Heart failure (HF) classification. Causes of chronic heart failure. How fast the problem develops

Such a distinction should simplify the diagnostic procedure and the choice of treatment tactics.

In domestic clinical practice, the classification of CHF according to Vasilenko-Strazhesko and the functional classification of the New York Heart Association are used.

CHF according to Vasilenko-Strazhesko (stages 1, 2, 3)

The classification was adopted in 1935 and is used to this day with some clarifications and additions. Based on the clinical manifestations of the disease during CHF, three stages are distinguished:

• I. Hidden circulatory failure without concomitant hemodynamic disorders. Symptoms of hypoxia appear with unusual or prolonged physical exertion. Shortness of breath, severe fatigue, tachycardia are possible. There are two periods A and B.

Stage Ia is a preclinical variant of the course, in which cardiac dysfunctions have almost no effect on the patient's well-being. An instrumental examination reveals an increase in the ejection fraction during physical exertion. At stage 1b (hidden CHF), circulatory failure manifests itself during exercise and resolves at rest.

The use of modern drugs and aggressive methods of treatment quite often eliminates the symptoms of CHF corresponding to stage 2b to the preclinical state.

New York (FC 1, 2, 3, 4)

The functional classification is based on exercise tolerance as an indicator of the severity of circulatory insufficiency. Determination of the patient's physical abilities is possible on the basis of a thorough history taking and extremely simple tests. On this basis, four functional classes are distinguished:

• I FC. Daily physical activity does not cause manifestations of dizziness, shortness of breath and other signs of myocardial dysfunction. Manifestations of heart failure occur against the background of unusual or prolonged physical exertion.
• II FC. Physical activity is partially limited. Everyday stress causes discomfort in the heart area or anginal pain, tachycardia attacks, weakness, shortness of breath. At rest, the state of health is normalized, the patient feels comfortable.
• III FC. Significant limitation of physical activity. The patient does not experience discomfort at rest, but everyday physical activity becomes unbearable. Weakness, pain in the heart, shortness of breath, tachycardia attacks are caused by loads less than usual.
• IV FC. Discomfort occurs with minimal physical exertion. Attacks of angina pectoris or other symptoms of heart failure may also occur at rest without visible prerequisites.

See the table of correspondence between the classifications of CHF according to NIHA (NYHA) and N.D. Strazhesko:

Functional classification is convenient for assessing the dynamics of the patient's condition during treatment. Since the gradation of the severity of chronic heart failure on a functional basis and according to Vasilenko-Strazhesko are based on different criteria and do not exactly correlate with each other, the stage and class for both systems are indicated when diagnosing.

Your attention to the video about the classification of chronic heart failure:

Chronic heart failure 1 degree 2 fc

Second functional class of exertional angina

Angina pectoris is a disease characterized by transient episodes of myocardial ischemia. They occur in conditions of emotional or physical stress, when the heart muscle requires more oxygen.

• The reasons
• Symptoms
• Diagnostics
• Treatment
• Consequences and prevention

The pathogenesis of angina pectoris is based on changes in arterial tone, as well as endothelial dysfunction of the coronary vessels. Tension or stress leads to vasoconstriction, which causes sudden myocardial ischemia. The level of exercise that causes ischemia and exertional angina is somewhat unpredictable.

Myocardial ischemia is associated with a violation of the contractile function of the heart muscle area, as well as with a change in the biochemical or electrical processes that occur in it. Due to oxygen deficiency in cardiomyocytes, the energy reserve is depleted, and other negative processes occur.

At the cellular level, the concentration of intracellular sodium increases, and potassium ions are lost. Transient ischemia is expressed in the development of an attack of angina pectoris, and stable ischemia leads to irreversible changes, that is, to a heart attack of the ischemic area of ​​the myocardium.

There are four functional classes of angina pectoris. The first of these is characterized by attacks that occur during very strong loads, for example, when walking fast or climbing stairs. 2 FC is characterized by limited physical activity, while attacks occur even when walking at a distance of more than five hundred meters.

Functional classes of exertional angina

The third class is characterized by significant limited activity, and in the fourth functional class, physical activity is so severely limited that seizures occur with minimal exertion or at rest. Let's take a closer look at 2 FCs of angina pectoris and first discuss the reasons that lead to the development of this disease.

The reasons

Let's single out several reasons that lead to a malfunction of the heart and to the occurrence of angina attacks:

1. Atherosclerosis. This is the most common reason. It is the atherosclerotic narrowing of the lumen of the coronary arteries by approximately fifty percent that leads to a discrepancy between the delivery of oxygen to the heart muscle and the need for it. It turns out that not the amount of oxygen that is necessary for the normal functioning of the heart is delivered.
2. Hypertrophic cardiomopathy, that is, an isolated lesion of the myocardium.
3. Pulmonary hypertension.
4. Severe arterial hypertension.
5. Stenosis of the aortic mouth.
6. Coronary spasm.
7. aortic insufficiency.

There are also risk factors. These include smoking, obesity and physical inactivity, heredity, diabetes and menopause. Hypoxia and severe anemia aggravate the course of angina pectoris.

It is worth highlighting the immediate causes that can lead to the development of attacks of angina related to FC 2:

• physical exercise;
• temperature changes;
• overeating;
• emotional disturbances and so on.

Symptoms

Angina pectoris 2 FC is characterized by symptoms such as:

• discomfort and tightness in the chest;
• heartache;
• dyspnea.

These manifestations are observed during such loads as climbing stairs or uphill, brisk walking, running, after overeating, in wind or cold. Such people are not strong, but still limited in activity. This is due to the fact that when walking at an average pace on flat terrain for five hundred meters, an attack begins to develop. This also happens when going up more than 1 floor, although some people show signs when going up to the fifth floor.

It turns out that for the occurrence of an attack, it is necessary to have factors in which the myocardium experiences a large need for oxygen. They, as already mentioned, can be different circumstances, although basically an attack develops during exercise. Some angina sufferers may feel reduced tolerance in the morning, but it returns to normal in the afternoon.

The severity of the clinical picture inherent in angina pectoris 2 FC depends on physical activity. Those who during the day often exceed the level of stress, suffer from attacks several times a day. If a person monitors the level of stress and does not exceed them, he may almost not feel angina attacks. This means that the severity of the disease is determined by the frequency of attacks.

Diagnostics

The most complete information is given by the ECG, which is removed during an attack. It is during this period that you can catch all the changes that indicate the presence of angina pectoris. In order to provoke ischemia, stress tests are used. Holter ECG monitoring allows you to detect painless and painful episodes of ischemia, and possible heart rhythm disturbances per day.

Since angina pectoris can be confused with other diseases, you should immediately consult a doctor and conduct a thorough diagnosis. The main difference between functional class 2 angina pectoris is that the attack stops after taking nitroglycerin or at rest.

Treatment

First of all, you need to know how to stop an attack that has begun. To do this, you need to eliminate the load that led to its occurrence, take a reclining position, provide air access and take a nitroglycerin tablet under the tongue.

Self-treatment of angina FC 2 is aimed at reducing the number of attacks, which will allow the patient to improve the quality of life. The doctor recommends lifestyle changes and avoiding stress that leads to seizures. In addition, he prescribes medications.

Drug therapy includes the use of the following drugs:

• nitrates - eliminate spasms of the coronary arteries;
• statins - lower cholesterol levels;
• beta-blockers, calcium antagonists - reduce the heart's need for oxygen;
• aspirin - prevents thrombosis.

Consequences and prevention

A more favorable prognosis can be said in the case of stable exertional angina. If angina pectoris arose for the first time, it is very difficult to predict the course. An even more serious prognosis can be given with unstable angina. Fatal infarction occurs in three percent of patients.

First of all, prevention is based on the elimination of risk factors. This means that you need to stop smoking, follow a diet, get rid of extra pounds, treat arterial hypertension, and so on. In order to prevent the occurrence of seizures or reduce their number, it is also necessary to lead a healthy lifestyle and follow the recommendations of a doctor.

Angina pectoris 2 FC is a disease, the development of which often depends on the person himself. It is worth making an effort, as the heart will not remind you of itself with unpleasant attacks, which will allow you to enjoy life more.

Features of hypertension of the 1st degree: its symptoms and treatment

1. Symptoms of hypertension 1 degree
2. Risks 1, 2 , 3 and 4
3. Diagnostics
4. What tests are needed?
5. Treatment
6. Complications
7. Prevention

High blood pressure often occurs in old age in both sexes, this leads to a disease of the cardiovascular system, which is called hypertension. Normal blood pressure (BP) occurs during the contraction of the heart, more precisely its left ventricle, blood from it enters the aorta, and then moves through the smaller arteries. The level of pressure is affected by the amount of tension, the volume of blood in small arteries and their tone.

Hypertension 1 degree, what is it?

It has another name - arterial hypertension. Its presence can be confirmed or refuted by tests and diagnostics of the body under the supervision of a doctor. An increase in pressure can be indicated by three consecutive control measurements, which are carried out using a tonometer.

Normal pressure can change its value up and down, depending on the state of the person, especially stressful situations and an unhealthy lifestyle affect it. In ordinary life, it rises during physical exertion, and during sleep it decreases, but normalizes during the day.

Its performance should be in the range of 60-90. If the blood pressure is higher than normal, this indicates that the person is suffering from hypertension.

A systematic increase in pressure refers to hypertension of the 1st degree. This is the mildest form, with it there is still no serious effect on the internal organs (heart, blood vessels and kidneys). The second degree is much more difficult, and the third is the most severe, with it there is a destruction of vital organs.

The first degree of the disease is treatable if you turn to a specialist in time and pass the necessary tests. The prerequisites for its diagnosis is the condition of the patient, who can feel the abnormalities described below in the body.

Symptoms of hypertension 1 degree

With it, the increase in pressure occurs periodically and itself returns to normal. The attack is accompanied by:

• Blurred vision;
• short dizziness;
• Headache in the back of the head;
• Quiet tinnitus;
• Increased heartbeat;
• Decline in strength;
• Heaviness in the limbs;
• increased sweating;
• swelling of the hands and feet;
• Memory deterioration.

If such symptoms began to appear with enviable regularity, then you should immediately begin to systematically measure your blood pressure, twice a day. For the first time in the morning, without even getting out of bed, in the evening put a tonometer near you, and when you wake up immediately take its measurements.

The second measurement should be taken during the day from 16:00 to 17:00. If during the week the pressure is constantly high, then you need to contact a specialist.

The first signs of hypertension 1 degree

This disease is insidious in that at the initial stage it occurs with virtually no obvious symptoms. This leads to the fact that people seek medical help late and have to treat it in a fluffy form.

In the meantime, she gives:

• To heart failure, which is expressed in edema and tachycardia, with it there is shortness of breath.
• Failures in the work of the kidneys, which do not have time to process the products that enter them, and accumulate fluid in themselves, therefore, urination failures occur. In neglected forms, this is expressed in the intoxication of the body with products formed after the breakdown of urea.
• Changes in the state of the vessels, accompanied by unbearable and persistent headaches.

Risks 1, 2 , 3 and 4

In addition to monitoring pressure, there is another important factor, by accurately determining the indication of which you can make the correct treatment for the patient, and it is called risk. Its value is made up of the summation of blood pressure readings, as well as aggravating factors, such as:

• Bad habits;
• Excess weight;
• Glucose level;
• Heredity;
• Age;
• An indicator of cholesterol in the blood;
• Associated diseases.

Risks are of four degrees, they are diagnosed when there is a certain percentage of the likelihood of complications affecting the vessels and the heart.

For grade 1 hypertension, symptoms and treatment in most cases correspond to grade 1 and 2 risk. Subsequent levels of risk come with aggravating factors that are rare in the initial stage. If a patient with hypertension excessively consumes alcohol, then it complicates the course of the disease.

Causes of hypertension of the 1st degree

Pathological abnormalities in the activity of the heart can be caused by various factors, and their dangerous combination. The reasons for the pressure surges are:

• Bad habits. Smoking causes constriction of blood vessels. Wrong nutrition.
• Physical passivity or vice versa excessive loads.
• Age: for women (over 50), for men (over 65). Although recently there has been a significant "rejuvenation" of this disease.
• hereditary predisposition. The more relatives suffer from this disease, the greater the likelihood of its occurrence.
• Pregnancy. At this wonderful time, mother experiences exorbitant physical exertion, hormonal failure and restructuring of the body, cases of nervous breakdowns are not uncommon. A mixture of these hazards results in pressure buildup.
• Taking medications that cause side effects in the form of increased pressure. It can be dietary supplements or oral contraceptives.
• Stress and constant psychological experiences lead to heart failure, in which adrenaline is released, and it constricts blood vessels.
• The presence of the following diseases: diabetes mellitus, atherosclerosis (formation of plaques on the inside of the vessels), kidney and hypothalamus disease, pyelonephritis.
• Deviation in the work of the thyroid gland and adrenal glands.
• A sharp change in climatic conditions.
• Excess salt. An ordinary food product, without which not a single dish can do, can, if it is overabundant, cause a spasm of the arteries and cause the accumulation of fluid in the body.
• Chronic fatigue and lack of sleep.

All these reasons can provoke the appearance of arterial hypertension of the 1st degree.

Diagnostics

People who have already experienced high blood pressure should be examined annually, the same applies to those who first showed signs of hypertension. To confirm the diagnosis previously made by the doctor, you need to undergo a hardware examination.

In addition to these studies, you need to visit an ophthalmologist who checks the fundus. The eyes, like the heart, are most often affected by hypertension. The expansion of the veins located in the retina of the eye can be irreversible, this change must be stopped if the vessels are detected in time to return to normal.

What tests are needed?

When the question arises whether hypertension of the 1st degree can be cured, the answer is yes, if all the necessary studies have been completed and tests have been passed, which include:

• Urinalysis;
• General and biochemical blood test;
• Hormone testing for women.

As a result of the first two analyzes, it is estimated:

• Metabolism of carbohydrates and glucose levels;
• The work of the kidneys in the presence of uric acid and creatinine;
• Electrolytic exchanges: sodium, potassium, phosphate and calcium;
• Fat deposits: the presence of cholesterol, triglycerides and HDL;
• The degree of damage to the heart and kidneys;
• condition of the vessel walls.

Hormonal examinations are used only for the weak half of humanity; for their conduct, blood is taken from a vein on certain days of the menstrual cycle:

• Prolactin and LH for 3-5 days;
• Progesterone and estradiol on the 20th day of the cycle;
• Testosterone, androstenedione, 17-OH progesterone on days 7-10.

These tests are necessary to establish a complete picture of the course of the disease and prescribe an effective treatment for grade 1 hypertension. Basically, everyone starts taking blood pressure lowering drugs, but they do not eliminate the causes of the disease, for this the doctor must prescribe complex therapy.

Treatment

When the results of tests and studies confirm the presence of hypertension, the question of how to treat grade 1 hypertension is immediately considered.

The doctor will advise you to change your lifestyle and introduce more rest into it, try to avoid stressful situations, supplement the day with physical exercises and walking, start eating right.

Diet for hypertension 1 degree

You need to reconsider your diet and, if possible, try not to use salt, replacing it with other products, such as vinegar or citric acid, but within reasonable limits. Diet is very important with high blood pressure, properly selected foods can help blood vessels, the main focus should be plant foods.

List of foods that lower blood pressure:

1. Green tea and hibiscus.
2. Gourds - melons and watermelons. They are known for their diuretic properties.
3. Dairy products, their main component is calcium, which actively lowers blood pressure. It is also found in almonds and green vegetables.
4. Foods containing magnesium: cereals (oats, buckwheat and wheat), walnuts, beans, beets, black currants and carrots.
5. Sour foods: grapefruit, celery, viburnum, chokeberry, quince and cranberries.
6. Calcium-rich foods include oranges, tuna, tomatoes, dried apricots, zucchini, and bananas.
7. Products that can thin the blood - garlic.

It is worth reducing and over time completely eliminating from the use of such products:

• Smoked meats, spicy and salty dishes;
• Foods high in caffeine;
• Fatty fish and ice cream;
• Foods with a high starch content: semolina, potatoes, white flour muffins and corn;
• Confectionery with butter cream;
• by-products;
• Sharp and specific spices.

If you stick to such a diet, you can not only help the vessels return to normal, but also significantly lose weight without exhausting yourself with endless diets on one product. The main feature of the treatment is to refuse products from the "black" list gradually so that the body can adapt to their absence.

When exercise and diet do not quite cope with the disease, it is necessary to supplement the treatment for grade 1 hypertension with drugs. But they should be prescribed by a doctor, under no circumstances should you self-medicate.

Drugs for hypertension 1 degree

The standard approach to drug treatment is to prescribe the following drugs:

• Neurotropic agents that relieve stress and soothe. These include: antidepressants (amitriptyline), tranquilizers (diazepam and trioxazine), and sedatives (valerian and bromine-based drugs).
• Diuretics, these tablets for hypertension of the 1st degree help to remove salt and excess water from the body. Effective are: furosemide, lasix, hydrochlorothiazide and amiloride.
• Vasodilator drugs: vasonite, molsidomine or apressin.

The choice of drugs and their dosage is fully prescribed by the doctor.

