ACUTE RESPIRATORY DISTRESS SYNDROME

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Introduction

Drug overdose

Reperfusion injury
transplantation)

(e.g.,

post-lung

Adverse effect of medication

ARDS was defined as a syndrome of
INTE

acute onset

with bilateral infiltrates on chest radiography RNAL

consistent with pulmonary edema
MEDI

pulmonary artery occlusion pressure less than or CINE

Pathology
equal to 18 mm Hg (or absence of clinical evidence of left
II
atrial hypertension)
hypoxemia as measured by the ratio of the
arterial partial pressure of oxygen (Pao2) to the fraction of
oxygen inspired (Fio2)
Pao2/Fio2 ratio of less than or equal to 300 define an entity
termed acute lung injury (ALI).

Timing

Acute Lung
Acute
injury

ARDS

Acute

Oxygenation

Pulmonary
Frontal Chest
Artery
Wedge
Radiograph
Pressure

Pao2/Fio2 Bilateral
300 m Hg
infiltrates

18 m Hg if
measured, or no
clinical evidence
of left atrial
hypertension

Pao2/Fio2 Bilateral
200 mm Hg infiltrates

18 mm Hg if
measured, or no
clinical evidence
of left atrial
hypertension

Fio2, fraction of oxygen inspired; Pao2, arterial Po2.

ARDS was the most severe form of ALI and was defined as
occurring if the Pao2/Fio2 ratio is less than or equal to 200

Note: Acute respiratory distress syndrome (ARDS) is an entity

characterized by diffuse alveolar injury, alveolar collapse or
consolidation, protein-rich lung edema, surfactant inactivation, and
inflammation.
Course and Pathophysiology

Exudative phase
The first 7 days of illness after exposure to a precipitating ARDS
risk factor; usually present within 1236 h after the initial insult
but symptoms can be delayed by 57 days

Alveolar capillary endothelial cells and type I pneumocytes

(alveolar epithelial cells) are injured loss of the normally tight
alveolar barrier to fluid and macromolecules.

Edema fluid rich in protein accumulates in the

interstitial and alveolar spaces.

Cytokines (e.g., IL-1, IL-8, and TNF-) and lipid mediators (e.g.,
leukotriene B4) are present.

In response to proinflammatory mediators, leukocytes

(especially neutrophils) traffic into the pulmonary interstitium
and alveoli.

Most severe form of AHRF

Decrease in mortality in late 1990s: 40-70% to 30-40%

Condensed plasma proteins aggregate with cellular debris and

Mortality: due mostly to sepsis or multiple organ failure

Primary pulmonary cause/AHRF causes < 20% of ARDS mortality

dysfunctional pulmonary surfactant to form hyaline membrane

whorls.
Pulmonary vascular injury: vascular obliteration by
microthrombi and fibrocellular proliferation

Diffuse interstitial and

alveolar infiltrates

Dependent alveolar
edema and
atelectasis
Clinical Disorders Commonly Associated with ARDS
Indirect Injury
Direct Injury
Sepsis

Pneumonia

Major trauma

Aspiration

Multiple blood transfusions

Pulmonary contusion

Pancreatitis

Toxic inhalation

Cardiopulmonary bypass

Near drowning

Proliferative Phase

Lasts from day 7 to day 21.

Most patients recover rapidly and are liberated from
mechanical ventilation during this phase but some may still
experience dyspnea, tachypnea, and hypoxemia or develop
progressive lung injury and early changes of pulmonary fibrosis.

 The first signs of resolution are often evident with the initiation Page
of lung repair, organization of alveolar exudates, and a shift
from a neutrophil to a lymphocyte-predominant pulmonary
infiltrate.
Proliferation of type II pneumocytes along alveolar basement
membranes to synthesize new pulmonary surfactant and
differentiate into type I pneumocytes.

INTE
RNAL
MEDI
(+) alveolar type III procollagen peptide - marker of pulmonary CINE
fibrosis; associated with a protracted clinical course and II

Lung protective strategy

Low tidal volume prevents the excessive global

increased mortality
Fibrotic Phase
Some patients will enter a fibrotic phase that may require longterm support on mechanical ventilators and/or supplemental
oxygen.

Alveolar edema and inflammatory exudates of earlier phases

are converted to extensive alveolar duct and interstitial fibrosis.

Acinar architecture is markedly disrupted, leading to
emphysema-like changes with large bullae.

Intimal fibroproliferation leads to progressive vascular occlusion

and pulmonary hypertension.

