Heart failure is a heart disease that is caused by poor circulation. The heart is not able to pump blood effectively, and therefore the circulation of oxygen and nutrients throughout the body is disrupted, resulting in blood stagnation. Among other things, heart failure can provoke coronary heart disease, heart disease, lung disease, myocarditis, rheumatism and arterial hypertension.

Prevention of heart failure

The main preventive actions are:

Heart failure can be caused by increased stress, so it is necessary to train the cardiovascular system. It is important that the exercises are dosed and individually selected.

In stable condition, doctors recommend walking for 20-30 minutes 3-5 times a week. An alternative is to ride a bike for 20 minutes five times a week. However, the duration of the load can be determined by the person himself, prerequisite All that remains is to ensure that your health does not deteriorate. The first signal that you should stop exercising is the appearance of slight shortness of breath.

In medicine, there are several classifications of heart failure. Recently, the most common one is the one proposed by the New York Heart Association.

Based on subjective indicators, four functional classes are distinguished:

I functional class– has no restrictions on physical activity. Habitual physical activity does not cause fatigue, weakness, shortness of breath or palpitations.

II functional class– restrained restriction physical activity. Patients at rest do not show pathological symptoms.

III functional class– obvious limitation of physical activity. A small physical activity causes the manifestation of clinical symptoms in patients.

IV functional class– the slightest physical activity causes chest discomfort. Signs appear even in calm state, and small physical activities can intensify symptoms.

Causes of heart failure

The main cause of heart failure is any pathological disease that impairs the functioning of the heart. In most cases, heart failure is a natural outcome of diseases of the heart and blood vessels. Sometimes illness can serve as the first signal of a serious heart disease.

After the onset of hypertension, quite a long time may pass before the first symptoms of heart failure appear. The disease can progress quite quickly, often we are not even talking about days or hours, but about minutes. In such cases, we can talk about acute failure. The remaining cases are classified as chronic heart failure.

The main directions of treatment of heart failure:

1. Symptomatic treatment – ​​elimination of symptoms.
2. Protecting the organs that are most affected by poor heart function. Most often these are the brain, kidneys and blood vessels.
3. Extending the patient's life and improving its quality.

Symptoms of chronic heart failure

In children, chronic deficiency is manifested by delayed physical development, anemia and lack of weight. In addition, the child may have impaired breathing, central and peripheral circulation.

In adults, chronic heart failure is accompanied by polycythemia and acrocyanosis. For patients of any age common symptom is pale skin.

In the early stage of chronic failure, the disease manifests itself only during physical activity. In the later stages, the symptoms are stable and can be expressed even when the patient takes a horizontal position, resulting in shortness of breath.

First aid for heart failure

First aid for heart failure should be aimed at improving the contractility of the heart. If heart failure is associated with angina pectoris, then the patient should place one nitroglycerin tablet under the tongue. The doctor, providing first aid, must use strophanitis, corglycon and digoxin.

Eufillin is effective in reducing blood stagnation in the pulmonary vessels. The medicine can be administered intravenously in the form of a 2.4% solution and intramuscularly in the form of a 24% solution. To increase oxygen levels, the patient is given humidified oxygen to breathe. Furosemide or novorit is also administered.

How to treat heart failure?

The most important thing in treating chronic heart failure is to relieve the patient of symptoms. The treatment used must fully comply with the subjective requirements of the patient.

The following methods are used to treat the disease:

It should be remembered that the treatment of acute heart failure is a difficult process, since it often involves the treatment of accompanying diseases.

folk remedies

Since the end of the 18th century, digitalis, also called digitalis, has been considered the most effective folk remedy for the treatment of heart failure. The peculiarity of foxglove is that it only affects sick heart and has no effect on the healthy. Digitalis preparations enhance the contractile function of the myocardium, the result of this effect is an increased amount of ejected blood.

Signs and treatment of heart failure

What is heart failure?

This is a disease accompanied by a certain set of symptoms, the development of which is caused by disruption of the processes of filling and emptying of the heart with the subsequent formation of hemodynamic disorders.

Distinguish following forms insufficiency:

Acute heart failure

This pathology is a serious, life-threatening condition. Characterized by rapid development clinics as a result of a sudden drop in myocardial contractile function and a decrease in cardiac output.

The reasons leading to the development of acute failure are:

• inflammatory, dystrophic heart diseases;
• bradyarrhythmias, tachyarrhythmias;
• myocardial infarction (large focal transmural);
• pulmonary embolism;
• hypertensive crisis;
• state of decompensation of chronic heart failure.

The following clinical forms of acute failure exist:

• congestive – includes right and left ventricular failure, manifested by stagnation of circulating blood;
• hypokinetic – accompanied by the development of cardiogenic shock.

Symptoms of acute heart failure:

Left ventricular cardiovascular failure leads to a delay in circulating blood in the pulmonary circle. At the same time, it develops acute edema lungs, which is manifested by the following symptoms:

1. Increasing shortness of breath, up to suffocation.
2. Forced position of the body while sitting, since in a horizontal position the ventilation of the lungs deteriorates.
3. Cough with foamy sputum.
4. Distant moist rales in the lungs when breathing.
5. Increased heart rate.
6. Cyanosis of the skin and mucous membranes.

With significantly severe hypertension, cardiopulmonary failure develops in the pulmonary vessels. The main cause of the development of this condition is pulmonary embolism. Symptoms of the pathology are:

• sudden onset of shortness of breath at rest;
• cyanosis of the lips;
• acute chest pain;
• with a pulmonary infarction - hemoptysis.

Right ventricular failure of the heart is manifested by stagnation of circulating blood in the area of ​​the systemic circulation, which can be determined by the appearance of the following symptoms:

• swelling of the neck veins;
• pain in the right hypochondrium due to the development of portal hypertension, venous stagnation and liver enlargement, which is accompanied by stretching of the capsule;
• in case of acute necrosis of the liver parenchyma, jaundice may appear;
• development of ascites (accumulation of fluid in abdominal cavity).

The total form of the disease is characterized by combined signs of hemodynamic disturbances.

Cardiogenic shock is manifested by symptoms such as:

• decline blood pressure, decrease in pulse pressure;
• decreased urine output or complete absence of urination;
• the appearance of sinus tachycardia;
• cold, sticky sweat;
• marbling of the skin.

Chronic heart failure (CHF)

It is more widespread and is the predominant form of the disease in clinical practice. The frequency of diagnosis increases with age. Thus, symptoms of CHF are most often detected in older people (in the age group of 60-80 years).

Reasons for the formation of CHF

Factors leading to the development of pathology include the following diseases:

• arterial hypertension;
• myocarditis, dilated cardiomyopathy;
• chronic ischemic heart disease: small-focal infarction, post-infarction cardiosclerosis;
• lung diseases (chronic obstructive pulmonary disease, pneumonia);
• diabetes mellitus

In men, symptoms of the disease more often develop after undergoing acute heart attack myocardium. In women, the leading factor in the formation of chronic heart failure is arterial hypertension in combination with diabetes mellitus. In children, the most common cause is congenital anomalies of the heart.

Signs of CHF

With a long course of the disease, there are dysfunctions of all parts of the heart. In the clinical picture, the main symptoms of heart failure can be identified:

• fatigue;
• shortness of breath, cardiac asthma;
• peripheral edema;
• heartbeat.

Most patients complain of fatigue. The presence of this symptom is due to the following factors:

• low cardiac output;
• insufficient peripheral blood flow;
• state of tissue hypoxia;
• development of muscle weakness.

Shortness of breath in heart failure increases gradually - it first occurs during physical activity, then appears with minor movements and even at rest. With decompensation of cardiac activity, so-called cardiac asthma develops - episodes of suffocation that occur at night.

Signs of cardiac asthma:

• acute, sudden onset;
• feeling of lack of air, difficulty breathing;
• the appearance of suffocation;
• first a dry cough, then there may be foamy sputum.

Peripheral edema includes:

• swelling of the legs (feet, legs) – symmetrical on both limbs, from barely noticeable in the form of a mark from the elastic of socks, to pronounced;
• accumulation of fluid between the layers of the pleura and pericardium;
• the appearance of ascites, anasarca.

The skin in the area of ​​edema has a bluish color. Tachycardia is a compensation reaction due to the presence of chronic oxygen starvation of tissues. Rhythm disturbances are often present (persistent or paroxysmal atrial fibrillation, ventricular extrasystole).

Classification of heart failure

Two complementary classifications have been widely used, reflecting the severity of existing changes.

The domestic classification (Vasilenko-Strazhesko) involves division into stages:

1. Stage 1 CHF – hemodynamic disturbances occur only during physical activity.
2. Stage 2a – there are symptoms of hemodynamic disturbances in one circle of blood circulation, and exercise tolerance is reduced.
3. Stage 2b – severe, there are pronounced hemodynamic disturbances in both circles;
4. Stage 3 – terminal, significant hemodynamic disturbances, structural changes in organs.

The New York Heart Association distinguishes 4 functional classes depending on exercise tolerance:

1. Functional class I (FC I) – physical activity is not limited.
2. Functional class II – physical activity is moderately limited.
3. III FC – there is a pronounced limitation.
4. IV FC – inability to make any movements without discomfort.

Causes of death in heart failure

Life-threatening conditions that require emergency care include:

• the appearance of ventricular arrhythmias;
• acute pulmonary edema;
• exudative pericarditis, accompanied by cardiac tamponade.

Treatment of heart failure

Indications for hospitalization are:

• acute heart failure clinic;
• newly diagnosed heart failure in people of working age;
• ineffectiveness of therapy, decompensated chronic failure.

Chronic heart failure in the compensation stage is treated on an outpatient basis. On prehospital stage the following methods are used:

1. Compliance with nutritional principles - the diet is enriched with foods high in potassium, salt intake is significantly limited, and fluid intake is monitored.
2. Dosed physical activity should be adequate to the patient’s capabilities; breathing exercises and walking are useful.
3. Drug therapy – using drugs with proven positive influence on prognosis and quality of life. These are drugs from the group of angiotensin-converting enzyme inhibitors, sartans, adrenergic blockers, aldosterone antagonists, cardiac glycosides. For significant edema, diuretics are prescribed, and diuretic herbs are additionally used. In addition, statins, nitrates, anticoagulants, and antiarrhythmic drugs are used.
4. Surgical methods - installation of an electrical pacemaker, implantable cardioverter-defibrillator, myocardial revascularization surgery.

Timely adequate treatment in the early stages of the disease can slow down the progression of the disease, improve the prognosis and have a significant impact on the quality and life expectancy of such patients.

Development of heart failure

In each specific case, the period during which heart failure develops may be different and depends on the type of cardiovascular disease. Heart failure is divided into left and right ventricular, depending on which of the ventricles of the heart is most affected by the effects of the disease.

At right ventricular heart failure Excessive fluid volume is retained in the vessels of the systemic circulation. The consequence of this is the development of edema, in the first stages - in the area of ​​​​the ankles and feet. In addition to the main symptoms, with right ventricular heart failure, the patient complains of rapid fatigue, which occurs due to insufficient oxygen saturation of the blood, a feeling of pulsation and fullness in the neck.

At left ventricular heart failure fluid is retained in the pulmonary circulation, resulting in a decrease in the level of oxygen entering the blood. The consequence of this is the development of shortness of breath, which intensifies with physical activity, the appearance fatigue and weaknesses.

The severity of symptoms and the order in which they occur depends on each individual case. Symptoms of an existing disease appear more quickly in right ventricular heart failure. This is explained by the fact that the left ventricle is the most powerful section of the heart. As a rule, it takes a long time before he begins to “lose ground.” However, when this does happen, the progression of heart failure occurs rapidly.

Symptoms of heart failure

Depending on which part of the heart is most affected, the symptoms of heart failure differ. Arrhythmias may appear. shortness of breath, darkening of the eyes, dizziness, fainting, pale skin, swelling of the neck veins, leg pain and swelling, ascites (free fluid in the abdominal cavity), enlarged liver. Even minor physical activity becomes unbearable for the patient. In the later stages of the disease, symptoms appear not only during exercise, but also at rest, resulting in the patient completely loses his ability to work. All organs and systems of the body, to a greater or lesser extent, feel the negative effects of insufficient blood circulation.

Depending on which side of the heart (or both) is damaged, symptoms will vary. At bad work right side the peripheral veins of the heart become overfilled with blood, which then leaks into the abdominal cavity (including the liver) and leg tissue. This leads to the liver increasing in size and swelling. When the left side is affected, the blood vessels of the heart and pulmonary circulation are filled with blood, some of which spreads to the lungs. This type of heart failure is characterized by a cough, rapid breathing, rapid heart rate, and pale or bluish skin. The severity of symptoms may vary, there are probability of death.

Diagnosis of heart failure

This disease is the result of various conditions and diseases, both cardiovascular and other origins. To identify existing heart failure, a routine examination by a doctor is often not enough, since it may be necessary to use certain diagnostic methods to clarify the reasons that caused it.

Help doctors identify all kinds of arrhythmias. symptoms of hypertrophy and ischemia (lack of blood supply) of the myocardium may ECG (electrocardiography). Typically, signs identified by ECG may indicate other diseases, since they are not unique to heart failure.

Based on the ECG, stress tests have been developed and are widely used, the essence of which is that the patient must overcome various levels of stress, gradually increasing. To carry out such tests, special equipment is used that helps to dose the load: treadmill - a treadmill, bicycle ergometry - a special modification of a bicycle. With the help of such tests, you can obtain data on what reserve capabilities the pumping function of the heart has.

