Bradycardia

Bradycardia is a decrease in heart rate to less than 60 beats per minute. In some cases, this and lower heart rate are considered a normal variant (trained athletes).

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Pulse in bradycardia

With bradycardia, the pulse is always slow. Usually, the indicators are about 50-60 beats per minute. Without treatment, the heartbeat slows down, and accordingly, the speed of blood flow through the vessels decreases. There is a danger for the cerebral cortex, since it is very sensitive to oxygen content. There is a decrease in the processes of removing by-products, carbon dioxide.

Good or bad?

It is impossible to give a clear answer to the question of whether bradycardia is good or bad. This is due to the fact that everything depends on the individual characteristics of a person, his well-being. Not only objective data are important, but also subjective sensations and the patient's well-being. Bradycardia is often observed in completely healthy people who have never complained about their heart or circulatory system.

Tachycardia and bradycardia syndrome

Tachycardia and bradycardia syndrome may accompany myocarditis, cardiomyopathy, heart defects, and even vegetative-vascular dystonia. Premature babies are at risk. Family history is also important: a tendency to arrhythmia, tachycardia, and bradycardia in grandparents and parents. People with a high risk of developing allergic reactions, with neuropsychiatric pathologies, and frequent stress are also at risk. A tendency to a slow heart rate is observed in people who are passive and phlegmatic by nature. The heart works more slowly in children with reduced body weight. Some medications and physiotherapy procedures can act in a similar way.

Epidemiology

According to statistics, every fourth person on the planet suffers from bradycardia. About two thirds of all cases of the disease are bradycardia, which develops against the background of cardiovascular diseases (66% of cases). About 6% of cases are bradycardia, which develops against the background of nervous and mental diseases, 3% are bradycardia against the background of hormonal imbalance and metabolic processes, about 15% are against the background of osteochondrosis, other forms of bradycardia account for 10% of cases.

Causes bradycardia

It is believed that bradycardia is caused by anatomical, physiological mechanisms, and the constitution of the human body. Practicing cardiologists only partially share this point of view. Of course, everyone confirms: this is a slowdown in the heart's work, and it can be considered both as a normal variant and as a pathology. But there is no unanimous opinion regarding which heart rate indicator should be taken as a critical limit. Some are inclined to believe that bradycardia should be considered a condition in which the heart rate reaches values below 60 beats per minute. Others are inclined to believe that bradycardia can be considered values below 50 beats per minute. Bradycardia requires mandatory diagnostics and, if necessary, treatment.

Heart disease causing bradycardia

The main causes of life-threatening bradycardia are: sick sinus syndrome, second-degree atrioventricular block (especially second-degree atrioventricular block, Mobitz type II), third-degree atrioventricular block with a wide QRS complex.

There are a number of diseases that cause bradycardia. For example, it can develop against the background of cardiac arrhythmia, angina pectoris, myocardial infarction, ischemic heart disease, endocarditis, pericarditis, and even hypotonic or hypertensive disease. In some cases, bradycardia can even be a harbinger of sudden death, heart failure.

Bradycardia and alcohol

There are also cases where alcohol causes bradycardia. This is observed with alcohol intoxication (if a person has consumed an excessive amount of alcohol), with regular and systematic alcohol consumption, against the background of alcoholism, when consuming low-quality alcohol, especially if the alcohol contains methanol, or the ethanol level is exceeded.

If a person has a history of heart disease, including bradycardia, alcohol should be excluded. It should also be taken into account that bradycardia may develop when taking certain medications and alcohol at the same time. Almost all alcohol poisoning, intoxication, and hangover syndromes are accompanied by bradycardia. This may be a temporary condition, or it may develop into a chronic pathology.

Drugs that cause bradycardia

There are a number of drugs that cause bradycardia: propanolol, enalapril, novocaine, quinidine, norpase, disopyramide, lidocaine, all potassium and magnesium preparations, calcium gluconate. Potentially, alcohol-containing infusions cause bradycardia.

