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

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

It is caused by intrapulmonary shunting of blood. Dyspnea and tachycardia are observed. The diagnosis is established by the results of arterial blood gas analysis and chest X-ray. In these cases, artificial ventilation itself is the most effective treatment method.

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Causes of acute hypoxemic respiratory failure

The most common causes are pulmonary edema, severe pneumonia, and ARDS. Pulmonary edema occurs when capillary hydrostatic pressure increases (in left ventricular failure or hypervolemia) or capillary permeability increases (in acute lung injury). The mechanism of lung injury may be direct (pneumonia, aspiration of acidic contents) or indirect (sepsis, pancreatitis, massive blood transfusion). In all forms of acute lung injury, the alveoli fill with protein-containing fluid, and impaired surfactant synthesis leads to alveolar collapse, a decrease in the volume of ventilated areas of the lungs, and increased intrapulmonary shunting.

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

Causes of acute hypoxemic respiratory failure

Diffuse lung injury

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

The most common

• Sepsis and systemic inflammatory response syndrome
• Aspiration of acidic gastric contents
• Multiple transfusions in hypovolemic shock

Less common causes

• Drowning
• Pancreatitis
• Air or fat embolism
• Cardiopulmonary shunt
• Drug reaction or overdose
• Leukoagglutination
• Inhalation injury
• Infusion of biologically active substances (eg, interleukin-2)
• Edema of unspecified or mixed etiology
• After straightening the atelectatic lung
• Neurogenic, after a seizure
• Associated with treatment aimed at relaxing the muscles of the uterus
• High-rise
• Alveolar hemorrhage
• Connective tissue diseases
• Thrombocytopenia
• Bone marrow transplant
• Infection in immunodeficiency
• Focal lung lesions
• Lobar pneumonia
• Lung contusion
• Atelectasis of a lung lobe
• ARDS - acute respiratory distress syndrome.

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Symptoms of acute hypoxemic respiratory failure

Acute hypoxemia may cause dyspnea, anxiety, and agitation. Impaired consciousness, cyanosis, tachypnea, tachycardia, and increased sweating may be observed. Heart rhythm and CNS function disturbances (coma) are possible. Diffuse rales are heard on auscultation, especially in the lower parts of the lungs. In severe ventricular failure, jugular vein distension is observed.

One of the simplest methods for diagnosing hypoxemia is pulse oximetry. Patients with low O2 saturation undergo arterial blood gas testing and chest X-ray. Oxygen insufflation must be provided until test results are available.

If supplemental oxygen does not result in saturation above 90%, right-to-left shunting may be the cause. However, if there is pulmonary infiltration on chest 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. Pulmonary edema against the background of high blood pressure is characterized by the presence of a third heart sound, filling of the jugular veins and peripheral edema, and on the radiograph - diffuse infiltration of the lung tissue, cardiomegaly and expansion of the vascular bundle. ARDS is characterized by diffuse infiltration of the peripheral parts of the lungs. Focal infiltrates are characteristic of lobar pneumonia, atelectasis and pulmonary contusion. Echocardiography or pulmonary artery catheterization are sometimes used to clarify the diagnosis.

Treatment of acute hypoxemic respiratory failure

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

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

NIPPV allows avoiding intubation in some patients, since drug therapy can lead to rapid improvement. IPAP is usually set at 10-15 cm H2O and EPAP at 5-8 cm H2O, the HO level is the lowest, allowing maintaining O2 saturation in the artery above 90%.

Several ventilation modes may be used. The most common mode of ventilation in acute situations is A/C, followed by volume-controlled ventilation. The initial settings are: tidal volume 6 ml/kg ideal body weight (see p. 453), respiratory rate 25 breaths per minute, FiO2 = 1.0, PEEP 5 to 8 cm H2O. PEEP may then be increased gradually by 2.5 cm, gradually decreasing the volume to a safe level. Another mode of ventilation may be PSV (with the same PEEP levels). The initial pressure should be sufficient to ensure complete exclusion of the respiratory muscles. This usually requires a support pressure of 10 to 20 cm H2O above the desired PEEP.

