Heart failure: symptoms, causes, treatment

Heart failure is associated with decreased heart function. The heart muscle cannot produce the energy needed to pump the required amount of blood throughout the body.

In Russia alone, about 7 million people suffer from heart failure. In people over 70, one in four people are affected, with men typically affected at a much younger age than women. The risk for men is approximately one and a half times higher than for women. In Russia, diseases of the circulatory system are the most common cause of death.

• What is heart failure?
• What causes heart failure?
• What are the types of heart failure and what are their symptoms? Left-sided heart failure
• Right-sided heart failure
• Global heart failure
• Systolic heart failure
• Diastolic heart failure
• Chronic heart failure
• Acute heart failure

What is heart failure?

With a healthy heart, oxygen-rich blood from the left ventricle is pumped through the body to the organs, providing them with oxygen and nutrients. After supplying the organs, low-oxygen blood returns from the body to the right side of the heart, from where it is transported to the lungs. In the lungs, the blood is enriched with oxygen so that it can again be pumped throughout the body through the left ventricle.

Heart failure is a weakening of the pumping function of the heart. Typically, either the right side of the heart is affected (right-sided heart failure) or the left side of the heart (left-sided heart failure). With advanced heart failure, both sides of the heart can be affected (global heart failure). Heart failure can also be chronic or acute in nature. Chronic heart failure is more common than acute heart failure, which occurs suddenly and unexpectedly. Acute heart failure can occur suddenly against the background of an acute cardiovascular accident and/or decompensated heart failure.

3. How to prevent worsening of the condition in heart failure?

To prevent congestive heart failure from progressing, it is important to monitor your health very closely. Do not violate the recommended medication regimen. And you need to regularly visit your doctor to make sure that the disease is not developing. Fluid retention in the body is one of the symptoms of heart failure and is a reason to immediately consult a doctor. Dizziness, weakness, shortness of breath can also be signs of heart failure, and if these symptoms reappear during treatment, do not delay a visit to a specialist.

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What are the types of heart failure and what are their symptoms?

Each type of heart failure has different symptoms, and the symptoms can vary in intensity. However, the main symptom of heart failure is difficulty breathing during exercise or at rest. Warning signs may include sweating with mild exercise, an inability to lie flat, tightness in the chest, or swelling in the legs.

Left-sided heart failure

The left side of the heart is responsible for pumping oxygen-rich blood throughout the body to the organs. In left-sided heart failure, the pumping function of the left ventricle is limited, resulting in insufficient oxygenated blood to be pumped throughout the body. Instead, the blood remains in the pulmonary circulation, which can lead to fluid in the lungs (pulmonary edema), difficulty breathing, throat irritation, a rattling sound when breathing, weakness, or dizziness.

It is most often caused by coronary artery disease (CHD), high blood pressure or a heart attack, and less commonly by problems with the heart muscle or heart valves.

Left-sided heart failure may present acutely or develop over time. It is usually first noticed by shortness of breath from physical activity. When severe, it can even lead to hypotension (low blood pressure) at rest.

Right-sided heart failure

The right side of the heart is responsible for returning low-oxygen blood back to the lungs. In right-sided heart failure, the right ventricle does not work properly. This causes increased pressure in the veins, forcing fluid into the surrounding tissue. This leads to swelling, especially in the feet, toes, ankles and legs. This can also lead to an urgent need to urinate at night when the kidneys receive better blood circulation.

The cause is most often an acute or chronic increase in pulmonary circulatory resistance. Caused by pulmonary diseases such as pulmonary embolism, asthma, severe emphysema, chronic obstructive pulmonary disease (COPD, most commonly due to tobacco use), or left-sided heart failure. Rare causes include heart valve problems or heart muscle disease.

Global heart failure

When both the left and right sides of the heart are affected, it is called global heart failure. There are symptoms of left and right heart failure.

Systolic and diastolic heart failure

Systolic heart failure is associated with loss of normal functioning of heart muscle cells or external impairment of pumping function. Blood enters the lungs, and the organs do not receive enough oxygen.

In diastolic heart failure, the elasticity of the ventricle is lost, causing it to not relax and fill appropriately. One of the most common causes of diastolic dysfunction is high blood pressure. Due to increased resistance in the arteries, the heart must work harder. The elasticity of the heart muscle decreases, and less blood can be pumped from the ventricles to the body between contractions. This results in the body not receiving enough blood and nutrients.

Heart valve disease can also cause the heart muscle to thicken. The heart muscles become stiffer and less elastic due to the accumulation of proteins. Symptoms range from cough to shortness of breath.

