Clinical variants of acute heart failure. Heart failure: main classification Treatment of acute heart failure

Acute heart failure (AHF) is a syndrome of rapid development of circulatory failure due to a decrease in the pumping function of one of the ventricles or filling them with blood. Acute heart failure is traditionally understood as the occurrence of acute (cardiogenic) shortness of breath, accompanied by signs of pulmonary congestion (with possible pulmonary edema).

There are two types of AHF - left ventricular and right ventricular. Acute left ventricular heart failure has the greatest clinical significance.

Causes of acute heart failure

All causes of AHF can be divided into 3 groups: 1 - causes leading to a sharp increase in afterload (PE, myocardial infarction of the pancreas), 2 - causes leading to a sharp increase in preload (excessive fluid intake, renal dysfunction with an increase in BCC, etc. ) and 3 - causes leading to an increase in cardiac output (sepsis, anemia, thyrotoxicosis, etc.). Causes of acute heart failure in last years mention nonsteroidal drugs and thiazolidinediones.

Clinical pictureAcute heart failure is characterized by one of 6 syndromes or a combination of them:

1. increase in edema, as a rule, is observed in patients with chronic heart failure; it is accompanied by increased dyspnea, the appearance of free fluid in the cavities, and often hypotension, which sharply worsens the prognosis;
2. pulmonary edema manifested by shortness of breath, orthopnea position, an increase in the number of moist rales above the angle of the scapula, a decrease in oxygen saturation arterial blood <90%; отличительная его особенность - отсутствие выраженных отеков и признаков застоя;
3. increase in blood pressure. As a rule, AHF develops in patients with preserved LV systolic function, accompanied by tachycardia and a sharp increase in peripheral vascular resistance. In a number of patients, pulmonary edema predominates in the clinical picture;
4. hypoperfusion of peripheral tissues and organs. If signs of organ and tissue hypoperfusion persist after the arrhythmia has been eliminated and preload increased, cardiogenic shock should be assumed. Systolic BP while<90 мм рт.ст., а среднее АД снижается на 30 мм рт.ст. и более; объем выделенной мочи <0,5 мл/кг за 1 час; кожные покровы холодные. Прогноз у таких больных крайне тяжелый;
5. with isolated right ventricular failure patients have reduced stroke volume in the absence of pulmonary edema and stagnation in the pulmonary circulation; characteristic increase in pressure in the right atrium, swelling of the veins of the neck, hepatomegaly;
6. acute coronary syndrome (ACS) clinically manifested in 15% of patients with AHF; often lead to AHF rhythm disturbances (atrial fibrillation, bradycardia, ventricular tachycardia) and local violations of the contractile function of the myocardium.

Classification of acute heart failure

In the clinic, it is customary to use the classifications of Killip (1967) for patients with AMI, ACS, Forrester (uses clinical symptoms and hemodynamic parameters in patients after AMI).

A modification of the Forrester classification is based on the concepts of "dry-wet" and "warm-cold". They are easy to identify during physical examination of the patient. Patients who meet the wet-cold criteria have the worst prognosis.

A distinctive feature of all studies of the outcomes of acute heart failure is the inclusion of hospitalized patients of older age groups with high comorbidity. The highest mortality (60%) was observed in patients with signs of cardiogenic shock, the lowest - in patients with AHF caused by increased blood pressure.

Pulmonary edema is always associated with poor prognosis. In 2/3 of patients hospitalized with AHF, pneumonia was noted.

Among all patients hospitalized for acute heart failure, the combined rate of death + rehospitalization was 30-50%, depending on age.

Symptoms and signs of acute heart failure

CARDIAC ASTHMA. The development of an attack can be facilitated by physical exertion or neuropsychic stress. Characteristic is an attack of suffocation, which develops more often at night.

The feeling of lack of air is accompanied by palpitations, sweating, a feeling of anxiety and fear. Shortness of breath is inspiratory in nature. Often worried about coughing with a small amount of light sputum, there may be streaks of blood in the sputum.

On examination - acrocyanosis, the skin is grayish-pale, covered with cold sweat. The patient, as a rule, takes a forced position, sitting with his legs down. In this position, part of the venous blood is deposited in the veins of the lower extremities, and thus its flow to the heart decreases.

Harsh breathing, a small amount of dry rales (due to secondary bronchospasm) are heard in the lungs, moist small bubbling rales in the lower sections. In the heart, auscultation determines the gallop rhythm, the accent of the second tone over the pulmonary artery. The pulse is frequent, weak filling, arrhythmia is possible. BP is often normal, but as asthma progresses, it may decrease. The number of breaths per minute reaches 30-40.
In case of progression of the disease and inadequacy of treatment, cardiac asthma can turn into alveolar edema, i.e. true pulmonary edema.

ALVEOLAR PULMONARY EDEMA. The condition of the patients is getting worse. Asphyxia increases, cyanosis increases, the respiratory rate reaches 40-60 per minute, swollen jugular veins, sweating are noted. A very characteristic symptom is gurgling breathing, which can be heard at a distance. With a cough, pink frothy sputum begins to stand out, its amount can reach 3-5 liters. This is because the protein, when combined with air, foams vigorously, as a result of which the volume of the transudate increases, which leads to a reduction in the respiratory surface of the lungs. During auscultation of the lungs, moist rales of various sizes are heard, first over the upper sections, and then over the entire surface of the lungs. Heart sounds are muffled, often a gallop rhythm, accent of the second tone over the pulmonary artery. The pulse is frequent, weak, arrhythmic. BP is usually low, but may be normal or high. The least favorable course of pulmonary edema against the background of low blood pressure. The picture of pulmonary edema usually increases within a few hours, but it can also be violent, and in some patients it acquires an undulating course.

Diagnosis of acute heart failure

Diagnosis of acute heart failure is difficult due to the obviousness of the clinical picture.

Methods of high diagnostic value are:

• collection of anamnesis (when possible) with clarification of hypertension, CHF and medications taken;
• palpation assessment of edema and temperature of the skin;
• determination of CVP (if catheterization is possible);
• auscultation of the heart with an assessment of: I tone; systolic murmur at the 1st point and its conduction; diastolic murmur at the 1st point; systolic and diastolic noise at the 2nd and 5th points; determination of III tone;
• auscultation of the lungs with an assessment of the number of moist rales in the lungs in relation to the angle of the scapula;
• examination of the neck - swollen veins of the neck;
• percussion determination of free fluid in the pleural cavities;
• ECG, chest x-ray;
• determination of рO 2 , рСО 2 , pH of arterial and venous blood;
• determination of levels of sodium, potassium, urea and creatinine, glucose, albumin, AJ1T, troponin; in patients with acute heart failure, an increase in the level of troponin is possible, which requires its subsequent dynamic control; an increase in the level in at least one of the subsequent samples indicates ACS;
• determination of natriuretic peptides; there is no consensus on the definition of BNP or NTpro-BNP; however, their normal value is possible with isolated right ventricular failure, and a retained elevated level at discharge indicates a poor prognosis;
• Echocardiography is a first-line study in patients with acute heart failure.

Diagnostic criteria for acute heart failure syndrome

1. Inspiratory or mixed type of suffocation.
2. Cough with light sputum in the stage of interstitial edema and with frothy sputum in the stage of alveolar edema.
3. Bubbling breath in the stage of alveolar edema.
4. Moist rales in the lungs.
5. Rg-logical signs of pulmonary edema.

Laboratory and instrumental research

Electrocardiographic study is the most accessible and quite informative method.

The ECG may show signs of myocardial infarction, post-infarction scar, rhythm and conduction disturbances.

Of the non-specific signs - a decrease in the amplitude of the "T" wave and the ST interval. In a hospital, patients undergo an Rg-logical examination of the lungs.

Stages of diagnostic search and differential diagnosis of acute heart failure syndrome

1. The basis of the diagnostic algorithm is to establish the presence of acute heart failure syndrome based on the clinical picture of cardiac asthma or pulmonary edema.
2. The second possible step in the diagnostic process may be taking into account the anamnestic data and physical examination in order to establish the cause of the syndrome.

To do this, it is first necessary to establish whether an asthma attack is a manifestation of heart failure, since this symptom also occurs in diseases of the respiratory system.

An attack of cardiac asthma must first be differentiated from an attack of bronchial asthma. This is especially important in cases where there is no anamnestic data on previous diseases.
The positive effect of treatment can also be used for the purpose of differential diagnosis.

An asthma attack with spontaneous pneumothorax occurs along with pain in the corresponding half of the chest. The examination reveals a tympanic percussion sound on the side of the lesion and a sharp weakening of breathing in the same place. Choking occurs with exudative pleurisy with a significant accumulation of fluid. The presence of fluid is recognized on the basis of a dull percussion sound, a sharp weakening of breathing and voice trembling.

Suffocation during obstruction of the respiratory tract by a foreign body is permanent, not amenable to drug therapy, accompanied by a strong cough.

Laryngeal involvement can also cause acute choking in cases of subglottic laryngitis, edema, or foreign body aspiration. They are characterized by stridor or stenotic breathing (difficult noisy breathing).

If an asthma attack is accompanied by the appearance of frothy (sometimes pink) sputum, bubbling breathing, the presence of a large number of wet rales of various sizes, then there is a picture of true or alveolar pulmonary edema. Diseases that cause pulmonary edema are varied.

