Acute heart failure

Acute heart failure is a symptomatic complex of rapidly developing systolic and / or diastolic heart function disorders. The main symptoms are:

• decreased cardiac output;
• insufficient perfusion of tissues;
• increased pressure in the capillaries of the lungs;
• stagnation in the tissues.

[1], [2], [3], [4], [5], [6], [7], [8]

What causes acute heart failure?

The main causes of the development of acute heart failure are: exacerbation of coronary heart disease (acute coronary syndrome, mechanical complications of myocardial infarction), hypertensive crisis, acute arrhythmia, decompensation of chronic heart failure, severe cardiac valve pathology, acute myocarditis, cardiac tamponade, aortic dissection, P.

Among non-cardiac causes of this pathology, volume overload, infection (pneumonia and septicemia), acute disorders of cerebral circulation, extensive surgical interventions, renal failure, bronchial asthma, drug overdose, alcohol abuse, pheochromocytoma are leading.

Clinical variants of acute heart failure

According to modern ideas on clinical and hemodynamic manifestations, acute heart failure is divided into the following types:

• Acute heart failure is decompensated (first arising or decompensated chronic heart failure).
• Hypertensive acute heart failure (clinical manifestations of acute heart failure in patients with a relatively preserved function of the left ventricle in combination with high blood pressure and a radiographic picture of venous stasis in the lungs or their edema).
• Pulmonary edema (confirmed by chest radiography) - severe respiratory distress with wet wheezing in the lungs, orthopnea and, as a rule, saturation of arterial blood with oxygen <90% when breathing room air before treatment.
• Cardiogenic shock is a clinical syndrome characterized by hypoperfusion of tissues due to heart failure, which persists after the correction of preload. Usually, there is arterial hypotension (SBP <90 mm Hg or a decrease in blood pressure> 30 mm Hg) and / or a decrease in the diuresis rate <0.5 ml / kg / h. Symptomatology can be associated with the presence of brady- or tachyarrhythmias, as well as a marked decrease in contractile dysfunction of the left ventricle (true cardiogenic shock).
• Acute heart failure with high cardiac output - usually in combination with tachycardia, warm skin and limbs, stagnation in the lungs and sometimes low blood pressure (an example of this kind of acute heart failure is septic shock).
• Acute right ventricular failure (low cardiac output syndrome in combination with increased pressure in the jugular veins, increased liver and arterial hypotension).

In view of clinical manifestations, acute heart failure is classified by clinical signs into left ventricular, right ventricular with low cardiac output, left or right ventricular failure with symptoms of blood stasis, and also by their combination (biventricular or total heart failure). Depending on the degree of development of disorders, compensated and decompensated circulatory insufficiency is also distinguished.

[9], [10], [11], [12],

Acute heart failure of neurogenic origin

Usually this type of heart failure develops in acute disorders of cerebral circulation. Damage to the central nervous system leads to a massive release of vasoactive hormones (catecholamines). Which causes a significant increase in pressure in the pulmonary capillaries. With sufficient duration of such a pressure jump, the fluid leaves the pulmonary capillaries. As a rule, acute damage to the nervous system is accompanied by a violation of the permeability of the capillary membrane. Intensive therapy in such cases should be directed, above all, to maintaining adequate gas exchange and reducing pressure in the pulmonary vessels.

[13]

Acute heart failure in patients with acquired heart defects

The course of acquired heart defects is often complicated by the development of acute circulatory disorders in a small circle - acute left ventricular failure. Especially characterized by the development of attacks of cardiac asthma with aortic stenosis.

Aortic heart defects are characterized by an increase in hydrostatic pressure in the small circle of the circulation and a significant increase in the final diastolic volume and pressure, as well as retrograde blood stasis.

Increase hydrostatic pressure in a small circle of more than 30 mm Hg. Art. Leads to active penetration of plasma into the alveoli of the lungs.

