This document discusses acute respiratory distress syndrome (ARDS). It begins by defining ARDS and describing its signs and symptoms. It then discusses the history of ARDS definitions and criteria. It outlines the pathophysiology and three phases of ARDS. Treatment strategies covered include mechanical ventilation, monitoring, infection control, and specific therapies. Prognosis and risk factors are also summarized.

1. Ahad Aftab Khan Lodhi, MD

3. 
Adult Respiratory
Distress Syndrome

Da Nang Lung

Transfusion Lung

Post Perfusion Lung


4. Acute respiratory distress
Cyanosis refractory to oxygen therapy
Decreased lung compliance
Diffuse infiltrates on chest radiograph
Difficulties:
 lacks specific criteria
 controversy over incidence and mortality

5. 1988: four-point lung injury score
 Level of PEEP
 PaO2 / FiO2 ratio
 Static lung compliance
 Degree of chest infiltrates
1994: consensus conference
simplified the definition

6. Acute onset
 may follow catastrophic event
Bilateral infiltrates on chest radiograph
PAWP < 18 mm Hg
Two categories:
 Acute Lung Injury - PaO2/FiO2 ratio < 300
 ARDS - PaO2/FiO2 ratio < 200

7. ALI
Acute Acute
PaO2/FiO2 < 200 < 300mmHg
B/l interstitial /alveolar Same
infiltrates
PCWP <18mmHg Same

8. The 1994 NAECC Definition Limitations
Descriptive definition - Permits inclusion of a multiplicity of clinical
entities ranging from autoimmune disorders to direct and indirect
Pulmonary injury
Does not address the cause of lung injury
Does not provide guidelines on how to define acute
The radiological criteria are not sufficiently specific
Does not account for the level of PEEP used, which affects the
Pao2/Fio2 ratio
Does not specify the presence of nonpulmonary organ system
dysfunction at the time of diagnosis
Does not include the different specific mechanistic pathways
involved in producing lung injury

9. The 1998 NAECC Updated
Recommendations
The collection of epidemiologic data should be based on the
1994 NAECC definitions.
The severity of ALI/ARDS should be assessed by the Lung Injury
Score (LIS) or by the APACHE III or SAPS II scoring systems.
The factors that affect prognosis should be taken into account.
The most important of these are incorporated into the GOCA
stratification system.
It will be also useful to record:
Information relating to etiology (at a minimum, direct or indirect cause)
Mortality,including cause of death,and whether death was associated with withdrawal
of care
Presence of failure of other organs and other time-dependent covariates
Follow-up information, including recovery of lung function and quality of life

11. 3 phases
- exudative (0-7 d)
- proliferative ( 7-21 d)
- fibrotic ( > 21 days)

12. Acute, exudative 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

13. Subacute, Proliferative phase:
 persistent hypoxemia
 development of hypercarbia
 fibrosing alveolitis
 further decrease in pulmonary
compliance
 pulmonary hypertension

14. Chronic phase
 obliteration of alveolar and
bronchiolar spaces and pulmonary
capillaries
Recovery phase
 gradual resolution of hypoxemia
 improved lung compliance
 resolution of radiographic
abnormalities

16. Inciting event
Inflammatory mediators
 Damage to microvascular endothelium
 Damage to alveolar epithelium
 Increased alveolar permeability results
in alveolar edema fluid accumulation

18. Type I cell
Alveolar
macrophage
Endothelial
Cell
RBC’s Type II
cell
Capillary

19. Type I cell
Alveolar
macrophage
Endothelial
Cell
RBC’s Type II
cell
Capillary
Neutrophils

20.  Target organ injury from host’s inflammatory
response and uncontrolled liberation of inflammatory
mediators
 Localized manifestation of SIRS
 Neutrophils and macrophages play major roles
 Complement activation
 Cytokines: TNF-α, IL-1β, IL-6
 Platelet activation factor
 Eicosanoids: prostacyclin, leukotrienes, thromboxane
 Free radicals
 Nitric oxide

21. Abnormalities of gas exchange
Oxygen delivery and
consumption
Cardiopulmonary interactions
Multiple organ involvement

22. Hypoxemia: HALLMARK of ARDS
 Increased capillary permeability
 Interstitial and alveolar exudate
 Surfactant damage
 Decreased FRC
 Diffusion defect and right to left shunt

23. Pathologic flow dependency
 Uncoupling of oxidative dependency
 Oxygen utilization by non-ATP producing
oxidase systems
 Increased diffusion distance for O2 between
capillary and alveolus

24. A = Pulmonary hypertension
resulting in increased RV afterload
B = Application of high PEEP
resulting in decreased preload
A+B = Decreased cardiac output

26. Routine blood counts
RFT
CXR
ABG
CT chest
BNP
2D Echo
BAL
PCWP

27. Can be difficult to do. Should always try to
make the diagnosis in light of the clinical
picture.
Need to determine Cardiogenic vs. Non-
cardiogenic edema.

