Coding for chronic heart failure in μb. Chronic heart failure (doctor's workbook) Chronic cardiopulmonary failure mkb 10

The clinical picture is characterized by the development of respiratory distress - the appearance at night (during sleep) of a dry cough, tachypnea and paroxysmal, increasing shortness of breath or suffocation due to the fact that the venous return of blood to the heart increases in the supine position, or in connection with an acute cardiac catastrophe that occurs. in a patient with CHF. There is a rapid increase in the load on the left side of the heart, with which it cannot cope. Additionally, during sleep, the sensitivity of the central nervous system decreases, which impairs gas exchange in the lungs; in the supine position, there is no compensatory increase in respiratory rate.
The attack sometimes passes quickly without treatment (“thanks to the open window”), but, as a rule, it tends to drag on - from ten minutes to several hours. The nature of the attacks, the severity of their course and the prognosis are varied. In some cases, an attack of CA has "harbingers" (in the previous 2-3 days the patient notes an increase in shortness of breath and the frequency of attacks of dry cough), while in others it does not (as in mitral stenosis).
The patient wakes up (often in fear), his breathing becomes frequent (RR up to 30-40 breaths per 1 min) and superficial (as in an "overheated or driven dog") due to irritation of the respiratory center. The patient occupies a forced position - orthopnea (sitting, with his legs down), sometimes with an emphasis on his hands to include auxiliary muscles in the act of breathing, which reduces blood stasis in the pulmonary circulation. Palpitations appear (or increase) (heart rate more than 120-150 beats / min), a strong feeling of lack of air - shortness of breath of an inspiratory or mixed type (patients “catch air with their mouths” and speak with difficulty), coughing.
At first it is dry (slight coughing), later it becomes productive, with a small amount of light-colored sputum, sometimes streaked with blood. Blood pressure can be high, and then sharply decrease before our eyes, signaling a collapse.
If a rapid rise in pressure is formed in the pulmonary circulation (more than 50 mm, which exceeds the capabilities of the Kitaev reflex), then rapid fluid retention in the interstitium begins. She enters it, but cannot return back due to high venous pressure. A small amount of fluid also enters the lumen of the alveoli, which causes an organic blockade of gas exchange (between the air and the capillary is not only the epithelium, but also a layer of liquid). This leads to an accelerating progression of dyspnea, which until a certain time is actually a compensatory mechanism.
Diagnostics includes a variety of research methods. Objectively, the face becomes pale with a cyanotic tint, the skin is covered with drops of cold sweat (this is due to a decrease in the functioning of the LV myocardium and an increase in sympathetic stimulation). The patient behaves uneasily, sometimes complains of pain in the heart (if CA has developed against the background of MI). On inspiration, retraction of the intercostal spaces and supraclavicular fossae is noted - a sign of high negative intrathoracic pressure necessary for breathing. The borders of the heart are more often displaced to the left.
Auscultation of the heart (sometimes difficult due to wheezing and a lot of wheezing) can reveal a symptom of the disease that caused ALVN, deafness of heart sounds, accent of the 2nd tone over LA, gallop rhythm. The pulse is frequent, weak filling, often alternating or filiform. If there is no CABG, then BP first rises (as a result of sympathetic stimulation), rarely remains normal, and then decreases.
When listening to the lungs, first determine the manifestations of broncho-obstructive syndrome (due to swelling of the respiratory mucosa) - an elongated and noisy exhalation, "hard" breathing, single and scattered dry rales (therefore, such patients are often and dangerously confused with patients suffering from true BA) or short-term crepitus due to fluid moistening of the walls of the alveoli. Later, silent, single moist or crepitant rales occur (due to the appearance of a small amount of fluid in the small bronchi, bronchioles and alveoli) immediately in the upper sections of the lungs, and then in the posterior sections of the lungs on both sides.
On a chest x-ray, signs of venous stasis, plethora are usually determined; expansion of the roots of the lungs; fuzziness and increased lung pattern (due to edematous infiltration of the peribronchial interstitial tissue), thin Kerley lines, reflecting swelling of the interlobar septa and elements of infiltration.
On the ECG, the amplitude of the teeth, the ST interval decrease, and changes characteristic of the underlying disease are also determined.

congestive heart disease

Right ventricular failure (secondary to left ventricular heart failure)

Left sided heart failure

Cardiac(s) or myocardial failure NOS

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to contact medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

Symptoms and treatment of chronic heart failure

Interesting! Huge amounts of money are allocated worldwide for the treatment of heart failure, for example, in the United States, costs are $40 billion annually. The percentage of morbidity is constantly increasing, more often people are hospitalized after 65 years.

Chronic insufficiency can be characterized as follows - it is the failure of the cardiovascular system. It is expressed in the impossibility of providing the necessary volume of blood to the internal organs and muscle tissues that need it. The chronic form develops in conditions of violation of cardiac functions, more precisely, the myocardium. Even with increased pressure, it cannot push all the blood out of the heart cavity.

Causes of the pathological process and how it occurs

The main cause is damage to the middle layer of the heart muscle, the aorta following directly from it, or the valves. This can occur in the presence of ischemia, inflammatory processes in the heart muscle, cardiomyopathy, as well as systemic disorders of the connective tissue of the body. Lesions can be toxic in nature. This occurs when poisoning with toxic substances, poisons, medicines.

Blood vessels, a large unpaired artery can be affected in such diseases:

• atherosclerosis;
• persistent increase in pressure;
• when blood sugar levels rise and there is a deficiency of the hormone insulin.

Chronic heart failure is also provoked by heart defects of congenital or acquired origin.

When blood circulation slows down, oxygen starvation of all the insides of the body begins. Their sequence depends on the amount of consumed substances and blood. One of the characteristic manifestations of this condition is shortness of breath during exertion and at rest. The patient may complain of not sound sleep, tachycardia and excessive fatigue.

The symptoms that are characteristic of this condition are determined by the functioning of which part of the heart is difficult. Sometimes cyanosis is observed, i.e. the acquisition of the skin on the fingers and lips of a gray-bluish hue. This indicates a lack of oxygen in distant parts of the body. Swelling of the legs and other parts of the body is caused by the fact that blood stagnates in the venous bed. If there is an overflow of the veins of the liver, then pain is noted in the region of the right hypochondrium.

As the pathological process develops, the above symptoms worsen.

CHF (Chronic heart failure) ICD-10

Chronic heart failure is a pathological condition in which there are problems with the nutrition of the heart, due to its insufficient blood supply.

CHF syndrome according to ICD-10 (International Classification of Diseases) is a pathology that occurs only against the background of other serious diseases.

It has many typical clinical signs that make it possible to suspect a disease, even without being a physician.

The essence of pathology, the mechanism of its development

Chronic heart failure can develop over months. This process is divided into several main stages:

• Due to heart disease or organ overload, the integrity of the myocardium is disrupted.
• The left ventricle contracts incorrectly, that is, weakly, due to which not enough blood enters the heart vessels.
• compensation mechanism. It is launched if necessary for the normal functioning of the heart muscle in difficult conditions. The layer on the left side of the organ thickens and hypertrophies, and the body releases more adrenaline. The heart begins to contract faster and stronger, and the pituitary gland produces a hormone, due to which the amount of water in the blood increases significantly.
• When the heart is no longer able to supply organs and tissues with oxygen, the body's reserves are exhausted. Oxygen starvation of cells occurs.
• Due to a serious violation of blood circulation, decompensation develops. The heart beats slowly and weakly.
• Heart failure occurs - the inability of the body to supply the body with oxygen and nutrients.

Classification

According to ICD-10, CHF is divided into three stages depending on the course of the disease:

• First. Clinical manifestations occur in a person only after physical exertion, and there are no signs of stagnation in the blood circulation.
• Second. There are signs of congestion in one or two circles of blood flow.
• Third. There are persistent violations and irreversible processes in the body.

Depending on the state of the left ventricle, two variants of CHF are distinguished:

• systolic function of the left lower chamber of the heart is preserved,
• there is left ventricular dysfunction.

Chronic heart failure is also divided into functional classes:

• I - ordinary physical activity does not provoke any clinical signs.
• II - during physical activity, symptoms of heart failure appear, so a person is forced to limit himself in work.
• III - the clinic is pronounced even with minor loads.
• IV - complaints occur in a patient at rest.

The reasons

The CHF code according to the ICD is I50. This syndrome, in fact, is an unfavorable outcome of most heart diseases, and in particular coronary artery disease and hypertension (up to 85% of cases). A quarter of cases of CHF incidence can be caused by such reasons:

Very rarely, chronic heart failure is caused by factors such as:

In any case, if a person suffers from any of the aforementioned disorders, his heart gradually becomes weaker and his pumping function deteriorates.

Clinical picture

Signs of chronic heart failure depend on the severity of the course of the disease and related disorders in the body. Typical complaints of patients with CHF are:

• development of shortness of breath. First, rapid breathing appears due to physical activity, later - even at rest;
• nocturnal suffocation - a phenomenon when the patient wakes up from the fact that he cannot breathe and feels the need to get out of bed;
• shortness of breath in an upright position (it happens that the patient has difficulty breathing in a standing or sitting position, but when he lies on his back, the respiratory rate returns to normal);
• general weakness and fatigue;
• dry cough arising from stagnation of blood in the lungs;
• nocturnal diuresis prevails over daytime (frequent urination at night);
• swelling of the legs (first, the feet and legs swell symmetrically, then the thighs);
• development of ascites (accumulation of fluid in the abdomen).

Another pronounced sign of chronic heart failure is orthopnea - the forced position of the patient, in which he lies with his head raised, otherwise he develops shortness of breath and dry cough.

Diagnostic Measures

When diagnosing a patient, one cannot do without a visual examination, in which the doctor will clearly see the typical symptoms of CHF - edema, pulsation and swelling of the veins, an increase in the abdomen. On palpation, “splash noises” are detected, which confirm the presence of free fluid in the peritoneum.

With the help of auscultation, accumulation of fluid in the lungs (wet rales) can be detected. The patient's heart and liver are enlarged.

To clarify the diagnosis, the doctor is assigned a number of hardware studies:

• electrocardiogram - reveals changes inherent in diseases that led to chronic heart failure;
• Ultrasound of the heart - allows you to detect expansion of the cavities of the body, signs of regurgitation (reflux of blood from the ventricles back into the atria), as well as to study the contractility of the ventricles;
• chest x-ray - helps to determine the size of the heart, as well as to detect congestion in the lungs.

Treatment

The main principle of the treatment of chronic heart failure is to slow the progression of the disease, as well as alleviate the symptoms. Conservative therapy involves lifelong use of heart drugs and other drugs that improve the patient's quality of life.

The drugs that a doctor prescribes for CHF include:

• ACE inhibitors, which lower the level of pressure inside the vessels;
• beta-blockers, which reduce the heart rate and overall vascular resistance, as a result of which blood can move freely through the arteries;
• cardiac glycosides, which increase the contractility of the heart muscle with a decrease in the frequency of contractions;
• anticoagulants that prevent thrombosis;
• calcium channel antagonists, which relax blood vessels and help lower blood pressure;
• nitrates, which reduce blood flow to the heart muscle;
• diuretics - are prescribed to relieve congested organs and reduce swelling.

Prevention

Primary prevention helps to prevent the development of diseases, the direct consequence of which is CHF.

If such a disease already occurs and it cannot be completely cured, secondary prevention is indicated for patients. It prevents the progression of CHF.

Patients with chronic heart failure should give up bad habits, take caffeine-containing products, reduce the amount of salt in the diet.

Nutrition should be fractional and balanced. You need to eat high-calorie, but easily digestible foods. You should limit physical activity and strictly follow all doctor's instructions.

Chronic heart failure ICD code 10

Types, symptoms and treatment of myocardial dystrophy of the heart

Myocardial dystrophy is a specific cardiac disease of non-inflammatory origin, which is characterized by a violation of metabolic processes in myocytes, cardiac muscle, changes in the contractility of the heart, and the development of heart failure. The code for this disease according to the International Classification of Diseases (ICD)10 revision (ICD10) is not assigned.

• Causes
• Disease classification
• Clinical picture
• Diagnostics
• Treatment
• Traditional medicine recipes
• Prevention

This disease responds well to treatment with timely and high-quality diagnosis.

Causes

Myocardial dystrophy, as an independent disease, occurs very rarely, it is mainly a secondary pathology. All causes of myocardial dystrophy that contribute to the violation of the trophism of the heart can be divided into two groups:

• cardiac - myocarditis, cardiomyopathy;
• non-cardiac - intoxication, anemia (microbial code 10-d64.9), metabolic disorders, infectious diseases, as a result of external factors, such as radiation, overheating, weightlessness and others.

One of the causes of myocardial dystrophy is myocarditis.

Under the influence of all of the above reasons, the cells of the heart muscle experience a lack of nutrients, oxygen, and intoxication from metabolic products. As a result, the cells of the active tissue of the heart die, and they are replaced by rough scar tissue. Accordingly, the functions of the heart muscle are inhibited:

As a result of these pathological processes, there is a violation of blood circulation in the body, from which all organs and systems of the human body suffer.

Disease classification

Cardiologists distinguish several types of heart dystrophy:

Hypertrophied heart is one of the types of organ dystrophy

According to the severity of the disease:

• Compensation - hemodynamics is maintained at a normal level, adren-dependent repolarization deviations are found in the heart tissues;
• Subcompensation - with dosed physical activity, the mechanisms of hemodynamics are strained, moderately severe myocardial dystrophy;
• Decompensation - with dosed physical activity, pronounced deviations of hemodynamics, persistent violations of repolarization, a sharp decrease in the contractile function of the heart muscle are observed.

Classification of myocardial dystrophy depending on the pathogenesis:

• primary myocardial dystrophy - the cause of the disease has not been established;
• secondary myocardial dystrophy - occurs against the background of another disease, as a complication.

Depending on the disease that caused the dystrophy of the heart:

• Dishormonal dystrophy occurs in men and women, and is associated with a violation of the production of sex hormones. This disease is accompanied by increased fatigue, sleep disturbance, constant thirst and a sharp decrease in weight, as well as pain in the region of the heart, aching and stabbing.
• Tonsillogenic myocardial dystrophy is a complication of tonsillitis, which is accompanied by impaired endurance, arrhythmia, and aching heart pain.
• Alcoholic myocardial dystrophy - develops as a result of prolonged (chronic) alcohol intoxication. Ethanol destroys the membranes of heart cells, reducing the amount of potassium and fatty acids in it. Hypokalemia is always accompanied by arrhythmia, shortness of breath. Moreover, pain in the region of the heart is practically absent.
• Diabetic cardiac dystrophy (code E10-E14 + with a common fourth sign. 5) - occurs in type I diabetes mellitus, accompanied by diabetic pathology of the coronary vessels, angina pectoris.
• Anemic myocardial dystrophy - often occurs during pregnancy (code O99.4). In most cases, in the later stages of pregnancy, late toxicosis joins it. But, obstetricians claim that myocardial dystrophy during pregnancy is not an indication for its termination.

Clinical picture

At an early stage of the disease, myocardial dystrophy does not make itself felt and is asymptomatic. In the absence of adequate treatment, heart failure may develop, which can be fatal. Therefore, it is urgent to contact a cardiologist if the first alarming symptoms occur:

• shortness of breath and palpitations that occur with the slightest physical exertion;
• increased fatigue and weakness;
• discomfort that is felt in the left half of the chest;
• paroxysms of nocturnal and evening coughing with much sputum.

Depending on the cause and type of disease, the symptoms of myocardial dystrophy may vary.

Diagnostics

The clinical picture of this disease is very similar to the symptoms of other cardiac diseases. Therefore, a highly qualified cardiologist should make a diagnosis by conducting a series of diagnostic procedures:

• X-ray examination;
• echocardiography;
• phonocardiography;
• general and biochemical blood test;
• MRI and CT.

Nuclear magnetic resonance imaging is considered a breakthrough in the diagnosis of myocardial dystrophy.

Radioactive phosphorus will be injected into the human body, the content of which will be studied in the cells of the heart muscle.

The most reliable instrumental diagnostic method is myocardial biopsy, but this type of diagnosis is not welcomed by cardiologists. The reason for this is the high likelihood of complications after the procedure.

Diagram of a heart biopsy

Treatment

Treatment of myocardial dystrophy depends on the severity and severity of the disease, taking into account the individual characteristics of the patient's body. That is why the course of treatment should be prescribed by a highly qualified cardiologist. The standard course of therapy has several directions:

• correction and treatment of the underlying disease;
• vitamin therapy;
• restorative therapy;
• sedatives;
• stimulation of metabolic processes in the myocardium.

With increasing heart failure, it is necessary to prescribe diuretics, potassium preparations and cardiac glycosides.

With timely diagnosis and treatment, myocardial dystrophy responds well to therapy.

In addition to medications, you need to change your lifestyle:

• balanced natural nutrition;
• high physical activity;
• to give up smoking;
• exclusion of alcohol;
• full healthy sleep;
• avoidance of stress.

Traditional medicine recipes

With the effectiveness of drug treatment, one should not deny the effect of treatment with folk remedies. But only on the recommendation of the attending physician, in no case on the advice of a neighbor. With myocardial dystrophy, treatment with folk remedies comes down to taking light soothing teas based on mint, lemon balm, motherwort. With swelling, renal diuretic fees will help. But all drugs must be prescribed by the attending physician!

Prevention

Preventive measures include:

• healthy fortified diet;
• proper sleep and rest;
• rejection of bad habits;
• when playing sports, the load should correspond to age and training;
• all endocrine, infectious and cardiac diseases should be treated in time under the supervision of a doctor.

Myocardial dystrophy: classification, treatment, symptoms

Myocardial dystrophy is a diagnosis that can be deciphered even by those whose interests do not in any way intersect with the study of medical terminology. Almost every person, passing an annual professional examination in a clinic, is faced with such concepts as a cardiologist, cardiogram, etc. The basis of these words is "cardio" - which in Greek means heart. Dystrophy is an equally well-known concept, which means "weakness as a result of malnutrition."

Definition

Myocardial dystrophy of the heart is a pathology in which the cells of the heart muscle (myocytes) are affected due to a violation of metabolic processes in them. The changes are both structural and functional. As a result, the heart is not able to fully perform its main function - pumping blood. With myocardial dystrophy, its contractility decreases. This is manifested in a violation of blood circulation through the vessels and insufficient supply of organs and tissues with oxygen.

At the same time, other important functions of the main pump are inhibited - automatism, conductivity, as well as excitability.

Myocardial dystrophy is a secondary pathology. It develops as a complication of other diseases.

Types of myocardial dystrophy

The classification of myocardial dystrophy divides the disease into several types.

dishormonal

With age, against the background of hormonal disruptions, dyshormonal myocardial dystrophy can develop. In males over 50 years of age, the causative factor is usually disturbances in the process of testosterone synthesis, in women after 45 years of age - hormonal disruptions associated with "entry" into the menopause, or with cycle failures due to diseases of the organs of the reproductive system.

Estrogens are hormones that regulate many metabolic processes in the body, including electrolyte and protein metabolism. With insufficient estrogen secretion, the heart muscle receives less glucose, iron, phosphorus, copper, fatty acids and energy.

In some cases, this type of myocardial dystrophy may be the result of thyroid diseases, accompanied by its hypo- or hyperfunction.

Dysmetabolic

With violations in metabolic processes that are associated with malnutrition, dysmetabolic myocardial dystrophy develops. In this case, first of all, protein and carbohydrate metabolism “suffer”.

The reasons for these violations can be:

• avitaminosis;
• amyloidosis;
• diabetes;
• eating food that is low in protein components and iron.

mixed

Anemia, endocrine pathologies, lack of vitamins, metabolic disorders associated with hyperfunction of the thyroid gland in combination can lead to the fact that a child (or an adult) will develop myocardial dystrophy of mixed genesis.

Myocardial dystrophy according to ICD-10 has no code.

Clinical manifestations

If myocardial dystrophy develops, the symptoms depend on which cause is the main cause of the disease. However, there are a number of signs characteristic of any type of this pathology:

• pain in the heart of a pressing or aching character;
• discomfort and tingling in the heart muscle;
• general weakness;
• chronic fatigue;
• shortness of breath that occurs with physical (even slight) overstrain;
• heart rhythm failures;
• swelling (more often on the lower extremities by the end of the day).

If myocardial dystrophy develops in an athlete, there is a strong and sudden fatigue after training.

Diagnostics

There are no specific methods for diagnosing myocardial dystrophy. If dystrophic changes in the heart are suspected, the doctor prescribes a complete examination to the patient, which necessarily includes an ultrasound examination of the heart muscle and an ECG.

Treatment of myocardial dystrophy

With myocardial dystrophy, treatment is aimed, first of all, at eliminating the root cause. If such therapy is not available, symptomatic treatment will bring only temporary relief.