First of all it is:

• diseases of the cardiovascular system - cardiogenic (hydrostatic) pulmonary edema, associated primarily with impaired myocardial contractility;
• respiratory diseases;
• kidney failure;
• poisoning and intoxication (including inhalation of toxic fumes);
• severe infectious diseases;
• allergy;
• infusion hyperhydration;
• diseases of the central nervous system (brain injury, acute cerebrovascular accident).

In all cases, pulmonary edema leads to severe ARF associated with a violation of the permeability of the alveolar-capillary membrane, a decrease in gas diffusion and damage to the surfactant.

3. Additional research methods will help establish the final diagnosis.

Acute left ventricular heart failure

With this type of heart failure, there is a decrease in the pumping function of the left ventricle.

The reasons

The main reasons include:

1. Myocardial infarction.
2. Arterial hypertension.
3. Atherosclerotic cardiosclerosis.
4. Valvular heart disease.
5. diffuse myocarditis.
6. Paroxysmal arrhythmias.

Development mechanism. First, the fluid impregnates the walls of the alveoli and accumulates in the interstitial tissue of the lungs (the stage of interstitial edema), and then it also appears in the lumen of the alveoli (the stage of alveolar edema).

There is a pronounced violation of gas exchange, increasing hypoxemia. It promotes the release of a large number of biologically active substances, such as histamine, serotonin, kinins, prostaglandins. This leads to an increase in vascular permeability, which creates conditions for the further progression of pulmonary edema.

Platelet aggregation increases, microatelectases develop, which reduce the respiratory surface of the lungs. Respiratory failure and hypoxemia contribute to the production of large amounts of adrenaline and norepinephrine. This leads to a further increase in capillary permeability and an increase in peripheral resistance. Increased afterload contributes to a decrease in cardiac output.

Clinical criteria for major diseases

MYOCARDIAL INFARCTION. As a rule, it begins with a pain syndrome, however, there is also a painless variant with an asthma attack (asthmatic variant). Myocardial infarction should be suspected in any case of dyspnoea in an elderly person, taking into account risk factors. Decisive diagnostic value is attached to the ECG study.

Interpretation of ECG data can be difficult in cases of small-focal and repeated myocardial infarctions. Then the final diagnostic conclusion can be made in a hospital based on a comparison of clinical and laboratory data obtained during the dynamic examination of the patient.

ARTERIAL HYPERTENSION. An asthma attack in hypertensive patients may occur during a hypertensive crisis, usually in the form of cardiac asthma. In the case of recurrent attacks of cardiac asthma in patients with arterial hypertension, it is necessary to exclude the presence of pheochromocytoma.

CARDIOSCLEROSIS. Acute left ventricular failure develops more often in patients with atherosclerotic cardiosclerosis. These can be variants of postinfarction cardiosclerosis and a variant without a scar. Anamnestic data and ECG signs of a scar can indicate a past heart attack: an abnormal Q wave or QS.

In cases of atherosclerotic cardiosclerosis without a scar, the age of the patient, the presence of other signs of coronary artery disease (angina pectoris, rhythm disturbances), and risk factors should be taken into account.

VALVULAR HEART DEFECTS. Often complicated by attacks of cardiac asthma. This can be observed with aortic heart disease, more often with aortic stenosis.
The mechanism of development of left ventricular failure in these defects is associated with overload of the left ventricular myocardium or volume (with aortic insufficiency) or pressure (with stenosis).

The cause of suffocation in them may also be pulmonary embolism as a result of stagnation in the systemic circulation. Most often, pulmonary edema develops in patients with mitral stenosis.

MYOCARDITIS. An asthma attack is often one of the early signs of severe diffuse myocarditis. An indication of the presence of an infection in the immediate anamnesis can be of great diagnostic value.
Patients with severe myocarditis, as a rule, have signs of both left and right ventricular failure. Auscultation of the heart can provide important diagnostic information: weakening of tones, especially the first one, gallop rhythm, various rhythm disturbances.

PAROXYSMAL RHYTHM DISORDERS. In many cases, they occur with symptoms of suffocation, and sometimes lead to pulmonary edema. A detailed presentation of the diagnosis of arrhythmias is presented in the "Arrhythmias" section, but here we will limit ourselves to only general remarks.

The occurrence of acute heart failure during paroxysmal tachycardia is determined primarily by the initial state of the myocardium, the duration of the attack and the heart rate. The likelihood of developing acute heart failure in patients with paroxysmal arrhythmias increases if they have valvular heart disease (especially mitral stenosis, atherosclerotic cardiosclerosis, thyrotoxicosis, WPW syndrome).
The most severe paroxysmal tachycardia occurs in children. In the elderly, acute heart failure against arrhythmia may be a manifestation of myocardial infarction. Paroxysmal arrhythmias in the elderly, in addition to acute heart failure, are complicated by transient disorders of cerebral circulation in the form of dizziness, visual impairment, and hemiparesis.

ACUTE RIGHT VENTRICULAR HEART FAILURE. The most common causes: thromboembolism of a large branch of the pulmonary artery, spontaneous pneumothorax.
In the study of the cardiovascular system, a weak frequent pulse, tachycardia, gallop rhythm are found. The liver is enlarged, painful on palpation. Rg-data are due to the underlying disease.

Paramedic tactics and emergency care for acute heart failure syndrome

Tactics of a paramedic in the syndrome of acute heart failure

1. Provide emergency care, taking into account the nosological form.
2. If a myocardial infarction is suspected, take an ECG and analyze the result.
3. Call an ambulance. Prior to the arrival of the ambulance, conduct dynamic monitoring of the patient, evaluate the results of the treatment and, if necessary, adjust it.

Emergency care for acute heart failure syndrome

Patients with acute heart failure need emergency medical care, so the professionally competent and clear actions of the paramedic largely determine the outcome of the disease.

1. The patient should be in a sitting position with lowered legs, which allows deposition of part of the blood in the veins of the lower extremities. The exception is patients with myocardial infarction and patients with low blood pressure, they are recommended a semi-sitting position. For the same purpose, the imposition of venous tourniquets can be recommended. Three tourniquets can be applied at the same time (leave one hand for IV injections). Transfer one of the tourniquets to the free limb every 15-20 minutes.

2. Drug therapy:

• Morphine in/in fractionally. It reduces shortness of breath by suppressing the respiratory center, reduces preload, relieves anxiety and fear. Contraindications to its appointment are respiratory rhythm disturbances, cerebral pathology, convulsions, airway obstruction.
• Nitroglycerin 0.5 mg sublingually twice with an interval of 15-20 minutes. In severe cases, the drug can be administered intravenously in saline or 5% glucose solution under the control of blood pressure. The drug, being a venous vasodilator, reduces pre- and afterload on the heart. Contraindications to the appointment of the drug are low blood pressure, stroke, shock, severe anemia, toxic pulmonary edema.
• Lasix is ​​administered at an initial dose of 20-40 mg IV. The effect is evaluated by diuretic action and improvement of clinical manifestations. The introduction of diuretics leads to a decrease in blood filling of the lungs, a decrease in pressure in the pulmonary artery and reduces the venous return of blood to the heart. Contraindications to the appointment of the drug are hypotension and hypovolemia.
• In patients with low blood pressure, dopamine is used, which is administered intravenously (250 mg of the drug is diluted in 500 ml of 5% glucose solution). The drug is contraindicated in thyrotoxicosis, pheochromocytoma, arrhythmias.
• Of the other means can be used: corticosteroids are used to reduce alveolar-capillary permeability. Their use is most justified in low blood pressure (for example, prednisolone 60-90 mg IV); in case of bronchial obstruction, inhalation of salbutamol 2.5 mg through a nebulizer. It is better to refuse the introduction of aminophylline because of the risk of developing arrhythmias and frequent side effects in the form of vomiting, tachycardia, and agitation.

3. Oxygen therapy.

4. Defoaming. The use of defoamers is of great importance in the treatment of pulmonary edema, since a large amount of foam in the alveoli reduces the respiratory surface of the lungs.

Indications for hospitalization

Acute heart failure requires mandatory hospitalization in the intensive care unit or cardioreanimation. The patient is transported in a semi-sitting or sitting position.

Emergency care sequence for various hemodynamic variants of pulmonary edema

1. Sitting position with lowered legs.
2. The introduction of narcotic analgesics and (or) neuroleptics, taking into account contraindications.
3. The introduction of inotropic drugs and drugs that cause unloading of the pulmonary circulation.
4. The use of defoamers.

Monitoring the condition of patients with acute heart failure

A patient with acute heart failure must be hospitalized either in the intensive care unit or in the intensive care unit. In this case, the patient is subject to either non-invasive or invasive monitoring. For the vast majority of patients, a combination of its two forms is desirable.

Non-invasive monitoring - determination of body temperature; the number of respiratory movements, the number of heartbeats, blood pressure, pO 2 (or oxygen saturation of arterial blood), the volume of urine excreted, ECG.

Pulse oximetry is mandatory for patients transferred to oxygen inhalation.

Invasive monitoring:

• catheterization of a peripheral artery is advisable in patients with unstable hemodynamics, if intra-arterial pressure can be measured in the ward (if equipment is available);
• catheterization of the central vein for the introduction of drugs, control of CVP, saturation of venous blood;
• pulmonary artery catheterization in everyday practice for the diagnosis of acute heart failure is not indicated. It is advisable to use a Swan-Gans catheter only if it is difficult to differentiate between pulmonary and cardiac pathology, in situations where the use of a thermodimotor is mandatory, and, if necessary, monitor end-diastolic pressure in the LV by the level of occlusion pressure in the pulmonary artery. Tricuspid regurgitation reduces the value of data obtained with a thermodimotor. Among the limitations of the use of the catheter should include situations caused by mitral stenosis, aortic regurgitation, primary pulmonary hypertension, when the pulmonary artery occlusion pressure is not equal to the end-diastolic pressure in the left ventricle (pulmonary artery catheterization has a recommendation class IIc, and a level of evidence B);
• Coronary angiography is indicated for ACS complicated by acute heart failure in all patients who do not have absolute contraindications. Carrying out on the basis of coronary angiography shunting or stenting significantly improves the prognosis.

