Treatment of respiratory failure

Treatment of patients with acute respiratory failure is performed in the intensive care unit or intensive care unit and provides for:

1. Elimination of the cause of acute respiratory failure (treatment of the underlying disease).
2. Providing airway patency.
3. Maintain the required level of ventilation.
4. Correction of hypoxemia and tissue hypoxia.
5. Correction of the acid-base state.
6. Maintaining hemodynamics.
7. Prevention of complications of acute respiratory failure.

The choice of specific methods for solving these problems depends on many factors: the nature and severity of the course of the underlying lung disease, such as developed respiratory failure, the initial functional state of the lungs and respiratory tract, blood gas composition, acid-base state, patient's age, systems and the like.

Providing airway patency

Providing free airway patency is the most important task of treating patients with acute respiratory failure, regardless of its genesis. For example, for many diseases that are the causes of parenchymal respiratory failure (chronic obstructive bronchitis, bronchial asthma, bronchiolitis, cystic fibrosis, central lung cancer, bronchopneumonia, pulmonary tuberculosis, etc.), a pronounced airway obstruction due to edema, infiltration of the mucosa , the presence of low secretion in the bronchi (sputum), spasm of smooth muscles of the bronchi and other causes. In patients with ventilation respiratory failure bronchial obstruction develops again. Against the background of a significant decrease in the respiratory volume and the weakening in connection with this of bronchial drainage. Thus, respiratory insufficiency of any nature (parenchymal or ventilation), one way or another, is accompanied by violations of bronchial patency, without which it is practically impossible to effectively treat respiratory failure.

Methods of natural sputum removal

The sanation of the tracheobronchial tree begins with the most simple methods - creating and maintaining the optimum humidity and temperature of the inhaled air, (humidifiers are used for humidifying and warming the air.) Deep breathing, cough reflex, percussion or vibratory chest massage also contribute to removal of sputum, eating the patient's condition allows these therapeutic measures to be implemented.Pustural drainage in a number of cases makes it possible to achieve a natural drift bronchiectasis, chronic obstructive bronchitis complicated by acute respiratory failure, nevertheless, in severe patients with respiratory failure, in patients in the unconscious state or in patients whose active movements are limited in connection with the continuous conduct of hemodynamic monitoring or receiving infusion therapy, the use of this method of cleansing the airways provides tsya impossible. The same applies to the technique of percussion or vibration massage of the chest, which in some patients with signs of bronchial obstruction has good results for years.

Bronchodilators and expectorants

To restore the patency of the airways use bronchodilators expectorant drugs. If a patient has signs of an active bacterial inflammatory process in the bronchi, it is advisable to use antibiotics.

Preferred is the inhalation of respiratory tract bronchodilators and expectorants, as well as isotonic fluids, which not only contributes to the more effective effect of these drugs on the mucous membrane of the trachea, bronchi and tracheobronchial contents, and is accompanied by the necessary moistening of the mucosa. Nevertheless, it should be remembered that conventional jet inhalers form large enough aerosol particles, which reach only the oropharynx, trachea or large bronchi. Unlike them, ultrasonic nebulizers create aerosol particles about 1-5 nm in size that penetrate into the lumen of not only large but also small bronchi and have a more pronounced positive effect on the mucous membrane.

As drugs with bronchodilator effect, patients with acute respiratory failure use anticholinergic drugs, euphyllin or beta2-adrenomimetics.

With severe bronchial obstruction, it is advisable to combine inhalational administration of beta2-adrenomimetics with ingestion or parenteral administration of other bronchodilators. Euphyllinum is initially administered at a saturating dose of 6 mg / kg in a small volume of 0.9% sodium chloride solution (slowly, for 10-20 minutes), and then continue to drip it intravenously at a maintenance dose of 0.5 mg / kg / patients over 70 years of age maintain a dose of euphyllin reduced to 0.3 mg / kg / h, and for patients with concomitant liver disease or chronic heart failure - up to 0.1-0.2 mg / kg / h. Expectorants often use ambroxol in a daily dose of 10-30 mg / kg (parenterally). If necessary, hydrocortisone is administered at a dose of 2.5 mg / kg parenterally every 6 hours or prednisolone orally at a daily dose of 0.5-0.6 mg / kg.

Improvements in the rheological properties of sputum can also be achieved with the use of infusion therapy, for example, isotonic sodium chloride solution, which contributes to moderate hemodilution and a decrease in the viscosity of phlegm.

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

Methods for compulsory airway cleansing

Tracheobronchial catheter. With insufficient effectiveness of these methods of airway sanitation (pulmonary drainage, chest massage, use of inhalers, etc.), severe obstruction of the bronchi and increasing respiratory insufficiency, resort to forced cleaning of the tracheobronchial tree. For this purpose, a plastic catheter with a diameter of 0.5-0.6 cm is inserted into the trachea and is guided through the nasal passage or mouth and then through the vocal cords to the trachea and, if necessary, into the cavity of the main bronchi. The connection of the catheter (probe) to the electric pump allows evacuating the sputum within the reach of the probe. In addition, being a strong mechanical stimulus, the probe usually causes the patient to have a strong reflex cough and separation of a significant amount of sputum, which allows to restore the patency of the airways.

