Heart failure. Acute heart failure diagnosis and treatment at the prehospital stage Classification of acute heart failure

Acute heart failure (AHF) - clinical syndrome complicating the course of various diseases. At the same time, at one end of the spectrum of causes of AHF is cardiogenic shock, which occurs with a critical decrease in myocardial contractility, at the other - pulmonary edema, which develops against the background of high blood pressure and tachycardia in hypertrophic obstructive cardiomyopathy.

Causes of the disease

The main diseases and conditions contributing to the development of AHF include the following:

Acute decrease in myocardial contractility due to its damage or “stunning” ( acute heart attack myocardium, myocardial ischemia, myocarditis, heart surgery, consequences of the use of artificial circulation, severe brain injury, toxic effects on the myocardium, etc.).

Increasing manifestations (decompensation) of chronic heart failure.

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

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

Hypertensive crisis.

Increased pressure in the pulmonary circulation (thromboembolism pulmonary artery, acute diseases lungs, etc.).

Tachy or bradyarrhythmias.

Mechanisms of occurrence and development of the disease (pathogenesis)

Speed ​​of progression matters pathological process. The likelihood of AHF occurring is highest during acute events (for example, with extensive myocardial infarction, paroxysmal tachyarrhythmia, the appearance of valvular regurgitation), when compensatory mechanisms do not have time to reduce the consequences of the emerging disorders. With a slower increase in changes clinical manifestations circulatory failure usually worsens less dramatically. Often one patient has a combination of several causes that mutually aggravate each other; Acute decompensation can be caused by the addition of an additional factor (for example, increased blood pressure or a paroxysm of tachyarrhythmia). In many cases, AHF occurs with a significantly reduced contractility of the left ventricular myocardium. However, there are situations in which the leading mechanism of the pathogenesis of AHF is damage to the right ventricle (for example, right ventricular myocardial infarction or PE, leading to a decrease in left ventricular filling pressure and cardiac output) or when there are no significant disturbances in myocardial contractility (for example, with tachyarrhythmia in patients with severe left ventricular myocardial hypertrophy or mitral stenosis, with the sudden appearance of disturbances in intracardiac hemodynamics). The outcome of AHF depends on the nature of the underlying disease and the reasons that caused decompensation. Thus, in survivors of an episode of AHF due to severe brain injury (when it is believed that due to the massive release of catecholamines, myocardial “stunning” occurs), contractile function can be completely restored and subsequent treatment will not be needed. On the other hand, the presence of serious heart disease often requires active interventions to prevent recurrent episodes of AHF. Knowing the reasons for the development of AHF in a particular patient allows us to develop optimal treatment tactics.

Clinical picture of the disease (symptoms and syndromes)

Killip classification based on clinical symptoms and chest x-ray results. The classification is used primarily for heart failure due to myocardial infarction, but can be used for de novo heart failure.

Classification by clinical severity

Classification of clinical severity is based on assessment of peripheral circulation (tissue perfusion) and pulmonary auscultation (pulmonary congestion). Patients are divided into the following groups:

Class I (Group A) (warm and dry);

Class II (Group B) (warm and humid);

class III (group L) (cold and dry);

Class IV (Group C) (cold and wet).

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

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

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

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

IV. Cardiogenic shock - insufficient perfusion of vital important organs and tissues, caused by a decrease in the pumping function of the heart after correction of preload. Regarding hemodynamic parameters, there are currently no clear definitions of this condition, which reflects the discrepancy in the prevalence and clinical outcomes of this condition. However, cardiogenic shock is usually characterized by decreased blood pressure (SBP 30 mm Hg) and/or low urine output, regardless of the presence of organ congestion. Cardiogenic shock is an extreme manifestation of small output syndrome.

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

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

Based on clinical and hemodynamic data, it is proposed to distinguish the following clinical variants of AHF.

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

2. Pulmonary edema - an episode of AHF, accompanied by severe respiratory failure and a decrease in arterial blood oxygen saturation< 90 % при дыхании комнатным воздухом до начала лечения. В его основе лежит увеличение давления в капиллярах легких, что приводит к выходу жидкой части крови в интерстициальное пространство и альвеолы.

3. Hypertensive crisis implies the occurrence of AHF (pulmonary edema) against the background of unusually high blood pressure with relatively preserved left ventricular function.

4. Acute decompensation of chronic heart failure is characterized by the occurrence of AHF that does not respond diagnostic criteria cardiogenic shock, pulmonary edema or hypertensive crisis.

Diagnosis of the disease

An ECG allows one to quickly identify the presence of ischemia and extensive necrosis of the myocardium (and compare them with the severity of hemodynamic disturbances), as well as rhythm and conduction disturbances. Echocardiography allows you to quickly assess myocardial contractility, identify damage to heart valves and regurgitation in them, atrial or ventricular septal defects, as well as external myocardial rupture and tamponade. Optimal diagnosis and treatment of persistent severe manifestations of AHF require accurate (invasive) assessment of several hemodynamic parameters - pulmonary artery wedge pressure and cardiac output (using a floating Swan-Ganz balloon catheter inserted into the pulmonary artery), as well as blood pressure (at systolic blood pressure below 80 mm Hg or cardiogenic shock, as well as the use of vasopressor agents or active vasodilators preferably using an arterial catheter). In a number of patients, it is necessary to determine arterial blood gases and acid-base balance; in milder cases, arterial oxygen saturation can be assessed using pulse oximetry.

Classification of T. killip(1967) is based on accounting clinical signs and chest x-ray results. There are four stages (classes) of severity:

Stage I - no signs of heart failure;

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

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

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

J.S. Forrester classification(1977) is based on taking into account clinical signs characterizing the severity of peripheral hypoperfusion, the presence of pulmonary congestion, reduced cardiac index (CI) ≤ 2.2 l/min/m2 and high blood pressure pulmonary artery wedge (PAWP) > 18 mm Hg. Art. There are normal (group I), pulmonary edema (group II), hypovolemic and cardiogenic shock (group III and IV, respectively).

Classification of "clinical severity" for patients hospitalized with acute decompensation of CHF. It is based on the assessment of peripheral perfusion and pulmonary congestion during auscultation:

Class I - no signs of peripheral hypoperfusion and pulmonary congestion (“warm and dry”);

Class II - no signs of peripheral hypoperfusion with pulmonary congestion (“warm and moist”);

Class III - signs of peripheral hypoperfusion without pulmonary congestion (“cold and dry”);

Class IV - signs of peripheral hypoperfusion with pulmonary congestion (“cold and wet”).

Widespread implementation of this classification into practice requires the accumulation of clinical experience.

Diagnosis of AHF is based on symptoms and findings additional methods examinations: electrocardiogram (ECG), chest x-ray, echocardiogram (EchoCG), determination of the level of biomarkers in the blood. It is necessary to evaluate the presence of systolic and/or diastolic dysfunction of the LV, as well as the leading clinical syndrome: low CO or symptoms of blood stasis, LV or RV failure.

Clinical assessment

During physical examination, you should pay attention Special attention for palpation and auscultation of the heart with determination of the quality of heart sounds, the presence of III and IV sounds, murmurs and their nature.

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

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

Chest X-ray

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

Laboratory research

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

Plasma levels of BNP and NT-proBNP increase due to their release from the ventricles of the heart in response to increased ventricular wall tension and volume overload. BNP levels > 100 pg/ml and NT-proBNP > 300 pg/ml have been proposed to be used to confirm and/or rule out CHF in patients hospitalized in the emergency department with shortness of breath. However, in elderly patients these indicators have not been sufficiently studied, and with the rapid development of AHF, their content in the blood upon admission to the hospital may remain normal. In other cases, normal levels of BNP or NT-proBNP can accurately exclude the presence of HF. If the concentration of BNP or NT-proBNP increases, it is necessary to ensure the absence of other diseases, including renal failure and septicemia. A high level of BNP or NT-proBNP indicates a poor prognosis.

EchoCG

EchoCG is necessary to determine the structural and functional changes underlying AHF. It is used to assess and monitor the local and general function of the ventricles of the heart, the structure and function of the valves, pericardial pathology, mechanical complications of myocardial infarction, volumetric formations hearts.

CO can be assessed by the speed of movement of the aortic or pulmonary contours. With a Doppler study, determine the pressure in the PA (by the stream of tricuspid regurgitation) and monitor the LV preload. However, the reliability of these measurements in AHF has not been verified using right heart catheterization.

Other diagnostic methods

Additional diagnostic methods are indicated for individual patients to clarify the cause of AHF and determine indications for invasive treatment.

In case of coronary circulation disorders, coronary angiography is necessary. This study is often indicated for long-standing AHF, the cause of which cannot be determined using other examination methods.

To clarify the nature of the lung disease and diagnose large pulmonary embolism, it can be used CT scan chest with or without contrast angiography, as well as scintigraphy.

If a dissecting aortic aneurysm is suspected, computed tomography, transesophageal echocardiography, and magnetic resonance imaging are indicated.

Pulmonary artery catheterization (PA) can help in diagnosing and monitoring the effectiveness of treatment for AHF.

Treatment of the disease

Conservative treatment

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

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

2. AHF leads to a progressive deterioration of blood oxygenation in the lungs, arterial hypoxemia and hypoxia of peripheral tissues. The simplest method of combating this manifestation of the disease is breathing 100% oxygen. The goal is to maintain arterial oxygen saturation >90%. It is optimal to use a mask with high speed oxygen supply (8-15 l/min). In some cases, more active respiratory support, even mechanical ventilation, may be required.

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

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

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

6. It is important to eliminate the causes underlying AHF in a particular patient.

Eliminate tachycardia or bradycardia if they cause AHF or aggravate it.

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

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

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

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

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

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

The main drugs used in the treatment of acute heart failure

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

Pressor (sympathomimetic) amines (norepinephrine, dopamine and, to a lesser extent, dobutamine), in addition to increasing myocardial contractility, can cause peripheral vasoconstriction, which, along with an increase in blood pressure, leads to a deterioration in the oxygenation of peripheral tissues. Treatment is usually started with small doses, which are gradually increased (titrated) if necessary until the optimal effect is obtained. In most cases, dose selection requires invasive monitoring of hemodynamic parameters with determination of cardiac output and pulmonary artery wedge pressure. A common disadvantage of drugs in this group is the ability to cause or worsen tachycardia (or bradycardia when using norepinephrine), cardiac arrhythmias, myocardial ischemia, as well as nausea and vomiting. These effects are dose-dependent and often prevent further dose increases.