In the early stages of the development of stenosis of the aortic estuary, the main manifestation of left ventricular failure is attacks of excruciating cough at night. As the disease progresses, typical clinical signs of cardiac asthma occur, up to the developed pulmonary edema. Arterial opinion is usually increased. Often, patients complain of pain in the heart.

The occurrence of attacks of suffocation is typical for pronounced mitral stenoses without concomitant right ventricular failure. With this type of heart disease, there is an obstruction to blood flow at the level of the atrioventricular (atrioventricular) aperture. With its sharp narrowing, the blood can not be pumped from the left atrium into the left ventricle of the heart and partially remains in the cavity of the left atrium and a small circle of blood circulation. Emotional stress or physical activity leads to an increase in right ventricular performance against the background of a constant and reduced capacity of the left atrioventricular aperture. Increased pressure in the pulmonary artery in these patients with physical exertion leads to fluid exudation in the interstitial lungs and the development of cardiac asthma. Decompensation of the possibilities of the heart muscle leads to the development of alveolar pulmonary edema.

In a number of cases, the picture of acute left ventricular failure in patients with mitral stenosis may also be caused by the mechanical closure of the left atrioventricular orifice by a movable thrombus. In this case, pulmonary edema is accompanied by the disappearance of the arterial pulse against the background of a strong palpitation and the development of a pronounced pain syndrome in the heart. Against the background of increased dyspnea and a clinical picture of reflex collapse, development of loss of consciousness is possible.

If the left atrioventricular aperture is closed for a long time, a rapid lethal outcome is possible.

[14], [15], [16], [17], [18]

Acute congestive heart failure of another genesis

A number of pathological conditions is accompanied by the development of acute mitral insufficiency, the main manifestation of which is cardiac asthma.

Acute mitral insufficiency develops as a result of rupture of the tendon chords of the mitral valve in bacterial endocarditis, myocardial infarction, Marfan syndrome, myxome heart and other diseases. A ruptured chord of the mitral valve with the development of acute mitral insufficiency can occur in healthy people.

Practically healthy people with acute mitral insufficiency mostly complain about suffocation during exercise. Relatively rare, they have a detailed picture of pulmonary edema. In the atrial region, systolic tremor is determined. Auscultatory hears a loud scraping systolic noise in the atrial region, which is well conducted in the vessels of the neck.

The size of the heart, including the left atrium, is not increased in this category of patients. In the event that acute mitral insufficiency occurs against the background of severe cardiac muscle pathology, usually severe pulmonary edema difficult to medicate therapy is developed. A classic example of this is the development of acute left ventricular failure in patients with myocardial infarction with papillary muscle damage.

[19], [20], [21], [22], [23], [24], [25], [26], [27]

Total acute heart failure

Total (biventricular) heart failure often develops when blood circulation is decompensated in patients with heart defects. It is also observed in endotoxicosis, myocardial infarction, myocarditis, cardiomyopathy and acute poisoning with poisons with cardiotoxic action

With total heart failure, clinical symptoms are combined, typical for both left- and right-ventricular failure. Characterized by shortness of breath, cyanosis of the lips and skin.

Acute insufficiency of both ventricles is characterized by rapid development of tachycardia, hypotension, circulatory and hypoxic hypoxia. Cyanosis, swelling of peripheral veins, enlargement of the liver, sharp overestimation of central venous pressure are observed. Intensive therapy is carried out according to the above principles, with emphasis on the prevalent type of insufficiency.

Assessment of the severity of myocardial damage

The severity of heart damage with myocardial infarction is usually evaluated according to the following classifications:

The classification of Killip T. Is based on taking into account the clinical signs and results of chest X-ray. There are four stages of gravity.

• Stage I - no signs of heart failure.
• Stage II - there are signs of heart failure (wet wheezing in the lower half of pulmonary fields, III tone, signs of venous hypertension in the lungs).
• Stage III - severe heart failure (obvious pulmonary edema, wet wheezing spreads to more than the lower half of the pulmonary fields).
• Stage IV - cardiogenic shock (SBP 90 mm Hg with signs of peripheral vasoconstriction: oliguria, cyanosis, sweating).