From medicines use:

• vitamin complexes;
• anabolic steroid;
• potassium orotate;
• inosine;
• cocarboxylase.

For the successful treatment of myocardial dystrophy, the patient needs to adjust the daily routine, not physically overstrain, forget about alcohol and cigarettes. Nutrition should be balanced and rich in vitamins. If there are chronic infectious foci, they need to be eliminated. In some cases, patients with a diagnosis of "myocardial dystrophy" are advised to change jobs in the presence of unfavorable conditions.

In the therapy of myocardial dystrophy, the use of stem cells gives a good effect. At the first stage, material is taken from the patient. Further, the most viable ones are isolated from the total number and grown. Then, in two stages, the resulting material is injected into the heart. There, new healthy cells begin to divide intensively, replacing the pathological area.

With timely started adequate treatment, the prognosis for myocardial dystrophy is favorable.

ICD coding for chronic heart failure

The disease is located in the class of pathologies of the circulatory organs, and the CHF code according to ICD 10 is as follows: I50. This section is divided into several varieties, where the forms of heart failure are indicated.

There are the following options for encoding the diagnosis according to the ICD:

• I0 - congestive heart failure. Another name for the pathological process is right ventricular failure. It is accompanied by stagnation of blood in the systemic circulation, as evidenced by edema in the lower extremities.
• I1 - left ventricular failure of the heart. The disease is also called cardiac asthma, as it leads to disorders in the pulmonary circulation. This also includes acute pulmonary edema, which is formed due to pulmonary hypertension.
• I9 - unspecified CHF. A mixed type of pathology, which occurs most often, since the processes in the small and large circles of blood circulation are closely related.

Sometimes chronic heart failure in ICD 10 has a code that belongs to a different category. For example, the occurrence of CHF in pathologies of the kidneys, lungs, hypertension, in the neonatal period and in people with heart prostheses. Separately encoded CHF in women due to ectopic pregnancy or abortion.

General information about the disease

In cardiology, CHF is rather not a separate disease, but a complication of already existing pathological processes.

Deficiency develops due to a long decompensated state, most often with heart disease.

The problem is that patients with cardiovascular pathology tend to ignore the symptoms of their disease for a long time and reject medical care. It is impossible to start the problem, since the result of the progression of the pathological process will be acute cardiovascular failure. This condition has two forms: unstable angina and myocardial infarction.

CHF is confirmed not only by a non-specific clinical picture, which may indicate dozens of other diseases, but also by instrumental research methods.

Cardiological diagnoses usually have a long wording, as they require clarification of the severity of the process, etiological factors and concomitant diseases related to the circulatory system.

When registering chronic insufficiency, the degree of development of the process is specified. In ICD 10, CHF does not require additional divisions, however, in the clinical practice of a cardiologist, one cannot do without them. The severity of the process depends on the dosage of drugs, recommendations for lifestyle and future forecasts.

After establishing this diagnosis, the main task of the medical staff is to maintain the body at the same level, since the problem cannot be completely cured, as well as to eliminate the risks for the development of acute coronary blood supply insufficiency.

ICD code 10 chronic heart failure

Chronic heart failure

CHRONIC HEART FAILURE

Chronic heart failure (CHF) is a disease with a complex of characteristic symptoms (shortness of breath, fatigue, decreased physical activity, edema, etc.) associated with inadequate perfusion of organs and tissues at rest or during exercise.

ICD-10 CODE

• I50.0 Congestive heart failure

Classification of CHF by the New York Heart Association by severity.

• I functional class. Ordinary physical activity is not accompanied by fatigue, palpitations, shortness of breath or angina pectoris. This functional class occurs in patients with heart disease that does not lead to limitation of physical activity.
• II functional class. At rest, patients feel well, but ordinary physical activity causes fatigue, shortness of breath, palpitations, or angina pectoris. This functional class occurs in patients with heart disease that causes mild limitation of physical activity.
• III functional class. This functional class occurs in patients with heart disease that causes significant limitation of physical activity. At rest, patients feel well, but a small (less than usual) exercise causes fatigue, shortness of breath, palpitations or angina pectoris.
• IV functional class. This functional class occurs in patients with heart disease, due to which they are unable to perform any kind of physical activity without discomfort. Symptoms of heart failure or angina occur at rest; with any physical activity, these symptoms are aggravated.

The classification of CHF by the Society of Heart Failure Specialists (Russia, 2002) is presented in Table. one.

Table 1. Classification of CHF by the Society of Heart Failure Specialists (Russia, 2002)

Functional classes of CHF

(may change with treatment)

(does not change during treatment)

HISTORY AND PHYSICAL EXAMINATION

The most frequent complaints of patients with CHF (in descending order of frequency): shortness of breath, fatigue, palpitations, peripheral edema, cough, wheezing in the lungs, orthopnea, swollen jugular veins, hepatomegaly, cardiomegaly.

LABORATORY RESEARCH METHODS

• Complete blood count (determining the level of hemoglobin, the number of erythrocytes, leukocytes and platelets).
• Biochemical blood test (study of the concentration of electrolytes, creatinine, glucose, activity of liver enzymes in the blood).
• General urine analysis.

INSTRUMENTAL RESEARCH METHODS

Criteria for the diagnosis of diastolic heart failure are given below (the presence of the first two criteria is mandatory).

• Symptoms and signs of heart failure.
• Normal or slightly impaired systolic function of the left ventricle (left ventricular ejection fraction equal to or greater than 45-50%).
• Detection of violations of the relaxation of the left ventricle with the help of echocardiography.

In patients with CHF, it is possible to use various options for a stress test: a 6-minute walk test, bicycle ergometry, treadmill, including blood gas analysis. In routine practice, in the absence of special equipment, a walking test for 6 minutes can be used to assess physical tolerance and objectify the functional status of patients.

• The patient must walk continuously for 6 minutes, moving between two points located at a known distance.
• The patient can stop at will.
• The distance traveled by the patient in 6 minutes correlates with other performance indicators.
• The parameters for assessing the test with a 6-minute walk are shown in Table. 2.

Table 2. Parameters for scoring the 6-minute walk test

according to the New York classification

Other studies (24-hour ECG monitoring, determination of the neurohormonal profile, radioisotope study) do not occupy an important place in the diagnosis of CHF. A test widely used in developed countries for diagnosing CHF - determining the level of brain natriuretic peptide - is not yet available in outpatient clinics in the Russian Federation.

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS

• Unknown etiology of heart failure.
• Systolic blood pressure less than 100 mm Hg.
• The content of creatinine in the blood is more than 150 µmol/l.
• The content of sodium in the blood is less than 135 mmol / l.
• The content of potassium in the blood is more than 6.0 mmol / l.
• Severe heart failure.
• Valvular heart disease as a cause of heart failure.

• Diet.
• Mode of physical activity.
• Psychological rehabilitation, organization of medical supervision, schools for patients with CHF.
• Drug therapy.
• Electrophysiological methods of treatment.
• Surgical, mechanical methods of treatment.

• Prevention of the development of clinically pronounced CHF (at the stage of asymptomatic cardiac dysfunction).
• Elimination of symptoms of CHF.
• Slowing down the progression of the disease.
• Improving the quality of life.
• Reducing the number of hospitalizations.
• Forecast improvement.

INDICATIONS FOR HOSPITALIZATION

• With the ineffectiveness of outpatient treatment of patients with functional class IV CHF, severe fatigue and decreased performance, as well as with the ineffectiveness of diuretics.
• When planning parenteral administration of diuretics, vasodilators or drugs with a positive inotropic effect under the control of hemodynamic parameters, requiring pulmonary artery catheterization.
• In patients with very low cardiac output who require positive inotropic therapy.

Hospitalization is necessary in the presence of life-threatening arrhythmias or arrhythmias that worsen the course of CHF.

• Limiting the intake of table salt, and the more so, the more pronounced the symptoms of the disease and congestion.
  • I functional class - do not eat salty foods (restriction to 3 g of table salt per day).
  • II functional class - do not eat salty foods and do not add salt to food (limitation to 1.5 g of table salt per day).
  • III-IV functional class - do not eat salty foods, do not add salt to food, eat foods with a reduced salt content and cook food without salt (limitation of less than 1 g of table salt per day).
• Limitation of fluid intake is relevant only in extreme situations in a decompensated state, in which intravenous administration of diuretics is necessary. In normal situations, the volume of fluid is not recommended to increase more than 2 liters per day.
• Food should be high-calorie, easy to digest and contain enough vitamins and protein.

• There is no evidence of benefit from vaccination. It is advisable to use vaccines against influenza and hepatitis B.
• It is not recommended to stay in conditions of high mountains, high temperatures, humidity. It is advisable to spend your holidays in a familiar climate zone. When choosing transport, preference should be given to aviation.
• Smoking is strictly and absolutely contraindicated for all patients with CHF.
• sexual activity. The use of phosphodiesterase-5 inhibitors (sildenafil, etc.) is not contraindicated, except in combination with long-acting nitrates.

All drugs for the treatment of CHF can be divided into three main categories: basic, additional and auxiliary (Table 3).

Table 3 Drugs for the treatment of chronic heart failure

• ACE inhibitors
• beta-blockers

• Diuretics (for swelling)
• Spironolactone (with III-IV functional classes)
• Cardiac glycosides (with CHF combined with atrial fibrillation; with CHF refractory to treatment)
• Angiotensin-II receptor antagonists (with intolerance to ACE inhibitors)
• Warfarin (for atrial fibrillation)

• Vasodilators
• Calcium channel blockers
• Antiarrhythmic drugs
• Acetylsalicylic acid
• Statins
• Non-glycoside inotropic agents

*** Impact on prognosis is unknown; their use is determined by the clinical picture.

ACE inhibitors

• ACE inhibitors are indicated for all patients with CHF (any etiology and stage of the process, including asymptomatic left ventricular dysfunction).
• ACE inhibitors improve the clinical picture, quality of life, slow down the progression of the disease, reduce morbidity and improve the prognosis of patients with CHF, i.e. allow you to achieve all goals in the treatment of CHF.
• These drugs are considered the most reasonable way to treat CHF with preserved systolic function of the heart.
• The absence of the appointment of ACE inhibitors cannot be considered justified and leads to a deliberate increase in the risk of death in patients with CHF.

In table. 4 shows the doses of the most studied ACE inhibitors in the treatment and prevention of CHF, used in Russia.

Table 4. Angiotensin-converting enzyme inhibitors prescribed for the treatment of chronic heart failure

Initial dose for arterial hypotension

• The need for the use of diuretics and vasodilators and their dosages should be assessed.
• Do not allow excessive diuresis before starting treatment; diuretics should be discontinued 24 hours before the first use of ACE inhibitors.
• Therapy should be started in the evening when the patient is in a horizontal position to minimize the risk of arterial hypotension.
• It is recommended to start treatment with low doses and increase them to maintenance levels.
• With a significant deterioration in kidney function (an increase in the concentration of creatinine in the blood by more than 30% of the original), it is necessary to reduce the dose by half, and if there is no improvement, stop the ACE inhibitor.
• Potassium-sparing diuretics should be avoided at the start of treatment, especially in patients with high levels of potassium in the blood (more than 5.0 mmol / l); however, this does not contradict the recommendations for the combined use of ACE inhibitors with high doses of spironolactone during decompensation and the combination of ACE inhibitors with low doses of aldosterone antagonists in long-term treatment of CHF.
• It is recommended to avoid prescription of NSAIDs.
• It is necessary to control blood pressure and electrolytes in the blood 1-2 weeks after each dose increase.

beta-blockers

• beta-blockers should be prescribed to all patients with CHF who do not have contraindications common to this group of drugs.
• beta-blockers should only be used in addition to ACE inhibitors.
• beta-blockers in addition to ACE inhibitors are indicated in all patients with asymptomatic left ventricular dysfunction after myocardial infarction.
• it is desirable to prescribe beta-blockers to patients who have achieved stabilization of the state (there are no signs of stagnation, there is no need for parenteral therapy).
• Only four beta-blockers are recommended for the treatment of CHF: bisoprolol, carvedilol, metoprolol succinate (sustained release) and nebivolol.
• Treatment with beta-blockers in CHF should begin with 12.5% ​​of the therapeutic dose. Doses are increased slowly (not more than 1 time in 2 weeks) until the optimum is reached (Table 5).
• With worsening heart failure, the development of arterial hypotension or bradycardia during dose titration, the following algorithm should be followed.
• With worsening heart failure, it is necessary first of all to increase the dose of diuretics and ACE inhibitors, if necessary, temporarily reduce the dose of beta-blocker.
• In case of arterial hypotension, it is shown first of all to reduce the dose of vasodilators, if necessary, temporarily reduce the dose of beta-blocker.
• In case of bradycardia, the dose should be reduced or drugs that reduce heart rate should be discontinued, if necessary, reduce the dose of a beta-blocker or cancel the latter if there are clear indications.
• Always consider re-prescribing a beta-blocker or increasing its dose after stabilization of the condition.
• If inotropic support is required during circulatory decompensation in patients on constant therapy with beta-blockers, the calcium sensitizer levosimendan is considered the drug of choice, since its hemodynamic effect does not depend on the degree of blockade of beta-adrenergic receptors.
• Contraindications to the appointment of beta-blockers in CHF are severe bronchial asthma and / or chronic obstructive pulmonary disease, symptomatic bradycardia, arterial hypotension.

Table 5. Beta-blockers for the treatment of chronic heart failure

Some patients may be treated with non-recommended beta-blockers (most often atenolol or short-acting metoprolol tartrate). In table. 6 shows the scheme of transfer to the recommended drugs.

Table 6. Scheme for switching patients with chronic heart failure from atenolol and metoprolol tartrate to recommended beta-blockers

• CHF III-IV functional class.
• Heart failure of unknown etiology.
• The presence of relative contraindications: bradycardia, arterial hypotension, poor tolerance of low doses of beta-blockers, concomitant chronic obstructive pulmonary disease.
• Information about the withdrawal of beta-blockers in the past due to adverse reactions or exacerbation of heart failure.

Aldosterone antagonists (spironolactone)

• Aldosterone antagonists are prescribed in addition to ACE inhibitors and beta-blockers in patients with functional class III-IV CHF.
• The recommended dose of spironolactone for chronic heart failure is 25 mg/day.

• These drugs are indicated only for patients with III-IV functional class of CHF.
• Treatment should only be started if the potassium level in the blood does not exceed 5.0 mmol / l, and the concentration of creatinine is less than 1.7 mg / dl.
• The recommended dosage of spironolactone for long-term use is 25 mg/day.
• Shown control of the content of potassium and creatinine in the blood every 4-6 weeks.
• If, after the start of treatment, the level of potassium in the blood exceeds 5.0-5.5 mmol / l, the dose of spironolactone should be reduced by 50%, and if the level of potassium is more than 5.5 mmol / l, spironolactone therapy should be discontinued.
• If after a month of therapy the symptoms of heart failure are still pronounced, the dose of spironolactone should be increased to 50 mg / day (subject to normokalemia). After increasing the dose of spironolactone, control of the concentration of potassium and creatinine in the blood is shown after 1 week.

Diuretics

• Treatment with diuretics begins only with clinical signs of stagnation (stage II A, functional class II).

Table 7. Diuretics in chronic heart failure

Algorithm for prescribing diuretics depending on the severity of CHF

• I and II functional class without edema - no need to treat with diuretics.
• II functional class (stagnation) - thiazide diuretics or loop diuretics (in small doses) are indicated.
• III functional class (decompensation) - loop diuretics are prescribed (combination with thiazide is possible) + aldosterone antagonists (in dozemg / day).
• III functional class (maintenance treatment) - loop diuretics (dose titration) + spironolactone (in doses/day) are recommended.
• IV functional class - shown loop diuretics + thiazide diuretics + aldosterone antagonists.

cardiac glycosides

• Cardiac glycosides are indicated for atrial fibrillation and symptomatic heart failure, regardless of the degree of cardiac dysfunction.
• Cardiac glycosides do not improve the prognosis, but help reduce the number of hospitalizations among patients with CHF and left ventricular systolic dysfunction with sinus rhythm.
• The main drug from the group of cardiac glycosides for the treatment of CHF is digoxin.
• The dose of digoxin for the treatment of CHF should not exceed 0.25 mg/day.
• A dose of digoxin 0.125-0.25 mg / day is taken in one dose daily, without gaps.
• The use of a loading dose of digoxin is not recommended.
• Predictors of the success of treatment with glycosides in patients with CHF are low ejection fraction of the left ventricle (less than 25%), cardiomegaly, non-ischemic etiology of the disease.

Angiotensin-II receptor antagonists

• Angiotensin-II receptor antagonists and ACE inhibitors are equally effective in reducing mortality and morbidity in CHF.
• Angiotensin-II receptor antagonists should be used as an alternative to ACE inhibitors when the latter are intolerant.
• The triple combination (ACE inhibitor + beta-blocker + angiotensin-II receptor antagonist) is not considered optimal. Only with intolerance to a beta-blocker should you switch to a combination of an ACE inhibitor + angiotensin-II receptor antagonist.

In table. 8 shows angiotensin-II receptor antagonists for the treatment of CHF.

Antiplatelet agents and anticoagulants

• Indirect anticoagulants (warfarin) should be given to all patients with CHF and atrial fibrillation.
• Regardless of the heart rate, indirect anticoagulants should be received by all patients with CHF who have had thromboembolic complications and / or with the presence of a floating thrombus in the cavity of the left ventricle.
• Indirect anticoagulants cannot be replaced by antiplatelet agents (acetylsalicylic acid, clopidogrel, ticlopidine) to reduce the risk of thromboembolic complications.
• For secondary prevention after myocardial infarction, either acetylsalicylic acid or indirect anticoagulants should be used (but not in combination due to a high risk of bleeding).
• The appointment of acetylsalicylic acid should be avoided in patients with frequent repeated hospitalizations due to worsening CHF.
• Therapy with indirect anticoagulants should be carried out under close supervision (1 time per month) of the international normalized ratio (INR). The safe and effective INR range is 2.0-3.0.

Vasodilators

• Nitrates are recommended to be prescribed in the presence of proven coronary artery disease and exertional angina, which is stopped by nitrates.
• Calcium channel blockers (dihydropyridine series - amlodipine or felodipine) can be used in the following clinical situations: the presence of resistant angina pectoris, concomitant persistent arterial hypertension, pulmonary hypertension, severe valvular regurgitation.

Antiarrhythmic drugs

• Only life-threatening and clinically manifest ventricular arrhythmias should be treated for CHF.
• Antiarrhythmic drugs of classes I and IV are contraindicated in patients with CHF.
• beta-blockers are the drug of choice for antiarrhythmic treatment.
• With the ineffectiveness of beta-blockers, class III drugs (amiodarone, sotalol) are indicated.
• Means of choice for the treatment of ventricular arrhythmias in patients with moderate CHF (I-II functional class) is amiodarone.
• In patients with severe CHF (III-IV functional class), amiodarone should not be used.
• The most justified method of preventing sudden death in patients with CHF and life-threatening arrhythmias is the installation of an implantable cardioverter-defibrillator.

Treatment of atrial fibrillation in patients with CHF

• In terms of the impact on mortality and morbidity, there is no difference between the tactics of maintaining sinus rhythm and the tactics of controlling heart rate. The expediency of restoring and maintaining sinus rhythm is determined by the doctor.
• Amiodarone is considered the most effective antiarrhythmic drug for maintaining sinus rhythm.
• To control heart rate in atrial fibrillation, the combination of beta-blocker + digoxin is most effective.

• NSAIDs.
• Tricyclic antidepressants.
• Antiarrhythmic drugs I and IV classes.
• Calcium channel blockers (verapamil, diltiazem, short-acting dihydropyridine drugs).
• Glucocorticoids. They are prescribed for symptomatic indications in cases of persistent arterial hypotension and severe edematous syndrome to facilitate the initiation of treatment with ACE inhibitors, diuretics and beta-blockers.

Patients should be informed of the importance of daily weight control during the treatment of heart failure. The patient should be weighed daily and record the result. With an increase in body weight by more than 2 kg in 1-3 days, the patient should contact the doctor.

Patients should be encouraged to follow a low-salt diet and limit fluid intake. Salt intake is recommended to be reduced to 3 g/day or less. In addition, it must be ensured that the patient fully understands all the details of his drug regimen.

The patient should be given the following information.

• How and when to take medication.
• A clear list of recommendations, including the name, dose and frequency of taking each drug.
• The most common side effects of drugs taken and the need to consult a doctor if they occur. Family members of patients with heart failure should be encouraged to learn the skills of cardiopulmonary resuscitation.

Mortality in patients with clinically severe heart failure within 1 year reaches 30%. The five-year survival rate of patients with CHF does not exceed 50%. The risk of sudden death in patients with CHF is 5 times higher than in the general population.