It should, however, be remembered that this method causes in some patients not only cough, but also a gag reflex, and in some cases - laryngospasm.

Microtracetostomy is a percutaneous catheterization of the trachea and bronchi, which is used in those cases when a prolonged permanent or periodic suction of tracheobronchial contents is planned, and there are no indications or technical possibilities for endotracheal intubation, fibroblochoscopy or artificial ventilation.

The patient after skin treatment and local anesthesia with a protected scalpel is punctured by the tracheal wall at the level between the cricoid cartilage and the first ring of the trachea. A flexible guide mandrin is inserted into the hole, along which a tracheostomy cannula of soft PVC with an internal diameter of 4 mm is inserted into the trachea. The introduction of a catheter into the trachea or bronchus usually causes a strong cough with sputum separation, which is aspirated through the probe.

In addition, the finding of a trachea or one of the main bronchi of a probe uses the introduction of liquids or medicinal substances into the trachea and bronchi that have a mucolytic, expectorant effect that improves the rheological properties of the sputum.

To this end, 50-150 ml of isotonic sodium chloride solution or 5% sodium bicarbonate solution together with solutions of antimicrobial agents (penicillin, furacillin, dioxidia, etc.) are injected into the tracheobronchial tree through the catheter. The rapid introduction of these solutions during deep inspiration also provokes a cough, which allows aspirating sputum and improving airway patency. If necessary, a small amount of mucolytics solution (for example, 5-10 mg of trypsin) is introduced through the intracerebral catheter (probe), which dilute sputum and facilitate its separation. The action lasts 2-3 hours, after which the procedure can be repeated.

In some cases, the catheter is carried to one of the main bronchi for the purpose of aspiration of bronchial contents and the administration of medicinal substances directly to the affected lung, for example, if the patient has atelectasis or abscesses. In general, the method of percutaneous catheterization of the trachea and bronchi with aspiration of the trachebronchial contents is quite effective and easy to perform, although complications may occur in the course of the surgery: erroneous insertion of the catheter into the esophagus, paratracheal tissue, development of pneumothorax, mediastinal emphysema, bleeding. In addition, with prolonged use of this technique, after 1-2 days, the mucosa of the trachea becomes less sensitive to mechanical stimulation by the catheter and fluid solutions and the cough reflex weakens. Fibroblochoscopy is the most effective method of sputum removal in the repair of the mucous membrane of the trachea and bronchi, although this is not the only task of this procedure. In this case, it becomes possible to sanitize the mucous membrane of not only the trachea and the main bronchus, but also other parts of the respiratory tract, up to the segmental bronchi. The technique of fibrobronchoscopy is less traumatic than micro tracheostomy, and, in addition, it has wide diagnostic capabilities.

Artificial ventilation (IVL). If an endotracheal catheter or fibrobronchoscope does not manage to provide adequate patency of the respiratory tract, and respiratory failure continues to increase, transebronchial tree is sanitized using endotracheal intubation and mechanical ventilation if the indications for the use of these methods of treatment did not arise earlier due to the increasing hypoxemia and hypercapnia.

Non-invasive ventilation

Mechanical ventilation (AV) is used in patients with acute respiratory failure to ensure sufficient ventilation volume (removal from the body of CO ₂ ) and adequate oxygenation (saturation of blood O ₂ ). The most common indication for ventilation is the inability of the patient to independently support these two processes.

Among the many types of ventilation are distinguished by invasive mechanical ventilation (through the endotracheal tube or tracheostomy) and noninvasive ventilation (through the facial mask). Thus, the term "non-invasive ventilation" is used to refer to artificial ventilation without invasive (endotracheal) penetration of the respiratory tract. The use of non-invasive ventilation in patients with acute respiratory insufficiency avoids many of the side effects of intubation of the trachea, tracheostomy and most invasive mechanical ventilation. For the patient, this method of treatment is more comfortable, allowing him to eat, drink, talk, expectorate sputum during this procedure.

For carrying out of non-invasive ventilation of lungs use 3 kinds of masks:

• nasal masks that cover only the nose;
• Oronasal masks that cover both the nose and mouth;
• mouthpieces, which are standard plastic tubes, held in position with a mouthpiece.

The latter method is usually used in the treatment of patients with chronic acute respiratory failure, when prolonged use of noninvasive ventilation is required. In acute acute respiratory failure more often use oronosal masks.

There are various regimes of non-invasive ventilation, among which the most widely used methods are the creation of positive pressure in the airways at different phases of the respiratory cycle (NPPV - noninvasive positive-pressure ventilation).

Ventilation with positive pressure during inspiration provides increased pressure in the airways during inspiration. This increases the pressure gradient between the convection and alveolar (diffusion, gas exchange) zones and thereby facilitates inhaling and oxygenation of the blood. This mode can be used for both fully controlled and for auxiliary ventilation of the lungs.

Ventilation with positive end-expiratory pressure (PEEP or PEEP positive end-expiratory pressure). This regime provides for the creation of a small positive pressure in the respiratory tract at the end of exhalation (usually not more than 5-10 cm H2O), which prevents the alveoli from collapsing (collapse), reduces the risk of the phenomenon of early expiratory closure of the bronchi, leads to atelectasis spreading and an increase FOE. Owing to the increase in the number and size of functioning alveoli, the veiltilation-perfusion ratio improves, the alveolar shunt decreases, which is the reason for improving oxygenation and reducing hypoxemia.

