Acute hypoxemic respiratory failure: causes, symptoms, diagnosis, treatment

Acute hypoxemic respiratory failure is a severe arterial hypoxemia refractory to oxygen treatment.

It is caused by intrapulmonary shunting of the blood. In this case, shortness of breath and tachycardia are observed. The diagnosis is established by the results of a study of arterial blood gases and chest X-ray. IVL in these cases is in itself the most effective method of treatment.

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

Causes of acute hypoxemia respiratory failure

The most common causes are pulmonary edema, severe pneumonia and ARDS. Lung edema develops with increased hydrostatic pressure in the capillaries (with left ventricular failure or hypervolemia) or increased capillary permeability (with acute lung damage). The mechanism of lung damage can be direct (pneumonia, aspiration of acidic contents) or mediated (sepsis, pancreatitis, massive blood transfusion). In all forms of acute lung damage, the alveoli are filled with a liquid containing the protein, and a disruption in the synthesis of the surfactant leads to collapsing of the alveoli, a decrease in the volume of the ventilated areas of the lungs, and increased intrapulmonary shunting.

As a result of disruption of transmembrane gas transfer, the blood perfusing such alveoli remains mixed venous, regardless of the amount of FiO2 of the inhaled mixture. This ensures a constant supply of deoxygenated blood into the pulmonary veins, causing arterial hypoxemia. Unlike acute hypoxemic respiratory failure, hypoxemia due to a mismatch between ventilation and perfusion (asthma / COPD) is well adjusted by increasing the oxygen concentration in the inspired air.

Causes of acute hypoxemia respiratory failure

Diffuse lung damage

• Cardiogenic (hydrostatic or high pressure) edema
• Left ventricular failure (with IHD, cardiomyopathy, valve damage)
• Overload volume (especially with concomitant diseases of the kidney and heart)
• Edema with increased capillary permeability against the background of low blood pressure (ARDS)

The most frequent

• Sepsis and Systemic Inflammatory Response Syndrome
• Aspiration of acidic stomach contents
• Multiple transfusions with hypovolemic shock

Less frequent causes

• Drowning
• Pancreatitis
• Air or fat embolism
• Cardiopulmonary shunt
• Reaction to drugs or overdose
• Leukoagglutination
• Inhalation trauma
• Infusion of biologically active substances (eg, interleukin-2)
• Edema of not specified or mixed etiology
• After spreading of the atelectasized lung
• Neurogenic, after convulsive seizure
• Associated with treatment aimed at relaxing the muscles of the uterus
• High-altitude
• Alveolar bleeding
• Diseases of connective tissue
• Thrombocytopenia
• Bone marrow transplantation
• Infection with immunodeficiency
• Focal lung lesions
• Lobar pneumonia
• Contusion of the lung
• Atelectasis of lobe fraction
• ARDS is an acute respiratory distress syndrome.

[9], [10], [11]

Symptoms of acute hypoxemia respiratory failure

Acute hypoxemia can cause shortness of breath, anxiety and agitation. There may be a violation of consciousness, cyanosis, tachypnea, tachycardia and increased sweating. There are violations of the rhythm of the heart and the functions of the central nervous system (coma). At auscultation, diffuse wheezing is heard, especially in the lower parts of the lungs. With severe ventricular failure, swelling of the jugular veins is observed.

One of the most simple methods for diagnosing hypoxemia is pulse oximetry. Patients with low oxygen saturation O2 conduct a study of arterial blood gases and chest X-ray. Before receiving the results of the studies, it is necessary to insufflate oxygen.

If the additional administration of oxygen does not lead to an increase in the saturation index above 90%, it can be assumed that the reason for this is a shunting of blood from right to left. However, in the presence of pulmonary tissue infiltration on the radiograph, the most likely cause of hypoxemia is alveolar edema.

After establishing the fact of acute hypoxemic respiratory failure, it is necessary to identify its causes, which can be pulmonary and extrapulmonary. For pulmonary edema against a background of increased blood pressure, the presence of a third heart tone, the filling of the jugular veins and peripheral edema, and on the roentgenogram - diffuse infiltration of the lung tissue, cardiomegaly and vascular bundle expansion. Diffuse infiltration of the peripheral parts of the lung is characteristic of ARDS. Focal infiltrates are characteristic for lobar pneumonia, atelectasis and concussion of the lungs. To clarify the diagnosis, sometimes echocardiography or catheterization of the pulmonary artery is used.

Treatment of acute hypoxemia respiratory failure

Treatment of acute hypoxemic respiratory failure begins with insufflation through the face mask of a high air flow containing 70-100% oxygen. If oxygen saturation does not increase by more than 90%, the need for mechanical ventilation is considered. The features of treatment depend on the actual clinical situation.

IVL in cardiogenic pulmonary edema. Ventilator has a positive effect on left ventricular failure due to several reasons. Positive inspiratory pressure reduces pre- and postnagruzku and relieves respiratory muscles, reducing the energy costs of breathing. With a decrease in the cost of breathing, cardiac output from the intensively working respiratory muscles is redistributed to the vital organs (brain, intestine, kidneys). EPAP or PEEP redistribute fluid in the lungs and promote the opening of collapsed alveoli.

NIPPV avoids intubation in some patients, as drug therapy can lead to a rapid improvement in the condition. Typically, IPAP is set at 10-15 cm of water. Art. And EPAP - 5-8 cm of water. The level of NO is the smallest, allowing to maintain the oxygen saturation in the artery above 90%.