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

Dopamine stimulates a- and b-adrenergic receptors, as well as dopaminergic receptors located in the vessels of the kidneys and mesentery. Its effect depends on the dose. With intravenous infusion at a dose of 2-4 mcg/kg per minute, the effect is mainly on dopaminergic receptors, which leads to dilation of the celiac arterioles and renal vessels. Dopamine can help increase the rate of diuresis and overcome diuretic refractoriness caused by reduced renal perfusion, and can also act on the renal tubules, stimulating natriuresis. However, as noted, improvements in glomerular filtration in patients with the oliguric stage of acute renal failure doesn't come. At doses of 5-10 mcg/kg/min, dopamine stimulates predominantly b1-adrenergic receptors, which increases cardiac output; Venoconstriction is also noted. At doses of 10-20 mcg/kg/min, stimulation of a-adrenergic receptors predominates, which leads to peripheral vasoconstriction (including celiac arterioles and renal vessels). Dopamine alone or in combination with other pressor amines is used to eliminate arterial hypotension, increase myocardial contractility, and also increase heart rate in patients with bradycardia that needs correction. If dopamine administration at a rate of more than 20 mcg/kg/min is required to maintain blood pressure in a patient with sufficient ventricular filling pressure, it is recommended to add norepinephrine.

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

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

Agents that increase the affinity of contractile myofibrils of cardiomyocytes for calcium. The only drug in this group that has reached the stage of widespread clinical use in AHF is levosimendan. Its positive inotropic effect is not accompanied by a noticeable increase in myocardial oxygen demand and an increase in sympathetic effects on the myocardium. Other possible mechanisms of action are selective inhibition of phosphodiesterase III, activation of potassium channels. Levosimendan has vasodilating and anti-ischemic effects; due to the presence of a long-acting active metabolite, the effect persists for some time after stopping the drug. In a relatively small (504 patients) randomized, double-blind, placebo-based clinical trial performed in Russia (RUSSLAN), the efficacy and safety of a 6-hour IV infusion of levosimendan was demonstrated in patients with left ventricular failure after recent myocardial infarction. Moreover, along with symptomatic improvement, a decrease in the overall mortality of these patients was noted, noticeable after 2 weeks. and persisted for at least 6 months. after starting treatment. A 24-hour infusion of the drug led to hemodynamic and symptomatic improvement and prevented repeated episodes of worsening disease in severe heart failure. Further study of levosimendan in a wider cohort of patients with AHF is planned (SURVIVE study). Levosimendan is approved for use in a number of European countries and was recently registered in Russia.

Digoxin has limited value in the treatment of AHF. The drug has a low therapeutic width and can cause severe ventricular arrhythmias, especially in the presence of hypokalemia. Its property of slowing atrioventricular conduction is used to reduce the ventricular rate in patients with persistent atrial fibrillation or flutter (see below).

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

Nitroglycerin causes relaxation of smooth muscle cells in the vascular wall, which leads to dilatation of arterioles and veins, including the vessels of the heart. When taking the drug under the tongue, the effect occurs within 1-2 minutes and can last up to 30 minutes. In case of AHF, this is the fastest and most affordable way to reduce the acute manifestations of the disease - if systolic blood pressure is above 100 mm Hg, you need to start taking nitroglycerin under the tongue (1 tablet containing 0.3-0.4 mg medicinal substance, every 5-10 minutes) until it becomes possible to administer it intravenously. Intravenous nitroglycerin infusion is usually started at 10-20 mcg/min and increased by 5-10 mcg/min every 5-10 min until the desired hemodynamic or clinical effect. Low doses of the drug (30-40 mcg/min) mainly cause venodilation, higher doses (150-500 mcg/min) also lead to dilatation of arterioles. When maintaining a constant concentration of nitrates in the blood for more than 16-24 hours, tolerance to them develops. Nitrates are effective for myocardial ischemia, emergency conditions arising from arterial hypertension, or congestive heart failure (including mitral or aortic regurgitation). When using them, arterial hypotension should be avoided (its likelihood is increased with hypovolemia, lower localization of myocardial infarction, right ventricular failure). Hypotension that occurs with the use of nitrates is usually eliminated by intravenous fluid administration; the combination of bradycardia and hypotension is treated with atropine. They may also contribute to the occurrence or aggravation of tachycardia, bradycardia, disruption of ventilation-perfusion relationships in the lungs and headache. Nitrates are considered contraindicated in cases of severe contractile dysfunction of the right ventricle, when its output depends on preload, with systolic blood pressure below 90 mm Hg, and also with a heart rate of less than 50 beats. per minute or severe tachycardia.

Sodium nitroprusside is similar to nitroglycerin in its effect on arterioles and veins. It is usually administered in doses of 0.1-5 mcg/kg/min (in some cases up to 10 mcg/kg/min) and should not be exposed to light. Used to treat emergency conditions arising from severe heart failure (especially associated with aortic or mitral regurgitation) and arterial hypertension. There is evidence of increased symptomatic efficacy (but not outcome) when treating conditions with low cardiac output and high peripheral resistance that do not respond to dopamine. Sodium nitroprusside should not be used if myocardial ischemia persists, as it can impair circulation in areas of the blood supply to significantly stenotic epicardial coronary arteries. With hypovolemia, sodium nitroprusside, like nitrates, can cause a significant decrease in blood pressure with reflex tachycardia, so the filling pressure of the left ventricle should be at least 16-18 mm Hg. Other side effects include worsening hypoxemia in pulmonary diseases (by eliminating hypoxic constriction of pulmonary arterioles), headache, nausea, vomiting and abdominal cramps. In case of liver or kidney failure, as well as when sodium nitroprusside is administered at a dose of more than 3 mcg/kg per minute for more than 72 hours, accumulation of cyanide or thiocyanate in the blood is possible. Cyanide intoxication is manifested by the occurrence of metabolic acidosis. At thiocyanate concentrations > 12 mg/dL, lethargy, hyperreflexia, and seizures occur. Treatment consists of immediately stopping the drug infusion; in severe cases, sodium thiosulfate is administered.

In decompensated heart failure, the effectiveness of a number of new vasodilators - endothelin receptor antagonists and natriuretic peptides - is being studied. One of the drugs belonging to the last group (nesiritide) in patients with acute decompensated heart failure in terms of its effect on hemodynamic parameters and clinical symptoms at least inferior to nitroglycerin at lower frequency side effects. In 2001, it was approved by the US Food and Drug Administration food products and drugs (FDA) for use for this indication. The effect of nesiritide on mortality has not yet been determined.

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

4. Furosemide is a loop diuretic with a direct venodilating effect. The latter effect occurs within the first 5 minutes after intravenous administration, while an increase in urine output occurs later. The initial dose is 0.5-1 mg/kg IV. If necessary, administration is usually repeated after 1-4 hours.

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

Treatment tactics for individual manifestations of acute heart failure

Pulmonary edema. The goal of treatment is to reduce the pressure in the capillaries of the lungs. Optimally achieve reduction in pulmonary artery wedge pressure< 20 (но не ниже 16-18) мм рт.ст., сердечного индекса более 2 л/мин.

Pulmonary edema, hypertensive crisis and acute decompensation of chronic heart failure are in many cases associated with the occurrence of severe peripheral vasoconstriction in patients with reduced contractile reserve of the left ventricle. An increase in afterload leads to a decrease in cardiac output and an increase in diastolic pressure in the left ventricle. Emergency treatment These variants of AHF are based on the use of powerful, rapidly acting vasodilators. After initial stabilization, treatment should be aimed at preventing recurrent episodes of severe vasoconstriction in combination with optimizing cardiac function.

First-line interventions are aimed at quickly reducing pressure in the capillaries of the lungs and eliminating hypoxia. In addition to IV morphine and a diuretic (furosemide), they also include placing the patient in a semi-sitting position with legs down and providing breathing with 100% oxygen. It is important to remember that holding the patient in a horizontal position (which often occurs during transport or when attempting to catheterize a central vein) can quickly lead to irreversible worsening of AHF, especially if active treatment has not yet been started. When systolic blood pressure is above 100 mm Hg. you should start taking nitroglycerin sublingually (1 tablet every 5-10 minutes) or use nitrates in the form of an aerosol until it is possible to perform an IV infusion of nitroglycerin or the systolic blood pressure decreases to less than 90 mm Hg. If there is no response to the first dose of furosemide within 20 minutes, it is recommended to administer a double dose of the drug. However, some studies suggest that the use of moderate doses of furosemide in combination with a high dose of nitrates is preferable to repeated IV administration of increased doses of furosemide (80 mg) in combination with a low dose of nitrates. Moreover, the most important predictor of success early treatment pulmonary edema was an opportunity to reduce mean blood pressure by 15-30% in the first 15-30 minutes.

Mechanical ventilation (with the possible creation of positive pressure at the end of expiration) is usually started when arterial blood oxygen saturation decreases to 90%, oxygen tension in arterial blood decreases to 60 mm Hg. when breathing 100% oxygen and optimal use of bronchodilators (in the presence of bronchospasm), as well as with clinical manifestations of brain hypoxia (drowsiness, lethargy), a progressive increase in carbon dioxide tension in the blood or an increase in acidosis. In milder cases, the effectiveness of continuous positive pressure breathing can be assessed. Data on the effectiveness of early initiation of noninvasive positive pressure ventilation are conflicting, and it has been suggested that it should be considered as a possible intervention in patients who do not respond to standard oxygen breathing and drug treatment.