• I0 - congestive heart failure. Another name for the pathological process is right ventricular failure. It is accompanied by stagnation of blood in the systemic circulation, as evidenced by edema in the lower extremities.
• I1 - left ventricular failure of the heart. The disease is also called cardiac asthma, as it leads to disorders in the pulmonary circulation. This also includes acute pulmonary edema, which is formed due to pulmonary hypertension.
• I9 - unspecified CHF. A mixed type of pathology, which occurs most often, since the processes in the small and large circles of blood circulation are closely related.

Sometimes in ICD 10 it has a code that refers to another rubric. For example, the occurrence of CHF in pathologies of the kidneys, lungs, hypertension, in the neonatal period and in people with heart prostheses. Separately encoded CHF in women due to ectopic pregnancy or abortion.

General information about the disease

In cardiology, CHF is rather not a separate disease, but a complication of already existing pathological processes.

Deficiency develops due to a long decompensated state, most often with heart disease.

The problem is that patients with cardiovascular pathology tend to ignore the symptoms of their disease for a long time and reject medical care. It is impossible to start the problem, since the result of the progression of the pathological process will be acute cardiovascular failure. This condition has two forms: unstable angina and myocardial infarction.

CHF is confirmed not only by a non-specific clinical picture, which may indicate dozens of other diseases, but also by instrumental research methods.

Cardiological diagnoses usually have a long wording, as they require clarification of the severity of the process, etiological factors and concomitant diseases related to the circulatory system.

When registering chronic insufficiency, the degree of development of the process is specified. In ICD 10, CHF does not require additional divisions, however, in the clinical practice of a cardiologist, one cannot do without them. The severity of the process depends on the dosage of drugs, recommendations for lifestyle and future forecasts.

After establishing this diagnosis, the main task of the medical staff is to maintain the body at the same level, since the problem cannot be completely cured, as well as to eliminate the risks for the development of acute coronary blood supply insufficiency.

Heart failure (I50)

Excluded:

• complicating conditions:
  • abortion, ectopic or molar pregnancy (O00-O07, O08.8)
  • obstetric surgery and procedures (O75.4)
• conditions due to hypertension (I11.0)
  • kidney disease (I13.-)
• consequences of heart surgery or in the presence of a heart prosthesis (I97.1)
• neonatal heart failure (P29.0)

congestive heart disease

Right ventricular failure (secondary to left ventricular heart failure)

Left sided heart failure

Cardiac(s) or myocardial failure NOS

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) is adopted as a single regulatory document for accounting for morbidity, reasons for the population to contact medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. №170

The publication of a new revision (ICD-11) is planned by WHO in 2017 2018.

With amendments and additions by WHO.

Processing and translation of changes © mkb-10.com

What is chronic heart failure according to ICD 10?

If a patient develops CHF, the ICD-10 has specific codes for this disease. Heart failure is a condition where the heart and circulatory system cannot provide normal blood flow. Such pathologies appear due to the fact that the heart does not contract as much as it is required. Because of this, a smaller volume of blood enters the arteries than is necessary to ensure the work of the whole organism.

Heart failure is called one of the most common pathologies. Moreover, in the ranking of diseases, it occupies one place with the most frequent infectious diseases. Among the entire population of the planet, approximately 3% of people suffer from this disease, and in patients over 65 years old, this figure rises to 10%. By the way, when compared in terms of costs, the amount allocated for the treatment of chronic heart failure is 2 times more than for various forms of cancer.

The International Classification of Diseases, known as the ICD-10, was developed by the World Health Organization. It is reviewed every 10 years, so that additions and changes were made to the already developed base.

The ICD-10 code for heart failure is I50.

Moreover, this group excludes a condition that has such a complication as abortion, molar or ectopic pregnancy. Surgical interventions and obstetric procedures are also excluded. It does not yet include a condition that is associated with hypertension or kidney pathologies. If the insufficiency of the functioning of the heart muscle is detected in a newborn, then the code P29.0 is assigned by an international organization. When such a pathology is caused in a person of any age by heart surgery or wearing a prosthesis, then code I97.1 is set.

Classification involves a more detailed division. Under the number I50.0, there is a failure of the functioning of the heart with a congestive character. If the patient has a left ventricular form of such a pathology, then code I50.1 is used. If the form of the disease has not been clarified, then the number I50.9 is written.

The chronic form of heart failure develops rather slowly - it will take several weeks and even months. There are several main phases in this process:

1. 1. Violation of the integrity of the myocardium. This is due to various heart diseases or organ overload.
2. 2. The contractile function of the left ventricle is impaired. This part of the organ contracts weakly, so that a small volume of blood is sent to the arteries.
3. 3. Compensation. This mechanism is triggered by the body when it is necessary to ensure the normal functioning of the heart in difficult conditions. The muscle layer on the left side becomes much thicker, as it begins to grow and hypertrophy. The body produces more adrenaline, which causes the heart to beat faster and harder. In addition, the pituitary gland produces a special dysuric hormone, which increases the amount of water in the blood.
4. 4. Reserves are exhausted. The heart can no longer supply the cells with oxygen and useful substances. Because of this, there is a lack of energy and oxygen.
5. 5. Decompensation. The blood flow is disturbed, but the body is no longer able to compensate for it. The muscle tissue of the heart can no longer fully work. Organ movements become slow and weak.
6. 6. Development of heart failure. The heart moves weakly, which is why all the cells of the body do not receive the necessary nutrients and oxygen.

The causes of heart failure are as follows:

1. 1. Diseases of the heart valves. Because of this, blood rushes in large quantities to the ventricles, which leads to congestion.
2. 2. Blood hypertension. With such a pathology, the outflow of blood from the region of the heart is disturbed, while the volume of blood in the organ increases. The heart has to work much harder, which causes overwork. In addition, the risk of stretching the valves increases.
3. 3. Narrowing of the mouth of the aorta. The diameter of the lumen narrows, which leads to the accumulation of blood in the region of the left ventricle. The pressure in this area increases, so that this part of the organ is stretched. This vascular problem causes the myocardium to become weaker.
4. 4. Dilated cardiomyopathy. This cardiac pathology is characterized by stretching of the wall of the organ, while thickening does not occur. The volume of blood during reflux from the heart to the artery decreases by 2 times.
5. 5. Myocarditis. A disease characterized by inflammatory processes in the tissues of the myocardium. It develops under the influence of various reasons. It leads to problems with contractility and conduction of the heart muscle. The walls are gradually stretched.
6. 6. Ischemia, myocardial infarction. This leads to problems in supplying the heart muscle with blood.
7. 7. Tachyarrhythmia. During diastole, the filling of the heart with blood is disturbed.
8. 8. Hypertrophic type cardiomyopathy. With such an ailment, the walls thicken, and the volume of the ventricles decreases.
9. 9. Graves' disease. With such a pathology, the human body contains a large amount of hormonal substances that are synthesized by the thyroid gland. This has a toxic effect on the tissues of the heart.
10. 10. Pericarditis. These are inflammatory processes in the pericardium. Usually they create mechanical obstacles to filling the ventricles and atria with blood.

Chronic heart failure varies by type. According to the contraction phase, the following violations are distinguished:

1. 1. Diastolic. By diastole, we understand the phase when the heart relaxes, but with pathology, the muscle loses its elasticity, so that it cannot stretch and relax.
2. 2. Systolic. During systole, the heart contracts, but in pathology, the heart chamber does it weakly.

The disease, depending on the cause, is of the following types:

1. 1. Reloading. The heart muscle is weakened due to significant overloads. For example, blood viscosity has increased, hypertension develops, or there are mechanical obstacles to the outflow of blood from the heart.
2. 2. Myocardial. It is assumed that the muscular layer of the organ is significantly weakened. This includes myocarditis, ischemia, defects.

As for the acute form of the disease, the left ventricular and right ventricular types are distinguished. In the first case, blood circulation in the coronary type vessels in the left ventricle is disturbed. In the second type, the patient has damage to the right ventricle, as the branches at the end of the pulmonary artery are clogged. In other words, it is called pulmonary embolism. This also happens with a heart attack on the right side of the heart. The course of the acute form of the disease is as follows:

• cardiogenic shock;
• swelling of the lungs;
• hypertensive crisis;
• high cardiac output on the background of heart failure;
• acute form of decompensation.

CHF manifests itself in the form of the following symptoms in a patient. Shortness of breath appears as a result of oxygen starvation of the brain. At first, it appears only during intense physical exertion, but then at rest. Further, the human body will no longer be able to endure physical activity. This leads to a feeling of weakness, pain in the sternum, shortness of breath. Then all the symptoms of cyanosis will be noticeable: pallor and blueness of the skin on the nose, fingers, earlobes. Often there is swelling of the lower extremities. Another characteristic sign of chronic heart failure is the stagnation of blood in the vessels of the internal organs, which causes problems with the central nervous system, kidneys, liver and organs of the gastrointestinal tract.

Failure of the functioning of the heart muscle, both acute and chronic, is a fairly common pathology. According to ICD-10, the I.50 code for such a disease is established, but its various varieties are distinguished, so you should always check this regulatory document.

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CHF (Chronic heart failure) ICD-10

Chronic heart failure is a pathological condition in which there are problems with the nutrition of the heart, due to its insufficient blood supply.

CHF syndrome according to ICD-10 (International Classification of Diseases) is a pathology that occurs only against the background of other serious diseases.

It has many typical clinical signs that make it possible to suspect a disease, even without being a physician.

The essence of pathology, the mechanism of its development

Chronic heart failure can develop over months. This process is divided into several main stages:

• Due to heart disease or organ overload, the integrity of the myocardium is disrupted.
• The left ventricle contracts incorrectly, that is, weakly, due to which not enough blood enters the heart vessels.
• compensation mechanism. It is launched if necessary for the normal functioning of the heart muscle in difficult conditions. The layer on the left side of the organ thickens and hypertrophies, and the body releases more adrenaline. The heart begins to contract faster and stronger, and the pituitary gland produces a hormone, due to which the amount of water in the blood increases significantly.
• When the heart is no longer able to supply organs and tissues with oxygen, the body's reserves are exhausted. Oxygen starvation of cells occurs.
• Due to a serious violation of blood circulation, decompensation develops. The heart beats slowly and weakly.
• Heart failure occurs - the inability of the body to supply the body with oxygen and nutrients.

Classification

According to ICD-10, CHF is divided into three stages depending on the course of the disease:

• First. Clinical manifestations occur in a person only after physical exertion, and there are no signs of stagnation in the blood circulation.
• Second. There are signs of congestion in one or two circles of blood flow.
• Third. There are persistent violations and irreversible processes in the body.

Depending on the state of the left ventricle, two variants of CHF are distinguished:

• systolic function of the left lower chamber of the heart is preserved,
• there is left ventricular dysfunction.

Chronic heart failure is also divided into functional classes:

• I - ordinary physical activity does not provoke any clinical signs.
• II - during physical activity, symptoms of heart failure appear, so a person is forced to limit himself in work.
• III - the clinic is pronounced even with minor loads.
• IV - complaints occur in a patient at rest.

The reasons

The CHF code according to the ICD is I50. This syndrome, in fact, is an unfavorable outcome of most heart diseases, and in particular coronary artery disease and hypertension (up to 85% of cases). A quarter of cases of CHF incidence can be caused by such reasons:

Very rarely, chronic heart failure is caused by factors such as:

In any case, if a person suffers from any of the aforementioned disorders, his heart gradually becomes weaker and his pumping function deteriorates.

Clinical picture

Signs of chronic heart failure depend on the severity of the course of the disease and related disorders in the body. Typical complaints of patients with CHF are:

• development of shortness of breath. First, rapid breathing appears due to physical activity, later - even at rest;
• nocturnal suffocation - a phenomenon when the patient wakes up from the fact that he cannot breathe and feels the need to get out of bed;
• shortness of breath in an upright position (it happens that the patient has difficulty breathing in a standing or sitting position, but when he lies on his back, the respiratory rate returns to normal);
• general weakness and fatigue;
• dry cough arising from stagnation of blood in the lungs;
• nocturnal diuresis prevails over daytime (frequent urination at night);
• swelling of the legs (first, the feet and legs swell symmetrically, then the thighs);
• development of ascites (accumulation of fluid in the abdomen).

Another pronounced sign of chronic heart failure is orthopnea - the forced position of the patient, in which he lies with his head raised, otherwise he develops shortness of breath and dry cough.

Diagnostic Measures

When diagnosing a patient, one cannot do without a visual examination, in which the doctor will clearly see the typical symptoms of CHF - edema, pulsation and swelling of the veins, an increase in the abdomen. On palpation, “splash noises” are detected, which confirm the presence of free fluid in the peritoneum.

With the help of auscultation, accumulation of fluid in the lungs (wet rales) can be detected. The patient's heart and liver are enlarged.

To clarify the diagnosis, the doctor is assigned a number of hardware studies:

• electrocardiogram - reveals changes inherent in diseases that led to chronic heart failure;
• Ultrasound of the heart - allows you to detect expansion of the cavities of the body, signs of regurgitation (reflux of blood from the ventricles back into the atria), as well as to study the contractility of the ventricles;
• chest x-ray - helps to determine the size of the heart, as well as to detect congestion in the lungs.

Treatment

The main principle of the treatment of chronic heart failure is to slow the progression of the disease, as well as alleviate the symptoms. Conservative therapy involves lifelong use of heart drugs and other drugs that improve the patient's quality of life.

The drugs that a doctor prescribes for CHF include:

• ACE inhibitors, which lower the level of pressure inside the vessels;
• beta-blockers, which reduce the heart rate and overall vascular resistance, as a result of which blood can move freely through the arteries;
• cardiac glycosides, which increase the contractility of the heart muscle with a decrease in the frequency of contractions;
• anticoagulants that prevent thrombosis;
• calcium channel antagonists, which relax blood vessels and help lower blood pressure;
• nitrates, which reduce blood flow to the heart muscle;
• diuretics - are prescribed to relieve congested organs and reduce swelling.

Prevention

Primary prevention helps to prevent the development of diseases, the direct consequence of which is CHF.

If such a disease already occurs and it cannot be completely cured, secondary prevention is indicated for patients. It prevents the progression of CHF.

Patients with chronic heart failure should give up bad habits, take caffeine-containing products, reduce the amount of salt in the diet.

Nutrition should be fractional and balanced. You need to eat high-calorie, but easily digestible foods. You should limit physical activity and strictly follow all doctor's instructions.

Mkb 10 chronic heart failure

Chronic heart failure

CHRONIC HEART FAILURE

Chronic heart failure (CHF) is a disease with a complex of characteristic symptoms (shortness of breath, fatigue, decreased physical activity, edema, etc.) associated with inadequate perfusion of organs and tissues at rest or during exercise.

ICD-10 CODE

• I50.0 Congestive heart failure

Classification of CHF by the New York Heart Association by severity.

• I functional class. Ordinary physical activity is not accompanied by fatigue, palpitations, shortness of breath or angina pectoris. This functional class occurs in patients with heart disease that does not lead to limitation of physical activity.
• II functional class. At rest, patients feel well, but ordinary physical activity causes fatigue, shortness of breath, palpitations, or angina pectoris. This functional class occurs in patients with heart disease that causes mild limitation of physical activity.
• III functional class. This functional class occurs in patients with heart disease that causes significant limitation of physical activity. At rest, patients feel well, but a small (less than usual) exercise causes fatigue, shortness of breath, palpitations or angina pectoris.
• IV functional class. This functional class occurs in patients with heart disease, due to which they are unable to perform any kind of physical activity without discomfort. Symptoms of heart failure or angina occur at rest; with any physical activity, these symptoms are aggravated.

The classification of CHF by the Society of Heart Failure Specialists (Russia, 2002) is presented in Table. one.

Table 1. Classification of CHF by the Society of Heart Failure Specialists (Russia, 2002)

Functional classes of CHF

(may change with treatment)

(does not change during treatment)

HISTORY AND PHYSICAL EXAMINATION

The most frequent complaints of patients with CHF (in descending order of frequency): shortness of breath, fatigue, palpitations, peripheral edema, cough, wheezing in the lungs, orthopnea, swollen jugular veins, hepatomegaly, cardiomegaly.

LABORATORY RESEARCH METHODS

• Complete blood count (determining the level of hemoglobin, the number of erythrocytes, leukocytes and platelets).
• Biochemical blood test (study of the concentration of electrolytes, creatinine, glucose, activity of liver enzymes in the blood).
• General urine analysis.

INSTRUMENTAL RESEARCH METHODS

Criteria for the diagnosis of diastolic heart failure are given below (the presence of the first two criteria is mandatory).

• Symptoms and signs of heart failure.
• Normal or slightly impaired systolic function of the left ventricle (left ventricular ejection fraction equal to or greater than 45-50%).
• Detection of violations of the relaxation of the left ventricle with the help of echocardiography.

In patients with CHF, it is possible to use various options for a stress test: a 6-minute walk test, bicycle ergometry, treadmill, including blood gas analysis. In routine practice, in the absence of special equipment, a walking test for 6 minutes can be used to assess physical tolerance and objectify the functional status of patients.

• The patient must walk continuously for 6 minutes, moving between two points located at a known distance.
• The patient can stop at will.
• The distance traveled by the patient in 6 minutes correlates with other performance indicators.
• The parameters for assessing the test with a 6-minute walk are shown in Table. 2.

Table 2. Parameters for scoring the 6-minute walk test

according to the New York classification

Other studies (24-hour ECG monitoring, determination of the neurohormonal profile, radioisotope study) do not occupy an important place in the diagnosis of CHF. A test widely used in developed countries for diagnosing CHF - determining the level of brain natriuretic peptide - is not yet available in outpatient clinics in the Russian Federation.

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS

• Unknown etiology of heart failure.
• Systolic blood pressure less than 100 mm Hg.
• The content of creatinine in the blood is more than 150 µmol/l.
• The content of sodium in the blood is less than 135 mmol / l.
• The content of potassium in the blood is more than 6.0 mmol / l.
• Severe heart failure.
• Valvular heart disease as a cause of heart failure.

• Diet.
• Mode of physical activity.
• Psychological rehabilitation, organization of medical supervision, schools for patients with CHF.
• Drug therapy.
• Electrophysiological methods of treatment.
• Surgical, mechanical methods of treatment.

• Prevention of the development of clinically pronounced CHF (at the stage of asymptomatic cardiac dysfunction).
• Elimination of symptoms of CHF.
• Slowing down the progression of the disease.
• Improving the quality of life.
• Reducing the number of hospitalizations.
• Forecast improvement.

INDICATIONS FOR HOSPITALIZATION

• With the ineffectiveness of outpatient treatment of patients with functional class IV CHF, severe fatigue and decreased performance, as well as with the ineffectiveness of diuretics.
• When planning parenteral administration of diuretics, vasodilators or drugs with a positive inotropic effect under the control of hemodynamic parameters, requiring pulmonary artery catheterization.
• In patients with very low cardiac output who require positive inotropic therapy.

Hospitalization is necessary in the presence of life-threatening arrhythmias or arrhythmias that worsen the course of CHF.

• Limiting the intake of table salt, and the more so, the more pronounced the symptoms of the disease and congestion.
  • I functional class - do not eat salty foods (restriction to 3 g of table salt per day).
  • II functional class - do not eat salty foods and do not add salt to food (limitation to 1.5 g of table salt per day).
  • III-IV functional class - do not eat salty foods, do not add salt to food, eat foods with a reduced salt content and cook food without salt (limitation of less than 1 g of table salt per day).
• Limitation of fluid intake is relevant only in extreme situations in a decompensated state, in which intravenous administration of diuretics is necessary. In normal situations, the volume of fluid is not recommended to increase more than 2 liters per day.
• Food should be high-calorie, easy to digest and contain enough vitamins and protein.

• There is no evidence of benefit from vaccination. It is advisable to use vaccines against influenza and hepatitis B.
• It is not recommended to stay in conditions of high mountains, high temperatures, humidity. It is advisable to spend your holidays in a familiar climate zone. When choosing transport, preference should be given to aviation.
• Smoking is strictly and absolutely contraindicated for all patients with CHF.
• sexual activity. The use of phosphodiesterase-5 inhibitors (sildenafil, etc.) is not contraindicated, except in combination with long-acting nitrates.

All drugs for the treatment of CHF can be divided into three main categories: basic, additional and auxiliary (Table 3).

