-fainting states and short-term loss of consciousness, cold sweat, pain in the heart, dizziness, instability of blood pressure. With severe bradycardia (heart rate less than 40 beats per minute), leading to the development of heart failure, an operation may be required to implant an electrocardiostimulator.

Regardless of the cause, bradycardia is based on a violation of the ability of the sinus node to produce electrical impulses with a frequency above 60 per minute or their inadequate propagation along the conductive pathways. A moderate degree of bradycardia may not cause hemodynamic disorders. A rare heart rhythm with bradycardia leads to a lack of blood supply and oxygen starvation of organs and tissues, disrupting their full functioning.

In physically trained people, physiological bradycardia occurs, considered as a variant of the norm: in a quarter of young healthy men, the heart rate is 50-60 per minute; during sleep, under the influence of physiological fluctuations of autonomic regulation, the heart rate decreases by 30%. However, more often bradycardia develops against the background of already existing pathological processes.

Classification of bradycardia

According to the localization of the detected disorders, sinus bradycardia is distinguished, associated with violations of automatism in the sinus node, and bradycardia in heart blockades (sinoatrial or atrioventricular), in which the conduction of impulses between the sinus node and the atria or atria and ventricles is disrupted. The heart rate may decrease under physiological conditions (in athletes, in sleep, at rest) - this is functional or physiological bradycardia; pathological bradycardia accompanies the course of various diseases.

Pathological bradycardia can occur in acute form (with myocardial infarction, myocarditis, intoxication, etc.) and disappear after the cure of the disease that caused it, or in chronic form (with age-related sclerotic heart diseases). For the reasons of the development of sinus bradycardia, the following forms are distinguished: extracardial (neurogenic), organic (with heart lesions), medicinal, toxic and sinus bradycardia of athletes. Sometimes, according to the etiology, bradycardia is divided into toxic, central, degenerative and idiopathic.

Causes of bradycardia

The extracardial form of bradycardia can develop with neurocirculatory dystonia, neuroses with autonomic dysfunction, pressure on the carotid sinus (when wearing a tight collar or tie), pressure on the eyeballs (Aschner reflex), increased intracranial pressure (with meningitis, brain contusion, subarachnoid hemorrhage, edema or brain tumor), gastric ulcer and duodenal ulcer. Bradycardia, which develops with myxedema, is proportional to the severity of hypothyroidism.

The causes of the organic form of bradycardia may be myocardial infarction, myocardiodystrophy, myocarditis, cardiosclerosis. These diseases lead to degenerative and fibrous changes in the sinus node or conduction disorders in the myocardium, accompanied by the development of bradycardia.

With an organic lesion of the rhythm driver, a syndrome of weakness of the sinus node develops, and the frequency of pulse generation in it decreases sharply. This condition is accompanied by sinus bradycardia - rhythmic, but very rare contractions of the heart; change of bradycardia and tachycardia or alternation of spontaneous rhythm drivers. The extreme degree of damage to the sinus node is manifested by the failure of the automatism function, as a result of which they cease to produce electrical impulses of the heart.

When the myocardial conduction pathways are affected, a blockade of impulses develops, as a result of which part of the signals generated by the sinus node is blocked and cannot reach the ventricles - bradycardia develops. Taking cardiac glycosides, quinidine, beta-blockers, sympatholytic drugs (for example, reserpine), calcium channel blockers (for example, verapamil, nifedipine), morphine can contribute to the development of the dosage form of bradycardia.

The toxic form of bradycardia develops with severe intoxication caused by sepsis, hepatitis, uremia, typhoid fever, poisoning with organophosphates, and slowing down the processes of automatism and conduction in the heart muscle. This group sometimes also includes bradycardia caused by hypercalcemia or severe hyperkalemia.

The so-called bradycardia of athletes is characterized by a heart rate of up to 35-40 per minute, even in the daytime. Its cause is the peculiarities of the autonomic regulation of the heart rate in people who are professionally engaged in sports. Also, natural aging processes in the body can lead to bradycardia; sometimes the causes of bradycardia remain unclear - in these cases, they speak of its idiopathic form.

