The disease is located in the class of pathologies of the circulatory system, and the CHF code according to ICD 10 is as follows: I50. This section is divided into several varieties, which indicate the forms of heart failure.

The following options for encoding the diagnosis according to the ICD are distinguished:

• I0 – congestive CHF. Another name for the pathological process is right ventricular failure. It is accompanied by stagnation of blood in the systemic circulation, as evidenced by swelling in the lower extremities.
• I1 – left ventricular failure of the heart. The disease is also called cardiac asthma, as it leads to disturbances in the pulmonary circulation. This also includes acute pulmonary edema, which is formed due to pulmonary hypertension.
• I9 – unspecified CHF. A mixed type of pathology, which occurs most often, since the processes in the pulmonary and systemic circulation are closely related.

Sometimes chronic heart failure in ICD 10 has a code that belongs to a different category. For example, the occurrence of CHF due to pathologies of the kidneys, lungs, hypertension, in the neonatal period and in people with cardiac prostheses. CHF in women due to ectopic pregnancy or abortion is separately coded.

General information about the disease

In cardiology, CHF is, rather, not a separate disease, but a complication of existing pathological processes.

Failure develops due to a long-term decompensated state, most often due to heart disease.

The problem is that patients with cardiovascular pathology tend to ignore the symptoms of their disease for a long time and reject medical help. The problem cannot be neglected, since the progression of the pathological process will result in acute cardiovascular failure. This condition has two forms: unstable angina and myocardial infarction.

CHF is confirmed not only by a nonspecific clinical picture, which may indicate dozens of other diseases, but also by instrumental research methods.

Cardiac diagnoses usually have a long formulation, as they require clarification of the severity of the process, etiological factors and concomitant diseases related to the circulatory system.

When registering chronic failure, the degree of development of the process is specified. In ICD 10, CHF does not require additional divisions, but in the clinical practice of a cardiologist one cannot do without them. The severity of the process depends on the dosage of drugs, lifestyle recommendations and future prognosis.

After establishing this diagnosis, the main task of the medical personnel is to maintain the body at the same level, since the problem cannot be completely cured, as well as to eliminate the risks for the development of acute insufficiency of coronary blood supply.

Chronic systolic heart failure is a clinical syndrome that complicates the course of a number of diseases and is characterized by the presence of shortness of breath during exercise (and then at rest), fatigue, peripheral edema and objective signs of impaired cardiac function at rest (for example, auscultatory signs, EchoCG data) .

Code according to the international classification of diseases ICD-10:

• I50 Heart failure

Statistics. Chronic systolic heart failure occurs in 0.4–2% of the population. Its prevalence increases with age: in people over 75 years of age it develops in 10% of cases.

Reasons

Etiology Heart failure with low cardiac output Myocardial damage: IHD (post-infarction cardiosclerosis, chronic myocardial ischemia) Cardiomyopathies Myocarditis Toxic effects (for example, alcohol, doxorubicin) Infiltrative diseases (sarcoidosis, amyloidosis) Endocrine diseases Nutritional disorders (vitamin B1 deficiency) Myocardial overload Arterial hypertension Rheumatic heart defects Congenital heart defects (for example, aortic stenosis) Arrhythmias Supraventricular and ventricular tachycardias Atrial fibrillation Heart failure with high cardiac output Anemia Sepsis Arteriovenous fistula.

Risk factors Refusal of the patient from pharmacotherapy Prescription of drugs with a negative inotropic effect, and their uncontrolled use Thyrotoxicosis, pregnancy and other conditions associated with increased metabolic needs Excess body weight Presence of chronic pathology of the heart and blood vessels (arterial hypertension, coronary artery disease, heart defects, etc.) .

Pathogenesis The pumping function of the heart is impaired, which leads to a decrease in cardiac output. As a result of a decrease in cardiac output, hypoperfusion of many organs and tissues occurs. A decrease in cardiac perfusion leads to activation of the sympathetic nervous system and an increase in heart rate. A decrease in kidney perfusion causes stimulation of the renin-angiotensin system. The production of renin increases, while excessive production of angiotensin II occurs, leading to vasoconstriction, water retention (edema, thirst, increased blood volume) and a subsequent increase in preload on the heart. A decrease in the perfusion of peripheral muscles causes the accumulation of under-oxidized metabolic products in them, and hypoxia leads to severe fatigue.

CLASSIFICATIONS

Classification of the XII All-Union Congress of Therapists in 1935 (N.D. Strazhesko, V.Kh. Vasilenko).

Stage I (initial) - latent heart failure, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).

Stage II (severe) - prolonged circulatory failure, hemodynamic disturbances (stagnation in the systemic and pulmonary circulation), dysfunction of organs and metabolism are also expressed at rest. Period A - the beginning of a long stage, characterized by mild hemodynamic disturbances, dysfunction of the heart or only their parts Period B is the end of a long stage, characterized by profound hemodynamic disturbances, the entire cardiovascular system is involved in the process.

Stage III (final, dystrophic) - severe hemodynamic disorders, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs.

Classification of the New York Heart Association (1964) Class I - ordinary physical activity does not cause significant fatigue, shortness of breath or palpitations Class II - mild limitation of physical activity: satisfactory health at rest, but ordinary physical activity causes fatigue, palpitations, shortness of breath or pain Class III - pronounced limitation of physical activity: satisfactory health at rest, but less than usual load leads to the appearance of symptoms Class IV - inability to perform any physical activity without deteriorating well-being: symptoms of heart failure are present even at rest and intensify with any physical activity.

The classification of the Society of Heart Failure Specialists (OSSN, 2002) was adopted at the All-Russian Congress of Cardiologists in October 2002. The convenience of this classification is that it not only reflects the state of the process, but also its dynamics. The diagnosis must reflect both the stage of chronic heart failure and its functional class. It is necessary to take into account that the correspondence between the stage and the functional class is not entirely clear - the functional class is set in the presence of slightly less pronounced manifestations than is necessary to assign the corresponding stage of heart failure.

Stages of chronic heart failure (may worsen despite treatment) Stage I - the initial stage of heart disease (damage). Hemodynamics are not affected. Latent heart failure Asymptomatic left ventricular dysfunction stage IIA - 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 stage IIB - severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels Stage III is the final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes target organs (heart, lungs, blood vessels, brain, kidneys). Final stage organ remodeling.

Functional classes of chronic heart failure (can change during treatment in both directions) FC I - 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 workload, but it may be accompanied by shortness of breath and/or delayed recovery FC II - slight limitation of physical activity: no symptoms at rest, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations FC III - noticeable limitation of physical activity: no symptoms at rest , physical activity of lesser intensity compared to usual exercise is accompanied by the appearance of FC IV symptoms - the inability to perform any physical activity without the appearance of discomfort; Symptoms of heart failure are present at rest and worsen with minimal physical activity.

Symptoms (signs)

Clinical manifestations

Complaints - shortness of breath, attacks of suffocation, weakness, fatigue Shortness of breath in initial stage heart failure occurs during physical activity, and with severe heart failure - at rest. It appears as a result of increased pressure in the pulmonary capillaries and veins. This reduces the extensibility of the lungs and increases the work of the respiratory muscles. Severe heart failure is characterized by orthopnea - a forced sitting position taken by the patient to facilitate breathing with severe shortness of breath. The deterioration of well-being in the supine position is due to the deposition of fluid in the pulmonary capillaries, leading to an increase in hydrostatic pressure. In addition, in the lying position, the diaphragm rises, which makes breathing somewhat difficult. Chronic heart failure is characterized by paroxysmal nocturnal shortness of breath (cardiac asthma), caused by the occurrence of interstitial pulmonary edema. At night, during sleep, an attack of severe shortness of breath develops, accompanied by coughing and the appearance of wheezing in the lungs. As heart failure progresses, alveolar pulmonary edema may occur. Rapid fatigue in patients with heart failure appears due to insufficient oxygen supply to skeletal muscles. Patients with chronic heart failure may experience nausea, decreased appetite, abdominal pain, abdominal enlargement (ascites) due to stagnation of blood in the liver and system portal vein From the side of the heart, pathological III and IV heart sounds can be heard. Moist rales are detected in the lungs. Hydrothorax is characteristic, often right-sided, resulting from an increase in pleural capillary pressure and extravasation of fluid into the pleural cavity.

Clinical manifestations of heart failure significantly depend on its stage. Stage I - signs (fatigue, shortness of breath and palpitations) appear during normal physical activity, there are no manifestations of heart failure at rest. Stage IIA - there are unexpressed hemodynamic disturbances. Clinical manifestations depend on which parts of the heart are predominantly affected (right or left). Left ventricular failure is characterized by stagnation in the pulmonary circulation, manifested by typical inspiratory shortness of breath with moderate physical exertion, attacks of paroxysmal nocturnal shortness of breath, and rapid fatigue. Swelling and enlargement of the liver are uncharacteristic. Right ventricular failure is characterized by the formation of congestion in the systemic circulation. Patients are concerned about pain and heaviness in the right hypochondrium, decreased diuresis. The liver is characterized by enlargement (the surface is smooth, the edge is rounded, palpation is painful). A distinctive feature of stage IIA heart failure is considered to be complete compensation of the condition during treatment, i.e. reversibility of manifestations of heart failure as a result of adequate treatment Stage IIB - there are profound hemodynamic disturbances, the entire circulatory system is involved in the process. Shortness of breath occurs with the slightest physical exertion. Patients are bothered by a feeling of heaviness in the right hypochondrium, general weakness, sleep disturbance. Orthopnea, edema, ascites are characteristic (a consequence of increased pressure in the hepatic veins and peritoneal veins - transudation occurs and fluid accumulates in the abdominal cavity), hydrothorax, hydropericardium Stage III - the final dystrophic stage with deep irreversible metabolic disorders. As a rule, the condition of patients at this stage is severe. Shortness of breath is pronounced even at rest. Characterized by massive edema, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium, edema of the genital organs). At this stage, cachexia occurs.

Diagnostics

Instrumental data

ECG. You can identify signs of blockade of the left or right branch of the His bundle, ventricular or atrial hypertrophy, pathological Q waves (as a sign of a previous MI), arrhythmias. A normal ECG casts doubt on the diagnosis of chronic heart failure.

EchoCG allows you to clarify the etiology of chronic heart failure and assess the functions of the heart, the degree of their impairment (in particular, determine the ejection fraction of the left ventricle). Typical manifestations of heart failure are expansion of the cavity of the left ventricle (as it progresses, expansion of other chambers of the heart), an increase in the end-systolic and end-diastolic dimensions of the left ventricle, and a decrease in its ejection fraction.

X-ray examination It is possible to detect venous hypertension in the form of a redistribution of blood flow in favor of the upper parts of the lungs and an increase in the diameter of blood vessels. When congestion in the lungs, signs of interstitial edema are revealed (Kerley lines in the costophrenic sinuses) or signs of pulmonary edema. Hydrothorax is detected (usually right-sided). Cardiomegaly is diagnosed with magnification. the transverse size of the heart is more than 15.5 cm in men and more than 14.5 cm in women (or with a cardiothoracic index of more than 50%).

Catheterization of the cardiac cavities reveals an increase in pulmonary capillary wedge pressure of more than 18 mm Hg.

Diagnostic criteria - Framingham criteria for the diagnosis of chronic heart failure, divided into major and minor Major criteria: paroxysmal nocturnal dyspnea (cardiac asthma) or orthopnea, swelling of the jugular veins, wheezing in the lungs, cardiomegaly, pulmonary edema, pathological III heart sound, increased central venous pressure (more than 160 mm water column), blood flow time more than 25 s, positive “hepatojugular reflux” Minor criteria: swelling in the legs, night cough, shortness of breath on exertion, liver enlargement, hydrothorax, tachycardia more than 120 per minute, decrease in vital capacity by 1/3 from maximum To confirm the diagnosis of chronic heart failure, either 1 major or 2 minor criteria are required. The symptoms detected must be related to heart disease.

