ARDS - Diagnosis and Management

DIAGNOSIS & MANAGMENT OF
Acute Respiratory Distress Syndrome
DR. VITRAG SHAH
FIRST YEAR FNB RESIDENT,
DEPARTMENT OF CCEM,
SGRH, DELHI
MODERATOR
DR.RAHUL
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SYMPTOMS…………
• Fever/chills
• Headache, myalgia
• Sore throat
• Cough
• Coryza
• Prostration
• Range of symptoms differs by age
– Vomiting & diarrhea in children/elderly
– Fever alone in infants
– May be atypical in elderly
• Serious complications can occur among high risk groups

OUTLINE
 What is ARDS
 Berlin vs AECC definition & LIS
 Risk Factors
 Etiology
 Clinical course & Pathophysiology
 Differential diagnosis
 Management
 General management & nursing care
 Role of NIV
 Ventilatory management
 Management of Refractory hypoxemia
 Non-Ventilatory management
 Other drugs/therapies
 Prognosis
 Future/Research & Role of stem cells
 References

WHAT IS ARDS??
 A type of inflammatory lung injury that is neither a
primary disease or a single entity.
 Rather, it is an expression of myriad other diseases
that produce diffuse inflammation in the lungs, often
accompanied by inflammatory injury in other organs
& it is also the leading cause of acute respiratory
failure.

 Physicians think they do a lot for a patient when they
give his disease a name --Immanuel Kant
 First described as clinical syndrome in 1967 by
Ashbaugh & Petty .
 Synonyms: Sponge Lung, Shock lung, Non-cardiogenic
pulmonary edema, Capillary leak syndrome, Traumatic
wet Lung, Adult hyaline membrane disease, ALI &
ARDS, and most recently, Only ARDS.

THE BERLIN DEFINITION:-
 The Berlin Definition of ARDS (published in 2012) replace the
American-European Consensus Conference’s definition of
ARDS (published in 1994).
 The European society of intensive care medicine endorsed by
The American Thoracic Society and The Society of Critical Care
Medicine developed the Berlin definition in 2012.
 The major changes to the Berlin Definition are that the term
“acute lung injury” has been eliminated, the pulmonary
capillary wedge pressure (ie, pulmonary artery occlusion
pressure) criteria has been removed, and minimal ventilator
settings have been added.

SpO2 can be substituted for the PaO2 to calculate the SpO2/FIO2 ratio, which may be
more a feasible method of identifying severely ill patients in these resource-limited
environments.

WHAT’S NOT INCLUDED…..
 The draft definition of severe ARDS included the more
extensive involvement on the frontal chest radiograph
(3 or 4 quadrants) { from those with the minimal
criterion of “bilateral opacities” (2 quadrants) },
respiratory system compliance (40 mL/cm H2O),
positive end expiratory pressure (10 cm H2O), and
corrected expired volume per minute (10 L/min).
 These variables were identified for further study
during the evaluation phase & not included in present
criteria.

PCWP:
 The problem is that the wedge pressure is not a measure
of capillary hydrostatic pressure,
 The PCWP is a measure of LAP and LAP cannot be the
same as the pulmonary capillary pressure in presence of
blood flow .
 If the wedge (left-atrial) pressure were equivalent to the
pressure in the pulmonary capillaries, there would be no
pressure gradient for flow in the pulmonary veins. Thus, the
capillary hydrostatic pressure must be higher than the wedge
pressure.So PCWP will underestimate the actual
capillary hydrostatic pressure.
 This difference is small in the normal lung, but in severe
ARDS, the capillary hydrostatic pressure can be double the
wedge pressure.
 Because of this discrepancy, the wedge pressure should
be abandoned as a diagnostic criterion for ARDS.

MURRAY LUNG INJURY SCORE (LIS)
 Radiography
 Oxygenation
 Compliance
 PEEP
 But doesn’t exclude left heart failure

 Risk Factors
 Older age
 Chronic alcohol abuse
 Metabolic acidosis
 Critical illness.
 Trauma patients
 >80% of cases are caused by:
 Sepsis
 Bacterial pneumonia
 Trauma
 Multiple transfusions
 Gastric acid aspiration
 Drug overdose

CLINICAL DISORDERS ASSOCIATED WITH THE
DEVELOPMENT OF ARDS
 Indirect insult
 Common
 Sepsis
 Severe trauma
 Shock
 Less common
 Acute pancreatitis
 Cardiopulmonary bypass
 Transfusion-related TRALI
 DIC
 Burns
 Head injury
 Drug overdose
Direct insult
 Common
 Aspiration pneumonia
 Pneumonia
Less common
 Inhalation injury
 Pulmonary contusions
 Fat emboli
 Near drowning
 Reperfusion injury

