Characteristic signs of acute heart failure. How acute heart failure manifests itself Acute sleep

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What are the types of heart failure?

The classification of heart failure is based primarily on the mechanisms of its development, as well as on the type of cardiac dysfunction that is observed.
Today there are several classifications of this syndrome. If we talk about the classification of this pathology depending on the speed of its development, then in this case it may be acute And chronic.
If we take into account the area of ​​the damaged area of ​​the heart, then this pathology may be right-hearted or right ventricular or left heart or left ventricular. Left ventricular heart failure is observed much more often than the right ventricular form. This is explained by the fact that the left ventricle is subjected to greater loads than the right, which, of course, “unsettles it.”

In medical practice there are also isolated heart failure. It can be either right or left ventricular, and in most cases it occurs in an acute form. But the chronic form of this disease, as a rule, is mixed.

What is acute and chronic heart failure?

Acute heart failure develops very quickly. The development of this state takes only a few minutes, sometimes hours. The obvious symptoms of this syndrome are considered to be pulmonary edema And cardiac asthma. Both of these conditions can cause the death of the patient, which is why in this case immediate medical assistance is necessary.

Pulmonary edema and cardiac asthma are accompanied by severe attacks of shortness of breath, as well as bluish skin. In addition, the patient experiences dizziness and moist rales in the lung area. Very often in such cases, patients lose consciousness. All these signs can occur along with a hypertensive crisis or myocardial infarction. If this happens, it means acute decompensation of the functioning of the heart. In some cases, an acute form of heart failure occurs against the background of complications of the chronic form of this disease.

The most common causes of the development of the acute form of this pathology include:

• Acute valvular insufficiency
• Cardiac tamponade
• Myocardial infarction
• Heart rhythm disturbance
• Pulmonary embolism
• Decompensation of chronic heart failure
• Heart injuries

The most common causes of chronic heart failure include:

• Cardiosclerosis
• Arterial hypertension
• Chronic ischemic heart disease
• Heart valve diseases
• Chronic cor pulmonale

Shortness of breath is considered to be one of the first signs of heart failure. At first, this condition makes itself felt only after excessive physical exertion. Then shortness of breath begins to “pursue” the patient, giving him no rest even in a supine position. In medicine, this condition is called orthopnea. In people suffering from a chronic form of this disease, this condition represents a kind of indicator of their functional potential. Since physical activity and shortness of breath are practically inseparable concepts, this was the impetus for classifying heart failure into so-called functional classes, abbreviated as FC.

I FC– the patient leads a normal life. Weakness in the muscles, shortness of breath, palpitations and some other symptoms occur only at the moment of physical stress.
II FC– the patient’s daily activity is practically unlimited. He experiences shortness of breath, as well as some other symptoms accompanying this condition, immediately during moderate physical activity. For example, while walking. At rest, no unpleasant symptoms are felt.
III FC– the patient’s physical activity undergoes a number of pronounced restrictions. Any even minor stress immediately causes palpitations, shortness of breath, and so on.
IV FC– all the symptoms inherent in heart failure make themselves felt even at rest. They become more noticeable even during normal conversation.
Shortness of breath in this condition occurs due to impaired blood circulation in the vessels of the lungs. This is explained by the fact that the heart can no longer normally distill the blood flowing to it.

Since there is stagnation of blood in the lungs, this leads to the development of other far from pleasant symptoms, one of which is:
Dry cough– In medicine, this condition is also called cardiac cough. In most cases, this symptom is observed in patients with chronic heart failure. A dry cough is the result of swelling of the lung tissue. Most often, a cough makes itself felt during physical activity or in a lying position, since at such moments the heart must work even faster. There are also cases when attacks of dry cough transform into cardiac asthma, that is, an attack of suffocation. This fact is a signal of the onset of acute heart failure.

Since therapy for the chronic form of this condition involves taking antihypertensive drugs, including ACE inhibitors ( Captopril), the use of which may cause a side effect such as a dry cough, it is best for patients to monitor symptoms of cough and consult their doctor about this. If the patient’s cough occurs precisely because of the medications, then the medications should be replaced.