Differential diagnosis Nephrotic syndrome- a history of edema, proteinuria, renal pathology Cirrhosis of the liver Occlusive lesions of the veins with subsequent development of peripheral edema.

Treatment It is necessary to first assess the possibility of influencing the cause of the deficiency. In some cases, an effective etiological intervention (for example, surgical correction of heart disease, myocardial revascularization in ischemic heart disease) can significantly reduce the severity of manifestations of chronic heart failure. In the treatment of chronic heart failure, non-drug and medicinal methods therapy. It should be noted that both types of treatment should complement each other.

Non-drug treatment Limiting the consumption of table salt to 5–6 g/day, fluids (up to 1–1.5 l/day) Optimizing physical activity Moderate physical activity is possible and even necessary (walking for at least 20–30 minutes 3–5 r/ weeks) Complete physical rest should be observed if the condition worsens (at rest the heart rate decreases and the work of the heart decreases).

Treatment

Drug therapy. The ultimate goal of treatment of chronic heart failure is to improve the quality of life and increase its duration.

Diuretics. When prescribing them, it is necessary to take into account that the occurrence of edema in heart failure is associated with several reasons (constriction of the renal vessels, increased secretion of aldosterone, increased venous pressure. Treatment with diuretics alone is considered insufficient. In chronic heart failure, loop (furosemide) or thiazide (for example, hydrochlorothiazide) diuretics. In case of insufficient diuretic response, loop diuretics and thiazides are combined. Thiazide diuretics are usually used in a dose of 25 to 100 mg/day. It should be remembered that when the renal GFR is less than 30 ml/min, it is not advisable to use thiazides. Loop diuretics begin to act faster; their diuretic effect is more pronounced, but less durable than that of thiazide diuretics. Furosemide is used at a dose of 20–200 mg/day intravenously, depending on the manifestations of edema syndrome and diuresis. It can be prescribed orally at a dose of 40–100 mg/day. .

ACE inhibitors cause hemodynamic unloading of the myocardium due to vasodilation, increased diuresis, and decreased filling pressure of the left and right ventricles. Indications for prescribing ACE inhibitors are clinical signs of heart failure, a decrease in left ventricular ejection fraction of less than 40%. When prescribing ACE inhibitors, certain conditions must be observed according to the recommendations of the European Society of Cardiology (2001): It is necessary to stop taking diuretics 24 hours before taking ACE inhibitors. Blood pressure should be monitored before and after taking ACE inhibitors. Treatment begins with small doses and is gradually increased. It is necessary to monitor renal function. (diuresis, relative density of urine) and the concentration of blood electrolytes (potassium, sodium ions) with increasing doses every 3–5 days, then every 3 and 6 months Co-administration of potassium-sparing diuretics should be avoided (they can only be prescribed for hypokalemia) Combined use should be avoided NSAIDs.

The first positive data have been obtained on the beneficial effect of angiotensin II receptor blockers (in particular, losartan) on the course of chronic heart failure as an alternative to ACE inhibitors in cases of intolerance or contraindications to their use.

Cardiac glycosides have a positive inotropic (increase and shorten systole), negative chronotropic (decreasing heart rate), negative dromotropic (slowing AV conduction) effect. The optimal maintenance dose of digoxin is considered to be 0.25–0.375 mg/day (in elderly patients 0.125–0.25 mg/day); The therapeutic concentration of digoxin in blood serum is 0.5–1.5 mg/l. Indications for the use of cardiac glycosides are tachysystolic atrial fibrillation and sinus tachycardia.

B - Adrenergic blockers The mechanism of beneficial action of  - adrenergic blockers in chronic heart failure is due to the following factors: Direct protection of the myocardium from the adverse effects of catecholamines Protection from catecholamine-induced hypokalemia Improvement of blood flow in the coronary arteries due to a decrease in heart rate and improved diastolic relaxation of the myocardium Reduction of the effect of vasoconstrictor systems (for example, due to a decrease in renin secretion) Potentiation of the vasodilating kallikrein - kinin system Increasing the contribution of the left atrium to the filling of the left ventricle due to improved relaxation of the latter Currently, carvedilol - b1 - and a1 - adrenergic blocker with vasodilating properties is recommended for use among b - adrenergic blockers for the treatment of chronic heart failure. The initial dose of carvedilol is 3.125 mg 2 times / day, followed by an increase in the dose to 6.25 mg, 12.5 mg or 25 mg 2 times / day in the absence of side effect in the form of arterial hypotension, bradycardia, decreased left ventricular ejection fraction (according to echocardiography) and other negative manifestations of the action of beta-blockers. Metoprolol is also recommended, starting with a dose of 12.5 mg 2 times / day, bisoprolol 1.25 mg 1 time / day under the control of ventricular ejection fractions with a gradual increase in dose after 1-2 weeks.

Spironolactone. It has been established that the administration of the aldosterone antagonist spironolactone at a dose of 25 mg 1–2 times a day (in the absence of contraindications) helps to increase the life expectancy of patients with heart failure.

Peripheral vasodilators are prescribed for chronic heart failure if there are contraindications or if ACE inhibitors are poorly tolerated. Of the peripheral vasodilators, hydralazine is used at a dose of up to 300 mg/day, isosorbide dinitrate at a dose of up to 160 mg/day.

Other cardiotonic drugs. b - Adrenergic agonists (dobutamine), phosphodiesterase inhibitors are usually prescribed for 1–2 weeks in the final stage of heart failure or in case of a sharp deterioration in the condition of patients.

Anticoagulants. Patients with chronic heart failure are at high risk of thromboembolic complications. Both pulmonary embolism due to venous thrombosis and thromboembolism of vessels in the systemic circulation caused by intracardiac thrombi or atrial fibrillation are possible. The administration of indirect anticoagulants to patients with chronic heart failure is recommended in the presence of atrial fibrillation and a history of thrombosis.

Antiarrhythmic drugs. If there are indications for the prescription of antiarrhythmic drugs (atrial fibrillation, ventricular tachycardia), it is recommended to use amiodarone at a dose of 100–200 mg/day. This drug has minimal negative inotropic effects, whereas most other drugs in this class reduce left ventricular ejection fraction. In addition, antiarrhythmic drugs themselves can provoke arrhythmias (proarrhythmic effect).

Surgical treatment

The choice of the optimal method of surgical treatment depends on the cause leading to heart failure. Thus, in case of ischemic heart disease, in many cases, myocardial revascularization is feasible, in case of idiopathic subaortic hypertrophic stenosis - septal myectomy, in case of valvular defects - prosthetics or reconstructive interventions on the valves, in case of bradyarrhythmias - pacemaker implantation, etc.

In case of heart failure refractoriness to adequate therapy, the main surgical treatment method is heart transplantation.

Methods of mechanical circulatory support (implantation of assisters, artificial ventricles and biomechanical pumps), previously proposed as temporary options before transplantation, have now acquired the status of independent interventions, the results of which are comparable to the results of transplantation.

To prevent the progression of cardiac dilatation, devices are implanted in the form of a mesh that prevents excessive expansion of the heart.

In case of cor pulmonale that is tolerant to treatment, transplantation of the heart-lung complex seems to be a more appropriate intervention.

Forecast. In general, the 3-year survival rate of patients with chronic systolic heart failure is 50%. The mortality rate from chronic systolic heart failure is 19% per year.

Factors whose presence correlates with a poor prognosis in patients with heart failure Reduced left ventricular ejection fraction by less than 25% Inability to climb one floor and move at a normal pace for more than 3 minutes Decrease in the content of sodium ions in the blood plasma less than 133 mEq/l Decrease in the concentration of potassium ions in the plasma blood less than 3 mEq/l Increased norepinephrine content in the blood Frequent ventricular extrasystole with daily monitoring ECG.

The risk of sudden cardiac death in patients with heart failure is 5 times higher than in the general population. Most patients with chronic heart failure die suddenly, mainly from ventricular fibrillation. Prophylactic administration of antiarrhythmic drugs does not prevent this complication.

ICD-10 I50 Heart failure

Medicines and Medicines are used for the treatment and/or prevention of chronic systolic heart failure.

Pharmacological group(s) of the drug.

Family doctor. Therapist (volume 2). Chronic renal failure ICD 10

Chronic renal failure

General information

There are various definitions chronic renal failure(CRF), however, the essence of any of them comes down to the development of a characteristic clinical and laboratory complex that arose as a result of the progressive loss of all renal functions.

Chronic renal failure (CRF) is the loss of homeostatic renal function due to renal disease for more than 3 months: decreased glomerular filtration and relative density (osmolarity), increased concentrations of creatinine, urea, potassium, phosphorus, magnesium and aluminum in blood serum, decreased blood calcium, acid-base imbalance (metabolic acidosis), development of anemia and arterial hypertension.

Epidemiology

The problem of chronic renal failure has been actively developed for several decades, due to the significant prevalence of this complication. Thus, according to the literature, the number of patients with chronic renal failure in Europe, the USA and Japan ranges from 157 to 443 per 1 million population. The prevalence of this pathology in our country is 212 per 1 million population among patients over 15 years of age. Among the causes of mortality, chronic renal failure ranks eleventh.

Etiology

CRF is based on a single morphological equivalent - nephrosclerosis. There is no form of kidney pathology that could not potentially lead to the development of nephrosclerosis, and, consequently, renal failure. Thus, chronic renal failure is the outcome of any chronic kidney disease.

CRF can be caused by primary kidney diseases, as well as secondary kidney damage as a result of long-term chronic disease of organs and systems. Direct damage to the parenchyma (primary or secondary), leading to chronic renal failure, is conventionally divided into diseases with predominant damage to the glomerular apparatus or tubular system, or a combination of both. Among glomerular nephropathies, the most common are chronic glomerulonephritis, diabetic nephropathy, amyloidosis, and lupus nephritis. More rare causes of chronic renal failure with damage to the glomerular apparatus are malaria, gout, prolonged septic endocarditis, and myeloma. Primary damage to the tubular system is most often observed in most urological diseases accompanied by impaired urine outflow, congenital and acquired tubulopathies (renal diabetes insipidus, Albright's tubular acidosis, Fanconi syndrome, which occurs as an independent hereditary disease or accompanies various diseases), poisoning with drugs and toxic substances. Vascular diseases can lead to secondary damage to the renal parenchyma - damage to the renal arteries, essential hypertension (primary nephroangiosclerosis), malformations of the kidneys and urinary tract (polycystic disease, renal hypoplasia, neuromuscular dysplasia of the ureters, etc.). Chronic isolated damage to any part of the nephron is actually the trigger for the development of chronic renal failure, however, in clinical practice, late stages of chronic renal failure are characterized by dysfunction of both the glomerular and tubular apparatus.