• Bisoprolol

Bisoprolol is prescribed one tablet 1-2 times a day. Normalizes the condition of the coronary vessels, improves automatism and other functions of the heart. Provides its nutrition and protection.

Bradycardia with high blood pressure, hypertension

It occurs in every second elderly person and every fourth teenager (due to hormonal changes, accelerated weight gain is also observed).

Hypotension and bradycardia

Hypotension is accompanied by bradycardia (reduced tone of blood vessels), since the blood flow slows down and its volume decreases. The force of ejection also decreases. Signs of bradycardia are lethargy and insufficient activity.

Bradycardia after myocardial infarction

Bradycardia is a natural phenomenon, since myocardial infarction is caused by circulatory failure and after it a focus of necrosis (death) of individual areas occurs.

Bradycardia in VSD

Bradycardia with VSD is observed in every second person (the heart experiences excessive stress and is unable to fully adapt to stress, which is due to structural pathology of the heart and insufficient development of blood vessels).

Bradycardia during surgery, under anesthesia

During anesthesia, bradycardia often develops, since the pulse decreases.

Bradycardia and the thyroid gland

Bradycardia in hypothyroidism is quite common, since it significantly depends on the hormonal background, nervous regulation, and even on the state of the immune system, the general physical form of a person. The thyroid gland indirectly causes bradycardia. It disrupts the hormonal background, which affects the main properties of the heart, vascular tone decreases. First, bradycardia develops, then arrhythmia and extrasystole gradually develop.

Bradycardia in osteochondrosis

Osteochondrosis is often accompanied by bradycardia, which is quite easy to explain. Osteochondrosis is a disease of the spine, which causes pain and tightness in the back, pinching and displacement of the vertebrae and blood vessels. All this entails a decrease in vascular and muscle tone, bradycardia. It is known that bradycardia against the background of osteochondrosis currently occurs in 40 to 80% of cases, that is, it occurs in every third or fourth person on the planet.

Bradycardia with neurosis

Neurosis is often accompanied by bradycardia, since this is a condition in which vascular tone, blood pressure, pulse, and other vital signs of the body are sharply affected.

Bradycardia after tachycardia

Bradycardia can be observed after tachycardia, and this condition is called tachycardia and bradycardia syndrome. When bradycardia develops, it is necessary to take vitamins. Heart diseases are associated primarily with a lack of vitamins B, H, PP. Basically, traditional treatment, surgical methods of treatment are used as a last resort. The main method of surgical treatment is the installation of a pacemaker to regulate the heart rhythm.

Risk factors

The risk group includes people prone to emotional reactions, suffering from neuroses, mental illnesses. Risk factors include heart and blood vessel diseases, hormonal disorders, age (most often found in adolescents, the elderly). Bradycardia is observed in premature babies due to the immaturity of the cardiovascular system and insufficient adaptation to new conditions of functioning (outside the mother's body).

Pathogenesis

The pathogenesis is based on a violation of vascular tone, a decrease in the strength of the cardiac impulse, which entails a decrease in tone, as well as a decrease in contractile activity and automatism of the heart. There is a decrease in the frequency of contraction of the heart muscle, as a result of which blood is less often ejected from the ventricle of the heart into the aorta. The internal organs receive much less oxygen and nutrients. The basis is also a decrease in the trophism of the heart itself.

Forms

Depending on the degree of danger, the following are distinguished:

• severe bradycardia (heart rate < 40 beats per minute), which is rarely physiological and rarely asymptomatic, almost always requires treatment;
• moderate bradycardia (heart rate 40-60 beats per minute), which requires immediate treatment only in the case of arterial hypotension (systolic blood pressure < 90 mm Hg), hemodynamic disturbances and heart failure.

Diagnostics bradycardia

Diagnosis of bradycardia is aimed at identifying the etiological and pathogenetic factors that trigger the development of pathology and support its course. It is important to make the correct diagnosis, since further treatment will be selected on this basis. There are also cases when treatment is not required at all, since bradycardia can be a natural physiological state of the body.