The mode of ventilator with PEEP is usually used to treat patients with acute parenchymal acute respiratory failure, signs of bronchial obstruction, low FAE, the tendency of patients to develop early bronchial expiratory collapse and impaired ventilation-perfusion relations (COPD, bronchial asthma, pneumonia, atelectasis, acute respiratory distress -syndrome, cardiogenic pulmonary edema, etc.).

It should be remembered that with ventilation in PEEP mode due to an increase in the mean intrathoracic pressure, the flow of venous blood to the right heart can be impaired, which is accompanied by hypovolemia and a decrease in cardiac output and blood pressure.

Ventilation with a constant positive pressure during inspiration and exhalation (CPAP) is characterized by the fact that positive pressure (above atmospheric pressure) is established throughout the entire breathing cycle. In most cases, the pressure during inspiration is maintained at a level of 8-11 cm of water at the station, and at the end of expiration (PEEP) 3-5 cm of water. Art. The frequency of breathing is usually set from 12-16 per minute to 18-20 per minute (in patients with weakened respiratory muscles)

With good tolerance, an increase in inspiratory pressure up to 15-20 cm of water is possible. St, and PEEP up to 8 10 cm of water. Art. The oxygen supply is carried out directly into the mask or into the inspiratory hose. The oxygen concentration is adjusted so that oxygen saturation (SaO ₂ ) is greater than 90%.

In clinical practice, other modifications of the described noninvasive positive pressure ventilation modes are also used.

The most common of the indications for NPPV are the known clinical and pathophysiological signs of respiratory failure. An important condition for conducting NPPV is the adequacy of the patient and his ability to cooperate with a doctor during the NPPV procedure, as well as the possibility of adequate sputum discharge. In addition, it is inappropriate to use the NPPV technique in patients with unstable hemodynamics, myocardial infarction or unstable angina, heart failure, uncontrolled arrhythmias, respiratory arrest, and the like.

Indications for NPPV in acute respiratory failure (S. Mehla, NS Hill, 2004 as modified)

Pathophysiological signs of respiratory failure	Hypoxemia without hypercapnia Acute (or acute in the background of chronic) hypercapnia Respiratory acidosis
Clinical signs of respiratory failure	Dyspnea Paradoxical movement of the abdominal wall Participation in the respiration of the assisted musculature
Patient Requirements	Respiratory protection Cooperation with a doctor Minimal tracheobronchial secretion Hemodynamic stability
Suitable categories of patients	COPD Bronchial asthma Cystic Fibrosis Pulmonary edema Pneumonia Discard intubation

When carrying out NPPV, blood pressure monitoring, heart rate, ECG, oxygen saturation and basic hemodynamic parameters are mandatory. When the patient's condition is stabilized, NPPV can be interrupted for short periods, and then completely discontinued, if the respiration rate does not exceed 20-22 per minute for self-breathing, oxygen saturation remains at a level greater than 90% and the gas composition of the blood is stabilized.

Non-invasive positive pressure ventilation (NPPV), providing indirect "access" to the respiratory tract (through the mask), is easier and more comfortable for the patient by the method of respiratory support and avoids a number of side effects and complications of endotracheal intubation or tracheostomy. However, the use of NPPV requires the presence of intact airways and adequate patient co-operation 2 by a doctor (S. Mehta, NS Hill, 2004).

Invasive pulmonary ventilation

Traditional invasive artificial ventilation (IVL), carried out with the help of an endotracheal tube or tracheostomy, is usually used in severe acute respiratory failure and in many cases prevents the rapid progression of the disease and even the death of the patient.

Clinical criteria for the transfer of patients to IVL is acute respiratory failure, accompanied by severe dyspnea (more than 30-35 per m), agitation, coma or sleep with secret consciousness, pronounced cyanosis or earthy color of the skin, excessive sweating, tachycardia or bradycardia, active participation in respiration of the auxiliary musculature and the appearance of paradoxical movements of the abdominal wall.

According to the data on the determination of the gas composition of blood and other functional methods of the study, the use of mechanical ventilation is shown when, in comparison with the proper values, the GEL is more than halved, oxygen saturation of arterial blood is less than 80%, PaO _{2 is} below 55 mm Hg. , RaCO ₂ above 53 mm Hg. Art. And the pH is below 7.3.

An important and sometimes decisive criterion for transferring a patient to IVL is the rate of deterioration of the functional state of the lungs and violations of the gas composition of the blood.

Absolute indications for mechanical ventilation are (SN Avdeev, AG Chucholin, 1998):

• stopping breathing;
• expressed disorders of consciousness (sopor, coma);
• unstable hemodynamics (systolic blood pressure <70 mm Hg, heart rate <50 per min or> 160 per min);
• fatigue of the respiratory musculature. Relative indications for mechanical ventilation are:
• respiratory rate> 35 per min;
• arterial blood pH <7.3;
• RaCO ₂ > 2 <55 mm Hg. St, despite carrying out oxygen therapy.