Today, the main and accessible to everyone method of identifying diseases, the symptom of which is heart failure, is EchoCG (echocardiography) - ultrasound examination of the heart. Using this procedure, you can not only find out the cause of heart failure, but also evaluate the ventricles of the heart for their contractile function. Today, using only echocardiography, it is possible to diagnose acquired or congenital heart disease, to suggest the presence of arterial hypertension, coronary heart disease and a number of other diseases. The EchoCG method can also be used to evaluate the effectiveness of prescribed treatment.

Examination of the chest organs using X-rays in case of heart failure helps to detect blood stagnation in the pulmonary circulation, as well as cardiomealgia (increase in the size of the heart cavities). A number of heart diseases (for example, valvular heart defects) have a unique X-ray picture. X-ray examination of the chest organs, like echocardiography, allows us to determine the effectiveness of treatment.

For a highly accurate assessment of the contractile function of the ventricles (including the volume of blood they contain), radioisotope methods for studying the heart (for example, radioisotope ventriculography) are used. These methods are based on the introduction and further distribution of radioisotope preparations throughout the body.

The PET (positron emission tomography) method is a nuclear diagnostic method, which is one of the most advanced achievements of modern medicine. This type of research is very expensive and is not very widespread today. The main opportunity of PET is to identify a section of viable myocardium in patients with heart failure using a certain radioactive “tag”, which will allow further adjustments to the prescribed treatment.

Treatment of heart failure

Acute heart failure requires hospitalization of the patient. It is imperative to follow a regimen with limited physical activity (the attending physician selects physical therapy); it is required to adhere to a diet that includes foods rich in proteins and vitamins and a limited salt content; if the patient has severe edema, a salt-free diet is prescribed. Diuretics, cardiac glycosides, calcium antagonists, vasodilators, and potassium supplements are also prescribed.

Modern pharmacology has made a huge step forward in prolonging and improving the quality of life of patients diagnosed with heart failure. But before proceeding directly to the treatment of heart failure, you need to exclude all possible factors which can cause its appearance (anemia. febrile conditions, stress, alcohol abuse, excessive consumption table salt, as well as taking medications that contribute to fluid retention in the body, etc.).

Treatment of heart failure involves not only getting rid of its immediate causes, but also correcting its manifestations. An important role in the treatment of heart failure is given to such a general measure as rest. Which does not at all imply that the patient should spend all the time lying down. There should be physical activity, but at the same time the patient should not get tired or experience unpleasant feelings. If the patient has difficulty withstanding stress, he should sit more, but not lie down. When there is no swelling or obvious shortness of breath, you should walk in the fresh air. It must be remembered that physical activity for patients with heart failure does not involve any elements of competition.

The bed on which a person with heart failure sleeps should have a raised head end, or he should be given a high pillow. If the patient has swelling of the legs, it is advised to sleep on a bed with the end of the leg raised or place a thin pillow under the legs (this will help reduce the manifestations of swelling).

Mandatory low salt diet. You should not add salt to already prepared food. It is extremely important to reduce excess weight, as it significantly increases the load on a diseased heart. However, if heart failure has developed sufficiently, weight may decrease on its own. To control your weight and detect fluid retention in the body in time, you need to weigh yourself at the same time of day every day.

Medicines that modern medicine offers for the treatment of heart failure are aimed at:

decreased vascular tone;

increased myocardial contractility;

elimination of sinus tachycardia;

reducing fluid retention in the body;

prevention of blood clots in the heart cavities.

If modern medications do not give the desired effect, surgery may be prescribed.

Article publication date: 12/18/2016

Article updated date: 12/18/2018

From this article you will receive comprehensive information about the disease heart failure: what causes it to develop, its stages and symptoms, how it is diagnosed and treated.

In heart failure, the heart is unable to fully cope with its function. Because of this, tissues and organs receive insufficient oxygen and nutrients.

If you suspect heart failure, do not delay contacting a cardiologist. If you contact it at an early stage, you can get rid of the disease completely. But with heart failure of degree 2 and higher, doctors usually give a less favorable prognosis: it is unlikely to be completely cured, but it is possible to stop its development. If you neglect your health and do not contact specialists, the disease will progress, which can lead to death.

Why does pathology occur?

The causes of heart failure can be congenital or acquired.

Causes of congenital pathology

Causes of acquired heart failure

• Chronic arterial hypertension (high blood pressure);
• vascular spasms;
• stenosis (narrowing) of blood vessels or heart valves;
• endocarditis – inflammation of the inner lining of the heart;
• myocarditis – inflammation of the heart muscle;
• pericarditis - inflammation serous membrane hearts;
• heart tumors;
• previous myocardial infarction;
• metabolic disorders.

Acquired heart failure mainly affects people over 50 years of age. Also at risk are smokers and those who abuse alcohol and (or) drugs.

Heart failure often occurs and progresses due to excessive physical activity in adolescence, when the load on the cardiovascular system is already high. To prevent heart failure, young athletes are advised to reduce the intensity of training at the age when puberty begins and the body is most active in growth. If at this age they appeared initial symptoms heart failure, most likely, doctors will prohibit sports for 0.5–1.5 years.

Classification and symptoms

Signs of heart failure may vary depending on the severity of the condition.

Classification of heart failure according to Vasilenko and Strazhesko:

Stage 1 (initial, or hidden)

Symptoms appear only during intense physical activity, which was previously achieved without difficulty. Signs: shortness of breath, palpitations. At rest, no circulatory disturbances are observed.

For patients with this stage of heart failure, there are no restrictions in terms of physical activity. They can do any job. However, it is still necessary to undergo a preventive examination with a cardiologist once every six months or a year; you may also need to take medications that support the functioning of the heart.

Treatment at this stage is effective and helps get rid of the disease.

Stage 2 A

Sports activities with such heart failure are prohibited, but physical education and moderate physical activity at work are not contraindicated.

Signs can be eliminated with proper treatment.

Stage 2 B

Blood circulation is impaired in both the small and large circles.

All symptoms appear at rest or after minor physical activity. This:

• cyanosis of the skin and mucous membranes,
• cough,
• dyspnea,
• wheezing in the lungs,
• swelling of the limbs,
• aching pain in the chest,
• liver enlargement.

Patients experience chest discomfort and shortness of breath even with the slightest physical exertion, as well as during sexual intercourse. Walking exhausts them. It is very difficult to climb up the stairs. Such patients are usually considered disabled.

Treatment helps reduce symptoms and prevent further development of heart failure.

Stage 3 (final, or dystrophic)

Due to severe circulatory disorders, the main symptoms intensify. Pathological changes in internal organs also develop (cardiac cirrhosis of the liver, diffuse pneumosclerosis, congestive kidney syndrome). Metabolic disorders progress, and depletion of body tissues develops.

Treatment of heart failure at this stage is usually ineffective. It helps to slow down the development of changes in internal organs, but does not entail a significant improvement in well-being.

Patients with stage 3 heart failure are not able to fully perform even everyday tasks (cooking, washing, cleaning). Patients are recognized as disabled.

The prognosis is unfavorable: the disease can lead to death.

Diagnosis of heart failure

Before starting treatment, the doctor needs to find out the severity and nature of the disease.

First of all, you will need to be examined by a therapist. Using a stethoscope, he will listen to the lungs for wheezing, and will also conduct a superficial examination to detect bluishness of the skin. Measure heart rate and blood pressure.

Sometimes additional tests are performed to determine the heart's response to physical activity.

Test	Progress	Evaluation of results
20 squat test	All heart rate measurements are carried out in 1 minute. Heart rate is measured at rest in a sitting position (result No. 1 – R No. 1). The patient squats 20 times in 30 seconds. Heart rate is measured immediately after squats (P No. 2). Heart rate is measured after 1 minute (P No. 3). Then after another 2 minutes (P No. 4).	Heart response to stress: P No. 2 is 25% more than P No. 1 - excellent, 25-50% more - normal, 51% or more more - bad. Cardiac recovery after exercise: P No. 3 is close to P No. 1 - excellent, P No. 4 is close to P No. 1 - normal, P No. 4 is more than P No. 1 - bad.
Ruffier-Dixon test	All heart rate measurements are taken for 15 seconds. Heart rate is measured after a 5-minute rest in a supine position (P1). The patient squats 30 times in 45 seconds. Heart rate is measured immediately after exercise (P2) (the patient lies down after squats). Wait 30 seconds. The last time the heart rate is measured is 15 seconds.	The result is calculated using the formula: (4 * (P1+P2+P3) – 200) / 10 Rating: less than 3 - excellent, from 3 to 6 - good, from 7 to 9 - normal, from 10 to 14 - bad, more than 15 - very bad. In patients with tachycardia, this test may give a biased poor result, so the first test is used.

The tests are used for patients whose wheezing in the lungs is mild. If the tests give poor results, the patient most likely has heart failure. If wheezing in the lungs is severe, no tests are required.

When the primary examination by the therapist is completed, he gives a referral to a cardiologist who will conduct further diagnostics and prescribe treatment.

• ECG - will help identify pathologies of the heart rhythm.
• 24-hour ECG (Holter mount or Holter) – electrodes are attached to the patient’s body and a device is attached to the belt that records heart function for 24 hours. During these days the patient leads his normal lifestyle. Such an examination helps to more accurately record arrhythmias if they manifest themselves in the form of attacks.
• (ultrasound of the heart) – necessary to identify structural pathologies of the heart.
• Chest X-ray. Helps identify pathological changes in the lungs.
• Ultrasound of the liver, kidneys. If the patient has heart failure stage 2 or higher, it is necessary to diagnose these organs.

Methods for diagnosing heart pathologies

Sometimes a CT or MRI of the heart, blood vessels or other internal organs may be needed.

After receiving the results of these diagnostic methods, the cardiologist prescribes treatment. It can be either conservative or surgical.

Treatment

Drug therapy

Conservative treatment includes taking various groups of drugs:

Group of drugs	Effect	Examples of drugs
Cardiac glycosides	Supports and improves the contractile function of the heart muscle	Digitoxin, Digoxin, Methyldigoxin, Strophanthin K
Nitrates	Filming painful sensations in the chest, dilate veins	Nitroglycerine
ACE inhibitors	Reduce blood pressure, dilate blood vessels, reduce the risk of cardiac arrest	Captopril, Lisinopril, Fosinopril
Beta blockers	Reduce blood pressure and slow heart rate	Metoprolol, Atenolol
Calcium antagonists	Dilate arteries, reduce blood pressure, eliminate arrhythmias	Verapamil, Cinnarizine, Diltiazem, Amlodipine, Nitrendipine
Diuretics	Remove excess fluid from the body, prevent the formation of edema, increase the effectiveness of drugs that lower blood pressure	Spironol, Uractone, Furosemide, Aldactone
Other	Stimulates metabolism in the myocardium	ATP, Riboxin, Carnitine

Drugs for the treatment of heart failure

If a patient has stage 1 heart failure that appears due to excessive physical exertion, the doctor may decide that the patient does not yet need to take serious medications. In this case, he will prescribe only medications that improve metabolism in the heart muscle, as well as B vitamins to strengthen the heart and blood vessels.

Surgical treatment

For some congenital or acquired heart defects, drug treatment is ineffective. It may relieve symptoms for a short time, but has no effect on the cause of the disease.

Plant	Recipe
Foxglove Purple – Contains Digitoxin	Take 1.5 tsp. (1 g) dry leaves. Pour 1 tbsp. boiling water Leave for 12 hours. Take 1 tsp. 2 times a day. Pay attention! Do not exceed the dosage under any circumstances. Foxglove is a plant that can poison you! For severe heart defects, after a heart attack, for stenosis coronary arteries and some types of arrhythmias are prohibited from using digitalis! Folk remedies, like medicines, can be hazardous to health if used incorrectly. Be sure to consult your doctor!
Woolly foxglove – contains digoxin, celanide
Lily of the valley - contains corglycone	Take 8-10 fresh flowers. Pour 1 tbsp. boiling water Leave for 1-2 hours. Drink in small portions throughout the day. Attention! Korglykon is contraindicated in WPW syndrome, as it causes attacks of tachycardia.

Herbs for treating heart failure

Diet and lifestyle for heart failure

First of all, you should give up bad habits if you have them. If you have heart failure of degree 2 or higher, exercise is contraindicated. Physical therapy Doctors recommend taking into account the patient’s well-being.

The diet should also be adjusted:

To reduce swelling and reduce the load on the kidneys, reduce the amount of water (you can drink no more than 0.75–1 liters per day).

To prevent a large amount of blood from rushing to your head, it is recommended to sleep with a large pillow under your head. And to prevent edema, you need another pillow - it is placed under your feet.

Acute heart failure (AHF) – emergency, which develops with a sudden disruption of the pumping function of the heart.

Acute myocardial dysfunction entails circulatory disorders in the systemic and pulmonary circulation; as the pathological condition progresses, multiple organ failure develops, i.e., gradual failure of all organs and systems occurs.

Acute heart failure can develop as a complication of cardiac diseases, sometimes occurring suddenly, without obvious preconditions for a catastrophe. Next, you will learn what are the signs of acute heart failure and symptoms before death.

Factors in the development of AHF are conventionally divided into several groups:

• Organic myocardial lesions;
• Other cardiovascular pathologies;
• Non-cardiac diseases that do not directly affect the heart or blood vessels.

