Treatment of respiratory failure

Treatment of patients with acute respiratory failure is carried out in the intensive care unit or resuscitation department and includes:

1. Elimination of the cause of acute respiratory failure (treatment of the underlying disease).
2. Ensuring airway patency.
3. Maintaining the required level of lung ventilation.
4. Correction of hypoxemia and tissue hypoxia.
5. Correction of acid-base balance.
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 underlying lung disease, the type of respiratory failure that has developed, the initial functional state of the lungs and respiratory tract, blood gas composition, acid-base balance, the patient's age, the presence of concomitant cardiovascular diseases, etc.

Ensuring airway patency

Ensuring free airway patency is the most important task in treating patients with acute respiratory failure, regardless of its genesis. For example, many diseases that cause parenchymatous respiratory failure (chronic obstructive bronchitis, bronchial asthma, bronchiolitis, cystic fibrosis, central lung cancer, bronchopneumonia, pulmonary tuberculosis, etc.) are characterized by pronounced airway obstruction caused by edema, mucous membrane infiltration, the presence of low secretion in the bronchi (sputum), spasm of the smooth muscles of the bronchi, and other causes. In patients with ventilatory respiratory failure, bronchial obstruction develops secondarily. Against the background of a significant decrease in respiratory volume and the resulting weakening of bronchial drainage. Thus, respiratory failure of any nature (parenchymal or ventilatory), one way or another, is accompanied by disturbances in bronchial patency, without the elimination of which effective treatment of respiratory failure is practically impossible.

Methods for Naturally Removing Phlegm

Sanitation of the tracheobronchial tree begins with the simplest methods - creating and maintaining optimal humidity and temperature of inhaled air (usual (flow-through, reversible) humidifiers are used to humidify and warm the air. Deep breathing of the patient, inducing a cough reflex, percussion or vibration massage of the chest also help remove sputum, if the patient's condition allows these therapeutic measures to be carried out. Pustural drainage in some cases allows for natural drainage of the bronchi and removal of sputum and can be used in the treatment of some patients with pneumonia, bronchiectasis, chronic obstructive bronchitis complicated by acute respiratory failure. However, in severe patients with respiratory failure, in unconscious patients or patients whose active movements are limited due to constant hemodynamic monitoring or receiving infusion therapy, the use of this method of clearing the airways is impossible. The same applies to the technique percussion or vibration massage of the chest, which has given good results in some patients with signs of bronchial obstruction.

Bronchodilators and expectorants

To restore the patency of the respiratory tract, bronchodilators (expectorants) are used. If the patient has signs of an active bacterial inflammatory process in the bronchi, it is advisable to use antibiotics.

Inhalation administration of bronchodilators and expectorants, as well as isotonic liquids, into the respiratory tract is preferable, which not only promotes a more effective effect of these drugs on the mucous membrane of the trachea, bronchi and tracheobronchial contents, but is also accompanied by the necessary moistening of the mucous membrane. However, it should be remembered that conventional jet inhalers form fairly large aerosol particles that reach only the oropharynx, trachea or large bronchi. In contrast, ultrasonic nebulizers create aerosol particles about 1-5 nm in size, which penetrate into the lumen of not only large but also small bronchi and have a more pronounced positive effect on the mucous membrane.

Anticholinergic drugs, euphyllin or beta2-adrenergic agonists are used as drugs with a bronchodilatory effect in patients with acute respiratory failure.

In case of severe bronchial obstruction, it is advisable to combine inhalation of beta2-adrenergic agonists with oral or parenteral administration of other bronchodilators. Euphyllin is initially administered at a saturating dose of 6 mg/kg in a small volume of 0.9% sodium chloride solution (slowly, over 10-20 min), and then its intravenous drip administration is continued at a maintenance dose of 0.5 mg/kg/h. In patients over 70 years of age, the maintenance dose of euphyllin is reduced to 0.3 mg/kg/h, and for patients with concomitant liver disease or chronic heart failure - to 0.1-0.2 mg/kg/h. Of the expectorants, ambroxol is most often used at a daily dose of 10-30 mg/kg (parenterally). If necessary, hydrocortisone is also prescribed 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.

Improvement of the rheological properties of sputum can also be achieved by using infusion therapy, for example, with isotonic sodium chloride solution, which promotes moderate hemodilution and a decrease in sputum viscosity.