The transfer of a patient to an invasive ventilator is generally shown with a pronounced and progressive ventilating (hypercapnic), parenchymal (hypoxemic) and mixed form of acute respiratory failure. At the same time, it should be remembered that this method of respiratory support for backward reasons is most effective in patients with ventilation form with acute respiratory failure, since ventilator influences predominantly on the exchange of gases in the convection zone. As is known, the parenchymal form of respiratory failure in most cases is caused not by a decrease in the volume of ventilation, but by a violation of ventilation-perfusion relations and other changes taking place in the alveolar (diffusion) zone. Therefore, the use of mechanical ventilation in these cases is less effective and, as a rule, can not completely eliminate hypoxemia. The increase in PAO ₂ in patients with parenchymal respiratory failure, which still occurs under the influence of ventilation, is mainly due to a decrease in the expenditure of respiration energy and a slight increase in the oxygen concentration gradient between the convection and alveolar (diffusion) zones associated with an increase in the oxygen content in the inhaled mixture and the application of the regimen Ventilator with positive pressure during inspiration. In addition, the use of the PEEP mode, which prevents the emergence of micro-teleclases, the collapse of the alveoli and the phenomenon of early expiratory closure of the bronchi, contributes to the increase in FDE, to some improvement in ventilation-perfusion relations and to a decrease in alveolar blood shunting. Due to this in a number of cases, it is possible to achieve a marked reduction in clinical and laboratory signs of acute respiratory failure.

Invasive mechanical ventilation is most effective in patients with ventilation form of acute respiratory failure. In the parenchymal form of respiratory failure, especially in severe violations of ventilation-perfusion relations, the listed modes of artificial ventilation, although they have a positive effect on PAO ₂, in some cases still can not be radically eliminated, arterial hypoxemia and are ineffective.

It should be true, "and to have the appearance that cases of mixed respiratory failure, which are characterized by violations both in the alveolar (diffusion) and convection zones, are often found in clinical practice, which always leaves hope for a positive effect of the use of artificial ventilation in these patients.

The main parameters of ventilation are (OA Dolina, 2002):

• minute volume of ventilation (MOB);
• respiratory volume (DO);
• respiratory rate (BH);
• pressure on inspiration and exhalation;
• the ratio of the time of inspiration and expiration;
• rate of gas injection.

All these parameters are in close relationship with each other. The choice of each of them depends on many factors considered, primarily on the form of respiratory failure, the nature of the underlying disease that caused acute respiratory failure, the functional state of the lungs, the age of the patients, and so on.

Typically, ventilation is performed in the mode of moderate hyperventilation, causing some respiratory alkalosis and associated violations of central regulation of respiration, hemodynamics, electrolyte composition and tissue gas exchange. The hyperventilation regimen is a forced measure associated with an unphysiological relationship between ventilation and blood flow in the lungs during artificial inspiration and expiration (G. Diette, R. Brower, 2004).

In clinical practice, a large number of ventilation regimens are used, described in detail in special guidelines for anesthesiology and resuscitation. The most common of these are controlled ventilation (CMV), controlled ventilation (ACV), intermittent mandatory ventilation (IMV), synchronized intermittent forced ventilation (SIMV - Synchronized intermittent mandatory) ventilation, ventilation with the support of inspiratory pressure (PSV - Pressure support ventilation), controlled by the pressure of the ventilation (PCV - Pressure control ventilation) and others.

Traditional controlled ventilation (CMV) is a fully controlled forced ventilation. This mode of artificial ventilation is used in patients who have completely lost their ability to breathe independently (patients with violations of central regulation of respiration, paralysis or severe fatigue of the respiratory muscles, as well as patients with respiratory depression caused by the use of muscle relaxants and drugs during surgical operations, etc.). . In these cases, the fan automatically injects a certain amount of air into the lungs at a certain frequency.

The regime of assisted controlled ventilation (ACV) is used in patients with acute respiratory failure, which retained the ability to independent, although not quite effective, breathing. When using this mode, set the minimum respiratory rate, respiratory volume and inspiratory speed. If the patient independently makes an adequate attempt at inspiration, the fan immediately "responds" to it by injecting a predetermined volume of air and, thus, "takes over" part of the work of breathing. If the frequency of spontaneous (independent) breaths is greater than the prescribed minimum respiratory rate, all respiratory cycles are ancillary. If, however, during a certain interval of time (t) there is no attempt at an independent inspiration, the fan automatically performs a "controlled" injection of air. Auxiliary controlled ventilation, in which the ventilator takes most or all of the breathing work, is often used in patients with neuromuscular weakness or with pronounced fatigue of the respiratory muscles.

The mode of intermittent forced ventilation (IMV) is based, in fact, on the same principles as auxiliary-controlled ventilation. The difference is that the fan does not respond to every attempt of the patient to take an independent breath, but only if the spontaneous breathing of the patient does not provide the given frequency and volume of ventilation. The device is switched on periodically for one forced breathing cycle. In the absence of attempts at a sound breathing, the fan performs "controlled breathing" in the forced mode.

