Diagnosis and treatment of acute heart failure. Heart failure

From this article you will receive comprehensive information about the disease heart failure: what causes it to develop, its stages and symptoms, how it is diagnosed and treated.

Article publication date: 12/18/2016

Article updated date: 05/25/2019

In heart failure, the heart is unable to fully cope with its function. Because of this, tissues and organs receive insufficient oxygen and nutrients.

If you suspect heart failure, do not delay contacting a cardiologist. If you contact it at an early stage, you can get rid of the disease completely. But with heart failure of degree 2 and higher, doctors usually give a less favorable prognosis: it is unlikely to be completely cured, but it is possible to stop its development. If you neglect your health and do not contact specialists, the disease will progress, which can lead to death.

Why does pathology occur?

The causes of heart failure can be congenital or acquired.

Causes of congenital pathology

Causes of acquired heart failure

• Chronic arterial hypertension (high blood pressure);
• vascular spasms;
• stenosis (narrowing) of blood vessels or heart valves;
• endocarditis – inflammation of the inner lining of the heart;
• myocarditis – inflammation of the heart muscle;
• pericarditis - inflammation of the serous membrane of the heart;
• heart tumors;
• previous myocardial infarction;
• metabolic disorders.

Acquired heart failure mainly affects people over 50 years of age. Also at risk are smokers and those who abuse alcohol and (or) drugs.

Heart failure often occurs and progresses due to excessive physical activity in adolescence, when the load on the cardiovascular system is already high. To prevent heart failure, young athletes are advised to reduce the intensity of training at the age when puberty begins and the body is most active in growth. If at this age the initial symptoms of heart failure appear, doctors will most likely ban sports for 0.5–1.5 years.

Classification and symptoms

Signs of heart failure may vary depending on the severity of the condition.

Classification of heart failure according to Vasilenko and Strazhesko:

Stage 1 (initial, or hidden)

Symptoms appear only during intense physical activity, which was previously achieved without difficulty. Signs: shortness of breath, palpitations. At rest, no circulatory disturbances are observed.

For patients with this stage of heart failure there are no restrictions in terms of physical activity. They can do any job. However, it is still necessary to undergo a preventive examination with a cardiologist once every six months or a year; you may also need to take medications that support the functioning of the heart.

Treatment at this stage is effective and helps get rid of the disease.

Stage 2 A

Sports activities with such heart failure are prohibited, but physical education and moderate physical activity at work are not contraindicated.

Signs can be eliminated with proper treatment.

Stage 2 B

Blood circulation is impaired in both the small and large circles.

All symptoms appear at rest or after minor physical activity. This:

• cyanosis of the skin and mucous membranes,
• cough,
• dyspnea,
• wheezing in the lungs,
• swelling of the limbs,
• aching pain in the chest,
• liver enlargement.

Patients experience chest discomfort and shortness of breath even with the slightest physical exertion, as well as during sexual intercourse. Walking exhausts them. It is very difficult to climb up the stairs. Such patients are usually recognized as incapacitated.

Treatment helps reduce symptoms and prevent further development of heart failure.

Stage 3 (final, or dystrophic)

Due to severe circulatory disorders, the main symptoms intensify. Pathological changes in internal organs also develop (cardiac cirrhosis of the liver, diffuse pneumosclerosis, congestive kidney syndrome). Metabolic disorders progress, and depletion of body tissues develops.

Treatment of heart failure at this stage is usually ineffective. It helps to slow down the development of changes in internal organs, but does not entail a significant improvement in well-being.

Patients with stage 3 heart failure are not able to fully perform even everyday tasks (cooking, washing, cleaning). Patients are recognized as disabled.

The prognosis is unfavorable: the disease can lead to death.

Diagnosis of heart failure

Before starting treatment, the doctor needs to find out the severity and nature of the disease.

First of all, you will need to be examined by a therapist. Using a stethoscope, he will listen to the lungs for wheezing, and will also conduct a superficial examination to detect bluishness of the skin. Measure heart rate and blood pressure.

Sometimes additional tests are performed to determine the heart's response to physical activity.

Test	Progress	Evaluation of results
20 squat test	All heart rate measurements are carried out in 1 minute. Heart rate is measured at rest in a sitting position (result No. 1 - R No. 1). The patient squats 20 times in 30 seconds. Heart rate is measured immediately after squats (P No. 2). Heart rate is measured after 1 minute (P No. 3). Then after another 2 minutes (P No. 4).	Heart response to stress: P No. 2 is 25% more than P No. 1 - excellent, 25-50% more - normal, 51% or more more - bad. Cardiac recovery after exercise: P No. 3 is close to P No. 1 - excellent, P No. 4 is close to P No. 1 - normal, P No. 4 is more than P No. 1 - bad.
Ruffier-Dixon test	All heart rate measurements are taken for 15 seconds. Heart rate is measured after a 5-minute rest in a supine position (P1). The patient squats 30 times in 45 seconds. Heart rate is measured immediately after exercise (P2) (the patient lies down after squats). Wait 30 seconds. The last time the heart rate is measured is 15 seconds.	The result is calculated using the formula: (4 * (P1+P2+P3) – 200) / 10 Rating: less than 3 - excellent, from 3 to 6 - good, from 7 to 9 - normal, from 10 to 14 - bad, more than 15 - very bad. In patients with tachycardia, this test may give a biased poor result, so the first test is used.

The tests are used for patients whose wheezing in the lungs is mild. If the tests give poor results, the patient most likely has heart failure. If wheezing in the lungs is severe, no tests are required.

When the primary examination by the therapist is completed, he gives a referral to a cardiologist who will conduct further diagnostics and prescribe treatment.

• ECG - will help identify pathologies of the heart rhythm.
• 24-hour ECG (Holter mount or Holter) – electrodes are attached to the patient’s body and a device is attached to the belt that records heart function for 24 hours. During these days the patient leads his normal lifestyle. Such an examination helps to more accurately record arrhythmias if they manifest themselves in the form of attacks.
• (ultrasound of the heart) – necessary to identify structural pathologies of the heart.
• X-ray chest. Helps identify pathological changes in the lungs.
• Ultrasound of the liver, kidneys. If the patient has heart failure stage 2 or higher, it is necessary to diagnose these organs.

Methods for diagnosing heart pathologies

Sometimes a CT or MRI of the heart, blood vessels or other internal organs may be needed.

After receiving the results of these diagnostic methods, the cardiologist prescribes treatment. It can be either conservative or surgical.

Treatment

Drug therapy

Conservative treatment includes taking various groups of drugs:

Group of drugs	Effect	Examples of drugs
Cardiac glycosides	Supports and improves the contractile function of the heart muscle	Digitoxin, Digoxin, Methyldigoxin, Strophanthin K
Nitrates	Relieves pain in the chest, dilates veins	Nitroglycerine
ACE inhibitors	Reduce blood pressure, dilate blood vessels, reduce the risk of cardiac arrest	Captopril, Lisinopril, Fosinopril
Beta blockers	Reduce blood pressure and slow heart rate	Metoprolol, Atenolol
Calcium antagonists	Dilate arteries, reduce blood pressure, eliminate arrhythmias	Verapamil, Cinnarizine, Diltiazem, Amlodipine, Nitrendipine
Diuretics	Remove excess fluid from the body, prevent the formation of edema, increase the effectiveness of drugs that lower blood pressure	Spironol, Uractone, Furosemide, Aldactone
Other	Stimulates metabolism in the myocardium	ATP, Riboxin, Carnitine

Drugs for the treatment of heart failure

If a patient has stage 1 heart failure that appears due to excessive physical exertion, the doctor may decide that the patient does not yet need to take serious medications. In this case, he will prescribe only medications that improve metabolism in the heart muscle, as well as B vitamins to strengthen the heart and blood vessels.

Surgery

For some congenital or acquired heart defects, drug treatment is ineffective. It may relieve symptoms for a short time, but has no effect on the cause of the disease.

Plant	Recipe
Foxglove Purple – Contains Digitoxin	Take 1.5 tsp. (1 g) dry leaves. Pour 1 tbsp. boiling water Leave for 12 hours. Take 1 tsp. 2 times a day. Note! Do not exceed the dosage under any circumstances. Foxglove is a plant that can poison you! In case of severe heart defects, after a heart attack, with coronary artery stenosis and certain types of arrhythmias, it is prohibited to use digitalis! Folk remedies, like medicines, can be hazardous to health if used incorrectly. Be sure to consult your doctor!
Woolly foxglove – contains digoxin, celanide
Lily of the valley - contains corglycone	Take 8-10 fresh flowers. Pour 1 tbsp. boiling water Leave for 1-2 hours. Drink in small portions throughout the day. Attention! Korglykon is contraindicated in WPW syndrome, as it causes attacks of tachycardia.

Herbs for treating heart failure

Diet and lifestyle for heart failure

First of all, you should give up bad habits if you have them. If you have heart failure of degree 2 or higher, exercise is contraindicated. Doctors recommend physical therapy taking into account the patient’s well-being.

The diet should also be adjusted:

To reduce swelling and reduce the load on the kidneys, reduce the amount of water (you can drink no more than 0.75–1 liters per day).

So that your head doesn't rush a large number of blood, it is recommended to sleep with a large pillow under your head. And to prevent edema, you need another pillow - it is placed under your feet.

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 modern classification There are two types of AHF - 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:

• angina pectoris,
• arterial hypertension,
• congenital or acquired heart defects,
• TELA,
• myocarditis of various etiologies,
• arrhythmia,
• myocardial infarction,
• cardiomyopathy,
• aortic aneurysm.

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:

• increased heart rate,
• dizziness,
• shortness of breath,
• discomfort behind the sternum,
• swelling of the veins of the neck,
• swelling,
• acrocyanosis,
• hepatomegaly,
• ascites,
• pallor,
• weakness,
• hyperhidrosis.

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:

• fighting bad habits,
• minimizing stress effects on the body,
• control blood pressure and cholesterol levels,
• adequate balanced nutrition,
• optimization of work and rest,
• full sleep,
• annual examination of the heart and blood vessels using the basic available techniques.

Acute heart failure is a deadly pathology that significantly complicates a person’s life and can lead to sudden death. Timely treatment mitigates the course of the pathology and makes the prognosis of the disease favorable. The main thing is to identify AHF in time and provide first aid correctly. Do not self-medicate, consult a specialist. They will prescribe a treatment regimen and select the correct dosage of drugs, taking into account the course of AHF and the individual characteristics of the body.

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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 with prehospital stage 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 oxygen consumption, diabetes 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 infarctions 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, AV block high degree) 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 to provide emergency assistance, 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

1. ECG: changes caused by underlying heart disease are usually observed, most often signs of myocardial ischemia, rhythm and conduction disturbances.
2. 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.
3. Echocardiography: detects functional abnormalities (systolic or diastolic dysfunction, valvular dysfunction) or anatomical changes of the heart (eg, mechanical complications of myocardial infarction).
4. 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.
5. 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 due to arterial hypertension and hypertension 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.

Goals of treatment 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. "

A. L. Vertkin, V. V. Gorodetsky, O. B. Talibov, A. V. Topolyansky

NNPO Emergency Medical Care, MGMSU

Acute heart failure (AHF), which is a consequence of impaired myocardial contractility and a decrease in systolic and cardiac output, is manifested by extremely severe clinical syndromes: cardiogenic shock, pulmonary edema, acute cor pulmonale.