Treatment of acute heart failure

There are 3 levels of goals for the treatment of acute heart failure.

First level goals (stage of manifestationacute heart failure, the patient is hospitalized in the intensive care unit or intensive observation):

• minimization of manifestations of decompensation (shortness of breath, edema, pulmonary edema, hemodynamic parameters);
• restoration of adequate oxygenation;
• improvement of blood supply to peripheral organs and tissues;
• restoration (stabilization) of kidney and myocardial function;
• the maximum reduction in the length of stay in the intensive care unit.

Goals of the second level - the patient is transferred from the intensive care unit:

• titration of drugs that reduce the mortality of patients with CHF;
• determination of indications for surgical interventions (resynchronization, ACCORN mesh, cardioverter-defibrillator);
• rehabilitation;
• reduction in hospital stay.

Goals of the third level - the patient was discharged from the hospital:

• mandatory participation of the patient in educational programs;
• compulsory physical rehabilitation;
• control of doses of life-saving drugs in the treatment of CHF;
• lifelong monitoring of the patient's condition.

The use of oxygen in the treatment of acute heart failure

Oxygen therapy is mandatory for all patients with acute heart failure who have arterial oxygen saturation.<95% (для пациентов с ХОБЛ <90%).

The strategy of choice is non-invasive oxygen therapy, without tracheal intubation. To do this, use face masks that allow you to create positive pressure at the end of exhalation. Non-invasive oxygenation (NIO) is the first line of treatment for patients with pulmonary edema and acute heart failure associated with increased blood pressure. NIO reduces the need for intubation and mortality on the first day after hospitalization, leads to an improvement in LV contractility and a decrease in afterload.

NIO should be used with caution in patients with cardiogenic shock and isolated right ventricular failure.

The impossibility with the help of NIO to increase the saturation to the target level or the severity of the patient's condition (inadequacy), which does not allow him to fully use the mask, are indications for intubation and transfer of the patient to mechanical ventilation.

NIE should be carried out for 30 minutes every hour, starting with a positive end-expiratory pressure of 5-7.5 cm of water. followed by its titration to 10 cm of water.

Side effects of NIO - increased right ventricular failure, dry mucous membranes (possibility of violating their integrity and attaching infection), aspiration, hypercapnia.

The use of morphine in the treatment of acute heart failure

Morphine should be used in a patient with AHF who is restless, agitated, and severely short of breath. The efficacy of morphine in acute heart failure has not been well studied. A safe dose is 2.5-5 mg intravenously slowly. Given the possible nausea and vomiting after the administration of morphine (especially with NIO), monitoring of the patient is mandatory.

Use of loop diuretics

Features of the use of loop diuretics inacute heart failure:

• the introduction of loop diuretics intravenously - the basis of the treatment of acute heart failure in all cases of volume overload and signs of stagnation;
• loop diuretics are not indicated in patients with systolic blood pressure<90 мм рт.ст., гипонатриемией и ацидозом;
• high doses of loop diuretics contribute to hyponatremia and increase the likelihood of hypotension in the treatment of ACE inhibitors and ARA
• the introduction of intravenous vasodilators reduces the dose of diuretics;
• it is advisable to start diuretic treatment with 20-40 mg of furosemide or 10-20 mg of torasemide intravenously.

After the introduction of a diuretic, control of urine volume is mandatory, if necessary, the introduction of a urinary catheter is indicated.

According to the level of excreted urine, the dose of diuretics is titrated upwards, however, the total dose of furosemvda for the first 6 hours of treatment should be<100 мг, а за 24 ч <240 мг.

• With renal refractory in patients with AHF, it is advisable to combine loop diuretics with HCTZ - 25 mg orally and aldosterone 25-50 mg orally. This combination is more effective and safer than large doses of the loop diuretic alone;
• Diuretic treatment always leads to the activation of neurohormones, contributes to hypokalemia and hyponatremia (monitoring of electrolyte levels is mandatory).
• The prospects for diuretic treatment of AHF are associated with the use of vasopressin receptor antagonists.

The use of vasodilators

Vasodilators reduce systolic blood pressure and filling pressure of the left and right ventricles, reduce dyspnea and total vascular resistance. Despite the decrease in blood pressure, including diastolic, coronary blood flow is maintained. Vasodilators reduce congestion in the ICC without increasing stroke volume and without increasing oxygen consumption Calcium antagonists are not indicated in the treatment of acute heart failure. The use of vasodilators is contraindicated in systolic blood pressure<90 мм рт.ст. из-за угрозы снижения кровоснабжения внутренних органов Контроль АД при применении вазодилататоров обязателен особенно у больных со сниженной функцией почек и аортальным стенозом.

Drugs with a positive effect in the treatment of acute heart failure

Positive inotropic drugs (PIP) should be used in all patients with low cardiac output, low blood pressure and signs of reduced blood supply to organs.

Identification during examination of a patient of wet and cold skin, acidosis, low GFR, elevated ALT, impaired consciousness and low systolic blood pressure are indications for the use of PIP. PIP treatment should be started as early as possible and stopped as soon as the patient's condition is stabilized. Unjustified continuation of PIP treatment leads to myocardial damage and increased mortality. A significant complication of PIP treatment is severe arrhythmias.

Vasopressors

Vasopressors (norepinephrine) are not recommended as first-line drugs in the treatment of acute heart failure. The use of vasopressors is justified in cardiogenic shock, when PIP treatment and fluid administration do not lead to a rise in blood pressure > 90 mm Hg. and signs of decreased blood supply to organs persist.

Features of correction of the condition of patients with acute heart failure

Decompensation of CHF. Treatment begins with loop diuretics and vasodilators. Diuretic infusion is preferred over bolus administration. The need to add a combined diuretic treatment should be assessed as early as possible.

With persistent hypotension, PIP is indicated.

Pulmonary edema. Treatment begins with an injection of morphine. Vasodilators are needed in normal or high blood pressure. Diuretics - in the presence of signs of stagnation and swelling.

PIP is added to the treatment of hypotension and signs of organ hypoperfusion.

With inadequate oxygenation - transfer to mechanical ventilation.

Acute heart failure due to hypertension, - vasodilators and small doses of diuretics (especially at the onset of stagnation in the ICC).

Cardiogenic shock. With systolic blood pressure<90 мм рт.ст. - внутривенно растворы, улучшающие реологию крови, 250 мл/10 мин и ПИП.

While maintaining hypoperfusion of organs and systolic blood pressure not higher than 90 mm Hg, - norepinephrine. In the absence of positive dynamics - intra-aortic counterpulsation and transfer to mechanical ventilation.

Right ventricular failure always suspicious for PE and right ventricular infarction (require special treatment regimens).

Acute heart failure in patients with ACS always suspicious for acute myocardial infarction or postinfarction defects (special treatment regimens).

• Interstitial pulmonary edema or cardiac asthma:
• Alveolar pulmonary edema.

By severity the following stages of AHF are distinguished (Killip classification):

I stage- no signs of heart failure.

II stage- mild AHF: there is shortness of breath, moist fine bubbling rales are heard in the lower parts of the lungs.

III stage- severe AHF: severe shortness of breath, a significant amount of moist rales over the lungs.

IV stage- a sharp fall in blood pressure (systolic blood pressure 90 mm Hg or less) up to the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, blackout.

Etiology of acute left ventricular heart failure:

1. IHD: acute coronary syndrome (protracted anginal attack, painless widespread myocardial ischemia), acute myocardial infarction (AMI).
2. Mitral valve insufficiency caused by detachment of the papillary muscle (with AMI) or detachment of the mitral valve chord (with infective endocarditis or chest trauma).
3. Stenosis of the left atrioventricular orifice associated with a tumor in any of the chambers of the heart (most often - left atrial myxoma), thrombosis of the mitral valve prosthesis, mitral valve damage in infective endocarditis.
4. Insufficiency of the aortic valve with rupture of the aortic valves, with a dissecting aneurysm of the ascending aorta.
5. Acutely increased heart failure in patients suffering from chronic heart failure (acquired or congenital heart defects, cardiomyopathy, postinfarction or atherosclerotic cardiosclerosis); this may be due to hypertensive crisis, paroxysmal arrhythmias, fluid volume overload resulting from inadequate diuretic or excessive fluid therapy.

Etiology of acute right ventricular heart failure:

1. AMI of the right ventricle.
2. Thromboembolism of the pulmonary artery (TELA).
3. Stenosing process in the right atrioventricular orifice (as a result of a tumor or vegetative growths in infective endocarditis of the tricuspid valve).
4. Asthmatic status.

Etiology of acute biventricular heart failure:

1. AMI with damage to the right and left ventricle.
2. Rupture of the interventricular septum in AMI.
3. Paroxysmal tachycardia.
4. Acute severe myocarditis.

Pathogenesis. Main development mechanisms:

• Primary myocardial damage, leading to a decrease in myocardial contractility (CHD, myocarditis).
• Pressure overload of the left ventricle (arterial hypertension, aortic valve stenosis).
• Left ventricular volume overload (aortic and mitral valve insufficiency, ventricular septal defect).
• Decreased filling of the ventricles of the heart (cardiomyopathy, hypertension, pericarditis).
• High cardiac output (thyrotoxicosis, severe anemia, cirrhosis of the liver).

