CHF in the stage of decompensation. Decompensated heart failure: treatment. Heart failure, causes, symptoms, treatment

Heart failure is a fairly common problem faced by great amount of people different ages and gender. Sometimes such diseases are diagnosed even in young people, their development can be provoked by hereditary predisposition, lifestyle, influence environment as well as natural wear and tear of organs. Enough serious illness of the cardiovascular system is decompensated heart failure, the prevention of which will avoid a lot of difficulties. Let's talk about this on the pages of the site www.rasteniya-lecarstvennie.ru, and also consider the symptoms of such pathological condition and also talk about how it is treated.

In general, heart failure is characterized as a condition in which the cardiovascular system is unable to fully provide the tissues and organs of the body with a sufficient amount of blood. If we talk about the decompensated form of such an ailment, then it is considered as the last, so-called terminal stage development of heart failure. With such a violation, the heart is completely unable to deliver a sufficient volume of blood to the tissues, even if the patient is at rest. At the same time, all internal mechanisms that previously provided compensation continue to function.

There are several types of decompensated heart failure: chronic and acute, as well as right or left ventricular failure. In most cases, an acute form of heart failure is decompensated, because the body has absolutely no time to adapt.

About how decompensated heart failure is corrected (symptoms)

For timely access to the doctor and carrying out adequate therapy it is extremely important to pay attention to the state of the body and manifestations of decompensated heart failure. In certain cases, the diagnosis is complicated by the fact that the clinical symptoms of one disease are superimposed on the signs of some other.

It should be borne in mind that there is not a single specific manifestation of heart failure, focusing on which you can make a 100% correct diagnosis.

In decompensated heart failure, the patient often has a history of myocardial injury or heart failure. The patient is also worried about shortness of breath in different time day (both day and night), as well as at rest and during physical activity.

A characteristic symptom of this pathological condition is also considered to be general weakness. Most patients experience increased swelling, an increase in body weight or volume abdominal cavity.

Conducting a physical examination helps to identify other manifestations of the disease. They are represented by an increase in pressure in jugular vein, wheezing in the lungs and hypoxia. Among characteristic symptoms there is also an arrhythmia in different options, decreased volume of urine formation, as well as constantly cold brushes and lower limbs. A correct diagnosis can be made only after a series of instrumental tests.

About how decompensated heart failure is corrected (treatment)

Correction of decompensated heart failure is aimed at eliminating the manifestations of stagnation, improving the volumetric parameters of the heart, as well as identifying the so-called decompensation trigger factors, and then eliminating them. Treatment also includes long-term drug therapy and the maximum possible reduction side effects. At acute form ailments are carried out resuscitation after which the patient is sent to hospital treatment.

modern medicine uses a lot therapeutic methods for the treatment of patients suffering from left ventricular systolic dysfunction. They are prescribed angiotensin-converting enzyme inhibitors, as well as angiotensin II receptor blockers. In addition, beta-blockers and aldosterone antagonists are actively used. Therapy may also include the use of cardioverters and defibrillators, which are implanted inside. Such measures help to reduce by an order of magnitude the likelihood of developing lethal outcome. Diuretics provide an increase in the amount of urine excreted from the body, thereby eliminating swelling and shortness of breath. Beta-blockers effectively optimize the activity of the heart, somewhat slowing down its rhythm. And taking an angiotensin-converting enzyme inhibitor helps to stop further development diseases, thereby reducing the mortality rate. Cardiac glycosides are often the drugs of choice.

In the event that the treatment is ineffective, the patient can be pumped out fluid from the abdominal cavity, which helps to slightly alleviate his condition for a while.

Inpatient treatment is indicated for patients with decompensated heart failure. Doctors carry out the correction of ailments that provoked such a violation, and also provide the patient with complete rest. shown diet food while smoking and alcohol are under strict prohibition.

Prevention of decompensated heart failure

The main measure for the prevention of decompensated heart failure is systematic observation by a cardiologist, and competent timely treatment of diseases of the cardiovascular system. In addition, in order to prevent such a disease, it is extremely important to conduct healthy lifestyle life, avoid stress and other overloads.

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Causes of the appearance of pathology

Consider what decompensated heart failure is, and as a result of which it occurs. There is a certain set of factors that provoke this phenomenon:

• congenital heart disease;
• heart surgery;
• inflammation of the heart muscle - myocarditis;
• ischemic disease;
• brain injury;
• hypertensive crisis;
• increased pressure in the pulmonary circulation;
• hypertrophic cardiomyopathy;
• arterial hypertension;
• aortic stenosis;
• bradyarrhythmia, tachyarrhythmia.

In addition to the causes directly related to disorders of the heart, it is necessary to identify external criteria that provoke the emergence and development of the problem:

• regular alcohol abuse;
• excess body fat;
• thyroid disease;
• liver failure;
• poisoning with toxins, poisons, chemicals;
• advanced form of bronchial asthma;
• errors in the selection of drugs.

These contributing factors only exacerbate the picture, postponing recovery, provoking complications and new diseases. The risk group includes patients diagnosed with diabetes mellitus, obesity, and those who are unable to get rid of bad habits. The vessels of such people are weak, many loads are beyond their strength, since the heart is hard to cope with its main tasks.

Varieties and symptoms of the disease

In any form, decompensated heart failure is manifested by the following symptoms:

• asthma attacks that occur mainly at night;
• swelling of the limbs;
• shortness of breath, manifested with minor physical exertion, it causes stagnation of blood in the lungs; without proper treatment, shortness of breath bothers a person even at rest;
• pain on the right side chest;
• memory impairment, retardation mental activity, blurred consciousness.

Depending on the stage of the disease, acute and chronic forms of DHF are distinguished.

Heart failure in the stage of decompensation can affect the right or left ventricles, in addition, there is a mixed form, when parts of the heart on both sides are affected.

