Treatment of chronic heart failure: breathe deeply

Chronic heart failure (CHF) is one of the main health problems in modern society. The disease affects 10 people out of 1000 after 65 years and 10% of the population after 80 years . The condition is typical for older people. It rarely appears at a young age.

The specialists at the Harmony Clinic have extensive experience working with patients diagnosed with heart failure. If you've recently been feeling heaviness and pain in your chest, suffering from loss of energy, shortness of breath and other symptoms of heart disease, make an appointment with a cardiologist. The doctor will conduct a professional examination, refer you for examination and develop an individual therapy regimen for a speedy recovery.

Heart failure

Heart failure is an acute or chronic condition caused by a weakening of myocardial contractility and congestion in the pulmonary or systemic circulation. It manifests itself as shortness of breath at rest or with slight exertion, fatigue, swelling, cyanosis (blueness) of the nails and nasolabial triangle. Acute heart failure is dangerous due to the development of pulmonary edema and cardiogenic shock, while chronic heart failure leads to the development of organ hypoxia. Heart failure is one of the most common causes of human death.

Classification of the disease

In ICD 10, chronic heart failure is coded 150, divided into systolic and diastolic forms. This is not the only division of pathology; there are other bases for classification. One of the most common divisions is by stages :

• Stage I - primary changes, decreased functionality of the left ventricle of the heart. At this moment, there are still no serious disturbances in blood flow, so symptoms of chronic heart failure do not appear.
• Stage II A - blood moves along the bed more slowly and can form areas of stagnation in the pulmonary fields or lower segment of the body.
• II B - hemodynamics suffer, affecting both circles of blood circulation at once. This stage is already characterized by noticeable changes in blood vessels and the heart muscle itself. The doctor can identify signs of the disease by recording extraneous whistling in the lungs and swelling of the lower extremities.
• Stage III - swelling spreads throughout the body. Now they appear not only in the legs, but also become noticeable in the hips and lumbar area. Fluid can accumulate in the peritoneum and spread throughout the body. At this stage, irreversible changes affect vital organs: the brain, heart, bronchopulmonary system, kidneys and liver.

There is a well-known classification by functional units or classes, which is determined by the general well-being of a sick person in response to physical activity. There are 4 stages of chronic heart failure. At the first stage, activity does not cause major changes. Shortness of breath may occur during intense activities, although in many situations there is no shortness of breath.

The second functional class can be determined by normal well-being during the period of rest and increased heartbeat under light loads. When moving to stage 3, the patient experiences significant limitations in physical activity. And at the 4th stage, loads are practically inaccessible, as they cause acute discomfort. Another popular gradation is the division by zones of heart damage. Thus, experts distinguish between left-, right- and two-ventricular heart failure.

Classification of heart failure

According to the nature of the course, the classification of heart failure involves division into:

• spicy;
• chronic.

Acute heart failure

According to ICD-10, the code corresponds to I50.9 Heart failure, unspecified. Acute circulatory failure often leads to death (death) in the absence of timely, competent therapy.

Acute heart failure occurs suddenly, minutes or hours after a heart attack, when the body can no longer compensate. Some symptoms include:

• severe difficulty breathing and/or coughing;
• Gurgling sound when breathing;
• Heart rhythm disturbances;
• Pallor;
• Cold sweat.

The development of acute heart failure can occur in two types:

• left type (acute left ventricular or left atrial failure);
• acute right ventricular failure.

Chronic heart failure

Chronic heart failure is a consequence of cardiovascular diseases. It develops gradually and progresses slowly. The wall of the heart thickens due to the growth of the muscle layer. The formation of capillaries that supply nutrition to the heart lags behind the growth of muscle mass. The nutrition of the heart muscle is disrupted, and it becomes stiff and less elastic. The heart cannot cope with pumping blood.

Diagnostics

The examination is carried out under the supervision of a cardiologist. An acute attack requires immediate action. Therefore, specialized actions are taken immediately, and then the results of instrumental methods are evaluated.