Classification of Forrester JS is based on the consideration of clinical signs characterizing the severity of peripheral hypoperfusion, the presence of stagnation in the lungs, reduced NI <2.2 l / min / m2 and elevated DZLA> 18 mm Hg. Art. Isolate the norm (group I), pulmonary edema (group II), hypovolemic - cardiogenic shock (groups III and IV, respectively).

[28], [29], [30], [31]

How is acute heart failure treated?

It is generally accepted to begin intensive therapy of acute heart failure with measures aimed at reducing post-loading on the left ventricle. It is used to give the patient a sedentary or semi-sitting position, oxygen therapy, provision of venous access (if possible, central vein catheterization), administration of analgesics and neuroleptics, peripheral vasodilators, euphyllin, gangliablocators, diuretics, vasopressors in indications.

Monitoring

All patients with acute heart failure showed monitoring of heart rate, blood pressure, saturation, respiratory rate, body temperature, ECG and diuresis control.

Oxygen therapy and respiratory support

To ensure adequate oxygenation of tissues, prevention of lung dysfunction and development of multiple organ failure, all patients with acute heart failure are indicated with oxygen therapy and respiratory support.

Oxygen therapy

The use of oxygen with a reduced cardiac output can significantly improve tissue oxygenation. Enter oxygen with a nasal catheter at a rate of 4-8 l / min for the first two days. The catheter is guided through the lower nasal passage to the khoan. Oxygen is fed through a rotameter. The flow rate of 3 l / min provides an inhaled oxygen concentration of 27% by volume, with 4-6 l / min - 30-40% by volume.

Reduction of foaming

To reduce the surface tension of the fluid in the alveoli, oxygen inhalation with a defoamer (30-70% alcohol or 10% alcohol solution of antifosilane) is indicated. These drugs have the ability to reduce the surface tension of the liquid, which helps to eliminate the bubbles of plasma swirling into the alveoli and improves the transport of gases between the lungs and blood.

Non-invasive respiratory support (without intubation of the trachea) is accomplished by maintaining a positive positive airway pressure (CPAP). The introduction of the oxygen-air mixture into the lungs can be carried out through the face mask. Carrying out this type of respiratory support can increase the functional residual volume of the lungs, increase the elasticity of the lungs, reduce the degree of involvement of the diaphragm in the act of breathing, reduce the work of the respiratory muscles and reduce their need for oxygen.

Invasive respiratory support

In the case of acute respiratory failure (respiratory rate more than 40 per minute, severe tachycardia, hypertension to hypotension, a drop in PaO2 below 60 mmHg, and an increase in RACO2 above 60 mmHg), and also because of the need for protection respiratory tract from regurgitation in patients with cardiac pulmonary edema, there is a need for invasive respiratory support of IVL with intubation of the trachea).

Artificial ventilation of the lungs in this category of patients improves oxygenation of the body by normalizing the gas exchange, improves the ventilation / perfusion ratio, reduces the body's oxygen demand (since the work of the respiratory muscle ceases). With the development of pulmonary edema, it is effective to carry out artificial ventilation of the lungs with pure oxygen at an elevated end-expiratory pressure (10-15 cm W). After relief of the emergency condition, it is necessary to reduce the concentration of oxygen in the inhaled mixture.

Increased end-expiratory pressure (PEEP) is an established component of intensive therapy for acute left ventricular heart failure. Nevertheless, at present there is convincing evidence that high positive airway pressure or overdischarge of lungs leads to the development of pulmonary edema due to increased pressure in the capillaries and an increase in the permeability of the capillary membrane. The development of pulmonary edema, apparently, depends primarily on the magnitude of peak airway pressure and whether there are any previous changes in the lungs. Overexpansion of the lungs in itself can cause increased membrane permeability. Therefore maintenance of the raised positive pressure in respiratory ways at carrying out of respiratory support should be spent under the careful dynamic control of a condition of the patient.

