ARDS

Sophie Tatishvili
JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669
J Emerg Crit Care Med 2017;1:25
Pressure-volume relationship in the lungs of a patient with
acute respiratory distress syndrome (ARDS).

At the lower inflection point,

collapsed alveoli begin to open
and lung compliance changes.
At the upper deflection point,
alveoli become overdistended.
The shape and size of alveoli are
illustrated at the top of the
figure.

Harrison's Manual of Medicine, 18e

DIAGNOSTIC CRITERIA FOR ARDS

John P. Kress, Jesse B. Hall

Clinical Disorders Commonly Associated with
ARDS

John P. Kress, Jesse B. Hall

Diagram illustrating the time course for the
development and resolution of ARDS
The exudative phase is notable
for early alveolar edema and
neutrophil-rich leukocytic
infiltration of the lungs, with
subsequent formation of
hyaline membranes from
diffuse alveolar damage.
Within 7 days, a proliferative
phase ensues with prominent
interstitial inflammation and
early fibrotic changes.
Approximately 3 weeks after
the initial pulmonary injury,
most patients recover.
However, some patients enter
the fibrotic phase, with
substantial fibrosis and bullae
formation.
John P. Kress, Jesse B. Hall
ARDS pathophysiology timeline
Chest x-ray

A representative
anteroposterior
chest x-ray in the
exudative phase of
ARDS shows
diffuse interstitial
and alveolar
infiltrates that can
be difficult to
distinguish from
left ventricular
failure.
 The normal alveolus (left side) and the injured alveolus in the acute
phase of acute lung injury and the acute respiratory distress syndrome .
In the acute phase of the syndrome (right side), there
is sloughing of both the bronchial and alveolar
epithelial cells, with the formation of protein-rich
hyaline membranes on the denuded basement
membrane. Neutrophils are shown adhering to the
injured capillary endothelium and marginating
through the interstitium into the air space, which is
filled with protein-rich edema fluid. In the air space,
an alveolar macrophage is secreting cytokines,
interleukin-1, 6, 8, and 10, (IL-1, 6, 8, and 10) and
tumor necrosis factor a (TNF-a), which act locally to
stimulate chemotaxis and activate neutrophils.
Macrophages also secrete other cytokines, including
interleukin-1, 6, and 10. Interleukin-1 can also
stimulate the production of extracellular matrix by
fibroblasts. Neutrophils can release oxidants,
proteases, leukotrienes, and other proinflammatory
molecules, such as platelet-activating factor (PAF).
A number of antiinflammatory mediators are also
present in the alveolar milieu, including interleukin-
1–receptor antagonist, soluble tumor necrosis factor
receptor, autoantibodies against interleukin-8, and
cytokines such as interleukin-10 and 11 (not shown).
The influx of protein-rich edema fluid into the
alveolus has led to the inactivation of
surfactant. MIF, Macrophage inhibitory factor.

(Modified from Ware LB, Matthay MA: N Engl J Med 342:1334-1349, 2000, with
permission of the publisher.)
A representative CT scan of the chest during the exudative phase
of ARDS, in which dependent alveolar edema and atelectasis
predominate.
 ARDS managemet
Clinical trials have
provided evidence-based
therapeutic goals for a
stepwise approach to the
early mechanical
ventilation, oxygenation,
and correction of
acidosis and diuresis of
critically ill patients with
ARDS. Fio2 , inspired
O2 percentage; MAP,
mean arterial pressure;
PBW, predicted body
weight; PEEP, positive
end expiratory pressure;
RR, respiratory rate;
Spo2 , arterial
oxyhemoglobin
saturation measured by
pulse oximetry.
Harrison's Manual of Medicine, 18e
Evidence-Based Recommendations for
ARDS

John P. Kress, Jesse B. Hall