Heart failure presentation. Nursing presentation "the importance of nursing in solving the problems of a patient with diseases of the cardiovascular system"
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Currently, non-communicable diseases such as diseases of the cardiovascular system, cancer, diabetes and chronic lung diseases, overtaking infectious diseases, are becoming the leading cause of death in the world. Cardiovascular diseases (hereinafter - CVD) are the main problem of state, medical and public organizations in industrialized countries due to high morbidity, disability and mortality among the population. The relevance of the chosen topic is due to the fact that CVD diseases have an increasing trend. In Russia, according to existing statistics, 10% of adolescents under 16 years old, 30% of the adult population under 45 years old, 80% of people over 55-60 years old suffer from CVD diseases. CVDs remain one of the leading causes of mortality in the population, which negatively affects the demographic situation and socio-economic indicators in Russia.
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There are very few studies devoted to this aspect of the management of patients with cardiovascular diseases. In addition, in them, the role of a nurse is assessed primarily from the position of a doctor's assistant, and not an independent participant in the treatment and diagnostic process. This determined the relevance and significance of the study. Analysis of the theoretical aspects of the problem of cardiovascular pathology made it possible to establish that this class of diseases is today very common in most countries of the world. It occupies one of the first places in the structure of the causes of mortality among the population, including in Russia.
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Research hypothesis. The study is based on the assumption that the problems of patients suffering from diseases of the cardiovascular system are very numerous and varied. It should be noted that they are not limited only to problems associated with damage to the circulatory organs directly, but reflect the systemic nature of the pathology. The correct organization of the nursing process plays an essential role in the treatment and prevention of diseases. The outcome of the disease largely depends on the activity of the nurse. Research methods. Analysis of scientific and methodological literature on the research topic, questioning (survey on the problem under study), study and generalization of information, statistical processing of the data obtained, generalization, analysis, systematization.
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The purpose of the work is to identify the main factors influencing the development of cardiovascular diseases and to study the role of a nurse in their treatment and prevention. Research objectives: 1. To analyze the scientific and methodological literature on this topic. 2. To characterize the role of cardiovascular diseases in the overall structure of mortality 3. To characterize the most clinically significant CVD diseases 4. To study the main problems of patients with CVS diseases and to identify the role of a nurse in solving them 5. To analyze the specifics of a nurse's activities in the treatment and prevention of CVD diseases 6. To summarize the existing experience of a nurse when working in cardiological patients. 7. To develop an algorithm for the activity of a nurse in the treatment and prevention of CVD diseases.
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The object of the research is patients suffering from cardiovascular diseases. The subject of the research is the role of a nurse in the treatment and prevention of CVD. Practical significance. The research results can be used to organize nursing care for patients with cardiovascular diseases and their complications. The results can be useful for the patients themselves to organize self-control.
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Today, chronic heart failure (CHF) is diagnosed in more than 23 million people in the world. As for our country, there are various functional classes of this disease. So, according to Rosstat, CHF I-II functional class (FC) is diagnosed in more than 5.1 million people, III-IV FC is diagnosed in 2.4 million people. The age range is as follows: in a person aged 45-54, CHF is found in 0.7%. The frequency of this pathology increases significantly in patients over the age of 75 years - it is diagnosed in 8.4% of individuals.
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The rate of recovery of the patient and the quality of his life, as well as the prognosis, and not only recovery, but sometimes life, largely depend on the success of solving the problems of a patient with CVD diseases. Nurses can be actively involved in solving these problems, as nursing personnel are now seen as a valuable resource for health care. - When solving the problems of patients with diseases of the cardiovascular system, the nurse defines short-term and long-term goals and implements the measures necessary to achieve them. - The main problems of patients with diseases of the cardiovascular system are pain in the region of the heart, a feeling of palpitations and interruptions in the work of the heart, headache and dizziness, shortness of breath, edema, psychological problems, etc. CCC, is that it must be able to quickly and flexibly respond to critical situations, must be able to provide urgent assistance, make a decision. - Emergency cardiac care - a complex of emergency measures, including diagnosis, treatment and prevention of acute circulatory disorders in cardiovascular diseases. The loss of time in the provision of emergency cardiac care can be irreparable.
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At this stage, the nurse collects information about the patient's health, living conditions, work, activities. This information can be both objective and subjective.
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At the second stage, the nurse analyzes the data obtained, identifies the patient's main problems, and formulates a nursing diagnosis. The patient's problems are different. Highlight existing and potential problems. Existing problems are real problems that the patient has at the current moment in time that bother him. Potential problems are problems that do not yet exist, but may arise in the near future. Timely prevention is essential to prevent potential problems from becoming existing ones. It is necessary to proceed from the fact that the patient always has several problems and they work together. The first step is to prioritize problems.
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After the nurse has identified the priority of the problems, divided them into primary and secondary, it is necessary to proceed to the formulation of a nursing diagnosis. A nursing diagnosis is different from a medical diagnosis. Nursing diagnosis is based on describing the patient's reactions and identifying the patient's problems. Nursing diagnosis does not have to be made using strict terminology. Basically, it is put on the basis of personal daily observations of the patient.
Slide 1 Slide description:CHRONIC HEART INSUFFICIENCY Lecture for 4th year students of the Faculty of Dentistry, associate professor of the Department of Internal Diseases of the Faculty of Dentistry and Pediatrics, Alekseeva D.V. Tver, 2011
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DEFINITION Heart failure is a syndrome characterized by the inability of the cardiovascular system to adequately provide organs and tissues of the body with blood and oxygen in an amount sufficient to maintain normal life
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Heart failure Acute and chronic
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CIRCULATIONS
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Heart failure is a syndrome! Nosological form - a specific disease isolated on the basis of an established cause (etiology), developmental features (pathogenesis), typical external manifestations and characteristic damage to organs and tissues Syndrome - a set of symptoms associated with a single pathogenesis
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STRUCTURE OF DIAGNOSIS Clinical diagnosis: Main disease: XXX Complications: Heart failure Concomitant diseases: YYY. ZZZ.
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Chronic heart failure (CHF) DEFINITION of CHF - from the modern clinical point of view, it is a disease with a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.), which are associated with inadequate perfusion of organs and tissues at rest or during exertion and often with fluid retention in the body. The root cause is impairment of the heart's ability to fill or empty due to myocardial damage, as well as an imbalance in the vasoconstrictor and vasodilating neurohumoral systems.
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STRUCTURE OF DIAGNOSIS Clinical diagnosis: Main disease: XXX Complications: Chronic heart failure (stage, functional class) Concomitant diseases: YYY. ZZZ.
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Epidemiology of CHF The prevalence of CHF in the population is 7% (7.9 million people). Clinically pronounced CHF occurs in 4.5% of the population (5.1 million people). Terminal CHF - in 2.1% (2.4 million people). The prevalence of CHF increases significantly with age. Among men, the prevalence of CHF is higher than among women in the age group under 60. The annual mortality rate for CHF as a whole is 6%, with clinically severe CHF it reaches 12%. Decompensation of CHF is the reason for hospitalization in cardiological hospitals of every second patient
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ETIOLOGY OF CHF Arterial hypertension is present in 88% of patients with CHF IHD is detected in 55% of patients with CHF Chronic obstructive pulmonary disease - 13% Diabetes mellitus - 11.9% of cases Past acute cerebrovascular accident - 10.3% of cases Permanent form of atrial fibrillation - 10, 3% Heart defects - 4.3% Myocarditis - 3.6% Dilated cardiomyopathy (including alcoholic) - 0.8%
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PATHOGENESIS AND PATHOPHYSIOLOGY CHF Model of pathogenesis - neurohumoral CHF - a complex of hemodynamic and neurohumoral reactions to heart dysfunction (E. Braunwald, 1989) Activation of the sympatho-adrenal system (SAS) and renin-angiotensin-aldosterone system half of the cases!) heart failure
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CLINICAL PICTURE OF CHF
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CLASSIFICATION of CHF (OSSN, 2002)
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CHF DIAGNOSTICS The reference points in the diagnosis of CHF are: 1. Typical complaints of the patient. 2. Physical examination data (examination, palpation, auscultation) - clinical signs. 3. Data of objective (instrumental) survey methods.
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CHF DIAGNOSTICS instrumental examination methods 1. Electrocardiography (normal ECG in CHF is an exception to the rule). 2. Chest X-ray (cardiomegaly and venous pulmonary congestion). 3. Echocardiography, including Doppler echocardiography (systolic - EF Slide 17 
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CHF DIAGNOSIS laboratory tests 1. A standard set of laboratory tests for CHF includes: a clinical blood test to determine the level of hemoglobin, the number of leukocytes and platelets, a biochemical blood test - electrolytes, creatinine, glucose, liver enzymes, general urine analysis 2. According to indications - C-reactive protein (exclusion of the inflammatory etiology of heart disease), thyroid-stimulating hormone (exclusion of hyper- or hypothyroidism), urea and uric acid. With a sharp deterioration in the condition - cardiospecific enzymes. 3. Natriuretic hormones - brain natriuretic peptide (BNP) and its N-terminal precursor (NT-proBNP).
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DIAGNOSTIC ALGORITHM FOR CHF
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CHF TREATMENT main goals Prevention of symptomatic CHF (for stage I CHF) Elimination of CHF symptoms (for stages IIA – III) Slowing the progression of the disease by protecting the heart and other target organs (brain, kidneys, blood vessels) (for stages I – III) Improvement quality of life (for stages IIA – III) Reduced hospitalizations (and costs) (for stages I – III) Improved prognosis (for stages I – III)
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CHF TREATMENT Ways to achieve goals Diet Mode of physical activity Psychological rehabilitation, organization of medical supervision, schools for CHF patients Drug therapy Electrophysiological methods of therapy Surgical, mechanical methods of treatment
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CHF TREATMENT Diet Restriction of salt intake Restriction of fluid intake - with decompensation Food should be high-calorie, easy to digest, with a sufficient content of vitamins, protein Weight control
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CHF TREATMENT Mode of physical activity Physical rehabilitation is recommended for all patients: Breathing exercises Walking Dosed physical training
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CHF TREATMENT Psychological rehabilitation and the creation of outpatient observation schools for patients with CHF Patient education !!!
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CHF TREATMENT Drug therapy
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SITUATION PROBLEM
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SITUATION PROBLEM
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SITUATION PROBLEM
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Lecture topic: CHRONIC HEART FAILURE. DEFINITION. CLASSIFICATION. CLINIC. DIAGNOSTICS. TREATMENT Assoc. RUDA M.M. - presentation
1 Topic of the lecture: CHRONIC HEART FAILURE. DEFINITION. CLASSIFICATION. CLINIC. DIAGNOSTICS. TREATMENT Assoc. RUDA M.M.
2 LECTURE OUTLINE Introduction Introduction Heart failure syndrome Heart failure syndrome Acute heart failure Acute heart failure Chronic heart failure Chronic heart failure etiology etiology Pathogenesis Pathogenesis Main clinical symptoms Main clinical symptoms Vascular insufficiency syndrome Vascular insufficiency syndrome
3 Heart Failure Syndrome Heart failure is a condition in which the heart is unable to provide a level of blood circulation adequate to the metabolic needs of the body. Heart failure is a pathological condition in which the heart is unable to provide a level of blood circulation adequate to the metabolic needs of the body.
4 Classification of acute HF Acute HF Left ventricular Cardiac asthma Pulmonary edema Right ventricular Pulmonary embolism
7 acute left ventricular failure According to the clinical course, they are distinguished: According to the clinical course, they are distinguished: instant (death occurs after a few minutes), acute (up to 1 hour), instant (death occurs after a few minutes), acute (up to 1 hour), protracted ( lasting up to 2 days) prolonged (lasting up to 2 days) recurrent course. The latter has a wave-like character, most often encountered in myocardial infarction. recurrent course. The latter has a wave-like character, most often encountered in myocardial infarction.
8 CLINIC Typical clinical signs are: Typical clinical signs are: severe respiratory failure, shortness of breath, sloughing up of pink foamy sputum, orthopedic, pale, skin covered with cold sweat. On examination, peripheral cyanosis. severe respiratory distress, shortness of breath, coughing up of pink frothy sputum, orthopedic, pale, skin covered with cold sweat. On examination, peripheral cyanosis. On auscultation, moist rales of various sizes are heard over most of the lungs, tachycardia, protodiastolic gallop rhythm and systolic murmur over the apex, blood pressure may increase or be sharply reduced (shock). On auscultation, moist rales of various sizes are heard over most of the lungs, tachycardia, protodiastolic gallop rhythm and systolic murmur over the apex, blood pressure may increase or be sharply reduced (shock). Chest X-ray reveals the presence of a "wet lung" syndrome. In the study of the gas composition of blood, severe or moderate hypoxemia, hypercapnia are determined, the pH of arterial blood decreases (respiratory acidosis). Chest X-ray reveals the presence of a "wet lung" syndrome. In the study of the gas composition of blood, severe or moderate hypoxemia, hypercapnia are determined, the pH of arterial blood decreases (respiratory acidosis).
9 CLINIC Intense pressing or stabbing pain in the chest Intense pressing or stitching pain in the chest Pale skin with a cyanotic tint Pale skin with a cyanotic tinge Swelling and pulsation of the cervical veins Swelling and pulsation of the cervical veins Pulse small frequent Pulse small A frequent Decrease tones above the pulmonary artery, gallop rhythm Strengthening II tone above the pulmonary artery, gallop rhythm Pleural friction noise Pleural friction noise
16 CHRONIC HEART INSUFFICIENCY Heart failure (HF) is a complex clinical syndrome that occurs as a result of any cardiac pathology that impairs the contractility of the ventricles, and leads to disruption of adequate blood supply to organs and tissues Heart failure (HF) is a complex clinical syndrome that occurs due to any cardiac pathology that impairs the contractility of the ventricles, and leads to disruption of adequate blood supply to organs and tissues
17 Etiology: myocardial diseases (myocarditis, cardiosclerosis, cardiomyopathy, myocardial dystrophy); myocardial diseases (myocarditis, cardiosclerosis, cardiomyopathy, myocardial dystrophy); heart defects, heart defects, increased blood pressure (hypertension, symptomatic arterial hypertension, pulmonary hypertension); increased blood pressure (hypertension, symptomatic arterial hypertension, pulmonary hypertension); violation of diastolic filling of the ventricles of the heart (exudative and adhesive pericarditis, violation of diastolic filling of the ventricles of the heart (exudative and adhesive pericarditis, restrictive cardiomyopathies, cardiac tamponade); restrictive cardiomyopathies, cardiac tamponade); excessive physical activity, excessive physical activity, intravenous administration of large amounts of fluid; intravenous administration of large amounts of fluid; pathological changes in the pulmonary circulation (pulmonary embolism, spontaneous pneumothorax, bilateral pneumonia). pathological changes in the pulmonary circulation (pulmonary embolism, spontaneous pneumothorax, bilateral pneumonia).
