Principles for the treatment of acute heart failure

Heart failure is an acute or persistent problem brought on by a weakening of the myocardial contractility and also blockage in the lung blood circulation or blood circulation system. It materializes itself as lack of breath at remainder or with a mild lots, tiredness, swelling, cyanosis (cyanosis) of the nails and also nasolabial triangular. Acute heart failure threatens for the growth of lung edema and also cardiogenic shock, persistent heart failure causes the growth of body organ hypoxia. Heart failure is one of the most usual reasons of human fatality.

A decline in the contractile (pumping) feature of the heart in heart failure causes the growth of a discrepancy in between the hemodynamic demands of the body and also the opportunity of the heart in their execution. This inequality appears by an excess of venous inflow to the heart and also the resistance that the myocardium requires to get over in order to remove blood right into the vascular bed over the capability of the heart to relocate blood to the arterial system.

Not being an independent illness, heart failure creates as a difficulty of numerous pathologies of capillary and also the heart: valvular heart illness, coronary artery illness, cardiomyopathy, arterial high blood pressure, etc.

In some conditions (for instance, arterial high blood pressure), the boost in heart failure happens progressively, over the years, while in others (acute coronary infarction), come with by the fatality of some useful cells, this time around is decreased to days and also hrs. With a sharp progression of heart failure (within minutes, hrs, days), they talk about its acute form. In other cases, heart failure is considered chronic.

Chronic heart failure affects from 0,5 to 2% of the population, and also after 75 years, its prevalence is about 10%. The significance of the problem of the incidence of heart failure is determined by a steady increase in the number of patients suffering from it, a high rate of mortality and disability of patients.

Heart failure >—
with systolic dysfunction
(PVlt; 40%)

left ventricular dysfunction
(PVgt; 40%)

CH classes

Classification of chronic heart failure (CHF)

initial, latent failure
blood circulation appearing only
during exercise (shortness of breath,
palpitations, excessive fatigue).
At rest, these phenomena disappear. Hemodynamics
not broken.

– pronounced long-term failure
blood circulation. Hemodynamic impairment
(stagnation in small and large circles
blood circulation), dysfunction
organs and metabolism are expressed in
peace, disability is severely limited.

PA – signs
circulatory failure expressed
moderately. Hemodynamic disorders only
in one of the departments of the cardiovascular
systems (in a small or large circle
blood circulation).

PB – ending
long stage. Deep violations
hemodynamics in which all
the cardiovascular system
(hemodynamic disturbances as in
large and in small circles of blood circulation).

W – final,
severe dystrophic stage
hemodynamic disorders. Persistent
irreversible metabolic changes
changes in the structure of organs and tissues,
complete disability.

detected by a variety of
physical exercise tests – using
bicycle ergometry. Samples of the Master, on
treadmill and others. The decrease is determined
MOS is also detected by
rheolipocardiography, echocardiography.

The second
Symptoms of HF become apparent
show up at rest. Disability
drops sharply or patients become
incapable of work. 2nd stage is divided
into two periods: 2a and 2B.

stage can go to stage 1B or
full compensation may even come
hemodynamics. The degree of reversibility 2B
stage less.
the healing process occurs or decreases
symptoms of heart failure or temporary transition 2B
stages in 2A and only very rarely in 1B

The third
dystrophic stage,
cirrhotic, cachectic, irreversible,

class I
(FC I)

Patients with
non-cardiac disease
restriction of physical activity.
Normal physical activity is not
causes neither fatigue nor palpitations,
not short of breath

class II

Patients with
heart disease that causes
slight physical limitation
activity. At rest, patients feel
yourself well. Regular physical
stress causes excessive fatigue
palpitations, shortness of breath, or angina pectoris

class III

Patients with
heart disease that causes
significant limitation of physical
activity. At rest, patients feel
yourself well. Small physical
stress causes fatigue
palpitations, shortness of breath, or angina pectoris

class IV

Patients with
heart disease due to which
they cannot even perform the minimum
physical activity. Fatigue,
palpitations, shortness of breath, and angina pectoris
observed at rest, at any load
these symptoms are aggravated

During treatment
stage HF is maintained, and FC changes,
showing the effectiveness of

diagnosis decision
combine stage definition and
functional class chronic
heart failure – for example:
CHD, chronic heart failure
IIB stage, II FC; Hypertrophic
cardiomyopathy, chronic cardiac
insufficiency of stage IIA, IV FC.