Main causes and pathogenesis

A decrease in myocardial contractility occurs either as a result of its overload, or due to a decrease in the functioning mass of the myocardium, a decrease in the contractile ability of myocytes, or a decrease in the compliance of chamber walls. These conditions develop in the following cases:

* in case of disturbance of diastolic and/or systolic function of the myocardium during infarction (the most common cause), inflammatory or dystrophic diseases of the myocardium, as well as tachy- and bradyarrhythmias;

* in case of sudden occurrence of myocardial overload due to a rapid significant increase in resistance in the outflow tract (in the aorta - hypertensive crisis in patients with compromised myocardium; in the pulmonary artery - thromboembolism of the branches of the pulmonary artery, a prolonged attack of bronchial asthma with the development of acute pulmonary emphysema, etc.) or due to volume loads (an increase in the mass of circulating blood, for example, with massive fluid infusions - a variant of the hyperkinetic type of hemodynamics);

* in case of acute disturbances of intracardiac hemodynamics due to rupture of the interventricular septum or the development of aortic, mitral or tricuspid insufficiency (septal infarction, infarction or avulsion of the papillary muscle, perforation of the valve leaflets in bacterial endocarditis, rupture of the chordae, trauma);

* with increased load (physical or psycho-emotional stress, increased inflow in a horizontal position, etc.) on the decompensated myocardium in patients with chronic congestive heart failure.

Classification

Depending on the type of hemodynamics, which ventricle of the heart is affected, as well as on some features of the pathogenesis, the following clinical variants of AHF are distinguished.

* With stagnant hemodynamics:

Right ventricular (venous congestion in the systemic circulation);

Left ventricular (cardiac asthma, pulmonary edema).

* With hypokinetic 1 type of hemodynamics (small output syndrome - cardiogenic shock):

Arrhythmic shock;

Reflex shock;

A true shock.

Since myocardial infarction is one of the most common causes of AHF, the table provides a classification of acute heart failure in this disease.

Possible complications

Any of the variants of AHF is a life-threatening condition. Acute congestive right ventricular failure, not accompanied by small output syndrome, in itself is not as dangerous as diseases leading to right ventricular failure.

Clinical picture

* Acute congestive right ventricular failure is manifested by venous congestion in the systemic circulation with increased systemic venous pressure, swelling of the veins (most noticeable in the neck), enlarged liver, and tachycardia. Edema may appear in the lower parts of the body (with prolonged horizontal position - on the back or side). Clinically, it differs from chronic right ventricular failure by intense pain in the liver area, aggravated by palpation. Signs of dilatation and overload of the right heart are determined (expansion of the borders of the heart to the right, systolic murmur over the xiphoid process and protodiastolic gallop rhythm, emphasis of the second tone on the pulmonary artery and corresponding ECG changes). A decrease in left ventricular filling pressure due to right ventricular failure can lead to a drop in left ventricular minute volume and the development of arterial hypotension, up to a picture of cardiogenic shock.

With pericardial tamponade and constrictive pericarditis, the pattern of large circle congestion is not associated with insufficiency of myocardial contractile function, and treatment is aimed at restoring diastolic filling of the heart.

Biventricular failure, an option when congestive right ventricular failure is combined with left ventricular failure, is not discussed in this section, since the treatment of this condition is not much different from the treatment of severe acute left ventricular failure.

* Acute congestive left ventricular failure clinically manifests itself as paroxysmal shortness of breath, painful suffocation and orthopnea, occurring more often at night; sometimes - Cheyne-Stokes breathing, cough (initially dry, and then with sputum, which does not bring relief), later - foamy sputum, often pink in color, pallor, acrocyanosis, hyperhidrosis and is accompanied by excitement, fear of death. In case of acute congestion, moist rales may not be heard at first, or a meager amount of fine bubbling rales is detected over the lower parts of the lungs; swelling of the mucous membrane of the small bronchi can manifest itself as a moderate picture of bronchial obstruction with prolongation of exhalation, dry wheezing and signs of pulmonary emphysema. A differential diagnostic sign that allows one to differentiate this condition from bronchial asthma can be the dissociation between the severity of the patient’s condition and (in the absence of pronounced expiratory dyspnea, as well as “silent zones”) the paucity of the auscultatory picture. Loud, varied moist rales over all the lungs, which can be heard at a distance (bubbling breathing), are characteristic of a detailed picture of alveolar edema. Possible acute expansion of the heart to the left, the appearance of a systolic murmur at the apex of the heart, a proto-diastolic gallop rhythm, as well as an emphasis on the second tone on the pulmonary artery and other signs of load on the right heart, up to the picture of right ventricular failure. Blood pressure can be normal, high or low, tachycardia is typical.

The picture of acute congestion in the pulmonary circulation, which develops with stenosis of the left atrioventricular orifice, essentially represents left atrial failure, but is traditionally considered together with left ventricular failure.

* Cardiogenic shock is a clinical syndrome characterized by arterial hypotension and signs of a sharp deterioration in microcirculation and tissue perfusion, including blood supply to the brain and kidneys (lethargy or agitation, drop in diuresis, cold skin covered with sticky sweat, pallor, marbled skin pattern); sinus tachycardia is compensatory in nature.

A decrease in cardiac output with a clinical picture of cardiogenic shock can be observed in a number of pathological conditions not associated with insufficiency of myocardial contractile function - with acute obstruction of the atrioventricular orifice by an atrial myxoma or a spherical thrombus/ball prosthesis thrombus, with pericardial tamponade, with massive pulmonary embolism. These conditions are often combined with the clinical picture of acute right ventricular failure. Pericardial tamponade and atrioventricular orifice obstruction require immediate surgical intervention; drug therapy in these cases can only worsen the situation. In addition, the picture of shock during myocardial infarction is sometimes imitated by dissecting aortic aneurysm; in this case, differential diagnosis is necessary, since this condition requires a fundamentally different therapeutic approach.

There are three main clinical variants of cardiogenic shock:

* arrhythmic shock develops as a result of a drop in cardiac output due to tachycardia/tachyarrhythmia or bradycardia/bradyarrhythmia; after stopping the rhythm disturbance, adequate hemodynamics are quickly restored;

* reflex shock (pain collapse) develops as a reaction to pain and/or sinus bradycardia resulting from a reflex increase in vagal tone and is characterized by a rapid response to therapy, primarily painkillers; observed with relatively small infarction sizes (often of the posterior wall), while there are no signs of congestive heart failure and deterioration of tissue perfusion; pulse pressure usually exceeds a critical level;

* true cardiogenic shock develops when the volume of damage exceeds 40-50% of the myocardial mass (more often with anterolateral and repeated infarctions, in people over 60 years of age, against the background of arterial hypertension and diabetes mellitus), is characterized by a detailed picture of shock, resistant to therapy, often combined with congestive left ventricular failure; depending on the selected diagnostic criteria, the mortality rate ranges from 80-100%.

In some cases, especially when it comes to myocardial infarction in patients receiving diuretics, the developing shock is hypovolemic in nature, and adequate hemodynamics are relatively easily restored due to replenishment of the circulating volume.

Diagnostic criteria

One of the most consistent signs of acute heart failure is sinus tachycardia (in the absence of sinus node weakness, complete AV block, or reflex sinus bradycardia); characterized by expansion of the borders of the heart to the left or right and the appearance of a third sound at the apex or above the xiphoid process.

* In acute congestive right ventricular failure, the following have diagnostic value:

o swelling of the neck veins and liver;

o Kussmaul's sign (swelling of the jugular veins on inspiration);

o intense pain in the right hypochondrium;

o ECG signs of acute overload of the right ventricle (type SI-QIII, increasing R wave in leads V1,2 and formation of a deep S wave in leads V4-6, depression of STI, II, a VL and elevation of STIII, a VF, as well as leads V1, 2; possible formation of blockade of the right bundle branch, negative T waves in leads III, aVF, V1-4) and signs of overload of the right atrium (high pointed waves PII, III).

* Acute congestive left ventricular failure is detected based on the following signs:

o shortness of breath of varying severity, up to suffocation;

o paroxysmal cough, dry or with foamy sputum, foaming from the mouth and nose;

o orthopnea position;

o the presence of moist rales heard over the area from the posterior-lower sections to the entire surface of the chest; local small-bubble rales are characteristic of cardiac asthma; with advanced pulmonary edema, large-bubble rales are heard over the entire surface of the lungs and at a distance (bubbling breathing).

* Cardiogenic shock at the prehospital stage is diagnosed based on:

o drop in systolic blood pressure less than 90-80 mmHg. Art. (or 30 mmHg below the “working” level in people with arterial hypertension);

o decrease in pulse pressure - less than 25-20 mm Hg. Art.;

o signs of impaired microcirculation and tissue perfusion - a drop in urine output of less than 20 ml/h, cold skin covered with sticky sweat, pallor, marbled skin pattern, in some cases - collapsed peripheral veins.

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%20%D0%BD%D0%BE%D1%80%D0%B0%D0%B4%D1%80%D0%B5%D0%BD%D0%B0%D0%BB%D0%B8%D0%BD %D0%B0%20(0.5-16%20%D0%BC%D0%BA%D0%B3/%D0%BC%D0%B8%D0%BD)%20%D0%B8%D0%BB %D0%B8%20%D0%B8%D1%85%20%D1%81%D0%BE%D1%87%D0%B5%D1%82%D0%B0%D0%BD%D0%B8%D1 %8F.%3C/p%3E%0D%0A%0D%0A%3Cp%3E*%20%D0%A1%D1%80%D0%B5%D0%B4%D1%81%D1%82%D0 %B2%D0%BE%D0%BC%20%D0%B1%D0%BE%D1%80%D1%8C%D0%B1%D1%8B%20%D1%81%20%D0%BF%D0 %B5%D0%BD%D0%BE%D0%BE%D0%B1%D1%80%D0%B0%D0%B7%D0%BE%D0%B2%D0%B0%D0%BD%D0%B8 %D0%B5%D0%BC%20%D0%BF%D1%80%D0%B8%20%D0%BE%D1%82%D0%B5%D0%BA%D0%B5%20%D0%BB %D0%B5%D0%B3%D0%BA%D0%B8%D1%85%20%D1%8F%D0%B2%D0%BB%D1%8F%D1%8E%D1%82%D1%81 %D1%8F "defoamers" - substances that ensure the destruction of foam by reducing surface tension. The simplest of these means is alcohol vapor, which is poured into a humidifier, passing oxygen through it, supplied to the patient through a nasal catheter or breathing mask at an initial rate of 2-3 l/min, and after a few minutes - at a rate of 6-8 l/min.

* Persistent signs of pulmonary edema with stabilization of hemodynamics may indicate an increase in membrane permeability, which requires the administration of glucocorticoids to reduce permeability (4-12 mg of dexamethasone).

* In the absence of contraindications, in order to correct microcirculatory disorders, especially with long-term intractable pulmonary edema, the administration of sodium heparin is indicated - 5 thousand IU intravenously as a bolus, then drip at a rate of 800 - 1000 IU/hour.

* Treatment of cardiogenic shock is to increase cardiac output, which is achieved in various ways, the significance of which varies depending on the clinical type of shock.

* In the absence of signs of congestive heart failure (shortness of breath, moist rales in the posterior lower parts of the lungs), the patient must be placed in a horizontal position.

* Regardless of the clinical picture, it is necessary to provide complete analgesia.

* Stopping rhythm disturbances is the most important measure to normalize cardiac output, even if adequate hemodynamics are not observed after restoration of normosystole. Bradycardia, which may indicate increased vagal tone, requires immediate intravenous administration of 0.3-1 ml of 0.1% atropine solution.

* If the clinical picture of shock is extensive and there are no signs of congestive heart failure, therapy should begin with the administration of plasma substitutes in a total dose of up to 400 ml under the control of blood pressure, heart rate, respiratory rate and auscultation of the lungs. If there is an indication that immediately before the onset of acute cardiac damage with the development of shock, there were large losses of fluid and electrolytes (long-term use of large doses of diuretics, uncontrollable vomiting, profuse diarrhea, etc.), then an isotonic solution is used to combat hypovolemia sodium chloride; the drug is administered in an amount of up to 200 ml over 10 minutes, repeated administration is also indicated.

