Acute Respiratory Distress Syndrome:

Supportive Care and Oxygenation in the

Intensive Care Unit

Hendri Pangestu
Let us start from definition
 ARDS is …
Acute syndrome
with diffuse lung infiltrates,
edema caused by increased alveolar-capillary
membrane permeability,
and decreased oxygenation
Introduction .
Acute respiratory distress syndrome (ARDS) is a life
threatening respiratory condition characterized by hypoxemia,
and stiff lungs; without mechanical ventilation most patients
would die.
Updated definition of ARDS .
ARDS is a syndrome with multiple risk factors that trigger the
acute onset of respiratory insufficiency.
The pathogenic mechanisms vary depending on the inciting
insult, but as demonstrated on autopsy findings, there are a
number of common pathological pulmonary features, such
as increased permeability as reflected by alveolar edema due
to epithelial and endothelial cell damage, and neutrophil
infiltration in the early phase of ARDS.
Anatomi Sistem Respirasi
• Traktus
Respiratorius sup.
– Hidung/mulut, faring dan
struktur sekitarnya
• Traktus
Respiratorius inf
Laring, trakea, bronchi,
alveolus
 PERTUKARAN GAS EKSTERNA

UDARA BEBAS:
PiO2 : 20.9 % x 760 = 159 mmHg
PiCO2 : 0.04 % x 760 = 0.3 mmHg
PiN2 : 78.6 % x 760 = 597 mmHg
PiH2O : 0.46 % x 760 = 3.5 mmHg

N2 H2O
ALVEOLUS
PAN2: PAH2O:
573 mmHg 47 mmHg
PROSES DIFUSI
PAO2: PACO2:
104 mmHg 40 mmHg

O2 O2
O2 CO2
PaO2:
PaO2: 104mmHg
40 mmHg CO2
CO2
PaCO2:
PaCO2:
40 mmHg
45 mmHg
KAPILER PARU
Oxygenation
In the Berlin definition, there is no use of the term Acute Lung
Injury (ALI). The committee felt that this term was used
inappropriately in many contexts and hence was not helpful.
In the Berlin definition, ARDS was classified as mild, moderate
and severe according to the value of PaO /FiO ratio (Table 1).
2 2

Importantly, the PaO /FiO ratio value is considered only with a

2 2

CPAP or PEEP value of at least 5 cmH O.

2
 Berlin Definition Key Components

1.Timing
2.Chest imaging
3.Origin of
edema
4.Oxygenation
 1. Timing

Acute;
onset within 1 week of a known clinical
insult or new or worsening respiratory
symptoms
 2. Chest imaging

bilateral opacities consistent with

pulmonary edema must be present,
not fully explained by cardiac failure or fluid
overload
and may be detected on CT or chest
radiograph, involving at least 3 quadrants
 3. Origin of edema

“must not be fully explained by cardiac

failure or fluid overload,”
— an “objective assessment“ (e.g.
echocardiogram) should be performed in
most cases if there is no clear cause such
as trauma or sepsis.
 4. Oxygenation

𝑷𝒂𝑶𝟐
PF ratio  𝑭𝒊𝑶𝟐 <300mmHg
with a minimum of 5 cmH20
PEEP (or CPAP)
 SEVERITY / CLASSIFICATION

ARDS Severity PaO2/FiO2* Mortality**

Mild 201-300 mmHg 27 %
Moderate 101-200 mmHg 32 %
Severe ≤ 100 mmHg 45 %
*on PEEP 5+;
**observed in cohort
 Induced factors :
Sepsis
Pneumonia CAP/HAP
Tuberculosis
Fluid overload
TRALI
Common risk factors for ARDS
 Transport oksigen

Mitok ATP = energy

ondria

O2
Sel
O2
O O2
2

O2

O2 O2

O2
 Difusi Abnormal
Alveolus normal Pneumonia/ARDS
Current therapies
Protective mechanical ventilation
In this trial, patients randomized to receive a lower tidal volume (Vt) [4-6 mL/kg predict body
weight (PBW), and maintenance of plateau pressure between 25 and 30 cmH2O had a
survival benefit.
Mortality was reduced from 40% in the conventional arm to 31% in the low Vt arm (CI, 2.4-
15.3%
difference between groups) . The benefit in terms of mortality and ventilation free days did
not appear to be related to the value of the lung compliance at baseline or to the underlying
risk factor for ARDS

Non conventional therapies in severe ARDS

Historically pron positioning, high frequency oscillatory ventilation and extracorporeal
membrane e have been proposed as non-conventional therapies for
oxygenation life- in severe ARDS patients
threatening refractory hypoxemia
ARDS therapies other than mechanical ventilation
In ARDS patients, alveolar edema formation caused by increased vascular permeability
may be worsened by higher hydrostatic pressure as a consequence of fluid overload. Of
note, positive fluid balance, higher values of central venous
and capillary wedge pressures are independent risk factors for mortality in critical
ill patients.
To examine whether a more fluid-conservative strategy would impact outcomes, ARDSnet
sponsored a RCT to evaluate the effects of fluid therapy strategy aimed to limit the net
fluid balance in ARDS patients without shock and renal failure requiring replacement
therapy .
Inhaled nitric oxide for its pulmonary vasodilator effects has been proposed to treat
refractory hypoxemia reestablishing an adequate ventilation perfusion matching.
Future non-ventilatory therapeutic options
Gene therapy for ALI/ARDS
Mesenchymal stem cells
 VENTILASI PARU
PROSES MEKANIK, KELUAR
MASUKNYA UDARA DARI
LUAR KE DALAM PARU DAN
SEBALIKNYA  YAITU
BERNAFAS
EKSTERNA
PERTUKARAN GAS
TERJADI ANTARA UDARA DALAM
ALVEOLUS DENGAN DARAH
PROSES DALAM KAPILER, PROSESNYA
DISEBUT DIFUSI
RESPIRASI
PERTUKARAN GAS
PERTUKARAN GAS ANTARA
INTERNA DARAH DENGAN SEL
JARINGAN/TISUE

UTILISASI O2
PEMAKAIAN OKSIGEN
DALAM SEL PADA REAKSI
PELEPASAN ENERGI
 Insult Mempengaruhi
Pertukaran gas oksigenisasi
Co-morbid
eksterna
Illness
es
Therapies
Injuries
Ventilation

Mempengaruhi
Pneumonia Kontraktility
/Hemodinamik

Sepsis
Sepsis berat Mempengaruhi
Pertukaran gas Utilisasi
Sepsis shock
interna oksigen /
MODF mitokondria
Semoga
bermanfaat