Second-line interventions usually begin somewhat later and last from several hours to several days. Due to the time delay before the start of treatment, these include intravenous infusion of nitroglycerin or sodium nitroprusside. It has been noted that the effectiveness of vasodilators decreases both with too low and too high doses of drugs. When using them, it is necessary to carefully monitor blood pressure; the dose is titrated until systolic blood pressure decreases by 10-15%, but not below 90 mm Hg, and until an optimal hemodynamic effect is achieved (clinical improvement may be delayed). For refractory or recurrent symptoms of AHF associated with low myocardial contractility, the administration of positive inotropic agents (dobutamine and/or dopamine) is indicated. The optimal duration of treatment with vasodilators and pressor amines is unclear; the need to continue their infusion after the elimination of acute manifestations of heart failure to prevent recurrent deterioration is not obvious (little studied). The indication for long-term use of nitrates is the need to control myocardial ischemia. Repeated administration of high doses of furosemide, even during a refractory episode of AHF, is suggested to be treated with caution, using the lowest dose that provides symptomatic improvement. It is important to remember that excessive diuresis can lead to hypovolemia and arterial hypotension, especially in patients receiving vasodilators and who initially did not have fluid retention in the body. To promptly recognize this condition, if it is impossible to control the filling pressure of the left ventricle, it is advisable to determine at least the central venous pressure. In case of severe bronchospasm, aminophylline may be required (administered intravenously at a loading dose of 5 mg/kg over 20-30 minutes, followed by infusion of 0.5-0.7 mg/kg/h); its use is undesirable for supraventricular tachyarrhythmias. It is important to be aware of signs of aminophylline overdose, including nausea, vomiting, tachycardia, tachyarrhythmias, tremor, restlessness, irritability and convulsions. An effective means of controlling myocardial ischemia when drug treatment is insufficiently effective, as well as the associated manifestations of AHF and severe arrhythmias, is IBD.

It is important to identify and eliminate the causes underlying AHF as quickly as possible (see above). After eliminating acute manifestations of heart failure, it is necessary to optimize the treatment of the disease that led to its development. In this case, you can start titrating the dose of the beta blocker no earlier than acute decompensation has been eliminated.

Arterial hypotension and cardiogenic shock. Arterial hypotension is diagnosed if systolic blood pressure does not exceed 80-90 mm Hg, and requires correction in cases when it is accompanied by a deterioration of the patient’s condition (i.e., it is symptomatic). However, sometimes the appearance of symptoms associated with a decrease in blood pressure may require intervention even in cases where the absolute values ​​of blood pressure exceed 90 mmHg. Thus, with significant myocardial damage, signs of peripheral hypoperfusion (including oliguria) can occur in the absence of arterial hypotension; in this case, as a rule, there is tachycardia. The use of a beta-blocker in this situation can provoke a detailed picture of cardiogenic shock.

A combination of bradycardia or atrioventricular block (with possible appearance ventricular arrhythmias) and low cardiac output (with the possible appearance of signs of peripheral hypoperfusion) can occur with the use of nitrates, morphine, during acute ischemia or in the early stages of myocardial infarction and is eliminated by raising the legs and IV atropine. This condition is considered a manifestation of the vasovagal reaction. In case of arterial hypotension or cardiogenic shock, you must first ensure that there is sufficient filling pressure in the ventricles of the heart (the absence of absolute or relative hypovolemia). In an emergency situation, if there is no pulmonary edema, it is advisable to quickly administer 250-500 ml of fluid intravenously, possibly repeatedly (carefully monitoring the degree of congestion in the lungs and at least central venous pressure). The appearance or worsening of pulmonary congestion suggests that the filling pressure of the left ventricle is not low. If a sufficient increase in blood pressure is not achieved, an infusion of a pressor agent should be started in a gradually increasing dose, the choice of which depends on the level of blood pressure. With very low systolic blood pressure, norepinephrine is used, with an increase in blood pressure to 80 mm Hg. they are trying to switch to dopamine, with a blood pressure of 90 mm Hg. add dobutamine and try to reduce the dose of dopamine. The use of IBD helps maintain a sufficient level of blood pressure.

In case of severe right ventricular failure (spread of necrosis to the right ventricle during myocardial infarction, massive pulmonary embolism), the use of vasodilators (nitrates, ACE inhibitors, etc.) and diuretics should be excluded. Sometimes an increase in blood pressure is facilitated by an increase in the preload of the right ventricle with the help of a fairly rapid intravenous injection of no more than 500 ml of fluid, possibly repeated. In this case, it is important to carefully monitor signs of pulmonary congestion, since in the simultaneous presence of left ventricular failure, accelerated administration of an excess amount of fluid can lead to its aggravation (up to pulmonary edema), as well as an increase in right ventricular afterload due to increased pressure in the pulmonary capillaries. If fluid administration is ineffective, IV dobutamine infusion should be started. It is also important to achieve the preservation of synchronous contractile activity of the right atrium and ventricle (eliminating paroxysms of supraventricular arrhythmias and, if necessary, using sequential atrioventricular electrical stimulation of the heart). If left ventricular contractile dysfunction occurs, it may be necessary to reduce afterload with sodium nitroprusside or IBD. PE with arterial hypotension or shock is an indication for thrombolytic therapy.

To correct the pumping function of the heart, in addition to normalizing blood pressure, other factors that can aggravate disturbances in myocardial contractility should be eliminated. In the presence of hypovolemia, it is important not only to adequately replenish the deficiency of intravascular fluid, but also to identify and, if possible, eliminate its cause. Continuous positive pressure breathing or mechanical ventilation may be required to correct hypoxemia. In case of myocardial ischemia, it is important to perform coronary angiography as soon as possible and the maximum possible revascularization of the myocardium (including with the help of coronary bypass surgery). It is believed that revascularization is justified up to 48 hours after the occurrence of myocardial infarction, up to 18 hours after the development of shock caused by extensive myocardial damage. This approach is considered justified in patients under 75 years of age; There is insufficient data to recommend it in the very elderly. Criteria to predict failure of revascularization in myocardial infarction with cardiogenic shock have not yet been developed. Obviously, patients who require prolonged cardiopulmonary resuscitation, have severe hypoxic brain damage and concomitant diseases with a low life expectancy are not suitable for early invasive treatment. Patients with myocardial infarction who have experienced cardiogenic shock are also indicated for coronary angiography; the need and method of revascularization depend on the characteristics of the coronary anatomy, as well as the persistence of myocardial ischemia (occurring spontaneously or during stress tests). Surgical correction of severe disorders of intracardiac hemodynamics and rapid elimination of cardiac tamponade may be required. Failure to stop the infusion of positive inotropic agents is one of the indications for heart transplantation. At the same time, it is obvious that invasive treatment is impossible in the vast majority of medical institutions. That's why great importance attached to such an organization of medical care that allows you to quickly transfer patients in need to hospitals with appropriate capabilities.

There are reports that in cardiogenic shock refractory to standard treatment, the nitric oxide synthase inhibitor L-NMMA may be effective.

AHF with rhythm and conduction disorders. Arrhythmia can be both the main cause of the development of AHF (especially in patients with contractile dysfunction of the left ventricle, severe myocardial hypertrophy, and heart defects), and a factor aggravating the course of AHF, which is based on other causes. In any case, one should strive to eliminate as quickly as possible newly emerging tachy- or bradyarrhythmias, accompanied by symptoms of AHF.

To quickly relieve paroxysmal tachyarrhythmia (atrial fibrillation/flutter, paroxysmal supraventricular tachycardia, sustained ventricular tachycardia) in the presence of AHF, synchronized electrical cardioversion is indicated. In most cases, depression of consciousness sufficient to perform the procedure can be achieved with the help of intravenous administration of diazepam, which, in comparison with other drugs used for this purpose, appears to be quite safe. The exception is supraventricular tachycardia that occurs due to increased automaticity (ectopic or polymorphic atrial tachycardia, nodal tachycardia), when electrical cardioversion is not effective. Amiodarone is indicated for drug elimination of arrhythmia in patients with AHF, as well as to increase the effectiveness of electrical cardioversion and prevent the resumption of arrhythmia after it. One of the possible schemes for rapid saturation with amiodarone involves an initial IV infusion of 5-7 mg/kg over 30-60 minutes, then 1.2-1.8 g/day as a continuous IV infusion or several oral doses before total dose 10 g, then maintenance dose 200-400 mg/day orally; another regimen, recommended for patients with severe impairment of myocardial contractility, involves an intravenous infusion of 150 mg of the drug over 10 minutes (if necessary, repeated at intervals of 10-15 minutes), then 1 mg/min for 6 hours, then 0. 5 mg/min for the remaining 18 hours; general daily dose should not exceed 2-2.2 g. For recurrent tachycardia with wide QRS complexes, the effectiveness of lidocaine can be assessed (iv 0.5-0.75 mg/kg every 5-10 minutes to a total dose of 3 mg/kg, then start intravenous infusion at a dose of 1-4 mg/min). It is important to consider that in cases of ventricular escape due to bradycardia or blockade, the administration of lidocaine can be fatal. Presence of polymorphic ventricular tachycardia(including tachycardia of the "pirouette" type) - an indication for the exclusion of drugs that prolong the QT interval, intravenous administration of magnesium, rapid pacing, as well as the use of isoproterenol (in preparation for the latter) and, possibly, lidocaine. In some cases, supraventricular tachycardia can be quickly eliminated using vagal tests, as well as intravenous bolus (over 1-3 s) administration of adenosine (6 mg, if arrhythmia persists, 12 mg after 1-2 minutes, repeated if necessary). The advisability of using other antiarrhythmic drugs in AHF is questionable; most of them are dangerous due to the high risk of proarrhythmic action and aggravation of myocardial contractility disorders. In cases where the duration of atrial fibrillation or atrial flutter paroxysm exceeds 48 hours, sinus rhythm must be urgently restored, despite the increased risk of arterial thromboembolism. In this case, in the absence of contraindications, before attempting to restore the rhythm, a continuous intravenous infusion of unfractionated heparin should be started and the therapeutic values ​​of activated partial thromboplastin time should be achieved (1.5-2 times higher than normal for the specific laboratory medical institution). On the same day, indirect anticoagulants are prescribed (warfarin is preferable, if it is unavailable, acenocoumarol). Heparin can be discontinued no earlier than a therapeutic effect is achieved indirect anticoagulants- international normalized ratio 2-3 in two consecutive analyzes with an interval of at least 24 hours. In the future, with continued sinus rhythm, these values ​​​​of the international normalized ratio must be maintained for at least 3-4 weeks.