Table 3 Drugs for the treatment of chronic heart failure

• ACE inhibitors
• beta-blockers

• Diuretics (for swelling)
• Spironolactone (with III-IV functional classes)
• Cardiac glycosides (with CHF combined with atrial fibrillation; with CHF refractory to treatment)
• Angiotensin-II receptor antagonists (with intolerance to ACE inhibitors)
• Warfarin (for atrial fibrillation)

• Vasodilators
• Calcium channel blockers
• Antiarrhythmic drugs
• Acetylsalicylic acid
• Statins
• Non-glycoside inotropic agents

*** Impact on prognosis is unknown; their use is determined by the clinical picture.

ACE inhibitors

• ACE inhibitors are indicated for all patients with CHF (any etiology and stage of the process, including asymptomatic left ventricular dysfunction).
• ACE inhibitors improve the clinical picture, quality of life, slow down the progression of the disease, reduce morbidity and improve the prognosis of patients with CHF, i.e. allow you to achieve all goals in the treatment of CHF.
• These drugs are considered the most reasonable way to treat CHF with preserved systolic function of the heart.
• The absence of the appointment of ACE inhibitors cannot be considered justified and leads to a deliberate increase in the risk of death in patients with CHF.

In table. 4 shows the doses of the most studied ACE inhibitors in the treatment and prevention of CHF, used in Russia.

Table 4. Angiotensin-converting enzyme inhibitors prescribed for the treatment of chronic heart failure

Initial dose for arterial hypotension

• The need for the use of diuretics and vasodilators and their dosages should be assessed.
• Do not allow excessive diuresis before starting treatment; diuretics should be discontinued 24 hours before the first use of ACE inhibitors.
• Therapy should be started in the evening when the patient is in a horizontal position to minimize the risk of arterial hypotension.
• It is recommended to start treatment with low doses and increase them to maintenance levels.
• With a significant deterioration in kidney function (an increase in the concentration of creatinine in the blood by more than 30% of the original), it is necessary to reduce the dose by half, and if there is no improvement, stop the ACE inhibitor.
• Potassium-sparing diuretics should be avoided at the start of treatment, especially in patients with high levels of potassium in the blood (more than 5.0 mmol / l); however, this does not contradict the recommendations for the combined use of ACE inhibitors with high doses of spironolactone during decompensation and the combination of ACE inhibitors with low doses of aldosterone antagonists in long-term treatment of CHF.
• It is recommended to avoid prescription of NSAIDs.
• It is necessary to control blood pressure and electrolytes in the blood 1-2 weeks after each dose increase.

beta-blockers

• beta-blockers should be prescribed to all patients with CHF who do not have contraindications common to this group of drugs.
• beta-blockers should only be used in addition to ACE inhibitors.
• beta-blockers in addition to ACE inhibitors are indicated in all patients with asymptomatic left ventricular dysfunction after myocardial infarction.
• it is desirable to prescribe beta-blockers to patients who have achieved stabilization of the state (there are no signs of stagnation, there is no need for parenteral therapy).
• Only four beta-blockers are recommended for the treatment of CHF: bisoprolol, carvedilol, metoprolol succinate (sustained release) and nebivolol.
• Treatment with beta-blockers in CHF should begin with 12.5% ​​of the therapeutic dose. Doses are increased slowly (not more than 1 time in 2 weeks) until the optimum is reached (Table 5).
• With worsening heart failure, the development of arterial hypotension or bradycardia during dose titration, the following algorithm should be followed.
• With worsening heart failure, it is necessary first of all to increase the dose of diuretics and ACE inhibitors, if necessary, temporarily reduce the dose of beta-blocker.
• In case of arterial hypotension, it is shown first of all to reduce the dose of vasodilators, if necessary, temporarily reduce the dose of beta-blocker.
• In case of bradycardia, the dose should be reduced or drugs that reduce heart rate should be discontinued, if necessary, reduce the dose of a beta-blocker or cancel the latter if there are clear indications.
• Always consider re-prescribing a beta-blocker or increasing its dose after stabilization of the condition.
• If inotropic support is required during circulatory decompensation in patients on constant therapy with beta-blockers, the calcium sensitizer levosimendan is considered the drug of choice, since its hemodynamic effect does not depend on the degree of blockade of beta-adrenergic receptors.
• Contraindications to the appointment of beta-blockers in CHF are severe bronchial asthma and / or chronic obstructive pulmonary disease, symptomatic bradycardia, arterial hypotension.

Table 5. Beta-blockers for the treatment of chronic heart failure

Some patients may be treated with non-recommended beta-blockers (most often atenolol or short-acting metoprolol tartrate). In table. 6 shows the scheme of transfer to the recommended drugs.

Table 6. Scheme for switching patients with chronic heart failure from atenolol and metoprolol tartrate to recommended beta-blockers

• CHF III-IV functional class.
• Heart failure of unknown etiology.
• The presence of relative contraindications: bradycardia, arterial hypotension, poor tolerance of low doses of beta-blockers, concomitant chronic obstructive pulmonary disease.
• Information about the withdrawal of beta-blockers in the past due to adverse reactions or exacerbation of heart failure.

Aldosterone antagonists (spironolactone)

• Aldosterone antagonists are prescribed in addition to ACE inhibitors and beta-blockers in patients with functional class III-IV CHF.
• The recommended dose of spironolactone for chronic heart failure is 25 mg/day.

• These drugs are indicated only for patients with III-IV functional class of CHF.
• Treatment should only be started if the potassium level in the blood does not exceed 5.0 mmol / l, and the concentration of creatinine is less than 1.7 mg / dl.
• The recommended dosage of spironolactone for long-term use is 25 mg/day.
• Shown control of the content of potassium and creatinine in the blood every 4-6 weeks.
• If, after the start of treatment, the level of potassium in the blood exceeds 5.0-5.5 mmol / l, the dose of spironolactone should be reduced by 50%, and if the level of potassium is more than 5.5 mmol / l, spironolactone therapy should be discontinued.
• If after a month of therapy the symptoms of heart failure are still pronounced, the dose of spironolactone should be increased to 50 mg / day (subject to normokalemia). After increasing the dose of spironolactone, control of the concentration of potassium and creatinine in the blood is shown after 1 week.

Diuretics

• Treatment with diuretics begins only with clinical signs of stagnation (stage II A, functional class II).

Table 7. Diuretics in chronic heart failure

Algorithm for prescribing diuretics depending on the severity of CHF

• I and II functional class without edema - no need to treat with diuretics.
• II functional class (stagnation) - thiazide diuretics or loop diuretics (in small doses) are indicated.
• III functional class (decompensation) - loop diuretics are prescribed (combination with thiazide is possible) + aldosterone antagonists (in dozemg / day).
• III functional class (maintenance treatment) - loop diuretics (dose titration) + spironolactone (in doses/day) are recommended.
• IV functional class - shown loop diuretics + thiazide diuretics + aldosterone antagonists.

cardiac glycosides

• Cardiac glycosides are indicated for atrial fibrillation and symptomatic heart failure, regardless of the degree of cardiac dysfunction.
• Cardiac glycosides do not improve the prognosis, but help reduce the number of hospitalizations among patients with CHF and left ventricular systolic dysfunction with sinus rhythm.
• The main drug from the group of cardiac glycosides for the treatment of CHF is digoxin.
• The dose of digoxin for the treatment of CHF should not exceed 0.25 mg/day.
• A dose of digoxin 0.125-0.25 mg / day is taken in one dose daily, without gaps.
• The use of a loading dose of digoxin is not recommended.
• Predictors of the success of treatment with glycosides in patients with CHF are low ejection fraction of the left ventricle (less than 25%), cardiomegaly, non-ischemic etiology of the disease.

Angiotensin-II receptor antagonists

• Angiotensin-II receptor antagonists and ACE inhibitors are equally effective in reducing mortality and morbidity in CHF.
• Angiotensin-II receptor antagonists should be used as an alternative to ACE inhibitors when the latter are intolerant.
• The triple combination (ACE inhibitor + beta-blocker + angiotensin-II receptor antagonist) is not considered optimal. Only with intolerance to a beta-blocker should you switch to a combination of an ACE inhibitor + angiotensin-II receptor antagonist.

In table. 8 shows angiotensin-II receptor antagonists for the treatment of CHF.

Antiplatelet agents and anticoagulants

• Indirect anticoagulants (warfarin) should be given to all patients with CHF and atrial fibrillation.
• Regardless of the heart rate, indirect anticoagulants should be received by all patients with CHF who have had thromboembolic complications and / or with the presence of a floating thrombus in the cavity of the left ventricle.
• Indirect anticoagulants cannot be replaced by antiplatelet agents (acetylsalicylic acid, clopidogrel, ticlopidine) to reduce the risk of thromboembolic complications.
• For secondary prevention after myocardial infarction, either acetylsalicylic acid or indirect anticoagulants should be used (but not in combination due to a high risk of bleeding).
• The appointment of acetylsalicylic acid should be avoided in patients with frequent repeated hospitalizations due to worsening CHF.
• Therapy with indirect anticoagulants should be carried out under close supervision (1 time per month) of the international normalized ratio (INR). The safe and effective INR range is 2.0-3.0.

Vasodilators

• Nitrates are recommended to be prescribed in the presence of proven coronary artery disease and exertional angina, which is stopped by nitrates.
• Calcium channel blockers (dihydropyridine series - amlodipine or felodipine) can be used in the following clinical situations: the presence of resistant angina pectoris, concomitant persistent arterial hypertension, pulmonary hypertension, severe valvular regurgitation.

Antiarrhythmic drugs

• Only life-threatening and clinically manifest ventricular arrhythmias should be treated for CHF.
• Antiarrhythmic drugs of classes I and IV are contraindicated in patients with CHF.
• beta-blockers are the drug of choice for antiarrhythmic treatment.
• With the ineffectiveness of beta-blockers, class III drugs (amiodarone, sotalol) are indicated.
• Means of choice for the treatment of ventricular arrhythmias in patients with moderate CHF (I-II functional class) is amiodarone.
• In patients with severe CHF (III-IV functional class), amiodarone should not be used.
• The most justified method of preventing sudden death in patients with CHF and life-threatening arrhythmias is the installation of an implantable cardioverter-defibrillator.

Treatment of atrial fibrillation in patients with CHF

• In terms of the impact on mortality and morbidity, there is no difference between the tactics of maintaining sinus rhythm and the tactics of controlling heart rate. The expediency of restoring and maintaining sinus rhythm is determined by the doctor.
• Amiodarone is considered the most effective antiarrhythmic drug for maintaining sinus rhythm.
• To control heart rate in atrial fibrillation, the combination of beta-blocker + digoxin is most effective.

• NSAIDs.
• Tricyclic antidepressants.
• Antiarrhythmic drugs I and IV classes.
• Calcium channel blockers (verapamil, diltiazem, short-acting dihydropyridine drugs).
• Glucocorticoids. They are prescribed for symptomatic indications in cases of persistent arterial hypotension and severe edematous syndrome to facilitate the initiation of treatment with ACE inhibitors, diuretics and beta-blockers.

Patients should be informed of the importance of daily weight control during the treatment of heart failure. The patient should be weighed daily and record the result. With an increase in body weight by more than 2 kg in 1-3 days, the patient should contact the doctor.

Patients should be encouraged to follow a low-salt diet and limit fluid intake. Salt intake is recommended to be reduced to 3 g/day or less. In addition, it must be ensured that the patient fully understands all the details of his drug regimen.

The patient should be given the following information.

• How and when to take medication.
• A clear list of recommendations, including the name, dose and frequency of taking each drug.
• The most common side effects of drugs taken and the need to consult a doctor if they occur. Family members of patients with heart failure should be encouraged to learn the skills of cardiopulmonary resuscitation.

Mortality in patients with clinically severe heart failure within 1 year reaches 30%. The five-year survival rate of patients with CHF does not exceed 50%. The risk of sudden death in patients with CHF is 5 times higher than in the general population.

Chronic heart failure mkb 10

Nebival: indications, contraindications, instructions

Beta-blockers are a group of choice in the treatment of hypertension in people with tachycardia, heart failure. The drugs are well combined with diuretics, which enhance the antihypertensive effect. The use of Nebival reduces the likelihood of developing severe cardiovascular diseases, the risk of sudden death. The medicine is prescribed by a doctor according to strict indications.

Mechanism of action

The biologically active substance of the drug is nebivalol, which consists of two parts that are different in chemical composition and mode of action. The drug belongs to the group of selective beta-blockers, it acts mainly on beta1-adrenergic receptors. After taking Nebival, the heart rate decreases, vasodilation occurs, and myocardial oxygen demand decreases. The drug does not affect beta2-adrenergic receptors, therefore the risk of bronchospasm, increased uterine tone is minimal.

Distribution in the body

After taking the drug, it is rapidly absorbed in the gastrointestinal tract. A notable advantage is that the medicine can be taken with or without food. Food does not affect the absorption process or the activity of Nebival. Metabolism occurs in the liver, the drug is excreted equally by the kidneys and intestines.

When choosing an antihypertensive agent, attention should be paid to the patient's metabolism. People with a slow metabolism should be prescribed low doses, since the bioavailability of the drug is high. If the metabolism is fast, the dose should be increased.

Indications and contraindications

The drug is used to reduce pressure in hypertension. In the complex treatment of chronic heart failure, mainly in the elderly (over 70 years), these tablets have a good effect.

In some cases, Nebival tablets are not recommended. To avoid side effects, deterioration of the condition, you must carefully read the instructions.

• Allergic reaction to one of the components of the drug.
• Acute violation of the liver or kidneys.
• Decreased blood pressure (systolic< 90 мм рт. ст.).
• Bradycardia (pulse less than 60).
• Atrioventricular block II-III degree, weakness of the sinus node.
• The drug is forbidden to be taken in acute heart failure, collapse, when it is necessary to administer drugs that increase the strength of heart contractions.
• Patients with bronchial asthma should stop taking the medicine. It is necessary to choose Nebival analogues or another antihypertensive agent.
• Lactase deficiency is a direct contraindication, it is also not recommended to use the medicine for people with malabsorption of galactose, glucose.
• The drug is not used in children (under 18 years of age).
• Pregnancy. Nebival negatively affects the development of the child. Before prescribing the remedy, you need to make sure that the woman is not pregnant. When breastfeeding, the drug is contraindicated.

Note! The day before the proposed operation with the use of anesthesia, Nebival's reception is canceled!

Release form and method of application

The tablets are round in shape with slightly beveled edges. The pack contains 2 blisters of 10 white tablets each. It is recommended to store at a temperature not higher than 25 degrees.

The dosage and frequency of administration directly depends on the pathology, the state of the kidneys, liver, and the presence of concomitant diseases.

Arterial hypertension

To reduce pressure, it is recommended to use 5 mg (1 tablet) of Nebival 1 time per day, the effectiveness will increase if the hours of admission are unchanged (for example, every day in the morning at 9.00). The drug acts gradually, normalization of pressure will occur in 1-2 weeks after the start of administration. Nebival is prescribed alone or in combination with other drugs, it goes well with diuretics (hydrochlorothiazide).

Chronic heart failure

In case of heart disease, the doctor selects the dose individually. You should start with 1.25 mg (quarter of a tablet) per day. After 14 days, the dose is gradually increased. The maximum dose is 10 mg. After each dose increase, the patient's condition should be monitored for 2-3 hours. Periodically, you need to measure pressure, heart rate, pay attention to the general condition of the patient, the presence of complaints.

The drug is also canceled gradually, one-stage cancellation often leads to a worsening of the condition.

In case of renal insufficiency, do not take more than 2.5 mg of the drug per day.

Adverse reactions

After you start taking Nebival, adverse reactions may occur, so you need to read the instructions before buying. If the condition worsens, any of the following symptoms occur, you should consult a doctor.

• A sharp drop in blood pressure, slowing atrioventricular impulse conduction, bradycardia (decrease in heart rate< 60), возникновение аритмии, боли в сердце.
• Headache, sleep disturbance, dizziness, mood deterioration.
• Nausea (rarely vomiting), loss of appetite, bloating, bowel problems (constipation or diarrhea).
• An allergic reaction is manifested by a rash on the body, itching, and sometimes Quincke's edema.
• In rare cases, shortness of breath, bronchospasm occurs.
• Increased fatigue, the occurrence of edema or pastosity of the limbs.

special instructions

Nebival can cause dizziness, it increases fatigue, therefore it is used with caution in patients whose work is related to precise actions, driving vehicles. Before using the drug, it is recommended to read the instructions or ask questions to the doctor.

The drug often causes exacerbation of allergic reactions, psoriasis.

Nebival does not affect glucose metabolism, but patients with diabetes mellitus, thyroid pathology should take the drug under medical supervision. The drug masks the manifestations of hypoglycemia, thyrotoxicosis: rapid heartbeat, breathing.

With caution, the drug is prescribed to patients with depression, myasthenia gravis.

Interaction

• It is forbidden to take Nebival with floktafenin and sultopride, in which case the risk of ventricular arrhythmia increases.
• Simultaneous administration with antiarrhythmic drugs, calcium channel blockers leads to impaired conduction (AV-blockade), a decrease in the contractile function of the heart, and hypotension.
• Central antihypertensive drugs (clonidine, methyldopa) in combination with Nebival increase heart failure by reducing the frequency and strength of heart contractions.
• Caution is required when prescribing Nebival together with insulin and other hypoglycemic drugs. Beta-adrenergic mask masks the symptoms of hypoglycemia.
• It is recommended that the dose of the antihypertensive drug be reduced if the patient is taking baclofen or amifostine. The risk of hypotension is significantly increased.
• Antidepressants, antipsychotics enhance the effect of the drug.
• Alcohol does not affect drug metabolism.

Overdose

With an increase in the maximum allowable dose (10 mg), the following symptoms occur several times: a sharp decrease in pressure, pulse, nausea, vomiting, cyanosis is possible. In severe cases, there is loss of consciousness, signs of heart failure, coma, cardiac arrest.

First aid

The main task is to neutralize the excess nebivalol in the body. For this purpose, gastric lavage is carried out, activated charcoal or other sorbents are prescribed. Further treatment is symptomatic. With severe hypotension, bradycardia, beta-agonists are administered, if the effect is not achieved, the use of dopamine, norepinephrine is necessary. In case of ventricular arrhythmia, it is necessary to administer lidocaine, if there are convulsions - diazepam.

Among the most common diseases in our time are diseases associated with the heart. Most often, with diseases of the heart muscle, the doctor ascertains the diagnosis - arrhythmia.

And no one will be afraid of this type of arrhythmia, like sinus tachycardia. It is interesting that at the present time these words do not plunge a person into shock. He accepts the diagnosis and begins to fight his disease.

• Forms of manifestation
• How dangerous is all this?
• Diagnostics
• Prevention and treatment

What do you need to know about the disease?

Everyone knows that before starting a fight against something or someone, it is necessary to study the situation from the inside, and only then rebuff the problem. So what is sinus tachycardia? Before dealing with this issue, it is worth making a reservation: many, speaking of this disease, use the term "sinus". But, even using the wrong meaning of the word, you will always be understood.

Tachycardia is one type of arrhythmia. It is worth noting that, in essence, this disease is only a symptom of problems in the body.

Thus, most often they do not treat the disease - tachycardia, but treat what caused it.

By nature, the problem is heart palpitations. The maximum heart rate within normal range is 90 beats per minute. Anything above this by at least 10 beats is considered abnormal and such a deviation is tachycardia.

There is an international classification of diseases of the 10th revision, or simply microbial 10. All diseases have their own microbial code 10, which will designate the disease in the same way in any country in the world. Thus, if you are diagnosed with sinus tachycardia, then in whatever country you are in America, Russia, England or Israel, this disease will have the same indicator for microbial 10 - I49.5.

Forms of manifestation

It occurs due to strong physical exertion, and the disease can also manifest itself due to great emotional experiences in a person’s life, or due to increased body temperature.

Neurogenic, psychogenic, centrogenic or constitutionally hereditary.

All this is the name of one form. Most often observed in people with an unstable nervous system. Accompanied by neurosis, depression, stress.

As the name implies, it occurs due to poisoning with some substances. Substances can influence from outside the body, such as alcohol and smoking. There may also be associated with internal problems of the body, for example, an imbalance of hormones in the body:

• thyrotoxicosis - the release of hormones due to a diseased thyroid gland. If the heart beats 90 to 120 times per minute, then it is working within normal limits. Even in sleep, such a frantic rhythm can persist. Although most often reduced;
• pheoromocytoma is a tumor of the adrenal glands. The released adrenal hormones simply poison the body and cause a rapid heartbeat;
• chronic infection - for example, tuberculosis (Koch's wand) or chronic tonsillitis caused by inflammation of the tonsils.

This means that the disease is caused either by taking drugs to combat lung disease, or drugs that affect the release of hormones. Or just an overdose.

It occurs due to a lack of oxygen for the sinus node. Most often it is manifested due to a disease of the lungs or bronchi. But sometimes it can also be the cause of poor oxygen delivery to the heart.

It occurs due to problems with the heart muscle.