Narcotic analgesics and antipsychotics

The introduction of narcotic analgesics and neuroleptics (morphine, promedol, droperidol), in addition to an anesthetic effect, causes venous and arterial dilatation, reduces the heart rate, has a sedative and euphoric effect. Morphine is administered fractionally intravenously at a dose of 2.5-5 mg until an effect or a total dose of 20 mg is achieved. Promedol is administered intravenously in a dose of 10-20 mg (0.5-1 ml of a 1% solution). To enhance the effect of intravenously administered droperidol in a dose of 1-3 ml of 0.25% solution.

Vasodilators

The most common method of correction of heart failure is the use of vasodilators to reduce the workload of the heart by reducing venous return (preload) or vascular resistance, to overcome which the heart pump (postload) works and the pharmacological stimulation to increase myocardial contractility (inotropic drugs of positive effect) .

Vasodilators - a means of choice for hypoperfusion, venous stasis in the lungs and a decrease in diuresis. Before the appointment of vasodilators with the help of infusion therapy, it is necessary to eliminate the existing hypovolemia.

Vasodilators are divided into three main subgroups, depending on the application points. The drugs with predominant venodilatory action (reducing preload) are distinguished, with predominantly arterio-damaging effect (reducing afterload) and having a balanced effect on systemic vascular resistance and venous return.

The drugs of the 1 st group include nitrates (the main representative of the group is nitroglycerin). They have a direct vasodilating effect. Nitrates can be taken under the tongue, in the form of an aerosol - a spray of nitroglycerin at 400 mcg (2 injections) every 5-10 minutes, or isosorbide dinitrate at 1.25 mg. The starting dose of nitroglycerin for intravenous administration in the development of acute left ventricular failure is 0.3 μg / kg / min with a gradual increase to 3 μg / kg / min until a clear effect on hemodynamics (or 20 μg / min with an increase in dose to 200 μg / min ).

Preparations of the 2-nd group - alpha-adrenergic blockers. They are rarely used in the treatment of pulmonary edema (phentolamine 1 ml 0.5% solution, tropafen 1 ml 1 or 2% solution, administered intravenously, intramuscularly or subcutaneously).

The drugs of the third group include sodium nitroprusside. It is a powerful balanced short-acting vasodilator, relaxing the smooth muscles of the veins and arterioles. Sodium nitroprusside serves as a means of choice in patients with severe hypertension against a background of low cardiac output. Before use, 50 mg of the drug is dissolved in 500 ml of 5% glucose (in 1 ml of this solution contains 6 μg of sodium nitroprusside).

The nitroprusside doses required to satisfactorily reduce the myocardial load in heart failure vary from 0.2 to 6.0 μg / kg / min or more, an average of 0.7 μg / kg / min.

Diuretics

Diuretics are an established component in the treatment of acute left ventricular failure. The most commonly used are high-speed drugs (lasix, ethacrynic acid).

Lasix is a short-acting loop diuretic. Oppresses the reabsorption of sodium and chlorine ions in the loop of Henle. With the development of pulmonary edema is administered intravenously in a dose of 40-160 mg. The introduction of a shock dose of lasix with subsequent infusion is more effective than repeated bolus administration.

Recommended doses are from 0.25 mg / kg of mass to 2 mg / kg of mass and higher if there is refractoriness. The introduction of Lasix causes a venodilating effect (after 5-10 minutes), rapid diuresis, reduces the volume of circulating blood. The maximum of their action is observed within 25-30 minutes after administration. Lasix is available in ampoules containing 10 mg of the drug. Similar effects can be achieved by intravenous administration of ethacrynic acid in a dose of 50-100 mg.

