A presentation by Jon Henrik Laake at the 2017 meeting of the Scandinavian Society of Anaestesiology and Intensive Care Medicine. All available content from SSAI2017: https://scanfoam.org/ssai2017/ Delivered in collaboration between scanFOAM, SSAI & SFAI.

1. ARDS
acute respiratory distress syndrome
Jon Henrik Laake
Chairman Clinical Practice Committee – SSAI
Rikshospitalet - Oslo University Hospital

2. Copenhagen 1952-3
”Supervised by anaesthetists
and dedicated nursing staff,
Bjørn Ibsen's techniques slashed
mortality rates from 87% to less
than 15% among patients with
bulbar poliomyelitis”

3. 7511
Saturday 12 August 1967
ACUTE RESPIRATORY DISTRESS
IN ADULTS
DAVID G. ASHBAUGH
M.D. Ohio State
ASSISTANT PROFESSOR OF SURGERY
D. BOYD BIGELOW
M.D. Colorado
ASSISTANT IN MEDICINE AND AMERICAN THORACIC SOCIETY-NATIONAL
TUBERCULOSIS ASSOCIATION FELLOW IN PULMONARY DISEASE
THOMAS L. PETTY
M.D. Colorado
ASSISTANT PROFESSOR OF MEDICINE
BERNARD E. LEVINE
M.D. Michigan
AMERICAN THORACIC SOCIETY-NATIONAL TUBERCULOSIS ASSOCIATION
FELLOW IN PULMONARY DISEASE*
From the Departments of Surgery and Medicine,
University ofColorado Medical Center, Denver, Colorado, U.S.A.
Summary
The respiratory-distress syndrome in 12
patients was manifested by acute onset of
tachypnœa, hypoxæmia, and loss of compliance after a
variety of stimuli; the syndrome did not respond to usual
and ordinary methods of respiratory therapy. The clinical
and pathological features closely resembled those seen in
infants with respiratory distress and to conditions in
congestive atelectasis and postperfusion lung. The
theoretical relationship of this syndrome to alveolar
surface active agent is postulated. Positive end-expiratory
pressure was most helpful in combating atelectasis and
hypoxæmia. Corticosteroids appeared to have value in the
treatment of patients with fat-embolism and possibly viral
pneumonia.
Introduction
IN the course of clinical and laboratory observations on
272 adult patients receiving respiratory support, a few
patients did not respond to usual methods of therapy.
They exhibited a clinical, physiological, and pathological
course of events that was remarkably similar to the
infantile respiratory distress syndrome (hyaline-membrane
disease). Difficult cases of respiratory failure in con-
junction with prolonged cardiopulmonary bypass (Baer
and Osborn 1960), with congestive atelectasis (Berry and
Sanislow 1963), with viral pneumonia (Petersdorf et al.
1959), and with fat-embolism (Ashbaugh and Petty 1966)
have been recorded; and in these cases the patho-
physiology of the illness closely resembled the infantile
respiratory distress syndrome and findings in patients
described here.
Patients
A similar pattern of acute respiratory distress was seen in
12 patients. The clinical pattern, which we will refer to as the
respiratory-distress syndrome, includes severe dyspnoea,
tachypnoea, cyanosis that is refractory to oxygen therapy, loss
* Present address: 909 East Brill Street, Phoenix, Arizona.
of lung compliance, and diffuse alveolar infiltration seen on
chest X-ray.
No patient had a previous history of respiratory failure.