In case of long-term rhythm disturbances, when their elimination is impossible or not justified, one should strive to reduce excessive tachycardia. Most often we are talking about atrial fibrillation or atrial flutter. For AHF in this situation, the treatment of choice is IV injections of digoxin. However, this drug has a number of disadvantages: on the one hand, the effect usually begins to appear only approximately 60 minutes after IV administration (and it may take up to 6 hours to achieve the maximum effect); on the other hand, the effectiveness of reducing the ventricular rate is significantly reduced at high sympathetic activity (which is inevitable in AHF). To quickly reduce the frequency of ventricular contractions, it is recommended to administer digoxin 0.25 mg every 2 hours up to a total dose of 1.5 mg; maintenance dose 0.125-0.25 mg/day. Beta-blockers do not have these disadvantages, but their use in acute manifestations of heart failure is contraindicated due to the negative effect on myocardial contractility. However, in some cases (for example, if it is necessary to quickly eliminate severe tachysystole while severe myocardial ischemia persists and there are no significant disturbances in myocardial contractility), the advisability of intravenous administration of a low dose of a beta-blocker can be discussed. However, this requires sufficient experience, certain knowledge of the causes of the development of AHF and extreme vigilance, since sometimes the administration of even a minimal dose of these drugs can lead to an irreversible worsening of heart failure.

It should also be taken into account that, as a rule, it is not possible to quickly reduce tachycardia in patients with AHF; Heart rate decreases gradually as acute manifestations of the disease are eliminated and sympathetic activity decreases. Obviously, there is no need to deal with arrhythmias that do not have significant clinical significance.

Bradycardia is understood not only as low absolute heart rate values ​​(less than 50-60 beats/min), but also as a rhythm that is too rare for the existing hemodynamic state (relative bradycardia; for example, heart rate 65 per minute in cardiogenic shock). The treatment of choice for eliminating symptomatic bradycardia is electrical endocardial pacing of the right ventricle. In preparation for this intervention, it is recommended to resort to transcutaneous electrical stimulation of the heart; it can be started quickly, but can be painful and is not always accompanied by adequate mechanical contractions of the heart. In milder cases or as a temporary measure, you can evaluate the effectiveness of IV infusion of dopamine, dobutamine, as well as IV administration of atropine (single dose of 0.5-1 mg at intervals of 3-5 minutes; peak action occurs within 3 min; exceeding the dose of 2.5-3 mg or 0.03-0.04 mg/kg for 2.5 hours is not recommended). For distal atrioventricular blocks (with wide QRS complexes), atropine is ineffective and is not recommended. In severe cases, indicate the possibility of intravenous infusion of adrenaline (2-10 mcg/min).

In all cases, before attempts to restore sinus rhythm, administer antiarrhythmics or digoxin, it is important to normalize the level of potassium and magnesium in the blood, maintaining their concentration above 4 and 1 mmol/l, respectively. To prevent the occurrence of arrhythmias, it is also necessary to monitor the content of potassium and magnesium in the blood during treatment, especially when diuretics are administered.

Surgery

Heart diseases in AHF that require surgical correction

Cardiogenic shock in acute myocardial infarction in patients with multivessel coronary artery disease.

Ventricular septal defect after MI.

Rupture of the free wall of the left ventricle.

Acute decompensation of valvular heart disease.

Failure and thrombosis artificial valve hearts.

Aortic aneurysm or its dissection and rupture into the pericardial cavity.

Acute mitral regurgitation with dysfunction or rupture of the papillary muscle due to ischemia, rupture of the myxomatous chord, endocarditis, trauma.

Acute aortic regurgitation due to endocarditis, aortic dissection, closed injury chest.

Rupture of sinus of Valsalva aneurysm.

Acute decompensation of chronic cardiomyopathy, requiring the use of mechanical methods of circulatory support.

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

Mechanical methods of supporting blood circulation

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

VACP is a standard component of the treatment of patients with cardiogenic shock or severe acute left ventricular failure with:

Lack of rapid response to fluid administration, treatment with vasodilators and inotropic support;

Severe mitral regurgitation or rupture of the interventricular septum to stabilize hemodynamics, allowing the necessary diagnostic and therapeutic measures to be performed;

Severe myocardial ischemia as preparation for coronary angiography (CAG) and revascularization.

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

Means of supporting the ventricles of the heart are mechanical pumps that partially replace the mechanical work of the ventricle. There are many models of such devices, some of which are designed for the treatment of CHF, while others are intended for short-term use in AHF. Their use is justified only in severe AHF that does not respond to standard treatment, including adequate fluid administration, diuretics, inotropes, vasodilators, VACP and, if necessary, mechanical ventilation.

Although temporary hemodynamic and clinical improvement may occur in many cases, the use of mechanical ventricular assist devices is indicated when restoring cardiac function is possible in:

Acute ischemia or MI;

Shock after heart surgery;

Acute myocarditis;

Acute heart valve dysfunction, especially without previous CHF, when improvement in ventricular function is expected, spontaneously or after myocardial revascularization or heart valve replacement;

Waiting for a heart transplant.

Contraindications include severe concomitant diseases. The main complications are thromboembolism, bleeding and infection. There are known cases of technical breakdowns of the device.

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

Main causes and pathogenesis

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

• in case of disturbance of diastolic and/or systolic function of the myocardium during infarction (the most common cause), inflammatory or dystrophic diseases of the myocardium, as well as tachy- and bradyarrhythmias;
• with the sudden occurrence of myocardial overload due to a rapid significant increase in resistance in the outflow tract (in the aorta - hypertensive crisis in patients with compromised myocardium; in the pulmonary artery - thromboembolism of the branches of the pulmonary artery, a prolonged attack of bronchial asthma with the development of acute emphysema, etc.) or due to stress volume (an increase in the mass of circulating blood, for example, with massive fluid infusions - a variant of the hyperkinetic type of hemodynamics);
• in case of acute disturbances of intracardiac hemodynamics due to rupture of the interventricular septum or the development of aortic, mitral or tricuspid insufficiency (septal infarction, infarction or avulsion of the papillary muscle, perforation of the valve leaflets in bacterial endocarditis, rupture of the chordae, trauma);
• with increasing load (physical or psycho-emotional stress, increased inflow in a horizontal position, etc.) on the decompensated myocardium in patients with chronic congestive heart failure.

Classification

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

Since one of the most common reasons The development of AHF is myocardial infarction; the table shows the classification of acute heart failure in this disease.

Possible complications

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

Clinical picture

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

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

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

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

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

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

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

There are three main clinical variants of cardiogenic shock:

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

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

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

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

Diagnostic criteria

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

• In acute congestive right ventricular failure, the following have diagnostic value:
  • swelling of the neck veins and liver;
  • Kussmaul's sign (swelling of the jugular veins on inspiration);
  • intense pain in the right hypochondrium;
  • ECG signs of acute overload of the right ventricle (type SI-QIII, increasing R wave in leads V1,2 and formation of a deep S wave in leads V4-6, depression of STI, II, a VL and elevation of STIII, a VF, as well as in leads V1, 2; blockade may form right leg His bundle, negative T waves in leads III, aVF, V1-4) and signs of right atrium overload (high pointed waves PII, III).
• Acute congestive left ventricular failure is detected based on the following signs:
  • shortness of breath of varying severity, up to suffocation;
  • paroxysmal cough, dry or with foamy sputum, foaming from the mouth and nose;
  • orthopnea position;
  • the presence of moist rales heard over the area from the posterior-lower sections to the entire surface of the chest; local small-bubble rales are characteristic of cardiac asthma; with advanced pulmonary edema, large-bubble rales are heard over the entire surface of the lungs and at a distance (bubbling breathing).
• Cardiogenic shock at the prehospital stage is diagnosed based on:
  • a drop in systolic blood pressure of less than 90-80 mmHg. Art. (or 30 mmHg below the “working” level in persons with arterial hypertension);
  • decrease in pulse pressure - less than 25-20 mm Hg. Art.;
  • signs of impaired microcirculation and tissue perfusion - a drop in diuresis of less than 20 ml/h, cold skin covered with sticky sweat, pallor, marbled skin pattern, in some cases - collapsed peripheral veins.

Treatment of acute heart failure

In any variant of AHF, in the presence of arrhythmias, it is necessary to restore an adequate heart rhythm.

If the cause of AHF development is myocardial infarction, then one of the most effective methods The fight against decompensation will be the rapid restoration of coronary blood flow through the affected artery, which can be achieved at the prehospital stage using systemic thrombolysis.

Inhalation of humidified oxygen through a nasal catheter at a rate of 6-8 l/min is indicated.

• Treatment of acute congestive right ventricular failure consists of correcting the conditions that caused it - pulmonary embolism, status asthmaticus, etc. This condition does not require independent therapy.

The combination of acute congestive right ventricular and congestive left ventricular failure serves as an indication for therapy in accordance with the principles of treatment of the latter.

When acute congestive right ventricular failure and small output syndrome (cardiogenic shock) are combined, the basis of therapy is inotropic agents from the group of pressor amines.

• Treatment of acute congestive left ventricular failure.

