Acute respiratory failure

from Wikipedia, the free encyclopedia
Classification according to ICD-10
J80 Respiratory distress syndrome in adults [ARDS]
ICD-10 online (WHO version 2019)

As acute respiratory failure , technical terminology also Acute Respiratory Distress Syndrome ( ARDS called), or acute respiratory distress syndrome , the massive response is lung to various damaging factors referred; regardless of whether the resulting pulmonary inflammatory mechanisms are primarily triggered pulmonarily or systemically. ARDS must have an identifiable, noncardiac cause.

Synonyms designations are adult respiratory distress syndrome (now obsolete. English Adult Respiratory Distress Syndrome ), acute progressive respiratory failure and shock lung .

definition

AECC definition (1994)

Diffuse lung infiltrates on the X-ray

In 1994, the definition of the ARDS, which has been in use since 1967, was refined at the American-European consensus conference (AECC definition). The following criteria were decisive:

With an index of 200 to 300 mmHg, however, one spoke of an ALI ( Acute Lung Injury ); for example, a PaO 2 of 90 mmHg to 30 percent O 2 (i.e. FiO 2 = 0.3) corresponds to an index of 300 mmHg.

Berlin definition (2011)

Since there had been some criticism of this definition for years, the European Society of Intensive Care Medicine, the American Thoracic Society and the Society of Critical Care Medicine adopted a new definition for the ARDS in Berlin in autumn 2011 in a consensus process. According to these criteria from 2011, a distinction is no longer made between ALI ( Acute Lung Injury ) and ARDS. The so-called Berlin definition of the ARDS (named after the place where the expert group met) specifies:

  1. Timing: Occurrence within a week,
  2. Radiology: bilateral infiltrates in the x-ray of the lungs or in the computed tomography without any other meaningful explanation,
  3. Cause: Respiratory failure is not explained by heart failure or hypervolaemia ,
  4. Oxygenation: with a positive end-expiratory pressure of> 5  cmH 2 O :
    1. mild ARDS if Horovitz quotient (see above) from 201 to 300  mmHg ;
    2. moderate ARDS if Horovitz quotient <200 mmHg;
    3. severe ARDS if Horovitz quotient <100 mmHg.

The current S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency from December 2017 uses this definition.

Causes and Risk Factors

Direct lung damage

Inhalation of toxic gases such as smoke gas ( inhalation trauma , toxic pulmonary edema ), infection of the lungs ( pneumonia ), aspiration of stomach contents, lung contusion , aspiration of salt or fresh water (almost drowning ), fat embolism, amniotic fluid embolism, inhalation of hyperbaric oxygen.

Indirect lung damage

Causes can include sepsis , bacteremia , endotoxinemia , severe trauma (especially multiple trauma ) with shock ("shock lung"), burns , (acute necrotizing) pancreatitis , severe course of tropical malaria , drugs and immunosuppression (for example after transplantation or radiation) . Other secondary factors such as chronic alcohol abuse , chronic lung diseases and low serum pH increase the risk of developing ARDS.

A transfusion-associated acute pulmonary insufficiency (TRALI) cannot be clinically differentiated from the ARDS, but is differentiated from the ARDS, as the prognosis with the TRALI is significantly better.

The stated incidence of ARDS varies between two and 28 cases per 100,000 inhabitants per year, depending on the study. Although the mortality rate has decreased in recent decades due to advances in supportive therapy, it is still around 40 percent.

Pathophysiology

microscopic view of a shock lung (pulmonary hyaline membrane)

In acute lung failure, this acute respiratory failure is caused by severe diffuse damage to the lung parenchyma . Further components are perfusion disorders , coagulation disorders , permeability disorders of the alveolar walls , pulmonary edema , breakdown of surfactant and connective tissue remodeling of lung tissue.

Functionally, the ARDS is characterized by:

  • an arterial hypoxemia varying severity
  • diffuse radiographic infiltration
  • Reduced elasticity ( compliance ) of the lungs and
  • a decreased functional residual capacity, d. That is, after “normal” exhalation, less air remains in the lungs than usual.

ARDS usually has three phases: the exudative phase , the early phase , and the late proliferative phase .

treatment

Patients with ARDS often have to be intubated and ventilated in a controlled manner as part of intensive care treatment , whereby differentiated ventilation patterns with PEEP are used. The ventilation parameters are adapted to the patient's condition depending on the situation. Since mechanical ventilation itself has a damaging effect on the lungs, the principles of lung protective ventilation must be taken into account: small tidal volumes, avoidance of high ventilation pressures and higher breathing rates. A procedure should be chosen that also allows spontaneous breathing, for example BIPAP ventilation .

The administration of corticosteroids can be useful. Hemodynamic disorders and changes are treated in a controlled manner according to the principles of intensive care. The most important part of the treatment concept is, if possible, eliminating the triggering cause ( causal therapy , e.g. the infection).