The right side of the heart is responsible for the systemic circulation. Decompensated heart failure of the right ventricle is manifested as follows:

• swollen legs;
• feel the heaviness right side chest;
• hydrothorax;
• ascites

Left ventricular failure leads to inadequate blood flow in a small circle, which can be identified by some of the signs:

• lungs swell;
• heaviness is felt in the whole body;
• often there are bouts of dry cough;
• the patient becomes short of breath even in the absence of any exertion.

Diagnostic methods

The patient examination program includes the following mandatory activities:

Hardware diagnostics in combination with urine and blood tests gives a comprehensive picture that provides the most precise definition causes of the problem, as well as denoting the stage, specifics, possible complications or related illnesses. These measures can help in the appointment of the most effective therapeutic regimen.

Basic principles of treatment and preventive measures

Decompensated heart failure should be treated as soon as possible. medical intervention, and the ongoing therapy pursues the most important goals, namely:

• normalization of blood and fluid volumes at which the heart will function adequately;
• elimination of congestion in organs;
• identification and elimination of decompensating factors that provoke or aggravate negative processes;
• minimizing side effects;
• selection of a long-term treatment program.

Immediately after diagnosing DHF, the patient is sent to the hospital, where he is prescribed the following groups of drugs:

• ACE inhibitors;
• "Morphine";
• Digoxin - for normalization heart rate;
• diuretics - in tablets or in the form of injections - eliminate swelling, shortness of breath, lower blood pressure;
• "Veroshpiron" - aldosterone receptor blocker;
• beta inhibitors that reduce energy needs hearts in contraction;
• cardiac glycosides stimulate cardiac output.

Sometimes it may be necessary to prescribe immunomodulators for recovery defensive forces body and hepatoprotectors to stimulate liver function. As for food, here, as in Everyday life, complete rest: no systems should be overloaded, including the digestive system. alcohol, smoking, spicy food and salt are completely excluded, as well as fatty foods, fried foods and red meat.

In some cases, the disease is so advanced that the patient requires surgery due to the high risk of cardiac arrest. Can be applied:

• shunting;
• coronary angioplasty;
• installation of a pacemaker;
• defibrillator implantation.

Every person with heart failure, knowing about decompensated heart failure, what it is, must follow a list of preventive measures to prevent the progression of the disease to the stage of decompensation:

1. Constant monitoring by the attending cardiologist with regular diagnostics of the state of the heart muscle (once a year).
2. Emotional and physical stress is strongly discouraged, although light gymnastics and daily walks are shown.
3. Fluid intake needs to be monitored.
4. The food here plays one of the critical roles. So, it is better to focus on vegetables, fruits and berries in a variety of forms and combinations. You can not include spices, salt, smoked meats in your diet, you should give up alcohol.
5. Do not allow excessive development of infections, try to treat them on time. Get vaccinated.
6. Engage in strengthening immunity.

A calm environment, conscientious intake of drugs and dietary nutrition can significantly reduce the risk of exacerbations and side effects during treatment.

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Kinds

By type, decompensated heart failure is divided into:

• acute and chronic;
• right ventricular and left ventricular.

Acute

The acute form is usually decompensated, since the body does not have time to cope with the ongoing changes.

With the development of acute forms, emergency medical care, resuscitation, and placement in a hospital are required.

Chronic

In the presence of cardiac pathologies, there is a possibility of developing decompensated chronic heart failure. Its signs in lesions of the left and right ventricles are similar.

Symptoms accompanying the chronic form:

• the occurrence and development of swelling of the lower extremities;
• swelling of the abdomen;
• swelling of the scrotum;
• swelling of the liver;
• swelling of the pericardium;
• shortness of breath even in the absence of exertion;
• tachycardia.

Depending on the localization of the lesion, left- and right-sided ventricular failure is distinguished. Accordingly, overstrain (for example, due to a decrease in the lumen of the aorta) of the left ventricle causes a left ventricular form of pathology. Another reason is the weakening of the contractile function of the myocardium, caused, for example, by a heart attack.

The right ventricular form develops due to excessive load to the right ventricle. The cause may be pulmonary hypertension, as a result of which blood flow slows down.

There is also a mixed form of pathology in which both ventricles are affected.

Symptoms of decompensated chronic insufficiency

Diagnosis requires the presence of certain symptoms. However, it must be borne in mind that the signs of one disease overlap with the symptoms of other pathologies. In addition, there is no clear-cut sign that would allow a diagnosis to be made with certainty.

When making a primary diagnosis, they are guided by the presence of the following symptoms:

• history of myocardial injury or heart failure;
• shortness of breath, which occurs regardless of the time of day and exerted loads;
• general weakness;
• swelling, weight gain, an increase in the abdominal cavity in volumes.

Breathing difficulties are often observed when the patient is in the supine position. This is caused by blood flow to the lungs.

There may also be clouding of consciousness caused by a deterioration in the blood supply to the brain.

With lesions localized on the right side, patients often complain of discomfort in the right hypochondrium.

During the examination, the doctor examines the patient's condition through a physical examination and draws attention to the following points:

• the presence of wheezing in the lungs, hypoxia;
• arrhythmia;
• decreased urine output;
• cold feet and hands.

Diagnostics

Diagnosis of the disease involves instrumental studies. For this purpose, the following methods can be used:

• electrocardiography;
• chest x-ray;
• determination of B-type natriuretic peptide or N-neutral.

Natriuretic peptides regulate water-salt exchange in the body. They begin to be produced with an increase in myocardial tension against the background of high pressure in the left ventricle.

In cardiovascular disorders, these peptides display indicators of the contractile activity of the heart muscle. Accurate data can be obtained through the study of B-type peptides.

Standard blood and urine tests are also performed. Indicators of the content of urea, creatinine, electrolytes, glucose, transaminase in the blood are revealed. As a result, the pressure of arterial blood gases and the state of the thyroid gland are determined.

In some cases, transthoracic echocardiography is prescribed, the results of which make it possible to determine the systolic and diastolic functions of the left ventricle, valves, pressure in the left atrium, right ventricle and vena cava.