Modification of this method of artificial ventilation is synchronized and intermittent forced ventilation (SIMV), at which the fan maintains periodic respiratory cycles synchronized with the efforts of the patient, if any. This avoids the automatic injection of air into the lungs in the middle or at the height of the patient's own spontaneous inspiration and reduces the risk of barotrauma. Synchronized intermittent forced ventilation is used in patients with tachypnea, who need significant fan support. In addition, the gradual increase in the intervals between the mandatory cycles facilitates the patient's withdrawal from the breathing apparatus during prolonged ventilation (OA Valley, 2002). Ventilation mode with inspiratory pressure support (PSV). In this mode, each patient's own inspiration is supported by a ventilator that responds to the patient's respiratory efforts, rapidly raising the pressure in the endotracheal tube of the level chosen by the physician. This pressure is maintained throughout the inhalation, after which the pressure in the tube drops to 0 or up to the PEEP required for adequate inhalation of the patient. Thus, in this mode of ventilation, the respiration rate, speed and duration of inspiration supported by the ventilator are completely determined by the patient. This mode of ventilation, which is the most comfortable for the patient, is often used to wean from the breathing apparatus, gradually reducing the level of pressure support.

It should be added that in these and many other modes of ventilation, PEEPs are often used - positive end-expiratory pressure. The advantages of this ventilation technique have been described above. The PEEP mode is used primarily in patients with alveolar shunt, early expiratory closure of the airways, collagen alveoli, atelectasis, and the like.

The regime of high-frequency ventilation (HF IVL) has a number of advantages in comparison with the described methods of volumetric ventilation and in recent years has acquired an increasing number of supporters. This mode combines a small tidal volume and a high frequency of ventilation. With the so-called jet HF IVL, the change in the phases of inspiration and expiration occurs at a frequency of 50-200 per min, and with oscillatory HF IVL reaches 1-3 thousand per min. The respiratory volume and, accordingly, the inspiratory-expiratory pressure drops in the lungs sharply decrease. The visceral-pulmonary pressure remains practically constant throughout the entire breathing cycle, which significantly reduces the risk of barotrauma and hemodynamic disorders. In addition, special studies have shown that the use of HF IVL, even in patients with parenchymal acute respiratory failure, increases RaO ₂ by 20-130 mm Hg. Art. More than using traditional volumetric ventilation. This proves that the effect of HF IVF extends not only to convection, but also to the alveolar (diffusion) zone, in which there is a significant improvement in oxygenation. In addition, this mode of artificial ventilation, apparently, is accompanied by an improvement in the drainage of minute bronchi and bronchioles.

When carrying out ventilation, remember the possible complications and undesirable effects of artificial ventilation, which include:

• spontaneous pneumothorax resulting from excessive increase in intrapulmonary pressure, for example, when using PEEP in patients with bullous pulmonary emphysema or with primary damage to lung tissue;
• violation of venous return of blood to the right heart, hypovolemia, reduction of cardiac output and blood pressure due to increased intrathoracic pressure;
• aggravation of violations of ventilation-perfusion relations as a result of compression of pulmonary capillaries and reduction of pulmonary blood flow;
• occurrence of respiratory alkalosis and associated violations of central regulation of respiration, hemodynamics, electrolyte composition and tissue gas exchange as a result of prolonged and insufficiently controlled hyperventilation;
• infectious complications (eg, nosocomial pneumonia, etc.);
• aspiration;
• complications of intubation in the form of esophagus ruptures, the emergence of mediastinal emphysema, subcutaneous emphysema,

To prevent these complications, it is necessary to carefully select the modes of ventilation and its basic parameters, as well as take into account all indications and contraindications for this method of treatment.

Oxygen therapy

The most important component of complex treatment of patients with respiratory failure of any genesis is oxygen therapy, the application of which in many cases is accompanied by significant positive results. At the same time, it should be remembered that the effectiveness of this method of treating respiratory failure depends on the mechanism of hypoxia and many other factors (OA Dolina, 2002). In addition, the use of oxygen therapy can be accompanied by undesirable side effects.

Indications for the appointment of oxygen therapy are clinico-laboratory signs of respiratory failure: dyspnea, cyanosis, tachycardia or bradycardia, decreased exercise tolerance, increased weakness, arterial hypotension or hypertension, impaired consciousness, as well as hypoxemia, decreased oxygen saturation, metabolic acidosis, etc.

There are several ways of oxygen therapy: inhalation oxygen therapy, hyperbaric, intravenous, extracorporeal oxygenation, the use of artificial oxygen carriers and antihypoxic drugs. The most widespread in clinical practice was inhaled oxygen therapy. Oxygen is iigalized through the nasal cannula, facial mask, intubation tube, tracheostomy cannulae, and the like. The advantage of using the nasal cannula was minimal discomfort for the patient, the ability to talk, cough, drink, and eat. The drawbacks of the method include the inability to increase the concentration of oxygen in the inspired air (FiO2) greater than 40%. The face mask gives a higher concentration of oxygen and provides a better moisturization of the inhaled mixture, but creates considerable discomfort. With intubation of the trachea, the oxygen concentration can be high.

When choosing the optimum oxygen concentration in the inspired air, the principle of minimum content should be followed, which can still provide at least the lower acceptable limit of PaO ₂ (about 60-65 mm Hg) and SaO ₂ (90%). The use of excessive concentrations of oxygen for many hours or days can have a negative effect on the body. Thus, if there is hypercapnia in patients with respiratory insufficiency, the use of high concentrations of oxygen with oxygen therapy leads not only to normalization, but also to an increase in the oxygen content in the blood (PaO2), which can smooth the clinical manifestations of respiratory failure during inhalation, despite the persistence of hypercapia. However, after the cessation of inhalation of oxygen, its negative effects, in particular the suppression of central hypoxic mechanisms of stimulation of respiration, can be affected. As a result, hypoventilation of the lungs is aggravated, the level of CO ₂ in the blood increases even more , respiratory acidosis develops and the clinical signs of acute respiratory failure increase.