CLINICAL COURSE AND
PATHOPHYSIOLOGY
The natural history of ARDS is marked by three phases
1. Exudative (First 7 days)
2. Proliferative (After 7-21 days)
3. Fibrotic (After 3-4 weeks)
Each with characteristic clinical and pathologic features

Alveolar
Damage
Capillary
Damage
Leakage
Oedema
Fluid
Inflammatory
Cellular
Infiltrates
V/Q
Mismatch
Atelectasis
↓Thoracic
Compliance
↑Dead Space
Hypoxic
Vasoconstriction
Hypoxia
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ARDS– PROBLEMS & CONCERNS
 Strain (stretch) due to over distension of compliant
alveoli leading to volutrauma.
 High inspiratory pressures (Pplat) leading to barotrauma.
 Release of inflammatory mediators from lung
(biotrauma)
 Shear stress due to complete closure & re-opening of
non-compliant alveoli (atelectrauma).

 Earliest clinical signs of ARDS are tachypnea &
progressive hypoxemia usually refractory to oxygen ,
which usually leads to diffuse pulmonary infiltrates in
chest x-ray within 24 hours & leading to respiratory failure
requiring mechanical ventilation within 48 hours of illness.

PROGRESSION OF ARDS:
If the injurious factor is not removed,
the amount of inflammatory mediators
released by the lungs in ARDS may
results in
 SIRS - Systemic inflammatory
response syndrome
 MODS - multi organ dysfunction
syndrome
This adds up to impaired oxygenation
which is the central problem of ARDS,
which further impairs oxygen delivery.

DIFFERENTIAL DIAGNOSIS
 Most common
 Cardiogenic pulmonary edema
 Diffuse pneumonia
 Alveolar hemorrhage
 Less frequent
 Acute interstitial lung diseases(e.g., acute interstitial
pneumonitis)
 Acute immunologic injury (e.g., hypersensitivity
pneumonitis)
 Toxin injury (e.g., radiation pneumonitis)
 Neurogenic pulmonary edema

1. CHEST X- RAY .
 A homogeneous infiltrate and the absence of
pleural effusions is more characteristic of
ARDS.
 Patchy infiltrates from the hilum, prominent
pleural effusions, cardiomegaly &
cephalization is more characteristic of
cardiogenic pulmonary edema.
 However, , pleural effusions can appear in
ARDS, and the view is that CXR are not
reliable for distinguishing ARDS from
cardiogenic pulmonary edema
ARDS vs Cardiogenic Pulmonary Edema

2. Severity of Hypoxemia:
 In the early stages of ARDS, the hypoxemia is often more
pronounced than the CXR abnormality
 In the early stages of cardiogenic pulmonary edema, the CXR
abnormalities are often more pronounced than the
hypoxemia.
 However, there are exceptions, and severe hypoxemia can
occur in cardiogenic pulmonary edema from a low cardiac
output

3. BNP
 In patients with hypoxic respiratory failure :
 An BNP level of less than 100 pg/mL in a patient
with bilateral infiltrates and hypoxemia favors the
diagnosis of ARDS/acute lung injury (ALI) rather
than cardiogenic pulmonary edema.

4. Bronchoalveolar Lavage:
The most reliable method for confirming or
excluding the diagnosis of ARDS .
A.) Neutrophils
 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
considered evidence of ARDS .

B.) Total Protein:
 Because inflammatory exudates are rich in proteinaceous
material, lavage fluid similarly rich in protein→ evidence of
lung inflammation.
 When the protein concentration in lung lavage fluid is
expressed as a fraction of the total protein concentration, the
following criteria can be applied
 Protein (lavage/serum) <0.5 = Hydrostatic edema
 Protein (lavage/serum) >0.7 = Lung inflammation
 Lung inflammation is expected to produce a protein
concentration that is greater than 70% of the protein
concentration in serum.

 Although not specific, BAL can be used as evidence of ARDS
if other causes of lung inflammation (e.g., pneumonia) can be
excluded on clinical grounds.
 BAL has not gained widespread acceptance as a diagnostic
tool for ARDS, because most ICU physicians use the
diagnostic criteria to evaluate possible ARDS.