The introduction of a catheter into the central vein or pulmonary artery allows you to determine the pressure that occurs when the chambers are filled, which makes it possible to determine the cardiac output.

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Clinical picture

In order to start effective treatment, a rapid diagnosis is necessary, which is possible if certain symptoms are present. The procedure is complicated by the fact that often the clinical manifestations of one disease are superimposed by signs of another.

Attention! Due to the heterogeneous nature of end-stage heart failure, there is no clear specific sign that would 100% confirm the diagnosis.

Decompensated heart failure has the following symptoms:

• history of myocardial injury or heart failure;
• shortness of breath in daytime and nocturnal, during exercise and at rest;
• general weakness;
• edema, an increase in body weight or volume of the abdominal cavity.

With the help of a physical examination, the following signs of the disease can be detected:

• increased pressure in the jugular vein;
• wheezing in the lungs, hypoxia;
• arrhythmia in any of its manifestations;
• decrease in the volume of urine formation;
• cold lower extremities and hands.

Diagnosis is impossible without instrumental tests. For example, to determine venous congestion and interstitial edema a chest x-ray is performed.

Research methods and principles

What is decompensated heart failure is understandable, this is when the cardiovascular system is unable to perform elementary functions. Widely used for diagnosis instrumental research. These include electrocardiography, chest x-ray, and measurement of B-type natriuretic peptide or N-neutral. Laboratory tests are carried out, namely blood/urine analysis. The level of urea, creatinine, electrolytes in the blood, transaminase, glucose is determined. These tests evaluate arterial blood gas pressure and evaluate thyroid function.

In some situations, transthoracic echocardiography is performed, it allows you to evaluate the systolic and diastolic functions of the left ventricle, valves, as well as filling pressure with blood in the left atrium, right ventricle and inferior vena cava. catheterization central vein or pulmonary artery provide valuable pressure information when filling the cardiac chambers, after which it is possible to easily calculate cardiac output.

Targets and drugs used in treatment

Having an accurate idea of ​​​​what this disease is, the goals become clear, the action of which is aimed at:

• elimination of manifestations of stagnation;
• optimization of volumetric performance indicators;
• detection, and in case of presence of trigger factors of decompensation, their elimination;
• optimization of long-term therapy;
• minimizing side effects.

In recent decades, therapeutic approaches to the treatment of patients with left ventricular systolic dysfunction have been well developed and applied. For this, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers, aldosterone antagonists, cardioverter defibrillators implanted inside are used. All this has shown considerable effectiveness in reducing the number of cases of death.

Patients diagnosed with decompensated heart failure are hospitalized. As far as possible, the diseases that cause heart failure are treated. The patient is provided with complete rest in order to reduce the load on the heart.

Important! In order to avoid thrombosis in the vessels of the lower extremities, being in bed should still be limited. It will be better if medical manipulations are carried out in a sitting position.

Regarding nutrition, it should be carried out in small portions, by the way, salt intake is strictly limited. Alcohol and smoking are strictly prohibited. For drug exposure, diuretics are used - drugs that increase the volume of urine excreted from the body, lower blood pressure and significantly reduce the severity of edema and shortness of breath. Beta-blockers normalize the work of the heart and slow down the rhythm of its work, but at the beginning of their administration, the control of the doctor is important. Angiotensin-converting enzyme inhibitors can stop the progression of the disease, thus reducing the mortality rate. The dosage of the above drugs should be carried out in strict accordance with the doctor's recommendations.

infocardio.ru

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Chronic heart failure (CHF) is one of the serious problems in many developed countries of the world. This is the only disease of cardio-vascular system whose prevalence continues to increase. The problem of the prevalence of CHF is more often determined by the increase in the life expectancy of people, that is, the “aging” of the population. The detection rate of CHF depends on the age of patients and almost doubles with every decade of life after the age of 45 years. A serious not only medical but also social problem is the treatment of patients with CHF, which requires large financial costs.

What is heart failure?

From a pathophysiological point of view, heart failure is the inability of the heart muscle, in the absence of a decrease in circulating blood volume and hemoglobin level, to supply tissues with blood in accordance with their metabolic needs at rest and / or during moderate exercise. Heart failure is a pathology that develops as a result of a decrease in the ability of the myocardium to contract. In this case, there is a discrepancy between the load imposed on the heart and the ability of the heart to perform its work. CHF develops as a result of violation of both functions of the heart: both systolic and diastolic.

Systolic function is an active process, as a result of which the heart muscle contracts, blood is pushed into the vessels and perfusion of internal organs and peripheral tissues is carried out. Impaired shock function, or systolic heart failure, is a consequence of CHF, regardless of the causes that caused the development given state. Traditionally, CHF is associated precisely with systolic insufficiency, which in the vast majority of cases causes the development of clinical symptoms that force the patient to consult a doctor.

Equally important for the normal functioning of the heart is its diastolic function, that is, the ability to relax. Violation of diastolic work, or diastolic heart failure, in some cases is the main one in the development and progression of CHF. With the development of diastolic insufficiency, the heart cavities are usually not expanded, the myocardium has normal contractility, but the filling of the ventricles with blood is impaired. This decrease in diastolic filling depends on both changes in the passive elasticity of the myocardium and changes in the mechanisms of its active relaxation. The leading factors determining changes in diastolic relaxation in CHF are disorders of calcium metabolism and energy supply, changes in sympathetic innervation, and myocardial remodeling processes.

In almost all diseases leading to the development of CHF, violations of both one and another function of the heart are detected. Therefore, among the pathophysiological causes of the development of CHF (both systolic and diastolic), the following can be distinguished.

• pressure overload (arterial hypertension, primary vascular pulmonary hypertension, stenosis of the aortic or pulmonary artery);
• volume overload (mitral, aortic, or tricuspid valve regurgitation, other birth defects hearts);
• combined overload.

Violations of heart rate (tachysystolic forms of cardiac arrhythmia, bradysystole). Age changes.

