Presentations on the topic of chronic heart failure. Presentation on nursing "the importance of nursing activities in solving the problems of a patient with diseases of the cardiovascular system" Mechanism of development of the disease

Lecture topic: CHRONIC HEART FAILURE. DEFINITION. CLASSIFICATION. CLINIC. DIAGNOSTICS. TREATMENT Assoc. RUDA M.M. - presentation

Hospital therapy CHRONIC HEART FAILURE Prof. Alyavi A. L. - presentation

Chronic heart failure. Diagnostics and treatment - presentation, report, project

Slide captions:

Chronic heart failure

Causes

Stage I

Stage II

Stage III

6-minute walk test

Main symptoms

Symptoms

Tachycardia

dyspnea

Cyanosis

Liver enlargement

Edema

Complaints at stage 1

Complaints at stage 2

Complaints at stage 3

Epidemiology

Forecast

Principles of treatment and patient care

Goals of therapy

Presentation on the topic: Chronic heart failure new recommendations OSCH - 2006

Presentation of chronic heart failure and cytokine system

Chronic heart failure - presentation

Presentations on the topic of chronic heart failure

Rice. 1. The role of cytokines in the development and presentation of chronic heart failure (according to R. Kelly, T. Smith (1997) as modified by E.L. Nasonova et al. (1999)

Scheme. Involvement of inflammatory mechanisms in the pathogenesis of chronic heart failure and its presentation (A.N. Korzh, 2003).

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Presentation on theme: "Chronic heart failure"— Presentation transcript:

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CHRONIC HEART FAILURE Lecture for 4th year students of the Faculty of Dentistry, Associate Professor of the Department of Internal Medicine, Dental and Pediatric Faculties Alekseev D.V. Tver, 2011

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DEFINITION Heart failure is a syndrome characterized by the inability of the cardiovascular system to adequately supply the organs and tissues of the body with blood and oxygen in quantities sufficient to maintain normal life functions.

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Heart failure Acute and chronic

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CIRCLES OF BLOOD CIRCULATION

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Heart failure is a syndrome! Nosological form - a specific disease isolated on the basis of an established cause (etiology), developmental characteristics (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 Associated diseases: YYY. ZZZ.

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Chronic heart failure (CHF) DEFINITION CHF - from a modern clinical point of view, is a disease with a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.), which are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body. The root cause is a deterioration in the ability of the heart to fill or empty, caused by myocardial damage, as well as an imbalance of 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 expressed 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. The prevalence of CHF among men is higher than among women in the age group under 60 years. The annual mortality rate for CHF in general is 6%, and for clinically significant CHF it reaches 12%. Decompensation of CHF is the reason for hospitalization in cardiology 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 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 OF CHF Pathogenesis model - neurohumoral CHF - a complex of hemodynamic and neurohumoral reactions to cardiac dysfunction (E. Braunwald, 1989) Activation of the sympathetic-adrenal system (SAS) and the renin-angiotensin-aldosterone system (RAAS) Systolic and diastolic (more 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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DIAGNOSIS OF CHF The reference points in diagnosing CHF are: 1. Characteristic complaints of the patient. 2. Physical examination data (inspection, palpation, auscultation) - clinical signs. 3. Data from objective (instrumental) examination methods.

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DIAGNOSIS OF CHF instrumental examination methods 1. Electrocardiography (normal ECG with CHF is an exception to the rule). 2. X-ray of the chest organs (cardiomegaly and venous pulmonary congestion). 3. Echocardiography, including Doppler EchoCG (systolic - EF Slide 17
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DIAGNOSIS OF CHF laboratory tests 1. The standard set of laboratory tests for CHF includes: clinical blood test with determination of hemoglobin level, number of leukocytes and platelets, biochemical blood test - electrolytes, creatinine, glucose, liver enzymes general urine test 2. According to indications - C-reactive protein (excluding inflammatory etiology of heart disease), thyroid-stimulating hormone (excluding hyper- or hypothyroidism), urea and uric acid. In case of a sharp deterioration of the condition, cardio-specific enzymes are used. 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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TREATMENT OF CHF main goals Prevention of the development of symptomatic CHF (for stage I CHF) Elimination of symptoms of CHF (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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TREATMENT OF CHF ways to achieve goals Diet Physical activity regimen Psychological rehabilitation, organization of medical supervision, schools for patients with CHF Drug therapy Electrophysiological methods of therapy Surgical, mechanical methods of treatment

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TREATMENT OF CHF Diet Limiting salt intake Limiting fluid intake - in case of decompensation Food should be high in calories, easily digestible, with sufficient vitamins and protein Control of body weight

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TREATMENT OF CHF Physical activity regimen Physical rehabilitation is recommended for all patients: Breathing exercises Walking Dosed physical training

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TREATMENT OF CHF Psychological rehabilitation and creation of outpatient observation schools for patients with CHF Patient education!!!

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TREATMENT OF CHF Drug therapy

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SITUATIONAL TASK

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SITUATIONAL TASK

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SITUATIONAL TASK

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1 Lecture topic: CHRONIC HEART FAILURE. DEFINITION. CLASSIFICATION. CLINIC. DIAGNOSTICS. TREATMENT Assoc. RUDA M.M.

2 LECTURE PLAN 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 pathological 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: instantaneous (death occurs within a few minutes), acute (lasting up to 1 hour), instantaneous (death occurs within a few minutes), acute (lasting up to 1 hour), prolonged ( lasting up to 2 days) protracted (lasting up to 2 days) recurrent course. The latter has a wave-like character and is most common in myocardial infarction. relapsing course. The latter has a wave-like character and is most common in myocardial infarction.

8 CLINIC Characteristic clinical signs are: Characteristic clinical signs are: severe respiratory failure, shortness of breath, coughing up pink frothy sputum, orthopnea, pale skin covered with cold sweat. On examination - peripheral cyanosis. severe respiratory failure, shortness of breath, coughing up pink frothy sputum, orthopnoea, pale skin covered with cold sweat. On examination - peripheral cyanosis. During auscultation, moist rales of varying caliber are heard over most of the lungs, tachycardia, protodiastolic gallop rhythm and systolic murmur over the apex; blood pressure may increase or be sharply decreased (shock). During auscultation, moist rales of varying caliber are heard over most of the lungs, tachycardia, protodiastolic gallop rhythm and systolic murmur over the apex; blood pressure may increase or be sharply decreased (shock). Chest x-ray reveals the presence of “wet lung” syndrome. When studying the gas composition of the blood, severe or moderate hypoxemia, hypercapnia are determined, and the pH of the arterial blood decreases (respiratory acidosis). Chest x-ray reveals the presence of “wet lung” syndrome. When studying the gas composition of the blood, severe or moderate hypoxemia, hypercapnia are determined, and the pH of the arterial blood decreases (respiratory acidosis).

9 CLINIC Intense pressing or stabbing pain in the chest Intense pressing or stabbing pain in the chest Pale skin with a cyanotic tint Pale skin with a cyanotic tint Swelling and pulsation of the neck veins Swelling and pulsation of the neck veins Pulse small, frequent Pulse small, frequent Reduced blood pressure Reduced blood pressure Strengthening II tones over the pulmonary artery, gallop rhythm Increased tone over the pulmonary artery, gallop rhythm Pleural friction noise Pleural friction noise

16 CHRONIC HEART FAILURE 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); disturbance of diastolic filling of the ventricles of the heart (exudative and adhesive pericarditis, disturbance of diastolic filling of the ventricles of the heart (exudative and adhesive pericarditis, restrictive cardiomyopathies, cardiac tamponade); restrictive cardiomyopathies, cardiac tamponade); over-the-top physical activity, over-the-top 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, double pneumonia). pathological changes in the pulmonary circulation (pulmonary embolism, spontaneous pneumothorax, double pneumonia).

18 IHD – 50 – 70% IHD – 50 – 70% Arterial hypertension – % Arterial hypertension – % Cardiomyopathies – 7 – 14% Cardiomyopathies – 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 Impaired pumping function of the heart Impaired pumping function of the heart Decreased tolerance to physical activity Decreased tolerance to physical activity Fluid retention in the body Fluid retention in the body Progressive course Progressive course Poor prognosis Poor prognosis

23 Pathogenesis. The main pathogenetic factors of chronic heart failure are: The main pathogenetic factors of chronic heart failure are: decreased cardiac output and perfusion of tissue organs; decreased cardiac output and perfusion of tissue organs; activation of the sympathoadrenal system; activation of the sympathoadrenal system; constriction of arterioles and venules; constriction of arterioles and venules; activation of the renin system – angiotensin - aldosterone activation of the renin - angiotensin - aldosterone system, sodium and water retention, sodium and water retention. The appearance of edema. The appearance of edema.

24 Classification. Clinical stage of heart failure; Clinical stage of heart failure; Variant of heart failure; Variant of heart failure; Patient functional class Patient functional class

25 Clinical stage of HF First stage - initial First stage - initial Second stage - severe long-term circulatory failure (divided into A and B) Second stage - severe 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 during physical exertion; at rest, hemodynamics, organ and metabolic functions are not impaired; working ability is reduced. Carrying out tests with dosed physical activity determines a decrease in tolerance to stress CH I (initial, latent) - the appearance of shortness of breath, tachycardia, fatigue only during physical exertion; at rest, hemodynamics, organ and metabolic functions are not impaired; working ability is reduced. Carrying out tests with dosed physical activity determines a decrease in stress tolerance

27 HF IIA (beginning of a long stage) – signs of stagnation in one of the blood circulation, which can be eliminated with therapy. Shortness of breath, palpitations, and discomfort in the heart area appear with ordinary minor physical exertion. Working capacity is reduced. Signs of congestion in the lungs (with left ventricular failure), or enlarged liver, pastosity or edema of the lower extremities (with right ventricular failure) are determined. HF IIA (the beginning of a long stage) are signs of stagnation in one of the blood circulation, which can be eliminated with therapy. Shortness of breath, palpitations, and discomfort in the heart area appear with ordinary minor physical exertion. Working capacity is reduced. Signs of congestion in the lungs (with left ventricular failure), or enlarged liver, pastosity or edema of the lower extremities (with right ventricular failure) are determined.