Complications

Hypertension of the 1st degree occurs with a slight increase in pressure, but despite this, it can cause serious complications:

• On the kidneys. In them, sclerosis of tissues and blood vessels occurs. Their activity and the function of urea distillation are disturbed, protein appears in the urine. The next step will be kidney failure.
• To the brain. Thrombosis appears in its vessels, vessels are disturbed, which first lead to small heart attacks occurring in the deep parts of the brain. High blood pressure can lead to stroke and heart attack. Due to impaired blood supply, the brain begins to decrease in size and can cause dementia.
• For vessels. They are located throughout the body, and the disease can affect completely different places. If it touches the retina of the eyes, it will result in loss of vision.
• On the heart. With hypertension, the load falls on the left ventricle of the heart, its muscle increases and leads to myocardial infarction. Also, this condition threatens the appearance of angina pectoris and even death.

Some of the above complications entail loss of working capacity and disability, which once again proves that it is better to treat the disease at its very beginning.

Do they take to the army with hypertension of the 1st degree?

In peacetime, conscripts with such a diagnosis, after being confirmed by appropriate examinations, may not be recognized as fit for military service. This is stipulated in article 43 on the schedule of diseases.

To receive an exemption, you need to have blood pressure readings within the limits indicated in the article, that is, 140/90 and above.

Prevention

If there is a predisposition to hypertension, then it is better to prevent it than to spend a lot of effort and money on treatment, the following actions will help:

• Regular exercise or walking;
• Maintaining your weight;
• To give up smoking;
• Undergo periodic blood sugar checks;
• Regularly measure blood pressure;
• After a busy day, arrange a rest;
• Sleep at least 8 hours a day;
• Do an ECG of the heart.

It is quite possible to cure hypertension of the 1st degree if desired. An integrated approach to treatment will not only relieve further suffering from the complications of this disease, but also prolong life.

What is heart failure: symptoms, signs and treatment of the disease

Heart failure - what is it? This is a pathological condition that appears in the event of a malfunction of the heart, when the blood is not pumped in the proper volume. Acute heart failure can lead to death in a short time, as there is a high probability of dangerous complications. Chronic HF develops gradually and leads to prolonged "starvation" of body tissues.

Causes of the disease

Why does heart failure occur? This condition occurs due to various etiological factors. Most often, the etiology of this disease is associated with atherosclerosis and arterial hypertension. Increased pressure in the bloodstream and atherosclerotic narrowing of the lumen of the vessels lead to the fact that it becomes difficult for the heart to push blood. The body's resources allow compensating for this pathological condition - at first there are no clinical symptoms of circulatory failure due to an increase in heart rate and an increase in the strength of heart contractions. When the myocardium is depleted, decompensation of the disease occurs - this is manifested by shortness of breath, edema, and a decrease in tolerance to physical stress. These are all symptoms of congestive heart failure (CHF).

The pathogenesis of heart failure also includes diseases accompanied by direct damage to the heart. These are myocarditis, valvular defects, infectious and autoimmune diseases, intoxications. In diseases of the lungs, an increase in pressure in the small circle can often occur. All these reasons lead to an increase in the load on the heart, due to which the efficiency of the organ is significantly reduced. This can also happen with fluid retention in the body, for example, with kidney disease.

In many cases, the causes of heart failure and the etiology of this condition are due to a past heart attack. Most often, this leads to acute heart failure with the rapid development of complications and the death of the patient.

Types of heart failure

This disease is classified according to the rate of development of the clinic:

• acute HF - progresses in a very short time (a few minutes - a few hours). Complications of this type of disease often become pulmonary edema or shock of a cardiogenic nature. The most common causes of AHF are heart attack, valve defects (aortic and mitral), damage to the walls of the heart;
• chronic HF - progresses over many months or years. The cause of CHF is compensated pathological conditions with damage to the heart and other organs (arterial hypertension, malformations, chronic lung diseases, etc.).

Classification

There are several ways to classify heart failure. Depending on the severity of the clinic, the following are distinguished:

• First degree - no clinical symptoms.
• In the second degree of heart failure, the symptoms are mild, wheezing may be present.
• The third degree is a more pronounced clinical picture, the presence of wheezing.
• The fourth degree of severity is characterized by the presence of complications, for example, cardiogenic shock, collapse (decrease in systolic blood pressure below 90 mm Hg).

According to the degree of patient's resistance to physical activity, heart failure is divided into four functional classes (FC):

• 1 FC - shortness of breath and other symptoms appear with severe physical exertion, for example, during the ascent to the third floor and above. Normal physical activity does not cause symptoms of the disease.
• 2 FC - moderate heart failure, it makes itself felt only after climbing two flights of stairs or when walking fast. The patient's daily activities may be slightly reduced.

• 3 FC - the symptoms of the disease become pronounced even with small physical exertion and during daily activities. At rest, shortness of breath completely disappears.
• 4 FC - in this case, shortness of breath and other manifestations disturb the patient at rest. The heart is under heavy stress, complications of heart failure are often observed.

Types of heart failure according to its classification by stages:

• The first stage is the onset of the disease. It is characterized by a latent course, the symptoms of circulatory failure occur only in cases where the patient experiences a pronounced physical or emotional stress. At rest, the activity of the circulatory system is not disturbed.
• The second stage is marked clinical manifestations. There are signs of prolonged stagnation of blood, this is noticeable in the absence of physical activity. Stagnation appears in the large and small circles of blood circulation, which is primarily manifested by edema. This stage is subdivided into IIA and IIB. The first is characterized by impaired function of only the left or right ventricle. In this case, shortness of breath appears during normal physical exertion for a person, its activity is markedly reduced. Outwardly, the patient has blue skin, swelling of the legs, enlarged liver and hard breathing. Stage IIB is characterized by a deeper degree of hemodynamic disturbances, the cause of which is stagnation in both circles of blood circulation.
• The third stage of the disease is terminal. In this case, the heart ceases to cope with its function, which leads to irreversible damage to the structure of internal organs, to the depletion of their resources.

Signs and symptoms of the disease

The clinical symptoms of heart failure are the same for both acute and chronic variant of this pathology. The difference lies in the rate of development of the manifestations of the disease and the body's ability to adapt to changes in hemodynamics. Therefore, in acute circulatory failure, full compensation does not occur, as a result of which the terminal stage quickly sets in and the risk of death increases. The chronic variant of the disease may not manifest itself for a long time, and therefore the diagnosis and treatment are often belated.

How to recognize heart failure? The clinical picture consists of symptoms associated with stagnation of blood in the vessels due to the inability of the heart muscle to fully perform its function. As a result, edema appears on the lower extremities and stagnation in the pulmonary circulation, which causes wheezing. The patient loses the ability to adequately cope with physical and emotional stress, so the conceived efforts of normal intensity lead to shortness of breath.

Stagnation of blood leads to disruption of oxygen transport in tissues - hypoxia develops, metabolism changes, cyanosis (cyanosis) of the skin of the extremities, nasolabial triangle appears.

Headache. This symptom is not characteristic of heart failure. Loss of consciousness, dizziness, darkening of the eyes are more likely.

Nausea and vomiting. Such manifestations of heart failure are also not characteristic of this disease. However, in rare cases, they may indicate the development of metabolic disorders.

Drowsiness. Decreased performance, fatigue and drowsiness may be the result of circulatory failure, which leads to a decrease in oxygen saturation of tissues.

Heart failure in newborns and adolescents

This disease in children and newborns is quite difficult to diagnose, as it often resembles manifestations of other pathologies. The cause of HF at an early age is usually associated with congenital diseases:

• heart defects;
• CNS lesions;
• glycogen disease, cardiac form;
• fibroelastosis of the endocardium.

It is also worth taking into account that this condition can occur with infectious diseases caused by viruses or bacteria.

There are no significant differences in how heart failure manifests itself in children. Usually the symptomatology consists in the appearance of shortness of breath and edema, increased heart rate. The main changes in the internal organs - the liver increases, the boundaries of the heart expand.

Heart failure in adolescents occurs when they have a heart defect. Signs of heart failure in adolescents do not differ from those in children and adults, which helps to establish the diagnosis.

Methods for diagnosing heart failure

Heart failure syndrome is a secondary disease that occurs against the background of other pathologies. In this regard, examination and diagnostic measures should be aimed primarily at identifying the cause of this condition. Early diagnosis of circulatory insufficiency is important, when there are no pronounced clinical symptoms.

For those patients who have been diagnosed with a heart attack and other myocardial diseases, arterial hypertension, it is important to pay attention to the presence of such a symptom as shortness of breath that occurs during physical exertion. Other characteristic signs that make it possible to suspect the presence of heart failure are edema in the lower extremities, expansion of the borders of the heart to the left side.

The pulse in patients with circulatory failure is usually low-amplitude. An increase in heart rate is also characteristic.

CBC in HF is nonspecific or reflects changes caused by the primary pathology. More specific are the analysis of blood gases and electrolytes. It is also important to determine the pH of the blood, the level of creatinine, urea and indicators of protein metabolism in biochemical analysis. It is possible to determine the level of cardiospecific enzymes, which can increase both in HF and in myocardial ischemia.

Diagnosis of heart failure is largely determined by the indications of instrumental research methods. According to the ECG, signs of myocardial hypertrophy are determined, which develops in response to an increased load on the heart muscle. You can also determine rhythm disturbances or signs of ischemia of the muscle tissue of the heart.

There are special stress tests, which are an ECG with physical activity. This is possible when using an exercise bike or treadmill. The load is gradually increased, due to which it is possible to determine the functional class of heart failure and the presence of signs of myocardial ischemia.

Echocardiography makes it possible to both determine heart failure and visualize the structure of the heart in order to determine the cause of its dysfunction. At the same time, echocardiography evaluates the functional state of the heart, for example, ejection fraction and other indicators of pumping function. MRI makes it possible to determine the presence of defects in this organ. X-ray of the lungs and chest organs shows the presence of stagnation in the pulmonary circulation.

To determine the degree of damage to other internal organs in severe circulatory failure, an abdominal ultrasound is performed. It shows changes in the spleen, liver, pancreas and other organs.

Ways to treat the disease

Treatment of heart failure involves conservative therapy. It includes the following areas:

• reduction of clinical manifestations of circulatory failure. For this, cardiac glycosides are prescribed - for AHF, intravenous fast-acting drugs are used, for CHF - long-acting drugs;
• reducing the load on the myocardium - this is achieved by using beta-blockers, which lower blood pressure and slow down the pulse;
• the appointment of diuretics in order to reduce the total amount of fluid in the body.

It is worth noting that it is impossible to cure heart failure, you can only reduce its symptoms and signs. The best results are obtained by the treatment of heart failure of the first degree. A patient who has taken all the recommended drugs in this case may not notice an improvement in his condition.

If the patient has a history of arrhythmia, which may have caused the development of myocardial insufficiency, then surgical treatment is possible. It consists in the implantation of an artificial pacemaker. Surgical treatment is also indicated in those cases. When there is a significant narrowing of the lumen of the arteries due to atherosclerosis, when there is a pathology of the valves.

What is dangerous heart failure, consequences and complications

Circulatory insufficiency is progressive in nature, as a result of which, in the absence of proper therapy for this condition, the patient's condition worsens over time, the degree of hemodynamic disorders increases, which often leads to death.

Frequent consequences of heart failure occur due to pulmonary edema, when there is stagnation in the pulmonary vessels, the liquid part of the blood penetrates into the tissues of this organ. Because of this, the ability of the lungs to saturate the blood with oxygen sharply decreases, hypoxia develops.

With circulatory failure, signs of cerebral ischemia may appear, which is manifested by fainting, dizziness, darkening in the eyes.

Heart failure of the 1st degree is usually the least likely to lead to serious consequences.

Disease prevention

Prevention of heart failure is based on the treatment of diseases, the development of which leads to circulatory failure - hypertension, valve defects, etc. On the other hand, it is important to adjust the patient's lifestyle in order to reduce the number of risk factors.

If the function of the heart is already impaired, then the prevention of heart failure should be aimed at maintaining the optimal level of daily physical activity, constant monitoring by a cardiologist, and taking prescribed drugs.

What to do with heart failure to increase the chances of recovery of the body? In addition to taking medications, correction of the patient's lifestyle plays an important role in the treatment of circulatory insufficiency. In order for the treatment to be effective, people with this disease must reduce their body weight to normal values, since excess weight is one of the most common causative factors for hypertension.

Patients with this pathology are advised to follow a diet. It consists primarily in limiting salt intake. Patients with heart failure should completely abandon this flavor enhancer, since salt reduces the excretion of fluid from the body, which leads to an increase in the load on the myocardium.

If the patient smokes or drinks alcohol, then these habits will have to be completely abandoned.

You also need to exercise regularly. Depending on the severity of the disease, the allowable volume of loads also changes. For example, in functional class III, regular walking for about 40 minutes is sufficient, and in milder cases of circulatory failure, special exercises can be added. Physiotherapy is prescribed by the attending physician, so you should not independently increase the daily amount of physical exercise without knowing the whole picture of the disease. At the same time, the symptoms and treatment of severe heart failure do not allow the patient to carry out this method of rehabilitation.

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Chronic heart failure (CHF) is a complex clinical syndrome that develops when the heart is unable to provide blood supply to organs and tissues at the level of normal metabolism.

Insufficient cardiac output is the main reason for the excitation of stress-organizing systems (sympathetic-adrenal, reninangiotensin-aldosterone, etc.), which leads to sodium and water retention, an increase in circulating blood volume, tachycardia, increased heart rate, and production of unusual under normal conditions or in excess amounts of biologically active substances (natriuretic peptides, endothelins, etc.).

In CHF, as a rule, there is systolic and diastolic dysfunction of the left ventricle (LV) or both ventricles, which often develops as a result of coronary artery disease or prolonged arterial hypertension. The LV cavities are dilated, the ejection fraction (EF) is reduced.

Clinical signs of CHF - shortness of breath, weakness, congestion, weight loss - progress over time. The prognosis is poor, mortality is the same as with cancer. The greater the dilatation of the heart, the lower the EF and the more severe the functional class of CHF, the worse the prognosis.

When diagnosing CHF, symptoms of heart failure and dysfunction of the heart (low EF, heart enlargement) are taken into account. In cases of uncertainty in the diagnosis of CHF, the benefit of diuretic therapy is visible.

To assess the function of the heart, echocardiography is chosen (EF, size of the cavities, mobility of the walls of the heart).

The severity of CHF is determined by 3 stages according to Strazhesko-Vasilenko or according to the New York classification, which distinguishes 4 functional classes depending on the patient's tolerance to physical activity.

Help for patients with CHF includes general measures (sodium restriction, fluids, complete proteins, physical activity), pharmacotherapy and surgical treatment (heart transplant, auxiliary heart). The main directions of pharmacotherapy: ACE inhibitors, diuretics, beta-blockers, cardiac glycosides. Aldosterone antagonists and angiotensin receptor blockers are increasingly being used as additional drugs.

Keywords: myocardial dysfunction, heart failure.

SUBJECT OF THE CHAPTER, CLINICAL SIGNIFICANCE

Chronic heart failure(CHF) can be the outcome of any cardiovascular disease. The prevalence of CHF in the general population is 1.5-2%, and among people over 65 years old - 6-10%. Despite significant advances in the treatment of cardiovascular diseases, the prevalence of CHF is not only not decreasing, but is steadily increasing, which is partly due to the aging of the population.

CHF is a complex clinical syndrome that occurs due to the inability of the heart to provide the body's needs for oxygen. In 80-90% of cases, CHF occurs in patients with left ventricular dysfunction. The main manifestations of heart failure are shortness of breath and weakness, which can limit the patient's physical activity, and fluid retention, which can lead to pulmonary congestion and peripheral edema. Both disorders can cause impairment of the patient's functional ability and quality of life, but do not necessarily dominate the clinical picture at the same time. Some patients have impaired exercise tolerance but minimal signs of fluid retention. Other patients complain mainly of edema, but practically do not complain of shortness of breath and weakness. Diagnosis of CHF should be based not only on the data of anamnesis and clinical examination, but also on the results of instrumental research methods.

CHF is characterized not only by a violation of the contractility of the heart muscle, but also by the reaction of other organs and systems to a decrease in the pumping function of the heart. This is manifested by activation of neurohumoral systems, peripheral vasoconstriction, sodium and water retention in the body, as well as changes in the function and structure of the liver, lungs, skeletal muscles and other organs.

CHF is characterized by a decrease in cardiac output and activation of neurohumoral systems with changes in tissues and organs due to inadequate metabolism.

In developed countries, CVD is the main cause of CHF. In second place is hypertension, in third - DCMP. Much less often, rheumatic heart disease became the cause of CHF.

The prognosis of CHF remains extremely serious, regardless of its etiology. After the onset of clinical symptoms, about 50% of patients with CHF die within 5 years.

In half of patients, the cause of death is heart failure refractory to therapy. Many patients die suddenly as a result of ventricular arrhythmias.

CHF is one of the most common causes of hospitalization and, among the elderly, the most common cause of hospitalization. About

1 / 3 patients need re-hospitalization within 6-12 months. The costs associated with hospitalization range from 2/3 to 3/4 of all costs for the treatment of patients with CHF.

Over the past two decades, the goals and principles of drug therapy have changed significantly. Previously, the main goals in the treatment of CHF were considered to improve impaired heart function (by prescribing cardiac glycosides) and removing excess sodium and water from the body (using diuretics). Modern drug therapy aims to improve the quality of life of patients with CHF, reduce the need for hospitalization, and increase the life expectancy of patients. Angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, aldosterone antagonists, and AT1-angiotensin receptor blockers, which suppress excessive activation of neurohumoral systems, occupied leading positions among medications.

TERMINOLOGY, PATHOGENESIS SCH

The term "chronic heart failure" (CHF) refers to a group of pathological conditions that differ in etiology and mechanism of development, in which the heart gradually loses the ability to provide adequate blood supply to organs and tissues. The terms CHF and chronic circulatory failure are identical. The term congestive heart failure is actually a synonym for CHF with severe signs of fluid stasis.

