Acute heart failure

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

• decreased cardiac output;
• insufficient tissue perfusion;
• increased pressure in the pulmonary capillaries;
• tissue congestion.

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What causes acute heart failure?

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

Among the non-cardiac causes of this pathology, the leading ones are volume overload, infections (pneumonia and septicemia), acute cerebrovascular accidents, extensive surgical interventions, renal failure, bronchial asthma, drug overdose, alcohol abuse, and pheochromocytoma.

Clinical variants of acute heart failure

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

• Acute decompensated heart failure (newly occurring or decompensation of chronic heart failure).
• Hypertensive acute heart failure (clinical manifestations of acute heart failure in patients with relatively preserved left ventricular function in combination with high blood pressure and radiographic evidence of venous congestion in the lungs or their edema).
• Pulmonary edema (confirmed by chest radiography) is severe respiratory distress with pulmonary rales, orthopnea, and typically arterial oxygen saturation <90% on room air prior to treatment.
• Cardiogenic shock is a clinical syndrome characterized by tissue hypoperfusion due to heart failure that persists after preload correction. Arterial hypotension (SBP < 90 mmHg or sBP > 30 mmHg) and/or decreased diuresis < 0.5 ml/kg/h are usually observed. Symptoms may be associated with the presence of brady- or tachyarrhythmias, as well as a marked decrease in left ventricular contractile dysfunction (true cardiogenic shock).
• Acute high output heart failure - usually associated with tachycardia, warm skin and extremities, pulmonary congestion, and sometimes low blood pressure (an example of this type of acute heart failure is septic shock).
• Acute right ventricular failure (low cardiac output syndrome combined with increased jugular venous pressure, liver enlargement and arterial hypotension).

Taking into account clinical manifestations, acute heart failure is divided by clinical signs into left ventricular, right ventricular with low cardiac output, left- or right-ventricular failure with symptoms of blood stagnation, as well as their combination (biventricular or total heart failure). Depending on the degree of development of disorders, compensated and decompensated circulatory failure are also distinguished.

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Acute heart failure of neurogenic origin

Typically, this type of heart failure develops with acute cerebrovascular accidents. 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. If such a pressure surge lasts long enough, fluid comes out of 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 aimed primarily at maintaining adequate gas exchange and reducing pressure in the pulmonary vessels.

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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 the pulmonary circulation - acute left ventricular failure. The development of attacks of cardiac asthma is especially characteristic in aortic stenosis.

Aortic heart defects are characterized by an increase in hydrostatic pressure in the pulmonary circulation and a significant increase in end-diastolic volume and pressure, as well as retrograde blood stagnation.

An increase in hydrostatic pressure in the pulmonary circulation of more than 30 mm Hg leads to active penetration of plasma into the alveoli of the lungs.

In the early stages of aortic stenosis, the main manifestation of left ventricular failure is attacks of painful coughing at night. As the disease progresses, typical clinical signs of cardiac asthma occur, up to full-blown pulmonary edema. Arterial pressure is usually elevated. Patients often complain of heart pain.

The occurrence of asthma attacks is typical for severe mitral stenosis without concomitant right ventricular failure. With this type of heart defect, there is an obstruction to blood flow at the level of the atrioventricular orifice. With its sharp narrowing, blood cannot be pumped from the left atrium to the left ventricle of the heart and partially remains in the cavity of the left atrium and the pulmonary circulation. Emotional stress or physical exertion leads to an increase in the productivity of the right ventricle against the background of unchanged and reduced throughput of the left atrioventricular orifice. An increase in pressure in the pulmonary artery in these patients during physical exertion leads to transudation of fluid into the interstitium of the lungs and the development of cardiac asthma. Decompensation of the capabilities of the heart muscle leads to the development of alveolar edema of the lungs.

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

If the closure of the left atrioventricular orifice persists for a long time, rapid death is possible.

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Acute heart failure of other genesis

A number of pathological conditions are 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 mitral valve chords in bacterial endocarditis, myocardial infarction, Marfan syndrome, cardiac myxoma and other diseases. Rupture of the mitral valve chords with the development of acute mitral insufficiency can also occur in healthy people.