In severe cases of ARDS treatment is with kinetic therapy (RotoRest therapy or supported prone position of the patient). This positioning therapy ensures that the breathing gas (usually with protective, controlled ventilation and the above-mentioned “high” analgesia sedation) is distributed homogeneously in the lungs. The prone position can be carried out in 135 ° and 180 ° body position. This opens dorsobasal atelectasis and improves oxygenation.

Mechanical ventilation

Gentle forms of ventilation are recommended in order to reduce additional lung damage from artificial ventilation.

Low tidal volumes

The ventilator should be set to a tidal volume of no more than 6 ml / kg of ideal body weight . These small tidal volumes reduce the regular overstretching and subsequent collapse of the alveoli . The ideal body weight is calculated using the following formulas:

Men Women
ideal body weight in kg = 50 + 0.91 × (height in cm - 152.4 cm) ideal body weight in kg = 45.5 + 0.91 × (height in cm - 152.4 cm)

A 165 cm tall woman, for example, has an ideal body weight of 57 kg and should be ventilated with a maximum tidal volume of 342 ml. For a 180 cm tall man, the ideal body weight would be 75.1 kg and the maximum tidal volume 451 ml.

There is high quality evidence for this recommendation based on scientific studies. By reducing the tidal volume from 12 ml / kg to 6 ml / kg alone, the mortality rate of patients in a study with 861 patients could be reduced from 39.8% to 31%. Another study with 485 patients showed that even a slightly increased tidal volume of 8.5 ml / kg led to a significant increase in mortality. This further supports the strict recommendation of a maximum tidal volume of 6 ml / kg, which can also be found in the current guidelines (from 2017) for the German-speaking area.

PEEP

Recommended combinations of oxygen concentration and PEEP (modified from)
FiO 2 PEEP in cmH 2 O
0.3 5
0.4 5-8
0.5 8-10
0.6 10
0.7 10-14
0.8 14th
0.9 14-18
1 18-24

To reduce the collapse of the alveoli in the low-pressure exhalation phase, a PEEP should be set during ventilation . The right PEEP level must be selected, as too high a PEEP can lead to circulatory problems due to venous congestion and also overinflate the alveoli. A PEEP that is too low cannot adequately prevent the alveoli from collapsing. The ideal level of PEEP can be limited by measuring methods by measuring a static pressure-volume curve during ventilation of the patient, or by lengthy trial and error of different PEEP levels and their effect on the blood gases . In a study on 549 patients, estimating the PEEP based on the ideal oxygen concentration of the inhaled air (FiO 2 ) has proven to be practicable and equivalent . The level of oxygen concentration in the exhaled air, which allows an adequate supply of oxygen to the body, is a factor in estimating the severity of ARDS. The higher this concentration has been set, the more severe the ARDS. The PEEP level can also be estimated from this.

HFOV

In order to improve the ventilation of the lungs in the case of acute lung failure, the High Frequency Oscillation Ventilation ( HFOV ), in German high frequency ventilation , was developed. A sufficiently high pressure (above the PEEP) to keep the alveoli open is maintained in the airways. In contrast to other ventilation methods, ventilation with high-frequency ventilation does not take place via breaths, whereby air is pressed into the lungs. Instead, there is a high gas flow in the ventilation system, which is set into vibrations (oscillations). This allows air to flow through the lungs without changes in pressure due to changes in volume. The hoped-for benefit of this system lies in the reduction of ventilation-associated lung damage by avoiding the peak pressures that occur with conventional ventilation. In clinical studies and meta-analyzes , however, it was shown that, in terms of mortality, high-frequency ventilation was not only consistently not better , but in some studies even worse than conventional lung-protective ventilation. In addition, some studies showed an increase in the duration of ventilation and the intensive care stay. For these reasons, the Austrian, Swiss and German specialist societies advise against the use of high-frequency ventilation in their 2017 guideline for the treatment of acute lung failure.

Prone position

In patients who are artificially ventilated in the supine position, the underlying lung sections are squeezed together by the weight and gradually take part in the gas exchange less and less because it does not reach any air. On the other hand, the free lung areas above get relatively too much air and are overstretched. In severe ARDS, the prone position is the first choice to improve this condition and should be done early because it significantly improves the chances of survival. The patient should remain in the prone position for 16 hours before turning onto their back again. The measure is more successful and has fewer complications if the upper body is also elevated. Continuous lateral rotation therapy can only be used as a less effective alternative if the prone position is not safe, for example due to instability of the spine or injuries to the abdomen or brain. These are special beds that automatically rock the patient from right to left and back again with a tilt of up to 60 °. For the therapy to be effective, the rotation should be carried out with only brief interruptions for at least 18-20 hours a day.