* The combination of cardiogenic shock with congestive heart failure or the lack of effect from the entire complex of therapeutic measures is an indication for the use of inotropic agents from the group of pressor amines, which, in order to avoid local circulatory disorders accompanied by the development of tissue necrosis, should be injected into the central vein:

o dopamine at a dose of up to 2.5 mg affects only dopamine receptors of the renal arteries; at a dose of 2.5-5 mcg/kg/min, the drug has a vasodilating effect; at a dose of 5-15 mcg/kg/min, it has a vasodilating and positive inotropic effect ( and chronotropic) effects, and at a dose of 15-25 mcg/kg/min - positive inotropic (and chronotropic), as well as peripheral vasoconstrictive effects; 400 mg of the drug is dissolved in 400 ml of a 5% glucose solution, while 1 ml of the resulting mixture contains 0.5 mg, and 1 drop - 25 mcg of dopamine. The initial dose is 3-5 mcg/kg/min with a gradual increase in the rate of administration until the effect is achieved, the maximum dose (25 mcg/kg/min, although the literature describes cases where the dose was up to 50 mcg/kg/min) or the development of complications (most often sinus tachycardia exceeding 140 beats per minute, or ventricular arrhythmias). Contraindications to its use are thyrotoxicosis, pheochromocytoma, cardiac arrhythmias, hypersensitivity to disulfide, previous use of MAO inhibitors; if the patient was taking tricyclic antidepressants before prescribing the drug, the dose should be reduced;

o the lack of effect from dopamine or the inability to use it due to tachycardia, arrhythmia or hypersensitivity is an indication for the addition or monotherapy with dobutamine, which, unlike dopamine, has a more pronounced vasodilatory effect and a less pronounced ability to cause an increase in heart rate and arrhythmia. 250 mg of the drug is diluted in 500 ml of a 5% glucose solution (1 ml of the mixture contains 0.5 mg, and 1 drop - 25 mcg of dobutamine); in monotherapy, it is prescribed at a dose of 2.5 mcg/kg/min, increasing every 15-30 minutes by 2.5 mcg/kg/min until an effect, side effect is obtained, or a dose of 15 mcg/kg/min is achieved, and with a combination of dobutamine with dopamine - in maximum tolerated doses; Contraindications to its use are idiopathic hypertrophic subaortic stenosis and stenosis of the aortic mouth. Dobutamine is not prescribed for systolic blood pressure

Differential diagnosis of acute coronary syndrome and acute heart failure

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Methods for identifying nonspecific indicators of tissue necrosis, inflammatory reaction and hyperenzyme for diagnosing acute myocardial infarction. Determination of the activity of the enzymes creatine phosphokinase and lactate dehydrogenase in blood serum.

presentation, added 07/09/2014

Diagnoses > Acute heart failure

This information cannot be used for self-medication!

Consultation with a specialist is required!

What is acute heart failure?

Doctors call acute heart failure a rapidly occurring disorder of the pumping function of the heart muscle, which entails a deterioration in the blood supply to all organs of the human body.

What are the reasons for its occurrence?

A heart attack with extensive myocardial damage, rupture of its wall or damage to the valve apparatus is the most common cause of this most dangerous pathology. In addition to it, other heart diseases lead to acute heart failure (AHF) - chronic heart failure at the stage of depletion of compensation mechanisms, severe arrhythmias, obstruction to blood flow, various valve lesions, myocarditis, pulmonary embolism, arterial hypertension, tamponade and cardiac injuries. Non-cardiac causes of AHF are also possible - thyrotoxicosis, anemia, kidney disease complicated by arterial hypertension.

Three forms of OSN

According to its clinical course, acute heart failure is divided into three forms - cardiac asthma, pulmonary edema and cardiogenic shock.

Stagnation of blood in the pulmonary artery system, caused by weakness of the contractile function of the myocardium or slowing of blood flow as a result of thrombosis, leads to the leakage of the liquid part of the blood into the pulmonary alveoli. As a result, oxygen exchange in them is disrupted, which leads to severe shortness of breath, even attacks of suffocation, especially at night. This process is called cardiac asthma.

Pulmonary edema is also manifested by severe shortness of breath, asthma and coughing. The cough is first dry, and then with copious production of foamy sputum. With this form of AHF, bubbling is heard in the patient’s chest, his skin turns pale, acquires a bluish tint, and becomes covered in cold sweat. The patient assumes the orthopneic position - sitting on the bed with his hands resting on its edge.

In cardiogenic shock, the patient suddenly becomes covered in cold, sticky sweat, the skin turns pale, and after 10–30 seconds there is loss of consciousness. In this form of AHF, blood pressure drops seriously (down to zero).

Possible complications

Given the exceptional severity of this pathology, the most serious complication that can occur is death. This outcome does not occur in all cases of AHF, but the prognosis for the patient’s life is always very serious and depends primarily on the timeliness of the start of treatment measures. Acute heart failure can become chronic or cause various thrombotic complications. The kidneys and lungs are often affected.

Treatment of AHF is a complex of emergency measures

The rapid development of AHF does not give doctors time to carry out any labor-intensive diagnostic studies. Pulmonary edema and cardiogenic shock are emergencies that require immediate medical attention, so doctors most often limit themselves to measuring blood pressure, electrocardiography and determining blood oxygen levels.

Treatment of acute heart failure should begin in the first minutes, or better yet, in the first seconds from its onset. The basic principles are blood saturation with oxygen, a decrease (with pulmonary edema) or an increase (with cardiogenic shock) of blood pressure. In case of pulmonary edema, diuretics and narcotics that eliminate shortness of breath must be prescribed. In case of cardiogenic shock, solutions are infused intravenously to replace blood loss. In parallel, diagnosis and treatment of the pathology that led to the development of AHF is carried out. If the heart stops, doctors immediately begin resuscitation measures.

Is it possible to prevent the development of acute heart failure?

Since this pathology most often develops against the background of chronic diseases, the best method of preventing AHF is periodic examinations by an appropriate specialist and taking preventive courses of treatment for the underlying disease. Quitting smoking and alcohol, normalizing body weight, and daily exercise in reasonable amounts increases the contractility of the heart, reducing the risk of developing acute heart failure in the future.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Acute transmural myocardial infarction of other specified locations (I21.2)

Cardiology

general information

Short description

Approved by the minutes of the meeting
Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan

No. 13 from 06/28/2013

Acute heart failure (AHF)- AHF is a clinical syndrome characterized by the rapid onset of symptoms that determine a violation of the systolic and/or diastolic function of the heart (reduced CO, insufficient tissue perfusion, increased pressure in the capillaries of the lungs, tissue congestion).
New-onset AHF (de novo) in patients without a known history of cardiac dysfunction is distinguished, as well as acute decompensation of CHF. With the rapid development of AHF, in contrast to gradually increasing symptoms and acute decompensation of CHF, there are usually no signs of fluid retention in the body (Recommendations of the European Society of Cardiology for the diagnosis and treatment of acute and chronic heart failure, 2012).

I. INTRODUCTORY PART

Protocol name: Protocol for diagnosis and treatment of acute heart failure

Protocol code:

ICD-10 codes:

I50 - Heart failure

I50.0 - Congestive heart failure

I50.1 - Left ventricular failure

I50.9 - Heart failure, unspecified

R57.0 - Cardiogenic shock

I21.0 - Acute transmural infarction of the anterior myocardial wall

I21.00 - Acute transmural infarction of the anterior myocardial wall with hypertension

I21.1 - Acute transmural infarction of the lower myocardial wall

I21.10 - Acute transmural infarction of the lower myocardial wall with hypertension

I21.2 - Acute transmural myocardial infarction of other specified locations

I21.20 - Acute transmural myocardial infarction of other specified locations with hypertension

I21.3 - Acute transmural myocardial infarction of unspecified localization

I21.30 - Acute transmural myocardial infarction of unspecified localization with hypertension

I21.4 - Acute subendocardial myocardial infarction

I21.40 - Acute subendocardial myocardial infarction with hypertension

I21.9 - Acute myocardial infarction, unspecified

I21.90 - Acute myocardial infarction, unspecified with hypertension

I22.0 - Repeated infarction of the anterior myocardial wall

I22.00 - Repeated infarction of the anterior myocardial wall with hypertension

I22.1 - Repeated infarction of the lower myocardial wall

I22.10 - Repeated infarction of the lower myocardial wall with hypertension

I22.8 - Repeated myocardial infarction of another specified location

I22.80 - Repeated myocardial infarction of another specified location with hypertension

I22.9 - Repeated myocardial infarction of unspecified localization

I22.90 - Repeated myocardial infarction of unspecified localization with hypertension

I23.0 - Hemopericardium as an immediate complication of acute myocardial infarction

I23.00 - Hemopericardium as an immediate complication of acute myocardial infarction with hypertension

I23.1 - Atrial septal defect as a current complication of acute myocardial infarction

I23.10 - Atrial septal defect as a current complication of acute myocardial infarction with hypertension

I23.2 - Ventricular septal defect as a current complication of acute myocardial infarction

I23.20 - Ventricular septal defect as a current complication of acute myocardial infarction with hypertension

I23.3 - Rupture of the cardiac wall without hemopericardium as a current complication of acute myocardial infarction

I23.30 - Cardiac wall rupture without hemopericardium as a current complication of acute myocardial infarction with hypertension

I23.4 - Rupture of the chordae tendineus as a current complication of acute myocardial infarction

I23.40 - Rupture of the chordae tendineus as a current complication of acute myocardial infarction with hypertension

I23.5 - Papillary muscle rupture as a current complication of acute myocardial infarction

I23.50 - Papillary muscle rupture as a current complication of acute myocardial infarction with hypertension

I23.6 - Thrombosis of the atrium, atrial appendage and ventricle of the heart as a current complication of acute myocardial infarction

I23.60 - Atrial thrombosis of the atrial appendage and ventricle of the heart as a current complication of acute myocardial infarction with hypertension

I23.8 - Other ongoing complications of acute myocardial infarction

I23.80 - Other ongoing complications of acute myocardial infarction with hypertension

I24.1 - Dressler's syndrome

I24.10 - Dressler's syndrome with hypertension

I24.8 - Other forms of acute coronary heart disease

I24.80 - Other forms of acute coronary heart disease with hypertension

I24.9 - Acute coronary heart disease, unspecified

I24.90 - Acute coronary heart disease, unspecified

Abbreviations used in the protocol:

AH - arterial hypertension

BP - blood pressure

APTT - activated partial thromboplastin time

BAB - beta blockers

VACP - intra-aortic counterpulsator

PAWP - pulmonary artery wedge pressure

ACE inhibitor - angiotensin-converting enzyme inhibitor

IHD - coronary heart disease

MI - myocardial infarction

LV - left ventricle

PA - pulmonary artery

HF - heart failure

CO - cardiac output

SBP - systolic blood pressure

SI - cardiac index

CPSP - spontaneous breathing with continuous positive pressure

NVPV - non-invasive positive pressure ventilation

IVS - interventricular septum

MOC - minute volume of blood circulation

CAG - caranaroangiography

TPVR - total peripheral vascular resistance

RV - right ventricle

TC - heart transplant

TLT - thrombolytic therapy

PE - pulmonary embolism

CHF - chronic heart failure

HR - heart rate

CVP - central venous pressure

ECG - electrocardiography

EX - pacemaker

ECMO - extracorporeal membrane oxygenation

EchoCG - echocardiography

NYHA - New York Heart Association

CPAP - continuous positive airway pressure

NIPPV - non-invasive positive pressure ventilation

Date of development of the protocol: April 2013.

Protocol users: cardiologists, cardiac surgeons, anesthesiologists-resuscitators, therapists

Disclosure of no conflict of interest: absent.

Table 1. Provoking factors and causes of acute heart failure

Classification

Clinical classification

Acute circulatory failure can manifest itself in one of the following conditions:

I. Acute decompensated heart failure(de novo or as decompensation of CHF) with characteristic complaints and symptoms of AHF, which is moderate and does not meet the criteria for cardiogenic shock, pulmonary edema or hypertensive crisis.

II. Hypertensive heart failure: complaints and symptoms of HF accompany high blood pressure with relatively preserved LV function. However, there are no signs of pulmonary edema on chest x-ray.