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Methods of forced airway clearance

Tracheobronchial catheter. If the above methods of respiratory tract sanitation (pustural drainage, chest massage, use of inhalers, etc.) are insufficiently effective, there is severe bronchial obstruction and increasing respiratory failure, forced cleaning of the tracheobronchial tree is used. For this purpose, a plastic catheter with a diameter of 0.5-0.6 cm is inserted into the trachea, which is passed through the nasal passage or mouth and then through the vocal cords into the trachea, and if necessary, into the cavity of the main bronchi. Attaching the catheter (probe) to an electric suction device allows evacuation of sputum within the reach of the probe. In addition, being a strong mechanical irritant, the probe usually causes a strong reflex cough in the patient and the separation of a significant amount of sputum, which helps restore the patency of the respiratory tract.

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

Microtracheostomy is a percutaneous catheterization of the trachea and bronchi, which is used in cases where long-term continuous or periodic suction of tracheobronchial contents is planned, and there are no indications or technical capabilities for endotracheal intubation, fiberoptic bronchoscopy or artificial ventilation of the lungs.

After the patient's skin has been treated and local anesthesia has been administered, a puncture is made in the tracheal wall with a protected scalpel at the level between the cricoid cartilage and the first tracheal ring. A flexible guide mandrin is inserted into the opening, through which a tracheostomy cannula made of soft polyvinyl chloride with an internal diameter of 4 mm is inserted into the trachea. Insertion of a catheter into the trachea or bronchus usually causes a strong cough with the separation of sputum, which is aspirated through a tube.

In addition, the location of the probe in the trachea or one of the main bronchi is used to introduce liquids or medicinal substances into the trachea and bronchi that have a mucolytic, expectorant effect, improving the rheological properties of sputum.

For this purpose, 50-150 ml of isotonic sodium chloride solution or 5% sodium bicarbonate solution together with antimicrobial solutions (penicillin, furacillin, dioxidium, etc.) are injected into the tracheobronchial tree through a catheter. Rapid administration of these solutions during deep inhalation also provokes coughing, which allows aspiration of sputum and improves airway patency. If necessary, a small amount of mucolytic solution (for example, 5-10 mg of trypsin) is injected through an intratracheal catheter (probe), which liquefies sputum and facilitates its separation. The effect lasts for 2-3 hours, after which the procedure can be repeated.

In some cases, a catheter is inserted into one of the main bronchi to aspirate bronchial contents and administer drugs directly to the affected lung, for example, if the patient has atelectasis or abscesses. In general, the technique of percutaneous catheterization of the trachea and bronchi with aspiration of tracheobronchial contents is quite effective and easy to perform, although complications are possible during the procedure: 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 tracheal mucosa becomes less sensitive to mechanical irritation by the catheter and liquid solutions, and the cough reflex weakens. Fiberoptic bronchoscopy is the most effective method of removing sputum and sanitizing the mucous membrane of the trachea and bronchi, although this is not the only goal of this procedure. In this case, it becomes possible to sanitize the mucous membrane not only of the trachea and main bronchus, but also of other parts of the respiratory tract, right down to the segmental bronchi. The fibrobronchoscopy technique is less traumatic than microtracheostomy, and, in addition, has broad diagnostic capabilities.

Artificial ventilation of the lungs (AVL). If an endotracheal catheter or a fiberoptic bronchoscope fails to provide sufficient patency of the airways, and respiratory failure continues to increase, tracheobronchial tree sanitation is used using endotracheal intubation and ALV, unless indications for the use of these treatment methods have arisen earlier due to increasing hypoxemia and hypercapnia.

Non-invasive ventilation

Artificial ventilation of the lungs (AVL) is used in patients with acute respiratory failure to ensure sufficient ventilation (removal of CO2 from the body ₎ and adequate blood oxygenation (blood saturation with O2 ₎. The most common indication for ALV is the patient's inability to independently maintain these two processes.

Among the many types of artificial ventilation, a distinction is made between invasive artificial ventilation (via an endotracheal tube or tracheostomy) and non-invasive artificial ventilation (via a face mask). Thus, the term "non-invasive ventilation" is used to denote artificial ventilation of the lungs without invasive (endotracheal) penetration into the respiratory tract. The use of non-invasive ventilation in patients with acute respiratory failure allows avoiding many side effects of tracheal intubation, tracheostomy, and invasive artificial ventilation itself. For the patient, this method of treatment is more comfortable, allowing him to eat, drink, talk, expectorate, etc. during this procedure.

To perform non-invasive ventilation of the lungs, 3 types of masks are used:

• 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 by a mouthpiece.

The latter method is usually used in the treatment of patients with chronic acute respiratory failure, when long-term use of non-invasive mechanical ventilation is required. In acute acute respiratory failure, oronasal masks are more often used.

