ACUTE RESPIRATORY DISTRESS

SYNDROME
MODERATOR: DR DIVYA KAVITA
PRESENTOR:DR GURLEEN KAUR
Acute Respiratory Distress
Syndrome
• ARDS is a final common state in acute lung injury characterized
by noncardiogenic pulmonary edema, heterogeneous consolidation,
decreased lung compliance, and severe hypoxemia.

• It is a syndrome that involves injury and increased

epithelial-endothelial permeability of the alveoli.
• Common sources of ARDS:
Infection- Noninfectious
related Gastric aspiration
Pneumonia Blood transfusions
Septicemia Multisystem
Severe sepsis trauma
Septic shock Pancreatitis
Drug overdose
Microscopic
appearance in
ARDS images of a normal
Microscopic
lung and a lung in the advanced
stages of ARDS, show a dense
infiltration of leukocytes and
proteinaceous material that fills
and obliterates the normal
architecture of the lungs.
Clinical
features
•
Earliest signs:
• Sudden hypoxemia
• Signs of respiratory distress (e.g., dyspnea, tachypnea)
•
CXR – initially normal  bilateral pulmonary infiltrates
within 24 hours.
•
Progressive hypoxemia requiring mechanical ventilation
occurs within the first 48 hours.
Clinical features and diagnostic criteria of
ARDS
1. Acute onset
2. Bilateral infiltrates on frontal CXR
3. PaO2/FiO2 =< 3oo with PEEP>=5mmHg
4. No evidence of left heart failure or fluid
overload
5. The presence of a predisposing condition
Berlin Criteria for grading severity in ARDS
MILD - PaO2/FiO2 201 to 300; PEEP > 5 cm of H2O
MODERATE - PaO2/FiO2 101 to 200; PEEP > 5 cm of
H2O SEVERE - PaO2/FiO2 <100; PEEP > 10 cm of H2O

This is not the diagnostic criteria for ARDS because Berlin criteria require a certain level of PEEP which needs
mechanical ventilation, and the diagnosis of ARDS can occur during spontaneous breathing.
Diagnostic
pitfalls
•
The lack of specificity in the criteria makes the diagnosis
difficult.
•
In a study, postmortem diagnoses of patients with a
premortem diagnosis of ARDS were made. Results:
Actual/Postmortem diagnosis % of
autopsies
ARDS 50%
Acute Pneumonia 25%
Pulmonary congestion 11%
Invasive Aspergillosis 6%
Pulmonary embolism 3%
Other 5%

This means that with the current diagnostic criteria, the diagnostic accuracy is only around 50%!
Radiological appearance
The infiltrate has a finely granular or The infiltration shows a hilar prominence
ground-glass appearance and is evenly and is confined to the lower lung fields,
distributed in all lung fields, with no with left hemidiaphragm obliteration s/o
evidence of pleural effusion. pleural effusion.

Because of such variability in the radiographic appearance of ARDS, it is not possible to identify ARDS
reliably using the chest x-ray alone.
Pulmonary Artery Wedge Pressure
(PAWP)
•
A PAWP of =< 18 mm of Hg is usually indicative of non-cardiogenic
pathology 
and thus helps in the diagnosis of ARDS.
•
But the PAWP is not a measure of Capillary Hydrostatic Pressure.
•
The PAWP is measured in the absence of blood fl ow when the static
column of blood between the catheter tip and left atrium results in an
equalization of pressures between the wedge pressure and left atrial
pressure. However, when fl ow resumes, the pressure in the pulmonary
capillaries must be higher than the left atrial pressure to provide a
pressure gradient for fl ow in the pulmonary veins. Therefore, the left
atrial (wedge) pressure is lower than the capillary hydrostatic pressure,
and this will lead to an overdiagnosis of ARDS.

Thus, PAWP is also not a reliable investigation to diagnose ARDS.

Bronchoalveolar Lavage
• Although rarely used, bronchoalveolar lavage is a reliable method for
distinguishing ARDS from cardiogenic pulmonary edema.
• This procedure is performed at the bedside using a flexible fiberoptic
bronchoscope that is advanced into one of the involved lung segments.
• Once in place, the lung segment is lavaged with isotonic saline, and the
lavage fluid is analyzed for the presence of neutrophils and protein.
• 1. In normal subjects, neutrophils make up less than 5% of the cells recovered in lung lavage
fluid, whereas in patients with ARDS, as many as 80% of the recovered cells are
neutrophils. A low neutrophil count in lung lavage fluid can be used to exclude the
diagnosis of ARDS, while a high neutrophil count is evidence of ARDS.
• 2. Because inflammatory exudates are rich in proteinaceous material, lung lavage fluid that is
rich in protein is used as evidence of ARDS. When the protein concentration in lung
lavage fluid is expressed as a fraction of the protein concentration in plasma, the following
criteria can be applied:
•
Hydrostatic Edema: Lavage fluid [protein] / plasma [protein] <0.5
•
ARDS: Lavage fluid [protein] / plasma [protein] >0.7
Ventilator management in ARDS
•
Conventional Mechanical Ventilation - Since the introduction of positive-
pressure mechanical ventilation, the use of large inflation volumes (tidal volumes) has been a
standard practice to reduce the tendency for atelectasis during mechanical ventilation. The
conventional tidal volumes are 12 to 15 mL/kg, which are twice the size of tidal volumes
achieved during quiet breathing (6 to 7 mL/kg). In patients with ARDS, these large inflation
volumes are delivered into lungs that have only a fraction of the normal functional lung
volume.
Thus conventional ventilatory settings should not be used in ARDS.