III. Pulmonary edema(confirmed by chest x-ray) is accompanied by severe respiratory distress, orthopnea, wheezing in the lungs, and the level of blood oxygen saturation before treatment is usually less than 90%.

IV. Cardiogenic shock- an extreme manifestation of AHF. This is a clinical syndrome in which, along with a decrease in systolic blood pressure to less than 90-100 mm Hg. signs of reduced perfusion of organs and tissues appear (cold skin, oligoanuria, lethargy and lethargy). At the same time, the cardiac index is reduced (usually 2.2 l/min per 1 m2) and the pulmonary artery wedge pressure is increased (> 18-20 mm Hg). The latter distinguishes cardiogenic shock from a similar condition that occurs during hypovolemia. The main link in the pathogenesis of cardiogenic shock is a decrease in cardiac output, which cannot be compensated by peripheral vasoconstriction, which leads to a significant decrease in blood pressure and hypoperfusion. Accordingly, the main goals of treatment are to optimize the filling pressure of the ventricles of the heart, normalize blood pressure and eliminate the causes underlying the decrease in cardiac output.

V. HF with high cardiac output characterized by increased IOC with usually increased heart rate (due to arrhythmias, thyrotoxicosis, anemia, Paget's disease, iatrogenic and other mechanisms), warm extremities, pulmonary congestion and sometimes decreased blood pressure (as in septic shock).

VI. Right ventricular heart failure characterized by low cardiac output syndrome due to pumping failure of the RV (myocardial damage or high load - PE, etc.) with increased venous pressure in the jugular veins, hepatomegaly and arterial hypotension.

Classification of T. killip(1967) is based on taking into account clinical signs and chest radiography results.

The classification is used primarily for heart failure due to myocardial infarction, but can be used for de novo heart failure.

There are four stages (classes) of severity:

stage I- no signs of heart failure;

stage II- HF (moist rales in the lower half of the pulmonary fields, III tone, signs of venous hypertension in the lungs);

stage III- severe HF (obvious pulmonary edema, moist rales extending to more than the lower half of the lung fields);

stage IV- cardiogenic shock (SBP 90 mm Hg with signs of peripheral vasoconstriction: oliguria, cyanosis, sweating).

J.S. Forrester classification(1977) is based on taking into account clinical signs characterizing the severity of peripheral hypoperfusion, the presence of pulmonary congestion, reduced cardiac index (CI) ≤ 2.2 l/min/m2 and increased pulmonary artery wedge pressure (PAWP) > 18 mm Hg. Art.

There are normal (group I), pulmonary edema (group II), hypovolemic and cardiogenic shock (group III and IV, respectively).

After stabilization of the condition, patients are assigned a functional class of heart failure according to NYHA

Table 2. NewYork Heart Association (NYHA) classification.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Table 1- List of basic and additional diagnostic measures

Diagnostic criteria

Complaints and anamnesis:

Complaints may include shortness of breath/suffocation, dry cough, hemoptysis, fear of death. With the development of pulmonary edema, a cough appears with foamy sputum, often pink in color. The patient takes a forced sitting position.

Physical examination:

During a physical examination, special attention should be paid to palpation and auscultation of the heart, determining the quality of heart sounds, the presence of III and IV sounds, murmurs and their nature.

It is important to systematically evaluate the state of peripheral circulation, skin temperature, and the degree of filling of the ventricles of the heart. RV filling pressure can be estimated using venous pressure measured in the superior vena cava. However, caution should be exercised when interpreting the result, since increased central venous pressure (CVP) may be a consequence of impaired distensibility of the veins and pancreas due to inadequate filling of the latter. Increased LV filling pressure is usually indicated by the presence of moist rales on pulmonary auscultation and/or signs of pulmonary congestion on chest x-ray. However, in a rapidly changing situation, clinical assessment of the degree of left heart filling may be erroneous.

table 2- Clinical and hemodynamic signs in different types of AHF

Note:* the difference between low CO syndrome and cardiogenic shock is subjective; when assessing a particular patient, these classification points may overlap.

Instrumental studies:

ECG

A 12-lead ECG allows you to determine the rhythm of the heart and sometimes helps to clarify the etiology of AHF.

Table 6. The most common ECG changes in heart failure.

Chest X-ray

Chest radiography should be performed as early as possible in all patients with AHF to assess the size and clarity of the heart shadow, as well as the severity of blood congestion in the lungs. This diagnostic test is used both to confirm the diagnosis and to evaluate the effectiveness of treatment. Chest x-ray can distinguish left ventricular failure from inflammatory pulmonary disease. It is important to consider that radiological signs of pulmonary congestion are not an accurate reflection of increased pulmonary capillary pressure. They may be absent with PAWP up to 25 mm Hg. Art. and respond late to favorable hemodynamic changes associated with treatment (a delay of up to 12 hours is possible).

Echocardiography (EchoCG)

EchoCG is necessary to determine the structural and functional changes underlying AHF. It is used to assess and monitor the local and general function of the ventricles of the heart, the structure and function of the valves, pericardial pathology, mechanical complications of myocardial infarction, and space-occupying lesions of the heart. CO can be assessed by the speed of movement of the aortic or pulmonary contours. With a Doppler study, determine the pressure in the PA (by the stream of tricuspid regurgitation) and monitor the LV preload. However, the reliability of these measurements in AHF has not been verified using right heart catheterization (Table 4).

Table 4- Typical abnormalities detected by echocardiography in patients with heart failure

The most important hemodynamic parameter is LVEF, which reflects the contractility of the LV myocardium. As an “average” indicator, we can recommend a “normal” level of LVEF of 45%, calculated by 2-dimensional echocardiography according to Simpson.

Transesophageal echocardiography

Transesophageal echocardiography should not be considered as a routine diagnostic method; it is usually resorted to only if an insufficiently clear image is obtained during transthoracic access, complicated by valvular damage, suspected malfunction of the mitral valve prosthesis, to exclude thrombosis of the left atrial appendage with a high risk of thromboembolism.

24-hour ECG monitoring (Holter monitoring)

Standard Holter ECG monitoring has diagnostic meaning only in the presence of symptoms, probably associated with the presence of arrhythmias (subjective sensations of interruptions, accompanied by dizziness, fainting, history of syncope, etc.).

Magnetic resonance imaging

Magnetic resonance imaging (MRI) is the most accurate method with maximum reproducibility of calculations for calculating heart volumes, wall thickness and LV mass, surpassing echocardiography and radioisotope angiography (RIA) in this parameter. In addition, the method allows you to detect thickening of the pericardium, assess the extent of myocardial necrosis, the state of its blood supply and features of functioning. Carrying out diagnostic MRI is justified only in cases where the information content of other imaging techniques is insufficient.

Radioisotope methods

Radionuclide ventriculography is considered a very accurate method for determining LVEF and is most often performed when studying myocardial perfusion to assess its viability and the degree of ischemia.

Indications for consultation with specialists:

1. Consultation with an arrhythmologist - the presence of heart rhythm disturbances (paroxysmal atrial tachycardia, atrial fibrillation and flutter, sick sinus syndrome), diagnosed clinically, according to ECG and XMECG data.

2. Consultation with a neurologist - the presence of episodes of seizures, the presence of paresis, hemiparesis and other neurological disorders.

3. Consultation with an infectious disease specialist - the presence of signs of an infectious disease (severe catarrhal symptoms, diarrhea, vomiting, rash, changes in biochemical blood parameters, positive results of ELISA tests for intrauterine infections, markers of hepatitis).

4. Consultation with an ENT doctor - nosebleeds, signs of upper respiratory tract infection, tonsillitis, sinusitis.

5. Consultation with a hematologist - the presence of anemia, thrombocytosis, thrombocytopenia, coagulation disorders, and other hemostasis abnormalities.

6. Consultation with a nephrologist - evidence of UTI, signs of renal failure, decreased diuresis, proteinuria.

7. Consultation with a pulmonologist - presence of concomitant lung pathology, decreased lung function.

8. Consultation with an ophthalmologist - routine examination of the fundus.

Laboratory diagnostics

In all cases of severe AHF, invasive assessment of arterial blood gas composition with determination of parameters characterizing it (PO2, PCO2, pH, base deficiency).
In patients without very low CO and shock with vasoconstriction, pulse oximetry and end-tidal CO2 may be an alternative. The balance of oxygen supply and the need for it can be assessed by SvO2.
In case of cardiogenic shock and long-term small output syndrome, it is recommended to determine PO2 of mixed venous blood in the PA.

Levels BNP and NT-proBNP in blood plasma increase due to their release from the ventricles of the heart in response to increased ventricular wall tension and volume overload. BNP levels > 100 pg/ml and NT-proBNP > 300 pg/ml have been proposed to be used to confirm and/or exclude CHF in patients hospitalized in the emergency department with shortness of breath.

However, in elderly patients these indicators have not been sufficiently studied, and with the rapid development of AHF, their content in the blood upon admission to the hospital may remain normal. In other cases, normal levels of BNP or NT-proBNP can accurately exclude the presence of HF.
If the concentration of BNP or NT-proBNP increases, it is necessary to ensure the absence of other diseases, including renal failure and septicemia. High level BNP or NT-proBNP indicates a poor prognosis.

Cardiac troponins are important in determining diagnosis and risk stratification, and in enabling the distinction between NSTEMI and unstable angina. Troponins are more specific and sensitive than traditional cardiac-specific enzymes such as creatine kinase (CK), myocardial isoenzyme MB (MB-CK), and myoglobin.

Elevated levels of cardiac troponins reflect myocardial cell damage, which in PD ACS may result from distal embolization of platelet thrombi from the site of plaque rupture or rupture. Accordingly, troponin can be considered as a surrogate marker of active thrombus formation. If there are signs of myocardial ischemia (chest pain, ECG changes, or new wall motion abnormalities), an increase in troponin levels indicates MI. In patients with MI, the initial increase in troponin levels occurs within ~4 hours of symptom onset. Elevated troponin levels can persist for up to 2 weeks due to proteolysis of the contractile apparatus. There are no significant differences between troponin T and troponin I.

In the blood of healthy people, even after excessive physical activity, the level of troponin T does not exceed 0.2 - 0.5 ng/ml, so its increase above this limit indicates damage to the heart muscle.

The following laboratory tests are also routinely performed in patients with suspected HF: general blood analysis(with determination of hemoglobin level, number of leukocytes and platelets), electrolyte blood test, serum creatinine and glomerular filtration rate (GFR), blood glucose, liver enzymes, urinalysis. Additional tests are performed depending on the specific clinical picture (Table 3).

Table 3- Typical deviations from normal laboratory parameters in patients with heart failure

Differential diagnosis

Differential diagnosis

Table 5- Differential diagnosis of acute heart failure with other cardiac and non-cardiac diseases

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Treatment

Treatment Goals

Purpose of emergency treatment- rapid stabilization of hemodynamics and reduction of symptoms (shortness of breath and/or weakness). Improvement of hemodynamic parameters, primarily CO and SV, PAWP and pressure in the RA.

Table 6- Treatment goals for AHF

Treatment tactics

Non-drug treatment

OSN is life-threatening condition and requires urgent treatment. The following are interventions indicated for most patients with AHF. Some of them can be performed quickly in any medical institution, others are available only to a limited number of patients and are usually performed after initial clinical stabilization.

1) In AHF, the clinical situation requires urgent and effective interventions and can change quite quickly. Therefore, with rare exceptions (nitroglycerin under the tongue or nitrates in the form of an aerosol), drugs should be administered intravenously, which, in comparison with other methods, provides the most rapid, complete, predictable and controllable effect.

2) AHF leads to a progressive deterioration of blood oxygenation in the lungs, arterial hypoxemia and hypoxia of peripheral tissues. The most important task in the treatment of AHF is to ensure adequate tissue oxygenation to prevent tissue dysfunction and the development of multiple organ failure. To achieve this, it is extremely important to maintain capillary blood saturation within normal limits (95-100%).