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

Positive inspiratory pressure ventilation provides increased pressure in the airways during inspiration. This increases the pressure gradient between the convection and alveolar (diffusion, gas exchange) zones, thereby facilitating inspiration and blood oxygenation. This mode can be used for both fully controlled and assisted ventilation.

Ventilation with positive end-expiratory pressure (PEEP). This mode involves creating a small positive pressure in the airways at the end of exhalation (usually no more than 5-10 cm H2O), which prevents the collapse of the alveoli, reduces the risk of the phenomenon of early expiratory bronchial closure, leads to the straightening of atelectasis and an increase in FRC. Due to the increase in the number and size of functioning alveoli, the ventilation-perfusion relationship improves, the alveolar shunt decreases, which is the reason for the improvement of oxygenation and the reduction of hypoxemia.

The PEEP mechanical ventilation mode is usually used to treat patients with parenchymatous acute respiratory failure, signs of bronchial obstruction, low FOE, a tendency of patients to develop early expiratory bronchial collapse and ventilation-perfusion disorders (COPD, bronchial asthma, pneumonia, atelectasis, acute respiratory distress syndrome, cardiogenic pulmonary edema, etc.).

It should be remembered that during mechanical ventilation in the PEEP mode, due to an increase in average intrathoracic pressure, the flow of venous blood to the right parts of the heart may be disrupted, which is accompanied by hypovolemia and a decrease in cardiac output and arterial pressure.

Continuous positive airway pressure (CPAP) ventilation is characterized by the fact that positive pressure (higher than atmospheric) is maintained throughout the entire respiratory cycle. In most cases, the pressure during inspiration is maintained at 8-11 cm H2O, and at the end of expiration (PEEP) - 3-5 cm H2O. The respiratory rate is usually set from 12-16 per minute to 18-20 per minute (in patients with weakened respiratory muscles)

If well tolerated, it is possible to increase the inhalation pressure to 15-20 cm H2O, and PEEP to 8-10 cm H2O. Oxygen is supplied directly to the mask or to the inhalation hose. The oxygen concentration is adjusted so that the oxygen saturation (SaO2 ₎ is above 90%.

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

The most common indications for NPPV are known clinical and pathophysiological signs of respiratory failure. An important condition for NPPV is the patient's adequacy and ability to cooperate with the physician during the NPPV procedure, as well as the ability to adequately remove sputum. 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, etc.

Indications for NPPV in acute respiratory failure (according to S. Mehla, NS Hill, 2004 in modification)

Pathophysiological signs of respiratory failure	Hypoxemia without hypercapnia Acute (or acute on the background of chronic) hypercapnia Respiratory acidosis
Clinical signs of respiratory failure	Dyspnea Paradoxical movement of the abdominal wall Participation of accessory muscles in breathing
Requirements for the patient	Respiratory protection ability Collaboration with a doctor Minimal tracheobronchial secretion Hemodynamic stability
Suitable categories of patients	COPD Bronchial asthma Cystic fibrosis Pulmonary edema Pneumonia Refusal to intubate

When performing NPPV, it is necessary to monitor blood pressure, heart rate, ECG, oxygen saturation and the main hemodynamic parameters. When the patient's condition stabilizes, NPPV can be interrupted for short periods and then completely stopped if, with spontaneous breathing, the respiratory rate does not exceed 20-22 per minute, oxygen saturation remains at a level greater than 90% and stabilization of the blood gas composition is observed.

Non-invasive positive pressure ventilation (NPPV), providing indirect "access" to the respiratory tract (through a mask), is a simpler and more comfortable method of respiratory support for the patient and allows avoiding a number of side effects and complications of endotracheal intubation or tracheostomy. At the same time, the use of NPPV requires the presence of intact airways and adequate cooperation of the patient and physician (S. Mehta, NS Hill, 2004).

Invasive ventilation

Traditional invasive mechanical ventilation (MV) using an endotracheal tube or tracheostomy is generally used in severe acute respiratory failure and in many cases can prevent rapid progression of the disease and even death of the patient.

The clinical criteria for transferring patients to artificial ventilation are acute respiratory failure, accompanied by severe dyspnea (more than 30-35 per minute), agitation, coma or sleep with decreased consciousness, severe increasing cyanosis or earthy color of the skin, increased sweating, tachycardia or bradycardia, active participation of accessory muscles in breathing and the occurrence of paradoxical movements of the abdominal wall.

According to the data of determining the gas composition of the blood and other functional research methods, the use of artificial ventilation is indicated when, in comparison with the required values, the vital capacity decreases by more than half, the oxygen saturation of arterial blood is less than 80%, PaO2 _is below 55 mm Hg, _PaCO2 is above 53 mm Hg and pH is below 7.3.