After restoration of basic vital signs, the following examination methods are indicated:

• Oral interview with a person. Complaints play a big role.
• Anamnesis collection.
• Measurement of blood pressure, heart rate.
• Auscultation. Listening to sound. Against the background of current defects, systolic murmur develops. The tones are dull, chaotic behavior is possible due to arrhythmias.
• Electrocardiography. Assessment of the functional state of the heart. Depression of the ST segment and deformation of the R, P, and S teeth occur.
• Echocardiography. Used to detect organic defects. Deviations are clearly visible during imaging.
• MRI or CT if indicated.
• Scintigraphy.
• Coronography.

This is enough in the system. It is possible to prescribe 24-hour monitoring to determine heart rate and blood pressure over a 24-hour period.

The examination takes place in an inpatient or outpatient setting. The first option is faster.

How is chronic heart failure classified?

In all cases when heart failure (symptoms and organ disorders) develops slowly, it is said to be chronic. As symptoms increase, this option is divided into stages. So, according to Vasilenko-Strazhesko there are three of them.

I (initial) stage - hidden signs of circulatory failure, manifested only during physical activity by shortness of breath, palpitations, excessive fatigue; at rest there are no hemodynamic disturbances.

Stage II (severe) – signs of prolonged circulatory failure and hemodynamic disorders (congestion of the pulmonary and systemic circulation) are expressed at rest; severe limitation of working capacity:

• Period II A – moderate hemodynamic disturbances in one part of the heart (left or right ventricular failure). Shortness of breath develops during normal physical activity, and performance is sharply reduced. Objective signs are cyanosis, swelling of the legs, initial signs of hepatomegaly, hard breathing.
• Period II B – deep hemodynamic disorders involving the entire cardiovascular system (large and small circle). Objective signs – shortness of breath at rest, severe edema, cyanosis, ascites; complete disability.

III (dystrophic, final) stage – persistent circulatory and metabolic failure, morphologically irreversible damage to the structure of organs (liver, lungs, kidneys), exhaustion.

Depending on the symptoms that appear at different stages of the disease, the severity of the patient, functional classes (types) of heart failure are distinguished:

I – the disease does not have any effect on the patient’s quality of life. Heart failure is stage 1 and does not limit the patient’s physical activity in any way. Stage 1 deficiency responds well to therapy.

II – the patient is not bothered by anything at rest; mild restrictions are recorded during physical activity.

III – there are no symptoms at rest, but there is a noticeable decrease in performance.

IV – chest pain and signs of heart failure are recorded at rest, the patient is partially or completely incapacitated.

Possible complications

Among the likely consequences of a long-term or, especially, acute course of the pathological process, the following are distinguished:

• Cardiogenic shock. Emergency condition. Accompanied by a critical drop in blood pressure and heart rate. Contractility is insufficient, blood ejection into the systemic circle is also insufficient. Hence the generalized dysfunction of the whole body.
• Cardiac arrest and sudden death without prospects for resuscitation.
• Heart attack. Acute myocardial malnutrition, necrosis of active muscle tissue (read about the first signs of pre-infarction here).
• Stroke. Similar phenomenon. Its essence lies in the death of nerve cells and the development of persistent neurological deficits. What nature depends on the localization. Disability often occurs.
• Pulmonary edema. As a result of insufficient gas exchange. May lead to death from asphyxia. Restoration is urgent.
• Attack of cardiac asthma.
• Vascular dementia due to damage to the arteries of the brain.

All of these conditions are potentially fatal. Treatment is immediate, in a specialized hospital. The risks are great, so first aid must also be provided. The outcome depends on the quality of the event.

Symptoms of heart failure

In the initial stages, symptoms of heart failure occur only during physical activity. Shortness of breath appears - breathing becomes too frequent and deep, and does not correspond to the severity of work or physical exercise. If the pressure in the vessels of the lungs increases, the patient is bothered by a cough, sometimes with blood.

After physical exertion, heavy meals and in a lying position, increased heart rate occurs. The patient complains of increased fatigue and weakness.

Over time, these symptoms intensify and begin to bother you not only during physical work, but also at rest.

Many patients with heart failure have decreased urine output and go to the toilet mostly at night. In the evenings, swelling appears on the legs, at first only on the feet, and over time it “rises” higher. The skin of the feet, hands, earlobes and tip of the nose takes on a bluish tint. If heart failure is accompanied by stagnation of blood in the liver vessels, a feeling of heaviness and pain occurs under the right rib.