18 IHD - 50 - 70% IHD - 50 - 70% Arterial hypertension -% Arterial hypertension -% Cardiomyopathy - 7 - 14% Cardiomyopathy - 7 - 14% Heart defects - 6 - 12% Heart defects - 6 - 12% Other causes - 5 - 10% Other reasons - 5 - 10%
20 CHF is a syndrome characterized by a violation of the pumping function of the heart; a violation of the pumping function of the heart; a decrease in exercise tolerance; a decrease in exercise tolerance; a decrease in exercise tolerance; fluid retention in the body; fluid retention in the body;
23 Pathogenesis. The main pathogenetic factors of chronic heart failure are: The main pathogenetic factors of chronic heart failure are: a decrease in cardiac output and tissue organ perfusion; a decrease in cardiac output and tissue organ perfusion; activation of the sympathoadrenal system, activation of the sympathoadrenal system, constriction of arterioles and venules; constriction of arterioles and venules - activation angiotensin - aldosterone activation of the renin - angiotensin - aldosterone system sodium and water retention sodium and water retention Emergence of edema. The appearance of edema.
24 Classification. Clinical stage of heart failure; Clinical stage of heart failure; Heart failure variant; Heart failure variant; Patient functional class Patient functional class
25 Clinical stage of heart failure First stage - initial First stage - initial Second stage - extended long-term circulatory failure (divided into A and B) Second stage - extended long-term circulatory failure (divided into A and B) Third stage - final, dystrophic Third stage - final , dystrophic
26 CH I (initial, latent) - the appearance of shortness of breath, tachycardia, fatigue only with physical exertion; at rest, hemodynamics, functions of organs and metabolism are not impaired; working capacity is reduced. Conducting tests with dosed physical activity determines a decrease in tolerance to loads of SN I (initial, latent) - the appearance of shortness of breath, tachycardia, fatigue only with physical exertion; at rest, hemodynamics, functions of organs and metabolism are not impaired; working capacity is reduced. Conducting tests with dosed physical activity determines a decrease in exercise tolerance
27 CH ІІА (the beginning of a long stage) - signs of stagnation in one of the circulatory circles, which can be eliminated during therapy. Shortness of breath, palpitations, unpleasant sensations in the region of the heart, appear with ordinary minor physical exertion. The ability to work is reduced. Signs of congestion in the lungs (with left ventricular failure), or enlargement of the liver, pastiness or edema of the lower extremities, (with right ventricular heart failure) are determined. СН ІІА (the beginning of a long stage) - signs of stagnation in one of the circulatory circles, which can be eliminated during therapy. Shortness of breath, palpitations, unpleasant sensations in the region of the heart, appear with ordinary minor physical exertion. The ability to work is reduced. Signs of congestion in the lungs (with left ventricular failure), or enlargement of the liver, pastiness or edema of the lower extremities, (with right ventricular heart failure) are determined.
29 СН ІІБ (end of long stage) - signs of stagnation in both circles of blood circulation are constant, do not completely disappear during treatment. СН ІІБ (end of a long stage) - signs of stagnation in both circles of blood circulation are constant, do not completely disappear during treatment. Shortness of breath, palpitations, precordial discomfort appear with the least physical exertion and even at rest. The ability to work is sharply reduced. Stagnant wheezing in the lungs, enlarged liver, swelling of the veins, constant edema, first on the lower extremities, and then on the whole body are determined. Shortness of breath, palpitations, precordial discomfort appear with the least physical exertion and even at rest. The ability to work is sharply reduced. Stagnant wheezing in the lungs, enlarged liver, swelling of the veins, constant edema, first on the lower extremities, and then on the whole body are determined.
32 HF III (final, dystrophic) - severe hemodynamic disorders with the development of irreversible changes in organs, complete disability blood circulation anasarca, ascites, hydrothorax, hydropericardium, severe dystrophic changes in various organs and tissues. Signs of stagnation in the small and large circulation of anasarca, ascites, hydrothorax, hydropericardium, severe dystrophic changes in various organs and tissues.
34 Variants of heart failure: Systolic - the cause of hemodynamic disturbance is due to insufficiency of the systolic function of the left ventricle. The main criterion is the value of fractional left ventricular ejection 50%. Diastolic - hemodynamic disorder is caused by a violation of diastolic filling of the left (or right) ventricles. The main criterion is the presence of clinical signs of heart failure, stagnation in the small circle (or in the small and large cola) circles with a preserved (50%) fraction of left ventricular injection.
35 Functional class of HF FC I - patients with heart diseases, in whom the usual performance does not lead to shortness of breath, fatigue and palpitations. Physical stress tolerance is normal. FC I - patients with heart disease, in whom the implementation of the usual does not lead to shortness of breath, fatigue and palpitations. Physical stress tolerance is normal. FC II - patients with moderate physical limitation. Shortness of breath, fatigue and palpitations occur with normal physical exertion. FC II - patients with moderate physical limitation. Shortness of breath, fatigue and palpitations occur with normal physical exertion. FC III - Patients with severe limitation of physical activity. Shortness of breath, fatigue and palpitations - with little physical exertion. FC III - Patients with severe limitation of physical activity. Shortness of breath, fatigue and palpitations - with little physical exertion. FC IV - patients in whom any level of physical activity causes subjective symptoms. FC IV - patients in whom any level of physical activity causes subjective symptoms.
39 Vascular insufficiency syndrome This is a pathological condition that occurs due to a decrease in the tone of the smooth muscles of the vascular wall or a decrease in the mass of circulating blood. This is a pathological condition that occurs due to a decrease in the tone of the smooth muscles of the vascular wall or a decrease in the mass of circulating blood. As a result, there is a discrepancy between the capacity of the vascular bed and the volume of circulating blood. As a result, there is a discrepancy between the capacity of the vascular bed and the volume of circulating blood.
40 Causes of violation of vascular tone innervation disorders of vascular tone innervation Disorders of vasomotor nerves function Disorders of vasomotor nerves function Vascular paresis due to toxic damage Vascular paresis due to toxic damage Decreased circulating blood volume (blood loss and dehydration) Decreased circulating blood volume (blood loss) and dehydration
41 Classification Fainting is a sudden short-term loss of consciousness due to cerebral ischemia. Fainting is a sudden short-term loss of consciousness due to cerebral ischemia. Collapse is a form of vascular insufficiency due to a sharp decrease in vascular tone and an acute decrease in the volume of circulating blood.Collapse is a form of vascular insufficiency due to a sharp decrease in vascular tone and an acute decrease in the volume of circulating blood
42 Shock is a serious life-threatening condition of a patient that arises as a result of the influence on the body of strong endogenous or exogenous irritants and is accompanied by progressive disturbance of vital functions of the body and critical disturbance of hemodynamics. Shock is a serious life-threatening condition of the patient, which arises as a result of the influence on the body of strong endogenous or exogenous irritants and is accompanied by progressive disruption of vital body functions and critical hemodynamic disturbance.
43 Forms of shock Hypovolemic Hypovolemic Traumatic Traumatic Cardiogenic Cardiogenic Vascular forms of shock Vascular forms of shock Infectious-toxic Infectious-toxic anaphylactic anaphylactic
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Hospital therapy CHRONIC HEART FAILURE Prof. Alyavi A. L. - presentation
1 Hospital therapy CHRONIC HEART FAILURE Prof. Alyavi A. L.
2 CHF is a syndrome that develops as a result of various diseases of the cardiovascular system, leading to a decrease in the pumping function of the heart, chronic hyperactivation of neurohormonal systems and manifested by shortness of breath, increased fatigue, limited physical activity and excessive fluid retention in the body. CHF is a syndrome that develops as a result of various diseases of the cardiovascular system, leading to a decrease in the pumping function of the heart, chronic hyperactivation of neurohormonal systems and manifested by shortness of breath, increased fatigue, limited physical activity and excessive fluid retention in the body.
3 The exceptional importance and attention to this pathology is caused by an increase in the number of patients with CHF, an increase in the number of patients with CHF, a poor prognosis of the disease, a poor prognosis of the disease, an increase in the number of hospitalizations due to exacerbation of CHF, an increase in the number of hospitalizations due to exacerbation of CHF, an unsatisfactory quality of life, an unsatisfactory quality of life, and an increase in costs for combating CHF with an increase in the cost of combating CHF
4 EPIDEMIOLOGY EPIDEMIOLOGY - The prevalence of clinically severe CHF in the population is about 2% - The prevalence of clinically severe CHF in the population is about 2% - Among people over 65 years old, it increases to 10%, and decompensation becomes the most common cause of hospitalization in elderly patients. - Among people over 65 years old, it rises to 10%, and decompensation becomes the most common reason for hospitalization of elderly patients. - The number of patients with asymptomatic left ventricular dysfunction is at least 4 times higher than the number of patients with clinically severe CHF. - The number of patients with asymptomatic left ventricular dysfunction is at least 4 times higher than the number of patients with clinically severe CHF. - Over 15 years, the number of hospitalizations diagnosed with CHF has tripled. - Over 15 years, the number of hospitalizations diagnosed with CHF has tripled. - The five-year survival rate of patients with CHF is still below 50%. - The five-year survival rate of patients with CHF is still below 50%. - The risk of sudden death is 5 times higher than in the population - The risk of sudden death is 5 times higher than in the population - The cost of treating patients with CHF in the United States is about $ 20 billion, while cancer patients spend $ 2.4 billion. - The cost of treating patients with CHF in the United States is about $ 20 billion, while cancer patients spend $ 2.4 billion.
5 Classification of V.Kh. Vasilenko and N.D. Strazhesko Adopted at the XII All-Union Congress of Physicians in 1935. STAGE I - initial latent circulatory failure, manifested only during physical exertion (shortness of breath, palpitations, excessive fatigue). STAGE I - initial latent circulatory failure, manifested only during physical exertion (shortness of breath, palpitations, excessive fatigue). At rest, these phenomena disappear. Hemodynamics is not impaired. At rest, these phenomena disappear. Hemodynamics is not impaired. STAGE II - severe long-term circulatory failure, hemodynamic disturbances are expressed at rest. STAGE II - severe long-term circulatory failure, hemodynamic disturbances are expressed at rest. Period A - signs of circulatory failure at rest are moderately expressed. Hemodynamic disorders only in one of the departments of the cardiovascular system (in the large or small circle of blood circulation). Period A - signs of circulatory failure at rest are moderately expressed. Hemodynamic disorders only in one of the departments of the cardiovascular system (in the large or small circle of blood circulation). Period B - the end of a long stage, pronounced hemodynamic disturbances in which the entire CVS is involved Period B - the end of a long stage, pronounced hemodynamic disturbances in which the entire CVS is involved (both large and small circulatory systems) (both large and small circulatory systems) STAGE III - terminal dystrophic with severe hemodynamic disturbances. Persistent changes in metabolism and irreversible changes in the structure of organs and tissues. STAGE III - terminal dystrophic with severe hemodynamic disturbances. Persistent changes in metabolism and irreversible changes in the structure of organs and tissues.
6 Classification of CHF of the New York Heart Association Classification of CHF of the New York Heart Association FC I. The patient has no limitations in physical activity. Normal exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. I FC. The patient has no limitations in physical activity. Normal exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but doing normal physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but doing normal physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. III FC. Pronounced limitation of physical activity. The patient feels comfortable only at rest, but less than usual, physical activity leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain. III FC. Pronounced limitation of physical activity. The patient feels comfortable only at rest, but less than usual, physical activity leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain. IV FC. Inability to perform any load without discomfort. Symptoms of heart failure or angina syndrome may manifest at rest. When the minimum load is performed, discomfort increases. IV FC. Inability to perform any load without discomfort. Symptoms of heart failure or angina syndrome may manifest at rest. When the minimum load is performed, discomfort increases.
7 Clinical picture The clinical picture - Progressive dyspnea. - Progressive shortness of breath. - Fast fatiguability. - Fast fatiguability. - Night attacks of cardiac asthma - Night attacks of cardiac asthma - Losing weight or, on the contrary, weight gain (due to edema) - Losing weight or, on the contrary, weight gain (due to edema) - Signs of left ventricular failure: - Signs of left ventricular failure: - tachycardia - tachycardia - decreased pulse filling - decreased pulse filling - tachypnea - tachypnea - moist rales in the lower lungs - moist rales in the lower lungs - with auscultation of the heart - gallop rhythm - with auscultation of the heart - gallop rhythm - deterioration of peripheral circulation - deterioration of peripheral circulation Signs of right ventricular failure: Signs of right ventricular failure
8 Laboratory and instrumental studies Laboratory and instrumental studies - Examination of renal function - Examination of renal function - Determination of serum electrolyte levels - Determination of serum electrolyte levels - Complete blood count - Complete blood count - Chest X-ray - Chest X-ray - ECG - ECG - Echocardiography - Echocardiography - Isotope ventriculography - Isotope ventriculography
9 Principles of treatment Principles of treatment - Explaining to the patient the need for continuous treatment - Explaining to the patient the need for continuous treatment - Identifying and, if possible, eliminating the cause of heart failure - Identifying and, if possible, eliminating the cause of heart failure - Carrying out non-drug treatment - Carrying out non-drug treatment - Carrying out drug treatment - Carrying out medication treatment
10 Non-drug treatment includes: regimen, in case of overweight - weight loss, limiting the consumption of sodium chloride (6-8 g per day), restriction of fluid to per day), restriction of fluid to 1.5 liters per day, if necessary, perform pleural puncture 1.5 liters per day, if necessary, perform pleural puncture and pericardiocentesis, puncture and pericardiocentesis
11 Drug treatment Drug treatment It has two basic principles: inotropic stimulation of the heart and unloading of cardiac activity. Of the positive inotropic agents for long-term treatment of CHF, cardiac glycosides are used. Unloading of the heart can be divided into four types: It implies two basic principles: inotropic stimulation of the heart and unloading of cardiac activity. Of the positive inotropic agents for long-term treatment of CHF, cardiac glycosides are used. Unloading of the heart can be divided into four types: - volumetric (diuretics are used) - volumetric (diuretics are used) - hemodynamic (long-acting vasodilators and dihydropyridines) - hemodynamic (long-acting vasodilators and dihydropyridines) - neurohumoral (ACE inhibitors, antagonists of receptors to A- , aldosterone antagonists - neurohumoral (ACE inhibitors, antagonists of receptors to A-P, aldosterone antagonists - myocardial (beta-blockers) - myocardial (beta-blockers)
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Chronic heart failure. Diagnostics and treatment - presentation, report, project
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Slide Description: Chronic heart failure. Diagnostics and treatment P.A. Lebedev Professor, DMN Head of the Department of Therapy and the Course of Functional Diagnostics, Institute of Postgraduate Education, Samara State Medical University
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The definition of CHF is "a pathophysiological syndrome in which, as a result of one or another disease of the cardiovascular system, there is a decrease in pumping function, which leads to an imbalance between the hemodynamic need of the body and the capabilities of the heart." The modern neurohumoral model of pathogenesis has proven that the development of CHF occurs according to the same pathophysiological laws, regardless of the etiology of damage.