The list is dominated by damage to the heart muscle, in particular myocardial infarction, in which muscle cells die. The larger the area of ​​necrosis, the higher the risk of developing AHF and the more severe its course. , burdened by AHF, - one of the most dangerous conditions with a high probability of death for the patient.

AHF can also be caused by inflammatory lesion myocardium - myocarditis. High risk development of AHF is also present during cardiac operations and when using artificial life support systems.

Acute heart failure is one of the most threatening complications of many vascular and cardiac diseases. Among them:

• Chronic heart failure (we talked about the reasons for its development);
• , congenital and acquired;
• leading to a critical acceleration or deceleration of heart rate;
• Arterial hypertension;
• Cardiomyopathies;
• Cardiac tamponade;
• Blood circulation disorders in the pulmonary circulation.

AHF often develops against the background of trauma or brain surgery, as a complication of infectious diseases, and also as a result of severe or chronic intoxication. The likelihood of myocardial dysfunction increases with certain endocrine diseases and kidney damage.

Accordingly, the risk group for developing AHF includes people who have a history of:

• Diseases of the heart and blood vessels;
• Bleeding disorders;
• Kidney diseases;
• Diabetes mellitus;
• Abuse of alcohol, tobacco, drugs, harmful conditions labor;
• Elderly.

Precursors of OSN

Acute heart failure can develop suddenly. In some cases, AHF and sudden coronary death are the first manifestations of asymptomatic coronary heart disease.

In approximately 75% of cases of AHF, alarming symptoms appear 10-14 days before the disaster, which are often perceived as a temporary minor deterioration of the condition. These could be:

• Increased fatigue;
• Heart rhythm disturbances, mainly;
• General weakness;
• Deterioration in performance;
• Dyspnea.

Attacks of dizziness and loss of coordination of movements are possible.

Manifestations

According to the location of the lesion, AHF can be right ventricular, left ventricular or total. When the functions of the right ventricle are impaired, symptoms indicating congestion in the big circle blood circulation:

• Sticky cold sweat;
• Acrocyanosis, less often – a yellowish tint to the skin;
• Swelling of the jugular veins;
• Shortness of breath not associated with physical activity, turning into suffocation as the condition progresses;
• , decreased blood pressure, thready pulse;
• Enlarged liver, pain in the right hypochondrium;
• Edema of the lower extremities;
• Ascites (fluid effusion into the abdominal cavity).

In left ventricular acute heart failure, progressive congestion develops in the pulmonary circulation and is manifested by the following symptoms:

• Shortness of breath, turning into suffocation;
• Pallor;
• Severe weakness;
• Tachycardia;
• Cough with foamy pinkish sputum;
• Gurgling wheezing in the lungs.

In the lying position, the patient's condition worsens; the patient tries to sit with his legs on the floor. The condition of AHF is accompanied by a fear of death.

It is customary to distinguish several stages in the development of AHF. The appearance of precursors in time coincides with the initial or latent stage. There is a decrease in performance; after physical or emotional stress, shortness of breath and/or tachycardia occurs. At rest, the heart functions normally and symptoms disappear.

The second stage is characterized by the manifestation of severe circulatory failure in both circles. At substage A, pallor of the skin and cyanosis are noticeable in the areas of the body furthest from the heart. Typically, cyanosis develops first at the tips of the toes, then the tips of the hands.

Signs of congestion appear, in particular moist rales in the lungs, the patient suffers from a dry cough, and possibly hemoptysis.

Swelling appears on the legs, the liver increases slightly in size. Symptoms indicating blood stagnation increase in the evening and fade away completely or partially the next morning.

Heart rhythm disturbances and shortness of breath occur with exertion.

At substage B, the patient is bothered by aching pain in the chest, tachycardia and shortness of breath are not associated with physical or emotional stress. The patient is pale, cyanosis affects not only the tips of the fingers, but also the ears, nose, and extends to the nasolabial triangle. Swelling of the legs does not go away after a night's rest and spreads to the lower part of the body.

Fluid accumulations form in the pleural and abdominal cavities. Due to stagnation of blood in the portal system, the liver becomes greatly enlarged and thickened, and pain is felt in the right hypochondrium. Impaired fluid removal from tissues leads to severe oliguria - insufficient urine output.

The third stage, also known as dystrophic or final stage. Circulatory failure leads to multiple organ failure, which is accompanied by increasing irreversible changes in the affected organs.

Diffuse pneumosclerosis, liver cirrhosis, and congestive kidney syndrome develop. Vital organs fail. Treatment at the dystrophic stage is ineffective, and death becomes inevitable.

First aid

When the first symptoms indicating heart failure appear, you must:

• Sit the victim in a comfortable position, with his back raised;
• Provide access to fresh air, unfasten or remove clothing items that restrict breathing;
• If possible, immerse your hands and feet in hot water;
• Call " Ambulance”, describing the symptoms in detail;
• if it is low, give a nitroglycerin tablet;
• 15-20 minutes after the onset of the attack, apply a tourniquet to the thigh, change the position of the tourniquet at intervals of 20-40 minutes;
• In case of cardiac arrest, artificial respiration and indirect cardiac massage should be started (if you have the skills to perform it).
• While the victim is conscious, you need to talk to him and calm him down.

The ambulance doctors who arrived at the scene must stabilize the patient’s condition. To do this, do:

• Oxygen therapy;
• Elimination of bronchospasms;
• Pain relief;
• Pressure stabilization;
• Increased breathing efficiency;
• Prevention of thrombotic complications;
• Elimination of edema.

All these actions fall within the competence of qualified medical personnel; specific drugs are selected individually depending on the patient’s condition.

What happens if you ignore signals?

If you do not pay attention to the threatening symptoms, pathological condition progresses quickly. The fatal stage of AHF can occur in a matter of hours or even minutes.

The more time passes from the onset of the first symptoms, the less likely the patient is to survive.

Near-death state

No one is safe from sudden death due to cardiac arrest. Approximately in 25% of cases this happens without any apparent reason, the patient does not feel anything. In all other cases, so-called prodromal symptoms or precursors appear, the appearance of which coincides in time with the latent stage of development of AHF.

What are the symptoms before death in acute cardiovascular failure? In half of cases, a seizure occurs before death acute pain in the heart area, tachycardia.

Ventricular fibrillation, lightheadedness, and severe weakness develop. Then comes loss of consciousness.

Immediately before death, tonic muscle contractions begin, breathing becomes frequent and heavy, gradually slows down, becomes convulsive and stops 3 minutes after the onset of ventricular fibrillation.

The skin turns pale, becomes cold to the touch, and acquires a grayish tint. The patient's pupils dilate and the pulse in the carotid arteries can no longer be felt.

Prevention

Prevention of AHF is especially important for people at risk. Persons suffering from cardiac diseases must undergo preventive examinations see a cardiologist and follow the doctor’s instructions.

Many patients are prescribed lifelong maintenance therapy.

It is very important to lead an active lifestyle, physical activity should cause a feeling of pleasant fatigue.

If possible, avoid emotional stress.

It is necessary to completely review the diet, give up fried, too spicy, fatty and salty foods, alcohol and tobacco in any form. More detailed recommendations regarding diet can only be given by the attending physician, based on the characteristics of past diseases and the general condition of the patient.

Useful video

You will learn a lot of additional information from the video:

Chronic heart failure (CHF) is a condition in which the volume of blood ejected by the heart for each heartbeat decreases, that is, the pumping function of the heart decreases, as a result of which organs and tissues lack oxygen. About 15 million Russians suffer from this disease.

Depending on how quickly heart failure develops, it is divided into acute and chronic. Acute heart failure can be caused by injury, toxins, heart disease, and can quickly be fatal without treatment.

Chronic heart failure develops over a long period of time and is manifested by 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

About the causes of this life-threatening condition, symptoms and treatments, including folk remedies we'll talk about it in this article.

Classification

According to the classification according to V. Kh. Vasilenko, N. D. Strazhesko, G. F. Lang, three stages are distinguished in the development of chronic heart failure:

• I Art. (HI) initial or latent deficiency, which manifests itself in the form of shortness of breath and palpitations only with significant physical activity that has not previously caused it. At rest, hemodynamics and organ functions are not impaired, work capacity is slightly reduced.
• Stage II - pronounced, prolonged circulatory failure, hemodynamic disturbances (stagnation in the pulmonary circulation) with little physical activity, sometimes at rest. At this stage, there are 2 periods: period A and period B.
• H IIA stage - shortness of breath and palpitations with moderate physical activity. Mild cyanosis. As a rule, circulatory failure is predominantly in the pulmonary circulation: periodic dry cough, sometimes hemoptysis, manifestations of congestion in the lungs (crepitus and silent moist rales in lower parts), palpitations, irregularities in the heart area. At this stage, initial manifestations of stagnation are observed in the systemic circulation (slight swelling in the feet and legs, slight enlargement of the liver). By morning these phenomena decrease. Working capacity sharply decreases.
• H IIB stage – shortness of breath at rest. All objective symptoms of heart failure increase sharply: pronounced cyanosis, congestive changes in the lungs, prolonged aching pain, interruptions in the heart area, palpitations; signs of circulatory failure in the systemic circulation, constant swelling of the lower extremities and torso, enlarged dense liver (cardiac cirrhosis of the liver), hydrothorax, ascites, severe oliguria are added. The patients are unable to work.
• Stage III (H III) - final, dystrophic stage of failure In addition to hemodynamic disturbances, morphologically irreversible changes in organs develop (diffuse pneumosclerosis, cirrhosis of the liver, congestive kidney, etc.). Metabolism is disrupted, and patients become exhausted. Treatment is ineffective.

Depending on phases of cardiac dysfunction are distinguished:

1. Systolic heart failure (associated with a violation of systole - the period of contraction of the ventricles of the heart);
2. Diastolic heart failure (associated with a violation of diastole - the period of relaxation of the ventricles of the heart);
3. Mixed heart failure (associated with disturbances of both systole and diastole).

Depending on zones of predominant blood stagnation are identified:

1. Right ventricular heart failure (with stagnation of blood in the pulmonary circulation, that is, in the vessels of the lungs);
2. Left ventricular heart failure (with stagnation of blood in the systemic circulation, that is, in the vessels of all organs except the lungs);
3. Biventricular (two-ventricle) heart failure (with blood stagnation in both circulation circles).

Depending on the results of a physical examination determine classes on the Killip scale:

• I (no signs of heart failure);
• II (mild HF, few wheezing);
• III (more severe heart failure, more wheezing);
• IV (cardiogenic shock, systolic blood pressure below 90 mmHg).

The mortality rate for people with chronic heart failure is 4-8 times higher than for their peers. Without proper and timely treatment in the stage of decompensation, the one-year survival rate is 50%, which is comparable to some cancer diseases.

Causes of chronic heart failure

Why does CHF develop, and what is it? Chronic heart failure is usually caused by damage to the heart or an impairment of its ability to pump enough blood through the vessels.

The main causes of the disease are called:

• coronary heart disease;
• heart defects.

There are also other provoking factors development of the disease:

• cardiomyopathy – myocardial disease;
• – heart rhythm disturbance;
• myocarditis – inflammation of the heart muscle (myocardium);
• cardiosclerosis – damage to the heart, which is characterized by the proliferation of connective tissue;
• smoking and alcohol abuse.

According to statistics, in men the most common cause of the disease is coronary heart disease. In women, this disease is caused mainly by arterial hypertension.

Mechanism of development of CHF

1. The throughput (pumping) capacity of the heart decreases – the first symptoms of the disease appear: exercise intolerance, shortness of breath.
   Compensatory mechanisms are activated aimed at preserving normal operation heart: strengthening the heart muscle, increasing adrenaline levels, increasing blood volume due to fluid retention.
2. Heart nutritional disorder: muscle cells have become much larger, and the number blood vessels increased slightly.
3. Compensatory mechanisms are exhausted. The work of the heart deteriorates significantly - with each beat it does not push out enough blood.

Signs

The main signs of the disease include the following symptoms:

1. Frequent shortness of breath is a condition when there is an impression of lack of air, so it becomes rapid and not very deep;
2. Increased fatigue, which is characterized by the rapidity of loss of strength when performing a particular process;
3. Increasing number of heart beats per minute;
4. Peripheral edema, which indicate poor removal of fluid from the body, begin to appear from the heels, and then move higher and higher to the lower back, where they stop;
5. Cough - from the very beginning of the clothes it is dry with this disease, and then sputum begins to be released.

Chronic heart failure usually develops slowly, and many people consider it a sign of aging in their bodies. In such cases, patients often wait until the last moment to see a cardiologist. Of course, this complicates and lengthens the treatment process.

Symptoms of chronic heart failure

The initial stages of chronic heart failure can develop according to the left and right ventricular, left and right atrial types. With a long course of the disease, there are dysfunctions of all parts of the heart. In the clinical picture, the main symptoms of chronic heart failure can be identified:

• fatigue;
• shortness of breath;
• peripheral edema;
• heartbeat.

Most patients complain of fatigue. The presence of this symptom is due to the following factors:

• low cardiac output;
• insufficient peripheral blood flow;
• state of tissue hypoxia;
• development of muscle weakness.

Shortness of breath in heart failure increases gradually - it first occurs during physical activity, then appears with minor movements and even at rest. With decompensation of cardiac activity, so-called cardiac asthma develops - episodes of suffocation that occur at night.

