Presentation on nursing "the importance of nursing activities in solving the problems of a patient with diseases of the cardiovascular system." Presentation: chronic heart failure Main drugs affecting the prognosis of patients with CHF

A syndrome expressed in 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. Heart failure is based on a violation of the pumping function of one or both ventricles.

or hyperthyroidism, heart damage due to diffuse connective tissue diseases, toxic-allergic lesions of the myocardium).

Hemodynamic overload of the heart muscle:

Impaired diastolic filling of the ventricles (adhesive pericarditis, hypertrophic and restrictive cardiomyopathies, myocardial storage diseases

Amyloidosis, hemochromatosis, glycogenosis).

Pathogenesis of heart failure

Decreased cardiac output

Stages of CHF

The initial stage of heart disease (damage). Hemodynamics are not disturbed, hidden heart failure.

Asymptomatic LV dysfunction.

Clinically pronounced stage of heart disease (damage). Hemodynamic disturbances in one of the blood circulation circles (moderately expressed).

Adaptive remodeling of the heart and blood vessels.

Stages of CHF (continued)

Severe stage of heart disease (damage), pronounced changes in hemodynamics in both circulations.

Maladaptive remodeling of the heart and blood vessels.

The final stage of cardiac damage, pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys).

The final stage of organ remodeling.

Functional classes of CHF

1 FC

There are no restrictions on physical activity: habitual physical activity is not accompanied by rapid fatigue, shortness of breath and palpitations. The patient can tolerate increased stress, but it may be accompanied by shortness of breath and/or delayed recovery.

Slight limitation of physical activity: no symptoms at rest, usual physical activity is accompanied by fatigue, shortness of breath or palpitations.

6 minute test

Determination of the functional class of heart failure according to the 6-minute test

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.

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

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.

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.

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).

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).

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 a narrowing 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 systems -> norepinephrine, causes a constriction of arterioles and venules -> an increase in the venous return of blood to the heart -> the flow 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 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 large amounts of blood to the decompensated leo"> hyperactivation of the sympathetic-adrenal system -> norepinephrine, causes constriction of arterioles and venules -> increase 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) -> hyperproduction of angiotensin 2 (acts vasopressive, 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 -> increases the formation of aldosterone -> increases sodium reabsorption -> activation of the production of antidiuretic hormone (ADH) - 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 narrowing of arterioles and venules -> increase in 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 -> increased venous return of blood to the heart -> influx of a large amount of blood to the decompensated leo"> !}

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 FK: 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.

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.

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.

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

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.

Regimen: 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.

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.

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.

3. Cardiac glycosides are medications 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.

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.

Prognosis 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.

1. Definition of CHF syndrome.

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

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

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

Presentation of chronic heart failure and cytokine system

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.

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)

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.

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

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

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

Good to know

© VetConsult+, 2016. All rights reserved. The use of any materials posted on the site is permitted provided there is a link to the resource. When copying or partially using materials from the pages of the site, be sure to place a direct hyperlink open to search engines, located in the subtitle or in the first paragraph of the article.

Chronic heart failure - presentation

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

1 Topic: Chronic heart failure Astana 2012

2 Chronic heart failure is the inability of the cardiovascular system to provide the organs and tissues of the body with a sufficient amount of blood. Chronic heart failure develops when 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.

Presentations on the topic of chronic heart failure

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.

Slide 1

Slide 2

Slide 3

Slide 4

Slide 5

Slide 6

Slide 7

Slide 8

Slide 9

Slide 10

Slide 11

Slide 12

Slide 13

Slide 14

Slide 15

Slide 16

Slide 17

Slide 18

Slide 19

Slide 20

Slide 21

Slide 22

Slide 23

Slide 24

Slide 25

Slide 26

Slide 27

Slide 28

Slide 29

Slide 30

Slide 31

Slide 32

Slide 33

Slide 34

Slide 35

Slide 36

Slide 37

Slide 38

Slide 39

Slide 40

Slide 41

Slide 42

Slide 43

Slide 44

Slide 45

Slide 46

Slide 47

Slide 48

Slide 49

Slide 50

Slide 51

Slide 52

Slide 53

Slide 54

Slide 55

Slide 56

Slide 57

Slide 58

Slide 59

Slide 60

Slide 61

Slide 62

Slide 63

Slide 64

Slide 65

Slide 66

Slide 67

Slide 68

Slide 69

Slide 70

Slide 71

Slide 72

Slide 73

Slide 74

Slide 75

Slide 76

Slide 77

Slide 78

Slide 79

Slide 80

Slide 81

Slide 82

Slide 83

Slide 84

Slide 85

Slide 86

Slide 87

Slide 88

Slide 89

Slide 90

Slide 91

Slide 92

Slide 93

Slide 94

Slide 95

Slide 96

Slide 97

Slide 98

Slide 99

Slide 100

Slide 101

Slide 102