Acute heart failure classification. Heart failure (HF) classification. Use of loop diuretics

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 edema lungs).

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 an increase in shortness of breath, 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 of 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 stage of the diagnostic process may be taking into account the anamnestic data and physical examination in order to establish the cause of the development 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.

Causes

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 patients with hypertension 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 an 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 the Swan-Gans catheter only when it is difficult to differentiate between pulmonary and cardiac pathology, in situations where the use of a thermodimotor is mandatory, and, if necessary, to monitor the 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, dryness of the mucous membranes (the possibility of violation of their integrity and 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 is an indication 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).

Acute heart failure, AHF is a polyetiological syndrome in which there are profound violations of the pumping function of the heart.

The heart loses its ability to provide blood circulation at a level necessary to maintain the functioning of organs and tissues.

Let's take a closer look at the classification of acute heart failure.

In cardiology, several methods are used to classify the manifestations of acute cardiovascular insufficiency. By type of hemodynamic disorder distinguish between congestive and hypokinetic acute heart failure(cardiogenic shock).

Depending on the localization of the lesion, the pathology is divided into right ventricular, left ventricular and mixed (total).

Left ventricular

With lesions of the left ventricle in the pulmonary circulation, stagnation is formed. The pressure in the pulmonary artery system increases, with an increase in pressure, the pulmonary arterioles narrow. External respiration and blood oxygen saturation are difficult.

The liquid part of the blood begins to sweat into the lung tissue or into the alveoli, interstitial edema (cardiac asthma) or alveolar edema develops. Cardiac asthma is also a form of acute failure.

Difficulty in breathing is manifested by shortness of breath, increasing to suffocation, in some patients Cheyne-Stokes breathing (intermittent breathing with periodic stops) is observed.

Breathlessness worsens when lying down, the patient tries to sit (orthopnea). In the early stages, moist rales are heard in the lower parts of the lungs, turning into fine bubbling.

Increasing obstruction of the small bronchi is manifested by dry wheezing, prolongation of exhalation, and symptoms of emphysema. Alveolar edema is indicated by loud moist rales over the lungs. In the severe stage, the patient's breathing becomes bubbling.

The patient suffers from dry cough, as the pathological condition progresses, scanty sputum is separated, turning into foamy. Sputum may be pink in color.

Oxygen starvation provokes an acceleration of myocardial contractions, the patient develops. The skin turns pale, profuse sweat appears, pronounced cyanosis is observed in the peripheral parts of the body.

BP values ​​remain within normal limits or decrease. The left ventricular form develops as a complication of arterial hypertension.

Right ventricular

Acute right ventricular failure develops with pneumothorax, decompression sickness, embolism of the trunk or branches of the pulmonary artery, total pneumonia. In violation of the functions of the right ventricle, stagnation is formed in the systemic circulation. The patient develops shortness of breath, swelling of the jugular veins is noticeable on inspiration.

The liver enlarges and thickens due to stagnation of blood in the portal system, it becomes painful.

Profuse cold sweat appears, acrocyanosis and peripheral edema appear.

As the swelling progresses, it spreads higher, the effusion of the liquid part of the blood into the abdominal cavity begins - ascites.

In some patients, the functioning of the stomach is disturbed - develops congestive gastritis. Blood pressure drops sharply until the development of cardiogenic shock. In response to the progressive lack of oxygen in the tissues, the frequency of respiration and heartbeat increase.

With total heart failure, symptoms of both forms are observed.

Killip classes

The classification is based on the clinical manifestations of pathology and its radiological signs. Based on these data, four stages of pathology are distinguished according to the increasing severity:

• I- there are no signs of heart failure;
• II- in the lower parts of the lung fields, moist rales are heard, signs of pulmonary circulation disorders appear;
• III- moist rales are heard in more than half of the lung fields, pronounced pulmonary edema;
• IV- cardiogenic shock, there are signs of peripheral vasoconstriction, cyanosis, systolic blood pressure is lowered to 90 mm Hg. Art. and below, sweat appears, the excretory function of the kidneys is impaired.