Symptoms of bradycardia

Moderate bradycardia is usually not accompanied by circulatory disorders and does not lead to the development of clinical symptoms. The occurrence of dizziness, weakness, semi-fainting and fainting states is observed with bradycardia with a heart rate of less than 40 beats per minute, as well as against the background of organic heart lesions. Also, with bradycardia, fatigue, difficulty breathing, chest pain, fluctuations in blood pressure, impaired concentration and memory, short-term vision disorders, episodes of confused thinking appear.

In general, the manifestations of bradycardia correspond to the severity of hemodynamic disorders developing against its background.

The brain is the first to react to the weakening of the contractile function of the myocardium and the slowing down of blood circulation, experiencing hypoxia. Therefore, bradycardia often leads to bouts of loss of consciousness, convulsions (seizures or Morgagni-Adams-Stokes prodromes), which can last from several seconds to 1 minute. This is the most dangerous condition in bradycardia, requiring urgent medical measures, because with a prolonged attack, respiratory arrest may occur.

Diagnosis of bradycardia

Characteristic signs of bradycardia are detected when collecting patient complaints and objective examination. During the examination, a rare pulse is determined, which, with sinus bradycardia, has the correct rhythm, heart tones of ordinary sonority are heard, respiratory arrhythmia is often detected. Patients with identified bradycardia are recommended to consult a cardiologist.

Electrocardiographic examination in bradycardia allows you to record a rare heart rate, the presence of sinoatrial or atrioventriuclear blockade. If episodes of bradycardia are not detected at the time of ECG registration, they resort to daily ECG monitoring.

In the organic form of bradycardia, ultrasound of the heart is performed. The ultrasound EchoCG method determines a decrease in the ejection fraction of less than 45%, an increase in the size of the heart, sclerotic and degenerative changes of the myocardium. With the help of exercise cycling ergometry, the increase in heart rate is estimated in connection with a given physical activity.

If it is impossible to detect transient blockages by ECG and Holter monitoring, transesophageal electrophysiological examination of the cardiac pathways is performed. With the help of the CPEFI, it is possible to determine the organic or functional nature of bradycardia.

Treatment of bradycardia

Functional and moderate bradycardia, not accompanied by clinical manifestations, do not require therapy. With organic, extracardial, toxic forms of bradycardia, the treatment of the underlying disease is carried out. In case of drug bradycardia, dosage adjustment or withdrawal of drugs that slow down the heart rate is required.

In case of manifestations of hemodynamic disorders (weakness, dizziness), the appointment of preparations of belladonna, ginseng root, eleutherococcus extract, isoprenaline, ephedrine, caffeine and others is carried out in individually selected doses. Indications for active treatment of bradycardia are the development of angina pectoris, arterial hypotension, fainting, heart failure, ventricular arrhythmia.

The occurrence of a Morgagni—Adams—Stokes attack requires consultation with a cardiac surgeon and a solution to the issue of implantation of an electrocardiostimulator - an artificial pacemaker that generates electrical impulses with a physiological frequency. An adequate and constant preset heart rate contributes to the restoration of normal hemodynamics.

Prognosis and prevention of bradycardia

The presence of organic heart lesions adversely affects the prognosis of the course of bradycardia. Significantly aggravates the possible consequences of bradycardia, the occurrence of Morgagni-Adams-Stokes attacks without resolving the issue of electrostimulation. The combination of bradycardia with heterotopic tachyarrhythmias increases the likelihood of thromboembolic complications. Against the background of a persistent decrease in the rhythm, the development of disability of the patient is possible. With the physiological form of bradycardia or its moderate nature, the prognosis is satisfactory.

Timely elimination of extracardial causes, organic heart lesions, toxic effects on the myocardium, the correct selection of dosages of medicines will prevent the development of bradycardia.