Paroxysmal (spontaneous, paroxysmal) nocturnal dyspnea can manifest itself in the form of:

• short attacks of paroxysmal nocturnal dyspnea that go away on their own;
• typical attacks of cardiac asthma;
• acute pulmonary edema.

Cardiac asthma and pulmonary edema are essentially acute heart failure that develops against the background of chronic heart failure. Cardiac asthma usually occurs in the second half of the night, but in some cases it is provoked by physical effort or emotional excitement during the day.

1. In mild cases the attack lasts several minutes and is characterized by a feeling of lack of air. The patient sits up and harsh breathing is heard in the lungs. Sometimes this condition is accompanied by a cough with a small amount of sputum. The attacks may be rare, occurring over a few days or weeks, but may also occur several times during the night.
2. In more severe cases, a severe, prolonged attack of cardiac asthma develops. The patient wakes up, sits down, bends his torso forward, rests his hands on his hips or the edge of the bed. Breathing becomes rapid, deep, usually with difficulty inhaling and exhaling. There may be no wheezing in the lungs. In some cases, bronchospasm may occur, increasing ventilation disturbances and respiratory work.

The episodes may be so unpleasant that the patient may be afraid to go to bed, even after symptoms have resolved.

Diagnosis of CHF

In diagnosis, you need to start with analyzing complaints and identifying symptoms. Patients complain of shortness of breath, fatigue, and palpitations.

The doctor checks with the patient:

1. How does he sleep?
2. Has the number of pillows changed over the past week?
3. Did the person begin to sleep sitting instead of lying down?

The second stage of diagnosis is physical examination including:

1. Skin examination;
2. Assessment of the severity of fat and muscle mass;
3. Checking for edema;
4. Pulse palpation;
5. Palpation of the liver;
6. Auscultation of the lungs;
7. Auscultation of the heart (1st sound, systolic murmur at the 1st point of auscultation, analysis of the 2nd tone, “gallop rhythm”);
8. Weighing (a 1% decrease in body weight over 30 days indicates the onset of cachexia).

Diagnostic goals:

1. Early detection of the presence of heart failure.
2. Clarification of severity pathological process.
3. Determination of the etiology of heart failure.
4. Assessment of the risk of complications and sudden progression of pathology.
5. Forecast assessment.
6. Assessment of the likelihood of complications of the disease.
7. Monitoring the course of the disease and timely response to changes in the patient’s condition.

Diagnostic tasks:

1. Objective confirmation of the presence or absence of pathological changes in the myocardium.
2. Identification of signs of heart failure: shortness of breath, fatigue, rapid heartbeat, peripheral edema, moist rales in the lungs.
3. Identification of the pathology that led to the development of chronic heart failure.
4. Determination of the stage and functional class of heart failure according to NYHA (New York Heart Association).
5. Identification of the predominant mechanism of development of heart failure.
6. Identification of provoking causes and factors aggravating the course of the disease.
7. Identification of concomitant diseases, assessment of their connection with heart failure and its treatment.
8. Collecting sufficient objective data to prescribe the necessary treatment.
9. Identification of the presence or absence of indications for the use of surgical treatment methods.

Diagnosis of heart failure must be carried out using additional methods examinations:

1. The ECG usually shows signs of myocardial hypertrophy and ischemia. Often this study reveals accompanying arrhythmia or conduction disturbance.
2. An exercise test is carried out to determine tolerance to it, as well as changes characteristic of coronary heart disease (deviation of the ST segment on the ECG from the baseline).
3. Daily Holter monitoring allows you to clarify the state of the heart muscle during typical patient behavior, as well as during sleep.
4. A characteristic sign of CHF is a decrease in ejection fraction, which can be easily seen with ultrasound. If you additionally perform Doppler sonography, heart defects will become obvious, and with the right skill, you can even identify their degree.
5. Coronary angiography and ventriculography are performed to clarify the condition of the coronary bed, as well as in terms of preoperative preparation during open heart surgery.

When diagnosing, the doctor asks the patient about complaints and tries to identify signs typical of CHF. Among the evidence for diagnosis, the discovery of a person's history of heart disease is important. At this stage, it is best to use an ECG or determine natriuretic peptide. If no deviations from the norm are found, the person does not have CHF. If manifestations of myocardial damage are detected, the patient should be referred for echocardiography to clarify the nature of cardiac lesions, diastolic disorders, etc.

At subsequent stages of diagnosis, doctors identify the causes of chronic heart failure, clarify the severity and reversibility of changes in order to determine adequate treatment. Additional studies may be prescribed.

Complications

Patients with chronic heart failure may develop dangerous conditions such as

• frequent and prolonged;
• pathological myocardial hypertrophy;
• numerous thromboembolism due to thrombosis;
• general exhaustion of the body;
• disturbance of heart rhythm and cardiac conduction;
• dysfunction of the liver and kidneys;
• sudden death from cardiac arrest;
• thromboembolic complications (pulmonary embolism).

Prevention of the development of complications includes taking prescribed medications, timely determination of indications for surgical treatment, prescribing anticoagulants according to indications, and antibiotic therapy for damage to the bronchopulmonary system.

Treatment of chronic heart failure

First of all, patients are advised to follow an appropriate diet and limit physical activity. You should completely avoid fast carbohydrates, hydrogenated fats, in particular those of animal origin, and also carefully monitor your salt intake. It is also necessary to immediately stop smoking and drinking alcohol.

All methods of therapeutic treatment of chronic heart failure consist of a set of measures that are aimed at creating necessary conditions in everyday life, contributing to a rapid reduction in the load on the S.S.S., as well as the use of medications designed to help the myocardium work and influence the disturbed processes of water-salt metabolism. The scope of treatment measures is determined by the stage of development of the disease itself.

Treatment of chronic heart failure is long-term. It includes:

1. Drug therapy, aimed at combating the symptoms of the underlying disease and eliminating the causes contributing to its development.
2. Rational mode, including restriction of work activity according to the forms and stages of the disease. This does not mean that the patient must remain in bed all the time. He can move around the room, and exercise therapy is recommended.
3. Diet therapy. It is necessary to monitor the caloric content of food. It must comply with the patient’s prescribed regimen. For obese people, the calorie content of food is reduced by 30%. On the contrary, patients with malnutrition are prescribed enhanced nutrition. If necessary, fasting days are carried out.
4. Cardiotonic therapy.
5. Treatment with diuretics, aimed at restoring water-salt and acid-base balance.

Patients with the first stage are fully able to work; in the second stage, there is limited ability to work or it is completely lost. But in the third stage, patients with chronic heart failure require constant care.

Drug treatment

Drug treatment of chronic heart failure is aimed at increasing contraction functions and ridding the body of excess fluid. Depending on the stage and severity of symptoms for heart failure, the following groups of drugs are prescribed:

1. Vasodilators and ACE inhibitors– angiotensin-converting enzyme (, ramipril) – reduce vascular tone, dilate veins and arteries, thereby reducing vascular resistance during heart contractions and helping to increase cardiac output;
2. Cardiac glycosides (digoxin, strophanthin, etc.)– increase myocardial contractility, increase its pumping function and diuresis, promote satisfactory exercise tolerance;
3. Nitrates (nitroglycerin, nitrong, sustak, etc.)– improve blood flow to the ventricles, increase cardiac output, dilate the coronary arteries;
4. Diuretics (, spironolactone)– reduce the retention of excess fluid in the body;
5. B-blockers ()– reduce heart rate, improve blood flow to the heart, increase cardiac output;
6. Drugs that improve myocardial metabolism(B vitamins, ascorbic acid, Riboxin, potassium preparations);
7. Anticoagulants ( , )– prevent thrombus formation in blood vessels.

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.

Triple therapy (ACEI + diuretic + glycoside) was the standard in the treatment of CHF in the 80s, and now remains an effective regimen in the treatment of CHF, but for patients with sinus rhythm It is recommended to replace the glycoside with a beta-blocker. The gold standard from the early 90s to the present is a combination of four drugs - ACE inhibitor + diuretic + glycoside + beta-blocker.

Prevention and prognosis

To prevent heart failure, you need proper nutrition, sufficient physical activity, and giving up bad habits. All diseases of the cardiovascular system must be promptly identified and treated.

The prognosis in the absence of treatment for CHF is unfavorable, since most heart diseases lead to its wear and tear and the development of severe complications. When carrying out drug and/or cardiac surgery, the prognosis is favorable, because there is a slowdown in the progression of the failure or a radical cure for the underlying disease.

Cardiac asthma(asthma cardiale; Greek asthma shortness of breath, suffocation) - attacks of suffocation from several minutes to several hours with myocardial infarction, cardiosclerosis, heart defects and other diseases associated with heart failure.

The occurrence of cardiac asthma is facilitated by an increase in blood circulation volume (for example, during physical exertion, fever), an increase in the mass of circulating blood (for example, during pregnancy, after introduction into the body large quantities fluids), as well as the horizontal position of the patient; this creates conditions for increased blood flow to the lungs. Due to stagnation of blood and increased pressure in the pulmonary capillaries, interstitial pulmonary edema develops, disrupting gas exchange in the alveoli and the patency of the bronchioles, which is associated with the occurrence of shortness of breath; in some cases, breathing problems are aggravated by reflex bronchospasm.

The occurrence of cardiac asthma in the daytime is usually directly related to physical or emotional stress, increased blood pressure, and an attack of angina pectoris; sometimes an attack is triggered by eating or drinking heavily. Before an attack develops, patients often feel chest tightness and palpitations. When cardiac asthma occurs at night (observed more often), the patient wakes up from a feeling of lack of air, difficulty breathing, tightness in the chest, and the appearance of a dry cough; he experiences anxiety, a feeling of fear, his face becomes covered with sweat. During an attack, the patient, as a rule, begins to breathe through his mouth and necessarily sits up in bed or stands up, since shortness of breath decreases with an upright position of the body (orthopnea). The number of respirations reaches 30 or more per minute; the ratio of the duration of exhalation and inhalation usually changes little. In the lungs you can hear - hard breathing, sometimes (with bronchospasm) dry wheezing (usually less abundant and less “musical” than with bronchial asthma), often fine bubbling moist rales in the subscapular areas on both sides or only on the right. Subsequently, a picture of alveolar pulmonary edema may develop with a sharp increase in shortness of breath, and the release of light or pink foamy liquid when coughing. Auscultation of the heart reveals changes characteristic of a mitral or aortic defect, and in the absence of a defect, a significant weakening of the first heart sound or its replacement by systolic murmur, an accentuation of the second sound over the pulmonary trunk, often a gallop rhythm. As a rule, there is tachycardia, and with atrial fibrillation there is a significant pulse deficit.

Heart failure- a complex of disorders caused mainly by a decrease in the contractility of the heart muscle. If medical care is not provided, death is possible.

Heart failure syndrome complicates many diseases of the cardiovascular system, and heart failure develops especially often in people suffering from coronary heart disease and hypertension. The main and most noticeable manifestations of heart failure syndrome include shortness of breath, which sometimes occurs even at rest or with minimal physical activity. In addition, the possibility of heart failure is indicated by increased heart rate, increased fatigue, limited physical activity, and excess fluid retention in the body, causing swelling. Insufficient blood supply to the body is also the basis for such a clear sign of heart failure as blueness of the nails or nasolabial triangle (not in the cold, but at normal temperature). The inevitable result of heart failure is the appearance in the body of various abnormalities in blood circulation, which are either felt by the patient himself or determined by a cardiologist during examination.

Heart failure can occur in chronic and acute forms. Chronic heart failure usually develops as a complication of any cardiovascular disease, and can exist in a latent, asymptomatic form for quite a long time. The acute form of heart failure develops rapidly - over a few days or even hours, usually against the background of an exacerbation of the underlying disease. In some cases, they speak of the congestive phase of heart failure: its cause is a slowdown in blood flow in organs and tissues, which leads to fluid retention in the tissues of the body. It is the stagnant phase that, in its extreme manifestation, leads to the occurrence of such a life-threatening symptom as pulmonary edema.

There is also another classification of heart failure - according to the place of formation, that is, depending on which part of the heart the blood supply is impaired. On this basis, heart failure is divided into left ventricular and right ventricular. The most characteristic sign of left ventricular heart failure is shortness of breath, and the most characteristic sign of right ventricular heart failure is swelling in the feet and ankles.

Heart failure syndrome, unfortunately, is quite widespread, especially among older people. Therefore, in our time, when all statistics talk about the general aging of the population, there is an increase in the number of patients. Thus, heart failure is detected in 3-5% of people over 65 years of age and in every tenth (!) person over 70 years of age. Heart failure is more common in women because men have a high mortality rate directly from vascular disease (myocardial infarction) before it develops into heart failure.

Most patients suffering from heart failure have a chronic form. It is important to emphasize that in this case, the symptoms of heart failure develop gradually, arise softly and therefore are often accepted by patients as natural. age-related changes(“I’m getting old... So my heart is playing tricks...”). In such cases, patients often wait until the last moment to see a cardiologist, or contact them belatedly. Of course, this complicates and lengthens the treatment process, because restoration of normal heart function and blood circulation in the initial period of heart failure is achieved more easily and with the help of smaller quantities of drugs than in the period of pronounced symptoms.

We should not forget that chronic heart failure is a progressive syndrome. Therefore, patients at the moment having “only” a latent form of chronic heart failure, within just a few years they can become the group of the most severely ill patients who are difficult to treat.