Acute left ventricular heart failure.

The main pathogenetic factor is a decrease in the contractility of the left ventricle with preserved or increased venous return, which leads to an increase in hydrostatic pressure in the pulmonary circulation system. With an increase in hydrostatic pressure in the pulmonary capillaries more than 25 - 30 mm Hg. there is an extravasation of the liquid part of the blood into the interstitial space of the lung tissue, which causes the development of interstitial edema. One of the important pathogenetic mechanisms is the foaming of the fluid that has entered the alveoli with each breath, which rises up, filling the bronchi of a larger caliber, i.e. alveolar pulmonary edema develops. So, from 100 ml of sweated plasma, 1 - 1.5 liters of foam is formed. Foam not only disrupts the airway, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance, increases hypoxia and edema.

Clinical picture:

Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of lack of air, dry cough. The patient is in a forced orthopnea position. Cyanosis and pallor of the skin, cold clammy sweat. Tachypnea, moist rales in the lower parts of the lungs, muffled heart sounds, tachycardia, accent of the second tone over the pulmonary artery.

Alveolar pulmonary edema is characterized by the development of a sharp attack of suffocation, a cough appears with the release of foamy pink sputum, "gurgling" in the chest, acrocyanosis, profuse sweating, tachypnea. In the lungs, mixed moist rales. Tachycardia, accent of the second tone over the pulmonary artery.

Acute right ventricular heart failure is a consequence of a sharp increase in pressure in the pulmonary artery system. Given the low prevalence of isolated right ventricular AMI and infectious lesions of the tricuspid valve, as a rule, in clinical practice, acute right ventricular failure occurs in combination with left ventricular failure.

Clinical picture: gray cyanosis, tachypne, acute enlargement of the liver, pain in the right hypochondrium, swelling of the jugular veins, peripheral and abdominal edema.

Acute biventricular heart failure: at the same time, symptoms of left and right ventricular failure appear.

With the diagnosis of acute cardiovascular insufficiency, emergency care consists in an urgent call for an ambulance. A heart attack is manifested in sudden disturbances in the work of the heart and is accompanied by a sharp deterioration in well-being, acute chest pain, weakness, loss of consciousness.

AHF is characterized by cardiogenic shock, pulmonary edema, cardiac asthma, and other signs requiring immediate medical attention.

Signs and symptoms of heart failure

Acute diseases of the cardiovascular system develop through several mechanisms that are associated with an increase in the load on the heart. When a person has shortness of breath, a feeling of tightness behind the sternum, a cough that is not associated with a cold, this may portend a heart attack.

Signs of acute cardiovascular insufficiency are determined during a medical examination, and the patient himself feels the symptoms. Before the onset of an attack of heart failure, the patient experiences fear, his skin turns blue, breathing quickens, blood pressure drops or rises.

Symptoms include:

• pulsating veins in the neck are visible;
• sudden pallor;
• bubbling breath;
• numbness in hands and feet;
• weakened heartbeat and rare pulse;
• drop in blood pressure;
• bluing of the skin of the face;
• darkening in the eyes;
• the appearance of a cough, with pink sputum;
• adoption of a forced sitting posture;
• severe muscle weakness;
• tachycardia;
• nausea;
• suffocation;
• cyanosis of the lips;
• fainting.

The most common diseases of the cardiovascular system are not always accompanied by signs and symptoms of insufficiency.

The following signs characterize cardiovascular insufficiency:

• a noticeable drop in blood pressure;
• the skin looks marbled, pale;
• vague consciousness;
• the patient has a cold sweat;
• increased levels of lactic acid in the blood;
• pronounced palpitations;
• capillaries are poorly filled with blood;
• very weakly filled pulse;
• intestinal peristalsis is absent;
• reduced function of urination;
• a sharp drop in body temperature in the armpit and on the limbs;
• cold hands and feet.

The difference between acute and chronic heart failure is the speed at which symptoms and signs appear. It means a heart attack, inflammation of the myocardium, severe arrhythmia.

The heart contracts weakly, the pressure drops sharply, the body lacks blood. Intensive care for acute cardiovascular failure is an emergency.

The mechanism of development of acute heart failure

A sharp violation of cardiac activity, called AHF, is very life-threatening.

The regularities of the development of this disease are revealed, which proceeds according to the following scheme:

• weak heartbeats;
• lack of blood in the arterial bed;
• organs and tissues lack nutrition and oxygen;
• blood pressure rises in the capillaries of the pulmonary system, due to a slowdown in venous outflow;
• blood stagnates in organs and tissues, causing swelling.

AHF is dangerous because if you do not provide emergency care to the patient, a quick death is likely.

The doctor knows that the severity of an attack of AHF depends on what type it is:

1. Right ventricular failure. Occurs with phenomena of blockage of the pulmonary artery (embolism), which causes damage to the right ventricle of the heart muscle in the form of a heart attack. This pathology severely limits the flow of blood from the vena cava to the lungs.
2. Left ventricular failure occurs when the right ventricle of the heart is functioning normally. In this case, the blood enters the lungs, the outflow from which is weakened. There is an overflow of blood vessels in the lungs. Since the left ventricle works poorly, the left atrium overflows with blood, stagnation occurs, blood fills the vessels of the lungs.

There are several options for the acute course of the disease:

1. Cardiogenic shock variant. Pathological decrease in blood pressure due to weak contraction of the left ventricle of the heart muscle. Clouded consciousness, muscle weakness, pallor of the skin, a strong decrease in the temperature of the extremities, and cold sweat are characteristic.
2. Pulmonary edema characterized by overflow of the alveoli in the lungs with the liquid part of the blood, which sweats through the walls of the pulmonary capillaries. The patient is suffocating, he does not have enough air. Weak rapid pulse.
3. Hypertensive crisis in its characteristics, it resembles pulmonary edema, although the right ventricle has no pathologies. Fluid leaking into the alveoli is caused by high blood pressure.
4. Abnormal heart failure, which is caused by increased cardiac activity with tachycardia and stagnation of blood in the lungs, high blood pressure.
5. Exacerbation of congestion in the heart muscle.

In case of a heart attack, when the general condition of the patient deteriorates sharply, fear seizes him, the attack is accompanied by pain in the heart and arrhythmia. Tests for acute cardiovascular insufficiency allow us to determine what type of cardiac pathology we are dealing with.

Classification of heart failure by types and causes

When there is literally not enough blood in the body to provide tissues and organs with nutrition and oxygen, they speak of heart failure. Symptoms of acute cardiovascular insufficiency are a necessary element for classification.

It can develop quickly, then the insufficiency is called acute and gradually, manifesting itself in a chronic form:

1. Acute heart failure is called acute because it can develop in a few minutes. In this case, phenomena of cardiogenic shock occur, in which the myocardium loses its ability to contract, the ejection of blood by the left ventricle becomes minimal, and there is an acute shortage of blood in the organs. Observe: a drop in the minute ejection of blood, an increase in the resistance of blood vessels to the movement of blood; heart rhythm is disturbed; there is tamponing of the ventricles with bleeding into the heart sac; blockage of the pulmonary artery (embolism).
2. Chronic heart failure develops gradually, over several months or even years. Contribute to the appearance of insufficiency, heart defects, high blood pressure, reduced hemoglobin in the blood, severe chronic lung diseases. It is characterized by the fact that the patient develops shortness of breath, increased fatigue, swelling throughout the body and in the internal organs, fluid is retained in the body. There are interruptions in the work of the heart, pain, it becomes impossible to perform even light physical work.

The classification of acute cardiovascular insufficiency is based on objective signs. The classification of 1935, when it was first applied, was obviously insufficient and incomplete. According to this classification, three stages are distinguished in the disease: At the first stage, neither doctors nor the patient himself observe obvious symptoms, and at the third stage all signs of pathology are already manifested.

Currently popular American classification:

• 1 class. The appearance of shortness of breath during moderate physical exertion, for example, when climbing stairs to the third floor. Under normal conditions, no discomfort is felt.
• 2 class. Shortness of breath is already caused by insignificant physical activity, for example, brisk walking. The patient tries to move less, as discomfort appears during loads.
• 3 class. At rest, the state of health is normal, however, already with normal walking, shortness of breath and palpitations appear. Any physical stress causes problems in the work of the heart.
• 4th grade. Shortness of breath appears at rest, cyanosis of the lips and pallor of the skin are observed. The slightest physical activity leads to shortness of breath and interruptions in the heart, pressure drops.

In medical practice, the classification of V. Kh. Vasilenko, N. D. Strazhesko, G. F. Lang is often used, according to which the disease is characterized by three stages.