Oxygen therapy. In patients with hypoxemia, you should ensure that there is no obstructed airway, then begin oxygen therapy with a high O2 content in the respiratory mixture, which is increased if necessary. The advisability of using increased O2 concentrations in patients without hypoxemia is controversial: such an approach can be dangerous.

Respiratory support without endotracheal intubation (non-invasive ventilation). For respiratory support without tracheal intubation, two modes are mainly used: spontaneous breathing mode with continuous positive airway pressure (CPAP). The use of CPAP can restore lung function and increase functional residual volume. At the same time, the compliance of the lungs improves, the transdiaphragmatic pressure gradient decreases, and the activity of the diaphragm decreases. All this reduces the work associated with breathing and reduces the metabolic needs of the body. The use of non-invasive methods in patients with cardiogenic pulmonary edema improves arterial blood pO2, reduces the symptoms of AHF, and can significantly reduce the need for tracheal intubation and mechanical ventilation.

Respiratory support with endotracheal intubation.

Invasive respiratory support (ventilation with tracheal intubation) should not be used to treat hypoxemia, which can be eliminated with oxygen therapy and non-invasive methods of ventilation.

Indications for mechanical ventilation with tracheal intubation are as follows:

Signs of weakness of the respiratory muscles - a decrease in respiratory rate combined with an increase in hypercapnia and depression of consciousness;

Severe breathing impairment (in order to reduce the work of breathing);

The need to protect the airways from regurgitation of gastric contents;

Elimination of hypercapnia and hypoxemia in unconscious patients after prolonged resuscitation or drug administration;

The need for sanitation of the tracheobronchial tree to prevent atelectasis and bronchial obstruction.

The need for immediate invasive ventilation may occur with pulmonary edema secondary to ACS.

3) It is necessary to normalize blood pressure and eliminate disorders that can cause a decrease in myocardial contractility (hypoxia, myocardial ischemia, hyper- or hypoglycemia, electrolyte disturbances, side effects or drug overdose, etc.). Attitude to the early introduction of special agents for the correction of acidosis (sodium bicarbonate, etc.) in last years Quite discreet. The decreased response to catecholamines in metabolic acidosis has been questioned. Initially, it is more important to maintain adequate ventilation of the pulmonary alveoli and restore sufficient perfusion of peripheral tissues as quickly as possible; further interventions may be required if hypotension and metabolic acidosis persist for a long time. To reduce the risk of iatrogenic alkalosis, it is recommended to avoid complete correction of base deficiency.

4) In the presence of arterial hypotension, as well as before prescribing vasodilators, it is necessary to ensure that there is no hypovolemia. Hypovolemia leads to insufficient filling of the heart chambers, which in itself causes a decrease in cardiac output, arterial hypotension and shock. A sign that low blood pressure is a consequence of impaired pumping function of the heart, and not of insufficient filling, is sufficient filling pressure of the left ventricle (pulmonary artery wedge pressure exceeding 18 mm Hg). When assessing the adequacy of filling the left ventricle in real clinical conditions, one often has to rely on indirect indicators (physical signs of pulmonary congestion, the degree of stretching of the neck veins, X-ray data), but they respond quite late to favorable hemodynamic changes caused by treatment. The latter may lead to the use of unreasonably high doses of drugs.

5) An effective means of increasing blood pressure, reducing left ventricular afterload and increasing perfusion pressure in the coronary arteries is intra-aortic balloon pump (IABP). This improves the contractility of the left ventricle and reduces myocardial ischemia.

In addition, IBD is effective in the presence of mitral regurgitation and ventricular septal defects. It is contraindicated in aortic regurgitation, aortic dissection and severe peripheral atherosclerosis. Unlike drug treatment, it does not increase myocardial oxygen demand (like positive inotropic agents), does not inhibit myocardial contractility, and does not reduce blood pressure (like drugs used to eliminate myocardial ischemia or reduce afterload). At the same time, this is a temporary measure that allows you to gain time in cases where it is possible to eliminate the causes of the developed condition (see below). In patients waiting surgical intervention, other methods of mechanical support (mechanical left ventricular bypass devices, etc.) may be required.

6) It is important to eliminate the causes underlying AHF in a particular patient. Eliminate tachycardia or bradycardia if they cause AHF or aggravate it.

If there are signs of acute persistent occlusion of a large epicardial coronary artery (the appearance of persistent ST segment elevations on the ECG), it is necessary to restore its patency as quickly as possible. There is evidence that in AHF, percutaneous angioplasty/stenting (possibly against the backdrop of intravenous administration of platelet glycoprotein IIb/IIIa receptor blockers) or coronary artery bypass surgery (with corresponding damage to the coronary arteries) is more effective than thrombolytic therapy, especially in the presence of cardiogenic shock.

In the presence of exacerbation of coronary artery disease, when according to the ECG there are no signs of persistent occlusion of a large epicardial coronary artery (unstable angina, including post-infarction, acute heart attack myocardium, not accompanied by ST segment elevations on the ECG) it is necessary to suppress myocardial ischemia as quickly as possible and prevent its reoccurrence. Symptoms of AHF in such patients are an indication for the maximum possible antithrombotic treatment (including a combination of acetylsalicylic acid, clopidogrel, heparin and, in some cases, intravenous infusion of a blocker of glycoprotein IIb/IIIa platelet receptors) and the earliest possible performance of coronary angiography followed by myocardial revascularization (method depends on coronary anatomy - percutaneous angioplasty/stenting or coronary artery bypass surgery). In this case, angioplasty/stenting of the coronary arteries in the early stages of the disease should be carried out without stopping treatment with the combination of the above drugs. When rapid coronary artery bypass surgery is possible, it is suggested that the administration of clopidogrel be postponed until the results of coronary angiography are available; if it turns out that the patient needs coronary bypass surgery and the operation is planned in the next 5-7 days, the drug should not be prescribed. If coronary artery bypass grafting can be performed within the next 24 hours, it is recommended to use unfractionated heparin rather than low molecular weight heparin.

Perform the most complete revascularization of the myocardium in patients with chronic forms of coronary artery disease (especially effective in the presence of viable hibernated myocardium).

Perform surgical correction of intracardiac hemodynamic disorders (valvular defects, atrial or ventricular septal defects, etc.); If necessary, quickly eliminate cardiac tamponade.

In a number of patients the only possible way The treatment is a heart transplant.

However, complex invasive diagnostic and therapeutic interventions are not considered justified in patients with end-stage concomitant diseases, when the underlying cause of AHF is unavoidable, or when corrective interventions or heart transplantation are impossible.

7) Diet of patients with AHF (after stabilization of the condition).

The main points are as follows:

Functional class I (FC) - do not eat salty foods (limit salt intake to 3 g NaCl per day);

II FC - do not add salt to food (up to 1.5 g of NaCl per day);

III FC - eat foods with reduced salt content and cook without salt (<1,0 г NaCl в день).

2. When limiting salt intake, limiting fluid intake is relevant only in extreme situations: with decompensated severe CHF, requiring IV administration of diuretics. In normal situations, it is not recommended to use a fluid volume of more than 2 l/day (maximum fluid intake is 1.5 l/day).

3. Food should be high in calories, easily digestible, with sufficient vitamins and protein.

4. NB! A weight gain of >2 kg in 1-3 days may indicate fluid retention in the body and an increased risk of decompensation!

5. The presence of obesity or overweight worsens the patient's prognosis and in all cases with a body mass index (BMI) of more than 25 kg/m2 requires special measures and caloric restriction.

8) Bed-based physical activity regimen

Physical rehabilitation is contraindicated for:

Active myocarditis;

Valve stenosis;

Cyanotic congenital defects;

Rhythm disturbances of high gradations;

Attacks of angina in patients with low ejection fraction (EF) of the left ventricle (LV).

Drug treatment of chronic heart failure

Essential medicines used in the treatment of acute heart failure.

1) Positive inotropic agents are temporarily used in AHF to increase myocardial contractility and their action is usually accompanied by an increase in myocardial oxygen demand.

Pressor (sympathomimetic) amines(norepinephrine, dopamine and, to a lesser extent, dobutamine), in addition to increasing myocardial contractility, can cause peripheral vasoconstriction, which, along with an increase in blood pressure, leads to a deterioration in oxygenation of peripheral tissues.

Treatment is usually started with small doses, which are gradually increased (titrated) if necessary until the optimal effect is obtained. In most cases, dose selection requires invasive monitoring of hemodynamic parameters with determination of cardiac output and pulmonary artery wedge pressure. A common disadvantage of drugs in this group is the ability to cause or worsen tachycardia (or bradycardia when using norepinephrine), cardiac arrhythmias, myocardial ischemia, as well as nausea and vomiting. These effects are dose-dependent and often prevent further dose increases.

Norepinephrine causes peripheral vasoconstriction (including celiac arterioles and renal vessels) due to stimulation of α-adrenergic receptors. In this case, cardiac output can either increase or decrease depending on the initial peripheral vascular resistance, the functional state of the left ventricle and reflex influences mediated through carotid baroreceptors. It is indicated for patients with severe arterial hypotension (systolic blood pressure below 70 mm Hg), with low peripheral vascular resistance. The usual starting dose of norepinephrine is 0.5-1 mcg/min; subsequently it is titrated until the effect is achieved and in case of refractory shock it can be 8-30 mcg/min.

Dopamine stimulates α- and β-adrenergic receptors, as well as dopaminergic receptors located in the vessels of the kidneys and mesentery. Its effect depends on the dose. With intravenous infusion at a dose of 2-4 mcg/kg per minute, the effect is mainly on dopaminergic receptors, which leads to dilation of the celiac arterioles and renal vessels. Dopamine can help increase the rate of diuresis and overcome diuretic refractoriness caused by reduced renal perfusion, and can also act on the renal tubules, stimulating natriuresis. However, as noted, there is no improvement in glomerular filtration in patients with the oliguric stage of acute renal failure. In doses of 5-10 mcg/kg per minute, dopamine stimulates mainly 1-adrenergic receptors, which helps to increase cardiac output; Venoconstriction is also noted. At doses of 10-20 mcg/kg per minute, stimulation of α-adrenergic receptors predominates, which leads to peripheral vasoconstriction (including celiac arterioles and renal vessels). Dopamine, alone or in combination with other pressor amines, is used to eliminate arterial hypotension, increase myocardial contractility, and also increase heart rate in patients with bradycardia that requires correction. If dopamine administration at a rate of more than 20 mcg/kg/min is required to maintain blood pressure in a patient with sufficient ventricular filling pressure, it is recommended to add norepinephrine.

Dobutamine- a synthetic catecholamine that mainly stimulates β-adrenergic receptors. In this case, myocardial contractility improves with an increase in cardiac output and a decrease in the filling pressure of the ventricles of the heart. Due to a decrease in peripheral vascular resistance, blood pressure may not change. Since the goal of dobutamine treatment is to normalize cardiac output, monitoring of this indicator is required to select the optimal dose of the drug. Doses of 5-20 mcg/kg per minute are usually used. Dobutamine can be combined with dopamine; it is able to reduce pulmonary vascular resistance and is the drug of choice in the treatment of right ventricular failure. However, already 12 hours after the start of the drug infusion, tachyphylaxis may develop.

Phosphodiesterase III inhibitors(amrinone, milrinone) have positive inotropic and vasodilating properties, causing predominantly venodilation and a decrease in pulmonary vascular tone. Just like pressor amines, they can aggravate myocardial ischemia and provoke ventricular arrhythmias. Their optimal use requires monitoring of hemodynamic parameters; pulmonary artery wedge pressure should not be lower than 16-18 mmHg. IV infusion of phosphodiesterase III inhibitors is usually used for severe heart failure or cardiogenic shock that does not adequately respond to standard treatment with pressor amines. Amrinone quite often causes thrombocytopenia, and tachyphylaxis can quickly develop. Recently, it was shown that the use of milrinone in worsening chronic heart failure does not lead to an improvement in the clinical course of the disease, but is accompanied by an increase in the incidence of persistent arterial hypotension requiring treatment and supraventricular arrhythmias.