Mechanical ventilation in ARDS. Almost all patients with ARDS require mechanical ventilation, which in addition to improving oxygenation reduces the need for oxygen, since it reduces the work of the respiratory muscles. The main condition of mechanical ventilation in this situation is maintaining a pressure plateau below 30 cm H2O and a tidal volume equal to 6 ml/kg of estimated body weight. These conditions help minimize further damage to lung tissue due to overstretching of the alveoli. To avoid the toxic effect of oxygen, the HO level should be below 0.7.

In some patients with ARDS, NIPPV may be used. However, unlike cardiac patients, this category of patients often requires higher EPAP (8-12 cm H2O) and inspiratory pressure (above 18-20 cm H2O). Ensuring these parameters leads to patient discomfort, the inability to maintain mask tightness and eliminate gas leaks. Necrosis may occur due to the need for strong pressure on the skin, and the breathing mixture will inevitably enter the stomach. If the condition worsens, these patients require intubation and transfer to mechanical ventilation. Critical hypoxemia may occur during intubation. Therefore, careful patient selection, monitoring and constant close observation are required to perform this method of respiratory support (see above).

Previously, CMV was used in patients with ARDS to normalize ABG values, without taking into account the negative effect of mechanical lung distension. It has now been proven that alveolar overdistension leads to lung injury, and this problem often occurs with the previously recommended tidal volume of 10-12 ml/kg. Since some alveoli are filled with fluid and are not ventilated, the remaining free alveoli participating in breathing will be overdistensed and damaged, which will lead to an increase in lung injury. A decrease in mortality is observed with a lower tidal volume - about 6 ml/kg of ideal body weight (see equation below). A decrease in tidal volume leads to the need to increase the respiratory rate, sometimes up to 35 per minute, to level out hypercapnia. This technique reduces the likelihood of lung injury associated with mechanical ventilation, is well tolerated by patients, although it can cause respiratory acidosis. Tolerance of elevated PCO2 concentrations is called permissive hypercapnia. Since hypercapnia can cause dyspnea and desynchronization with the respirator, patients are given analgesics (morphine) and high doses of sedatives (propofol is started at a dose of 5 mcg/kg/min, gradually increasing until the effect is achieved or to a dose of 50 mcg/kg/min; due to the possibility of hypertriglyceridemia, triglyceride levels should be monitored every 48 hours). This ventilation mode often requires the use of muscle relaxants, which do not add comfort to patients and, with prolonged use, can cause subsequent muscle weakness.

PEEP improves oxygenation by increasing the area of the ventilated lung due to the involvement of additional alveolar volume in breathing and allows for a decrease in HO2. Some researchers have selected PEEP based on O2 saturation and lung compliance, but this has advantages over selection based on O2 saturation at HO2 values below toxic levels. A PEEP level of 8-15 cm H2O is commonly used, although in severe cases it may be necessary to increase it to more than 20 cm H2O. In these cases, the focus should be on other ways to optimize oxygen delivery and consumption.

The best indicator of alveolar overdistension is plateau pressure measurement, which should be performed every 4 hours or after each change in PEEP and tidal volume. The goal is to reduce the plateau pressure to less than 30 cm H2O. If the pressure exceeds these values, the tidal volume should be reduced by 0.5-1.0 ml/kg to a minimum of 4 ml/kg, while increasing the respiratory rate to compensate for the minute respiratory volume, monitoring the respiratory waveform curve for complete expiration. The respiratory rate can be increased to 35 breaths per minute until air traps in the lungs due to incomplete expiration. If the plateau pressure is below 25 cm H2O and the tidal volume is less than 6 ml/kg, the tidal volume can be increased to 6 ml/kg or until the plateau pressure exceeds 25 cm H2O. Some researchers suggest that pressure-controlled ventilation is more protective of the lungs, although there is no convincing evidence to support this point of view.

For patients with ARDS, the following tactic of mechanical ventilation is recommended: A/C is initiated with a tidal volume of 6 ml/kg ideal body weight, a respiratory rate of 25 breaths per minute, a flow rate of 60 l/min, FiO2 of 1.0, PEEP of 15 cm H2O. As soon as O2 saturation exceeds 90%, FiO2 is reduced to a nontoxic level (0.6). PEEP is then reduced by 2.5 cm H2O until the minimum PEEP level is reached that allows maintaining O2 saturation at 90% with FiO2 of 0.6. The respiratory rate is increased to 35 breaths per minute to achieve a pH above 7.15.