home Folk remedies Causes of acute heart failure. Characteristic signs of acute heart failure. Acute right ventricular failure

Causes of acute heart failure. Characteristic signs of acute heart failure. Acute right ventricular failure

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Introduction

Acute heart failure can be: left ventricular (left type), right ventricular (right type) and total.

Acute heart failure can fundamentally develop in two ways - heart failure manifested in connection with stagnation and heart failure manifested by symptoms of a rapid drop in cardiac output. The pathogenesis is based on the same processes, but the manifestations are different: acute heart failure is manifested by either pulmonary edema and cardiac asthma or cardiogenic shock.

Treatment of acute left ventricular failure at the prehospital stage is carried out in the following areas:

relief of “respiratory panic” (opioids); reducing preload (diuretics, nitrates, opioids); reduction of afterload (nitrates, vasodilators); inotropic stimulation of the heart (catecholamines, cardiac glycosides, non-glycoside inotropic drugs); reducing pressure in the pulmonary artery system (nitrates, prostacyclin, furosemide, opioids); defoaming (ethyl alcohol vapor, synthetic defoaming agents); oxygen therapy, artificial pulmonary ventilation (ALV).

1. Acute heart failure

Symptoms of acute left ventricular failure.

The earliest clinical sign is tachycardia, which is characterized by a progressive course, discrepancy between body temperature and psycho-emotional state.

Almost simultaneously with tachycardia, tachypnea-type shortness of breath develops, decreasing with oxygen therapy and with an elevated position of the upper body.

The nature of shortness of breath is inspiratory, however, against the background of impaired bronchial patency of reflex genesis, an expiratory component is added.

Paroxysmal shortness of breath is a sign of cardiac asthma or pulmonary edema, and it may be accompanied by a cough that worsens with changes in body position, various wet and dry wheezing, foamy discharge from the trachea, and vomiting.

Patients are pale, the skin is covered with cold sweat, acrocyanosis and cyanosis of the mucous membranes are noted.

The size of the heart is determined by the nature of the underlying disease. Auscultatory signs are muffled or dull heart sounds, gallop rhythm, the appearance of noise or weakening of the previously occurring intensity, arrhythmias.

Observed fainting may be a manifestation of acute left ventricular failure, or may be caused by sudden brain hypoxia due to low cardiac output or asystole (with atrioventricular blockade, sick sinus syndrome, long Q-T interval syndrome, idiopathic hypertrophic subaortic stenosis).

Other signs of acute left ventricular failure include anxiety, agitation, nausea, vomiting, convulsions, and in the terminal period bradycardia, brandypnea, muscle hypotension, and areflexia appear.

Acute right ventricular failure.

Its causes can be cardinal (pulmonary artery stenosis, Ebstein's disease, atrial septal defect, pulmonary embolism, exudative pericarditis) and extracardiac (pneumonia, lobar emphysema, diaphragmatic hernia, bronchial asthma, etc.).

Clinical symptoms are moderate tachycardia, dyspnea-type shortness of breath, enlarged liver, less often spleen, swelling of the neck veins.

Edema syndrome acquires diagnostic significance only in combination with hematomegaly, shortness of breath and other symptoms of decompensation. Isolated peripheral edema never occurs in acute heart failure in children.

Electrocardiography, chest radiography and echocardiography are of important diagnostic value.

Urgent Care.

It is necessary to give an elevated position to the upper body, establish oxygen therapy with its concentration in the inhaled air of at least 30–40%, and in case of pulmonary edema, use defoamers and nasotracheal suction. Nutrition until recovery from a critical condition should be parenteral.

Of the cardiac glycosides, strophanthin and korglycon are used.

Doses of strophanthin (single): 0.05% solution intravenously, administration of the drug can be repeated 3-4 times a day.

Doses of korglykon (single): 0.06% solution intravenously for children, the drug is administered no more than 2 times a day in a 20% glucose solution. You can also use intravenous administration of digoxin at a saturation dose of 0.03–0.05 mg/kg evenly over 2 days in three doses (the higher the body weight, the lower the saturation dose per 1 kg of weight). After 2 days, he switches to a maintenance dose of cardiac glycosides, which is equal to 1/1–1/6 of the saturation dose, given in two doses per day. Contraindications to the prescription of glycosides are bradycardia, atrioventricular block, ventricular tachycardia; They should be used with caution in septic endocarditis, anuria, and exudative pericarditis. At the same time, Lasix or furosemide is prescribed intravenously at a dose of 2–4 mg/(kg day) and aminophylline (2.4% solution, 0.3–5 ml intravenously); you should remember the possibility of increasing tachycardia and hypotension.

For pulmonary edema and cardiac asthma, intravenous administration of a mixture of standard solutions of aminazine, pipolfen, promedol together with rheopolyglucin is effective. It is necessary to relieve psychomotor agitation and anxiety, which is achieved by administering seduxen, narcotic analgesics (fentanyl 0.001 mg/kg, promedol 1% solution and neuroleptics (droperidol - 0.25% solution)

To reduce the permeability of alveolar-capillary membranes and combat hypotension, glucocorticoids are administered intravenously - prednisolone up to 3-5 mg (kg per day), the initially administered dose can be half the daily dose.

To eliminate concomitant vascular insufficiency, which worsens cardiac function and contributes to the aggravation of metabolic acidosis, careful administration of fluid under the control of diuresis is indicated. It is recommended to alternate the administration of a polarizing mixture (10% glucose solution - 10-15 ml/kg, insulin - 2-4BD, panangin - 1 ml for 1 year of life or potassium chloride solution, 0.25% novocaine solution - 2-5 ml) 2 once a day with a solution of rheopolyglucin, hemodez, plasma; for persistent acidosis, administration of a 4% solution of sodium bicarbonate is indicated.

During asystole, mouth-to-mouth breathing is performed, chest compressions are performed, a 1% solution of calcium chloride, a 10% solution of adrenaline hydrochloride and a 0.1% solution of atropine sulfate in 10 ml of 10% glucose are injected intravenously or better intracardially.

Hospitalization in all cases of heart failure is urgent in a therapeutic (cardiology) hospital.

failure heart attack cardiac thromboembolism

2. Features of the treatment of acute heart failure that developed against the background of a hypertensive crisis

Hypertensive crises are vascular crises in patients with hypertension, most often developing in the form of acute disorders of cerebral hemodynamics or acute heart failure against the background of a pathological increase in blood pressure.

A hypertensive cardiac crisis develops as a result of acute dystrophy of the myocardium of the left ventricle of the heart from hyperfunction, which occurs in conditions of an extreme increase in blood pressure due to a sharp increase in peripheral resistance to blood flow during a crisis due to acute systemic arteriolar hypertension. The development of heart failure is facilitated by low severity of myocardial hypertrophy (which is possible, for example, during a crisis course of the disease) and a decrease in energy production in the myocardium (for example, oxygen deficiency with increased consumption, diabetes mellitus or other causes of impaired utilization of energy substances).

Symptoms: with blood pressure above 220/120 mm Hg. Art. acute left ventricular heart failure develops: orthopnea, cardiac asthma, tachycardia, weakening of the first heart sound (sometimes gallop rhythm), accent of the second sound over the pulmonary trunk, hard breathing and moist rales in the lungs

Treatment

Intravenous stream slowly 2 ml of 0.25% solution of droperidol, 40 mg of furosemide, 1 ml of 0.06% solution of corglycone; sublingually 10 mg of phenigidine (chew capsule or tablet) or nitroglycerin (1 tablet every 10 minutes) until the patient’s condition improves or (or then) intravenously 300 mg of diazoxide or intravenous drip (in 250 ml of 5% glucose solution) 2–4 ml 5% pentamine solution or 50 mg sodium nitroprusside at an initial rate of 5–10 drops per 1 minute under constant blood pressure monitoring; intramuscular injection of 1 ml of 5% pentamine solution is acceptable. Inhalation through a nasal oxygen catheter with a constant flow of 2–4 ml per 1 min, beta-blockers

All patients with hypertensive cardiac crisis are subject to emergency hospitalization. Emergency care should be provided on site and when transporting the patient to the hospital. The set of measures to stop a crisis includes pathogenetic therapy: general for all G. k. (tranquilizing and antihypertensive therapy) and specific for certain options (use of vasoactive drugs depending on the type of angiodystonia that forms the crisis), as well as symptomatic therapy aimed at eliminating dangerous for life or especially painful manifestations of the crisis for the patient.

Tranquilizing therapy is carried out in all cases, even if the crisis was not preceded by mental trauma, since the crisis itself corresponds to a situation of stress. Treatment begins with intravenous administration of 10 mg of seduxen. At the beginning of a crisis, in the absence of pronounced manifestations of anxiety and restlessness, seduxen in the same dose can be given orally. Neuroleptic drugs, of which droperidol (5 mg intravenously) is the most preferable, have an advantage over seduxen only in the following cases: with developing pulmonary edema, frequent painful vomiting, severe pain syndrome (headache, angina), the presence of severe depression in the patient due to severe mental trauma. Aminazine should not be prescribed due to its cardiotoxic effect. In the early phases of G.'s development, psychotherapy and the use of tranquilizers cause a decrease in blood pressure in almost half of the cases even before the use of antihypertensive drugs.