Over time, heart failure leads to poor circulation in the brain. The patient becomes irritable, quickly gets tired during mental stress, and often becomes depressed. He sleeps poorly at night and is constantly sleepy during the day.

Symptoms of right ventricular acute heart failure are caused by stagnation of blood in the veins of the systemic circulation:

• Increased heartbeat is the result of deterioration of blood circulation in the coronary vessels of the heart. Patients experience increasing tachycardia, which is accompanied by dizziness, shortness of breath and heaviness in the chest.
• Swelling of the neck veins, which increases with inspiration, is explained by an increase in intrathoracic pressure and difficulty in blood flow to the heart.
• Edema. A number of factors contribute to their appearance: slower blood circulation, increased permeability of capillary walls, interstitial fluid retention, and impaired water-salt metabolism. As a result, fluid accumulates in cavities and limbs.
• A decrease in blood pressure is associated with a decrease in cardiac output. Manifestations: weakness, pallor, increased sweating.
• There is no congestion in the lungs.

Chronic heart failure develops in the right and left atrial, right and left ventricular types. Chronic heart failure, according to various authors, is observed in 0.5–2% of the population. The incidence increases with age; after 75 years, the pathology occurs in 10% of people. Chronic left ventricular failure develops as a complication of coronary heart disease, arterial hypertension, mitral valve insufficiency, aortic disease and is associated with stagnation of blood in the pulmonary circulation. It is characterized by gas and vascular changes in the lungs.

Clinically manifested:

• increased fatigue;
• dry cough (rarely with hemoptysis);
• attacks of palpitations;
• cyanosis;
• attacks of suffocation, which often occur at night;
• shortness of breath.

In chronic left atrial insufficiency in patients with mitral valve stenosis, congestion in the pulmonary circulation system is even more pronounced. The initial signs of heart failure in this case are cough with hemoptysis, severe shortness of breath and cyanosis. Gradually, sclerotic processes begin in the vessels of the small circle and in the lungs. This leads to the creation of an additional obstacle to blood flow in the pulmonary circle and further increases the pressure in the pulmonary artery basin. As a result, the load on the right ventricle increases, causing the gradual formation of its failure.

Chronic right ventricular failure usually accompanies emphysema, pneumosclerosis, mitral heart defects and is characterized by the appearance of signs of blood stagnation in the systemic circulatory system. Patients complain of shortness of breath during exercise, enlargement and distension of the abdomen, a decrease in the amount of urine discharge, the appearance of edema of the lower extremities, heaviness and pain in the right hypochondrium.

Publications in the media

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, echocardiographic data) . Statistical data. 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.

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, defects hearts, 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 renal perfusion causes stimulation of the renin-angiotensin systems. 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, as well as 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 activity (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 hearts or only parts of them •• Period B - 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.

New York Heart Association classification (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 - severe 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 impaired. 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 - the final stage of cardiac damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys). The final stage of organ remodeling.

• Functional classes of chronic heart failure (can change during treatment in either direction) •• 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: there are no symptoms at rest, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations •• FC III - noticeable limitation of physical activity: at rest there are no symptoms, physical activity of lesser intensity compared to usual exercise is accompanied by the appearance of symptoms •• FC IV - inability to perform any physical activity without discomfort; Symptoms of heart failure are present at rest and worsen with minimal physical activity.

Clinical manifestations • Complaints - shortness of breath, attacks of suffocation, weakness, fatigue • • Shortness of breath in the initial stage of heart failure occurs during physical activity, and in case of 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 health 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, loss of appetite, abdominal pain, abdominal enlargement (ascites) due to blood stagnation in the liver and portal vein system •• 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 concerned about a feeling of heaviness in the right hypochondrium, general weakness, and sleep disturbances. 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 profound 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.

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 redistribution of blood flow in favor of the upper parts of the lungs and an increase in the diameter of blood vessels •• With congestion in the lungs, signs of interstitial edema are detected (Kerley lines in the costophrenic sinuses) or signs of pulmonary edema •• Hydrothorax is detected ( most often right-sided) •• Cardiomegaly is diagnosed when the transverse size of the heart increases by more than 15.5 cm in men and more than 14.5 cm in women (or when the cardiothoracic index is 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, distention 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 of the 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 • Liver cirrhosis • Occlusive lesions of the veins with subsequent development of peripheral edema. Treatment • It is necessary to first evaluate the possibility of influencing the cause of the deficiency. In some cases, 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 drug therapy methods are distinguished. 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, liquid (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/week) •• Complete physical rest should be observed if the condition worsens (at rest the heart rate decreases and the work of the heart decreases).