The Killip classification of acute heart failure was developed to assess the patient's condition with myocardial infarction, but can be used in cases of pathological conditions that have arisen after.

By clinical severity

Proposed in 2003 to assess the condition of patients with acute decompensation of chronic heart failure. It is based on symptoms of peripheral circulatory disorders and auscultatory signs of congestion in the small circle. According to these criteria, four classes of severity of the condition are distinguished:

• I- congestion is not determined, peripheral blood circulation is normal. The skin is dry and warm.
• II- symptoms of stagnation of blood in the pulmonary circle are detected, there are no visible signs of impaired venous outflow. The skin is warm and moist.
• III- Peripheral circulatory insufficiency is determined without concomitant violation of venous outflow in the small circle. The skin is dry and cold.
• IV- signs of insufficiency of peripheral circulation are accompanied by congestion in the lungs.

Several clinical variants of the pathology are possible:

• Decompensated, develops as a complication of a chronic form of pathology or for other reasons. The symptoms and complaints of the patient correspond to the typical clinic of moderate AHF.
• Hypertensive heart failure. BP is greatly elevated with relatively preserved left ventricular function. There are no signs of pulmonary edema on x-rays. The patient's symptoms and complaints are typical of AHF.
• . It is manifested by disturbances in the rhythm and frequency of breathing, wheezing, orthopnea are heard in the lungs, gas exchange in the lungs is difficult. X-rays confirm accumulation of fluid in the lungs.
• Cardiogenic shock. An extreme manifestation of the syndrome of low cardiac output. Systolic blood pressure drops to critical values, blood supply to tissues and organs is severely impaired. The patient exhibits symptoms of progressive renal impairment.
• High cardiac output syndrome. Accompanied by manifestations of stagnation of blood in the pulmonary circulation. The patient's extremities are warm, possibly lowering blood pressure.
• Right ventricular. The volume of cardiac output is reduced, the pressure in the arterial bed is increased. Increased pressure in the jugular veins, stagnation in the portal system of the liver leads to the development of hepatomegaly.

Any possible classification is more or less conditional and is intended to simplify the diagnosis and choice of treatment tactics in emergency situations.

Learn more about heart failure in this video:

- an acute or chronic condition caused by a weakening of myocardial contractility and congestion in the pulmonary or systemic circulation. Manifested by shortness of breath at rest or with slight exertion, fatigue, edema, cyanosis (cyanosis) of the nails and nasolabial triangle. Acute heart failure is dangerous for the development of pulmonary edema and cardiogenic shock, chronic heart failure leads to the development of organ hypoxia. Heart failure is one of the most common causes of human death.

General information

- an acute or chronic condition caused by a weakening of myocardial contractility and congestion in the pulmonary or systemic circulation. Manifested by shortness of breath at rest or with slight exertion, fatigue, edema, cyanosis (cyanosis) of the nails and nasolabial triangle. Acute heart failure is dangerous for the development of pulmonary edema and cardiogenic shock, chronic heart failure leads to the development of organ hypoxia. Heart failure is one of the most common causes of human death.

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

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

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

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

Causes of heart failure

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

Risk factors

Factors provoking the development of heart failure cause its manifestation with a decrease in the compensatory mechanisms of the heart. Unlike causes, risk factors are potentially reversible, and reducing or eliminating them can delay worsening heart failure and even save a patient's life.

These include:

• overstrain of physical and psycho-emotional capabilities
• arrhythmias, PE, hypertensive crises, progression of coronary artery disease;
• pneumonia, SARS, anemia, renal failure, hyperthyroidism
• taking cardiotoxic drugs, drugs that promote fluid retention (NSAIDs, estrogens, corticosteroids), which increase blood pressure (isadrine, ephedrine, adrenaline)
• severe and rapidly progressive weight gain, alcoholism
• a sharp increase in BCC with massive infusion therapy
• myocarditis, rheumatic fever, infective endocarditis
• non-compliance with recommendations for the treatment of chronic heart failure.

Pathogenesis

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

In chronic heart failure, changes that develop in the heart are compensated for a long time by its intense work and adaptive mechanisms of the vascular system: an increase in the strength of heart contractions, an increase in rhythm, a decrease in pressure in diastole due to the expansion of capillaries and arterioles, which facilitates the emptying of the heart during systole, an increase in perfusion fabrics.