• Treatment of acute congestive heart failure begins with the administration of sublingual nitroglycerin at a dose of 0.5-1 mg (1-2 tablets) and placing the patient in an elevated position (with an unexpressed picture of congestion - an elevated head end, with extensive pulmonary edema - a sitting position with legs down) ; These measures are not performed in cases of severe arterial hypotension.
• Universal pharmacological agent in acute congestive heart failure, furosemide is used, due to venous vasodilation already 5-15 minutes after administration, causing hemodynamic unloading of the myocardium, which increases over time due to the diuretic effect that develops later. Furosemide is administered intravenously as a bolus and is not diluted; the dose of the drug ranges from 20 mg for minimal signs of congestion to 200 mg for extremely severe pulmonary edema.
• The more pronounced the tachypnea and psychomotor agitation, the more indicated is the addition of a narcotic analgesic to therapy (morphine, which, in addition to venous vasodilation and reducing preload on the myocardium, already 5-10 minutes after administration reduces the work of the respiratory muscles, suppressing the respiratory center, which provides an additional reduction load on the heart. A certain role is also played by its ability to reduce psychomotor agitation and sympathoadrenal activity; the drug is administered intravenously in fractional doses of 2-5 mg (for which 1 ml of a 1% solution is taken, diluted with isotonic sodium chloride solution, bringing the dose to 20 ml and administered 4-10 ml) with repeated administration if necessary after 10-15 minutes Contraindications are respiratory rhythm disturbances (Cheyne-Stokes breathing), depression respiratory center, acute obstruction respiratory tract, chronic cor pulmonale, cerebral edema, poisoning with substances that depress breathing.
• Severe congestion in the pulmonary circulation in the absence of arterial hypotension or any degree of acute congestive left ventricular failure during myocardial infarction, as well as pulmonary edema against the background of a hypertensive crisis without cerebral symptoms, are an indication for intravenous drip administration of nitroglycerin or isosorbide dinitrate. The use of nitrate drugs requires careful monitoring of blood pressure and heart rate. Nitroglycerin or isosorbide dinitrate is prescribed at an initial dose of 25 mcg/min, followed by an increase every 3-5 minutes by 10 mcg/min until the desired effect is achieved or side effects appear, in particular a decrease in blood pressure to 90 mm Hg. Art. For intravenous infusion every 10 mg of the drug is dissolved in 100 ml of 0.9% sodium chloride solution, so one drop of the resulting solution contains 5 mcg of the drug. Contraindications to the use of nitrates are arterial hypotension and hypovolemia, pericardial constriction and cardiac tamponade, pulmonary artery obstruction, and inadequate cerebral perfusion.
• Modern methods of drug treatment have minimized the importance of bloodletting and the application of venous tourniquets to the extremities, however, if adequate drug therapy is impossible, these methods of hemodynamic unloading not only can, but should be used, especially with rapidly progressing pulmonary edema (bloodletting in a volume of 300- 500 ml).
• In case of acute congestive left ventricular failure combined with cardiogenic shock, or with a decrease in blood pressure during therapy that did not give positive effect, non-glycoside inotropic agents are additionally prescribed - intravenous drip administration of dobutamine (5-15 mcg/kg/min), dopamine (5-25 mcg/kg/min), norepinephrine (0.5-16 mcg/min) or a combination thereof.
• A means of combating foaming during pulmonary edema are “defoamers” - substances that ensure the destruction of foam by reducing surface tension. The simplest of these means is alcohol vapor, which is poured into a humidifier, passing oxygen through it, supplied to the patient through a nasal catheter or breathing mask at an initial rate of 2-3 l/min, and after a few minutes - at a rate of 6-8 l/min.
• Persistent signs of pulmonary edema with stabilization of hemodynamics may indicate an increase in membrane permeability, which requires the administration of glucocorticoids to reduce permeability (4-12 mg of dexamethasone).
• In the absence of contraindications, in order to correct microcirculatory disorders, especially with long-term intractable pulmonary edema, the administration of sodium heparin is indicated - 5 thousand IU intravenously as a bolus, then drip at a rate of 800 - 1000 IU/hour.

• Treatment of cardiogenic shock involves increasing cardiac output, which is achieved by different ways, the significance of which varies depending on the clinical type of shock.

• In the absence of signs of congestive heart failure (shortness of breath, moist rales in the posterior lower parts of the lungs), the patient must be placed in a horizontal position.
• Regardless of the clinical picture, it is necessary to provide complete analgesia.
• Stopping rhythm disturbances is the most important event to normalize cardiac output, even if adequate hemodynamics are not observed after restoration of normosystole. Bradycardia, which may indicate increased vagal tone, requires immediate intravenous administration 0.3-1 ml of 0.1% atropine solution.
• If the clinical picture of shock is extensive and there are no signs of congestive heart failure, therapy should begin with the administration of plasma expanders in a total dose of up to 400 ml under the control of blood pressure, heart rate, respiratory rate and auscultation of the lungs. If there is an indication that immediately before the onset of acute cardiac damage with the development of shock, there were large losses of fluid and electrolytes (long-term use of large doses of diuretics, uncontrollable vomiting, profuse diarrhea, etc.), then an isotonic solution is used to combat hypovolemia sodium chloride; the drug is administered in an amount of up to 200 ml over 10 minutes, repeated administration is also indicated.
• The combination of cardiogenic shock with congestive heart failure or the lack of effect from the entire complex of therapeutic measures is an indication for the use of inotropic agents from the group of pressor amines, which, in order to avoid local circulatory disorders accompanied by the development of tissue necrosis, should be injected into the central vein:
  • dopamine at a dose of up to 2.5 mg affects only dopamine receptors of the renal arteries; at a dose of 2.5-5 mcg/kg/min, the drug has a vasodilating effect; at a dose of 5-15 mcg/kg/min, it has a vasodilating and positive inotropic (and chronotropic) effects, and at a dose of 15-25 mcg/kg/min - positive inotropic (and chronotropic), as well as peripheral vasoconstrictive effects; 400 mg of the drug is dissolved in 400 ml of a 5% glucose solution, while 1 ml of the resulting mixture contains 0.5 mg, and 1 drop - 25 mcg of dopamine. The initial dose is 3-5 mcg/kg/min with a gradual increase in the rate of administration until the effect is achieved, the maximum dose (25 mcg/kg/min, although the literature describes cases where the dose was up to 50 mcg/kg/min) or the development of complications (most often sinus tachycardia exceeding 140 beats per minute, or ventricular arrhythmias). Contraindications to its use are thyrotoxicosis, pheochromocytoma, cardiac arrhythmias, hypersensitivity to disulfide, previous use of MAO inhibitors; if the patient was taking tricyclic antidepressants before prescribing the drug, the dose should be reduced;
  • the lack of effect from dopamine or the inability to use it due to tachycardia, arrhythmia or hypersensitivity is an indication for the addition or monotherapy with dobutamine, which, unlike dopamine, has a more pronounced vasodilatory effect and a less pronounced ability to cause an increase in heart rate and arrhythmia. 250 mg of the drug is diluted in 500 ml of a 5% glucose solution (1 ml of the mixture contains 0.5 mg, and 1 drop - 25 mcg of dobutamine); in monotherapy, it is prescribed at a dose of 2.5 mcg/kg/min, increasing every 15-30 minutes by 2.5 mcg/kg/min until the effect is achieved, side effect or achieving a dose of 15 mcg/kg/min, and when combining dobutamine with dopamine - in the maximum tolerated doses; Contraindications to its use are idiopathic hypertrophic subaortic stenosis and stenosis of the aortic mouth. Dobutamine is not prescribed for systolic blood pressure< 70 мм рт. ст.
  • in the absence of effect from the administration of dopamine and/or a decrease in systolic blood pressure to 60 mm Hg. Art. norepinephrine can be used with a gradual increase in dosage ( maximum dose- 16 mcg/min). Contraindications to its use are thyrotoxicosis, pheochromocytoma, previous use of MAO inhibitors; If you have previously taken tricyclic antidepressants, the dose should be reduced.
• If there are signs of congestive heart failure and in the case of using inotropic drugs from the group of pressor amines, the administration of peripheral vasodilators - nitrates (nitroglycerin or isosorbide dinitrate at a rate of 5-200 mcg/min) is indicated.
• In the absence of contraindications, in order to correct microcirculatory disorders, especially with long-term intractable shock, heparin is indicated - 5 thousand IU intravenously as a bolus, then drip at a rate of 800 - 1 thousand IU/hour.
• If there is no effect from adequately administered therapy, the use of intra-aortic balloon counterpulsation is indicated, the purpose of which is to achieve temporary stabilization of hemodynamics before the possibility of more radical intervention (intra-coronary balloon angioplasty, etc.) arises.

Indications for hospitalization

After relief of hemodynamic disturbances, all patients with acute heart failure are subject to hospitalization in cardiac intensive care units. In the torpid course of AHF, hospitalization is carried out by specialized cardiology or resuscitation teams. Patients with cardiogenic shock should, whenever possible, be hospitalized in hospitals where there is a cardiac surgery department.

A. L. Vertkin, Doctor of Medical Sciences, Professor
V. V. Gorodetsky, Candidate of Medical Sciences
O. B. Talibov, Candidate of Medical Sciences

1 The clinical picture of cardiogenic shock can develop with a hypovolemic type of hemodynamics: against the background of active diuretic therapy preceding a heart attack, profuse diarrhea, etc.

Heart failure is not a separate disease, but a complex of dangerous symptoms associated with disruption of the heart and blood supply to all organs and tissues.

Depending on the rate of development of the condition, chronic and acute heart failure are distinguished. The acute form progresses faster, has more severe symptoms and is considered more life-threatening. Most often it develops against the background of an existing disease.

Acute heart failure is one of the most common causes of death in cardiovascular diseases. Very often it develops against the background of another disease and is accompanied by acute clinical manifestations. In the absence of qualified medical care, this condition quickly leads to death.

The classification of acute heart failure is based not only on symptoms, but also on the location of the lesion, the speed and mechanism of development.

The most common causes of AHF are the following diseases and conditions:

• . During a heart attack, the blood supply to the myocardium is disrupted, as a result of which the tissue begins to partially die. The most common cause of heart attack is thrombosis. A common consequence of a heart attack is heart failure. Due to myocardial necrosis, the heart cannot sufficiently perform its functions.
• Myocarditis. This is inflammation of the myocardium, which, if left untreated, can also lead to AHF. In acute and severe myocarditis, heart failure develops quickly, which can lead to the death of the patient.
• Trauma and heart surgery. In some cases, surgery and serious chest injuries can lead to the development of acute heart failure.
• Hypertonic disease. Severe hypertension can lead to hypertensive crisis, a condition that is accompanied by a sharp and strong jump in blood pressure. This condition is considered life-threatening and can lead to tissue damage to the heart and brain, severe AHF, and death.
• Pulmonary embolism. In this disease, blood clots block the pulmonary artery, which leads to a sharp increase in arterial and venous pressure and acute heart failure.
• It is worth remembering that AHF can also be caused by a non-cardiac disease, for example, a pulmonary infection, brain injury, or stroke.

The symptoms of AHF differ depending on which ventricle is affected. The most common symptoms are shortness of breath and dry cough, swelling, bluish skin, wheezing in the chest, and foam at the mouth. AHF develops very quickly, so when the first signs appear, it is necessary to take the patient to the hospital as quickly as possible.

