Respiratory failure - Overview of information

Respiratory failure syndrome can complicate the course of most acute and chronic respiratory diseases and is one of the main reasons for repeated hospitalizations, decreased ability to work, physical activity at home and premature death of patients. At the same time, it should be borne in mind that respiratory failure is often encountered in the practice of anesthesiologists, resuscitators, neurologists, traumatologists, surgeons and doctors of other specialties, which is explained by the variety of its causes, which are not always associated with respiratory pathology.

Respiratory failure is a condition of the body in which either the maintenance of normal gas composition of the blood is not ensured, or this is achieved by abnormal functioning of the external respiratory system, leading to a decrease in the functional capabilities of the body.

Normal respiratory function is ensured by: central regulation by the respiratory center (irritant carbon dioxide); the state of the impulse conduction system along the anterior roots of the spinal cord; the state of conductivity at the level of the neuromuscular synapse and muscle mediators; the state and function of the costal framework; changes in the functional state of the pleural cavity, diaphragm, lungs, patency of the airways; the state of the inhaled gas mixture. The state of cardiac activity and blood flow in the pulmonary circulation are of great importance in the development of respiratory failure.

In pathological conditions at these levels, the normal gas composition of the blood can be maintained for a long time by the tension of compensatory mechanisms: an increase in the frequency and depth of breathing, an increase in heart rate and blood flow velocity, increased kidney function to remove acidic metabolic products, an increase in the oxygen capacity of the blood, and others with the formation of latent respiratory failure. With decompensation, a pronounced picture of respiratory failure develops with the development of hypoxic syndrome.

Respiratory failure is classified by many systems, but there is no single international one yet.

From a practical point of view, the most acceptable classification is that of B.E. Votchal (1972). By genesis, there are: centrogenic respiratory failure (with damage to the respiratory center); neuromuscular (with damage to the conduction pathways and muscles); thoracodiaphragmatic (with damage to the costal frame or dysfunction of the diaphragm); bronchopulmonary - obstructive respiratory failure caused by obstruction of the airways (bronchospasm, inflammation, foreign bodies, tumors, asphyxia, etc.), restrictive, caused by pathology of the alveoli (inflammation, alveolar edema or tumor, etc.) or compression of the lung, pleural effusion, diffusion, developing with pathology of microcirculation in the lungs or destruction of surfactant. According to the course, respiratory failure can be acute (ARF) and chronic (CRF). In terms of severity, it can be compensated, with a decrease in the partial pressure of oxygen in arterial blood to 80 mm Hg; subcompensated - up to 60 mm Hg; decompensated with a decrease in PaO2 below 60 mm Hg and the development of hypoxic syndrome.

Chronic respiratory failure is diagnosed by therapists if the cause is not surgical thoracic pathology, usually benign or malignant tumors. Sometimes the surgeon has to determine the severity of the disease. According to B.E. Votchala, there are 4 degrees:

• I - shortness of breath when running and quickly climbing stairs;
• II - shortness of breath during normal activities in everyday life (moderate walking, cleaning, etc.);
• III - shortness of breath with little exertion (dressing, washing);
• IV - shortness of breath at rest.

Many pulmonologists and therapists use the so-called “everyday” classification of the severity of chronic respiratory failure - the appearance of shortness of breath with moderate climbing up the stairs:

• Grade I - shortness of breath at the level of the third floor;
• II degree - at the level of the second floor;
• III degree – at the level of the first floor.

Acute respiratory failure of various genesis may be encountered in the practice of any surgeon. Centrogenic acute respiratory failure is observed in craniocerebral trauma, brain compression syndrome, inflammation, poisoning. The neuromuscular form is more common in cervical spine trauma and spinal cord injuries, and rarely in myasthenia, syringomyelia, botulism, and tetanus. Thoracodiaphragmatic (parietal) acute respiratory failure is typical for rib fractures, especially with a violation of the rib cage framework, diaphragmatic hernias, diaphragmatic relaxation, and diaphragmatic compression by distended intestinal loops.

Bronchopulmonary acute respiratory failure is the most common in the practice of surgeons. The restrictive form is most often observed in pneumothorax, pleurisy, hemothorax, alveolar cancer, pneumonia, abscesses and gangrene of the lungs and other diseases of the parenchymatous part of the pulmonary coat. In addition to the clinical picture of acute respiratory failure, chest X-ray is performed to identify the cause. Other studies are carried out according to indications by thoracic surgeons.