29 HF IIB (end of a long stage) – signs of stagnation in both circulation circles are constant and do not completely disappear with treatment. HF IIB (end of a long stage) – signs of stagnation in both circulation circles are constant and do not completely disappear with treatment. Shortness of breath, palpitations, precordial discomfort appear with the least physical stress and even at rest. Working capacity is sharply reduced. Congestive wheezing in the lungs, enlarged liver, swollen veins, constant swelling, first in the lower extremities, and then throughout the body, are detected. Shortness of breath, palpitations, precordial discomfort appear with the least physical stress and even at rest. Working capacity is sharply reduced. Congestive wheezing in the lungs, enlarged liver, swollen veins, constant swelling, first in the lower extremities, and then throughout the body, are detected.

32 HF III (terminal, dystrophic) – severe hemodynamic disorders with the development of irreversible changes in organs, complete loss of ability to work HF III (terminal, dystrophic) – severe hemodynamic disorders with the development of irreversible changes in organs, complete loss of ability to work Signs of stagnation in the small and large circle blood circulation anasarca, ascites, hydrothorax, hydropericardium, severe dystrophic changes in various organs and tissues. Signs of stagnation in the pulmonary and systemic circulation are 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 systolic function of the left ventricle. The main criterion is the ejection fraction of the left ventricle 50%. Diastolic - hemodynamic disorder is caused by a violation of the diastolic filling of the left (or right) ventricles. The main criterion is the presence of clinical signs of heart failure, congestion in the small circle (or in the small and large circles) with preserved (50%) left ventricular ejection fraction.

35 Functional class of HF FC I – patients with heart diseases in whom the usual activities do not lead to shortness of breath, fatigue and palpitations. Tolerance to physical stress is normal. FC I – patients with heart diseases in whom performing routine exercises does not lead to shortness of breath, fatigue and palpitations. Tolerance to physical stress is normal. FC II – patients with moderate physical limitations. Shortness of breath, fatigue and palpitations occur with normal physical exertion. FC II – patients with moderate physical limitations. 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 minor physical exertion. FC III – Patients with severe limitation of physical activity. Shortness of breath, fatigue and palpitations - with minor 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, a discrepancy arises between the capacity of the vascular bed and the volume of circulating blood. As a result, a discrepancy arises between the capacity of the vascular bed and the volume of circulating blood.

40 Causes of disturbances in the innervation of vascular tone disturbances in the innervation of vascular tone Disorders of the function of the vascular motor nerves Disorders of the function of the vasomotor nerves Vascular paresis due to toxic damage Vascular paresis due to toxic damage Reduction in the volume of circulating blood (blood loss and dehydration) Reduction in the volume of circulating blood (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 caused by a sharp decrease in vascular tone and an acute decrease in the volume of circulating blood Collapse is a form of vascular insufficiency caused by a sharp decrease in vascular tone and an acute decrease in the volume of circulating blood

42 Shock is a severe life-threatening condition of the patient that occurs as a result of the influence of strong endogenous or exogenous stimuli on the body and is accompanied by a progressive disruption of the vital functions of the body and a critical disturbance of hemodynamics. Shock is a severe, life-threatening condition of the patient that occurs as a result of the influence of strong endogenous or exogenous stimuli on the body and is accompanied by a progressive disruption of the vital functions of the body and a critical disturbance of hemodynamics.

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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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, limitation of 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, limitation of 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; unsatisfactory quality of life; fight against CHF increasing costs for the fight against CHF

4 EPIDEMIOLOGY EPIDEMIOLOGY - The prevalence of clinically significant CHF in the population is about 2% - The prevalence of clinically significant CHF in the population is about 2% - Among people over 65 years of age it increases to 10%, and decompensation becomes the most common cause of hospitalization in elderly patients. - Among persons over 65 years of age it increases to 10%, and decompensation becomes the most common cause of hospitalization in elderly patients. - The number of patients with asymptomatic left ventricular dysfunction is at least 4 times higher than the number of patients with clinically significant CHF. - The number of patients with asymptomatic left ventricular dysfunction is at least 4 times higher than the number of patients with clinically significant CHF. - Over 15 years, the number of hospitalizations with a diagnosis of CHF has tripled. - Over 15 years, the number of hospitalizations with a diagnosis of 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 by V.Kh. Vasilenko and N.D. Strazhesko Adopted at the XII All-Union Congress of Therapists in 1935. STAGE I – initial latent circulatory failure, manifested only during physical activity (shortness of breath, palpitations, excessive fatigue). STAGE I – initial latent circulatory failure, manifested only during physical activity (shortness of breath, palpitations, excessive fatigue). With rest, these phenomena disappear. Hemodynamics are not impaired. With rest, these phenomena disappear. Hemodynamics are 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 disturbances in only one part of the cardiovascular system (in the systemic or pulmonary circulation). Period A – signs of circulatory failure at rest are moderately expressed. Hemodynamic disturbances in only one part of the cardiovascular system (in the systemic or pulmonary circulation). Period B – the end of a long stage, pronounced hemodynamic disturbances in which the entire cardiovascular system is involved Period B – the end of a long stage, pronounced hemodynamic disturbances in which the entire cardiovascular system is involved (both systemic and pulmonary circulation) (both systemic and pulmonary circulation) STAGE III – final dystrophic with severe hemodynamic disturbances. Persistent changes in metabolism and irreversible changes in the structure of organs and tissues. STAGE III – final dystrophic with severe hemodynamic disturbances. Persistent changes in metabolism and irreversible changes in the structure of organs and tissues.

6 Classification of CHF by the New York Heart Association Classification of CHF by the New York Heart Association I FC. The patient does not experience restrictions in physical activity. Normal exercise does not cause weakness (lightheadedness), palpitations, shortness of breath or anginal pain. I FC. The patient does not experience restrictions 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 performing normal physical activities causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but performing normal physical activities causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain. III FC. Marked limitation of physical activity. The patient feels comfortable only at rest, but less physical activity than usual leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain. III FC. Marked limitation of physical activity. The patient feels comfortable only at rest, but less physical activity than usual leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain. IV FC. Inability to perform any activity without discomfort. Symptoms of heart failure or angina may occur at rest. When performing a minimum load, discomfort increases. IV FC. Inability to perform any activity without discomfort. Symptoms of heart failure or angina may occur at rest. When performing a minimum load, discomfort increases.

7 Clinical picture Clinical picture - Progressive shortness of breath. - Progressive shortness of breath. - Fast fatiguability. - Fast fatiguability. - Night attacks of cardiac asthma - Night attacks of cardiac asthma - Weight loss or, on the contrary, weight gain (due to edema) - Weight loss 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 parts of the lungs - moist rales in the lower parts of the 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: - distension of the jugular veins - distension of the jugular veins - swelling (especially in the ankles) - swelling (especially in the ankles) - hepatomegaly - hepatomegaly - ascites - ascites

8 Laboratory and instrumental studies Laboratory and instrumental studies - Study of kidney function - Study of kidney function - Determination of the level of serum electrolytes - Determination of the level of serum electrolytes - 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 - Carry out non-drug treatment - Carry out non-drug treatment - Carry out drug treatment - Carry out medication treatment

10 Non-drug treatment includes: regimen, for overweight - weight loss, limiting the consumption of table salt (6-8 g per day), limiting fluids to Non-drug treatment includes: regimen, for overweight - losing weight, limiting the consumption of table salt (6-8 g per day), fluid restriction to 1.5 l per day, if necessary, perform pleural puncture 1.5 l per day, if necessary, perform pleural puncture and pericardiocentesis puncture and pericardiocentesis

11 Drug treatment Drug treatment Implies two basic principles: inotropic stimulation of the heart and unloading of cardiac activity. Of the positive inotropic agents, cardiac glycosides are used for long-term treatment of CHF. Cardiac unloading can be divided into four types: Implies two basic principles: inotropic stimulation of the heart and unloading of cardiac activity. Of the positive inotropic agents, cardiac glycosides are used for long-term treatment of CHF. Cardiac unloading can be divided into four types: - volumetric (diuretics are used) - volumetric (diuretics are used) - hemodynamic (vasodilators and long-acting dihydropyridines) - hemodynamic (vasodilators and long-acting dihydropyridines) - neurohumoral (ACE inhibitors, A-P receptor antagonists , aldosterone antagonists - neurohumoral (ACE inhibitors, AP receptor antagonists, aldosterone antagonists - myocardial (beta-blockers) - myocardial (beta-blockers)

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Chronic heart failure. Diagnostics and treatment P.A. Lebedev Professor DMN Head of the Department of Therapy and Functional Diagnostics Course IPO SamSMU

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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, a decrease in pumping function occurs, 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 uniform pathophysiological laws, regardless of the etiology of the damage.

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Classification of CHF I Initial stage of heart damage. Hemodynamics are not impaired. Hidden heart failure. Asymptomatic LV dysfunction. II A Clinically pronounced stage of heart disease. Hemodynamic disturbances in one of the blood circulation circles are moderately expressed. Adaptive remodeling of the heart and blood vessels IIB Severe stage of heart disease. Severe hemodynamic disturbances in both circulation circles. Maladaptive remodeling of the heart and blood vessels. III Final stage of cardiac damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, brain, kidneys, lungs). The final stage of organ remodeling. Functional symptoms of CHF (I - I V) Example: CHF II B IIFcl, CHF IIA I I I Fcl

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criteria used to determine the diagnosis of CHF

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Electrocardiography This is the most accessible instrumental method that allows you to objectively assess the condition 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 EPOCHA-O-CHF study, the most common deviation from the norm on a standard ECG in patients with CHF are signs of LV hypertrophy (LVH) and deviation of the electrical axis of the heart to the left, which occur in 50-70% of those examined.