In this case, swelling usually occurs on the legs. At first they form in the ankle area. In the evenings they most often become larger, but in the mornings they practically disappear. If the disease is not treated, then it is quite possible for swelling to spread to the thighs and lower legs, as well as to some other parts of the body. In addition to edema, patients may also experience trophic changes in the skin. This could be hair loss, skin pigmentation, nail deformation, and so on.

Muscle weakness is another symptom of chronic heart failure. It occurs as a result of a decrease in the blood supply to the muscles. In such cases, patients indicate excessive fatigue, as well as very severe muscle weakness, which occurs mainly during physical activity.

Pain in the right hypochondrium - this symptom of chronic heart failure is extremely rare. It occurs due to stagnation of blood in the systemic circulation, namely in the liver area. If a patient experiences this kind of pain, then he most often also experiences swelling in the legs, swelling of the jugular veins, as well as hydrothorax and ascites. All these signs of this syndrome can be combined with other unpleasant symptoms that arise due to the underlying pathology that provoked heart failure. As soon as a person notices one of these signs, he should immediately seek help from a doctor.

conclusions

• In acute heart failure, there is a sharp change in the functioning of the heart;
• The obvious signs of this condition are considered to be: loss of consciousness, severe shortness of breath, which develops into an attack of suffocation, the onset of a dry cough;
• Chronic heart failure is accompanied by fairly slow disruptions in the functioning of the heart, which make themselves felt as a result of the presence of some chronic cardiovascular pathology such as angina pectoris, hypertension, and so on;
• The main signs of the chronic form of this disease include: cardiac cough, swelling of the legs, shortness of breath, muscle weakness;
• If you have this disease, you need qualified help from medical specialists.

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

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

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

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

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

Cardiogenic causes

Heart diseases leading to acute disruption of myocardial contractile activity:

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

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

Extracardiac causes

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

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

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

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

Symptoms

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

Symptoms of right ventricular AHF

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

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

Symptoms of left ventricular AHF

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

Patients complain of:

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

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

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

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

Diagnostics

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

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

Treatment

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

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

Drug therapy:

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

Prevention

Measures to prevent the development of acute heart failure.

Acute heart failure (AHF) is an emergency condition that develops when the pumping function of the heart is severely impaired.

Acute myocardial dysfunction entails circulatory disorders in the systemic and pulmonary circulation; as the pathological condition progresses, multiple organ failure develops, i.e., gradual failure of all organs and systems occurs.

Acute heart failure can develop as a complication of cardiac diseases, sometimes occurring suddenly, without obvious preconditions for a catastrophe. Next, you will learn what are the signs of acute heart failure and symptoms before death.

Factors in the development of AHF are conventionally divided into several groups:

• Organic myocardial lesions;
• Other cardiovascular pathologies;
• Non-cardiac diseases that do not directly affect the heart or blood vessels.

The list is dominated by damage to the heart muscle, in particular myocardial infarction, in which muscle cells die. The larger the area of ​​necrosis, the higher the risk of developing AHF and the more severe its course. , burdened by AHF, - one of the most dangerous conditions with a high probability of death for the patient.

Inflammatory damage to the myocardium – myocarditis – can also lead to AHF. A high risk of developing AHF is also present during cardiac surgery and when using artificial life support systems.

Acute heart failure is one of the most threatening complications of many vascular and cardiac diseases. Among them:

• Chronic heart failure (we talked about the reasons for its development);
• , congenital and acquired;
• leading to a critical acceleration or deceleration of heart rate;
• Arterial hypertension;
• Cardiomyopathies;
• Cardiac tamponade;
• Blood circulation disorders in the pulmonary circulation.

AHF often develops against the background of trauma or brain surgery, as a complication of infectious diseases, and also due to severe or chronic intoxication. The likelihood of myocardial dysfunction increases with certain endocrine diseases and kidney damage.

Accordingly, people who have a history of:

• Diseases of the heart and blood vessels;
• Bleeding disorders;
• Kidney diseases;
• Diabetes;
• Abuse of alcohol, tobacco, narcotic substances, harmful working conditions;
• Elderly.

Precursors of OSN

Acute heart failure can develop suddenly. In some cases, AHF and sudden coronary death are the first manifestations of asymptomatic coronary heart disease.