Chronic and acute heart failure

Chronic heart failure is a progressive disease that takes months or years to develop and is more common than acute heart failure. In chronic heart failure, symptoms are often not taken seriously because the body is able to compensate over a long period of time or symptoms are associated with increasing age. Symptoms reflect either left- or right-sided heart failure.

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.

ABOUT HEART FAILURE AND THE USE OF DIURETICS

Some patients with CHF have very moderate manifestations of cardiac decompensation. It is important for the doctor to overcome the stereotype that dictates the prescription of diuretics to any patient diagnosed with CHF. Diuretics are indicated only for patients with CHF who have clinical signs and symptoms of excessive fluid retention in the body.

The features of diuretic therapy, its components and errors in prescribing certain diuretics will be discussed1.

In the practice of modern cardiologists and therapists in the treatment of heart failure, sufficient attention is paid to diuretic therapy. For the effective action of diuretics, it is important: entry into the body, adsorption and entry into the bloodstream, filtration and penetration into the renal tubules, active influence on specific transporters (electrolyte carriers in the apical membrane of renal tubule cells).

Table Classification of diuretics, their quality indicators

Today, thiazide and loop diuretics . What is the difference?

Thiazide diuretics act on the cortical segment of the loop of Hengle in the area of ​​the distal tubules, blocking the activity of the sodium-chloride transporter. Their effect on Na+ reabsorption and, therefore, on diuresis is moderate and is observed with normal renal function (creatinine clearance greater than 30 ml/min.). Thiazide diuretics suppress the reabsorption of sodium, increasing the excretion of it and other ions in the urine, they practically do not disturb the acid-base balance, compared with loop diuretics, they begin to act later (2 hours after administration, but have a longer effect (12–36 h), reduce glomerular filtration, reduce Ca+ excretion in the urine, do not have a “rebound” effect. They are indicated for edema of any level, hypertension, and diabetes insipidus.

Important! Thiazide diuretics are not prescribed for significant renal failure, severe diabetes mellitus, or gout with kidney damage.

The most powerful are loop diuretics , which block the activity of a special Na+/2Cl-/K+ transporter in tubular cells throughout the entire ascending segment of the loop of Hengle. The diuretic effect of loop diuretics is stronger and persists even with reduced renal function (with creatinine clearance not lower than 5 ml/min.). When using these diuretics, the effect occurs quickly and does not last long, so they require repeated doses throughout the day. It has been established that loop diuretics interfere with Na+ reabsorption and increase glomerular filtration. Loop diuretics are prescribed for edema caused by CHF, dysfunction of the liver, kidneys, and endocrine glands. They are indicated for edema of the brain, lungs, and to relieve hypertensive crises. The action of loop diuretics can provoke a pronounced deficiency of Na+ K+ Mg+ Cl- ions, dehydration, decreased tolerance to carbohydrates, and increased concentrations of uric acid and lipids in the blood serum. Ethacrynic acid may cause ototoxic effects.

Important! Loop diuretics are contraindicated in severe diabetes mellitus, uric acid diathesis, severe liver and kidney damage. These diuretics should not be used during lactation if you are intolerant to sulfonamide drugs.

RECOMMENDATIONS OF AN EXPERT

When using loop and thiazide diuretics in the blood, the concentration of cholesterol, beta-lipoproteins, and triglycerides increases, therefore, when prescribing diuretics, lipids in the diet should be limited, and, if necessary, combine them with angiotensin-converting enzyme inhibitors (ACE inhibitors). Another complication of treatment with loop and thiazide diuretics is hyperuricemia (increased levels of uric acid in the blood serum), in order to avoid it requires a corrective diet with limited purines, as well as the use of diuretics with ACE inhibitors. This combination - capozide + ACE inhibitors - is effective, both components enhance each other’s effect and is safe, because allows you to avoid many adverse reactions characteristic of diuretic therapy.

Diuretic treatment tactics include two phases: active and maintenance .

The task of the active phase is to eliminate excess accumulation of fluid in the body, manifested in the form of edema. In this phase, it is necessary to create forced diuresis, with urine excreted exceeding the fluid consumed by 800–1000 ml per day. In parallel, body weight should decrease daily by no more than 750–1000 g.

After achieving optimal dehydration, the patient is transferred to the maintenance stage of treatment. During this period, the amount of fluid drunk should not exceed the volume of urine excreted, and body weight should remain stable. The main thing in the maintenance phase of treatment is the daily use of selected doses of diuretics.

It is important to remember that the practice of prescribing “shock” doses of diuretics (once every few days) is flawed and is difficult for patients to tolerate. It is better to recommend the patient the drug “ Hypothiazide ” - 12.5-25 mg per day than 40-80 mg of the drug “ Lasix” once every 5 days.

