2. History
In 1967, Ashbaugh and colleagues reported the clinical
characteristics of 12 patients with sudden respiratory failure that
they called ARDS
No underlying cardiac or pulmonary disease
Rapidly developed acute hypoxemia, stiff lungs, and diffuse
bilateral alveolar infiltrates on chest x-ray a few days following
exposure to a precipitating factor.
Autopsies revealed a characteristic histological pattern of diffuse
alveolar damage (DAD) including hyaline membrane formation,
oedema, cell necrosis, or fibrosis (Ashbaugh et al. 1967)
3. First clinical definition - AECC
(1994)
Acute onset of hypoxemia
PaO2 to FiO2 ratio ≤ 200 mmHg regardless of PEEP level,
Presence of bilateral infiltrates on chest radiograph, and
Pulmonary artery wedge pressure ≤ 18 mmHg or no clinical signs of
cardiogenic pulmonary oedema
ALI ( acute lung injury)
ARDS
5. Timing of onset
By definition, respiratory symptoms must commence within 7 days of a clinical insult
Disease processes developing over several weeks like idiopathic pulmonary fibrosis,
nonspecific interstitial pneumonitis and granulomatosis with polyangiitis can be excluded
by accurately timing the respiratory symptoms
6. Diseases with acute onset that may
mimic ARDS
Alveolar hemorrhage due to vasculitis
Drug-induced pulmonary toxicity
Acute eosinophilic pneumonia
Organizing or diffuse interstitial pneumonia
A complete diagnostic workup should include
Echo,BAL and chest CT scan
7. ARDS is an acute inflammatory lung condition
ARDS is not a disease
Always precipitated by an underlying process
• Pneumonia
• Aspiration of gastric contents
• Contusion,near
drowning,inhalational injury
pulmonary
• sepsis, pancreatitis, major
trauma, transfusion-related
acute lung injury, severe burns,
or drug overdose.
Extra
pulmonary
8. Pathophysioogy
ARDS is characterized by a marked reduction in lung compliance
DAD is the morphological hallmark of the lung in ARDS
Diffuse alveolar damage is defined by the presence of hyaline
membranes associated with interstitial oedema, cell necrosis and
proliferation and then fibrosis at a later stage
10. Mechanisms of hypoxemia in ARDS
Loss of lung volume due to alveolar
oedema and collapse
intrapulmonary shunt and marked
alteration in (VA/Q ratio)
Surfactant deficiency
impairment to the hypoxic pulmonary
vasoconstriction response
Pulmonary hypertension and positive
pressure ventilation
Opening of patent foramen ovale
intracardiac shunt
Increase in the physiological dead space
occurs
Alteration in lung diffusion
11. Traditional ventilator settings
TV 12 – 15 ml/kg
PEEP 0 - 5 CM H20
FiO2 0.8 - 1.0
PaCO2 < 50, PO2 > 80, spO2 > 98%
Ventilator induced lung
injury(VILI)
14. “Baby lung”
Using CT scan, Gattinoni found that compliance correlated with the normally aerated lung and
that the specific compliance (compliance divided by functional residual capacity) was actually
normal.
The "baby lung" is a physiological concept
The remaining normally aerated lung accessible to ventilation is considerably reduced and of
similar size as that of a baby
ARDS lung is not "stiff" but instead small, with nearly normal intrinsic elasticity
23. Oxygenation strategies
The first-line strategy in supporting hypoxemic patients is to provide oxygen
oxygen mask
oxygen mask plus reservoir
High flow canula – 1st line strategy for oxygenation
25. NIV
No strong evidence for the use of noninvasive ventilation (NIV)
Intubation rates of 40-50% in cases of moderate and severe ARDS
Risk of delaying intubation by masking signs of respiratory distress
Worsening VILI
poor tolerance of the facemask is frequent
26. When to intubate?
Whatever oxygenation strategy is used, intubation should not be delayed.
RR > 35-40 breaths/min
Clinical signs of respiratory distress
Severe hypoxemia defined as PaO2 < 60 mm Hg or SpO2 < 90% despite high FiO2
Respiratory acidosis, and copious secretions
Non-respiratory indications for invasive ventilation are altered consciousness and the
occurrence of shock
27. Targets of mechanical ventilation
To achieve adequate gas exchange whilst avoiding VILI
28. Lung protective ventilation
Low VTs ( 4 - 6 ml/kg of ideal body weight)
High PEEP levels ( 11- 16 cm h2O)
Strict monitoring of plateau pressure to avoid exceeding 30 cm H2O
29. Mode of ventilation
Worldwide assist-control in volume-controlled ventilation
(VCV) is the most commonly used mode
No difference in outcomes between VCV and (PCV
Whatever the ventilator mode used, VTs and end-inspiratory plateau
pressure should be limited and continuously monitored.