Obstructive respiratory failure may occur with bronchospasm, tongue retraction, bronchial tree malformations (diverticula, tracheal prolapse), bronchial tumors, fibrinous-ulcerative and adhesive bronchitis. Rarely, asphyxia occurs. External; asphyxia develops with suffocation. In surgical practice, regurgitation (Mendelson's syndrome) may occur due to the entry of vomitus, blood (hemoaspiration) into the airways, or abundant secretion of bronchial secretions that close the lumen of the bronchi (atelectasis). Foreign bodies and burns may occur, but this is very rare, since the lungs are protected by a reflex spasm of the vocal cords. Acute obstruction develops suddenly: breathing is severely labored, shallow, often arrhythmic, auscultation is not performed or cacophony with a bronchial component is heard. Emergency radiography and bronchoscopy not only allow for a topical diagnosis. Radiologically, obstruction is manifested by pulmonary atelectasis (homogeneous intense darkening with a shift of the mediastinum toward the darkening).

Asphyxia from drowning should be considered as a separate issue. There are three types of drowning:

1. True drowning with water entering the airways occurs in 75-95% of cases, when after a short cessation of breathing the reflex spasm of the vocal cords is removed and with an involuntary inhalation a large amount of water enters the bronchi and alveoli. It is accompanied by a sharply expressed purple cyanosis, swelling of the veins of the neck and extremities, and the release of a foamy pink liquid from the mouth.
2. Asphyxial drowning, which occurs in 5-20% of cases, when a sharp reflex laryngospasm is observed with a small but sudden flow of water into the throat or nose. In this case, water does not enter the lungs, but goes into the stomach, overflowing it. Sometimes vomiting with regurgitation can occur, then this type of drowning turns into true drowning. In asphyxial drowning, cyanosis is blue, white or light pink "fluffy" foam comes out of the mouth and nose.
3. "Syncopal" drowning is observed in 5-10% of cases. It occurs with reflex cardiac and respiratory arrest due to sudden immersion in cold water. It can also occur with emotional shock, injection of a cold solution into a vein, injection of a cold solution into the ear, nose or throat ("laryngopharyngeal shock").

Respiratory failure is a life-threatening impairment of O2 consumption and CO2 production. It may involve impaired gas exchange, decreased ventilation, or both. Common manifestations may include dyspnea, accessory muscle involvement, tachycardia, increased sweating, cyanosis, and impaired consciousness. Diagnosis is based on clinical and laboratory data, arterial blood gas testing, and radiographic examination. Treatment is performed in the intensive care unit and includes correction of the causes of respiratory failure, O2 inhalation, sputum removal, and respiratory support if necessary.

During respiration, oxygenation of arterial blood and elimination of CO2 from venous blood occur _. Therefore, respiratory failure is distinguished as a result of inadequate oxygenation or inadequate ventilation, although both disorders are often present.

Artificial lung ventilation (ALV) can be non-invasive and invasive. The choice of treatment method is based on knowledge of the respiratory mechanisms.

Respiratory failure is a condition in which the lungs are unable to provide normal gas composition of arterial blood, resulting in hypercapnia and/or hypoxemia. According to another frequently used definition proposed by E. Campbell, respiratory failure is a condition in which, under resting conditions, the partial pressure of oxygen (PaO2) in arterial blood is below 60 mm Hg and/or the partial pressure of carbon dioxide (PaCO2) is above 49 mm Hg.

Both definitions essentially refer to the most severe cases of decompensated respiratory failure, which manifests itself at rest. However, from a clinical point of view, it is important to determine respiratory failure at the earliest possible stages of development, when diagnostically significant changes in the gas composition of arterial blood are detected not at rest, but only with an increase in the activity of the respiratory system, for example, during physical exertion. In this regard, we like the definition of respiratory failure proposed more than half a century ago (1947) at the XV All-Union Congress of Therapists: "Respiratory failure is a condition in which either the maintenance of normal gas composition of arterial blood is not ensured, or the latter is achieved due to abnormal functioning of the external respiratory apparatus, leading to a decrease in functional capabilities." According to this definition, two stages of respiratory failure syndrome development can be distinguished: compensated and decompensated.

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Methods and modes of mechanical ventilation

Ventilators control the pressure or volume of inspiration, or both. There is a certain relationship between pressure and volume: a certain pressure corresponds to a certain volume and vice versa. The parameters set on the device differ in different modes, but they are based on the respiratory rate, total ventilation volume, flow rate, waveform, and the ratio of inspiratory and expiratory duration (I/E).

Volume-controlled ventilation. In this ventilation mode, the patient is supplied with a given volume of air, while the pressure in the airways may vary. This type of mechanical ventilation is used in assist-control (A/C) and synchronized intermittent mandatory ventilation (SIMV).