In the latter case, the patient lives in a vicious cycle. He spends the day of taking the diuretic near the toilet due to excessive diuresis. On the 2nd day, the patient is completely overwhelmed, thirsty, and suffers from electrolyte imbalance (even to the point of seizures). On the 3rd day the patient begins to recover. On the 4th day he could feel cheerful, but over the days that have passed since the start of taking the drug, the accumulating fluid again causes overhydration and shortness of breath, which will require repeating the “shock” diuresis on the morning of the 5th day.

ALGORITHM FOR PRESCRIPTION OF DIURETICS DEPENDING ON THE SEVERITY OF CHF

• Functional class I (no edema) - you can do without diuretics;
• Functional class II (stagnation) - thiazide or loop diuretics are indicated in small doses, with a glomerular filtration rate of 30 ml/min. the use of thiazide diuretics is not recommended;
• III functional class (maintenance treatment) - loop diuretics + spironolactone are recommended;
• IV functional class - loop + thiazide diuretics + aldosterone antagonists are indicated.

INTERACTION OF DIURETICS WITH OTHER medicinal products, MECHANISM OF ACTION OF DIURETICS

In order to avoid unwanted effects, you must follow several recommendations:

• the combined use of thiazide diuretics and cardiac glycosides increases the toxicity of the latter due to hypokalemia;
• the combination of thiazide drugs with antihypertensives has an increased hypotensive effect;
• when diuretics are prescribed simultaneously with glucocorticoids, the likelihood of hyperglycemia is high;
• Furosemide increases the ototoxic effect of aminoglycosides, increasing the risk of developing glycoside intoxication;
• When loop diuretics are combined with nonsteroidal anti-inflammatory drugs (NSAIDs), the diuretic effect is weakened.

I am glad that the percentage of choice of Torasemide for initial therapy has become quite high - 68%, for Indapamide - only 13%. It is necessary to use new generation loop diuretics, such as Torasemide , Britomar, . It is noticed that:

• Torsemide is able to block aldosterone receptors.

In American studies, it was emphasized that there was a 56% reduction in re-hospitalization compared with the use of furosemide;

• the combination of thiazide and loop diuretics with ACE inhibitors leads to an increased diuretic effect.

ACE inhibitors can be prescribed to patients with CHF with a systolic pressure level above 85 mmHg. Art. At initially low blood pressure, the activity of ACE inhibitors remains. The prescription of ACE inhibitors is necessary with a gradual reduction in the starting dose. To exclude hypertension, the first dose of ACE inhibitors should be administered 24 hours after heavy diuresis;

• Spironolactone increases the concentration of cardiac glycosides in the blood and enhances the hypotensive effect of antihypertensive drugs.

With the simultaneous administration of spironolactone and non-steroidal anti-inflammatory drugs, the diuretic effect is reduced;

• ACE inhibitors, as an addition to the treatment of edema, not only improve the general condition of the patient, but also reduce the risk of hospitalization;
• normalization of the protein profile is necessary, namely the use of Albumin (200–400 ml/day), possibly together with diuretics, which increases the rate of their filtration;
• if the blood pressure level is sufficient, it is possible to additionally prescribe drugs that increase the glomerular filtration rate.

Only a third of surveyed doctors (30%) prescribe the maximum tolerated dose;

• if the absorption of the drug is impaired, the dose of the diuretic prescribed orally can be increased as desired, but success will not be achieved, and only transferring the patient to parenteral treatment will provide an adequate diuretic response;
• in case of systemic hypotension, the dose of diuretics and vasodilators should be increased no more than once a week;
• in case of intolerance to ACE inhibitors, sartan preparations that do not have indications for heart failure ( Eprosartan, Candesartan , etc.) should not be prescribed to patients with heart failure;

Only sartans in a number of studies have proven their effectiveness in patients with heart failure from functional classes I to IV. But you need to know that not all sartans have indications for heart failure ; only 59% of medical specialists know this;

• in practice, underestimation of heart rate control in patients with heart failure has been observed.

The good news is that 9 out of 10 doctors know that heart rate control is needed, but low doses of beta blockers, when the heart rate (according to outpatient records) is more than 70, the doses of beta blockers are not optimized in 76% of cases. The use of the drug Ivab Radin (Coraxan), the first representative of a new class of drugs - if-channel inhibitors, has increased the survival rate of patients with CHF;

• irresponsible ignorance of the role of mineralocorticoid receptors in the treatment of patients with heart failure. According to studies, it was found that 47% of surveyed doctors use drugs of this group ( Spironolactone ) in the treatment of heart failure from functional classes II to IV.