MANAGEMENT OF ARDS
 General principles & supportive care
 Role of NIV
 Lung-Protective Ventilation Protocol
• LVV & VILI
• Permissive hypercapnia
• PEEP & Open lung ventilation
• Lung Recruitment - Recruitment maneuvers
• Mode of ventilator
• Approach to patient-ventilator dyssynchrony
• Role of Neuromuscular blockers
 Management of Refractory Hypoxemia
• Prone Position
• Other Modes of ventilation
• IRV
• Inhaled Nitric Oxide
• ECMO
 Non Ventilatory Management
 Fluid management
 Diuretics
 Steroids
 Blood Transfusion cut-off
 Choice of Inotropic agent
 Other drugs/Therapies
 Prognosis
 Future/Research & Role of stem cell

Management of ARDS:-
General Principles:
(1) Early recognition and treatment of the underlying medical
and surgical disorders (e.g., sepsis, aspiration, trauma);
(2) Minimizing procedures and their complications;
(3) Prophylaxis against venous thromboembolism,
gastrointestinal bleeding, and central venous catheter
infections;
(4) Prompt recognition of nosocomial infections; and
provision of adequate nutrition, Glucose control.
(5) Use of sedatives and neuromuscular blockade
(6) Hemodynamic management
(7) Ventilatory strategies to decrease tidal volume (Vt) while
maintaining adequate oxygenation

MANAGEMENT OF HYPOXEMIA
 Decrease oxygen consumption
 Increase oxygen delivery
 Ventilatory strategies (LPV)

DECREASE OXYGEN CONSUMPTION
 In diseases with severe pulmonary shunting,
increasing the saturation of mixed venous blood
(SvO2 ) may increase the SaO2 . Therapies that
decrease oxygen consumption may improve SvO2
(and SaO2 subsequently) by decreasing the amount
of oxygen extracted from the blood.
 Common causes of increased oxygen consumption
include fever, anxiety and pain, and use of
respiratory muscles; therefore, arterial saturation
may improve after treatment with anti-pyretics,
sedatives, analgesics, or paralytics

INCREASE OXYGEN DELIVERY
 DO 2 = 10 x CO x (1.34 x Hgb x SaO 2 + 0.003 x
PaO 2 )
 where DO 2 is oxygen delivered, CO is cardiac
output, Hgb is hemoglobin concentration, SaO 2 is
the arterial oxygen saturation, and PaO 2 is the
partial pressure of oxygen in arterial blood. As a
result, in addition to low SaO 2 , DO 2 may be
decreased by a low Hgb and a low CO. In turn, a
low DO 2 may decrease SvO 2 .

ROLE OF NIV
 No trials have compared NIV to invasive mechanical
ventilation, and the only evidence at present is studies such
as that by “Ferrer et al” in which NIPPV is compared with
supplemental oxygen by face mask alone. In this particular
trial, NIPPV was associated with decreased need for
intubation compared with oxygen by face mask in the
overall study population, but among patients with ARDS,
there were no differences in outcomes.
 Their use should only be considered in patients with mild
disease (PaO2/FIO2 > 200 and no other organ dysfunction)
and immunocompromised patients who are
hemodynamically stable, able to tolerate wearing a face
mask, and able to maintain a patent airway.

PaO2 55-80 mmhg

The slope of this relationship represents the compliance of the respiratory system, and the goal
should be to ventilate patients on the steepest portion of the relationship where smaller pressure
changes are necessary to achieve the desired tidal volume. Lowering the tidal volume helps avoid
the upper, flat portion of this relationship (A), where large changes in pressure are necessary to
achieve small volume changes. Application of positive end-expiratory pressure helps avoid the
lower, flat portion of this relationship (B) by preventing repetitive opening and closing of the
alveoli.

Lung-Protective Ventilation:
 Since the introduction of positive-pressure mechanical
ventilation, large inflation volumes(TV) were used to ↓
tendency for atelectasis during MV.
 The standard tidal volumes were 10 to 15 mL/kg, which
are twice the size of tidal volumes used during quiet
breathing (6 to 7 mL/kg).
 In patients with ARDS, these large inflation volumes are
delivered into lungs that have a marked ↓in functional
volume. → VOLUTRAUMA.

 CXR in ARDS show homogeneous pattern
of lung infiltration.
 CT images reveal that the lung infiltration in
ARDS is not spread evenly throughout the
lungs, but rather is confined to dependent
lung regions
 The remaining area of uninvolved lung is
the functional portion of the lungs in ARDS.(
baby lungs)
 The large inflation volumes delivered by
mechanical ventilation cause overdistention
and rupture of BABY LUNG→ Ventilator-
induced lung injury.