•
Functional volume in ARDS –
•
CXR shows a homogenous pattern of lung infiltration, but, CT scan reveals that
the lung infiltration is confined to dependent lung regions.
CT Scan in
ARDS
The dense consolidation in
posterior lung regions (which
the
are
the dependent lung regions in the
supine position) and the normal or
uninvolved lung are restricted to
the anterior half of the thorax.
The uninvolved areas represent
the functional portion of the lungs
and the portion that receives the
inflation volumes.
Therefore, the high inflation volumes
used during conventional mechanical
ventilation are being delivered to a
markedly reduced volume of available
lung aka BABY LUNGS, and this
results in overdistension and rupture
of the distal airspaces.
Ventilator-induced lung injury
• Excessive inflation of the distal airspaces produces stress fractures in the alveolar-
capillary interface, and this leads to infiltration of the lung parenchyma and distal
airspaces with an inflammatory exudate. This condition is known as ventilator-
induced lung injury (VILI). The lung injury is volume-related rather than pressure-
related and is called volutrauma .

• During conventional, high-volume mechanical ventilation, proinflammatory

cytokines can appear in the lungs and systemic circulation, even though there is no
structural damage in the lungs. This pro-inflammatory condition is known as
biotrauma .
• It can lead to neutrophil activation and inflammatory infiltration in the lungs.
• The systemic inflammatory response associated with biotrauma can promote inflammatory injury in
other organs, which means that mechanical ventilation can be a source of inflammatory-
mediated multiorgan failure!

• The decrease in lung distensibility in ARDS can result in the collapse of small
airways at the end of expiration. When this occurs, mechanical ventilation can be
associated with cyclic opening and closing of small airways, and this process can be a
source of lung injury. This type of lung injury is called atelectrauma .
Lung-protective
ventilation
• Lung protective ventilation employs
low tidal volumes (6 mL/kg) to limit the
risk of volutrauma and biotrauma, and
uses positive end-expiratory pressure
(PEEP) to limit the risk of atelectrauma.
• The tidal volume in this protocol is 6
mL/kg, based on predicted body weight ,
which is the body weight associated
with normal lung volumes.
Positive End-expiratory
pressure
• Lung protective ventilation employs a positive end-expiratory
pressure (PEEP) of at least 5 cm H2O to prevent the collapse of small
airways at the end of expiration. The goal is to prevent the cyclic
opening and closing of small airways and reduce the risk of
atelectrauma.

• In situations where a toxic level of inhaled oxygen (FIO2 >50%) is

needed to maintain the target SpO2 of 88–95%, PEEP levels above 5 cm
H2O can be used to improve arterial oxygenation and reduce the FIO 2
to safer levels. However, it is important to emphasize that increases
in PEEP can reduce the cardiac output.
Permissive
hypercapnia
• One of the consequences of low tidal volume ventilation is a
decrease in CO2 elimination in the lungs, which can result in
hypercapnia and respiratory acidosis.

• Because of the benefits of low-volume ventilation, hypercapnia is

allowed to persist as long as there is no evidence of harm. This
practice is known
as permissive hypercapnia.

• Data from clinical trials of permissive hypercapnia show that arterial

PCO 2 levels of 60–70 mm Hg and arterial pH levels of 7.2–7.25 are
safe for most patients.
Non-ventilatory management

• The treatment of ARDS begins by treating the inciting condition (e.g.,

septicemia), if possible.

• Therapies directed at the ARDS have been marked by failure more

than success. The failed therapies in ARDS include surfactant (in
adults), inhaled nitric oxide, pentoxyphylline, ibuprofen, prostaglandin
E1, and antifungal agents (to inhibit thromboxane).

• Clinical benefits have been reported with fluid management that

avoids fluid accumulation in the lungs, and with high-dose
corticosteroids in severe or unresolving ARDS.
Fluid management

• The lung consolidation in ARDS is an inflammatory exudate, and

should not be influenced by fluid balance.

• However, avoiding a positive fluid balance will prevent

unwanted fluid accumulation in the lungs, which could aggravate the
respiratory insufficiency in ARDS. Avoiding a positive fluid balance in
patients with ARDS can reduce the time on mechanical ventilation, and
can even reduce mortality.

• However, it is also important to avoid fluid deficits and maintain

intra-vascular volume because the positive intrathoracic
pressures during mechanical ventilation will magnify the tendency
for the cardiac output to decrease in response to deficits in
intravascular volume.
Corticosteroid
therapy
• There is a long history of clinical trials evaluating steroid therapy in
ARDS, and the aggregated results of these studies show no consistent
survival benefit associated with steroid therapy .