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. If the diuretic response is insufficient, loop diuretics and thiazides are combined •• Thiazide diuretics. Hydrochlorothiazide is usually used in a dose of 25 to 100 mg/day. It should be remembered that if 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 IV, depending on the manifestations of edema 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 with gradual their increase •• It is necessary to monitor renal function (diuresis, relative density of urine) and the concentration of blood electrolytes (potassium, sodium ions) while increasing the dose every 3–5 days, then every 3 and 6 months •• Avoid co-administration of potassium-sparing diuretics (their can be prescribed only for hypokalemia) •• Concomitant use of NSAIDs should be avoided.

• 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-blockers •• The mechanism of beneficial action of β-blockers in chronic heart failure is due to the following factors ••• Direct protection of the myocardium from the adverse effects of catecholamines ••• Protection against catecholamine-induced hypokalemia ••• Improvement of blood flow in the coronary arteries due to a decrease in heart rate and improvement diastolic relaxation of the myocardium ••• Reducing the effect of vasoconstrictor systems (for example, due to decreased 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 from b -adrenergic blockers for the treatment of chronic heart failure, carvedilol is recommended for use - a b1- and a1-blocker with vasodilating properties. 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 effects in the form of arterial hypotension, bradycardia, decreased left ventricular ejection fraction (according to EchoCG) and other negative manifestations of the action of b-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 . β-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 patient’s condition.

• 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). Surgery

• 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 refractory to adequate therapy, the main surgical treatment 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. Overall, 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, the presence of which correlates with a poor prognosis in patients with heart failure •• Decrease in left ventricular ejection fraction of 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 blood plasma less than 133 mEq /l •• Decrease in the concentration of potassium ions in the blood plasma less than 3 meq/l •• Increase in the content of norepinephrine in the blood •• Frequent ventricular extrasystole during daily ECG monitoring.

• 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

Causes of heart failure

The main causes of heart failure are:

• coronary heart disease and myocardial infarction;
• dilated cardiomyopathy;
• rheumatic heart defects.

In elderly patients, the causes of heart failure are often type II diabetes mellitus and arterial hypertension. Type 2 diabetes mellitus can lead to the development of heart failure.

There are a number of factors that can reduce the compensatory mechanisms of the myocardium and provoke the development of heart failure. These include:

• pulmonary embolism (PE);
• severe arrhythmia;
• psycho-emotional or physical stress;
• progressive coronary heart disease;
• hypertensive crises; acute and chronic renal failure;
• severe anemia;
• pneumonia; severe ARVI;
• hyperthyroidism;
• long-term use of certain medications (adrenaline, ephedrine, corticosteroids, estrogens, non-steroidal anti-inflammatory drugs);
• infective endocarditis;
• rheumatism; myocarditis;
• a sharp increase in the volume of circulating blood due to incorrect calculation of the volume of intravenously administered fluid;
• alcoholism;
• rapid and significant weight gain.

Eliminating risk factors can prevent the development of heart failure or slow its progression.

How is heart failure diagnosed?

Diagnosis begins with a comprehensive assessment of a person's medical history, paying particular attention to symptoms (onset, duration, manifestation). This helps classify the severity of the symptom. The heart and lungs are examined. If a heart attack or rhythm disorder is suspected, a 12-lead resting ECG is performed. In addition, echocardiography and complete blood count. The need for catheterization is determined individually.

In diagnosis, you need to start with analyzing complaints and identifying symptoms. Patients complain of shortness of breath, fatigue, and palpitations.

The doctor asks the patient:

1. How does he sleep?
2. Has the number of pillows changed over the past week?
3. Did the person begin to sleep sitting instead of lying down?

The second stage of diagnosis is a physical examination, including:

1. Skin examination;
2. Assessment of the severity of fat and muscle mass;
3. Checking for edema;
4. Pulse palpation;
5. Palpation of the liver;
6. Auscultation of the lungs;
7. Auscultation of the heart (1st sound, systolic murmur at the 1st point of auscultation, analysis of the 2nd tone, “gallop rhythm”);
8. Weighing (a 1% decrease in body weight over 30 days indicates the onset of cachexia).