Patients complain
general weakness, decline, or loss
disability, shortness of breath, palpitations,
decreased daily urine

associated with stagnation of blood in a small circle
circulatory obstructive
sufficient oxygen
blood. In addition, the lungs become
rigid, which leads to a decrease
respiratory excursions. Arose
hypoxemia leads to insufficient
oxygen supply to organs and tissues,
increased accumulation in the blood
carbon dioxide and other metabolic products
substances that irritate the respiratory
center. As a result,
dyspnoe and tachypnoe.

shortness of breath occurs during physical
energized, then at rest. To the patient
easier to breathe upright
in bed he prefers
headboard position
and with severe shortness of breath he takes
sitting down
legs (orthopnea position).

congestion in the lungs occurs
dry or mucous cough
sputum, sometimes with blood. Stagnation
in bronchi may be complicated by attachment
infections and the development of congestive bronchitis
with the release of mucopurulent
sputum. Percussion
over the lungs a box is defined
tint of sound.

Sweating transudate,
which by gravity descends into
lower parts of the lungs, will cause blunting
percussion sound. Auscultatory:
hard is audible over the lungs
breathing, in the lower parts – weakened
vesicular. In the same departments may
to listen to small and medium bubbles
deaf wet rales.

congestion in the lower parts of the lungs leads
to the development of connective tissue. At
such pneumosclerosis rales become
persistent, very rough (crackling). IN
the power of hypoventilation and blood stasis in
lower parts of the lungs against the background of a decrease
body defenses easily joins
infection – the course of the disease is complicated
hypostatic pneumonia.

from the side of the heart:
borders are shifted to the right or left in
depending on left failure
or right ventricle. With prolonged
total heart failure can be significant
enlarged heart with displacement
borders in all directions, up to development
cardiomegaly (cor bovinum).

a symptom of heart failure is tachycardia.
It serves as a manifestation of compensatory
mechanism providing an increase in IOC
blood. Tachycardia may occur with
physical activity going on and
after its termination. Subsequently she
becomes constant.
Arterial pressure
decreases, diastolic remains
normal. Pulse pressure decreases.

heart failure is characteristic
peripheral cyanosis
– cyanosis of lips, earlobes, chin,
fingertips. It is associated with insufficient
blood oxygen saturation which
intensively absorbed by tissues during
slow motion of blood on the periphery.
Peripheral Cold Cyanosis
– limbs, protruding parts of the face

and an early symptom of congestion
in the pulmonary circulation is
as CH increases. First, the liver is swollen,
painful, its edge is rounded.
prolonged congestion in the liver
overgrowth of the connective occurs
tissue (liver fibrosis develops).
It becomes tight, painless,
its size decreases after taking
diuretic drugs.

stagnation in a big circle
circulatory overflow observed
blood superficial
The cervical vein swelling is best seen.
Swollen veins on the hands are often visible.
Healthy veins sometimes swell.
with arms down, but when raised
hands they fall. With heart failure, veins do not fall
even when raising them above horizontal

the result of slowing blood flow in
kidneys decreases their water excretion
function. There is oliguria,
which may
be of different sizes, but as
daily development of the disease
diuresis is reduced to 400-500 ml per day.
Nocturia observed
– advantage of night diuresis over
daytime, due to improved work
hearts at night. Relative
urine density increases
congestive proteinuria detected
and microhematuria.

of the most common symptoms of stagnation
blood in the pulmonary circulation
are swelling
which are localized in the lower sections,
starting from the bottom
limbs. In the initial stages, in
areas of the ankles, feet. As
progression of HF swelling spread
on the shins, hips. Then arise in
subcutaneous tissue of the genital organs,
belly, back.

If the patient is long
was in bed, early localization
edema is the lower back, sacrum. At
large swelling they spread
on the subcutaneous tissue of the whole organism
– there is anasarka. Free from
swelling remains the head, neck, most
upper torso.
the initial stages of HF swelling appear
at the end of the day, disappear by morning.

Oh hidden
swelling can be judged by weight gain
body, decrease daily diuresis,
nocturia. Cardiac edema is inactive.
They change their localization little with
a change in the position of the patient.
swelling. They become especially dense
on legs with development in places of edema
connective tissue.

(sweating in the pleural cavity). So
how pleural vessels relate to
large (parietal
pleura) and to the small (visceral pleura)
circulatory system, hydrotorx can
occur with blood stasis as in one,
so in the second round of blood circulation.
light and sometimes shifting under pressure
mediastinal organs, it worsens
patient, increases shortness of breath.

Acute and chronic heart failure are distinguished by the rate of increase in signs of decompensation.