Antihypertensive therapy is carried out using fast-acting drugs under the control of blood pressure dynamics. The pressure cuff placed on the patient's shoulder is not removed until the crisis is relieved; Blood pressure is measured during the expected period of action of the administered drugs, but not less than every 5–7 minutes, since the dynamics of blood pressure may not depend on drug therapy.

In the absence of these drugs or their ineffectiveness in the next 10 minutes after administration, as well as in cases of developed hypertensive cardiac disease, ganglion blockers or sodium nitroprusside (indicated only in hypertensive cardiac crisis) should be used intravenously by drip in a controlled blood pressure mode. For this purpose, 2–3 ml of a 5% solution of pentamine or 50 mg of sodium nitroprusside (niprid, nanipruss) are diluted in 250 ml of a 5% glucose solution. The infusion is started at a slow rate (5–10 drops per minute), increasing it if necessary under continuous monitoring of blood pressure dynamics until the desired level is reached (not lower than 160 ± 10 mm Hg for systolic blood pressure). The bottle with sodium nitroprusside solution should be wrapped in foil; the total amount of this drug per infusion should not exceed 3 mg per 1 kg of the patient’s body weight. If the infusion rate of sodium nitroprusside is excessive, collapse occurs; patients also feel palpitations, heat in the body, chest pain (without ECG changes), weakness, sometimes agitation, vomiting are observed, and cerebrovascular accidents are possible.

Symptomatic therapy for hypertensive cardiac crisis is aimed at eliminating pulmonary edema and left ventricular heart failure. Lasix, corglycone or strophanthin, oxygen therapy are used, and, if necessary, also antianginal drugs and antiarrhythmic drugs.

3. Features of the treatment of acute heart failure that develops against the background of myocardial infarction

Acute heart failure is a consequence of myocardial necrosis and leads to a decrease in the pumping function of the heart and the development of hypoxia - an early and permanent sign of circulatory failure in acute myocardial infarction.

Acute heart failure during myocardial infarction. Myocardial infarction is the most common cause of acute heart failure. Heart failure during myocardial infarction develops due to decreased contractility (systolic dysfunction) and decreased compliance (diastolic dysfunction) of the left ventricle.

Despite the restoration of blood flow in the infarction zone, restoration of diastolic and systolic function can occur after only a few days or even weeks (stunned myocardium).

Depending on what part of the myocardium fails to function (including acute infarction, scarring, viable but ischemic myocardium with poor contractility), manifestations range from mild pulmonary congestion to severely decreased cardiac output and cardiogenic shock.

Cardiogenic shock is usually caused by damage to at least 40% of the left ventricular myocardium, but can occur with relatively small infarcts if the right ventricle is involved or if there are mechanical complications such as papillary muscle dysfunction or ventricular septal rupture.

In addition to left ventricular ischemia and mechanical defects, low cardiac output may be caused by bradyarrhythmias (eg, high-degree AV block) and tachyarrhythmias (atrial fibrillation and flutter, supraventricular and ventricular tachycardia).

Hospital mortality ranges from 6% with preserved left ventricular function to 80% with cardiogenic shock.

Before the doctor arrives:

The patient is provided with maximum physical and mental rest: he should be laid down and, if possible, calmed down.

If suffocation or lack of air occurs, the patient must be given a semi-sitting position in bed.

Although nitroglycerin does not completely eliminate pain in I. m., its repeated use is advisable and necessary.

Distractions also bring noticeable relief: mustard plasters on the heart and sternum, heating pads on the legs, warming the hands.

A patient in the acute period of the disease needs constant monitoring. The first attack is often followed by repeated, more severe ones. The course of the disease may be complicated by acute heart failure, cardiac arrhythmias, etc.

Many medications used in this case are only applicable under medical supervision. Therefore, the patient can receive full treatment only in a hospital setting, and if a myocardial infarction is suspected, he should be urgently hospitalized.

Identification of the initial stage of heart failure is important for the timely administration of ACE inhibitors, which can have a positive effect on the course of the disease.

For the prevention and treatment of acute congestive heart failure, nitrates, diuretics, ACE inhibitors, and in especially severe cases, sodium nitroprusside are of primary importance.

The use of cardiac glycosides for emergency care, especially in the first days of myocardial infarction, with diastolic heart failure and with preserved sinus rhythm, is ineffective. In the acute stage of the disease, even small doses of cardiac glycosides can contribute to the occurrence or worsening of arrhythmias, including ventricular fibrillation.

From the first days of myocardial infarction, activation of neurohormonal systems occurs (increased levels of renin, angiotensin II, aldosterone, norepinephrine, atrial natriuretic peptide). The severity and duration of neurohumoral stimulation depend on the degree of damage to the left ventricle and the use of a number of drugs (in particular, diuretics and peripheral vasodilators). Subsequently, to maintain cardiac output, the mass of the heart muscle, volumes and pressure in the left ventricle change compensatoryly. Neurohumoral activity, the development of heart failure, dilatation and hypertrophy of the left ventricle can be favorably influenced by prescribing ACE inhibitors.

Captopril (Capoten) is a first generation ACE inhibitor. Captopril is prescribed from the 3rd day of the disease, starting with 6.25 mg 3 times a day (18.75 g/day), and then 25–50 mg per dose (75–100 mg/day).

4. Features of the treatment of acute heart failure that develops against the background of thromboembolism

Pulmonary embolism (PE) is a syndrome caused by embolism of the pulmonary artery or its branches by a thrombus and is characterized by acutely occurring severe cardiorespiratory disorders; with embolism of small branches - symptoms of the formation of hemorrhagic pulmonary infarctions.

Treatment of acute right ventricular failure includes treatment of the main cause that led to right ventricular failure (thromboembolism of the branches of the pulmonary artery, status asthmaticus, etc.), elimination of hypoxia, and effects on blood flow in the pulmonary artery bed. This condition does not require independent therapy.

The main directions of treatment for PE at the prehospital stage include pain relief, prevention of continued thrombosis in the pulmonary arteries and repeated episodes of PE, improvement of microcirculation (anticoagulant therapy), correction of right ventricular failure, arterial hypotension, hypoxia (oxygen therapy), relief of bronchospasm. In order to prevent recurrence of pulmonary embolism, strict bed rest is necessary; Patients are transported on recumbent stretchers.

In case of thromboembolism of large branches of the pulmonary artery, narcotic analgesics are used to relieve severe pain, as well as to unload the pulmonary circulation and reduce shortness of breath, optimally morphine intravenously. 1 ml of a 1% solution is diluted with isotonic sodium chloride solution to 20 ml (1 ml of the resulting solution contains 0.5 mg of the active substance) and 2–5 mg are administered every 5–15 minutes until pain and shortness of breath are eliminated, or until side effects appear ( arterial hypotension, respiratory depression, vomiting).

It is advisable to use direct anticoagulants - intravenous heparin in a dose of 5000 IU or low molecular weight heparins. Heparin does not lyse the thrombus, but stops the thrombotic process and prevents the growth of the thrombus distal and proximal to the embolus. By weakening the vasoconstrictor and bronchospastic effect of thorombocyte serotonin and histamine, heparin reduces spasm of the pulmonary arterioles and bronchioles. Having a beneficial effect on the course of phlebothrombosis, heparin serves to prevent recurrent pulmonary embolism.

To improve microcirculation, rheopolyglucin is additionally used - 400 ml is administered intravenously at a rate of up to 1 ml per minute; the drug not only increases the volume of circulating blood and increases blood pressure, but also has an antiaggregation effect. Complications are usually not observed; allergic reactions to reopolyglucin are quite rare.

With the development of bronchospasm and stable blood pressure, a slow (stream or drip) injection of 10 ml of a 2.4% solution of aminophylline is indicated.

Conclusion

Acute heart failure is a sudden decrease in the contractile function of the heart, which leads to disruption of intracardiac hemodynamics, blood circulation in the pulmonary and systemic circulation, which can lead to dysfunction of individual organs.

The variety of causes of heart failure explains the existence of various clinical and pathophysiological forms of this pathological syndrome, each of which is characterized by predominant damage to certain parts of the heart and the action of various mechanisms of compensation and decompensation.

In most cases (about 70–75%), we are talking about a predominant violation of the systolic function of the heart, which is determined by the degree of shortening of the heart muscle and the magnitude of cardiac output (CO).

Today, cardiovascular diseases are the number one killer in all developed and many developing countries. Heart failure is the third leading cause of hospitalization and the first among people over 65 years of age. In the age group over 45 years, the incidence doubles every 10 years.

Among the causes leading to the development of acute heart failure, myocardial infarction ranks first. In this case, a large number of muscle fibers are switched off from work.