1 patient gave a history of mild asthma since childhood but had
no disability or recent attacks. Another patient had a chronic
cough that was attributed to cigarette smoking. The remaining
10 patients did not have any previous pulmonary disease.
Severe trauma preceded respiratory distress in 7 patients
(table i). Viral infection in 4 patients and acute pancreatitis in
1 patient were precipitating factors in the remainder. Respira-
tory distress occurred as early as one hour and as late as
ninety-six hours after the precipitating illness or injury. Shock
of varying degree and duration was present in 5 patients and
excessive fluid administration occurred in 7 patients. 4 patients
developed acidosis with pH less than 7-3 before the onset of
respiratory distress.
Methods
All patients were admitted to intensive-care units of the
surgical or medical services. Blood-gas studies were performed
on arterial blood drawn by percutaneous puncture of either
brachial or femoral artery. In most instances, blood was drawn
only during a steady state. P a02 measurements were determined
with a Clark electrode and oxygen saturation was measured on
TABLE I-ACUTE RESPIRATORY DISTRESS
7511
Summary
The respiratory-distress syndrome in 12
patients was manifested by acute onset of
tachypnœa, hypoxæmia, and loss of compliance after a
variety of stimuli; the syndrome did not respond to usual
and ordinary methods of respiratory therapy. The clinical
and pathological features closely resembled those seen in
infants with respiratory distress and to conditions in
congestive atelectasis and postperfusion lung. The
theoretical relationship of this syndrome to alveolar
surface active agent is postulated. Positive end-expiratory
pressure was most helpful in combating atelectasis and
hypoxæmia. Corticosteroids appeared to have value in the
treatment of patients with fat-embolism and possibly viral
pneumonia.
Introduction
IN the course of clinical and laboratory observations on
272 adult patients receiving respiratory support, a few
patients did not respond to usual methods of therapy.
They exhibited a clinical, physiological, and pathological
course of events that was remarkably similar to the
infantile respiratory distress syndrome (hyaline-membrane
disease). Difficult cases of respiratory failure in con-
junction with prolonged cardiopulmonary bypass (Baer
and Osborn 1960), with congestive atelectasis (Berry and
Sanislow 1963), with viral pneumonia (Petersdorf et al.
1959), and with fat-embolism (Ashbaugh and Petty 1966)
have been recorded; and in these cases the patho-
physiology of the illness closely resembled the infantile
respiratory distress syndrome and findings in patients
described here.
Patients
A similar pattern of acute respiratory distress was seen in
12 patients. The clinical pattern, which we will refer to as the
respiratory-distress syndrome, includes severe dyspnoea,
tachypnoea, cyanosis that is refractory to oxygen therapy, loss
* Present address: 909 East Brill Street, Phoenix, Arizona.
artery. instances,
only during a steady state. P a02 measurements were determined
with a Clark electrode and oxygen saturation was measured on
TABLE I-ACUTE RESPIRATORY DISTRESS