Signs and danger of the disease

Of course, sinus tachycardia, like any other disease, can be identified by symptoms. Signs of this disease include:

• The main symptom is fast, palpitations.
• Shortness of breath, here is another indicator of the presence of the disease. If you have not been engaged in any physical activity, but the feeling is as if it is squeezing the chest and it has become difficult to breathe, this is sinus tachycardia.
• Dizziness.
• Frequent state of weakness of the body.
• Sometimes loss of consciousness.
• Contractive pain in chest. The time should not exceed 5 minutes. The symptom is inherent in people with coronary heart disease.

How dangerous is all this?

Sinus tachycardia is striking in its unusualness. Initially, it is not a disease. It would seem, what if the heart beats faster. Logically, this should be even more useful, but not everything is so smooth here.

The more often the heart contracts, the less it has time to saturate the blood with oxygen, therefore, such contractions are more harmful and dangerous. The longer the disease lasts, the more the body and the heart lack oxygen. Each time more and more likely to damage organs due to lack of oxygen.

As a result, tachycardia, which is not a sign of heart disease, can lead to ischemia of the heart muscle and life-threatening consequences.

Diagnostics

Such a disease is diagnosed by carrying out the following actions:

The anamnesis of the patient's complaints is collected.

They will ask you to tell how long ago you felt problems, can you compare what such manifestations are connected with. Are there any complaints about something else besides the heart.

The second step is to collect an anamnesis related to the life of the applicant.

What a person does, what harmful substances he encounters in his life. Whether there are any bad habits or heart disease in close relatives.

Then a physical examination will be carried out.

Particular attention will be paid to the skin, whether everything is fine with the hairline and nails. Are there any wheezing or excessive movements when breathing.

A general blood test is taken.

To identify diseases that could serve as the appearance of a rapid heartbeat.

General urine analysis.

Here it is checked whether there are any problems with the urinary system. After all, if there are problems, then poisoning can occur and, as a result, the appearance of signs of a rapid heartbeat.

The next step will be a biochemical blood test.

It is taken in order to exclude or, on the contrary, confirm diseases that cause a rapid pulse. According to this analysis, it is possible to determine in which direction to look for the problem.

According to the indications of hormones, it is possible to determine which organ problems caused heart disease. For example, if the adrenal hormones are more than expected, then a decision will be made to identify the reason for the failure and how to cure it.

An ECG is used to confirm the diagnosis and determine the severity of the disease.

The cardiogram will show the frequency with which the heart muscle contracts. If the contraction occurs more than 100 times per minute, then such indications will be considered tachycardia. After all, a normal human heartbeat is from 60 to 90 beats per minute.

According to Holter, daily monitoring of the electrocardiogram is carried out.

Observation is carried out from 24 hours to 72. This analysis allows you to see how often sinus tachycardia occurs, how long it lasts and what is causing it.

EchoCG - determines whether everything is normal with the structure of the heart.

According to the testimony of this apparatus, it is possible to determine the size of the heart chambers, the thickness of the walls of the myocardium, and problems with the valve apparatus. If the readings deviate from the norm, then measures are taken to restore the body's work with such problems.

Consultation with a psychotherapist.

This is necessary for people with a neurogenic cause of the problem. Such a specialist can determine that the complications are not caused by a disease of some organs, but by the mental state of the patient.

Prevention and treatment

As a rule, in order to get rid of a rapid heart rate, it is initially necessary to overcome the diseases and problems that cause it.

To reduce the rapid pulse itself, in addition to the medicines prescribed by the doctor, you can use a set of additional measures to prevent the disease.

It is necessary to exclude all contact with harmful substances that can poison the body. It will be necessary to quit bad habits.

To get a better effect, you need to use light physical activity, such as walking. But at the same time, overexerting the body is very dangerous. It is worth compiling a healthy menu, and eliminating foods that affect the heartbeat from the diet.

The whole set of measures should be discussed with the doctor and only he can determine what will be useful in your case. Discuss with the treating specialist the possibility of using such folk methods as decoctions, tinctures, aromatherapy and massages.

• Do you often experience discomfort in the area of ​​the heart (pain, tingling, squeezing)?
• You may suddenly feel weak and tired...
• Feeling high pressure all the time...
• There is nothing to say about shortness of breath after the slightest physical exertion ...
• And you have been taking a bunch of medications for a long time, dieting and watching your weight ...

What is an ischemic attack?

TIA (transient ischemic attack) is an acute but short-term episode of neurological dysfunction caused by damage to the blood supply to one part of the brain.

If we talk about the concept of ischemia in general, then this is a violation of the blood flow in a certain area of ​​\u200b\u200bthe body or throughout the organ. This pathology can occur suddenly in the intestines, in cartilage and bone structures, but the most complex cases are noted in the heart and brain.

TIA is popularly called a microstroke for the similarity of symptoms, but this is not entirely true. The average duration of an ischemic attack is 12 minutes, and if the symptoms do not go away within a day, then this is another diagnosis - an ischemic stroke. The difference between the two is well described in various medical literature. Ischemic attack symptoms are obvious.

It is most correct to call a transient ischemic attack a harbinger of an acute stroke, which can occur very soon, within a couple of months.

TIA classification - frequency, severity, ICD-10

According to how easy or severe the disease is, the following types are distinguished:

• a mild form of the course of TIA (after 10 minutes the patient feels as usual);
• form of moderate severity (manifestations of TIA do not go away for several hours);
• severe form of the course of TIA (signs persist for a day).

According to the frequency of TIA, the following types of it are distinguished:

• rare (not more than 2 times a year);
• average frequency (every 2 months);
• frequent (more than once a month).

According to ICD-10 (this is an international classification system for diseases in which a code is assigned to each type of disease), TIA has the following classification:

1. G 45.0 - syndrome of the vertebrobasilar arterial system.
2. G 45.4 - TGA syndrome. By the way, many researchers consider this syndrome to be part of epileptic disorders and do not refer to ischemia.
3. G 45.1 - carotid artery syndrome (in the carotid basin).
4. G 45.2 - multiple and bilateral arterial syndromes.
5. G 45.3 - syndrome of transient blindness.
6. G unspecified TIA.
7. G 45.8 - other TIAs pass under this code.

Symptoms of the disease

The manifestations of an ischemic attack will depend on which artery the disorder occurred in. The general symptoms are:

• weakness, paralysis of the face or limbs, usually on one side of the body;
• distorted slurred speech;
• blindness in one or both eyes, double vision;
• dizziness;
• difficulty swallowing;
• tinnitus and severe hearing loss.

Symptoms by type of TIA

If there is a violation of the passage of the vessel in the basin of the carotid arteries (TIA in the carotid basin), then this will result in such manifestations:

• lack or decrease in the ability to control limbs (usually one side);
• slurred speech, incomprehension of addressed speech (dysarthria and aphasia);
• violation of fine motor skills;
• severe visual impairment;
• constant desire to sleep;
• confusion.

TIA in the vertebral artery system (in the vertebrobasilar basin) manifests itself in the following:

• vomit;
• dizziness;
• lack of coordination;
• hemianopsia, photopsia;
• split before the eyes;
• facial paralysis.

Transient monocular blindness is manifested by a feeling as if there is a curtain in front of the eyes, covering one eye for a short time. This form of TIA can occur suddenly, or it can be caused by bright lights, a too hot bath or bath, or a sharp turn. In addition, there may be impaired coordination and motor skills.

Transient global amnesia is another type of TIA. She has one symptom - loss of memory for recent events. And what happened a long time ago, the patient remembers. A person in this case is confused, repeats the same questions, disoriented in time and space.

Causes of TIA

Thrombi are the most common culprit in a transient ischemic attack. Blood clots can form as a result of past atherosclerosis or diseases of the cardiovascular system (myocardial infarction, atrial fibrillation, atrial myxoma). A clot can block blood flow to part of the brain. Brain cells are affected within a few seconds of blockage. This causes symptoms in the parts of the body controlled by these cells. After that, the blood flow returns, and the symptoms disappear.

Violation of blood flow can occur in one of the vascular pools, which in the human body are divided into two types:

The first is between the vertebral arteries. It supplies blood to the brain stem. The second is located between the two carotid arteries. It supplies blood to the cerebral hemispheres.

Sometimes a TIA is caused by a sudden drop in blood pressure, which reduces blood flow to the brain.

Well, the undoubted "companions" of any vascular pathology, dramatically increasing the chances of a transient ischemic attack:

• smoking;
• high cholesterol;
• excessive consumption of alcohol;
• diabetes;
• overweight.

Diagnosis of TIA

TIA is insidious in that it lasts for several minutes, and when the ambulance arrives, the patient, as a rule, refuses to be hospitalized, since all the symptoms have passed. But you must definitely go to the hospital, as an ischemic attack can happen again.

The following tests are considered on an emergency basis:

• biochemical blood test with determination of glucose and cholesterol levels;
• complete blood count;
• analysis of the level of electrolytes in the blood serum (iron, calcium, potassium, sodium, magnesium, chlorine, phosphorus);
• coagulation studies, or coagulogram;

The following tests are helpful and can often be done urgently:

• sedimentation rate of erythrocytes;
• cardiac enzymes - proteins that are released into the blood when the heart is malfunctioning;
• lipid profile, or lipidogram - a special blood test that reflects the level of concentration of fats and lipoproteins.

Additional lab tests ordered as needed (based on medical history) include the following:

• screening for hypercoagulable conditions (especially in young patients without known vascular risk factors);
• serological reaction to syphilis;
• analysis for the presence of antiphospholipid antibodies;
• hemoglobin electrophoresis;
• serum protein electrophoresis;
• examination of the cerebrospinal fluid.

The following examinations must be carried out within 24 hours:

1. Magnetic resonance imaging (MRI), a modern, but already very well studied and widely used safe method of radiation diagnostics.
2. Non-contrast computed tomography is a type of CT scan, but done without an intravenous infusion of radiopaque agents.
3. Carotid dopplerography of the neck, also called duplex scanning, ultrasonography, is an accurate, completely painless and harmless procedure that examines the shape of blood vessels.
4. CT angiography (CTA) - this use of computed tomography gives good visibility of blood vessels and features of blood flow.
5. Magnetic resonance angiography (MRA) is a type of MRI for obtaining an image with the lumen of blood vessels for the presence of plaques in them.
6. Doppler ultrasonography (UZDG), today it is one of the safest methods that provide maximum information about the state of the vascular system.
7. Echocardiography, to check your heart shape and its blood flow, is an ultrasound examination of the heart and heart valves.
8. PET of the brain stands for Positron Emission Tomography. This is the latest diagnostic method used to assess not the structure of the brain tissue, as magnetic resonance and computed tomography does, but the functional functioning of the brain.

Various types of treatment for the disease

Many doctors agree that it is not TIA that should be treated, but the main culprit - atherosclerosis. The disease must be treated medically, sometimes surgically.

You also need to change your lifestyle in favor of a healthy one.

Medical treatment, i.e. drug treatment should be started urgently and include the following groups of drugs:

• drugs that lower the level of "bad" cholesterol (Caduet, Mevacor);
• nootropics and neuroprotectors (Baclofen, Pronoran, Cinnarizine, Pantogam);
• blood-thinning drugs (Curantil, Trental);
• drugs that lower blood pressure (enalapril, Micardis, Valsacor);
• antioxidants (Mexidol);
• metabolites (Cytoflavin);
• sedatives (Pipolfen, Validol, Proroxan);
• sleeping pills (Melaxen, Donormil);
• drugs to reduce sugar (Maninil, Siofor).

After completing a comprehensive course of treatment, the patient must be under the supervision of a local doctor.

Surgical treatment may be justified if a person has a narrowing of the carotid artery, which is located in the neck. When medications don't help, a doctor may recommend a surgery called a carotid endarterectomy. What this operation is can be described quite simply. Such an intervention is the process of cleansing the carotid arteries from fatty deposits and plaques. Thus, blood flow is restored, and the risk of a recurrence of an ischemic attack is significantly reduced. Such an operation is very effective, but also has risks: stroke and re-occlusion of the carotid artery, bleeding, infections.

Surgical treatment of ischemic stroke cannot be prescribed to everyone.

There are quite a lot of contraindications for its implementation, including hypertension, acute heart failure, Alzheimer's disease, oncology in the late stages, and a recent myocardial infarction.

Disease prevention

How can TIA be prevented? If you search for data on the topic "ischemic attack treatment", then almost every medical manual talks about the necessary prevention of ischemic stroke. Precautions must be taken to prevent TIA. If you have already been a victim of an ischemic attack, then you are doubly at risk of a stroke.

You can do the following to prevent a transient ischemic attack:

• avoid active and passive smoking;
• follow the principles of proper nutrition: vegetables and fruits with a minimum of harmful fatty foods;
• lead physical activity;
• limit or eliminate alcohol consumption;
• limit your salt intake;
• control the level of sugar;
• control blood pressure;
• eliminate stressful situations.

Consequences of an ischemic attack

The prognosis here is quite unfavorable. Usually there are no more than 2-3 ischemic attacks, then a severe stroke necessarily occurs, which can lead to disability or even death. 10% of those who have experienced an ischemic attack during the first or second day get a stroke in the form of a cerebral stroke or myocardial infarction. Unfortunately, a huge number of people after suffering an ischemic stroke do not go to doctors, which makes the prognosis for recovery sharply negative and subsequently leads to serious problems.

TIA is not dangerous to human life, but it is a dire warning before a more serious problem. If this pathology is not treated, then in the near future a powerful ischemic attack of the brain can occur again.

Cerebral ischemia is a type of cerebrovascular disease, a fairly common severe pathology. Disciculatory encephalopathy is the name of a chronic disease that is used in domestic medicine. What it is? Cerebral ischemia is an extremely urgent neurological problem. This is a severe brain disorder. Today, in the conclusions of professionals, this diagnosis is very common. Disciculatory encephalopathy affects about 6% of the world's population. The number of such patients is constantly growing.

Etiology of dysciculatory encephalopathy

The causes of ischemia are varied. Various diseases lead to pathology. What is ischemic brain disease?

Causal factors of circulatory encephalopathy are the following disorders:

• vascular atherosclerosis;
• hypertension;
• atrial fibrillation;
• diseases of the blood vessels;
• damage to the endocrine system;
• ailments of the spine;
• cervical pathology.

Blood flow in the brain tissue depends on the level of red blood cells. Improper nutrition is the cause of high cholesterol. There is damage to the vessels of the head. The age factor is of great importance. In adults, ischemia of the cerebral vessels is often found. Young people suffer from this disease less. Old age is a contributing factor.

Pathogenesis of dysciculatory encephalopathy

The accumulation of cholesterol deposits in the blood vessels leads to pathology. There are irreversible changes. Ischemic cerebrovascular accident develops. A vessel clogged with a cholesterol plaque cannot perform its functions. If there is a blockage of the arteries, a narrowing of their lumen, oxygen starvation of the tissues develops. Brain cells damaged by nutritional deficiencies do not regenerate. Even one damaged vessel often leads to catastrophic consequences.

Classification of pathology

ICD-10 lists cerebral ischemia as a chronic form of cerebral pathology. Symptoms and treatment of dysciculatory encephalopathy are within the competence of a neurologist. Treating ischemia is difficult and time consuming. There is a multifocal or diffuse lesion, ischemic brain disease develops. Cerebrovascular pathology is manifested by clinical, neurological, neuropsychological, mental disorders in the body.

Cerebral ischemia is diagnosed by a professional. The acute form of cerebrovascular pathology is a consequence of oxygen starvation. A sudden onset develops. The chronic form of the pathology is formed gradually in conditions of impaired blood circulation in the vessels of the head.

Clinical picture

Signs of cerebral ischemia occur gradually or instantly.

Disciculatory encephalopathy is manifested by the following symptoms:

• pain syndrome;
• frequent dizziness;
• constant noise in the head;
• gradual deterioration of memory performance;
• low level of attention, decreased performance;
• cognitive impairment.

At an early stage, cerebral ischemia is manifested by a violation of the functions of the nervous system. There is a rapid pronounced fatigue. Memory is greatly deteriorating. This leads to a significant decrease in performance. However, usually people at this stage do not complain. Often patients do not turn to a neurologist.

Disciculatory encephalopathy - brain damage of the 1st degree. A neurasthenic syndrome develops. In general, the patient's health is normal, but a person may complain of a slight malaise. The early stage of the pathology is characterized by chills, mood swings, irritability, nervous excitement, and sleep disturbance. If adequate treatment is not carried out, the patient's condition worsens.

Stage 2 of the disease develops. There are severe neurological disorders. Pathological reflexes are noted. The patient is disturbed by numbness, a feeling of cold in the feet and palms. This is a clear manifestation of pathology. Complaints of feeling unwell are becoming more frequent. Walk is disturbed. Cerebellar disturbances appear. The patient experiences constant drowsiness. The disease of the 2nd degree is characterized by a progressive decrease in memory. All signs of the 1st degree of brain failure are also preserved, but patients notice these defects less. At stage 2, transient ischemic attacks are noted.

In the 3rd phase of tissue ischemia, memory deteriorates, dementia develops. Violated social and labor adaptation of the patient. Such a patient needs constant monitoring and care. At stage 3, patients present very few complaints. This is due to the fact that they have a reduced critical attitude towards their condition. In this phase, the headaches go away. But the human condition is grave. Patients often have severe strokes, vascular dementia, parkinsonism.

Diagnostic procedures

How can a correct diagnosis be made? The neurologist evaluates the painful symptoms and prescribes treatment when he listens to the patient's complaints. If at least 2 of the characteristic symptoms appear constantly during the last months, such complaints should be the reason for an in-depth examination of the cardiovascular system.

When signs of coronary artery disease of the brain appear, laboratory blood tests are performed. Hardware studies include ultrasound, high-frequency ultrasound tomography, electroencephalography, dopplerogram of the brain, cardiography. The results of these studies can show the localization of the lesion.

Tactics of medical measures

If there are symptoms of cerebral ischemia, what should be done? How to cure the patient? The most effective method of treatment is the use of special preparations, which are selected individually by the attending doctor. The main task of a specialist is the treatment of vascular pathology. With ischemia of the cerebral vessels, treatment is required immediately.

It is important to relieve the symptoms of dysciculatory encephalopathy in order to improve the quality of life of patients. It is necessary to increase the blood supply to the inner ear, to reduce the activity of the vestibular centers. This will help get rid of dizziness. Given the patient's condition, the neurologist prescribes Piracetam, Betagistim, Gingko Biloba. Betagistim is the main drug indicated for use. It normalizes the electrical activity of the vestibular centers of the brain, peripheral receptors, improves the blood supply to the inner ear.

Vestibo normalizes vestibular functions. This drug is necessarily included in the therapeutic course for 2 or 3 stages of cerebral ischemia. Vestibo, Actovegin significantly reduce tinnitus, as aerobic metabolism increases. Actovegin is a drug that shows a good result.

When using these drugs, the processes of improving blood flow occur. The energy resources of cells increase. The transport of oxygen is activated. Improved metabolic processes. Damage to brain neurons is prevented by neuroprotectors. Neuromodulatory drugs, vasoactive drugs, neurotrophic cerebroprotectors, neuropeptides are used.

Such medications neutralize the pathogenic factor, limit and stop damage to brain tissue. Cinnarizine, Vinpocetine, Nimodipine are calcium channel blockers. These drugs increase cerebral blood flow because they dilate the blood vessels in the brain. The doctor prescribes according to the testimony of Neuromedin, Pramipex, physiotherapy, therapeutic massage. Special vestibular gymnastics is performed. Effective spa treatment. With signs of cerebral ischemia, symptoms, treatment are the competence of the doctor.

What are the complications of the disease? Disciculatory encephalopathy can lead to stroke, heart attack. This often causes changes in body functions, daily activities. Patients with cerebral ischemia need complex treatment. It is important to prevent disciculatory encephalopathy. Prevention starts as early as possible. It is required in every possible way to avoid stress, control weight, and exercise. The use of tobacco, alcoholism is contraindicated. Cerebral ischemia is dangerous.

If characteristic symptoms of cerebral ischemia occur, the patient should go to a neurologist. The patient should be shown to a specialist. Early detection of pathology, treatment of coronary disease helps to maintain a decent standard of living.

Short description

Chronic systolic heart failure- a clinical syndrome that complicates the course of a number of diseases and is characterized by the presence of shortness of breath during exercise (and then at rest), fatigue, peripheral edema, and objective signs of cardiac dysfunction at rest (for example, auscultatory signs, echocardiography - data).

Code according to the international classification of diseases ICD-10:

• I50 Heart failure

Statistical data. Chronic systolic heart failure occurs in 0.4-2% of the population. With age, its prevalence increases: in people older than 75 years, it develops in 10% of cases.