28. Cardiogenic Non-Cardiogenic
Diffuse Bilateral patchy
Bilateral infiltrates
infiltrates homogenously
predominately in lung bases.
distributed throughout the
Kerley B’s. Cardiomegaly.
lungs. No Kerley B’s.

29. Non-cardiogenic
Patchy infiltrates in Homogenous pluffy
bases shadows
Effusions + Effusions –
Kerley B lines + Kerley B lines –
Cardiomegaly + Cardiomegaly –
Pulmonary vascular No pulm.vascular
redistribuition redistribuition
Excess fluid in alveoli Protein,inflammatory
cells,fluid

30. late

31. Cardiogenic Non-Cardiogenic
No septal thickening. Diffuse
Septal thickening. More severe in alveolar infiltrates.
lung bases. Atelectasis of dependent lobes
usually seen .

32. RESPIRATORY SUPPORT
Conventional mechanical ventilation
Newer modalities:
High frequency ventilation
 ECMO
Innovative strategies
 Nitric oxide
 Liquid ventilation
 Exogenous surfactant

33. Monitoring:
 Respiratory
 Hemodynamic
 Metabolic
 Infections
 Fluids/electrolytes

34. Treatment of underlying cause
Cardio-pulmonary support
Specific therapy targeted at lung injury
Supportive therapy.

35. In the early stages of ARDS the hypoxia may be
corrected by 40 to 60% inspired oxygen .
If the patient is well oxygenated on <= 60 %
inspired oxygen and apparently stable without CO2
retention then ward monitoring may be feasible
but close observation( 15 to 30 Min), continuous
oximetry, and regular blood gases are required

36. Inadequate oxygenation ( PaO2- < 60 with FiO2
>=0.6)
Rising or elevated PaCO2 ( > 50mmHg)
 Clinical signs of incipient respiratory failure

37. The Aims are to increase PaO2 while
minimizing the risk of further lung injury
(ventilator induced lung injury)

39. Spontaneous breathing trial daily
PaO2/FiO2 less than previous day
Systolic BP > 90 without vasopressors
No neuromuscular blockade
2 hr trial- with T piece with 1-5cm water CPAP.
ABG,RR,SPO2 monitoring
If tolerated for 30 mt,consider extubation

40. RECOMMENDATION
S
 MECHANICAL VENTILATION
Low tidal volume A
Minimize LAFP B
High PEEP C
Prone position C
Recruitment maneuvers C
High frequency ventilation D
 Glucocorticoids D
 Sufactant D
replacement,inhaled
NO,others

41. Low tidal volume mechanical ventilation
 In ARDS there is a large amount of poorly compliant
(i.e. non-ventilating) lung and a small amount of
healthy, compliant lung tissue. Large tidal volume
ventilation can lead to over-inflation of the healthy
lung tissue resulting in ventilator-induced lung
injury of that healthy tissue.
PEEP
 Setting a PEEP prevents further lung injury due to
shear forces by keeping airways patent during
expiration

42. High TV vs low TV (12ml/kg vs 6ml/kg)
- 861 pts
- mortality rate 39.2 % vs 31%
High PEEP vs low PEEP
13cm H20 vs 8 cm H20 –NO difference
Amato etal- optimal PEEP- 15cm H20

43. Inverse ratio ventilation
- reduce peak airway pressure
- I: E – 1:1 & 4:1
- severe hypoxemic resp.failure
Permissive hypercapnea
- controlled hypoventilation
- PaCO2 upto 55mmhg
- pH upto 7.25
 Proning

44. High flow ventilation
ECMO
Partial fluid ventilation (PLV)

46.  Fluids –
- conservative management
- normal or low LAFP
- reduce icu stay,duration of ventilation
 Steroids
- Meduri et al study
- methyprednisolone-2mg/kg
& taper to .5-1mg/kg in 1-2wk

47. Empirical antibiotics
Culture sensitivity & change antibiotics
Avoid nephrotoxic drug
Enteral feeding

48. NO
Ketoconazole
Albuterol
Pentoxyphylline
NSAIDS
N-acetyl cysteine

49. Mortality ranges-26 %-44%
Risk factors-
- advanced age
- CKD,CLD
- Chronic immunosuppression
- chronic alcohol abuse
ARDS from direct lung injury has double
mortality