An important and, at times, decisive criterion for transferring a patient to mechanical ventilation is the rate of deterioration of the functional state of the lungs and disturbances in the gas composition of the blood.

Absolute indications for artificial ventilation are (S.N. Avdeev, A.G. Chucholin, 1998):

• respiratory arrest;
• severe disturbances of consciousness (stupor, coma);
• unstable hemodynamics (systolic blood pressure < 70 mmHg, heart rate < 50 bpm or > 160 bpm);
• fatigue of the respiratory muscles. Relative indications for artificial ventilation are:
• respiratory rate > 35 per min;
• arterial blood pH < 7.3;
• PaCO2 > ₂ <55 mmHg, despite oxygen therapy.

Transfer of the patient to invasive mechanical ventilation is generally indicated in cases of severe and progressive ventilatory (hypercapnic), parenchymatous (hypoxemic) and mixed forms of acute respiratory failure. At the same time, it should be remembered that this method of respiratory support is, for obvious reasons, most effective in patients with the ventilatory form of acute respiratory failure, since mechanical ventilation affects primarily the gas exchange in the convection zone. As is known, the parenchymatous form of respiratory failure in most cases is caused not by a decrease in ventilation volume, but by a violation of ventilation-perfusion relations and other changes occurring in the alveolar (diffusion) zone. Therefore, the use of mechanical ventilation in these cases is less effective and, as a rule, cannot completely eliminate hypoxemia. The increase in PaO2 _in patients with parenchymatous respiratory failure, which nevertheless occurs under the influence of artificial ventilation, is mainly due to a decrease in the energy expenditure of respiration and some 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 use of the artificial ventilation mode with positive pressure during inhalation. In addition, the use of the PEEP mode, which prevents the occurrence of microatelectasis, alveolar collapse and the phenomenon of early expiratory bronchial closure, contributes to an increase in FRC, some improvement in ventilation-perfusion relations and a decrease in alveolar shunting of blood. Due to this, in some cases it is possible to achieve a noticeable decrease in the clinical and laboratory signs of acute respiratory failure.

Invasive artificial ventilation is most effective in patients with the ventilatory form of acute respiratory failure. In the case of the parenchymatous 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 cannot radically eliminate arterial hypoxemia and are ineffective.

It should, however, be kept in mind that in clinical practice, cases of mixed respiratory failure are more often encountered, which are characterized by disturbances in both the alveolar (diffusion) and convection zones, which always leaves hope for a positive effect of the use of artificial ventilation in these patients.

The main parameters of artificial ventilation are (O.A. Dolina, 2002):

• minute ventilation volume (MOV);
• tidal volume (TV);
• respiratory rate (RR);
• pressure during inhalation and exhalation;
• ratio of inhalation and exhalation time;
• gas injection rate.

All the listed parameters are closely interconnected with each other. The choice of each of them depends on many factors taken into account, 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, etc.

Usually, artificial ventilation is carried out in a mode of moderate hyperventilation, causing some respiratory alkalosis and associated disturbances in the central regulation of respiration, hemodynamics, electrolyte composition and tissue gas exchange. The hyperventilation mode is a forced measure associated with the non-physiological relationship between ventilation and blood flow in the lungs during artificial inhalation and exhalation (G. Diette, R. Brower, 2004).

In clinical practice, a large number of modes of mechanical ventilation are used, which are described in detail in special guidelines on anesthesiology and resuscitation. The most common of them are continuous mandatory ventilation (CMV), assist control ventilation (ACV), intermittent mandatory ventilation (IMV), synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation (PSV), pressure control ventilation (PCV), 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 the ability to breathe independently (patients with disorders of central regulation of breathing, paralysis or severe fatigue of the respiratory muscles, as well as patients with respiratory depression caused by the use of muscle relaxants and narcotics during surgery, etc.). In these cases, the ventilator automatically blows the required portion of air into the lungs at a certain frequency.

Assisted-controlled ventilation (ACV) is used in patients with acute respiratory failure who retain the ability to breathe independently, although not entirely effectively. In this mode, a minimum respiratory rate, tidal volume, and inspiratory flow rate are set. If the patient independently makes an adequate attempt to inhale, the ventilator immediately “responds” to it by insufflating a predetermined volume of air and, thus, “takes over” part of the work of breathing. If the frequency of spontaneous (independent) inhalations is greater than the prescribed minimum respiratory rate, all respiratory cycles are assisted. If, however, there is no attempt at independent inhalation within a certain time interval (t), the ventilator automatically carries out “controlled” insufflation of air. Assisted-controlled ventilation, in which the ventilator takes over most or all of the work of breathing, is often used in patients with neuromuscular weakness or with severe fatigue of the respiratory muscles.