The reasons

Etiology. Heart failure with low cardiac output.. Myocardial damage: ... CHD (post-infarction cardiosclerosis, chronic myocardial ischemia) ... Cardiomyopathies ... Myocarditis ... Toxic effects (eg, alcohol, doxorubicin) ... Infiltrative diseases (sarcoidosis) , amyloidosis) ... Endocrine diseases ... Nutritional disorders (vitamin B1 deficiency) .. Myocardial overload ... Arterial hypertension ... Rheumatic heart defects ... Congenital heart defects (for example, aortic stenosis) .. Arrhythmias. .. Supraventricular and ventricular tachycardias... Atrial fibrillation. Heart failure with high cardiac output. Anemia.. Sepsis.. Arteriovenous fistula.

Risk factors. Refusal of the patient from pharmacotherapy. Appointment of drugs with a negative inotropic effect, and their uncontrolled intake. Thyrotoxicosis, pregnancy and other conditions associated with increased metabolic demands. Overweight. The presence of chronic pathology of the heart and blood vessels (arterial hypertension, coronary artery disease, heart defects, etc.).

Pathogenesis. The pumping function of the heart is impaired, which leads to a decrease in cardiac output. As a result of a decrease in cardiac output, hypoperfusion of many organs and tissues occurs .. A decrease in heart perfusion leads to activation of the sympathetic nervous system and an increase in heart rate .. A decrease in kidney perfusion causes stimulation of the renin-angiotensin system. The production of renin increases, while an excess production of angiotensin II occurs, leading to vasoconstriction, water retention (edema, thirst, increased BCC) and a subsequent increase in preload on the heart. to severe fatigue.

CLASSIFICATIONS

Classification of the XII All-Union Congress of Therapists in 1935 (N.D. Strazhesko, V.Kh. Vasilenko).

Stage I (initial) - latent heart failure, manifested only during exercise (shortness of breath, tachycardia, fatigue).

Stage II (expressed) - prolonged circulatory failure, hemodynamic disorders (stagnation in the systemic and pulmonary circulation), dysfunction of organs and metabolism are expressed even at rest. Period A - the beginning of a long stage, characterized by mild hemodynamic disorders, impaired heart function or only parts of them.. Period B - the end of a long stage, characterized by profound hemodynamic disturbances, the entire CVS is involved in the process.

Stage III (final, dystrophic) - severe hemodynamic disturbances, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs.

New York Heart Association classification(1964). Class I - ordinary physical activity does not cause severe fatigue, shortness of breath or palpitations. Class II - mild limitation of physical activity: satisfactory state of health at rest, but ordinary physical activity causes fatigue, palpitations, shortness of breath or pain. Class III - severe limitation of physical activity: satisfactory state of health at rest, but the load is less than usual leads to the appearance of symptoms. Class IV - the impossibility of performing any physical activity without a deterioration in well-being: symptoms of heart failure are present even at rest and intensify with any physical activity.

Heart Failure Society Classification(OSNN, 2002) adopted at the All-Russian Congress of Cardiology in October 2002. The convenience of this classification is that it not only reflects the state of the process, but also its dynamics. The diagnosis must reflect both the stage of chronic heart failure and its functional class. It should be borne in mind that the correspondence between the stage and the functional class is not quite clear - the functional class is set in the presence of several less pronounced manifestations than is necessary to set the corresponding stage of heart failure.

. Stages of chronic heart failure(may worsen despite treatment) .. Stage I - the initial stage of the disease (lesion) of the heart. Hemodynamics is not disturbed. Hidden heart failure Asymptomatic dysfunction of the left ventricle. IIA stage - a clinically pronounced stage of the disease (lesion) of the heart. Violations of hemodynamics in one of the circles of blood circulation, expressed moderately. Adaptive remodeling of the heart and blood vessels. Stage IIB is a severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels. Stage III - the final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys). The final stage of organ remodeling.

. Functional classes of chronic heart failure(may change during treatment both in one direction and the other) .. I FC - there are no restrictions on physical activity: habitual physical activity is not accompanied by rapid fatigue, the appearance of shortness of breath or palpitations. The patient tolerates the increased load, but it may be accompanied by shortness of breath and / or delayed recovery of strength .. II FC - a slight limitation of physical activity: at rest there are no symptoms, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations .. III FC - a noticeable limitation of physical activity: at rest, there are no symptoms, physical activity of less intensity compared to habitual loads is accompanied by the appearance of symptoms .. IV FC - the inability to perform any physical activity without the appearance of discomfort; symptoms of heart failure are present at rest and worsen with minimal physical activity.

Symptoms (signs)

Clinical manifestations

. Complaints- shortness of breath, asthma attacks, weakness, fatigue .. Shortness of breath in the initial stage of heart failure occurs during exercise, and with severe heart failure - at rest. It appears as a result of an increase in pressure in the pulmonary capillaries and veins. This reduces the extensibility of the lungs and increases the work of the respiratory muscles .. Severe heart failure is characterized by orthopnea - a forced sitting position taken by the patient to facilitate breathing with severe shortness of breath. Deterioration of well-being in the supine position is due to the deposition of fluid in the pulmonary capillaries, leading to an increase in hydrostatic pressure. In addition, in the supine position, the diaphragm rises, which makes breathing somewhat difficult. Chronic heart failure is characterized by paroxysmal nocturnal dyspnea (cardiac asthma), due to the occurrence of interstitial pulmonary edema. At night, during sleep, an attack of severe shortness of breath develops, accompanied by coughing and the appearance of wheezing in the lungs. With the progression of heart failure, alveolar pulmonary edema may occur.. Rapid fatigue in patients with heart failure appears due to insufficient oxygen supply to skeletal muscles. in the liver and portal vein system. From the side of the heart, pathological III and IV heart sounds can be heard. In the lungs, moist rales are determined. Hydrothorax is characteristic, more often right-sided, resulting from an increase in pleural capillary pressure and extravasation of fluid into the pleural cavity.

. Clinical manifestations of heart failure significantly depend on its stage... Stage I - signs (fatigue, shortness of breath and palpitations) appear during normal physical activity, there are no manifestations of heart failure at rest .. Stage IIA - there are unexpressed hemodynamic disturbances. Clinical manifestations depend on which parts of the heart are predominantly affected (right or left) ... Left ventricular failure is characterized by stagnation in the pulmonary circulation, manifested by typical inspiratory dyspnea with moderate physical exertion, attacks of paroxysmal nocturnal dyspnea, and rapid fatigue. Edema and enlargement of the liver are uncharacteristic ... Right ventricular failure is characterized by the formation of congestion in the systemic circulation. Patients are concerned about pain and heaviness in the right hypochondrium, a decrease in diuresis. An increase in the liver is characteristic (the surface is smooth, the edge is rounded, palpation is painful). A distinctive feature of stage IIA heart failure is the complete compensation of the condition during treatment, i.e. reversibility of manifestations of heart failure as a result of adequate treatment. Stage IIB - there are profound hemodynamic disturbances, the entire circulatory system is involved in the process. Shortness of breath occurs with the slightest physical exertion. Patients are concerned about the feeling of heaviness in the right hypochondrium, general weakness, sleep disturbance. Orthopnea, edema, ascites are characteristic (a consequence of an increase in pressure in the hepatic veins and peritoneal veins - extravasation occurs, and fluid accumulates in the abdominal cavity), hydrothorax, hydropericardium .. Stage III - the final dystrophic stage with deep irreversible metabolic disorders. As a rule, the condition of patients in this stage is severe. Shortness of breath is expressed even at rest. Characterized by massive edema, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium, edema of the genital organs). At this stage, cachexia occurs.

Diagnostics

instrumental data

. ECG. it is possible to identify signs of blockade of the left or right leg of the His bundle, ventricular or atrial hypertrophy, pathological Q waves (as a sign of a previous MI), arrhythmias. A normal ECG casts doubt on the diagnosis of chronic heart failure.

. echocardiography allows you to clarify the etiology of chronic heart failure and evaluate the functions of the heart, the degree of their violation (in particular, to determine the ejection fraction of the left ventricle). Typical manifestations of heart failure are the expansion of the cavity of the left ventricle (as it progresses, the expansion of other chambers of the heart), an increase in the final systolic and final diastolic sizes of the left ventricle, and a decrease in its ejection fraction.

. X-ray examination.. It is possible to identify venous hypertension in the form of a redistribution of blood flow in favor of the upper sections of the lungs and an increase in the diameter of the vessels .. With stagnation in the lungs, signs of interstitial edema are detected (Kerley lines in the rib-diaphragmatic sinuses) or signs of pulmonary edema .. Hydrothorax is detected (usually right-sided) .. Cardiomegaly is diagnosed with an increase in the transverse size of the heart of more than 15.5 cm in men and more than 14.5 cm in women (or with a cardiothoracic index of more than 50%).

. Cardiac catheterization allows to detect an increase in the wedge pressure of the pulmonary capillaries more than 18 mm Hg.

Diagnostic criteria - Framingham criteria for the diagnosis of chronic heart failure, subdivided into major and minor. Major criteria: paroxysmal nocturnal dyspnea (cardiac asthma) or orthopnea, jugular vein swelling, rales in the lungs, cardiomegaly, pulmonary edema, abnormal III heart sound, increased CVP (more than 160 mm H2O), blood flow time more than 25 s, positive "hepatojugular reflux". Minor criteria: swelling in the legs, nocturnal cough, shortness of breath on exertion, liver enlargement, hydrothorax, tachycardia over 120 per minute, decrease in VC by 1/3 of the maximum. To confirm the diagnosis of chronic heart failure, either 1 major or 2 minor criteria are required. The signs to be determined must be related to heart disease.

Differential Diagnosis. Nephrotic syndrome - a history of edema, proteinuria, renal pathology. Cirrhosis of the liver. Occlusive lesions of the veins with the subsequent development of peripheral edema.

Treatment. It is necessary first of all to assess the possibility of influencing the cause of the insufficiency. In some cases, an effective etiological effect (for example, surgical correction of heart disease, myocardial revascularization in IHD) can significantly reduce the severity of manifestations of chronic heart failure. In the treatment of chronic heart failure, non-drug and drug therapies are distinguished. It should be noted that both types of treatment should complement each other.

Non-drug treatment. Limiting the use of table salt to 5-6 g / day, liquids (up to 1-1.5 l / day). Optimization of physical activity .. Moderate physical activity is possible and even necessary (walking for at least 20-30 minutes 3-5 r / week) .. Complete physical rest should be observed when the condition worsens (at rest, the heart rate decreases and the work of the heart decreases).

Treatment

Drug therapy. The ultimate goal of treating chronic heart failure is to improve the quality of life and increase its duration.

Diuretics. When prescribing them, it must be taken into account that the occurrence of edema in heart failure is associated with several reasons (narrowing of the renal vessels, increased secretion of aldosterone, increased venous pressure. Treatment with diuretics alone is considered insufficient. In chronic heart failure, loop (furosemide) or thiazide (for example, hydrochlorothiazide) diuretics In case of insufficient diuretic response, loop diuretics and thiazides are combined. they begin to act faster, their diuretic effect is more pronounced, but less prolonged than that of thiazide diuretics.Furosemide is used at a dose of 20-200 mg/day IV, depending on the manifestations of edematous syndrome and diuresis.It is possible to prescribe it orally at a dose of 40- 100 mg/day

ACE inhibitors cause hemodynamic unloading of the myocardium due to vasodilation, increased diuresis, and a decrease in filling pressure of the left and right ventricles. Indications for the appointment of ACE inhibitors are clinical signs of heart failure, a decrease in the left ventricular ejection fraction of less than 40%. When prescribing ACE inhibitors, certain conditions must be observed according to the recommendations of the European Society of Cardiology (2001) .. It is necessary to stop taking diuretics 24 hours before taking ACE inhibitors .. Blood pressure should be monitored before and after taking ACE inhibitors .. Treatment begins with small doses with gradual their increase .. It is necessary to monitor kidney function (diuresis, relative density of urine) and the concentration of blood electrolytes (potassium, sodium ions) with an increase in dose every 3-5 days, then every 3 and 6 months. Co-administration of potassium-sparing diuretics (their can be prescribed only for hypokalemia) .. It is necessary to avoid the combined use of NSAIDs.

The first positive data have been obtained on the beneficial effect of angiotensin II receptor blockers (in particular, losartan) on the course of chronic heart failure as an alternative to ACE inhibitors in case of their intolerance or contraindications to prescription.

Cardiac glycosides have a positive inotropic (increase and shorten systole), negative chronotropic (decrease in heart rate), negative dromotropic (slow AV conduction) action. The optimal maintenance dose of digoxin is 0.25-0.375 mg/day (in elderly patients 0.125-0.25 mg/day); The therapeutic concentration of digoxin in the blood serum is 0.5-1.5 mg/L. Indications for the appointment of cardiac glycosides are tachysystolic form of atrial fibrillation, sinus tachycardia.

B — Adrenoblockers. relaxation of the myocardium... Decrease in the effect of vasoconstrictor systems (for example, due to a decrease in renin secretion)... Potentiation of the vasodilating kallikrein-kinin system... Increase in the contribution of the left atrium to the filling of the left ventricle by improving the relaxation of the latter.. Currently from b - blockers for the treatment of chronic heart failure is recommended for use carvedilol - b1 - and a1 - adrenoblocker with vasodilating properties. The initial dose of carvedilol is 3.125 mg 2 r / day, followed by an increase in dose to 6.25 mg, 12.5 mg or 25 mg 2 r / day in the absence of side effects in the form of arterial hypotension, bradycardia, a decrease in the ejection fraction of the left ventricle (according to EchoCG) and other negative manifestations of the action of b-blockers. Metoprolol is also recommended, starting with a dose of 12.5 mg 2 r / day, bisoprolol 1.25 mg 1 r / day under the control of ventricular ejection fractions with a gradual increase in dose after 1-2 weeks.

Spironolactone. It has been established that the appointment of the aldosterone antagonist spironolactone at a dose of 25 mg 1-2 r / day (in the absence of contraindications) contributes to an increase in the life expectancy of patients with heart failure.

Peripheral vasodilators are prescribed for chronic heart failure if there are contraindications or if ACE inhibitors are poorly tolerated. Of the peripheral vasodilators, hydralazine is used at a dose of up to 300 mg / day, isosorbide dinitrate at a dose of up to 160 mg / day.

. Other cardiotonic drugs. b - Adrenomimetics (dobutamine), phosphodiesterase inhibitors are usually prescribed for 1-2 weeks in the final stage of heart failure or with a sharp deterioration in the condition of patients.

Anticoagulants. Patients with chronic heart failure are at high risk of thromboembolic complications. Both pulmonary embolism due to venous thrombosis and thromboembolism of the vessels of the systemic circulation due to intracardiac thrombi or atrial fibrillation are possible. The appointment of indirect anticoagulants in patients with chronic heart failure is recommended in the presence of atrial fibrillation and thrombosis in history.

Antiarrhythmic drugs. If there are indications for the appointment of antiarrhythmic drugs (atrial fibrillation, ventricular tachycardia), it is recommended to use amiodarone at a dose of 100-200 mg / day. This drug has a minimal negative inotropic effect, while most other drugs in this class reduce the left ventricular ejection fraction. In addition, antiarrhythmic drugs themselves can provoke arrhythmias (proarrhythmic effect).

Surgery

The choice of the optimal method of surgical treatment depends on the cause leading to heart failure. So, in many cases, with IHD, myocardial revascularization is feasible, with idiopathic subaortic hypertrophic stenosis - septal myectomy, with valvular defects - prosthetics or reconstructive interventions on the valves, with bradyarrhythmias - pacemaker implantation, etc.

In case of refractoriness of heart failure to adequate therapy, the main surgical treatment is heart transplantation.

Methods of mechanical circulatory support (implantation of assistants, artificial ventricles and biomechanical pumps), previously proposed as temporary options before transplantation, have now acquired the status of independent interventions, the results of which are comparable to those of transplantation.

To prevent the progression of cardiac dilatation, devices are implanted in the form of a mesh that prevents excessive expansion of the heart.

In treatment-tolerant cor pulmonale, transplantation of the heart-lung complex seems to be a more appropriate intervention.

Forecast. In general, the 3-year survival rate for patients with chronic systolic heart failure is 50%. Mortality from chronic systolic heart failure is 19% per year.

Factors, the presence of which correlates with a poor prognosis in patients with heart failure .. Decrease in the left ventricular ejection fraction less than 25% .. Inability to rise one floor and move at a normal pace for more than 3 minutes. l .. Decrease in the concentration of potassium ions in blood plasma less than 3 meq / l .. Increase in the content of norepinephrine in the blood .. Frequent ventricular extrasystole during daily ECG monitoring.

The risk of sudden cardiac death in patients with heart failure is 5 times higher than in the general population. Most patients with chronic heart failure die suddenly, mainly from the onset of ventricular fibrillation. Prophylactic administration of antiarrhythmic drugs does not prevent this complication.

ICD-10. I50 Heart failure

Medicines and Medications are used for the treatment and / or prevention of "Chronic systolic heart failure".

Pharmacological group(s) of the drug.

Family doctor. Therapist (vol. 2). Chronic renal failure mkb 10

Chronic renal failure

general information

There are various definitions of chronic renal failure (CRF), however, the essence of any of them is the development of a characteristic clinical and laboratory complex resulting from the progressive loss of all renal functions.

Chronic renal failure (CRF)- this is the loss of homeostatic functions of the kidneys against the background of renal disease for more than 3 months: a decrease in glomerular filtration and relative density (osmolarity), an increase in the concentration of creatinine, urea, potassium, phosphorus, magnesium and aluminum in blood serum, a decrease in blood calcium, a violation of acid- alkaline balance (metabolic acidosis), the development of anemia and arterial hypertension.

Epidemiology

The problem of CRF has been actively developed for several decades, due to the high prevalence of this complication. Thus, according to the literature, the number of patients with CRF in Europe, the USA and Japan ranges from 157 to 443 per 1 million population. The prevalence of this pathology in our country is 212 per 1 million population among patients older than 15 years. Among the causes of lethality, CRF ranks eleventh.

Etiology

CRF is based on a single morphological equivalent - nephrosclerosis. There is no such form of kidney pathology that could not potentially lead to the development of nephrosclerosis, and, consequently, renal failure. Thus, CRF is the outcome of any chronic kidney disease.

CRF can be caused by primary kidney diseases, as well as their secondary damage as a result of a long-term chronic disease of organs and systems. Direct damage to the parenchyma (primary or secondary), leading to chronic renal failure, is conditionally divided into diseases with a primary lesion of the glomerular apparatus or tubular system, or a combination of both. Among glomerular nephropathy, the most common is chronic glomerulonephritis, diabetic nephropathy, amyloidosis, lupus nephritis. Malaria, gout, protracted septic endocarditis, multiple myeloma are more rare causes of chronic renal failure with damage to the glomerular apparatus. The primary lesion of the tubular system is most often observed in most urological diseases accompanied by a violation of the outflow of urine, congenital and acquired tubulopathies (renal diabetes insipidus, Albright tubular acidosis, Fanconi syndrome, which occurs as an independent hereditary disease or accompanies various diseases), drug poisoning and toxic substances. Secondary damage to the kidney parenchyma can be caused by vascular diseases - damage to the renal arteries, essential hypertension (primary nephroangiosclerosis), malformations of the kidneys and urinary tract (polycystic, renal hypoplasia, neuromuscular dysplasia of the ureters, etc.). Chronic isolated damage to any part of the nephron is actually a trigger for the development of chronic renal failure, however, in clinical practice, the late stages of chronic renal failure are characterized by dysfunction of both the glomerular and tubular apparatus.