The syndrome of acute cardiovascular insufficiency manifests itself gradually:

1. I (HI). It is defined as the initial, in a different way, latent chronic heart failure. At this stage, the disease is imperceptible to the patient, only with physical exertion of medium strength and intensity, shortness of breath and palpitations appear. There is a general decrease in performance
2. Shortness of breath becomes noticeable during physical exertion of low intensity. Under tension, the phenomena of lack of air and frequent weak pulse become constant. At this stage, period A and period B are distinguished.
3. H IIA stage. Manifested by heart failure in the small (pulmonary) circulation. Cyanosis of the lips and pallor of the skin appear during exercise. The heart beats rapidly, shortness of breath is accompanied by coughing and wheezing in the lungs, clearly audible. Efficiency is reduced, edema appears on the legs and feet in the evening.
4. H IIB stage. Pain is felt in the heart, shortness of breath appears at rest, the skin becomes blue. The legs swell, the liver becomes enlarged and dense, fluid appears in the abdomen. Patients become disabled, they have frequent attacks and exacerbations.
5. Stage III (H III). This is what is called the dystrophic stage. Signs of circulatory failure are pronounced. Pneumosclerosis is found in the lungs, kidneys and liver (cirrhosis), constant heartbeat and shortness of breath are affected. Patients become emaciated, they lose their appetite, sleep is disturbed. Pain in the heart, noticeable interruptions, a drop in blood pressure make the prognosis unfavorable. Treatment at this stage is problematic.

Classification of the disease depending on heart failure is:

1. Systolic (due to problems with contractions of the muscles of the ventricles of the heart).
2. Diastolic (disturbances occur in the cardiac pause phase)
3. Mixed (disturbances affect all phases of the cardiac cycle).

The prevalence of diseases of the cardiovascular system has made it possible to develop effective methods of treatment and clarify the classification of the disease.

Depending on which area of ​​the circulatory system is subjected to stagnant processes, types of insufficiency are recorded according to their localization:

1. Right ventricular (stagnation is observed in the pulmonary circulation);
2. Left ventricular (congestive manifestations in all organs and systems of the body);
3. Biventricular (blood stasis is observed both in the large and in the small circles of blood circulation).

There is a classification of acute coronary syndrome (ACS) to determine the suspected myocardial infarction, or angina, according to the Killip scale.

Table. Mortality rating scale classification:

Among the causes of sudden death of people, acute heart failure is in the first place, so it is important to identify it at the stage of compensation. First aid for acute cardiovascular insufficiency is what all doctors are taught, regardless of specialization.

The origin of cardiac pathology determines its form:

1. Heart failure of myocardial origin. It occurs as a result of pathology in the muscular wall of the heart. It is caused by failures in the energy processes of the myocardium. In this case, interruptions in the work of the heart are observed both during systole and diastole.
2. Heart failure caused by overload with strong physical exertion or the development of heart disease. It also occurs with chronic malnutrition and overwork.
3. When the symptoms and signs of both the myocardial form and the congestion form are combined, then combined heart failure occurs.

The classification of this dangerous disease made it possible to develop effective methods of treatment in order to save the patient from inevitable death.

Therapeutic measures for acute diseases of the heart and blood vessels

Treatment of acute cardiovascular insufficiency is carried out depending on which syndrome manifests itself during an attack. For each disease, a detailed instruction has been developed, which describes the sequence of the use of drugs and methods.

Doctors strictly adhere to the developed methods of treatment, since the cost of errors in treatment is high. Acute cardiovascular failure occurs suddenly, and emergency care is to follow medical instructions.

Table. Treatment of manifestations of acute heart failure:

Resuscitation in acute cardiovascular failure is to restore the functions of blood circulation and heart function. It is carried out by resuscitation doctors armed with appropriate medical equipment and medicines. The nursing process in acute cardiovascular insufficiency consists in carrying out a system of therapeutic measures as prescribed by a cardiologist.

The treatment of cardiovascular diseases, especially AHF, is one side of the general treatment and prevention measures. The modern understanding of the medical business involves, along with the treatment of patients, to promote and prevent dangerous diseases and their manifestations.

In this sense, the prevention of acute cardiovascular insufficiency is an important and necessary link in the complex treatment of heart disease. Heart disease is prevented by taking good care of your health.

Emergency care algorithm for acute heart failure

Acute heart failure is a polyetiological symptom complex that occurs as a result of a violation of myocardial contractility, leading to a decrease in blood supply to organs (insufficiency of ejection) and relative stagnation of blood in the venous system and in the pulmonary circulation (insufficiency of inflow).

Pulmonary edema is the accumulation of fluid in the interstitial tissue and / or alveoli of the lungs as a result of plasma extravasation from the vessels of the pulmonary circulation.

ETIOLOGY AND PATHOGENESIS

Myocardial contractility is reduced as a result of:
■ decrease in the functioning mass of the myocardium,
■ hemodynamic overload of the left or right heart,
■ reducing the compliance of the chamber walls.

Causes of acute heart failure

■ Impaired diastolic and/or systolic myocardial function in: □ myocardial infarction (most common cause); □ inflammatory or degenerative diseases of the myocardium; □ tachycardia, tachy- and bradyarrhythmia.

■ Sudden overload of the myocardium in: □ hypertensive crisis; □ heart defects; □ severe anemia; □ hyperthyroidism; hypervolemia.

■ Acute disorders of intracardiac hemodynamics in case of: □ rupture of the interventricular septum; □ septal myocardial infarction; □ infarction or avulsion of the papillary muscle; □ bacterial endocarditis with perforation of valve leaflets; □ rupture of chords; □ injury.

■ Increased load on the decompensated myocardium in patients with severe chronic congestive heart failure with:
□ physical activity,
□ psycho-emotional stress,
□ fever,
□ an increase in BCC (for example, when drinking too much liquid or massive infusions);
□ increase inflow in a horizontal position, etc.

■ Overdose of drugs.

With left ventricular acute heart failure:

■ pressure increases in the pulmonary circulation, the pulmonary artery system;
■ pulmonary arterioles constrict in response to increased pressure in the left atrium;
■ worsening external respiration and blood oxygenation;
■ develops interstitial edema (cardiac asthma syndrome), and then - alveolar edema (pulmonary edema syndrome).

With right ventricular acute heart failure:

■ the ability of the heart to pump blood into the pulmonary circulation is reduced or lost;
■ there is venous congestion in the systemic circulation;
■ acute respiratory failure develops.

CLASSIFICATION

According to the type of hemodynamics, the following variants of acute heart failure are distinguished:

■ Congestive type: left ventricular acute heart failure (cardiac asthma, pulmonary edema) and right ventricular acute heart failure (venous stasis in the systemic circulation);
■ Hypokinetic type: cardiogenic shock.

In myocardial infarction, there are 4 classes of acute heart failure.

Classification of acute heart failure in myocardial infarction

CLINICAL PICTURE

Left ventricular acute heart failure is characterized by the appearance of several of the following symptoms:

■ increasing shortness of breath of varying severity (up to suffocation);
■ orthopnea position;
■ sometimes Cheyne-Stokes breathing (alternating short periods of hyperventilation with respiratory arrest);

■ cough (first dry, and then with sputum), later - frothy sputum, often painted pink;

■ feeling of fear, anxiety, fear of death;
■ pallor;
■ acrocyanosis;
■ pouring sweat;
■ tachycardia (up to 120-150 per minute);
■ normal or reduced blood pressure;

■ moist rales may not be heard at first or a meager amount of fine bubbling rales over the lower parts of the lungs is determined; swelling of the mucous membrane of small bronchi can be manifested by a moderate pattern of bronchial obstruction with lengthening of expiration, dry rales and signs of emphysema;
■ in case of alveolar edema, voiced wet rales of various sizes are detected over all lungs, which can be heard at a distance (bubbling breath).

Right ventricular acute heart failure:

■ shortness of breath;
■ swelling of the neck veins;
■ congestion in the veins of the upper half of the body;
■ symptom of Kussmaul (swelling of the jugular veins on inspiration);
■ liver enlargement;
■ intense pain in the right hypochondrium, aggravated by palpation;
■ swelling in the lower parts of the body (in a horizontal position - on the back or side), ascites;
■ in some cases, dyspepsia (congestive gastritis);
■ more pronounced cyanosis;
■ tachycardia;
■ possible development of arterial hypotension up to the picture of shock.

In global acute heart failure, a combination of the above symptoms is observed.

DIFFERENTIAL DIAGNOSIS

It is carried out with non-cardiogenic pulmonary edema, which develops due to an increase in the permeability of the alveolar membranes (with pneumonia, sepsis, aspiration, pancreatitis, poisoning with irritating and toxic gases, etc.) and is called adult respiratory distress syndrome. Features of therapy include the rejection of the use of nitrates and cardiac glycosides. The feasibility of prescribing glucocorticoids to reduce membrane permeability and stimulate the formation of pulmonary surfactant should be evaluated.

ADVICE TO THE CALLER

■ Help the patient to assume a sitting position with legs down.

■ Keep warm and quiet.

■ For chest pain, give the patient nitroglycerin under the tongue (1-2 tablets or spray 1-2 doses), if necessary, repeat the dose after 5 minutes.

■ If the duration of an angina attack is more than 15 minutes, let the patient chew 160-325 mg of acetylsalicylic acid.

■ Find medications the patient is taking, previous ECGs, and show them to EMS staff.

■ Avoid food and drink.

■ Do not leave the patient unattended.

Attention! With hypotension (cardiogenic shock), the position with a raised leg end of nitroglycerin is contraindicated!

ACTIONS ON A CALL

Diagnostics

REQUIRED QUESTIONS

■ How long does shortness of breath bother you?

■ Was the onset sudden or did the dyspnoea increase gradually?

■ What are the conditions for shortness of breath (at rest, during exercise, etc.)?

■ What symptoms preceded the present condition (chest pain,

palpitations, hypertensive crisis, etc.)?

■ What drugs did the patient take on their own and their effectiveness?

■ Has the patient had a recent myocardial infarction, an episode of congestive heart failure?

■ Does the patient have diabetes?

INSPECTION AND PHYSICAL EXAMINATION

■ Assessment of the general condition and vital functions: consciousness, respiration, blood circulation.