4. 1964
in vivo
1968
1971
1975
in vivo
1974
vs
1989
1988
n
vivo 19971985
2015
2014vs
2002
vs
2000 2013
2005 2016
2010
1970
1976
1988
1986 1990
1994
1998
In vivo
2005
Heterogeneous Gas
Distribu<on 2015
In vivo
2009
1967
2012
Page 29 of 30
AJRCCM Articles in Press. Published on 01-February-2017 as 10.1164/rccm.201612-2415CI
Copyright © 2017 by the American Thoracic Society
Laffey JG and Kavanagh BP Am J Respir Crit Care Med. 2017 Jul 1;196(1):18-28.

6. ARDS pathophysiology
 Oxygenation failure
 Ventilatory failure
 V/Q disturbances
 Pulmonary hypertension
 Inflammation
 Coagulopathy
 Pulmonary Oedema
 Adjunct organ failure
 Genetics
 Lung mechanics
Therapy ?

9. Intervention Recommendation QoE Outcome Comment
Pressure and volume limitation
(PVL)
Strong
Moderate to
high
Death 
PEEP > 5 cm Weak Moderate
O2 
LOS 
Non-invasive ventilation No recommendation No data
FiO2 No recommendation Absent No trials
Spontaneous breathing modes No recommendation Absent No trials
Pressure vs volume control Weak Very low
Irrelevant with
modern ventilators
Prone positioning Weak Low
O2 
Death 
Inconsistent results
Recruitment manoeuvres Weak Very low O2  Rescue therapy
HFOV Strong against High
LOS 
Death 
PVL better
QoE = Quality of evidence LOS = length of stay O2 = oxygenation

10. Respiratory failure

11. ARDS – The Berlin definition:
• Acute respiratory failure not explained by heart failure or
volume overload
• Decreased arterial PO2/FiO2 ratio:
• mild ARDS: ratio is 201 - 300 mmHg (≤ 39.9 kPa)
• moderate ARDS: 101 - 200 mmHg (≤ 26.6 kPa)
• severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)
(a minimum PEEP of 5 cmH2O is required; it may be
delivered noninvasively with CPAP to diagnose mild ARDS).
ARDS Definition Task Force, Ranieri VM, Rubenfeld GD, Thompson BT,
Ferguson ND, Caldwell E, Fan E, Camporota L, Slutsky AS. Acute
respiratory distress syndrome: the Berlin Definition. JAMA, June 20,
2012—Vol 307, No. 23 pages 2526–33.

12. Study or Subgroup
Brower 2004
Meade et al 2008
Mercat et al 2008
Total (95% CI)
Total events
Heterogeneity: Chi² = 0.00, df = 2 (P = 1.00); I² = 0%
Test for overall effect: Z = 1.76 (P = 0.08)
Events
69
173
136
378
Total
276
475
385
1136
Events
75
205
149
429
Total
273
508
382
1163
Weight
17.8%
46.8%
35.4%
100.0%
M-H, Fixed, 95% CI
0.91 [0.69, 1.21]
0.90 [0.77, 1.06]
0.91 [0.75, 1.09]
0.90 [0.81, 1.01]
Year
2004
2008
2008
Experimental Control Risk Ratio Risk Ratio
M-H, Fixed, 95% CI
0.01 0.1 1 10 100
Favours high PEEP Favours low PEEP
Forest plot of comparison: High PEEP vs Low PEEP, outcome: Hospital mortality [death
before discharge].
”Patient-important” vs ”surrogate” end-points
Study or Subgroup
Brower 2004
Villar et al 2006
Meade et al 2008
Mercat et al 2008
Huh 2009
Total (95% CI)
Heterogeneity: Chi² = 28.52, df = 4 (P < 0.00001); I² = 86%
Test for overall effect: Z = 15.26 (P < 0.00001)
Mean [PaO2/FiO2]
220
139
187
218
161
SD [PaO2/FiO2]
89
43
69
97
65
Total
244
50
464
378
30
1166
Mean [PaO2/FiO2]
168
124
149
150
137
SD [PaO2/FiO2]
66
54
61
69
48
Total
230
45
498
371
27
1171
Weight
16.7%
8.4%
48.4%
22.7%
3.8%
100.0%
IV, Fixed, 95% CI [PaO2/FiO2]
52.00 [37.95, 66.05]
15.00 [-4.77, 34.77]
38.00 [29.75, 46.25]
68.00 [55.96, 80.04]
24.00 [-5.48, 53.48]
44.69 [38.95, 50.43]
Year
2004
2006
2008
2008
2009
Experimental Control Mean Difference Mean Difference
IV, Fixed, 95% CI [PaO2/FiO2]
-100 -50 0 50 100
Favours low PEEP Favours high PEEP
Forest plot of comparison: High PEEP vs Low PEEP, outcome: Oxygenation efficiency
[PO2/FiO2].