Practically healthy individuals with acutely developed mitral insufficiency mainly complain of suffocation during physical exertion. Relatively rarely, they have a detailed picture of pulmonary edema. Systolic tremor is determined in the atrial region. Auscultation reveals a loud scraping systolic murmur in the atrial region, which is well transmitted to the neck vessels.

The size of the heart, including the left atrium, is not increased in this category of patients. If acute mitral insufficiency occurs against the background of severe pathology of the heart muscle, severe pulmonary edema usually develops, which is difficult to treat with medication. A classic example of this is the development of acute left ventricular failure in patients with myocardial infarction with damage to the papillary muscles.

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Total acute heart failure

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

Total heart failure combines clinical symptoms typical of both left- and right-sided ventricular failure. Dyspnea, cyanosis of the lips and skin are characteristic.

Acute failure of both ventricles is characterized by rapid development of tachycardia, hypotension, circulatory and hypoxic hypoxia. Cyanosis, swelling of peripheral veins, liver enlargement, and a sharp increase in central venous pressure are observed. Intensive care is carried out according to the above principles, with an emphasis on the predominant type of failure.

Assessment of the severity of myocardial damage

The severity of heart damage in myocardial infarction is usually assessed according to the following classifications:

The Killip T. classification is based on clinical signs and chest X-ray results. Four stages (classes) of severity are distinguished.

• Stage I - no signs of heart failure.
• Stage II - there are signs of heart failure (moist rales in the lower half of the lung fields, third tone, signs of venous hypertension in the lungs).
• Stage III - severe heart failure (obvious pulmonary edema; moist rales extend to more than the lower half of the lung fields).
• Stage IV - cardiogenic shock (SBP 90 mmHg with signs of peripheral vasoconstriction: oliguria, cyanosis, sweating).

The Forrester JS classification is based on clinical signs characterizing the severity of peripheral hypoperfusion, the presence of pulmonary congestion, decreased CI < 2.2 l/min/m2 and increased PAOP> 18 mm Hg. A distinction is made between the norm (group I), pulmonary edema (group II), and hypovolemic-cardiogenic shock (groups III and IV, respectively).

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How is acute heart failure treated?

It is generally accepted to begin intensive therapy of acute heart failure with measures aimed at reducing the afterload on the left ventricle. This includes placing the patient in a sitting or semi-sitting position, oxygen therapy, providing venous access (central vein catheterization if possible), administering analgesics and neuroleptics, peripheral vasodilators, euphyllin, ganglionic blockers, diuretics, and, if indicated, vasopressors.

Monitoring

All patients with acute heart failure are recommended to have their heart rate, blood pressure, oxygen saturation, respiratory rate, body temperature, ECG, and diuresis monitored.

Oxygen therapy and respiratory support

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

Oxygen therapy

The use of oxygen in the presence of decreased cardiac output can significantly improve tissue oxygenation. Oxygen is administered via a nasal catheter at a rate of 4-8 l/min for the first two days. The catheter is inserted through the lower nasal passage to the choanae. Oxygen is supplied via a rotameter. A flow rate of 3 l/min provides an inspired oxygen concentration of 27 vol.%, at 4-6 l/min - 30-40 vol.%.

Reduced foaming

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

Non-invasive respiratory support (without tracheal intubation) is performed by maintaining increased positive airway pressure (CPAP - Continuous Positive Airway Pressure). The oxygen-air mixture can be administered into the lungs through a face mask. This type of respiratory support allows for an increase in the functional residual volume of the lungs, an increase in lung elasticity, a decrease in the degree of diaphragm involvement in the act of breathing, a decrease in the work of the respiratory muscles and a decrease in their need for oxygen.

Invasive respiratory support

In case of acute respiratory failure (respiratory rate over 40 per minute, severe tachycardia, transition from hypertension to hypotension, drop in PaO2 below 60 mm Hg and increase in PaCO2 above 60 mm Hg), as well as due to the need to protect the airways from regurgitation in patients with cardiac pulmonary edema, there is a need for invasive respiratory support (MV with tracheal intubation).

