There may be no subjective sensations of slowing of the heart rhythm, and if they exist, regardless of their type, they appear the same. Isolation of different types of bradycardia matters not so much for patients as for the doctor in the context of determining treatment tactics.
Classify this deviation in the number of heartbeats from the reference value for various reasons. So, for reasons causing bradycardia, emit:
- physiological, which is a variant of the norm;
- pharmacological or drug, arising as a side effect from medication, often incorrect;
- pathological, manifested as a result of heart disease (intracardiac) and lesions of other organs (extracardiac), which can indirectly provoke a delayed heartbeat (sometimes they do not secrete medication in a separate form). 
Pathological bradyarrhythmias are also classified for more specific causes. Toxic, endocrine, neurogenic, drug, myogenic (based on organic lesions of the heart muscle) are distinguished.
Bradycardia is interpreted as absolute, that is, determined constantly, at any position of the body and the patient's condition, the presence or absence of previous physical and mental stress, as well as relative, caused by certain circumstances - trauma, illness, medication, stress, physical exertion.
In some patients, the causes of slow heartbeats remain unclear even with the use of all possible at the present level of research. Idiopathic bradycardia is diagnosed in such patients. It can also be observed continuously or periodically. If, besides reducing the pulse, the person is no longer bothered, then treatment is not required in this case.
According to the localization of the source of violations, sinus bradycardia is associated with a decrease in the activity of the pacemaker cells of the sinus node, which do not produce the necessary number of impulses for a minute with their rhythm and coordination preserved. Such work of the myocardium is often an individual feature, a variant of the norm that does not cause hemodynamic disturbances, and does not require the adoption of therapeutic measures.
Sinus (sinus) node can work as expected. In this case, the cause of a rare pulse is the blockade of nerve fibers that transmit electrical impulses. Transmission may be disrupted at different sites from the atria to the ventricles (atrioventricular block) and in the area between the sinoatrial node and the right atrium (sinoauricular blockade). The transmission of an electrical impulse can be partially blocked when they are carried out, but more slowly or not all, and also completely, which is a lethal threat.
Bradycardia (bradyarrhythmia) can be compensated, which means the body's ability to block this deviation without pathological consequences. It is a random find. Drug therapy in such cases is not required, you just need to know about such features of your body and periodically monitor your condition.
Decompensated state requires medical care, because the symptoms of a slow heart rate, insufficient blood volumes entering the systemic circulation and the associated hypoxia bother the patient, and self-compensation is no longer possible.
This type of slow heartbeat is considered a variant of the norm, caused by the influence of certain physiological conditions. Such physiological features are inherent in trained people accustomed to regular and significant physical exertion. Functional bradycardia is observed in this category of the population at rest and is expressed in slowing heart rate, sometimes very significant. A trained heart, accustomed to working in conditions of overload, provides normal hemodynamics, for example, during a night's sleep with rare jolts, as it contracts powerfully and strongly, pushing a large volume of blood with one jerk.
This type of heart work can be constitutional and genetic in nature and can be observed in members of the same family. These people are usually naturally physically well developed and, consequently, lead an active lifestyle.
The bradycardia of athletes and the genetically determined feature of the body reflects the powerful work of a well-trained heart during the rest period and is expressed in the relative hypotension of the sympathetic division of the autonomic nervous system against the background of the dominant activity of the vagus nerve. Such a vegetative imbalance is resistant. However, the detection of a slow pulse in people with such features requires examination to rule out intracardiac lesions.
Slow heart rate can be caused by age-related changes and hormonal imbalances: rapid physical growth during the period of growing up, pregnancy and aging of the body.
Reflex bradycardia also refers to physiological. It occurs as a reaction to a decrease in body temperature or stimulation of the vagus nerve - artificially caused by pressing the carotid artery or the eyes, while massaging the chest in the area above the heart.