This is facilitated by other negative effects of hyperoxia:

• retention of carbon dioxide in tissues due to the fact that as the concentration in the blood of oxyhemoglobin increases, the content of reduced hemoglobin, which is known to be one of the most important "carriers" of carbon dioxide, is significantly reduced;
• exacerbation of ventilation-perfusion ratios in the lungs due to oppression of the mechanism of hypoxic pulmonary vasoconstriction, because perfusion of poorly ventilated areas of lung tissue increases under the influence of high concentrations of oxygen; In addition, developing absorption micro-teleclases contribute to an increase in alveolar blood shunting;
• damage to the pulmonary parenchyma with superoxide radicals (destruction of the surfactant, damage to the ciliated epithelium, disturbance of the drainage function of the respiratory tract, and development of absorption micro-teleclactases against this background)
• blood denitrogenation (leaching of nitrogen), which leads to edema and fullness of the mucous membranes;
• hyperoxic damage to the central nervous system and others.

When administering inhalation of oxygen, it is advisable to adhere to the following recommendations (AP Zipber, 1996):

• The most rational way for long-term oxygen therapy is the minimum concentration of oxygen in the inspired air, which provides the lower permissible limit of oxygen parameters, and not the normal and, especially, excessive.
• If, when breathing air, PaO ₂ <65 mm Hg. Pa. ₂ (in venous blood) <35 mm Hg. And there is no hypercapnia (PaCO ₂ <40 mm Hg), high concentrations of oxygen can be used without fear of respiratory depression.
• If, when breathing air, PaO ₂ <65 mm Hg. , PaCO ₂ <35 mm Hg. And PaCO ₂ > 45 mm Hg. Art. (hypercapnia), the oxygen concentration in the inspired air should not exceed 40%, or oxygen therapy with higher concentrations should be combined with mechanical ventilation.

Before transferring the patient to mechanical ventilation, it is advisable to test the non-invasive ventilation mode, which usually allows to reduce the concentration of oxygen in the inhaled mixture. The increase in pulmonary volumes, which makes oxygene therapy more effective and prevents atelectasis due to hyperoxia, can be achieved by the PEEP.

Maintaining hemodynamics

The most important condition for effective therapy of patients with acute respiratory failure is the maintenance of adequate hemodynamics. For this purpose, mandatory monitoring of blood pressure, heart rate, CVP, DZLA and cardiac output is performed in intensive care or intensive care units in severe patients. In patients with acute respiratory failure, the most frequent changes in hemodynamics are the occurrence of hypovolemia. This is facilitated by high intrathoracic pressure in patients with obstructive and restrictive lung diseases, which limits the flow of blood to the right heart and leads to a decrease in BCC. The choice of an inadequate regime of mechanical ventilation can also contribute to increasing airway and chest pressure.

Recall that the hypovolemic type of circulation that develops in such patients is characterized by a sharp decrease in CVP (<5 mm Hg), DZLA and diastolic pressure in the pulmonary artery (<9 mm Hg) and SI (<1.8 -2.0 l / min × m ² ), as well as systolic blood pressure (<90 mm Hg) and pulse pressure (<30 mm Hg).

The most characteristic hemodynamic signs of hypovolemia are:

• Low values of CVP (<5 mm of mercury) and, respectively, collapsed peripheral veins during examination.
• Decrease in DZLA or diastolic pressure in the pulmonary artery and the absence of wet wheezing and other signs of blood congestion in the lungs.
• Decreased SI and systolic and pulse blood pressure.

Treatment of patients with hypovolaemia should be directed, first of all, to an increase in the venous return to the heart, to achieve the optimal level of ZDL (15-18 mm Hg) and restore the pump function of the left ventricle, mainly by increasing the preload and the inclusion of the Starling mechanism.

To this end, patients with hypovolemia are prescribed infusions of 0.9% solution of sodium chloride or low molecular weight dextrans, for example, rheopolyglucin or dextran 40. The latter not only effectively compensate intravascular volume of blood, but also improve the rheological properties of blood and microcirculation. Treatment is carried out under the control of CVP. DZLA, SI and AD. The introduction of fluid is stopped when the systolic blood pressure rises to 100 mm Hg. Art. And above and / or with an increase in DZLA (or diastolic pressure in the pulmonary artery) to 18-20 mm Hg. , the appearance of dyspnea and wet wheezing in the lungs and an increase in CVP.

Correction of the acid-base state

Significant violations of the blood gas composition in patients with respiratory failure are often accompanied by severe acid-base disorders, which, as a rule, has a negative effect on metabolic processes in the lungs and other internal organs, the state of regulation of respiration and the cardiovascular system, and the effectiveness of treatment of patients. Inadequately selected parameters of oxygen therapy and ventilation in patients with acute or chronic respiratory failure can also lead to significant violations of blood pH.