To make a correct diagnosis, you need to see a cardiologist who will conduct an examination, if necessary, prescribe appropriate laboratory tests, instrumental studies. If necessary, he will refer you for consultation with other specialists. Often you have to see an endocrinologist, since bradycardia often develops against the background of thyroid dysfunction, or with diabetes.

What awaits you at the appointment? In any case, the first thing the doctor will do is conduct a survey and examination (collect anamnesis). The main method is a standard examination (the doctor listens to the heart tones, listens for wheezing, whistling, noise, determines the rhythm, strength, intensity of the heartbeat, the zone of cardiac dullness). A timely visit to the doctor allows already at the stage of early examination to assume the presence or absence of pathology, make a preliminary diagnosis and select methods of further research to confirm or refute this diagnosis.

Tests

The main methods are considered to be instrumental, in particular, ECG. Laboratory tests are prescribed less often, but they can also be very informative for any heart pathology. As with other diseases, tests are usually prescribed for any diagnosis. A clinical blood test is often prescribed (since blood is the main biological fluid of the body, reflecting all changes in the body). Much depends on the composition, concentration, thickness, viscosity of the blood. In particular, this affects the intensity of the heart.

Let's look at the main indicators that may indicate pathological bradycardia:

• A decrease in the number of platelets (red blood platelets that determine the function of blood clotting and its viscosity).
• An increase in the number of leukocytes may indicate the development of an inflammatory process, increased stress, maladaptation. A decrease in the number of leukocytes may indicate anemia, leukemia, oncological processes, immunodeficiency.
• An increase in the number of neutrophils may indicate the presence of heart inflammation.
• A decrease in neutrophils indicates tension in the immune system, protracted inflammatory processes, and the presence of a progressive infection, in which it is already detected in the blood.
• An increased number of eosinophils and basophils may indicate an allergic reaction, parasitic infection, or the presence of protozoa in the body. An increase in eosinophils is also observed during blood transfusions, during pregnancy, after operations, and organ and tissue transplants.
• ESR – erythrocyte sedimentation rate indicates in which direction and with what intensity inflammatory and autoimmune processes are occurring in the body.
• The development of bradycardia may also be indicated by a number of changes in the biochemical state of the blood: an increase in the enzymatic activity of creatine phosphokinase, aspartate aminotransferase, and lactate dehydrogenase.

Instrumental diagnostics

Instrumental methods cannot be avoided to examine the condition of the heart. The main method is to measure the pulse and pressure using a tonometer. To do this, the tonometer tourniquet is applied to the arm (to the brachial vein, artery), after which the vessel is compressed. The chamber is inflated, a phonendoscope is applied to the vessel to listen to heartbeats. When the chamber is deflated, the pulse and pressure are counted (the readings are displayed on the display).

The second method is an electrocardiogram, which records the heart rhythm. The doctor then deciphers it and makes a diagnosis. In rare cases, echocardiography is used, which allows identifying the causes of bradycardia, ultrasound of the heart, computer or magnetic resonance imaging.

Sinus bradycardia on ECG

On the ECG, sinus bradycardia can be recognized by such signs as an increase in the interval between the two upper teeth R - R, which occurs due to the interval T - P. The interval P - Q is of normal duration, or slightly exceeds the norm (up to 0.21 - 0.22 sec.). One of the main symptoms is a heart rate of less than 60 per 1 min.

Differential diagnosis

Differential diagnostics consists of differentiating the signs of bradycardia and the signs of other diseases that have similar signs. It is very important to differentiate the pathological condition and the norm, although the line between them can be very thin. This is due to the fact that treating a healthy heart can be dangerous, since such treatment, on the contrary, can provoke some disease, up to myocardial infarction. The main methods of differential diagnostics:

• electrocardiogram method,
• echocardiography method,
• electrophysiological methods,
• functional tests.

The clinical picture of the pathology and anamnesis data are important. Bradycardia may be a hereditary pathology, so genetic screening may be required.