■ The position of the patient: the presence of orthopnea.

■ Visual assessment: skin (pale, high humidity), the presence of acrocyanosis, swelling of the cervical veins and veins of the upper half of the body, peripheral edema (lower limbs, ascites).

■ Calculation of respiratory rate: tachypnea.

■ Pulse examination: correct or incorrect.

■ Calculation of heart rate: tachycardia or rarely bradycardia.

■ Measurement of blood pressure: the presence of hypotension (with severe myocardial damage) or hypertension (with a stress response of the body); decrease in SBP< 90 мм рт.ст. является признаком шока.

■ Percussion: the presence of an increase in the boundaries of relative cardiac dullness to the left or right (cardiomegaly).

■ Palpation may reveal displacement of the apex beat, an enlarged painful liver.

■ Auscultation of the heart and blood vessels

□ With left ventricular acute heart failure - protodiastolic gallop rhythm, systolic murmur at the apex of the heart;

□ In right ventricular acute heart failure - accent II tone on the pulmonary artery, gallop rhythm, systolic murmur over the xiphoid process.

■ Auscultation of the lungs: the presence of moist rales.

INSTRUMENTAL STUDIES

Registration of an ECG in 12 assignments. A constant symptom of acute heart failure is tachycardia.

■ ECG signs of right ventricular acute heart failure:

□ type SI-QIII,

□ increase in the R wave in leads V 1.2,

□ deep S wave in leads V 4-6,

□ ST depression in leads I, II, aVL, and STB elevation in leads III, aVF, V 1.2

□ blockade of the right leg of the bundle of His, □ negative T waves in leads III, aVF, V 1-4,

□ high P waves in leads II, III.

■ ECG signs of left ventricular acute heart failure:

□ bifurcation and increase in the amplitude of the P wave in leads I, II aVL, V 5.6,

□ an increase in the amplitude and duration of the second negative phase of the P wave or the formation of a negative P wave in lead V 1;

■ In the presence of ECG taken earlier, it is necessary to evaluate the previous pathology of the heart and evaluate the newly appeared changes.

■ If arrhythmia and conduction disturbances are detected, appropriate treatment is carried out (see the article "Violations of the heart rhythm and conduction").

Treatment

In any clinical variant of acute heart failure, an urgent correction of the condition that caused it is indicated, and the patient is hospitalized in a hospital.

Correction of the causes of acute heart failure

4.5 ACUTE HEART FAILURE

DEFINITION.

Acute heart failure, which occurs as a result of a violation of myocardial contractility, a decrease in systolic and cardiac output, is manifested by several extremely severe clinical syndromes: cardiogenic shock, pulmonary edema, acute decompensated cor pulmonale, etc.

ETIOLOGY AND PATHOGENESIS.

The contractility of the myocardium decreases either as a result of its overload with an increase in the hemodynamic load on the left or right heart, or due to a decrease in the functioning mass of the myocardium or a decrease in the compliance of the chamber wall. Acute heart failure develops when:

Violation of the diastolic and / or systolic function of the myocardium, due to the development of a heart attack (the most common cause), inflammatory or degenerative diseases of the myocardium, as well as tachy- and bradyarrhythmias;

Sudden occurrence of overload of the myocardium of the corresponding part of the heart due to a rapid significant increase in resistance in the outflow tract (in the aorta - a hypertensive crisis; in the pulmonary artery - massive thromboembolism of the branches of the pulmonary artery, a protracted attack of bronchial asthma with the development of acute emphysema, etc.) or volume load (increase masses of circulating blood, for example, with massive fluid infusions - a variant of the hyperkinetic type of hemodynamics);

Acute disorders of intracardiac hemodynamics due to rupture of the interventricular septum or the development of aortic, mitral or tricuspid insufficiency (septal infarction, infarction or separation of the papillary muscle, bacterial endocarditis with perforation of the valve leaflets, rupture of chords, trauma);

Increased load (physical or psycho-emotional stress, increased inflow in a horizontal position, etc.) on the decompensated myocardium in patients with more or less severe chronic congestive heart failure due to congenital or acquired heart defects, postinfarction cardiosclerosis, hypertrophic or dilated cardiomyopathy.

The fall in the contractile function of the myocardium leads to a number of compensatory changes in hemodynamics:

To maintain cardiac output, with a decrease in stroke volume, the heart rate increases, which is accompanied by a shortening of diastole, a decrease in diastolic filling, and leads to an even greater drop in stroke volume;

With a decrease in ventricular contractility, pressure in the atria and veins increases, resulting in stagnation in that part of the bloodstream that precedes the decompensated myocardial chamber. Increased venous pressure contributes to an increase in diastolic filling of the corresponding chamber and, according to the Frank-Starling law, to shock ejection, but an increase in preload leads to an increase in myocardial energy consumption and progression of decompensation. Acute congestive left ventricular failure is manifested by an increase in pressure in the pulmonary artery system (which is aggravated by the Kitaev reflex - narrowing of the pulmonary arterioles in response to an increase in pressure in the left atrium), worsening of external respiration and blood oxygenation, and, when hydrostatic pressure in the pulmonary capillaries exceeds oncotic and osmotic pressure , leads first to interstitial, and then to alveolar pulmonary edema;

With a decrease in cardiac output, maintaining a sufficient level of blood pressure is carried out by increasing peripheral resistance. However, this leads to an increase in afterload and a deterioration in tissue perfusion (including perfusion of vital organs - the heart, kidneys, and brain), which is especially pronounced when compensatory mechanisms are insufficient and blood pressure decreases.

An increase in peripheral resistance, shunting and sequestration of blood and a slowdown in tissue blood flow, which are primarily characteristic of shock, contribute to the sweating of the liquid part of the blood into the tissue, which leads to hypovolemia, hemoconcentration, deterioration of the rheological properties of the blood and creates conditions for the development of thrombotic complications.

With various clinical variants, individual variants of hemodynamic disturbances may come to the fore.

CLINICAL PICTURE AND CLASSIFICATION.

Depending on the type of hemodynamics, the affected chamber of the heart and some features of pathogenesis, the following clinical variants of acute heart failure are distinguished:

Since myocardial infarction is one of the most common causes of acute heart failure, its classification in this disease is of interest (Table 8).

Table 8Classification of acute heart failure in myocardial infarction (based on Killip T. & Kimball J., 1967)

Acute congestive right ventricular failure

manifested by venous congestion in the systemic circulation with an increase in systemic venous pressure, swelling of the veins (best seen in the neck) and liver, and tachycardia; edema may appear in the lower parts of the body (in a horizontal position - on the back or side). Clinically, it differs from chronic right ventricular failure by intense pain in the liver, 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 II tone on the pulmonary artery and corresponding ECG changes). A decrease in the filling pressure of the left ventricle due to right ventricular failure can lead to a drop in the minute volume of the left ventricle and the development of arterial hypotension up to the picture of cardiogenic shock (see).

With pericardial tamponade, constrictive pericarditis, the picture of stagnation in a large circle is not associated with contractile insufficiency of the contractile function of the myocardium, and the treatment is aimed at restoring the diastolic filling of the heart.

Biventricular failure, when congestive right ventricular failure accompanies left ventricular failure, is not considered in this section, since its treatment differs little from that of severe acute left ventricular failure.

Acute congestive left ventricular failure

clinically manifests: paroxysmal shortness of breath, painful suffocation and orthopnea, occurring more often at night, sometimes - Cheyne-Stokes breathing, cough (first dry, and then with sputum, which does not bring relief), later - frothy sputum, often colored pink, pallor, acrocyanosis, hyperhidrosis and is accompanied by excitement, fear of death. In acute congestion, moist rales may not be heard at first, or a meager amount of finely bubbling rales over the lower sections of the lungs is determined; swelling of the mucosa of small bronchi can be manifested by a moderate pattern of bronchial obstruction with prolonged exhalation, dry rales and signs of emphysema. For differential diagnostics with bronchial asthma, dissociation between the severity of the condition and (in the absence of a pronounced expiratory nature of dyspnea and "silent zones") the scarcity of the auscultatory picture can serve. Voiced wet rales of various sizes over all the lungs, which can be heard at a distance - bubbling breathing, are characteristic of a detailed picture of alveolar edema. There may be an acute expansion of the heart to the left, the appearance of a systolic murmur at the apex of the heart, a protodiastolic gallop rhythm, as well as an accent of II tone on the pulmonary artery and other signs of stress on the right heart, up to a picture of right ventricular failure; possible tachycardia up to 120-150 per minute. Blood pressure, depending on the initial level, can be normal, high or low.

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

Cardiogenic shock

Clinical syndrome characterized by arterial hypotension (SBP less than 90-80 mm Hg, or 30 mm Hg below the "working" level in persons with arterial hypertension, a decrease in pulse pressure and signs of a sharp deterioration in microcirculation and tissue perfusion, in including blood supply to the brain and kidneys (lethargy or agitation, diuresis drop of less than 20 ml per hour, cold skin covered with sticky sweat, pallor, gray cyanosis, marble skin pattern); sinus tachycardia, which has a compensatory character.

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 opening with atrial myxoma or a thrombus of a prosthetic valve, with pericardial tamponade, with massive pulmonary embolism. These conditions are often combined with the clinical picture of acute right ventricular failure. Pericardial tamponade and obstruction of the atrioventricular orifice require immediate surgical intervention; drug therapy in these cases can only aggravate the situation. Besides, the picture of a shock at a myocardial infarction sometimes imitates a dissecting aortic aneurysm (see), which requires differential diagnosis, since it needs a fundamentally different therapeutic approach.