Respiratory acidosis (pH <7.35, BE in norm or> 2.5 mmol / l, SB in norm or> 25 mmol / l) in patients with acute respiratory insufficiency develops as a result of severe hypoventilation of the lung developing in patients with pneumothorax, pleural effusion, trauma of the chest, with pulmonary atelectasis, pneumonia, pulmonary edema, bronchial status. The cause of respiratory acidosis may be a depression of the central mechanisms of regulation of respiration (respiratory center depression), as well as prolonged oxygen therapy using a respiratory mixture with a high oxygen content. In all these cases, respiratory acidosis is combined with an increase in RaCO ₂ in the blood> 45 mm Hg. Art. (hypercapnia).

The best way to correct respiratory acidosis in patients with acute respiratory failure are measures aimed at improving ventilation of the lungs (non-invasive or invasive artificial ventilation) and, of course, treatment of the underlying disease. If necessary, stimulation of the respiratory center (naloxone, nalorphy) is carried out.

Respiratory alkalosis (pH> 7.45, BE in norm or <-2.5 mmol / l, SB in norm or <21 mmol / l) sometimes develops in patients with acute respiratory failure during the ventilation period, if not entirely well chosen the main parameters of this procedure, which leads to the emergence of hyperventilation of the lungs. Respiratory alkalosis is combined with a decrease in PaCO2 <35 mm Hg. Art. (hypocapnia) and moderate deficiency of bases.

Correction of respiratory alkalosis provides, first of all, optimization of the parameters of ventilation and a reduction in the frequency of respiration and respiratory volume.

Metabolic acidosis (pH <7.35, BE <-2.5 mmol / L and SB <21 mmol / L) develops in patients with severe respiratory failure and severe tissue hypoxia, which is accompanied by the accumulation in the tissues of a large number of under-oxidized metabolic products and organic acids. In this case, as a result of compensatory hyperventilation of the lungs (if it is possible), the Raco ₂ <35 mm Hg decreases . Art. And hypocapnia develops.

To eliminate metabolic acidosis, first of all, competent correction of hemodynamics, microcirculation and water-electrolyte metabolism is necessary. The use of bicarbonate buffers (4.2% and 8.4% sodium bicarbonate, 3.6% trisamine-THAM solution, 1% lactosol solution) is recommended only at critical pH values, as its rapid normalization can lead to disruption of compensation processes, osmolality disorders , electrolyte metabolism and tissue respiration. It should not be forgotten that in most cases metabolic acidosis at the initial stages of its development is a compensatory reaction of the organism to a pathological process aimed at preserving optimal oxygenation of tissues.

Correction of metabolic acidosis by intravenous injection of buffer solutions should be started in those cases when the pH is in the range of 7.15-7.20.

To calculate the dose of intravenously administered buffer solutions, the following formulas are proposed:

1. 4.2% solution of NaHCO ₃ (ml) = 0.5 x (WE weight of body);
2. 8.4% solution of NaHCO ₃ (ml) = 0.3 x (WE weight of body);
3. 3.6% THAM (ml) = BE x body weight.

In this case, BE is measured in mmol / l, and body weight - in kg.

Intravenous infusions of buffer solutions require careful monitoring of the dynamics of electrolyte blood composition and pH. For example, when sodium bicarbonate solution is introduced, a significant increase in the sodium content in the blood plasma is possible, which can cause a hyperosmolar condition, respectively, an increased risk of pulmonary edema, brain, arterial hypertension, etc. In case of an overdose of sodium bicarbonate, there is a danger of metabolic alkalosis development, which is accompanied by aggravation of tissue hypoxia and respiratory center depression due to displacement of the hemoglobin oxygenation curve to the left and increase in the affinity of hemoglobin to oxygen.

Prolonged oxygen therapy and IVL at home in patients with chronic respiratory failure

[8], [9], [10], [11], [12], [13]

Long-term oxygen therapy at home

Prolonged hypoxia of various organs and tissues in patients with chronic respiratory insufficiency, as is known, leads to the development of a number of serious morphological and functional disorders: pulmonary arterial hypertension, chronic pulmonary heart, hemodynamic, neuropsychic disorders, acid-base disorder and electrolyte exchange , and in severe cases to polyorganism insufficiency. Chronic hypoxia is naturally accompanied by a decrease in the quality of life and the survival of patients.

To prevent hypoxic damage to organs and tissues in patients with severe chronic respiratory failure in recent years, more and more long-term oxygen therapy at home. The concept of long-term oxygen therapy was first proposed in 1922 by D. Barach, but it was not until the 1970s and 1980s that it became more widespread in the world.

Long-term oxygen therapy is currently the only acceptable method of treatment at home, which can reduce the mortality of patients with chronic respiratory failure, for example, prolonging the life of patients with COPD for 6-7 years. At the same time, the life expectancy significantly improves if the duration of oxygen therapy exceeds 15 hours per day (MRC Trial study - British Medical Research Council, 1985).

Prolonged for many months and years, oxygen therapy increases the oxygen content in the arterial blood, leading to an increase in its delivery to the heart, the brain and other vital organs. In addition, prolonged oxygen therapy is accompanied by a decrease in dyspnea, increased exercise tolerance, decreased hematocrit, improved function and metabolism of the respiratory muscles, improved neuropsychological status of patients, and reduced hospitalization rates (RL Meredith, J, K. Stoller, 2004).