Decrease in the activity of the sinoatrial node may occur as a result of the treatment course with certain drugs. Most often, this type of cardiotoxic effect is caused by: β-blockers, calcium antagonists, cardiac glycosides, opiates. The development of undesirable effects usually occurs with improper dosing, self-medication, non-compliance with the recommended duration of treatment. If the drug causes a slow work of the heart, it is necessary to discuss with the doctor dose adjustment or replacement (cancellation) of the drug.
In addition to drugs, the cardiotoxic effect in the form of bradycardia can develop in heavy smokers, alcoholics, and with various infections and poisonings. 
Slow pulse can be determined in any one position of the body, and in another - to correspond to the norm. Usually, when an irregular heart function is detected in a patient, during diagnosis, the pulse is counted in different positions - standing, lying, changing positions.
Vertical bradycardia is diagnosed in cases where the patient's pulse slows down while standing or on the move. If the patient lies down, his heart rate returns to normal. This feature is referred to as sinus bradyarrhythmia. More common in children. Severe bradycardia manifests characteristic symptoms, mild and moderate can occur with subtle symptoms and be a variant of the norm.
The vertical position of the electrical axis of the heart on the cardiogram, like any other, can be combined with any heart rhythm.
The slowing of the heart rate in the prone position occurs quite often and, in most cases, is an individual feature of this organism. A person is determined to lie bradycardia, while in a standing position, on the move, or in a loaded state, the pulse rate increases. If such changes are not accompanied by pathological symptoms of cerebral hypoxia, then there should be no cause for concern.
Slowing the pulse during sleep is a completely acceptable phenomenon. Night bradycardia is typical for trained people, when the heart compensates for the lack of physical activity by slowing the pulse. Rare powerful impulses are enough to ensure normal blood flow. This condition is also called rest bradycardia. It can be observed not only when the patient is sleeping, and when just resting in a relaxed state.
This form of slow work of the heart muscle accompanies noncardiac diseases causing hypertonus of the vagus nerve. 
Direct irritation of the vagus nerve causes neuroses, tumors of the mediastinum or brain, meningitis, cholelithiasis, inflammatory diseases of the stomach and intestines, inflammation of the middle ear, acute widespread glomerulonephritis, hepatitis and hepatosis, and serious infectious diseases. These extracardiac pathologies may be accompanied by rare contractions of the heart muscle. Vagal bradycardia is common in children and adolescents and is one of the manifestations of vascular dystonia. Accompanied by sleep disorders, severe fatigue, moodiness, poor appetite.
Hypertension of the vagus nerve, caused by any reasons, provokes the development of the weakness of the sinoatrial node and sinus bradyarrhythmia at any age. Clinically, this condition manifests itself with non-specific symptoms - low blood pressure, general weakness, dizziness, sweating, shortness of breath, temporary impairment of consciousness; in more severe cases, hypoglycemia and Morgagni-Adams-Stokes syndrome may develop.
Neurogenic bradycardia can develop in acute myocardial infarction affecting cardiomyocytes located along the lower wall of the heart muscle.
The dominance of the vagus nerve is also manifested in physiological bradycardia, however, if it has a pathological origin, then the condition will progress without treatment. Therefore, when a slow pulse is detected even in trained individuals, it is recommended to be examined to exclude organic intra-and extracardiac pathologies.
Any violation of the contractile activity of the heart affects such an indicator of its work as the amount of arterial blood emitted by the heart muscle in one contraction (systolic volume). Therefore, the expression systolic bradycardia is not correct. Perhaps it means that with a moderate degree of decrease in the number of heartbeats, the body can activate a compensatory mechanism in the form of an increase in systolic volume. At the same time, organs and tissues do not experience hypoxia, since the amount of arterial blood ejected by powerful but rare strokes is enough to ensure normal hemodynamics in a particular person.
However, such a compensatory mechanism is not included in all. For many, the systolic volume does not change, and with a decrease in the heart rate, hypoxia and symptoms of circulatory insufficiency gradually develop.