In approximately 75% of cases of AHF, alarming symptoms appear 10-14 days before the disaster, which are often perceived as a temporary minor deterioration of the condition. It can be:

• Increased fatigue;
• Heart rhythm disturbances, mainly;
• General weakness;
• Deterioration in performance;
• Dyspnea.

Attacks of dizziness and loss of coordination of movements are possible.

Manifestations

According to the location of the lesion, AHF can be right ventricular, left ventricular or total. When the functions of the right ventricle are impaired, symptoms indicating congestion in the systemic circulation predominate:

• Sticky cold sweat;
• Acrocyanosis, less often – a yellowish tint to the skin;
• Swelling of the jugular veins;
• Shortness of breath not associated with physical activity, turning into suffocation as the condition progresses;
• , decreased blood pressure, thready pulse;
• Enlarged liver, pain in the right hypochondrium;
• Edema of the lower extremities;
• Ascites (fluid effusion into the abdominal cavity).

In left ventricular acute heart failure, progressive congestion develops in the pulmonary circulation and is manifested by the following symptoms:

• Shortness of breath, turning into suffocation;
• Pallor;
• Severe weakness;
• Tachycardia;
• Cough with foamy pinkish sputum;
• Gurgling wheezing in the lungs.

In the lying position, the patient's condition worsens; the patient tries to sit with his legs on the floor. The condition of AHF is accompanied by a fear of death.

It is customary to distinguish several stages in the development of AHF. The appearance of precursors in time coincides with the initial or latent stage. There is a decrease in performance; after physical or emotional stress, shortness of breath and/or tachycardia occurs. At rest, the heart functions normally and symptoms disappear.

The second stage is characterized by the manifestation of severe circulatory failure in both circles. At substage A, pallor of the skin and cyanosis are noticeable in the areas of the body furthest from the heart. Typically, cyanosis develops first at the tips of the toes, then the tips of the hands.

Signs of congestion appear, in particular moist rales in the lungs, the patient suffers from a dry cough, and possibly hemoptysis.

Swelling appears in the legs, the liver increases slightly in size. Symptoms indicating blood stagnation increase in the evening and fade away completely or partially the next morning.

Heart rhythm disturbances and shortness of breath occur with exertion.

At substage B, the patient is bothered by aching pain in the chest, tachycardia and shortness of breath are not associated with physical or emotional stress. The patient is pale, cyanosis affects not only the tips of the fingers, but also the ears, nose, and extends to the nasolabial triangle. Swelling of the legs does not go away after a night's rest and spreads to the lower part of the body.

Fluid accumulations form in the pleural and abdominal cavities. Due to stagnation of blood in the portal system, the liver becomes greatly enlarged and thickened, and pain is felt in the right hypochondrium. Impaired fluid removal from tissues leads to severe oliguria - insufficient urine output.

The third stage, also known as dystrophic or final stage. Circulatory failure leads to multiple organ failure, which is accompanied by increasing irreversible changes in the affected organs.

Diffuse pneumosclerosis, liver cirrhosis, and congestive kidney syndrome develop. Vital organs fail. Treatment at the dystrophic stage is ineffective, and death becomes inevitable.

First aid

When the first symptoms indicating heart failure appear, you must:

• Sit the victim in a comfortable position, with his back raised;
• Provide access to fresh air, unfasten or remove clothing items that restrict breathing;
• If possible, immerse your hands and feet in hot water;
• Call an ambulance, describing the symptoms in detail;
• if it is low, give a nitroglycerin tablet;
• 15-20 minutes after the onset of the attack, apply a tourniquet to the thigh, change the position of the tourniquet at intervals of 20-40 minutes;
• In case of cardiac arrest, artificial respiration and indirect cardiac massage should be started (if you have the skills to perform it).
• While the victim is conscious, you need to talk to him and calm him down.

The ambulance doctors who arrived at the scene must stabilize the patient’s condition. To do this, do:

• Oxygen therapy;
• Elimination of bronchospasms;
• Pain relief;
• Pressure stabilization;
• Increased breathing efficiency;
• Prevention of thrombotic complications;
• Elimination of edema.

All these actions fall within the competence of qualified medical personnel; specific drugs are selected individually depending on the patient’s condition.

What happens if you ignore signals?

If you do not pay attention to the threatening symptoms, the pathological condition progresses quickly. The fatal stage of AHF can occur in a matter of hours or even minutes.