Summary. To achieve positive results in the treatment of CHF, the doctor should inform the patient about how and when to take medications, familiarize him with a list of recommendations, including the dose and frequency of taking each drug, and also give the patient an idea of ​​the most common side effects of diuretics and the need for See a doctor if they occur.

—— 1 Prepared based on the introduction by Anna Ivanovna Chesnikova , Chairman of the Rostov Regional Research Society of Therapists, Doctor of Medical Sciences, Professor, at a symposium within the framework of the XI National Congress of Therapists

What classes is heart failure divided into?

There are several classifications of heart failure:

1. Classification according to V. Kh. Vasilenko, N. D. Strazhesko, G. F. Lang;
2. Classification of acute heart failure according to the Killip scale;
3. And the most common is the New York Heart Association classification.

According to the New York Heart Association (NYHA) functional classification, heart failure is classified into classes I-IV depending on the severity of symptoms and limitation of physical activity.

Heart failure is divided into four classes depending on the severity of symptoms:

• NYHA I: heart disease without any restrictions on physical activity. Normal activity does not cause increased fatigue, palpitations, or difficulty breathing.
• NYHA II: Heart disease causing moderate limitation in daily activities. No symptoms at rest.
• NYHA III: Heart disease causing marked limitation in daily activities. Simple activities such as brushing your teeth, eating, or talking cause fatigue, palpitations, or difficulty breathing. There are no symptoms at rest.
• NYHA IV: Heart disease that causes symptoms at rest (and with any degree of light physical activity).

Heart failure significantly reduces quality of life. Patients often experience great frustration with physical limitations and tend to withdraw from social life. For this reason, psychological disorders such as depression are often present in addition to the expected physical symptoms.

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.

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.

Diuretics in the treatment of cardiovascular pathology

S – diameter of vessels.
The rheological properties of blood are determined by hematocrit (polycythemia), blood viscosity (hyperlipidemia, hyperfibrinogenemia, hyperglycemia), erythrocyte mobility, platelet aggregation state, etc.

Thus, there are 5 main areas of application of therapeutic interventions in the treatment of HF and hypertension:

1) sympatho-adrenal system - blockade of a- and b-adrenergic receptors;

2) kidneys – diuretics;

3) renin–angiotensin–aldosterone system – ACE inhibitors and vascular AT1 receptor blockers;

4) vascular system - peripheral vasodilators, in particular anti-calcium drugs;

5) blood rheology – antiplatelet agents, hypolipidemic, hypoglycemic, etc.

Modern cardiology cannot be imagined without β-blockers, of which more than 20 names are known, ACE inhibitors [5]. However, currently diuretics occupy a priority place in the treatment of dilated cardiopathy and hypertension

.

In the treatment of hypertension, there are three main goals: immediate, intermediate and final [1,6,7].

Immediate goal

antihypertensive therapy - reducing blood pressure to a “normal” level (< 130/85 mm Hg), and, if possible, an “optimal” level (< 120/80 mm Hg).

Interim goal

– prevention of target organ damage (central nervous system, heart, kidneys).

Final goal

– improve the quality and increase the life expectancy of patients with hypertension through the prevention or regression of cardiovascular complications.

Accumulated clinical experience indicates that thiazide diuretics have fairly high antihypertensive activity, not inferior to β-blockers, calcium antagonists, ACE inhibitors and α1-blockers. Numerous studies have shown that when treated with thiazide diuretics, systolic blood pressure decreases by an average of 10–20 mmHg, and diastolic blood pressure by 5–15 mmHg. [8–10].

Comparative studies have shown that there is no significant difference in the antihypertensive activity of low (<25 mg hydrochlorothiazide per day or equivalent doses of other drugs) and high doses (>25 mg) thiazide diuretics. Based on pooled data from 31 studies, high doses of thiazide diuretics reduced blood pressure levels by an average of 18/11 mmHg, and low doses by 13/9 mmHg. At the same time, low doses of diuretics are much better tolerated by patients and are not accompanied by significant electrolyte and metabolic disturbances [11].

Unlike beta-blockers, diuretics are equally effective in preventing cardiovascular complications in both middle-aged and elderly patients with hypertension. In 18 randomized studies in which diuretics and beta-blockers were used in the treatment of hypertension in patients over 60 years of age, it was found that diuretics effectively prevent the development of primary and recurrent cerebrovascular accidents [12]. However, unlike beta-blockers, diuretics are more effective in preventing the risk of coronary heart disease and death, which makes them first-line drugs in the initial treatment of hypertension.