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A standard diagnostic laboratory test for a patient with HF should include hemoglobin levels, red blood cell, white blood cell and platelet counts, plasma electrolytes, creatinine, glucose, liver enzymes and urinalysis. Also, if necessary, it is possible to determine the level of C-reactive protein (excluding the inflammatory etiology of heart disease), thyroid-stimulating hormone (excluding hyper- or hypothyroidism), urea and uric acid

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The importance of echocardiography Echocardiography allows you to solve the main diagnostic problem - to clarify the very fact of dysfunction and its nature, as well as to conduct a dynamic assessment of the state of the heart and hemodynamics. The most important hemodynamic parameter is LVEF, which reflects the contractility of the LV myocardium. Determination of LVEF allows one 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 of indicating the preservation of systolic function. 50%, calculated by 2-dimensional echocardiography according to Simpson. The degree of decrease in LVEF is associated with the severity of systolic dysfunction and is used to determine the risk of surgical treatment; the dynamics of LVEF is an indicator of disease progression and the effectiveness of therapy; low LVEF is a marker of a negative prognosis.

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In half of the patients with signs of CHF there is no systolic dysfunction, diastole disorders are more closely associated with the severity of the patients’ clinical condition, the degree of decrease in exercise tolerance, and quality of life than systole disorders. The dynamics of diastolic parameters can serve as a criterion for the effectiveness of treatment and a marker of prognosis in patients with CHF.

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To diagnose primary diastolic HF, three conditions are required: 1. The presence of symptoms and signs of HF. 2. Normal or slightly impaired LV systolic function (LVEF.50%). 3. Detection of impaired LV relaxation and/or distensibility.

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Hypertrophic cardiomyopathy Frequency 1:500 in the US population The most common cause of death in athletes and people under 40 years of age VS predominates among the causes of mortality The highest incidence of VS at the age of 15-30 years Characteristically often combined with myocardial ischemia

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Nitroglycerin for myocardial infarction Class 1 Patients with ischemic pain should receive NTG sublingually every 5 minutes up to 3 times, after which a decision should be made on intravenous infusion of NTG. Indications for intravenous infusion of NTG include recurrent anginal pain, hypertension, and pulmonary congestion.

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Contraindications to IGT Systolic blood pressure less than 90 mm Hg or a decrease in blood pressure by 30 mm Hg or more from the initial level, severe bradycardia less than 50 beats per minute or tachycardia more than 100 beats per minute, suspected right ventricular myocardial infarction

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Levosimendan (Simdax) Indications: acute left ventricular failure during myocardial infarction Contraindications: arterial hypotension, tachycardia, history of ventricular flutter-fibrillation, mechanical obstruction preventing filling and ejection from the LV, severe renal and hepatic failure There is no information on the possibility of use in HCM, severe failure mitral valve

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Parameters of physical activity and oxygen consumption in patients with different FCs of CHF (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?

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State budgetary educational institution of secondary vocational education of the Department of Health of the city of Moscow “Medical College No. 5” Separate unit No. 4 For theoretical classes Topic: “Nursing care for chronic heart failure” Teacher Molodova E.Yu.

Relevance of the topic Currently, the main problem of population mortality is cardiovascular diseases. In the Russian Federation, the prevalence of chronic heart failure (CHF) is 7%. Every year around the world the number of CHF increases 3 times. The one-year mortality rate of patients with severe CHF reaches 25–30%; up to 1000 patients die in one year.

The concept of chronic heart failure. Chronic heart failure is the final point in the formation of a large number of diseases affecting the heart. It develops with pathology of the function of the heart, namely its muscular layer - the myocardium. In this case, the heart muscle is unable to expel blood from the heart into the vessels under increased pressure.

Etiology of chronic heart failure ischemic heart disease arterial hypertension diabetes mellitus previous myocardial infarction arrhythmias atherosclerosis smoking alcohol abuse obesity age 60-75 years

Dyspnea; - Nocturnal paroxysmal shortness of breath; - Orthopnea; - Non-productive (dry) cough during exercise and/or at night; - Weakness, fatigue during physical activity; - Nocturia / oliguria; - Abdominal complaints; - Symptoms from the central nervous system. Subjective symptoms - Bilateral peripheral edema; - Hepatomegaly; - Swelling and pulsation of the neck veins; - Ascites; - Arrhythmias; - Hydrothorax; - Listening to bilateral moist rales in the lungs; - Expansion of the percussion boundaries of the heart; Objective signs

Functional classes (New York Heart Association - NYHA): 1 FC - without restriction of physical activity. Ordinary physical activity does not cause fatigue, palpitations, shortness of breath, or angina; FC 2 – minor limitation of physical activity. There are no symptoms at rest, habitual physical activity is accompanied by shortness of breath, fatigue or rapid heartbeat; 3 FC – noticeable limitation of physical activity. At rest there are no unpleasant sensations, physical activity of lesser intensity is accompanied by the appearance of symptoms; 4 FC – inability to perform any physical activity. Symptoms are present at rest and worsen with minimal physical activity.

Complications of chronic heart failure: Sudden cardiac death; Pulmonary edema; Cardiogenic shock; Kidney failure; Liver failure, impairment of all liver functions due to blood stagnation; Cardiac cachexia, exhaustion of the body due to poor circulation, loss of body weight, thinning of the skin with the appearance of poorly healing ulcers.

Diagnostics. Physical examination: Examination Percussion Auscultation Laboratory tests: Complete blood count / biochemical; General urine analysis / daily diuresis.

Instrumental studies: Magnetic resonance imaging; Electrocardiography; CT scan; Chest X-ray; Echocardiography; Stress echocardiography; 6-minute walk test. Magnetic resonance imaging of the heart

Computed tomography Electrocardiography Chest X-ray

Stress echocardiography Echocardiography

Invasive diagnostic procedures: Right-sided and left-sided cardiac catheterization; Coronary angiography. Coronary angiography

Drug therapy The main drugs of drug treatment: ACE inhibitors Beta-blockers Calcium channel blockers Aldosterone antagonists Diuretics Cardiac glycosides Angiotensin 2 receptor antagonists

Electrophysiological methods of therapy Implantation of pacemakers that create an electrical impulse and transmit it to the heart muscle.

Surgical, mechanical methods of treatment: Coronary artery bypass grafting Coronary stenting Mammarocoronary bypass grafting Surgical correction of heart valves Wrapping the heart with an elastic mesh frame Heart transplantation Coronary stenting Coronary artery bypass grafting

Nursing process in chronic heart failure. Stages of the nursing process: Stage 1 - collection of information, assessment of the condition; Stage 2 - identification of the patient’s problems, interpretation of the data obtained; Stage 3 - planning nursing care for the patient. Stage 4 - implementation of the drawn up nursing intervention plan; Stage 5 - assessment of the effectiveness of care and the results of the listed stages.

Identifying patient problems Shortness of breath; Edema; Weakness, fatigue during physical activity; Sleep and appetite disturbances; Risk of complications, bedsores; The need for frequent visits to the toilet, with frequent urination (when taking diuretics). Risk of developing congestive pneumonia. Lack of knowledge about your disease.

Nursing Care Planning Follow all physician orders. Provide assistance in self-care and hygiene measures. Organize and control meals. Organization of dosed physical activity, exercise therapy. Teach the patient/family to monitor: body weight, dynamics of edema, condition of the skin in the area of edema. - measure blood pressure, respiratory rate, pulse, temperature - determine daily diuresis and water balance; - prevent bedsores, congestive pneumonia, constipation

Fundamentals of anatomy and physiology of the cardiovascular systemThe heart is a hollow muscular
body performing
pump function. In an adult
its volume and mass are
on average 600-800 cm3 and 250330 g The heart consists of
four cameras - left
atrium (LA), left
ventricle (LV), right
atrium (AA) and right
ventricle (RV), all of them
separated by partitions.
The RA includes the vena cava, the LA
- pulmonary veins. From RV and LV
come out accordingly
pulmonary artery (pulmonary
trunk) and ascending aorta.

Conditionally, in the body
a person is separated
small and large circles
blood circulation In small
circle of blood circulation -
right ventricle
pulmonary vessels and left
atrium - occurs
exchange of blood with external
environment. It's in the lungs
she gets enough
oxygen and
exempt from
carbon dioxide.
Big circle
represented by left
ventricle, aorta,
arteries, veins and
right atrium, he
created for
implementation
blood supply of all
body.

Pathological condition
in which the CVS is not
capable of delivering
organs and tissues
required amount
blood for their normal
functioning at rest
and under load
(physical,
emotional and
diseases).

Chronic failure
blood circulation develops when
the heart is affected and impaired
contractile function.

Heart damage due to myocarditis,
diffuse atherosclerotic and
post-infarction cardiosclerosis, defects
hearts and pericarditis, etc.

Initial (hidden). Subjective
(shortness of breath, palpitations, weakness) and
objective signs of NK appear
only during physical activity. IN
At rest there are no symptoms.

The presence of subjective and objective
signs of NK as in physical
under load and at rest.
IIA- The phenomenon of stagnation and disruption
organ functions are poorly expressed or
moderate, more often manifested moderately.
IIB - congestion is pronounced
stronger and always present at rest.

Final (dystrophic). Total
heart failure.
Marked congestion in organs,
multiple organ failure
due to structural and morphological changes.

0 FC – patient passes
in 6 minutes more than 550m;
1 FC – the patient passes
550-426m;
2 FC – the patient passes
425-301m;
3 FC – the patient passes
300-151m;
4 FC – the patient passes
150m or less

The first clinical signs
chronic cardiac
failures are: tachycardia,
shortness of breath, cyanosis and edema.

shortness of breath on exertion or (in
in advanced cases) at rest;
cardiopalmus;
pale or bluish skin tone,
especially those far from the heart
areas of the body (fingers, toes, lips);
swelling (primarily of the legs);
pain in the right hypochondrium,
associated with congestion of the liver veins;
increased fatigue.