Extracorporeal membrane oxygenation

So-called extracorporeal membrane oxygenation (ECMO) is often used as a rescue measure for critically ill patients. The blood is diverted from the body, the gas exchange takes place on a machine, and the now oxygen-rich blood is returned to the patient's bloodstream. Because of the risks involved in the procedure, it should only be used in severe cases in which adequate oxygen saturation cannot be achieved in the blood despite optimized ventilation and positioning measures (Horovitz quotient <80mmHg) and other factors (such as fluid overload, pneumothorax ) are excluded. Since the gas exchange in the lungs is to be supported, a so-called veno-venous ECMO is recommended, i.e. the blood is taken from a large vein and also reintroduced via a vein. A veno-arterial ECMO is useful in cardiovascular failure.

Medical therapy

There is no established drug therapy for acute lung failure. In practice, corticosteroids (such as cortisone) are often used to reduce tissue damage caused by inflammatory processes. However, there is no conclusive data on this. Other therapies, such as the use of beta-2 sympathomimetics to widen the airways or surfactant , have been tried, but discarded because of negative effects.

See also

Web links

Individual evidence

  1. ↑ LB Ware, MA Matthay: The Acute Respiratory Distress Syndrome. In: NEJM . 4-5-2000; 342 (18), pp. 1334-1349. PMID 10793167
  2. ↑ M. Leuwer, H. Trappe, TH Schürmeyer, O. Zuzan: Checklist for interdisciplinary intensive care medicine. 2nd Edition. Thieme-Verlag, 2004, ISBN 3-13-116912-5 .
  3. ↑ David Ashbaugh, D. Bigelow, T. Petty, B. Levine: Acute respiratory distress in adults. In: The Lancet . Volume 7511, No. 2, 1967, pp. 319-323. PMID 4143721
  4. ↑ G. Bernard, A. Artigas, K. Brigham, J. Carlet, K. Falke, L. Hudson, M. Lamy, J. Legall, A. Morris, R. Spragg: The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. In: Am J Respir Crit Care Med. 149 (1994) 3 Pt 1, pp. 818-824. PMID 7509706
  5. ^ V. Marco Ranieri, B. Taylor Thompson, Niall D. Ferguson, Ellen Caldwell, Eddy Fan, Luigi Camporota, Arthur S. Slutsky: Acute Respiratory Distress Syndrome - The Berlin Definition . In: JAMA . tape 307 , no. 23 , May 21, 2012, ISSN  0098-7484 , p. 2526-2533 , doi : 10.1001 / jama.2012.5669 .
  6. ↑ S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , p. 11.
  7. ↑ Malaria. Statements by the Blood Working Group of the Federal Ministry of Health . In: Bundesgesundheitsbl - Health Research - Health Protection . tape 51 , 2008, p. 236–249 , doi : 10.1007 / s00103-008-0453-5 ( rki.de [PDF; 1.7 MB ]).
  8. ↑ Hilmar Burchardi: Etiology and pathophysiology of acute respiratory failure (ARI). In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unchanged edition, ibid. 1994, ISBN 3-540-57904-4 , pp. 47-91; here: pp. 49-53 and 68-74, in particular pp. 53 and 68 f.
  9. ^ P. Marino: The ICU book. Practical intensive care medicine. 3. Edition. Urban & Fischer bei Elsevier, 2002, ISBN 3-437-23160-X .
  10. ↑ Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. In: New England Journal of Medicine. 342, 2000, pp. 1301-1308, doi: 10.1056 / NEJM200005043421801 .
  11. ↑ DM Needham, E. Colantuoni, PA Mendez-Tellez, VD Dinglas, JE Sevransky, CR Dennison Himmelfarb, SV Desai, C. Shanholtz, RG Brower, PJ Pronovost: Lung protective mechanical ventilation and two year survival in patients with acute lung injury : prospective cohort study. In: BMJ. 344, 2012, pp. E2124 – e2124, doi: 10.1136 / bmj.e2124 .
  12. ↑ S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , p. 91.
  13. ↑ a b Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory Distress Syndrome. In: New England Journal of Medicine. 351, 2004, pp. 327-336, doi: 10.1056 / NEJMoa032193 .
  14. ↑ S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , p. 70 f.
  15. ↑ S2e guideline: Positioning therapy and early mobilization for prophylaxis or therapy of pulmonary dysfunction , status 04/2015, pp. 10–29.
    S3 guideline for invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , pp. 181–186.
  16. ↑ S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , pp. 192–195.
  17. ↑ Michael A. Matthay, Rachel L. Zemans, Guy A. Zimmerman, Yaseen M. Arabi, Jeremy R. Beitler: Acute respiratory distress syndrome . In: Nature Reviews. Disease Primers . tape 5 , no. 1 , March 14, 2019, ISSN  2056-676X , p. 18 , doi : 10.1038 / s41572-019-0069-0 , PMID 30872586 , PMC 6709677 (free full text).
  18. ↑ S3 guideline on invasive ventilation and the use of extracorporeal procedures in acute respiratory insufficiency. 1st edition, long version, as of December 4, 2017 , pp. 163–165.