According to the definition of WHO experts (1964), heart failure (HF) is a multisystem disease in which the primary dysfunction of the heart causes a number of hemodynamic, nervous and humoral adaptive reactions aimed at maintaining blood circulation in accordance with the needs of the body.

The experts of the European Society of Cardiology (2001) define HF as a pathophysiological syndrome in which dysfunction of the heart leads to the inability of the heart to pump blood at a rate sufficient to meet the needs of tissue metabolism.

In the vast majority of cases, CHF is caused by damage to the myocardium of one or both ventricles of the heart; this is the so-called myocardial heart failure. In myocardial CHF, LV function is impaired in most cases, which is not surprising, since CAD and hypertension are the most common causes of CHF in many countries around the world. Isolated right ventricular failure is not common and is associated mainly with chronic pulmonary hypertension in patients with obstructive pulmonary disease. In myocarditis, dilated, hypertrophic, and alcoholic cardiomyopathies, the myocardium of both the left and right ventricles is simultaneously affected, although dysfunction of one of the ventricles may predominate.

CHF is usually caused by damage to the myocardium of one left or both ventricles of the heart.

Myocardial HF should be distinguished from cases of development of clinical symptoms and signs of CHF in patients without damage to the ventricular myocardium, for which the term circulatory insufficiency is used. Examples of circulatory CHF are valvular heart disease, constrictive and effusion pericarditis, severe anemia, etc. To CHF do not apply cases of circulatory insufficiency, which is associated with peripheral vasodilation (for example, with septic shock) or changes in circulating blood volume (hemorrhagic shock, liver and kidney disease with fluid retention).

Myocardial CHF can be conditionally divided into three groups: left-sided, right-sided and bilateral (or total). Left sided heart failure almost always due to damage to the left ventricle (with the exception of cases of isolated mitral stenosis) and is characterized by congestion in the lungs, arterial hypotension and reduced blood supply to vital organs and extremities.

Right sided heart failure characterized by increased central venous pressure, peripheral edema and ascites, which are caused by damage to the right ventricle (isolated tricuspid valve stenosis is extremely rare).

About total or congestive heart failure they say in those cases when there are simultaneously clinical manifestations of left- and right-sided heart failure.

In patients with left ventricular failure, it is necessary to establish what form of LV dysfunction is present - systolic or diastolic. To clarify the etiology and pathophysiological type of CHF, a targeted history taking, physical examination, electrocardiography, chest x-ray, and especially echocardiography are necessary.

CLASSIFICATION

For more than 60 years in our country, to characterize the severity of CHF, the classification of stages of circulatory insufficiency proposed by N.D. Strazhesko and V.Kh. Vasilenko in 1935. According to this classification, the following forms of circulatory failure are distinguished.

1. Acute circulatory failure; may be caused by acute failure of the heart or any of its departments (left or right ventricle, left atrium) or caused by acute vascular insufficiency (collapse, shock).

2. Chronic circulatory failure; There are three stages in its development.

First stage (initial)- latent circulatory failure, manifested only during physical exertion; at rest, hemodynamics and organ functions are not impaired; work capacity is reduced.

Second stage- severe circulatory failure; violations of hemodynamics (stagnation in the small or large circle of blood circulation) and disorder of the functions of organs are expressed at rest; patients' ability to work is severely limited. In this stage, two periods are distinguished: A - hemodynamic disturbances are weakly expressed; and B - with profound hemodynamic disturbances.

Third stage- final, dystrophic stage; in addition to severe hemodynamic disturbances, there are irreversible morphological changes in the organs.

As criteria for distinguishing between stages of CHF, such simple indicators as signs of fluid retention and the need for diuretics can be successfully used. In the first stage of CHF, there is no fluid retention, and therefore diuretics are never prescribed. Stage II CHF is characterized by fluid retention in the body. Patients with CHF II A stage diuretics are prescribed periodically,

and patients with CHF stage II B usually require constant intake of diuretics. Patients with stage III CHF often develop refractoriness to diuretics, and even their constant intake does not always provide an unedematous state.

When using the classification of N.D. Strazhesko and V.Kh. Vasilenko, it is desirable to indicate in the diagnosis the year when this stage of CHF was established.

In the United States and Western Europe, the classification of the New York Heart Association (NYHA), which assesses the degree of limitation of physical activity of a patient with CHF, has become widespread (Table 3.1.).

Table 3.1

Classification of the severity of CHF by the New York Heart Association (NYHA) *

Note.*New York Heart Association.

Determining the functional class according to the NYHA classification in patients with CHF in everyday clinical practice causes difficulties in such concomitant diseases as obstructive pulmonary disease, severe anemia, renal failure, liver cirrhosis, etc., which can simulate heart failure. In elderly and senile patients, detrained, leading a sedentary lifestyle due to intermittent claudication, joint diseases or the consequences of cerebrovascular accident, it is not always possible to prove the connection of symptoms caused by physical activity with damage to the heart.

To classify the severity of CHF, a division at stage 1-3 according to Strazhesko-Vasilenko and the degree of physical activity restriction I-IV (New York Heart Association) can be used.

In the guidelines of the American College of Cardiology and the American Heart Association (2001), it is proposed to use another classification of CHF stages, which significantly expands the circle of patients with CHF by those with a high risk of developing heart failure and asymptomatic, which is important for early diagnosis and prevention of this condition. This classification distinguishes 4 stages - A, B, C, D.

To stage A include patients who do not have structural or functional lesions of the heart and have never had signs or symptoms of CHF, but have a disease that is closely associated with the onset of heart failure. These can be the following conditions and diseases: systemic arterial hypertension, coronary artery disease, diabetes mellitus, therapy with cardiotoxic drugs, history of alcoholism, family history of cardiomyopathy.

To stage B refers to patients who have never had signs or symptoms of heart failure, but have structural heart disease that is closely associated with the development of heart failure. Typical examples are: LV hypertrophy or fibrosis, LV dilatation or decreased contractility, asymptomatic valvular heart disease, history of myocardial infarction.

To stage C includes patients who have or have recently had symptoms of HF associated with structural heart disease, such as dyspnea or weakness due to LV systolic dysfunction, as well as asymptomatic patients who are being treated for past symptoms of HF.

To Stage D include patients with severe structural heart disease and severe symptoms of heart failure at rest, despite maximum therapy. These are patients who are frequently hospitalized for CHF, awaiting a heart transplant, receiving continuous infusions of non-glycoside inotropic drugs, attached to a heart-lung machine, or in hospice care for CHF.

When formulating a diagnosis in patients with left ventricular heart failure, along with the etiology of CHF and its stage, if possible, indicate the pathophysiological type of CHF (systolic or diastolic dysfunction, a state with high cardiac output), the functional and metabolic class of XCH, and whether the patient is receiving appropriate therapy or no.

An approximate formulation of a detailed diagnosis in patients with CHF could look like this: CAD, exertional angina II FC. Postinfarction cardiosclerosis after transmural myocardial infarction of the anterior wall of the left ventricle (1995). Chronic heart failure stage II B (1996), III-IV FC (January 2001).

Such a diagnosis both describes the patient's condition at the present time and characterizes the development of CHF after myocardial infarction.

To characterize the course of right ventricular heart failure, the classification of N.D. Strazhesko and V.Kh. Vasilenko does not fit. In patients with chronic cor pulmonale, it is not possible to determine the functional class, since it is impossible to distinguish between symptoms associated with heart and respiratory failure.

ORIGIN OF CHF

CHF is the outcome of a wide variety of diseases, not only diseases of the circulatory system, but also respiratory diseases (for example, chronic obstructive pulmonary disease), some endocrine, rheumatic, hematological, oncological and surgical diseases (hyper- and hypothyroidism, pheochromocytoma, diffuse diseases of the connective tissue). tissue, severe anemia, chronic leukemia, pulmonary thromboembolism

artery, cardiotoxic effect of drugs used in the treatment of cancer, etc.).

Heart diseases, which are the most common causes of CHF, are shown in Table. 3.2.

Table 3.2

Major heart conditions that can cause heart failure

CAD and arterial hypertension occur in most patients with CHF. The likelihood of developing heart failure in patients with arterial hypertension increases by 2-6 times in the presence of a history of myocardial infarction, electrocardiographic signs of LV hypertrophy, valvular heart disease, and diabetes mellitus.

Unlike CAD and hypertension, valvular heart disease does not play a significant role in the development of CHF in the general population. As for DCM, the literature data regarding its significance as a cause of CHF in the general population are very contradictory.

(from 0 to 11%). In some Western European countries, DCM is the second most common (after CAD) cause of CHF.

In this case, DCM refers to diseases with dilatation of the heart due to inflammatory processes, family genetic or unidentified (idiopathic) causes. Cardiac dilatation in CAD can be considered as ischemic DCM (see Chapter 1, Volume 3).

CVD and arterial hypertension are the most common causes of CHF.

PATHOPHYSIOLOGY OF CHF

In most patients with “myocardial” CHF due to LV dysfunction, cardiac output sooner or later decreases, although in the early stages of CHF development, due to the inclusion of cardiovascular and neuroendocrine compensatory mechanisms at rest, it can remain normal for a long time. In CHF that develops in patients with hyperthyroidism (thyrotoxicosis) or severe anemia, cardiac output may be increased.

Left ventricular dysfunction in patients with CHF may be systolic or diastolic.

They often coexist. Only in patients with coronary artery disease who have undergone extensive transmural myocardial infarction, one can confidently speak of predominantly systolic LV dysfunction caused by the death of contractile fibers. CHF caused by LV systolic dysfunction is characterized by a combination of impaired central and peripheral hemodynamics and excessive activation of a number of neurohumoral systems. Changes in hemodynamics and neurohumoral activation reflect the desire of the body, with a reduced contractility of the heart muscle, to maintain cardiac output and blood supply to vital organs at the proper level, and therefore, in case of LV dysfunction, they should be considered as one of the most important compensatory-adaptive mechanisms.

Activation of neurohumoral systems is aimed at foreign and chronotropic stimulation of the heart muscle, an increase in

load on the left ventricle, maintaining sufficient glomerular filtration and systemic blood pressure, as well as the redistribution of gradually decreasing cardiac output in favor of vital organs by reducing the blood supply to the extremities and subcutaneous tissue. An excess of neurohormones such as norepinephrine, angiotensin, aldosterone and endothelin-1 stimulates cardiomyocyte hypertrophy.

The most important indicator of LV systolic dysfunction is a decrease in its ejection fraction, which is most often measured by echocardiography and less often by radionuclide ventriculography. LV systolic dysfunction is also characterized by dilatation of its cavity and the appearance of a third heart sound. Dilatation of the LV (or both ventricles) is indicated by an increase in the cardiothoracic index (normally less than 0.5), an increase in the end diastolic size of the LV cavity (more than 5.5-6.0 cm) and a decrease in the shortening fraction of its anterior-posterior size (less 25-30%).

An indicator of LV systolic dysfunction in CHF is a decrease in EF and LV dilatation.

LV diastolic dysfunction is more likely in patients with coronary artery disease in combination with arterial hypertension, diabetes mellitus or obesity. The hypertonic heart is typically characterized by LV diastolic dysfunction, which, at the stage of its decompensation, is accompanied by LV systolic dysfunction.

Clinical symptoms and signs of CHF in the absence of heart disease and with normal or near-normal LV ejection fraction suggest diastolic dysfunction. With LV diastolic dysfunction, the value of its ejection fraction does not change or increases; the final diastolic size of the LV cavity is not increased, and in some cases even reduced. Doppler echocardiography is required to diagnose LV diastolic dysfunction.

LV diastolic dysfunction in CHF is manifested by a violation of its filling at the beginning of diastole (with sinus rhythm) or during the entire diastole (atrial fibrillation).

With Doppler echocardiography, signs of LV diastolic dysfunction are changes in the ratio of the magnitudes of the first filling wave to the atrial filling wave (E/A), deceleration time, and time of isovolumic relaxation. However, the interpretation of echocardiographic parameters of LV diastolic function is difficult, especially in patients with atrial fibrillation.

Patients with CHF usually have both systolic and diastolic LV dysfunction.

FORECAST

The prognosis for CHF remains extremely serious. According to the Framingham study, about 80% of men and 65% of women die within 6 years after the onset of clinical manifestations of CHF. Mortality in patients with CHF is 4-8 times higher than in the general population of persons of the same age. Mortality from CHF is comparable or even exceeds that of the most malignant forms of cancer (breast cancer, prostate cancer and colorectal cancer).

The life prognosis of patients with CHF depends on the etiology. Thus, mortality in CHF of ischemic etiology is 1.4-3.8 times higher than in patients with CHF of other etiology.

The long-term prognosis of the life of patients with CHF largely depends on the severity of clinical symptoms, and in particular on the degree of limitation of physical activity, expressed by the value of the functional class. The higher the functional class of patients with CHF, the higher the mortality rate. Thus, the overall mortality of patients with functional class II CHF is from 5 to 15% per year, with functional class III CHF - from 20 to 50% per year and with functional class IV CHF - from 30 to 70%.

Type 2 diabetes mellitus is an independent risk factor for the development of CHF and is associated with increased mortality in patients with CHF.

Thanks to modern surgical and medical treatment, the development of left ventricular heart failure began to lose its three-stage character. The life expectancy of patients with CHF has increased, but all

a smaller number survive to the dystrophic stage of the disease. Currently, up to half of patients with CHF die suddenly and a decreasing number of patients with CHF die from progressive, refractory therapy for heart failure. Even in patients with end-stage CHF, pronounced stagnation occurs now in a few cases.

Mortality in CHF is high and comparable to mortality from cancer.

DIAGNOSIS OF CHF

The main goals of diagnosing CHF are formulated in Table. 3.4.

Table 3.4

The main goals of diagnosing chronic heart failure

1. Prove that the patient has heart failure.

2. Establish the presence of heart disease by the data of anamnesis, clinical examination and the results of non-invasive research methods.

3. Exclude other diseases that can simulate the symptoms and signs of heart failure.

4. Establish the etiology of heart failure.

5. Determine the forms of heart failure (left-, right-sided or total), pathophysiological type of LV dysfunction (systolic or diastolic) and its severity.

6. Assess the severity of clinical symptoms and the degree of limitation of physical activity.

7. Identify factors that cause progression of heart failure or contribute to its decompensation.

8. Identify comorbidities that may affect the course and outcome of heart failure and the choice of drugs.

9. Assess the functional state of the kidneys, liver and other organs that may affect the choice of therapy.

10. Assess the possible impact of drugs taken by the patient on the course of heart failure and the choice of drugs for its treatment.

11. Evaluate the immediate and long-term prognosis and the possibility of improving it with the help of drug therapy or surgery.

The diagnosis of CHF should be based both on the data of the anamnesis and clinical examination, and on the results of instrumental research methods.

Clinical examination

The classic symptoms of CHF are shortness of breath, weakness and swelling of the legs (Table 3.5).

Nocturnal asthma attacks have greater sensitivity and specificity, as well as predictive value. Edema is an insensitive sign of heart failure and can be associated with massive obesity, diseases of the liver (cirrhosis of the liver), kidneys (diffuse glomerulonephritis, nephrotic syndrome, renal failure) and thyroid gland (hypothyroidism), etc.

The main clinical signs of CHF are due to cardiomegaly (eg, displacement of the apex beat, III heart sound), congestion (edema, swollen jugular veins, moist rales in the lungs) and activation of the sympathetic nervous system (tachycardia). The significance of these signs in the diagnosis of CHF is not the same.

Lateral and downward displacement of the apex beat may indicate dilatation of the left ventricle. However, in 40-50% of patients, the apex beat cannot be determined. Cardiac percussion is a more reliable method for detecting cardiac dilatation. The presence of a third heart sound has a high specificity in diagnosing CHF, however, the reliability of this sign is limited due to differences in the skill of physicians in auscultation of the heart. Swollen jugular veins have a high specificity in diagnosing CHF in patients with established heart disease. However, swelling of the cervical veins can cause not only heart disease, but also bronchopulmonary diseases. Moist rales in the lungs are also a highly specific diagnostic sign, but have low sensitivity and prognostic value in the diagnosis of CHF. Tachycardia is a sensitive, although not very specific sign of CHF. Often it is not a sign of heart failure, but a manifestation of non-cardiac diseases (thyrotoxicosis, anemia, lung disease, neurocirculatory dystonia, etc.).

Measuring blood pressure in a patient with suspected congestive heart failure can help determine the type of LV dysfunction. So, systolic blood pressure is below 90 mm Hg. usually combined with

systolic LV dysfunction. On the contrary, systemic blood pressure, equal to 160/90 mm Hg. and more or diastolic blood pressure above 105 mm Hg. rather, it indicates LV diastolic dysfunction.

The classic symptoms of CHF are shortness of breath, weakness, and swelling.

For the diagnosis of CHF, objective evidence of the presence of serious damage to the heart and dysfunction of the heart muscle is required, which, as a rule, cannot be obtained without the use of instrumental research methods.

The European Society of Cardiology Heart Failure Working Group recommends the diagnosis of heart failure based on the presence of three criteria: (1) symptoms of heart failure (at rest or during exercise); (2) objective evidence of cardiac dysfunction (at rest); (3) the positive effect of therapy aimed at treating heart failure (in cases where the diagnosis is in doubt). Criteria 1 and 2 are mandatory for a diagnosis of heart failure.

In patients with CHF, there is a progressive loss of body weight up to the development of cachexia.

