ARDS is defined by acute onset hypoxemia caused by bilateral lung infiltrates from non-cardiogenic pulmonary edema. The Berlin definition categorizes ARDS as mild, moderate, or severe based on oxygenation levels. Mechanical ventilation can worsen lung injury so strategies aim to limit tidal volumes and pressures while using PEEP to recruit alveoli. Additional techniques like prone positioning, inhaled nitric oxide, and alternative modes may help in severe cases but require more study.

2. ARDS.. Definition
•ARDS: acute respiratory distress syndrome
Criteria :
- Acute onset
- Bilateral infiltrates on chest radiograph
- Exclusion of left Atrial hypertension
Two categories..
Acute Lung Injury - PaO2/FiO2ratio <300
RDS - PaO2/FiO2ratio <200
American European consensus conference (AECC) 1994

3. Other CriteriaChest
Radiograph
OxygenationSource
Impaired pulmonary
compliance
Marked difference in
inspired vs. arterial
oxygen tensions
Diffuse alveolar
infiltrates on frontal
chest radiograph
Cyanosis refractory
to oxygen therapy
Petty and
Ashbau,
1971
PEEP and respiratory
system compliance
(by quintiles)
Preexisting direct or
indirect lung injury
Nonpulmonary organ
dysfunction
No. of quadrants
of alveolar
consolidation
on frontal chest
radiograph
Hypoxemia
(PaO2/FIO2),
by quintiles
Murray et
al,
Older diagnostic Criteria for ARDS

4. Other CriteriaChest
Radiograph
OxygenationSource
PCWP <18 mm Hg
if measured or
no clinical evidence
of left atrial
hypertension
Bilateral infiltrates
on
frontal chest
radiography
ALI:
PaO2/FIO2 <300,
regardless of PEEP
level
ARDS, PaO2/FIO2
<200,
regardless of PEEP
level
Bernard
et al,
Older diagnostic Criteria for ARDS

5. ARDS… ‘Berlin definition’
Adopted in 2011; initiated by European Society Of
Intensive Care Medicine
3 mutually exclusive categories.. based on PaO2/FIO2 (at
PEEP> 5)
• Mild- Between 300 and 200 mmHg.
• Moderate- Between 100 and 200 mmHg.
• Severe- Less than 100 mmHg.
Initially 4 ancillary criterions( radiographic severity, respiratory
system compliance, PEEP, and corrected expired minute
volume) were also included, but later dropped as they did not
contribute to predictive validity of severe ARDS.
JAMA. 2012;307(23):2526-2533/ doi:10.1001/jama.2012.5669

6. ARDS… ‘Berlin definition’ Differences
• Acute Lung Injury.. No longer exists. It is replaced by
mild ARDS.
• Onset must be within 7 days of some defined event,
like sepsis, pneumonia or worsening of respiratory
symptoms.
• Bilateral opacities consistent with Pulmonary edema
must be present, but may be detected on CT scan.
• There is no need to exclude heart failure in this new
definition. Patients with CHF or high PCOP can still
have ARDS.
JAMA. 2012;307(23):2526-2533/ doi:10.1001/jama.2012.5669

7. ARDS.. Etiology
Direct Injury
Common Causes
• Pneumonia 28%
• Gastric aspiration 14%
Less Common Causes
• Pulmonary contusion
• Fat emboli
• Near drowning
• Inhalational injury
Indirect Injury
Common Causes
•Sepsis 32%
•Shock after severe trauma 5%
Less Common Causes
•Cardiopulmonary Bypass
•Drug overdose
•Acute pancreatitis
•Massive blood transfusions
Davis et al., J Peds1993;123:35

8. ARDS.. Stages
Acute, exudative - inflammatory phase
• Rapid onset of respiratory failure after trigger
• Diffuse alveolar damage with inflammatory cell
infiltration
• Hyaline membrane formation
• Capillary injury
• Protein-rich edema fluid in alveoli
• Disruption of alveolar epithelium

9. ARDS.. Stages
Sub-acute, Proliferative phase:4-10 days
• Persistent hypoxemia
• Development of hypercarbia
• Further decrease in pulmonary compliance
• Pulmonary hypertension

10. ARDS.. Stages
Chronic phase above 10 days
• Fibrosing alveolitis
• Obliteration of alveolar and bronchiolar spaces
and pulmonary capillaries
Recovery phase
• Gradual resolution of hypoxemia
• Improved lung compliance
• Resolution of radiographic abnormalities

13. ARDS.. Pathophysiology
• Abnormalities of gas exchange
• Oxygen delivery and consumption
• Cardiopulmonary interactions
• Multiple organ involvement

14. Abnormalities in Gas Exchange
Hypoxemia: HALLMARK of ARDS
• Increased capillary permeability
• Interstitial and alveolar exudate
• Surfactant damage
• Decreased FRC
• Diffusion defect and right to left shunt

15. Oxygen delivery and consumption
• VO2 is dependent on DO2 over a wide range of DO2
values in acute respiratory failure. This dependency
phenomenon is much stronger in ARDS than in
respiratory failure due to other causes.
• Because of alterations in ventricular function, DO2 may
be inadequate to satisfy oxygen demand and may
contribute to multiple-system organ failure (MSOF).
• Due to the abnormal dependency of VO2 on DO2,
changes in the oxygenation status may not be reflected by
changes in mixed venous oxygen saturation in ARDS

16. Cardiopulmonary interactions
• A = Pulmonary hypertension resulting in
increased RV afterload
• B = Application of high PEEP resulting in
decreased preload
• A+B = Decreased cardiac output

17. Innovations:
•iNO
•PLV
•Proning
•Surfactant
•Anti-
Inflammatory
Gentle ventilation:
•Permissive
hypercapnia
•Low tidal volume
•Open-lung
•HFOV
ARDS
Extra Corporeal Membrane Oxygenator
ARDS.. Therapies

18. Mechanical Ventilation in ARDS
Injurious ventilator
associated lung injury
Necessary to reverse
Hypoxaemia

19. • The lung with ALI or ARDS are particularly
prone to ventilator associated lung injury:
(Baby lung)
 Collapsed, consolidated, less compliant areas
(Dependant)
 Normal areas (non dependant)

20. A, The chest radiograph shows bilateral pulmonary infiltrates that appear to be diffuse.
B, A computed tomographic scan of the thorax from the same patient demonstrates
that the distribution of the bilateral infiltrates is predominantly in dependent regions with
more normal-appearing lung in nondependent regions.