Pathogenesis

Regardless of the etiological factor, the mechanism of development of chronic renal failure is based on a decrease in the number of active nephrons, a significant decrease in the glomerular filtration rate in an individual nephron, and a combination of these indicators. Complex mechanisms Kidney damage includes many factors (impaired metabolic and biochemical processes, blood clotting, impaired urine passage, infection, abnormal immune processes), which, when interacting with other diseases, can lead to chronic renal failure. In the development of chronic renal failure the most important point is a slow, hidden impairment of all renal functions, of which the patient is usually unaware. However, modern examination methods make it possible to identify the hidden stage, since the changes that occur in the body when the functional capacity of the kidneys is impaired are now well known. This is what it is important task clinician, which allows him to take preventive and therapeutic measures aimed at preventing premature development end-stage renal failure. The kidneys have significant reserve capabilities, as evidenced by the preservation and maintenance of the life of the body with the loss of 90% of nephrons. The adaptation process is carried out by strengthening the function of the remaining nephrons and restructuring the entire organism. With the progressive death of nephrons, the glomerular filtration rate decreases, the water-electrolyte balance is disturbed, and metabolic products, organic acids, phenolic compounds, some peptides and other substances are retained in the body, which determine the clinical picture of chronic renal failure and the patient's condition. Thus, disruption of the excretory and secretory functions of the kidneys contributes to the development of pathological changes in the body, the severity of which depends on the intensity of nephron death and determines the progression of renal failure. With chronic renal failure, one of the most important functions of the kidneys is disrupted - maintaining water-salt balance. Already in the early stages of chronic renal failure, especially caused by diseases with predominant damage to the tubular apparatus, there is a violation of the concentrating ability of the kidneys, which is manifested by polyuria, nocturia, a decrease in urine osmolarity to the level of the osmotic concentration of blood plasma (isosthenuria) and with advanced damage - hyposthenuria (osmotic concentration of urine below the osmotic concentration of blood plasma). Polyuria, which is persistent even with fluid restriction, may be due to both a direct decrease in tubular function and a change in osmotic diuresis. Important function kidneys is to maintain electrolyte balance, especially ions such as sodium, potassium, calcium, phosphorus, etc. With chronic renal failure, sodium excretion in the urine can be increased or decreased. In a healthy person, 99% of the sodium filtered through the glomeruli is reabsorbed in the tubules. Diseases with predominant damage to the tubular-interstitial system lead to a decrease in its reabsorption by up to 80%, and, consequently, an increased excretion. Increased sodium excretion in urine does not depend on its introduction into the body, which is especially dangerous when recommended in similar situations the patient restricts salt intake. However, predominant damage to the glomeruli, a decrease in the glomerular filtration rate, especially with preserved tubular function, can lead to sodium retention, which entails the accumulation of fluid in the body and increased blood pressure. Up to 95% of potassium introduced into the body is removed by the kidneys, which is achieved by its secretion in the distal tubules. In chronic renal failure, the regulation of potassium balance in the body is carried out through its excretion by the intestines. Thus, when GFR decreases to 5 ml/min, about 50% of incoming potassium is excreted in the feces. An increase in potassium in plasma can be observed in the oligoanuric phase of chronic renal failure, as well as during exacerbation of the underlying disease, with increased catabolism. Since the main amount of potassium in the body is in the intracellular space (in plasma - about 5 mmol/l, in intracellular fluid - about 150 mmol/l), in some situations (febrile state, surgery, etc.) against the background of chronic renal failure may occur hyperkalemia, which threatens the patient's life. The state of hypokalemia in patients with chronic renal failure is observed much less frequently and may indicate a deficiency of total potassium in the body and a sharp impairment of the secretory ability of the distal tubules. Disturbances in the functions of the glomerular and tubular apparatus already in the early stages of chronic renal failure lead to hyperchloremic acidosis, hyperphosphatemia, a moderate increase in magnesium in the blood serum and hypocalcemia.

Increased blood concentrations of urea, amino nitrogen, creatinine, uric acid, methylguanidine, phosphates, etc. An increase in amino nitrogen levels may be associated with increased protein catabolism due to its excess intake or its sharp limitation during fasting.

Urea is the end product of protein metabolism and is formed in the liver from the nitrogen of deaminated amino acids. In conditions of renal failure, there is not only a difficulty in its secretion, but also, for reasons still unknown, an increase in its production by the liver.

Creatinine is formed in the muscles of the body from its precursor creatinine. The content of creatinine in the blood is quite stable; an increase in creatinemia in parallel with an increase in the level of urea in the blood occurs, as a rule, when glomerular filtration decreases to 20-30% of the normal level.

Excessive production of parathyroid hormone has attracted even more attention as a possible major toxin in uremia. This is confirmed by the effectiveness of at least partial parathyroidectomy. More and more facts are emerging indicating the toxicity of substances of unknown nature, the relative molecular weight of which is 100-2000, as a result of which they are called “medium molecules”. They accumulate in the blood serum of patients with chronic renal failure. However, it is becoming increasingly clear that azotemia (uremia) syndrome is not caused by one or more toxins, but depends on the restructuring of cells of all tissues and changes in transmembrane potential. This occurs as a result of disturbances in both kidney function and the systems that regulate their activity.

Its causes are blood loss, shortened life span of red blood cells due to protein and iron deficiency in the body, toxic effects of nitrogen metabolism products, hemolysis (glucose-6-phosphate dehydrogenase deficiency, excess guanidine), low erythropoietin. The growth of medium molecules also inhibits erythropoiesis.

Osteodystrophy

Osteodystrophy caused by impaired metabolism of calciferol. In the kidneys, the active metabolite 1,25-dehydroxycalciferol is formed, which affects calcium transport by regulating the synthesis of specific proteins that bind it. In chronic renal failure, the transfer of calciferol into metabolically active forms is blocked. The water-electrolyte balance remains close to physiological for a long time, right up to the terminal phase. In conditions of impaired ion transport in the tubules, with tubular defects, the loss of sodium increases, which, if its replenishment is insufficient, leads to the syndrome of hyponatremia. Hyperkalemia is regarded as the second most important sign of chronic renal failure. This is due not only to increasing catabolism, characteristic of renal failure, but also to increased acidosis, and most importantly, to changes in the distribution of potassium outside and inside cells.

Changes in the CBS occur due to a violation of the “carbonic acid – bicarbonate” function. With various variants of renal dysfunction, depending on the nature of the process, one or another type of impairment of CBS may be observed. With glomerular, the possibility of acidic valencies entering the urine is limited; with tubular, ammonia acidogenesis is preferentially activated.

Arterial hypertension

In its occurrence, there is no doubt the role of inhibition of the production of vasodilators (kinins). The imbalance of vasoconstrictors and vasodilators in chronic renal failure is caused by the kidney's loss of the ability to control sodium levels in the body and the volume of circulating blood. In the terminal phase of chronic renal failure, a persistent hypertensive reaction can be adaptive, maintaining filtration pressure. In these cases sharp decline blood pressure can be fatal.

According to ICD-10, chronic renal failure is classified as follows:

N18 Chronic renal failure.

N18.0 – End-stage kidney damage.

N18.8 – Other chronic renal failure.

N18.9 – Chronic renal failure not specified.

N19 – Renal failure not specified.

Diagnostics

Diagnosis of chronic renal failure with known renal disease is not difficult. Its degree, and, consequently, severity, is determined by an increase in the concentration of creatinine in the blood serum and a decrease in GFR. As should be clear from what was stated earlier, it is very important to monitor the state of electrolyte and acid-base metabolism and promptly register disturbances in the activity of the heart and lungs.

Diagnosis of chronic renal failure is mainly laboratory. The first symptom is a decrease in the relative density of urine to 1.004-1.011, regardless of the amount of diuresis. It must be borne in mind that the presence of sugar and protein in the urine can increase the relative density of urine (every 1% sugar - by 0.004 and 3 g/l - by 0.01).

A study of electrolyte balance to determine the level of decline in renal function is not very informative. The same can be said with regard to the degree of anemia, and, even more so, the level of blood pressure.

Accurate assessment of kidney function, taking into account the condition of other organs, the degree of dystrophic processes in the body when deciding on the prospects for a kidney transplant.

In general therapeutic practice, one may encounter creatininemia without a specific renal disease. This is observed in congestive heart failure. Usually creatininemia does not exceed 0.6-0.8 mmol/l. A more significant increase can be observed with rapidly increasing decompensation of cardiac activity, for example, in patients with complicated myocardial infarction. A feature of such creatininemia is the unusual preservation of quite high density urine. Renal failure occurs when the “renal quota” of cardiac output decreases to 7.8%. The deterioration of renal hemodynamics is associated with an increase in venous pressure, and the decrease in renal blood flow outpaces the reduction in glomerular filtration, so that the filtration fraction is usually increased. Deterioration of renal hemodynamics is accompanied by redistribution of renal blood flow. The outer part of the cortex suffers the most. Saving increased density urine is associated with a slowdown in blood flow, especially in the medulla.

Thus, “chronic” creatinemia, unusual for extrarenal causes, without the development of diffuse nephrosclerosis, not accompanied by its usual isosthenuria, has a certain diagnostic and prognostic significance for cardiac patients. This type of renal failure does not require special treatment. Another feature of decreased renal function in congestive heart failure is the appearance and increase of proteinuria. As a rule, blood plasma proteins are released, but the culprit is impaired tubular reabsorption of protein. The histopathological picture of such a congested kidney reveals varicose veins. The glomeruli are enlarged in size, the capillary loops are wide and contain red blood cells. The stroma of the kidney is swollen, the tubules are somewhat dilated, their epithelium is in a state of dystrophy, many tubules show signs of atrophy. Focal interstitial fibrosis and arteriosclerosis.

Clinical criteria

Main manifestations:

Symptoms of endogenous intoxication;

Oliguria;

Nausea;

Macrohematuria or microhematuria;

Urinary problems;

Itchy skin;

Bleeding.

Already the first communication with the patient and clarification of such data from the anamnesis as the duration of the nephrological disease, the presence or absence of chronic glomerulo- or pyelonephritis, arterial hypertension, the duration of these diseases, the frequency of exacerbations of glomerulo- or pyelonephritis, the amount of urine excreted per day, as well as the identification of early symptoms of chronic renal failure, allow one to suspect renal failure and outline a plan for diagnostic and therapeutic measures.

An indication in the anamnesis of the duration of a nephrological disease of more than 5-10 years gives grounds to suspect the presence of renal failure and perform all diagnostic studies, confirming or rejecting this diagnosis. Analysis of studies showed that total impairment of renal function and identification of the stage of chronic renal failure are possible with the use of traditional methods urine and blood tests.

Asthenic syndrome: weakness, fatigue, drowsiness, decreased hearing, taste.

Dystrophic syndrome: dry and painful itching of the skin, traces of scratching on the skin, weight loss, possible real cachexia, muscle atrophy.

Gastrointestinal syndrome: dry, bitter and unpleasant metallic taste in the mouth, lack of appetite, heaviness and pain in the epigastric region after eating, often diarrhea, possible increase in the acidity of gastric juice (due to reduced destruction of gastrin in the kidneys), in late stages There may be gastrointestinal bleeding, stomatitis, mumps, enterocolitis, pancreatitis, liver dysfunction.

Cardiovascular syndrome: shortness of breath, pain in the heart, arterial hypertension, left ventricular myocardial hypertrophy, in severe cases - attacks of cardiac asthma, pulmonary edema; with advanced chronic renal failure - dry or exudative pericarditis, pulmonary edema.

Anemic-hemorrhagic syndrome: pale skin, nasal, intestinal, stomach bleeding, skin hemorrhages, anemia.

Osteoarticular syndrome: pain in the bones, joints, spine (due to osteoporosis and hyperuricemia).

Damage to the nervous system: uremic encephalopathy (headache, memory loss, psychosis with obsessive fears, hallucinations, convulsive attacks), polyneuropathy (paresthesia, itching, burning sensation and weakness in the arms and legs, decreased reflexes).

Urinary syndrome: isohyposthenuria, proteinuria, cylindruria, microhematuria.