Pathogenesis

Regardless of the etiological factor, the mechanism of development of CRF is based on a decrease in the number of active nephrons, a significant decrease in the glomerular filtration rate in a single nephron, and on a combination of these indicators. The complex mechanisms of kidney damage include many factors (impaired metabolic and biochemical processes, blood clotting, impaired passage of urine, infection, abnormal immune processes), which, when interacting with other diseases, can lead to chronic renal failure. In the development of chronic renal failure, the most important point is the slow, hidden violation of all renal functions, which the patient is usually unaware of. However, modern examination methods make it possible to identify a latent stage, since the changes that occur in the body in violation of the functional ability of the kidneys are now well known. This is an important task of the clinician, which allows him to take preventive and therapeutic measures aimed at preventing the premature development of end-stage renal failure. The kidneys have significant reserve capacity, as evidenced by the preservation and maintenance of the life of the body with the loss of 90% of nephrons. The process of adaptation is carried out by strengthening the function of the remaining nephrons and restructuring the whole organism. With the progressive death of nephrons, the glomerular filtration rate decreases, the water-electrolyte balance is disturbed, there is a delay in the body of metabolic products, organic acids, phenolic compounds, some peptides and other substances that cause the clinical picture of CRF and the patient's condition. Thus, a violation of the excretory and secretory functions of the kidneys contributes to the development of pathological changes in the body, the severity of which depends on the intensity of nephron death and determines the progression of renal failure. With CRF, one of the most important functions of the kidneys is disturbed - maintaining the water-salt balance. Already in the early stages of chronic renal failure, especially due to diseases with a predominant lesion of the tubular apparatus, there is a violation of the concentration ability of the kidneys, which is manifested by polyuria, nocturia, a decrease in the osmolarity of urine to the level of the osmotic concentration of the blood plasma (isostenuria) and, with a far advanced lesion, hypostenuria (osmotic concentration of urine below the osmotic concentration of blood plasma). Polyuria, which is permanent even with fluid restriction, may be due to both a direct decrease in tubular function and a change in osmotic diuresis. An important function of the kidney is to maintain electrolyte balance, especially ions such as sodium, potassium, calcium, phosphorus, etc. In chronic renal failure, sodium excretion in the urine can be increased and decreased. In a healthy person, 99% of the sodium filtered through the glomeruli is reabsorbed in the tubules. Diseases with a predominant lesion of the tubular-interstitial system lead to a decrease in its reabsorption up to 80%, and, consequently, its increased excretion. Strengthening the excretion of sodium in the urine does not depend on its introduction into the body, which is especially dangerous when recommending in such situations the patient limit salt intake. However, the predominant damage to the glomeruli, a decrease in the glomerular filtration rate, especially with preserved tubular function, can lead to sodium retention, which leads to the accumulation of fluid in the body, an increase in blood pressure. Up to 95% of the potassium introduced into the body is removed by the kidneys, which is achieved by its secretion in the distal tubules. In chronic renal failure, the regulation of the balance of potassium in the body is carried out by removing it from the intestines. So, with a decrease in GFR to 5 ml / min, about 50% of the incoming potassium is excreted in the feces. An increase in plasma potassium can be observed in the oligoanuric phase of chronic renal failure, as well as during an exacerbation of the underlying disease, with increased catabolism. Since the main amount of potassium in the body is located in the intracellular space (in plasma - about 5 mmol / l, in the intracellular fluid - about 150 mmol / l), in some situations (fever, surgery, etc.) hyperkalemia, threatening the life of the patient. The state of hypokalemia in patients with chronic renal failure is much less common and may indicate a deficiency of total potassium in the body and a sharp violation of the secretory ability of the distal tubules. Violations of the functions of the glomerular and tubular apparatus already in the early stages of chronic renal failure lead to hyperchloremic acidosis, hyperphosphatemia, a moderate increase in magnesium in the blood serum and hypocalcemia.

An increase in the concentration of urea, amino nitrogen, creatinine, uric acid, methylguanidine, phosphates, etc. in the blood. An increase in the level of amino nitrogen may be associated with increased protein catabolism due to its excessive intake, or its sharp restriction during starvation.

Urea is the end product of protein metabolism, formed in the liver from the nitrogen of deaminated amino acids. In conditions of renal insufficiency, not only the difficulty of its excretion is noted, but also, for still unknown reasons, an increase in its production by the liver.

Creatinine is formed in the muscles of the body from its precursor creatinine. The content of creatinine in the blood is quite stable, the increase in creatinemia in parallel with the increase in the level of urea in the blood occurs, as a rule, with a decrease in glomerular filtration to 20-30% of the normal level.

Even more attention is drawn to the excess production of parathyroid hormone as a possible main toxin in uremia. This is confirmed by the effectiveness of at least partial parathyroidectomy. There are more and more facts indicating the toxicity of substances of unknown nature, the relative molecular weight of which is 100-2000, as a result of which they are called "medium molecules". They accumulate in the blood serum of patients with CRF. However, it is becoming more and more obvious that the syndrome of azotemia (uremia) is not caused by one or more toxins, but depends on the rearrangement of cells in all tissues and changes in the transmembrane potential. This occurs as a result of violations of both the function of the kidneys and the systems that regulate their activity.

Its causes are blood loss, shortening of the life span of erythrocytes due to protein and iron deficiency in the body, toxic effects of nitrogen metabolism products, hemolysis (glucose-6-phosphate dehydrogenase deficiency, excess guanidine), reduced erythropoietin. The growth of medium molecules also inhibits erythropoiesis.

Osteodystrophy

Osteodystrophy caused by a violation of the metabolism of calciferol. In the kidneys, the active metabolite 1,25-dehydroxycalciferol is formed, which affects calcium transport by regulating the synthesis of specific proteins that bind it. With chronic renal failure, the translation of calciferol into exchange-active forms is blocked. The water-electrolyte balance remains close to physiological for a long time, up to the terminal phase. Under conditions of violation of ion transport in the tubules, with tubular defects, the loss of sodium increases, which, if its replenishment is insufficient, leads to the syndrome of hyponatremia. Hyperkalemia is regarded as the second most important sign of CRF. This is due not only to the increasing catabolism characteristic of renal failure, but also to an increase in acidosis, and most importantly, to a change in the distribution of potassium outside and inside the cells.

The change in CBS occurs due to a violation of the function "carbonic acid - bicarbonate". With various variants of impaired renal function, depending on the nature of the process, one or another type of violation of the KOS can be observed. With glomerular - the possibility of entering the urine of acidic valences is limited, with tubular - there is a predominant inclusion of ammonio-acidogenesis.

Arterial hypertension

In its occurrence, the role of inhibition of the production of vasodilators (kinins) is undoubted. The imbalance of vasoconstrictors and vasodilators in chronic renal failure is due to the loss of the ability of the kidney to control sodium levels in the body and the volume of circulating blood. In the terminal phase of chronic renal failure, a persistent hypertension reaction can be adaptive, maintaining filtration pressure. In these cases, a sharp drop in blood pressure can be fatal.

According to ICD-10, CRF is classified as follows:

N18 Chronic renal failure.

N18.0 - End-stage kidney disease.

N18.8 - Other chronic renal failure

N18.9 Chronic renal failure not specified.

N19 - Renal failure not specified.

Diagnostics

Diagnosis of chronic renal failure with known renal disease is not difficult. Its degree, and, consequently, its severity, is determined by an increase in the concentration of creatinine in the blood serum and a decrease in GFR. As it should be clear from the above, it is very important to monitor the state of electrolyte, acid-base metabolism, timely register violations of the heart and lungs.

Diagnosis of CRF is mainly laboratory. The first symptom is a decrease in the relative density of urine to 1.004-1.011, regardless of the magnitude of diuresis. It must be borne in mind that the presence of sugar and protein in the urine can increase the relative density of urine (each 1% sugar - by 0.004 and 3 g / l - by 0.01).

The study of electrolyte balance to establish the level of decline in kidney function is not very informative. The same can be said about the degree of anemia, and, moreover, the level of blood pressure.

An accurate assessment of kidney function, taking into account the state of other organs, the degree of dystrophic processes in the body become very important when deciding on the prospects for kidney transplantation.

In general therapeutic practice, one may encounter creatininemia without a specific renal disease. This is seen in congestive heart failure. Usually creatininemia does not exceed 0.6-0.8 mmol / l. A more significant increase can be observed with rapidly increasing cardiac decompensation, for example, in patients with complicated myocardial infarction. A feature of such creatininemia is the unusual preservation of a sufficiently high density of urine. Renal failure occurs when the "renal quota" of cardiac output is reduced to 7.8%. The deterioration of renal hemodynamics is associated with an increase in venous pressure, and the decrease in renal blood flow outstrips the reduction in glomerular filtration, so that the filtration fraction is usually increased. The deterioration of renal hemodynamics is accompanied by a redistribution of renal blood flow. The outer part of the cortical layer suffers the most. Preservation of increased urine density is associated with a slowdown in blood flow, especially in the medulla.

Thus, “chronic” creatinemia, unusual for extrarenal causes, without the development of diffuse nephrosclerosis, not accompanied by its usual isosthenuria, has a certain diagnostic and prognostic value for cardiac patients. Such renal failure does not require special treatment. Another feature of the decrease in kidney function in congestive heart failure is the appearance and increase of proteinuria. As a rule, plasma proteins are secreted, but the culprit is impaired tubular reabsorption of the protein. The histopathological picture of such a congestive kidney reveals varicose veins. The glomeruli are enlarged, the capillary loops are wide and contain erythrocytes. The stroma of the kidney is edematous, the tubules are somewhat dilated, their epithelium is in a state of dystrophy, and many tubules show signs of atrophy. Focal interstitial fibrosis and arteriosclerosis.

Clinical Criteria

Main manifestations:

- symptoms of endogenous intoxication;

- oliguria;

- nausea;

- macrohematuria or microhematuria;

- violation of urination;

- itching of the skin;

- bleeding.

Already the first communication with the patient and clarification of such data from the anamnesis as the duration of the nephrological disease, the presence or absence of chronic glomerulo- or pyelonephritis, arterial hypertension, the duration of these diseases, the frequency of exacerbations of glomerulo- or pyelonephritis, the amount of urine excreted per day, as well as the identification of early symptoms of chronic renal failure, allow to suspect renal failure and outline a plan for diagnostic and therapeutic measures.

An indication in the anamnesis of the duration of the nephrological disease for more than 5-10 years gives grounds to suspect the presence of renal failure and to perform all diagnostic studies confirming or rejecting this diagnosis. The analysis of studies showed that the total impairment of kidney function and the detection of the stage of chronic renal failure are possible using traditional methods for examining urine and blood.

Asthenic syndrome: weakness, fatigue, drowsiness, hearing loss, taste.

Dystrophic Syndrome: dryness and excruciating itching of the skin, traces of scratching on the skin, weight loss, real cachexia, muscle atrophy is possible.

Gastrointestinal syndrome: dryness, bitterness and an unpleasant metallic taste in the mouth, lack of appetite, heaviness and pain in the epigastric region after eating, often diarrhea, an increase in the acidity of gastric juice (by reducing the destruction of gastrin in the kidneys), in the later stages there may be gastrointestinal bleeding , stomatitis, parotitis, enterocolitis, pancreatitis, liver dysfunction.

Cardiovascular Syndrome: shortness of breath, pain in the heart, arterial hypertension, left ventricular myocardial hypertrophy, in severe cases - attacks of cardiac asthma, pulmonary edema; with advanced CRF - dry or exudative pericarditis, pulmonary edema.

Anemia-hemorrhagic syndrome: skin pallor, nasal, intestinal, gastric bleeding, skin hemorrhages, anemia.

Osteoarticular syndrome: pain in the bones, joints, spine (due to osteoporosis and hyperuricemia).

Damage to the nervous system: uremic encephalopathy (headache, memory loss, psychoses with obsessive fears, hallucinations, convulsive seizures), polyneuropathy (paresthesia, itching, burning sensation and weakness in the arms and legs, decreased reflexes).

urinary syndrome: isohypostenuria, proteinuria, cylindruria, microhematuria.

Early clinical signs of CKD- polyuria and nocturia, hypoplastic anemia; then general symptoms join - weakness, drowsiness, fatigue, apathy, muscle weakness. Subsequently, with a delay of nitrogenous slags, there are skin itching (sometimes painful), nasal, gastrointestinal, uterine bleeding, subcutaneous hemorrhages; "uremic gout" may develop with joint pain, tophi. Uremia is characterized by dyspeptic syndrome - nausea, vomiting, hiccups, loss of appetite, up to disgust for food, diarrhea. The skin is pale yellowish in color (a combination of anemia and delayed urochromes). The skin is dry, with traces of scratching, bruises on the arms and legs; tongue - dry, brown. With the progression of chronic renal failure, symptoms of uremia increase. Sodium retention leads to hypertension, often with malignant features, retinopathy. Hypertension, anemia, and electrolyte shifts cause damage to the heart. In the terminal stage, fibrinous or effusion pericarditis develops, indicating a poor prognosis. As uremia progresses, neurological symptoms increase, convulsive twitches appear, encephalopathy intensifies, up to the development of uremic coma, with strong noisy acidotic breathing (Kussmaul breathing). The tendency of patients to infections is characteristic; pneumoniae is common.

Laboratory Criteria

Clinical analysis of urine- proteinuria, hypoisostenuria, cylindruria, possible abacterial leukocyturia, hematuria.

Blood analysis:

clinical- anemia, an increase in the erythrocyte sedimentation rate (ESR), moderate leukocytosis is possible, a shift of the leukocyte formula to the left, thrombocytopenia is possible;

biochemical- an increase in the levels of urea, creatinine, residual nitrogen in the blood, an increase in total lipids, B-lipoproteins, hyperkalemia, hypocoagulation, hypocalcemia, hyperphosphatemia, hypodysproteinemia, hypercholesterolemia are possible.

Laboratory diagnostics

– Clinical blood test, with the determination of platelets;

- biochemical blood test, with the determination of the level of creatinine, urea, cholesterol, proteinogram, electrolytes (potassium, calcium, phosphorus, sodium, chlorine);

- determination of daily protein excretion;

- determination of the functional state of the kidneys (glomerular filtration rate);

- acid-base state;

- ALT, AST;

- X-ray examination of the kidneys, bones, lungs.

Additional laboratory and instrumental studies

- Ferritin;

— percentage (%) of transferrin saturation;

- determination of parathyroid hormone;

- determination of urinary calcium excretion;

- determination of blood amylase;

— protein-sedimentary samples;

- determination of fibrin degradation products in blood serum;

— radionuclide studies (indirect renoangiography, dynamic and static renoscintigraphy);

- puncture biopsy of the kidney;

- functional studies of the bladder;

- echoencephalogram;

- echocardiography with an assessment of the functional state of the heart, dopplerography of blood vessels.

Differential Diagnosis

Diagnosis of chronic renal failure in clinicians does not cause any particular difficulties due to the characteristic clinical picture and laboratory changes in the blood and urine. The only thing to always remember is that such a clinic may be due to an exacerbation of chronic renal failure as a result of an occlusive factor and the development of an acute inflammatory process in the upper or lower urinary tract. Under these conditions, the true stage of chronic renal failure can be established only after the restoration of the passage of urine and the elimination of the acute inflammatory process. For nephrologists, it is important to diagnose the early and pre-dialysis stages of chronic renal failure, which allows you to outline treatment tactics and determine the prognosis of nephrological disease.

Identification of CRF, as a rule, is carried out in parallel with the diagnosis of a nephrological disease and includes the history of the disease, clinical manifestations, changes in general blood and urine tests, as well as specific studies aimed at identifying the total kidney function and methods to assess the morphological and functional kidney parameters.

Expert advice

— Optometrist: condition of the fundus;

— neuropathologist: the presence of uremic and hypertensive encephalopathy;

— gastroenterologist: the presence of complications from the gastrointestinal tract (gastritis, hepatitis, colitis, etc.);

— cardiologist: symptomatic arterial hypertension, hypertensive heart;

— cardiac surgeon: uremic pericarditis (puncture);

- urologist: the presence of stones in the pyelocaliceal section of the kidneys, ureters, etc.

Goals

Based on the classification, the treatment of CRF is indicated already with a glomerular filtration rate of less than 60 ml / min, which corresponds to a creatinine level of 140 μmol / l for men and 105 μmol / l for women (renoprotection is indicated from a GFR level of about 90 ml / min). It is recommended to stabilize blood pressure to target numbers< 130/80 мм рт.ст. а при протеинурии – < 125/75 мм рт.ст.

Diagnosis and management of complications.

Level of treatment

Outpatient: general practitioner, family doctor, specialist cardiologist, gastroenterologist, etc.; inpatient - indications for inpatient treatment.

Patients with CRF are subject to dispensary observation by a nephrologist, and in his absence, by a general practitioner at the place of residence.

Dispensary observation should include: examination of patients with chronic renal failure stage I 3 times a year, with chronic renal failure stage II - 6 times a year, and with chronic renal failure stage III - monthly, appointment of an adequate regimen, employment and selection of rational dietary and therapeutic measures; identification and elimination of factors that contribute to the progression of chronic renal failure. In the event of intercurrent diseases, patients are examined additionally. Patients with stage IV CKD should be treated with hemodialysis or peritoneal dialysis, or symptomatic therapy (if there are contraindications for renal replacement therapy (RRT) at the place of residence.

Treatment Methods

Basic drug therapy(in accordance with international standards and protocols approved by the Ministry of Health of Ukraine: specifically, the pharmacological group of drugs, dose, duration of the course) and additional.

Surgical treatment or other types of treatment (indications).

The main objectives of dietary treatment for chronic renal failure is to reduce the intake of protein with food - a low-protein diet (LPD); control of fluid intake; reduction in the use of foods that contain Na +, K +, Mg2 +, Cl-, phosphates.

Protein restriction

A low-protein diet (NBD) helps to inhibit the progression of chronic renal failure: intraglomerular hypertension and glomerular hypertrophy, proteinuria decrease, the incidence of secondary hyperparathyroidism decreases, and the level of nitrogen metabolism products decreases.

Correction of calcium phosphate disorders

Elevated serum phosphorus levels and the development of secondary hyperparathyroidism (SHPT) not only contribute to the development of osteopathy, but also affect the progression of CKD. With GFR indicators of 40-50 ml/min, the amount of phosphorus in the daily diet should not exceed 800-1000 mg. With GFR below 40 ml / min, in addition to dietary restriction of phosphorus to 1 g / day, phosphate binders (PBS) are prescribed: phosphate binders.

Blood pressure (BP) and proteinuria control

ACE inhibitors (ACE inhibitors):

- enalapril - from 5 to 40 mg / day;

- perindopril - from 2 to 8 mg / day;

- quinapril - from 5 to 20 mg / day;

- moexipril - from 3.75 to 15 mg / day;

- ramipril - from 2.5 to 10 mg / day;

- spirapril - from 3 to 6 mg / day.

Angiotensin II receptor blockers (ARBII):

- valsartan - from 80 to 160 mg / day;

- losartan - from 25 to 100 mg / day;

- candesartan - from 8 to 32 mg / day;

- irbesartan - from 150 to 300 mg / day;

- telmisartan - from 40 to 80 mg / day;

- eprosartan - from 400 to 1200 mg / day.

Calcium channel blockers:

- amlodipine - from 5 to 10 mg / day;

- lercanidipine - from 5 to 10 mg / day;

- diltiazem - from 30 to 90 mg / day three times;

- diltiazem retard - from 90 to 300 mg / day twice;

- verapamil - from 40 to 120 mg / day from 2 to 3 times a day;

- verapamil retard - from 240 to 480 mg / day.

ACE inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) more significantly than diuretics, calcium antagonists and b-blockers, reduce proteinuria and microalbuminuria.

Calcium channel blockers. namely, the nifedipine group (dihydropyridine) effectively reduce blood pressure, but do not affect the level of proteinuria and the progression of chronic renal failure, which is associated with their ability to sharply reduce the tone of the afferent arteriole and increase water hammer at high systemic blood pressure. On the contrary, non-hydropyridine calcium channel blockers (verapamil, diltiazem) have practically no effect on the mechanism of renal autoregulation, help reduce proteinuria, and inhibit glomerular fibrosis. Achieving target blood pressure in chronic kidney disease occurs with the appointment of several drugs.

Anemia correction

Body iron saturation is controlled by target trough serum erythropoietin levels above 100 ng/mL and transferrin saturation > 20%. Iron preparations, if necessary, are prescribed in a dose of more than 200-300 mg of elemental iron per day. In parallel, other drugs are used that are mandatory in the treatment of anemia:

- folic acid - from 5 to 15 mg / day;

- pyridoxine (vitamin B6) - from 50 to 200 mg / day.

The main type of replacement therapy for erythropoietin deficiency anemia is the appointment of erythropoietin:

- Eprex - from 20 to 100 U / kg three times a week;

- recormon - from 20 to 100 U / kg three times a week.

Correction of hyperazotemia

In order to reduce the level of azotemia, the toxic load of uremia, drugs are used that enhance their excretion.

Hypoazotemic phytopreparations:

- hofitol - from 2 to 3 tablets three times a day for 15 minutes. before meals or 2 ampoules twice a day intramuscularly or intravenously daily for 14-21 days;

- lespenephril (lespeflan) - from 3 to 6 teaspoons per day or intravenously at the rate of 1 ml / kg of the patient's weight.

Enterosorption with the use of enterosorbents - 1.5-2 hours before or after food and medicines:

- activated carbon - up to 5 g from 3 to 4 times / day;

- spherical carbonite - up to 5 g from 3 to 4 times / day;

- enterosgel - 1 tablespoon (15.0 g) 3 to 4 times / day;

- sorbigel - 1 tablespoon (15.0 g) 3 to 4 times / day;

- enterodesis - 5 ml per 1000 ml of water 3 to 4 times / day;

- polyphepan - 1 tablespoon (15.0 g) 2 to 4 times / day or at the rate of 0.5 g / kg of body weight / day.