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

A modification of this method of artificial ventilation is synchronized and intermittent mandatory ventilation (SIMV), in which the ventilator maintains periodic respiratory cycles synchronized with the patient's efforts, if any. This avoids automatic blowing of air into the lungs in the middle or at the height of the patient's spontaneous inhalation and reduces the risk of barotrauma. Synchronized intermittent mandatory ventilation is used in patients with tachypnea who require significant ventilatory support. In addition, a gradual increase in the intervals between forced cycles facilitates the patient's weaning from mechanical breathing during prolonged mechanical ventilation (OA Dolina, 2002). Pressure support ventilation mode on inspiration (PSV). In this mode, each spontaneous breath of the patient is supported by a ventilator, which responds to the patient's respiratory efforts, quickly increasing the pressure in the endotracheal tube to the level selected by the doctor. This pressure is maintained throughout the entire inhalation, after which the pressure in the tube drops to 0 or to the PEEP required for adequate inhalation of the patient. Thus, in this mode of ventilation, the respiratory 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 for weaning from mechanical breathing, gradually reducing the level of pressure support.

It should be added that the above and many other modes of artificial ventilation often use PEEP - positive end-expiratory pressure. The advantages of this ventilation technique were described above. The PEEP mode is used primarily in patients with alveolar shunt, early expiratory closure of the airways, collapsed alveoli, atelectasis, etc.

The high-frequency ventilation mode (HFMV) has a number of advantages over the described methods of volumetric ventilation and has been gaining more and more supporters in recent years. This mode combines a small tidal volume and a high ventilation frequency. With the so-called jet HFMV, the change in the inhalation and exhalation phases occurs with a frequency of 50-200 per minute, and with oscillatory HFMV it reaches 1-3 thousand per minute. The tidal volume and, accordingly, the inspiratory-expiratory pressure drops in the lungs are sharply reduced. The intrapulmonary pressure remains almost constant during the entire respiratory cycle, which significantly reduces the risk of barotrauma and hemodynamic disorders. In addition, special studies have shown that the use of HFMV even in patients with parenchymatous acute respiratory failure allows increasing PaO ₂ by 20-130 mm Hg more than with traditional volumetric ventilation. This proves that the effect of HF ALV extends not only to the convection zone, but also to the alveolar (diffusion) zone, where oxygenation is significantly improved. In addition, this mode of artificial ventilation is apparently accompanied by improved drainage of the smallest bronchi and bronchioles.

When performing artificial ventilation, one should remember about possible complications and undesirable effects of artificial ventilation, which include:

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

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

Oxygen therapy

The most important component of the complex treatment of patients with respiratory failure of any genesis is oxygen therapy, the use 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 may be accompanied by undesirable side effects.

Indications for the administration of oxygen therapy are clinical and laboratory signs of respiratory failure: dyspnea, cyanosis, tachycardia or bradycardia, decreased tolerance to physical activity, increasing weakness, arterial hypotension or hypertension, impaired consciousness, as well as hypoxemia, decreased oxygen saturation, metabolic acidosis, etc.

There are several methods of oxygen therapy: inhalation oxygen therapy, hyperbaric, intravenous, extracorporeal oxygenation, the use of artificial oxygen carriers and antihypoxic agents. Inhalation oxygen therapy is the most widely used in clinical practice. Oxygen is inhaled through nasal cannulas, a face mask, an endotracheal tube, tracheostomy cannulas, etc. The advantage of using nasal cannulas was minimal discomfort for the patient, the ability to speak, cough, drink, and eat. The disadvantages of the method include the inability to increase the concentration of oxygen in the inhaled air (FiO2) to more than 40%. A face mask provides a higher concentration of oxygen and ensures better humidification of the inhaled mixture, but creates significant discomfort. During tracheal intubation, the oxygen concentration can be high.