Agents that increase the affinity of contractile myofibrils of cardiomyocytes for calcium. The only drug in this group that has reached the stage of widespread clinical use in AHF is levosimendan. Its positive inotropic effect is not accompanied by a noticeable increase in myocardial oxygen demand and an increase in sympathetic effects on the myocardium. Other possible mechanisms actions - selective inhibition of phosphodiesterase III, activation of potassium channels. Levosimendan has vasodilating and anti-ischemic effects; due to the presence of a long-acting active metabolite, the effect persists for some time after stopping the drug. Digoxin has limited value in the treatment of AHF. The drug has a low therapeutic width and can cause severe ventricular arrhythmias, especially in the presence of hypokalemia. Its property of slowing atrioventricular conduction is used to reduce the frequency of ventricular contractions in patients with persistent atrial fibrillation or flutter.

2) Vasodilators are able to quickly reduce pre- and afterload due to the expansion of veins and arterioles, which leads to a decrease in pressure in the capillaries of the lungs, a decrease in peripheral vascular resistance and blood pressure. They should not be used for arterial hypotension.

Isosorbide dinitrate peripheral vasodilator with a predominant effect on venous vessels. Antianginal agent. The mechanism of action is associated with the release of the active substance nitric oxide in the smooth muscles of blood vessels. Nitric oxide causes activation of guanylate cyclase and increases cGMP levels, which ultimately leads to smooth muscle relaxation. Under the influence of isosorbide dinitrate, arterioles and precapillary sphincters

They relax to a lesser extent than large arteries and veins.
The effect of isosorbide dinitrate is associated mainly with a decrease in myocardial oxygen demand due to a decrease in preload (dilatation of peripheral veins and a decrease in blood flow to the right atrium) and afterload (reduction in peripheral resistance), as well as with a direct coronary dilation effect. Promotes redistribution of coronary blood flow in areas with reduced blood supply. Reduces pressure in the pulmonary circulation.
Intravenous infusion is usually started at 10-20 mcg/min and increased by 5-10 mcg/min every 5-10 minutes until the desired hemodynamic or clinical effect is achieved. Low doses of the drug (30-40 mcg/min) mainly cause venodilation, higher doses (150-500 mcg/min) also lead to dilatation of arterioles. When maintaining a constant concentration of nitrates in the blood for more than 16-24 hours, tolerance to them develops. Nitrates are effective for myocardial ischemia, emergency conditions arising from arterial hypertension, or congestive heart failure (including mitral or aortic regurgitation). When using them, arterial hypotension should be avoided (its likelihood is increased with hypovolemia, lower localization of myocardial infarction, right ventricular failure). Hypotension that occurs with the use of nitrates is usually eliminated by intravenous fluid administration; the combination of bradycardia and hypotension is eliminated by atropine. They may also contribute to the occurrence or aggravation of tachycardia, bradycardia, disruption of ventilation-perfusion relationships in the lungs and headache.
Nitrates are considered contraindicated in cases of severe contractile dysfunction of the right ventricle, when its output depends on preload, with systolic blood pressure below 90 mm Hg, and also with a heart rate of less than 50 beats. per minute or severe tachycardia.

Sodium nitroprusside its effect on arterioles and veins is similar to nitroglycerin. It is usually administered in doses of 0.1-5 mcg/kg per minute (in some cases up to 10 mcg/kg per minute) and should not be exposed to light.

Used to treat emergency conditions arising from severe heart failure (especially associated with aortic or mitral regurgitation) and arterial hypertension. There is evidence of increased symptomatic efficacy (but not outcome) when treating conditions with low cardiac output and high peripheral resistance that do not respond to dopamine.
Sodium nitroprusside should not be used if myocardial ischemia persists, since it can worsen blood circulation in areas of the blood supply of significantly stenotic epicardial coronary arteries. With hypovolemia, sodium nitroprusside, like nitrates, can cause a significant decrease in blood pressure with reflex tachycardia, so the filling pressure of the left ventricle should be at least 16-18 mm Hg.
Other side effects include worsening hypoxemia in pulmonary disease (by relieving hypoxic constriction of pulmonary arterioles), headache, nausea, vomiting, and abdominal cramps. In case of liver or kidney failure, as well as when sodium nitroprusside is administered at a dose of more than 3 mcg/kg per minute for more than 72 hours, accumulation of cyanide or thiocyanate in the blood is possible. Cyanide intoxication is manifested by the occurrence of metabolic acidosis. At thiocyanate concentrations >12 mg/dL, lethargy, hyperreflexia, and seizures occur.

Treatment consists of immediately stopping the drug infusion; in severe cases, sodium thiosulfate is administered.

3) Morphine- a narcotic analgesic, which, in addition to analgesic, sedative effects and increased vagal tone, causes venodilation.

It is considered as the drug of choice for relieving pulmonary edema and eliminating chest pain associated with myocardial ischemia and not resolving after repeated administration of sublingual nitroglycerin.
To the main side effects include bradycardia, nausea and vomiting (resolved by atropine), respiratory depression, as well as the occurrence or worsening of arterial hypotension in patients with hypovolemia (usually eliminated by raising the legs and intravenous fluid administration).
It is administered intravenously in small doses (10 mg of the drug is diluted in at least 10 ml of physiological solution, approximately 5 mg is administered intravenously slowly, then, if necessary, 2-4 mg at intervals of at least 5 minutes until the effect is achieved).

4) Furosemide- a loop diuretic with a direct venodilating effect. The latter effect occurs within the first 5 minutes after intravenous administration, while an increase in urine output occurs later.

The initial dose is 0.5-1 mg/kg IV. If necessary, administration is usually repeated after 1-4 hours.

5) Beta-blockers.
The use of drugs in this group in AHF associated with impaired myocardial contractility is contraindicated. However, in some cases, when pulmonary edema occurs in a patient with subaortic or isolated mitral stenosis and is associated with the occurrence of tachysystole, often in combination with elevated blood pressure, the administration of a beta-blocker helps relieve the symptoms of the disease.
Three drugs are available for intravenous use in Russia - propranolol, metoprolol and esmolol. The first two are administered in small doses at intervals sufficient to assess the effectiveness and safety of the previous dose (changes in blood pressure, heart rate, intracardiac conduction, manifestations of AHF). Esmolol has a very short half-life (2-9 minutes), so its use is considered preferable in acute patients with a high risk of complications.

6) Anticoagulants.

Anticoagulants are indicated for patients with ACS, atrial fibrillation, artificial heart valves, deep vein thrombosis of the lower extremities and pulmonary embolism. There is evidence that subcutaneous administration of low molecular weight heparins (enoxaparin 40 mg 1 time / day, dalteparin 5000 IU 1 time / day) can reduce the incidence of deep vein thrombosis of the lower extremities in patients hospitalized with an acute therapeutic disease, incl. severe heart failure. Large studies have not been conducted to compare the preventive effectiveness of low molecular weight heparins and unfractionated heparin (5000 IU subcutaneously 2-3 times a day) in AHF.

7) Fibrinolytic therapy.

Patients with ST-segment elevation MI who are eligible for PCI require mechanical (catheter) reperfusion (primary coronary intervention) within 60 minutes of seeking help. If primary PCI is not possible, restoration of blood flow in the infarct-related artery can be achieved by pharmacological reperfusion (fibrinolysis) within 30 minutes after the first contact with the patient.

Despite the limited effectiveness and high risk of bleeding, fibrinolysis at the prehospital stage should be considered as a priority treatment method, if all conditions for its implementation are available (trained personnel with the ability to interpret ECG). The bolus drug (tenecteplase) has ease of administration and a better prognostic option with a lower risk of bleeding.

In the absence of contraindications, it is necessary to begin throbbolytic therapy (TLT) under the following conditions:

If the time from the onset of an anginal attack is 4-6 hours, at least does not exceed 12 hours;

The ECG shows ST segment elevation >0.1 mV in at least 2 consecutive chest leads or 2 limb leads, or a new left bundle branch block (LBBB) appears.

The administration of thrombolytics is justified at the same time when there are ECG signs of true posterior MI (high R waves in the right precordial leads V1-V2 and ST segment depression in leads V1-V4 with an upward directed T wave).

Recombinant tissue plasminogen activator (Alteplase) is administered intravenously (the drug is first dissolved in 100-200 ml of distilled water or 0.9% sodium chloride solution) according to the “bolus + infusion” scheme. The dose of the drug is 1 mg/kg body weight (but not more than 100 mg): 15 mg is administered as a bolus; subsequent infusion of 0.75 mg/kg body weight over 30 minutes (but not more than 50 mg), then 0.5 mg/kg (but not more than 35 mg) over 60 minutes (total infusion duration - 1.5 hours).

Streptokinase is administered intravenously at a dose of 1,500,000 IU over 30-60 minutes in a small amount of 0.9% sodium chloride solution. The development of hypotension and acute allergic reactions is often noted. You should not re-introduce streptokinase (check your medical history) due to the appearance of antibodies that can affect its activity and the development of allergic reactions, including anaphylactic shock.

Tenecteplase (Metalise) intravenously 30 mg at body weight<60 кг, 35 мг при 60-70 кг, 40 мг при 70-80 кг; 45 мг при 80-90 кг и 50 мг при массе тела >90 kg, the required dose is administered as a bolus over 5-10 seconds. For administration, a previously installed venous catheter can be used, but only if it is filled with a 0.9% sodium chloride solution; after administering Metalyse, it must be thoroughly washed (in order to complete and timely delivery of the drug to the blood). Metalyse is not compatible with dextrose solution, and should not be administered via a dextrose-containing dropper. No other medications should be added to the injection solution or to the infusion line. Given the longer half-life of elimination from the body, the drug is used in the form of a single bolus, which is especially convenient for pre-hospital treatment.

Absolute contraindications to fibrinolytic therapy:

Previous hemorrhagic stroke or cerebrovascular accident of unknown origin.

Ischemic stroke suffered within the last 6 months, with the exception of ischemic stroke that occurred within 3 hours, which can be treated with thrombolytics.

Recent major trauma/surgery/head injury (within the last 3 months).

Brain tumor, primary or metastatic.

Changes in the structure of cerebral vessels, the presence of arteriovenous malformation, arterial aneurysms.

Suspicion of dissecting aortic aneurysm.

Gastrointestinal bleeding within the past month.

Presence of signs of bleeding or hemorrhagic diathesis (except menstruation).

Punctures in areas that cannot be compressed (for example, liver biopsy, lumbar puncture).

Relative contraindications to fibrinolytic therapy:

Transient ischemic attack in the last 6 months.

Refractory arterial hypertension (systolic blood pressure ≥180 mm Hg and/or diastolic blood pressure ≥110 mm Hg).

Taking indirect anticoagulants (warfarin) (the higher the INR, the higher the risk of bleeding).

State of pregnancy or within 1 week after birth.

Liver disease in an advanced stage.

Exacerbation peptic ulcer or duodenum.

Infectious endocarditis.

Ineffectiveness of resuscitation measures. Traumatic or prolonged (> 10 min) cardiopulmonary resuscitation.

For streptokinase - previous use (> 5 days ago and up to one year or more) or an allergic reaction to it.

The criteria for successful fibrinolysis are a decrease in the ST segment displacement on the ECG by more than 50% within 60-90 minutes (must be documented in the medical history), the occurrence of typical reperfusion arrhythmias, and the disappearance of chest pain.

Features of treatment of AHF depending on the cause of decompensation

Eliminating the cause of decompensation is the most important component of treating AHF and preventing its relapse. Non-cardiac diseases can seriously complicate the course of AHF and complicate its treatment.

IHD

It is the most common cause of AHF, which can be represented by left ventricular failure with low CO, left ventricular failure with symptoms of blood stasis, and right ventricular failure. All patients with exacerbation of coronary artery disease are advised to undergo coronary angiography as soon as possible.

