This document discusses acute respiratory distress syndrome (ARDS). It defines ARDS as diffuse inflammatory lung injury leading to impaired gas exchange. ARDS is not a primary disorder but occurs due to infectious or non-infectious conditions like pneumonia or sepsis. Treatment involves treating the underlying cause, mechanical ventilation with a protective strategy using low tidal volumes and high PEEP, fluid management to avoid positive balance, and possibly steroids in moderate to severe cases. Outcomes are improved by following evidence-based guidelines for ARDS therapies.

1. Dr. Mohamed El Sayed
Lecturer of Anesthesia and intensive care
ALS provider –ACLS provider –ATLS provider

2.  Definition
 Causes
 Clinical features
 Diagnosis
 Treatment

3. Diffuse inflammatory injury of the lungs 
Neutrophil degranulation damages the capillary
endothelium, leading to exudation of protein-
rich fluid that fills the distal airspaces and
impairs pulmonary gas exchange.
 10 % of ICU admissions
 25 % of prolonged mechanical ventilation
 Most (>90%) cases of ARDS appear within one
week of a known predisposing condition
 80% of cases require mechanical ventilation

4.  ARDS is not a primary disorder, but is a
consequence of a variety of infectious and
noninfectious conditions
 The most frequent offenders are
1. Pneumonia, 59 %
2. Extra-pulmonary sepsis 16 %
3. Aspiration of gastric secretions 14 %
 Tendency to triggera systemic inflammatory
response.

8.  Anterior sub-pleural consolidations
 Absence or reduction of lung sliding
 “Spared areas” of normal parenchyma
 Pleural line abnormalities (irregular
thickened fragmented pleural line)
 Non-homogeneous distribution of B-
lines (a characteristic ultrasound finding
suggestive of fluid accumulation in the
lungs)

10. Dense
consolidation
in the posterior
lung regions

11.  Decreased PaO2/FiO2 ratio (a decreased
PaO2/FiO2 ratio indicates reduced arterial
oxygenation from the available inhaled
gas):
◦ Mild ARDS: 201 – 300 mmHg (≤ 39.9 kPa)
◦ Moderate ARDS: 101 – 200 mmHg (≤ 26.6 kPa)
◦ Severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)
 Note that the 2012 "Berlin criteria" are a
modification of the prior 1994 consensus
conference definitions

12.  Treatment of the underlying cause is crucial.
 Appropriate antibiotics therapy is started as
soon as cultures results are available, or if
infection is suspected (whichever is earlier).
 Empirical therapy may be appropriate if local
microbiological surveillance is efficient.
 Mechanical ventilation
 Fluid management
 Steroids
 Others

13. Goals of MV
 (a) limit the stretchimposed on the distal
airspaces during lung inflation ( volutrauma )
 (b) prevent the distal airspacesfrom collapsing
during lung deflation. ( Atlectotrauma)
 Protective lung strategy 
1. Low TV
2. Platue pressure < 30
3. Low fiO2
4. PEEP
5. RECRUITMENT

17.  mean airway pressure (to promote
recruitment (opening) of easily collapsible
alveoli and predictor of hemodynamic
effects) and
 Plateau pressure  (best predictor of alveolar
over-distention)
 Ideal body weight rather than actual weight).
 improved mortality when people with ARDS
 Permissive hypercarbia  according to Ph

18.  PEEP  keep alveoli open
 At least 5 cm H2O
 high PEEP levels does not improve outcomes in
ARDS.
 For cases of hypoxemia that require potentially toxic
concentrations of inhaled O2 (FIO2 >60%),
incremental increases in PEEP can help to improve
arterial oxygenation and reduce the inhaled O2 to
lower (nontoxic) levels.
 maximum “safe” level of PEEP is reached when
the plateau pressure reaches 30 cm H2O.

19.  The limits of tolerance to hypercapnia are
unclear,
 clinical trials of permissive hypercapnia show
that an arterial PCO2 of 60–70 mm Hg and an
arterial are safe for most patientspH of 7.2–
7.25

20.  APRV is a modified form of continuous
positive airway pressure
 periods of spontaneous breathing with high-
level CPAP, interrupted by brief periods of
pressure release to atmospheric pressure.
 The high CPAP level improves arterial
oxygenation by opening collapsed alveoli
(alveolar recruitment), and the pressure
release is designed to facilitate CO2 removal
 The increase in arterial oxygenation occurs
gradually, over 24 h

21. Ventilator Settings
 high and low airway pressures, and the time
spent at each pressure level.
 The high airway pressure = end-inspiratory
alveolar pressure during CMV
 The low airway pressure = zero.
 The time spent at the high airway pressure
is usually 85–90% of the total cycle time.
 Recommended times are 4–6 seconds for
the high pressure level, and 0.6 to 0.8
seconds for the low pressure level

22. Advantages
 a. APRV can achieve nearly complete recruitment of
collapsed alveoli, more than can be achieved with
HFOV or high-level PEEP.
 b. APRV can increase cardiac output despite the high
airway pressures that are used. This is attributed to
the marked alveolar recruitment that occurs with
APRV, which also reopens blood vessels and
increases pulmonary blood flow.
Disadvantages
 a. The benefits of APRV are lost if the patient has no
spontaneous breathing efforts.
 b. Severe asthma and COPD are relative
contraindications to APRV because of the inability to
empty the lungs rapidly during the pressure release
phase.

24.  Clinical studies have shown that avoiding a
positive fluid balance in patients with ARDS
can reduce the duration of mechanical
ventilation and improve survival rates
 A simple protocol for fluid management,
developed by the ARDS Network

26.  Steroid therapy can be used for the early
treatment of moderate-to-severe ARDS, and for
unresolving ARDS.
 While there is no consistent survival benefit
attributed to steroid therapy in ARDS, there are
other potential benefits, including
◦ a shorter duration of mechanical ventilation,
◦ improved gas exchange
◦ shorter stay in the ICU

27. Early cases of ARDS :
 PaO2/FIO2 is <200 mm Hg with PEEP of 10 cm H2O
 a Methylprednisolone
 1 mg/kg (ideal body weight) over 30 minutes,
 1 mg/kg/day by continuous infusion for 14 days,
 followed by a gradual taper over the next 14 days.
Long standing ARDS > 14 day
 7–14 days after the onset of illness = irreversible pulmonary fibrosis
 a Methylprednisolone
 2 mg/kg (ideal body weight) over 30 minutes,
 2 mg/kg/day by continuous infusion for 14 days,
 1 mg/kg/day (continuous infusion) for the next 7 days,
 gradual taper that ends 2 weeks after extubation.
 There is no evidence that this regimen increases the risk
of infection

28.  Intra-tracheal surfactant (in adults),
 Inhaled nitric oxide,
 intravenous N-acetylcysteine,
 ibuprofen,
 Prostaglandin E infusions,
 Atrial natriuretic peptide,
 Monoclonal anti-endotoxin antibodies
 Neutrophil elastase inhibitors
 immune-modulating feeding

29. Evidence –Based Recommendations for ARDS
Therapies
recommendationtreatment
A
C
C
D
Mechanical ventilation:
• Low tidal volume
• High-PEEP or “ open-lung”
• Prone position
• High- frequency ventilation and ECMO
B
Minimize left atrial filling pressures
Cglucocorticoids
DSurfactant replacement ,inhaled nitric oxide and other
anti-inflammatory therapy ( e.g
Ketoconazole,PGE,NSAIDs)
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31. Thank you