In the early stages of cardiac
deficiency is
compensatory mechanism
aimed at maintaining
normal heart function. At
progression of cardiac
insufficiency tachycardia becomes
permanent and loses its
compensatory properties. She herself
helps weaken the myocardium. On
this stage requires treatment
disturbed heart rhythm.

Appears at the beginning only when
physical activity, at stage 2 already in
resting position. The appearance of shortness of breath
early stages of cardiac
deficiency contributes to stagnation in
ICC - initially of a transitory nature,
occurring only during physical
load. Night cough may occur
the first symptom of the initial transition
stage into a more pronounced, weakening
left ventricle.

Occurs in the early stages of
load, and then at rest. At
heart failure occurs
peripheral cyanosis as opposed to
central, conditioned
respiratory diseases.

Clinical symptom of deficiency
right ventricle.
At grade 1 - not palpable
At grade 2 – a protruding,
diseased liver.
At 3 tbsp - dense, with a pointed edge
liver (cardiac cirrhosis)

Arise as a result of a violation
contractile function of the myocardium,
decreased renal blood flow, etc.
Diuresis becomes small, urine
has a high concentration, contains
protein, red blood cells.
1st stage – swelling is not noticeable
Stage 2-3 – edema manifests itself in the form of ascites
and hydrothorox

Poor sleep, mild cyanosis, decreased
ability to work.
During period A – no complaints, but
physical and emotional stress
lead to increased blood pressure and decreased
cardiac output by 10-20%.
During period B – characterized by all
symptoms 1 tbsp. turning into
stagnation of the ICC under load conditions.

Shortness of breath occurs quickly and is constant
tachycardia, increased heart size,
shortness of breath, cough with sputum. Violation
organ and metabolic functions.
During period A – the beginning of the stage, violations
hemodynamics are insignificant, disturbance
functions of the heart or its department, congestive
liver phenomena.
During period B – the end of the second stage:
profound hemodynamic disturbances, swelling on
legs, congestion of the liver, its
significant increase.

The above phenomena are significantly
increase: increased cyanosis, shortness of breath
observed in a state of rest, swelling
reach the lower back, abdominal cavity
and chest. Patients can sleep
only in a semi-sitting position.
The heart is significantly enlarged, the pulse
arrhythmic, weak filling,
soft. Patients die while growing
phenomena of insufficiency
blood circulation

CHF affects 0.4% to 2% of adults
population. Among older people
75 years its prevalence may
reach 10%. Risk with age
development of heart failure
gradually increases. Among all
patients visiting medical
Russian institutions, 38.6% available
signs of chronic heart disease
insufficiency.

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

The goals of treatment for CHF are:
eliminating or minimizing clinical
symptoms of CHF - increased fatigue,
palpitations, shortness of breath, swelling;
protection of target organs - blood vessels, heart,
kidneys, brain (similar to
hypertension therapy), as well as prevention
development of striated hypotrophy
muscles;
improving quality of life;
increase in life expectancy
reduction in the number of hospitalizations.

1. Definition of CHF syndrome.

3. Causes, pathogenesis of CHF.
4. Classification of CHF.
5. Clinic, treatment.

CHRONIC HEART FAILURE new recommendations OSCH - 2006 Professor of the Department of Hospital Therapy E.I. Tarlovskaya

The main causes of CHF in Europe is coronary artery disease and myocardial infarction (up to 60-70%) DCM Heart defects hypertension (over 70 years of age)

“Trigger” factors provoking the appearance/worsening of HF Transient myocardial ischemia Tachy-bradyarrhythmias PA thromboembolism Increased mitral regurgitation Renal dysfunction Thyroid pathology Side effects of medications Excessive consumption of NaCl and water Respiratory infection (every 4 decompensations) Alcohol abuse New!

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 they use NSAIDs More often they are hospitalized

Criteria used to determine the diagnosis of CHF Symptoms Shortness of breath (slight to suffocation) Fatigue Palpitations Cough Orthopnea

Criteria used to determine the diagnosis of CHF Clinical signs Pulmonary congestion (wheezing, R-graphy) Peripheral edema Tachycardia (>90 per min) Swollen neck veins Hepatomegaly Gallop rhythm (S3) Cardiomegaly (CTI - 60%, EDV - 67 mm, percussion – border of the OST anterior PL)

Criteria used to determine the diagnosis of CHF Objective signs of cardiac dysfunction ECG, R-graphy of the chest Systolic dysfunction (decreased LVEF)* Diastolic dysfunction** (Doppler echocardiography, increased PAWP) BNP hyperactivity

ECG in patients with CHF Signs of LVH Deviation of el. left axis Signs of cicatricial damage to the myocardium (predictor of low contractility) LBP block (predictor of low contractility) ECG signs of LA and RA overload (predictor of diastolic dysfunction) Atrial fibrillation (common cause of decompensation)

ECHO cardioscopy (normal) LV systolic function EF=SV/EDV; EF (according to Teicholtz) = 55-60% EF (according to Simpson) = 50-55% LV diastolic function E/A ratio = 1-2, LVVIVR (LV isovolumetric relaxation time)<92 мс (<30); <100 мс (30-50 л); <105 мс (>50 l)

Laboratory diagnostics Hemoglobin Red blood cells White blood cells Platelets Electrolytes (K+!) Creatinine Glucose Liver enzymes General urine analysis Natriuretic peptide

Natriuretic peptide specificity - 90% A close relationship between NUP and the severity of HF has been proven. Definition of NUP - laboratory test for the presence of HF NUP - assessment of the severity of HF NUP - prognosis of the patient with HF NUP - treatment effectiveness

Coronary angiography and ventriculography Indications: Differential diagnosis of ischemic cardiomyopathy Refractory heart failure of unknown etiology Severe mitral regurgitation Aortic valve damage

Coronary angiography and ventriculography Contraindications: Terminal CHF Revascularization, surgery, heart transplant is not planned

Myocardial biopsy Indications: Unclear genesis of CHF (subject to the exclusion of ischemic cardiomyopathy) Limitation: Aggressive invasive nature Low sensitivity (especially with mosaic myocardial damage) Lack of uniform generally accepted diagnostic criteria

Diagnostic algorithm for CHF Symptoms or signs of CHF Objective examination, ECG, R-graphy, NUP normal EchoCG normal CHF unlikely Etiology, severity, trigger factors Choice of treatment

Surgical treatment of CHF Myocardial revascularization operations Surgery to correct mitral regurgitation Heart transplantation – has no serious future Implantation of a circulatory support device “LV bypass”

Left ventricular assist Improves the prognosis of patients with critical CHF The method is superior in its effectiveness (impact on survival) to all therapeutic methods of treatment The main limitation in Russia is the high cost

Mechanical treatments Use of restrictive external elastic mesh to limit cardiac dilatation No significant clinical studies

Electrophysiological methods of treating CHF Cardiac resynchronization therapy Three-chamber cardiac stimulation Elimination of asynchrony in the heart

Cardiac resynchronization therapy Improves quality of life Slows cardiac remodeling Reduces readmissions Reduces mortality (ECC Guidelines, 2005)

Cardiac resynchronization therapy, indications for 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 CRT + CD mode reduces overall mortality in patients with CHF by 43%

Additional drugs Statins - for all patients with ischemic etiology of CHF For stage III CHF. and cardiac fibrosis of the liver with cholesterol less than 4 mmol/l - do not use

Additional agents Indirect anticoagulants (WARFARIN) - for patients with CHF with atrial fibrillation (permanent and recurrent with frequent attacks, more often than once every 3 months) Warfarin cannot be replaced by aspirin, clopidogrel and their combination

Additional means 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 subcutaneously for 2-3 weeks

Auxiliary agents are used not for the treatment of CHF, but for special indications PVD (nitrates) - for concomitant angina BMCC (amlodipine, felodipine) - for severe angina and persistent hypertension AAP - for life-threatening VAs 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 for CHF Nitrates can be prescribed for CHF only in the presence of proven coronary artery disease and angina pectoris, which resolves only with nitro drugs. In all other cases, nitrates for CHF are not indicated. Nitrates can negatively affect the prognosis of patients with CHF, complicating the use of ACE inhibitors

Blockers of slow calcium channels in CHF Only long-acting dihydroperidines - amlodipine (NORVASK) and felodipine (PLENDIL) Short-acting dihydroperidines - contraindicated Verapamil and diltiazem can be used only in stages I - IIA. (I-II FC)

Slow calcium channel blockers for CHF Indications for amlodipine and felodipine (against the background of basic treatment): Persistent angina Persistent hypertension High pulmonary hypertension Severe valvular regurgitation

The cardiodepressive properties of cytokines, their ability to influence myocardial remodeling, and participation in both systolic and diastolic dysfunction have been established experimentally and clinically. The 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 studies confirming the participation of the cytokine system TNF-α, IL-1β, IL-6 in the pathogenesis of CHF, there are studies in which no significant manifestations of cytokineogenesis were found in CHF. Despite individual differences in the vascular effects of cytokines, one should remember the existence of a single functional complex of cytokines or the “tandem of TNF-α, IL-1β, 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-α system and other cytokines (IL-1β, IL-6, IFN-g) regarding the expression of the inducible form of NO synthetase (NOS2) in cardiomyocytes and endothelial cells of myocardial microvessels. NO and the toxic product formed during the interaction of NO and superoxide anions, peroxynitrite, have the ability to significantly reduce myocardial contractility.