If heart failure is suspected, diuretics are usually used as trial therapy. So, a pronounced diuretic effect after taking 20-40 mg of furosemide and a noticeable decrease in shortness of breath and (or) edema speak in favor of the diagnosis of CHF. To clarify the origin of dyspnea and trial therapy, adrenergic blockers and nitrates are also used (if dyspnea is suspected to be the equivalent of angina pectoris), beta-sympathomimetics (if obstructive pulmonary disease is suspected), corticosteroids (if allergic alveolitis is suspected) and antibiotics (if for a lung infection).

Symptomatic therapy of heart failure, improving the patient's condition, may make it difficult to diagnose CHF, so therapy should be started only when there are already sufficiently certain grounds to suspect the presence of CHF.

Symptoms of heart failure and objective signs of cardiac dysfunction are mandatory criteria for the diagnosis of CHF.

Among the instrumental methods for diagnosing heart failure, the most common are electrocardiography, chest x-ray, and echocardiography. Radionuclide methods, magnetic resonance imaging and X-ray contrast ventriculography provide fairly accurate information about the state of heart function, however, due to their high cost, they are not widely used in everyday clinical practice.

Electrocardiography

Although ECG changes in CHF are nonspecific, electrocardiography can provide important information about the possible etiology of CHF. For example, a pathological tooth Q indicates a transmural myocardial infarction, and segment changes ST and prong T- for myocardial ischemia. The specificity of the presence of pathological teeth Q in the ECG leads from the anterior wall and the blockade of the left branch of the His bundle reaches almost 80% in CHF due to LV systolic dysfunction. Pathological teeth Q in other leads, a more sensitive, but less specific sign of CHF due to LV systolic dysfunction.

High R-wave voltage, reflecting LV hypertrophy, suggests that hypertonic heart, aortic stenosis, or hypertrophic cardiomyopathy is the cause of CHF due predominantly to LV diastolic dysfunction. On the contrary, the low voltage of the teeth R often observed in pericarditis, amyloidosis and hypothyroidism. Deviation of the electrical axis to the right, blockade of the right leg of the His bundle and signs of right ventricular hypertrophy are characteristic of CHF caused by right ventricular dysfunction.

A normal ECG is not characteristic of serious heart disease and gives reason to doubt the correctness of the diagnosis of CHF.

A normal ECG gives reason to doubt the diagnosis of CHF.

Chest X-ray

Chest x-rays can show dilatation of the heart and individual chambers, as well as signs of pulmonary venous congestion and interstitial and alveolar pulmonary edema. Dilatation of the heart can be recognized either by an increase in the transverse dimension (more than 15.5 cm in men and more than 14.5 cm in women), or by an increase in the cardiothoracic index (the ratio of the size of the heart to the size of the chest in direct projection) of more than 0.5 (or fifty%). However, determining the size of the heart on a chest x-ray is not entirely informative, since they can be normal even in patients with proven heart failure. In particular, heart size is usually normal in CHF due to LV diastolic dysfunction, such as in patients with hypertensive heart disease or hypertrophic cardiomyopathy.

Literature data regarding the diagnostic value of some instrumental signs in case of suspected CHF are summarized in Table. 3.6.

Chest x-ray can help diagnose left atrial enlargement with mitral valve disease, valvular or pericardial calcification, LV aneurysm, and pericardial effusion that looks like a general enlargement of the heart.

echocardiography

echocardiography- the only reliable method for diagnosing cardiac dysfunction that can be used in everyday clinical practice. It allows not only to directly detect dysfunction of the heart muscle, but also to determine its cause. In many cases, the simultaneous use of M-mode echocardiography, two-dimensional echocardiography and Doppler sonography eliminates invasive studies. Echocardiography allows you to determine the functional integrity of the valves, the size of the chambers of the heart, hypertrophy of the walls of the ventricles, local (regional, segmental) contractility, as well as assess systolic and diastolic functions.

The most characteristic sign of heart failure due to CAD, DCM and some valvular heart disease is dilatation of the LV cavity (end diastolic

size 6.0 cm). In the area of ​​the transferred transmural myocardial infarction, a local (regional) violation of LV contractility can be detected. Violations of local LV contractility are most characteristic of CAD; their detection helps in the differential diagnosis of coronary artery disease from DCMP of another origin, in which there is a total violation of contractility of both the left and right ventricles.

If heart failure is suspected, it is important to measure the size of the LV cavity and evaluate its function. With standard M-mode echocardiography, LV end-diastolic and end-systolic dimensions can be measured. The final diastolic size correlates well with the volume of the LV cavity and its shortening fraction, determined by the formula:

end diastolic size - end systolic size end diastolic size

Normally, the shortening fraction of the anteroposterior size of the left ventricle exceeds 25-30%.

Impaired LV systolic function, which is considered characteristic of CAD and DCM, is manifested by dilatation of its cavity and a decrease in ejection fraction.

LV EF is determined by the formula:

to end diastolic volume - end systolic volume end diastolic volume

LV EF less than 45% is considered one of the most important signs of its systolic dysfunction, and less than 35-40% indicates severe LV systolic dysfunction.

There are significant differences in the value of LV EF in patients with CHF, depending on the instrumental method used to assess LV function.

An ejection fraction of less than 35-40% indicates severe LV systolic dysfunction.

Echocardiography allows to determine the presence and degree of LV hypertrophy and helps in the differential diagnosis

hypertensive heart and hypertrophic cardiomyopathy. Doppler echocardiography makes it possible to assess LV diastolic function, which is often impaired in myocardial ischemia, hypertension and hypertrophic cardiomyopathy, as well as in patients with valvular heart disease.

Doppler echocardiography can accurately diagnose heart defects and assess their severity. Therefore, echocardiography can help determine indications for surgical treatment of acquired and congenital heart defects, which are potentially avoidable causes of CHF. Echocardiography also reveals pericardial effusion, LV aneurysm, and thrombi in the heart cavities.

Transesophageal echocardiography

Transesophageal echocardiography allows a more detailed assessment of the structure and function of the heart and is used in cases where, due to a poor “window”, transthoracic examination is insufficiently informative. In particular, it allows better diagnosis of intracardiac thrombi, which often form in patients with CHF and atrial fibrillation.

Stress echocardiography

Dobutamine stress echocardiography is helpful in the diagnosis of potentially reversible LV systolic dysfunction in patients with ischemic DCM.

Other Methods

Other research methods are of limited value in the diagnosis of heart failure and are used only for certain indications. For example, coronary angiography is performed in patients with CAD to determine the possibility of revascularization of the ischemic myocardium. Cardiac catheterization is performed to measure pressure in the cavities of the heart and pulmonary artery, to take a biopsy specimen from the endomyocardium to diagnose specific lesions of the heart muscle, and to conduct an electrophysiological study in repeated life-threatening ventricular arrhythmias.

Radioisotope myocardial scintigraphy with thallium-201 in combination with physical activity reveals the reversible nature of myocardial ischemia, and therefore, the possibility of the patient undergoing myocardial revascularization.

Radioisotope ventriculography is used to evaluate LV function.

Spiroveloergometry proved to be useful in the differential diagnosis of heart failure and respiratory failure and in the objective assessment of the severity of heart failure.

24-hour ECG monitoring is performed in patients with palpitations and episodes of loss of consciousness, which may be associated with cardiac arrhythmias.

In instrumental and biochemical studies, it is important to diagnose concomitant diseases and, in particular, diseases that can simulate symptoms and signs of heart failure or contribute to its decompensation (Table 3.6).

In cases where the diagnosis of heart failure is beyond doubt, it is necessary to evaluate the severity of clinical symptoms and the degree of limitation of physical activity.

CHF TREATMENT

The immediate goal of treating patients with CHF is to eliminate the symptoms of the disease in the form of shortness of breath, attacks of cardiac asthma, fluid retention in the body. Another important goal is to increase the level of physical activity and quality of life. In this case, the treatment should prolong the life of the patient. It is necessary to minimize the risks of unwanted side effects depending on the drugs used, their doses and tactics of use. The physician should also strive to reduce the cost of treatment, ensure a reduction in the frequency of hospitalizations and minimize the ratio between the price and effectiveness of therapy. Since most of the funds spent on treatment fall on the hospital period (about 70%), a modern doctor needs to pay more attention to the outpatient stage of treatment. The goals of CHF treatment also include the control and prevention of diseases leading to cardiac dysfunction and HF, as well as the prevention of progression of HF if cardiac dysfunction is already established.

General measures

Patients are recommended a diet with limited salt. The more severe the heart failure and the greater the degree of fluid retention in the body, the stricter the control of salt intake should be. Restriction of fluid intake is indicated during the period of increasing signs of heart failure, however, even in a compensated patient, fluid intake should not exceed 1-1.5 liters per day.

The diet of a patient with CHF should correspond to the degree of development of fatty tissue. Patients with obesity or overweight should eat food with a reduced calorie content. Food

a patient with pathological weight loss should be high-calorie, easily digestible, with a sufficient content of vitamins and protein.

As CHF progresses, patients lose lean body mass, which includes all tissue except for adipose tissue. About 30% of lean mass is in skeletal muscle. The loss of muscle mass leads to a further increase in weakness, fatigue, shortness of breath, and a deterioration in exercise tolerance.

Loss of lean body mass constitutes an important CHF syndrome with a complex pathogenesis, in the origin of which chronic disturbances in the blood supply to organs and tissues, as well as impaired function of the small intestine with loss of nutrients, matter.

Therefore, patients with CHF are recommended to use special nutritional supplements with easy digestibility (nutritional mixtures) that can be absorbed in conditions of impaired function of the small intestine (protein hydrolysates or whole proteins - milk and egg albumins, maltodextrins and disaccharides, vegetable oils, vitamins, trace elements: nutrilan , nutrison, berlamin modulator, pentamen, etc.). Properly administered nutritional support leads to an increase in lean body mass. Techniques have been developed to assess nutrient loss and support.

In recent years, the attitude to the regimen of physical activity of patients with CHF has been significantly revised. Only in some severe pathological conditions (active myocarditis, valvular stenosis, cyanotic congenital malformations, severe arrhythmias, angina attacks in patients with low LV ejection fraction) requires restriction of physical activity. The rest of the patients with CHF show regular physical activity (from breathing exercises to regular dosed walking and special physical training).

The conditions for starting aerobic physical training are listed below:

Compensation for CHF for at least 3 weeks;

Ability to speak without shortness of breath;

Respiratory rate less than 30 per minute;

Fatigue is small;

Cardiac index more than 2 liters per minute / square meter. pove.body;

Central venous pressure less than 12 mm Hg. Absolute contraindications for starting physical training are:

Progressive shortness of breath in the last 3-5 days,

Signs of myocardial ischemia at low load (less than 50 watts),

uncontrolled diabetes,

acute diseases,

Embolism.

Relative contraindications are:

Recent use of dobutamine;

Decreased systolic blood pressure during exercise;

IV functional class of heart failure;

Ventricular extrasystoles of high grades at rest or during exercise;

heart rate lying more than 100 per minute;

General bad condition.

Physical training is initially carried out under medical supervision, and then independently and without supervision, but with periodic monitoring in a medical center. Training helps to preserve muscle mass, improve muscle function and exercise tolerance.

Regular physical activity contributes to the preservation of muscle mass in patients with CHF and inhibits the development of physical incapacity.

Medical treatment

Most patients should receive a combination of four classes of drugs - an ACE inhibitor, a diuretic, a cardiac glycoside, and a beta-blocker. As additional means in the treatment of patients with CHF, aldosterone antagonists, angiotensin receptor blockers, nitrates, non-glycoside positive inotropic agents, as well as anticoagulants and antiarrhythmics are prescribed.

ACE inhibitors are among the first prescribed drugs, and in this, as shown by the CIBIS III study (comparing the effectiveness of initial therapy with enalapril or concor), they have an equal position with beta-blockers. Due to a wide range of hemodynamic and neurohumoral effects, ACE inhibitors have a beneficial effect on symptoms.

HF, improve the clinical condition of patients, reduce the need for hospitalization and improve the prognosis of life. ACE inhibitors are indicated for all patients with CHF, regardless of etiology, stage of the process and type of decompensation. In Russia, the drugs listed in Table 1 are used to treat CHF. 3.8.

Low blood pressure (less than 100 mm Hg) is often an obstacle to the appointment of ACE inhibitors. In order to reduce the likelihood of a significant decrease in blood pressure at the first dose or when it is increased, it is recommended to reduce the intake of diuretics or refrain from using them on the day of the appointment of the ACE inhibitor, and treatment should begin in the evening, when the patient is already in bed. Perindopril reduces blood pressure to a lesser extent in patients with CHF compared to other inhibitors.

Treatment begins with small doses, stepwise increasing to maintenance. Drugs are prescribed constantly, for a long time, in fact

for life. Side effects requiring discontinuation of the drug are rare: hypotension (3-4%), dry cough (2-3%) and azotemia (1-2%).

If a patient with CHF does not receive treatment with ACE inhibitors, then with rare exceptions, this is a medical error.

Diuretics are indicated for all patients with signs of sodium and water retention in the body. When prescribing diuretics, the symptomatic effect occurs faster than when prescribing other classes of drugs. Only diuretics effectively control fluid retention in the body. Thiazide (hypothiazid) or loop (furosemide, uregit) diuretics are usually used. Potassium-sparing drugs (triamterene, amiloride) have practically ceased to be used due to the potassium-sparing properties of ACE inhibitors. The choice of the optimal dose of diuretics and the frequency of their appointment is determined by the degree of fluid retention in the body. When conducting therapy with diuretics, it is necessary to regularly assess the clinical signs of fluid retention in the body, determine body weight and measure daily diuresis. The greater the degree of fluid retention, the more active the therapy should be. During the period of active therapy, daily diuresis should exceed the amount of fluid consumed per day. After elimination of edema, they switch to maintenance therapy, the task of which is to maintain an edematous state. This requires smaller doses of diuretics, but often they have to be prescribed daily to avoid recurrence of edema.

Aldosterone antagonists (veroshpiron, aldactone) occupy a special place among diuretics. Due to their potassium-sparing action, these drugs are widely used as diuretics that potentiate the effect of thiazide and loop diuretics. With the advent of ACE inhibitors, aldosterone antagonists have become much less commonly used. However, their neuromodulatory antialdosterone effect leads to an additional beneficial effect on patient survival. During an exacerbation of CHF, aldactone is used in high doses up to 150-300 mg, followed by a transition to long-term maintenance therapy at doses of 12.5-50 mg per day.

Beta-blockers, suppressing the activity of the sympathoadrenal system, reduce tachycardia, have antiarrhythmic and antifibrillatory effects. With long-term therapy, they increase cardiac output, block negative cardiac remodeling, normalize LV diastolic function, and reduce myocardial ischemia and hypoxia. Their ability to reduce the mortality of patients and slow down the progression of CHF has been proven. For the treatment of patients with CHF, beta-blockers are recommended, the effectiveness of which has been proven in multicenter controlled trials. These include the cardioselective drugs bisoprolol, metoprolol, and nebivolol, as well as the non-cardioselective drug with additional alpha1-blocker properties, carvedilol (Table 3.9). The effectiveness of nebivolol has been proven in the group of elderly patients with coronary artery disease.

Table 3.9

Doses of beta-blockers in CHF

Treatment should be started with small doses (1/8 of the therapeutic dose), which are increased slowly to the target therapeutic dosages. Transient hypotension, bradycardia, and worsening heart failure may occur at the start of therapy and during the titration period, but disappear with prolonged therapy.

Here is a scheme for prescribing Concor to patients with CHF III-IV of functional classes, which was used in the CIBIS-II study:

1.25 mg - 1 week, 2.5 mg - 2nd week, 3.75 mg - 3rd week, 5 mg - 4-7 weeks, 7.5 mg - 8-11 weeks,

10 mg is a further maintenance dose.

Beta-blockers can be used in patients of any functional class and with low ejection fraction (in the COPERNICUS study, the use of carvedilol proved to be effective in patients with functional class IV CHF, even in the subgroup with an ejection fraction of less than 15%)!

Cardiac glycosides in patients with CHF are the drug of choice in the presence of atrial fibrillation, although they can also be used in sinus rhythm. They have three main mechanisms of action - they have positive inotropic, negative chronotropic and neuromodulatory effects. The latter effect is most characteristic of low doses of glycosides. At present, high, so-called saturating, doses of cardiac glycosides, which threaten the occurrence of severe arrhythmias, have been completely abandoned. A huge number of varieties of prescribed cardiac glycosides are gone. Today, the main drug is digoxin at a dose of 0.25 mg per day (in patients with a large body weight, 1-1/2 tablets are prescribed, in the elderly, 1/2-1/4 tablets). In chronic renal failure, the dose of digoxin is reduced in proportion to creatinine clearance (a switch to digitoxin with a hepatic elimination route is possible). Cardiac glycosides improve clinical symptoms, quality of life, and reduce the need for hospitalizations.

Angiotensin receptor blockers have their own points of application as a neurohormonal modulator, complementing the action of ACE inhibitors and replacing them. Evidence is gradually accumulating that the angiotensin receptor blockers losartan, valsartan and candesartan have an independent beneficial effect on the course of CHF and patient survival.