Early clinical signs of chronic renal failure are polyuria and nocturia, hypoplastic anemia; then general symptoms appear - weakness, drowsiness, fatigue, apathy, muscle weakness. Subsequently, with the retention of nitrogenous wastes, skin itching (sometimes painful), nasal, gastrointestinal, uterine bleeding, subcutaneous hemorrhages; “uremic gout” may develop with joint pain and tophi. Uremia is characterized by dyspeptic syndrome - nausea, vomiting, hiccups, loss of appetite, even aversion to food, diarrhea. The skin is pale yellowish in color (a combination of anemia and urochrome retention). Skin – dry, with scratch marks, bruises on arms and legs; tongue – dry, brown. As chronic renal failure progresses, the symptoms of uremia increase. Sodium retention leads to hypertension, often with malignant features and retinopathy. Hypertension, anemia and electrolyte imbalances cause heart damage. In the terminal stage, fibrinous or effusion pericarditis develops, indicating an unfavorable prognosis. As uremia progresses, neurological symptoms increase, convulsive twitching appears, encephalopathy intensifies, up to the development of uremic coma, with strong noisy acidotic breathing (Kussmaul breathing). Patients are prone to infections; Pneumonia is common.

Laboratory criteria

Clinical urine analysis - proteinuria, hypoisosthenuria, cylindruria, possible abacterial leukocyturia, hematuria.

Blood test:

clinical – anemia, increased erythrocyte sedimentation rate (ESR), possible moderate leukocytosis, shift of the leukocyte formula to the left, possible thrombocytopenia;

biochemical - increased levels of urea, creatinine, residual nitrogen in the blood, increased total lipids, B-lipoproteins, hyperkalemia, hypocoagulation, hypocalcemia, hyperphosphatemia, possible hypodysproteinemia, hypercholesterolemia.

Laboratory diagnostics

Clinical blood test, with platelet determination;

Biochemical blood test, with determination of the level of creatinine, urea, cholesterol, protein profile, electrolytes (potassium, calcium, phosphorus, sodium, chlorine);

Determination of daily protein excretion;

Determination of the functional state of the kidneys (glomerular filtration rate);

Acid-base state;

ALT, AST;

X-ray examination of the kidneys, bones, lungs.

Additional laboratory and instrumental studies

Ferritin;

Percentage (%) transferrin saturation;

Determination of parathyroid hormone;

Determination of calcium excretion in urine;

Determination of blood amylase;

Protein-sedimentary samples;

Determination of fibrin degradation products in blood serum;

Radionuclide studies (indirect renoangiography, dynamic and static renoscintigraphy);

Needle biopsy of the kidney;

Functional studies of the bladder;

Echoencephalogram;

Echocardiography with assessment of the functional state of the heart, Dopplerography of blood vessels.

Differential diagnosis

Diagnosis of chronic renal failure does not pose any particular difficulties for clinicians due to the characteristic clinical picture and laboratory changes in the blood and urine. The only thing you should always remember: such a clinic may be caused by an exacerbation of chronic renal failure as a result of an occlusive factor and the development of an acute inflammatory process in the upper or lower urinary tract. In these conditions, the true stage of chronic renal failure can be established only after restoration of urine passage and elimination of the acute inflammatory process. For nephrologists, it is important to diagnose the early and pre-dialysis stages of chronic renal failure, which makes it possible to outline treatment tactics and determine the prognosis of nephrological disease.

Detection of chronic renal failure, as a rule, is carried out in parallel with the diagnosis of nephrological disease and includes a history of the disease, clinical manifestations, changes in general blood and urine tests, as well as specific studies aimed at identifying total renal function and methods for assessing morphological and functional kidney parameters.

Specialist consultations

Ophthalmologist: condition of the fundus;

Neurologist: presence of uremic and hypertensive encephalopathy;

Gastroenterologist: presence of complications from the gastrointestinal tract (gastritis, hepatitis, colitis, etc.);

Cardiologist: symptomatic arterial hypertension, hypertensive heart;

Cardiac surgeon: uremic pericarditis (puncture);

Urologist: the presence of stones in the pelvicalyceal part of the kidneys, ureters, etc.

Based on the classification, treatment of chronic renal failure is indicated from a glomerular filtration level of less than 60 ml/min, which corresponds to a creatinine level of 140 µmol/l for men and 105 µmol/l for women (renoprotection is indicated from a GFR level of about 90 ml/min). It is recommended to stabilize blood pressure to target values

Diagnosis and management of complications.

Treatment level

Outpatient: therapist, family doctor, cardiologist, gastroenterologist, etc.; inpatient – ​​indications for inpatient treatment.

Patients with chronic renal failure are subject to dispensary observation by a nephrologist, and in his absence, by a general practitioner at their place of residence.

Dispensary observation should include: examination of patients with stage I chronic renal failure 3 times a year, with stage II chronic renal failure - 6 times a year, and with stage III chronic renal failure - monthly, prescription of an adequate regimen, employment and selection of rational dietary and therapeutic measures; identification and elimination of factors that contribute to the progression of chronic renal failure. If intercurrent diseases occur, patients are examined additionally. Patients with stage IV chronic renal failure should be treated with hemodialysis or peritoneal dialysis, or symptomatic therapy (if there are contraindications for renal replacement therapy (RRT) at the place of residence.

Treatment methods

Basic drug therapy (in accordance with international standards and protocols approved by the Ministry of Health of Ukraine: specifically pharmacological group drugs, dose, course duration) and additional.

Surgical treatment or other types of treatment (indications).

The main goals of dietary treatment for chronic renal failure are to reduce protein intake with food - low protein diet (LPD); control of fluid intake; reducing the consumption of foods that contain Na+, K+, Mg2+, Cl-, phosphates.

Limiting protein intake

A low-protein diet (LPD) helps slow down the progression of chronic renal failure: intraglomerular hypertension and glomerular hypertrophy, proteinuria are reduced, the incidence of secondary hyperparathyroidism is reduced, and the level of nitrogen metabolic products is reduced.

Correction of calcium phosphate disorders

Elevated serum phosphorus levels and the development of secondary hyperparathyroidism (SHPT) not only contribute to the development of osteopathy, but also affect the progression of chronic renal failure. With GFR levels of 40-50 ml/min, the amount of phosphorus in daily ration should not exceed 800-1000 mg. When GFR is below 40 ml/min, in addition to dietary phosphorus restriction to 1 g/day, phosphate binders (PBPs) are prescribed: phosphate binders.

Control of blood pressure (BP) and proteinuria levels

ACE inhibitors (ACEI):

Enalapril – from 5 to 40 mg/day;

Perindopril – from 2 to 8 mg/day;

Quinapril – from 5 to 20 mg/day;

Moexipril – from 3.75 to 15 mg/day;

Ramipril – from 2.5 to 10 mg/day;

Spirapril - from 3 to 6 mg/day.

Angiotensin II receptor blockers (ARBs):

Valsartan – from 80 to 160 mg/day;

Losartan – from 25 to 100 mg/day;

Candesartan – from 8 to 32 mg/day;

Irbesartan – from 150 to 300 mg/day;

Telmisartan – from 40 to 80 mg/day;

Eprosartan – from 400 to 1200 mg/day.

Calcium channel blockers:

Amlodipine – from 5 to 10 mg/day;

Lercanidipine – from 5 to 10 mg/day;

Diltiazem – from 30 to 90 mg/day three times;

Diltiazem retard – from 90 to 300 mg/day twice;

Verapamil - from 40 to 120 mg/day 2 to 3 times a day;

Verapamil retard – from 240 to 480 mg/day.

ACE inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) reduce proteinuria and microalbuminuria more significantly than diuretics, calcium antagonists and b-blockers.

Calcium channel blockers. namely, the nifedipine group (dihydropyridine), effectively reduce blood pressure, but do not affect the level of proteinuria and the progression of chronic renal failure, which is associated with their ability to sharply reduce the tone of the afferent arteriole and increase water hammer at high systemic blood pressure. On the contrary, non-hydropyridine calcium channel blockers (verapamil, diltiazem) have virtually no effect on the mechanism of renal autoregulation, help reduce proteinuria, and inhibit glomerular fibrosis. Achieving target blood pressure in chronic kidney disease occurs when several drugs are prescribed.

Correction of anemia

The saturation of the body with iron is controlled by target minimum indicators serum erythropoietin concentrations greater than 100 ng/ml and transferrin saturation levels > 20%. If necessary, iron supplements are prescribed in a dose of more than 200-300 mg of elemental iron per day. In parallel, other drugs are used that are mandatory in the treatment of anemia:

Folic acid– from 5 to 15 mg/day;

Pyridoxine (vitamin B6) – from 50 to 200 mg/day.

The main type of replacement therapy for erythropoietin deficiency anemia is the administration of erythropoietin:

Eprex – from 20 to 100 U/kg three times a week;

Recormon - from 20 to 100 U/kg three times a week.

Correction of hyperazotemia

In order to reduce the level of azotemia, the toxic load of uremia, drugs are used that enhance their excretion.

Hypoazotemic herbal remedies:

Hofitol - from 2 to 3 tablets three times a day for 15 minutes. before meals or 2 ampoules twice a day intramuscularly or intravenously daily for 14-21 days;

Lespenefril (lespeflan) – from 3 to 6 teaspoons per day or intravenously at the rate of 1 ml/kg of the patient’s weight.

Enterosorption using enterosorbents - 1.5-2 hours before or after meals and medications:

Activated carbon– up to 5 g 3 to 4 times/day;

Spherical carbonite – up to 5 g 3 to 4 times/day;

Enterosgel – 1 tablespoon (15.0 g) 3 to 4 times a day;

Sorbigel – 1 tablespoon (15.0 g) 3 to 4 times/day;

Enterodesis - 5 ml per 1000 ml of water 3 to 4 times a day;

Polyphepan - 1 tablespoon (15.0 g) 2 to 4 times/day or at the rate of 0.5 g/kg body weight/day.

Intestinal dialysis with the introduction into the colon through a probe of 8 to 10 liters of solution, which contains: sucrose - 90 g/l; glucose – 8 g/l, potassium chloride– 0.2 g/l, sodium bicarbonate – 1 g/l, sodium chloride – 1 g/l.

Correction of dyslipidemia

The target level of LDL cholesterol in adults with chronic kidney disease is 1 mmol/l (40 mg/dl); TG

Lovastatin – from 10 to 80 mg/day;

Simvastatin – from 10 to 40 mg/day;

Pravastatin – from 10 to 40 mg/day;

Atorvastatin – from 10 to 40 mg/day;

Fluvastatin – from 10 to 40 mg/day.

Statins block a key enzyme for cholesterol synthesis in the liver and have a pronounced lipid-lowering effect. Desired LDL cholesterol level –

Gemfibrozil – 600 mg twice a day;

Fenofibrate – 200 mg/day.

Fibrates are prescribed when TG levels are > 5.7 mmol/L (500 mg/dL), with dosage adjusted according to renal function. The combination of fibrates and statins is not advisable because there is a high risk of rhabdomyolysis.

Indications for active methods of treatment of chronic renal failure:

Serum creatinine level is above 0.528 mmol/l (in diabetic nephropathy - above 0.353 mmol/l), an arteriovenous fistula is applied, with a further increase in creatinine - “introduction” to hemodialysis;

Pericarditis, neuropathy, encephalopathy, hyperkalemia, high hypertension, impairment of CBS in patients with chronic renal failure.

Today in Ukraine the following active methods of treatment of chronic renal failure are used: chronic hemodialysis in combination with hemosorption and hemofiltration, peritoneal dialysis and kidney transplantation.

The prognosis is poor, improves with the use of replacement therapy renal therapy(RRT) and kidney transplantation.

Prevention

Timely detection and treatment of nephrological diseases leading to the development of chronic renal failure, such as acute glomerulo- and pyelonephritis, diabetic nephropathy.

Chronic heart failure. Definition. Classification. Clinic. Diagnostics. Treatment.