Artificial ventilation of the lungs in this category of patients improves oxygenation of the body by normalizing gas exchange, improves the ventilation/perfusion ratio, and reduces the body's need for oxygen (since the work of the respiratory muscles stops). In the development of pulmonary edema, artificial ventilation of the lungs with pure oxygen with increased pressure at the end of exhalation (10-15 cm Hg) is effective. After the emergency condition has been relieved, it is necessary to reduce the concentration of oxygen in the inhaled mixture.

Elevated end-expiratory pressure (PEEP) is a well-established component of intensive care for acute left ventricular heart failure. However, there is now convincing evidence that high positive airway pressure or lung overinflation leads to the development of pulmonary edema due to increased capillary pressure and increased capillary membrane permeability. The development of pulmonary edema appears to depend primarily on the magnitude of peak airway pressure and whether there are any previous changes in the lungs. Lung overinflation itself may cause increased membrane permeability. Therefore, maintaining elevated positive airway pressure during respiratory support should be done under close dynamic monitoring of the patient's condition.

Narcotic analgesics and neuroleptics

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

Vasodilators

The most common method of correcting heart failure is the use of vasodilators to reduce the workload of the heart by reducing venous return (preload) or vascular resistance, which the cardiac pump is designed to overcome (afterload) and pharmacological stimulation to increase myocardial contractility (positive-acting inotropic drugs).

Vasodilators are the drug of choice for hypoperfusion, pulmonary venous congestion, and decreased diuresis. Before prescribing vasodilators, existing hypovolemia must be corrected with infusion therapy.

Vasodilators are divided into three main subgroups depending on the points of application. There are drugs with a predominantly venodilating effect (reducing preload), with a predominantly arteriodilating effect (reducing afterload) and those with a balanced effect on systemic vascular resistance and venous return.

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

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

Sodium nitroprusside is a drug of the 3rd group. It is a powerful, balanced, short-acting vasodilator that relaxes the smooth muscles of veins and arterioles. Sodium nitroprusside is the drug of choice in patients with severe hypertension against the background of low cardiac output. Before use, 50 mg of the drug is dissolved in 500 ml of 5% glucose (1 ml of this solution contains 6 mcg of sodium nitroprusside).

The doses of nitroprusside required to satisfactorily reduce the load on the myocardium in heart failure vary from 0.2 to 6.0 mcg/kg/min or more, averaging 0.7 mcg/kg/min.

Diuretics

Diuretics are a well-established component in the treatment of acute left ventricular failure. Fast-acting drugs (lasix, ethacrynic acid) are most often used.

Lasix is a short-acting loop diuretic. It inhibits the reabsorption of sodium and chloride in the loop of Henle. In the development of pulmonary edema, it is administered intravenously at a dose of 40-160 mg. The introduction of a loading dose of Lasix followed by infusion is more effective than repeated bolus administration.

Recommended doses are from 0.25 mg/kg body weight to 2 mg/kg body weight and higher in the presence of refractoriness. The introduction of Lasix causes a venodilating effect (after 5-10 minutes), rapid diuresis, and reduces the volume of circulating blood. The maximum effect 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 at a dose of 50-100 mg.

Diuretics in patients with acute coronary syndrome are used with great caution and in small doses, as they can cause massive diuresis with subsequent reduction in circulating blood volume, cardiac output, etc. Refractoriness to the therapy is overcome by combination therapy with other diuretics (torasemide, hydrochlorothiazide) or dopamine infusion.

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Inotropic support

The need for inotropic support arises with the development of the "low cardiac output" syndrome. The most commonly used drugs are chemotherapy, dobutamine, and adrenaline.

Dopamine is administered intravenously by drip at a rate of 1-3 to 5-15 mcg/kg/min. Dobutamine at a dose of 5-10 mcg/kg/min is highly effective in acute heart failure refractory to therapy with cardiac glycosides.

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

Levosimendan increases the sensitivity of 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 dilation of veins and arteries (including coronary arteries).

Levosimendan is indicated for 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 mcg/kg over 10 minutes, followed by continuous infusion at a rate of 0.05-0.1 mcg/kg min.

Adrenaline is used as an infusion at a rate of 0.05-0.5 mcg/kg/min for profound arterial hypotension (systolic blood pressure < 70 mm Hg) refractory to dobutamine.