Heart failure can be caused by certain heart rhythm disturbances or blockages of the heart's afferent pathways. Thromboembolism of the pulmonary artery or its branches can also cause acute heart failure. This is a very dangerous condition. It is necessary to immediately take measures to restore heart function - increase LV contractility with medication or through counterpulsation (in case of a heart attack), restore heart rhythm (in case of arrhythmias), dissolve a blood clot (in case of thrombosis).

Literature

Eliseev O.M. Handbook of emergency and first aid. Rostov n/a. Rostov University, 1994 – 217 p.

Oskolkova M.K. Functional diagnosis of heart diseases.

M. 2004 – 96 p.

Ruksin V.V. Emergency cardiology, St. Petersburg, Nevsky dialect, 2002 – 74 p.

Directory of General Practitioners. In 2 volumes. / Ed. Vorobyova N.S. – M. Eksmo Publishing House, 2005 – 310 p.

Acute heart failure (AHF) - treatment, diagnosis and clinical picture

AHF can develop de novo, that is, in a person without a history of cardiac dysfunction, or as acute decompensation of chronic heart failure.

1) which lead to a rapid increase in symptoms: acute coronary syndrome (myocardial infarction or unstable angina, leading to ischemia and dysfunction of a significant portion of the myocardium, mechanical complications of fresh myocardial infarction, right ventricular myocardial infarction), hypertensive crisis, cardiac arrhythmia and conduction disturbances, thromboembolism pulmonary artery, cardiac tamponade, aortic dissection. cardiomyopathy in pregnant women, complications of surgical interventions, tension pneumothorax;

2) which lead to a slower increase in symptoms: infections (including myocarditis and infective endocarditis), pheochromocytoma, overhydration, high cardiac output syndrome (severe infection, especially sepsis, thyrotoxic crisis, anemia, arteriovenous fistulas, Paget's disease; usually , AHF develops due to pre-existing heart damage), exacerbation of CHF.

A common cause, especially in older people, is coronary heart disease. In younger people, the following predominate: dilated cardiomyopathy, cardiac arrhythmias, congenital and acquired heart defects. myocarditis.

CLINICAL PICTURE AND TYPICAL COURSE

1. Subjective and objective symptoms:

1) reduced cardiac output (peripheral hypoperfusion) - fatigue, weakness, confusion, drowsiness; pale, cold, moist skin, sometimes acrocyanosis, thready pulse, hypotension, oliguria;

2) retrograde stagnation:

a) in the systemic circulation (right ventricular failure) - peripheral edema (loose edema around the bones or sacral region; may not have time to appear), dilatation of the jugular veins and palpation pain in the epigastrium (due to liver enlargement), sometimes - transudate in the serous cavities (pleural , abdominal, pericardial);
b) in the pulmonary circulation (left ventricular failure → pulmonary edema) - shortness of breath, rapid breathing and shortness of breath in a sitting position, moist rales over the pulmonary fields;

3) the underlying disease causing CHF.

Based on the presence of symptoms of peripheral hypoperfusion, the patient is characterized as “cold” (with hypoperfusion) or “warm” (without hypoperfusion), and based on symptoms of blood stagnation in the pulmonary circulation - as “wet” (with stagnation) or “dry” (without stagnation).

2. Clinical forms of AHF (according to ESC standards, 2008):

1) exacerbation or decompensation of CHF - symptoms of blood stagnation in the systemic and pulmonary circulation;
2) pulmonary edema;
3) CHF with high blood pressure - subjective and objective symptoms of heart failure are accompanied by high blood pressure and, as a rule, preserved systolic function of the left ventricle, signs of increased tone of the sympathetic nervous system, with tachycardia and spasm of blood vessels; the patient may be in a state of normovolemia or only slight overhydration; objective symptoms of pulmonary edema often appear without symptoms of stagnation in the systemic circulation;
4) cardiogenic shock - tissue hypoperfusion due to hypertension, typical systolic blood pressure<90 мм рт. ст. 30 мм рт.»>or a decrease in mean arterial pressure of >30 mm Hg. Art. anuria or oliguria, often - heart rhythm disturbances; Symptoms of organ hypoperfusion and pulmonary edema develop rapidly;
5) isolated right ventricular AHF - small output syndrome without pulmonary edema, increased pressure in the jugular veins with or without hepatomegaly;
6) AHF with ACS.

Diagnosis of acute heart failure

Based on subjective and objective symptoms, as well as the results of additional studies.

Supporting research

ECG: changes caused by underlying heart disease are usually observed, most often signs of myocardial ischemia, rhythm and conduction disturbances.
X-ray of the chest: in addition to the symptoms of the underlying disease, it can reveal congestion in the pulmonary circulation, fluid in the pleural cavities and enlargement of the chambers of the heart.
Echocardiography: detects functional abnormalities (systolic or diastolic dysfunction, valvular dysfunction) or anatomical changes of the heart (eg, mechanical complications of myocardial infarction).
Laboratory tests: basic - complete blood count, blood levels of creatinine, urea, potassium and sodium, glucose, cardiac troponins, liver enzyme activity, arterial blood gasometry (in patients with slight shortness of breath, pulse oximetry can be replaced, except in cases of shock with very low cardiac output release and peripheral vasospasm). Determination of natriuretic peptides (BNP / NT-proBNP) is suitable for the differential diagnosis of cardiac (increased concentration) and cardiac causes of shortness of breath; remember that in patients with rapidly increasing pulmonary edema or acute mitral regurgitation, peptide parameters at the time of hospitalization may still be within normal limits.
Endomyocardial biopsy

Treatment of acute heart failure

General principles

1. Goals of emergency treatment. control of subjective symptoms, especially shortness of breath. and stabilization of the hemodynamic state.

2. Pathogenetic treatment: apply in every case.

3. Careful monitoring: respiration, heart rate, ECG and blood pressure. Perform the study regularly (for example, every 5-10 minutes), and in unstable patients - constantly, until the drug doses and the patient’s condition stabilize. If there is no strong vasospasm and significant tachycardia, blood pressure measurements using non-invasive automatic devices are reliable. In case of AHF, monitoring of the rhythm and ST segment is necessary, especially if its cause is GCS or arrhythmia. In patients receiving oxygen, monitor SaO2 regularly using a heart rate monitor (eg every hour), or better yet, continuously.

Invasive hemodynamic monitoring is sometimes necessary, especially in situations where congestion and hypoperfusion coexist and an unsatisfactory response to pharmacological treatment, as it helps in choosing the appropriate treatment; it can be done with:

1) a Swan-Hans catheter inserted into the pulmonary artery - to measure pressure in the superior vena cava, right atrium, right ventricle and pulmonary artery, wedge pressure in the capillaries of the lungs and determine cardiac output, as well as oxygen saturation of mixed venous blood;
2) a catheter inserted into the central vein - to measure central venous pressure (CVP) and oxygen saturation of hemoglobin in venous blood (SvO2) in the superior vena cava or right atrium;
3) a catheter inserted into a peripheral artery (usually radial) to continuously measure blood pressure.

4. Actions depending on the clinical form of GHF

1) exacerbation or decompensation of CHF → vasodilators + loop diuretics (in patients with impaired renal function or those taking diuretics for a long time, consider using diuretics in large doses); inotropic drugs for hypotension and organ hypoperfusion;

2) pulmonary edema;

3) GSN with high blood pressure → vasodilators (careful monitoring required); diuretics in small doses in patients with hyperhydration or pulmonary edema;

4) cardiogenic shock;

5) isolated right ventricular AHF → store right ventricular preload; Avoid, if possible, the use of vasodilators (opioids, nitrates, ACE inhibitors, ARBs) and diuretics; Careful infusion of solutions (with careful monitoring of hemodynamic parameters), sometimes dopamine in a small dose, can be effective;

6) GHF that developed during ACS → to determine the cause of AHF, perform echocardiography; in case of STEMI or NSTEMI → coronary angiography and revascularization procedure; in case of mechanical complications of fresh myocardial infarction → urgent surgery.

Pharmacological treatment

1. Vasodilators: mainly indicated in patients with symptoms of hypoperfusion and congestion, without hypotension; avoid in patients with systolic blood pressure<110 мм рт. ст. Уменьшают систолическое артериальное давление, давление наполнения левого и правого желудочков, а также периферическое сосудистое сопротивление; уменьшают одышку. Обязательный мониторинг артериального давления. Особенно осторожно назначайте пациентам со значительным митральным или аортальным стенозом.

1) IV nitroglycerin (Nitroglycerin) - first 10-20 mcg/min, if necessary increase by 5-10 mcg/min every 3-5 minutes to the maximum hemodynamically tolerated dose (more than 200 mcg/min); possibly po or in aerosol 400 mcg every 5-10 minutes; After 24-48 hours of administration at high doses, tolerance develops, so use intermittently. If systolic blood pressure decreases<90 мм рт. ст. → уменьшите дозу, а если в дальнейшем снижается — прекратите инфузию.

2) IV sodium nitroprusside (Niprusid) - initially 0.3 mcg/kg/min, up to max. 5 mcg/kg/min; recommended for patients with severe AHF with arterial hypertension and GHF as a result of mitral regurgitation. Do not use in AHF developing due to ACS, given the risk of a steal effect; with long-term treatment, especially in patients with severe renal or hepatic insufficiency, symptoms of the toxic effects of its metabolites - thiocyanide and cyanide (abdominal pain, confusion, convulsions) may develop.