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Classification of CHF I The initial stage of heart damage. Hemodynamics is not impaired. Latent heart failure, asymptomatic LV dysfunction. II А Clinically expressed stage of heart disease. Hemodynamic disturbances in one of the circles of blood circulation are moderately expressed. Adaptive remodeling of the heart and blood vessels IIB Severe stage of heart disease. Severe hemodynamic disturbances in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels. III The final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organisms (heart, brain, kidneys, lungs). The final stage of organ remodeling. Functional classes of CHF (I - I V) Example: CHF II B IIFkl, CHF IIA I I I Fkl
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criteria used in determining the diagnosis of CHF
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Electrocardiography This is the most accessible instrumental method that allows you to objectively assess the state of the heart. Myocardial dysfunction, one way or another, will always be reflected on the ECG: a normal ECG in CHF is an exception to the rule (negative predictive value> 90%). According to the EPOCH-O-CHF study, the most frequent deviations from the norm on the standard ECG in CHF patients are signs of LV hypertrophy (LVH) and deviation of the electrical axis of the heart to the left, which are found in 50–70% of those examined.
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The standard diagnostic set of laboratory tests in a patient with heart failure should include the determination of hemoglobin level, the number of red blood cells, leukocytes and platelets, the concentration of plasma electrolytes, creatinine, glucose, hepatic enzymes and a general urinalysis. Also, if necessary, it is possible to determine the level of C-reactive protein (exclusion of the inflammatory etiology of heart disease), thyroid-stimulating hormone (exclusion of hyper- or hypothyroidism), urea and uric acid
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The value of echocardiography EchoCG allows solving the main diagnostic problem - to clarify the fact of dysfunction and its nature, as well as to conduct a dynamic assessment of the state of the heart and hemodynamics.The most important hemodynamic parameter is LVEF, which reflects the contractility of the LV myocardium. Determination of LVEF makes it possible to differentiate patients with systolic dysfunction from those with preserved systolic function. The level of LVEF can be recommended as an indicator with a high probability indicating the preservation of systolic function. 50%, calculated by the method of 2D echocardiography according to Simpson. The degree of LVEF reduction is associated with the severity of systolic dysfunction and is used to determine the risk of surgical treatment; dynamics of left ventricular ejection fraction is an indicator of disease progression and effectiveness of therapy; low left ventricular ejection fraction is a marker of a negative prognosis.
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In half of patients with CHF signs, there is no systolic dysfunction, diastole disorders are more closely associated with systole disorders, associated with the severity of the patients' clinical condition, the degree of decreased exercise tolerance, and quality of life. The dynamics of diastolic parameters can serve as a criterion for the effectiveness of treatment and a marker for the prognosis of patients with CHF.
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Three conditions are required to diagnose primary diastolic HF: 1. The presence of symptoms and signs of HF. 2. Normal or slightly impaired LV systolic function (LVEF 50%). 3. Identification of impaired relaxation of the LV and / or its extensibility.
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Hypertrophic CMF Frequency 1: 500 in the US population The most common cause of death in athletes and people under 40 years of age VS prevails among the causes of mortality The highest frequency of VS at the age of 15-30 years A frequent combination with myocardial ischemia is characteristic
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Nitroglycerin for myocardial infarction Class 1 Patients with ischemic pain should receive sublingual NTG every 5 minutes up to 3 times, after which an intravenous infusion of NTG should be decided. Indications for intravenous infusion of IGT include recurrent anginal pain, hypertension, and pulmonary congestion.
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Contraindications to NTG Systolic blood pressure less than 90 mm Hg or a decrease in blood pressure by 30 mm Hg or more from baseline, severe bradycardia less than 50 beats per minute or tachycardia more than 100 per minute, suspicion of right ventricular myocardial infarction
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Levosimendan (Simdax) Indications: acute left ventricular failure in myocardial infarction Contraindications: arterial hypotension, tachycardia, history of flutter-fibrillation of ventricles, mechanical obstruction preventing filling and ejection from the LV, severe renal and hepatic insufficiency mitral valve
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Parameters of physical activity and oxygen consumption in patients with different FC CHS (according to NYHA) FC Dist. 6-min (m) O2 consumption (max) ml. kg - 1. min – 1 0> 551> 22.1 1 426–550 18.1–22.0 2 301–425 14.1–18.0 3 151–300 10.1–14.0 4
What is the upper or lower heart pressure
instituteDepartment of Hospital Therapy with courses in Endocrinology, Hematology and Clinical Laboratory
diagnostics
Head of the Department of Hospital Therapy with the Course of Clinical Laboratory Diagnostics, Doctor of Medical Sciences, Professor
P.P. Ogurtsov.
Chronic cardiac
failure
The presentation was prepared by: Stepanyan Lyusine Nairievna
Group: ML-502
Lecturer: Doctor of Medical Sciences, Professor Ivanov Gennady Georgievich
Chronic heart failure
CHF is a disease with a complex of characteristic symptoms (shortness of breath,fatigue and decreased physical activity, edema, etc.), which are associated
inadequate perfusion of organs and tissues at rest or during exertion and often with a delay
body fluids.
The underlying cause is impairment of the heart's ability to fill or
emptying due to myocardial damage, as well as imbalance
vasoconstrictor and vasodilating neurohumoral systems.
Etiology of CHF
The main reasons for the development of CHF in the Russian Federation are:AH (95.5%),
Ischemic heart disease (69.7%),
postponed myocardial infarction or ACS (15.3%),
Diabetes mellitus (15.9%).
The combination of ischemic heart disease and hypertension occurs in most patients with CHF.
There is an increase in the number of patients with heart defects (4.3%) with
the predominance of degenerative aortic valve disease.
Less common causes of CHF are
transferred myocarditis (3.6%), cardiomyopathies, toxic lesions
myocardium of various etiologies, including iatrogenic genesis (chemotherapy,
radiation damage to the myocardium and others), anemia (12.3%).
Common causes of CHF also include COPD (13%), chronic and
paroxysmal atrial fibrillation (12.8%), acute
cerebrovascular accident (10.3%)
CHF pathogenesis
Pathophysiology of CHF
CHF is a pathophysiological syndrome in which, as a result of one or anotherdiseases of the cardiovascular system or under the influence of other etiological
causes there is a violation of the ability of the heart to fill or empty,
accompanied by an imbalance of neurohumoral systems (RAAS, sympathoadrenal system, natriuretic peptide system, kinin-kallikrein
system), with the development of vasoconstriction and fluid retention, which leads to
further dysfunction of the heart (remodeling) and other organs
(proliferation), as well as the mismatch between the provision of organs and tissues
the body with blood and oxygen with their metabolic needs.
Classification of CHF by LV ejection fraction:
CHF with low EF (less than 40%) (CHFF)CHF with intermediate EF (from 40% to 49%) (CHF)
CHF with preserved EF (50% or more) (CHFF)
CHF classification
Functional classes (may change during treatment in one or the otherside)
CHF classification
(May get worse despite treatment)Clinical manifestations
Typical SymptomsSpecific signs
Dyspnea
Orthopnea
Night attacks
cardiac asthma
Poor portability
physical activity
Fatigue, tiredness,
increase in time
recovery after
termination of load
Swelling of the ankles
Swelling of the neck veins
Hepatojugular reflux
Apical displacement
push to the left
Gallop Rhythm (appearance
III tone)
Systolic murmur on
apex of the heart
Physical examination
Inspection: pallor of the skin,acrocyanosis, cyanosis of mucous membranes,
symmetrical pastiness of the lower
limbs (lower leg, ankle),
symmetrical edema, anasarca,
swollen neck veins (lying, standing).
Palpation of the abdomen: the liver protrudes from under the costal arch.
Percussion of the heart and abdomen: increase
the boundaries of the relative dullness of the heart,
an increase in the size of the liver (by
Kurlov), finding a free
fluid in the abdomen.
Physical examination
Lung auscultation:wheezing in the lungs (symmetrical from
lower sections to the entire surface
lungs),
weakening and absence
respiratory noise in the lower
parts of the lungs.
Auscultation of the heart:
weakening of the I tone at the top,
the presence of a gallop rhythm (III tone),
the presence of noise relative
inadequacies
atrioventricular valves.
Laboratory diagnostics
General blood analysisTo exclude anemia and other causes leading to shortness of breath, an extended
general blood analysis.
Blood chemistry
the content of sodium, potassium, calcium, urea in the blood, hepatic
enzymes, bilirubin, ferritin and the calculation of the total iron-binding capacity of the blood,
calculation of GFR based on the content of creatinine in the blood according to the CKD-EPI formula, the ratio
urine albumin / creatinine and assessment of thyroid function.
The listed studies are shown in the following cases: before starting admission
diuretics, RAAS suppressants, and anticoagulants to control their safety, for
identifying treatable causes of heart failure (e.g. hypocalcemia and thyroid dysfunction)
glands) and concomitant diseases (for example, iron deficiency) to determine
forecast.
Laboratory diagnostics
Natriuretic hormonesStudy of blood levels of natriuretic hormones (BNP and
NTproBNP) is indicated to rule out an alternate cause of dyspnea and
determining the forecast.
The level of BNP more than 35 pg / ml is diagnostically significant, the level
NT-proBNP - more than 125 pg / ml.
Instrumental diagnostics
Electrocardiogram (ECG)12-lead ECG is recommended for determining
heart rate, heart rate, width and shape of the QRS complex, and
also identify other important violations. ECG helps
determine the further treatment plan and evaluate
forecast. A normal ECG virtually eliminates
the presence of systolic heart failure.
Transthoracic echocardiography
Transthoracic echocardiography is recommended for assessing
structure, systolic and diastolic function
myocardium, incl. in patients on
treatments potentially damaging the myocardium
(for example, chemotherapy), as well as to identify and
valvular pathology assessment, prognosis assessment.
Additional technologies (including tissue
dopplerography, indicators of myocardial deformation, in
incl. Strain and Strain rate) can be included in the EchoCG protocol
studies in patients at risk of developing heart failure for
detecting myocardial dysfunction in preclinical
stages
Instrumental diagnostics
Chest x-ray detects cardiomegaly(cardiothoracic index more than 50%), venous congestion or pulmonary edema.
Magnetic resonance imaging (MRI)
Cardiac MRI is recommended for assessing the structure and function of the myocardium (including
right sections) with a poor acoustic window, as well as in patients with difficult
combined congenital heart disease (taking into account
restrictions / contraindications for MRI), as well as for the characteristics of the myocardium in
suspected myocarditis, amyloidosis, Chagas disease, Fabry disease,
non-compact myocardium, hemochromatosis.
Instrumental diagnostics
Coronary angiographyCoronary angiography is recommended for assessing
lesions of the coronary arteries in patients with
angina pectoris, which in the future
revascularization can be performed
myocardium.
Left and right heart catheterization
recommended before heart transplant or
device implantation for long-term
circulatory support to assess
functions of the left and right heart, as well as
pulmonary vascular resistance.
Stress EchoCG, SPECT, PET
To assess myocardial ischemia and viability
can be applied:
stress echocardiography with physical or pharmacological
load, single-photon emission
computed tomography (SPECT), positron emission tomography (PET) in patients with heart failure and
IHD for making a decision on revascularization.
Instrumental diagnostics
Holter ECG monitoringHolter ECG monitoring is not routinely used in patients with CHF and is indicated only
in the presence of symptoms suspected of being associated with cardiac arrhythmias and
conduction (for example, with palpitations or fainting). In patients with AF, with
24-hour ECG monitoring monitors the frequency of ventricular contractions.
ECG-guided exercise testing
Exercise tests under ECG control provide an objective
assessment of exercise tolerance, as well as to find out the presence of myocardial ischemia.
Instrumental diagnostics
Cardiopulmonary Exercise Testing (CPT)Testing helps to find out what is associated with shortness of breath - with a pathology of the heart
or lungs, it is also important when considering transplantation
or the installation of an artificial LV for the purpose of physical training.
CPT is carried out in two main modes:
on the treadmill
track
(treadmill)
bicycle ergometer
Treadmill test
The treadmill allows you to exerciseconstantly increasing load through
a combination of increasing speed and degree
increasing the angle of inclination of the surface.
Protocols with a progressive increase in load
are very popular and are matched in
each case depending on
the severity of the patient's condition.
As a rule, an increase in load occurs
gradually at intervals of 6 to 60 seconds.
The choice of protocol should be
individualized and, in most cases,
oriented in such a way that
the duration of the study ranged from 8
up to 12 minutes before symptoms of physical
weakness preventing you from continuing
further testing.
Lowest treadmill speed
(1 - 1.2 km / h) can be used as base
level for load testing.
Bicycle ergometry
The ergometer is preferred for patientswith disturbed gait or balance, and
also for obesity, orthopedic
violations and at the same time
echocardiographic study.
Ergometer requires less space
to conduct research, it
the cost price is lower when it is used
fewer
artifacts during ECG recording.
Modern bicycle ergometers with electronic
braking system can provide
the same level of physical activity
at different pedaling speeds.
6-minute walk test (6MTH)
Distance 6MTH can be used to determinefunctional class of CHF and the volume of physical training.
The scale for assessing the severity of heart failure
dynamicsevaluate the effectiveness
ongoing treatment of CHF.
Treatment
Conservative treatmentTreatment objectives:
preventing the progression of CHF
(at I FC),
reduction of symptoms,
improving the quality of life,
inhibition and reverse development
remodeling of target organs,
decrease in the number of hospitalizations,
decrease in mortality.
Limiting salt intake
With CHF I FC should not be used
salty food (sodium up to 3 g / day, which
corresponds to 7.5 g of salt),
at II FC - do not add salt to food (sodium
1.5-2 g, which corresponds to 4-5 g of salt),
FC III – IV - use products with
reduced salt and cook
dishes without salt (sodium - 1 g, which
corresponds to<3 г соли).
During active diuretic therapy
moderate sodium and salt restriction
(sodium<3 г, соль <7 г), после достижения
payments according to FC HSN.
Non-drug treatment of CHF
Limiting fluid intakeLimiting fluid intake is relevant only in extreme situations: when
decompensated severe course of CHF, requiring intravenous administration of diuretics.
In normal situations, the volume of fluid is less than 2 l / day (minimum intake
liquid - 1.5 l / day).
Non-drug treatment of CHF
Limiting alcohol intakeAlcohol is strictly prohibited for the sick
with alcoholic cardiomyopathy.
In patients with ischemic origin
CHF use up to 20 ml of ethanol in
day can improve
forecast.
Non-drug treatment of CHF
Body weight controlWeight gain> 2 kg in 1–3 days is likely to indicate fluid retention.
the body and the risk of developing decompensation.
The presence of obesity or overweight worsens the prognosis of a patient with CHF, and in all cases
BMI more than 25 kg / m2 requires special measures and restriction of caloric intake.
Progressive decrease in body weight (with a baseline BMI less than 19 kg / m2),
due to the loss of both adipose tissue and muscle mass is called cardiac
cachexia - documented unintentional weight loss of 5 kg or more or more,
than 7.5% of the original weight in a compensated state for 6 months.
In the treatment of such patients, a combination of drug correction is necessary
neurohormonal disorders, cytokine blockade and nutritional support.
