• Patient presentation and
• First described in 1967 by Ashbaugh
Consensus after 1994
• In 1994 a new definition was
recommended by the American-
European Consensus Conference
ARDS is characterized by
• Acute onset
• Bilateral infiltrates on chest
• Pulmonary artery wedge pressure
< 18 mmHg; if unavailable, then
lack of clinical evidence of left
ventricular failure suffices
• PaO2:FiO2 < 200 mmHg
• The annual incidence of ARDS 1.5 to 13.5
people per 100,000 in the general
population. In mechanically ventilated
population is much higher.
• (ALI) of 16.1% in ventilated patients
admitted for more than 4 hours.
• More than half these patients may develop
- Brun-Buisson et al. (2004)
• Mechanical ventilation, sepsis, pneumonia, shock,
aspiration, trauma (especially pulmonary contusion),
major surgery, massive transfusions, smoke
inhalation, drug reaction or overdose, fat emboli and
reperfusion pulmonary edema after lung
transplantation or pulmonary embolectomy. Pneumonia
and sepsis are the most common triggers, and
pneumonia is present in up to 60% of patients.
• Elevated abdominal pressure of any cause is also
probably a risk factor for the development of ARDS,
particularly during mechanical ventilation
• Severe pneumonia.
• Near drowning.
• Inhalation of toxins and other irritants
such as smoke.
• Lung injury and bruising.
• Oxygen toxicity.
• Fat embolism- Where bubbles of fat
travel through the bloodstream and block
• Shock- Including septic shock and shock due to trauma.
• Diabetic Ketoacidosis.
• Hypersensitivity reactions.
• Drugs reactions due to aspirin, heroin or paraquat.
• Multiple blood transfusions.
• Acute liver failure.
• Obstetric complications- Problems during pregnancy or
delivery such as preeclampsia.
• Cardiac surgery and other complicated surgeries.
Patient presentation and
• ARDS usually occurs within 24 to 48
hours of the initial injury or illness.
• The patient usually presents with
shortness of breath, tachypnea, and
symptoms related to the underlying
cause, i.e. shock
Patient presentation and
• Arterial blood gas analysis
• Chest X-ray
• Pulmonary artery catheter for
measuring the pulmonary artery
• CT scanning
• Diffuse inflammation of lung
• Typical histological presentation
involves diffuse alveolar damage and
hyaline membrane formation in
• Endothelial dysfunction, fluid
extravasation from the capillaries and
impaired drainage of fluid from the lungs.
• This pulmonary edema increases the
thickness of the alveolo-capillary space.
• This impairs gas exchange leading to
hypoxia, increases the work of breathing,
eventually induces fibrosis of the airspace.
• Dysfunction of type II pulmonary
epithelial cells, with a concomitant
reduction in surfactant production.
• Edema and decreased surfactant
production by type II pneumocytes
may cause whole alveoli to collapse,
or to completely flood.
• This loss of aeration contributes further
to the right-to-left shunt, resulting in
massive intrapulmonary shunting.
• The loss of aeration may follow
different patterns according to the
nature of the underlying disease, and
• In pneumonia-induced ARDS,
infiltrates are usually distributed to
the lower lobes, in their posterior
segments, and they roughly
correspond to the initial infected
• In sepsis or trauma-induced ARDS,
infiltrates are usually more patchy
and diffuse. The posterior and basal
segments are always more affected,
but the distribution is even less
• Mechanical ventilation
• When sepsis is diagnosed,
appropriate protocols should be
• The overall goal is to maintain acceptable gas
exchange and to minimize adverse effects in its
• Three parameters are used:
PEEP, to maintain maximal recruitment of
Mean airway pressure (to promote recruitment
and predictor of hemodynamic effects)
Plateau pressure (best predictor of alveolar
VARIABLES NIH-ARDS NETWORK PROTOCALS
TIDAL VOLUME ≤6 ml/kg
PLEATAU PRESSURE ≤30 cm H2O
VENTILATION SET 6-35/ min to achieve pH ≥7.30
RATE/ pH GOAL
INSPIRATORY Flow to achieve I:E Ratio 1:1-1:3
OXYGENATION PaO2 ≥55mmHg,SpO2 ≥88%
FiO2/PEEP 0.3/5, 0.4/5-8, 0.5/8-10, 0.6/10,
0.7/10-14, 0.8/14, 0.9/14-18,1/18-24
WEANING When FiO2/PEEP 0.4/8 ,with PSV
• Low tidal volume ventilation
• Plateau pressure less than 30 cm
H2O was a secondary goal,
• APRVis the primary mode of choice
when ventilating a patient with ARDS
AIRWAY PRESSURE RELEASE
• A CPAP circuit with release valve at
expiratory limb –driven by time
• APRV is a CPAP system causing
. alveolar ventilation by briefly
• Release valve opens for 1-2sec.
• Pr drops to lower level-low CPAP(0to-
• Lung volume less than FRC in expiration
• alveolar ventilation & CO2 elimination
• Reapplication of CPAP by closing valve-
Higher CPAP(10to 12 cm H2O)
• FRC & oxygenation.
• Lesser PIP ,so less hemo dynamic
• To alveolar ventilation in ALI of
mild to moderate.
• A weaning mode.