Auxiliary agents include drugs of various classes and directions of action, which are designed to influence concomitant diseases and emerging complications. Peripheral vasodilators (most often nitrates) are often prescribed for angina. Blockers of slow calcium

channels (most often long-acting dihydropyridines) may be indicated for persistent arterial hypertension and severe angina pectoris. Antiarrhythmic drugs (usually class III) are prescribed in the presence of life-threatening ventricular arrhythmias. Disaggregants (aspirin and others) are used in patients who have had a heart attack, are prescribed at the risk of thromboembolic complications in patients with atrial fibrillation, intracardiac thrombosis, after operations on the heart valves and with dilatation of the heart cavities. Non-glycoside inotropic agents (sympathomimetics, phosphodiesterase inhibitors, drugs that increase the sensitivity of cardiomyocytes to calcium) are prescribed for persistent hypotension and low cardiac output during exacerbation of CHF. Statins are used for hyper- and dyslipidemia, and cytoprotectors (trimetazidine) are used to improve the function of cardiomyocytes in patients with CAD. The practitioner should avoid polypharmacy and dwell on the necessary drugs.

New directions of CHF pharmacotherapy are being developed: the use of endothelin receptor blockers (bosentan), inhibitors of vasopeptidase-atrial natriuretic peptide and brain natriuretic peptide (neseritide), blockers of tissue necrotizing factor receptors, erythropoietins, statins, drugs that slow down the heart rate (ivabradine), etc.

The main direction of treatment of patients with CHF is pharmacotherapy with the use of ACE inhibitors, diuretics, beta-blockers and cardiac glycosides. Angiotensin II receptor blockers and aldosterone antagonists are increasingly being used.

Surgical, mechanical and electrophysiological methods of treatment are used quite rarely for a number of reasons. Myocardial revascularization is used most often, but the mortality of patients increases as the ejection fraction decreases. Correction of mitral regurgitation is effective in a carefully selected group of patients. Heart transplant surgery can give brilliant results. However, for many reasons, this operation does not have a serious prospect and is being replaced by alternative use of circulatory assist devices. The latter provide hemodynamic unloading of the heart and

restoration of its contractility, which further allows the patient to do without hemodynamic support and even without drug therapy for several months. Biventricular resynchronization of the ventricles of the heart, which is devoted to a special section in Volume 4, is very promising.

The phrase "heart failure" is widely used by many people. However, it is often used not quite correctly, implying the majority of cardiac pathologies. Understanding the causes and mechanism of heart failure contributes to the timely detection of problems and an increase in the patient's life expectancy.

Heart failure (HF) is a set of symptoms that may include:

• shortness of breath
• orthopnea;
• weakness;
• increased fatigue;
• heartbeat;
• night cough;
• the appearance of edema;
• swelling of the neck veins.

Thus, it is not an independent disease. Doctors understand heart failure as a set of symptoms that are associated with inadequate perfusion of organs and tissues at rest or during exercise, and often with fluid retention in the body.

Important: effective treatment of HF symptoms is possible only if the underlying disease is eliminated.

What causes heart failure

In the mechanism of occurrence of the above symptoms, the following sequence can be distinguished:

1. Some diseases lead to damage and weakening of the myocardium - the main muscle of the heart.
2. Pathologies of the myocardium become the reason that the body is not able to fully meet the body's needs for blood supply.
3. Poor blood supply leads to malnutrition of internal organs and tissues.
4. Blood stagnation occurs in the body, which provokes pathological processes at the place of their formation.

The main and less common causes are shown in the table:

With any variant of the violation, acidosis, hypoxia of tissues and internal organs, and metabolic disorders appear.

Features of the course of heart failure

Over the years, the symptoms progress, signaling the emergence of new problems in the body. The lack of adequate treatment leads to a deterioration in the patient's health and aggravation of pathological processes.

Heart failure can be acute or chronic.

The acute form is a consequence of problems with myocardial contraction, which are accompanied by a decrease in minute and systolic blood volume. The acute form can occur due to the ingress of toxins, the presence of cardiac diseases, injuries. It is manifested by critical conditions: cardiogenic shock, cardiac asthma, acute kidney failure, pulmonary edema. Lack of treatment can lead to death.

The chronic form develops for a long time and is explained by the presence of the underlying cause that caused the pathology of the myocardium. Symptoms appear gradually, worsening over time. The severity of the process and the number of symptoms determine the stage of chronic heart failure.

Important: treatment of the chronic form, as a rule, is long and complex. Often patients have to completely change their lifestyle.

Classification

There are two classifications that give a clear understanding of how much the pathological process is running and how serious the patient's condition is. In general, they are very similar and are often equivalent. However, the first evaluates the stage of heart failure in terms of the doctor and visible symptoms, and the second takes into account complaints and functional limitations in the patient's life. For clarity, they are presented in the form of a table:

For the most accurate description of the patient's condition, doctors combine both models, indicating both the stage and the functional class.

Symptoms

Based on in which circle of blood circulation problems appear, the symptoms of the second stage may differ slightly.

Symptoms that appear with pathologies of a small circle of blood flow:

• increased fatigue, irritability;
• increased heart rate after physical activity;
• orthopnea;
• nocturnal attacks of suffocation;
• dyspnea;
• orthopnea;
• weakness;
• heartbeat;
• night cough;
• the appearance of edema;
• swelling of the neck veins;
• cyanosis.

Symptoms that appear with pathologies of the pulmonary circulation:

• shortness of breath after exercise or heavy meals;
• pallor of the skin, acrocyanosis, cyanosis of the mucous membranes;
• loss of appetite;
• wheezing in the lungs (symmetrical from the lower sections to the entire surface of the lungs);
• weakening of the first tone at the apex of the heart, the presence of a gallop rhythm,
  presence of noise of relative insufficiency of atrioventricular valves.

At stage 2a, disturbances are noticeable only in one of the circles of blood circulation. At the last stage of the second stage, which is classified as grade 2b, the problems affect both circles of blood circulation. Symptoms become serious and significantly impair the quality of life of the patient. According to foreign classification 2b, the degree corresponds not to the second, but to the third functional class due to the severity of the course.

The second stage is decisive for the outcome of the disease. During this period, the symptoms are already quite clearly visible and should alert the patient. A timely visit to a doctor in the second stage allows you to start the right treatment, which is likely to lead to full compensation. If treatment is not started, then the symptoms will begin to worsen and pass into the third stage, the treatment of which is impossible for modern medicine.

Important: the patient needs to morally tune in to treatment and want to recover. This will help you follow the doctor's recommendations exactly and not skip taking medications. A frivolous approach to treatment makes it practically useless.

Treatment

Heart failure is difficult to cure completely. In most cases, doctors manage to achieve an improvement in the patient's condition and return to the first stage. It is much easier to prevent the occurrence of heart failure, so it is very important to take specific preventive measures, take care of heart health and treat other diseases in time.

At the second stage II FC from drug therapy are prescribed:

• diuretics (diuretics);
• ACE inhibitors;
• statins;
• beta blockers;
• cardiac glycosides;
• omega-3 PUFAs;
• anticoagulants and antiaggregants;
• antiarrhythmics, etc.

Important: only a doctor can choose the right group, generation and brand of the drug. For heart problems, taking medicine that someone else suggested could cost you your life!

In addition to drug therapy, much attention is paid to:

1. Mode of physical activity. The doctor adjusts the dose and frequency of exercise.
2. Diet. The diet includes ingredients that are good for the heart, and excludes all unhealthy foods and drinks. For stage 2 CHF, recommendations for salt intake are no more than 1.5 g per day.
3. Quit smoking.
4. The psychological state of the patient. This will allow you to consciously treat the treatment and reduce the level of daily stress that has a negative impact on heart health.

An important point at all stages, especially the second, is the treatment regimen. This concept includes medical recommendations and patient adherence to treatment. Doctors teach the patient and his relatives to control the course of heart failure, determine severe conditions and provide first aid. The patient receives complete information about the disease. The treatment becomes more understandable for him, and the symptoms less frightening.

Video - Chronic heart failure: epidemiology, diagnosis, treatment

The most obvious signs of heart failure are shortness of breath and swelling. Shortness of breath occurs due to stagnation of blood in the pulmonary vessels and with an increased need for oxygen in the body. Edema appears due to stagnation in the blood in the venous bed.

CHF develops gradually, so there are several stages of this disease. There are different principles for dividing heart failure into stages, one of the most convenient and understandable classifications was developed by the New York Heart Association. It distinguishes four functional classes of patients with CHF:

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 - a pronounced 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 - the inability to perform any load without the appearance of discomfort. Symptoms of heart failure or angina syndrome may occur at rest. When performing a minimum load, discomfort increases.

What is chronic heart failure?

The state of chronic heart failure occurs when the heart ceases to adequately supply tissues and organs with blood, and therefore with oxygen and nutrients.

Why does this happen?

In chronic insufficiency, the heart muscle (myocardium) is not able to develop the proper efforts to expel blood from the left ventricle. The causes of such a violation may be associated with damage to the myocardium itself, the aorta (the main artery coming directly from the heart) and heart valves.

The myocardium is affected in ischemic heart disease, myocarditis (inflammation of the heart muscle), cardiomyopathies, and systemic connective tissue diseases. There is also toxic damage to the myocardium in case of poisoning with poisons, toxins and drugs.

Damage to the aorta and arteries occurs in atherosclerosis, arterial hypertension, diabetes mellitus and some other diseases.

Unoperated heart defects (congenital and acquired) also lead to heart failure.

What's happening?

Slowed blood circulation causes chronic oxygen starvation of organs and tissues, which causes a characteristic manifestation of heart failure - shortness of breath during exercise or (in advanced cases) at rest. A person complains of fatigue, poor sleep, rapid heartbeat (tachycardia).

Lack of oxygen in the most distant parts of the body from the heart (fingers, toes, lips) leads to the fact that the skin on them acquires a gray-bluish tint (cyanosis). Insufficient cardiac output leads not only to a decrease in the volume of blood entering the arterial bed, but also to stagnation of blood in the venous bed. This leads to edema (primarily in the legs), as well as pain in the right hypochondrium, associated with overflow of the liver veins.

In the most severe stage of heart failure, all of the above symptoms increase.

Cyanosis and shortness of breath bother a person even in a state of complete rest. He is compelled to spend the whole day in a sitting position, because in the lying position the dyspnea increases, and he can even sleep only while sitting. Edema spreads to the entire lower body, fluid also accumulates in the body cavities (abdominal, pleural).

Diagnosis

The diagnosis is made on the basis of an examination by a cardiologist and additional examination methods, such as an electrocardiogram in various variations: daily ECG monitoring and a treadmill test. The contractility and size of the heart, the amount of blood ejected into the aorta can be determined using an echocardiogram. It is possible to carry out cardiac catheterization (a thin tube is inserted through a vein or artery directly into the heart, this procedure allows you to measure the pressure in the heart chambers and identify the place of blockage of blood vessels).

Treatment

Heart failure is much easier to prevent than to cure.

Its prevention includes the treatment of arterial hypertension, the prevention of atherosclerosis, a healthy lifestyle, exercise, smoking cessation and diet.

If heart failure still develops, the cardiologist prescribes treatment. This usually includes diuretics (to reduce the volume of blood pumped), ultraselective beta-blockers (to reduce the heart's oxygen demand), metabolic therapy, and, of course, treatment of the underlying disease.

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Classification of chronic heart failure - signs, degrees and functional classes

The classification of clinical forms and variations of chronic heart failure is necessary to distinguish between the causes of occurrence, the severity of the patient's condition, and the characteristics of the course of the pathology.

Such a distinction should simplify the diagnostic procedure and the choice of treatment tactics.

In domestic clinical practice, the classification of CHF according to Vasilenko-Strazhesko and the functional classification of the New York Heart Association are used.

CHF according to Vasilenko-Strazhesko (stages 1, 2, 3)

The classification was adopted in 1935 and is used to this day with some clarifications and additions. Based on the clinical manifestations of the disease during CHF, three stages are distinguished:

• I. Hidden circulatory failure without concomitant hemodynamic disorders. Symptoms of hypoxia appear with unusual or prolonged physical exertion. Shortness of breath, severe fatigue, tachycardia are possible. There are two periods A and B.

Stage Ia is a preclinical variant of the course, in which cardiac dysfunctions have almost no effect on the patient's well-being. An instrumental examination reveals an increase in the ejection fraction during physical exertion. At stage 1b (hidden CHF), circulatory failure manifests itself during exercise and resolves at rest.

The use of modern drugs and aggressive methods of treatment quite often eliminates the symptoms of CHF corresponding to stage 2b to the preclinical state.

New York (FC 1, 2, 3, 4)

The functional classification is based on exercise tolerance as an indicator of the severity of circulatory insufficiency. Determination of the patient's physical abilities is possible on the basis of a thorough history taking and extremely simple tests. On this basis, four functional classes are distinguished:

• I FC. Daily physical activity does not cause manifestations of dizziness, shortness of breath and other signs of myocardial dysfunction. Manifestations of heart failure occur against the background of unusual or prolonged physical exertion.
• II FC. Physical activity is partially limited. Everyday stress causes discomfort in the heart area or anginal pain, tachycardia attacks, weakness, shortness of breath. At rest, the state of health is normalized, the patient feels comfortable.
• III FC. Significant limitation of physical activity. The patient does not experience discomfort at rest, but everyday physical activity becomes unbearable. Weakness, pain in the heart, shortness of breath, tachycardia attacks are caused by loads less than usual.
• IV FC. Discomfort occurs with minimal physical exertion. Attacks of angina pectoris or other symptoms of heart failure may also occur at rest without visible prerequisites.

See the table of correspondence between the classifications of CHF according to NIHA (NYHA) and N.D. Strazhesko:

Functional classification is convenient for assessing the dynamics of the patient's condition during treatment. Since the gradation of the severity of chronic heart failure on a functional basis and according to Vasilenko-Strazhesko are based on different criteria and do not exactly correlate with each other, the stage and class for both systems are indicated when diagnosing.

Your attention to the video about the classification of chronic heart failure:

What does CHF 1 degree 1 FC mean

The quality and activity of each person's life is directly dependent on how his heart is able to perform the functions assigned to it.

Chief among these is the ability to pump oxygenated blood throughout the body. In violation of this function, we can talk about the development of chronic heart failure.

Many patients, after being discharged from the hospital or examined by the attending physician, cannot understand what the entry in the CHS 1 degree 1 fc card means?

In order to answer this question, it is necessary to study in detail the classification of the disease, the causes and symptoms of its development.

What is this disease

The essence of this disease lies in the fact that the volume of blood that is ejected by the heart with each contraction is significantly reduced.

As a result of this violation, the internal organs of a person and all tissues of the body do not receive the required amount of blood enriched with oxygen. According to statistics, approximately 15 million people in our country suffer from chronic heart failure.

One of the main features of CHF is that it has the ability to develop over a long period of time (from 6 months to several years).

There are several reasons or factors that can trigger the development of the disease. Among the most important are the following:

• development of coronary heart disease;
• high blood pressure (hypertension);
• acquired or congenital heart defects;
• the presence of a disease such as diabetes;
• change in thickness or improper performance of myocardial function;
• various types of arrhythmias;
• myocarditis (inflammation of the heart muscle);
• proliferation of connective tissue of the myocardium;
• excessive consumption of alcoholic beverages;
• smoking, etc.

If we talk about the reasons that provoke the development of chronic heart failure in women, then the main one is high blood pressure, and in men - coronary heart disease.

Symptoms

Symptoms of the disease appear depending on the degree of its development. The clinical picture of CHF is characterized by the following features:

• a person gets tired quickly;
• against the background of frequent shortness of breath, cardiac asthma may develop;
• edema of the upper and lower extremities is observed;
• strong and frequent beating or fluttering of the heart.

I would like to note that such a symptom as fatigue is characteristic of all stages of the development of the disease. There are the following reasons for this:

• the heart with each contraction throws out an insufficient amount of blood;
• internal organs and the brain do not receive enough oxygenated blood, resulting in development of processes such as hypoxia and weakness of skeletal muscles.

If we talk about shortness of breath, then its intensity and frequency is increasing. In the early stages of the development of the disease, it can manifest itself only with great physical exertion. In more complex phases, it can appear even if the person is at complete rest.

In the case of decompensation of the heart muscle, attacks of shortness of breath torment patients even at night. This condition has the following manifestations:

• small seizures that go away on their own;
• attacks that resemble asthmatic in nature;
• in the form of acute pulmonary edema.

Against the background of chronic heart failure, diseases such as asthma, acute heart failure, or pulmonary edema develop. As for cardiac asthma, it can manifest itself in two forms:

1. Light. The attack of suffocation lasts for several minutes with little intensity. In a sitting position, the patient is heard in the lungs hard breathing.
2. Heavy. The attack tends to continue for a long period of time. The patient's breathing becomes very rapid and difficult. The presence of wheezing in the lungs is not always observed. The frequency of such attacks can be so strong that the patient tries to sleep sitting up.

The danger of chronic heart failure is that it develops so slowly and the symptoms are so mild that most people attribute their condition to old age or body fatigue.

This leads to the fact that people turn to the attending physician too late, when the disease is already intensively developing.

This state of affairs significantly complicates the treatment process and makes it much longer.

The development process of CHF

As mentioned earlier, chronic heart failure develops very slowly and gradually. Experts distinguish the following main stages of its development:

1. The heart stops pumping oxygen-enriched blood in the volume necessary for the normal functioning of the body.
2. As a result, the first symptoms of the disease begin to appear: shortness of breath and fatigue during heavy physical exertion. At this stage, the body activates its compensatory abilities, which lead to an increase in the amount of adrenaline in the blood, and fluid retention in the tissues.
3. There is an active process of growth of the muscle tissue of the heart, which is accompanied by an insufficient number of blood vessels. As a result, the heart receives an insufficient amount of blood, and the walls of the myocardium and ventricles thicken greatly, complicating the contraction of the heart.
4. The internal resources of the body are running out, which leads to disruption of the functioning of the heart.