All drugs for the treatment of CHF and decreased LVEF can be divided into two main categories, according to the degree
evidenceI-ACE (inhibitor
angiotensin-converting enzyme)
ARA (AT-II receptor antagonist) =
Sartan
ARNI (receptor antagonist
neprizilina)
BAB (β-blocker)
AMKR (mineralocorticoid antagonist
receptors)
Ivabradine (If-channel inhibitor)
The main drugs affecting the prognosis of patients with CHF
ACE I (angiotensin converting enzyme inhibitor)ACE inhibitors in maximum tolerated doses are used in all patients
CHF I – IV FC and with LVEF<40 % для снижения риска смерти, повторных госпитализаций и
improving the clinical condition.
Refusal to prescribe i-ACE to patients with low and intermediate LVEF cannot
considered justified when SBP is> 85 mm Hg. and leads to increased risk
death of patients with CHF (recommendation class Ia, level of evidence A).
ACE inhibitors have not yet been proven to improve the prognosis of patients with
SNpFV. However, due to the improvement in the functional status of patients and
reducing the risk of involuntary hospitalizations and ACE are shown to all
patients with HFPS (recommendation class IIa, level of evidence B).
Dosing regimen I-ACE
The main drugs affecting the prognosis of patients with CHF
ARA (AT-II receptor antagonist) = SARTANESARA in the maximum tolerated doses are used in patients with CHF I – IV
FC with LVEF<40 % для снижения комбинации риска смерти и
hospitalizations for CHF with intolerance to I-ACE (class
Recommendations IIa, level of evidence A).
ARA has not been shown to improve the prognosis of patients with HFsPV and
SNpFV. The use of ARA candesartan in patients with HFsPH and HFPS
may reduce hospital admissions (grade IIb, grade
evidence B), and with intolerance to ACE inhibitors in such patients
Candesartan may be the drug of choice (recommendation class
IIa, level of evidence B).
ARA dosage regimen
The main drugs affecting the prognosis of patients with CHF
ARNI (neprisilin receptor antagonist) -SacubitrilARNI are recommended for patients with CHF II-III FC with LVEF<40% стабильного течения(без
decompensation, administration of IV or doubling the dose of oral diuretics and with
SBP> 100 mm Hg. Art.), with the portability of i-ACE (or ARA).
Transfer of this category of patients to ARNI (at a dose of 100 mg x 2 times a day no earlier than
less than 36 hours after the last dose of ACE I (ARA), followed by titration
doses up to the optimal 200 mg x 2 times a day) is made for additional
reducing the risk of death and subsequent hospitalizations due to worsening of the course
CHF (recommendation class I, level of evidence B).
It is possible to consider the use of ARNI in patients with CHF II-III FC with LVEF<35%
stable course as a starting therapy (instead of i-ACE) to reduce
risk of death and hospitalization due to worsening of CHF (class
of recommendation IIa, level of evidence C).
The combination of two blockers of the renin-angiotensin system (excluding AMKR) is not
recommended for the treatment of patients with CHF due to a significant increase in serious
adverse events including symptomatic hypotension and impairment of function
kidney (recommendation class III, level of evidence A).
Uperio, Inresto
Valsartan + Sacubitril (Valsartanum + Sacubitrilum)The main drugs affecting the prognosis of patients with CHF
BAB (β-blocker)BAB are used in all patients with CHF II – IV FC and LVEF<40 % для
reducing the risk of death and re-hospitalization with an ACE inhibitor
(ARA) and AMKR (recommendation class I, level of evidence A). BAB
prescribed starting from 1/8 of the average therapeutic dose, optimally
after reaching the state of compensation, and are slowly titrated to
as portable as possible.
BAB can be prescribed to patients with HFPS and HFPS for the purpose of
decrease in heart rate and severity of LVH.
α-β-blocker carvedilol, in addition to reducing heart rate, has
positive effect on LV relaxation indices in patients with
SNsFV.
Dosing regimen of BAB
The main drugs affecting the prognosis of patients with CHF
AMKR in doses of 25-50 mg / day is used in all patients with CHF II-IV FC and
LVEF<40 % для снижения риска смерти, повторных госпитализаций и
improvement of the clinical condition together with i-ACE (ARA) and BAB (class
Recommendations I, level of evidence A).
MCR antagonists can be prescribed for patients with HFsPH and HFPS
to reduce the number of hospitalizations for CHF (recommendation class
IIa, level of evidence B).
Thus, a triple neurohormonal blockade: ACE inhibitors (with
intolerance to ARA) or ARNI (with stable CHF with SBP> 100 Hg) in
combination with BAB and AMKR is the basis of HFNEF therapy and, in total,
45% reduce mortality in patients with CHF I – IV FC.
AMCR (mineralocorticoid receptor antagonist)
In the case of stable CHF, spironolactone (12.5-50 mg) and eplerenone (25-50mg) are recommended to reduce the risk of death and hospitalization
patients with CHF II – IV FC.
The main drugs affecting the prognosis of patients with CHF
Ivabradine (If-channel inhibitor)Ivabradine is used in patients with CHF II – IV FC and LVEF<40 % c
sinus rhythm and heart rate> 70 beats / min with intolerance to BAB for
reduce the risk of death and hospitalization (recommendation class IIa, level
proof C).
Diuretics
Ivabradin
Cardiac glycosides
Omega-3 PUFA
Heparin / LMWH and UAC
Drugs that affect the prognosis of patients with CHF and are used in certain clinical situations.
DiureticsDiuretics are used in all patients
CHF II – IV FC with LVEF<40 % и
signs of stagnation for improvement
clinical symptoms and reduction
risk of repeated hospitalizations (class
Diuretics may be prescribed if
fluid retention in the body
patients with HFFV / HFFV, but they should be
use with care not to
cause excessive decline
LV preload and cardiac fall
emission (recommendation class IIb, level
proof C);
Diuretics
Degitration therapy in the active phase (withpresence of stagnant phenomena) is carried out with
excess of excreted urine over drunk
liquid no more than 1-1.5 liters per day during
avoiding electrolyte, hormonal,
arrhythmic and thrombotic complications.
Torasemide loop diuretics are combined
or Furosemide with a diuretic dose of AMKR (100-300 mg / day).
After reaching euvolemia, diuretics
are prescribed daily in minimal doses,
to maintain a balanced
diuresis (torasemide or furosemide).
To maintain optimal acid-base sensitivity to loops
diuretics and normalization of renal blood flow,
once every 2 weeks, 4-5 day courses are recommended
ICAG (carbonic anhydrase inhibitor) acetozolamide
(0.75 / day). (recommendation class I, level
proof C).
Drugs that affect the prognosis of patients with CHF and are used in certain clinical situations.
Cardiac glycosidesDigoxin is prescribed for patients with CHF with LVEF<40 % и синусовым ритмом при недостаточной
the effectiveness of the main remedies for decompensation to reduce the risk of repeated
hospitalizations (recommendation class IIa, level of evidence B).
The appointment of digoxin is carried out by monitoring the level of the drug in the blood (at a concentration
more than 1.1–1.2 ng / ml, dosage reduction is necessary) both in sinus rhythm and in AF
(optimal values of the concentration of digoxin in the blood<0,9 нг/мл) при отсутствии
contraindications (recommendation class I, level of evidence C).
If it is impossible to determine the concentration of digoxin, taking the drug can be
continued in small doses (0.25-0.125 mcg) if there is no data on glycoside
intoxication (with MT<60 кг (особенно у женщин), в возрасте >75 years old and with GFR<60
(ml / min / 1.73 m2) no more than 0.125 mg).
Drugs that affect the prognosis of patients with CHF and are used in certain clinical situations.
Omega-3 PUFA (polyunsaturated fatty acids)Omega-3 PUFAs should be considered in patients with CHF
II – IV FC and LVEF<40 % для снижения риска смерти, в т. ч. внезапной и
re-hospitalizations, in addition to basic treatments
CHF (recommendation class IIa, level of evidence B).
Drugs that affect the prognosis of patients with CHF and are used in certain clinical situations.
OACG should be prescribed for patients with CHF II – IV FC to reduce the risk of death
and hospitalizations for AF (grade I recommendation, level of evidence A) or
intracardiac thrombosis (recommendation class IIa, level of evidence A).
OACG should not be used in all patients with CHF I – IV FC with sinus rhythm
without signs of intracardiac thrombus, since they do not reduce the risk
thromboembolism with increased risk of bleeding (recommendation class III,
Evidence level B).
Oral anticoagulants (OACG)
For patients with CHF and nonvalvular AF who are indicated (numberCHA2DS2VASc score> 2) anticoagulant therapy should be preferred
prescribing new oral anticoagulants (NOACs) instead of antagonists
vitamin K (AVK), given the greater reduction in the risk of death and
thromboembolic complications while reducing the risk
bleeding, especially intracranial (recommendation class IIa,
Evidence level B).
The use of PLA is contraindicated in the presence of mechanical valves
and mitral stenosis with valve overlaps (recommendation class
III, level of evidence B).
Regardless of the risk of thromboembolism, the NOAC should not be used in
patients with AF and GFR<30 мл / мин/1,73 м2 (класс рекомендаций III,
Evidence level A).
Drugs that affect the prognosis of patients with CHF and are used in certain clinical situations.
HeparinPrescribing heparin or low molecular weight heparins (LMWH) for at least 7 days
should be considered in patients with CHF II – IV FC with LVEF<40% при наличии венозного
thrombosis, PE, or decompensation requiring bed rest (≥3
days), to reduce the risk of thromboembolism, improve the prognosis and reduce the risk
hospitalizations (recommendation class I, level of evidence C) followed by
transfer to AVK (with INR control) or OACG (recommendation class I, level
proof B).
In the presence of venous thrombosis and PE in patients with CHF, an alternative
therapy with factor X-a inhibitors instead of heparin with transfer to VKA: apixaban 10
mg x 2 times a day for 7 days with subsequent transfer to 5 mg x 2 times a day
(recommendation class I, level of evidence B) or rivaroxaban 15 mg x 2 times daily in
within 21 days with transfer to 20 mg x 1 time per day (recommendation class I, level
proof B).
Duration of anticoagulant therapy in the first episode of venous thrombosis or PE
is up to 3 months (recommendation class I, level of evidence A), and when
repeated episodes should be of longer duration (recommendation class I, level
evidence B), PLA should be preferred in these cases (recommendation class IIa,
level of evidence B), and if anticoagulant therapy is not possible,
prescribe aspirin (recommendation class IIb, level of evidence B).
Antiarrhythmics
BMCC (blockers of slow
calcium channels)
Iron preparations
Statins (HMG-CoA reductases)
Aspirin
Peripheral vasodilators
Coenzyme Q-10
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
AntiarrhythmicsAntiarrhythmics (amiodarone, sotalol) do not affect the prognosis of patients with CHF and
can only be used to eliminate symptomatic ventricular
cardiac arrhythmias (class of recommendation IIb, level of evidence B).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
BMCC (slow calcium blockerschannels)
Dihydropyridine BMCCs (amlodipine and
felodipine) do not affect the prognosis
patients with CHF.
These drugs may be prescribed in the background
the main therapy of CHF for additional
control of blood pressure, pressure in the pulmonary artery and
valvular regurgitation (recommendation class IIb,
Evidence level B).
Patients with HFpEF and HFfV calcium antagonists
verapamil and diltiazem are contraindicated (class
Recommendations III, level of evidence C).
Prescribing verapamil and diltiazem to patients with
HFPS to reduce heart rate can be
recommended only in case of intolerance
BAB and in the absence of severe CHF,
manifested, for example, by fluid retention,
and LVEF> 50% (recommendation class IIb, level
proof C).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
Iron preparationsIntravenous trivalent iron supplementation should be
considered in patients with CHF and hemoglobin levels<120 г/л для
reducing symptoms and improving physical tolerance
stress (recommendation class IIa, level of evidence A).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
Statins (HMG-CoA reductases)Statin use has not been shown to affect
prognosis of patients with CHF, but led to
decrease in the number of hospitalizations for
ischemic ethology.
The primary prescription of statins may be
considered in patients with CHF ischemic
etiology (recommendation class IIb, level
proof of A).
Primary prescription of statins to patients with CHF
non-ischemic etiology is not recommended
(recommendation class III, level of evidence
B).
Previously prescribed statin therapy for patients with
ischemic etiology of CHF should be
continued (recommendation class IIa, level
proof B).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
AspirinThe appointment of aspirin does not affect the prognosis of patients with CHF and, in some cases, weakens
the action of the main means of treatment.
Therefore, the appointment of aspirin can only be considered in patients who have undergone
ACS no more than 8 weeks ago and underwent percutaneous procedures
intravascular exposure (recommendation class IIb, level of evidence B).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
Peripheral vasodilatorsConvincing data on the effect of vasodilators (including nitrates and their
combination with hydralazine) is not, and their use can only be considered
to eliminate angina pectoris if other methods are ineffective (class
of recommendations IIb, level of evidence B).
Drugs that do not affect the prognosis of patients with CHF and are used to improve symptoms
Coenzyme Q-10The use of coenzyme Q-10 in addition to
the main remedies for the treatment of CHF
can lead to an increase in LVEF and
elimination of symptoms and even how
shown in a relatively small
volume randomized
clinical trial, reduce
mortality. Therefore, the application
coenzyme Q-10 can be considered
as an adjunct to basic therapy
CHF (recommendation class IIb, level
proof B).
Surgery
Angina pectorisIn the presence of angina pectoris or multivessel disease in patients with CHF
with low LVEF with ineffectiveness of HTM can be considered
coronary revascularization.
Surgery
Valvular heart diseaseSituations are possible when it is difficult
recognizable heart valve defects,
leading to heart failure or
increasing its severity.
Patients with CHF and lesions of the valve (valves)
hearts are a high-risk group.
In such a situation, the decision is made
consultation with a thorough assessment of the attitude
risk / benefit with the participation of experts in the field
treatment of valvular heart disease: a cardiologist, a specialist in the field of CHF, a cardiac surgeon,
specialist in transcatheter implantation
artificial valves, a specialist in
imaging methods, anesthesiologist, if
necessary, a gerontologist and a resuscitator.
Artificial left ventricle
Artificial LV placement should be considered in patients withterminal LVEFF (with optimal drug and
non-drug therapy) as a "bridge to transplantation" for
improving symptoms, reducing the risk of hospitalization and sudden death in
patients with indications for heart transplant.
Artificial LV placement should be considered in patients with
terminal LVEFF, persisting despite optimal
drug and non-drug therapy, in patients who are not
are candidates for heart transplant.
Electrophysiological methods
The use of all electrophysiological methods for the treatment of CHF shouldstart only against the background of OMT with its insufficient effectiveness.
It is not an alternative, but an addition to the most active therapy.
sick. Implantation of CRT and ICD devices is recommended for patients
who have a life expectancy of at least one year after
device implantation.
Cardiac Resynchronization Therapy (CRT)
Cardiac applicationresynchronization therapy (CRT)
- software cardiac stimulation synchronizes the operation of the cameras
heart and provides sustainable
improvement in the overwhelming
most patients with
chronic cardiac
insufficiency for which
conventional medication
has ceased to be effective.