TNF-α-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 the SAS and RAAS, is essential in the development of decreased exercise tolerance. The latter is associated with a weakening of vascular dilation in response to physiological stimuli, a decrease in strength and endurance, and an increase in skeletal muscle catabolism. It has been established that NO induction in response to TNF cytokine system is associated with increased cardiomyocyte apoptosis. An important aspect of the role of the cytokine system in CHF is their prognostic value. The prognostic significance of increased cytokine levels in patients with CHF was studied in the SOLVD studies, which showed that a TNF-α level of less than 6.5 pg/ml is prognostically more favorable, and increased levels of the TNF-α and IL-6 system cytokines are independent predictors death of patients with severe CHF. In the VEST study, circulating levels of proinflammatory cytokines (TNF-α system, IL-6) and cytokine receptors were independent predictors of mortality in patients with severe chronic heart failure with the presentation of 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 activation of the immune system and lead to an increase in TNF-α and other pro-inflammatory cytokines (Fig. 1). This “sequence” of events is indirectly confirmed by the directly proportional dependence of the TNF- level on severity of chronic heart failure and its presentation. However, most researchers assign the expression of proinflammatory cytokines the role of the root cause of the development and progression of CHF.

Thus, the mechanism for the implementation of the hemodynamic and clinical influence of proinflammatory cytokines in CHF consists of four components:

negative inotropic effect
cardiac remodeling (irreversible dilatation of cavities and hypertrophy of cardiomyocytes
disorders of endothelium-dependent dilatation of arterioles
enhancing the process of apoptosis of cardiomyocytes and peripheral muscle cells

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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 the function of the heart, namely its muscular layer (myocardium), is impaired. In this case, the heart muscle (myocardium) is unable to expel (push) blood from the heart into the vessels under increased pressure. In other words, the heart is “like a pump”, it does not cope with its job and cannot pump blood well.

3 Main causes: Myocardial infarction. Because damage to the heart during a heart attack or the remaining scar after it prevents the heart muscle from contracting fully 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 a congenital disorder or acquired change in the “architecture” of the heart. Cardiomyopathies, by expanding, narrowing and thickening the walls of the heart, reduce the contractility of the myocardium.

5 Cardiac (related to heart disease) Myocardial infarction. Cardiac arrhythmias. Non-cardiac (diseases not related to the heart). Respiratory tract infections, pneumonia. Diseases of the thyroid gland (thyrotoxicosis). Chronic renal failure. Physical and emotional stress. Abuse of alcohol, liquids, salt. 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 amiodarone). Nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoid hormones. Calcium antagonists (medicines used to treat hypertension). Antitumor agents. Sympathomimetics are drugs that stimulate a certain part of the nervous system (terbutaline, tyramine). Antidepressants (tricyclics). Antimalarial drugs. Drugs (heroin). Vasodilators (vasodilators - diazoxide, hydralazine). Analgesics (acetamifene). Medicines that lower blood pressure (reserpine). Physical effects (radiation, high and low temperatures, 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. Thus, in the early stages of failure, tissue metabolism or microcirculation is disrupted, which is especially pronounced at the time of physical stress (N.D. Strazhesko, V.Kh. Vasilenko, R.G. Mezhebovsky, L.P. Pressman, etc.). The development of oxygen starvation of tissues due to the slow transport of blood oxygen is to a certain extent compensated by the increased use of oxygen by tissues, which leads to an increase in the arteriovenous difference in oxygen content. However, a decrease in oxygen tension in venous blood below 20 mmHg. Art. incompatible with life due to paralysis of vital centers in the medulla oblongata. The immediate result of a discrepancy between the supply of oxygen and the need for it in tissues is a disruption of carbohydrate metabolism, phosphorylation processes, and protein synthesis. This leads to irreversible degenerative processes in organs. Disruption of microcirculation is facilitated by sodium and water retention 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 makes it even more difficult to supply tissues with oxygenated blood. Retrograde long-term 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 hemodynamic condition and worsens the course of the disease.

hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes constriction of arterioles and venules -> increased venous return of blood to the heart -> influx of a large amount of blood to the decompensated lion" title = "Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> norepinephrine , causes a narrowing of arterioles and venules -> an increase in the venous return of blood to the heart -> the influx of a large amount of blood to the decompensated leo" class = "link_thumb"> 8 Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes a narrowing of arterioles and venule -> increase in venous return of blood to the heart -> influx of a large amount of blood to the decompensated left ventricle. Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of the renal arterioles -> activation of the renin-angiotensin system (RAS) -> overproduction of angiotensin 2 (acts vasopressively, narrows small arteries) -> local (cardiac) tissue RAS is activated ( progression of its hypertrophy). Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of the renal arterioles -> activation of the renin-angiotensin system (RAS) -> overproduction of angiotensin 2 -> increased formation of aldosterone -> increased sodium reabsorption -> activation of antidiuretic hormone (ADH) 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 constriction of arterioles and venules -> increase in venous return of blood to the heart -> influx of a large amount of blood to the decompensated leo"> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes constriction of arterioles and venules -> increased venous return of blood to the heart -> influx of a large amount of blood to the decompensated left ventricle. Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of the renal arterioles -> activation of the renin-angiotensin system (RAS) -> overproduction of angiotensin 2 (acts vasopressively, narrows small arteries) -> local (cardiac) tissue RAS is activated ( progression of its hypertrophy). Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> spasm of the renal arterioles -> activation of the renin-angiotensin system (RAS) -> overproduction of angiotensin 2 -> increased formation of aldosterone -> increased sodium reabsorption -> activation of antidiuretic hormone (ADH) 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 constriction of arterioles and venules -> increased venous return of blood to the heart -> influx of a large amount of blood to the decompensated leo » title=”Deterioration of blood supply to organs and tissues -> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes constriction of arterioles and venules -> increase in venous return of blood to the heart -> influx of a large amount of blood to the decompensated leo”>

10 Functional classification of chronic heart failure of the New York Heart Association (NYHA, 1964): 1 FC: Physical activity does not cause oral discomfort (increased fatigue, shortness of breath, palpitations, etc.) 2 FC: Physical activity causes moderate, insignificant discomfort 3 FC: Physical activity causes significant discomfort. The patient feels well at rest. 4 FC: Minimal physical activity causes discomfort, which 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 early), first indicate the stage and period according to the classification of N.D. Strazhesko, then according to NYHA, for example: CHF 2a, FC 3.

13 Crepitation and fine bubbling rales in the lower parts of both lungs, which do not disappear after vigorous coughing and are not caused by inflammatory infiltration in the lungs. Dilatation of the left ventricle. The emphasis of the second tone is on the pulmonary artery. The appearance of a pathological III tone and a proto-diastolic gallop rhythm (left ventricular, better audible in the region of 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 (blue lips, ears, tip of the nose, cold cyanotic hands, feet), swollen veins of the neck, hydrothorax, congestive hepatomegaly, positive Plesch test (hepato-jugular, abdomino-jugular reflux). Peripheral edema (primarily in the area of the legs, feet, with further spread upward), ascites, and possible development of cirrhosis of the liver. Dilatation of the right ventricle (not always determined by percussion due to the often accompanying emphysema and forward rotation of the heart by the right ventricle) Epigastric pulsation, synchronous with the activity of the heart (caused by contraction of the right ventricle). Systolic murmur of tricuspid regurgitation (relative tricuspid valve regurgitation due to severe dilatation of the right ventricle) Right ventricular protodiastolic gallop rhythm

15 Laboratory tests: Complete blood count (hematocrit, red blood cells and hemoglobin). Biochemical blood test (determination of liver enzymes, cholesterol). Content of thyroid hormones in the blood.

16 Instrumental studies: ECG (electrocardiography). Echocardiography (ultrasound) of the heart (determines myocardial contractility). Catheterization of the heart cavities. Coronary angiography (X-ray contrast method for studying 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. If the condition is preserved (stable), exercise up to 45 minutes a day (according to how you feel). Physical rest during exacerbation of symptoms.

18 Mode: the patient’s activity should not exceed the capabilities of the cardiovascular system. At stage I of CHF, semi-bed rest is prescribed for 5-7 days, then increased physical activity is limited: at stage II (period A), semi-bed rest is indicated, and at stages 11B and III, bed rest is indicated. The duration of bed rest depends on the course of CHF. With very strict and prolonged bed rest, the risk of developing phlebothrombosis and pulmonary embolism increases. These patients are prescribed breathing exercises and frequent changes in body position. Mental peace is achieved by observing a therapeutic regimen and using sedatives (bromides, valerian, motherwort, minor tranquilizers). The diet should be rich in vitamins, which are administered in double doses; salt and liquid restriction is indicated. It is necessary to monitor bowel function. In stage I CHF, the amount of table salt is reduced to 5-6 g per day (10 tables). At stages II and III - up to 3 g/day (10a table). In case of severe edematous syndrome, a sharply hypochloride diet is indicated - no more than 1 g of salt per day. Along with salt restriction, fluid restriction is necessary (up to 1 l/day). Against the background of this diet, fasting days (milk, curd, fruit, etc.) are prescribed, which are especially indicated for patients with excess body weight.

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 (adenosine converting enzyme inhibitors) are a group of medications that help: Reduce the risk of sudden death. Slowing the progression of CHF. Improvement of the course of the disease. Improving the patient's quality of life. These include: Captopril. Quinapril. Enalapril. Ramipril. Fosinopril. Lisinopril. The effect of the therapy may appear within 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. Reduce the volume of fluid in the body. Reduces the load on the heart. Dilate blood vessels. Quickly, effectively and safely eliminate fluid retention in the body, regardless of the cause of CHF. These include: Furosemide. Lasix. Hydrochlorothiazide. Spironaloctone. Torsemide. Triamterene. Amiloride.

21 3. Cardiac glycosides are drugs that are the “gold standard” in the treatment of CHF. Increase myocardial contractility. Improving blood circulation. Reduces the load on the heart. They have a diuretic effect. Slow down heart rate. Reduce the risk of hospitalization. These include: Digoxin. Digitoxin. Korglykon.

22 4. Antiarrhythmic drugs are drugs that prevent the development of arrhythmia and reduce the risk of sudden death. These include Amiodarone. 5. Anticoagulants are medications that prevent blood thickening and the formation of 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 use of medications that improve metabolism, nourish the heart muscle and protect it from ischemic effects. These include: ATP (adenosine triphosphoric acid). Cocarboxylase. Potassium preparations (panangin, asparkam, calyposis). Magnesium preparations. Thiotriazolin. Vitamin E. Riboxin. Mildronate. Preductal MR. Mexican.