Extracardiac causes (compression of the heart by exudate or tumor, changes in the pericardium, cardiac tamponade, dysfunction endocrine organs, hypothyroidism, diabetes mellitus, etc.).

Despite the variety of causes leading to the formation of heart failure, the development of CHF goes through three main stages: initial, adaptive and final:

1. 1. At the initial stage, myocardial damage occurs, or the heart begins to experience an increased hemodynamic load, resulting in the development of myocardial dysfunction, the essence of which lies in the discrepancy between cardiac output and the metabolic needs of organs and tissues. The consequence of a decrease in cardiac output is a decrease in perfusion of organs and tissues.
2. 2. The adaptive stage is characterized by the organism getting used to the changed conditions of functioning. The initial stage of heart failure proceeds without significant violations of intracardiac and systemic hemodynamics. This happens as a result of the inclusion of adaptation mechanisms. Mechanisms of adaptation, or compensation, in CHF cover all functional systems from the cellular level to the whole organism. Adaptive mechanisms of CHF include changes in neuroendocrine regulation, alternative and replacement metabolic pathways, cardiac factors - the Frank-Starling law, remodeling processes of both the myocardium and its components at the cellular and molecular levels.
3. 3. At the final stage, the CHF phenotype is formed. As a result of the implementation of compensatory-adaptive reactions at various levels in many patients, the functional state of most body systems remains practically normal until a certain time. But over time, supporting mechanisms are transformed into pathogenetic factors. As a result of “switching on” several mechanisms (prolonged activation or hyperactivation of neurohumoral systems, heart remodeling, etc.), further deterioration in myocardial functioning occurs and irreversible changes in the heart develop, that is, a CHF phenotype is formed.

Heart failure is acute and chronic:

• Acute heart failure occurs as a result of any catastrophe: severe cardiac arrhythmias (paroxysmal tachycardia, ventricular fibrillation and others), myocardial infarction, acute myocarditis, acute weakening of the contractile function of the myocardium in patients with heart defects, embolism of the pulmonary artery trunk.
• Chronic develops gradually over a long period of time. The reasons may be aortic defect, mitral insufficiency, hypertonic disease, emphysema, pneumosclerosis.

Heart failure is also differentiated according to the parts of the heart.

Allocate compensated and decompensated heart failure:

• Compensated CHF is an early, latent form of cardiac dysfunction, when the metabolic needs of organs and tissues in the rest phase are provided by activation compensatory mechanisms.
• Decompensated - these are manifest forms of a pathological condition, when the disease manifests itself in a number of symptoms. Dyspnea, with or without signs of increased fluid volume (edema) is the most common clinical symptom of heart failure. A high degree of dyspnea does not correlate with the degree of left ventricular (LV) dysfunction that caused it, which is more significant indicator forecast.

Pathophysiology of heart failure

The pathophysiology of CHF is considered to be a complex and complex process. CHF is a combination of manifestations of primary pathological influences and a whole complex of compensatory mechanisms. Despite the fact that the clinical diagnosis of CHF syndrome usually does not cause great difficulties, the subtle pathophysiological and biochemical changes that occur in this case are much more difficult to study. Taking into account the first conceptual models of (cardiac and cardiorenal) pathogenesis, the main reason for the occurrence of CHF belonged to a decrease in the contractile activity of the heart, as well as the exchange of electrolytes and water in the body. The widespread use of this concept led to the active use of cardiac glycosides in the clinic, and then diuretics for the treatment of congestive syndrome.

In the mid 70s. In the 20th century, the cardiocirculatory model was the most famous. When myocardial dysfunction occurs, compensatory changes in hemodynamics are formed, which are divided into heterometric (increase in preload, myocardial hypertrophy) and homeometric (increase in the frequency of cardiac activity cycles, increase in large peripheral resistance). These changes in hemocirculation, primarily aimed at increasing shock value and / or maintenance of blood pressure with a decrease in cardiac output due to the mechanisms of Frank-Starling (increased strength and speed of contraction of the heart muscle with an increase in fiber length), Bowdich (increased strength and speed of contractions of the heart muscle with an increase in heart rate), Anrep (increase in strength contraction of the heart with an increase in afterload), then they begin to have a negative effect, contributing to the development of cardiac decompensation.

From a hemodynamic point of view, the combination of a decrease in myocardial attracting function and changes in peripheral circulation associated with a change in pre- and post-exercise characteristics is considered main reason manifestations of CHF. According to this idea, drugs that affect both central and peripheral hemodynamics were introduced into the practice of treating CHF. However, numerous clinical studies have led to disillusionment with inotropic stimulants (sympathomimetics, phosphodiesterase inhibitors) and a far from unambiguous assessment of the efficacy and safety of vasodilators in reducing left ventricular function. The progression of CHF is not as closely related to the state of the attracting function of the heart, as previously thought. The state of the attracting function of the left ventricle is not closely related to exercise tolerance.

80s - early 90s characterized by the creation of a neurohormonal theory of the pathogenesis of CHF. The neurohumoral model is widely known and consistent with the results of many trials that have demonstrated an increase in the survival of patients with CHF after neurohumoral unloading of the heart with angiotensin-converting enzyme blockers (ACE inhibitors). Good results in the use of ACE inhibitors have accelerated the search for other neurohumoral stimulants for the treatment of patients with CHF, the possibility of using non-peptide receptor antagonists to angiotensin II subtype I is being actively studied. Creating new groups pharmacological preparations for the treatment of CHF is closely related to the success of pathophysiology and biochemistry in considering the role of neurohumoral changes in the pathogenesis and sanogenesis of CHF.

The list of neuroendocrine systems activated (at the vascular and, more importantly, at the local level) in CHF is quite extensive. Among the most studied regulatory systems related to the neurohumoral theory of CHF pathogenesis are reninangiotensin, aldosterone, sympathetic-adrenal, endothelin, kallikrein-kinin, natriuretic, vasopressin, adrenomedullin, neuroendopeptidase. Data concerning new groups of mediators that are activated in CHF are of interest not only from the point of view of pathophysiology, but are of great importance in improving the treatment of the disease.