Intestinal dialysis with the introduction into the colon through a probe from 8 to 10 liters of a solution that contains: sucrose - 90 g / l; glucose - 8 g / l, potassium chloride - 0.2 g / l, sodium bicarbonate - 1 g / l, sodium chloride - 1 g / l.

Correction of dyslipidemia

Target LDL-C in adults with chronic kidney disease< 2,6 ммоль/л; уровень ХС ЛПВП >1 mmol/l (40 mg/dl); TG< 2,3 ммоль/л.

Statins:

- lovastatin - from 10 to 80 mg / day;

- simvastatin - from 10 to 40 mg / day;

- pravastatin - from 10 to 40 mg / day;

- atorvastatin - from 10 to 40 mg / day;

- fluvastatin - from 10 to 40 mg / day.

Statins block the key enzyme of cholesterol synthesis in the liver and have a pronounced lipid-lowering effect. Desired level of LDL cholesterol -< 2,6 ммоль/л.

Fibrates:

- gemfibrozil - 600 mg twice a day;

- fenofibrate - 200 mg / day.

Fibrates are prescribed for triglycerides > 5.7 mmol/l (500 mg/dl), dosed according to renal function. The combination of fibrates and statins is not desirable, as there is a high risk of developing rhabdomyolysis.

Indications for active treatment of CRF:

- serum creatinine level - above 0.528 mmol / l (with diabetic nephropathy - above 0.353 mmol / l), an arteriovenous fistula is superimposed, with a further increase in creatinine - “input” into hemodialysis;

- pericarditis, neuropathy, encephalopathy, hyperkalemia, high hypertension, impaired acid-base balance in patients with chronic renal failure.

Today, the following active methods of treating CRF are used in Ukraine: chronic hemodialysis in combination with hemosorption and hemofiltration, peritoneal dialysis and kidney transplantation.

The prognosis is poor and improves with renal replacement therapy (RRT) and kidney transplantation.

Prevention

Timely detection and treatment of nephrological diseases leading to the development of CRF, such as acute glomerulo- and pyelonephritis, diabetic nephropathy.

Chronic heart failure. Definition. Classification. Clinic. Diagnostics. Treatment.

Relevance of the problem

The prevalence of clinically significant chronic heart failure (CHF) in the population is at least 1.5-3.0%. Among people over 65 years of age, the incidence of CHF increases to 6-10%, and decompensation becomes the most common cause of hospitalization of elderly patients. The number of patients with asymptomatic dysfunction of the left ventricle is at least 4 times higher than the number of patients with clinically severe CHF. In 15 years, the number of hospitalizations diagnosed with CHF has tripled, and in 40 years it has increased 6 times. Five-year survival of patients with CHF is still below 50%. The risk of sudden death is 5 times higher than in the general population. In the United States, there are more than 2.5 million patients with CHF, about 200 thousand patients die annually, the 5-year survival rate after the onset of signs of CHF is 50%.

Chronic heart failure (CHF) is a cardio-caused violation of (pumping) function with corresponding symptoms, consisting in the inability of the circulatory system to deliver the amount of blood necessary for their normal functioning to organs and tissues. Thus, this is a disproportion between the state of blood circulation and metabolism, which increases with an increase in the activity of vital processes; pathophysiological condition in which dysfunction of the heart does not allow it to maintain the level of blood circulation necessary for metabolism in tissues.

CHF can develop against the background of almost any disease of the cardiovascular system, but the main three are the following nosological forms:

- Ischemic heart disease (CHD)

— Arterial hypertension

- Heart defects.

ischemic heart disease. From the existing classification, acute myocardial infarction (AMI) and ischemic cardiomyopathy (ICMP is a nosological unit introduced into clinical practice by ICD-10) are especially common, leading to the development of CHF. The mechanisms of occurrence and progression of CHF due to AMI are due to a change in the geometry and local contractility of the myocardium, called the term "left ventricular (LV) remodeling", with ICMP there is a decrease in total myocardial contractility, called the term "hibernation ("hibernation") of the myocardium".

Arterial hypertension. Regardless of the etiology of hypertension, there is a structural restructuring of the myocardium, which has a specific name - "hypertensive heart". The mechanism of CHF in this case is due to the development of LV diastolic dysfunction.

Heart defects. Until now, Ukraine has been characterized by the development of CHF due to acquired and uncorrected rheumatic malformations.

A few words must be said about dilated cardiomyopathy (DCM) as a cause of CHF. DCM is a rather rare disease of unspecified etiology that develops at a relatively young age and quickly leads to cardiac decompensation.

Establishing the cause of CHF is necessary for the choice of treatment tactics for each individual patient.

Pathogenetic aspects of heart failure

From the point of view of modern theory, the main role in the activation of compensatory mechanisms (tachycardia, the Frank-Starling mechanism, constriction of peripheral vessels) is played by hyperactivation of local or tissue neurohormones. These are mainly the sympathetic-adrenal system (SAS) and its effectors - norepinephrine and adrenaline and the renin-angiotensin-aldosterone system (RAAS) and its effectors - angiotensin II (A-II) and aldosterone, as well as the system of natriuretic factors. The problem is that the “launched” mechanism of neurohormone hyperactivation is an irreversible physiological process. Over time, short-term compensatory activation of tissue neurohormonal systems turns into its opposite - chronic hyperactivation. The latter is accompanied by the development and progression of systolic and diastolic dysfunction of the left ventricle (remodeling).

If the heart is damaged, the stroke volume of the ventricle will decrease, and the end-diastolic volume and pressure in this chamber will increase. This increases the end-diastolic stretch of the muscle fibers, which leads to greater systolic shortening (Starling's law). The Starling mechanism helps preserve cardiac output. but the resulting chronic rise in diastolic pressure will be transmitted to the atria, pulmonary veins, or veins of the systemic circulation. Increasing capillary pressure is accompanied by fluid extravasation with the development of edema. Reduced cardiac output, especially with a decrease in blood pressure, activates the SAS, stimulating myocardial contractions, heart rate, venous tone, and a decrease in kidney perfusion leads to a decrease in glomerular filtration rate, reabsorption of water and sodium chloride, and activation of the RAAS.

Tissue hypoxia in CHF is not only the resulting link in pathogenesis, but also a factor that has a direct provoking effect on other leading components of it - a decrease in the pumping capacity of the heart, preload, afterload, and heart rhythm. Hypoxia is a complex multi-component, multi-stage process. The direct primary effects of hypoxia are directed at targets localized at various levels: organismal, systemic, cellular, and subcellular. At the subcellular level, hypoxia initiates the development of apoptosis.

The result of the described processes is an increase in peripheral vascular resistance and circulating blood volume with a corresponding increase in afterload and preload.

Heart failure clinic

Most patients develop primary left heart failure. The most common complaint is inspiratory dyspnea, initially associated with exercise and progressing to orthopnea, paroxysmal postural, to dyspnea at rest. Characterized by complaints of unproductive cough, nocturia. Patients with CHF note weakness, fatigue, which are the result of reduced blood supply to the skeletal muscles and the central nervous system.

With right ventricular failure, there are complaints of pain in the right hypochondrium due to stagnation in the liver, loss of appetite, nausea due to intestinal edema or reduced gastrointestinal perfusion, peripheral edema.

On examination, it can be noted that some patients, even with severe CHF, look good at rest, while others have shortness of breath when talking or with minimal activity; patients with a long and severe course look cachexic, cyanotic.

In some patients, tachycardia, arterial hypotension, a drop in pulse pressure, cold extremities, and sweating (signs of SAS activation) are found.

Examination of the heart reveals a cardiac impulse, an extended or elevating apical impulse (ventricular dilatation or hypertrophy), a weakening of the I tone, a protodiastolic gallop rhythm.

With left ventricular failure, hard breathing, dry rales (congestive bronchitis), crepitus in the basal sections of the lungs are heard, dullness in the basal sections (hydrothorax) can be determined.

With right ventricular heart failure, swollen jugular veins, liver enlargement are detected; a slight pressure on it can increase the swelling of the jugular veins - a positive hepatojugular reflex. Ascites and anasarca appear in some patients.

Diagnosis of heart failure

The final clinical diagnosis of heart failure can only be established by taking into account instrumental data, primarily EchoCG, as well as X-ray of the chest, ECG, and laboratory research data.

With the help of echocardiography, the following are assessed: the condition of the valves, the presence of shunts, aneurysms, the condition of the pericardium, the presence of a tumor or thrombi, as well as contractile function (diffuse changes or regional disorders, their quantitative assessment), the presence of myocardial hypertrophy, chamber dilatation, determine the global systolic function — FV.

An important role in the diagnosis of heart failure is played by X-ray examination of the OGP: - assessment of the size of the heart (cardiothoracic index); - the presence and severity of stagnation in the lungs; - differential diagnosis with diseases of the respiratory system; -diagnosis and control of the effectiveness of treatment of complications of heart failure (pneumonia, hydrothorax, pulmonary embolism).

An integral part of the examination in HF syndrome is the ECG, which allows to detect hypertrophy, ischemia, focal changes, arrhythmias and blockade, and is also used to control therapy with B-blockers, diuretics, cardiac glycosides, amiodarone.

The 6-minute walk test is used to determine functional class (FC) in patients. This method has been widely used in the last 4-5 years in the USA, including in clinical trials. The condition of patients who are able to overcome from 426 to 550 m in 6 minutes corresponds to mild CHF; from 150 to 425 m - medium, and those who are not able to overcome even 150 m - severe decompensation. Thus, the functional classification of CHF reflects the ability of patients to perform physical activity and outlines the degree of changes in the functional reserves of the body. This is especially significant in assessing the dynamics of the patients' condition.

Laboratory examination for heart failure includes a complete blood count (hemoglobin, erythrocytes, leukocytes, platelets, hematocrit, ESR), a general urinalysis, a biochemical blood test (electrolytes -K +, Na +, creatinine, bilirubin, liver enzymes - ALT, AST, alkaline phosphatase , glucose).

CH classification

In Ukraine, the classification of the Ukrainian Association of Cardiology of 2006 is used, according to which HF stages are distinguished (based on the classification of V.Kh. Vasilenoko-N.D. Strazhesko), dysfunction variants (according to echocardiography) and functional classes (according to the NYHA classification)

The functional classification of the New York Heart Association is the most convenient and meets the requirements of practice, assuming the allocation of four functional classes according to the ability of patients to endure physical activity. This classification is recommended for use by WHO. The principle underlying it is an assessment of the patient's physical (functional) capabilities, which can be identified by a doctor with a targeted, thorough and accurate history taking, without the use of complex diagnostic techniques.

Four functional classes (FC) of CHF have been identified.

I FC. The patient does not experience restrictions in physical activity. Ordinary exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but the performance of ordinary physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

III FC. Severe limitation of physical activity. The patient feels comfortable only at rest, but less than usual physical activity leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain.

IV FC. Inability to perform any load without discomfort. Symptoms of heart failure or angina syndrome may occur at rest. When performing a minimum load, discomfort increases.

It is the dynamics of FC during treatment that allows us to objectively decide whether our therapeutic measures are correct and successful. The conducted studies also proved the fact that the definition of FC to a certain extent predetermines the possible prognosis of the disease.

In clinical practice, determining the variant of myocardial dysfunction is crucial for a differentiated approach to treatment tactics. Clinically, both systolic and diastolic variants are manifested by the same type of symptoms - shortness of breath, cough, wheezing, orthopnea. In the absence of EchoCG data, you can try to determine the variant of dysfunction using clinical and radiological data, taking into account the etiology of heart failure, auscultatory data, determining the boundaries of the heart percussion and radiographically, as well as ECG data (hypertrophy, dilatation, cicatricial changes in their localization, the presence of signs of cardiac aneurysm, etc. .).

Treatment of CHF.

The goals of HF treatment are:

Elimination or minimization of clinical symptoms of CHF - increased fatigue, palpitations, shortness of breath, edema;

protection of target organs - blood vessels, heart, kidneys, brain (similar to hypertension therapy), as well as

Prevention of the development of malnutrition of the striated muscles;

improving the quality of life,

increase in life expectancy

Reducing the number of hospitalizations.

There are non-drug and drug treatments.

Non-drug methods

Diet. The main principle is to limit the intake of salt and, to a lesser extent, fluids. At any stage of CHF, the patient should take at least 750 ml of fluid per day. Restrictions on salt intake for patients with CHF I FC - less than 3 g per day, for patients with ІІ-ІІІ FC - 1.2-1.8 g per day, for patients with FC IV - less than 1 g per day.

Physical rehabilitation. Options - walking or an exercise bike for 20-30 minutes a day up to five times a week with the implementation of self-monitoring of well-being, heart rate (load is considered effective when 75-80% of the patient's maximum heart rate is reached).

Medical treatment of heart failure

The entire list of drugs used to treat CHF is divided into three groups: main, additional, auxiliary.

The main group of drugs fully meet the criteria of "medicine of evidence" and is recommended for use in all countries of the world: ACE inhibitors, diuretics, SG, ß-blockers (in addition to ACE inhibitors).

An additional group, the efficacy and safety of which has been proven by large studies, however, requires clarification (meta-analysis): aldosterone antagonists, angiotensin I receptor antagonists, CCBs of the latest generation.

Auxiliary drugs, their use is dictated by certain clinical situations. These include peripheral vasodilators, antiarrhythmics, antiplatelet agents, direct anticoagulants, non-glycoside positive inotropic agents, corticosteroids, statins.

Despite the large selection of drugs, polypharmacy (unjustified prescription of a large number of groups of drugs) is unacceptable in the treatment of patients. At the same time, today, at the level of the polyclinic link, the main group of drugs for the treatment of CHF does not always occupy a leading position, sometimes preference is given to drugs of the second and third groups.

Principles of the combined use of basic drugs for the treatment of heart failure.

1. Monotherapy in the treatment of CHF is rarely used, and in this capacity only ACE inhibitors can be used in the initial stages of CHF.

2. Dual therapy with ACE inhibitor + diuretic is optimal for patients with CHF P-III FC NYHA with sinus rhythm; the use of the diuretic + glycoside scheme, which was extremely popular in the 1950s and 1960s, is not currently used.

3. Triple therapy (ACE inhibitor + diuretic + glycoside) - was the standard in the treatment of CHF in the 80s, and now remains an effective regimen in the treatment of CHF, however, for patients with sinus rhythm, it is recommended to replace the glycoside with a ß-blocker.

4. The gold standard from the early 90s to the present is a combination of four drugs - ACE inhibitor + diuretic + glycoside + ß-blocker.

Acute vascular insufficiency

Under this term, several acute circulatory disorders are collected, which are not included in the concept of either circulatory arrest or shock. The boundary with the latter is so poorly defined that one term is often used instead of another.

Collapse is a condition in which a disorder of the peripheral circulation occurs as a result of a gross violation of the ratio between the capacity of the vascular bed and the volume of circulating blood.

This definition refers to the defeat of the body with intact defense mechanisms. The outcome of the collapse is difficult to predict. It can lead to death, recovery without consequences, or go into shock.

pathological physiology

The main manifestation of the collapse is a drop in blood pressure, usually below 10.7 kPa (80 mm Hg. Art.) or 2/3 below the patient's normal blood pressure with the disappearance of the peripheral pulse. A characteristic feature of this hypotension is its sudden appearance due to poor adaptation of the body. This is one of the factors that distinguishes it from shock, in which the activation of protective mechanisms leads to a slow development of the pathological state of the present syndrome.

The absence of this "defensive reaction" is characteristic of some tissues and systems:

Myocardium, from where the bradycardia of the heart arises during the collapse;

Peripheral circulation (pale, cold, without cyanosis, marble-colored skin);

Venous circulation (venous pressure is low, the veins do not fill under the tourniquet);

Cerebral circulation (frequent memory impairment, agitation and delirium, sometimes convulsions and even fainting);

Renal circulation (with collapse, there is almost always oligo- or anuria);

Neurovegetative system (excessive sweating, pallor of the face, nausea).

The reasons for the collapse are numerous. It may be the result of:

a) acute hypovolemia due to bleeding, extracellular dehydration (in particular, with hyponatremia);

b) a decrease in cardiac output due to a violation of the heart rhythm in the direction of acceleration (ventricular tachycardia, rotation of the apex of the heart) or its decrease (nodal or sinus bradycardia, atrioventricular block);

c) circulatory disorders due to difficult filling of the cavities of the heart, for example, with cardiac tamponade;

d) a decrease in peripheral resistance due to a secondary reaction of the vasovasal reflex in a labile patient under emotional stress;

e) hyperventilation, which occurs during artificial ventilation in patients suffering from pulmonary insufficiency with hypercapnia, as well as when using vasodilators.

These factors may be combined. It is this combination that is observed in the collapse that appears in the initial stage of myocardial infarction (it should be distinguished from cardiogenic shock). As a result of poisoning with barbiturates during collapse, fluid may accumulate in the splanchnicus zone; it is also characterized by the inhibitory effect of drugs on the myocardium.

The state of shock is characterized by a syndrome, the clinical essence of which is manifested by diffuse damage to brain cells and a secondary discrepancy between tissue blood supply to the needs of the body. It sometimes leads to death on its own. However, the stage of its irreversibility in humans has not yet been clearly defined.

Due to the difficulty of clinically defining "shock", numerous definitions have been proposed, of which Wilson's definition is the most accepted. According to him, a patient in a state of shock is characterized by the presence of three or more signs:

Systolic pressure is equal to or less than 10.7 kPa (80 mmHg);

Insufficient blood supply to the tissues, which is manifested by wet, cold, cyanotic, marble skin coloration or a decrease in the cardiac index below 2.5 l / min

Diuresis less than 25 ml/h;

Acidosis with a bicarbonate content of less than 21 mmol / l and lactic acidemia more than 15 mg per 100 ml.

Causes of shock

Maintaining adequate hemodynamics in the body is the result of a rational interaction between three main factors: bcc, cardiac output and peripheral vascular resistance. A pronounced change in one of these factors can lead to a “shock state”.

hypovolemic shock

Hypovolemic shock develops with a decrease in the volume of BCC by 20%. This acute volume loss may be the result of the following factors:

More or less significant external bleeding

Internal bleeding occurring in a cavity (abdomen, esophagus) or tissue (hematoma). So, for example, a fracture of the femur is accompanied by blood loss of up to 1000 ml, a fracture of the pelvic bones - from 1500 to 2000 ml;

Plasma loss (burn, pancreatitis);

Loss of water (electrolytes, such as sodium),

Cardiogenic shock

Shock as a result of heart failure can occur for two reasons.

Due to the insufficiency of myocardial function and development as a result of this critical decrease in cardiac output. Decompensation occurs when the heart fails or its rhythm is disturbed (slow or frequent). Myocardial infarction resulting from one of these mechanisms is a fundamentally remote cause of cardiogenic shock.

Obstruction of contraction or systolic ejection results in underfilling or failure of a component of another mechanism that allows a grouping of rather unrelated causes such as pericardial tamponade, pulmonary embolism, aortic rupture, intracardiac thrombosis, and tumor.

Toxic-infectious shock

Toxic-infectious (bacterial) shock is, at least in the initial stage, a rather frequent shock caused by impaired peripheral circulation.

Gram-negative organisms (Enterobacteriaceae and especially Pseudomonas) usually cause shock, but septicemia caused by Gram-positive organisms (specifically staphylococci) can also cause bacterial shocks. Often this shock is the first sign of a septic condition, but it can also appear during its development. In the pathogenesis, studied mainly in animals, a change in the mechanisms of microcirculation is noted. Peripheral vasoconstriction is followed by a stage of atony with opening of arterioles and blockage of veins. This leads to significant stasis, predominant in the area of ​​the celiac zone, and, consequently, to hypovolemia, which results in a decrease in MOS. This decrease in MOS can also be facilitated by direct damage to the myocardium by bacterial toxins. Bacterial endotoxins (staphylococcus exotoxins) act as a "trigger" for these disorders, releasing vasoactive substances such as histamine, kinins, and catecholamines.

Anaphylactic shock

Anaphylactic shock is the result of the interaction of circulating or tissue antigens with antibodies and develops according to a mechanism similar to bacterial shock.

neurogenic shock

Under this term, disorders of various origins are combined, following damage to the central nervous system or resulting from direct damage to the brain due to damage to the brain substance or pharmacological effects (ganglioblockers). Both of these reasons lead to a decrease in VP and a secondary fall in MOS, followed by a decrease in blood pressure. Inhibition of reflex vasoconstriction does not allow correcting these disorders.

There are also shock states, the mechanisms of which are more complex. This applies to shocks observed in massive barbiturate poisoning, where in addition to the neurogenic cause of shock, there is a direct negative inotropic effect of the drug on the myocardium. The state of shock in a person with polytrauma occurs as a result of the appearance of two components: hypovolemia and neurovegetative reaction. Shock in pancreatitis is due to hypovolemia, to which a toxic element is added, which, in all likelihood, causes vasoplegia.