As evidence, we cite data from a study conducted several years ago in the UK. According to these data, patient survival within a year after the appearance of the first signs (symptoms) of heart failure was 57% for men and 64% for women. And after five years, these figures had dropped to 25% and 38%, respectively. In other words, 5 years after the first symptoms of heart failure appeared, only one out of four men and only every third woman remained alive! Do you need any other evidence that at the slightest suspicion of heart failure, you must IMMEDIATELY consult a cardiologist, and the case of heart failure is truly one of those cases when “delay is like death”!

Therefore, people who begin to notice “pranks” behind their hearts should always remember: early diagnosis heart failure, and, consequently, early start treatment is the key to success in treating the syndrome. Currently, thanks to a major leap in knowledge in cardiology, heart failure can be kept “in check” for a long time. Medicines selected especially for you by a professional cardiologist will not only significantly prolong your life, but will also make it comfortable, harmonious, and free. And a patient suffering from heart failure will no longer burden the lives of those close to him.

As for acute heart failure, this is a serious but rare form of the disease. It appears unexpectedly or sudden attack Choking (cardiac asthma), often at night, and requires emergency medical attention. Acute heart failure can be complicated by pulmonary edema. In such a case, the cardiologist eliminates the swelling on the spot, but, nevertheless, hospitalization of the patient is required.

Classification of heart failure:

There is a lot of debate in the cardiology community regarding the classification of chronic heart failure. In our country, the classification of V.Kh. Vasilenko and N.D. Strazhesko, proposed by them at the XII Congress of Therapists in 1935, that is, more than half a century ago, has been used for a long time, and is still used today.

According to this classification, chronic heart failure is divided into three stages: from the initial stage, with practically unexpressed symptoms, to the final dystrophic stage with severe circulatory disorders. This classification of heart failure was the first of its kind, was widely used and was long considered ideal. However, with the development of the capabilities of cardiology in the diagnosis and treatment of heart failure, the Vasilenko-Strazhesko classification, which does not provide the ability to assess the dynamics of the process of heart failure, has become somewhat outdated.

Currently, in our country, the classification of heart failure proposed by the New York Heart Association (NYHA) is increasingly used. According to this classification, patients with heart failure syndrome are divided into four functional classes (FC).

Class 1. There are no restrictions on physical activity and no impact on the patient’s quality of life.

Class 2. Weak restrictions on physical activity and complete absence of inconvenience during rest.

Class 3. A noticeable decrease in performance, symptoms disappear during rest.

Class 4. Complete or partial loss of function, symptoms of heart failure and chest pain occur even during rest.

An easy and convenient way to determine the FC of each patient is also proposed - the so-called six-minute walk test. To carry out the test, it is enough to ask the patient to walk for six minutes at a comfortable pace along a hospital corridor of a known length and measure the time spent on this. This is sufficient to calculate the maximum oxygen consumption during exercise, and, as a result, to correctly recognize the stage of heart failure. Patients passing in 6 min. more than 551 m have no signs of heart failure; those who walk a distance from 426 to 550 m belong to FC I, those who walk a distance from 301 to 425 m belong to FC II, from 151 to 300 m belong to FC III, and patients who walk less than 150 m in 6 minutes belong to FC IV. Recently, Russian doctors are increasingly turning to this simple classification scheme.

Symptoms and signs of heart failure:

The significance of symptoms and signs in heart failure cannot be overestimated, because it is they, first of all, that allow the cardiologist to make the correct diagnosis and prescribe treatment. Manifestations of heart failure are a slowdown in the speed of general blood flow, a decrease in the amount of blood ejected by the heart, an increase in pressure in the heart chambers, and the accumulation of excess blood volumes that the heart cannot cope with in the so-called “depots” - the veins of the legs and abdominal cavity.

Here are the symptoms most often encountered by heart failure patients and cardiologists:

— Shortness of breath

- Weakness and fatigue

— Heartbeat

— Blueness, peripheral cyanosis and acrocyanosis

— Nocturia

The different symptoms of failure depend on which side of the heart is involved. For example, the left atrium receives oxygenated blood from the lungs and pumps it into the left ventricle, which in turn pumps blood to the rest of the organs. In case left side If the heart cannot effectively pump blood, the blood is backed up into the pulmonary vessels, and excess fluid penetrates through the capillaries into the alveoli, causing breathing difficulties. Other symptoms of left-sided heart failure include general weakness and excessive mucus production.

Right-sided insufficiency occurs when there is difficulty in the outflow of blood from the right atrium and right ventricle, which happens, for example, when the heart valve is not functioning properly. As a result, pressure increases and fluid accumulates in the veins of the liver and legs, which end in the right chambers of the heart. The liver becomes enlarged, painful, and the legs become very swollen. With right-sided insufficiency, a phenomenon called nocturia is observed.

In congestive heart failure, the kidneys cannot handle large volumes of fluid, and kidney failure develops. Salt, which is normally excreted by the kidneys along with water, is retained in the body, causing even greater swelling. Kidney failure is reversible and disappears with successful treatment of the main cause - heart failure.

It is important to note that almost all symptoms and clinical signs, even the “classic triad” - shortness of breath, swelling of the legs and moist rales in the lungs, not to mention fatigue and palpitations, are often found in other diseases or are leveled out by the treatment, which makes them insufficient for the diagnosis of chronic heart failure. An accurate diagnosis can only be made by a cardiologist and only using special examination methods.

Causes of heart failure:

As mentioned above, these are, first of all, various diseases of the cardiovascular system.

The most common cause of heart failure is a narrowing of the arteries that supply oxygen to the heart muscle. Vascular diseases develop at a relatively young age, sometimes they remain unattended, and then manifestations of congestive heart failure often occur in older people.

Chronic heart failure syndrome can complicate the course of almost all diseases of the cardiovascular system. But its main causes, accounting for more than half of all cases, are ischemic (coronary) heart disease and arterial hypertension, or a combination of these diseases. Often, cardiologists in their practice note the occurrence of heart failure syndrome during heart attacks and angina pectoris.

Other reasons causing the development of heart failure are changes in the structure of the heart valves, hormonal disorders(for example, hyperthyroidism - excessive function of the thyroid gland), infectious inflammation of the heart muscle (myocarditis). Myocarditis can manifest itself as a complication of almost any infectious disease: diphtheria, scarlet fever, polyarthritis, lacunar tonsillitis, pneumonia, polio, influenza, etc. It is this fact that serves as further confirmation that there are no “frivolous” viral infections, and each requires qualified treatment. Otherwise, they cause serious complications on the heart and blood vessels.

During pregnancy in women with various vascular or heart diseases, increased load on the heart can also trigger the development of heart failure. Chronic heart failure can also be caused by alcohol and drug addiction, excessive physical activity, and even a sedentary lifestyle. Thus, a recent study in the United States identified the causes of sudden deaths of taxi drivers from heart failure. It turned out that heart failure is provoked by the formation of blood clots as a result of slow blood flow and blockage of blood vessels due to prolonged sitting in the car.

There is a high risk of heart failure syndrome in diabetes mellitus and diseases of the endocrine system in general. In general, we can say that heart failure is provoked by diseases in which the heart muscle is overloaded with pressure (as in hypertension) or volume (heart valve insufficiency), as well as direct myocardial diseases (myocarditis, heart attack). In addition, any factors that cause excessive stress on the heart and blood vessels can put a patient at risk.

Among the factors contributing to the exacerbation and progression of heart failure, in the first place, as you might guess, is the exacerbation or progression of the underlying disease of the cardiovascular system, as well as the addition of other diseases of the same or other systems and organs. First of all, as mentioned, this concerns diseases of the endocrine system and respiratory organs. Exacerbation of existing heart failure is caused by situations that weaken the body’s immune and nervous systems: physical overexertion, malnutrition, vitamin deficiencies, intoxication, severe stressful situations. Finally, we present this fact for those who like self-medication; taking certain antiarrhythmic drugs with a negative inotropic effect can provoke the progression of heart failure.

Consequences of heart failure:

Heart failure syndrome is the most difficult test for the human body, and this is not surprising. Chronic heart failure is a “time bomb” in the body. People tend to pay attention only to pronounced symptoms that clearly define the disease. The child has a rash, which means you need to show him to the doctor, it could be scarlet fever. A severe cough and pain in the side are a sure sign of pneumonia, which you also cannot ignore. But shortness of breath, fatigue, palpitations - somehow all this is not serious, and it can indicate almost any disease. So it turns out that until chronic heart failure reaches a severe stage, the patient has the opportunity to simply not pay attention to its symptoms. But we must not forget that heart failure is a PROGRESSIVE syndrome, and when the patient finally thinks about possible problems and consequences, it may already be too late. But treatment of heart failure, begun in the earliest stages, significantly improves the patient’s life prognosis; in most cases, heart failure syndrome is successfully cured in the early stages.

Cardiologists cannot predict the consequences of heart failure unambiguously and in absentia. The prognosis for each individual patient depends on the severity of the disease, concomitant diseases, age, effectiveness of therapy, lifestyle and much more. But in general, the consequences of heart failure can be extremely unfavorable. In the United States, for example, heart failure is the leading cause of hospitalization for people over 65 years of age. In patients with heart failure syndrome, the risk of death increases with myocardial infarction and stroke. And in general, diseases of the cardiovascular system complicated by heart failure are more severe and less easily cured. This applies primarily to hypertension, coronary heart disease and angina.

Symptoms and clinical signs - Diagnosis of chronic heart failure

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Symptoms and clinical signs of chronic heart failure

The significance of symptoms and clinical signs is extremely high, since they allow the doctor to suspect the presence of CHF in a patient and, therefore, organize the diagnostic process with maximum determination and specificity in order to confirm or refute the diagnostic hypothesis. The intensive development of science and technology has contributed to the creation and implementation of numerous informative instrumental and laboratory methods for studying patients with diseases of the cardiovascular system. However, immediate clinical examination the patient is the first stage of diagnosis. Unfortunately, we often have to deal with the fact that the clinical examination of the patient is replaced by one or another paraclinical tests. And if such a vicious approach is practiced long enough, it can lead to the atrophy of the doctor’s so-called “bedside” diagnostic skills.

Sometimes a patient comes to see a cardiologist or therapist with complaints indicating a disease of the cardiovascular system (for example, pain in the heart, “interruptions” in the heart, headache associated with increased blood pressure), in which there is a high probability of developing CHF. A nosological diagnosis (in particular, ischemic heart disease) in a case where there are no manifest manifestations of heart failure “helps” the syndromic diagnosis of the initial stage of heart failure.

In most textbooks on internal medicine a description of the presence and severity of symptoms (complaints) and clinical signs of heart failure is given depending on the stage and form (left-, right-ventricular) CHF. As a matter of fact, it is the analysis of symptoms and clinical signs that allows one to determine the stage of the pathological process right at the bedside of a patient with chronic heart failure.

Dyspnea, as mentioned above, is the most “popular” finding in CHF. To the Bolshoi medical encyclopedia(2nd ed.) N. Savitsky gives the following definition of shortness of breath (dyspruxn; from the Greek dyspnoia - difficulty breathing, shortness of breath) - “difficulty breathing, characterized by a violation of its frequency, depth and rhythm, accompanied by a complex of unpleasant sensations in the form of tightness in the chest , lack of air, which can lead to a painful feeling of suffocation.”

Inspiratory dyspnea (or, according to James Mackenzie, “thirst for air”) in patients with chronic heart failure has a complex origin (the significance of each factor individually varies in different patients and with various diseases cardiovascular system) and there are still unresolved questions regarding its genesis. Apparently, in the formation of shortness of breath, in addition to the stagnation of blood “above” the weakened part of the heart (LV) with an increase in pressure in the pulmonary capillaries, due to which its appearance is traditionally explained, other, incompletely studied factors may also take part. In particular, the perception of difficulty breathing largely depends on the diffusion capacity of the lungs (shortness of breath is more severe, the more severe the hypoxemia), the reaction of the central nervous system on changes in blood composition (hypoxemia, hypercapnia, acidosis, etc.), the state of peripheral and respiratory muscles and the patient’s weight. The accumulation of fluid in the pleural and abdominal cavities, which impedes the respiratory excursion of the lungs, contributes to the appearance of shortness of breath. It is also possible that this symptom is based on a decrease in lung compliance and an increase in intrapleural pressure, which leads to an increase in the work of the respiratory muscles and auxiliary muscles. It should be added that in patients with long-term congestion of the lungs, their congestive (indurative) sclerosis develops - brown compaction (induration) of the lungs.

The sensitivity, specificity and prognostic significance of shortness of breath have already been discussed above (Table 1, 7.2). The main thing to remember is the low specificity of this symptom.

Naturally, in the initial stage of CHF, shortness of breath is absent at rest and appears only with intense muscle tension(climbing stairs or uphill, when walking quickly over long distances). Patients move freely around the apartment and can take any position convenient for themselves. As heart failure progresses, shortness of breath is observed even with minor exertion (even when talking, after eating, while walking around the room), then it becomes constant. And finally, the patient receives some relief only in a forced vertical position - a state of orthopnea. In this case, shortness of breath becomes the most serious symptom of heart disease for the patient. Severe forms of CHF are characterized by the development of painful shortness of breath at night (see below “orthopnea” and “cardiac asthma”). Very often, patients avoid the position on the left side, as this causes discomfort from the heart, which they usually cannot describe well, and shortness of breath increases (it is assumed that in this position there is a closer fit of the dilated heart to the anterior chest wall). Many patients with chronic heart failure find relief from staying in front of an open window.