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

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

Cardiac glycosides

Cardiac glycosides (digoxin, strophanthin, corglycon) are able to normalize the myocardium's need for oxygen in accordance with the volume of work and increase load tolerance with the same energy expenditure. 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 (lanicor) is administered in a dose of 1-2 ml of 0.025% solution, strophanthin - 0.5-1 ml of 0.05% solution, corglycon - 1 ml of 0.06% solution.

In acute left ventricular failure, after rapid digitalization, an increase in arterial pressure is observed. Moreover, its growth occurs mainly due to an increase in cardiac output with an insignificant (about 5%) increase in the resistance of peripheral vessels.

Indications for the use of cardiac glycosides include supraventricular tachyarrhythmia and atrial fibrillation, when the ventricular rate cannot be controlled by other drugs.

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

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Features of intensive care of acute heart failure in myocardial infarction

The main method of preventing the development of acute heart failure in patients with myocardial infarction is timely reperfusion. Percutaneous coronary intervention is considered preferable. If there are appropriate indications, emergency coronary bypass grafting is justified in patients with cardiogenic shock. If these treatment methods are unavailable, then thrombolytic therapy is indicated. Emergency myocardial revascularization is also indicated in the presence of acute heart failure that has complicated acute coronary syndrome without elevations of the 5T segment on the electrocardiogram.

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

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Intensive care of acute heart failure in patients with heart defects

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

• in order to reduce the blood flow to the right heart, the patient should be in a sitting or semi-sitting position;
• inhale oxygen passed through alcohol or antifomsilane;
• administer intravenously 1 ml of 2% promedol solution;
• administer 2 ml of 1% lasix solution intravenously (in the first 20-30 minutes, the venodilating effect of the drug is observed, later a diuretic effect develops);
• If the measures taken are insufficient, the introduction of peripheral vasodilators with the point of application in the venous section of the vascular bed (nitroglycerin, naniprus, etc.) is indicated.

A differentiated approach should be taken 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 predominant failure or isolated mitral valve failure. In patients with "pure" or predominant stenosis, acute left ventricular failure is caused not so much by deterioration of the contractile function of the left ventricle as by disturbances in intracardiac hemodynamics due to impaired blood outflow from the pulmonary circulation with preserved (or even enhanced) contractile function of the right ventricle. The use of cardiac glycosides in this case, by enhancing the contractile function of the right ventricle, can also intensify an attack of cardiac asthma. It should be noted here that in some cases an attack of cardiac asthma in patients with isolated or predominant mitral stenosis can be caused by a decrease in the contractile function of the left atrium or increased cardiac work due to a high heart rate. In these cases, the use of cardiac glycosides against the background of measures to relieve the pulmonary circulation (diuretics, narcotic analgesics, venous vasodilators, ganglionic blockers, etc.) is entirely justified.

Treatment tactics for acute heart failure in hypertensive crisis

The goals of intensive therapy for acute left ventricular failure in the context of hypertensive crisis:

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

Emergency measures: oxygen therapy, non-invasive ventilation with maintenance of positive airway pressure and administration of antihypertensive drugs.

General rule: rapid (within a few minutes) reduction of systolic or diastolic blood pressure - 30 mm Hg. After that, a slower reduction of blood pressure to the values that existed before the hypertensive crisis is indicated (usually within a few hours). It is a mistake to reduce blood pressure to "normal numbers", since this can lead to a decrease in organ perfusion and an improvement in the patient's condition. For an initial rapid reduction of blood pressure, it is recommended to use:

• intravenous administration of nitroglycerin or nitroprusside;
• intravenous administration of loop diuretics;
• intravenous administration of a long-acting dihydropyridine derivative (nicardipine).
• If it is impossible to use intravenous means
• A 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 serious impairment of left ventricular contractility with tachycardia.

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

Treatment tactics for acute heart failure with cardiac rhythm and conduction disorders

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

General treatment rules: oxygenation, respiratory support, achieving analgesia, maintaining normal concentrations of potassium and magnesium in the blood, eliminating myocardial ischemia. Table 6.4 provides basic treatment measures for stopping acute heart failure caused by disturbances in cardiac rhythm or conduction.

If bradycardia is resistant to atropine, transcutaneous or transvenous cardiac pacing should be attempted.