Also, with prolonged tachyarrhythmias, the duration of the cardiac diastolic period is shortened, causing a decrease in the volume of blood filling the ventricles. Over time, because of this, the systolic volume and the minute volume of blood circulation decrease, which provokes the development of signs of bradycardia.
A moderate slowdown on the expiration of the pulse is typical for children and puberty, people with hypertonicity of the autonomic nervous system. At the same time, while inhaling, the pulse rate in patients with respiratory arrhythmia rises.
The pathogenesis of such an abnormal respiratory rhythm is not associated with organic intracardiac disorders. Respiratory arrhythmia does not lead to the development of impaired blood flow and does not cause the development of persistent dyspnea, cardiogenic shock and swelling. The heart rhythm remains sinus, normal, only on the electrocardiogram is an increase in the length of the gap RR, corresponding to the exhalation. Respiratory bradycardia is not considered a true arrhythmia. It can be called a sinus diagnosis as the heart maintains a normal sinus rhythm (a sinoatrial node emits impulses).
Respiratory bradycardia in some can be observed continuously, in others - to be periodic. It manifests itself by slowing the pulse during exhalation, sometimes by complete fading, and by an increase in inhalation, especially if it is deep.
Asymptomatic, the presence of undesirable symptoms of hypoxia is likely to indicate the presence of any cardiac or extracardiac pathology. Often accompanied by neurocirculatory dystonia. Usually noticeable manifestations of accelerated inhalation pulse, as well as hyperhidrosis, cold hands and feet, some discomfort behind the sternum, feeling of lack of air.
In children and adolescents, respiratory bradycardia is often associated with intensive growth, in expectant mothers - with changes in hormonal levels, increased stress on the body. In these categories of the population, the symptoms of respiratory bradycardia after some time self pass.
It is worth alarming when an accidentally detected slow pulse associated with the respiratory cycle is accompanied by severe discomfort — severe weakness, symptoms of hypoxia, pre-fainting and fainting. 
Arrhythmia and bradycardia (bradyarrhythmia)
The human heart works automatically, never stopping, throughout life. Rare slow pulse (bradycardia), as well as frequent - heart pounding, directly jumping out of the chest (tachycardia), extraordinary impulses (extrasystoles) or fading halfway (blockade) are types of rhythmic anomalies of the heart muscle (arrhythmia).
Sometimes the heart rhythm is disturbed in all - with surges of emotions, physical exertion. Many have deviations from standard indicators, but do not feel them. Rhythm failures occur for various reasons and, accordingly, have different consequences. Physiological changes are not dangerous, and the most noticeable and frequently occurring disorder is accelerated heartbeat or tachycardia. Slow rhythm and other disorders are not so noticeable, especially in the embryonic state. If an electrocardiogram or home tonometer shows the presence of any type of arrhythmia, you should consult a cardiologist and follow his advice on further actions.
The term bradyarrhythmia is a complete synonym for bradycardia, therefore, all that has already been and will be said about the slow rhythm of the heart relates to this formulation of the diagnosis.
Extrasystole and bradycardia
Extrasystoles - extraordinary impulses that occur outside the heart rhythm in ectopic foci of hyperactivity, located in any part of the conducting system outside the sinoatrial node (atria, ventricles, atrioventricular node). These impulses are transmitted through the myocardium, causing it to contract when the atria and ventricles relax, when they are filled with blood. An extraordinary extrasystolic ejection of blood has a volume below the norm, in addition, the next release also already has a lower volume. Frequent extrasystoles can lead to a significant decrease in hemodynamic parameters.
In bradycardia, when the activity of the sinus node is reduced or the conduction of impulses is disturbed, passive ectopic non-sinus rhythms have a substitutive character that excites heart contractions. Their protective function in the absence of impulses of the main pacemaker is beyond doubt. New impulse centers begin to function independently, going out of control of the sinus node. The reasons for this are all the same factors that lead to the development of bradycardia.