The best mechanical ventilation would provide adequate gas

exchange with the lowest amount of VILI
Mechanical Ventilation
Ventilator-induced lung injury

ARDS Netowrk: tidal volume 6 ml/kg vs. 12 ml/kg

Mortality: 31% vs. 40%

Prevention of alveolar collapse

Set positive end-expiratory pressure (PEEP) to

Physiologic consequences: increased risk of pneumothorax,

reductions in lung compliance, and increased pulmonary dead
space.
General principles of management
1. The 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. The prompt recognition of nosocomial infections; and
5. Provision of adequate nutrition.
Barotrauma
1970s-

Low PEEP and high tidal volume: larger tidal

volumes (10 to 15 per kilogram) are preferable, having
been used in several thousand ventilated patients with no
evidence of development of pulmonary damage

The main concerns were the presumed harm of

high inspiratory oxygen fraction and the hemodynamic
impairment

It was later recognized in experimental and

clinical settings that high-volume/high-pressure mechanical
ventilation could severely damage the lung parenchyma
Volutrauma
1980s-

The focus shifted from the potential harm of

pressure to the harm of volume (overdistention)

Application of computed tomography (CT) and

the quantitative approach to CT analysis led to the concept
of baby lung

High pressure or excessive distention applied to a

small fraction of the lung parenchyma (with a size similar
to the lung of a baby) unavoidably leads to structural
lesions of the lung regions open to ventilation
Biotrauma/atelectrauma

stress and strain of the baby lung

Higher PEEP prevents the regional excessive
stress and strain by avoiding alveolar collapse and
reopening during mechanical ventilation
The literature to date supports that the harm of mechanical
ventilation is due to excessive global or regional stress and
strain

a physical rupture of the lung

mechanically induced inflammation of the lung

parenchyma, constituting VILI

minmize fiO2 and maximize PaO2

Inverse ratio ventilation, I:E > 1:1
Prone position ventilation (?)

Other MV Strategies

High-frequency ventilation (HFV), i.e., (520 cycles per second)

and low tidal volumes (12 mL/kg).

extracorporeal membrane oxygenation (ECMO)

partial liquid ventilation (PLV) with perfluorocarbon
adjunctive ventilator therapies not routinely used
Supportive Care

One of the first goals of therapy in ARDS is to treat the

underlying cause

Additional treatment focuses on preventing complications and

providing supportive care to allow time for the body to heal

Source control in patients with sepsis

antibiotics
surgical dbridement
drainage

DVT prophylaxis

Ulcer prophylaxis
Supportive: Sedation
Balance patient comfort and the ability to assess neurologic
status

Complications

hypotension

slow ventilator weaning

inability to assess neurologic status

worsening of critical care myopathy

Daily interruption of sedative infusions

stopping an infusion until the patient is awake

and then restarting the drug
decrease the duration of mechanical ventilation
and length of stay in the ICU

Supportive: Nutrition

Patients commonly do not receive adequate nutrition in both

medical and surgical ICUs

Nutritional support protocols increase the proportion of
patients adequately fed

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INTE
RNAL
Enteral feeding with certain nutrients and antioxidants
MEDI
improved gas exchange, lowered the requirement for
mechanical ventilation, decreased the length of ICU stay, and CINE
II
reduced the incidence of new organ failure
Fluid Management
Glucocorticoids not recommended
Inhaled nitric oxide not recommended
Surfactant repalcement
Other anti-inflammatory therapy

Initial Management of ARDS

Intervention

Goals

Initiate
volume/pressure
limited ventilation

Tidal volume < 6ml/kg PBW

Plateau pressure <30 cm H2O
RR <35 bpm

Oxygenate

FiO2 < 0.6

PEEP < 10 cm H2O
SpO2 88-95%

Minimize Acidosis

pH > 7.3
RR < 35 bpm

Diuresis

MAP > 65mm Hg

Avoid hypoperfusion

Prognosis/Mortality
Mortality 41-65%

>80% from non-pulmonary causes (sepsis)

Major Risk Factors for ARDS Mortality
Advanced age

Preexisting organ dysfunction

Chronic liver disease
Cirrhosis
Chronic alcohol abuse
Chronic immunosuppression
Sepsis
Chronic renal disease
Any nonpulmonary organ failure
Increased APACHE II scores
Direct lung injury

ARDS Survivors

Recovery of maximum lung function in 6 months

Over a third with normal spirometry and diffusing capacity 1
year after extubation

Burden of emotional and respiratory symptoms

Depression and posttraumatic stress disorder