Relevance of the problem

The prevalence of clinically significant chronic heart failure (CHF) in the population is at least 1.5-3.0%. Among people over 65 years of age, the incidence of CHF increases to 6-10%, 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. Over 15 years, the number of hospitalizations with a diagnosis of CHF has tripled, and over 40 years it has increased 6 times. 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 general population. In the United States, there are more than 2.5 million patients with CHF; about 200 thousand patients die annually; the 5-year survival rate after the onset of signs of CHF is 50%.

Chronic heart failure (CHF) is a cardiac-related disorder of (pumping) function with corresponding symptoms, consisting in the inability of the circulatory system to deliver to organs and tissues the amount of blood necessary for their normal functioning. Thus, this is a disproportion between the state of blood circulation and metabolism, which increases with the increase in the activity of life processes; a pathophysiological condition in which impaired cardiac function prevents it from maintaining the level of blood circulation necessary for tissue metabolism.

CHF can develop against the background of almost any disease cardiovascular system, however, the main three are the following nosological forms:

Coronary heart disease (CHD)

And arterial hypertension

With heart defects.

IHD. From the existing classification, acute myocardial infarction (AMI) and ischemic cardiomyopathy (ICMP - a nosological unit introduced into clinical practice by ICD-10) most often lead to the development of CHF. The mechanisms of the onset and progression of CHF due to AMI are caused by changes in the geometry and local contractility of the myocardium, called the term “remodeling of the left ventricle” (LV), with ICMP there is a decrease in the total contractility of the myocardium, called the term “hibernation (sleep) of the myocardium.”

Arterial hypertension. Regardless of the etiology of hypertension, a structural restructuring of the myocardium occurs, which has a specific name - “hypertensive heart”. The mechanism of CHF in this case is due to the development of LV diastolic dysfunction.

Heart defects. To date, Ukraine has been characterized by the development of CHF due to acquired and uncorrected rheumatic defects.

A few words need to be said about dilated cardiomyopathy (DCM) as a cause of CHF. DCM is a rather rare disease of unspecified etiology, which develops at a relatively young age and quickly leads to cardiac decompensation.

Establishing the cause of CHF is necessary to select treatment tactics for each individual patient.

Pathogenetic aspects of heart failure

From the point of view modern theory, the main role in the activation of compensatory mechanisms (tachycardia, Frank-Starling mechanism, constriction of peripheral vessels) is played by hyperactivation of local or tissue neurohormones. This is mainly the sympathetic-adrenal system (SAS) and its effectors - norepinephrine and adrenaline and the renin-angiotensin-aldosterone system (RAAS) and its effectors - angiotensin II (A-II) and aldosterone, as well as the system of natriuretic factors. The problem is that the “triggered” mechanism of hyperactivation of neurohormones is irreversible physiological process. Over time, short-term compensatory activation of tissue neurohormonal systems turns into its opposite - chronic hyperactivation. The latter is accompanied by the development and progression of systolic and diastolic dysfunction of the left ventricle (remodeling).

If the heart is damaged, the stroke volume of the ventricle will decrease, and the end-diastolic volume and pressure in this chamber will increase. This increases end-diastolic stretch muscle fibers, which leads to greater systolic shortening (Starling's law). The Starling mechanism helps maintain cardiac output. but the resulting chronic rise in diastolic pressure will be transmitted to the atria, pulmonary veins, or veins of the systemic circulation. Increasing capillary pressure is accompanied by transudation of fluid with the development of edema. Reduced cardiac output, especially with a decrease in blood pressure, activates the SAS, which stimulates myocardial contractions, heart rate, venous tone, and a decrease in renal perfusion leads to a decrease in the rate of glomerular filtration, reabsorption of water and sodium chloride, and activation of the RAAS.

Tissue hypoxia in CHF is not only the resulting link in the pathogenesis, but also a factor that has a direct provoking effect on its other leading components - a decrease in the pumping ability of the heart, preload, afterload and heart rhythm. Hypoxia is a complex multicomponent, multistage process. The direct primary effects of hypoxia are directed at targets localized at a variety of levels: organismal, systemic, cellular and subcellular. At the subcellular level, hypoxia initiates the development of apoptosis.

The result of the described processes is an increase in peripheral vascular resistance and circulating blood volume with a corresponding increase in afterload and preload.

Heart Failure Clinic

In most patients, left heart failure primarily develops. The most common complaint is inspiratory dyspnea, initially associated with exercise and progressing to orthopnea, paroxysmal postural dyspnea, and dyspnea at rest. Complaints of nonproductive cough and nocturia are typical. Patients with CHF note weakness and fatigue, which are the result of reduced blood supply to skeletal muscles and the central nervous system.

With right ventricular failure, there are complaints of pain in the right hypochondrium due to congestion in the liver, loss of appetite, nausea due to intestinal edema or reduced gastrointestinal perfusion, peripheral edema.

Upon examination, it can be noted that some patients, even with severe CHF, look good at rest; in others, shortness of breath appears when talking or minimal activity; patients with long-term and severe course look cachectic and cyanotic.

In some patients, tachycardia, arterial hypotension, a drop in pulse pressure, cold extremities, and sweating are found (signs of SAS activation).

When examining the heart, a cardiac impulse, an expanded or elevating apical impulse (dilatation or hypertrophy of the ventricles), weakening of the first tone, and a protodiastolic gallop rhythm are revealed.

With left ventricular failure, hard breathing, dry wheezing (congestive bronchitis), crepitus in the basal parts of the lungs are heard, and dullness in the basal parts (hydrothorax) can be detected.

In right ventricular HF, swollen jugular veins, enlarged liver; slight pressure on it can increase the swelling of the jugular veins - a positive hepatojugular reflex. Ascites and anasarca appear in some patients.

Diagnosis of heart failure

The final clinical diagnosis of HF can only be established by taking into account instrumental data, primarily echocardiography, as well as radiography of the OGK, ECG, data laboratory methods research.

Using echocardiography, the following are assessed: the condition of the valves, the presence of shunts, aneurysms, the condition of the pericardium, the presence of a tumor or blood clots, as well as contractile function (diffuse changes or regional disorders, their quantitative assessment), the presence of myocardial hypertrophy, chamber dilation, and determine global systolic function - FV.

An important role in the diagnosis of heart failure is played by x-ray examination of the heart chamber: - assessment of heart size (cardiothoracic index); -presence and severity of congestion in the lungs; -differential diagnosis with diseases of the respiratory system; - diagnosis and monitoring of the effectiveness of treatment of complications of heart failure (pneumonia, hydrothorax, pulmonary embolism).

An integral part of the examination for HF syndrome is an ECG, which allows to identify hypertrophy, ischemia, focal changes, arrhythmias and blockades, and is also used to monitor therapy with B-blockers, diuretics, cardiac glycosides, and amiodarone.

A 6-minute walk test is used to determine functional class (FC) in patients. This method has been widely used in the last 4-5 years in the USA, including in clinical studies. The condition of patients who are able to overcome from 426 to 550 m in 6 minutes corresponds to mild CHF; from 150 to 425 m - moderate, and those who are not able to overcome 150 m - severe decompensation. Thus, functional classification of CHF reflects the ability of patients to perform physical activity and outlines the degree of changes in the functional reserves of the body. This is especially significant when assessing the dynamics of patients' condition.

Laboratory examination for HF includes a general blood test (hemoglobin, red blood cells, leukocytes, platelets, hematocrit, ESR), a general urine test, a biochemical blood test (electrolytes -K +, Na +, creatinine, bilirubin, liver enzymes - ALT, AST, alkaline phosphatase, glucose).

Classification of heart failure

In Ukraine, the classification of the Ukrainian Association of Cardiologists of 2006 is used, according to which the stages of heart failure are distinguished (based on the classification of V.Kh. Vasilenoko-N.D. Strazhesko), variants of dysfunction (according to EchoCG data) and functional classes (according to the NYHA classification)

The most convenient and meets the needs of practice is the functional classification of the New York Heart Association, which involves the identification of four functional classes according to the ability of patients to tolerate physical activity. This classification is recommended for use by WHO. The principle underlying it is an assessment of the patient’s physical (functional) capabilities, which can be identified by a doctor with a focused, thorough and careful history taking, without the use of complex diagnostic equipment.

Four functional classes (FC) of CHF have been identified.

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.

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.

It is the dynamics of FC during treatment that allows us to objectively decide whether our therapeutic measures are correct and successful. The conducted studies also proved the fact that the determination of FC to a certain extent predetermines and possible prognosis diseases.

In clinical practice, a differentiated approach to therapeutic tactics has a definition of the variant of myocardial dysfunction. Clinically, both systolic and diastolic variants are manifested by the same type of symptoms - shortness of breath, cough, wheezing, orthopnea. In the absence of EchoCG data, you can try to determine the type of dysfunction using clinical and radiological data, taking into account the etiology of heart failure, auscultatory data, determination of the boundaries of the heart by percussion and radiological examination, as well as ECG data (hypertrophy, dilatation, cicatricial changes, their localization, the presence of signs of cardiac aneurysm, etc. .).

Treatment of CHF.

The goals of treatment for heart failure are:

elimination or minimization clinical symptoms 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 of the development of hypotrophy of striated muscles;

·improving quality of life,

· increased life expectancy

· reduction in the number of hospitalizations.

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 g per day, for patients with FC II-III - 1.2-1.8 g per day, for FC IV - less than 1 g 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 CH

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, SG, ß-blockers (in addition to ACE inhibitors).

An additional group, the effectiveness and safety of which has been proven by large studies, but requires clarification (meta-analysis): aldosterone antagonists, angiotensin I receptor antagonists, latest generation CCBs.

Ancillary drugs, their use is dictated by certain clinical situations. These include peripheral vasodilators, antiarrhythmics, antiplatelet agents, direct anticoagulants, non-glycoside positive inotropes, corticosteroids, and statins.

Despite the large selection of medications, polypharmacy (unjustified prescription of a large number of groups of drugs) is unacceptable in the treatment of patients. At the same time, today at the polyclinic level the main group of drugs for the treatment of CHF does not always occupy leading positions; sometimes preference is given to drugs of the second and third groups.

Principles of combined use of basic drugs for the treatment of heart failure.

1. Monotherapy in the treatment of CHF is rarely used, and only ACE inhibitors can be used in this capacity in the initial stages of CHF.

2. Dual therapy with an ACEI + diuretic is optimal for patients with NYHA class P-III CHF in sinus rhythm; the use of a diuretic + glycoside regimen, extremely popular in the 50-60s, is not currently used.

3. Triple therapy (ACEI + diuretic + glycoside) was the standard in the treatment of CHF in the 80s, and now remains an effective regimen in the treatment of CHF, however, for patients with sinus rhythm, it is recommended to replace the glycoside with a ß-blocker.

4. The gold standard from the early 90s to the present is a combination of four drugs - ACE inhibitor + diuretic + glycoside + ß-blocker.

Acute vascular insufficiency

This term includes several acute circulatory disorders that are not included in the concept of either circulatory arrest or shock. The boundary with the latter is so poorly defined that one term is often used instead of the other.

Collapse is a condition in which a disorder of peripheral circulation occurs as a result of a gross violation of the relationship between the capacity of the vascular bed and the volume of circulating blood.

This definition means damage to the body with intact defense mechanisms. The outcome of the collapse is difficult to predict. It can lead to death, recovery without consequences, or go into shock.

Pathological physiology

The main manifestation of collapse is a drop in blood pressure, usually below 10.7 kPa (80 mm Hg) or 2/3 lower than the patient’s normal blood pressure with the disappearance of the peripheral pulse. A characteristic feature of this hypotension is its sudden appearance due to poor adaptation of the body. This is one of the factors that distinguishes it from shock, in which the activation of protective mechanisms leads to a delayed development of the pathological state of the present syndrome.