There are three main clinical variants of cardiogenic shock:

- arrhythmic shock develops as a result of a fall in cardiac output due to tachycardia / or bradycardia / bradyarrhythmia; after stopping the rhythm disturbance, adequate hemodynamics is restored quite quickly;

- reflex shock(pain collapse) develops as a reaction to pain and is characterized by a rapid response to analgesic therapy; absence of signs of congestive heart failure, deterioration of tissue perfusion (in particular, gray cyanosis); pulse pressure usually exceeds a critical level;

- true cardiogenic shock develops with a lesion volume exceeding 40-50% of the mass of the left ventricular myocardium (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 criteria for diagnosing this condition, the reported mortality rates (in the absence of surgical treatment) range from 80-100%.

In some cases, especially with the development of myocardial infarction in patients treated with diuretics, the developing shock has the character hypovolemic, and adequate hemodynamics is relatively easy to restore by replenishing the circulating volume.

DIAGNOSTIC CRITERIA.

One of the most persistent signs of acute heart failure is sinus tachycardia (in the absence of sick sinus syndrome, complete AV block, or reflex sinus bradycardia); characterized by the expansion of the boundaries of the heart to the left or right and the appearanceIIItone at the apex or above the xiphoid process.

In acute congestive right ventricular failure have diagnostic value:

Swelling of the neck veins and liver,

Kussmaul's symptom (swelling of the jugular veins on inspiration),

Intense pain in the right hypochondrium,

ECG signs of acute overload of the right ventricle (type S 1 -Q 3, an increase in the R wave in leads V I, II and the formation of a deep S wave in leads V 4-6, ST depression I, II, aVL and ST elevation III, aVF, as well as in leads V 1.2; it is possible to form a blockade of the right leg of the His bundle, negative T waves in leads III, aVF, V 1-4) and the right atrium (high peaked teeth P II, III).

In acute congestive left ventricular failure have diagnostic value.

Different severity of shortness of breath up to suffocation,

Paroxysmal cough, dry or frothy sputum, foaming from the mouth and nose,

- orthopnea position,

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

Cardiogenic shock at the prehospital stage is diagnosed on the basis of:

Falling SBP less than 90-80 mm Hg. (or 30 mm Hg below the "working" level in persons with arterial hypertension),

Decrease in pulse pressure - less than 25-20 mm Hg,

- signs of impaired microcirculation and tissue perfusion - a drop in diuresis of less than 20 ml per hour, cold skin covered with sticky sweat, pallor, gray cyanosis, marble skin pattern, in some cases collapsed peripheral veins.

ALGORITHM FOR THE TREATMENT OF ACUTE HEART FAILURE AT THE PRE-HOSPITAL STAGE.

In any clinical variant of acute heart failure, an early correction of the condition that led to the development of such a formidable complication is indicated:

If the cause is heart rhythm disturbances, the basis for normalizing hemodynamics and stabilizing the patient's condition is the restoration of normal heart rate.

a) With paroxysms of tachycardia and tachyarrhythmia, electropulse therapy is indicated, and if it is impossible to carry it out as soon as possible, specific antiarrhythmic therapy, depending on the nature of the rhythm disorder (see Chap. “”)

b) In case of a tachysystolic form of a constant form of atrial fibrillation, atrial fibrillation of unknown duration or paroxysm of atrial fibrillation more than a day old, it is necessary to carry out rapid digitalization by administering digoxin IV in an initial dose of 1 ml of a 0.025% solution,

c) with sinus bradycardia and sinoatrial blockade, it is enough to increase the heart rate by intravenous administration of 0.3-1 ml of a 0.1% atropine solution. With its ineffectiveness and with other bradyarrhythmias - a slow rhythm from the AV connection (substituting), AV blockade of II-III degree, elktrocardiostimulation is indicated. The impossibility of its implementation serves as an indication for drug treatment (for more details, see chapter “”);

If the cause is myocardial infarction, then one of the most effective methods of dealing with decompensation is the speedy restoration of coronary blood flow through the affected artery, which in prehospital care can be achieved using systemic thrombolysis (see Chap. "");

If acute was the result of acutely developed disorders of intracardiac hemodynamics due to trauma, myocardial rupture, damage to the valvular apparatus, emergency hospitalization by a special team to a specialized surgical hospital for surgical care is indicated.

However, in practice it is more often necessary to limit (at least at the first stage of assistance) to pathogenetic and symptomatic therapy. The main task in this case is to maintain an adequate pumping function of the heart, for which various approaches are used depending on the clinical variant of acute heart failure. In any case, oxygen therapy plays a certain role in the fight against hypoxemia - inhalation of humidified oxygen through a nasal catheter at a rate of 6-8 l / min.

Treatment of acute congestive right ventricular failure consists in the correction of the conditions that are its cause - pulmonary embolism (see), asthmatic status (see), etc. This condition does not need self-therapy.

The combination of acute congestive right ventricular failure with congestive left ventricular failure is an indication for therapy according to the principles of treatment of the latter.

The combination of acute congestive right ventricular failure with low output syndrome (cardiogenic shock), due to a decrease in blood supply to the pulmonary circulation and the left ventricle, may require infusion of fluids, sometimes in conjunction with inotropic therapy.

In the treatment of acute congestive left ventricular failure highlight the following areas:

1. Reducing the preload on the myocardium and pressure in the pulmonary artery, for which they use the appropriate position of the body and medications that have a venous vasodilating effect - lasix, morphine, nitrates.

2. Dehydration.

3. Suppression of the respiratory center, which reduces the work of the respiratory muscles and thereby provides physical peace to the patient. Suppression of the respiratory center contributes to the relief of the so-called "respiratory panic" (inadequately deep and frequent breathing), leading to a further increase in shifts acid-base balance.

4. Anti-foaming.

5. Inotropic therapy (according to strict indications).

6. The fight against increased membrane permeability (with the ineffectiveness of standard therapy).

7. Correction of microcirculatory disorders (as an auxiliary measure).

1. Treatment of acute congestive heart failure begins with the appointment of sublingual nitroglycerin at a dose of 0.5-1 mg (1-2 tablets) and giving the patient an elevated position (with an unexpressed picture of stagnation - a raised head end, with expanded pulmonary edema - a sitting position with legs down) ; these measures are not performed with severe arterial hypotension.

2. A universal pharmacological agent for acute congestive heart failure is furosemide (, urix), which reduces the hemodynamic load on the myocardium due to venous vasodilation already 5-15 minutes after i / v administration. Thanks to the diuretic action that develops later, the preload is reduced even more. Furosemide is administered as an intravenous bolus without dilution at a dose of 20 mg with minimal signs of congestion up to 200 mg with extremely severe pulmonary edema.

3. The more pronounced tachypnea and psychomotor agitation, the more indicated the addition of a narcotic analgesic, morphine, to therapy, which, in addition to venous vasodilation and a decrease in preload on the myocardium, already 5-10 minutes after administration reduces the work of the respiratory muscles, suppresses the respiratory center, which provides an additional reduction in load on the heart. A certain role is also played by its ability to reduce psychomotor agitation and sympathoadrenal activity; the drug is used intravenously in fractional doses of 2-5 mg (for which 1 ml of a 1% solution is adjusted to 10 ml with isotonic sodium chloride solution and injected in 2-5 ml) with repeated administration if necessary after 15 minutes. Contraindications are respiratory rhythm disturbances (Cheyne-Stokes breathing), marked depression of the respiratory center, acute airway obstruction, chronic decompensated cor pulmonale, cerebral edema.

4. Severe congestion in the pulmonary circulation in the absence of arterial hypotension, resistant to ongoing therapy, or any degree of acute congestive left ventricular failure in myocardial infarction, as well as pulmonary edema against the background of a hypertensive crisis without cerebral symptoms, are indications for intravenous drip of nitroglycerin or isosorbide dinitrate. Infusion is carried out under constant control of blood pressure and heart rate at an initial dose of 10-15 mcg / min, followed by an increase in it every 3-5 minutes by 10 mcg / min until the desired effect is achieved or side effects appear, in particular, a decrease in blood pressure to 90 mm Hg . Art. (every 10 mg of the drug is diluted in 100 ml of a 0.9% sodium chloride solution; 1 drop of the resulting solution contains 5 μg of the drug). Contraindications to the use of nitrates are uncompensated arterial hypotension, hypovolemia, pericardial constriction and cardiac tamponade, pulmonary artery obstruction, inadequate cerebral perfusion.

5. With the development of acute left ventricular failure against the background of a hypertensive crisis with cerebral symptoms, an intravenous drip of a mixed myotropic vasodilator sodium nitroprusside (50 mg in 250 ml of 5% glucose solution) is indicated under the control of blood pressure and heart rate at an initial dose of 0.5 μg / kg min, or 20 mcg / min with its increase every 5 minutes by 5 mcg / min until the expected effect is achieved (average dose - 1-3 mcg / kg min), the maximum rate of administration (5 mcg / kg min) or the development of side effects. Unlike nitrates, sodium nitroprusside not only reduces preload, but by increasing arterial inflow to tissues, in particular, increasing cerebral and renal blood flow, it also reduces afterload, which leads to a reflex increase in cardiac output. Sodium nitroprusside more often than nitrates causes the "steal" syndrome; contraindications to its use are aortic coarctation, arteriovenous shunts, it requires special care in old age.