A/C is the simplest and most effective method of mechanical ventilation. Each attempt to inhale is detected by a trigger, and the device delivers a set volume of air. In the absence of independent attempts to inhale, the device performs forced ventilation at a set frequency of inhalations.

SIMV delivers a set number and volume of breaths synchronized with the patient. Unlike A/C, spontaneous inhalation attempts are not supported, but the inhalation valve opens and allows spontaneous inhalation. This mode remains popular, although it does not provide respiratory support and is not effective in weaning the patient from mechanical ventilation.

Pressure-cycled ventilation. This mode includes pressure control ventilation (PCV), pressure support ventilation (PSV), and several noninvasive face mask options. In all cases, the ventilator delivers a specific inspiratory pressure while the volume can be varied. Changes in the mechanics of the respiratory system can lead to unrecognized changes in minute ventilation. Because this mode limits the pressure at which the lungs expand, it may theoretically be useful in RD-SV; however, its clinical advantages over A/C have not been demonstrated.

PCV is similar to A/C; each inspiratory attempt that exceeds the set trigger sensitivity limit is maintained with pressure for a certain time, and a minimum respiratory rate is maintained.

In PSV, there is no minimum respiratory rate; all breaths are initiated by the patient. The pressure delivered is typically turned off when the inspiratory attempt is complete. Thus, the longer or stronger the inspiratory attempt, the greater the resulting inspiratory volume. This mode is typically used when weaning a patient off mechanical ventilation. A similar mode is continuous positive airway pressure (CPAP), which maintains a constant pressure throughout the respiratory cycle. Unlike PSV, which may have different inspiratory and expiratory pressures, CPAP maintains a constant pressure.

Noninvasive positive pressure ventilation (NIPPV) is the application of positive pressure during ventilation through a tightly fitting mask over the nose or nose and mouth. It is used as a variant of PSV in spontaneously breathing patients. The physician sets the inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). Since the airway is unprotected, NIPPV can be used in patients with intact protective reflexes and in a fully conscious state to avoid aspiration. NIPPV should be avoided in hemodynamically unstable patients and in gastric congestion. In addition, IPAP should be set below the esophageal opening pressure (20 cm H2O) to avoid air entering the stomach.

Ventilator settings. Ventilator settings are adjusted based on the situation. Tidal volume and respiratory rate determine minute ventilation. Typically, tidal volume is 8-9 ml/kg ideal body weight, although some patients, especially those with neuromuscular diseases, benefit from higher tidal volumes to prevent atelectasis. Certain disorders (eg, ARDS) require lower tidal volumes.

The sensitivity of the trigger is set so that it can detect spontaneous attempts to inhale. Usually, the sensitivity is set at -2 cm H2O. If the limit is set too high, weakened patients will not be able to initiate inhalation. If the sensitivity is set too low, this will lead to hyperventilation.

The inhalation/exhalation ratio with normal breathing mechanics is set at 1:3. In patients with asthma or COPD in the acute stage, the ratio should be 1:4 or higher.

The flow rate is usually set at about 60 L/min, but it can be increased to 120 L/min in patients with obstructed airflow.

PEEP increases the lung volume at the end of expiration and prevents the pulmonary airspaces from closing at the end of expiration. PEEP is usually set at 5 cm H2O to avoid atelectasis, which may occur after intubation or with prolonged supine positioning. Higher values improve oxygenation in patients with impaired alveolar ventilation, such as in cardiogenic pulmonary edema and ARDS, by redistributing fluid from the alveoli to the interstitium and opening collapsed alveoli. PEEP allows a decrease in FiO2 in the presence of adequate arterial oxygenation, which in turn reduces the likelihood of oxygen-induced lung injury when prolonged ventilation with a high FiO2 (> 0.6) is required. PEEP increases intrathoracic pressure by inhibiting venous return, which may cause hypotension in hypovolemic patients.

Complications of artificial ventilation

Complications may be associated with tracheal intubation or mechanical ventilation. The former may include sinusitis, ventilator-associated pneumonia, tracheal stenosis, vocal cord injury, and tracheoesophageal or tracheovascular fistulae. Complications of mechanical ventilation include pneumothorax, hypotension, and ventilator-associated lung injury (VALI), the latter due to damage to the airways or lung parenchyma due to cyclic airspace closure and opening, excessive lung distension, or both.