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

  • on the left type (acute left ventricular or left atrial insufficiency)
  • acute right ventricular failure

In the development of chronic heart failure according to the classification of Vasilenko-Strazhesko, there are three stages:

I (initial) stage – hidden signs of circulatory failure, manifested only in the process of physical exertion by shortness of breath, palpitations, excessive fatigue; at rest hemodynamic disturbances are absent.

II (expressed) stage – signs of prolonged circulatory failure and hemodynamic disturbances (congestive phenomena of the small and large circles of blood circulation) are expressed at rest; severe disability:

  • Period II A – moderate hemodynamic disturbances in one part of the heart (left or right ventricular failure). Dyspnea develops with normal physical activity, working capacity is sharply reduced. Objective signs are cyanosis, swelling of the legs, the 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; total disability.

III (dystrophic, final) stage – persistent insufficiency of blood circulation and metabolism, morphologically irreversible disturbances in the structure of organs (liver, lungs, kidneys), exhaustion.

Causes of heart failure

Among the most common causes of heart failure that occur in 60-70% of patients are called myocardial infarction and coronary heart disease. They are followed by rheumatic heart diseases (14%) and dilated cardiomyopathy (11%). In the age group over 60, in addition to coronary heart disease, heart failure also causes hypertension (4%). In elderly patients, type 2 diabetes and its combination with arterial hypertension are a common cause of heart failure.

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Risk Factors

Factors that provoke the development of heart failure, cause its manifestation with a decrease in the compensatory mechanisms of the heart. Unlike causes, risk factors are potentially reversible, and their reduction or elimination can delay the aggravation of heart failure and even save the patient’s life.

  • overstrain of physical and psycho-emotional capabilities
  • arrhythmias, pulmonary embolism, hypertensive crises, progression of coronary heart disease;
  • pneumonia, SARS, anemia, renal failure, hyperthyro >1.
    The main trigger of CHF is
    myocardial contractility
    and a drop in cardiac output,
    which causes a decrease in perfusion row
    organs and activation of compensatory
    mechanisms (sympathetic adrenal
    renin-angiotensin-aldosterone systems
    systems, etc.).

Catecholamines (norepinephrine) cause
peripheral vasoconstriction of arterioles
and venules increase venous return
to the heart and level to normal reduced
cardiac output (compensatory
reaction). However, further activation
sympathetic adrenal system leads
to the progression of heart failure (catecholamines
activate RAAS, tachycardia worsens
filling the heart with diastole, etc.
decompensation reactions).

Renal arteriole spasm hypoperfusion
kidney on the background of heart failure 
activation of RAAS 
hyperproduction of angiotensin II
(powerful vasopressor; potentiates
hypertrophy and myocardial remodeling)
and aldosterone (increases reabsorption
sodium and plasma osmolality, activates
ADH products that delays
water). BCC increase on the one hand
normalizes cardiac output (compensation),
on the other, it potentiates dilation and
heart damage (decompensation).

An important role in the development of heart failure
also endothelial vascular dysfunction
(decrease in endothelial production
Vasorelaxing factor), overproduction
a number of cytokines: IL, TNF-
(disrupts the transport of calcium ions inward
cells, inhibits PVA dehydrogenase,
leading to ATP deficiency, triggers apoptosis

By origin:
due to volume overload, due to
primary myocardial pressure overload

In the heart cycle:
systolic type, diastolic
form, mixed form

According to the clinical version:
left ventricular, right ventricular,
biventricular (total)

In terms of cardiac output:
low cardiac output, high
cardiac output

The development of acute heart failure is often observed against the background of myocardial infarction, acute myocarditis, severe arrhythmias (ventricular fibrillation, paroxysmal tachycardia, etc.). In this case, a sharp drop in the minute release and blood flow into the arterial system occurs. Acute heart failure is clinically similar to acute vascular failure and is sometimes referred to as acute cardiac collapse.

In chronic heart failure, the changes developing in the heart are compensated for a long time by its intensive work and adaptive mechanisms of the vascular system: an increase in the force of contractions of the heart, an increase in rhythm, a decrease in pressure in the diastole due to the expansion of capillaries and arterioles, facilitating the emptying of the heart during systole, and an increase in perfusion tissues.

A further increase in the phenomena of heart failure is characterized by a decrease in the volume of cardiac output, an increase in the residual amount of blood in the ventricles, their overflow during diastole, and overstretching of the myocardial muscle fibers. Constant overstrain of the myocardium, trying to push blood into the vascular bed and maintain blood circulation, causes its compensatory hypertrophy. However, at a certain point, the stage of decompensation begins, due to the weakening of the myocardium, the development of processes of dystrophy and sclerosis in it. The myocardium itself begins to experience a lack of blood supply and energy supply.