21. Ventilator associated lung injury
 High inflation pressure Barotrauma
 Over distension Volutrauma
 Repetitive opening & closing of alveoli
Atelect-trauma
 SIRS & cytokines release Biotrauma.

22. Ventilator--Associated Lung Injury
• Barotrauma - Extra-alveolar air (pneumo-…)
• Volutrauma - Regional lung over-distension
(stretch injury)
• Alelectrauma - Cyclic closure & reopening of
terminal units (shear injury)
• Biotrauma - Inflammatory mediators
transmigrate to systemic circulation, causing
multiple organ-system failure

23. Lung Protection strategy
• Implemented immediately on intubation
• Limit tidal volume 6-8 ml/kg
• PEEP above inflection point
• FiO2 <0.6 and saturation (88-90%)
• Permissive hypercapnia
NIH study NEJM 2000;342:1301-8

24. Lung protective ventilation strategy
 Pressure & volume limitation
 Higher PEEP
 Recruitment maneuvers
(Dynamic process of reopening collapsed alveoli
through increase in trans pulmonary pressure)

25.  Which Recruitment maneuvers to be Used ?
1. The most well Known method of recruitment maneuver is
sustained application of CPAP of 30- 50 Cm H2O for 30
seconds
2. Periodic recruitment with a series of traditional sigh breaths
3. Intermittently raising PEEP over several breaths
4. Extended sigh maneuver with step wise increase in PEEP
while Vt is decreased
5. Intermittent application of pressure controlled ventilation
with incremental high PEEP
Lung protective ventilation etiology

26.  Permissive hypercapnea (acute respiratory acidosis)
Treatment : Increase respiratory rate in a stepwise up to 35
Bicarbonate infusion
Increase Vt
 Worsened oxygenation & transient desaturation
 Increased sedation or analgesia
 Hypotension & arrhythmias
 Barotraumas (Pneumothorax)
 Bacterial translocation
Consequences of lung protective ventilation

27. • High-frequency Ventilation
(Jet, Oscillation, or Percussive ventilation)
• HFOV allows for higher mean airway pressures
& markedly reduced tidal volumes (1-3 ml/kg)
Lung recruitment & reduce lung injury.
Alternative Approaches to Lung Protection

28. High frequency oscillatory ventilation
(HFOV)
• Advantage:-
Can provide enhanced gas exchange
Protective lung strategy for poor compliance of
lung
• Disadvantage:-
High lung volume may cause decreased venous
return and hypotension
IV fluids and vasopressors may be required

29. Gas entering the lungs travels centrally, while gas
leaving the lungs swirls around it

30. Airway pressure release ventilation (APRV)
• It provides two levels of airway pressure (P high & P low)
during two time periods (T high & T low) , usually a long
Thigh & short Tlow with spontaneous breathing during
both.
• Advantages: Decrease barotrauma, provide better V/P
matching, cardiac filling & patient comfort.
Alternative Approaches to Lung Protection

31. APRV

32. APRV Cautions
• Hemodynamic compromise
• Changing expiratory time constant
• Change in resistance
• Change in compliance
• Auto-PEEP
• Excessive release VT??

33. Open lung ventilation technique
• Advantages of high PEEP to
• Recruit more alveoli
• Reduce atelactasis
• Reduce stretch sheering injury
• Disadvantages
• Reduces cardiac output
• Increases airway pressure
Alternative Approaches to Lung Protection

34.  Prone positioning:
Recruitment of dorsal (nondependent) atelectatic lung
units, improved respiratory mechanics, decreased
ventilation- perfusion mismatch, increased secretion
drainage, reduced and improved distribution of
injurious mechanical forces
(Pelozi P et al, 2002)
Adjunctive therapies to lung-protective
Ventilation

35. Inhaled nitric oxide :
Selective VD in ventilated lung units improving
V/Q mismatch, decrease PaO2 & pulmonary
hypertension ( no sustained clinical benefit)
(Tayler RW et al, 2004)
Adjunctive therapies to lung-protective
Ventilation

36. Irrespective of this controversy as to whether the exact
ARDSNet protocol should be adopted, the existing
evidence supports that clinicians should change their
practice and adopt volume and pressure limited
ventilation for patients with ALI or ARDS.
As additional evidence emerges, ongoing reassessment
and evolution of these protocols will be necessary.

37. 1. Mechanical ventilation, although life saving, can
contribute to patient morbidity and mortality
2. Volume and pressure limited ventilation clearly leads to
improved patient survival
3. The role of re-cruitment maneuvers, higher levels of
PEEP, or both remain controversial
4. At this time, use of alternative modes of ventilation
(e.g., HFOV) and adjunctive therapies (e.g., inhaled nitric
oxide and prone positioning) should be limited to future
clinical trials and rescue therapy for patients with ALI or
ARDS with life threatening hypoxemia failing maximal
conventional lung protective ventilation.
Conclusions and Future Considerations

38. A
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39. ARDS
Patient
Manage
ment
Protocol

40. The Puzzle keep getting tougher with each step…