When choosing the optimal concentration of oxygen in the inhaled air, one should adhere to the principle of its minimum content, which can still provide at least the lower permissible limit of PaO ₂ (about 60-65 mm Hg) and SaO ₂ (90%). The use of excess oxygen concentrations for many hours or days can have a negative effect on the body. Thus, if patients with respiratory failure have hypercapnia, the use of high oxygen concentrations in oxygen therapy leads not only to normalization, but also to an increase in the oxygen content in the blood (PaO2), which can smooth out the clinical manifestations of respiratory failure during inhalation, despite the persistence of hypercapia. However, after the cessation of oxygen inhalation, its negative effects may occur, in particular, the suppression of central hypoxic mechanisms of respiratory stimulation. As a result, hypoventilation of the lungs worsens, 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 also facilitated by other negative effects of hyperoxia:

• retention of carbon dioxide in tissues due to the fact that with an increase in the concentration of oxyhemoglobin in the blood, the content of reduced hemoglobin, which is known to be one of the most important “carriers” of carbon dioxide, is significantly reduced;
• worsening of ventilation-perfusion relations in the lungs due to the suppression of the mechanism of hypoxic pulmonary vasoconstriction, since under the influence of high concentrations of oxygen, perfusion of poorly ventilated areas of lung tissue increases; in addition, developing absorption microatelectases contribute to an increase in alveolar shunting of blood;
• damage to the lung parenchyma by superoxide radicals (destruction of surfactant, damage to the ciliated epithelium, disruption of the drainage function of the respiratory tract and the development of absorption microatelectasis against this background)
• denitrogenation of the blood (washing out of nitrogen), which leads to swelling and plethora of the mucous membranes;
• hyperoxic CNS damage and others.

When prescribing oxygen inhalations, it is advisable to adhere to the following recommendations (A.P. Zipber, 1996):

• The most rational way for long-term oxygen therapy is a minimum concentration of oxygen in the inhaled air, ensuring the lower permissible limit of oxygen parameters, and not normal and, especially, excessive.
• If, when breathing air, _PaO2 < 65 mm Hg, PaO2 ₍ in venous blood) < 35 mm Hg, and there is no hypercapnia (PaCO2 _< 40 mm Hg), high concentrations of oxygen can be used without fear of respiratory depression.
• If, when breathing air, _PaO2 < 65 mmHg, PaCO2 _< 35 mmHg, and PaCO2 _> 45 mmHg (hypercapnia), the concentration of oxygen in the inhaled air should not exceed 40%, or oxygen therapy with higher concentrations should be combined with mechanical ventilation.

Before transferring the patient to artificial ventilation, it is advisable to try a noninvasive ventilation mode, which usually allows for a decrease in the oxygen concentration in the inhaled mixture. An increase in lung volumes, which makes oxygen therapy more effective and prevents the occurrence of atelectasis due to hyperoxia, can be achieved using the PEEP mode.

Maintaining hemodynamics

The most important condition for effective therapy of patients with acute respiratory failure is maintaining adequate hemodynamics. For this purpose, in intensive care units or resuscitation units in severe patients, mandatory monitoring of blood pressure, heart rate, central venous pressure, cardiac output and cardiac output is carried out. In patients with acute respiratory failure, the most frequent changes in hemodynamics consist of the occurrence of hypovolemia. This is facilitated by high intrathoracic pressure in patients with obstructive and restrictive lung diseases, which limits blood flow to the right heart and leads to a decrease in circulating blood volume. The choice of an inadequate mode of mechanical ventilation can also contribute to an increase in pressure in the airways and chest.

Let us recall that the hypovolemic type of blood circulation developing in such patients is characterized by a sharp decrease in CVP (< 5 mm Hg), PAOP and diastolic pressure in the pulmonary artery (< 9 mm Hg) and CI (< 1.8-2.0 l/min × m2 ⁾, as well as systolic blood pressure (< 90 mm Hg) and pulse pressure (< 30 mm Hg).

The most characteristic hemodynamic signs of hypovolemia are:

• Low CVP values (< 5 mmHg) and, accordingly, collapsed peripheral veins on examination.
• A decrease in the PAP or diastolic pressure in the pulmonary artery and the absence of wet rales and other signs of blood congestion in the lungs.
• Reduction of SI and systolic and pulse arterial pressure.

Treatment of patients with hypovolemia should be aimed primarily at increasing venous return to the heart, achieving an optimal level of PAOP (15-18 mm Hg) and restoring the pumping function of the left ventricle primarily by increasing preload and activating the Starling mechanism.

For this purpose, patients with hypovolemia are prescribed infusions of 0.9% sodium chloride solution or low-molecular dextrans, such as rheopolyglucin or dextran 40. The latter not only effectively replace the intravascular blood volume, but also improve the rheological properties of the blood and microcirculation. Treatment is carried out under the control of CVP, PAOP, SI and BP. Fluid administration is stopped when systolic blood pressure increases to 100 mm Hg and above and/or when PAOP (or diastolic pressure in the pulmonary artery) increases to 18-20 mm Hg, dyspnea and moist rales in the lungs appear and CVP increases.