23 Projections It is estimated that about 50% of patients diagnosed with heart failure live with this 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 has the following goals: improving the functioning of the left ventricle of the heart, restoring work capacity and improving the patient’s quality of life. Treatment of heart failure, begun at the earliest stages, significantly improves the patient's life prognosis.

Times of Day

Additional results

On this page you can download a presentation on the topic “Chronic heart failure (CHF).” The presentation provides a definition of CHF, 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. Pathanatomical changes.
3. Causes, pathogenesis of CHF.
4. Classification of CHF.
5. Clinic, treatment.

List of abbreviations

Introduction

Chapter 1. Chronic heart failure

1 Etiology

2 Clinical picture

3 Classification of CHF

4 Diagnostics

5 Treatment

Chapter 2. Nursing care for CHF

1 Nursing process

2 Nursing interventions

Chapter 3. Scientific research work

1 Analysis of statistical data

2 Survey results

Bibliography

Annex 1

List of abbreviations

BP - blood pressure

ACEI - angiotensin-converting enzyme inhibitor

IHD - coronary heart disease

LV - left ventricle

HF - heart failure

ESR - erythrocyte sedimentation rate

CVS - cardiovascular system

FC - functional class

CHF - chronic heart failure

HR - heart rate

ECG - electrocardiography

EchoCG - echocardiography

Introduction

Cardiovascular diseases rank first in prevalence among the population of economically developed countries. They remain the leading cause of disability and mortality. If previously they were associated with old age, now even middle-aged people are familiar with pain in the heart, irregular heart rhythms and pills for angina attacks. Diseases of the cardiovascular system are numerous. Some of them are diseases primarily of the heart, others - mainly of arteries or veins, and others affect the cardiovascular system as a whole. The outcome of the most common of them, such as coronary heart disease and arterial hypertension, is chronic heart failure.

Chronic heart failure is a syndrome that occurs when a person has systolic and (or) diastolic dysfunction, accompanied by chronic hyperactivation of neurohormonal systems, and clinically manifested by shortness of breath, weakness, palpitations, limitation of physical activity, and pathological fluid retention in the body.

In other words, CHF is a pathological condition consisting in the inability of the circulatory system to deliver to organs and tissues the amount of blood that is necessary for normal functioning.

The mortality rate of the Russian population is one of the highest among European countries. According to WHO, by 2030, about 23.3 million people will die from cardiovascular diseases, mainly from CHF. Therefore, CHF is much easier to prevent than to cure.

Relevance of the topic

The number of people suffering from CVS pathology is steadily increasing, and therefore the number of hospitalizations in hospitals is increasing. A sick person changes a lot compared to what he was before the illness, and hospitalization is additional stress.

Nurses play one of the leading roles in providing patient care. The nursing process is one of the basic concepts of modern nursing models. In accordance with the requirements of the State educational standard for nursing, the nursing process is a method of organizing and performing nursing care for a patient, aimed at meeting the physical, psychological, social needs of the individual, family and society. The goal of the nursing process is to maintain and restore the patient's independence and meet the basic needs of the body. The nursing process requires from the nurse not only good technical training, but also a creative attitude towards patient care, the ability to work with the patient as an individual, and not as an object of manipulation. The constant presence of the nurse and her contact with the patient make the nurse the main link between the patient and the outside world.

The functions of a nurse are varied and her activities concern not only the diagnostic and treatment process, but also patient care in order to prevent diseases leading to CHF and the progression of the disease itself.

Proper organization of cardiac care and provision of quality care will help reduce mortality and increase life expectancy.

Goals and objectives.

Purpose of the work: to study the features of care for patients with chronic heart failure to organize a qualified nursing process.

Research objectives:

study the nursing process in chronic heart failure;

analyze the number of patients hospitalized in the city’s cardiology departments with diseases leading to chronic heart failure;

assess the level of awareness of patients in the cardiology department about their disease, and their willingness to comply with the recommendations of the doctor and nurse in order to optimize care;

identify factors contributing to the progression of chronic heart failure.

Subject of research: nursing care for patients with chronic heart failure.

Object of study:

patients of the cardiology department of the City Hospital No. 1;

patients of the cardiology department of the City Hospital No. 2.

Materials and methods.

Materials:

sources of literary publications;

Internet sites;

statistical data from MBUZ “GB No. 1” and “GB No. 2”;

own research using a survey of patients from the cardiology departments of the Municipal Hospital No. 1 and Municipal Hospital No. 2.

prepared a literature review;

analyzed statistical data;

conducted a survey of patients with subsequent analysis of the results;

formulated conclusions and proposals.

Chapter 1. Chronic heart failure

1 Etiology

In most developed countries, the causes of chronic heart failure are the following diseases:

IHD, including myocardial infarction;

Hypertonic disease;

Cardiomyopathies;

Acquired and congenital heart defects;

Pericarditis;

Chronic cor pulmonale.

According to the Framingham Study, the role of arterial hypertension, diabetes mellitus and obesity in the occurrence of chronic heart failure has increased significantly. These conditions are not only risk factors for the development of coronary artery disease, but also themselves cause myocardial damage. In Russia, the importance of hypertensive heart and alcoholic myocardial damage in the development of heart failure is underestimated. Many patients do not admit that they abuse alcohol for a long time, so they are often diagnosed with other diseases. In some regions of the world, the role of heart defects and myocardial lesions of various nature remains high in the etiology of chronic heart failure.

Rare causes of chronic heart failure:

Thyrotoxicosis;

Severe anemia;

Take-take;

Paget's disease;

Severe obesity;

Chronic liver diseases;

Arteriovenous shunts;

Pregnancy;

Hypernephroma.

Most of the above diseases are chronic and characterized by progression. There are various factors that contribute to the occurrence and progression of heart failure:

Arrhythmias, primarily atrial fibrillation, lead to impaired cardiac function as a result of an increase in heart rate or, less commonly, a decrease (for example, with complete transverse block).

Pulmonary embolism leads to increased load on the right ventricle and is accompanied by tachycardia and fever.

Acute infectious diseases, including respiratory viral infections, change metabolism and increase the hemodynamic load on the heart.

Hyperkinetic blood circulation is observed during pregnancy, anemia, hyperthyroidism, etc. and can cause the development of heart failure in the presence of any heart disease.

The reasons for the increase in heart failure may be physical or emotional stress, increased salt intake, cessation of cardiotonic or diuretic drugs, or taking drugs that reduce myocardial contractile function. Estrogens, androgens, glucocorticosteroids, non-steroidal anti-inflammatory drugs cause sodium and water retention in the body.

A hypertensive crisis leads to a significant increase in the load on the myocardium.

1.2 Clinical picture

Manifestations of chronic heart failure are variable and depend on the characteristics of heart damage and the inclusion of compensatory mechanisms. They are characterized by a number of general signs, as well as symptoms of blood stagnation in the pulmonary and systemic circulation.

Shortness of breath is the main symptom of heart failure associated with stagnation of blood in the lungs. Initially, shortness of breath appears only during physical activity and disappears with rest. It should be borne in mind that shortness of breath during physical exertion also occurs in poorly trained people with a healthy heart. Therefore, it is necessary to pay attention to a decrease in exercise tolerance and the appearance of shortness of breath or a feeling of lack of air with significantly less physical effort than before. The basis of shortness of breath is a change in the gas composition of the blood, hypoxemia, as well as a decrease in the compliance of the lungs, associated with blood stagnation and interstitial edema and requiring increased work of the respiratory muscles. Dyspnea at rest is usually accompanied by tachypnea.

Orthopnea - relief of breathing in a position with a raised head or sitting. In this position, venous flow to the right heart is reduced, which leads to a decrease in pulmonary capillary pressure. Orthopnea decreases with increasing right ventricular failure and blood stagnation in the systemic circulation.

Cardiac asthma is characterized by attacks of shortness of breath, suffocation or lack of air and refers to manifestations of acute left ventricular failure. Attacks of cardiac asthma usually occur at night as a result of a rapid increase in blood stagnation in the pulmonary circulation. In addition to shortness of breath and suffocation, a cough with sputum is observed; upon auscultation, harsh breathing is detected, then moist rales appear. A prolonged attack of cardiac asthma can be complicated by pulmonary edema as a result of the transition of the liquid part of the blood from the vascular bed and interstitial tissue into the airways. The development of cardiac asthma is facilitated by a decrease in ventilation during sleep due to a decrease in the sensitivity of the respiratory center to changes in the gas composition of the blood and a decrease in the contractile function of the myocardium. In addition, in the horizontal position of the patient, blood leaves the depot with an increase in the volume of circulating blood.

Silent moist rales in the lungs are observed in chronic left ventricular failure and are heard in the lower parts of the lungs.

Congestive bronchitis in patients with heart failure leads to a cough with the release of mucous sputum. The sputum often contains streaks of blood, which is associated with small hemorrhages in the edematous mucous membrane of the bronchi.

Periodic Cheyne-Stokes breathing occurs mainly in patients with cerebral vascular atherosclerosis due to cerebral hypoperfusion and a decrease in the sensitivity of the respiratory center to changes in the gas composition of the blood. It is characterized by periods of apnea, i.e. lack of breathing for several seconds, while the oxygen content in the arterial blood drops and carbon dioxide increases.

Sinus tachycardia is a characteristic symptom of heart failure. Initially, it is an adaptive reaction, providing an increase in minute volume of blood circulation during physical activity, but at rest it persists much longer than in healthy people. Later, tachycardia becomes even more stable. Pulse pressure may be reduced, reflecting a decrease in stroke volume. Sometimes diastolic pressure increases as a consequence of widespread vasoconstriction and a reflex from the stretching mouths of the vena cava. A tendency to sinus tachycardia and especially atrial fibrillation, as well as arterial hypotension, is an unfavorable prognostic sign in patients with heart failure.