The absence of this “protective reaction” is typical for some tissues and systems:

Myocardium, where cardiac bradycardia originates during collapse;

Peripheral blood circulation (pale, cold, without cyanosis, marble-colored skin);

Venous circulation (venous pressure is low, the veins are not filled under the tourniquet);

Cerebral circulation (frequent memory impairment, agitation and delirium, sometimes convulsions and even fainting);

Renal circulation (with collapse there is almost always oligo- or anuria);

Neurovegetative system ( increased sweating, pale face, nausea).

The causes of collapse are numerous. It may be the result of:

a) acute hypovolemia due to bleeding, extracellular dehydration (in particular, with hyponatremia);

b) a decrease in cardiac output due to heart rhythm disturbances towards increased speed ( ventricular tachycardia, rotation of the apex of the heart) or its slowdown (nodal or sinus bradycardia, atrioventricular block);

c) circulatory disorders due to difficulty filling the cavities of the heart, for example, with cardiac tamponade;

d) a decrease in peripheral resistance due to a secondary reaction of the vasovasal reflex in a labile patient under emotional stress;

e) hyperventilation, which occurs when artificial ventilation in patients suffering pulmonary insufficiency with hypercapnia, as well as when using vasodilators.

These factors can be combined. It is this combination that is observed during collapse, which appears in the initial stage of myocardial infarction (it should be distinguished from cardiogenic shock). As a result of barbiturate poisoning during collapse, fluid accumulation in the splanchnicus zone is possible; it is also characterized by the inhibitory effect of drugs on the myocardium.

The state of shock is characterized by a syndrome, the clinical essence of which is manifested by diffuse damage to brain cells and a secondary discrepancy between the tissue blood supply and the needs of the body. It sometimes leads to death on its own. However, the stage of its irreversibility in humans has not yet been clearly defined.

Due to difficulties clinical definition Numerous definitions of "shock" have been proposed, of which Wilson's is the most accepted. According to him, a patient in a state of shock is characterized by the presence of three or more signs:

Systolic pressure is equal to or less than 10.7 kPa (80 mmHg);

Insufficient blood supply to tissues, which is manifested by wet, cold, cyanotic, marbled skin or a decrease in cardiac index below 2.5 l/min

Diuresis less than 25 ml/h;

Acidosis with a bicarbonate content of less than 21 mmol/l and lactic acidemia of more than 15 mg per 100 ml.

Causes of shock

Maintaining adequate hemodynamics in the body is the result of a rational interaction between three main factors: blood volume, cardiac output and peripheral vascular resistance. A pronounced change in one of these factors can lead to a “state of shock.”

Hypovolemic shock

Hypovolemic shock develops when the volume of the bcc decreases by 20%. This acute volume loss may result from the following factors:

More or less significant external bleeding -

Internal bleeding occurring in a cavity (abdominal cavity, food canal) or tissue (hematoma). For example, a fracture of the femur is accompanied by blood loss of up to 1000 ml, a fracture of the pelvic bones - from 1500 to 2000 ml;

Plasma loss (burn, pancreatitis);

Loss of water (electrolytes, e.g. sodium),

Cardiogenic shock

Shock as a result of heart failure can occur for two reasons.

Due to insufficient myocardial function and the development of a critical decrease in cardiac output as a result. Decompensation occurs when the heart fails or its rhythm is disturbed (slow or rapid). Myocardial infarction resulting from one of these mechanisms is a fundamentally remote cause of cardiogenic shock.

Preventing contraction or systolic ejection entails insufficient filling or leads to failure of a component of another mechanism, which allows for the grouping of rather unrelated causes such as pericardial tamponade, pulmonary embolism, aortic rupture, intracardiac thrombosis and tumor.

Toxic-infectious shock

Toxic-infectious (bacterial) shock is, at least in the initial stage, a fairly common shock caused by impaired peripheral circulation.

Shock is usually caused by gram-negative microorganisms (enterobacteria and especially pseudomonas), but septicemia caused by gram-positive microorganisms (especially staphylococci) can also cause bacterial shock. This shock is often the first sign of a septic condition, but it can occur as it progresses. In pathogenesis, studied mainly in animals, changes in microcirculation mechanisms are noted. Following peripheral vasoconstriction, there is a stage of atony with the opening of arterioles and blockage of veins. This leads to significant stasis, predominant in the celiac zone, and consequently to hypovolemia, which results in a decrease in MOS. This decrease in MOS can also be facilitated by direct damage to the myocardium by bacterial toxins. Bacterial endotoxins (staphylococcal exotoxins) act as a trigger for these disorders by releasing vasoactive substances such as histamine, kinins and catecholamines.

Anaphylactic shock

Anaphylactic shock is the result of the interaction of circulating or tissue antigens with antibodies and develops according to a mechanism similar to bacterial shock.

Neurogenic shock

This term combines disorders of various origins, following damage to the central nervous system or resulting from direct damage to the brain due to damage to the brain substance or pharmacological effects (ganglioblockers). Both of these reasons lead to a decrease in BP and a secondary drop in MVR with a subsequent decrease in blood pressure. Inhibition of reflex vasoconstriction does not allow these disorders to be corrected.

There are also shock states, the mechanisms of which are more complex. This applies to the shocks observed in massive barbiturate poisoning, where, in addition to the neurogenic cause of shock, there is a direct negative inotropic effect of the drug on the myocardium. A state of shock in a person with polytrauma occurs as a result of the appearance of two components: hypovolemia and a neurovegetative reaction. Shock with pancreatitis is caused by hypovolemia, to which a toxic element is added, which most likely causes vasoplegia.

heal-cardio.ru

CHF according to ICD-10

Chronic heart failure is a pathological condition in which problems arise with the nutrition of the heart due to its insufficient blood supply.

CHF syndrome according to ICD-10 (international classification of diseases) is a pathology that occurs only against the background of other serious diseases.

It has many typical clinical signs by which one can suspect the disease, even without being a doctor.

The essence of the pathology, the mechanism of its development

Chronic heart failure can develop over months. This process is divided into several main stages:

• Due to heart disease or organ overload, the integrity of the myocardium is compromised.
• The left ventricle contracts incorrectly, that is, weakly, which is why not enough blood enters the heart vessels.
• Compensation mechanism. It is triggered when the normal functioning of the heart muscle is necessary. harsh conditions. The layer on the left side of the organ thickens and hypertrophies, and the body releases more adrenaline. The heart begins to beat faster and stronger, and the pituitary gland produces a hormone that causes the amount of water in the blood to increase significantly.
• When the heart is no longer able to supply organs and tissues with oxygen, the body's reserves are exhausted. Oxygen starvation of cells occurs.
• Due to serious circulatory disorders, decompensation develops. The heart beats slowly and weakly.
• Heart failure occurs - the inability of the organ to supply the body with oxygen and nutrients.

Classification

According to ICD-10, CHF is divided into three stages depending on the course of the disease:

• First. Clinical manifestations occur in humans only after physical exertion, and there are no signs of stagnation in the blood circulation.
• Second. In one or two circles of the blood flow there are signs of stagnation.
• Third. Persistent disorders and irreversible processes in the body are observed.

Depending on the condition of the left ventricle, there are two types of CHF:

• systolic function of the left lower chamber of the heart is preserved,
• left ventricular dysfunction is observed.

Chronic heart failure is also divided into functional classes:

• I – ordinary physical activity does not provoke any clinical signs.
• II – during physical activity, symptoms of heart failure appear, so a person is forced to limit himself in work.
• III – the clinic is clearly expressed even with minor loads.
• IV – complaints arise in the patient at rest.

Reasons

The ICD code for CHF is I50. This syndrome, in fact, is an unfavorable outcome of most heart diseases, and especially coronary artery disease and hypertension (up to 85% of cases). A quarter of cases of CHF can be caused by the following reasons:

• myocarditis,
• cardiomyopathy,
• endocarditis,
• heart muscle defects.

Very rarely, factors such as:

• arrhythmia,
• pericarditis,
• rheumatism,
• diabetes mellitus,
• excess weight,
• metabolic disorder,
• anemia,
• heart tumors,
• chemotherapy,
• pregnancy.

In any case, if a person suffers from any of the above-mentioned disorders, his heart gradually becomes weaker and its pumping function deteriorates.

Clinical picture

Signs of chronic heart failure depend on the severity of the disease and associated violations in the body. Typical complaints of patients with CHF are:

• development of shortness of breath. First, rapid breathing appears due to physical activity, later – even at rest;
• night suffocation is a phenomenon when the patient wakes up from the fact that he cannot breathe and feels the need to get out of bed;
• shortness of breath in an upright position (it happens that the patient has difficulty breathing while standing or sitting, but when he lies on his back, the breathing rate normalizes);
• general weakness and fatigue;
• dry cough resulting from stagnation of blood in the lungs;
• nocturnal diuresis prevails over daytime diuresis (frequent urination at night);
• swelling of the legs (first the feet and legs swell symmetrically, then the thighs);
• development of ascites (fluid accumulation in the abdomen).

Another pronounced sign of chronic heart failure is orthopnea - a forced position of the patient in which he lies with his head elevated, otherwise he will experience shortness of breath and a dry cough.

Diagnostic measures

When diagnosing a patient, one cannot do without a visual examination, during which the doctor will clearly see the typical symptoms of CHF - swelling, pulsation and swelling of the veins, enlarged abdomen. On palpation, “splashing noises” are detected, which confirm the presence of free fluid in the peritoneum.

Auscultation can reveal fluid accumulation in the lungs (moist rales). The patient's heart and liver are enlarged in size.

To clarify the diagnosis, the doctor prescribes a number of hardware tests:

• electrocardiogram - reveals changes inherent in diseases that led to chronic heart failure;
• Ultrasound of the heart - allows you to detect expansion of the organ cavities, signs of regurgitation (reflux of blood from the ventricles back into the atria), and also study the contractility of the ventricles;
• Chest x-ray - helps to determine the size of the heart, as well as detect congestion in the lungs.

Treatment

The main principle of treatment for chronic heart failure is to slow the progression of the disease as well as relieve symptoms. Conservative therapy involves lifelong use of heart medications and other medications that improve the patient’s quality of life.

The drugs prescribed by the doctor for CHF include:

• ACE inhibitors, which lower the level of pressure inside blood vessels;
• beta blockers, which reduce heart rate and overall vascular resistance, allowing blood to move freely through the arteries;
• cardiac glycosides, which increase the contractility of the heart muscle while reducing the contraction frequency;
• anticoagulants that prevent thrombosis;
• calcium channel antagonists, which relax blood vessels and help lower blood pressure;
• nitrates, which reduce blood flow to the heart muscle;
• diuretics - prescribed to relieve congestion in organs and reduce swelling.

Prevention

Primary prevention allows you to prevent the development of diseases, the direct consequence of which is CHF.

If such a disease already exists and cannot be completely cured, secondary prevention is indicated for patients. It prevents the progression of CHF.

Patients with chronic heart failure should give up bad habits, take caffeine-containing products, and reduce the amount of salt in the diet.

Meals should be fractional and balanced. You need to eat high-calorie, but easily digestible foods. You should limit physical activity and strictly follow all doctor's instructions.

vseoserdce.ru

Coding of chronic heart failure in the ICD

The disease is located in the class of pathologies of the circulatory system, and the CHF code according to ICD 10 is as follows: I50. This section is divided into several varieties, which indicate the forms of heart failure.