Thus, thiazide diuretics are prescribed in small doses (no more than 25 mg per day), have fairly high antihypertensive activity and are well tolerated. This is the only class of antihypertensive drugs known to improve long-term prognosis in patients with hypertension.

Thiazide and thiazide-like diuretics can be divided into two generations. The first generation is derivatives of benzothiadiazone (hydrochlorothiazide, etc.) and phthelimidine (chlorthalidone, etc.); the second generation is chlorobenzamide derivatives (indapamide, etc.), which in chemical structure are a chlorobenzamide derivative containing a methylindoline group.

The hemodynamic effect of indapamide-like diuretics is due to their pharmacological action. In particular, indapamide

- a moderate saluretic diuretic associated with inhibition of the reabsorption of Na+, Cl–, H+ and, to a lesser extent, K+ and Mg2+ in the proximal and distal tubules of the short segment of the nephron. At the same time, indapamide eliminates the excess content of sodium ions in the vascular wall (due to its high lipophilicity), increases the synthesis of prostaglandin E2 and prostacyclin I2, inhibits the influx of Ca ions into vascular smooth muscle cells, which causes their dilation and reduces their sensitivity to pressor agents (catecholamines, thromboxane) . The total hemodynamic effect of indapamide is manifested as:

• vasodilating effect
• decrease in OPSS
• lowering systemic blood pressure
• changes in the viscosity properties of blood due to inhibition of platelet aggregation activity.

The effect of indapamides on blood pressure without a significant effect on diuresis is manifested in a daily dose of 2.5 mg, with an increase in which the diuretic effect becomes dominant.

In its hypotensive activity, indapamide is 30 times superior to the effect of spironolactones, 100 times superior to furosemide, and 300 times superior to chlorthalidone when used in comparable doses [13]. One of the identified antihypertensive effects of indapamide is its effect on renal production and release of prostaglandins, inhibition of the formation of the vascular vasoconstrictor thromboxane. Under the influence of indapamide in patients with essential arterial hypertension, the release of prostaglandin E2, which has vasodilating activity, increased. The effect of indapamide inhibiting the synthesis of thromboxane A2 in human platelets and stimulating the release of vasodilating prostacyclin I2 was verified in vitro [14].

The therapeutic efficacy of indapamide diuretics has been demonstrated in a number of large randomized studies. Their ability to prevent the development of coronary artery disease by reducing myocardial mass in hypertension

.
This property, atypical for other classes of diuretics, makes indapamide a unique drug with a cardioprotective effect
, the severity of which is not inferior to beta-blockers and ACE inhibitors.

Particular attention is drawn to the fact that indapamide-like diuretics do not have a withdrawal syndrome and do not cause adverse metabolic disorders: they do not have a negative effect on glucose metabolism and blood lipid levels. Recent studies have shown that indapamide helps normalize glucose metabolism in type 2 diabetics

, preventing diabetic nephropathy. A similar pattern was noted in the study of cholesterol and triglyceride metabolism in patients with dyslipoproteinemia. Indapamide reduces the level of atherogenic low-density cholesterol and triglycerides, while simultaneously increasing the concentration of high-density lipoproteins [15].

Thus, indapamide, combining all the positive pharmacodynamic, pharmacokinetic and economic advantages, in the absence of side effects of other diuretics, is a drug that is promising in terms of therapeutic tactics in patients with hypertension and chronic heart failure.

CHF is quite often a consequence of arterial hypertension syndrome and remains one of the main causes in the structure of causes of disability and mortality from cardiovascular pathology. Currently, the drugs of choice in the treatment of CHF with LV systolic dysfunction are ACE inhibitors, and for diastolic dysfunction - diuretics. The basis of CHF in most patients with hypertension is a violation of the diastolic and systolic function of the left ventricle, therefore the most promising is combined treatment with ACE inhibitors and diuretics. Taking into account the above, for the treatment of CHF, preference should be given to thiazide-like diuretics - indapamides

with moderate strength and long-lasting action [16]. Indapamide, reducing the level of intracellular calcium while maintaining the magnesium content, reduces the rigidity of the vascular wall and promotes more effective relaxation of the cardiomyocyte in diastole. At the same time, the synthesis of prostacyclins increases, platelet aggregation and the release of thromboxane A2 decrease, which overall has a positive hemodynamic effect by reducing afterload for the LV.

Indapamide, improving microcirculation in the kidney, eliminates microalbuminuria, which is a marker of generalized vascular damage and a predictor of cardiovascular and renal complications.

Thus, the use of diuretics, in particular indapamide-like ones, is relevant and promising in the prevention and treatment of hypertension and CHF.
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