If heart failure is suspected, the electrolyte and gas composition of the blood, acid-base balance, urea, creatinine, cardio-specific enzymes, and indicators of protein-carbohydrate metabolism are determined.

Based on specific changes, an ECG helps to identify hypertrophy and insufficiency of blood supply (ischemia) of the myocardium, as well as arrhythmias. Based on electrocardiography, various stress tests using an exercise bike (veloergometry) and a treadmill (treadmill test) are widely used. Such tests with a gradually increasing level of load make it possible to judge the reserve capabilities of heart function.

Using ultrasound echocardiography, it is possible to determine the cause of heart failure, as well as evaluate the pumping function of the myocardium. Using cardiac MRI, coronary heart disease, congenital or acquired heart defects, arterial hypertension and other diseases are successfully diagnosed. X-ray of the lungs and chest organs in heart failure determines congestive processes in the pulmonary circulation, cardiomegaly.

Causes

The development of left ventricular failure is caused by cardiac events. Possible diseases include:

Mitral valve defects

MV stenosis or MV prolapse. Developmental defects in one word. The anatomical structure covers the entrance to the left ventricle, preventing blood from returning to the atrium.

As a result of loose closure of the valves, regurgitation occurs - a reverse flow of liquid tissue. Hence the overload, impaired contractility and dilatation changes. Treatment is surgical, according to indications.

Attention:

At the first symptoms of LVN, the need for surgery is unconditional. Urgent therapy. The prospects for recovery depend on existing anatomical disorders. They are irreversible.

Aortic valve defects

Causes the onset of left ventricular failure even more often. The essence is approximately the same. A pathological narrowing of the valve of the body's largest artery occurs.

The blood comes back into the chamber, the volume of ejection into the large circle is insufficient. Hence the functional and then organic deviations.

Treatment is surgical. If possible, valve repair is performed. If ineffective or inappropriate, prosthetics are indicated.

The prognosis at an early stage is good. Maintenance therapy is required, but the dangers as such are minimal. Read more about aortic valve stenosis in this article.

Arterial hypertension

Patients with a stable increase in pressure suffer from LVH almost three times more often. Why are the statistics so unfavorable?

We are talking about an organic disorder of cardiac structures. During a prolonged increase in tonometer readings, the load on the left ventricle increases.

Myocardial muscle mass increases, but chamber volume and functionality decrease. Hence the decrease in blood output into the aorta.

The process moves further along the chain. A persistent disruption of the functioning of cardiac structures occurs. As the myopathy progresses, it worsens.

The disease develops relatively slowly, and severe left ventricular failure occurs several years later. Therefore, there is time for diagnosis and treatment.

Myocarditis

Inflammation of the muscle layer of the heart. The condition is provoked by an autoimmune or, more often, an infectious factor.

Outside of quality care, preferably in a hospital setting, the likelihood of tissue destruction and death is maximum. The outcome is disability.

Prosthetics may be a treatment option, but will not guarantee complete recovery.

Throughout the entire period of supervision, constant monitoring of the condition is required. Therefore, they try not to keep such patients at home. The risks of sudden death from cardiac arrest or other complications are too great.

Previous myocardial infarction

Acute malnutrition of the muscle layer. Even if the patient is lucky and survives, no one guarantees a favorable outcome in the future. It is necessary to evaluate the extent of the lesion, general health, and the quality of treatment.

In 100% of cases, a heart attack leaves scars; this is post-infarction cardiosclerosis. Hence the guaranteed failure, coronary artery disease, of varying severity.

Lifelong maintenance therapy under the supervision of a specialist is required. Complex cases are difficult to resolve.

Cardiomyopathy

The growth of the muscle layer of the organ (hypertrophic cardiomyopathy), or its stretching - dilatation.

These defects are almost impossible to radically correct. They often turn out to be the result of intoxication, viral and bacterial pathologies, and other processes.

With the help of medications, you can slow down the development of the condition, even to a complete stop. The prognosis in this case is much better.

Congenital and acquired heart defects

Genetic or spontaneously arising during life or intrauterine development. Treatment methods vary and depend on many factors.

The causes of the pathological process are excluded one by one. If defects and functional abnormalities are identified, urgent treatment is indicated. Delay reduces your chances of survival.