CPT / CPT-D implantation is shown
patients with sinus rhythm,
with HF-nFV II – IV FC with LVEF
≤35%, LBBB at duration
complex QRS ≥150ms with the aim
improving the clinical course of heart failure and
decrease mortality
An implantable cardiac defibrillator (ICD) is recommended for patients with a life expectancy of more than 1 year for secondary
prevention of sudden cardiac death (SCD) survivors of ventricular fibrillation orventricular tachycardia with unstable hemodynamics, or loss of consciousness, which
occurred 48 hours after myocardial infarction (MI), as well as if not
reversible causes of these rhythm disturbances.
Acute decompensation of CHF
The term "acute decompensatedheart failure "(ADF)
it is customary to call the period of CHF,
which is characterized by fast
worsening of cardiac symptoms
failure, which requires urgent
hospitalization of the patient and
intensive care.
Every episode of ADHD worsens the prognosis
a patient with CHF and requires both
specialized treatment and
temporary correction of the previous
CHF therapy.
Reasons for ADF:
rapid progressionCHF itself,
onset of acute conditions
(AMI, TELA, acute valvular
defeats, etc.),
background decompensation
exacerbation of concomitant
pathology (pneumonia, other
infections, dysfunction
kidney, anemia, adenoma
prostate gland,
paroxysmal fibrillation
atria, diabetes mellitus decompensation and
etc.)
Symptoms of ADHD
Diagnosis of ADF
X-ray of the lungsallows you to determine the severity
stagnant phenomena, identify the presence
fluid in the pleural cavity and
diagnose cardiomegaly, and
also not cardiovascular
diseases causing
progression of CHF (for example,
pneumonia) (recommendation class I,
level of evidence C).
It should be remembered that the severity of ADF is not
always correlates with
radiographic picture and that
X-ray of the lungs in position
lying down has less
diagnostic value than
research in a standing position.
Diagnosis of ADF
Electrocardiogram (ECG)ECG detects the presence of ischemia
myocardium, atrial fibrillation and others
causes of ADF.
ECG in 12 standard leads is necessary
register within 10 minutes after contacting
medical personnel if there is a suspicion of ACS or
arrhythmias, and within 30 minutes in other cases.
Echocardiography (EchoCG)
Echocardiography eliminates life-threatening
conditions (AMI, PE, aortic dissection), determine
LVEF, heart size, systolic pressure in
pulmonary artery, make an indirect assessment
pulmonary artery occlusion pressure and
central venous pressure.
Diagnosis of ADF
Natriuretic peptidesDetermination of natriuretic peptides
allows you to exclude non-heart reasons
symptoms regarded as a manifestation
progression of CHF (recommendation class I,
Evidence level A).
At the level of BNUP<100 пк/мл и/или NT-proBNP
<300 пк/мл наличие ОДСН маловероятно.
Cardiac troponin
The test is used to exclude ACS and
determining the prognosis of patients.
Creatinine and electrolytes
The test is used for selection and correction
therapy; it is recommended to carry out 1 time in 1-2
days and more often if necessary
Indications for hospitalization
Indications for hospitalization (transfer) inintensive care unit
include:
hemodynamic instability or
severe (progressive) shortness of breath
, and / or recurrent life-threatening
arrhythmia, and / or
other life-threatening conditions:
OKS,
hypertensive crisis,
heart ruptures as complications of ACS,
chest injury
acute insufficiency of heart valves,
TELA.
Primary management of patients hospitalized for ADF
Prescribing drugs in patients with ADHD
Oxygen therapyDiuretics
Vasodilators
Drugs with a positive
inotropic action
Oxygen therapy
Percutaneous monitoring recommendedblood oxygen saturation (recommendation class
I, level of evidence C).
Venous blood pH measurement and determination
partial pressure of CO2 in venous blood
should be considered in patients with acute
pulmonary edema or COPD.
In patients with cardiogenic shock for
determination of indicators of acid-base
states recommended to use
arterial blood.
Routine oxygen therapy is not advisable in
patients with ADHD who do not have hypoxemia, since
it can lead to vasoconstriction and decrease
cardiac output (recommendation class I, level
proof C).
Oxygen therapy
Oxygen therapy is indicated for SpO2<90% или PaO2 <60mmHg Art. in order to correct hypoxemia (class
Recommendations I, level of evidence C).
Non-invasive ventilation with positive
pressure (CPAP therapy and BiPAP therapy) should
be considered in patients with respiratory
distress (NPV> 25 per minute, SpO2<90%), ее следует
start as early as possible in order to reduce
the severity of respiratory distress and reduction
intubation needs (recommendation class IIa,
Evidence level B).
Non-invasive ventilation of the lungs can lower blood pressure, in
connection with which it should be used with caution in
patients with hypotension.
Intubation is indicated for respiratory failure
with hypoxemia (PaO2<60 мм рт.ст. (8 кПа), гиперкапнией
(PaCO2> 50 mmHg (6.65 kPa) and acidosis (pH<7,35)
in the absence of the possibility of non-invasive correction
ventilation disorders (recommendation class I,
level of evidence C).
Diuretics for ADF
Diuretics are indicated in the presence of edema syndrome.With AHF (ODSF), diuretics are prescribed according to the principle
quantum satis (how much you need) to get FAST
guaranteed diuretic response.
Optimal intravenous bolus use
effective doses of torasemide or furosemide.
With refractoriness, use several tactics of it
overcoming:
The addition of small doses of thiazide diuretics to
addition to loop diuretics;
The use of loop diuretics in combination with
large (150–300 mg) doses of AMKR;
Use of active diuretics with inhibitors
carbonic anhydrase (acetazolamide), which allows
avoid the development of alkalosis, in which
the effect of thiazide and loop diuretics weakens.
Vasodilators for ADF
Vasodilators are indicated in the treatment of ADF, since due to venodilationreduce preload and pressure in the pulmonary circulation (ICC),
stopping the symptoms of pulmonary edema.
At the same time, due to dilatation of arterioles and reduction of post-load,
vasodilators facilitate emptying of the compromised LV.
The use of nitroglycerin, isosorbide dinitrate, sodium nitroprusside
can only be considered in patients with BP ≥100 mmHg. Art. Application
serelaxin (a vasodilator and diuretic with additional organ protection
targets - kidneys, liver), the only drug that improves long-term
prognosis of patients with ADF should be considered in patients with SBP> 125 mm
rt. Art.
Prescribing vasodilators should be based on the recommendations presented in Table 3.
There are currently no doctors in the arsenal
"Pure" drugs with a positive
inotropic effect.
Preparations can be conditionally divided into:
derivatives of catecholamines (dopamine,
dobutamine),
positive inotropic with
vasodilating effect
(levosimendan, milrinone),
cardiac glycosides,
each of which has features
actions.
The drugs are indicated for patients with low
cardiac output, persisting
phenomena of stagnation, hypoperfusion, despite
for the use of vasodilators and / or
diuretics.
Drugs with positive inotropic action
The use of drugs with a positiveinotropic effect is not advisable
in patients without symptomatic hypotension
and / or hypoperfusion.
Long-term use of drugs with
positive inotropic effect (for
excluding digoxin) negatively
affects the prognosis of patients with CHF,
therefore their application should
be limited only to the acute period
hypopefusion and symptomatic
hypotension not corrected
drugs of other classes.
Slide 2
Help patients use the internet to learn about their condition
- Dear friends, now Russian patients with heart failure have access to a unique source of information, which is used by patients in England, Germany, France and Spain.
- Together with the European Heart Failure Association, the Society of Heart Failure Specialists of Russia translated and adapted a pan-European website for patients.
Slide 3
Fundamentals of anatomy and physiology of the cardiovascular system
Slide 4
Anatomy of the heart
- The heart is a hollow muscular organ that acts as a pump. In an adult, its volume and weight are on average 600-800 cm3 and 250-330 g.
- The heart consists of four chambers - the left atrium (LA), left ventricle (LV), right atrium (RV), and right ventricle (RV), all of which are separated by septa. The LA includes the hollow veins, the LA - the pulmonary veins. The pulmonary artery (pulmonary trunk) and the ascending aorta leave the RV and LV, respectively.
- Conventionally, in the human body, small and large circles of blood circulation are divided. In the pulmonary circulation - the right ventricle, pulmonary vessels and the left atrium - there is an exchange of blood with the external environment. It is in the lungs that it is saturated with oxygen and freed from carbon dioxide. The large circle is represented by the left ventricle, aorta, arteries, veins and the right atrium, it is designed to provide blood supply to the entire body.
Slide 5
Physiology of the heart.
- The amount of blood expelled by S. in 1 min is called the minute volume of S. (MO). It is the same for the right and left ventricles. When a person is at rest, MO averages 4.5-5 liters of blood. The amount of blood ejected by S. in one contraction is called the systolic volume; it is on average 65-70 ml.
- The aorta and arteries of the body are a pressure reservoir in which blood is under high pressure (for a person, the norm is about 120/70 mm Hg). The heart throws blood into the arteries in separate portions. In this case, the elastic walls of the arteries are stretched. Thus, during diastole, the energy accumulated by them maintains the blood pressure in the arteries at a certain level, which ensures the continuity of blood flow in the capillaries. The level of blood pressure in the arteries is determined by the relationship between MO and the resistance of the peripheral vessels. The latter, in turn, depends on the tone of the arterioles, which are, in the words of IM Sechenov, "taps of the circulatory system." Increasing the tone of the arterioles makes it difficult for blood to drain from the arteries and increases blood pressure; a decrease in their tone has the opposite effect.
- Coronary circulation, blood supply to the heart muscle, is carried out through the arteries and veins communicating with each other, penetrating the entire thickness of the myocardium.
- The arterial blood supply to the human heart occurs mainly through the right and left coronary (coronary) arteries, extending from the aorta at its beginning.
Slide 6
Chronic heart failure
Slide 7
The prevalence of CHF and its implications for the health care system
According to the data of epidemiological studies of the last 5 years, conducted in our country, it was revealed that:
- in 2002 in the Russian Federation there were 8.1 million people with clear signs of CHF, of which 3.4 million had terminal, III – IV FC disease.
- in 2003, decompensation of CHF caused hospitalizations in hospitals with cardiological departments for almost every second patient (49%), and CHF appeared in the diagnosis in 92% of patients hospitalized in such hospitals.
- In 4/5 of all patients with HF in Russia, this disease is associated with AH and in ⅔ of patients with IHD.
- More than 55% of patients with overt heart failure have almost normal myocardial contractility (LVEF> 50%) and the number of such patients will steadily increase.
- The one-year mortality rate of patients with clinically expressed HF reaches 26-29%, that is, in one year in the Russian Federation, from 880 to 986 thousand HF patients die.
Slide 8
What is CHF
CHF is a disease with a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.), which are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body. The root cause is impairment of the heart's ability to fill or empty due to myocardial damage, as well as an imbalance in the vasoconstrictor and vasodilating neurohumoral systems.
Slide 9
Causes of CHF
CHF syndrome can complicate the course of almost all diseases of the cardiovascular system, but the main causes of CHF, accounting for more than half of all cases, are:
- Ischemic (coronary) heart disease (CHD)
- Arterial hypertension
- a combination of these diseases, as well
- Valvular heart disease
Non-ischemic cardiomyopathies, including both diopathic dilated cardiomyopathy (DCM), and specific, of which cardiomyopathy is the most widespread as an outcome of myocarditis and alcoholic cardiomyopathy.
Slide 10
Clinical signs of CHF
- Weakness, fatigue and limited activity.
- Dyspnea.
- Palpitations.
- Lung congestion.
- Swelling.
Slide 11
CHF treatment goals
- Improved prognosis (life extension).
- Elimination of symptoms of the disease - shortness of breath, palpitations, increased fatigue and fluid retention in the body.
- Protection of target organs (heart, kidneys, brain, blood vessels, muscles) from damage.
- Reducing the number of hospitalizations.
- Improving the "quality of life".
Slide 12
The pathogenesis of heart failure in various diseases
Slide 13
Classification of CHF OSSN 2002 =
Slide 14
Methods for assessing the severity of CHF =
- Assessment of the severity of the patient's condition and especially the effectiveness of the treatment is an urgent task.
- It is the dynamics of PK during treatment that makes it possible to objectively decide whether the therapeutic measures are correct and successful.
- The use of a simple and affordable 6-minute corridor walk test makes it possible to quantitatively measure the severity and dynamics of the condition of a patient with CHF during treatment and his tolerance to physical activity.
Slide 15
Determining the distance of a six-minute walk
- This method has been widely used in the last 4–5 years in international practice and allows assessing the patient's tolerance to physical activity using minimal technical means.
- The essence of the method is that you need to measure how much distance the patient is able to walk within 6 minutes. All that is required is a watch with a second hand and a tape measure. The easiest way is to mark the hospital or outpatient corridor in advance and ask the patient to move along it for 6 minutes. If the patient walks too quickly and is forced to stop, this pause naturally starts at 6 minutes. As a result, you will determine the physical tolerance of your patient to stress. Each FC CHF corresponds to a certain distance of 6-minute walk
Slide 16
Other ways to assess the clinical condition of patients with CHF
- In addition to the dynamics of FC and tolerance to loads, the following are used to control the condition of patients with CHF:
- Assessment of the patient's clinical condition (the severity of shortness of breath, diuresis, changes in body weight, the degree of congestion, etc.);
- Dynamics of LVEF (in most cases, according to the results of echocardiography);
- Assessment of the patient's quality of life, measured in points using special questionnaires, the most famous of which is the questionnaire of the University of Minnesota, developed specifically for patients with CHF.
Slide 17
The concept of "quality of life"
- The patient's ability to live the same full life as his healthy peers in similar economic, climatic, political and national conditions.
- In other words, the doctor must remember the desire of his patient with CHF, who is already doomed to take medications, often quite unpleasant, to live a full life. This concept includes physical, creative, social, emotional, sexual, political activity. It must be remembered that changes in "quality of life" do not always parallel clinical improvement. For example, the appointment of diuretics is usually accompanied by clinical improvement, but the need to be "tied" to the toilet, the numerous adverse reactions inherent in this group of drugs, definitely worsen the "quality of life".
Slide 18
6 ways to achieve your goals in the treatment of decompensation
- Diet
- Physical activity regimen
- Psychological rehabilitation, organization of medical supervision, schools for patients with CHF
- Drug therapy
- Electrophysiological methods of therapy
- Surgical, mechanical treatments
As you can see, drug treatment is, although a very important component, it is in the fourth position on this list. Ignoring non-drug methods of combating CHF makes it difficult to achieve ultimate success and reduces the effectiveness of therapeutic (drug) effects.
Slide 19
Diet of CHF patients
The diet of patients with CHF should be high-calorie, easily digestible. The best option is to use nutritional mixtures in the diet. In food, the amount of salt should be limited as much as possible - this is much more effective than limiting fluid intake. The patient should take at least 750 ml of liquid at any stage of CHF.