Ventilator-Induced Lung Injury
MECHANISM
 The following mechanisms of lung injury have been described:
1) Atelectrauma : collapse of alveoli and surfactant depletion. Ventilation with high FiO2
aggravates alveolar collapse due to absorption atelectasis
2) Oxygen toxicity : While this is well known, it is not clear what concentration of oxygen is
toxic over what period of time. It is generally assumed that FiO2 <0.6 is not toxic, however
an attempt must be made to maintain the FiO2 as low as possible.
3)Volutrauma : Ventilation at high volumes and pressures can lead to alveolar
overdistension, causing increased permeability pulmonary edema in the uninjured lung and
enhanced edema in the injured lung.
4)Cyclical shear stress injury : Cyclic opening and closing of atelectatic alveoli during
mechanical ventilation create tremendous shear stress at their junctions with open alveoli.
This results in damage to the capillary endothelium and the alveolar membrane.
5)Biotrauma : Alveolar over-distension along with the repeated collapse and reopening of
the alveoli can result in a whole cascade of proinflammatory cytokines which induce both a
pulmonary and systemic cytokine response, aggravating lung injury and causing systemic
multiorgan dysfunction.
6)Barotrauma : Pneumothorax, pneumomediastinum, interstitital emphysema.

Lung-Protective Ventilation:

Low-Volume Ventilation(LVV)
LVV protocol is designed to achieve three
goals :
 Maintain a tidal volume of 6 mL/kg using
predicted body weight,
 Keep the end-inspiratory plateau pressure
below 30 cm H2O, and
 Avoid severe respiratory acidosis.

MEDIAN ORGAN FAILURE
FREE DAYS
6ml/kg.
12ml/kg
.

Permissive Hypercapnia
 One of the consequences of low volume ventilation is a
reduction in CO2 elimination via the lungs leading to
hypercapnia and respiratory acidosis. Allowing hypercapnia
to persist in favor of maintaining lung-protective low-volume
ventilation is known as permissive hypercapnia.
 The degree of hypercapnia can be minimized by using the
highest respiratory rate that does not induce auto-PEEP
and shortening the ventilator tubing to decrease dead
space. In addition, changing from a heat and moisture
exchanger to a heated humidifier appears to decrease
hypercapnia by decreasing dead space ventilation

 One of the more troublesome side effects of hypercapnia
is brainstem respiratory stimulation with subsequent
hyperventilation, which often requires neuromuscular
blockade to prevent ventilator asynchrony.
 Data from clinical trials of permissive hypercapnia show
that arterial PCO2 levels of 60 to 70 mm Hg and
arterial pH levels of 7.2 to 7.25 are safe for most
patients .

OPEN LUNG VENTILATION
 It is a stratergy that combines low tidal volume ventilation & enough
applied PEEP to maximize alveolar recruitment. The LTVV aims to
mitigate alveolar overdistention, while the applied PEEP seeks to
minimize cyclic atelectasis. Togather , these effects are expected to
decrese the risk of ventilator associated lung injury.
 LTVV is applied as described and applied PEEP is set at least 2 cm
above the lower inflection point of the pressure volume curve are
used. Applied PEEP of 16 cm H 2 O is used if the lower inflection point
is uncertain.
 Alternative approach : PEEP set at a high level following a recruitment
maneuver and then incrementally decreased until both the static lung
compliance decreased and the sPO2 decreased by 2% from the
previous measurement. The PEEP is then set 2 cm H 2 O above this
level.
 PEEP adjustment based on the PEEP–FIO2 protocol used in ARMA is
likely the most feasible approach until more data are available.

STRATEGY………..?
Aerated
Non aerated
recruitable
Non aerated
Non recruitable

Titration of PEEP by oxygenation after assessment of lung recruitability. PEEP/FIO2
tables are from the ALVEOLI Trial. Adjust PEEP and FIO2 using the two tables as
guidelines to maintain PaO2 between 55 and 80 mmHg or SpO2 between 88% and
95%.
*Consider the using lower PEEP table as a guideline for PEEP titration for
patients who have active barotrauma or adverse PEEP-induced cardiovascular
changes.
(or decrease in PaCO2 at constant minute ventilation and tidal
volume)

Positive End-Expiratory Pressure:
The high PEEP approach is a type of open lung ventilation
that does not require pressure-volume curves. This is
advantageous because pressure-volume curves are
difficult to construct and generally require neuromuscular
blockade.
Significance of PEEP:
Applied PEEP opens collapsed alveoli, which decreases
alveolar overdistension because the volume of each
subsequent tidal breath is shared by more open alveoli. If
the alveoli remain open throughout the respiratory cycle,
cyclic atelectasis is also reduced. Alveolar overdistension
and cyclic atelectasis are the principal causes of ventilator-
associated lung injury.