Indications for the appointment of long-term oxygen therapy for patients with chronic respiratory failure are (WJ O'Donohue, 1995):

• the values of PaO ₂  at rest are less than 55 mm Hg. Art. Or SaO ₂ less than 88%;
• values of PaO ₂ at rest from 56 to 59 mm Hg. Art. Or SaO ₂ less than 89% in the presence of clinical and / or electrocardiographic signs of a chronic pulmonary heart (compensated or decompensated) or secondary erythrocytosis (hematocrit 56% or more).

The task of oxygen therapy in patients with chronic respiratory failure is correction of hypoxemia and reaching values of PaO ₂ greater than 60 mm Hg. Art. And arterial blood saturation (SaO ₂ ) is more than 90%. It is considered optimal to maintain RaO ₂ within the range of 60-65 mm Hg. Art. Due to the sinusoidal form of the dissociation curve of oxyhemoglobin, an increase in PaO _{2 of} more than 60 mm Hg. Art. Leads only to an insignificant increase in SaO ₂ and the oxygen content in the arterial blood, but can lead to a delay in carbon dioxide. Thus, patients with chronic respiratory failure and indicators PaO ₂ > 60 mm Hg. Art. Prolonged oxygen therapy is not indicated.

With the appointment of long-term oxygen therapy, in most cases, select small streams of oxygen - 1-2 liters per minute, although in the most severe patients the flow can be increased by 1.5-2 times. Usually, oxygen therapy is recommended for 15 or more hours per day, including during night sleep. Inevitable interruptions between oxygen therapy sessions should not exceed 2 h.

As oxygen sources for prolonged oxygen therapy at home, it is most convenient to use special oxygen concentrators, which allow you to separate oxygen from the air and concentrate it. The arrangement of these autonomous devices can provide a sufficiently high oxygen content in the inspired gas mixture (40% to 90%) at a rate of 1-4 l / min. As systems for the delivery of oxygen to the respiratory tract, nasal cannulas, simple masks or Venturi masks are most often used.

Just like in patients with acute respiratory failure, the choice of oxygen concentration in the inhaled gas mixture during long-term oxygen therapy depends on the form of respiratory failure, the gas composition of the blood and the acid-base state. Thus, in patients with severe ventilation disorders and arterial hypoxemia combined with hypercapnia and / or peripheral edema caused by a decompensated pulmonary heart, oxygen therapy even with an oxygen-air mixture of 30-40% may be accompanied by hypoventilation, an even greater increase in RACO ₂, respiratory acidosis and even development of coma, which is associated with the oppression of the normal reaction of the respiratory center to hypercapnia. Therefore, in these cases it is recommended to use 24-28% oxygen-air mixture and careful control of acid-base state and gas composition of blood during treatment.

Long-term mechanical ventilation at home

A more effective method of treating patients with severe ventilation disorders and night and daytime hypercapnia is chronic respiratory support with portable ventilators. Long-term home ventilation is a method of long-term respiratory support for patients with a stable course of chronic respiratory failure who do not need intensive care. This method of treatment, especially in combination with rational oxygen therapy, can significantly increase the life expectancy of patients with chronic respiratory failure, improve their quality of life and improve the function of the respiratory apparatus. As a result of the systematic application of this method of treatment, hypercapnia, hypoxemia, lowering of the respiratory muscles, restoring the sensitivity of the respiratory center to CO _2, and the like decrease . The five-year survival rate of patients receiving long-term home ventilation is 43%,

Prolonged mechanical ventilation is shown, in particular, non-smoking patients who have a steady state (non-acute) The expressed ventilation disorders: FEV1 of less than 1.5 l and FVC less than 2 L and severe arterial hypoxemia (PaO ₂ <55 mm Hg.). With or without hypercapnia. One of the criteria for selecting patients for low-flow oxygen therapy is swelling as a manifestation of pulmonary hypertension and circulatory insufficiency.

The main indications for prolonged home ventilation.

Clinical

• Pronounced dyspnea at rest
• Weakness, a significant decrease in exercise tolerance
• Sleep disorders caused by hypoxemia
• Personality changes associated with chronic hypoxemia
• Signs of pulmonary hypertension and pulmonary heart, not amenable to conservative therapy

Functional

• FEV1 <1.5 L or / and FVC <2 L or / and
• PaO ₂ <55 mm Hg. Art. Or Sa2 <88% or
• PaO ₂ in the range from 55-59 mm Hg. Art. In combination with signs of a compensated or decompensated pulmonary heart, edema or hematocrit more than 55% and / or
• PaCO ₂ > 55 mm Hg. Art. Or
• RaCO ₂ in the range from 50 to 54 mm Hg. Art. In combination with nocturnal desaturation (SAO ₂ <88% or
• RaCO ₂ in the range from 50 to 54 mm Hg. Art. In combination with frequent episodes of hospitalization of the patient for hypercapnic respiratory failure (more than 2 episodes for 12 months)

Chronic respiratory support should be carried out at night, and then for several hours during the day. The parameters of home ventilation are usually selected in advance in a hospital setting, using principles.

Unfortunately, in Ukraine the described effective methods of long-term respiratory support in patients with chronic respiratory failure have not yet found wide application.