At this stage, neurohumoral mechanisms are included in the pathological process. Activation of the mechanisms of the sympathetic-adrenal system causes vasoconstriction on the periphery, which helps to maintain stable blood pressure in the mainstream of a large circle of blood circulation with a decrease in cardiac output. Renal vasoconstriction that develops with this leads to renal ischemia, which contributes to interstitial fluid retention.

Increased pituitary secretion of antidiuretic hormone increases the processes of water reabsorption, which entails an increase in the volume of circulating blood, an increase in capillary and venous pressure, and increased transudation of fluid in the tissue.

T.O., severe heart failure leads to gross hemodynamic disorders in the body:

Gas exchange disorder

When the blood flow slows down, tissue uptake of oxygen from the capillaries increases from 30% normal to 60-70%. The arteriovenous difference in blood oxygen saturation increases, which leads to the development of acidosis. The accumulation of under-oxidized metabolites in the blood and the increase in the work of the respiratory muscles cause activation of the main metabolism.

A vicious circle arises: the body experiences an increased need for oxygen, and the circulatory system is unable to satisfy it. The development of the so-called oxygen debt leads to the appearance of cyanosis and shortness of breath. Cyanosis in heart failure can be central (with congestion in the pulmonary circulation and impaired blood oxygenation) and peripheral (with slower blood flow and increased oxygen utilization in tissues). Since circulatory failure is more pronounced on the periphery, in patients with heart failure there is acrocyanosis: cyanosis of the extremities, ears, and tip of the nose.


Edema develops as a result of a number of factors: interstitial fluid retention with increasing capillary pressure and slowing blood flow; delays in water and sodium in violation of water-salt metabolism; violation of oncotic blood plasma pressure in the disorder of protein metabolism; decrease inactivation of aldosterone and antidiuretic hormone with a decrease in liver function.

Edema in heart failure is initially hidden, expressed by a rapid increase in body weight and a decrease in the amount of urine. The appearance of visible edema begins with the lower extremities if the patient is walking, or from the sacrum if the patient is lying. In the future, abdominal dropsy develops: ascites (abdominal cavity), hydrothorax (pleural cavity), hydropericardium (pericardial cavity).

stagnant organ changes

Congestion in the lungs is associated with impaired hemodynamics of the pulmonary circulation. They are characterized by stiffness of the lungs, a decrease in the respiratory excursion of the chest, limited mobility of the pulmonary edges. It manifests itself as congestive bronchitis, cardiogenic pneumosclerosis, hemoptysis. Stagnation of a large circle of blood circulation causes hepatomegaly, which is manifested by heaviness and pain in the right hypochondrium, and then cardiac fibrosis of the liver with the development of connective tissue in it.

The expansion of the cavities of the ventricles and atria in heart failure can lead to relative insufficiency of the atrioventricular valves, which is manifested by swelling of the veins of the neck, tachycardia, and expansion of the borders of the heart. With the development of congestive gastritis, nausea, loss of appetite, vomiting, a tendency to constipation, flatulence, loss of body weight appear. With progressive heart failure, a severe degree of exhaustion develops – cardiac cachexia.

Stagnant processes in the kidneys cause oliguria, an increase in the relative density of urine, proteinuria, hematuria, and cylindruria. Violation of the functions of the central nervous system in heart failure is characterized by rapid fatigue, decreased mental and physical activity, increased irritability, sleep disturbance, and depressive states.

Symptoms of heart failure

Acute heart failure

Acute heart failure is caused by a weakening of the function of one of the departments of the heart: the left atrium or ventricle, the right ventricle. Acute left ventricular failure develops in diseases with a predominant load on the left ventricle (hypertension, aortic defect, myocardial infarction). With weakening of the functions of the left ventricle, pressure in the pulmonary veins, arterioles and capillaries increases, their permeability increases, which leads to sweating of the liquid part of the blood and the development of first interstitial and then alveolar edema.

The clinical manifestations of acute left ventricular failure are cardiac asthma and alveolar pulmonary edema. An attack of cardiac asthma is usually triggered by physical or psychological stress. An attack of sudden suffocation often occurs at night, forcing the patient to wake up in fear. Cardiac asthma is manifested by a feeling of lack of air, palpitations, cough with difficult sputum, sharp weakness, cold sweat.