With the development of hypoxia of the central nervous system in severe CHF and especially in cases complicated by atherosclerosis of the cerebral arteries, periodic Cheyne-Stokes breathing may occur.

Orthopnea (from the Greek “orthos” - straight and “rpol” - breathing) is a high degree of shortness of breath with a forced (semi-sitting or sitting) position of the patient. Orthopnea is not only a highly specific (see Table 7.2) symptom of CHF, but also its objective sign, detected during examination of the patient. Patients with severe CHF often sit in a chair, on a bed (if they still have the strength to sit down), lowering their legs and leaning forward, leaning on the back of a chair, an advanced table, or reclining on pillows (a high headboard is created with the help of several pillows or a rolled-up table). mattress). Any attempt to lie down causes them to experience a sharp increase in shortness of breath. Sometimes (in cases of untreated or “refractory” CHF) severe shortness of breath forces the patient to spend all the time - day and night (this is the only way he can short time fall asleep) - sitting. He wakes up feeling short of breath if his head slips off the pillows. Sleepless nights may continue for weeks until the patient receives relief from CHF therapy. This phenomenon is especially characteristic of left heart failure. Orthopnea is explained by the fact that in the vertical position of the patient, blood moves (deposited in the veins of the lower torso and limbs) with a decrease in venous return to the right atrium, and, consequently, the pulmonary circulation becomes less full-blooded. Improving respiratory function in an upright position is facilitated by the creation better conditions for the movement of the diaphragm, as well as for the work of auxiliary respiratory muscles. Orthopnea usually disappears (or becomes significantly less severe) with increasing right ventricular heart failure secondary to left ventricular failure.

Cardiac asthma (from the Greek “asthma” - suffocation, heavy breathing) - acute suffocation in a “heart” patient. An attack of severe cardiogenic shortness of breath, reaching the level of suffocation, indicates acute left ventricular heart failure (the most striking clinical manifestation of interstitial pulmonary edema), which can develop in the absence of pre-existing CHF and be the first manifestation of cardiac dysfunction. However, most cardiologists note a high positive predictive value of cardiac asthma when diagnosing chronic heart failure. Cardiac asthma can occur at any time of the day, but most often develops at night in a horizontal position. In this situation, blood leaves the depot, so-called hidden edema - extracellular fluid accumulated during the day in the tissues of predominantly the lower half of the body due to increased venous pressure - passes into the vascular bed, and a weakening of respiratory function, decreased gas exchange, and increased tone are also observed vagus nerve and bronchoconstriction. The patient awakens (if he could fall asleep before) usually after nightmares with a feeling of suffocation, tightness in the chest, fear of death, and is forced to sit up in bed. He is afraid to move, holds his hands on the bed, breathes slowly or rapidly ( breathing movements are carried out without hindrance!), often accompanied by a cough with serous sputum. If simple inspiratory dyspnea in a patient with chronic heart failure can decrease after the patient takes a vertical position on the edge of the bed, with his legs down, then in the case of acute left ventricular heart failure, severe shortness of breath and cough often persist in this position. The main cause of cardiac asthma is the discrepancy between LV dysfunction and the satisfactory “pumping” function of the right ventricle into the pulmonary circle in case of failure of the Kitaev reflex. If active therapy for heart disease is not carried out, then once it begins, attacks of cardiac asthma tend to recur more and more often. With the weakening of the contractility of the right ventricle, the addition of tricuspid valve insufficiency (this gave rise to calling it the “safety valve of the heart”) and with the development of chronic stasis as a result morphological changes in the lungs, as well as with sclerosis of the branches pulmonary artery when the failure of the Kitaev reflex is lost clinical significance, relapses of cardiac asthma usually stop or their frequency is reduced. There is a common misconception among doctors that cardiac asthma is one of the criteria for stage IIB CHF, while as heart failure progresses from stage II A to stage IIB, the relevance of asthma attacks (acute heart failure!) becomes less important.

Cough (tussis). Dyspnea in patients with chronic left ventricular heart failure is often accompanied (especially at night) by a cough, dry or unproductive with mucous, difficult to separate sputum (in patients with acute left ventricular heart failure, sputum is usually not viscous and is easily excreted in the form of a thin, foamy liquid). Cough (this is a reflex act) is explained by swelling of the mucous membrane of the “congestive” bronchi (bronchitis cyanotica) or irritation of the recurrent nerve, dilated left atrium. Overflow of blood small vessels lungs may be accompanied by diapedesis of red blood cells or even minor hemorrhage and the appearance of hemoptysis (blood in the sputum). During microscopy, in addition to red blood cells, such sputum may contain so-called “heart defect cells” (hemosiderophages).

According to the IMPROVEMENT study, fatigue is the second most sensitive symptom of heart failure after shortness of breath (Table 1), which is found in most patients even with initial symptoms of CHF. However, weakness or fatigue in patients with chronic heart failure is given unfairly little attention in many medical guidelines. Sometimes even this symptom is not classified as the main complaint of a patient with chronic heart failure, but as a “general” one (along with sweating, dizziness, irritability). There is no exact data on the specificity of the symptom under discussion, but, apparently, it is not great, since it can be observed in many other diseases. As with shortness of breath, the pathophysiology of fatigue does not have a trivial explanation. It should be noted that shortness of breath, caused by stagnation in the pulmonary circulation, is often an early sign of diastolic CHF, and increased fatigue, which is associated with impaired blood supply skeletal muscles, most often occurs with systolic CHF. Despite the fact that traditionally cardiac dysfunction is given a central place in the development of CHF, in lately Disorders of peripheral blood flow (in this case, in skeletal muscles) are becoming increasingly important in its pathophysiology.

Palpitations (palpitatio cordis - cardiac race) is the third most frequently detected symptom of CHF (Table 7.1), which is expressed in the patient feeling each contraction of his heart. More often, palpitations are felt with tachycardia (hence the synonym - cardiac race), but it can also be with a normal heart rate and even bradycardia. Apparently, for the sensation of heartbeat, not only the frequency of heart contractions matters, but also their nature and the state of the nervous system (persons with increased excitability of the nervous system complain of heartbeat more often). It is known that in normal conditions a person does not feel the activity of his heart, as well as the motor activity of other internal organs, since most of the reflexes from the somatic organs are closed in the reflex arcs of the areas of the central nervous system located below the cerebral cortex, and therefore are not recognized by the person in sensory perception. A change in the strength and quality of these reflexes in diseases of the cardiovascular system leads to the fact that they reach the cerebral cortex. However, sometimes with severe damage to the heart, rapid and strong contractions, which can be seen by shaking the chest wall, there are no complaints of heartbeat.

In the initial stages of CHF, the heart rate at rest does not deviate from the norm, and tachycardia occurs only during physical activity, but in contrast to the physiological increase in heart rate in patients with heart failure, it normalizes not after stopping the exercise, but after 10 minutes or later. As CHF progresses, palpitations and tachycardia are also observed at rest. Tachycardia is a compensatory hemodynamic reaction aimed at maintaining a sufficient level of stroke (Bowditch mechanism) and minute blood volume, the effectiveness of which is rated low by most researchers (except for situations with heart valve insufficiency) - it quickly becomes untenable, leading to even greater myocardial fatigue. In patients with CHF, tachycardia is explained by humoral (activation of the sympathoadrenal system, etc.), reflex

Patients with chronic heart failure may also experience “interruptions” in the work of the heart, cardiac arrest with its subsequent with a strong blow, sudden increase in heart rate and other subjective manifestations of rhythm and conduction disturbances.

Edema (from the Greek oidax - swell in lat. oedema - tumor, edema), detected by patients with chronic heart failure, indicates that the volume of extracellular fluid has increased by more than 5 liters and the stage of “hidden edema” has already been passed. Hidden edema can be detected by weighing or using the McClure-Aldrich test by increasing the rate (normally 40-60 minutes) of resorption of 0.2 ml saline solution(in the classic version, 0.8% NaCl solution), injected intradermally with a thin needle into the most superficial layer of the epidermis (the tip of the needle should be visible!) with the formation of a “lemon peel”, usually on the volar surface of the forearm. Also, hidden edema is indicated by a sharp increase in diuresis after the use of diuretics or cardiac glycosides.

There is a pronounced dependence of edema on the position of the body: it spreads from bottom to top. Cardiac edema is localized at first only in sloping areas - symmetrically, in areas located the lowest. In the early stages, when the patient is in a vertical position (in a lying patient, swelling begins in the lower back!), there is only swelling of the dorsum of the feet, which appears in the evening and disappears by the morning (a characteristic complaint is “shoes become tight in the evening”). As they develop, they spread to ankle joints (at the condyles), then rise to the lower leg and higher, gripping the arms and genitals. Subsequently, swelling of the legs becomes permanent and spreads to the lower abdomen and lower back up to anasarca (swelling usually does not occur on the face, neck and chest!). If a patient with already developed persistent swelling of the legs is transferred to bed rest, then they can significantly decrease and even disappear, but they appear or increase (move) in the lumbosacral region. With the long-term existence of edema, trophic changes in the skin, cracks (with massive edema, the skin often bursts and fluid leaks out of the tears), and dermatitis occur.

The pathogenesis of edema in patients with chronic heart failure can be satisfactorily explained on the basis of Starling's hydrodynamic concepts. However, the mechanical (hydrodynamic) factor is not the only one, and sometimes, apparently, the main one. The causes of edema in these patients are very diverse - a whole complex of neurohumoral, hemodynamic and metabolic factors are important.

Edema is traditionally associated with right ventricular failure, but it can also occur with decreased contractility of the left ventricle. Edema, caused predominantly by right ventricular failure and venous stagnation, usually appears later than the liver enlarges, they are extensive, dense to the touch, the skin over them is thinned, cyanotic, with trophic changes. Edema with left ventricular dysfunction occurs earlier than venous stasis, is small, soft, removable, located in areas of the body remote from the heart, the skin over them is pale. If the first type of edema depends on venous stagnation, then the second type of edema is the result of hypoxemic disorders, porosity of the capillary walls as a result of slow blood circulation.

Edema (both in history and according to physical examination) is an insensitive sign of CHF (see Table 2) and can be associated with disturbances of local venous or lymphatic outflow (in particular, varicose veins with venous insufficiency of degree II-III), diseases liver and kidneys, etc. Therefore, the cardiac genesis of edema is established only on the basis of a comprehensive examination of the patient.

A feeling of heaviness (with slowly developing congestion) or pain (with rapidly developing congestion) in the right hypochondrium in patients with right ventricular heart failure usually precedes the appearance of edema, since the liver is the first to respond to failure of the right half of the heart. These symptoms are caused by stretching of the liver capsule when the hepatic veins and capillaries are overflowing with blood (with rapid enlargement of the liver, stretching of the Glissonian capsule is accompanied by fairly intense pain in the right hypochondrium). With progression of CHF, prolonged stagnation (“ nutmeg liver", cardiac cirrhosis) symptoms of liver dysfunction appear - icterus of the skin and mucous membranes. Portal hypertension occurs - at the initial stage, the patient is bothered by a feeling of bloating and fullness in the abdomen, then he notices an increase in the abdomen in volume (due to the accumulation of ascitic fluid). In this case, it is extremely rare that the complaints of a patient with chronic heart failure may be supplemented by a feeling of heaviness in the left hypochondrium (due to an enlarged spleen).

Nausea, vomiting, loss of appetite, constipation, flatulence and other symptoms of gastric and intestinal dyspepsia are almost constant companions of congestive heart failure. The functions of the gastrointestinal tract in CHF are always impaired to a greater or lesser extent, both due to hypoxia and reflex influences. Often, dyspeptic disorders are a manifestation of the side effects of medications used to treat heart disease (in particular, aspirin, cardiac glycosides).

Decreased diuresis (of course not during the period of swelling) and nocturia. Impaired renal function occurs due to a significant (almost half) decrease in renal blood flow, reflex spasm of the renal arterioles and increased pressure in the renal veins (the mechanism of these phenomena was discussed above). As a result of a simultaneous (but not uniform) decrease in glomerular filtration and an increase in tubular reabsorption of sodium and water, the daily amount of urine decreases, and the urine becomes concentrated with a high relative density. Urine is released mainly at night due to some improvement in the blood supply to the kidneys at rest and in a horizontal position, and the release of edematous fluid into the blood at this moment. In addition, central dysregulation of the diuresis rhythm appears to be important.

Changes in body weight. Sudden weight gain (sometimes 2 kg or more in 2-3 days) is a sign of increasing cardiac decompensation. Various metabolic changes in patients with chronic heart failure, barely noticeable at the beginning, in stage III lead to extremely severe nutritional disorders of all tissues and organs - a progressive decrease in body weight is observed (so-called cardiac cachexia develops, which is masked for some time by the presence of edema).

Complaints from patients with chronic heart failure about decreased mental performance and mood, irritability, insomnia at night, and then drowsiness during the day are associated with a change that occurs early after a circulatory disorder. functional state central nervous system.

Taking an anamnesis (all types) is an important part of the examination of a patient with a disease of the cardiovascular system. In this case, the following are identified: risk factors or history of coronary artery disease; the presence of arterial hypertension, diabetes, valve pathology; family history of cardiomyopathy; the presence of recent pregnancy, a viral (“cold”) disease, risk factors for contracting AIDS and associated diseases; diseases of the thyroid gland and others systemic diseases; presence and degree of alcohol dependence. When collecting a clinical history, it is important to find out the characteristics and sequence of symptoms in a given patient. It is always important to establish the time of onset of each symptom and its relationship to the expected time of heart disease, likely provoking factors for the first manifestation and exacerbations of CHF, indications for therapeutic interventions and their effectiveness.