These are the main stages of the development of the disease. Their duration is different for each person. It depends on the general condition of the patient, his lifestyle and other factors.

Classification

In the medical practice of our country, two classifications of chronic heart failure are used. They have some differences, but mostly complement each other.

The first classification was developed by such scientists as N.D. Strazhesky and V.Kh. Vasilenko with the participation of G.F. Lang and approved by the XII All-Union Congress of Therapists, which took place in 1935. This classification is based on the functional and morphological stages of the dynamics of the disease. According to its CHF is divided into the following stages:

1 stage. Patients do not feel almost any symptoms indicating the development of their disease. With heavy physical exertion, they experience slight fatigue and weakness.

In rare cases, tachycardia and dizziness appear.

2 stage. Signs of the disease begin to manifest themselves even when patients are at rest. But their intensity is very weak, and long-term short-term.

3 stage. Patients complain of severe shortness of breath, dizziness, weakness. In most cases, there is blueness of the upper and lower extremities, swelling of the face and extremities.

This classification is mainly used to characterize total chronic heart failure. But in the case of the development of right ventricular HF in patients, it does not give a clear picture of the progression of the disease.

In this case, another classification of CHF looks more reasonable, which is based on functional changes in the body. It was approved by the International and European Society of Cardiology in 1964 at the New York Heart Association. This designation is used to designate it - NYHA. There are such FC according to NYHA CHF:

1 FC. In patients with CHF 1 FC 1, there is no decrease in labor and physical activity. At low loads, such signs of the disease as shortness of breath, weakness, fatigue, dizziness are not observed. Heart failure 1 degree is asymptomatic.

11 FC. Shortness of breath, fatigue, palpitations, dizziness are manifested in patients even with a small and moderate load. In a calm state, such signs are not observed.

111 FC. Labor activity in patients is limited. With a small load, all the symptoms of the disease begin to appear.

1V FC. Any load brings discomfort to patients, a feeling of pain behind the sternum, blueness and swelling of the face, upper and lower extremities.

In practice, the following ratio of two classifications of chronic heart failure is used:

• CHF 1 tbsp. – FC 1 according to NYHA;
• CHF 2 tbsp. – FC 11 by NYHA;
• CHF 3 tbsp. – FC 111 by NYHA;
• CHF 3a Art. – FC 1V by NYHA.

The first and second classifications have the right to exist and are actively used in practice, both domestic and foreign. Both of them complement each other and help to more accurately characterize the patient's condition, determine the stage and complexity of the development of chronic heart failure.

In order to avoid a severe form of CHF development, as well as to prevent the development of complications, it is necessary to contact your doctor, even with the slightest suspicion of an illness. This will only simplify and speed up the healing process. Be healthy!

Chronic heart failure 1 degree 2 fc

Second functional class of exertional angina

Angina pectoris is a disease characterized by transient episodes of myocardial ischemia. They occur in conditions of emotional or physical stress, when the heart muscle requires more oxygen.

• The reasons
• Symptoms
• Diagnostics
• Treatment
• Consequences and prevention

The pathogenesis of angina pectoris is based on changes in arterial tone, as well as endothelial dysfunction of the coronary vessels. Tension or stress leads to vasoconstriction, which causes sudden myocardial ischemia. The level of exercise that causes ischemia and exertional angina is somewhat unpredictable.

Myocardial ischemia is associated with a violation of the contractile function of the heart muscle area, as well as with a change in the biochemical or electrical processes that occur in it. Due to oxygen deficiency in cardiomyocytes, the energy reserve is depleted, and other negative processes occur.

At the cellular level, the concentration of intracellular sodium increases, and potassium ions are lost. Transient ischemia is expressed in the development of an attack of angina pectoris, and stable ischemia leads to irreversible changes, that is, to a heart attack of the ischemic area of ​​the myocardium.

There are four functional classes of angina pectoris. The first of these is characterized by attacks that occur during very strong loads, for example, when walking fast or climbing stairs. 2 FC is characterized by limited physical activity, while attacks occur even when walking at a distance of more than five hundred meters.

Functional classes of exertional angina

The third class is characterized by significant limited activity, and in the fourth functional class, physical activity is so severely limited that seizures occur with minimal exertion or at rest. Let's take a closer look at 2 FCs of angina pectoris and first discuss the reasons that lead to the development of this disease.

The reasons

Let's single out several reasons that lead to a malfunction of the heart and to the occurrence of angina attacks:

1. Atherosclerosis. This is the most common reason. It is the atherosclerotic narrowing of the lumen of the coronary arteries by approximately fifty percent that leads to a discrepancy between the delivery of oxygen to the heart muscle and the need for it. It turns out that not the amount of oxygen that is necessary for the normal functioning of the heart is delivered.
2. Hypertrophic cardiomopathy, that is, an isolated lesion of the myocardium.
3. Pulmonary hypertension.
4. Severe arterial hypertension.
5. Stenosis of the aortic mouth.
6. Coronary spasm.
7. aortic insufficiency.

There are also risk factors. These include smoking, obesity and physical inactivity, heredity, diabetes and menopause. Hypoxia and severe anemia aggravate the course of angina pectoris.

It is worth highlighting the immediate causes that can lead to the development of attacks of angina related to FC 2:

• physical exercise;
• temperature changes;
• overeating;
• emotional disturbances and so on.

Symptoms

Angina pectoris 2 FC is characterized by symptoms such as:

• discomfort and tightness in the chest;
• heartache;
• dyspnea.

These manifestations are observed during such loads as climbing stairs or uphill, brisk walking, running, after overeating, in wind or cold. Such people are not strong, but still limited in activity. This is due to the fact that when walking at an average pace on flat terrain for five hundred meters, an attack begins to develop. This also happens when going up more than 1 floor, although some people show signs when going up to the fifth floor.

It turns out that for the occurrence of an attack, it is necessary to have factors in which the myocardium experiences a large need for oxygen. They, as already mentioned, can be different circumstances, although basically an attack develops during exercise. Some angina sufferers may feel reduced tolerance in the morning, but it returns to normal in the afternoon.

The severity of the clinical picture inherent in angina pectoris 2 FC depends on physical activity. Those who during the day often exceed the level of stress, suffer from attacks several times a day. If a person monitors the level of stress and does not exceed them, he may almost not feel angina attacks. This means that the severity of the disease is determined by the frequency of attacks.

Diagnostics

The most complete information is given by the ECG, which is removed during an attack. It is during this period that you can catch all the changes that indicate the presence of angina pectoris. In order to provoke ischemia, stress tests are used. Holter ECG monitoring allows you to detect painless and painful episodes of ischemia, and possible heart rhythm disturbances per day.

Since angina pectoris can be confused with other diseases, you should immediately consult a doctor and conduct a thorough diagnosis. The main difference between functional class 2 angina pectoris is that the attack stops after taking nitroglycerin or at rest.

Treatment

First of all, you need to know how to stop an attack that has begun. To do this, you need to eliminate the load that led to its occurrence, take a reclining position, provide air access and take a nitroglycerin tablet under the tongue.

Self-treatment of angina FC 2 is aimed at reducing the number of attacks, which will allow the patient to improve the quality of life. The doctor recommends lifestyle changes and avoiding stress that leads to seizures. In addition, he prescribes medications.

Drug therapy includes the use of the following drugs:

• nitrates - eliminate spasms of the coronary arteries;
• statins - lower cholesterol levels;
• beta-blockers, calcium antagonists - reduce the heart's need for oxygen;
• aspirin - prevents thrombosis.

Consequences and prevention

A more favorable prognosis can be said in the case of stable exertional angina. If angina pectoris arose for the first time, it is very difficult to predict the course. An even more serious prognosis can be given with unstable angina. Fatal infarction occurs in three percent of patients.

First of all, prevention is based on the elimination of risk factors. This means that you need to stop smoking, follow a diet, get rid of extra pounds, treat arterial hypertension, and so on. In order to prevent the occurrence of seizures or reduce their number, it is also necessary to lead a healthy lifestyle and follow the recommendations of a doctor.

Angina pectoris 2 FC is a disease, the development of which often depends on the person himself. It is worth making an effort, as the heart will not remind you of itself with unpleasant attacks, which will allow you to enjoy life more.

Features of hypertension of the 1st degree: its symptoms and treatment

1. Symptoms of hypertension 1 degree
2. Risks 1, 2 , 3 and 4
3. Diagnostics
4. What tests are needed?
5. Treatment
6. Complications
7. Prevention

High blood pressure often occurs in old age in both sexes, this leads to a disease of the cardiovascular system, which is called hypertension. Normal blood pressure (BP) occurs during the contraction of the heart, more precisely its left ventricle, blood from it enters the aorta, and then moves through the smaller arteries. The level of pressure is affected by the amount of tension, the volume of blood in small arteries and their tone.

Hypertension 1 degree, what is it?

It has another name - arterial hypertension. Its presence can be confirmed or refuted by tests and diagnostics of the body under the supervision of a doctor. An increase in pressure can be indicated by three consecutive control measurements, which are carried out using a tonometer.

Normal pressure can change its value up and down, depending on the state of the person, especially stressful situations and an unhealthy lifestyle affect it. In ordinary life, it rises during physical exertion, and during sleep it decreases, but normalizes during the day.

Its performance should be in the range of 60-90. If the blood pressure is higher than normal, this indicates that the person is suffering from hypertension.

A systematic increase in pressure refers to hypertension of the 1st degree. This is the mildest form, with it there is still no serious effect on the internal organs (heart, blood vessels and kidneys). The second degree is much more difficult, and the third is the most severe, with it there is a destruction of vital organs.

The first degree of the disease is treatable if you turn to a specialist in time and pass the necessary tests. The prerequisites for its diagnosis is the condition of the patient, who can feel the abnormalities described below in the body.

Symptoms of hypertension 1 degree

With it, the increase in pressure occurs periodically and itself returns to normal. The attack is accompanied by:

• Blurred vision;
• short dizziness;
• Headache in the back of the head;
• Quiet tinnitus;
• Increased heartbeat;
• Decline in strength;
• Heaviness in the limbs;
• increased sweating;
• swelling of the hands and feet;
• Memory deterioration.

If such symptoms began to appear with enviable regularity, then you should immediately begin to systematically measure your blood pressure, twice a day. For the first time in the morning, without even getting out of bed, in the evening put a tonometer near you, and when you wake up immediately take its measurements.

The second measurement should be taken during the day from 16:00 to 17:00. If during the week the pressure is constantly high, then you need to contact a specialist.

The first signs of hypertension 1 degree

This disease is insidious in that at the initial stage it occurs with virtually no obvious symptoms. This leads to the fact that people seek medical help late and have to treat it in a fluffy form.

In the meantime, she gives:

• To heart failure, which is expressed in edema and tachycardia, with it there is shortness of breath.
• Failures in the work of the kidneys, which do not have time to process the products that enter them, and accumulate fluid in themselves, therefore, urination failures occur. In neglected forms, this is expressed in the intoxication of the body with products formed after the breakdown of urea.
• Changes in the state of the vessels, accompanied by unbearable and persistent headaches.

Risks 1, 2 , 3 and 4

In addition to monitoring pressure, there is another important factor, by accurately determining the indication of which you can make the correct treatment for the patient, and it is called risk. Its value is made up of the summation of blood pressure readings, as well as aggravating factors, such as:

• Bad habits;
• Excess weight;
• Glucose level;
• Heredity;
• Age;
• An indicator of cholesterol in the blood;
• Associated diseases.

Risks are of four degrees, they are diagnosed when there is a certain percentage of the likelihood of complications affecting the vessels and the heart.

For grade 1 hypertension, symptoms and treatment in most cases correspond to grade 1 and 2 risk. Subsequent levels of risk come with aggravating factors that are rare in the initial stage. If a patient with hypertension excessively consumes alcohol, then it complicates the course of the disease.

Causes of hypertension of the 1st degree

Pathological abnormalities in the activity of the heart can be caused by various factors, and their dangerous combination. The reasons for the pressure surges are:

• Bad habits. Smoking causes constriction of blood vessels. Wrong nutrition.
• Physical passivity or vice versa excessive loads.
• Age: for women (over 50), for men (over 65). Although recently there has been a significant "rejuvenation" of this disease.
• hereditary predisposition. The more relatives suffer from this disease, the greater the likelihood of its occurrence.
• Pregnancy. At this wonderful time, mother experiences exorbitant physical exertion, hormonal failure and restructuring of the body, cases of nervous breakdowns are not uncommon. A mixture of these hazards results in pressure buildup.
• Taking medications that cause side effects in the form of increased pressure. It can be dietary supplements or oral contraceptives.
• Stress and constant psychological experiences lead to heart failure, in which adrenaline is released, and it constricts blood vessels.
• The presence of the following diseases: diabetes mellitus, atherosclerosis (formation of plaques on the inside of the vessels), kidney and hypothalamus disease, pyelonephritis.
• Deviation in the work of the thyroid gland and adrenal glands.
• A sharp change in climatic conditions.
• Excess salt. An ordinary food product, without which not a single dish can do, can, if it is overabundant, cause a spasm of the arteries and cause the accumulation of fluid in the body.
• Chronic fatigue and lack of sleep.

All these reasons can provoke the appearance of arterial hypertension of the 1st degree.

Diagnostics

People who have already experienced high blood pressure should be examined annually, the same applies to those who first showed signs of hypertension. To confirm the diagnosis previously made by the doctor, you need to undergo a hardware examination.

In addition to these studies, you need to visit an ophthalmologist who checks the fundus. The eyes, like the heart, are most often affected by hypertension. The expansion of the veins located in the retina of the eye can be irreversible, this change must be stopped if the vessels are detected in time to return to normal.

What tests are needed?

When the question arises whether hypertension of the 1st degree can be cured, the answer is yes, if all the necessary studies have been completed and tests have been passed, which include:

• Urinalysis;
• General and biochemical blood test;
• Hormone testing for women.

As a result of the first two analyzes, it is estimated:

• Metabolism of carbohydrates and glucose levels;
• The work of the kidneys in the presence of uric acid and creatinine;
• Electrolytic exchanges: sodium, potassium, phosphate and calcium;
• Fat deposits: the presence of cholesterol, triglycerides and HDL;
• The degree of damage to the heart and kidneys;
• condition of the vessel walls.

Hormonal examinations are used only for the weak half of humanity; for their conduct, blood is taken from a vein on certain days of the menstrual cycle:

• Prolactin and LH for 3-5 days;
• Progesterone and estradiol on the 20th day of the cycle;
• Testosterone, androstenedione, 17-OH progesterone on days 7-10.

These tests are necessary to establish a complete picture of the course of the disease and prescribe an effective treatment for grade 1 hypertension. Basically, everyone starts taking blood pressure lowering drugs, but they do not eliminate the causes of the disease, for this the doctor must prescribe complex therapy.

Treatment

When the results of tests and studies confirm the presence of hypertension, the question of how to treat grade 1 hypertension is immediately considered.

The doctor will advise you to change your lifestyle and introduce more rest into it, try to avoid stressful situations, supplement the day with physical exercises and walking, start eating right.

Diet for hypertension 1 degree

You need to reconsider your diet and, if possible, try not to use salt, replacing it with other products, such as vinegar or citric acid, but within reasonable limits. Diet is very important with high blood pressure, properly selected foods can help blood vessels, the main focus should be plant foods.

List of foods that lower blood pressure:

1. Green tea and hibiscus.
2. Gourds - melons and watermelons. They are known for their diuretic properties.
3. Dairy products, their main component is calcium, which actively lowers blood pressure. It is also found in almonds and green vegetables.
4. Foods containing magnesium: cereals (oats, buckwheat and wheat), walnuts, beans, beets, black currants and carrots.
5. Sour foods: grapefruit, celery, viburnum, chokeberry, quince and cranberries.
6. Calcium-rich foods include oranges, tuna, tomatoes, dried apricots, zucchini, and bananas.
7. Products that can thin the blood - garlic.

It is worth reducing and over time completely eliminating from the use of such products:

• Smoked meats, spicy and salty dishes;
• Foods high in caffeine;
• Fatty fish and ice cream;
• Foods with a high starch content: semolina, potatoes, white flour muffins and corn;
• Confectionery with butter cream;
• by-products;
• Sharp and specific spices.

If you stick to such a diet, you can not only help the vessels return to normal, but also significantly lose weight without exhausting yourself with endless diets on one product. The main feature of the treatment is to refuse products from the "black" list gradually so that the body can adapt to their absence.

When exercise and diet do not quite cope with the disease, it is necessary to supplement the treatment for grade 1 hypertension with drugs. But they should be prescribed by a doctor, under no circumstances should you self-medicate.

Drugs for hypertension 1 degree

The standard approach to drug treatment is to prescribe the following drugs:

• Neurotropic agents that relieve stress and soothe. These include: antidepressants (amitriptyline), tranquilizers (diazepam and trioxazine), and sedatives (valerian and bromine-based drugs).
• Diuretics, these tablets for hypertension of the 1st degree help to remove salt and excess water from the body. Effective are: furosemide, lasix, hydrochlorothiazide and amiloride.
• Vasodilator drugs: vasonite, molsidomine or apressin.

The choice of drugs and their dosage is fully prescribed by the doctor.