The program to isolate the pathogenetic mechanisms of CHF did not stop there. Not so long ago, a young theory of CHF progression was presented, the basis of which is the assumption of immune activation and systemic inflammation as signs poor prognosis and high cardiovascular risk. According to this theory, the non-specific triggering of macrophages and monocytes, working with strong shifts in microcirculation, is an activator of the creation of pro-inflammatory cytokines responsible for the evolution of LV dysfunction.

"Assistance" immune system with the pathogenesis of CHF may seem unusual. But immune defense of the organism is activated not only when interacting with infectious agents, but also when arterial blood supply is disturbed, hemodynamic overload and other effects on the heart, which are the initial link in the development of diastolic and / or shock impaired function.

Thanks to the successful development of the ideas of molecular biology, promoting research in the field of genetics, in recent times papers devoted to the study of the contribution genetic reasons in the development of CHF. This was facilitated by the formation of the theory of "phenotypic modulation", based on data from basic research in such sciences as genetics and cell biology. Phenotypic modulation refers to the competence of cells to change their phenotype and function within the same tissue.

The current theory of the pathogenesis of CHF combines all the concepts written above on the basis of their complementarity, since it is not necessary to rely on the fact that with the help of a single sufficiently logical theory of pathogenesis it is possible to explain all the disorders in a patient with heart failure and, moreover, solve all the problems of treatment , influencing the only mechanism for the formation and progression of circulatory failure.

Neurohumoral activation in CHF

Changes in the activity of neurohumoral systems are one of the leading adaptive mechanisms aimed at maintaining cardiac output and blood pressure, which is necessary to ensure normal tissue perfusion. In some cases, neurohumoral activation can serve as a factor in long-term adaptation. However, neurohumoral activation as a result of a permanent excessive regulatory response ultimately has Negative influence on the activity of the cardiovascular system and becomes one of the leading pathogenetic mechanisms of CHF.

During the evolution of CHF, three stages of neurohumoral activation can be distinguished:

1. 1. Deterioration of myocardial function leads to a decrease in cardiac output and a decrease in blood pressure. The latter, due to the effect on arterial baroreceptors, leads to an increase in efferent sympathetic self-activation, which results in rapid rise volume of blood in the cavities of the heart and activation of cardiopulmonary baroreceptors in order to reduce sympathetic activation and increase the production of atrial natriuretic hormone. An increase in the latter is aimed at reducing the activation of the sympathetic-adrenal system (SAS) and preventing an increase in RAAS activity.
2. 2. Over time, the blocking effect of cardiopulmonary baroreceptors on the SAS decreases, and sympathetic innervation(primarily the heart) increases. Efferent renal sympathetic innervation leads to activation of the RAAS, which is initially opposed by the atrial natriuretic peptide system. However, its inhibitory effect quickly decreases, and RAAS activity increases.
3. 3. The activity of the SAS and RAAS is significantly increased, which leads to a further decrease in cardiac output and an increase in sodium reabsorption. Increased sensitivity of carotid chemoreceptors metabolic changes in muscles with triggering of muscle chemoreceptors even at small exercise. All these changes lead to a further increase in the neurohumoral activity of both circulating and local tissue systems. The production of various endogenous vasoactive substances, mainly of vasoconstrictor action, is enhanced. At the same time, the processes of cell proliferation, protein biosynthesis and collagen formation (fibrosis) are activated, that is, the processes of remodeling of the heart and blood vessels begin.

Cardiac compensatory mechanisms

The main cardiac compensatory mechanisms are the Frank-Starling mechanism and myocardial remodeling.

The amount of muscle contraction is determined by its length before contraction. As the fiber length increases, increased force of contraction and an increase in stroke volume. This mechanism is associated with tonogenic dilatation of the ventricle of the heart and belongs to the cardiac factors of immediate adaptation. The effectiveness of the Frank-Starling mechanism significantly decreases under conditions of a decrease in myocardial contractility and with a significant increase in diastolic pressure in the ventricles of the heart. An increase in diastolic pressure in the ventricle above a certain limit no longer leads to an increase in the length of muscle fibers and a further increase in cardiac output does not occur.

LV remodeling in heart failure is a set of changes in its shape, internal volume and weight of the myocardium, arising as a response to inadequate hemodynamic conditions for the functioning of the heart or its damage. In the clinically advanced phase of LV systolic insufficiency, the remodeling phenomenon is embodied in its hypertrophy, dilatation, and geometric deformation.

The process of increasing hypertrophy of the heart muscle is a prolonged adaptation of the myocardium to an increase in hemodynamic load or local damage to cardiomyocytes. The development of hypertrophy is a compensatory-adaptive mechanism aimed, on the one hand, at reducing intramyocardial tension due to wall thickening, and, on the other hand, at maintaining the ability to develop sufficient intraventricular pressure in systole. However, already in the very process of development of hypertrophy, the foundations are laid for further myocardial decompensation.

The most important factor that determines the development of myocardial decompensation is the violation of the ratio between the contractile elements and the capillary network and energy imbalance in the hypertrophied myocardium. In hypertrophy, the development of capillaries lags far behind the increase in muscle fibers. The lag in the increase in the number of capillaries is one of the reasons for the development of energy deficiency in the hypertrophied myocardium.

The development of cavity dilatation is the second end mechanism of cardiac remodeling. Enlargement of the cavities and their changed geometry allows, at a certain stage, to maintain a more or less adequate cardiac output. This is achieved as a result of an increase in the volume of blood inside the heart. The heart, due to the increase in residual volume, is able to expel large quantity blood at a much lower amplitude of contraction. However, the formation of dilatation usually occurs already in conditions of a significant breakdown of energy metabolism in the heart muscle, and a further increase in the heart cavities is accompanied by an increase in intramyocardial tension and increased activation of tissue neurohumoral systems, which quickly leads to the depletion of myocardial energy reserves.