Types of OSN

There are several classifications of OSN. This condition can have different stages and clinical manifestations, so several different classifications are often used to characterize it.

Depending on the criterion (etiology, flow rate, primary lesion, etc.), the following classifications of acute heart failure are distinguished:

1. By origin. There are myocardial, overload and mixed heart failure depending on the cause that led to this condition. Myocardial heart failure occurs when the heart muscle is damaged, overload - when there is a heavy load on the heart, mixed - when myocardial damage and overload are combined.
2. According to the speed of development. Acute heart failure always occurs quickly, which is where its danger lies. The duration of symptoms development ranges from a couple of minutes to 2-3 hours. If heart failure proceeds slowly, developing over months or years, it is classified as a chronic form of the disease.
3. According to the mechanism of development. There are primary and secondary OSN. The primary type is also called cardiogenic, it develops as a result of disruption of the heart, a decrease in its contractile function, most often develops simultaneously with coronary heart disease and leads to myocardial infarction. Secondary, or non-cardiogenic, heart failure develops as a result of impaired blood flow to the heart muscle, observed with collapse or extensive blood loss.
4. According to the affected part of the heart. There are left ventricular and right ventricular heart failure. They differ symptomatically. Left ventricular AHF is caused by dysfunction of the left ventricle and often occurs during myocardial infarction, accompanied by shortness of breath or suffocation, cough, and arrhythmia. Right ventricular AHF occurs when the right ventricle of the heart is overloaded and is accompanied by cyanosis of the skin, swelling of the jugular veins, and a thread-like pulse.

Only a doctor can diagnose heart failure. It is necessary to diagnose and classify AHF as soon as possible after the onset of symptoms. Help for AHF should be provided to the patient within an hour.

Classification according to Killip and clinical severity

The Killip classification is based on the severity of AHF. There are several stages on this scale, which allows you to make a forecast.

The Killip scale is most often used in acute heart failure secondary to myocardial infarction, but can also be used in other forms of AHF.

According to the Killip classification, there are 4 stages of acute heart failure:

• Stage 1. This stage is asymptomatic. At acute form The disease does not last long, since the speed of development of the disease is high and the first signs begin to appear quite quickly.
• Stage 2. At the second stage, pulmonary circulation disturbances are observed, that is, wheezing appears in the chest, which is clearly audible, and shortness of breath. But at this stage, the symptoms of the disease are still weakly expressed, so AHF can easily be confused with another disease.
• Stage 3. Pulmonary wheezing is heard more clearly, shortness of breath becomes stronger. Moist rales are present in more than half of the lung fields, and pulmonary edema begins.
• Stage 4. At the last stage, cardiogenic shock occurs, when an extreme degree of left ventricular failure is observed, the functioning of not only the heart, but also other organs is disrupted, the vessels narrow, the blood vessels fall, and the excretory function of the kidneys worsens.

To clarify the stage, not only the clinical picture is often used, but also radiographic data. The prognosis largely depends on the stage of the disease, age and individual characteristics of the patient.

According to studies, the majority of patients who applied for medical care with stages 2,3,4 of the disease, were elderly and had a history of diabetes mellitus.

There is another classification, which is based on the development of symptoms of AHF. This is a classification according to Vasilenko, Strazhesko, Lang. There are 3 stages of the disease: the first, initial or hidden, the second pronounced and the third dystrophic.

At the first stage, only mild shortness of breath and rapid heartbeat appear. In the second stage, shortness of breath becomes stronger and is observed even at rest. At the third stage, irreversible changes begin in the internal organs due to circulatory problems.

Consequences and prevention of AHF

Since AHF occurs at lightning speed, the most dangerous consequence is a fatal outcome that can occur within a few hours or within a few minutes. A prognosis can be given only after resuscitation measures have been provided.

Heart failure itself is already a complication of many heart diseases. In severe form, AHF leads to cardiogenic shock, pulmonary edema and death. The prognosis is almost always unfavorable. About 50% of all cases of AHF lead to sudden death. About 17% of all hospitalized patients with AHF die within a year.

This condition is difficult to treat because the consequences are often irreversible. Therefore, doctors recommend not to neglect preventive measures:

1. Regular examination. Twice a year you need to undergo a preventive examination, donate blood, check the condition of the heart and blood vessels, monitor cholesterol levels and blood pressure.
2. Rejection of bad habits. Alcohol and smoking negatively affect the condition of the heart and blood vessels. Bad habits can lead to a number of diseases, so it is advisable to limit them or eliminate them altogether.
3. Proper nutrition. The diet should be balanced and contain enough protein and vitamins to maintain normal heart function. It is also important to monitor the level. If it is consistently elevated, you need to stop eating fatty meat.
4. Moderate physical exercise. The development of heart failure is influenced not only by physical inactivity, but also excess weight. It is necessary to move enough, but not to overload. It is recommended to constantly include cardio training in your daily routine, appropriate for your age and health status.
5. Lack of emotional overload. It is advisable to avoid stress and long-term depression.

More information about heart failure can be found in the video:

If you follow the rules of prevention, the likelihood of developing cardiovascular diseases decreases. It is especially important to pay attention preventive measures those people who have a hereditary predisposition to acute heart failure and other heart diseases.

Patients with acute heart failure may have one of the following: clinical conditions:

Acute decompensation of heart failure (first-time heart failure or decompensation of CHF) with clinical manifestations of AHF that are moderate and are not signs of CABG, OA or hypertensive crisis,

Hypertensive heart failure - signs and symptoms of heart failure are accompanied by high blood pressure and relatively preserved LV function with radiological signs of acute OA,

Pulmonary edema (confirmed by X-ray), accompanied by severe pulmonary distress syndrome, with the appearance of wheezing in the lungs and orthopnea, oxygen saturation (Sa02 less than 90%) in air before the course,

Cardiogenic shock is a sign of impaired tissue perfusion (SBP less than 90 mm Hg, low diuresis less than 0.5 ml/kg h, pulse rate more than 60 beats/min) caused by HF after preload correction with or without signs of congestion in vital signs. organs;

Heart failure due to high cardiac output, usually with high heart rate (due to arrhythmias, thyrotoxicosis, anemia), with warm peripheral areas, pulmonary congestion and sometimes low blood pressure (as in septic shock).

Killip's classification is used mainly to determine the clinical severity of myocardial damage due to myocardial infarction: K I - there are no clinical signs of HF or cardiac decompensation; By II - there is HF (moist rales mainly in the lower pulmonary fields, gallop rhythm, the presence of pulmonary venous hypertension); KIII - severe HF (true AH with moist rales throughout all lung fields); KIV - cardiogenic shock (SBP less than 90 mm Hg and signs of peripheral vasoconstriction - oliguria, cyanosis, sweating).

Categories: Family Medicine/Therapy. Emergency Medicine

print version

A patient with acute heart failure may have one of the following conditions:

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

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

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

IV. Cardiogenic shock is insufficient perfusion of vital organs and tissues caused by a decrease in the pumping function of the heart after correction of preload. Regarding hemodynamic parameters, there are currently no clear definitions of this condition, which reflects the discrepancy in the prevalence and clinical outcomes of this condition. However, cardiogenic shock is usually characterized by decreased blood pressure (SBP 30 mm Hg) and/or low urine output, regardless of the presence of organ congestion. Cardiogenic shock is an extreme manifestation of small output syndrome.

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

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

The Killip classification is based on clinical symptoms and chest x-ray findings. The classification is used primarily for heart failure due to myocardial infarction, but may be used for de novo heart failure.

Classification by clinical severity

Classification of clinical severity is based on assessment of peripheral circulation (tissue perfusion) and pulmonary auscultation (pulmonary congestion). Patients are divided into the following groups:

Class I (Group A) (warm and dry);

Class II (Group B) (warm and humid);

class III (group L) (cold and dry);

Class IV (Group C) (cold and wet).

Classification of chronic heart failure

Clinical stages:I; IIA; IIB; III

CH I, CH IIA; SN IIB; HF III meets the criteria of stages I, IIA, IIB and III chronic failure blood circulation according to N.D. classification Strazhesko and V.Kh. Vasilenko (1935):

I - initial circulatory failure; manifests itself only during physical activity (shortness of breath, tachycardia, fatigue); at rest, hemodynamics and organ functions are not impaired.

II - severe long-term circulatory failure; hemodynamic disturbances (stagnation in the pulmonary and systemic circulation, etc.), dysfunction of organs and metabolism, manifested at rest; period A - the beginning of the stage, hemodynamic disturbances are moderate; note a dysfunction of the heart or only some of its parts; period B - the end of a long stage: profound hemodynamic disturbances, the whole the cardiovascular system.

III - final, dystrophic circulatory failure; severe hemodynamic disturbances, persistent changes in metabolism and organ functions, irreversible changes in the structure of tissues and organs.

CH options:

With LV systolic dysfunction: LVEF Ј 45%;

With preserved LV systolic function: LVEF > 45%.

Functional class (FC) of patients according to NYHA criteria:

FC I - patients with heart disease in whom normal physical activity does not cause shortness of breath, fatigue or palpitations.

FC II - patients with heart disease and moderate limitation of physical activity. Shortness of breath, fatigue, and palpitations are noted when performing normal physical activities.

III FC - patients with heart disease and severe limitation of physical activity. At rest there are no complaints, but even with minor physical exertion shortness of breath, fatigue, and palpitations occur.

IV FC - patients with heart disease in whom any level of physical activity causes the above subjective symptoms. The latter also occur in a state of rest.

The term “Patient FC” is an official term that indicates the patient’s ability to perform household physical activity. To determine FC from I to IV in patients, the current classification uses the NYHA criteria, verified using the method of determining maximum oxygen consumption.

Degrees of acute heart failure. Stevenson's classification of acute heart failure

Classification. which is contained in the guidelines, allocates patients based on clinical presentation. According to the works of Cotter G. Gheorghiade M. et al. The European Society of Cardiology (ESC) guidelines for the diagnosis and treatment of AHF present 6 groups of patients with typical clinical and hemodynamic characteristics. The first three groups of patients (with ADHF, hypertensive AHF and AHF with pulmonary edema) account for > 90% of cases of AHF.