Treatment bradycardia

Severe bradycardia or central hemodynamic disturbances with moderate bradycardia are treated with intravenous administration of 0.5 mg (0.5 ml of 0.1% solution) of atropine. If necessary, repeated administrations of atropine are administered up to a maximum dose of 3 mg (3 ml of 0.1% solution). In patients with myocardial infarction, atropine should be administered with caution, since atropine-induced tachycardia can worsen myocardial ischemia and increase the extent of damage.

If atropine has a positive effect and there are no hemodynamic disturbances, the risk of asystole should be assessed. The main criteria for the risk of asystole are:

• asystole that has already occurred in the recent past;
• second-degree atrioventricular block Mobitz II, complete transverse block with wide QRS complexes;
• cessation of ventricular activity (ventricular pause) exceeding 3 seconds.

If there is a significant risk of asystole, a resuscitation team or a specialist should be called to perform cardiac pacing.

Temporary endocardial stimulation is optimal. It is performed by inserting an endocardial electrode into the right heart through the lumen of the catheter (by catheterization of the superior vena cava via subclavian or jugular access). If temporary endocardial stimulation is impossible, transcutaneous cardiac stimulation is indicated. If cardiac stimulation is impossible or ineffective, intravenous administration of adrenaline at a rate of 2-10 mcg/min is recommended (by titration until an adequate hemodynamic response is achieved).

Fist pacing may be used as a temporary measure to treat conditions such as ventricular activity or severe bradycardia while preparations are underway for other methods of pacing the heart.

If the treatment is ineffective, the beta-adrenergic stimulant isoprenaline is indicated, which is capable of exerting a stimulating effect on the myocardium. The drug is administered intravenously by drip titration at a rate of 2-20 mcg/min. In cases where severe bradycardia is caused by the use of beta-blockers or calcium antagonists, intravenous glucagon is indicated. The drug is capable of exerting an ino- and chronotropic effect on the heart due to an increase in the formation of cAMP, i.e. it causes an effect similar to beta-adrenergic receptor agonists, but without their involvement.

In case of intoxication with beta-blockers, glucagon is administered at a rate of 0.005-0.15 mg/kg with a transition to maintenance infusion intravenously by drip at a rate of 1-5 mg/h.

In case of calcium antagonist intoxication, the drug is administered intravenously as a bolus at a dose of 2 mg. Maintenance doses are selected individually depending on the patient's condition. There is no point in administering atropine to patients after a heart transplant. Due to myocardial denervation, administering atropine to them will not lead to an increase in the heart rate, but can cause a paradoxical atrioventricular block.

Complete atrioventricular block with non-widened QRS complexes is not an absolute indication for cardiac pacing. In these cases, the rhythm comes from the atrioventricular junction and can provide sufficient hemodynamic stability and organ perfusion. As a rule, such patients have a good effect from atropine administration, and the risk of asystole in them is considered low.

Sometimes cardiac arrest is caused by Adams-Stokes-Morgagni syndrome, which is characterized by the cessation or sharp slowing of effective contractile activity of the heart. An attack occurs during the period of extinction of the His bundle conduction during the transition of incomplete atrioventricular block to complete, as well as with a sharp suppression of ventricular automatism or the occurrence of asystole and ventricular fibrillation in patients with a permanent form of complete block. In this case, pronounced bradycardia is observed, ventricular contractions sharply slow down, reaching 20-12 per 1 minute, or stop completely, which leads to a disruption of the blood supply to the organs, especially the brain.

The syndrome manifests itself in attacks of loss of consciousness, sudden pallor, respiratory arrest and convulsions. Attacks last from several seconds to several minutes and pass on their own or after appropriate treatment, but sometimes end fatally.

Adams-Stokes-Morgagni syndrome is most often observed in patients with atrioventricular block grades II-III, but sometimes it also occurs with syndromes of sinus node weakness, premature ventricular excitation, paroxysmal tachycardia, and attacks of atrial tachyarrhythmia.

When an attack of Adams-Stokes-Morgagni syndrome develops, resuscitation measures must be carried out, as with any circulatory arrest. However, there is rarely a need for full resuscitation, since cardiac activity is most often restored after indirect cardiac massage.