Decompensation

Prolonged disruption of the activity of the cardiovascular apparatus eventually leads to the disruption of compensatory mechanisms and the manifestation of symptoms of decompensated heart failure. The immediate cause of the increase in the CHF clinic may be different moments, many of which usually do not lead to CHF on their own. The doctor most often encounters the following situation: pulmonary embolism, myocardial infarction, infection, anemia, thyrotoxicosis, pregnancy, cardiac arrhythmias (even a typical increase in heart rate), inflammation of the heart muscle, endocardium, multiple organ hypertension, severe physical, emotional, nutritional and other (including medication) external stresses.

It is important to note that the prognosis in patients with heart failure, the initial mechanism of which is known and is removed in any way (including intensive treatment) is better than in patients in whom the underlying cause could not be identified.

Despite advances in the treatment of heart failure, the prognosis in these patients remains unfavorable.

Decompensated heart failure is a disease of the cardiovascular system and is characterized by an inability to supply tissues and organs. necessary quantity blood for normal functioning. This is the last stage of the pathological process, in which pathofunctional changes occur. With progression, it does not cope with its main function either during the normal course of life and physical exertion, but also at rest.

This diagnosis says that the heart can no longer supply other organs. necessary blood, decompensated insufficiency is already a state when the compensatory mechanism and reserves cannot compensate for insufficient blood supply. Damage to the heart at this stage is already so serious and irreversible that the body cannot replace this deficiency with anything.

There is a division of decompensated heart failure into types according to the location of damage and the form of the course of the disease. It can be right ventricular or left ventricular, as well as acute or chronic stages.

It is decompensated heart failure that is the result of an acute and rapid development of pathology, when the body does not have time to rebuild and adapt to forced changes.

acute form

It can occur in both the left ventricle and the right. Left-sided localization occurs as a result of myocardial infarction, with mitral valve stenosis. The inability of the heart to pump blood leads to congestion and congestion of the vessels in the lungs. As a result, it leads to pulmonary edema, causing pulmonary insufficiency.

In the right ventricle, an acute form of decompensated insufficiency occurs for a number of other reasons:

• pulmonary embolism;
• myocardial infarction involving the septum between the ventricles.

At this stage, in an acute form, stagnation occurs in the systemic circulation of the body, blood begins to accumulate not only in the lungs, but also in the liver, causing its swelling. These stagnant processes and the inability of the heart to pump blood cause liver failure, swelling or infarction of the lung, which cause death.

Only timely medical care will help to avoid a fatal outcome. After emergency care, treatment in a hospital is necessary.

Chronic form

The disease in this case occurs against the background of old ailments of the heart and blood vessels, as a rule, not treated. Hypertension, arrhythmia, angina pectoris, bradycardia and other diseases without effective treatment lead to decompensated heart failure, which gradually becomes chronic, gradually destroying the heart to the end. It is impossible to understand which part suffered more without examinations, since the symptoms manifest themselves in the same way for disorders in the work of both ventricles.

Main features chronic form decompensated heart failure are swelling of the limbs and liver, as well as abdominal organs, liver, pericardium. For men, swelling of the scrotum is characteristic. Symptoms are accompanied by tachycardia and shortness of breath even at rest. This condition is due to the deterioration of the heart muscle.

Temporary measures in the case of chronic heart failure include symptom reduction and maintenance therapy of the heart muscle at any stage. Radioprotectors are used to regulate the heart rhythm, and edema is removed with diuretics. If necessary, fluid is pumped out to alleviate the patient's condition and reduce the load on. Since the disease develops in stages, urgent medical attention is not required.

The reasons

Despite the many causes of pathology, all of them are not fully understood. First of all, the causes of decompensation of the work of the heart are diseases of the cardiovascular system:

• dysfunctional valve disorders;
• cardiac ischemia;
• cardiomyopathy;
• hypertension;
• arrhythmia;
• atherosclerosis.

The progression of insufficiency is due to a number of characteristic factors:

• diseases of the endocrine system;
• regular bouts of hypertension;
• anemia;
• infectious diseases;
• inflammatory processes;
• excessive physical activity;
• taking various drugs;
• bad habits - smoking, alcohol.

Such a systemic disruption of the heart as a result leads to damage to the heart muscle and the development of decompensation. At this stage, the depletion of the walls of the heart and the progression of the process leads to dystrophic changes, chronic heart failure starts. The myocardium suffers from oxygen starvation, the shell does not receive enough nutrients and cannot fully perform the necessary functions.

Symptoms

It is impossible to diagnose chronic heart failure, knowing only the symptoms, but this should be the reason for contacting a specialist and undergoing complete examination to establish the exact causes of the pathology and the stage of development of the disease. Difficulties in diagnosis lie in the imposition of symptoms of insufficiency and the causes of the disease. But also decompensated heart failure is often accompanied by disturbances in the work of other body systems.

The peculiarity of this form of heart failure is that even at the last stage there is no definite sign of the disease and it is not possible to confirm the diagnosis.

And yet, decompensated heart failure has its own characteristic symptoms:

• shortness of breath at rest and exertion;
• myocardial damage in the past;
• muscle weakness;
• swelling of the limbs;
• an increase in the volume of the abdominal cavity.

At the initial examination, there is also increased pressure in the jugular vein and wheezing in the lungs. The patient is worried about arrhythmias various forms and feeling of coldness in the extremities. There is also a clear violation of urination and urinary retention. On the initial stage these manifestations are almost imperceptible.

With the defeat of the left side of the heart muscle with the progression of the disease, it is also involved, correcting its side. The defeat of the right ventricle proceeds separately and only at the last stage all parts of the heart are affected. By this time it is already a chronic form.