Subjectively, the extrasystole is perceived as a heart beat into the inner wall of the chest. Such sensations arise from the active contraction of the muscles of the ventricles after they relax. Patients may complain about the feeling that the heart is tumbling or turning over, they hear its uneven work. Some patients do not notice at all extrasystoles, but may note a feeling of fear, fear of death, sweating, weakness, discomfort in the chest, inability to inhale. It is difficult for the extrasystole of the face to suffer from neurocirculatory dystonia.
Atrial premature beats have in most cases a functional character, it is practically not detectable in case of serious heart damage. Whereas the inclusion of cardiomynocytes in action — atrioventricular (atrioventricular) node rhythm drivers and, especially, ventricles of the heart (idioventricular type rhythms) are characteristic of serious cardiac pathologies and manifest symptoms of bradycardia corresponding to the severity of the underlying disease. In patients with a long-term atrioventricular rhythm, resistant heart failure, frequent attacks of angina pectoris, and syncope at the height of Morgagni-Edems-Stokes syndrome develop.
Ventricular extrasystole and bradycardia
In more than 2/3 episodes, ectopic foci of hyperactivity form in the muscle layer of the ventricles. Idioventricular rhythm arises. The most dangerous ventricular extrasystole, which has developed against the background of heart disease.
In severe bradycardia, there are significant circulatory disorders that require resuscitation. Life threatening conditions develop:
- ventricular paroxysmal tachycardia - attacks of an increase in the number of contractions of these parts of the heart muscle (up to 200 beats / min), the consequence of which is acute ventricular failure, arrhythmogenic shock;
- fibrillation of the ventricles or a similar condition to it - flutter, in which myocardial contractions are ineffective and the blood practically does not enter the systemic circulation;
- asystolia of the ventricles - cessation of cardiac activity, coma.
The idioventricular rhythm, the source of which is located in the ventricular myocardium, in combination with atrial asystole, in most cases indicates a death condition.
Atrial fibrillation and bradycardia - a dangerous combination, especially in cases where the pulse is rare and also not rhythmic. In such cases, patients are recommended to implant a pacemaker.
In atrial fibrillation, the heart “beats up” the blood, increasing its viscosity. At this point, blood clots form in the left atrium — emboli, which through the bloodstream can enter the brain and cause cerebral arteries thrombosis, blockage or rupture of them, and pulmonary arteries. Patients with atrial fibrillation are prescribed blood-thinning drugs, for example, cardio-aspirin or cardio-magnil.
Bradycardia and asystole
Cardiac arrest, the complete absence of its electrical activity, and, as a result, the cessation of blood flow in the vessels of the body - this is asystole. It may be temporary - after a very short stop, blood circulation is resumed. Asystole lasting up to three seconds feels like dizziness, up to nine - loss of consciousness occurs. If the circulation stops for a quarter of a minute, you can die. Ambulance usually does not have time to come.
Causes of primary asystole is called ischemic heart disease and impaired cardiac conduction. Slow pulse precedes cardiac arrest.
Secondary develops in different states. Cardiographic rhythms suggesting an approaching cardiac arrest - ventricular fibrillation or lack of pulse during ventricular tachycardia; no pulse while maintaining conductivity.
Brachardia and bradycardia
A long-lasting and rather pronounced slow heartbeat is complicated by insufficient oxygenation of organs and tissues, including the cardiac muscle, which must work day and night, without stopping. The heart suffers from hypoxia, cardiomyocytes die and ischemic foci are formed. Bradycardia contributes to the development of such a form of coronary heart disease as angina pectoris or angina pectoris, as it was called earlier due to the fact that episodes of sudden pain are felt, pressure on the chest, as if something heavy is falling on her that does not allow to inhale (large toad). Rare heartbeats lead to a decrease in the volume of blood pumped by the heart.
Symptoms of angina pectoris in combination with bradycardia signals the body's inability to regulate the blood circulation process independently. In the absence of medical care, the state of the body worsens, areas of ischemia increase, the heart loses working capacity, the whole body suffers. If at first the symptoms of stenocardia appear during the actions of the patient associated with a certain tension, later - the attacks begin to bother and during rest.