Timely reperfusion in case of AMI with ST segment elevations on the ECG can prevent AHF or improve its course. Percutaneous coronary intervention is preferable; if indicated, emergency coronary artery bypass grafting is justified in patients with cardiogenic shock. If invasive treatment is not available or involves significant loss of time, TLT should be performed. Urgent myocardial revascularization is also indicated in cases of acute heart failure that complicates myocardial infarction, without ST segment elevations on the ECG. as well as in case of NS with severe myocardial ischemia.

The occurrence of AHF during exacerbation of coronary artery disease can be facilitated by reflex reactions, as well as disturbances of heart rhythm and conduction. Therefore, both adequate pain relief and rapid elimination of arrhythmias leading to hemodynamic disturbances are important.

In true cardiogenic shock, temporary stabilization can be achieved by maintaining adequate chamber filling, VACP, drug inotropic support, and mechanical ventilation. For left ventricular failure with symptoms of blood stagnation acute treatment the same as for other causes of this variant of AHF. Because inotropic agents can be dangerous, the possibility of VACP should be discussed. Subsequently, along with adequate myocardial revascularization, β-blockers and RAAS inhibitors are indicated.

More detailed approaches to the treatment of AHF during exacerbation of coronary artery disease are set out in the VNOK recommendations for the treatment of myocardial infarction with ST segment elevations on the ECG and ACS without persistent ST segment elevations on the ECG (Cardiology. - 2004. - No. 4 (appendix). - P. 1-28 ).

Pathology of the heart valve apparatus

The cause of AHF may be dysfunction of the heart valves during exacerbation of coronary artery disease (usually mitral regurgitation), acute mitral or aortic regurgitation of another etiology (endocarditis, trauma), aortic or mitral stenosis, thrombosis of an artificial valve, dissecting aortic aneurysm.

For infective endocarditis main reason development of AHF is heart valve insufficiency. The severity of cardiac dysfunction may be exacerbated by myocarditis. In addition to standard treatments for AHF, antibiotics should be prescribed. For a quick diagnosis, consultation with a specialist is indicated.

Severe acute mitral or aortic insufficiency requires emergency surgical treatment. With long-standing mitral regurgitation in combination with reduced SI and low EF, emergency surgery, as a rule, does not improve the prognosis. In these cases, preliminary stabilization of the condition with VACP can be of great importance.

Thrombosis of artificial heart valve

AHF in these patients often leads to death. In all patients with suspected prosthetic valve thrombosis, a chest x-ray and echocardiography should be performed. The optimal treatment remains unclear. For left heart valve thrombosis, surgical intervention is the method of choice. TLT is used for right heart valve thrombosis and in cases where surgery is high-risk.

For TLT, a recombinant tissue plasminogen activator inhibitor (10 mg IV bolus followed by an infusion of 90 mg over 90 minutes) and streptokinase (250,000-500,000 IU over 20 minutes followed by an infusion of 1,000,000-1.5,000,000) are used. ME for 10 hours). After administration of the thrombolytic, it is necessary to begin an intravenous infusion of unfractionated heparin in a dose that ensures an increase in aPTT by 1.5-2 times from normal (control) values ​​for a given laboratory. An alternative is to prescribe urokinase at a dose of 4400 IU/(kg·h) without heparin for 12 hours or 2000 IU/(kg·h) in combination with unfractionated heparin for 24 hours.

TLT is ineffective if there is overgrowth fibrous tissue with small areas of secondary thrombosis. In patients with very large and/or mobile thrombi, TLT is associated with an increased risk of thromboembolic complications and stroke. In these cases, surgical treatment is possible. To clarify the nature of the valve lesion, transesophageal echocardiography is preliminary indicated. After TLT, repeat echocardiography is necessary. The advisability of surgical intervention should be considered if TLT fails to eliminate the occlusion.

An alternative method is to administer additional doses of thrombolytic. Although the mortality rate during emergency surgery in patients with hemodynamic instability III-IV, according to the New York Heart Association (NYHA) classification (pulmonary edema, arterial hypotension), is high, TLT can lead to loss of time and further increase the risk of surgical treatment in case of her failure. According to non-randomized studies, in less severe patients, long-term antithrombotic and/or TLT may be as effective as surgical treatment.

Dissecting aortic aneurysm

Dissecting aortic aneurysm is accompanied by AHF in the presence of HA, acute valvular regurgitation, cardiac tamponade, and myocardial ischemia. If a dissecting aortic aneurysm is suspected, an emergency consultation with a surgeon is necessary. The morphology and function of the aortic valve, as well as the presence of pericardial fluid, are best assessed by transesophageal echocardiography. Surgical intervention is usually performed for health reasons.

Cardiac tamponade

Cardiac tamponade is a decompensated phase of its compression caused by the accumulation of fluid in the pericardium. With “surgical” tamponade (bleeding), intrapericardial pressure increases quickly - from several minutes to hours, while with “therapeutic” tamponade (inflammation) this process takes from several days to weeks. Hemodynamic impairment is an absolute indication for pericardiocentesis. In patients with hypovolemia, temporary improvement can be achieved by intravenous fluid administration, leading to an increase in the filling pressure of the ventricles of the heart.

In case of wounds, rupture of a ventricular aneurysm, or hemopericardium due to aortic dissection, surgery is necessary to eliminate the source of bleeding. Whenever possible, the cause of pericardial effusion should be treated.

AHF is one of the most common complications of hypertensive crises.

Clinical signs of AHF during hypertensive crisis include only pulmonary congestion, which can be minor or severe, up to sudden pulmonary edema.

In patients hospitalized with pulmonary edema due to a hypertensive crisis, there are often no significant changes in LV systolic function; more than half have LVEF > 45%. Diastolic disorders are often observed, in which the processes of myocardial relaxation worsen.

The goal of treatment of acute pulmonary edema due to hypertension is to reduce pre- and afterload on the LV, myocardial ischemia and eliminate hypoxemia by maintaining adequate ventilation of the lungs. Treatment should be started immediately in the following order: oxygen therapy, PPD or other modes of non-invasive ventilation, if necessary, mechanical ventilation, usually for a short period, in combination with IV administration of antihypertensive drugs.

Antihypertensive therapy should cause a fairly rapid, within a few minutes, reduction in SBP or DBP by 30 mm Hg. Subsequently, a slower decrease in blood pressure to the values ​​​​that occurred before the hypertensive crisis is shown, usually within a few hours. You should not try to reduce blood pressure to normal values, as this may lead to a decrease in organ perfusion. An initial rapid reduction in blood pressure can be achieved by prescribing the following drugs, either individually or in combination (if hypertension remains):

IV administration of isosorbide dinitrate, nitroglycerin or nitroprusside;

IV administration of loop diuretics, especially in patients with fluid retention and a long history of CHF;

It is possible to administer a long-acting dihydropyridine derivative (nicardipine) intravenously. However, with a hemodynamic effect similar to nitrates, drugs in this group can cause hypersympathicotonia (tachycardia), increase blood shunting in the lungs (hypoxemia), and also cause complications in the central nervous system.

A rapid reduction in blood pressure can be achieved by taking captopril under the tongue. Apparently, its use can be justified if it is impossible to administer drugs intravenously, as well as the unavailability or insufficient effectiveness of inhaled forms of nitrates.

β-Blockers should not be used for pulmonary edema, except in cases where AHF is combined with tachycardia in patients without serious impairment of LV contractility, for example, with diastolic HF, mitral stenosis. A hypertensive crisis with pheochromocytoma can be eliminated by intravenous administration of 5-15 mg of phentolamine with mandatory blood pressure monitoring; repeated administration is possible after 1-2 hours.

Kidney failure

Minor and moderate changes in renal function are usually asymptomatic and well tolerated by patients; however, even a slightly increased level of creatinine in the blood serum and/or a decrease in GFR are independent risk factors for an unfavorable prognosis in AHF.

In the presence of acute renal failure, diagnosis and treatment of concomitant pathology are necessary: ​​anemia, electrolyte disturbances and metabolic acidosis. Renal failure affects the effectiveness of therapy for heart failure, which involves the use of digoxin, ACE inhibitors, angiotensin receptor blockers, and spironolactone. An increase in serum creatinine by more than 25-30% and/or a concentration greater than 3.5 mg/dL (266 µmol/L) is a relative contraindication to continued ACE inhibitor therapy.

Moderate to severe renal failure [serum creatinine levels greater than 2.5–3 mg/dL (190–226 μmol/L)] is associated with decreased response to diuretics. In these patients, there is often a need to continually increase the dose of loop diuretics and/or add a diuretic with a different mechanism of action. This in turn can cause hypokalemia and an even greater decrease in GFR. The exception is torasemide, the pharmacological properties of which are practically independent of renal dysfunction, since the drug is 80% metabolized in the liver.

Patients with severe renal dysfunction and refractory fluid retention may require continuous venovenous hemofiltration.

Combination with inotropic agents increases renal blood flow, improves renal function, and restores the effectiveness of diuretics. Hyponatremia, acidosis, and uncontrolled fluid retention may require dialysis. The choice between peritoneal dialysis, hemodialysis and ultrafiltration usually depends on the technical equipment of the hospital and the level of blood pressure.

Lung diseases and bronchial obstruction

When ASI is combined with broncho-obstructive syndrome, it is necessary to use bronchodilators. Although drugs in this group may improve cardiac function, they should not be used to treat AHF.
Albuterol is usually used (0.5 ml of a 0.5% solution in 2.5 ml of saline via a nebulizer over 20 minutes). The procedure can be repeated every hour for the first few hours, and then according to indications.

Heart rhythm disturbances

Heart rhythm disturbances can be the main cause of AHF in patients with both preserved and impaired cardiac function, and also complicate the course of already developed AHF. To prevent and successfully eliminate heart rhythm disturbances, it is necessary to maintain normal concentrations of potassium and magnesium in the blood.

Bradyarrhythmias

Treatment usually begins with intravenous administration of 0.25-5 mg of atropine, repeated if necessary up to a maximum dose of 2 mg. For atrioventricular dissociation with rare ventricular activity in patients without myocardial ischemia, intravenous infusion of isoproterenol at a dose of 2-20 mcg/min can be used.

Low heart rate during atrial fibrillation can be temporarily eliminated by intravenous administration of theophylline at a rate of 0.2-0.4 mg/(kg·h), first as a bolus, then as an infusion. If there is no response to drug treatment, an artificial cardiac pacemaker should be used. If myocardial ischemia is present, it should be eliminated as quickly as possible.

Supraventricular tachyarrhythmias

Atrial fibrillation and atrial flutter. It is necessary to monitor heart rate, especially in the presence of diastolic myocardial dysfunction. However, in restrictive heart failure or cardiac tamponade, when the heart rate decreases rapidly, the patient's condition may suddenly worsen.

Depending on the clinical situation, it is possible to maintain normosystole with persistent arrhythmia or restore and maintain sinus rhythm. If the rhythm disturbance is paroxysmal in nature, after stabilization of the condition, the advisability of drug or electrical cardioversion should be considered. If the paroxysm lasts less than 48 hours, the use of anticoagulants is not necessary.

Table 7. - Treatment of arrhythmias in AHF

If the arrhythmia lasts longer than 48 hours, it is necessary to use anticoagulants and maintain normosystole with appropriate medications for at least three weeks before cardioversion. In more severe cases: with arterial hypotension, severe pulmonary congestion, emergency electrical cardioversion is indicated against the background of the administration of a therapeutic dose of heparin. The duration of anticoagulant use after successful cardioversion should be at least 4 weeks. In patients with persistent atrial fibrillation and flutter, the advisability of using anticoagulants depends on the risk of arterial thromboembolism and is discussed in the relevant guidelines.

To reduce heart rate and prevent recurrence of arrhythmia, β-blockers are used. Rapid digitalization should also be considered, especially when atrial fibrillation is secondary to AHF. Amiodarone is commonly used for drug cardioversion and to prevent recurrence of the arrhythmia.