All these symptoms only give reason to suspect insufficiency, but even a gradual development always occurs against the background of obvious heart problems, so a doctor is consulted at an early stage. The acute form is known for its sudden onset and the ambulance that arrived at the scene takes the patient to the hospital, where they carry out a complete diagnosis.

Diagnostics

After collecting an anamnesis and examining the patient, a series of diagnostic measures. To detect abnormalities in the work of the heart, instrumental examination, and do a series of laboratory tests. There is no one way to determine decompensated heart failure; an integrated approach is used here.

Of the main ways to confirm the diagnosis, it should be noted:

• x-ray examination of the heart and abdomen;
• ultrasound examination;
• electrocardiography;
• echocardiogram;
• general urine analysis;
• complete blood count and biochemistry.

The main goal of diagnostics is to detect pathological processes, evaluate general condition heart, stage of development and extent of damage. It is also important to determine the location of violations and the cause of their occurrence.

Instrumental methods make it possible to visualize the damaged organ as much as possible, and clinical studies to assess the degree of damage and the state of the body as a whole. But it is also important to find out if other health problems have arisen against the background of heart failure. Decompensation in most cases disrupts the functioning of the urinary system and respiratory organs.

The disease is very dangerous and poses a threat not only to health, but also to human life, therefore timely diagnosis and effective treatment can prevent serious consequences and complications.

Treatment Methods

Because of high danger acute and chronic decompensated heart failure requires urgent medical care. For the chronic form during an exacerbation, you also need urgent care, after all, at some point the heart will not withstand the load.

Therapeutic tactics is based on a number of measures to stabilize the condition:

• normalization of blood flow;
• elimination of symptoms;
• maintenance therapy for the damaged organ.

Of course, it is better not to bring the heart to such a state, and the prevention of the disease is much easier than the treatment and helps to avoid consequences. If time has been lost, it is important to start treatment as soon as possible. At right approach and effective treatment can prolong the life of the patient for many years.

Treatment of decompensated heart failure is aimed at reducing the load on the damaged heart. It is important to reduce the flow of fluid into the body and remove the excess. To do this, limit the intake of salt, which retains fluid and prescribe diuretics to get rid of the excess. This will help relieve swelling, restore breathing and ease overload on the heart muscle. If diuretics are used in complex treatment, funds are taken orally, if this measure is necessary, injections are prescribed.

In order for the heart to be able to pump fluid, it is necessary to increase the contractile function, but not speed up the heartbeat. For these purposes, pacemakers are used. It is equally important to reduce arterial pressure and expand the vessels. Vasodilators are used to reduce the intensity of the work of the heart. Congestive processes increase the risk of blood clots, so anticoagulants are an integral part of therapy.

Concept definition

Congestive heart failure is one of the stages of chronic heart failure (CHF), in which there is a decrease in the pumping function of the heart, as a result of which it is not able to provide metabolism in tissues and organs at the desired level. Blood in the truest sense of the word “stagnates”, without providing nutrients not only the whole body, but also the heart muscle itself - the myocardium. From such vicious circle The patient's condition is only getting worse. Currently, the concept of congestive or decompensated heart failure is included in the concept of "acute heart failure".

2 Prevalence and causes of the disease

According to studies, approximately 20 percent of hospitalizations are CHF. The results of the Framingham Study state that five-year survival since the diagnosis was made, it is 75 percent in men and 62 percent in women. During the first year after diagnosis, 26-29 percent of patients with CHF die.

The main causes of decompensated heart failure are coronary heart disease (CHD), arterial hypertension, cardiomyopathy, heart disease various etiologies, arrhythmias, toxic effect alcohol and some medicines on the heart muscle, anemia, thyrotoxicosis, pericarditis, valve defects, pulmonary hypertension (increased pressure in the pulmonary artery), etc.

3 Compensatory mechanisms in CHF

Decompensated heart failure does not develop overnight or momentarily. It is preceded by stages of chronic heart failure, including asymptomatic or latent heart failure. Despite the fact that CHF is already taking place, the circulatory system includes compensatory mechanisms aimed at keeping the heart in “shape”. The main point in CHF is a violation of the pumping function of the heart and a drop in cardiac output.

Cardiac output is the total volume of blood pumped by the left and right ventricles per minute. On the early stages a decrease in the pumping function in tissues in response to oxygen deficiency (hypoxia), a red blood germ is stimulated - the formation of erythrocytes, which are oxygen carriers, and oxygen absorption is optimized in tissues. But such “rescue” mechanisms cannot compensate for heart failure for a long time.

In response to a decrease in pumping function and increasing hypoxia, the heart muscle begins to hypertrophy (thicken) and increase the minute volume (cardiac output) by increasing the heart rate and expanding the cavities with an increase in their volume. In this case we are talking about pathological hyperfunction of the heart, which, unlike physiological, is continuous. Under the conditions of the underlying disease, which caused the launch of such compensatory mechanisms, the heart gradually wears out and, if the disease is not treated, it passes to the stage of decompensation.

4 Symptoms

The clinical picture of heart failure in the stage of decompensation emerges gradually and is directly related to the functional state of the circulatory system.

The first stage of decompensated heart failure is characterized by a decrease in exercise tolerance (reduced exercise tolerance). Patients complain of palpitations, shortness of breath during exercise. Swelling may appear on the legs by the end of the day.

The second stage "A" has clinical picture depending on in which circle of blood circulation there are stagnation. With stagnation in a small circle, shortness of breath with moderate physical exertion (FN) comes to the fore; at night, asthma attacks accompanied by a dry cough with hemoptysis may disturb. Skin pale, possible bluish tint of the earlobes, tip of the nose, fingertips. With stagnation in a large circle, patients complain of shortness of breath during exercise, pain in the right hypochondrium. Urination at night may appear or become more frequent, patients are worried about thirst.

The second stage "B" is characterized by stagnation in small and big circles circulation. Circulatory insufficiency is aggravated, stagnation is observed in other organs and systems.