The following options for encoding the diagnosis according to the ICD are distinguished:

• I0 – congestive CHF. Another name for the pathological process is right ventricular failure. It is accompanied by stagnation of blood in the systemic circulation, as evidenced by swelling in the lower extremities.
• I1 – left ventricular failure of the heart. The disease is also called cardiac asthma, as it leads to disturbances in the pulmonary circulation. This also includes acute pulmonary edema, which is formed due to pulmonary hypertension.
• I9 – unspecified CHF. A mixed type of pathology, which occurs most often, since the processes in the pulmonary and systemic circulation are closely related.

Sometimes chronic heart failure in ICD 10 has a code that belongs to a different category. For example, the occurrence of CHF in pathologies of the kidneys, lungs, hypertension, in the neonatal period and in people with cardiac prostheses. CHF in women due to ectopic pregnancy or abortion is separately coded.

General information about the disease

In cardiology, CHF is, rather, not a separate disease, but a complication of existing pathological processes.

Failure develops due to a long-term decompensated state, most often due to heart disease.

The problem is that patients with cardiovascular pathology tend to ignore the symptoms of their disease for a long time and reject medical help. The problem cannot be neglected, since the progression of the pathological process will result in acute cardiovascular failure. This condition has two forms: unstable angina and myocardial infarction.

CHF is confirmed not only by a nonspecific clinical picture, which may indicate dozens of other diseases, but also by instrumental research methods.

Cardiological diagnoses usually have a long formulation, as they require clarification of the severity of the process, etiological factors and concomitant diseases related to the circulatory system.

When registering chronic failure, the degree of development of the process is specified. In ICD 10, CHF does not require additional divisions, but in the clinical practice of a cardiologist one cannot do without them. The severity of the process depends on the dosage of drugs, lifestyle recommendations and future prognosis.

After establishing this diagnosis, the main task of the medical personnel is to maintain the body at the same level, since the problem cannot be completely cured, as well as to eliminate the risks for the development of acute insufficiency of coronary blood supply.

mkbkody.ru

Chronic heart failure: classification and features of treatment of the disease

Content

• Type classification
• Diagnosis
• Methods of influence

Interesting! Worldwide, huge amounts of money are spent on the treatment of heart failure. cash, for example in the USA the costs are 40 billion dollars annually. The incidence rate is constantly increasing; people over 65 years of age are more often hospitalized.

Chronic failure can be characterized as follows - it is a failure of the cardiovascular system. It is expressed in the inability to provide the necessary volume of blood to the internal organs and muscle tissues that need it. The chronic form develops in conditions of impaired cardiac function, or more precisely, the myocardium. Even with increased pressure, it cannot push all the blood out of the heart cavity.

Human heart

Causes of the pathological process and how it occurs

The main reason is a lesion of the middle layer of the heart muscle, the aorta, the next one directly from it, or the valves. This can occur in the presence of ischemia, inflammatory processes in the heart muscle, cardiomyopathy, as well as systemic disorders connective tissue body. The lesions may be toxic. This occurs during poisoning toxic substances, poisons, medications.

Blood vessels and the large azygos artery can be affected by the following diseases:

Atherosclerosis

• atherosclerosis;
• persistent increase in pressure;
• when blood sugar levels rise and there is a deficiency of the hormone insulin.

Chronic heart failure is also provoked by heart defects of congenital or acquired origin.

When blood circulation slows down, oxygen starvation of all the insides of the body begins. Their order depends on the amount of substances and blood consumed. One of the characteristic manifestations of this condition is shortness of breath during exercise and at rest. The patient may complain of poor sleep, tachycardia and excessive fatigue.

The symptoms that are characteristic of this condition are determined by which part of the heart is difficult to function. Sometimes cyanosis is observed, i.e. acquisition of a gray-bluish tint to the skin on the fingers and lips. This indicates a lack of oxygen in distant parts of the body. Swelling of the legs and other parts of the body is caused by blood stagnating in the venous bed. If the liver veins overflow, pain is noted in the area of ​​the right hypochondrium.

As the pathological process develops, the above symptoms worsen.

Classification of the disease

According to the ICD 10 code, chronic failure can be in the following forms:

• common heart failure (150);
• stagnant (150.0);
• left ventricular (150.1);
• unspecified (150.9).

The protracted form of the painful condition is characterized by the fact that the pathology develops gradually. Its development can take several weeks, months, years.

According to classifications, chronic heart failure is divided into IV functional classes:

1. the load is not accompanied by particular fatigue or angina pectoris. There are no noticeable palpitations, shortness of breath, or activity restrictions;
2. when at rest, the patient feels well, but when exerting himself there is discomfort (fatigue, difficulty breathing, chest pain);
3. significant restrictions on physical activity appear;
4. a person is not able to carry out a basic action without unpleasant sensations. All symptoms can occur even at rest, and with stress they intensify.

Often, when stage 1 chronic heart failure is present, the patient may not have any idea what is happening to him. Therefore, the visit to the doctor is delayed, which can negatively affect your health.

Survey

Chronic heart failure symptoms and treatment are closely related, but before moving on to therapy, you need to make a correct diagnosis. The process takes into account clinical manifestations and medical history. You can’t do without additional research, they can be instrumental and laboratory. In the first case, this is an electrocardiogram, and in the second - a general blood test, biochemical, as well as determining the level of hormones secreted thyroid gland into the blood.

What can a doctor do?

After the doctor has made a diagnosis based on research results, examination data and dialogue with the patient, he begins to develop therapy. In the first place is the condition that must be met for successful treatment. Meaning correct definition the underlying disease that led to the deficiency.

Treatment of deficiency consists in the fact that the patient must receive a complex of certain drugs. For this we use:

• diuretics;
• angiotensin-converting enzyme inhibitors;
• aldosterone antagonists;
• cardiac glycosides;
• β-blockers and calcium channel blockers;
• peripheral vasodilators.

The effectiveness of the above drugs has been repeatedly proven.

Treatment of chronic heart failure

When monitoring the treatment of a patient, the doctor focuses on such quality criteria as a decrease in the severity or complete elimination of symptoms, an increase in the left ventricular ejection fraction, and the elimination of signs of fluid retention. An indicator of the effectiveness of therapy is an increase in the period between hospitalizations and an improvement in the quality of life in general. Drug therapy is based on two principles. This means that inotropic stimulation of the heart and unloading of cardiac activity is carried out. Diet is important. For CHF, it must be high in calories, contain a minimum amount of salt, and be well absorbed. Chronic heart failure is not a death sentence. The main thing is to start her treatment on time, follow the doctor’s recommendations, organize proper diet and lead a healthy lifestyle. Symptoms of heart attack in women

If a patient develops CHF, ICD-10 has special codes for this disease. Heart failure is a condition where the heart and circulatory system I cannot maintain normal blood flow. Such pathologies appear due to the fact that the heart does not contract as strongly as required. Because of this, less blood enters the arteries than is necessary to ensure the functioning of the entire body.

Existing classification

Heart failure is called one of the most common pathologies. Moreover, in the ranking of diseases it ranks with the most common infectious diseases. Among the entire population of the planet, approximately 3% of people suffer from this disease, and in patients over 65 years of age, this figure increases to 10%. By the way, if we compare costs, the amount allocated for the treatment of chronic heart failure is 2 times larger than for various forms of cancer.

The International Classification of Diseases, known as ICD-10, was developed by the World Health Organization. It is revised every 10 years, so additions and changes have been made to the already established base.

The ICD-10 code for heart failure is I50.

Moreover, a condition that has a complication such as abortion, molar or ectopic pregnancy is excluded from this group. Surgical interventions and obstetric procedures are also excluded. This does not include a condition that is associated with hypertension or renal pathologies. If insufficient functioning of the heart muscle is detected in a newborn, then international organization code P29.0 is assigned. When such a pathology is caused in a person of any age by heart surgery or wearing a prosthesis, then code I97.1 is set.

Classification involves a more detailed division. The number I50.0 indicates insufficient functioning of the heart with a congestive nature. If the patient has a left ventricular form of this pathology, then code I50.1 is used. If the form of the disease could not be clarified, then the number I50.9 is written.

The mechanism of pathology development

The chronic form of heart failure develops quite slowly - it will take several weeks or even months. There are several main phases in this process:

1. 1. Violation of the integrity of the myocardium. This occurs due to various heart diseases or organ overload.
2. 2. Violated contractile function left ventricle. This part of the organ contracts weakly, so that a small volume of blood is sent into the arteries.
3. 3. Compensation. This mechanism is triggered by the body when it is necessary to ensure the normal functioning of the heart in difficult conditions. The muscle layer on the left side becomes much thicker, as it begins to grow and hypertrophy. The body produces more adrenaline, which causes the heart to contract faster and stronger. In addition, the pituitary gland produces a special dysuric hormone, which increases the amount of water in the blood.
4. 4. Reserves are being depleted. The heart can no longer supply cells with oxygen and nutrients. Because of this, there is a lack of energy and oxygen.
5. 5. Decompensation. The blood flow is disrupted, but the body is no longer able to compensate for it. The muscle tissue of the heart can no longer function fully. The movements of the organ become slow and weak.
6. 6. Development of heart failure. The heart moves weakly, which is why all the cells of the body do not receive the necessary nutrients and oxygen.

The causes of heart failure are as follows:

1. 1. Heart valve diseases. Because of this, blood rushes in large quantities to the ventricles, which leads to overload.
2. 2. Blood hypertension. With this pathology, the outflow of blood from the heart area is disrupted, and the volume of blood in the organ increases. The heart has to work much harder, which causes fatigue. In addition, the risk of valve stretching increases.
3. 3. Narrowing of the aortic mouth. The diameter of the lumen narrows, which leads to the accumulation of blood in the left ventricle. The pressure in this area increases, so that this part of the organ is stretched. This vascular problem causes the myocardium to become weaker.
4. 4. Dilated cardiomyopathy. This cardiac pathology is characterized by stretching of the organ wall, but no thickening occurs. The volume of blood when thrown from the heart into the artery decreases by 2 times.
5. 5. Myocarditis. A disease characterized by inflammatory processes in myocardial tissue. Develops under the influence of various reasons. Leads to problems with contractility and conduction of the heart muscle. The walls gradually stretch.
6. 6. Ischemia, myocardial infarction. This leads to problems in supplying the heart muscle with blood.
7. 7. Tachyarrhythmia. During diastole, the filling of the heart with blood is disrupted.
8. 8. Cardiomyopathy of the hypertrophic type. With this disease, the walls thicken and the volume of the ventricles decreases.
9. 9. Graves' disease. With this pathology, the human body contains a large amount of hormonal substances that are synthesized thyroid gland. This has a toxic effect on heart tissue.
10. 10. Pericarditis. This inflammatory processes on the pericardium. Usually they create mechanical obstacles to the filling of the ventricles and atria with blood.

Types of chronic illness

Chronic heart failure varies by type. According to the contraction phase, the following violations are distinguished:

1. 1. Diastolic. Diastole refers to the phase when the heart relaxes, but with pathology, the muscle loses its elasticity, so that it cannot stretch and relax.
2. 2. Systolic. During systole, the heart contracts, but with pathology, the heart chamber does this weakly.

Depending on the cause, the disease can be of the following types:

1. 1. Reloading. The heart muscle is weakened due to significant overload. For example, blood viscosity has increased, hypertension develops, or there are mechanical obstacles to the outflow of blood from the heart.
2. 2. Myocardial. It is assumed that the muscle layer of the organ is significantly weakened. This includes myocarditis, ischemia, and defects.

As for the acute form of the disease, there are left ventricular and right ventricular types. In the first case, blood circulation in the coronary vessels in the left ventricle is disrupted. In the second type, the patient has damage to the right ventricle, as the branches at the end of the pulmonary artery are blocked. In other words, it is called pulmonary embolism. This also happens with a heart attack on the right side of the heart. The course of the acute form of the disease is as follows:

• cardiogenic shock;
• swelling of the lungs;
• hypertensive crisis;
• high cardiac output due to heart failure;
• acute form of decompensation.