Diuretics in patients with acute coronary syndrome are used with great caution and in small doses, since they can cause massive diuresis, followed by a decrease in the volume of circulating blood, cardiac output, and the like. Refractory to ongoing therapy is overcome by combined therapy with other diuretics (torasemide, hydrochlorothiazide) or infusion of dopamine.

[32], [33], [34], [35], [36], [37], [38], [39]

Inotropic support

The need for inotropic support arises with the development of the syndrome of "small cardiac output". Most often used drugs such as chemistry, dobutamine, adrenaline.

Dopamine is administered intravenously drip at a rate of 1-3 to 5-15 μg / kg / min. Highly effective in acute heart failure refractory to the therapy with cardiac glycosides dobutamine in a dose of 5-10 μg / kg / min.

Levosimendan is a representative of a new class of drugs - calcium sensitizers. It has an inotropic and vasodilating action, which is fundamentally different from other inotropic drugs.

Levosimendan increases the sensitivity of the contractile proteins of cardiomyocytes to calcium without changing the concentration of intracellular calcium and cAMP. The drug opens potassium channels of smooth muscles, resulting in the expansion of veins and arteries (including coronary arteries).

Levosimendan is indicated in acute heart failure with low cardiac output in patients with left ventricular systolic dysfunction in the absence of severe arterial hypotension. It is administered intravenously at a loading dose of 12-24 μg / kg for 10 minutes followed by a prolonged shfusion at a rate of 0.05-0.1 μg / kg min.

Adrenaline is applied in the form of infusion at a rate of 0.05-0.5 mcg / kg / min with deep hypotension (BP <70 mm Hg) refractory to dobutamine.

Norepinephrine is administered intravenously drip in a dose of 0.2-1 μg / kg / min. For a more pronounced hemodynamic effect, norepinephrine is combined with dobutamine.

The use of inotropic drugs increases the risk of heart rhythm disturbances in the presence of electrolyte disorders (K + less than 1 mmol / l, Mg2 + less than 1 mmol / l).

Cardiac glycosides

Cardiac glycosides (digoxin, strophanthin, korglikon) are able to normalize myocardial oxygen demand in accordance with the volume of work and increase the tolerance of loads at the same energy inputs. Cardiac glycosides increase the amount of intracellular calcium, regardless of adrenergic mechanisms, and increase the contractile function of the myocardium in direct proportion to the degree of damage.

Digoxin (lanicore) is administered in a dose of 1-2 ml 0, O25% solution, strophantine 0.5-1 ml 0.05% solution, korglikon - 1 ml 0.06% solution.

In acute left ventricular failure, after a digitalization at a rapid pace, there is an increase in blood pressure. And its growth occurs mainly due to an increase in cardiac output with a slight (about 5%) increase in peripheral vascular resistance.

Indications for the use of cardiac glycosides are supraventricular tachyarrhythmia and atrial fibrillation, when the frequency of ventricular contractions can not be controlled by other drugs.

The use of cardiac glycosides for the treatment of acute heart failure with a preserved sinus rhythm is currently considered inappropriate.

[40], [41], [42], [43], [44], [45], [46], [47], [48]

Features of intensive therapy of acute heart failure with myocardial infarction

The main way to prevent the development of acute heart failure in patients with myocardial infarction is timely reperfusion. Preferred is percutaneous coronary intervention. If there is appropriate evidence in patients with cardiogenic shock, an emergency coronary bypass is justified. If these treatments are not available, then thrombolytic therapy is indicated. Urgent myocardial revascularization is also indicated in the presence of acute heart failure, which complicated acute coronary syndrome without the rise of the 5T segment of the electrocardiogram.

Adequate anesthesia and rapid elimination of cardiac arrhythmias leading to hemodynamic disturbances are extremely important. Achieving temporary stabilization of the patient's condition is accomplished by maintaining adequate filling of the heart chambers, drug inotropic support, intra-aortic counterpulsation and artificial ventilation.