Complications

Hypertension of the 1st degree occurs with a slight increase in pressure, but despite this, it can cause serious complications:

• On the kidneys. In them, sclerosis of tissues and blood vessels occurs. Their activity and the function of urea distillation are disturbed, protein appears in the urine. The next step will be kidney failure.
• To the brain. Thrombosis appears in its vessels, vessels are disturbed, which first lead to small heart attacks occurring in the deep parts of the brain. High blood pressure can lead to stroke and heart attack. Due to impaired blood supply, the brain begins to decrease in size and can cause dementia.
• For vessels. They are located throughout the body, and the disease can affect completely different places. If it touches the retina of the eyes, it will result in loss of vision.
• On the heart. With hypertension, the load falls on the left ventricle of the heart, its muscle increases and leads to myocardial infarction. Also, this condition threatens the appearance of angina pectoris and even death.

Some of the above complications entail loss of working capacity and disability, which once again proves that it is better to treat the disease at its very beginning.

Do they take to the army with hypertension of the 1st degree?

In peacetime, conscripts with such a diagnosis, after being confirmed by appropriate examinations, may not be recognized as fit for military service. This is stipulated in article 43 on the schedule of diseases.

To receive an exemption, you need to have blood pressure readings within the limits indicated in the article, that is, 140/90 and above.

Prevention

If there is a predisposition to hypertension, then it is better to prevent it than to spend a lot of effort and money on treatment, the following actions will help:

• Regular exercise or walking;
• Maintaining your weight;
• To give up smoking;
• Undergo periodic blood sugar checks;
• Regularly measure blood pressure;
• After a busy day, arrange a rest;
• Sleep at least 8 hours a day;
• Do an ECG of the heart.

It is quite possible to cure hypertension of the 1st degree if desired. An integrated approach to treatment will not only relieve further suffering from the complications of this disease, but also prolong life.

What is heart failure: symptoms, signs and treatment of the disease

Heart failure - what is it? This is a pathological condition that appears in the event of a malfunction of the heart, when the blood is not pumped in the proper volume. Acute heart failure can lead to death in a short time, as there is a high probability of dangerous complications. Chronic HF develops gradually and leads to prolonged "starvation" of body tissues.

Causes of the disease

Why does heart failure occur? This condition occurs due to various etiological factors. Most often, the etiology of this disease is associated with atherosclerosis and arterial hypertension. Increased pressure in the bloodstream and atherosclerotic narrowing of the lumen of the vessels lead to the fact that it becomes difficult for the heart to push blood. The body's resources allow compensating for this pathological condition - at first there are no clinical symptoms of circulatory failure due to an increase in heart rate and an increase in the strength of heart contractions. When the myocardium is depleted, decompensation of the disease occurs - this is manifested by shortness of breath, edema, and a decrease in tolerance to physical stress. These are all symptoms of congestive heart failure (CHF).

The pathogenesis of heart failure also includes diseases accompanied by direct damage to the heart. These are myocarditis, valvular defects, infectious and autoimmune diseases, intoxications. In diseases of the lungs, an increase in pressure in the small circle can often occur. All these reasons lead to an increase in the load on the heart, due to which the efficiency of the organ is significantly reduced. This can also happen with fluid retention in the body, for example, with kidney disease.

In many cases, the causes of heart failure and the etiology of this condition are due to a past heart attack. Most often, this leads to acute heart failure with the rapid development of complications and the death of the patient.

Types of heart failure

This disease is classified according to the rate of development of the clinic:

• acute HF - progresses in a very short time (a few minutes - a few hours). Complications of this type of disease often become pulmonary edema or shock of a cardiogenic nature. The most common causes of AHF are heart attack, valve defects (aortic and mitral), damage to the walls of the heart;
• chronic HF - progresses over many months or years. The cause of CHF is compensated pathological conditions with damage to the heart and other organs (arterial hypertension, malformations, chronic lung diseases, etc.).

Classification

There are several ways to classify heart failure. Depending on the severity of the clinic, the following are distinguished:

• First degree - no clinical symptoms.
• In the second degree of heart failure, the symptoms are mild, wheezing may be present.
• The third degree is a more pronounced clinical picture, the presence of wheezing.
• The fourth degree of severity is characterized by the presence of complications, for example, cardiogenic shock, collapse (decrease in systolic blood pressure below 90 mm Hg).

According to the degree of patient's resistance to physical activity, heart failure is divided into four functional classes (FC):

• 1 FC - shortness of breath and other symptoms appear with severe physical exertion, for example, during the ascent to the third floor and above. Normal physical activity does not cause symptoms of the disease.
• 2 FC - moderate heart failure, it makes itself felt only after climbing two flights of stairs or when walking fast. The patient's daily activities may be slightly reduced.

• 3 FC - the symptoms of the disease become pronounced even with small physical exertion and during daily activities. At rest, shortness of breath completely disappears.
• 4 FC - in this case, shortness of breath and other manifestations disturb the patient at rest. The heart is under heavy stress, complications of heart failure are often observed.

Types of heart failure according to its classification by stages:

• The first stage is the onset of the disease. It is characterized by a latent course, the symptoms of circulatory failure occur only in cases where the patient experiences a pronounced physical or emotional stress. At rest, the activity of the circulatory system is not disturbed.
• The second stage is marked clinical manifestations. There are signs of prolonged stagnation of blood, this is noticeable in the absence of physical activity. Stagnation appears in the large and small circles of blood circulation, which is primarily manifested by edema. This stage is subdivided into IIA and IIB. The first is characterized by impaired function of only the left or right ventricle. In this case, shortness of breath appears during normal physical exertion for a person, its activity is markedly reduced. Outwardly, the patient has blue skin, swelling of the legs, enlarged liver and hard breathing. Stage IIB is characterized by a deeper degree of hemodynamic disturbances, the cause of which is stagnation in both circles of blood circulation.
• The third stage of the disease is terminal. In this case, the heart ceases to cope with its function, which leads to irreversible damage to the structure of internal organs, to the depletion of their resources.

Signs and symptoms of the disease

The clinical symptoms of heart failure are the same for both acute and chronic variant of this pathology. The difference lies in the rate of development of the manifestations of the disease and the body's ability to adapt to changes in hemodynamics. Therefore, in acute circulatory failure, full compensation does not occur, as a result of which the terminal stage quickly sets in and the risk of death increases. The chronic variant of the disease may not manifest itself for a long time, and therefore the diagnosis and treatment are often belated.

How to recognize heart failure? The clinical picture consists of symptoms associated with stagnation of blood in the vessels due to the inability of the heart muscle to fully perform its function. As a result, edema appears on the lower extremities and stagnation in the pulmonary circulation, which causes wheezing. The patient loses the ability to adequately cope with physical and emotional stress, so the conceived efforts of normal intensity lead to shortness of breath.

Stagnation of blood leads to disruption of oxygen transport in tissues - hypoxia develops, metabolism changes, cyanosis (cyanosis) of the skin of the extremities, nasolabial triangle appears.

Headache. This symptom is not characteristic of heart failure. Loss of consciousness, dizziness, darkening of the eyes are more likely.

Nausea and vomiting. Such manifestations of heart failure are also not characteristic of this disease. However, in rare cases, they may indicate the development of metabolic disorders.

Drowsiness. Decreased performance, fatigue and drowsiness may be the result of circulatory failure, which leads to a decrease in oxygen saturation of tissues.

Heart failure in newborns and adolescents

This disease in children and newborns is quite difficult to diagnose, as it often resembles manifestations of other pathologies. The cause of HF at an early age is usually associated with congenital diseases:

• heart defects;
• CNS lesions;
• glycogen disease, cardiac form;
• fibroelastosis of the endocardium.

It is also worth taking into account that this condition can occur with infectious diseases caused by viruses or bacteria.

There are no significant differences in how heart failure manifests itself in children. Usually the symptomatology consists in the appearance of shortness of breath and edema, increased heart rate. The main changes in the internal organs - the liver increases, the boundaries of the heart expand.

Heart failure in adolescents occurs when they have a heart defect. Signs of heart failure in adolescents do not differ from those in children and adults, which helps to establish the diagnosis.

Methods for diagnosing heart failure

Heart failure syndrome is a secondary disease that occurs against the background of other pathologies. In this regard, examination and diagnostic measures should be aimed primarily at identifying the cause of this condition. Early diagnosis of circulatory insufficiency is important, when there are no pronounced clinical symptoms.

For those patients who have been diagnosed with a heart attack and other myocardial diseases, arterial hypertension, it is important to pay attention to the presence of such a symptom as shortness of breath that occurs during physical exertion. Other characteristic signs that make it possible to suspect the presence of heart failure are edema in the lower extremities, expansion of the borders of the heart to the left side.

The pulse in patients with circulatory failure is usually low-amplitude. An increase in heart rate is also characteristic.

CBC in HF is nonspecific or reflects changes caused by the primary pathology. More specific are the analysis of blood gases and electrolytes. It is also important to determine the pH of the blood, the level of creatinine, urea and indicators of protein metabolism in biochemical analysis. It is possible to determine the level of cardiospecific enzymes, which can increase both in HF and in myocardial ischemia.

Diagnosis of heart failure is largely determined by the indications of instrumental research methods. According to the ECG, signs of myocardial hypertrophy are determined, which develops in response to an increased load on the heart muscle. You can also determine rhythm disturbances or signs of ischemia of the muscle tissue of the heart.

There are special stress tests, which are an ECG with physical activity. This is possible when using an exercise bike or treadmill. The load is gradually increased, due to which it is possible to determine the functional class of heart failure and the presence of signs of myocardial ischemia.

Echocardiography makes it possible to both determine heart failure and visualize the structure of the heart in order to determine the cause of its dysfunction. At the same time, echocardiography evaluates the functional state of the heart, for example, ejection fraction and other indicators of pumping function. MRI makes it possible to determine the presence of defects in this organ. X-ray of the lungs and chest organs shows the presence of stagnation in the pulmonary circulation.

To determine the degree of damage to other internal organs in severe circulatory failure, an abdominal ultrasound is performed. It shows changes in the spleen, liver, pancreas and other organs.

Ways to treat the disease

Treatment of heart failure involves conservative therapy. It includes the following areas:

• reduction of clinical manifestations of circulatory failure. For this, cardiac glycosides are prescribed - for AHF, intravenous fast-acting drugs are used, for CHF - long-acting drugs;
• reducing the load on the myocardium - this is achieved by using beta-blockers, which lower blood pressure and slow down the pulse;
• the appointment of diuretics in order to reduce the total amount of fluid in the body.

It is worth noting that it is impossible to cure heart failure, you can only reduce its symptoms and signs. The best results are obtained by the treatment of heart failure of the first degree. A patient who has taken all the recommended drugs in this case may not notice an improvement in his condition.

If the patient has a history of arrhythmia, which may have caused the development of myocardial insufficiency, then surgical treatment is possible. It consists in the implantation of an artificial pacemaker. Surgical treatment is also indicated in those cases. When there is a significant narrowing of the lumen of the arteries due to atherosclerosis, when there is a pathology of the valves.

What is dangerous heart failure, consequences and complications

Circulatory insufficiency is progressive in nature, as a result of which, in the absence of proper therapy for this condition, the patient's condition worsens over time, the degree of hemodynamic disorders increases, which often leads to death.

Frequent consequences of heart failure occur due to pulmonary edema, when there is stagnation in the pulmonary vessels, the liquid part of the blood penetrates into the tissues of this organ. Because of this, the ability of the lungs to saturate the blood with oxygen sharply decreases, hypoxia develops.

With circulatory failure, signs of cerebral ischemia may appear, which is manifested by fainting, dizziness, darkening in the eyes.

Heart failure of the 1st degree is usually the least likely to lead to serious consequences.

Disease prevention

Prevention of heart failure is based on the treatment of diseases, the development of which leads to circulatory failure - hypertension, valve defects, etc. On the other hand, it is important to adjust the patient's lifestyle in order to reduce the number of risk factors.

If the function of the heart is already impaired, then the prevention of heart failure should be aimed at maintaining the optimal level of daily physical activity, constant monitoring by a cardiologist, and taking prescribed drugs.

What to do with heart failure to increase the chances of recovery of the body? In addition to taking medications, correction of the patient's lifestyle plays an important role in the treatment of circulatory insufficiency. In order for the treatment to be effective, people with this disease must reduce their body weight to normal values, since excess weight is one of the most common causative factors for hypertension.

Patients with this pathology are advised to follow a diet. It consists primarily in limiting salt intake. Patients with heart failure should completely abandon this flavor enhancer, since salt reduces the excretion of fluid from the body, which leads to an increase in the load on the myocardium.

If the patient smokes or drinks alcohol, then these habits will have to be completely abandoned.

You also need to exercise regularly. Depending on the severity of the disease, the allowable volume of loads also changes. For example, in functional class III, regular walking for about 40 minutes is sufficient, and in milder cases of circulatory failure, special exercises can be added. Physiotherapy is prescribed by the attending physician, so you should not independently increase the daily amount of physical exercise without knowing the whole picture of the disease. At the same time, the symptoms and treatment of severe heart failure do not allow the patient to carry out this method of rehabilitation.

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Chronic heart failure(CHF) - a cardially caused violation of the (pumping) function with the corresponding symptoms, which consists in the inability of the circulatory system to deliver the amount of blood necessary for their normal functioning to the organs and tissues.
Thus, this is a disproportion between the state of blood circulation and the metabolism of substances, 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.
From the modern clinical point of view, CHF is a disease with a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.), which are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body.

The root cause is a deterioration in the ability of the heart to fill or empty, due to damage to the myocardium, as well as an imbalance in the vasoconstrictor and vasodilating neurohumoral systems. It would seem a trifle: before the syndrome, now the disease.
It would be hard to imagine if there were no data that CHF is clearly associated with the gender of specific genes, and this already “pulls” for nosology.

Chronic heart failure is characterized by recurrent episodes of exacerbation (decompensation), manifested by a sudden or, more often, a gradual increase in symptoms and signs of CHF.

Epidemiology. The prevalence of clinically pronounced CHF in the population is at least 1.8-2.0%.
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 LV dysfunction 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%.

The reasons. CHF can develop against the background of almost any disease of the cardiovascular system, however, the main three are the following supra-nosological forms: coronary artery disease, arterial hypertension and 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) most often lead 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, Russia 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 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.
The fundamental "novelty" of modern ideas about the pathogenesis of CHF is associated with the fact that not all patients have symptoms of decompensation as a result of a decrease in the pumping (propulsive) ability of the heart.
Important factors in the development and progression of CHF are a decrease in cardiac output (in most patients), sodium retention and excess fluid in the body.

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. Basically, these are the sympathetic-adrenal system (SAS) and its effectors - norepinephrine and adrenaline and the renin-angiotensin-aldosterone system (RAAS) and its effectors - angiotensin II (A-11) 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 LV dysfunction (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 Sterling mechanism helps maintain CO, but the resulting chronic rise in diastolic pressure will be transmitted to the atria, pulmonary veins, or systemic veins. Increasing capillary pressure is accompanied by fluid extravasation with the development of edema. Reduced CO, especially with a decrease in blood pressure, activates the SAS, simulating 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 the rest of its leading components - 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 [Boitsov S.A. 1995].

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

CHF 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 are allocated (FC) CHF.
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.

The easiest way to determine the FC in patients is by the distance of a 6-minute walk.
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.

Clinical manifestations. 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; 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 CHF.
stopping the diagnosis of CHF is possible in the presence of 2 key criteria:
1) characteristic symptoms of heart failure (mainly shortness of breath, fatigue and limitation of physical activity, swelling of the ankles);
2) objective evidence that these symptoms are related to damage to the heart and not to any other organs (eg, lung disease, anemia, kidney failure).

It should be emphasized that CHF symptoms may be present at rest and/or during exercise.
At the same time, objective signs of cardiac dysfunction must be detected at rest.
This is due to the fact that the appearance of such a sign (for example, low LV EF) during exercise (for example, in a patient with coronary artery disease) may not be a sign of HF, but of coronary insufficiency.
By analogy with LV EF, this also applies to other objective signs of myocardial damage.

In doubtful cases, the diagnosis of HF can be confirmed by a positive response to therapy, in particular, to the use of diuretics.

A standard diagnostic set of laboratory tests in a patient with HF should include determination of hemoglobin, red blood cells, white blood cells, and platelets, plasma electrolytes, creatinine, glucose, liver enzymes, and urinalysis.
Also, as necessary, it is possible to determine the level of C-reactive protein (exclusion of inflammatory etiology of heart disease), thyroid-stimulating hormone (exclusion of hyper- or hypothyroidism), urea and plasma uric acid. With a sharp deterioration in the patient's condition, it is advisable to assess the content of cardiospecific enzymes in order to exclude acute MI.

Anemia refers to a factor that aggravates the course of CHF. Elevated hematocrit may indicate a pulmonary origin of dyspnea, as well as be a consequence of cyanotic heart defects or pulmonary arteriovenous fistula.

An increase in the level of creatinine in a patient with CHF can be:
associated with primary pathology of the kidneys;
a consequence of a concomitant disease or condition (hypertension, diabetes, advanced age);
a consequence of heart failure (renal hypoperfusion, congestive kidney);
associated with excessive intake of diuretics and / or iALF.

With stagnation of blood in the liver, an increase in the activity of liver enzymes can be observed.
Urinalysis is useful to detect proteinuria and glucosuria, which will allow us to conclude that there may be an independent primary renal pathology or DM - conditions that provoke the development or aggravate the course of HF.

Hyponatremia and signs of renal dysfunction in HF indicate a poor prognosis.

Echocardiography. This is an imaging technique, which is given a paramount role in the diagnosis of CHF due to its ease of implementation, safety and ubiquity.
Echocardiography allows solving the main diagnostic problem - to clarify the very fact of dysfunction and its nature, as well as to conduct a dynamic assessment of the state of the heart and hemodynamics.