The clinical picture of angina pectoris is a sudden attack of severe pain, accompanied by feelings of heaviness in the chest, the inability to breathe deeply, chest pain, the pain may irradiate to the left arm, under the scapula, to the jaw, strong weakness is felt, shortness of breath - just the legs do not hold, the skin pales, the heart is intermittent. There may be nausea, and with a strong attack - vomiting.
In the initial stages, the symptoms are not pronounced and may not all be present. The main symptom is a sudden attack of severe pressing or arching pain. Seeing a doctor at the first signs of a developing pathology will help get rid of it in the shortest possible time; in severe stages a pacemaker may need to be implanted.
Bradycardia and heart block
Non-sinus type of slow heartbeat is associated with the occurrence of obstacles to the passage of impulses, blockade of electrical impulses in different parts of the nerve fibers of the cardiac conduction system.
The causes of cardiac conduction disorders are different - organic lesions of the heart, intoxication with toxic substances and medicines. Sometimes even healthy people have blockades.
The transfer of a pulse can be interrupted at any part of the conduction. The main generator (pacemaker) - sinus (sinoatrial, sinusatrial) node generates electrical pulses with the highest frequency. The atrioventricular or atrioventricular node following it can replace, if necessary, the sinoatrial and produce impulses, but with a frequency of less than ten to twenty. When the nodes fail, the nerve fibers of the His bundle and / or Purkinje fibers are included in the work, however, they generate rare impulses corresponding to pronounced bradycardia.
However, even if the sinus node generates impulses with the necessary frequency, due to obstacles in the way (blockades), they will not reach the destination point. Transmission is blocked at different levels: between the sinoatrial node and the atria, from one atrium to another. Below the atrioventricular node, the conduction defect can be at different sites, and the conductivity can also be broken at the level of some leg of the His bundle.
Complete atrioventricular block (III degree) is the most dangerous. These parts of the heart begin to work autonomously from each other, being excited and relaxing with the frequency set by the ectopic foci that have arisen in them. Complete disorganization of myocardial electrical activity occurs.
Lighter degrees of blockade: the first, when the impulses do reach the end point, but with a slight delay, and the second, when not all impulses reach the end point.
Asymptometry is characteristic of milder forms, severe blockade bradycardia is characterized by symptoms of insufficient blood supply in the first place - the brain, attacks of hypertension, angina pectoris, and heart failure can be added to the medications.
Bradycardia and left ventricular hypertrophy
Oxygenated blood is released into the aorta from the left ventricle. This part of the heart provides oxygenation of organs and tissues of the whole organism. Hypertrophy (increase in size, thickening of the walls) often develops in completely healthy individuals who regularly train the heart muscle and thereby cause an increase in the weight and volume of an intensively working organ, the so-called sports heart. Due to this, the volume of arterial blood ejected into the bloodstream increases and the pulse slows down, since there is no need for its frequent ejections. This is a natural process that does not cause hemodynamic disturbances.
Left ventricular hypertrophy may develop to compensate for pathological processes that impede the release of blood into the aorta, and overcome the resistance of the vessels. Aortic abnormalities, valvular defects, hypertrophic cardiomyopathy, arterial hypertension, atherosclerosis, and other organic myocardial damage may be accompanied by left ventricular hypertrophic changes.
These diseases often develop for a long time asymptomatically, manifested only by a decrease in the pulse. By itself, bradycardia does not lead to hypertrophic changes, but rather is their symptom.
Therefore, a low pulse, especially a constant, serious reason for a thorough examination. Such a non-invasive diagnostic procedure such as an ultrasound of the heart can see changes in the structure of the myocardium in the early stages.