The salt restriction has 3 levels:
- 1st - restriction of foods containing a large amount of salt, the daily intake of sodium chloride is less than 3 g / day (with I FC CHF)
- 2nd - plus not salting food and using salt with a low sodium content in its preparation, daily consumption of sodium chloride 1.2-1.8 g / day (II - W FC CHF);
- 3rd - plus cooking without salt, the daily intake of sodium chloride is less than 1 g / day (IV FC).
Slide 20
Trophological status
The concept that characterizes the state of health and physical development of the body associated with nutrition.
It is necessary to distinguish between the following pathological conditions in a patient with CHF:
- obesity
- overweight
- normal weight
- cachexia.
Slide 21
- Obesity or overweight worsens the prognosis of a patient with CHF and in all cases of body mass index (BMI) more than 25 kg / m 2 requires special measures and restriction of caloric intake.
- Pathological weight loss, obvious or subclinical signs of which are found in 50% of patients with CHF.
Progressive weight loss due to the loss of both adipose tissue and muscle mass is called cardiac cachexia. The clinician verifies pathological weight loss in all cases:
- documented unintentional body weight loss of 5 kg or more or more than 7.5% of the initial (weight without edema, i.e. the patient's weight in a compensated state)
- body weight for 6 months with an initial BMI less than 19 kg / m2.
The body mass index is calculated as: BMI = body weight (kg) / height (m2). The development of cachexia, as a rule, indicates a critical activation of neurohormonal systems (primarily renin-angiotensin-aldosterone) involved in the progression of decompensation and inadequate growth of cytokine activity (primarily tumor necrosis factor-α). In the treatment of such patients, a combination of drug correction of neurohormonal disorders (evidence grade A), cytokine blockade (grade C evidence) and nutritional support is necessary.
Slide 22
Cachexia
Loss of muscle mass is a serious problem for people with heart failure. It is important to understand that often the loss of muscle mass can be invisible to the eye, due to the excess amount of subcutaneous fat or the presence of edema. In heart failure, especially in patients of functional class III and IV, there is often a pronounced loss of muscle mass, which worsens the prognosis of their life, quality of life and aggravates the course of the disease.
Slide 23
Nutritional support for CHF patients
- Before the appointment of nutritional support, it is necessary to calculate the true energy requirement (IPE).
- IPE is defined as the product of the basal metabolic rate (ROE) and the patient's activity factor. ROE is calculated using the Harris – Benedict equation:
- Men: ECE = 66.47 + 13.75 H weight (kg) + 5 H height (m) - 6.77 H age (years)
- Women: EOE = 66.51 + 9.56 H weight (kg) + 1.85 H height (m) - 4.67 H age (years)
- The activity factor (FA) is determined depending on the patient's physical activity: bed rest - 1.2, moderate physical activity - 1.3, significant physical activity - 1.4.
- With a body weight of less than 10–20% of the norm, the body weight deficit (DMT) is 1.1, 20–30% - 1.2, more than 30% - 1.3.
- IPE = OOE CH FA CH DMT
Slide 24
Principles of introducing enteral nutrition into the diet
- Start nutritional support with low doses (no more than 5-10% of the true energy requirement).
- Be sure to add enzyme preparations (1-2 tablets / day).
- Gradually increase the volume of energy replenishment due to the nutrient mixture (the volume of the injected mixture should be increased once every 5–7 days).
- 1st week - 5-10% of energy demand
- 2nd week - 10–20% of energy consumption
- 3rd week - 20-30% of energy consumption
Monitoring the effectiveness of nutritional support should be carried out already from the first week of therapy and include the dynamics of anthropometric indicators (BMI, BMI, shoulder muscle circumference), laboratory control and assessment of the tolerance of nutrient mixtures.
In patients with circulatory decompensation, when absorption rates deteriorate sharply, the use of oligomeric nutritional mixtures is optimal (Peptamen, level of evidence C)
Slide 25
Alcohol
- Alcohol is strictly prohibited for patients with alcoholic and dilated cardiomyopathy.
- In patients with ischemic genesis of CHF, drinking up to 200 ml of wine or 60 ml of spirits per day can improve the prognosis.
- For all other patients with CHF, limiting alcohol intake is in the form of usual recommendations, although the use of large volumes (for example, beer) should be limited if possible.
Slide 26
Physical activity regimen
Physical rehabilitation of patients takes an important place in the complex treatment of patients with CHF. This means walking, or treadmill, or cycling 5 times a week for 20 - 30 minutes. Upon reaching 80% of the maximum heart rate (HR) or upon reaching 50-70% of the maximum oxygen consumption. The duration of such a course of training in controlled studies reached 1 year, although longer use is possible in practice. With prolonged training, normal activity can be restored, the activity of neurohormones can be reduced and the sensitivity to drug therapy can be restored.
Slide 27
Training organization methodology
- Deterioration of the condition - increased shortness of breath, tachycardia, progression of fatigue, decrease in total body weight - is the basis for moving to the previous stage, or returning to breathing exercises.
- A complete rejection of physical activity is undesirable and should be considered as a last resort.
- The main thing for choosing a mode of exercise is to determine the initial tolerance using a 6-minute test, to recommend physical activity in the form of walking
Slide 28
The method of carrying out physical activity in the form of walking
- Stage I. Entry. The duration of the stage is 6-10 weeks. The frequency of classes is 5 times a week. Travel speed - 25 min / 1 km. Distance - 1 km. With a stable clinical picture, a transition to stage II is possible.
- Stage II. The duration of the stage is 12 weeks. The frequency of classes is 5 times a week. Travel speed - 20 min / 1 km. Distance - 2 km. In case of a stable clinical condition, a transition to a permanent form of training. For patients who have walked 500 meters or more in 6 minutes, dynamic physical activity is shown, for example, walking with a progressive increase in load up to a speed of 6 km / h and a duration of up to 40 minutes a day. Titration of the load up to 6–8 months.
Slide 29
Drug therapy for patients with CHF
- All medicines for the treatment of CHF can be divided into 3 categories.
- The main ones, the effect of which has been proven, is beyond doubt and which are recommended all over the world are:
- ACE inhibitors - are indicated for all patients with CHF, regardless of the etiology, stage of the process and the type of decompensation;
- Diuretics - are indicated for all patients with clinical symptoms of CHF associated with excessive sodium and water retention in the body;
- Cardiac glycosides - in small doses and with caution in sinus rhythm, although with atrial fibrillation they remain the means of choice;
- Beta-blockers - "on top" (optional) on an ACE inhibitor.
- As you can see, only 4 classes of drugs belong to the main means of treating CHF.
Slide 30
Additional, the effectiveness and safety of which has been shown in large studies, but requires clarification:
- antagonists of receptors for ALD (aldactone), used together with an ACE inhibitor in patients with severe CHF;
- ARA II (losartan and others), used in patients poorly tolerating an ACE inhibitor;
Slide 31
Auxiliary, the effect of which and the effect on the prognosis of patients with CHF are not known (not proven), but their use is dictated by certain clinical situations:
- peripheral vasodilators - (nitrates) with concomitant angina pectoris;
- antiarrhythmics - for life-threatening ventricular arrhythmias;
- aspirin - in patients after AMI;
- corticosteroids - with persistent hypotension; non-glycoside inotropic stimulants - with exacerbation of CHF, proceeding with persistent hypotension;
- indirect anticoagulants - with dilatation of the heart, intracardiac thrombosis, atrial fibrillation and after operations on the heart valves;
- statins - for hyper- and dyslipoprotedemia.
- blockers of slow calcium channels (amlodipine), used "on top" on an ACE inhibitor for valvular regurgitation and non-ischemic etiology of CHF.
Slide 32
- Angiotensin-converting enzyme inhibitors
- First appeared in clinical practice in the mid-70s, ACE inhibitors (the first was captopril) remain the greatest achievement in the treatment of cardiovascular diseases in the last quarter of the XX century. they were called both the "cornerstone of the treatment of CHF" (E. Braunwald, 1991), and the "gold standard of therapy" (T. Cohn, 1998), even the entire last period in the treatment of CHF was defined as the "era of ACE inhibitors" (M. Packer, 1995). Currently, the most studied ACE inhibitors (for example, captopril and enalapril) have 4 indications for use, which include, along with CHF, also arterial hypertension, AMI, diabetic nephropathy and coronary artery disease.
Slide 33
- ACE inhibitors block the activity of angiotensin-converting enzyme (ACE) or kininase II. As a result, the formation of A II is disrupted and at the same time the destruction of bradykinin decreases. A II is a powerful vasoconstrictor, a stimulator of cell proliferation and, in addition, promotes the activation of other neurohormonal systems such as ALD and catecholamines. Therefore, ACE inhibitors have vasodilating, diuretic, effects and can reduce cell proliferation in target organs.
- An increase in the content of bradykinin both in plasma and locally in organs and tissues of the body blocks the processes of remodeling, irreversible changes that occur in CHF in the myocardium, kidneys, and vascular smooth muscles.
Slide 34
- Practical issues of the use of ACE inhibitors in CHF (doses, treatment tactics, precautions)
- The appointment of all ACE inhibitors begins with small doses, with their gradual (no more than once every 2-3 days, and even less often with systemic hypotension - no more than once a week) titration to optimal (average therapeutic) doses
- ACE inhibitors can be prescribed to patients with CHF at SBP levels above 85 mm Hg. Art. With an initially low systolic blood pressure (85-100 mm. Hg), the effectiveness of an ACE inhibitor remains, therefore they should always and must be prescribed, reducing the starting dose by half (for all ACE inhibitors). The risk of hypotension increases in the most severe patients with CHF IV FC with a combination of ACE inhibitors with PVD (nitrates, BMCC) and when administered after abundant diuresis. To avoid hypotension, the first dose of an ACE inhibitor should be prescribed at least 24 hours after profuse diuresis, having previously canceled vasodilating agents
Slide 35
It must be remembered that neither hypotension nor the initial manifestations of renal dysfunction are contraindications for the appointment of an ACE inhibitor, but only require more frequent monitoring, especially in the first days of treatment. It is possible not to prescribe an ACE inhibitor only 5-7% of patients with CHF who have an intolerance to these drugs.
Slide 36
- Retention of fluid in the body and the formation of edema syndrome is a typical and best-known manifestation of CHF. Therefore, dehydration therapy is one of the most important components of the successful treatment of patients with CHF.
- However, it must be remembered that complex neurohormonal mechanisms are involved in the development of edematous syndrome and thoughtless dehydration causes only side effects and "rebound" fluid retention.
- Diuretic therapy. Diuretics are divided into groups, according to the localization of action in the nephron. The weakest of the diuretics, carbonic anhydrase inhibitors (acetozolamide), act on the proximal tubules. On the cortical part of the ascending knee of Henle's loop and the initial part of the distal tubules - thiazide and thiazide-like diuretics (hypothiazide, indapamide, chlorthalidone). On the entire ascending knee of the loop of Henle, the most powerful loop diuretics (furosemide, ethacrynic acid, bumetanide, torasemide **). On the distal tubules - competitive (spironolactone) and non-competitive (triamterene) aldosterone antagonists, belonging to the group of potassium-sparing diuretics.
Slide 37
The fundamental points in the treatment of diuretics are:
- the use of diuretics together with an ACE inhibitor;
- the appointment of the weakest of the effective diuretics in this patient.
- the appointment of diuretics should be carried out daily in minimum doses that allow achieving the necessary positive diuresis (for the active phase of treatment, usually + 800, + 1000 ml, for the maintenance phase + 200 ml with body weight control.
It should be remembered that, despite the fastest (of all the main means of treating CHF) clinical effect, diuretics lead to hyperactivation of neurohormones (in particular, RAAS) and an increase in sodium and water retention in the body.
- Diuretic therapy. Torasemide is a typical loop diuretic that blocks sodium and water reabsorption in the ascending part of Henle's loop. In terms of pharmacokinetic properties, it is superior to furosemide, Torasemide has better and predictable absorption compared to furosemide, and its bioavailability does not depend on food intake and is almost twice as high as that of furosemide
- In renal failure, the half-life of torasemide does not change (metabolism in the liver = 80%). The main positive difference between torasemide and other loop diuretics is its additional effects, in particular those associated with the simultaneous blockade of the RAAS.
Slide 38
Slide 39
Slide 40
An example of a dose titration for bisoprolol:
- 1.25 mg - 2 weeks;
- then 2.5 mg until the fourth week;
- 3.75 mg up to 6 weeks,
- 5 mg up to 8 weeks,
- 7.5 mg until week 10 and then finally 10 mg by week 12 of treatment.
With doubtful tolerance, the titration periods will be intervals of 4 weeks, the optimal dose will be achieved only by 24 weeks, that is, six months after the start of therapy. Patients with CHF do not need to rush to titrate the dose of BAB.
Slide 41
Psychological aspects of teaching patients with CHF
Slide 42
Patient education
Defined as a process of increasing knowledge and skills, which is aimed at changing attitudes towards one's disease and correcting behavioral stereotypes necessary to maintain or improve health
Slide 43
Slide 44
8 rules of communication:
- Patients should be encouraged to share their thoughts and thoughts about what they hear. In a group, everyone's opinion is important, and for this everyone should have the opportunity to express themselves. Maintain respect for every statement. If someone expresses a wrong judgment, then you can react something like this: "Many would agree with you, but it is known that ...". In this way, you will save the person from feeling guilty about the wrong answer.
- Ask questions that leave room for choice "What is your opinion?" Ask only one question, and do not burden the audience with a group of questions that follow one after the other. Pause after asking the question for at least half a minute.
- Encourage the participants of the meeting in every possible way, try to work to ensure that everyone has a positive attitude towards the material under discussion and a desire to use this knowledge in their lives.
Slide 45
8 rules of communication
- Try not to interrupt the speaker, but do not let the conversation go beyond the topic or the rules. If the patient touches on a problem close to the subject, you can briefly highlight it, taking the initiative and return to the topic of the lesson, or noting that the question is important and interesting, promise to return to it later.
- Encourage listeners to understand your message, including through examples and illustrations.
- Treat all participants with respect, without exception. If you show “unfriendly” behavior towards at least one of them, then the rest of the audience will be ready for such treatment from your side.
- As you ask a question, watch for signs of confusion, fear, or an inability to respond to the person you are contacting. If so, after a while, say, “You seem to be pondering my question carefully. Do you need more time or someone else wants to speak up? "
- The examples given should be formulated in a positive way, talking about how to do the right thing. Examples of other patients' mistakes can lead patients to think about complications and problems. They may also fear that later on their mistakes will also be discussed publicly.
Slide 46
Age features
- Age characteristics are a complex of physical, cognitive, intellectual, motivational, emotional properties characteristic of most people of the same age. In each age period, the views on oneself and one's life priorities change, the hierarchy of value goals, leading activities and motivation change. Views on the world, on others, on life and health, and even on age itself are changing.
- In conditions of severe somatic illness, a new life situation arises, creating deficit conditions for the development of personality. The problem of survival, overcoming or coping with difficult circumstances and maintaining the basic life values, the integrity of the individual is a difficult task. At different age stages, people cope with it in different ways. A 35-year-old and 60-year-old patient cannot be compared either physically, psychologically or socially.