The more time passes from the onset of the first symptoms, the less likely the patient is to survive.

Near-death state

No one is immune from sudden death due to cardiac arrest. Approximately in 25% of cases this happens without any apparent reason, the patient does not feel anything. In all other cases, so-called prodromal symptoms or precursors appear, the appearance of which coincides in time with the latent stage of development of AHF.

What are the symptoms before death in acute cardiovascular failure? In half of the cases, before death, an attack of acute pain in the heart region, tachycardia, occurs.

Ventricular fibrillation, lightheadedness, and severe weakness develop. Then comes loss of consciousness.

Immediately before death, tonic muscle contractions begin, breathing becomes frequent and heavy, gradually slows down, becomes convulsive and stops 3 minutes after the onset of ventricular fibrillation.

The skin turns pale, becomes cold to the touch, and acquires a grayish tint. The patient's pupils dilate and the pulse in the carotid arteries can no longer be felt.

Prevention

Prevention of AHF is especially important for people at risk. Persons suffering from cardiac diseases must undergo preventive examinations with a cardiologist twice a year and follow the doctor’s instructions.

Many patients are prescribed lifelong maintenance therapy.

It is very important to lead an active lifestyle, physical activity should cause a feeling of pleasant fatigue.

If possible, avoid emotional stress.

It is necessary to completely review the diet, give up fried, too spicy, fatty and salty foods, alcohol and tobacco in any form. More detailed recommendations regarding diet can only be given by the attending physician, based on the characteristics of past diseases and the general condition of the patient.

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Introduction

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

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

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

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

1. Acute heart failure

Symptoms of acute left ventricular failure.

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

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

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

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

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

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

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

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

Acute right ventricular failure.

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

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

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

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

Urgent Care.

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

Of the cardiac glycosides, strophanthin and korglycon are used.

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

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

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

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

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

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

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

failure heart attack cardiac thromboembolism

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

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

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

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

Treatment

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Before the doctor arrives:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Conclusion

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

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

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

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

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

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

Literature

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

Oskolkova M.K. Functional diagnosis of heart diseases.

M. 2004 – 96 p.

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

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

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

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

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

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

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

CLINICAL PICTURE AND TYPICAL COURSE

1. Subjective and objective symptoms:

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

2) retrograde stagnation:

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

3) the underlying disease causing CHF.

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

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

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

Diagnosis of acute heart failure

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

Supporting research

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

Treatment of acute heart failure

General principles

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

2. Pathogenetic treatment: apply in every case.

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

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

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

4. Actions depending on the clinical form of GHF

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

2) pulmonary edema;

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

4) cardiogenic shock;

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

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

Pharmacological treatment

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

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

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

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

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

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

5. Other drugs

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

Auxiliary treatment

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

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

Surgery

Indications:

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

SPECIAL SITUATIONS

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

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

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

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

The most interesting news

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

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

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

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

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

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

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

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

Treatment of acute heart failure.

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

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

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

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

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

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

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

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

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

Causes of AHF:

1) leading to a rapid increase in symptoms: acute coronary syndrome (myocardial infarction or unstable angina, leading to ischemia and dysfunction of a large area of ​​the myocardium, mechanical complications of acute coronary syndrome, right ventricular myocardial infarction), hypertensive crisis, cardiac arrhythmia and conduction disturbances, pulmonary embolism arteries, cardiac tamponade, aortic dissection, peripartum cardiomyopathy, stress-induced cardiomyopathy (takotsubo), surgical complications, tension pneumothorax;

2) leading to a slower increase in symptoms: infections (including myocarditis (except giant cell) and infective endocarditis), metabolic and hormonal disorders (for example, thyroid dysfunction, pheochromocytoma, ketoacidosis in diabetes mellitus), overhydration, high blood pressure syndrome cardiac output (severe infection, especially sepsis, thyrotoxic crisis, anemia, arteriovenous fistulas, Paget's disease).

AHF usually develops as a result of existing heart damage. It is possible to distinguish variants of AHF depending on the underlying cause or provoking factors, for example, AHF in acute pulmonary embolism, acute decompensation of CHF.