Migration pacemaker and bradycardia
In case of disorders of the automatism of the sinoatrial node or blockades of electrical impulses, other centers of automatism, located outside the main source of impulses, begin to replace the myocardial excitation. Bradycardia promotes the penetration of passive ectopic rhythms and complexes, one of which is the migratory or sliding rhythm (migration of the heart rhythm driver). This phenomenon consists in the gradual movement of the source of impulses from the synoptic node to the atrioventricular node, and then in the opposite direction. Each cycle begins in a new place: from the synopatrial node, different atrial structural elements, from the atrioventricular node. The most common displacement of the pacemaker: sinus → atrioventricular and back. The pulsation generator shifts gradually, which on the cardiogram looks like various modifications of the P wave, reflecting atrial contraction.
Migratory rhythm can be observed in healthy individuals with a dominant vagal tone.
Heart disease can also cause the formation of a migratory rhythm: sick sinus syndrome, inflammation of the heart muscle, ischemic disease, rheumatic defects. Cardiac complications from infectious diseases can also trigger this phenomenon.
Slow pulse is often recorded on the background of a stressful situation in children prone to the development of affective-respiratory attacks. At risk - children who have undergone pathological childbirth, severe infectious diseases and intoxications, suffering from somatic diseases. Increases the likelihood of attacks of pathological pregnancy of the mother and pedagogical neglect of the child.
The diagnosis of paroxysmal bradycardia is not correct, pediatricians love it to distinguish precisely such attacks from other forms of slow heart work.
In some children, any slight excitement can lead to the development of affective-respiratory attack. The development of paroxysm occurs according to the following scheme: the first phase of the so-called white attack (the skin of the child becomes very pale) begins with a quiet murmur, the parasympathetic division of the autonomic nervous system is activated. Then the automatism of the sinus node is disturbed and the pulse rate is greatly reduced, the blood pressure may fall. The child dies down, goes limp and loses consciousness. Seizures may occur. All this happens very quickly, in just a few seconds. Bradycardia can lead to an attack of asystole.
In children with heart pathologies, a blockage of cardiac conduction at various levels may occur. Basically, stressful situations precede attacks - fear, anger, intense anxiety, but sometimes it is not possible to establish a provoking factor.
A child, even after one such attack, must be shown to a cardiologist and carefully examined for various pathologies.
Bradycardia in the morning
Morning slow pulse can be physiological. At night, the heart is slow, there is no stress and an increased need for oxygen, so morning bradycardia, while the body is not yet involved in the daily rhythm, should not be disturbed, if it is not accompanied by symptoms of hypoxia, severe arrhythmia - then acceleration of the heart rhythm up to flicker, then noticeable reduction and stoppage of the pulse. Some may experience bouts of sudden fear of death, dizziness, convulsions, wheezing when breathing, shortness of breath.
Severe symptoms in the morning after a night's rest, not provoked by agitation, even if the state normalizes during the day, should be a reason for going to the doctor. Self-medication is dangerous in this case.
Acute transient disruption of the heart rhythm in the direction of slowing down can be caused by temporary external causes (fright, strong emotion). This condition often occurs in children and appears as a result of breath holding.
In early childhood (up to three years), bradycardia attacks are observed in children before bedtime, especially after a day filled with emotional outbursts and experiences (visiting a performance, children's holiday, entertainment complex). At bedtime, emotions fade away and this leads to a slowdown in heart activity.
Such transient attacks are not accompanied by severe symptoms, maximum weakness, drowsiness, sometimes fainting, and, as a rule, their causes on the surface. They are more common in children, but may appear in hyperemotional adults.
If transient bradycardia is accompanied by symptoms indicating a violation of hemodynamics, not provoked by external causes, then you should consult a doctor.
Against the background of severe bradycardia, oxygen starvation of the brain develops, and it consumes a lot of oxygen, the lack of which leads to dizziness, fainting and convulsions. These are standard manifestations of severe bradycardia, the complications of which may be acute disorders of the cerebral circulation.
There is also feedback. Slow heart rate can be a symptom of cerebral catastrophes: ischemic and hemorrhagic stroke, cerebral artery thrombosis. Cerebrovascular bradycardia is one of the symptoms of post-stroke stupor or coma.