Cyanosis of the lips and nails is associated with insufficient arterialization of the blood and increased use of oxygen in peripheral tissues, which leads to an increase in the content of reduced hemoglobin in the blood.

Alternating pulse is not common and is characterized by alternating pulse waves of normal and low amplitude, which is caused by a periodic decrease in the contractility of the left ventricular myocardium with a decrease in blood ejection.

Stagnation of blood in the systemic circulation is manifested by an enlarged liver, peripheral edema and swelling of the neck veins. The liver is usually dense to the touch. When pressing on it, even greater swelling of the neck veins is noted. Prolonged stagnation of blood in the liver leads to portal hypertension, enlarged spleen and ascites. Morphological examination reveals hypoxia of liver cells with more pronounced changes in the central zones, sometimes even with areas of necrosis of the lobules, especially when congestion is combined with small output syndrome. These changes may be accompanied by jaundice due to an increase in the level of direct bilirubin and an increase in the activity of aminotransferases in the serum.

Swelling appears first on the feet and ankles, later on the legs, especially in the evening. When lying down for a long time, swelling appears in the lower back. Edema is associated with an increase in hydrostatic pressure in small peripheral vessels and capillaries, an increase in the permeability of their walls due to hypoxemia, and sodium and water retention. Edema syndrome is often combined with pleural effusion (hydrothorax), usually right-sided. It is associated with an increase in pleural capillary pressure and extravasation of fluid into the pleural cavity. Pleural veins belong to both the large (parietal pleura) and small (visceral leaf) circulation circles. Therefore, hydrothorax can develop with venous stagnation in both circulation circles. When blood stagnates in the systemic circulation, stagnant gastritis often develops with atrophy of the gastric glands. In the terminal stage, cardiac cachexia is observed as a result of anorexia, malabsorption due to stagnation of blood in the intestinal veins.

With stagnation in the kidneys, proteinuria may appear, sometimes accompanied by slight azotemia. The density of urine is usually high.

Ascites occurs as a result of fluid transudation at elevated pressure in the portal veins and peritoneal veins. Ascites is most pronounced in patients with damage to the tricuspid valve and constrictive pericarditis.

Signs of decreased cardiac output are sometimes detected in the absence of pronounced stagnation of blood in the pulmonary circulation. The most pronounced decrease in blood flow in the skeletal muscles, which leads to weakness, fatigue, and in the long term - a decrease in muscle mass and the development of cardiac cachexia. In patients with heart failure, the hands may be pale and cold to the touch due to decreased blood flow along with increased sympathetic activity.

In more severe cases, signs of insufficient blood supply to the liver (“ischemic hepatitis”) and kidneys appear.

1.3 Classification of CHF

Table 1.1.

Stages of CHF (may worsen despite treatment)		Functional classes of CHF (can change during treatment in both directions)
	The initial stage of heart disease (damage). Hemodynamics are not impaired. Hidden heart failure. Asymptomatic LV dysfunction.		There are no restrictions on physical activity: habitual physical activity is not accompanied by rapid fatigue, shortness of breath or palpitations. The patient can tolerate increased stress, but it may be accompanied by shortness of breath and/or delayed recovery.
	Clinically pronounced stage of heart disease (damage). Hemodynamic disturbances in one of the blood circulation circles, expressed moderately. Adaptive remodeling of the heart and blood vessels.		Minor limitation of physical activity: no symptoms at rest, usual physical activity is accompanied by fatigue, shortness of breath or palpitations.
	Severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels.		Noticeable limitation of physical activity: there are no symptoms at rest, physical activity of less intensity compared to usual exercise is accompanied by the appearance of symptoms.
	The final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys).		Inability to perform any physical activity without discomfort; HF symptoms are present at rest and worsen with minimal physical activity.

4 Diagnostics

Diagnostic goals:

§ Early detection of the presence of heart failure.

§ Clarification of the severity of the pathological process.

§ Determination of the etiology of heart failure.

§ Assessing the risk of complications and sudden progression of pathology.

§ Forecast assessment.

§ Assessment of the likelihood of complications of the disease.

§ Monitoring the course of the disease and timely response to changes in the patient’s condition.

Diagnostic tasks:

§ Objective confirmation of the presence or absence of pathological changes in the myocardium.

§ Identification of the pathology that led to the development of chronic heart failure.

§ Determination of the stage and functional class of heart failure.

§ Identification of the predominant mechanism of development of heart failure.

§ Identification of provoking causes and factors aggravating the course of the disease.

§ Identification of concomitant diseases, assessment of their connection with heart failure and its treatment.

§ Collection of sufficient objective data to prescribe the necessary treatment.

Laboratory data.

General blood analysis. It is possible that iron deficiency anemia may develop in advanced heart failure due to impaired absorption of iron in the intestine or insufficient intake of iron from food (patients often have decreased appetite, they eat little, including not consuming enough foods containing iron). Initially existing severe anemia (as an independent disease) can lead to the development of CHF with high cardiac output. With cachexia, an increase in ESR may be observed. With decompensated chronic pulmonary heart disease, an increase in the level of hemoglobin, hematocrit, and red blood cells is possible. Due to the low level of fibrinogen in the blood, ESR decreases in severe CHF.

General urine analysis. Proteinuria and cylindruria may appear as markers of impaired renal function in CHF (“congestive kidney”).

Blood chemistry. A decrease in the content of total protein and albumin is possible (due to impaired liver function, due to the development of malabsorption syndrome; hypoproteinemia is expressed in cachexia); increased levels of bilirubin, alanine and aspartic aminotransferases, thymol test, γ-glutamyl transpeptidase, LDH, decreased prothrombin levels (these changes are due to impaired liver function); increased levels of cholesterol (with significant impairment of liver function - hypocholesterolemia), triglycerides, low- and very low-density lipoproteins, decreased high-density lipoproteins (in the elderly and with coronary heart disease); in severe CHF, an increase in the blood level of the cardiospecific MB fraction of creatine phosphokinase is possible; decrease in the content of potassium, sodium, chlorides, magnesium (especially with massive diuretic therapy); increased levels of creatinine and urea (a sign of impaired renal function; with severe liver damage, a decrease in urea levels is possible).

Instrumental research.

Electrocardiography.

Myocardial dysfunction, one way or another, will always be reflected on the ECG: a normal ECG with CHF is an exception to the rule. To objectify CHF, one should also take into account such ECG changes as signs of scarring of the myocardium and left bundle branch block as predictors of low myocardial contractility in coronary heart disease. An ECG also reveals various heart rhythm disturbances. The effect on the ECG of electrolyte imbalance, which may occur, should be taken into account, especially with frequent and prolonged use of diuretics.

X-ray of the chest organs.

The main radiographic signs confirming the presence of CHF are cardiomegaly and venous pulmonary stasis.

Cardiomegaly is caused by myocardial hypertrophy and dilatation of the cavities of the heart. Cardiomegaly can be judged based on an increase in the cardiothoracic index of more than 50%. or if there is an increase in the diameter of the heart of more than 15.5 cm in men and more than 14.5 cm in women. However, the size of the heart may be normal or slightly enlarged even with a pronounced clinical picture of CHF (with diastolic CHF). Normal heart sizes are not typical for systolic CHF.

Venous congestion - venous congestion of the lungs - is a characteristic sign of CHF. A decrease in the contractility of the LV myocardium increases the LV filling pressure and then the average pressure in the left atrium and in the pulmonary veins, as a result of which blood stagnation develops in the venous bed of the pulmonary circle. Subsequently, as CHF further progresses, pulmonary arterial hypertension, caused by spasm and morphological changes in arterioles, joins venous stagnation. The initial stage of venous congestion in the lungs is characterized by perivascular edema, dilation of the pulmonary veins, especially in the upper lobes, and redistribution of blood flow to the upper parts of the lungs. There are signs of pulmonary hypertension (expansion of the trunk and large branches of the pulmonary artery; depletion of the pulmonary pattern at the periphery of the pulmonary fields and increased transparency due to a pronounced narrowing of the peripheral branches of the pulmonary artery; enlargement of the right ventricle; increased pulsation of the pulmonary artery trunk. Hydrothorax is often detected, more often on the right. Cardiac radiography helps in identifying the underlying disease that led to the development of CHF (for example, post-infarction LV aneurysm, exudative pericarditis).

Echocardiography.

Echocardiography allows you to solve the main diagnostic problem - to clarify the very fact of cardiac dysfunction and its nature, as well as to conduct a dynamic assessment of the state of the heart and hemodynamics. Currently, tissue Doppler echocardiography is used to identify local disturbances in myocardial perfusion in CHF.

Radioisotope ventriculography allows one to accurately measure LVEF and LV final volumes and is considered a good method for assessing RV function. Radioisotope myocardial scintigraphy with technetium allows assessing LV function. Radioisotope scintigraphy of the myocardium with thallium makes it possible to assess the viability of the myocardium, identify foci of ischemia and fibrosis, and, in combination with physical activity, determine the reversible nature of ischemia and the effectiveness of treatment. The information content of radioisotope research methods exceeds that of Echo-CG.

Magnetic resonance imaging is the most accurate method with maximum reproducibility of calculations for calculating the volume of the heart, the thickness of its walls and the mass of the LV, superior in this parameter to Echo-CG and radioisotope research methods. In addition, the method makes it possible to detect thickening of the pericardium, assess the extent of myocardial necrosis, the state of its blood supply and features of functioning. However, given the high cost and low availability, diagnostic MRI is justified only in cases where other imaging techniques are insufficiently informative.

General research methods.

Pulmonary function assessment.

This test is useful to exclude pulmonary origin of shortness of breath. It has been established that forced vital capacity and forced expiratory volume in 1 second correlate with peak oxygen consumption in patients with CHF. With CHF, the expiratory rate in 1 second and forced vital capacity may decrease, but not to the same extent as with obstructive pulmonary diseases. There is also a decrease in the vital capacity of the lungs. After successful treatment of CHF, these indicators may improve, probably due to an improvement in the condition of the respiratory muscles, a decrease in shortness of breath and general weakness.