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

CLINICAL PICTURE AND NATURAL COURSE

1. Subjective and objective symptoms:

1) retrograde stagnation:

a) in the systemic circulation (right ventricular failure) - peripheral edema (edema of a pasty consistency around the bones or sacral area; may not have time to appear), dilation of the jugular veins and palpation pain in the epigastrium (due to liver enlargement), sometimes - transudate in the serous cavities ( pleural, abdominal, pericardial);

b) in the pulmonary circulation (left ventricular failure → pulmonary edema) - shortness of breath, rapid breathing and shortness of breath in a sitting position, moist rales over the pulmonary fields

2) decrease in cardiac output (peripheral hypoperfusion; rare, indicate a worse prognosis) - fatigue, feeling of weakness, amentia, drowsiness; the skin is pale, cold, moist, sometimes peripheral cyanosis, thready pulse, hypotension, oliguria;

3) the underlying disease that caused AHF.

According to the ESC recommendations (2016), it is recommended to use the classification of patients based on the so-called. hemodynamic profile. Presence or exclusion of stagnation (stagnation = wet profile vs. no stagnation = dry profile) and peripheral hypoperfusion(peripheral hypoperfusion = cold profile vs correct peripheral perfusion = warm profile), primarily based on an objective examination (sometimes additionally with laboratory tests), determines the diagnosis of 4 main patient profiles and makes it possible to develop further tactics (→). Attention: hypoperfusion is not synonymous with hypotension - most patients have blood pressure within normal limits or elevated.

Figure 2.19-2. Treatment algorithm for patients with acute heart failure depending on the clinical picture at the early stage of the disease (based on ESC 2016 recommendations, modified)

2. OSN can proceed as follows:

1) exacerbation or decompensation of CHF- symptoms of blood stagnation in the systemic and pulmonary circulation;

2) pulmonary edema;

3) - subjective and objective symptoms of HF are accompanied by high blood pressure and, as a rule, preserved systolic function of the left ventricle, signs of increased tone of the sympathetic nervous system, with tachycardia and spasm of blood vessels; the patient may be in a state of normovolemia or only slight overhydration; objective symptoms of pulmonary edema often appear without symptoms of stagnation in the systemic circulation;

4) cardiogenic shock- tissue hypoperfusion due to AHF, typically systolic blood pressure<90 мм рт. ст. или снижение среднего артериального давления на >30 mmHg Art., anuria or oliguria, often - heart rhythm disturbances; Symptoms of organ hypoperfusion and pulmonary edema develop rapidly;

5) isolated right ventricular AHF - small output syndrome without pulmonary edema, increased pressure in the jugular veins with or without liver enlargement;

6) AHF with ACS.

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

Additional research methods

1. ECG: changes caused by underlying heart disease are usually observed, more often signs of myocardial ischemia, rhythm and conduction disturbances.

2 . Chest X-ray: in addition to the symptoms of the underlying disease, it can reveal congestion in the pulmonary circulation, fluid in the pleural cavities and enlargement of the chambers of the heart.

3. Echocardiography: identifies functional abnormalities (systolic or diastolic dysfunction, valvular dysfunction) or anatomical changes in the heart (eg, mechanical complications of myocardial infarction).

4.  Ultrasound of the chest: makes it possible to visualize interstitial pulmonary edema; Abdominal ultrasound - performed to measure the width of the inferior vena cava and assess ascites.

5. Laboratory research: mandatory - complete blood count, concentrations of creatinine, urea, potassium and sodium, glucose, cardiac troponins, activity of liver enzymes in the blood, arterial blood gasometry (in patients with slight shortness of breath, it can be replaced by pulse oximetry, except in cases of shock with very low cardiac output and peripheral vasospasm). Determination of brain natriuretic peptide (BNP/NT-proBNP) will help in the differential diagnosis of cardiac (increased concentration) and non-cardiac causes of shortness of breath; Remember that in patients with rapidly increasing pulmonary edema or acute mitral regurgitation, peptide concentrations may still be within normal limits at the time of hospitalization. Determination of D-dimer - indicated in patients with suspected acute pulmonary embolism.

6. Endomyocardial biopsy: readings → .

Diagnostic tactics

It should be determined quickly (max. within 120 minutes) whether AHF is a consequence of a disease that requires specific actions: coronary angiography and possibly revascularization in the case of ACS or cardiac surgery in the case of myocardial rupture, aortic dissection, cardiac tumor or dysfunction of the native or artificial valve.