Correction of acid-base balance

Significant disturbances of the blood gas composition in patients with respiratory failure are often accompanied by pronounced disturbances of the acid-base balance, 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 artificial ventilation in patients with acute or chronic respiratory failure can also lead to significant disturbances of blood pH.

Respiratory acidosis (pH < 7.35; BE normal or > 2.5 mmol/l; SW normal or > 25 mmol/l) in patients with acute respiratory failure develops as a result of severe hypoventilation of the lungs, which develops in patients with pneumothorax, pleural effusion, chest trauma, pulmonary atelectasis, pneumonia, pulmonary edema, bronchial status. Respiratory acidosis can be caused by depression of the central mechanisms of respiratory regulation (depression of the respiratory center), as well as long-term oxygen therapy using a breathing mixture with a high oxygen content. In all these cases, respiratory acidosis is combined with an increase in PaCO2 _in the blood > 45 mm Hg (hypercapnia).

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

Respiratory alkalosis (pH > 7.45; BE normal or < -2.5 mmol/l; SB normal or < 21 mmol/l) sometimes develops in patients with acute respiratory failure during mechanical ventilation if the main parameters of this procedure are not chosen very well, which leads to the development of hyperventilation of the lungs. Respiratory alkalosis is combined with a decrease in PaCO2 < 35 mm Hg (hypocapnia) and moderate base deficit.

Correction of respiratory alkalosis involves, first of all, optimizing the parameters of mechanical ventilation and reducing the respiratory rate and tidal volume.

Metabolic acidosis (pH < 7.35, BE < -2.5 mmol/l and SW < 21 mmol/l) develops in patients with severe respiratory failure and pronounced tissue hypoxia, which is accompanied by the accumulation of a large amount of underoxidized metabolic products and organic acids in the tissues. As a result of compensatory hyperventilation of the lungs (if possible), PaCO2 decreases to _< 35 mm Hg and hypocapnia develops.

To eliminate metabolic acidosis, first of all, it is necessary to properly correct hemodynamics, microcirculation and water-electrolyte balance. The use of bicarbonate buffers (4.2% and 8.4% sodium bicarbonate, 3.6% trisamine solution - THAM, 1% lactosol solution) is recommended only at critical pH values, since its rapid normalization can lead to a breakdown of compensation processes, disturbances in osmolarity, electrolyte balance 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 body to a pathological process, aimed at maintaining optimal tissue oxygenation.

Correction of metabolic acidosis with intravenous administration of buffer solutions should be initiated in cases where the pH is in the range of 7.15-7.20.

To calculate the dose of intravenously administered buffer solutions, it is suggested to use the following formulas:

1. 4.2% NaHCO3 solution ₍ ml) = 0.5 x (BE × body weight);
2. 8.4% NaHCO3 solution ₍ ml) = 0.3 x (BE × body weight);
3. 3.6% TNAM (ml) = BE x body weight.

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

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

Long-term oxygen therapy and mechanical ventilation at home in patients with chronic respiratory failure

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Long-term oxygen therapy at home

Long-term hypoxia of various organs and tissues in patients with chronic respiratory failure is known to lead to the development of a number of serious morphological and functional disorders: pulmonary arterial hypertension, chronic pulmonary heart disease, hemodynamic, neuropsychiatric disorders, acid-base balance and electrolyte metabolism disorders, and in severe cases to multiple organ failure. Chronic hypoxia is naturally accompanied by a decrease in the quality of life and survival of patients.

In order to prevent hypoxic damage to organs and tissues in patients with severe chronic respiratory failure, long-term oxygen therapy at home has been increasingly used in recent years. The concept of long-term oxygen therapy was first proposed in 1922 by D. Barach, but it only became more widespread in the world in the 1970s and 1980s.

Long-term oxygen therapy is currently the only acceptable home treatment method capable of reducing mortality in patients with chronic respiratory failure, for example, prolonging the life of COPD patients by 6-7 years. At the same time, the life prognosis is significantly improved if the duration of oxygen therapy exceeds 15 hours per day (MRC Trial - British Medical Research Council, 1985).

Long-term, over many months and years, oxygen therapy increases the oxygen content in arterial blood, leading to an increase in its delivery to the heart, brain and other vital organs. In addition, long-term oxygen therapy is accompanied by a decrease in dyspnea, an increase in exercise tolerance, a decrease in hematocrit, an improvement in the function and metabolism of the respiratory muscles, an improvement in the neuropsychological status of patients, and a decrease in the frequency of hospitalizations (RL Meredith, J,K. Stoller, 2004).