The patient takes the position of orthopnea – sitting with legs down. On examination, the skin is pale with a grayish tint, cold sweat, acrocyanosis, severe shortness of breath. A weak, frequent filling of an arrhythmic pulse, expansion of the borders of the heart to the left, deaf heart tones, gallop rhythm is determined; blood pressure tends to decrease. In the lungs, hard breathing with single dry rales.

A further increase in congestive phenomena of the small circle contributes to the development of pulmonary edema. Sharp asphyxiation is accompanied by a cough with the release of an abundant amount of foamy pink sputum (due to the presence of an impurity of blood). In the distance, bubbling breathing with moist rales is heard (a symptom of a “boiling samovar”). The patient’s position is orthopnea, the face is cyanotic, the neck veins swell, cold sweat covers the skin. The pulse is threadlike, arrhythmic, frequent, Blood pressure is reduced, in the lungs are moist rales of various sizes. Pulmonary edema is an emergency condition requiring intensive care measures, because it can lead to death.

Acute left atrial heart failure occurs with mitral stenosis (left atrial ventricular valve). Clinically manifested by the same conditions as acute left ventricular failure. Acute right ventricular failure often occurs with thromboembolism of large branches of the pulmonary artery. Stagnation develops in the vascular system of a large circle of blood circulation, which is manifested by swelling of the legs, pain in the right hypochondrium, a feeling of fullness, swelling and pulsation of the cervical veins, shortness of breath, cyanosis, pain or pressure in the heart. The peripheral pulse is weak and frequent, blood pressure is sharply reduced, CVP is increased, the heart is expanded to the right.

With diseases that cause decompensation of the right ventricle, heart failure manifests itself earlier than with left ventricular failure. This is due to the large compensatory capabilities of the left ventricle, the most powerful part of the heart. However, with a decrease in left ventricular function, heart failure progresses at a catastrophic rate.

Chronic heart failure

The initial stages of chronic heart failure can develop according to the left and right ventricular, left and right atrial types. With aortic defect, mitral valve insufficiency, arterial hypertension, coronary insufficiency, congestion in the vessels of the small circle and chronic left ventricular failure develop. It is characterized by vascular and gas changes in the lungs. Shortness of breath occurs, asthma attacks (usually at night), cyanosis, palpitations, coughing (dry, sometimes with hemoptysis), and increased fatigue.

Even more pronounced congestion in the pulmonary circulation develops in patients with chronic left atrial insufficiency in patients with mitral valve stenosis. Shortness of breath, cyanosis, cough, hemoptysis appear. With prolonged venous congestion in the vessels of the small circle, sclerosis of the lungs and blood vessels occurs. There is an additional, pulmonary obstruction to blood circulation in the small circle. Increased pressure in the pulmonary artery system causes an increased load on the right ventricle, causing its insufficiency.

With a predominant lesion of the right ventricle (right ventricular failure), congestion develops in a large circle of blood circulation. Right ventricular failure can accompany mitral heart defects, pneumosclerosis, emphysema, etc. There are complaints of pain and heaviness in the right hypochondrium, the appearance of edema, decreased urine output, bursting and an increase in the abdomen, shortness of breath with movements. Cyanosis develops, sometimes with a jaundice-cyanotic hue, ascites, cervical and peripheral veins swell, and the liver grows in size.

Functional insufficiency of one part of the heart cannot remain isolated for a long time, and over time, total chronic heart failure develops with venous congestion in the mainstream of the small and large circles of blood circulation. Also, the development of chronic heart failure is noted with damage to the heart muscle: myocarditis, cardiomyopathy, coronary heart disease, intoxication.


Since heart failure is a secondary syndrome that develops with known diseases, diagnostic measures should be aimed at its early detection, even in the absence of obvious signs.

When collecting a clinical history, attention should be paid to fatigue and dyspnea, as the earliest signs of heart failure; the patient has coronary heart disease, hypertension, myocardial infarction and rheumatic fever, cardiomyopathy. Identification of swelling of the legs, ascites, rapid low-amplitude pulse, listening to the III cardiac sound and displacement of the borders of the heart are specific signs of heart failure.

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

ECG for specific changes helps to detect hypertrophy and insufficient blood supply (ischemia) of the myocardium, as well as arrhythmias. Based on electrocardiography, various load tests are widely used with the use of an exercise bike (bicycle ergometry) and a treadmill (treadmill test). Such tests with a gradually increasing load level make it possible to judge the reserve possibilities of heart function.