Advantages to APRV ventilation
• decreased airway pressures,
• decreased minute ventilation,
• decreased dead-space ventilation,
• promotion of spontaneous breathing, near
elimination of neuromuscular blockade
• almost 24 hour a day alveolar recruitment,
• decreased use of sedation,
• positive effect on cardiac output (due to the
negative inflection from the elevated baseline
with each spontaneous breath).
• A patient with ARDS on average spends 8 to 11
days on a mechanical ventilator; APRV may reduce
this time significantly.
•PC-IRV / VC-IRV
• Ti with set pr opening of stiff alveoli
units improved oxygenation
• Te not allowing alveoli to collapse
development of intrinsic PEEP
reduction of shunting
Improve oxygenation by
•Reducing intra pulmonary shunting
•Improvement of V/Q matching
•Decreased dead space ventilation
•Increased MAP & intrinsic PEEP
Useful when high FiO2 & high PEEP to be
Inverse ratio ventilation
• Inverse ratio ventilation is reserved for severe cases when
it is impossible to oxygenate the patient adequately.
• Treatment involves increasing the amount of time that the
ventilator is inspiring versus expiring.
• Patients normally spend more time exhaling than inhaling, at
a ratio of about 3:1. Increasing the amount of time spent
inhaling re-expands more collapsed alveoli than positive
• This is an uncomfortable technique and usually requires
sedation and a muscle-paralyzing drug that keeps the
respiratory muscles from resisting the unnatural inverse
• Distribution of lung infiltrates in
acute respiratory distress syndrome
• Repositioning into the prone position
(face down) might improve
oxygenation by relieving atelectasis
and improving perfusion.
• Improved V/P in previously atelectactic areas due
to uniform distribution of plural pr -Lamm etall
• Requires atleast more than 6 hrs/ day of prone
• A significant decrease in right ventricular
enlargement and a significant reduction in septal
dyskinesia, after 18 h of prone positioning.-Vielliard
• No improvement in mortality in clinical trials
• Several studies have shown that
pulmonary function and outcome are
better in patients that lost weight or
wedge pressure was lowered by
diuresis or fluid restriction
• Steroids cause a suppression of
inflammation during the fibroproliferative
phase of ARDS. The initial regimen
consists of mps 2 mg/kg daily. After 3-5
days a response must be apparent. In 1-2
weeks the dose can be tapered to mps 0.5-
1.0 mg daily. In the absence of results
steroids can be discontinued.-Meduri et al
• ARDSnet LAZARUS study demonstrated
that they are not efficacious in ARDS.
• Inhaled nitric oxide (NO) potentially acts as
selective pulmonary vasodilator. Rapid binding to
hemoglobin prevents systemic effects. It should
increase perfusion of better ventilated areas.
There are no large studies demonstrating positive
• Almitrine bismesylate stimulates chemoreceptors
in carotic and aortic bodies. It has been used to
potentiate the effect of NO, presumably by
potentiating hypoxia-induced pulmonary
vasoconstriction. In case of ARDS it is not known
whether this combination is useful.
• To date no prospective controlled clinical
trial has shown a significant mortality
benefit of exogenous surfactant in ARDS
• IV N-Acetyl-Cysteine which may
increase the lung surfactants
Newer /Near future
• Antioxidant Therapy -N-acetylcysteine and procysteine,
oxygen free-radical scavengers and precursors for
glutathione, were efficacious in some experimental studies
• Prostaglandin Agonists/Inhibitors: Prostaglandin E1 is a
vasodilator that blocks platelet aggregation and decreases
• Ibuprofen- an inhibitor of the cyclooxygenase pathway
• Ketoconazole, a potent inhibitor of thromboxane and
• Pentoxifylline is a phosphodiesterase inhibitor that inhibits
neutrophil chemotaxis and activation in animal models of
• Lisofylline inhibited release of TNF, IL-1, and IL-6,
• Anti–IL-8 Therapy
Enhanced Resolution of
Alveolar fluid clearance depends primarily on active
sodium transport across the alveolar epithelium
• Salmeterol, a lipid-soluble ß2-agonist
• Intra-alveolar terbutaline administration
markedly increased alveolar fluid clearance
• Dobutamine, ß2-adrenergic agonist, markedly
increased alveolar and lung fluid clearance in an
experimental rat model
• Dopamine, when administered at 5 µg/kg/min IV,
increased alveolar fluid clearance in an isolated
perfused rat model by increasing the activity of
. Na-K ATP pumps.
Enhanced Repair of the
Alveolar Epithelial Barrier
• Studies suggest that hepatocyte
growth factor and keratinocyte
growth factor are major mitogens
for alveolar epithelial type II cells
• Pulmonary: barotrauma (volutrauma),
pulmonary embolism (PE), pulmonary
fibrosis, ventilator-associated pneumonia
• Gastrointestinal: hemorrhage (ulcer),
dysmotility, pneumoperitoneum, bacterial
• Cardiac: arrhytmias, myocardial
• Renal: acute renal failure (ARF), positive
• Mechanical: vascular injury, pneumothorax
(by placing pulmonary artery catheter),
tracheal injury/stenosis (result of
intubation and/or irritation by
• Nutritional: malnutrition (katabolic state),