30. Gas exchange targets
Target a PaO2 of at least 60 mm Hg and SaO2 of at least 90%
No studies have shown that increasing PaO2 improves outcome
Protective ventilation using low VTs may induce respiratory acidosis
pH should usually be maintained above 7.2.
31. Driving pressure
Driving pressure (plateau pressure – PEEP) major determinant of outcome
it has been suggested that the mechanical power transferred to the respiratory system from
the ventilator plays a key factor in VILI
Not only the strain (change in lung volume) but both high flow and respiratory rate are
potentially harmful to the lungs
34. Recruitment maneuvers
Transient increases in trans-pulmonary pressure in an attempt to open collapsed alveoli.
When performing a recruitment manoeuvre the pressure reached at the end of inspiration
surpasses the recommended safety thresholds for short time periods
Sigh breaths, extended sigh breaths,
Increased inspiratory pressures and PEEP,
Sustained inflation
Staircase Recruitment Manoeuvre. There is currently minimal evidence to recommend a
particular method of recruitment.
35. Recruitment maneuvers
Oxygenation benefits may be short-lived and of uncertain signifiance,
There are no studies showing patient outcome benefits,
It is uncertain how to differentiate responders from non-responders
There is no evidence for when, how often they should be performed
There is no evidence of reducing VILI
The ART trial found increased mortality with staircase recruitment manoeuvre. Experts
made recently a conditional recommendation for using recruitment maneuver (Fan et al.
2017
Recruitment maneuvers can be considered as rescue therapyin the most
severely hypoxemic patients
No single method can be recommended.
36. Proning
Advocated for almost 40 years
Oxygenation improves dramatically
The dorsum of the lung has a larger volume than the anterior and apical areas
Better ventilating the dorsal regions of the lung in the prone position improves ventilation,
reduces intrapulmonary shunt leading to an improvement in V/Q matching.
39. Hemodynamics of proning
Afterload to the right ventricle is reduced
Lower pulmonary vascular resistance
Reduced levels of PEEP
Improves preload
42. PROSEVA trial
PROSEVA: Prone Positioning in Severe Acute Respiratory Distress
Syndrome
Guerin et al for the PROSEVA Study Group. NEJM 2013;368:2159-68.
Proning in severe ARDS reduces mortality without an
increase in adverse outcomes. Further studies are required to confirm
these findings but in the mean time these results are difficult to ignore
44. Early application of airway pressure release ventilation may
reduce the duration of mechanical ventilation in
acute respiratory distress syndrome
Zhou. Intensive Care Medicine 2017; 43:1648-1659.
46. Sedation
The use of sedation improves patient tolerance of positive pressure
ventilation and allows resting of respiratory muscles and the reduction of
oxygen consumption by these muscles.
47. Neuro muscular blockers
Neuromuscular blocking agent cisatracurium used for 48 hours in severe ARDS
patients Improved oxygenation ( ACURASYS trial)
Reduced lung and systemic inflammation
Improved patient survival after adjusting for confounding factors
48. steroids
Clear indications for steroid therapy for diseases that may mimic ARDS
include
Alveolar hemorrhage due to vasculitis,
Drug-induced toxic pneumonia with a lymphocytic pattern
Organized pneumonia
Acute eosinophilic pneumonia
49. Steroids in ARDS
Use of steroids in ARDS is unresolved
Mortality was significantly higher when steroid therapy was started 2 weeks after the
onset
Studies showing beneficial outcomes started low dose steroids early in the course of the
disease
High doses of steroids has been associated with either worse outcomes
50. Other adjunct therapies
HFOV - High frequency oscillatory ventilation - found harmful
Inhaled nitric oxide - no proven benefit
Restricted fluid regimen - beneficial
51. SUMMARY
Bed side echo ,BAL and CT thorax for complete work up
HFNC is first line oxygenation method in mild ARDS
Do not delay intubation
Lung protective ventilation strategy
Recruitment during early disease as rescue oxygenation
Early proning in case of poor response
Consider early ecmo if poor response to proning
52. This Photo by Unknown Author is licensed under CC BY-NC-ND