Using ultrasound echocardiography, it is possible to establish the cause of heart failure, as well as evaluate the pumping function of the myocardium. With the help of heart MRI, IHD, congenital or acquired heart defects, arterial hypertension and various other diseases are successfully diagnosed. Radiography of the lungs and chest organs in heart failure determines congestive processes in the small circle, cardiomegaly.

CT OGK S. Dilation of the lobar pulmonary arteries (red arrows), expansion of the right ventricle (green arrow), bilateral effusion in the chest cavity (yellow arrows) in a patient with congestive events in the pulmonary circulation

Radioisotope ventriculography in patients with heart failure allows a high degree of accuracy to assess the contractility of the ventricles and determine their volumetric capacity. In severe forms of heart failure, ultrasound of the abdominal cavity, liver, spleen, and pancreas is performed to determine damage to internal organs.

Heart failure treatment

With heart failure, treatment is carried out aimed at eliminating the primary cause (coronary heart disease, hypertension, rheumatism, myocarditis, etc.). In case of heart defects, cardiac aneurysm, adhesive pericarditis, which create a mechanical barrier to the heart, they often resort to surgical intervention.

In acute or severe chronic heart failure, bed rest is prescribed, complete mental and physical rest. In other instances, you should adhere to moderate loads that do not interfere with well-being. Fluid intake is limited to 500-600 ml per day, salt – 1-2 g. A fortified, easily digestible diet food is prescribed.

Pharmacotherapy of heart failure can extend and also significantly improve the condition of patients and their quality of life.

With heart failure, the following groups of drugs are prescribed:

  • cardiac glycosides (digoxin, strophanthin, etc.) – boost myocardial contractility, increase its pumping function and diuresis, contribute to satisfactory tolerance of physical activity;
  • vasodilators and ACE inhibitors – angiotensin-converting enzyme (enalapril, captopril, lisinopril, perindopril, ramipril) – reduce vascular tone, expand veins and arteries, thereby reducing vascular resistance during heart contractions and contributing to an increase in cardiac output;
  • nitrates (nitroglycerin and its prolonged forms) – improve blood supply to the ventricles, increase cardiac output, and expand the coronary arteries;
  • diuretics (furosemide, spironolactone) – reduce the retention of excess fluid in the body;
  • Β-adrenoblockers (carvedilol) – reduce the heart rate, improve blood circulation in the heart, increase cardiac output;
  • anticoagulants (acetylsalicylic acid, warfarin) – prevent blood clots in blood vessels;
  • drugs that improve myocardial metabolism (B vitamins, ascorbic acid, inosine, potassium preparations).

With the development of an attack of acute left ventricular failure (pulmonary edema), the patient is hospitalized and provides emergency treatment: diuretics, nitroglycerin, drugs that increase cardiac output (dobutamine, dopamine) are administered, oxygen is inhaled. With the development of ascites, puncture removal of fluid from the abdominal cavity is carried out, with the occurrence of hydrothorax, pleural puncture is performed. Due to severe tissue hypoxia, oxygen therapy is prescribed to clients with heart failure.

Prognosis and also prevention

The five-year survival threshold for clients with heart failure is 50%. The long-lasting prognosis is variable, it is affected by the severity of heart failure, concomitant background, the effectiveness of therapy, lifestyle, etc. The treatment of heart failure in the early stages can fully compensate for the condition of patients; the worst prognosis is observed in phase III heart failure.

Prevention of heart failure is the prevention of the development of the diseases causing it (IHD, hypertension, heart defects, etc.), as well as factors contributing to its occurrence. In order to avoid the progression of already developed heart failure, it is necessary to observe the optimal regime of exercise, taking the prescribed drugs, continuous tracking by a cardiologist.

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Tatyana Jakowenko

Editor-in-chief of the Detonic online magazine, cardiologist Yakovenko-Plahotnaya Tatyana. Author of more than 950 scientific articles, including in foreign medical journals. He has been working as a cardiologist in a clinical hospital for over 12 years. He owns modern methods of diagnosis and treatment of cardiovascular diseases and implements them in his professional activities. For example, it uses methods of resuscitation of the heart, decoding of ECG, functional tests, cyclic ergometry and knows echocardiography very well.

For 10 years, she has been an active participant in numerous medical symposia and workshops for doctors - families, therapists and cardiologists. He has many publications on a healthy lifestyle, diagnosis and treatment of heart and vascular diseases.

He regularly monitors new publications of European and American cardiology journals, writes scientific articles, prepares reports at scientific conferences and participates in European cardiology congresses.