The third stage replaces the previous stage in conditions of progression of heart failure. Being in a long-term "deficiency" of oxygen, during internal organs irreversible changes occur with a decrease in their function. The above symptoms (shortness of breath, cough, hemoptysis) appear at rest, edema of the legs and abdominal edema increase. The function of the digestive and urinary systems is disturbed. Food is poorly digested, nausea, vomiting appear, liquid stool. "cardiac cachexia" develops.

5 Diagnostics

In the diagnosis of CHF, the major and minor criteria proposed in the Framingham study are used.

Major (major) criteria:

• paroxysmal shortness of breath at night and forced sitting position patient,
• swollen jugular veins,
• wet rales in the lungs,
• enlargement of the chambers of the heart (cardiomegaly),
• pulmonary edema,
• gallop rhythm,
• an increase in venous pressure above 160 mm Hg,
• hepatojugular reflex (swelling of the veins of the neck with pressure on the right hypochondrium),
• blood flow time is above 25 seconds.

Small Criteria:

• swelling of the lower extremities,
• night cough,
• dyspnea during exercise
• liver enlargement,
• fluid in the pleural cavity
• an increase in heart rate (HR) above 120 per minute in sinus rhythm,
• decrease in lung capacity.

Second important point in the diagnosis is the relationship of symptoms with heart disease. For this, a number of studies are used - electrocardiography, echocardiographic examination of the heart, chest x-ray, laboratory tests, etc.

6 Treatment of congestive heart failure

In the treatment of congestive CHF, non-drug and drug methods are used. The goal of treatment is to eliminate symptoms, improve prognosis, and reduce the number of hospitalizations of patients. In the first case (not drug treatment) attention is paid to the control of body weight (BW), restriction of physical activity, restriction of salt intake, restriction of fluid intake. In drug treatment, therapy of the underlying pathology is mandatory. The main drugs in the treatment of congestive CHF are cardiac glycosides, angiotensin-converting enzyme inhibitors (ACE inhibitors), antiarrhythmic and diuretic drugs.

Malfunctions in the activity of the heart is a fairly common problem that a huge number of people of different ages and gender face. Sometimes such diseases are diagnosed even in young people, their development can be provoked by hereditary predisposition, lifestyle, environmental influences, as well as natural wear and tear of organs. A fairly serious disease of the cardiovascular system is decompensated heart failure, the prevention of which will avoid a lot of difficulties. Let's talk about this on the pages of the site www.site, and also consider the symptoms of such a pathological condition, and also talk about how it is treated.

In general, heart failure is characterized as a condition in which the cardiovascular system is unable to fully provide the tissues and organs of the body with a sufficient amount of blood. If we talk about the decompensated form of such an ailment, then it is considered as the last, so-called terminal stage of the development of heart failure. With such a violation, the heart is completely unable to deliver a sufficient volume of blood to the tissues, even if the patient is at rest. At the same time, all internal mechanisms that previously provided compensation continue to function.

There are several types of decompensated heart failure: chronic and acute, as well as right or left ventricular failure. In most cases, an acute form of heart failure is decompensated, because the body has absolutely no time to adapt.

About how decompensated heart failure is corrected (symptoms)

For a timely visit to the doctor and adequate therapy, it is extremely important to pay attention to the state of the body and the manifestations of decompensated heart failure. In certain cases, the diagnosis is complicated by the fact that the clinical symptoms of one disease are superimposed on the signs of some other.

It should be borne in mind that there is not a single specific manifestation of heart failure, focusing on which you can make a 100% correct diagnosis.

In decompensated heart failure, the patient often has a history of myocardial injury or heart failure. Also, the patient is worried about shortness of breath at different times of the day (both day and night), as well as at rest and during physical exertion.

A characteristic symptom of this pathological condition is also considered to be general weakness. Most patients experience increased swelling, an increase in body weight or volume of the abdominal cavity.

Conducting a physical examination helps to identify other manifestations of the disease. They are represented by increased pressure in the jugular vein, wheezing in the lungs and hypoxia. Among the characteristic symptoms is also arrhythmia in different variants, a decrease in the volume of urine formation, as well as constantly cold hands and lower limbs. A correct diagnosis can be made only after a series of instrumental tests.

About how decompensated heart failure is corrected (treatment)

Correction of decompensated heart failure is aimed at eliminating the manifestations of stagnation, improving the volumetric parameters of the heart, as well as identifying the so-called decompensation trigger factors, and then eliminating them. Also, treatment involves long-term drug therapy and the maximum possible reduction of side effects. In the acute form of the disease, resuscitation measures are carried out, after which the patient is sent for inpatient treatment.

Modern medicine uses many therapeutic methods to treat patients suffering from left ventricular systolic dysfunction. They are prescribed angiotensin-converting enzyme inhibitors, as well as angiotensin II receptor blockers. In addition, beta-blockers and aldosterone antagonists are actively used. Therapy may also include the use of cardioverters and defibrillators, which are implanted inside. Such measures help to reduce the likelihood of a fatal outcome by an order of magnitude. Diuretics provide an increase in the amount of urine excreted from the body, thereby eliminating swelling and shortness of breath. Beta-blockers effectively optimize the activity of the heart, somewhat slowing down its rhythm. And taking an angiotensin-converting enzyme inhibitor helps to stop the further development of the disease, thereby lowering the death rate. Cardiac glycosides are often the drugs of choice.

In the event that the treatment is ineffective, the patient can be pumped out fluid from the abdominal cavity, which helps to slightly alleviate his condition for a while.

Inpatient treatment is indicated for patients with decompensated heart failure. Doctors carry out the correction of ailments that provoked such a violation, and also provide the patient with complete rest. Diet food is shown, and smoking and alcohol are strictly prohibited.

Prevention of decompensated heart failure

The main measure for the prevention of decompensated heart failure is systematic observation by a cardiologist, and competent timely treatment of diseases of the cardiovascular system. In addition, to prevent such a disease, it is extremely important to lead a healthy lifestyle, avoid stress and other overloads.