Slide 47
Attitude to health
It is useful to know about the type of patient's attitude to their health. It is possible to generalize a person's behavior in relation to treatment to two types - positive, aimed at fulfilling the doctor's recommendations, lifestyle changes to maintain health, and negative, characterized by actions that sacrifice health value to other interests. It is important to be able to determine in a conversation with a patient the type of this attitude, the value attitudes that underlie it, the conditions that affect it. Usually, people with severe chronic illness take treatment seriously. But in real life, the high significance of this or that factor is not always confirmed by appropriate actions. Women tend to value their health more highly and make efforts to preserve and maintain it. Also, the value of health is higher for men who have never married than for married men. The value of health is related to the well-being of people. The higher the per capita income, the greater the value of health. In families with low income, it is 38.3%, and in families with a higher one - 61.9%. Attitudes toward illness and treatment are influenced by the person’s experience with spouse, family, and neighbors. This factor becomes especially significant for the perception of health in women.
Slide 48
Perception type.
A person perceives the world around him with the help of all his senses, but at the same time unconsciously gives preference to one and not to others. This innate feature dictates which way of cognition to choose - visual, auditory or tactile - and predetermines the choice of the object of attention, the speed of perception, and the type of memory. This predominance does not exclude other sensations, but most affects the perception of a given person, and the significance of this circumstance was realized only recently. There are 3 types of people on the leading channel of perception: agents - the sensory channel, viewers - the visual channel, listeners - the auditory channel and the 4th type of people who do not have a leading channel - logicians.
Slide 49
- The visual viewer, having come to the appointment, will sit further away and will carefully look into the eyes during a conversation, but become silent if the doctor looks away to make an entry in the medical record. Dislikes touching and breaking personal boundaries. For such a patient, visually recorded signs are important, so he will be more worried about edema or age spots than about violation of internal organs. It is easy to answer the question: "How does it look?", And with difficulty to the question: "What kind of pain?" While convincing him of the need for treatment, try to show him all the perspectives, "paint a clear picture" of recovery. Give him more written and visual recommendations.
- On the contrary, the kinesthetic agent will sit closer and easily describe his state of health in sensations. Ask him: "What are you feeling now?" and don't be afraid to move over and touch him. A kind touch can calm him down. If such a patient stops you in the corridor to ask about something important, he will get very close to you and may even hold you by the floor of the dressing gown. He, most likely, will gladly go to physical therapy or massage, but he will only remember what he did himself. Exercises "by ear" or from a book he will remember much worse.
Slide 50
Perception type
- Audial listeners are people with well-developed speech and auditory memory. They talk with pleasure and take offense and do not trust those specialists who cannot tell them in detail about their disease and the course of treatment. Do not send them to read a stand in the hallway, a poster, or a special brochure - it is better to comment on the text, giving explanations. When planning a conversation with such a patient, set aside a little more time for him in advance so as not to offend him by abruptly ending the conversation.
- Digital logicians also need to tell in detail and clearly about the stage of their disease, consequences and prospects, and clearly and consistently explain the treatment plan. They value instructions and recommendations, both written and verbal, especially clearly structured ones. The clearer and more logical you conduct a conversation with them, the more confidence you will have in them.
Slide 51
Emotional states
- Any serious medical illness leads to changes in the emotional sphere. Chronic heart failure is accompanied by physical suffering, changes in the usual way of life, sometimes a loss of social status, a decrease in the level of material well-being. In everyday life, a sick person is faced with a deterioration in the quality of life, and during hospitalization - also with the need to adapt to new conditions and people, which gives rise to a feeling of fear.
- In patients with CHF, manifestations of depressive disorders are common. A vicious circle arises: acute stress and long-term depressive disorders contribute to disturbances in the functioning of the cardiovascular system, and heart disease causes increased stress and depression.
- Depressive states often lead patients to a refusal to cooperate with medical professionals, active or latent resistance to the implementation of the doctor's recommendations. Patients with chronic heart failure have a significant increase in the risk of readmission and death when depressive disorders are present.
Slide 52
Depression
Difficulties arise in the diagnosis of depressive disorders, since many of the symptoms are similar to the main complaints of patients with heart failure: weakness, fatigue, depression, sleep disturbance, appetite, anxiety, irritability, decreased interests ... Often such patients do not notice an improvement in well-being and fear mistakes in diagnosis or treatment. They, or their relatives insist on additional examination, and reject the offer to take antidepressants with indignation. In these cases, a careful and well-reasoned persuasion is required to try, since with the correct appointment, positive changes occur quite quickly. It should be explained to the patient and his family that somatic illness has weakened the nervous system, and nervous tension and fatigue aggravate somatic disorders.
Slide 53
Cognitive impairments
- Severe chronic heart failure can cause ischemic brain disorders, accompanied by impaired cognitive processes (memory, attention, thinking), in severe cases, confusion, delirious or other psychotic symptoms. Disruption of metabolic processes, massive and prolonged intoxication lead to a decrease in the intellectual and operational-technical capabilities of patients.
- Asthenic states have various manifestations, but excessive fatigue, sometimes in the morning, difficulty concentrating, and slowing down of perception are always typical. Spontaneous lethargy occurs without exertion or with light exertion, lasts for a long time and does not go away after rest. Emotional lability, increased vulnerability and resentment, pronounced distraction are also characteristic. Patients cannot stand even a slight mental stress, get tired quickly, get upset over any trifle. You can ask them for no more than 5-10 minutes, the speech should be slow and calm, after that it is recommended to give the patient a rest or listen to him if he is ready to talk to you, but not insist on keeping the topic of the conversation. If you have not finished collecting the necessary information, then ask relatives, or return to questions after the patient has rested for at least five minutes.
Slide 54
Motivation
- Yes! I do exercise every day! Yes! I don't eat fatty foods! Yes! I keep track of the amount of salt!
- May I ask now, how are you doing with this?
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What do we want to achieve or 12 components of effective self-control of patients with chronic diseases
- the ability to recognize symptoms and respond to their appearance;
- the ability to properly use drug therapy;
- the ability to relieve emergency conditions;
- adherence to diet and exercise regime;
- effective interaction with healthcare professionals;
- use of public resources;
- adaptation to work;
- maintaining a relationship with a spouse;
- the ability to manage the psychological response to illness.
Slide 56
Literature
- National guidelines for the diagnosis and treatment of CHF (Approved by the Congress of Cardiologists of the Russian Federation in October 2003) Heart Failure Journal. 2003; 4 (6): 276-297.
- Ageev F.T., Danielyan M.O., Mareev V.Yu. et al. Patients with chronic heart failure in Russian outpatient practice: features of the contingent, diagnosis and treatment (based on the study EPOCHA-O-CHF). Heart Failure Journal. 2004; 5 (1): 4-7.
- Cleland JG, Swedberg K, Follath F et al. The EuroHeart Failure survey program a survey on the quality of care amongpatients with heart failure in Europe. Part 1: patient characteristics and diagnosis. Eur Heart J. 2003; 24 (5): 442-463.
- Mareev V.Yu., Danielyan M.O., Belenkov Yu.N. On behalf of the EPOCH-O-CHF research working group. Comparative characteristics of patients with CHF, depending on the value of EF according to the results of the Russian multicenter study EPOCHA-O-CHF. Heart Failure Journal. 2006.
- Arutyunov G.P., Kostyukevich O.I. Nutrition of patients with chronic heart failure, nutritional support problems, resolved and unresolved aspects. Heart Failure Journal. 2002; 3 (5): 245–248.
- Influence of therapeutic education of patients with chronic heart failure on their quality of life and the need for early repeated hospitalizations S.R. Gilyarevsky, V.A. Orlov, L.K. Hamaganova, E.Yu. Sycheva, E.M. Seredenina, O. A. Boeva Heart Failure No. 4 T.2
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1. Definition of CHF syndrome.
3. Causes, pathogenesis of CHF.
4. Classification of CHF.
5. Clinic, treatment.
Presentation on the topic: Chronic heart failure new recommendations of the OSSN - 2006
CHRONIC HEART FAILURE new recommendations of the OSSN - 2006 Professor of the Department of Hospital Therapy E.I. Tarlovskaya
The main causes of CHF in Europe IHD and MI (up to 60-70%) DCM Heart defects AH (over 70 years)
"Triggering" factors provoking the appearance / aggravation of heart failure Transient myocardial ischemia Tachy-bradyarrhythmias Thromboembolism LA Increased mitral regurgitation Renal dysfunction Thyroid pathology Side effects of drugs Excessive use of NaCl and water Respiratory infection (every 4 alcohol decompensation) Abuse!
Features of HF in women Women with HF are older than men More often the cause of HF is hypertension and diabetes More often diastolic HF More often HF is combined with depression More often NSAIDs are used More often hospitalized
Criteria used to diagnose CHF Symptoms Shortness of breath (mild to choking) Fatigue Heartbeat Cough Orthopnea
Criteria used to determine the diagnosis of CHF Clinical signs Pulmonary congestion (wheezing, R-graphy) Peripheral edema Tachycardia (> 90 bpm) Swollen cervical veins Hepatomegaly Gallop rhythm (S3) Cardiomegaly (CTI - 60%, CDRlzh - 67 mm, percussion - front OST border PL)
Criteria used to determine the diagnosis of CHF Objective signs of cardiac dysfunction ECG, chest R-graph Systolic dysfunction (decreased EF) * Diastolic dysfunction ** (Doppler echocardiography, increased PAA) BNP hyperactivity
ECG in patients with CHF Signs of LVH Deviation el. left axis Signs of cicatricial myocardial damage (predictor of low contractility) Blockade of LBPH (predictor of low contractility) ECG signs of LA and RL overload (predictor of diastolic dysfunction) Atrial fibrillation (common cause of decompensation)
ECHO cardioscopy (norm) LV systolic function EF = SV / EDV; EF (Teicholz) = 55-60% EF (Simpson) = 50-55% LV diastolic function E / A ratio = 1-2, LVIVRL (LV isovolumetric relaxation time)<92 мс (<30); <100 мс (30-50 л); <105 мс (>50 l)
Laboratory diagnostics Hemoglobin Erythrocytes Leukocytes Platelets Electrolytes (K +!) Creatinine Glucose Liver enzymes General urine analysis Natriuretic peptide
Natriuretic peptide specificity - 90% A close relationship between NP and the severity of heart failure has been proven.
Coronary angiography and ventriculography Indications: Differential diagnosis of ischemic CMP Refractory heart failure of unknown etiology Severe mitral regurgitation Aortic valve disease
Coronary angiography and ventriculography Contraindications: Terminal CHF Revascularization, surgery, heart transplant are not planned
Myocardial biopsy Indications: Unclear genesis of CHF (subject to exclusion of ischemic CMP) Limitation: Aggressive invasive nature Low sensitivity (especially in mosaic myocardial damage) Lack of uniform generally accepted diagnostic criteria
Diagnostic algorithm of CHF Symptoms or signs of CHF Objective examination, ECG, R-graphy, NP norm EchoCG norm CHF is unlikely Etiology, severity, triggering factors Treatment choice
Surgical treatment of CHF Myocardial revascularization surgery Operation to correct mitral regurgitation Heart transplantation - has no serious future Implantation of a circulatory assist device "LV bypass"
The accessory left ventricle Improves the prognosis of patients with critical heart failure The method surpasses all therapeutic methods in its effectiveness (impact on survival) of all therapeutic methods of treatment The main limitation in Russia is the high cost
Mechanical treatments Use of a restrictive external elastic mesh to restrict cardiac dilatation No relevant clinical studies
Electrophysiological methods of CHF treatment Cardiac resynchronization therapy Three-chamber cardiac stimulation Elimination of asynchrony in the work of the heart
Cardiac resynchronization therapy Improves quality of life Slows down remodeling of the heart Decreases readmission rates Decreases mortality (ESC Recommendations, 2005)
Cardiac resynchronization therapy, indications of CHF II - IV FC resistant to optimal standard therapy for LVEF< 35% КДР ЛЖ >55 mm QRS duration> 120 ms
Implantation of a cardioverter - defibrillator SCD-HeFT Patients with CHF who survived cardiac arrest Patients with CHF and paroxysms of sustained VT Patients with CHF after MI with EF<35% и ЖЭ IV – V градации Увеличение выживаемости!
Implantation of a cardioverter - defibrillator and pacemaker for cardiac resynchronization therapy COMPANION The CPT + CD mode reduces the overall mortality of patients with CHF by 43%
Additional funds Statins - for all patients with ischemic etiology of CHF With CHF III Art. and cardiac fibrosis of the liver with cholesterol less than 4 mmol / l - do not use
Additional funds Indirect anticoagulants (VARFARIN) - for patients with CHF with atrial fibrillation (permanent and recurrent with frequent attacks, more often 1 time in 3 months) Warfarin cannot be replaced with aspirin, clopidogrel and their combination
Additional funds To prevent thrombosis and embolism in patients with CHF who are on bed rest, treatment with low molecular weight heparins Enoxyparin (Clexane) 40 mg 1 time / day s / c for 2-3 weeks can be effective
Auxiliary agents are used not for the treatment of CHF, but for special indications PVP (nitrates) - with concomitant angina BMCC (amlodipine, felodipine) - with severe angina pectoris and persistent hypertension AAP - with life-threatening VA Aspirin (other antiplatelet agents) - for patients after MI Non-glycoside inotropic stimulants - with exacerbation of CHF, occurring with low cardiac output and persistent hypotension
Nitrates in CHF Nitrates can be prescribed for CHF only in the presence of proven coronary artery disease and angina pectoris, which passes only from nitro drugs In all other cases, nitrates in CHF are not indicated Nitrates can negatively affect the prognosis of patients with CHF, making it difficult to use an ACE inhibitor
Slow calcium channel blockers in CHF Only prolonged-release dihydroperidines - amlodipine (NORVASK) and felodipine (PLEENDIL) Short-acting dihydroperidins - are contraindicated Verapamil and diltiazem can be used only in I-IIA st. (I-II FC)
Slow calcium channel blockers in CHF Indications for amlodipine and felodipine (against the background of the main treatment): Persistent angina pectoris Persistent hypertension High pulmonary hypertension Severe valvular regurgitation
Presentation of Chronic Heart Failure and the Cytokine System
Experimentally and clinically, the cardiodepressive properties of cytokines, their ability to influence myocardial remodeling, participation in both systolic and diastolic dysfunction have been established. An important prognostic value of IL-1 and IL-6 has been shown, which make it possible to determine further course and presentation of chronic heart failure... Along with the works confirming the participation of the system of cytokines TNF-, IL-1, IL-6 in the pathogenesis of CHF, there are works in which significant manifestations of cytokinogenesis in CHF were not found. Despite individual differences in the vascular effects of cytokines, it should be remembered that there is a single functional complex of cytokines or "tandem TNF-, IL-1, IL-6", which are almost always formed and act in combination and constitute a single cytokine network of interconnected components. at different levels. The pathogenetic mechanisms underlying cytokine-induced myocardial pathology are very diverse (Fig. 1.2). One of them may be associated with the synergistic activity of the TNF-system and other cytokines (IL-1, IL 6, IFN-g) in relation to the expression of the inducible form of NO synthetase (NOS2) in cardiomyocytes and endothelial cells of myocardial microvessels. NO and a toxic product formed during the interaction of NO and superoxide anions, peroxynitrite, have the ability to significantly reduce myocardial contractility.