Patients with low EF should not use class I antiarrhythmic drugs, verapamil and diltiazem. In rare cases, verapamil may be considered in patients without a significant decrease in LV contractility to control heart rate or eliminate paroxysmal supraventricular tachycardia with narrow QRS complexes.

Ventricular arrhythmias.

Ventricular fibrillation and sustained ventricular tachycardia require immediate EIT and, if necessary, respiratory support.

Amiodarone and β-blockers can prevent their reoccurrence.

In case of recurrence of severe ventricular arrhythmias and hemodynamic instability, it is necessary to immediately perform CAG and electrophysiological studies.

Other types of treatment:- as a treatment option, after the transition to the terminal stage of CHF, this is the implantation of mechanical auxiliary devices left ventricular support, as well as heart transplantation (for more details, see treatment of CHF).

Surgical intervention

1) Emergency coronary angiography should be performed as soon as possible in patients with severe angina, profound or dynamic ECG changes, severe arrhythmias, or hemodynamic instability on admission or during the follow-up period. These patients account for 2-15% of patients admitted with a diagnosis of BP ST ACS.
Patients at high thrombotic risk and at high risk of developing MI should undergo angiographic testing without delay. Especially in the presence of clinical symptoms of HF or progressive hemodynamic instability (shock) and life-threatening cardiac arrhythmias (VF-ventricular fibrillation, VT-ventricular tachycardia) (Table 8).

Table 8- Predictors of high thrombotic risk or high risk of myocardial infarction, which are an indication for emergency coronary angiography


Patients with persistent ischemic symptoms and signs of ST segment depression in the anterior precordial leads (particularly in combination with elevated troponin), which may indicate probable posterior transmural ischemia, should undergo emergency coronary angiography (<2 ч).
Patients with persistent symptoms or documented troponin elevations in the absence of diagnostically significant ECG changes also require urgent coronary angiography to identify acute thrombotic occlusion in the left circumflex artery. Especially in cases where the differential diagnosis of another clinical situation remains unclear.

2) Surgical treatment. For some diseases underlying the occurrence of AHF, urgent surgical intervention can improve the prognosis (Table 9). Surgical treatment methods include myocardial revascularization, correction of anatomical heart defects, including valve replacement and reconstruction, and mechanical means of temporary circulatory support. The most important diagnostic method when determining indications for surgery is echocardiography.

Table 9- Heart diseases in AHF requiring surgical correction

3) Heart transplantation. The need for heart transplantation usually occurs in severe acute myocarditis, postpartum cardiomyopathy, and major myocardial infarction with a poor prognosis after revascularization.
Heart transplantation is not possible until the patient's condition is stabilized with mechanical circulatory support.

4) Mechanical methods of supporting blood circulation. Temporary mechanical circulatory support is indicated for patients with AHF who do not respond to standard treatment, when it is possible to restore myocardial function, surgical correction of existing disorders with a significant improvement in cardiac function, or heart transplantation are indicated.

Levitronix devices- refers to devices that provide hemodynamic support (from several days to several months), with minimal trauma to blood cellular elements. Without oxygenation.
Intra-aortic balloon counterpulsation (IABP)
A standard component of treatment for patients with cardiogenic shock or severe acute LV failure in the following cases:
- lack of rapid response to fluid administration, treatment with vasodilators and inotropic support;
- severe mitral regurgitation or rupture of the interventricular septum to stabilize hemodynamics, allowing the necessary diagnostic and therapeutic measures to be performed;
- severe myocardial ischemia (as preparation for coronary angiography and revascularization).

VACP can significantly improve hemodynamics, but it should be performed when it is possible to eliminate the cause of AHF - myocardial revascularization, heart valve replacement or heart transplantation, or its manifestations can regress spontaneously - myocardial stunning after AMI, open heart surgery, myocarditis.
VACP is contraindicated in aortic dissection, severe aortic regurgitation, severe peripheral arterial disease, intractable causes of heart failure, and multiple organ failure.

Extracorporeal membrane oxygenation (ECMO)
ECMO is the use of mechanical devices to temporarily (from several days to several months) support the function of the heart and/or lungs (in whole or in part) during cardiopulmonary failure, which leads to restoration of organ function or its replacement
Indication for ECMO for heart failure in adults - cardiogenic shock:
- Insufficient tissue perfusion manifesting as hypotension and low cardiac output despite adequate volume control
- Shock persists despite administration of volume, inotropes and vasoconstrictors, and intra-aortic balloon pumping if necessary

Implantation of VAD assistive devices:
The use of these devices in the treatment of severe heart failure is considered in two aspects. The first is a “bridge” to heart transplantation, i.e. the device is used temporarily while the patient awaits a donor heart. The second is a “bridge” to recovery, when, thanks to the use of an artificial ventricle of the heart, the function of the heart muscle is restored.

5) Ultrafiltration
Venovenous isolated ultrafiltration is sometimes used to remove fluid in patients with HF, although it is usually used as a reserve therapy for diuretic resistance.

Preventive actions:
The basis of emergency cardiology should be the active prevention of emergency cardiac conditions.
There are three areas for preventing cardiac emergencies:
- primary prevention of cardiovascular diseases;
- secondary prevention for existing cardiovascular diseases;
- emergency prevention during exacerbation of cardiovascular diseases.

Emergency prevention— a set of emergency measures to prevent the occurrence of a cardiac emergency or its complications.
Emergency prevention includes:
1) immediate measures to prevent the development of an emergency cardiac condition with a sharp increase in the risk of its occurrence (with a worsening of the course of cardiovascular disease, anemia, hypoxia; before inevitable high physical, emotional or hemodynamic stress, surgical intervention, etc.);
2) a set of self-help measures used by patients with cardiovascular diseases in the event of an emergency condition within the framework of an individual program previously developed by a doctor;
3) the earliest possible and minimally sufficient emergency medical care;
4) additional measures to prevent the development of complications of emergency cardiac conditions.

The development of individual self-help programs for patients with cardiovascular diseases by the attending physician can be of significant benefit.

The basis of emergency cardiac care is the elementary organization and equipment of the diagnostic and treatment process, and most importantly, specialists with clinical thinking, practical experience and dedication.

Indicators of treatment effectiveness and safety of diagnostic and treatment methods described in the protocol
Criteria for the effectiveness of treatment of patients with AHF:
Evaluation of the effectiveness of treatment for AHF:
1. achieving symptomatic improvement;
2. long-term survival of patients after AHF;
3. increase in life expectancy.

Drugs (active ingredients) used in treatment

Pulmonary edema due to heart failure, hypertensive crisis

Increasing manifestations (decompensation) of chronic heart failure

Violation of the integrity of the valves or chambers of the heart; cardiac tamponade

Severe myocardial hypertrophy (especially with the presence of subaortic stenosis).

Increased pressure in the pulmonary circulation (pulmonary embolism, acute lung diseases, etc.).

Tachy or bradyarrhythmias.

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. 1. European Society of Cardiology guidelines for the diagnosis and treatment of acute and chronic heart failure, Eur Heart J 2012. 2. Review of the 2010 American Heart Association guidelines for CPR and emergency cardiovascular care. 3. Journal “Cardiovascular Therapy and Prevention” 2006; 5 (6), Appendix 1. 4. Principles of treatment of acute heart failure Yavelov I.S. Center for Atherosclerosis, Research Institute of Physico-Chemical Medicine, Ministry of Health of the Russian Federation, Moscow, Journal “Emergency Medicine”1-2(32-33) 2011 / Practical recommendations. 5. Givertz M., Colucci W., Braunwald E. Clinical Aspects of Heart failure: High-Output Failure; Pulmonary Edema // Heart Disease. A Textbook of Cardiovascular Medicine/Ed. by E. Braunwald, D. Zipes, P. Libby. - 6th Edition. -W.B. Saunders Co, 2001. - 534-561. 6. Bristow M. Management of Heart Failure // Heart Disease. A Textbook of Cardiovascular Medicine/Ed. by E. Braunwald, D. Zipes, P. Libby. - 6th Edition. -W.B. Saunders Co. - 635-651. 7. Cotter G., Moshkovitz Y., Milovanov O. et al. Acute heart failure: a novel approach to its pathogenesis and treatment // Eur. J. Heart F. - 2002. - 4. - 227-234. 8. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Management of acute myocardial infarction in patient presenting with St-segment elevation // Eur. Heart J. - 2003. - 24. - 28-66. 9. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. International Consensus on Science. The American Heart Association in Collaboration With the International Liaison Committee on Resuscitation (ILCOR) // Circulation. - 2000. - 102, suppl. I-1-I-384. 10. Menon V., Hochman J. Management of cardiogenic shock complicating acute myocardial infarction // Heart. - 2002. - 88. - 531-537. 11. 1999 Updated ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). Web Version. 12. Lee T. Management of Heart Failure. Guidelines // Heart Disease. A Textbook of Cardiovascular Medicine/Ed. by E. Braunwald, D. Zipes, P. Libby. - 6th Edition. -W.B. Saunders Co, 2001. - 652-658. 13. Braunwald E., Antman E., Beasley J. et al. ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina ). 2002, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf. 14. The Task Force on the Management of Acute Coronary Syndromes of the European Society of Cardiology. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation // Eur. Heart J. - 2002. - 23. - 1809-40. 15. Richenbacher W., Pierce W. Treatment of Heart Failure: Assisted Circulation // Heart Disease. A Textbook of Cardiovascular Medicine/Ed. by E. Braunwald, D. Zipes, P. Libby. - 6th Edition. -W.B. Saunders Co, 2001. - 600-614. 16. ACC/AHA Guideline Update for the Management of Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction-2002: Summary Article A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina) // Circulation. - 2002, October 1. - 1893-1900. 17. Bristow M., Port D., Kelly R. Treatment of Heart Failure: Pharmacological Methods // Heart Disease. A Textbook of Cardiovascular Medicine/Ed. by E. Braunwald, D. Zipes, P. Libby. - 6th Edition. -W.B. Saunders Co, 2001. - 562-599. 18. Cuffe M., Califf R., Adams K. Jr. et al., for the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: A randomized controlled trial // JAMA. - 2002. - 287. - 1541-1547. 19. Moiseyev V., Poder P., Andrejevs N. et al. on behalf of RUSSLAN Study Investigators. Safety and efficacy of a novel calcium sensitizer, levosimendan, in patients with left ventricular failure due to an acute myocardial infarction. A randomized, placebo-controlled, double-blind study (RUSSLAN) // Eur. Heart J. - 2002. - 23. - 1422-1932. 20. Publication Committee for the VMAC Investigators. Intravenous nesiritide vs nitroglycerin for the treatment of decompensated congestive heart failure: A randomized controlled trial // JAMA. - 2002. - 287. - 1531-1540. 21. Task Force Report. Guidelines on diagnosis and management of acute pulmonary embolism // Eur. Heart J. - 2000. - 21. - 1301-1336. 22. Cotter G., Kaluski E., Blatt A. et al. L-NMMA (a nitric oxide synthase inhibitor) is effective in the treatment of cardiogenic shock // Circulation. - 2000. - 101. -1358-1361. 23. ACC/AHA/ESC Guidelines for the management of patients with atrial fibrillation. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation). Developed in Collaboration With the North American Society of Pacing and Electrophysiology // Eur. Heart J. - 2001. - 22. - 1852-1923. 24. European Resuscitation Council. Guidelines for Resuscitation. - Edition, 1996. 25. Ansell J., Hirsh J., Dalen J. et al. Managing Oral Anticoagulant Therapy // Chest. - 2001. - 119. - 22S-38S.
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Adenosine

Alteplase

Amiodarone

Amrinone

Atropine

Vasopressin injection

Heparin sodium

Dalteparin

Digoxin

Dobutamine

Dopamine

Isoproterenol

Isosorbide dinitrate

Captopril

Levosimendan

Lidocaine

Metoprolol

Milrinone

Morphine

Sodium nitroprusside

Nicardipine

Nitroglycerine

Norepinephrine

Propranolol

Salbutamol