2. Diuretics: indicated mainly in patients with AHF with symptoms of overhydration - stagnation in the pulmonary circulation or peripheral edema. In high doses, they may cause transient deterioration of renal function. Algorithm for treatment with diuretics in patients with AHF, drugs. When using diuretics: monitor diuresis (insertion of a urinary catheter may be indicated) and adjust the dose based on clinical response; limit sodium intake, monitor blood serum concentrations of creatinine, potassium and sodium every 1-2 days, depending on diuresis, adjusting potassium and magnesium losses.

3. Inotropic drugs: indicated mainly for AHF with peripheral hypoperfusion and hypotension (systolic pressure<85 мм рт. Ст.); проводите мониторинг ЭКГ учитывая высокую вероятность появления тахикардии, ишемии сердечной мышцы и нарушений ритма.

4. Vasopressors: Give if hypotension and hypoperfusion persist despite proper hydration.

5. Other drugs

1) Among antiarrhythmic drugs, the only drug that is effective in most cases of supraventricular and ventricular arrhythmias and does not have a negative inotropic effect is amiodarone;
2) In patients taking β-blockers for a long time for CHF who are hospitalized due to worsening heart failure, β-blockers generally do not need to be discontinued unless there is a need to use drugs with a positive inotropic effect. For bradycardia or decreased systolic pressure<100 мм рт. ст. → уменьшите дозу β-блокатора. Если β-блокатор отменен → примените его снова после стабилизации гемодинамического состояния пациента;
3) In patients taking ACEIs/ARBs for a long time, do not discontinue these medications unless absolutely necessary (withdrawal, for example, in a patient in shock), however, do not start their use in the acute phase of heart failure. If indicated, and in the absence of contraindications, begin treatment with ACE inhibitors/ARBs before discharge from the hospital;
4) Prescribe thromboprophylaxis with heparin or other anticoagulants;
5) During the stabilization period in patients without contraindications, after assessing renal function and potassium concentration, add an aldosterone antagonist to treatment;
6) In patients with treatment-resistant hyponatremia, tolvaptan can be prescribed.

Auxiliary treatment

1. Ventilatory support: consider (primarily non-invasive, if necessary invasive) if SaO2 persists despite maintaining airway and oxygen supply<90%).

2. Devices that support cardiac function: used in AHF (except for conditions with increased cardiac output) resistant to drug treatment, if restoration of effective cardiac function is possible, or it is necessary to maintain blood circulation at the time of heart transplantation or other intervention. which can restore heart function.

Surgery

Indications:

1) extensive (affecting a large number of vessels) coronary heart disease, causing severe myocardial ischemia;
2) acute mechanical complications of myocardial infarction;
3) acute mitral or aortic regurgitation caused by endocarditis or trauma or aortic dissection (applies to the aortic valve);
4) some complications of PCI.

SPECIAL SITUATIONS

1. Prosthetic valve thrombosis: often leads to death. If this complication is suspected, immediately perform an echocardiographic examination.

1) Thrombosis of the artificial valve of the right side of the heart or high surgical risk → prescribe fibrinolytic treatment: alteplase (boost IV 10 mg followed by infusion of 90 mg over 90 minutes) or streptokinase (250-500 thousand IU over 20 minutes followed by infusion of 1 -1500000 IU over 10 hours, after which use UFH);

2. Acute renal failure. accompanying hypertension, leads to metabolic acidosis and electrolyte disturbances, which can induce arrhythmias, reduce the effectiveness of treatment and worsen the prognosis. 190 µmol/l. Moderate or severe renal impairment (serum creatinine level >190 µmol/L) is associated with a worse response to diuretics. If overhydration persists despite appropriate pharmacological treatment, consider continuous venovenous hemofiltration.

3. Bronchospasm: if a patient with AHF occurs, administer salbutamol (Ventolin Nebula) 0.5 ml of a 0.5% solution (2.5 mg) in 2.5 ml of 0.9% NaCl during a 20-minute nebulization; subsequent doses every hour for the first few hours, later as needed.

The most interesting news

Diagnosis of acute heart failure. Treatment of acute heart failure.

Diagnosis of acute heart failure is based on symptoms and clinical data verified by appropriate examinations (ECG, chest x-ray, echocardiography, biomarkers, etc.). When conducting a clinical assessment, it is important to systematically study peripheral blood flow and temperature, and venous filling. Thus, filling of the pancreas during pancreatic decompensation is usually assessed by CVP in the jugular vein. When interpreting the data, it should be taken into account that high central venous pressure in AHF may be a consequence of a reflex decrease in the consistency of the veins and the pancreas due to its inadequate filling. According to auscultation of the lungs, the filling pressure of the left ventricle is indirectly assessed (when it increases, moist rales are usually heard).

Definition quality of heart sounds. gallop rhythm and valvular murmurs are also very important for the diagnosis and clinical assessment of AHF. Assess the severity of manifestations of atherosclerosis (this is important in older people), manifested by insufficient pulse and the presence of murmurs in the carotid artery.

A normal ECG is not typical for acute heart failure. ECG changes help to assess the rhythm and etiological factor of AHF, as well as the condition and load of the heart parts. ECG changes can be indicators of acute myocardial injury, perimyocarditis, pre-existing pathology (HCH, LVH or DCM).

X-ray examination of the chest should be carried out early in all patients with AHF to verify pre-existing lung pathology and the presence of congestive changes in the heart (determining its size and shape). X-ray data make it possible to differentiate the diagnosis of left heart failure of inflammatory origin and infectious lung diseases. Spiral CT of the lungs helps in the diagnosis of pulmonary embolism or pulmonary pathology. Echocardiography helps to assess regional and global contractility of the RV and LV, the condition of the valves, pericardial pathology, mechanical complications of MI and the level of PH.

Blood gas analysis allows you to assess blood oxygenation and acid-base balance (it can be replaced by pulse oximetry in mild cases of acute heart failure).

Everyone patients with acute heart failure The following laboratory tests are indicated: aPTT, PSA, D-dimer, cardiac troponin, assessment of urea, creatinine, potassium and sodium levels, and urinalysis.

In difficult cases angiography and pulmonary artery catheterization(DPA) allow us to clarify the genesis of acute heart failure.

Treatment of acute heart failure.

Treatment goals for acute heart failure- reduction in the severity of symptoms (dyspnea, weakness, clinical manifestations of HF, increased diuresis) and stabilization of the hemodynamic state (increased cardiac output and/or stroke volume, decreased PAWP).

Conduct body temperature monitoring a, RR, heart rate, blood pressure, ECG, electrolyte levels, creatinine and glucose.

Patients with acute heart failure often susceptible to infectious complications (usually respiratory and urinary tract), septicemia, or nasocomial infection with gram-positive microbes. Therefore, if necessary, they are prescribed early AB treatment. AHF in patients with diabetes is often accompanied by metabolic disorders (hyperglycemia often occurs). A normal level of glycemia increases the survival of patients with diabetes in severe condition.

Negative heat and nitrogen balance(due to reduced intestinal absorption) are unfavorable prognostic factors in AHF. Treatment should be aimed at maintaining heat and nitrogen balance. There is an association between AHF and renal failure. Both conditions may be causative, aggravating, or influencing the outcome of the other condition. Preservation of renal function is the main requirement when choosing adequate treatment tactics in patients with AHF.

Patients with acute heart failure Non-invasive ventilatory support with positive airway pressure is often necessary. This allows you to improve oxygenation and reduce the manifestations of AHF, and avoid many infectious and mechanical complications.

It is generally accepted to prescribe morphine and its analogues (causing venodilation, dilatation of small arteries and a decrease in heart rate) in the initial stages of treatment of severe AHF, especially in patients with shortness of breath and psychomotor agitation.

Anticoagulant therapy indicated in the treatment of ACS with HF, as well as in AF Vasodilators (improving peripheral circulation and reducing preload) are indicated for most patients with AHF as 1st line drugs for hypoperfusion, accompanied by adequate blood pressure, congestion and low diuresis. Nitrates reduce congestion in the lungs without significantly affecting the stroke volume of the heart and without leading to an increase in myocardial oxygen demand, especially in patients with ACS. The dose of nitrates should be reduced if SBP becomes less than 90 mm Hg, and administration should be discontinued if blood pressure continues to decrease.

— Return to the table of contents of the section “ Cardiology. "

One of the most severe circulatory disorders is acute cardiovascular failure, or AHF for short. This disease is most often a complication of other diseases and consists of circulatory disorders due to the fact that the heart cannot cope with its pumping function or is not sufficiently filled with blood and does not supply the body tissues with it in the required quantity. This condition threatens the patient’s life, so immediate hospitalization of the patient and placement in the intensive care unit is required. It is desirable that this be a specialized cardiology hospital, which has all the capabilities to diagnose and treat just such problems.