• There is evidence of other benefits provided by steroid therapy in

ARDS, and these include a reduction in markers of inflammation (both
pulmonary and systemic inflammation), improved gas exchange,
shorter duration of mechanical ventilation, and shorter length of stay
in the ICU.
Steroid therapy is currently recommended only in cases of early severe ARDS and
unresolving ARDS.
Early severe ARDS

• In early severe ARDS, defined as a PaO2/FIO2 <200 mm Hg with PEEP

of 10 cm H2O, the following steroid regimen in recommended:
•
Methylprednisolone: Start with an IV loading dose of 1 mg/kg (ideal
body weight) over 30 minutes, then infuse at 1 mg/kg/day for 14 days,
then gradually taper the dose over the next 14 days and discontinue
therapy. Five days after the patient is able to ingest oral medications,
the dose can be given orally (as prednisone or prednisolone) as a
single daily dose.
Unresolving ARDS
• ARDS has a fibrinoproliferative phase that begins 7–14 days after the onset of
illness, and eventually results in irreversible pulmonary fibrosis. High-dose steroid
therapy started in the developing phase of fibrinoproliferation can help to halt the
progression to pulmonary fibrosis. In cases where ARDS does not begin to resolve
after 7 days, high-dose steroid therapy is recommended, but should begin no
later than 14 days after the onset of illness. The following steroid regimen is
recommended:
•
Methylprednisolone: Start with an IV loading dose of 2 mg/kg (ideal body
weight) over 30 minutes, then infuse at 2 mg/kg/day for 14 days, and 1 mg/kg/day
for the next 7 days. After this, gradually taper the dose and discontinue therapy at 2
weeks after extubation. Five days after the patient is able to ingest oral
medications, the dose can be given orally (as prednisone or prednisolone) as a
single daily dose.
The risks of high-dose steroid therapy include worsening glycemic control and prolonged
neuromuscular weakness when combined with neuromuscular blocking agents.
There is no evidence of an increased risk of nosocomial infections with the steroid regimens.
Refractory hypoxemia

• A minority (10 to 15%) of patients with ARDS develop severe

hypoxemia that is refractory to oxygen therapy and mechanical
ventilation. This condition is an immediate threat to life, and the
following “rescue therapies” can produce an immediate
improvement in arterial oxygenation.

Unfortunately, these rescue measures often provide l i t l e or no survival benefit.

High-Frequency Oscillatory
Ventilation
•
High frequency oscillatory ventilation (HFOV) delivers small tidal volumes (1–2
mL/kg) using rapid pressure oscillations (300 cycles/min).
•
The small tidal volumes limit the risk of volutrauma, and the rapid
pressure oscillations create a mean airway pressure that prevents small
airway collapse and limits the risk of atelectrauma.
•
When used in patients with severe ARDS, HFOV can improve arterial
oxygenation, but there is no documented survival benefit.

HFOV requires a specialized ventilator (Sensormedics 3100B, Viasys Healthcare, Yorba Linda,
CA), and may not be available in all hospitals.
Inhaled Nitric Oxide

• Inhaled nitric oxide (5–10 ppm) is a selective pulmonary

vasodilator that can improve arterial oxygenation in ARDS by
increasing flow to areas of high dead space ventilation.

• However, the increase in arterial oxygenation is temporary (1–4

days), and there is no associated survival benefit.

• Adverse effects of inhaled nitric oxide include methemoglobinemia

(usually mild) and renal dysfunction.

An added risk is the potential for nitric oxide to form peroxynitrite, a potent toxin
capable of oxidant cell injury.
Prone positioning

• Switching from the supine to prone position can improve pulmonary

gas exchange by diverting blood away from poorly aerated lung regions
in the posterior thorax and increasing blood flow in aerated lung
regions in the anterior thorax.

• Prone positioning has had little impact on mortality in ARDS, but a

recent study combining lung protective ventilation with prone
positioning showed a lower than expected mortality rate in patients
with severe ARDS (PaO 2/FIO2 <100 mm Hg).

Prone positioning is labor intensive and creates problems with nursing care (e.g.,
airway care and skin care), but it may be the only measure available for refractory
hypoxemia in hospitals with limited resources.
ECMO

• Extracorporeal membrane oxygenation (ECMO) has had variable

success in patients with refractory hypoxemia, and is a consideration
only in medical centers with established ECMO programs, and only when
other rescue therapies have failed.
Other treatment points

• In patients requiring ICU stay with mechanical ventilation for ARDS,

cisatracurium is preferred NMBD because of its anti-inflammatory
•
properties.
The preferred opioid in ARDS is Remifentanil due to its neutrophil
response- attenuating properties.
• Aggressive plasma transfusion should be avoided.

• Weaning-off – The most effective strategy is the daily scheduled

use of spontaneous breathing trials (SBTs) to assess whether the
patient is ready for extubation.

• The ideal nursing care requirement is employing at least 3 para-

medical officers at all times with a patient of ARDS.
 THANK
YOU