When acute hypotension occurs in a patient on mechanical ventilation, the first step is to exclude tension pneumothorax. Hypotension most often results from decreased venous return with increased intrathoracic pressure when high PEEP is used or in a patient with asthma/COPD, and is particularly common in hypovolemia. Hypotension may also result from the sympatholytic effect of sedatives used during intubation and ventilation. Once tension pneumothorax and ventilator-related causes of hypotension have been excluded, the patient should be disconnected from the ventilator and manual bag ventilation should be performed at 2-3 breaths per minute with 100% oxygen while hypovolemia is corrected (500-1000 ml saline in adults, 20 ml/kg in children). If the condition improves rapidly, a relationship between the clinical problem and the mechanical ventilation is assumed, and adjustment of ventilation parameters is required.

As with all critically ill patients, prophylaxis against deep vein thrombosis and gastrointestinal bleeding is necessary. In the former case, prophylaxis is carried out with heparin at a dose of 5000 units subcutaneously twice a day or compression devices (bandages, stockings, etc.) are used. For the prevention of gastrointestinal bleeding, H2 blockers (eg, famotidine 20 mg orally or intravenously twice a day) or sucralfate (1 g orally 4 times a day) are prescribed. Proton pump inhibitors should be used in patients with active bleeding or if they have been previously prescribed.

The most effective way to reduce the risk of complications is to reduce the duration of mechanical ventilation.

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Mechanism of respiration

Normally, during inhalation, negative pressure is created in the pleural cavity, the pressure gradient between the atmospheric air and the lungs creates an air flow. During artificial ventilation, the pressure gradient is created by the device.

Peak pressure is measured at the opening of the airways (PaO2) and is created by the ventilator. It represents the total pressure required to overcome the resistance of the inhaled flow (resistance pressure), the elastic recoil of the lungs and chest (elastic pressure) and the pressure in the alveoli at the beginning of inspiration (positive end-expiratory pressure PEEP). Thus:

Resistance pressure is the product of conduction resistance and airflow. In mechanical ventilation, airflow must overcome the resistance of the breathing circuit, the endotracheal tube, and, most importantly, the patient's airway. Even when these factors are constant, increasing airflow increases resistance pressure.

Elastic pressure is a derivative of the elasticity of the lung tissue, the chest wall, and the volume of insufflated gas. At constant volume, elastic pressure increases with decreased lung compliance (as in fibrosis) or limited chest or diaphragm excursion (as in tense ascites).

The pressure at the end of expiration in the alveoli is normally equal to atmospheric pressure. However, if air does not completely escape from the alveoli due to airway obstruction, resistance to airflow, or shortened expiratory time, the pressure at the end of expiration will exceed atmospheric pressure. This pressure is called intrinsic or autoPEEP to distinguish it from the external (therapeutic) PEEP created by the ventilator.

At any increase in peak pressure (e.g. above 25 cm H2O), it is necessary to assess the relative contribution of resistance pressure and elastic pressure by measuring plateau pressure. To do this, the expiratory valve is left closed for an additional 0.3-0.5 s after inspiration, holding the exhalation. During this period, the airway pressure decreases because the air flow stops. As a result of this maneuver, the pressure at the end of inspiration is the elastic pressure (assuming that the patient does not attempt spontaneous inhalation or exhalation). The difference between the peak and plateau pressures is the resistance pressure.

Increased resistance pressure (e.g., greater than 10 cm H2O) indicates obstruction of the endotracheal tube due to increased secretion, clot formation, or bronchospasm. Increased elastic pressure (greater than 10 cm H2O) indicates decreased lung compliance due to edema, fibrosis, or atelectasis of a lung lobe; large-volume pleural effusion or fibrothorax; and extrapulmonary causes: encircling burn or chest wall deformity, ascites, pregnancy, or severe obesity.

Intrinsic PEEP can be measured in a patient without spontaneous ventilation with end-expiratory hold. Immediately before inspiration, the expiratory valve is closed for 2 s. The flow decreases, eliminating the resistance pressure; the resulting pressure reflects the alveolar pressure at the end of expiration (intrinsic PEEP). A non-quantitative method for assessing intrinsic PEEP is based on determining traces of expiratory flow. If the expiratory flow continues until the beginning of the next inspiration or the patient's chest does not assume its original position, this means that there is intrinsic PEEP. The consequences of increased intrinsic PEEP are an increase in the inspiratory work of the respiratory system and a decrease in venous return.

The detection of intrinsic PEEP should prompt a search for the cause of airway obstruction, although high minute ventilation (>20 L/min) itself can cause intrinsic PEEP in the absence of airflow obstruction. If the cause is flow limitation, then inspiratory time or respiratory rate can be reduced, thereby increasing the expiratory fraction of the respiratory cycle.