According to the phases of cardiac contraction where the disorder occurs:

systolic (inability of the heart to eject the required amount of blood from the ventricle);
diastolic (inability of the ventricles to completely fill with blood).

For the reason that caused the disease:

failure that occurred for the first time in people who had no previous heart pathologies;
acute failure, which was a consequence of acute decompensation of previously existing chronic heart failure.

According to the predominantly affected part of the heart:

right-sided;
left-handed.

Causes of acute heart failure

For a condition such as acute heart failure, the pathogenesis may include complications from various ailments in which circulatory impairment occurs due to a weakening of the pumping function of the heart and its less filling with blood.

It should be emphasized that in such a pathological condition as acute heart failure, the causes of its occurrence, as well as the mechanisms of its development, may differ; moreover, it can develop against the background of other diseases, seriously aggravating their course. What causes acute heart failure? These may be cardiac reasons and situations that have nothing to do with the heart.

Etiology of acute heart failure associated with cardiac problems:

Cardiac ailments leading to a sharp decrease in the contractility of the myocardium (as a result of its “stunning” or damage) - among them are myocarditis, acute myocardial infarction, consequences of connection to a heart-lung machine, consequences of cardiac surgery.
Decompensation (increasing phenomena) of chronic heart failure, that is, a condition in which the heart is not able to adequately supply the body with blood.
Cardiac tamponade.
Violation of the integrity of the heart chambers or valves.
Hypertensive crisis.
Severe hypertrophy (thickening of the walls) of the myocardium.
Diseases leading to increased pressure in the pulmonary circulation: acute diseases, pulmonary embolism.
Cardiac arrhythmias (tachycardia or bradycardia).

The causes of acute heart failure may not be cardiac in nature:

extensive surgery;
cerebral stroke (lack of blood circulation leading to the death of certain parts of the brain and disruption of its functioning);
infections;
myocardial poisoning with alcohol or drug overdose;
severe brain injury;
consequences of electric pulse therapy – electrical injury resulting from exposure to an electric current on the patient’s body.

Symptoms of acute heart failure

It is important to know the main signs of acute heart failure, which can be very diverse, since they are caused by different causes of this pathology, and also because the degree of dysfunction of one of the ventricles can be different. According to the symptoms, AHF can be divided into right ventricular and left ventricular, although there are cases when failures occur in both ventricles, and then they speak of biventricular failure. The latter can be caused by myocarditis, myocardial infarction, resulting in damage to both ventricles or mechanical complications after acute MI (rupture of the interventricular septum) and a number of other diseases.

Left ventricular AHF

The main cause of left ventricular failure is considered to be LV myocardial dysfunction due to hypertensive crisis, MI, and cardiac arrhythmias. Its extreme manifestation can be called cardiogenic shock. Its symptoms are:

arrhythmia and increased heart rate;
the occurrence of shortness of breath, quickly developing into suffocation;
characteristic wheezing in the lungs;
productive cough with the formation of foam, which has a pinkish tint due to the blood present in it;
pale skin and severe weakness.

Mostly, left ventricular failure is characterized by pulmonary symptoms. The patient tries to sit down and lower his legs to the floor.

Right ventricular AHF

Acute right ventricular heart failure is caused by RV myocardial infarction, pulmonary embolism, status asthmaticus, and cardiac tamponade. Her symptoms are as follows:

chest pain;
cold clammy sweat;
shortness of breath in the absence of physical activity, which due to bronchospasm turns into suffocation;
swelling of the jugular veins of the neck;
the skin becomes yellowish or bluish;
thready pulse with rapid heartbeat, hypotension;
accumulation of fluid in the abdominal cavity;
swelling of the lower extremities;
liver enlargement and pain in the right hypochondrium.

Symptoms of acute heart failure before death

Sometimes symptoms of acute cardiovascular failure begin to appear just half an hour to an hour before death, that is, the disease can develop at lightning speed.

In the most severe cases, the symptoms of acute heart failure before death are as follows:

cold clammy sweat;
sudden pallor of the skin;
foamy discharge from the mouth (often with blood);
the development of hurricane pulmonary edema leads to an attack of suffocation and respiratory arrest;
further death occurs from acute heart failure as a result of cardiac arrest.

Video about acute heart failure:

Diagnosis of acute heart failure

Obviously, the diagnosis of acute heart failure, which includes the following measures, is of utmost importance:

Of course, the question of how to treat acute heart failure is always relevant. Because it is a life-threatening condition, intensive care is often required for acute cardiovascular failure. With any degree of AHF, it is necessary to quickly improve the patient’s condition, which caused such a serious complication.

Treatment depending on the underlying cause

In acute heart failure, treatment is used that is aimed at reducing shortness of breath and quickly stabilizing the patient's condition. Better results can be achieved in specialized intensive care units.

If a heart rhythm disturbance has led to AHF, then in order to stabilize the patient’s condition and normalize his hemodynamics, it is necessary to quickly restore his heart rate, bringing it to its normal level.

If the cause is myocardial infarction (death of a section of the heart muscle due to insufficient blood supply), the most effective treatment of acute heart failure in this case involves actions aimed at quickly restoring blood flow in the affected artery. In first aid settings, this can be achieved through systemic thrombolysis, used in the first hours after a heart attack and consisting in dissolving the blood clot with thrombolytic drugs administered intravenously.

In acute heart failure, inhalation of humidified oxygen (oxygen therapy) is prescribed, and in severe cases it is necessary to resort to respiratory support and artificial ventilation.

Drug treatment

Medicines for acute heart failure are also used:

Morphine is used at an early stage, especially if the patient is in pain and appears agitated.
Even before the ambulance arrives, nitro drugs should be given, and then doctors administer them intravenously.

Various tablets for acute heart failure can be used at its initial stage, depending on its severity:

thiazide-like or loop diuretics;
venous vasodilators (nesiritide, sodium nitroprusside);
vasopressors (dopamine);
intropic agents (dobutamine);
improving myocardial contraction, anticoagulants that prevent thromboembolic complications from developing.

Surgery

When there are symptoms of acute heart failure, and conservative treatment due to the characteristics of the diseases that caused it turns out to be ineffective, then the only option left is emergency surgery. In this case, the following may apply:

correction of anatomical cardiac defects (reconstruction and valve replacement);
myocardial revascularization;
temporary circulatory support using mechanical means (intra-aortic balloon counterpulsation).

Patients with AHF stay in the hospital for an average of 10-14 days.

After stabilization of the patient's condition, the next stage of therapy is the prescription of ACE inhibitors and angiotensin-sensitive receptor blockers, mineralcorticoid receptor antagonists, and beta-blockers. If the contractility of the heart decreases (according to Echo-CG, the ejection fraction is less than 40%), then digoxin is prescribed.

When the acute period of heart failure has been overcome, a stable regimen of using diuretics has been found for at least two days, clinical recommendations for acute heart failure are as follows:

Unconditional cessation of smoking and drugs.
Alcohol is allowed only in very moderate quantities (and patients with alcoholic cardiomyopathy will have to abstain from alcohol altogether). Sometimes the restrictions look like this: men are allowed 2 glasses of wine a day, and women only one.
A person should exercise moderate physical activity every day, do aerobic exercise for half an hour a day, and walk in the fresh air - depending on how he feels.

Complications

AHF itself usually becomes a complication after certain diseases and pathological conditions. When heart failure itself is treated, thromboembolic complications, severe conduction and rhythm disturbances may well develop, and the disease can progress to the most severe forms (pulmonary edema, cardiogenic shock), up to sudden cardiac arrest.

Forecast

The prognosis of AHF is determined by the disease that provokes it. The prognosis for heart failure is always unfavorable, so acute heart failure is mentioned quite often as a cause of death.

Within a year after hospitalization with AHF, 17% of patients die, as well as 7% of those observed as outpatients. Very often (30-50%) those suffering from acute heart failure suddenly die from severe cardiac arrhythmias.

Therefore, it is very important for patients undergoing outpatient treatment to regularly take prescribed medications and maintain a healthy lifestyle.

Have you or your loved ones already been diagnosed with acute heart failure? How did you fight this illness? Tell us about it in the comments - help other readers!

Acute heart failure (AHF) is an emergency condition caused by a sudden decrease in the contractility of the heart, acute disruption of its function and insufficient blood supply to internal organs. This pathology develops suddenly for no apparent reason or is a consequence of cardiovascular disorders existing in the body.

According to the modern classification of AHF, there are two types - right ventricular and left ventricular.

The causes of acute heart failure are very diverse. These include injuries, intoxication, and heart disease. Without treatment, the pathology quickly leads to death.

The primary causes of AHF are myocardial diseases caused by acute infection or intoxication due to poisoning. An inflammatory process develops, cardiomyocyte dystrophy, hypoxia develops, and neurohumoral regulation is disrupted. Secondary causes include pathologies that do not directly affect the myocardium, but contribute to its overstrain, fatigue and oxygen starvation. This occurs with hypertension, atherosclerosis, and paroxysmal arrhythmia.