Rice. 1. The role of cytokines in the development and presentation of chronic heart failure (according to R. Kelly, T. Smith (1997) modified by E.L. Nasonova et al. (1999)
TNF--dependent expression of NOS2 in endothelial and smooth muscle cells of the vascular wall, combined with a decrease in the expression of the "constitutive" form of NO and activation of SAS and RAAS, is essential in the development of a decrease in exercise tolerance. The latter is associated with a weakening of vascular dilatation in response to physiological stimuli, a decrease in strength and endurance, and an increase in skeletal muscle catabolism. It was found that the induction of NO in response to TNF cytokine system is associated with an increase in cardiomyocyte apoptosis. An important aspect of the role of the cytokine system in CHF is their prognostic value. The predictive value of an increase in cytokine levels in patients with CHF was studied in the SOLVD studies, in which it was shown that a TNF-level less than 6.5 pg / ml is prognostically more favorable, and increased levels of cytokines of the TNF-and IL-6 system are independent predictors. death of patients with severe CHF. In the VEST study, circulating levels of proinflammatory cytokines (TNF-, IL-6 systems) and cytokine receptors were independent predictors of mortality in patients with severe chronic heart failure presenting with clinical symptoms. Increased stagnation and increasing ischemia of peripheral tissues and the myocardium itself, autoimmune disorders, endotoxemia characteristic of heart failure, can become the root cause of the activation of the immune system and lead to an increase in TNF-and other pro-inflammatory cytokines (Fig. 1). This "sequence" of events is indirectly confirmed by the directly proportional dependence of the TNF-level on the severity of chronic heart failure and its presentation... However, most researchers assign the expression of proinflammatory cytokines to the role of the root cause of the development and progression of CHF.
Scheme. Involvement of mechanisms of inflammation in the pathogenesis of chronic heart failure and its presentation (A.N. Korzh, 2003).
Thus, the mechanism for the realization of the hemodynamic and clinical effect of pro-inflammatory cytokines in CHF consists of four components:
- negative inotropic action
- remodeling of the heart (irreversible dilatation of cavities and hypertrophy of cardiomyocytes
- disorders of endothelium-dependent dilatation of arterioles
- enhancement of the process of apoptosis of cardiomyocytes and cells of peripheral muscles
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Chronic heart failure - presentation
Presentation on theme: "Chronic Heart Failure" - Presentation transcript:
1 Topic: Chronic heart failure Astana 2012
2 Chronic heart failure is the inability of the cardiovascular system to provide the organs and tissues of the body with a sufficient amount of blood. Chronic heart failure develops when there is a violation of the function of the heart, namely, its muscular membrane (myocardium). In this case, the heart muscle (myocardium) is not able to expel (push) blood from the heart into the vessels, under increased pressure. In other words, the heart is "like a pump", does not cope with its work and cannot pump blood well.
3 Main reasons: Myocardial infarction. Because, damage to the heart during a heart attack or the remaining scar after it, prevents the heart muscle from fully contracting and reduces the contractility of the myocardium. Arterial hypertension. Because a systematic increase in blood pressure does not allow the heart muscle to contract adequately. Heart defects prevent proper blood circulation due to congenital disorders or acquired changes in the "architecture" of the heart. Expanding cardiomyopathies, narrowing the volume and thickening the walls of the heart, reduce the contractility of the myocardium.
5 Cardiac (associated with heart disease) Myocardial infarction. Arrhythmias of the heart. Noncardiac (non-heart disease). Respiratory tract infections, pneumonia. Diseases of the thyroid gland (thyrotoxicosis). Chronic renal failure. Physical and emotional stress. Alcohol, liquid, salt abuse. Pulmonary embolism (blockage of the blood supply to the lungs by a blood clot).
6 Medicines that can provoke the development of CHF: Arrhythmic drugs (except for amiodarone). Non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoid hormones. Calcium antagonists (medicines used to treat hypertension). Antineoplastic agents. Sympathomimetics are medicinal substances that stimulate a specific part of the nervous system (terbutaline, tyramine). Antidepressants (tricyclic). Antimalarial drugs. Drugs (heroin). Vasodilators (vasodilators - diazoxide, hydralazine). Analgesics (acetamifen). Blood pressure lowering agents (reserpine). Physical effects (radiation, high and low temperature, cigarette smoke).
7 Due to the weakening of the contractile force of the myocardium, the effective blood volume decreases, which reduces the flow of oxygen to the tissues and the outflow of metabolic products from them. So, in the early stages of insufficiency, tissue metabolism or microcirculation is disturbed, which is especially pronounced at the time of physical stress (ND Strazhesko, V.Kh. Vasilenko, RG Mezhebovsky, LP Pressman, etc.). The development of tissue oxygen starvation due to the slowed transport of oxygen in the blood is to a certain extent compensated by the increased use of oxygen by the tissues, which leads to an increase in the arteriovenous oxygen content difference. However, the decrease in oxygen tension in the venous blood below 20 mm Hg. Art. incompatible with life due to paralysis of the vital centers in the medulla oblongata. The immediate result of a mismatch between the supply of oxygen and the need for it in tissues is a violation of carbohydrate metabolism, phosphorylation processes, and protein synthesis. This leads to irreversible degenerative processes in the organs. Disruption of microcirculation is facilitated by the retention of sodium and water in the body of a patient with chronic circulatory failure. The latter leads to an increase in the extra- and intracellular volume of fluid. This further complicates the supply of oxygenated blood to the tissues. Long-term retrograde stagnation of blood in vital organs (lungs, liver) leads to the development of fibrosis in them, damage to functioning cells, which in turn aggravates the state of hemodynamics, worsens the course of the disease.
hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes narrowing of arterioles and venules -> an increase in venous return of blood to the heart -> inflow of large amounts of blood to the decompensated lion "title =" Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> noradrenaline , causes a narrowing of arterioles and venules -> an increase in venous return of blood to the heart -> an influx of large amounts of blood to a decompensated lion "class =" link_thumb "> 8 Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> noradrenaline, causes narrowing of arterioles and venules -> increased venous return of blood to the heart -> large flow of blood to the decompensated left ventricle. Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of renal arterioles -> activation of the renin-angiotensin system (RAS) -> hyperproduction of angiotensin 2 (acts vasopressively, constricts small arteries) -> local (cardiac) tissue RAS ( the progression of his hypertrophy). Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of renal arterioles -> activation of the renin-angiotensin system (RAS) -> hyperproduction of angiotensin 2 -> increased formation of aldosterone -> increased sodium reabsorption -> activation of antidiuretic hormone production ) - vasopressin -> water retention in the body -> the appearance of edema. Angiotensin 2 and aldosterone -> myocardial remodeling -> death of cardiomyocytes -> fibrosis aldosterone hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes narrowing of arterioles and venules -> increased venous return of blood to the heart -> large blood flow to the decompensated lion "> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes narrowing of arterioles and venules -> increased venous return of blood to the heart -> large amount of blood flow to the decompensated left ventricle. Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of renal arterioles -> activation of the renin-angiotensin system (RAS) -> hyperproduction of angiotensin 2 (acts vasopressively, constricts small arteries) -> local (cardiac) tissue RAS ( the progression of his hypertrophy). Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of renal arterioles -> activation of the renin-angiotensin system (RAS) -> hyperproduction of angiotensin 2 -> increased formation of aldosterone -> increased sodium reabsorption -> activation of antidiuretic hormone production ) - vasopressin -> water retention in the body -> the appearance of edema. Angiotensin 2 and aldosterone -> myocardial remodeling -> death of cardiomyocytes -> fibrosis aldosterone "> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes narrowing of arterioles and venules -> increased venous return of blood to the heart -> large blood flow to the decompensated lion »Title =" Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causing narrowing of arterioles and venules -> increased venous return of blood to the heart -> large blood flow to the decompensated lion ">
10 Functional classification of chronic heart failure by the New York Cardiological Association (NYHA, 1964): 1 FC: Exercise does not cause discomfort in the mouth (increased fatigue, shortness of breath, palpitations, etc.) 2 FC: Exercise causes moderate, insignificant discomfort 3 FC: Physical activity causes significant discomfort. The patient feels well in the middle. 4 FC: Minimal physical activity causes discomfort that is present at rest and increases with activity.
11 Relative correspondence of stages according to N.D. Strazhesko and NYHA: CHF 1a stage 1 FC according to NYHA CHF 1b stage 2 FC according to NYHA CHF 2a stage 3 FC according to NYHA CHF 2b - 3 stages 4 FC according to NYHA Classification of chronic heart failure (CHF): When formulating a diagnosis, two classifications are taken into account, (described earlier), first the stage and period according to the classification of N.D. Strazhesko, then NYHA, for example: CHS 2a, 3 FC.
13 Crepitus and small bubbling rales in the lower parts of both lungs, which do not disappear after vigorous coughing up and are not caused by inflammatory infiltration in the lungs. Dilation of the left ventricle. Accent II tone on the pulmonary artery. The appearance of a pathological III tone and a protodiastolic gallop rhythm (left ventricular, better heard in the apex of the heart). Alternating pulse. Absence of peripheral edema, congestive hepatomegaly, ascites.
14 The main clinical symptoms of chronic right ventricular failure: Severe acrocyanosis (bluish lips, auricles, tip of the nose, cold cyanotic hands, feet), swollen neck veins, hydrothorax, congestive hepatomegaly, positive Plesch test (hepato-jugular, reflux-jugular). Peripheral edema (primarily in the area of the legs, feet, with further spread upward), ascites, possibly the development of liver cirrhosis. Dilation of the right ventricle (not always determined by percussion due to the often concomitant emphysema and forward rotation of the heart by the right ventricle) Epigastric pulsation, synchronous with the activity of the heart (due to the contraction of the right ventricle). Systolic murmur of tricuspid regurgitation (relative insufficiency of the tricuspid valve due to severe dilatation of the right ventricle) Right ventricular protodiastolic gallop rhythm
15 Laboratory tests: Complete blood count (hematocrit, erythrocytes and hemoglobin). Biochemical blood test (determination of liver enzymes, cholesterol). The content of thyroid hormones in the blood.
16 Instrumental studies: ECG (electrocardiography). ECHOKG (ultrasound) of the heart (determine the contractility of the myocardium). Cardiac catheterization. Coronary angiography (X-ray contrast method for examining the vessels of the heart). Phonocardiography (determination of heart sounds and heart murmurs). Chest X-ray. CT scan.
17 Non-drug treatment of CHF Lifestyle correction. Rational nutrition Elimination of bad habits. With a preserved (stable) state, exercise up to 45 minutes a day (according to your well-being). Physical rest with exacerbation of symptoms.
18 Mode: the patient's activity should not exceed the capabilities of the cardiovascular system. At stage I of CHF, a semi-bed rest is prescribed for 5-7 days, then increased physical activity is limited: at stage II (period A), a semi-bed rest is shown, and at 11B and III stages - bed rest. The duration of bed rest depends on the course of CHF. With a very strict and prolonged bed rest, the risk of developing phlebothrombosis and pulmonary embolism increases. These patients are shown breathing exercises and frequent changes in body position. Mental peace is achieved by observing a medical-protective regimen and the use of sedatives (bromides, valerian, motherwort, small tranquilizers). The diet should be rich in vitamins, which are given in a double dose, and salt and fluid restriction is indicated. It is necessary to monitor bowel function. At stage I of CHF, the amount of table salt is reduced to 5-6 g per day (10 table). At stages II and III, up to 3 g / day (10a table). With pronounced edematous syndrome, a sharply hypochlorite diet is indicated - no more than 1 g of salt per day. Along with limiting salt, it is necessary to restrict fluid (up to 1 l / day). Against the background of this diet, fasting days are prescribed (milk, cottage cheese, fruit, etc.), which are especially indicated for patients with overweight.
19 Drug treatment of chronic heart failure (CHF) Aimed at reducing the manifestations of the disease and improving the quality of life, prognosis for future life and the fight to reduce the risk of sudden death from CHF. 1. ACE inhibitors (inhibitors of adenosine converting enzyme) - a group of drugs that contribute to: Reducing the risk of sudden death. Slowing down the progression of CHF. Improving the course of the disease. Improving the patient's quality of life. These include: Captopril. Quinapril. Enalapril. Ramipril. Fozinopril. Lisinopril. The effect of the therapy can be seen as early as the first 48 hours.
20 2. Diuretics (diuretics) They can significantly improve the condition of a patient with CHF. Quickly relieve swelling, within a few hours. Decreases the volume of fluid in the body. Reduces stress on the heart. Expand blood vessels. Quickly, effectively and safely eliminate fluid retention in the body, regardless of the cause of CHF. These include: Furosemide. Lasix. Hydrochlorothiazide. Spironalokton. Torasemide. Triamteren. Amiloride.
21 3. Cardiac glycosides are drugs that are the "gold standard" in the treatment of CHF. Increase myocardial contractility. Improving blood circulation. Reduces stress on the heart. They have a diuretic effect. Slow down the heart rate. Reduces the risk of hospitalization. These include: Digoxin. Digitoxin. Korglikon.
22 4. Antiarrhythmic drugs - drugs that prevent the development of arrhythmias and reduce the risk of sudden death. These include - Amiodarone. 5. Anticoagulants - drugs that prevent blood clots and blood clots. These include - Warfarin. It is indicated for patients after thromboembolism, atrial fibrillation (with atrial fibrillation), for the prevention of thrombosis and sudden death. 6. Metabolic therapy is the intake of drugs that improve metabolism, nutrition of the heart muscle and protect it from ischemic effects. These include: ATP (adenosine triphosphoric acid). Cocarboxylase. Potassium preparations (Panangin, Asparkam, Kalipoz). Magnesium preparations. Thiotriazoline. Vitamin E. Riboxin. Mildronate. Preduct MR. Mexicor.
23 Predictions It is estimated that about 50% of patients diagnosed with heart failure live with the disease for more than 5 years. However, the prognosis for each individual patient depends on the severity of the disease, concomitant diseases, age, effectiveness of therapy, lifestyle and much more. Treatment of this disease pursues the following goals: improving the work of the left ventricle of the heart, restoring the ability to work and improving the patient's quality of life. Treatment of heart failure, started at the earliest stages, significantly improves the patient's life prognosis.
Chronic Heart Failure Presentations
On this page you can download a presentation on "Chronic heart failure (CHF)". The presentation gives the definition of CHF, the classification of CHF, the main causes of CHF, symptoms and treatment of chronic heart failure. The lecture contains photographs of patients with CHF with clinical manifestations. Slides - 22.
1. Definition of CHF syndrome.
2. Pathological changes.
3. Causes, pathogenesis of CHF.
4. Classification of CHF.
5. Clinic, treatment.