CHF manifests itself in the form of the following symptoms in the patient. Shortness of breath appears as a result oxygen starvation brain. At first it appears only during intense physical activity, but then also at rest. Then the human body will no longer be able to tolerate physical activity. This leads to a feeling of weakness, pain in the sternum, and shortness of breath. Then all the symptoms of cyanosis will be noticeable: pallor and blueness skin on the nose, fingers, earlobes. Swelling of the lower extremities often occurs. Another characteristic sign of chronic heart failure is stagnation of blood in the vessels of internal organs, which causes problems with the central nervous system, kidneys, liver and gastrointestinal tract.

Failure of the heart muscle to function, both acute and chronic, is a fairly common pathology. According to ICD-10, code I.50 has been established for this disease, but there are different types of it, so you should always check this regulatory document.

The clinical picture is characterized by the development of respiratory distress - the appearance at night (during sleep) of a dry cough, tachypnea and paroxysmal, increasing shortness of breath or suffocation due to the fact that in the supine position the venous return of blood to the heart increases, or in connection with an acute cardiac catastrophe that occurs in a patient with CHF. There is a rapid increase in the load on the left side of the heart, which it cannot cope with. Additionally, during sleep, the sensitivity of the central nervous system decreases, which impairs gas exchange in the lungs; in the supine position there is no compensatory increase in RR.
  The attack sometimes passes quickly without treatment (“thanks to the open window”), but, as a rule, it tends to drag on - from ten minutes to several hours. The nature of the attacks, their severity and prognosis are varied. In some cases, an attack of KA has “precursors” (in the previous 2-3 days the patient notes an increase in shortness of breath and the frequency of dry cough attacks), but in others it does not (as with mitral stenosis).
  The patient wakes up (often in fear), his breathing becomes frequent (RR up to 30-40 respiratory movements per minute) and shallow (like an “overheated or driven dog”) due to irritation respiratory center. The patient takes a forced position - orthopnea (sitting, with legs down), sometimes with emphasis on the arms to include auxiliary muscles in the act of breathing, which reduces blood stagnation in the pulmonary circulation. Palpitations appear (or intensify) (heart rate more than 120-150 beats/min), a strong feeling of lack of air - shortness of breath of inspiratory or mixed type (patients “gasp for air” and speak with difficulty), hacking cough.
  At first it is dry (slight coughing), later it becomes productive, with a small amount of light sputum, sometimes streaked with blood. Blood pressure can be high and then drop sharply before our eyes, signaling collapse.
  If a rapid rise in pressure in the pulmonary circulation is formed (more than 50 mm, which exceeds the capabilities of the Kitaev reflex), then rapid fluid retention in the interstitium begins. She enters it, but cannot return back due to high venous pressure. A small amount of liquid also enters the lumen of the alveoli, which causes an organic blockade of gas exchange (not only the epithelium, but also a layer of liquid appears between the air and the capillary). This leads to an accelerating progression of shortness of breath, which until a certain time is actually a compensatory mechanism.
  Diagnostics includes a variety of research methods. Objectively, the face becomes pale with a cyanotic tint, the skin is covered with drops of cold sweat (this is due to a decrease in the functioning of the LV myocardium and an increase in sympathetic stimulation). The patient behaves restlessly, sometimes complaining of pain in the heart (if CA developed against the background of MI). On inhalation, retraction of the intercostal spaces and supraclavicular fossae is noted - a sign of high negative intrathoracic pressure necessary for breathing. The borders of the heart are often shifted to the left.
  During auscultation of the heart (sometimes it is difficult due to whistling and a lot of wheezing), one can identify a symptom of the disease that caused CVD, dullness of heart sounds, emphasis of the 2nd tone over the PA, gallop rhythm. The pulse is frequent, weak in filling, often alternating or thread-like. If there is no CABG, then blood pressure initially increases (as a result of sympathetic stimulation), less often remains normal, and then decreases.
  When listening to the lungs, the manifestations of broncho-obstructive syndrome (due to swelling of the mucous membrane of the respiratory tract) are first determined - prolonged and noisy exhalation, “hard” breathing, isolated and scattered dry wheezing (therefore, such patients are often and dangerously confused with patients suffering from true asthma) or short-term crepitus due to the fluid moistening the walls of the alveoli. Later, silent, single moist or crepitating rales occur (due to the appearance of a small amount of fluid in the small bronchi, bronchioles and alveoli) immediately in the upper parts of the lungs, and then in the posterior lower parts of the lungs on both sides.
  A chest x-ray usually shows signs of venous congestion and congestion; expansion of the roots of the lungs; blurred and increased pulmonary pattern (due to edematous infiltration of the peribronchial interstitial tissue), thin Kerley lines, reflecting swelling of the interlobar septa and elements of infiltration.
  On the ECG, the amplitude of the waves and the ST interval decrease, and changes characteristic of the underlying disease are also determined.

Cerebral ischemia is a type of cerebrovascular disease and a fairly common severe pathology. Discyclatory encephalopathy is the name of a chronic disease that is used in domestic medicine. What is it? Cerebral ischemia is an extremely pressing neurological problem. This is a severe disorder of brain activity. Nowadays, this diagnosis is found quite often in the opinions of professionals. Dyscyclic encephalopathy affects about 6% of the world's population. The number of such patients is constantly growing.

Etiology of dyscirculatory encephalopathy

The causes of ischemia are varied. Various diseases lead to pathology. What is ischemic brain disease?

The causative factors of circulatory encephalopathy are the following disorders:

• vascular atherosclerosis;
• hypertension;
• atrial fibrillation;
• blood vessel diseases;
• damage to the endocrine system;
• diseases of the spine;
• cervical pathology.

Blood flow in brain tissue depends on the level of red blood cells. Poor nutrition causes high cholesterol. Damage to the blood vessels of the head occurs. The age factor is of great importance. Cerebral vascular ischemia is common in adults. Young people suffer from this disease less. Old age is a provoking factor.

Pathogenesis of discirculatory encephalopathy

The accumulation of cholesterol deposits in blood vessels leads to pathology. Irreversible changes are taking place. A disorder develops cerebral circulation according to the ischemic type. A vessel clogged with cholesterol plaque cannot perform its functions. If the arteries become blocked, their lumen narrows, oxygen starvation of the tissues develops. Brain cells damaged due to nutritional deficiency do not recover. Even one damaged vessel often leads to catastrophic consequences.

Classification of pathology

ICD-10 lists cerebral ischemia as a chronic type of cerebral pathology. Symptoms and treatment of dyscirculatory encephalopathy are the responsibility of a neurologist. Treating ischemia is difficult and time consuming. Multifocal or diffuse damage occurs, and ischemic cerebral disease develops. Cerebrovascular pathology is manifested by clinical, neurological, neuropsychological, and mental disorders in the body.

Cerebral ischemia is diagnosed by a professional. The acute form of cerebrovascular pathology is a consequence of oxygen starvation. A sudden attack develops. The chronic form of the pathology develops gradually in conditions of impaired blood circulation in the vessels of the head.

Clinical picture

Signs of cerebral ischemia appear gradually or instantly.

Dyscyclic encephalopathy is manifested by the following symptoms:

• pain syndrome;
• frequent dizziness;
• constant noise in the head;
• gradual deterioration of memory indicators;
• low level of attention, decreased performance;
• cognitive impairment.

At an early stage, cerebral ischemia is manifested by dysfunction of the nervous system. Rapid, severe fatigue appears. Memory deteriorates greatly. This leads to a significant decrease in performance. However, people usually do not complain at this stage. Often patients do not consult a neurologist.

Discyclatory encephalopathy - brain damage of the 1st degree. Development is happening neurasthenic syndrome. In general, the patient’s health is normal, but the person may complain of slight malaise. The early stage of the pathology is characterized by chills, sudden changes mood, irritability, nervous agitation, sleep disturbance. If adequate treatment is not carried out, the patient's condition worsens.

Stage 2 of the disease develops. Severe neurological disorders occur. Pathological reflexes are noted. The patient is bothered by numbness and a feeling of cold in the feet and palms. This is a clear manifestation of pathology. Complaints about feeling unwell. Gait is disturbed. Cerebellar disorders appear. The patient experiences constant drowsiness. Stage 2 disease is characterized by progressive memory loss. All signs of stage 1 brain failure also remain, but patients notice these defects less. At stage 2, transient ischemic attacks are noted.

In phase 3 of tissue ischemia, memory deteriorates and dementia develops. The patient's social and work adaptation is disrupted. Such a patient needs constant monitoring and care. At stage 3, patients show very few complaints. This is explained by the fact that their critical attitude towards their condition decreases. During this phase, headaches disappear. But the person’s condition is grave. Patients often experience severe strokes, vascular dementia, parkinsonism.

Diagnostic procedures

How can a correct diagnosis be made? The neurologist evaluates painful symptoms and prescribes treatment after listening to the patient’s complaints. If at least 2 of the characteristic symptoms appear continuously over the past months, such complaints should be the reason for an in-depth examination of the cardiovascular system.

When signs appear coronary disease blood vessels, laboratory blood tests are performed. Hardware studies include ultrasound, high-frequency ultrasound tomography, electroencephalography, Dopplerogram of the brain, and cardiography. The results of these studies may indicate the location of the lesion.

Treatment tactics

If symptoms of cerebral ischemia appear, what should you do? How to cure a patient? The most effective treatment method is to use special drugs, which are selected individually by the treating doctor. The main task of a specialist is treatment vascular pathology. In case of cerebral vascular ischemia, treatment is required immediately.

It is important to reduce the symptoms of dyscirculatory encephalopathy to improve the quality of life of patients. It is necessary to increase the blood supply to the inner ear and reduce the activity of the vestibular centers. This will help get rid of dizziness. Considering the patient’s condition, the neurologist prescribes Piracetam, Betagistim, Gingko Biloba. Betagistim is the main drug indicated for use. It normalizes the electrical activity of the vestibular centers of the brain, peripheral receptors, and improves blood supply to the inner ear.

Vestibo normalizes vestibular functions. This drug must be included in the therapeutic course at stages 2 or 3 of cerebral ischemia. Vestibo and Actovegin significantly reduce tinnitus as aerobic metabolism increases. Actovegin is a drug that shows good results.

When using these drugs, processes improve blood flow. The energy resources of cells increase. Oxygen transport is activated. Metabolic processes improve. Neuroprotectors prevent damage to brain neurons. Neuromodulatory drugs, vasoactive drugs, neurotrophic cerebroprotectors, and neuropeptides are used.

Such medications neutralize the pathogenic factor, limit and stop damage to brain tissue. Cinnarizine, Vinpocetine, Nimodipine are calcium channel blockers. Such medications increase cerebral blood flow because they dilate blood vessels in the brain. The doctor prescribes Neuromedin, Pramipex, physiotherapy, according to indications, therapeutic massage. Special vestibular gymnastics are performed. Effective sanatorium-resort treatment. If there are signs of cerebral ischemia, symptoms and treatment are the responsibility of the doctor.

What are the complications of the disease? Discyclatory encephalopathy can lead to stroke and heart attack. This often causes changes in body functions and daily activities. Patients with cerebral ischemia require complex treatment. Prevention of dyscirculatory encephalopathy is important. Prevention begins as early as possible. It is necessary to avoid stress in every possible way, control weight, and exercise. The use of tobacco and addiction to alcoholic beverages are contraindicated. Cerebral ischemia is dangerous.

If characteristic symptoms of cerebral ischemia occur, the patient should go to a neurologist. The patient should be shown to a specialist. Early detection of pathology and treatment of coronary disease helps maintain a decent standard of living.