The main causes of acute right ventricular heart failure are diseases in which there is systolic overload and a decrease in diastolic filling of the right ventricle. Acute left ventricular heart failure develops with dysfunction of the left ventricle of the heart.

Cardiogenic causes

Heart diseases leading to acute disruption of myocardial contractile activity:

These diseases lead to a weakening of the force of myocardial contractions, a decrease in the amount of blood ejected, slowing of blood flow, pulmonary hypertension, blood stasis and soft tissue swelling.

Extracardiac causes

Diseases and factors leading to the development of acute heart failure:

dyscirculatory disorders in the brain,
excessive consumption of alcoholic beverages,
smoking,
nervous overexcitement,
bronchial asthma,
intoxication,
endocrinopathies,
taking cytostatics, antidepressants, glucocorticoids,
medical therapeutic and diagnostic manipulations on the heart,
pulmonary pathology,
acute infectious diseases,

Under the influence of provoking factors, vascular resistance increases, hypoxia occurs, the heart begins to work more intensely, the myocardium thickens, and the ability to contract is impaired.

Acute heart failure in young children is a consequence of congenital heart defects, and in adolescents - the toxic effect of toxic substances on the myocardium.

Symptoms

Common signs of acute heart failure include: shortness of breath, cardialgia, weakness, fatigue, confusion, drowsiness, pale skin, acrocyanosis, thready pulse, fluctuations in blood pressure, edema. Without proper treatment, the pathology leads to dangerous consequences, often incompatible with life.

Symptoms of right ventricular AHF

Acute right ventricular heart failure is a form of the disease caused by stagnation of blood in the veins of the systemic circulation. Clinically, it manifests itself with the following symptoms:

Symptoms of left ventricular AHF

The cause of the pathology is stagnation of blood in the pulmonary circle. Acute left ventricular heart failure occurs in one of the following forms: “cardiac asthma”, cardiogenic shock, pulmonary edema.

Patients complain of:

shortness of breath,
wet cough with foamy sputum,
moist wheezing in the lungs, audible at a distance - the sound of bursting bubbles,
attacks of suffocation at night,
pain behind the sternum, radiating to the scapula,
dizziness.

Patients take a forced sitting position with their legs down. Their respiratory muscles are under constant tension, and fainting is possible.

Left ventricular failure, if untreated, leads to impaired cerebral circulation and ends with pulmonary edema, a change in the rhythm of breathing until it stops completely.

In the absence of timely and adequate therapy, acute decompensated heart failure develops. This is the terminal stage of pathology, when the heart ceases to cope with its functions and does not provide the body with normal blood circulation even at rest. Decompensation develops rapidly and often ends in the death of patients. Symptoms of acute heart failure before death: sudden paleness of the skin, cold sticky sweat, foam at the mouth, attacks of suffocation, cardiac arrest.

Diagnostics

Diagnosis of acute cardiovascular failure begins with listening to the patient’s complaints, collecting an anamnesis of life and illness. During the examination, cardiologists determine cyanosis, swelling of the neck veins, and a weak and rapid pulse. Then auscultation of the heart and lungs, palpation of the liver, ECG examination and additional instrumental diagnostic methods are performed.

Auscultation - listening to heart sounds. In this case, a weakening of the 1st tone, a bifurcation of the 2nd tone on the pulmonary artery, the appearance of the 4th heart sound, diastolic murmur, and arrhythmia are detected.
The electrocardiogram shows signs of hypertrophy and overload of the ventricles of the heart, impaired blood supply to the heart muscle, and myocardial ischemia.
ECHO-CG with Dopplerography allows us to establish a decrease in the volume of blood ejected from the ventricles, thickening of the walls of the ventricles, hypertrophy of the heart chambers, a decrease in myocardial contractile activity, expansion of the pulmonary aorta, disruption of the heart valves, and pulmonary hypertension. Echocardiography detects functional disorders and anatomical changes of the heart.
Using coronary angiography, the location and degree of narrowing of the coronary artery supplying the heart muscle is determined.
Computed tomography allows you to create a 3-dimensional model of the heart on a computer monitor and identify all existing pathological changes.
MRI of the heart is the most informative and popular research method, which is used independently or in addition to ultrasound, x-ray or CT of the heart. This test is safe and does not cause radiation exposure. It shows a full, three-dimensional image of the organ under study in any of the given planes, allowing you to assess their volume, condition and functionality.

Treatment

Acute arterial insufficiency is a deadly condition that requires emergency medical care. When the first symptoms of the disease appear, you must urgently call an ambulance.

Before the ambulance arrives, a patient with acute heart failure must be provided with emergency care. He is given a sitting position with his legs down, an air flow into the room is provided, and, if necessary, an antihypertensive drug is given, Nitroglycerin under the tongue, an Aspirin tablet. To drain blood from the lungs, patients are given a hot foot bath.

Drug therapy:

Sympathomimetics increase cardiac output, narrow the lumen of the veins, and stimulate venous blood flow. This group includes “Dopamine”, “Mezaton”, “Methoxamine”.
Nitrates – “Nitroglycerin”, “Sodium nitroprusside”. They expand the lumen of blood vessels, lower blood pressure, and improve cardiac output. The drugs are taken sublingually or administered intravenously.
Antiplatelet agents prevent platelet aggregation and prevent the formation of blood clots - “Aspirin”, “Curantil”, “Cardiomagnyl”.
Anticoagulants change blood viscosity, inhibiting clotting processes. Direct anticoagulants - Heparin, Fraxiparin and indirect - Warfarin.
Beta blockers slow the heart rate, reduce myocardial oxygen demand and blood pressure. These include Metoprolol, Bisoprolol, Propranolol.
Calcium channel blockers are used for arrhythmias and hypertension - Verapamil, Nifedipine.
Cardiotonic drugs are administered intravenously in a stream - “Amrinon” and “Milrinon”.
Diuretics remove excess fluid from the body, reduce the load on the heart and eliminate edema - Furosemide, Hypothiazide, Indapamide, Veroshpiron.
To reduce pain, take tablet analgesics - “Baralgin”, “Sedalgin”. If there is no effect, the patient is administered narcotic analgesics - “Promedol”, “Omnopon” in combination with a tranquilizer.
Cardiac glycosides increase the strength and efficiency of heart contractions, stimulate heart function - “Korglikon”, “Strofanthin”.
Antiarrhythmic drugs - Amiodarone, Novocainamide.

Prevention

Measures to prevent the development of acute heart failure.

Acute heart failure is one of the most severe circulatory disorders, a life-threatening condition that requires emergency treatment, hospitalization in an intensive care unit (department) and preferably in a hospital with the necessary diagnostic and treatment capabilities.

Acute heart failure is a complication of various diseases, consisting in circulatory disorders due to a decrease in the pumping function of the heart or a decrease in its filling with blood.

Of particular importance is the division of acute heart failure into systolic (inability to eject the required amount of blood from the ventricle) and diastolic (inability to fully fill the ventricles with blood), left-sided and right-sided.

Causes of acute heart failure

Acute heart failure can complicate the course of many diseases or conditions; its causes and development mechanisms are different.

Among the reasons are the following: decompensation of chronic heart failure, acute myocardial infarction, mechanical complications of acute myocardial infarction (eg: ventricular septal rupture, mitral valve chordae rupture, right ventricular infarction), right ventricular myocardial infarction, rapidly progressive arrhythmia or severe bradycardia, acute pulmonary embolism, hypertensive crisis, cardiac tamponade, aortic dissection, birth cardiomyopathy, obstruction of blood flow (narrowing of the aortic orifice and mitral orifice, hypertrophic cardiomyopathy, tumors, blood clots), valvular insufficiency (mitral or aortic), dilated cardiomyopathy, myocarditis, cardiac injury.

Non-cardiac causes include: infections, especially pneumonia, sepsis, poor adherence to treatment, volume overload, severe stroke, surgery and perioperative problems, renal dysfunction, exacerbation of asthma, chronic obstructive pulmonary disease, anemia, medications (non-steroidal anti-inflammatory drugs, corticosteroids, drug interactions), hypo- or hyperfunction of the thyroid gland, alcohol abuse and drugs.

Symptoms of acute heart failure

Symptoms are varied and depend on the causes of the disease and the degree of dysfunction of the left or right ventricles. Depending on the main symptoms, acute heart failure is divided into left and right ventricular failure; in some situations, right and left ventricular failure may occur simultaneously (biventricular failure).

Biventricular failure occurs during myocardial infarction with damage to the right and left ventricles, with mechanical complications of acute myocardial infarction (rupture of the interventricular septum), myocarditis, etc.

The main cause of acute left ventricular failure and is dysfunction of the left ventricular myocardium (myocardial infarction, hypertensive crisis, cardiac arrhythmia). The following symptoms are characteristic: increasing shortness of breath, worsening in a lying position, up to suffocation. The extreme manifestation of acute left ventricular failure is cardiogenic shock.

Acute right ventricular failure occurs with pulmonary embolism, right ventricular myocardial infarction, cardiac tamponade, status asthmaticus. Main symptoms: swelling and increased pulsation of the neck veins, edema, enlarged liver.