Differential diagnosis

Causes of non-cardiogenic pulmonary edema → (signs that help distinguish non-cardiogenic pulmonary edema from cardiogenic →), acute respiratory failure, interstitial lung diseases (with an acute course) → .

General principles

1.  Admission to the intensive care unit(general or cardiological) patients who have ≥1 of the criteria:

1) the need for intubation;

2) SpO2<90 % несмотря на оксигенотерапию;

3) respiratory rate >25/min;

4) heart rate<40 или >130/min;

5) systolic blood pressure<90 мм рт. ст.;

2. Goals of emergency treatment: control of subjective symptoms, primarily shortness of breath, and stabilization of hemodynamic status.

3. General scheme of therapeutic tactics for AHF, depending on the presence of symptoms of hypoperfusion and/or stagnation →.

4. Etiotropic treatment: apply in every case.

5. Careful monitoring: respiration, heart rate, ECG and blood pressure. Perform the study regularly (for example, every 5-10 minutes), and in unstable patients - constantly, until the drug doses and the patient’s condition stabilize. If there is no strong vasospasm and significant tachycardia, blood pressure measurements using non-invasive automatic devices are reliable. In case of AHF, monitoring of the rhythm and ST segment on the ECG is necessary, especially if its cause is ACS or arrhythmia. In patients receiving oxygen, monitor SpO2 with a pulse oximeter (eg, hourly), preferably continuously.

Occasionally, invasive hemodynamic monitoring may be necessary, especially in situations where congestion and hypoperfusion coexist, as well as an unsatisfactory response to pharmacological treatment, as this assists in the selection of appropriate treatment; it can be done with:

1) a Swan-Hans catheter inserted into the pulmonary artery - to measure pressure in the superior vena cava, right atrium, right ventricle and pulmonary artery, wedge pressure in the capillaries of the lungs and determine cardiac output →, as well as oxygen saturation of mixed venous blood;

2) a catheter inserted into the central vein - to measure central venous pressure (CVP) and oxygen saturation of hemoglobin in venous blood (SvO2) in the superior vena cava or right atrium;

3) a catheter inserted into a peripheral artery (usually the radial one) to continuously measure blood pressure.

4. Algorithm of action, depending on the clinical form of AHF

1) exacerbation or decompensation of CHF → vasodilators + loop diuretics (in patients with impaired renal function or long-term use of diuretics, consider the use of diuretics in large doses); inotropic drugs in case of hypotension and symptoms of organ hypoperfusion;

2) pulmonary edema → ;

Figure 2.19-3. Algorithm of action for acute pulmonary edema (according to ESC 2016 recommendations, modified)

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

4) cardiogenic shock→ ;

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

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

Pharmacological treatment

1. Vasodilators: mainly indicated for patients with symptoms of hypoperfusion and congestion, without hypotension; avoid in patients with systolic blood pressure<90 мм рт. ст. Уменьшают систолическое артериальное давление, давление наполнения левого и правого желудочков, а также периферическое сосудистое сопротивление; уменьшают одышку. Обязателен мониторинг артериального давления. Особенно осторожно назначайте пациентам с выраженным митральным или аортальным стенозом.

1) IV nitroglycerin - initially 10-20 mcg/min, if necessary increase by 5-10 mcg/min every 3-5 minutes to the maximum hemodynamically tolerated dose (max. 200 mcg/min); possibly po or in an aerosol 400 mcg every 5–10 min; Tolerance develops after 24–48 hours of administration at high doses, so use intermittently. If systolic blood pressure decreases<90 мм рт. ст. → уменьшите дозу, а если давление продолжает снижаться - прекратите инфузию.

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

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

Figure 2.19-4. Algorithm for diuretic treatment of patients with AHF (according to ESC 2008 recommendations, modified)

3. Inotropic drugs: indicated mainly for AHF with peripheral hypoperfusion and hypotension (systolic pressure 90 mm Hg); do not use routinely if hypotension is due to hypovolemia or other reversible cause; monitor the ECG, given the high likelihood of tachycardia, cardiac muscle ischemia and rhythm disturbances. Drugs and dosage →.

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