If possible, you should clarify the data of laboratory instrumental and other clinical studies that were carried out on the patient during the period of the present illness, obtain extracts from old medical records, copies of tests, electrocardiograms, etc. The information obtained often becomes one of the keys to recognizing CHF and largely determines the initial choice of medical actions.

It is necessary to ask the patient about physical and intellectual development, previous diseases, bad habits, living conditions, unfavorable professional factors. It is important to obtain information about the patient’s parents, relatives of the first and second degrees of kinship, find out their age, diseases, and if they died, then from what and at what age.

Clinical signs

Objective examination data can be varied. The main “findings” of the objective examination are presented in Fig. 1.

Figure 1. Main clinical signs of CHF

During a general examination of a patient with moderately severe CHF at rest, it is usually not possible to identify any signs of heart disease. When examining a patient with manifest CHF, the following signs can be detected:

1. Forced position of the patient (see above shortness of breath, orthopnea)
2. Cyanosis (Latin cyanosis - cyanosis from the Greek kyaneos - dark blue) - bluish discoloration of the skin is considered a common sign of CHF. However, we are not aware of any high-quality studies that accurately establish the sensitivity and specificity of this clinical sign. The appearance of cyanosis in patients with chronic heart failure is associated with a decrease in blood flow velocity and an increase in oxygen absorption in tissues, as well as insufficient arterialization of blood in the pulmonary capillaries, resulting in an increase in the content of reduced hemoglobin in the blood (has a blue color). The severity of cyanosis and its nature also depend on functional and organic changes small arteries(angiospasm, obliterating endarteritis, etc.), the diameter of small venules, the activity of arteriovenous anastomoses (the “short circuit” phenomenon), the first manifestations of cyanosis in patients with CHF are called acrocyanosis (from the Greek asgop - edge, limb + kyaneos - dark -blue), that is, cyanosis of the areas of the body farthest from the heart (tip of the nose, earlobes, lips, fingernails and toenails). The occurrence of acrocyanosis is caused mainly by a slowdown in blood flow and therefore it is peripheral in nature (it is often called peripheral cyanosis). Distinguish peripheral cyanosis from central cyanosis caused by respiratory disease (it is necessary to remember functional and structural changes in the lungs in patients with chronic left ventricular failure, leading to impaired blood oxygen saturation, which significantly complicates differential diagnosis), can be done using two techniques: 1) massage the earlobe until a “capillary pulse” appears - in the case of peripheral cyanosis, the cyanosis of the earlobe disappears, and in the case of central cyanosis, it remains; 2) allow the patient to breathe pure oxygen for 5-12 minutes - if after this cyanosis does not disappear, then it is of a peripheral (cardiac) nature.

With increasing cardiac weakness and oxygen deficiency, cyanosis increases (from barely noticeable cyanosis to a dark blue color) and becomes widespread (all skin and mucous membranes acquire a bluish tint) - central cyanosis, when saturation arterial blood oxygen drops to 80% and below. In its pathophysiological essence (impaired blood arterialization) and clinical manifestations, the latter is very close to that observed in patients with respiratory diseases. Particularly severe central cyanosis is observed in patients with congenital heart defects in the presence of an arteriovenous connection (“black heart patients”). The so-called “blue type” defects include tetralogy of Fallot (pulmonary artery outlet stenosis, ventricular septal defect, aortic dextroposition, right ventricular hypertrophy), Eisenmenger complex (subaortic ventricular septal defect, aorta “riding” over this defect, hypertrophy and dilatation of the right ventricle, normal or dilated pulmonary artery), Ebstein’s disease (dysplasia and displacement of the tricuspid valve into the cavity of the right ventricle), stenosis pulmonary artery, common arterial (aortopulmonary) trunk, atresia of the tricuspid valve, variants of transposition of the great vessels, defects of the interatrial and interventricular septum. Cyanosis can also occur due to poisoning with substances that form methemoglobin, sulfagemoglobin (sulfonamides, phenacetin, aniline, nitrobenzene, berthollet salt, arsenic hydrogen, nitrates and nitrites, etc.).

Pale skin and mucous membranes in patients with chronic heart failure can be combined with cyanosis (so-called “pale cyanosis”) with aortic heart defects (aortic stenosis, aortic valve insufficiency), collapse, heavy bleeding, infective endocarditis. With mitral orifice stenosis, pallor is combined with a purple-red “blush” on the cheeks - “mitral butterfly”.

1. Jaundice (Greek icteros). Jaundice staining of the skin and mucous membranes (primarily the sclera) in patients with severe chronic right ventricular heart failure is explained by the development of congestive fibrosis (“cardiac cirrhosis”) in the liver. Jaundice in patients with chronic heart failure is usually mild (rarely up to 68-85 µmol/l). However, sometimes, against the background of chronic stagnation in the liver, jaundice quickly and significantly increases - “bilirubinemic crisis.” The latter is associated with paroxysmal deterioration of intrahepatic circulation, developing following decompensation of cardiac activity. With infective endocarditis, the yellowness of the skin is combined with its pallor, and then the color resembles the color of “coffee with milk”. In such cases, petechiae with a pale center (Lukin-Libman symptom) can be found on the skin and especially on the conjunctiva of the lower eyelid.
2. “Corvisart's face” (Jean Nicolas Corvisart) is characteristic of significant untreated or refractory CHF. It is swollen, flabby, yellowish-pale with a bluish tint, its expression is apathetic, indifferent, drowsy, its eyes are sticky, dull, its mouth is constantly half-open, its lips are cyanotic.

Fingers in the form of " drumsticks“occurs with CHF developing in patients with infective endocarditis and some congenital heart defects.

1. Edema (see also “edema” above in the “Symptoms” section) in patients with chronic heart failure can be so pronounced that it can be detected during a general examination. However, even before pronounced swelling visible to the eye appears, one can notice by palpation the pastiness (from the Latin pastosus - pasty, flabby) of the tissues (primarily in the ankle area, on the back of the foot, shins) - when pressed, it appears gradually (within 1- 2 min) disappearing fossa, which is detected only by palpation. Massive, widespread swelling of the subcutaneous fat of the trunk and limbs, usually accompanied by ascites and hydrothorax, is called anasarca (from the Greek ana - on, up, up + sarx, sarcos - meat). The skin with edema, especially of the lower extremities, is pale, smooth and tense. With long-lasting edema, it becomes rigid, inelastic and acquires a brown tint due to diapedesis of red blood cells from stagnant capillaries. With pronounced edema, linear breaks may appear in the subcutaneous tissue of the abdomen, reminiscent of scars after pregnancy. A comparison of the sensitivity and specificity of edema detected by patient complaints and those detected during physical examination is presented in Table. 2.
2. Cardiac cachexia (from the Greek cachexia - exhaustion). Significant weight loss and the development of cachexia are observed in advanced stages of CHF and, in the case of treated cardiac decompensation, usually indicate the final (irreversible) stage of the disease. A patient with anasarca seems to “dry up” - “dry dystrophic type” according to V. Kh. Vasilenko:
3. activation of metabolism under the influence of additional work performed by the respiratory muscles, on the one hand, increased oxygen demand by the hypertrophied myocardium, on the other, and constant feeling discomfort associated with severe heart failure; 2) lack of appetite, nausea and vomiting caused by central disorders, intoxication with cardiac glycosides or congestive hepatomegaly and a feeling of heaviness in the abdominal cavity; 3) some malabsorption in the intestine caused by interstitial stagnation in the veins; 4) enteropathy leading to protein loss, which can be observed in individuals suffering from severe right ventricular CHF. Great value The development of cachexia in patients with chronic heart failure is attributed to changes in cytokine status (see above). Explicit or subclinical signs of malnutrition are found in 50% of patients with severe CHF. The development of pathological weight loss should be suspected in the case. a) body weight is less than 90% of ideal; b) with documented unintentional weight loss of at least 5 kg or more than 7.5% of the initial “dry” weight (without edema) during the last 6 months; c) mass index (weight/height2)<22 кг/м2.

Swelling and pulsation of the neck veins, dilatation of the veins of the arms, which do not collapse when raising the arm. In a healthy person, the veins of the neck can only be visible if he is in a supine position. If the overflow and expansion of the neck veins is noticeable in a vertical position, it means that there is a general (right ventricular heart failure, as well as diseases that increase pressure in the chest and impede the outflow of venous blood through the vena cava) or local (compression of the vein from the outside - tumor, scars, etc. or its blockage by a blood clot) venous stagnation. Moreover, if in severe diseases of the respiratory system the neck veins swell only when exhaling, due to an increase in intrathoracic pressure and difficulty in blood flow to the heart, then in CHF the swelling of the neck veins is constantly observed. The Austrian pathologist G. Gflitner proposed for clinical practice a simple method for approximate determination of the level of pressure in the right atrium - the higher the hand must be raised in order for the superficial veins of the hand to collapse, the higher the pressure in the right atrium (the height to which the hand is raised from level of the right atrium, expressed in millimeters, approximately corresponds to the value of venous pressure).

In patients with chronic heart failure, pulsation of the jugular veins can be seen in the neck area - the venous pulse. The swelling and collapse of the jugular veins during one cardiac cycle is due to the dynamics of blood outflow into the right atrium in different phases of systole and diastole of the heart (slowing down of blood flow in the jugular vein and its slight swelling during atrial systole and acceleration during ventricular systole with its collapse). In healthy people, the physiological negative venous pulse is usually not visualized and can only be analyzed when it is graphically recorded. If there is difficulty in the outflow of venous blood into the right atrium, a pathological venous pulse is detected during a routine examination. Pulsation of the jugular veins, coinciding in time with ventricular systole (the carotid artery pulsates outward from the jugular veins), is called a positive venous pulse and usually indicates tricuspid valve insufficiency - the 1st symptom of Bamberger (Bamberger I). However, the cause of noticeable pulsation of the jugular veins may be hypertrophy and insufficiency of the left ventricle, even in the absence of insufficiency of the right chambers, due to the transmission of pressure through the interventricular septum.

To determine the nature of the venous pulse, the jugular vein must be pressed with a finger. If the vein pulsation remains below the point of compression, then the venous pulse is positive; if absent, it is negative.

1. Plesh's symptom is swelling of the jugular veins when pressing on the liver from bottom to top (hepatojugular reflux), which is observed with severe right ventricular heart failure (in particular, with tricuspid valve insufficiency).
2. Palpation and percussion of the heart in patients with chronic heart failure can detect signs of cardiomegaly - displacement of the apical impulse (normally located in the 5th intercostal space 1-1.5 cm medial to the left midclavicular line) outward from the left midclavicular line and below fifth intercostal space; diffuse (more than 2 cm2) nature of the apical impulse (with concentric hypertrophy of the LV - “lifting”, with eccentric hypertrophy - “dome-shaped”); the so-called cardiac impulse (pulsation of the enlarged right ventricle to the left of the sternum, spreading to the epigastric region); expansion of the boundaries of relative dullness of the heart. To determine the proper maximum size of the heart, the patient’s height is divided by 10 and 3 cm is subtracted for the length and 4 cm for the diameter. With the development of heart disease in childhood, signs of cardiomegaly can be detected already when examining the heart area - protrusion of the chest (“heart hump”).

Tachycardia, arrhythmia, weakening of the sonority of heart sounds (hydropericardium must be excluded) and protodiastolic gallop rhythm, caused by a pathological (significantly enhanced) III tone, are often heard in CHF, but are not, however, specific signs for it. Noteworthy is the data that pathological III tone often occurs in patients with reduced systolic function, while IV tone can be determined when the compliance of the ventricular wall is impaired (diastolic dysfunction). Auscultation can also reveal “direct” and additional signs of heart valve disorders. Listening to heart murmurs may be a key point in diagnosing a heart defect underlying CHF, or may indicate the presence of functional (relative) mitral and tricuspid regurgitation as a result of dilatation of the ventricles and/or atria (hence, the valve ring in the area of ​​the atrioventricular junction), or dysfunction of the papillary muscles.

1. Systemic blood pressure is elevated in patients with acute decompensation or poorly controlled hypertension, but low blood pressure with low pulse pressure is more common in advanced disease. There is an opinion that blood pressure decreases when left ventricular heart failure predominates, and when right ventricular heart failure predominates, it may increase slightly (“congestive hypertension”). However, the validity of this judgment is not always confirmed in clinical practice.

Katzenstein's symptom (M. Katzenstein) - after compression of the femoral artery, blood pressure in a healthy person increases, and in the presence of weakness of the heart muscle, it decreases.

1. Physical examination of the respiratory organs in patients with chronic heart failure may reveal signs of pulmonary congestion with wet and dry rales, as well as the presence of fluid in the pleural cavity.

The appearance of silent moist rales, mainly in the phase of inspiration and/or crepitation (crepitatio - crackling) over the basal sections (especially on the side on which the patient lies) of the lungs in patients with left ventricular heart failure is associated with high pressure in the pulmonary veins, capillaries and the accumulation of small the amount of secretion in the lumen of the small bronchi (fine rales) or alveoli (crepitus). In patients with extremely severe decompensation of the left ventricle and cardiac asthma, in addition to moist rales (up to “bubbling” rales in the late phase of development of pulmonary edema), which are heard over all pulmonary fields, high-pitched dry rales, caused by congestion of the bronchial mucosa and accumulation of viscous transudate in the lumen of the bronchi. At the same time, such wheezing can be caused not only by left ventricular failure (rule out obstructive bronchial diseases!).