Considering the above, the main signs of acute heart failure are: heavy, rapid breathing (more than 24 per minute), noisy breathing - shortness of breath, even suffocation. A clear increase in shortness of breath and cough in a horizontal position. A sitting position and a position with the head of the bed raised alleviates the patient's condition. When breathing, moist wheezing becomes audible, interrupted by coughing; in the terminal stage, foam appears at the mouth. The position of the patient resting his straight arms on his knees or sitting to facilitate breathing.

Heart failure can develop very quickly and within 30-60 minutes lead to the death of the patient.

First aid

If the above symptoms appear, you must:

Call an ambulance,
give the patient a sitting position,
place your feet in heat (a heating pad, a container of hot water),
measure blood pressure when systolic pressure is above 100 mm Hg, give 1 tablet of nitroglycerin under the tongue or 1 inhalation under the tongue, if the patient’s condition improves, repeat taking nitroglycerin after 10 minutes, then every 10 minutes until the ambulance arrives. If there is no effect, do not give nitroglycerin again.
try to calm the patient.

Diagnostics

Diagnosis begins with a survey to clarify the possible causes, followed by an examination, where the doctor can note the presence of edema, swelling and pulsation of the neck veins, pallor of the skin, palpation reveals an enlarged liver, moisture in the skin, auscultation - wheezing in the lungs, rhythm disturbances, the appearance of additional tones and murmurs in the heart.

clinical blood test (to determine the presence of inflammation, anemia),
General urine test (to assess the condition of the kidneys).
Biochemical blood test: urea, creatinine (to assess the functional state of the kidneys), transaminases (to assess the condition of the liver), potassium, sodium levels (to exclude electrolyte disturbances, to assess kidney function),
blood sugar level,
troponin (to rule out damage to the heart muscle),
D-dimer (if pulmonary embolism is suspected),
arterial blood gases (in severe heart failure),
brain natriuretic peptide (pro-BNP, increases in heart failure).
A 12-lead electrocardiogram (ECG) allows you to evaluate the heart rhythm and the presence of myocardial ischemia.
A survey X-ray of the chest organs is performed to assess the size and boundaries of the heart and the severity of congestion in the lungs.

Echocardioscopy (ECHO-CS) is necessary to assess structural and functional changes in the heart (condition of valves, cardiac muscle, pericardium, pulmonary artery diameter, pulmonary artery pressure, mechanical complications of myocardial infarction, heart tumors, etc.).

In some situations, it may be necessary to perform coronary angiography - an examination of the blood vessels of the heart. If pulmonary embolism is suspected, spiral computed tomography and lung scintigraphy are performed. A magnetic resonance imaging study may be necessary to rule out a dissecting aortic aneurysm.

All patients are required to monitor blood pressure around the clock, pulse oximetry (determining oxygen saturation of hemoglobin in the blood), and ECG.

Treatment of acute heart failure

The main goal of treatment is to quickly stabilize the condition and reduce shortness of breath. The best treatment results are achieved in specialized emergency departments.

Oxygen therapy(inhalation of humidified oxygen), in severe cases, respiratory support and artificial ventilation may be required.

Drug treatment: morphine is indicated at the early stage of acute heart failure, especially in the presence of pain, agitation of the patient; nitro drugs are started before the ambulance arrives, then intravenous administration is continued. Depending on the severity, other drugs may be used at the initial stage: venous vasodilators (sodium nitroprusside, nesiritide), diuretics (loop, thiazide-like), intropic drugs that improve cardiac muscle contraction (dobutamine), vasopressors (dopamine). Drugs for the prevention of thromboembolic complications (anticoagulants).

For some diseases underlying heart failure, it is necessary emergency surgery. Possible surgical methods include: myocardial revascularization, correction of anatomical defects of the heart (valve replacement and reconstruction), mechanical means of temporary circulatory support (intra-aortic balloon counterpulsation).

The next stage of treatment after stabilization of the condition includes the appointment of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers, beta-blockers, mineralocorticoid receptor antagonists. If the contractility of the heart decreases, digoxin is prescribed (if the ejection fraction according to ECHO-CS is less than 40%).

Before discharge, it should be ensured that the acute period of heart failure has resolved and a stable regimen of diuretics has been established for at least 48 hours.

The average length of hospital stay is 10-14 days. Continue treatment (including beta blockers, ACE inhibitors or angiotensin receptor blockers, mineralocorticoid antagonists) on an outpatient basis. After discharge from the hospital, patients are observed by a cardiologist at their place of residence. Timely correction of therapy, dynamic ECG, ECHO-CS, as well as monitoring of laboratory parameters (electrolytes, creatinine, pro-BNP) help reduce the number of patient hospitalizations and improve the patient’s quality of life.

The doctor will also give specific recommendations on diet, level of physical activity, explain the need to take medications, pointing out possible side effects, and note conditions the occurrence of which should alert the patient.

Diet: Limit fluid to 1.5–2 L/day to reduce symptoms and fluid retention. Weight-based fluid restriction (30 ml/kg body weight, 35 ml/kg if body weight >85 kg) may reduce thirst and monitor and prevent malnutrition.

Eating Healthy Foods: limiting fats of animal origin in favor of eating poultry, fish (preferably sea), but no more than 2 times a week, fresh vegetables, fruits, herbs, seafood; avoiding fried foods, giving preference to stewed and steamed foods, if necessary, limiting salt to 1 g per day.

Be sure to control your weight. If you gain more than 2 kg in 3 days, consult a doctor.

Quitting smoking and drug use is mandatory, and moderate alcohol consumption is possible (complete abstinence is recommended in patients with alcoholic cardiomyopathy). In other cases, the following rule may apply: 2 units of alcohol per day for men and 1 unit per day for women (1 unit = 10 ml of pure alcohol, for example 1 glass of wine).

Required daily physical activity, aerobic physical activity 30 minutes a day according to condition (walking in the fresh air, Nordic walking).

Carry out immunization against influenza viruses and pneumococcal infections, since any viral or bacterial infections can lead to a worsening of the condition.

Monitor and adapt fluid intake when traveling, particularly during flights and in hot climates. Beware of adverse reactions from sun exposure when taking certain medications (eg, amiodarone).

Possible complications

Acute heart failure itself is a complication of many diseases and conditions. However, in the process of treating heart failure itself, severe rhythm and conduction disturbances, thromboembolic complications, progression of the disease to the most severe forms (cardiogenic shock, pulmonary edema), and sudden cardiac death may occur.

Forecast

The prognosis of heart failure is always determined by the disease from which it developed. Heart failure always has a poor prognosis. Within one year, 17% of hospitalized and 7% of outpatients with heart failure die. In 30-50% of cases, patients die suddenly from severe arrhythmias.

To summarize, I would like to note the particular importance of regularly taking recommended medications on an outpatient basis and maintaining a healthy lifestyle. Remember that strict adherence to the doctor’s recommendations will help avoid repeated hospitalizations and improve the patient’s quality of life.

Cardiologist Chuguntseva M.A.

– 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.

General information

A decrease in the contractile (pumping) function of the heart in heart failure leads to the development of an imbalance between the hemodynamic needs of the body and the ability of the heart to fulfill them. This imbalance is manifested by an excess of venous inflow to the heart and the resistance that must be overcome by the myocardium to expel blood into the vascular bed over the ability of the heart to move blood into the arterial system.

Not being an independent disease, heart failure develops as a complication of various pathologies of blood vessels and the heart: valvular heart disease, coronary artery disease, cardiomyopathy, arterial hypertension, etc.

In some diseases (for example, arterial hypertension), the increase in heart failure occurs gradually, over years, while in others (acute myocardial infarction), accompanied by the death of some functional cells, this time is reduced to days and hours. With a sharp progression of heart failure (within minutes, hours, days), they speak of its acute form. In other cases, heart failure is considered chronic.

Chronic heart failure affects 0.5 to 2% of the population, and after 75 years its prevalence is about 10%. The significance of the problem of the incidence of heart failure is determined by the steady increase in the number of patients suffering from it, the high mortality and disability rates of patients.

Causes of heart failure

Among the most common causes of heart failure, occurring in 60-70% of patients, are myocardial infarction and coronary artery disease. These are followed by rheumatic heart disease (14%) and dilated cardiomyopathy (11%). In the age group over 60 years, in addition to ischemic heart disease, heart failure is also caused by hypertension (4%). In elderly patients, a common cause of heart failure is type 2 diabetes mellitus and its combination with arterial hypertension.

Risk factors

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

These include:

overstrain of physical and psycho-emotional capabilities
arrhythmias, pulmonary embolism, hypertensive crises, progression of ischemic heart disease;
pneumonia, ARVI, anemia, renal failure, hyperthyroidism
taking cardiotoxic drugs, drugs that promote fluid retention (NSAIDs, estrogens, corticosteroids), increasing blood pressure (isadrine, ephedrine, adrenaline)
pronounced and rapidly progressive weight gain, alcoholism
a sharp increase in blood volume during massive infusion therapy
myocarditis, rheumatism, infective endocarditis
non-compliance with recommendations for the treatment of chronic heart failure.