6. Modern vasodilatory therapy, including powerful diuretics, has reduced to a minimum the significance of bloodletting and venous tourniquets on the limbs, however, if it is impossible to conduct adequate therapy due to the lack of drugs, these methods not only can, but should be used, especially with rapidly progressive pulmonary edema ( bloodletting in the amount of 300-500 ml).

7. In acute congestive left ventricular failure, combined with cardiogenic shock or with a decrease in blood pressure during therapy that did not give a positive effect, the addition of non-glycoside inotropic agents is indicated for treatment - intravenous administration of dobutamine at a dose of 2.5-10 mcg / kg min, dopamine 5 -20 mcg/kg/min. Persistent hypotension with SBP below 60 mmHg. requires the addition of an infusion of norepinephrine.

8. The means of directly combating foaming in pulmonary edema are "foam suppressants" - substances that ensure the destruction of the foam, reducing surface tension. The simplest of these means is alcohol vapor. Alcohol is poured into the humidifier, passing oxygen through it, supplied to the patient through a nasal catheter or breathing mask at an initial rate of 2-3 liters, and after a few minutes - at a rate of 6-8 liters of oxygen per 1 minute (less effective is the use of cotton wool moistened with alcohol, embedded in a mask) the disappearance of bubbling breathing is observed in terms of 10-15 minutes to 2-3 hours; the simplest method - spraying alcohol in front of the patient's mouth using any pocket inhaler or conventional spray - is the least effective; in extreme cases, intravenous administration of 5 ml of 96% ethanol in the form of a 33% solution is possible.

9. The remaining signs of pulmonary edema with stabilization of hemodynamics may indicate an increase in membrane permeability, which requires the administration of glucocorticoids with a membrane-stabilizing purpose (4-12 mg of dexamethasone).

10. In the absence of contraindications, in order to correct microcirculatory disorders, especially with long-term intractable pulmonary edema, the appointment of heparin is indicated - 5000 IU intravenously as a bolus, then drip at a rate of 1 thousand IU / hour with continued therapy in a hospital (see Chap. "").

B. Treatment of cardiogenic shock is to increase cardiac output and improve peripheral blood flow in the following ways.

1. Relief of adverse reflex effects on hemodynamics.

2. Fight against heart rhythm disorders.

3. Ensuring adequate venous return and diastolic filling of the left ventricle, combating hypovolemia and violations of the rheological properties of blood.

4. Restoration of adequate tissue perfusion of vital organs.

5. Stimulation of myocardial contractility by non-glycoside inotropic agents.

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 or even the Trendelenburg position (with the head end lowered), which contributes to an increase in venous return, an increase in cardiac output, and also an improvement in cerebral blood flow during centralized circulation.

Regardless of the characteristics of the clinical picture, it is necessary to provide full-fledged analgesia (see Chap. “”).

The relief of rhythm disturbances (see above) is the most important measure for the normalization of cardiac output, even if after the restoration of normosystole there is no restoration of adequate hemodynamics. Bradycardia may indicate an increased tone of the vagus and requires immediate intravenous administration of 0.5-1 ml of a 0.1% atropine solution.

To combat hypovolemia that occurs with right ventricular infarction or with previous dehydration (long-term use of diuretics, profuse sweating, diarrhea), intravenous administration of isotonic sodium chloride solution in an amount of up to 200 ml in 10-20 minutes is used with repeated administration of a similar dose in the absence of effect or complications.

The lack of effect from the entire complex of therapeutic measures, including the active fight against hypovolemia, or the combination of cardiogenic shock with congestive heart failure is an indication for the use of inotropic agents from the group of pressor amines.

a) dopamine (dopmin) at a dose of 1-5 mcg/kg min has a vasodilatory effect, at a dose of 5-15 mcg/kg min - vasodilating and positive inotropic (and chronotropic) effects, and at a dose of 15-25 mcg/kg min - positive inotropic (and chronotropic) and peripheral vasoconstrictive effects. 200 mg of the drug is dissolved in 400 ml of 5% glucose solution (1 ml of the 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 reached, the maximum dose (25 mcg / kg min) or the development of complications (most often sinus tachycardia exceeding 140 in 1 minute, or ventricular arrhythmias). Contraindications to its use are thyrotoxicosis, pheochromocytoma, cardiac arrhythmias, hypersensitivity to disulfide, previous intake of MAO inhibitors; with a previous intake of tricyclic antidepressants, doses should be reduced.

b) dobutamine (dobutrex), unlike dopamine, does not affect dopaminergic receptors, has a more powerful positive inotropic effect and a less pronounced ability to increase heart rate and cause arrhythmias. 250 mg of the drug is diluted in 500 ml of 5% glucose solution (1 ml of the mixture contains 0.5 mg, and 1 drop - 25 μg of dobutamine); in monotherapy, it is prescribed at a dose of 2.5 mcg / kg / min. with an increase every 15-30 minutes. at 2.5 mcg/kg/min. until an effect, side effect or dose of 15 mcg / kg / min is obtained, and in the case of a combination of dobutamine with dopamine - at the maximum tolerated doses. Contraindications to its appointment are idiopathic hypertrophic subaortic stenosis, stenosis of the aortic mouth;

c) if it is not possible to use other pressor amines or if dapamine and dobutamine are ineffective, norepinephrine can be used at an increasing dose not exceeding 16 µg / min (in the case of combination with dobutamine or dopamine infusion, the dose should be halved). Contraindications to its use are, pheochromocytoma, preceding the intake of MAO inhibitors; with a previous intake of tricyclic antidepressants, doses should be reduced;

In the presence of signs of congestive heart failure and in the case of the use of inotropic agents from the group of pressor amines, the introduction of peripheral vasodilators - nitrates (nitroglycerin or isosorbide dinitrate at a rate of 5-200 μg / min) or sodium nitroprusside (at a dose of 0.5-5 μg / kg /min).

In the absence of contraindications, in order to correct microcirculatory disorders, especially in long-term intractable shock, the appointment of heparin is indicated - 5000 IU intravenously as a bolus, then drip at a rate of 1 thousand IU / hour with continued therapy in a hospital (see Chap. "").

COMMON THERAPY ERRORS.

Acute heart failure is a life-threatening condition, and therefore erroneous therapy can be fatal. All identified therapy errors are due to outdated recommendations, partially preserved in some modern standards of medical care at the prehospital stage.

The most common mistake in all clinical variants of acute heart failure is the appointment of cardiac glycosides. In conditions of hypoxemia, metabolic acidosis and electrolyte disorders, which are invariably present in acute heart failure and cause increased sensitivity of the myocardium to digitalis, glycosides increase the risk of developing serious arrhythmias. In this case, the inotropic effect is achieved late and affects both the left and right ventricles, which can lead to an increase in pulmonary hypertension.

Dangerous in acute heart failure are attempts to stop paroxysmal arrhythmias with drugs, and not by electrical cardioversion, since most of the antiarrhythmic drugs used have a pronounced negative inotropic effect (exceptions are with paroxysmal ventricular tachycardia and magnesium sulfate with ventricular paroxysmal tachycardia of the “pirouette” type). Equally dangerous are drug attempts to combat bradyarrhythmias, taken instead of pacing, which is not always effective and can be fraught with the development of fatal arrhythmias or an increase in myocardial oxygen demand.

In acute left ventricular failure (both in low ejection syndrome and congestive hemodynamics), glucocorticoid hormones are still widely used. In cardiogenic shock, they are inferior to modern drugs in terms of the effectiveness of their effect on hemodynamics, but against the background of their use in large doses, potassium deficiency is exacerbated and the risk of developing arrhythmias up to fatal increases, and in myocardial infarction, myocardial ruptures become more frequent and scarring processes worsen (their use may be justified). only in acute myocarditis).

In congestive left ventricular failure, eufillin is traditionally used to reduce pressure in the pulmonary artery system, stimulate diuresis and unload, because modern drugs with vasodilating and diuretic activity (see above) are much more effective in this respect and, unlike eufillin, do not increase myocardial oxygen demand and do not have an arrhythmogenic effect. Recommendations for the use of aminophylline to combat broncho-obstruction accompanying edema also seem unconvincing, since obstruction is caused not so much by bronchospasm as by mucosal edema. In addition, obstruction, by increasing expiratory resistance, increases pressure in the alveoli, which partially prevents further exudation of fluid.

In cardiogenic shock, mezaton is relatively often used, which has very narrow indications only for the reflex nature of arterial hypotension due to peripheral vasodilation. Mezaton does not increase cardiac output, but causes only peripheral vasoconstriction, which in most cases leads to aggravation of circulatory disorders in vital organs, an increase in the load on the myocardium and a worse prognosis.

Relatively often, one has to deal with the introduction of pressor amines in cardiogenic shock without a preliminary attempt to compensate for hypovolemia, which, with inadequate BCC, is fraught with the development of a critical state of microcirculation with a fatal worsening of the prognosis. However, excessive use of plasma substitutes can provoke the development of congestive heart failure.

Unlike chronic, in acute right ventricular failure, bloodletting should not be resorted to.

INDICATIONS FOR HOSPITALIZATION.

Acute circulatory failure is a direct indication for hospitalization in the intensive care unit (block) or cardioreanimation.

If possible, patients with cardiogenic shock should be hospitalized in a hospital with a cardiac surgery department, because. current ideas about the treatment of this condition are unambiguously associated with aortic balloon counterpulsation and early surgical intervention.

Transportation is carried out on a stretcher in a horizontal position (with cardiogenic shock and right ventricular failure) and in a sitting position - with congestive left ventricular failure.