TITRATING PEEP BY ESOPHAGEAL PRESSURE
 Esophageal pressure is an estimate of pleural pressure.
It can be measured with an esophageal balloon catheter
and then used to calculate the transpulmonary pressure.
 Transpulmonary pressure = airway pressure -
pleural pressure
 The transpulmonary pressure can then be adjusted by
titrating applied PEEP, since airway pressure is related
to applied PEEP. Titrating applied PEEP to an end-
expiratory transpulmonary pressure between 0 and 10
cm H 2 O may reduce cyclic alveolar collapse, while
maintaining an end-inspiratory transpulmonary pressure
≤25 cm H 2 O may reduce alveolar overdistension.

• PEEP by acting as a “stent” to keep small airways open
at the end of expiration and ↓ shear forces.
• Advantages of PEEP:
• PEEP ↑arterial oxygenation by ↓ intra pulmonary
shunting.
• Allows reduction in (FiO2) to safer levels hence
↓oxygen toxicity.
• PEEP can also open collapsed alveoli and reverse
atelectasis - known as lung recruitment, and it
increases the available surface area in the lungs for
gas exchange

Pitfalls of PEEP:
 Increased applied PEEP has the potential to cause
pulmonary barotrauma or ventilator-associated lung
injury by increasing the plateau airway pressure and
causing alveolar overdistension. It also has the
potential to decrease blood pressure by reducing
cardiac output.
“High applied peep should be administered to the
patients with refractory hypoxemia before implimenting
other rescue interventions because ARDS patients are a
heterogenous group , some of whom may have large
areas of recruitable lung that will respond to applied
PEEP.”

LUNG RECRUITMENT
 If there is recruitable lung, then PEEP will have a favorable
effect and will improve gas exchange in the lungs. However if
there is no recruitable lung, PEEP can overdistend the lungs
(because the lung volume is lower if areas of atelectasis
cannot be aerated) and produce an injury similar to ventilator-
induced lung injury.
 Areas of atelectasis that contain pockets of aeration are most
likely to represent recruitable lung, whereas areas of
atelectasis that are airless are unlikely to be recruitable.
 The impact of routine recruitment maneuvers on clinical
outcomes is unclear, although one meta-analysis found that
recruitment maneuvers did not affect mortality, length of
hospital stay, or the incidence of barotrauma, despite
improving the PaO 2 .

RECRUITMENT MANEUVERS (RMS)
Current evidence suggests that that RMs should not be routinely used on all
ARDS patients unless severe hypoxemia persists or as a rescue maneuver to
overcome severe hypoxemia, to open the lung when setting PEEP, or following
evidence of acute lung derecruitment such as a ventilator circuit disconnect
• Vital capacity maneuver (inflation of the lungs up to 40 cm H2O,
maintained for 15 - 26 seconds)
• Intermittent sighs
• Intermittent increase of PEEP
• Continuous positive airway pressure (CPAP) of 35-40cm of H20
for 40 seconds.
• Increasing the ventilatory pressures to a plateau pressure of 50 cm
H2O for 1-2 minutes .
• One study found that most of the alveolar recruitment occurred
during the first ten seconds of the maneuver . This was followed by
a decrease in the blood pressure, which recovered within 30 seconds
after the recruitment maneuver. Significant airway overdistention
does not occur while single recruitment manuevre and recruited
alveoli tend to remain open when lower pressure are instituted.

RECRUITMENT MANEUVERS
Anesthesiology 2002, 96:795–802.
CPAP : 35-40 cm H20 for 30-40 seconds

RECRUITMENT MANEUVERS
Anesthesiology 2002, 96:795–802.
Curr Opin Crit Care 2003; 9:22–27
Crit Care Med 2004; 32: 2371–77
Intermittent Sigh
Intermittent PEEP
Progressive PEEP

MODE OF VENTILATOR
Randomized, controlled trials demonstrating superiority of volume
assist control over other modes in the management of ARDS are
lacking at this time, but it is the mode used in the majority of major
clinical trials in patients with ARDS and was the mode used in the
ARMA trial, which, as noted above, showed a clear mortality benefit.
PCV : Variable flow, so more comfortable if dyssynchrony, prolong i
time for oxygenation, control peak pressures

NEUROMUSCULAR BLOCKERS
 Administration of short-term (up to 48 hours)
neuromuscular blockade to patients with ARDS who
have severe gas exchange abnormalities (eg, PaO 2
/FiO 2 ≤120 mmHg) is probably safe and potentially
beneficial.
 Improvements in patient–ventilator synchrony and
elimination of muscle activity and the associated oxygen
consumption,
 Papazian L, Forel JM, Gacouin A, et al. Neuromuscular
blockers in early acute respiratory distress syndrome. N
Engl J Med 2010; 363:1107.