The most important hemodynamic parameter is the LV EF, which reflects the contractility of the LV myocardium.
It is better to determine the normal level of LV EF for each laboratory.
This is due to the population characteristics of the population, equipment, counting methods, etc.
In the literature, "normal" levels range from EF > 50% (MONICA, V-HeFT-I) to > 35% (SOLVD).

As an “average” indicator, we can recommend a “normal” LV EF > 45%, calculated by the 2-dimensional echocardiography no Simpson.
Methods for assessing the severity of CHF. Assessment of the severity of the patient's condition and especially the effectiveness of the treatment is an urgent task for every practitioner.
From this point of view, a single universal criterion for the condition of a patient with CHF is needed.
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. The use of a simple and affordable 6-minute corridor walk test makes it possible to quantitatively measure the severity and dynamics of the state of a patient with CHF during treatment and his tolerance to physical activity.
In addition to the dynamics of FC and exercise tolerance, to monitor the condition of patients with CHF, an assessment of the patient's clinical condition (severity of dyspnea, diuresis, changes in body weight, degree of congestion, etc.) is used; dynamics of LV EF (in most cases according to the results of echocardiography); assessment of the quality of life of the patient, measured in points using special questionnaires, the most famous of which is the questionnaire of the University of Minnesota, designed specifically for patients with CHF.

Forecast. The annual mortality rate in patients with CHF of functional class I according to the classification of the New York Heart Association (FC NYHA) is about 10%, with II FC - 20%, with III FC - 40%, with IV FC - more than 60%. Despite the introduction of new methods of therapy, the mortality rate of patients with CHF does not decrease.

Treatment of CHF.
The goals of CHF treatment are to eliminate or minimize the 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 striated muscles; improving the quality of life, increasing 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 1 FC - less than 3 g per day, for patients with II-III FC - 1.2-1.8 g per day, for IV FC - less than 1 g per day.

Physical rehabilitation. Options - walking or 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 CHF.
The entire list of drugs used to treat CHF is divided into three groups: main, additional, auxiliary.

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

An additional group, the efficacy and safety of which has been proven by large studies, however, requires clarification (carrying out a meta-analysis): aldosterone antagonists, A-H 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, and statins.

Despite the large selection of drugs in the treatment of patients, polypharmacy (unjustified prescription of a large number of groups of drugs) is unacceptable.

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.

Below is a description of the drugs of the main group.

ACE inhibitors. In Russia, the efficacy and safety of the following ACE inhibitors in the treatment of CHF has been fully proven: captopril, enalapril, ramipril, fosinopril, trandolapril.
The appointment of an ACE inhibitor is indicated for all patients with CHF, regardless of the stage, functional class, etiology and nature of the process.
Non-appointment of ACE inhibitors leads to an increase in mortality in patients with CHF. The earliest appointment of ACE inhibitors, already in FC I CHF, can slow down the progression of CHF.
ACE inhibitors can be prescribed to patients with CHF at blood pressure levels above 85 mm Hg. Art.
With an initially low blood pressure (85-100 mm Hg), the effectiveness of ACE inhibitors is preserved, so they should always be prescribed, reducing the starting dose by half (for all ACE inhibitors).

Arterial hypotension may occur immediately after the start of ACE inhibitor therapy due to the rapid effect on circulating neurohormones.
With therapy in titrating doses, this effect either does not occur or decreases at most by the end of the second week of therapy.
And the long-term effect of ACE inhibitors is realized through the blockade of tissue neurohormones.
Minimization of arterial hypotension is achieved by refusing the simultaneous appointment of ACE inhibitors and vasodilators of b-blockers, CCBs, nitrates), after stabilization of the level of blood pressure, if necessary, you can return to the previous therapy; refusal of previous active diuretic therapy, especially the day before, in order to avoid the potentiating effect of drugs.

In patients with initial hypotension, short-term use of small doses of steroid hormones - 10-15 mg / day is possible, however, if the initial systolic blood pressure (BP) is less than 85 mm Hg. Art., ACE inhibitor therapy is not indicated.

The start of therapy with any ACE inhibitor should begin with the minimum (starting) doses, which are discussed below.
Possible adverse reactions, in addition to arterial hypotension, when prescribing an ACE inhibitor (in the amount of not more than 7-9% of the reasons for withdrawal) are: dry cough, an increase in the degree of CRF in the form of azotemia, hyperkalemia.
Dry cough, which occurs in about 3% of cases, is due to the blockade of the destruction of bradykinin in the bronchi.
The possibility of prescribing an ACE inhibitor in the presence of chronic bronchitis or bronchial asthma has been proven, while the degree of cough does not increase.
Fosinopril has the least risk of this side effect.

With a decrease in glomerular filtration rate below 60 ml / min, the doses of all ACE inhibitors should be halved, and with a decrease below 30 ml / min by 3/4. The same applies to the treatment of elderly patients with CHF, in which renal function is usually impaired.

An exception is fosinopril, the dose of which does not need to be adjusted in renal insufficiency and in elderly patients, since it has two routes of excretion from the body - the kidneys and the gastrointestinal tract.
Spirapril also has a balanced dual route of excretion from the body, which also makes it possible to recommend it to patients with renal insufficiency.

Basic principles of dosing ACE inhibitors. There is a concept of starting and maximum (target) doses for each specific drug. Doubling the dose of the drug is carried out no more than 1 time per week (titration), provided that the patient feels well, there are no adverse reactions, and the level of blood pressure is at least 90 mm Hg. Art.
Antagonists of AN receptors (candesartan) - can be used along with ACE inhibitors as a first-line agent for blockade of the RAAS in patients with clinically severe decompensation.
Do not lose their effectiveness in women (unlike ACE inhibitors).
At the same time, a preventive effect in preventing symptomatic CHF has not been proven, and there is no effectiveness in CHF with preserved LV systolic function, when the effectiveness of ACE inhibitors is preserved.
The ability to prevent the development of CHF in patients with diabetic nephropathy has been proven for another representative of the class of angiotensin II receptor antagonists (ArATP) - losartan.

Aldosterone antagonists(spironolactone) has been successfully used in complex diuretic therapy for severe CHF as a potassium-sparing diuretic since the mid-1960s.
The indication for such use of the drug is the presence of decompensated CHF, hyperhydration and the need for treatment with active diuretics. It is as a reliable partner of thiazide and loop diuretics that the appointment of spironolactone should be considered.
In the period of achieving compensation (especially in patients with CHF III-IV FC), the use of spironolactone is absolutely necessary and you can not be afraid of combining its high doses with ACE inhibitors or ArATP if active diuretics are used correctly in parallel and positive diuresis is achieved.
However, after reaching the state of compensation, the use of high doses of spironolactone is stopped and the issue of long-term administration of low doses of the drug as an additional neurohormonal modulator is considered.
Only the combination of high doses of spironolactone and high doses of ACE inhibitors is not recommended for long-term treatment of CHF. To achieve a state of compensation during exacerbation of CHF and hyperhydration, such a combination, as mentioned above, is indicated, but requires careful monitoring of potassium and creatinine levels.
With exacerbation of decompensation phenomena, spironolactone is used in high doses (100-300 mg, or 4-12 tablets, administered once in the morning or in two doses in the morning and afternoon) for a period of 1-3 weeks until compensation is achieved.
After this, the dose should be reduced.
The criteria for the effectiveness of the use of spironolactone in the complex treatment of persistent edematous syndrome are: an increase in diuresis within 20-25%; reduction of thirst, dry mouth and the disappearance of a specific "liver" odor from the mouth; stable concentration of potassium and magnesium in plasma (no decrease) despite the achievement of positive diuresis.
In the future, for long-term treatment of patients with severe decompensation of III-IV FC, it is recommended to use small (25-50 mg) doses of spironolactone in addition to ACE inhibitors and β-blockers as a neurohumoral modulator, which allows more complete blocking of the RAAS, improve the course and prognosis of patients with CHF.
The concentration of spironolactone in the blood plasma reaches a plateau by the third day of treatment, and after discontinuation (or a decrease in the dose of the drug), its concentration and effect disappear (decrease) after three days.
Of the based adverse reactions of spironolactone (except for possible hyperkalemia and an increase in creatinine levels), the development of gynecomastia (up to 10% of patients) should be noted.
In the presence of an elevated serum creatinine level (> 130 μmol / l), a history of renal failure, hyperkalemia, even moderate (> 5.2 μmol / l), the combination of aldosterone antagonists with ACE inhibitors requires careful clinical and laboratory monitoring.

Diuretics (diuretics).

The main indication for the appointment of diuretics is the clinical signs and symptoms of excessive fluid retention in the body of a patient with CHF. However, it should be remembered that diuretics have two negative properties - they hyperactivate the neurohormones of the renin-angiotensin-aldosterone system, and also cause electrolyte disturbances.

Principles of diuretic therapy:
- combined with ACE inhibitors, which allows to reduce the dose of diuretics with the same clinical effect;
- the weakest of the effective diuretics is prescribed in order to prevent the development of the patient's dependence on diuretics, as well as to be able to have a reserve for the type and dose of the diuretic during the period of CHF decompensation;
- are prescribed daily in the minimum dose with the achievement of a positive fluid balance in diuresis in the phase of therapy for decompensation of CHF 800-1000 ml, with maintenance therapy - 200 ml under the control of body weight.

Characteristics of the most commonly used diuretics.

Currently, two groups of diuretics are mainly used - thiazide and loop.
From the group of thiazide diuretics, preference is given to hydrochlorothiazide, which is prescribed for moderate CHF (NYHA II-III FC). At a dose of up to 25 mg per day, it causes a minimum of adverse reactions; at a dose of more than 75 mg, diselectrolyte disorders can be recorded.
The maximum effect is 1 hour after administration, the duration of action is 12 hours.

One of the most powerful loop diuretics is furosemide, the initial effect is after 15-30 minutes, the maximum effect is after 1-2 hours, the duration of action is 6 hours.
The diuretic effect also persists with reduced kidney function. The dose varies from the severity of CHF symptoms - from 20 to 500 mg per day.
Recommended to take in the morning on an empty stomach.

Ethacrynic acid is a drug similar to furosemide, however, due to its action on various enzymatic systems of the loop of Henle, it can be used in the development of refractoriness to furosemide, or combined with it for persistent edema.
Dosage - 50-100 mg per day, the maximum dose is 200 mg.
Recommended to take in the morning on an empty stomach.

Dehydration therapy for CHF has two phases - active and maintenance.
In the active phase, the excess of excreted urine over the ingested liquid should be 1-2 liters per day, with a decrease in weight daily ~ 1 kg. No rapid dehydration can be justified and only leads to hyperactivation of neurohormones and rebound fluid retention in the body.

In the maintenance phase, diuresis should be balanced and body weight stable with regular (daily) diuretic administration.
The most common mistake in the appointment of diuretics in Russia is an attempt to "shock" diuresis (once every few days).

It is difficult to imagine a more erroneous treatment strategy, both taking into account the quality of life of the patient and the progression of CHF.

Algorithm for prescribing diuretics(depending on the severity of CHF) appears as follows:
IFC - do not treat with diuretics,
II FC (without stagnation) - do not treat with diuretics,
II FC (stagnation) - thiazide diuretics, only if they are ineffective, loop diuretics can be prescribed,
III FC (decompensation) - loop (thiazide) + aldosterone antagonists, in doses of 100-300 mg / day,
III FC (maintenance treatment) - thiazide (loop) + spironolactone (small doses) + acetazolamide (0.25 x 3 times / day for 3-4 days, every 2 weeks),
IV FC - loop + thiazide (sometimes a combination of two loop diuretics furosemide and uregit) + aldosterone antagonists + carbonic anhydrase inhibitors (acetazolamide 0.25 x 3 times / day for 3-4 days, every 2 weeks).

With refractory edematous syndrome, there are the following methods for overcoming resistance to the use of diuretics:
- the use of diuretics only against the background of ACE inhibitors and spironolactone;
- the introduction of a larger (twice as high as the previous ineffective dose) dose of a diuretic and only in / in (some authors suggest administering furosemide (lasix) twice a day and even constantly in / in drip);
- a combination of diuretics with drugs that improve filtration (with blood pressure more than 100 mm Hg. Art.
- eufillin 10 ml of a 2.4% solution intravenously drip and immediately after the dropper - lasix or SG, with lower blood pressure - dopamine 2-5 mcg / min);
- the use of diuretics with albumin or plasma (possible together, which is especially important for hypoproteinemia, but also effective in patients with normal plasma protein levels);
- with severe hypotension - a combination with positive inotropic agents (dobutamine, dopamine) and, in extreme cases, with glucocorticoids (only for the period of critical hypotension);
- a combination of diuretics according to the principles indicated above; mechanical methods of fluid removal (pleural, pericardial puncture, paracentesis) - are used only for vital indications; isolated ultrafiltration (contraindications - valvular stenosis, low cardiac output and hypotension).

cardiac glycosides.
Currently, the most common cardiac glycoside in Russia is digoxin, the only drug from the group of positive inotropic agents that remains in wide clinical practice for long-term treatment of CHF.

Non-glycoside agents that increase myocardial contractility adversely affect the prognosis and life expectancy of patients and can be used in the form of short courses in decompensated CHF.
The effect of SG is currently associated not so much with their positive inotropic effect, but with a negative chronotropic effect on the myocardium, as well as with the effect on the level of neurohormones, both circulating and tissue, as well as with the modulation of the baroreflex.

Based on the characteristics described above, digoxin is a first-line drug in patients with CHF in the presence of a permanent tachysystolic form of AF.
In sinus rhythm, the negative chronotropic effect of digoxin is weak, and myocardial oxygen consumption increases significantly due to the positive inotropic effect, which leads to myocardial hypoxia.

Thus, it is possible to provoke various rhythm disturbances, especially in patients with ischemic etiology of CHF.

So, the optimal indications for prescribing SG are as follows: permanent tachysystolic form of MA; severe CHF (III-IV functional class NYHA); ejection fraction less than 25%; cardiothoracic index over 55%; non-ischemic etiology of CHF (DCMP, etc.).

Principles of treatment at the present time: the appointment of small doses of SG (digoxin no more than 0.25 mg per day) and, which is desirable, but problematic in all-Russian practice, under the control of the concentration of digoxin in the blood plasma (no more than 1.2 ng / ml).
When prescribing digoxin, it is necessary to take into account its pharmacodynamics - plasma concentration increases exponentially by the eighth day from the start of therapy, therefore, such patients should ideally perform daily ECG monitoring in order to control rhythm disturbances.
A meta-analysis of studies on digoxin, conducted according to the rules of evidence-based medicine, showed that glycosides improve the quality of life (through the reduction of CHF symptoms); the number of hospitalizations associated with exacerbation of CHF is reduced; however, digoxin does not affect the prognosis in patients.

b-blockers.
In 1999, in the USA and European countries, and now in Russia, b-blockers are recommended for use as the main means for the treatment of CHF.

Thus, the postulate about the impossibility of prescribing drugs with a negative inotropic effect to patients with CHF was refuted.
The effectiveness of the following drugs has been proven:
- carvedilol - has, along with b-blocking activity, antiproliferative and antioxidant properties;
- bisoprolol - the most selective b1-receptor selective b-blocker;
- metoprolol (retard form with slow release) - a selective lipophilic b-blocker.

Principles of therapy with b-blockers.
Before the appointment of b-blockers, the following conditions must be met:
- the patient should be on a regulated and stable dose of an ACE inhibitor that does not cause arterial hypotension;
- it is necessary to strengthen diuretic therapy, since due to a temporary short-term decrease in pumping function, an exacerbation of CHF symptoms is possible;
- if possible, cancel vasodilators, especially nitropreparations, with hypotension, a short course of corticosteroid therapy (up to 30 mg per day orally) is possible;
- the starting dose of any b-blocker in the treatment of CHF is 1/8 of the average therapeutic dose: 3.125 mg for carvedilol; 1.25 - for bisoprolol; 12.5 - for metoprolol; doubling the dosages of b-blockers no more than once every two weeks, provided the patient is stable, there is no bradycardia and hypotension;
achievement of target doses: for carvedilol - 25 mg twice a day, for bisoprolol - 10 mg per day once (or 5 mg twice), for slow-release metoprolol - 200 mg per day.

The principles of the combined use of fixed assets for the treatment of CHF,
Monotherapy in the treatment of CHF is rarely used, and only ACE inhibitors can be used in this capacity in the initial stages of CHF.
Dual therapy with ACE inhibitor + diuretic - optimally suited for patients with CHF II-III FC NYHA with sinus rhythm;
the diuretic + glycoside regimen, extremely popular in the 1950s and 1960s, is not currently used.

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

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

The effect and influence of auxiliary agents on the prognosis of patients with CHF are not known (not proven), which corresponds to the level of evidence C. Actually, these drugs do not need (and are impossible) to treat CHF itself, and their use is dictated by certain clinical situations that complicate the course of decompensation itself :
peripheral vasodilators (PVD) = (nitrates) used for concomitant angina;
slow calcium channel blockers (CBCC) - long-acting dihydroperidines for persistent angina and persistent hypertension;
antiarrhythmic drugs (except for BAB, which are among the main drugs, mainly class III) for life-threatening ventricular arrhythmias;
aspirin (and other antiplatelet agents) for secondary prevention after myocardial infarction;
non-glycoside inotropic stimulants - with exacerbation of CHF, occurring with low cardiac output and persistent hypotension.