Several ventilation modes can be used. Most often in acute situations, A / C is used, and then the ventilator with volume control is used. The initial settings are: a tidal volume of 6 ml / kg of ideal body weight (see page 453), a respiration rate of 25 per minute, FiO = 1.0, PEEP of 5 to 8 cm of water. Art. Then PEEP can be gradually increased by 2.5 cm, gradually reducing the software to a safe level. Another mode of ventilation can be PSV (with the same PEEP levels). The initial pressure should be sufficient to ensure the complete exclusion of the work of the respiratory musculature. Usually for this it is necessary to provide a support pressure of 10-20 cm of water. Art. Above the required PEEP.

IVL with ARDS. Virtually all patients with ARDS need ventilation, which, in addition to improving oxygenation, reduces the need for oxygen, as it reduces the work of the respiratory muscles. The main condition for ventilation in this situation is maintaining the pressure plateau below the level of 30 cm of water. Art. And a tidal volume equal to 6 ml / kg of calculated body weight. These conditions allow minimizing further damage to lung tissue due to overexertion of the alveoli. To avoid toxic effects of oxygen, the NO level should be below 0.7.

Some patients with ARDS may use NIPPV. However, in contrast to cardiac patients, this category of patients often requires a higher level of EPAP (8-12 cm H2O) and inspiratory pressure (above 18-20 cm H2O). Providing these parameters leads to patients' discomfort, impossibility to maintain a tightness of the mask and to exclude gas leaks. Because of the need for a strong pressure on the skin may occur necrosis, in addition, the respiratory mixture will necessarily enter the stomach. If the condition worsens, these patients need intubation and transfer to mechanical ventilation. In the process of intubation, they may experience critical hypoxemia. Therefore, this method of respiratory support requires careful selection of patients, monitoring and constant close monitoring (see earlier).

Earlier, patients with ARDS used CMV, whose goal was to normalize ABG, while not taking into account the negative effect of mechanical stretching of the lungs. It has now been proven that overgrowth of the alveoli leads to lung damage and this problem often occurs when applying the recommended tidal volume of 10-12 ml / kg. Due to the fact that the part of the alveoli is filled with liquid and not ventilated, the remaining alveoli participating in the respiration will overstretch and become damaged, which will lead to aggravation of lung lesions. Decrease in mortality is observed when using a smaller tidal volume - about 6 ml / kg of ideal body weight (see equation below). Reduction of the respiratory volume leads to the need to increase the respiratory rate, sometimes up to 35 per minute, to level hypercapnia. This technique reduces the likelihood of lung injury associated with mechanical ventilation, is satisfactorily tolerated by patients, although it may be the cause of respiratory acidosis. The tolerability of elevated concentrations of PCO2 is called permissible hypercapnia. Since hypercapnia can cause shortness of breath and desynchronization with a respirator, patients are prescribed analgesics (morphine) and high doses of sedatives (propofol is started to be injected at a dose of 5 μg / kg / min, gradually increasing to obtain an effect or up to a dose of 50 μg / kg / min; because of the possibility of hypertriglyceridemia, the level of triglycerides must be monitored every 48 hours). This ventilation mode often requires the use of muscle relaxants, which do not add comfort to patients, with prolonged use may cause subsequent muscle weakness.

PEEP improves oxygenation by increasing the areas of the ventilated lung due to the involvement of additional alveolar volume in the respiration and allows to reduce HO2. Some researchers selected PEEP based on the determination of O2 saturation and lung extensibility, but this had advantages when compared with the selection for O2 saturation with HO2 values below the toxic values. Typically, the PEEP level of 8-15 cm of water is used. Although in severe cases it may be necessary to increase it by more than 20 cm of water. Art. In these cases, the focus should be on other ways to optimize oxygen delivery and consumption.

The best indicator of overgrowth of the alveoli is the measurement of plateau pressure, which must be done every 4 hours or after each change in PEEP and respiratory volume. The goal is to reduce the plateau pressure less than 30 cm of water. Art. If the pressure exceeds these values, it is necessary to reduce the tidal volume by 0.5-1.0 ml / kg to a minimum value of 4 ml / kg, while increasing the respiratory rate to compensate for the minute volume of respiration, controlling the presence of a complete exhalation in the respiratory wave curve. The frequency of breathing can be increased to 35 per minute, until air gas traps in the lungs appear due to incomplete exhalation. If the plateau pressure is below 25 cm of water. Art. And a tidal volume of less than 6 ml / kg, it is possible to increase the tidal volume to 6 ml / kg or until the plateau pressure exceeds 25 cm of water. Art. Some researchers suggest that ventilation with pressure control better protects the lungs, although there is no convincing evidence for this point of view.

For patients with ARDS, the following ventilatory tactic is recommended: A / C with a respiratory volume of 6 ml / kg of ideal body weight, a respiration rate of 25 per minute, a flow rate of 60 l / min, FiO2 1.0, a PEEP of 15 cm of water. Art. Once the O2 saturation exceeds 90%, FiO2 decreases to a non-toxic level (0.6). Then the PEEP is reduced by 2.5 cm of water. Art. Up to the minimum level of PEEP that allows maintaining O2 saturation at 90% with FiO2 0.6. The respiratory rate increases to 35 per minute to reach a pH above 7.15.