An increase in pleural capillary pressure in CHF and the penetration of fluid into the pleural cavities lead to the accumulation of pleural effusion (in the right pleural cavity more often than in the left), which can be established using known physical diagnostic techniques (lag of the “sick” half of the chest in the act of breathing , a sharp weakening or absence of vocal tremor over the area of ​​fluid accumulation, a dull sound or absolute dullness is determined by percussion, during auscultation, breathing and bronchophony are sharply weakened or absent). It is a common idea that since the pleural veins drain into the veins of both the systemic and pulmonary circulation, hydrothorax develops in both left and right ventricular CHF. However, A.G. Chuchalin believes that in patients with pulmonary hypertension with signs of right ventricular heart failure, fluid accumulation in the pleural cavity does not occur, and hydrothorax is associated with left ventricular dysfunction!

1. Hepatomegaly is the first symptom of liver congestion and represents the classic manifestation of right ventricular failure.

The liver is called the "reservoir" for stagnant blood and the pressure gauge of the right atrium. Increased central venous pressure is transmitted to the hepatic veins and interferes with blood flow to the central part of the lobule - central portal hypertension develops. The latter is accompanied by hypoxia, which over time causes atrophy and even necrosis of hepatocytes with replacement fibrosis and impaired liver architecture (up to the development of cardiac cirrhosis).

In the initial period of right ventricular CHF, the liver (painful on palpation!) protrudes only slightly from under the costal arch, its edge is rounded, smooth, and the surface is soft. Characteristic variability of its size is associated with the state of hemodynamics and the effectiveness of treatment. In the future, the organ can reach enormous sizes and “sink” below the iliac crest. The Plesch symptom is determined (see above). The edge of the liver becomes sharper, the surface becomes dense. In this case, the intensity of pain during palpation may decrease. Cardiologists and hepatologists note a variety of clinical manifestations of congestive liver: a clinical situation with severe CHF, manifested by anasarca and ascites and a slight enlargement of the liver, is possible, and, on the contrary, pronounced hepatomegaly with mildly expressed other phenomena of congestion.

With prolonged right ventricular CHF, such as, for example, in patients with damage to the tricuspid valve or chronic constrictive pericarditis, splenomegaly may develop simultaneously with hepatomegaly.

Systemic venous hypertension may also manifest as liver pulsations. True venous (for example, in patients with insufficiency of the right atrioventricular valve) or arterial pulsation coinciding with the apical impulse (for example, in case of aortic valve insufficiency) pulsation of the liver itself should be distinguished from the so-called transfer pulsation in cases where heart contractions are transmitted to it.

1. Ascites (Latin ascites - abdominal dropsy from the Greek ascos - leather bag for wine or water) in a patient with right ventricular CHF develops as a result of extravasation of fluid from the veins of the liver and peritoneum, the pressure in which is increased. As a rule, massive ascites is diagnosed in patients with tricuspid valve disease or chronic constrictive pericarditis. Ascites that develops after a long period of edema in patients with cardiac cirrhosis of the liver is often refractory to digitalis-diuretic therapy.

During examination with the patient in an upright position, the abdomen with severe ascites looks saggy; in a horizontal position, the stomach is flattened, and its lateral sections bulge (“frog belly”). With so-called tense ascites, the shape of the abdomen depends little on the position of the patient (there is so much fluid in the peritoneal cavity that it does not move). The navel protruding in the patient's vertical position allows one to distinguish an enlarged abdomen with ascites from that with significant obesity.

Conn's sign (N. Conn) is a sign of severe swelling of the scrotum in patients with ascites: the patient lies on his back with his legs widely abducted.

Detecting a large amount of free fluid in the abdominal cavity (more than 1.5 liters) does not cause difficulties. A percussion examination of the abdomen of a patient in a horizontal position on his back reveals dullness over the lateral areas, and intestinal tympanitis in the middle. Moving the patient to the left side causes a dull sound to shift downwards, and it is detected above the left half of the abdominal cavity, and in the area of ​​the right flank - a tympanic sound. To detect a small amount of fluid, percussion is used with the patient standing: with ascites, a dull or dull sound appears in the lower abdomen, disappearing in a clinostatic position.

Pitfield's symptom I (R.L. Pitfield) is a sign of ascites: if a sitting patient percusses the quadratus lumborum muscle with one hand, then the second hand, palpating the anterior abdominal wall, perceives weak vibrations.

The second issue of the journal “Heart Failure” for 2003 presents a scale for assessing the clinical condition in CHF, modified by V. Yu. Mareev, which consists of 10 categories and can be a good alternative to the six-minute walk test (see below) in objectifying the functional class of CHF in the case of inability for any reason to execute the latter:

1. Shortness of breath: 0 - no; 1 - under load; 2 - at rest.
2. Has your weight changed over the past week: 0 – no; 1 - increased.
3. Complaints about interruptions in heart function: 0 - none; 1 - yes.

IV What position is he in bed: 0 - horizontal; 1 - with a raised head end (+ 2 pillows); 2-1 + night suffocation; 3 - sitting.

1. Swollen neck veins: 0 - none; 1 - lying down; 2 - standing.
2. Wheezing in the lungs: 0 - no; 1 - lower sections (up to 1/3); 2 - to the shoulder blades (up to 2/3); 3 - over the entire surface of the lungs.
3. Presence of gallop rhythm: 0 - no; 1 - yes.
4. Liver: 0 - not enlarged; 1 - up to 5 cm; 2 - more than 5 cm.
5. Edema: 0 - no; 1 - pasty; 2 - swelling; 3 - anasarca.
6. Blood pressure level: 0 - >120 mm Hg; 1 - 100-120 mmHg; 2 -<120 мм рт.ст.

During the interview and examination of the patient, the doctor evaluates the clinical condition in all 10 categories of the scale. Mathematical processing of the study results consists of calculating the sum of points corresponding to the severity of clinical manifestations of CHF. In total, the maximum patient can score is 20 points (“critical” CHF). 0 points indicates a complete absence of signs of CHF. The results obtained are assessed as follows:

1. FC - up to 3.5 points
2. FC - 3.5-5.5 points
3. FC-5.5-8.5 points
4. FC - more than 8.5 points
5. Instrumental and laboratory diagnostics of chronic heart failure

The main instrumental methods for diagnosing CHF are non-invasive - ECG, echocardiography, chest radiography. According to indications, this minimum required set of studies is supplemented with more complex diagnostic techniques - stress tests, coronary angiography, cardiac catheterization, invasive hemodynamic monitoring using a Swan-Hans catheter, radioisotope methods, magnetic resonance imaging, endomyocardial biopsy, etc. However, they are rarely used , since the necessary information about cardiac dysfunction can be obtained using simple non-invasive studies and primarily echocardiography.

1. ECG. Although this method does not provide direct data on the state of the systolic and diastolic functions of the heart, its sensitivity in detecting CHF is so great that a normal ECG gives reason to doubt the correct diagnosis. The probability of absence of LV systolic dysfunction (negative predictive value) with a normal ECG exceeds 90%. In other words, no more than 10% of patients with chronic heart failure fall under the exception to the rule “myocardial dysfunction, one way or another, will always be reflected on the ECG.”

The most important ECG changes for objectifying CHF are presented in Table. 6.

Table 6. ECG changes in patients with chronic heart failure

Heart failure. signs

With moderate heart failure, patients usually do not experience much discomfort at rest, except when they have to remain in a horizontal position for more than a few minutes. In more severe heart failure, pulse pressure decreases, reflecting a decrease in stroke volume. In some cases, as a result of generalized vasoconstriction, diastolic blood pressure increases. The patient becomes noticeable cyanosis of the lips and nail beds, sinus tachycardia. In heart failure, systemic venous pressure is often pathologically high, which is manifested primarily by swelling of the jugular veins to varying degrees. In the early stages of heart failure, resting venous pressure remains normal. However, it can increase significantly during or immediately after cessation of physical activity, as well as with pressure on the anterior abdominal wall (positive abdominojugular reflex).

Loud III and IV tones are often heard in heart failure, but are not, however, specific signs for it. An alternating pulse is possible, i.e. a regular rhythm, against the background of which there are strong and weak contractions of the heart, and therefore, waves of peripheral pulses of different strengths. Alternating pulse can be recorded using sphygmomanometry, and in more severe cases, with simple palpation. It often occurs after extrasystoles and is usually observed in patients with cardiomyopathies, arterial hypertension or coronary heart disease. The reason for this lies in a decrease in the number of contractile fibers during weak contraction and/or fluctuations in the end-diastolic volume of the left ventricle.

Moist rales in the lower parts of the lungs. In patients with heart failure and high pressure in the pulmonary veins and capillaries, moist crackles on inspiration and dullness on percussion of the posterior lower parts of the lungs are often detected. In patients with pulmonary edema, coarse and whistling rales, sometimes accompanied by expiratory shortness of breath, are heard over both pulmonary fields. At the same time, such wheezing can be caused not only by left ventricular failure.

Cardiac edema. The location of cardiac edema usually depends on body position. If the patient can move, then edema is more often found in symmetrical areas of the lower extremities, in particular in the pretibial region and ankles, and if he is on bed rest, then in the sacral area. Palpable swelling on the face and hands in heart failure appears rarely and only in the later stages of the disease.

Hydrothorax and ascites. An increase in pleural capillary pressure in congestive heart failure and the penetration of fluid into the pleural cavities leads to the accumulation of pleural effusion. Since the pleural veins drain into the veins of both systemic and pulmonary circulation, hydrothorax develops with a noticeable increase in pressure in both venous systems, but can be a consequence of venous hypertension in any one of them: in the right pleural cavity more often than in the left. Ascites also develops as a result of extravasation of fluid from the veins of the liver and peritoneum, the pressure in which is increased (Chapter 39). As a rule, massive ascites is diagnosed in patients with damage to the right atrioventricular (tricuspid) valve and constrictive pericarditis.

Congestive hepatomegaly. Systemic venous hypertension is also manifested by dilatation, tension and pulsation of the liver. These changes can be observed in patients with ascites, but also in less severe forms of heart failure, regardless of the cause. With prolonged severe hepatomegaly, such as in patients with damage to the right atrioventricular (tricuspid) valve or chronic constrictive pericarditis, splenomegaly may simultaneously develop.

Jaundice. Signs of jaundice appear in the later stages of congestive heart failure. Its appearance is based on an increase in the levels of both direct and indirect bilirubin due to impaired liver function under the influence of stagnation of blood circulation in it and hepatocellular hypoxia, which leads to central lobar atrophy. At the same time, the concentrations of serum enzymes, in particular CGOT and SGPT, increase. In cases of acute liver congestion, jaundice can be severe and be accompanied by a significant increase in enzyme levels.

Cardiac cachexia. In severe chronic heart failure, significant weight loss and the development of cachexia can be observed. This occurs due to 1) activation of metabolism under the influence of additional work performed by the respiratory muscles, on the one hand, increased oxygen demand from the hypertrophied myocardium, on the other, as well as a constant feeling of discomfort associated with severe heart failure; 2) lack of appetite, nausea and vomiting caused by central disorders, intoxication with cardiac glycosides or congestive hepatomegaly and a feeling of heaviness in the abdominal cavity; 3) some malabsorption in the intestine caused by intestinal stagnation in the veins; 4) enteropathy leading to protein loss, which can be observed in individuals suffering from severe failure of the predominantly right heart.

Other manifestations. As a result of a decrease in the volume of circulating blood, the limbs become cold, become pale in color, and the skin becomes moist. Diuresis decreases; the specific gravity of urine increases, protein appears in it, and the sodium content decreases; prerenal azotemia is detected.

In patients with long-term severe heart failure, impotence and mental depression are common.

Heart failure. X-ray studies.

In addition to the enlargement of one or another chamber of the heart, the damage to which led to heart failure, signs of changes in the blood vessels of the lungs are detected, caused by increased pressure in their system (Chapter 179). In addition, chest x-ray can reveal pleural and interlobar effusions.

Heart failure. differential diagnosis.

The diagnosis of congestive heart failure can be established in the presence of its clinical manifestations in combination with characteristic symptoms of one or another etiological form of heart disease. Since chronic heart failure is often accompanied by enlargement of the heart, the preservation of normal sizes in all chambers of the heart casts doubt on this diagnosis, but in no case rejects it. Heart failure can be difficult to distinguish from lung disease. Differential diagnosis in this case is discussed in Chap. 26. Pulmonary embolism manifests itself with many symptoms characteristic of heart failure. However, hemoptysis, pleural chest pain, superior displacement of the right ventricle, and the characteristic mismatch of ventilation and perfusion of the lungs detected during lung scanning argue in favor of pulmonary embolism (Chapter 211).

Swelling of the ankles may be caused by varicose veins, a manifestation of cyclic edema, or the result of gravitational effects (Chapter 28). But in none of these cases will the edema be accompanied by hypertension of the jugular veins at rest or when pressing on the anterior abdominal wall. The renal nature of edema is usually confirmed by renal function tests and laboratory urine tests. Edema caused by kidney disease is rarely combined with increased venous pressure. Liver enlargement and ascites also occur in patients with liver cirrhosis, but in this case the jugular venous pressure remains within normal limits, and the positive abdominojugular reflex is absent.