Patients with ADHF usually have moderate or mild signs and symptoms of congestion and usually do not exhibit signs of other groups. Patients with hypertensive AHF are characterized by relatively preserved LV systolic function, clearly elevated blood pressure, symptoms and manifestations acute edema lungs. In the third group of patients (with AHF and pulmonary edema), a clinical picture is observed, which is dominated by severe respiratory disorders: shortness of breath, signs of pulmonary edema (PE) (confirmed by an objective examination and chest x-ray) and hypoxemia (O2 saturation when breathing room air up to treatment usually

Low cardiac output syndrome in patients with AHF is determined by signs of tissue hypoperfusion, despite adequate preload, and is a condition widely ranged in severity (from low CO syndrome to severe cardiogenic shock). The dominant factor in these cases is the degree of global hypoperfusion and the risk of target organ damage against the background of reduced CO. AHF with high CO remains a rare case of HF, usually characterized by warm extremities, pulmonary congestion, and (sometimes) low BP, as in sepsis, in the setting of elevated CO and high heart rate. Underlying conditions may include cardiac arrhythmias, anemia, thyrotoxicosis and Paget's disease.

Right ventricular AHF is diagnosed more often for two reasons: patients with chronic obstructive pulmonary disease (COPD) develop cor pulmonale; widespread prevalence of pulmonary hypertension. Patients experience increased jugular venous pressure, signs of right ventricular congestion (manifested by hepatomegaly, edema) and signs of low CO syndrome with hypotension. This classification serves as a basis for the development of specific therapeutic strategies as well as future research.

Another clinically relevant and widely used classification was developed by Stevenson et al. This classification allows patients to be assessed using clinical symptoms indicating the presence of hypoperfusion (cold) or the absence of hypoperfusion (warm), the presence of congestion at rest (wet) or the absence of congestion at rest (dry). In one study, patients with clinical profile A (warm and dry) had a 6-month mortality rate of 11%, and those with clinical profile C (cold and wet) had a 40% mortality rate. It follows that clinical profiles A and C may play a prognostic role. These profiles are also used when choosing therapy, which will be discussed further.

heal-cardio.ru

Classification of acute heart failure - severity of the disease

Acute heart failure, AHF, is a polyetiological syndrome in which profound disturbances in the pumping function of the heart occur.

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

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

Main types

In cardiology, several methods are used to classify the manifestations of acute cardiovascular vascular insufficiency. Based on the type of hemodynamic disturbance, a distinction is made between congestive and hypokinetic acute heart failure (cardiogenic shock).

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

Left ventricular

With lesions of the left ventricle, stagnation occurs in the pulmonary circulation. The pressure in the pulmonary artery system increases, and as pressure increases, the pulmonary arterioles narrow. External breathing and oxygen saturation of the blood are difficult.

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

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

In the lying position, shortness of breath intensifies, the patient tries to sit (orthopnea). On early stages In the lower parts of the lungs, moist rales are heard, turning into fine rales.

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

The patient is tormented by a dry cough; as the pathological condition progresses, scanty sputum is released, turning into foamy sputum. The sputum may be pink in color.

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

Blood pressure levels remain within normal limits or decrease. The left ventricular form develops as a complication coronary disease heart disease, myocardial infarction, aortic disease, arterial hypertension.

Right ventricular

Acute right ventricular failure develops with pneumothorax, decompression sickness, embolism of the trunk or branches of the pulmonary artery, and total pneumonia. When the functions of the right ventricle are impaired, stagnation occurs in the systemic circulation. The patient develops shortness of breath, and upon inhalation, swelling of the jugular veins is noticeable.

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

Profuse cold sweat appears, acrocyanosis and peripheral edema appear.

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

In some patients, the functioning of the stomach is disrupted - congestive gastritis develops. Blood pressure drops sharply until cardiogenic shock develops. In response to the progressive lack of oxygen in the tissues, the respiratory rate and heart rate increase.

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

Killip classes

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

• I – signs of heart failure do not appear;
• II – in the lower parts of the pulmonary fields, moist rales are heard, signs of pulmonary circulation disorders appear;
• III – moist rales are heard in more than half of the lung fields, severe pulmonary edema;
• IV – cardiogenic shock, signs of peripheral vasoconstriction, cyanosis appear, systolic blood pressure is reduced to 90 mm Hg. Art. and below, sweat appears, the excretory function of the kidneys is impaired.

The Killip classification of acute heart failure is designed to assess the patient's condition during myocardial infarction, but can be used in cases of pathological conditions arising for other reasons.

According to 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 pulmonary circulation. According to these criteria, four classes of severity of the condition are distinguished:

• I – congestion is not detected, peripheral blood circulation is normal. The skin is dry and warm.
• II – symptoms of blood stagnation in the pulmonary circle are detected, visible signs violations venous outflow No. The skin is warm and moist.
• III – failure of peripheral circulation is determined without concomitant disturbance of venous outflow in the pulmonary circle. The skin is dry and cold.
• IV – signs of peripheral circulatory failure are accompanied by congestion in the lungs.

There are several possible clinical options for the course of the pathology:

• Decompensated, develops as a complication of a chronic form of pathology or for other reasons. The patient's symptoms and complaints correspond to the typical clinical picture of moderate AHF.
• Hypertensive heart failure. Blood pressure is highly 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 for AHF.
• Pulmonary edema. It manifests itself as 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 fluid accumulation in the lungs.
• Cardiogenic shock. An extreme manifestation of low cardiac output syndrome. Systolic blood pressure drops to critical values, the blood supply to tissues and organs is severely impaired. The patient exhibits symptoms of progressive renal dysfunction.
• Increased cardiac output syndrome. Accompanied by manifestations of blood stagnation in the pulmonary circulation. The patient's extremities are warm, and blood pressure may decrease.
• Right ventricular. Cardiac output is reduced, arterial pressure is increased. The pressure in the jugular veins increases, congestion in the portal system of the liver leads to the development of hepatomegaly.

Any possible classification is, to one degree or another, conditional and is intended to simplify diagnosis and choice of treatment tactics in emergency situations.

Learn more about heart failure in this video:

No comments yet

oserdce.com

Acute heart failure: types, symptoms, emergency care:

Acute heart failure in children and adults is often one of the syndromes of many diseases. These may be myocarditis, ischemic heart disease, cardiosclerosis, hypertension and other ailments. Thus, acute circulatory disorders are caused by all those reasons that lead to the loss of the ability of the heart muscle to contract. As a rule, only the left or right ventricle is affected, and not both at once. The latter is more often affected in childhood.

Right ventricular acute heart failure: etiology

Its cause may be bronchial asthma, blockage of the pulmonary artery by an embolus or its narrowing, or pneumonia. It can also occur with the rapid transfusion of a large volume of liquid, for example, a glucose solution. The vessels of the pulmonary circulation sharply contract due to a sudden increase in the load on the right ventricle. Its contractility decreases and stagnation develops in those vessels through which blood flows to the corresponding half of the heart.

Right ventricular acute heart failure: symptoms

The patient experiences shortness of breath, blood pressure constantly decreases, and venous pressure increases sharply. There is expansion of the heart to the right side, cyanosis, and tachycardia.
Superficial veins swell due to blood overflow, the liver enlarges, and the legs swell.

Right ventricular acute heart failure: help

Drugs are prescribed that are aimed at eliminating arrhythmia, spasm, and also toning the work of the heart muscle. In this case, blood transfusions or other fluids are contraindicated. The fact is that additional filling of the vascular bed will only complicate the activity of the heart muscle.

Left ventricular acute heart failure: etiology

It may be caused by hypertension or aortic defects. Blood flows to the left ventricle from the corresponding atrium and pulmonary veins. His muscle is not able to pump it. As a result, this blood stagnates in the vessels of the pulmonary circulation and pressure increases. It rises due to overflow in the left half of the heart. At this time, the functional right ventricular muscle continues to actively redirect blood to the pulmonary circulation for some time. At the same time, the pressure in it increases even more. The result of the ongoing process is cardiac asthma, which often develops into pulmonary edema.

Left ventricular acute heart failure: symptoms

Attacks of dizziness, loss of consciousness, severe shortness of breath that occurs even in a lying position. Since the blood in the pulmonary circulation is very stagnant, the plasma sweats into the alveoli. As a result, hemoptysis begins. The fact that a severe attack has progressed to pulmonary edema is indicated by increased shortness of breath, the appearance of foamy sputum in the large quantities, rapid weak pulse, decreased diuresis, drop in blood pressure.

Left ventricular acute heart failure: help

The main goal of the measures taken is to increase the ability of the heart muscle to contract, increase the stroke volume of the organ, increase diuresis and dilate the pulmonary vessels. In addition to administering drugs, breathing is monitored during hypoxia, and exudate is sucked out of the respiratory tract. Vasoconstrictors are contraindicated.

www.syl.ru

Acute heart failure - symptoms, treatment, causes and signs

Acute heart failure (AHF) is a condition that occurs as a result of a sharp weakening of the contractile function of the heart muscle, accompanied by stagnant processes in the pulmonary and systemic circulation, as well as disruption of intracardiac dynamics. Acute heart failure leads to extremely severe complications due to dysfunction internal organs due to the inability of the myocardium to provide the necessary blood supply.

The condition can arise as an exacerbation of chronic heart failure or appear spontaneously in individuals without a history of cardiac dysfunction. Acute heart failure ranks first among the causes of hospitalization and mortality in many countries of the world.

Causes of acute heart failure and risk factors

The causes contributing to the occurrence of acute heart failure are divided into three groups:

• those that lead to an increase in cardiac output;
• those that lead to a sharp and significant increase in preload;
• those that lead to a sharp and significant increase in afterload.

Among them are the most common causes of acute heart failure:

• aortic dissection;
• pulmonary embolism;
• heart defects (congenital and acquired);
• unstable angina;
• anemia;
• arrhythmias;
• hypertensive crisis;
• cardiac tamponade;
• complications of coronary heart disease (heart attack, acute coronary syndrome);
• tension pneumothorax;
• overhydration;
• exacerbation of chronic obstructive pulmonary disease;
• cardiomyopathy in women during pregnancy;
• heavy infectious diseases; and etc.

AHF can develop against the background of sepsis, thyrotoxicosis and other severe pathological conditions.