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

• _{resting PaO2} values less than 55 mmHg or SaO2 _less than 88%;
• values of _PaO2 at rest from 56 to 59 mmHg or SaO2 _less than 89% in the presence of clinical and/or electrocardiographic signs of chronic pulmonary heart disease (compensated or decompensated) or secondary erythrocytosis (hematocrit 56% or more).

The objective of oxygen therapy in patients with chronic respiratory failure is to correct hypoxemia and achieve PaO2 values _greater than 60 mm Hg and arterial blood saturation (SaO2 _{) greater than 90%. MaintainingPaO2} within 60-65 mm Hg is considered optimal. Due to the sinusoidal shape of the oxyhemoglobin dissociation curve, an increase in _PaO2 greater than 60 mm Hg leads to only a slight increase in SaO2 _and arterial blood oxygen content, but may lead to carbon dioxide retention. Thus, long-term oxygen therapy is not indicated for patients with chronic respiratory failure and PaO2 values _> 60 mm Hg.

When prescribing long-term oxygen therapy, in most cases small oxygen flows are chosen - 1-2 liters per minute, although in the most severe patients the flow can be increased by 1.5-2 times. Usually, it is recommended to use oxygen therapy for 15 or more hours per day, including during night sleep. The inevitable breaks between oxygen therapy sessions should not exceed 2 hours.

As sources of oxygen for long-term oxygen therapy at home, it is most convenient to use special oxygen concentrators, which allow separating oxygen from atmospheric air and concentrating it. The design of these autonomous devices can provide a sufficiently high oxygen content in the inhaled gas mixture (from 40% to 90%) at a rate of 1-4 l/min. Nasal cannulas, simple masks or Venturi masks are most often used as systems for delivering oxygen to the respiratory tract.

As 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, blood gas composition and acid-base balance. Thus, in patients with severe ventilation disorders and arterial hypoxemia combined with hypercapnia and/or peripheral edema caused by decompensated pulmonary heart disease, oxygen therapy with even a 30-40% oxygen-air mixture can be accompanied by hypoventilation, an even greater increase in PaCO2 _, respiratory acidosis and even the development of coma, which is associated with the suppression of the normal reaction of the respiratory center to hypercapnia. Therefore, in these cases, it is recommended to use a 24-28% oxygen-air mixture and carefully monitor the acid-base balance and blood gas composition during treatment.

Long-term mechanical ventilation at home

A more effective method of treating patients with severe ventilation disorders and night and day hypercapnia is chronic respiratory support using portable ventilators. Long-term home ventilation is a method of long-term respiratory support for patients with stable chronic respiratory failure who do not require 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 enhance the function of the respiratory system. As a result of the systematic use of this method of treatment, there is a decrease in hypercapnia, hypoxemia, a decrease in the work of the respiratory muscles, restoration of the sensitivity of the respiratory center to CO ₂, etc. Five-year survival of patients receiving long-term home ventilation is 43%,

Long-term mechanical ventilation is indicated primarily for non-smoking patients who, in a stable condition (outside of an exacerbation), have pronounced ventilation disorders: FEV1 less than 1.5 l and FVC less than 2 l and severe arterial hypoxemia (PaO2 _< 55 mm Hg) with or without hypercapnia. One of the criteria for selecting patients for low-flow oxygen therapy is edema as a manifestation of pulmonary hypertension and circulatory failure.

Main indications for long-term home ventilation.

Clinical

• Severe shortness of breath at rest
• Weakness, significant decrease in exercise tolerance
• Sleep disorders caused by hypoxemia
• Personality changes associated with chronic hypoxemia
• Signs of pulmonary hypertension and pulmonary heart disease that are not amenable to conservative therapy

Functional

• FEV1< 1.5 L or/and FVC <2 L or/and
• PaO2 < 55 mmHg or SaO2 < 88% _or
• PaO2 within 55-59 mm Hg in combination with signs of compensated or decompensated pulmonary heart disease, edema or hematocrit greater than 55% and/ _or
• PaCO ₂ > 55 mm Hg. Art. or
• PaCO2 within the range of ₅₀ to 54 mmHg in combination with nocturnal desaturation (SaO2 _< 88% or
• PaCO2 within the range of ₅₀ to 54 mm Hg in combination with frequent episodes of hospitalization of the patient due to hypercapnic respiratory failure (more than 2 episodes within 12 months)

Chronic respiratory support should be provided at night and then for a few hours during the day. Home ventilation parameters are usually selected in advance in a hospital setting using the 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.