[49], [50], [51], [52], [53], [54]

Intensive therapy of acute heart failure in patients with heart defects

When developing an attack of cardiac asthma in a patient with mitral heart disease, it is recommended:

• in order to reduce the flow of blood to the right heart, the patient should be in a sitting or semi-sitting position;
• Inhalate oxygen, passed through alcohol or antifosilan;
• Enter intravenously I ml of a 2% solution of promedol;
• Enter intravenously 2 ml of I% solution of lasix (in the first 20-30 minutes the venodilating effect of the drug is observed, later the diuretic effect develops);
• when the measures performed are insufficient, the introduction of peripheral vasodilators with a point of application in the venous section of the vascular bed (nitroglycerin, nanipruss, etc.) is shown.

It should be differentiated approach to the use of cardiac glycosides in the treatment of left ventricular failure in patients with mitral heart defects. Their use is indicated in patients with a predominance of insufficiency or an isolated mitral valve insufficiency. In patients with "pure" or predominant stenosis, acute left ventricular failure is due not so much to a deterioration in the contractility of the left ventricle, but to disturbances of intracardiac hemodynamics due to a violation of outflow of blood from the small circle with preserved (or even strengthened) contractile function of the right ventricle. The use of cardiac glycosides in this case, by strengthening the contractile function of the right ventricle, can also increase the attack of cardiac asthma. Here it should be stipulated that in some cases, the onset of cardiac asthma in patients with isolated or predominant mitral stenosis may be due to a decrease in the contractile function of the left atrium or increased heart function due to a high heart rate. In these cases, the use of cardiac glycosides against the background of measures to discharge the small circle of circulation (diuretics, narcotic analgesics, venous vasolatators, ganglion blockers, etc.) is fully justified.

Tactics of treatment of acute heart failure in hypertensive crisis

Intensive care for acute left ventricular failure in the context of hypertensive crisis:

• reduction of pre- and post-loading on the left ventricle;
• prevention of myocardial ischemia development;
• elimination of hypoxemia.

Immediate measures: oxygen therapy, non-invasive ventilation, maintaining positive airway pressure and administering antihypertensive agents.

The general rule is that a rapid (in a few minutes) decrease in the BP of the system or AD diastas is 30 mm Hg. Art. After that, a slower decrease in blood pressure to the values that occurred before the hypertensive crisis (usually a few hours) is shown. It is a mistake to lower blood pressure to "normal numbers", as this can lead to a reduction in organ perfusion and improvement in the patient's condition. For the initial rapid reduction in blood pressure, it is recommended to use:

• intravenous administration of nitroglycerin or nitroprusside;
• intravenous injection of loop diuretics;
• intravenous administration of a long-acting dihydropyridine derivative (nicardipine).
• If it is not possible to use funds for intravenous administration
• relatively rapid reduction in blood pressure can be achieved with
• taking captopril sublingually. The use of beta-blockers is indicated in the case of a combination of acute heart failure without a serious violation of the contractility of the left ventricle with tachycardia.

Hypertensive crisis, caused by pheochromocytoma, can be eliminated by intravenous administration of phentolamine in a dose of 5-15 mg (with repeated administration after 1-2 hours).

Tactics of treatment of acute heart failure in heart rhythm and conduction disorders

Heart rhythm and conduction disorders often serve as a direct cause of the development of acute heart failure in patients with a variety of cardiac and extracardiac diseases. Intensive therapy in the development of fatal arrhythmias is carried out according to a universal algorithm for the treatment of cardiac arrest.

General treatment rules: oxygenation, respiratory support, achievement of analgesia, maintenance of normal concentration of potassium and magnesium in the blood, elimination of myocardial ischemia. Table 6.4 shows the basic treatment measures for the management of acute heart failure due to heart rhythm disturbances or conduction of the heart.

If the bradycardia is resistant to atropine, then percutaneous or transvenous electrical pacing should be undertaken.