Acute heart failure of the left type (left ventricular) is formed in such pathologies when the load falls predominantly on the left ventricle: myocardial infarction, hypertonic disease, aortic heart disease.

Acute heart failure of the right type (right ventricular) can be caused by exudative pericarditis, stenosis of the pulmonary artery, or adhesive pericarditis.

Forms of the disease

Due to the variety of causes contributing to the occurrence of acute heart failure, it is classified depending on the predominant lesions of certain parts of the heart and the mechanisms of compensation/decompensation.

By type of hemodynamics:

1. Acute heart failure with congestive hemodynamics.
2. Acute heart failure with hypokinetic type of hemodynamics (cardiogenic shock, small output syndrome).

Stagnation, in turn, is divided into:

• acute heart failure of the left type (left ventricular or left atrial);
• acute heart failure of the right type (right ventricular or right atrial);
• total (mixed) acute heart failure.

Hypokinetic (cardiogenic shock) occurs the following types:

• true shock;
• reflex;
• arrhythmic.

According to the standards of the European Society of Cardiology (adopted in 2008), acute heart failure is divided into the following forms:

• exacerbation of chronic heart failure;
• pulmonary edema;
• cardiogenic shock;
• isolated right ventricular acute heart failure;
• acute heart failure in acute coronary syndrome;
• chronic heart failure with hypertension.

Stages

Classification by severity is based on assessment of peripheral circulation:

• class I (group A, “warm and dry”);
• class II (group B, “warm and humid”);
• class III (group L, “cold and dry”);
• class IV (group C, “cold and wet”).

Depending on the radiological signs and manifestations of acute heart failure (Killip classification), the following are distinguished:

• class I – without manifestations of signs of heart failure;
• class II - moist rales in the lower parts of the lungs, symptoms of pulmonary circulation disorders;
• class III - moist rales in the lungs, pronounced signs of pulmonary edema;
• class IV – cardiogenic shock, peripheral vasoconstriction, impaired renal excretory function, hypotension.

The Killipp classification was developed to assess the condition of patients with acute heart failure that developed against the background of myocardial infarction, but can also be used for other types of pathology.

Symptoms of acute heart failure

In acute heart failure, patients complain of weakness and confusion. There is pallor of the skin, the skin is moist and cold to the touch, there is a decrease in blood pressure, a decrease in the amount of urine excreted (oliguria), and a thread-like pulse. Symptoms of the underlying disease against which AHF developed may appear.

In addition, acute heart failure is characterized by:

• peripheral edema;
• pain in the epigastric region on palpation;
• dyspnea;
• wet rales.

Acute left ventricular failure

Manifestations of left-type AHF are alveolar and interstitial pulmonary edema (cardiac asthma). Interstitial pulmonary edema develops more often against the background of physical and/or nervous tension, but can also manifest itself during sleep in the form of sudden suffocation, provoking a sudden awakening. During an attack, there is a lack of air, a hacking cough with characteristic shortness of breath, general weakness, and pale skin. Due to a sharp increase in shortness of breath, the patient takes a forced position, sitting with his legs down. Breathing is harsh, pulse is arrhythmic (gallop rhythm), weak filling.

With the progression of congestion in the pulmonary circulation, pulmonary edema develops - acute pulmonary failure, which is caused by significant sweating of transudate into the lung tissue. Clinically, this is expressed by suffocation, cough with the release of copious amounts of foamy sputum mixed with blood, moist rales, facial cyanosis, nausea, and vomiting. The pulse is thready, blood pressure decreases. Pulmonary edema refers to emergency conditions requiring immediate intensive care due to the high probability of death.

Acute left ventricular failure may manifest as syncope caused by cerebral hypoxia due to asystole or decreased cardiac output.

Acute right ventricular failure

Acute heart failure of the right type develops against the background of pulmonary embolism. Congestion in the systemic circulation is manifested by shortness of breath, cyanosis of the skin, edema lower limbs, intense pain in the heart and right hypochondrium. Blood pressure decreases, pulse is frequent, filling is weak. There is an enlargement of the liver, as well as (less commonly) the spleen.

Signs of acute heart failure due to myocardial infarction range from mild pulmonary congestion to a sharp decrease in cardiac output and manifestations of cardiogenic shock.

Diagnostics

To make a diagnosis of AHF, complaints and medical history are collected, during which the presence of diseases against which the pathology developed is clarified, paying special attention to the medications taken. Then carry out:

• objective examination;
• auscultation of the heart and lungs;
• electrocardiography;
• echocardiography;
• stress tests based on electrocardiography (treadmill test, bicycle ergometry);
• X-ray examination of the chest organs;
• magnetic resonance imaging of the heart;
• general analysis blood;
• biochemical blood test (levels of glucose, electrolytes, creatinine, urea, liver transaminases, etc.);
• determination of blood gas composition.

If necessary, coronary angiography is performed; in some cases, endomyocardial biopsy may be required.

Ultrasound is performed to determine damage to internal organs abdominal cavity.

With the aim of differential diagnosis shortness of breath in acute heart failure and shortness of breath due to non-cardiac causes, natriuretic peptides are determined.

Treatment of acute heart failure

Patients with AHF must be admitted to a cardiac intensive care unit or intensive care unit.

The prehospital emergency care scheme for patients with left-type acute heart failure includes:

• relief of attacks of so-called respiratory panic (if necessary, with the help of narcotic analgesics);
• inotropic stimulation of the heart;
• oxygen therapy;
• artificial ventilation;
• reduction of pre- and afterload on the heart;
• decrease in pressure in the pulmonary artery system.

Urgent measures for stopping an attack of acute right ventricular failure include:

• elimination of the main cause against which it arose pathological condition;
• normalization of blood supply to the pulmonary vascular bed;
• eliminating or reducing the severity of hypoxia.

Treatment of acute heart failure in the cardiac intensive care unit is carried out under invasive or non-invasive continuous monitoring:

• invasive - catheterization of a peripheral artery or central vein is performed (according to indications), with the help of a catheter, blood pressure and venous blood saturation are monitored, and injections are also administered medications;
• non-invasive – blood pressure, body temperature, number of respiratory movements and heartbeats, urine volume are monitored, and an ECG is performed.

Treatment of acute heart failure in the cardiac intensive care unit is aimed at minimizing cardiac dysfunction, improving blood counts, optimizing blood supply to tissues and organs, and saturating the body with oxygen.

To relieve vascular insufficiency, fluid administration is used under the control of diuresis. When cardiogenic shock develops, vasopressor drugs are used. For pulmonary edema, diuretics, oxygen inhalations, and cardiotonic medications are indicated.

Until the patient recovers from a critical condition, parenteral nutrition is indicated.

When transferred from the intensive care unit, the patient is rehabilitated. At this stage of treatment, the need for surgical interventions is determined.

The treatment regimen for acute heart failure is selected depending on etiological factors, forms of the disease and the patient’s condition and is carried out through oxygen therapy, as well as taking medications from the following main groups:

• loop diuretics;
• vasodilators;
• inotropic drugs; and etc.

Drug therapy is supplemented by prescription vitamin complexes, patients are also prescribed a diet.

If acute heart failure has developed against the background of heart defects, cardiac aneurysm and some other diseases, the issue of surgical treatment.

After discharge from the hospital, physical rehabilitation of the patient continues, and further monitoring of his health status is carried out.

Possible complications and consequences

Acute heart failure is dangerous precisely because of the high risk of developing life-threatening conditions:

• cardiogenic shock;
• pulmonary edema;
• atrial fibrillation;
• atrioventricular block;
• thromboembolism.

Forecast

With cardiogenic shock, the mortality rate reaches 80%.

The five-year survival rate for patients who have suffered acute heart failure is 50%.

The long-term prognosis depends on the presence of concomitant diseases, the severity of heart failure, the effectiveness of the treatment used, the general condition of the patient, his lifestyle, etc.

Timely adequate treatment of pathology in the early stages gives positive results and provides a favorable prognosis.

Prevention

In order to prevent the development, as well as to prevent the progression of acute heart failure that has already occurred, it is recommended to adhere to a number of measures:

Decompensated heart failure - what is it?

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

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

Stage I– no signs of heart failure.

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

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

IV stage– a sharp decrease 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 avulsion of the papillary muscle (in AMI) or avulsion of the mitral valve chord (in 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, or damage to the mitral valve due to infective endocarditis.
4. Aortic valve insufficiency due to rupture of the aortic valves, with dissecting aneurysm of the ascending aorta.
5. Acutely increased heart failure in patients suffering from chronic heart failure (acquired or congenital heart defects, cardiomyopathy, post-infarction or atherosclerotic cardiosclerosis); this may be due to hypertensive crisis, paroxysmal arrhythmia, fluid volume overload as a result of inadequate diuretic or excessive infusion therapy.

Etiology of acute right ventricular heart failure:

1. AMI of the right ventricle.
2. Pulmonary embolism (PE).
3. Stenotic 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 involving the right and left ventricles.
2. Rupture of the interventricular septum during AMI.
3. Paroxysmal tachycardia.
4. Acute severe myocarditis.

Pathogenesis. Basic development mechanisms:

• Primary myocardial damage, leading to a decrease in myocardial contractility (IHD, myocarditis).
• Left ventricular pressure overload ( arterial hypertension, aortic valve stenosis).
• Volume overload of the left ventricle (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, liver cirrhosis).

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. When the hydrostatic pressure in the pulmonary capillaries increases by more than 25 - 30 mm Hg. transudation of the liquid part of the blood occurs 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 liquid that enters the alveoli with each breath, which rises upward, 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 are formed. Foam not only disrupts the airway, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance and increases hypoxia and edema.

Clinical picture:

Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of lack of air and a dry cough. The patient is in a forced position of orthopnea. Cyanosis and pallor of the skin, cold sticky 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 with the release of foamy sputum appears Pink colour, “bubbling” in the chest, acrocyanosis, profuse sweating, tachypnea. There are various moist rales in the lungs. 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, tachypnea, acute enlargement of the liver, pain in the right hypochondrium, swelling of the jugular veins, peripheral and cavitary edema.

Acute biventricular heart failure: Symptoms of left and right ventricular failure appear simultaneously.