13. Nitric oxide – inhaled vasodilator

14. Study or Subgroup
Michael 1998
Troncy 1998
Dellinger 1998
Lundin 1999
Payen 1999
Metha 2001
Gerlach 2003
Park 2003
Taylor 2004
Total (95% CI)
Total events
Heterogeneity: Tau² = 0.00; Chi² = 0.59, df = 8 (P = 1.00); I² = 0%
Test for overall effect: Z = 1.17 (P = 0.24)
Events
11
9
43
41
48
4
3
4
44
207
Total
20
15
158
93
98
8
20
11
192
615
Events
9
8
20
35
46
3
4
2
39
166
Total
20
15
75
87
105
6
20
6
193
527
Weight
6.6%
6.6%
12.6%
21.9%
29.5%
2.3%
1.4%
1.4%
17.7%
100.0%
M-H, Random, 95% CI
1.22 [0.65, 2.29]
1.13 [0.60, 2.11]
1.02 [0.65, 1.61]
1.10 [0.78, 1.55]
1.12 [0.83, 1.50]
1.00 [0.35, 2.88]
0.75 [0.19, 2.93]
1.09 [0.28, 4.32]
1.13 [0.77, 1.66]
1.10 [0.94, 1.29]
Year
1998
1998
1998
1999
1999
2001
2003
2003
2004
Experimental Control Risk Ratio Risk Ratio
M-H, Random, 95% CI
0.1 0.2 0.5 1 2 5 10
Favours NO Favours Control
NO versus Placebo – mortality at end of follow-up
• Rebound effect?
• Toxic effects of NO? (concentration dependent?)
• Metabolites / reactants ONOO-
• Reduction in perfusion pressure in kidneys?
• Confounded by fluid therapy (lowered CVP)?

15. Adhikari NK, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, Park KJ, Mehta S, Slutsky AS, Friedrich JO.
Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic
review and meta-analysis. Crit Care Med. 2014 Feb;42(2):404-12.
Inhaled nitric oxide does not reduce mortality in patients with acute
respiratory distress syndrome regardless of severity:

16. ”Benefits vs harms”
Nitric oxide vs placebo; Outcome: p/f ratio
Study or Subgroup
Dellinger 1998
Gerlach 2003
Lundin 1999
Mehta 2001
Michael 1998
Park 2003
Troncy 1998
Total (95% CI)
Heterogeneity: Tau² = 15.41; Chi² = 6.62, df = 6 (P = 0.36); I² = 9%
Test for overall effect: Z = 4.37 (P < 0.0001)
Mean
166
142
138
115
92
254.2
189.8
SD
54
46
48
48
30
109.5
40.1
Total
120
20
78
8
16
11
15
268
Mean
131
129
131
96
72
247.8
166.3
SD
43
43
53
29.3
26
89.1
53.2
Total
57
20
66
6
16
6
15
186
Weight
31.1%
10.5%
25.6%
5.0%
19.7%
0.9%
7.2%
100.0%
IV, Random, 95% CI
35.00 [20.24, 49.76]
13.00 [-14.60, 40.60]
7.00 [-9.64, 23.64]
19.00 [-21.69, 59.69]
20.00 [0.55, 39.45]
6.40 [-89.88, 102.68]
23.50 [-10.21, 57.21]
20.67 [11.39, 29.95]
Experimental Control Mean Difference Mean Difference
IV, Random, 95% CI
-100 -50 0 50 100
Favours Control Favours NO
Study or Subgroup
Dellinger 1998
Lundin 1999
Taylor 2004
Total (95% CI)
Total events
Heterogeneity: Tau² = 0.00; Chi² = 0.88, df = 2 (P = 0.64); I² = 0%
Test for overall effect: Z = 2.65 (P = 0.008)
Events
20
28
10
58
Total
120
93
192
405
Events
7
12
6
25
Total
57
87
193
337
Weight
29.6%
51.1%
19.3%
100.0%
M-H, Random, 95% CI
1.36 [0.61, 3.02]
2.18 [1.19, 4.02]
1.68 [0.62, 4.52]
1.80 [1.17, 2.79]
NO Control Risk Ratio Risk Ratio
M-H, Random, 95% CI
0.1 0.2 0.5 1 2 5 10
Favours NO Favours control
Nitric oxide vs placebo; Outcome: Acute kidney injury

17. Handling oxygenation targets in adults with acute hypoxaemic
respiratory failure in the intensive care unit: A randomised clinical
trial of a lower versus a higher oxygenation target
Protocol version 1.0, 30th
of January 2017
Applicable protocol registration numbers:

18. (RR) with 95% confidence interval (Cl) for dichotomous outcomes. We assessed our
intervention effects with either random-effects model or fixed-effects model. Based on the
above parameters we concluded that the meta-analysis of these three trials did not provide a
significant difference between the intervention and the control group on all cause mortality on
maximum follow up (Figure 1.a,b,c,d,).
Figure 1a: Random Effect
Figure 1b: Random Effect (swapped)
Analysis courtesy of Sara Russo Krauss and Olav Lilleholt Schjørring
(HOT-ICU investigators)
Barbateskovic M, Schjørring OL, Jakobsen JC, et al. Higher versus lower inspiratory
oxygen fraction or targets of arterial oxygenation for adult intensive care patients
(protocol). Cochrane database systematic review. 2017(4).
Higher versus lower oxygen targets in respiratory failure

19. Baby lung

20. Baby lung
Gattinoni et al.

21. Normal Rat Lungs and Rat Lungs after Receiving High-Pressure Mechanical
Ventilation at a Peak Airway Pressure of 45 cm of Water.
Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from
experimental studies. Am J Respir Crit Care Med 1998;157:294-323.

23. Study or Subgroup
Amato et al 1998
Brochard et al 1998
Stewart 1998
Brower 1999
ARDS network 2000
Villar et al 2006
Total (95% CI)
Total events
Heterogeneity: Chi² = 11.38, df = 5 (P = 0.04); I² = 56%
Test for overall effect: Z = 3.16 (P = 0.002)
Events
11
27
30
13
133
17
231
Total
29
58
60
26
452
50
675
Events
17
22
28
12
170
25
274
Total
24
58
60
26
429
45
642
Weight
6.6%
7.8%
10.0%
4.3%
62.0%
9.4%
100.0%
M-H, Fixed, 95% CI
0.54 [0.31, 0.91]
1.23 [0.80, 1.89]
1.07 [0.74, 1.55]
1.08 [0.62, 1.91]
0.74 [0.62, 0.89]
0.61 [0.38, 0.98]
0.80 [0.70, 0.92]
Year
1998
1998
1998
1999
2000
2006
Protective ventilation Control Risk Ratio Risk Ratio
M-H, Fixed, 95% CI
0.1 0.2 0.5 1 2 5 10
Favours PVL Favours Control
Forest plot of comparison:
Pressure and volume limitation (Protective ventilation) vs Control,
outcome: Mortality at end of each study period.

24. Study or Subgroup
1.5.1 low-pressure control (< or = 31 cm H2O)
Stewart 1998
Brochard et al 1998
Brower 1999
Subtotal (95% CI)
Total events
Heterogeneity: Chi² = 0.24, df = 2 (P = 0.89); I² = 0%
Test for overall effect: Z = 0.95 (P = 0.34)
1.5.2 high-pressure control (> 31 cm H2O)
Amato et al 1998
ARDS network 2000
Villar et al 2006
Subtotal (95% CI)
Total events
Heterogeneity: Chi² = 1.33, df = 2 (P = 0.51); I² = 0%
Test for overall effect: Z = 3.58 (P = 0.0003)
Total (95% CI)
Total events
Heterogeneity: Chi² = 9.24, df = 5 (P = 0.10); I² = 46%
Test for overall effect: Z = 2.69 (P = 0.007)
Test for subgroup differences: Chi² = 7.46, df = 1 (P = 0.006), I² = 86.6%
Events
30
27
13
70
13
133
17
163
233
Total
60
58
26
144
29
432
50
511
655
Events
28
22
12
62
17
170
25
212
274
Total
60
58
26
144
24
429
45
498
642
Weight
10.1%
7.9%
4.3%
22.3%
6.7%
61.5%
9.5%
77.7%
100.0%
M-H, Fixed, 95% CI
1.07 [0.74, 1.55]
1.23 [0.80, 1.89]
1.08 [0.62, 1.91]
1.13 [0.88, 1.45]
0.63 [0.39, 1.02]
0.78 [0.65, 0.93]
0.61 [0.38, 0.98]
0.74 [0.63, 0.87]
0.83 [0.72, 0.95]
Year
1998
1998
1999
1998
2000
2006
Experimental Control Risk Ratio Risk Ratio
M-H, Fixed, 95% CI
0.1 0.2 0.5 1 2 5 10
Favours PVL Favours Control
Forest plot of comparison:
Pressure and volume limitation (Protective ventilation) vs Control,
Outcome: Mortality at different plateau pressure in control groups.