REFRACTORY HYPOXEMIA
 Following modalities are used for Refractory
Hypoxemia apart from N-M Blockers, High PEEP
& other recruitment maneuvers
 Prone Position
 Other modes of ventilator
 IRV
 Inhaled Nitric Oxide
 ECMO

Prone position:
 In several trials, MV in the prone position improves
oxygenation. Other purported benefits include improvements
in secretion clearance, increased end-expiratory volume,
and decreased mechanical compression of the lungs by the
heart.
 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.
 The latest PROSEVA (Proning Severe ARDS Patients) trial
confirmed these benefits in a formal randomized study. The
bulk of data indicates that in severe acute respiratory
distress syndrome, carefully performed prone positioning
offers an absolute survival advantage of 10–17%, making
this intervention highly recommended in this specific
population subset.
 Can be hazardous, leading to accidental endotracheal
extubation, loss of central venous catheters, and orthopedic
injury, pressure sores etc.

POSSIBLE MECHANISMS
 Recruitment of dependent lung zones,
 Increased functional residual capacity (FRC)
 Improved diaphragmatic excursion
 Increased cardiac output
 Improved ventilation-perfusion matching
 Relief of compression of the lung by the heart and
Mediastinal structures

OTHER MODES OF MV :
 AIRWAY PRESSURE RELEASE VENTILATION
(APRV):
 Another “open lung” approach
 It is a pressure control mode with spoteneous breaths;
CPAP released periodicaly.
 Two CPAP levels Higher CPAP is baseline pressure
 Intermittent, brief release of Paw from higher CPAP
level to lower CPAP level
 Decrease in Paw augments TV
 Spontaneous breathing at both upper & lower CPAP
 Available on few ventilators
 Like BiPAP/BiLevel but time at the lower pressure
(“release time”) is usually short  0.6-1sec

APRV
Airway Pressure Release Ventilation
From Mosby’s R. C. Equip. 6th ed. 1999.

Inverse ratio ventilation (IRV)
 Oxygenation can also be improved by increasing mean airway
pressure with "inverse ratio ventilation."
 The inspiratory (I) time is lengthened so that it is longer than the
expiratory (E) time (I:E ratio as high as 7:1 have been used).
 When the inspiratory time is increased, there is an obligatory
decrease in the expiratory time. This can lead to air trapping,
auto-PEEP, barotrauma, hemodynamic instability, and
decreased oxygen delivery.
 ↓ FIO2 to 0.60 to avoid possible oxygen toxicity,
 But no mortality benefit in ARDS has been demonstrated.

o There are potential side effects associated with
prolonging the inspiratory time that should be
considered.
o In addition, a prolonged inspiratory time may require
significant sedation or neuromuscular blockage,
particulary if the inspiratory time surpasses the
expiratory time.

 High-frequency ventilation (HFV) –
 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.
 HFOV requires a specialized ventilator
 Partial liquid ventilation (PLV) with perfluorocarbon,
an inert, high-density liquid that easily solubilizes
oxygen and carbon dioxide, has revealed promising
preliminary data on pulmonary function in patients with
ARDS, but no survival benefit.

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. iNO flows only into well
ventilated areas, so improves shunt.
 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.

EXTRA CORPOREAL MEMBRANE OXYGENATION:-
 Extracorporeal membrane oxygenation (ECMO) is the use of
a modified heart–lung machine to provide respiratory,
circulatory, or both support at the bedside, usually for at least
a number of days or even weeks.
 Extracorporeal membrane oxygenation (ECMO) uses
technology derived from cardiopulmonary bypass (CPB) that
allows gas exchange outside the body. In addition, circulatory
support can also be provided.
 ECMO is a valuable option for the management of severe but
reversible causes of respiratory failure or cardiogenic shock
refractory to conventional treatment.
 Veno-venous ECMO is designed to provide gas exchange,
while veno-arterial ECMO provides both gas exchange and
haemodynamic support.
 Acute respiratory distress syndrome associated with
pneumonia (viral or bacterial) is the most common cause of
refractory hypoxemia that requires ECMO support.

