Acute respiratory failure - diagnosis and treatment

Acute respiratory failure develops quickly and potentially reversely.

Acute respiratory distress syndrome (ARDS) - criteria (according to the Berlin definition, 2012):

1) manifestation - within a week from the onset of the disease, or the appearance or intensification of subjective symptoms from the respiratory system;

2) pathological changes in visual examinations of the lungs (RG or CT) - bilateral darkening, which can not be explained by the presence of fluid in the pleural cavities, atelectasis or the presence of nodular shadows;

3) the cause of pulmonary edema - respiratory failure can not be completely explained by cardiac insufficiency and hyperhydration; if there are no risk factors for ARDS? see below, an objective assessment (eg, echocardiographic) is needed to rule out hydrostatic edema;

4) oxygenation of arterial blood, estimated on the basis of the ratio PaO2 to the oxygen content in the respiratory mixture, can be represented as a decimal fraction (FiO2) (in a healthy person, breathes atmospheric air: PaO2 = 97 mm Hg, FiO2 = 021 ; PaO2 /FiO2 = 470 mm Hg, at an altitude> 1000 meters above sea level, use the formula PaO2 /FiO2? Atmospheric pressure in mmHg /760) with mechanical ventilation of the lungs. On this basis, differentiate ARDS (ARDS):

a) light - 200 mm of mercury. Art.

b) moderate severity - 100 mm Hg. Art.

c) Heavy - PaO2 /FiO2? 100 mm Hg. article, with PEEP? 5 cm H2O.

The causes of acute hypoxemia:



1) diffuse changes in the lungs:

  • a) pulmonary edema - caused by: increased hydrostatic pressure in the pulmonary vessels (left ventricular failure, hyperhydration); increased permeability of the air-blood barrier (ARDS, drowning, after reperfusion of the lungs[после трансплантации легкого или ликвидации артериальной эмболии]); unexplained or combined etiology (decompression[после декомпрессии пневмоторакса], postobturation[после устранения причины ателектаза], neurogenic, after a stroke, after application of tocolytic drugs);

  • b) alveolar bleeding - vasculitis and connective tissue diseases, hemorrhagic diathesis (in particular, DIC syndrome);


  • 2) focal changes in the lungs - pneumonia with severe current, atelectasis (including due to obstruction of the respiratory tract by foreign body, tumor or secretions), lung trauma;

    3) diseases of the pleura - pneumothorax (especially intense or massive), a large amount of fluid in the pleural cavity;

    4) a decrease in pulmonary blood flow - embolism of the pulmonary artery, shock.

    What causes acute hypoventilation? see above.

    The causes of GDDS are identical with their risk factors:

    1) pulmonary - aspiration of gastric contents, pneumonia, chest trauma and lung contusion, inhalation of smoke or toxic substances, chest irradiation, barotrauma with mechanical ventilation, drowning, vasculitis of pulmonary vessels;

    2) extrapulmonary - sepsis, shock, acute pancreatitis, polytrauma, numerous fractures (fat embolism), massive burns, craniocerebral trauma and increased intracranial pressure, numerous transfusions of blood products (acute posttransfusion lung injury - TRALI[transfusion related acute lung injury]), Complications in pregnancy (eclampsia, amniotic fluid embolism), tumor disintegration syndrome, after extracorporeal circulation, reactions to drug administration and drug poisoning.

    Pathogenesis of ARDS: an uncontrolled inflammatory process? damage to the air-blood barrier (endothelium of blood vessels and pneumocytes)? transudation of protein enriched with protein and shaped elements of blood into the lumen of the alveoli (formation of hyaline membranes)? destruction and reduction of surfactant synthesis? collapse and edema of the alveoli (exudative stage), destruction of the walls of the alveoli due to inflammatory edema? violation of gas exchange and reduced lung compliance? respiratory failure (dominated by hypoxemia) and pulmonary hypertension (acute). At the second or third week granulation tissue is formed (the proliferation stage), then it is possible to restore damaged cells or collagen synthesis by fibroblasts (fibrosis stage).

    CLINICAL PICTURE AND TYPICAL CURRENT



    Subjective symptoms: dyspnea; Depending on the cause, cough, fever, chest pain, hemoptysis and other symptoms may occur. Objective symptoms: symptoms of hypoxia (cyanosis, tachycardia, tachypnea) and symptoms of the underlying disease (upper airway obstruction, bronchial obstruction, pulmonary edema, inflammatory infiltrate, atelectasis, pneumothorax, fluid in the pleural cavity, etc.); Sometimes it is possible to observe the increased work of additional respiratory muscles and the paradoxical respiratory movements of the walls of the chest and abdomen. Without treatment, acute respiratory failure leads to death.

    DIAGNOSIS



    1. Exclude other, other than respiratory failure, possible causes of dyspnea.

    2. Determine the cause of acute respiratory failure (? See above); First of all:

  • 1) evaluate the respiratory system - look for symptoms of obstruction of the upper and severe obturation of the lower respiratory tract, atelectasis, pneumonia, pneumothorax, fluid in the pleural cavities;

  • 2) evaluate the circulatory system - find out if there is cardiogenic pulmonary edema or pulmonary embolism;

  • 3) exclude or Diagnose sepsis, if sepsis is diagnosed - find the cause.


  • auxiliary research

    1. Pulse oximetry: reduction of SaO2.

    2. Laboratory research:

  • 1) gasometry of blood - hypoxemia, in some cases, hypercapnia and acidosis;

  • 2) a general analysis of peripheral blood and a biochemical study - the presence of disorders, depending on the etiology.


  • 3. Microbiological studies: Since the frequent cause is infection, try to identify the etiologic factor (prescribe material from the respiratory tract[напр., Полученного при бронхофиброскопия], Blood cultures).

    4. Visual studies: thoracic thoracic gland - changes depending on the etiology (inflammatory infiltrates in the lungs, atelectasis, pneumothorax, fluid in the pleural cavity, with ARDS, non-specific pattern of pulmonary edema - diffuse blackout and alveolar consolidation with air bronchogram spreading from the periphery of the lungs to roots). CT of the chest - a typical, though not specific, sign of ARDS on HRCT is considered a symptom of "crazy paving".

    TREATMENT



    1. Restoration of airway passages (more often necessary in unconscious patients): depending on the situation - manual, intubation, the introduction of the mouth and throat tube or other device, conicotomy, tracheotomy (the method of choice for massive swelling of the larynx and prolonged mechanical ventilation).

    2. Oxygenotherapy for the treatment of hypoxemia in the regime of necessity with a high concentration of oxygen in the respiratory mixture (if necessary, 100%).

    3. Mechanical ventilation of the lungs: invasive or non-invasive; if ineffective? consider the need for extracorporeal lung function support (ECLA, ECMO).

    4. Treatment of the underlying disease: pharmacological and invasive - eg, Decompression of pneumothorax, drainage of the pleural cavity.

    5. Respiratory physiotherapy: including postural drainage.

    6. Nutrition: diet, prevents hypotrophy, with a decrease in the proportion of carbohydrates, to reduce the formation of CO2.

    COMPLICATIONS

    The consequences of hypoxemia and hypercapnia; bleeding from the upper parts of the digestive tract - from stress ulcers, or due to hemorrhagic gastritis (prophylaxis), venous thromboembolic disease.