25. Serpa Neto A et al. JAMA. 2012 Oct 24;308(16):1651-9.

26. 0%
5%
10%
15%
20%
25%
0 1 2 3 4 5 6 7 8 9 10
Probability
Deaths
Deaths in ARDS using different ventilation strategies
p = 40 % p = 30 %
”In my experience…”

27. Volumbegrenset ventilasjon
0
100
200
300
400
500
600
700
140 145 150 155 160 165 170 175 180 185 190 195 200 205 210
Høyde (cm)
Tidalvolum(6mL/kgpredikertvekt)
Kvinner
Menn
Kvinner: 45.5 + 0.91 x (høyde i cm - 152.4)
Menn: 50 + 0.91 x (høyde i cm - 152.4)
Kvinner Menn
Høyde
Predikert
vekt TV
Predikert
vekt TV
140 34 205 39 232
145 39 233 43 260
150 43 260 48 287
155 48 287 52 314
160 52 314 57 341
165 57 342 61 369
170 62 369 66 396
175 66 396 71 423
180 71 424 75 451
185 75 451 80 478
190 80 478 84 505
195 84 506 89 533
200 89 533 93 560
205 93 560 98 587
210 98 587 102 614

28. Study or Subgroup
Guerin 2004
Guerin 2013
Voggenreiter 2005
Total (95% CI)
Total events
Heterogeneity: Chi² = 13.70, df = 2 (P = 0.001); I² = 85%
Test for overall effect: Z = 2.20 (P = 0.03)
Events
179
56
1
236
Total
413
237
21
671
Events
159
94
3
256
Total
377
229
19
625
Weight
62.7%
36.1%
1.2%
100.0%
M-H, Fixed, 95% CI
1.03 [0.87, 1.21]
0.58 [0.44, 0.76]
0.30 [0.03, 2.66]
0.86 [0.74, 0.98]
Prone ventilation Control Risk Ratio Risk Ratio
M-H, Fixed, 95% CI
0.02 0.1 1 10 50
Favours prone Favours control
Study or Subgroup
Guerin 2013
Total (95% CI)
Heterogeneity: Not applicable
Test for overall effect: Z = 4.53 (P < 0.00001)
Mean
14
SD
9
Total
237
237
Mean
10
SD
10
Total
229
229
Weight
100.0%
100.0%
IV, Fixed, 95% CI
4.00 [2.27, 5.73]
4.00 [2.27, 5.73]
Prone ventilation Control Mean Difference Mean Difference
IV, Fixed, 95% CI
-10 -5 0 5 10
Favours control Favours prone
Study or Subgroup
Fernandez 2008
Guerin 2013
Mancebo 2006
Total (95% CI)
Heterogeneity: Chi² = 5.77, df = 2 (P = 0.06); I² = 65%
Test for overall effect: Z = 1.35 (P = 0.18)
Mean
15.9
24
27.9
SD
11.1
22
18.5
Total
21
237
76
334
Mean
11.3
26
22
SD
7.6
27
14.1
Total
19
229
60
308
Weight
26.0%
44.3%
29.6%
100.0%
IV, Fixed, 95% CI
4.60 [-1.25, 10.45]
-2.00 [-6.48, 2.48]
5.90 [0.42, 11.38]
2.06 [-0.92, 5.04]
Prone ventilation Control Mean Difference Mean Difference
IV, Fixed, 95% CI
-20 -10 0 10 20
Favours prone Favours control
Study or Subgroup
Fernandez 2008
Guerin 2004
Guerin 2013
Mancebo 2006
Total (95% CI)
Total events
Heterogeneity: Chi² = 1.95, df = 3 (P = 0.58); I² = 0%
Test for overall effect: Z = 0.66 (P = 0.51)
Events
0
22
15
7
44
Total
21
413
237
76
747
Events
1
28
13
4
46
Total
19
378
229
60
686
Weight
3.2%
60.3%
27.3%
9.2%
100.0%
M-H, Fixed, 95% CI
0.30 [0.01, 7.02]
0.72 [0.42, 1.23]
1.11 [0.54, 2.29]
1.38 [0.42, 4.50]
0.87 [0.59, 1.30]
Prone ventilation Control Risk Ratio Risk Ratio
M-H, Fixed, 95% CI
0.01 0.1 1 10 100
Favours prone Favours control
Forest plot of comparison:
Prone positioning vs Control
outcome:
Mortality at 90 Days.
Ventilator Free Days
ICU Days Survivors
Barotrauma