Pathogenesis

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, there is a sharp drop in minute output and blood flow into the arterial system. Acute heart failure is clinically similar to acute vascular failure and is sometimes referred to as acute cardiac collapse.

In chronic heart failure, 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 strength of heart contractions, an increase in rhythm, a decrease in pressure in diastole due to the expansion of capillaries and arterioles, which facilitates emptying of the heart during systole, and an increase in perfusion fabrics.

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 moment, a stage of decompensation occurs, due to the weakening of the myocardium, the development of the processes of degeneration 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 in the periphery, which helps maintain stable blood pressure in the systemic circulation while reducing cardiac output. The resulting renal vasoconstriction leads to renal ischemia, which contributes to interstitial fluid retention.

An increase in the secretion of antidiuretic hormone by the pituitary gland 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 into the tissue.

Thus, severe heart failure leads to severe hemodynamic disturbances in the body:

Gas exchange disorder

When blood flow slows down, tissue absorption of oxygen from capillaries increases from 30% normally 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 increased work of the respiratory muscles cause activation of the basal 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 stagnation in the pulmonary circulation and impaired blood oxygenation) and peripheral (with slow blood flow and increased utilization of oxygen in the tissues). Since circulatory failure is more pronounced in the periphery, patients with heart failure experience acrocyanosis: cyanosis of the extremities, ears, and tip of the nose.

Edema

Edema develops as a result of a number of factors: interstitial fluid retention with increased capillary pressure and slower blood flow; water and sodium retention due to impaired water-salt metabolism; disturbances in the oncotic pressure of blood plasma due to protein metabolism disorders; reducing the inactivation of aldosterone and antidiuretic hormone with decreased liver function.

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

stagnant changes in organs

Congestion in the lungs is associated with impaired hemodynamics of the pulmonary circulation. They are characterized by rigidity of the lungs, decreased respiratory excursion of the chest, and limited mobility of the pulmonary edges. Manifested by congestive bronchitis, cardiogenic pneumosclerosis, hemoptysis. Congestion of the systemic circulation causes hepatomegaly, manifested by heaviness and pain in the right hypochondrium, and then cardiac fibrosis of the liver with the development of connective tissue in it.

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 boundaries of the heart. With the development of congestive gastritis, nausea, loss of appetite, vomiting, a tendency to constipation, flatulence, and weight loss appear. With progressive heart failure, a severe degree of exhaustion develops - cardiac cachexia.

Congestive processes in the kidneys cause oliguria, increased relative density of urine, proteinuria, hematuria, and cylindruria. Dysfunction of the central nervous system in heart failure is characterized by rapid fatigue, decreased mental and physical activity, increased irritability, sleep disorders, and depressive states.

Classification

According to the rate of increase in signs of decompensation, acute and chronic heart failure are distinguished.

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

left type (acute left ventricular or left atrial failure)
acute right ventricular failure

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

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

II (pronounced) stage– signs of prolonged circulatory failure and hemodynamic disorders (stagnation 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 disorders of the structure of organs (liver, lungs, kidneys), exhaustion.

Symptoms of heart failure

Acute heart failure

Acute heart failure is caused by weakening of the function of one of the parts 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 disease, myocardial infarction). When the functions of the left ventricle are weakened, the 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.

Clinical manifestations of acute left ventricular failure are cardiac asthma and alveolar pulmonary edema. An attack of cardiac asthma is usually provoked by physical or neuropsychic 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 phlegm difficult to clear, severe weakness, and cold sweat.

The patient assumes an orthopneic position - sitting with legs down. On examination - pale skin with a grayish tint, cold sweat, acrocyanosis, severe shortness of breath. A weak, fast-filling arrhythmic pulse, expansion of the borders of the heart to the left, dull heart sounds, and a gallop rhythm are detected; blood pressure tends to decrease. There is harsh breathing in the lungs with isolated dry wheezing.

Further increase in pulmonary congestion contributes to the development of pulmonary edema. Sharp suffocation is accompanied by a cough with the release of copious amounts of foamy pink sputum (due to the presence of blood). From a distance, bubbling breathing with moist wheezing can be heard (a symptom of a “boiling samovar”). The patient's position is orthopneic, the face is cyanotic, the veins of the neck are swollen, the skin is covered with cold sweat. The pulse is threadlike, arrhythmic, frequent, blood pressure is reduced, and there are moist rales of various sizes in the lungs. Pulmonary edema is an emergency condition that requires intensive care measures, as it can be fatal.

Acute left atrial heart failure occurs with mitral stenosis (left atrioventricular 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 the systemic circulation, which is manifested by swelling of the legs, pain in the right hypochondrium, a feeling of distension, swelling and pulsation of the neck veins, shortness of breath, cyanosis, pain or pressure in the heart area. The peripheral pulse is weak and frequent, blood pressure is sharply reduced, central venous pressure is increased, the heart is enlarged to the right.

In diseases that cause decompensation of the right ventricle, heart failure manifests itself earlier than in left ventricular failure. This is explained by 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 disease, mitral valve insufficiency, arterial hypertension, coronary insufficiency, congestion in the pulmonary vessels and chronic left ventricular failure develop. It is characterized by vascular and gas changes in the lungs. There is shortness of breath, attacks of suffocation (usually at night), cyanosis, attacks of palpitations, cough (dry, sometimes with hemoptysis), increased fatigue.

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

With predominant damage to the right ventricle (right ventricular failure), congestion develops in the systemic circulation. Right ventricular failure can accompany mitral heart defects, pneumosclerosis, pulmonary emphysema, etc. There are complaints of pain and heaviness in the right hypochondrium, the appearance of edema, decreased diuresis, distension and enlargement of the abdomen, shortness of breath with movements. Cyanosis develops, sometimes with an icteric-cyanotic tint, ascites, the cervical and peripheral veins swell, and the liver increases in size.

The functional failure of one part of the heart cannot remain isolated for a long time, and over time, total chronic heart failure develops with venous stagnation in the pulmonary and systemic circulation. Also, the development of chronic heart failure is observed with damage to the heart muscle: myocarditis, cardiomyopathy, ischemic heart disease, intoxication.

Diagnostics

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 artery disease, hypertension, previous myocardial infarction and rheumatic attack, cardiomyopathy. Detection of swelling of the legs, ascites, rapid low-amplitude pulse, listening to the third heart 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, 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.

Treatment of heart failure

In case of heart failure, treatment is aimed at eliminating the primary cause (ischemic heart disease, hypertension, rheumatism, myocarditis, etc.). For heart defects, cardiac aneurysm, adhesive pericarditis, which create a mechanical barrier to the functioning of the heart, surgical intervention is often resorted to.

In case of acute or severe chronic heart failure, bed rest and complete mental and physical rest are prescribed. In other cases, you should adhere to moderate loads that do not disturb your well-being. Liquid consumption is limited to 500-600 ml per day, salt - 1-2 g. A fortified, easily digestible diet is prescribed.

Pharmacotherapy for heart failure can prolong and significantly improve the condition of patients and their quality of life.

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

cardiac glycosides (digoxin, strophanthin, etc.) – increase myocardial contractility, increase its pumping function and diuresis, and promote satisfactory exercise tolerance;
vasodilators and ACE inhibitors - angiotensin-converting enzyme (enalapril, captopril, lisinopril, perindopril, ramipril) - reduce vascular tone, dilate veins and arteries, thereby reducing vascular resistance during heart contractions and helping to increase cardiac output;
nitrates (nitroglycerin and its prolonged forms) - improve blood flow to the ventricles, increase cardiac output, dilate the coronary arteries;
diuretics (furosemide, spironolactone) – reduce the retention of excess fluid in the body;
B-blockers (carvedilol) – reduce heart rate, improve blood flow to the heart, increase cardiac output;
anticoagulants (acetylsalicylic acid, warfarin) – prevent thrombus formation in blood vessels;
drugs that improve myocardial metabolism (B vitamins, ascorbic acid, inosine, potassium preparations).

When an attack of acute left ventricular failure (pulmonary edema) develops, the patient is hospitalized and given emergency treatment: diuretics, nitroglycerin, drugs that increase cardiac output (dobutamine, dopamine), and oxygen inhalations are administered. If ascites develops, fluid is removed by puncture from the abdominal cavity; if hydrothorax occurs, pleural puncture is performed. Patients with heart failure due to severe tissue hypoxia are prescribed oxygen therapy.

Prognosis and prevention

The five-year survival rate for patients with heart failure is 50%. Long-term prognosis is variable, it is influenced by the severity of heart failure, concomitant background, effectiveness of therapy, lifestyle, etc. Treatment of heart failure in the early stages can completely compensate for the patient’s condition; The worst prognosis is observed in stage III heart failure.

Measures to prevent heart failure include preventing the development of diseases that cause it (coronary artery disease, hypertension, heart defects, etc.), as well as factors that contribute to its occurrence. To avoid the progression of already developed heart failure, it is necessary to adhere to the optimal regime of physical activity, take prescribed medications, and constant monitoring