NON-VENTILATORY MANAGEMENT
 Fluid management
 Diuretics
 Steroids
 Blood Transfusion cut-off
 Choice of Inotropic agent

Fluids management:
 Patients with ARDS should receive intravenous fluids
only sufficient to achieve an adequate cardiac output,
tissue oxygen delivery, and organ function, as
assessed by urine output, acid-base status, and
arterial pressure.
 Once the patient is beyond the early, resuscitative
phase of their illness, efforts should be made to
decrease the amount of volume administered and
maintain an even balance between the volume of
fluid administered to and eliminated from the patient,
referred to as “euvolemia”. The benefits of this
approach were demonstrated in the Fluid and
Catheter Treatment Trial (FACTT) .There were no
differences in 60-day mortality between the two
groups, but the conservative approach was
associated with improved gas exchange and shorter
duration of mechanical ventilation without increasing
the incidence of acute kidney injury or other non-
pulmonary organ failures.
 Goal: MAP ≥ 65mmHg, avoid hypoperfusion

 Fluid management in ARDS is usually aimed at reducing
extravascular lung water with diuretics. While this approach
has shown modest benefits in clinical measures like lung
compliance, gas exchange, and length of time on the
ventilator, but little survival benefit.
 The first problem with the use of diuretic therapy in ARDS
is the nature of the lung infiltration. While diuretics can
remove the watery edema fluid that forms as a
consequence of heart failure, the lung infiltration in ARDS
is an inflammatory process, and diuretics don't reduce
inflammation.
 Diuretic therapy can be tailored to achieve the lowest
cardiac filling pressures that do not compromise cardiac
output and systemic oxygen transport.
ROLE OF DIURETICS

 The golden rule is that hydrostatic pressures should be
kept as low as possible, provided that oxygen delivery to
the tissues is not compromised .
 As techniques to monitor the regional circulation become
available, titration of fluid requirements will become more
precise.
 There is no place for systematic fluid restriction and
diuretics to eliminate edema, as the function of other
tissues may deteriorate with inadequate perfusion.

ROLE OF STEROIDS
IN UNRESOLVING ARDS
Because of apparent benefit in small trials, it was thought that
there might be a role for high-dose corticosteroid therapy in
patients with late (fibroproliferative phase) ARDS. However, an
ARDS Study Network trial of methylprednisolone for patients
with ARDS persisting for at least 7 days demonstrated no
benefit in terms of 60-day mortality.Patients treated later in the
course of ARDS, 14 days after onset, had worsened mortality
with corticosteroid therapy.
The benefit of steroids in ARDS may be explained by the
ability of steroids to promote collagen breakdown and inhibit
fibrosis
One of the successful regimens involved methylprednisolone in
a dose of 1-2 mg/kg/day.

1.Steinberg KP, Hudson LD, Goodman RB, et al found
that in the subgroup of patients randomized 7 to 13 days
after the onset of ARDS, methylprednisolone caused a
non-statistically significant reduction in 60-day mortality
(27 versus 36 percent) and 180-day mortality (27 versus
39 percent). In contrast, among patients randomized more
than 14 days after the onset of ARDS, methylprednisolone
increased 60-day mortality (35 versus 8 percent) and 180-
day mortality (44 versus 12 percent). Methylprednisolone
increased ventilator-free days, shock-free days,
oxygenation, lung compliance, and blood pressure, but
also increased neuromuscular weakness.
2. In a double-blind trial, patients with early ARDS (defined
as ≤72 hours), Meduri GU, Golden E, Freire AX, et al
found that glucocorticoid therapy reduced the duration of
mechanical ventilation, length of ICU stay, and ICU
mortality (21 versus 43 percent).

HEMOGLOBIN
 Transfusion is often recommended to keep the Hb
above 10 g/dL, but this practice has no scientific
basis or documented benefit, even in ventilator-
dependent patients.
 Considering that blood transfusions can cause
ARDS, it is wise to avoid transfusing blood products
in patients with ARDS AND threshold should be 7
g/dL.
 If there is no evidence of tissue dysoxia or
impending dysoxia (e.g., an oxygen extraction ratio
>50%), there is no need to correct anemia with
blood transfusions.

INOTROPIC AGENT
 Cardiac output may be augmented by raising filling
pressures if they are low (if pulmonary edema is not
exacerbated) or by using inotropic agents. However,
raising oxygen delivery to supernormal levels is not
clinically useful and may be harmful in some
circumstances.
 If volume infusion is not indicated, dobutamine is
preferred over vasodilators for augmenting the cardiac
output because vasodilators will increase
intrapulmonary shunt and will add to the gas exchange
abnormality in ARDS. Dopamine should be avoided in
ARDS because it constricts pulmonary veins, and this
will cause an exaggerated rise in the pulmonary
capillary hydrostatic pressure.