30. ARDS was underdiagnosed, with 64.2% of all patients with ARDS
being clinician-recognized. Clinician recognition of ARDS ranged from
51.3% (95% CI, 47.5%-55.0%) for mild ARDS to 78.5% (95% CI, 74.8%-
81.8%) for severe ARDS
Clinician recognition of ARDS at the time of fulfillment of ARDS
criteria was 34.0% (95% CI, 32.0-36.0), suggesting that diagnosis of
ARDS was frequently delayed.
Extent of ARDS
Recognition
All
(n=2377)
Mild
(n=714)
30.0%
Moderate
(n=1106)
46.5%)
Severe
(n=557)
(23.4%)
P value
ARDS
Recognition at
any time
No. (%)
1525
(64.2%)
366
(51.3%)
722
(65.3%)
437
(78.5%)
<0.001

31. LUNG-SAFE

32. LUNG-SAFE

33. LUNG-SAFE

34. LUNG-SAFE

35. John G. Laffey, Giacomo Bellani et al (2016) Potentially modifiable factors contributing to outcome from acute
respiratory distress syndrome: the LUNG SAFE study. Intensive Care Med DOI 10.1007/s00134-016-4571-5
LUNG-SAFE

36. LUNG-SAFE

37. John G. Laffey, Giacomo Bellani et al (2016) Potentially modifiable factors contributing to outcome from acute
respiratory distress syndrome: the LUNG SAFE study. Intensive Care Med DOI 10.1007/s00134-016-4571-5

38. Jean-Louis Vincent et al. (2006) Sepsis in European intensive care units:
Results of the SOAP study Crit Care Med 2006; 34:344–353

39. Severe
ARDS
TV 6 mL/kg
pCO2 
pH
Renal
compensation
pH
Hemodynamic
stability
Limitation of
vasopressors, fluids
Resolution of
pulmonary
oedema

40. Severe
ARDS
TV 6 mL/kg
pCO2 
pH
Renal
compensation
pH
Hemodynamic
instability
Vasopressors
Fluids
✗

41. ECCO2r: Patients with combined acute
respiratory failure and kidney injury
• Gentle ventilation may cause severe
acidosis
• Removal of limited amount of CO2
may be sufficient to stabilise
patients
• Pediatric oxygenator
• Not useful for oxygenation failure
• Does not replace ECMO

42. ECMO – LAST RESORT?

43. Breathe!

44. Glutamin Glutamin Glutamin
Glutamat
a-KG
PAG
NH4+NH4+
HCO3- HCO3-
Krebs
syklus
ATP
OAA
NH4+NH4+
CO2 + H20 =Na+
H+
Na+
GDH
prox tubuli epitel blod
pH pH