How is heart failure treated?

For chronic heart failure, medications (such as ACE inhibitors, beta blockers and diuretics) are used. Medicines are used to prevent complications and improve quality of life. ACE inhibitors and beta blockers can prolong life, but they must be taken regularly to achieve a beneficial effect.

In addition, rhythm therapy (to treat cardiac arrhythmias) and implantation of a three-chamber pacemaker are used. The latter ensures timely activation of the atria and both ventricles. A defibrillator is also often implanted as part of a pacemaker to counteract dangerous heart rhythm disturbances in the setting of severe heart failure. This treatment is also known as resynchronization therapy. An important part of successful treatment is physical therapy.

In the treatment of heart failure, a properly organized diet plays an important role. Dishes should be easily digestible. The diet should include fresh fruits and vegetables as a source of vitamins and microelements. The amount of table salt is limited to 1-2 g per day, and liquid intake to 500-600 ml.

Pharmacotherapy, which includes the following groups of drugs, can improve the quality of life and prolong it:

• cardiac glycosides – enhance the contractile and pumping function of the myocardium, stimulate diuresis, and increase the level of exercise tolerance;
• ACE inhibitors (angiotensin-converting enzyme) and vasodilators - reduce vascular tone, expand the lumen of blood vessels, thereby reducing vascular resistance and increasing cardiac output;
• nitrates - dilate the coronary arteries, increase cardiac output and improve blood filling of the ventricles;
• diuretics – remove excess fluid from the body, thereby reducing swelling;
• β-blockers - increase cardiac output, improve the filling of the heart chambers with blood, reduce the heart rate;
• anticoagulants - reduce the risk of blood clots in blood vessels and, accordingly, thromboembolic complications;
• agents that improve metabolic processes in the heart muscle (potassium supplements, vitamins).

If cardiac asthma or pulmonary edema (acute left ventricular failure) develops, the patient requires emergency hospitalization.

Prescribed drugs that increase cardiac output, diuretics, nitrates. Oxygen therapy is mandatory. Removal of fluid from body cavities (abdominal, pleural, pericardial) is carried out by puncture.

First aid for an attack

There is little you can do on your own. The goal is to stabilize the patient's condition. There is no chance of elimination without special intervention. The main thing to do is to call a team of doctors.

Before the ambulance arrives, the emergency algorithm is as follows:

• Sit the patient down and place a cushion made from available materials under his back. A blanket or clothing will do.
• Be sure to lower your arms and legs. There should be no intense peripheral circulation, as this will negatively affect the state of the cardiovascular system.
• Open a vent or window to provide fresh air into the room.
• Against the background of pain, give a Nitroglycerin tablet. One.
• Measure blood pressure.
• If symptoms of cardiogenic shock develop (loss of consciousness, indifference to what is happening, a sharp drop in blood pressure and heart rate), the patient must be taken to the hospital as quickly as possible. If possible, it is better to do this on your own, without waiting for an ambulance.

Prevention and prognosis

To prevent heart failure, you need proper nutrition, sufficient physical activity, and giving up bad habits. All diseases of the cardiovascular system must be promptly identified and treated.

The prognosis in the absence of treatment for CHF is unfavorable, since most heart diseases lead to its wear and tear and the development of severe complications. When carrying out drug and/or cardiac surgery, the prognosis is favorable, because the progression of the insufficiency slows down or a radical cure for the underlying disease occurs.

The mechanism of pathology development

Normally, blood moves from the right side of the heart to the left ventricle, then is released into the aorta and moves in a large circle, providing nutrition to all organs and systems, including the brain.

LVAD develops as a result of exposure to a negative factor, usually mitral or aortic valve insufficiency or pathology of the interventricular septum.

The result of the violation is, on the one hand, a decrease in myocardial contractility as a result of overload. Accordingly, not enough blood is released.

On the other hand, stagnation of liquid connective tissue, which leads to dilatation (expansion) of cardiac structures and an even greater decrease in the organ’s ability to function normally.

The heart cannot function like this for a long time. Therefore, within a few years, death occurs. The progression is rapid.

The condition needs to be treated from the very first months, or preferably weeks, in a hospital setting. The basis of therapy is eliminating the cause of the phenomenon.