OTHER DRUG THERAPY – UNPROVEN BENIFIT
INHALED VASODILATORS : PGE1 (pulmonary vasodilatation
and anti-inflammatory effects on neutrophils/macrophages) ,
Aerosolized PGI2 (selective pulmonary vasodilatation of
ventilated lung areas), NO
GM-CSF
Almitrine (selective pulmonary vasoconstrictor of
nonventilated lung areas)
Surfactant (prevents alveolar collapse and protects against
intrapulmonary injury and infection)
Antioxidants - dietary oil supplementation – Omega-3 fatty
acid, N-acetylcysteine (protect the lung from free oxygen
radical production)
Anti-inflammatory drugs (Lisofylline, Ibuprofen, ketoconazole,
Statin)
No recommendation can be made for their use - Rescue
modality in the patient with refractory hypoxia?

Mortality:
 Recent mortality estimates for ARDS range from
26 to 58% with substantial variability.
 The underlying cause of the ARDS is the most
common cause of death among patients who die
early. In contrast, nosocomial pneumonia and
sepsis are the most common causes of death
among patients who die later in their clinical
course . Patients uncommonly die from
respiratory failure.
 Thus, improvement in survival is likely secondary
to advances in the care of septic/infected
patients and those with multiple organ failure.

Functional Recovery in ARDS Survivors
o ARDS pts experience prolonged
respiratory failure and remain dependent on
mechanical ventilation for survival.
o Patients usually recover their max lung
function within 6 mnths.
o One year after endotracheal extubation,
over a 1/3 of ARDS survivors have normal
spirometry values and diffusion capacity.
o Most of the remaining patients have only
mild abnormalities in their pulmonary
function.

 Recovery of lung function is strongly associated with the
extent of lung injury in early ARDS
 When caring for ARDS survivors it is important to be
aware of the burden of emotional and respiratory
symptoms.
 There are significant rates of depression and
posttraumatic stress disorder in ARDS survivors

FUTURE DIRECTIONS:
 With the high mortality rates associated
with ARDS and sepsis, the search
continues to identify targets.
 Effective anti-sepsis interventions may
reduce the incidence of ARDS and
improve outcomes from it.
 1) Antibodies against macrophage
migration inhibitory factor (MIF),
 2) Antibodies against high-mobility group
B-1 protein (HMGB1),
 3.) Stem cell therapy (MSC)

ROLE OF STEM CELLS – PHASE-I CLINICAL
TRAIL GOING ON
 Stem cells constitute a promising therapeutic strategy for patients
suffering from ALI/ARDS.
 MSCs appear closest to clinical translation, given the evidence
that they may favourably modulate the immune response to
reduce lung injury, while maintaining host immune-competence
and also facilitating lung regeneration and repair.
 However, gaps remain in our knowledge regarding the
mechanisms of action of MSCs, the optimal MSC administration
and dosage regimens, and the safety of MSCs in critically ill
patients. It is anticipated that these remaining knowledge deficits
will be addressed in ongoing and future studies.
 Other stem cells, such as ESCs and iPCs, are at an earlier stage
in the translational process, but offer the hope of directly
replacing injured lung tissue.
 Ultimately, lung-derived stem cells may offer the greatest hope
for lung diseases, given their role in replacing and repairing the
native damaged lung tissues.

 JAMA, June 20, 2012—Vol 307, No. 23 : Berlin Definition
 Harrison‘s Principles Of Internal Medicine 19th Edition
 The ICU Book, 3rd Edition - Paul L. Marino
 UpToDate : www.uptodate.com
 eMedicine : www.medscape.com
 Mechanical ventilation 3rd Edition - David W Chang
 Susen Pilbeam Text Book Of Mechanical Ventiltor
 Human Mesenchymal Stem Cells For Acute Respiratory Distress
Syndrome (START)Clinicaltrial :
http://clinicaltrials.gov/show/NCT01775774
 M, Luks Andrew. 2013. "Ventilatory strategies and supportive care in
acute respiratory distress syndrome." Influenza and other respiratory
viruses 7 Suppl 3: 8-17. doi:10.1111/irv.12178.
 Carl F. Haas, MLS, RRT “Mechanical Ventilation with Lung Protective
Strategies: What Works?” Crit Care Clin 27 (2011) 469–486

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ARDS - Diagnosis and Management

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