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

At this stage, neurohumoral mechanisms are included in the pathological process. Activation of the mechanisms of the sympathetic-adrenal system causes vasoconstriction in the periphery, which contributes to the maintenance of stable blood pressure in the systemic circulation with a decrease in cardiac output. The resulting renal vasoconstriction leads to renal ischemia, which contributes to interstitial fluid retention.

An increase in the secretion of antidiuretic hormone by the pituitary gland increases the processes of water reabsorption, which leads to an increase in the volume of circulating blood, an increase in capillary and venous pressure, and increased fluid transudation into the tissues.

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

Gas exchange disorder

When the blood flow slows down, the absorption of oxygen from the capillaries by the tissues increases from 30% in the norm to 60-70%. The arteriovenous difference in blood oxygen saturation increases, which leads to the development of acidosis. The accumulation of underoxidized metabolites in the blood and increased work of the respiratory muscles cause activation of the basal metabolism.

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

Edema

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

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

stagnant changes in organs

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

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

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

Classification

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

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

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

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

I (initial) stage- hidden signs of circulatory insufficiency, manifested only during physical exertion by shortness of breath, palpitations, excessive fatigue; at rest hemodynamic disturbances are absent.

II (expressed) stage- signs of prolonged circulatory insufficiency and hemodynamic disorders (stagnation of small and large circles of blood circulation) are expressed at rest; severe disability:

• Period II A - moderate hemodynamic disturbances in one part of the heart (left or right ventricular failure). Shortness of breath develops during normal physical activity, performance is sharply reduced. Objective signs - cyanosis, swelling of the legs, initial signs of hepatomegaly, hard breathing.
• Period II B - deep hemodynamic disorders involving the entire cardiovascular system (large and small circle). Objective signs - shortness of breath at rest, pronounced edema, cyanosis, ascites; complete disability.

III (dystrophic, final) stage- persistent circulatory and metabolic failure, morphologically irreversible damage to the structure of organs (liver, lungs, kidneys), exhaustion.

Heart failure symptoms

Acute heart failure

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

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

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

A further increase in stagnation of the small circle contributes to the development of pulmonary edema. Acute suffocation is accompanied by a cough with the release of copious amounts of frothy pink sputum (due to the presence of an admixture of blood). In the distance, bubbling breathing with moist rales is heard (a symptom of a “boiling samovar”). The position of the patient is orthopnea, the face is cyanotic, the veins of the neck swell, the skin is covered with cold sweat. The pulse is threadlike, arrhythmic, frequent, blood pressure is reduced, in the lungs there are wet rales of various sizes. Pulmonary edema is an emergency requiring intensive care measures, as it can be fatal.

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

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

Chronic heart failure

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

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

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

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

Diagnostics

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

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

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

ECG for specific changes helps to detect hypertrophy and insufficiency of blood supply (ischemia) of the myocardium, as well as arrhythmias. On the basis of electrocardiography, various stress tests are widely used using an exercise bike (bicycle ergometry) and a “treadmill” (treadmill test). Such tests with a gradually increasing level of load make it possible to judge the reserve capacity of the heart function.

Heart failure treatment

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

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

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

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

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

With the development of an attack of acute left ventricular failure (pulmonary edema), the patient is hospitalized and provided with emergency therapy: diuretics, nitroglycerin, drugs that increase cardiac output (dobutamine, dopamine), oxygen inhalations are administered. With the development of ascites, a puncture removal of fluid from the abdominal cavity is performed; if hydrothorax occurs, a pleural puncture is performed. Due to severe tissue hypoxia, patients with heart failure are prescribed oxygen therapy.

Forecast and prevention

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

Measures to prevent heart failure is to prevent the development of diseases that cause it (IHD, hypertension, heart defects, etc.), as well as factors contributing to its occurrence. In order to avoid the progression of already developed heart failure, it is necessary to comply with the optimal regimen of physical activity, taking prescribed drugs, and constant monitoring.

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

• 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.