Load tests.

Carrying out stress tests in patients with CHF is justified not to clarify the diagnosis, but to assess the patient’s functional status and the effectiveness of treatment, as well as to determine the degree of risk. However, a normal stress test result in a patient not receiving specific treatment almost completely excludes the diagnosis of CHF.

It is recommended to carry out bicycle ergometry and treadmill test, especially under the control of gas exchange indicators (spiroveloergometry). Oxygen consumption at the height of maximum load most accurately characterizes the functional class of CHF. Carrying out tests with physical activity is possible only if the patient’s condition is stable for at least 2 weeks (no complaints at rest, no signs of pulmonary congestion, etc.), no need to use inotropic agents and diuretics intravenously, and a stable level of creatinine in the blood. For everyday practice, the 6-minute walk test is recommended as a standard routine test.

5 Treatment

In some cases, timely diagnosis of the cause of decompensation and a specific effect on it can significantly (and sometimes radically) influence the development and progression of heart failure.

Treatment goals:

1. Prevention of the development of symptoms of chronic heart failure (for the first stage of chronic heart failure).

2. Elimination of clinical symptoms of heart failure (shortness of breath, increased fatigue, tachycardia, edema syndrome, etc.) - for stages IIA-III.

Slowing the progression of the disease by protecting target organs (heart, kidneys, brain, blood vessels, skeletal muscles) - for stages I-III.

Improved quality of life (for stages IIA-III), reduced frequency of hospitalizations (for stages I-III).

Improving the prognosis of the disease - prolonging life (for stages I-III).

There are non-drug and drug treatment methods.

Non-drug methods.

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

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

Drug treatment of CHF.

It should be noted that any treatment algorithms should be based on “evidence-based medicine,” that is, when the effectiveness of drugs has been proven in international studies.

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

The main group of drugs fully meet the criteria of “evidence-based medicine” and are recommended for use in all countries of the world: ACE inhibitors, diuretics, cardiac glycosides, beta-blockers (in addition to ACE inhibitors).

According to indications, it is possible to prescribe an additional group of drugs, the effectiveness and safety of which has been proven by large studies, but requires clarification (meta-analysis), these are aldosterone antagonists, angiotensin II receptor antagonists, calcium channel blockers of the latest generation.

Auxiliary drugs, the effectiveness of which has not been proven, but their use is dictated by certain clinical situations, are peripheral vasodilators, antiarrhythmics, antiplatelet agents, direct anticoagulants, non-glycoside positive inotropes, corticosteroids, statins.

Despite the large selection of drugs in the treatment of patients, polyp is unacceptable<#"876636.files/image002.gif">

The number of patients with hypertension admitted to the cardiology department for the period from 2009 to 2013.

Conclusions: the maximum number of hospitalized patients with hypertension was observed in 2009 and amounted to 682 people. By 2013, the number of patients had dropped to 493 people.

The minimum number of hospitalized people was in 2011 and amounted to 439 people.

Diagram 2.3.

The number of patients with acute myocardial infarction admitted to the cardiology department for the period from 2009 to 2013.

Conclusions: the maximum number of hospitalized patients with acute myocardial infarction was observed in 2011 and amounted to 431 people. By 2013, the number of patients decreased to 399 people.

The minimum number of hospitalized people was in 2010 and amounted to 364 people.

Diagram 3.3.

The number of patients with coronary artery disease admitted to the cardiology department for the period from 2009 to 2013.

Conclusions: the maximum number of hospitalized patients with coronary artery disease was observed in 2010 and amounted to 2611 people. By 2013, the number of patients had decreased slightly to 2,528 people.

In 2012, there was a sharp decline in hospitalized patients and the minimum number was 2,308 people.

Diagram 4.3.

The number of patients with angina admitted to the cardiology department for the period from 2009 to 2013.

Conclusions: The maximum number of hospitalized patients with angina pectoris was observed in 2010 and amounted to 1053 people. By 2013, the number of patients had dropped significantly to a minimum of 856 hospitalizations.

Over the entire period, the number of patients admitted to the hospital with unstable angina exceeded the number of patients with stable angina. The maximum number of people hospitalized with unstable angina was in 2013 and amounted to 626 people. The minimum number of hospitalized people was in 2011 and amounted to 561 people.

The maximum number of hospitalized patients with stable angina was in 2010 - 2011. and amounted to 489 people. The minimum number of hospitalized people was in 2013 and amounted to 230 people.

2 Survey results

Diagram 5.3.

Conclusion: the results of the survey showed that almost everyone knows the technique of measuring blood pressure, Ps and absolutely everyone knows their normal values. Consequently, if their health worsens, patients can control their condition.

Diagram 6.3.

Conclusion: only 59% of all respondents are familiar with treatment table No. 10 prescribed for their illness and only 48% follow the diet. But a lot depends on nutrition. Proper nutrition will help stop the development of the disease, and improper nutrition will aggravate it and lead to complications. Therefore, monitoring the diet for CHF is one of the most important parts of the treatment process.

Diagram 7.3.

Diagram 8.3.

Conclusion: obesity has a direct effect on the heart with the development of structural and functional changes. Among patients, only 53% know that obesity is a factor influencing the development of CHF. 22% of whom control their body weight. As weight increases, blood pressure increases, which, along with the need to provide blood to the increased mass, forces the weakened heart to work under increased load. To activate weight loss in patients, fasting days are recommended, but only 28% of all patients comply with this recommendation.

Diagram 9.3.

Conclusion: the motor mode trains the cardiovascular system, increases its ability to adapt and the contractile function of the myocardium. But, unfortunately, only 37% do it.

Diagram 10.3. Diagram 11.3.

Conclusion: with CHF, water-salt metabolism is disrupted, sodium ions (table salt) are retained in the body, which leads to fluid accumulation and edema. And this, in turn, complicates the work of an already diseased heart. Therefore, it is necessary to limit table salt and liquid in the diet. Only 25% fulfill this important point. To determine fluid retention in the body, a method for determining water balance is used, which patients can use independently at home. But, apparently, this method is not common among patients and 6% know about it.

Diagram 12.3.

Conclusion: another important problem is following the doctor’s recommendations and fulfilling all appointments. While in the hospital, everything is controlled by a nurse. As soon as patients are discharged, they forget about many things, or do not consider it necessary to do them. According to the survey results, 67% always follow the doctor’s recommendations and 94% do not stop taking medications, following the prescriptions.

Diagram 13.3.

Conclusion: all 100% of respondents know about the dangers of smoking and alcohol on the progression of CHF. Alcohol disrupts the activity of the autonomic nervous system, and therefore the rate of contraction of the heart muscle decreases. Under the influence of smoking components, the sympathetic nervous system is activated, which is manifested by an increase in blood pressure and heart rate, which increases the myocardial need for oxygen. Despite awareness, 28% still have bad habits.

nursing care heart failure

This thesis examined the features of care for patients with CHF for the organization of a qualified nursing process.

An important role in the treatment of patients with CHF is nursing care for the patient. Although the nurse does not independently treat the patient, but only carries out the doctor’s orders, her role is very great, since, being constantly near the patient, she notices all the changes occurring in his condition. The role of a nurse during a patient’s stay in a hospital is the ability to correctly build relationships with a particular patient, depending on his personal qualities and state of health, correctly and timely assess changes in the patient’s condition, organize quality care and, together with the doctor, carry out adequate treatment and emergency measures.

While the patient is being treated in a hospital, he is under the supervision of doctors, and under the supervision of a nurse he carries out all the doctor’s prescriptions. As soon as the patient is discharged from the hospital, everything changes. Doctors' recommendations are forgotten, medications are not taken regularly, and the condition is not monitored. It is nurses who play the leading role in teaching and counseling patients and their relatives in care and self-care skills at home. This work should be carried out both by a local nurse at the stage of outpatient care, and by a hospital nurse during the patient’s hospital stay.

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Dvoinikova S.I. Organization of nursing activities. GEOTAR-Media. 2014-245s

Kuleshova L.I., Pustovetova E.V. Fundamentals of Nursing. Course of lectures, nursing technologies. Phoenix, 2013.-215s

Lychev. V. G., Karmanov V. K. Nursing in therapy. With a course of primary medical care: textbook - 2nd ed., revised. And additional - M.:FORUM: INFRA-M, 2013-544p.

Moiseev V.S., Moiseev S.V., Kobalava Zh.D. Heart disease: A guide for doctors. - M.: Medical Information Agency LLC, 2008. - 528 p.

Smoleva E.V. Therapy with a course of primary health care. - Ed. 11th.-Rostov-on-Don: Phoenix, 2013.-285 p.

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Additional sources

Annex 1

To improve the quality of care, as well as drug and non-drug treatment, it is advisable to recommend that the patient keep a self-monitoring diary.

A self-monitoring diary is a document necessary for both the doctor and the patient. Keeping such a diary helps you become more disciplined, improve the quality of treatment, and analyze the patient’s health status.

What you need to know about self-control? First of all, self-control must be systematic and long-term. Observations made without a system from time to time will not bring any benefit. Only regular and detailed filling out of a self-monitoring diary makes it possible to learn to control the dynamics of the patient’s condition without the constant help of doctors.

Regular entries help:

monitor vital signs

record data on changes in state

determine the effectiveness of treatment

select the dose of drugs

monitor medication intake

Self-observation is reflected in your self-control diary: this diary will contain indicators that it is advisable to record at the same hours, using the same method, under similar conditions.

The meaning of self-control is to acquire the skills of a patient to correctly assess his condition and competently adjust treatment. Naturally, only a specialist can fully determine the treatment, however, as experience shows, when the patient consciously manages the disease, being a full participant in the process along with the doctor, he gets much better results than simply blindly following (if at all) the instructions of the attending physician . And, therefore, only a person who is in control of the situation will feel confident.

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