Acute Respiratory

Distress Syndrome
PATHOPHYSIOLOGY
Presented by:
Ms. Evelyn Olita, RN
 Causes

DIRECT LUNG INJURY INDIRECT LUNG INJURY

COMMON COMMON
 PNA  Sepsis*
 Aspiration  Severe trauma with shock and
multiple transfusions
LESS COMMON
 Pulm contusion LESS COMMON
 Fat emboli  Cardiopulm bypass
 Near-drowning  Acute pancreatitis
 Inhalation injury  Transfusions
 Reperfusion injury (transplant  Drug overdose
etc)
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 Pathophysiology

 Diffuse alveolar damage

 Lung capillary damage

 Inflammation/pulmonary edema

 Resulting severe hypoxemia and

decreased lung compliance
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 Pathophysiology

Occurs in Stages
1. Exudative ( Acute Phase)
2. Proliferative Phase
3. Fibrotic Phase
4. Recovery Phase

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 Exudative Phase (Acute Phase)
 Alveolar-capillary barrier is formed by
microvascular endothelium and alveolar
epithelium
 Under normal conditions epithelial barrier
is much less permeable than endothelium
 Epithelium is made up of type I and II cells
 Type I cells are injured easily and Type II
cells are more resistant
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 Exudative Phase
 In ALI/ARDS – damage to either one occurs
resulting in increased permeability of the barrier
 Influx of protein-rich edema fluid into the alveolar
space
 Injury of Type I cells results loss of epithelial
integrity and fluid extravasation (edema)
 Injury of Type II cells then impairs the removal of
the edema fluid

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 Exudative Phase

 Dysfunction of Type II cells also leads to

reduced production and turnover of surfactant
which leads to alveolar collapse
 If severe injury to epithelium occurs –
disorganized/insufficient epithelial repair occurs
resulting in fibrosis
 In addition to inflammatory process, there is
evidence that the coagulation system is also
involved
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Exudative Phase

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 Fibrotic Phase
 After acute phase, some patient will have
uncomplicated course and rapid resolution

 Some patients will progress to fibrotic lung

injury

 Such injury occurs histologically as early

as 5-7 days
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 Fibrotic Phase
 Intense inflammation leads to obliteration
of the normal lung architecture
 Alveolar space is filled with mesenchymal
cells and their products
 Reepithelialization and new blood vessel
formation occurs in disorganized manner
 Fibroblasts also proliferate, collagen is
deposited resulting in thickening of
interstitium
 Fibrosing alveolitis and cyst formation
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 Proliferative Phase
 With intervention (mechanical ventilation)
there is clearance of alveolar fluid
 Soluble proteins are removed by diffusion
between alveolar epithelial cells
 Insoluble proteins are removed by
endocytosis and transcytosis through
epithelial cells and phagocytosis through
macrophages
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 Proliferative Phase
 Type II cells begin to differentiate into
Type I cells and reepithelialize denuded
alveolar epithelium

 Further epithelialization leads to increased

alveolar clearance

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Proliferative Phase

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 Consequences
 Impaired gas exhange leading to severe
hypoxemia - 2/2 ventilation-perfusion mismatch,
increase in physiologic deadspace
 Decreased lung compliance – due to the
stiffness of poorly or nonaerated lung
 Pulm HTN – 25% of pts, due to hypoxic
vasoconstriction, Vascular compression by
positive airway compression, airway collapse
and lung parenchymal destruction

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 Clinical Features
 Pts are critically ill
 develop rapidly worsening tachypnea, dyspnea,
hypoxia requiring high conc of O2
 Occurs within hours to days ( usually12-48
hours) of inciting event
 Early clinical features reflects precipitants of
ARDS
 Physical exam shows cyanosis, tachycardia,
tachypnea and diffuse rales and other signs of
inciting event
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THANK YOU!!!

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COMMON DIAGNOSTIC
TEST/LABORATORY
FINDINGS in ARDS

PRESENTED BY;
MS. ROWENA FINIANOS, RN

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 Work Up
 ARDS is a clinical diagnosis
 No specific lab abnormality beyond
disturbance in gas exchange is evident
 Radiologic findings may be consistent but
not diagnostic
 Work up therefore is useful in identifying
inciting event or excluding other causes of
lung injury
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 Work Up
Useful diagnostic workup may include;
- CBC, Renal function test, Coagulation Profile, LFTs,
Liver Enzymes, Pancreatitic enzymes
- Arterial blood gas
- Blood culture
- Urine Analysis and Culture
- Toxicology screen
- CXR
- CT
- Bronchoscopy/Bronchial Airway Lavage
- CVP
- PCWP fibno
 Diagnostic Test Findings
1. ARTERIAL BLOOD GAS (ABG) analysis
results vary depending on progression.
Results initially reflect respiratory alkalosis
As ARDS worsens, respiratory acidosis is
evidenced by increasing PaCO2(>45mmHg)
Metabolic Acidosis is evidenced by
decreasing HCO3(<22mEq/L) and a
declining PaO2 despite oxygen therapy

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2. Serial chest X-RAYS vary depending
on the stage of the disorder
Bilateral infiltrates are shown in early
stages
In later stages, lung fields with a
ground- glass appearance and
“whiteouts” of both lung fields(with
irreversible hypoxemia) may be
observed

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3. CVP/ Pulmonary Artery Catheterization
- Helps identify the cause of pulmonary
edema (cardiac vs. non-cardiac) by
measuring pulmonary artery wedge
pressure(PAWP) which is usually low to
normal
4. Sputum analysis, including Gram stain
and culture and sensitivity, identifies
causative organisms

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5.Blood cultures identify
infectious organisms
6.Toxicology testing screens
for drug ingestion
7.Serum amylase rules out
pancreatitis.

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 CXR findings
diffuse, fluffy alveolar infiltrates with prominent air
bronchograms

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CT findings

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 Treatment

 No specific therapy for ARDS exists

 Mainstay of treatment is supportive care

 Treat underlying/inciting conditions

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 Treatment - Ventilation
Goals of ventilation in ARDS are to:
 Maintain oxygenation by keeping O2 sats
at 85-90%
 Avoiding oxygen toxicity and
complication of mechanical ventilation –
decreasing FiO2 to less than 65% within
the 1st 24-48 hours

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 How to select vent settings
 PEEP/FiO relationship to maintain
2

adequate PaO2/SpO2
 PaO2 goal: 55-80mmHg or SpO2 88-95%
use FiO2/PEEP combination to achieve
oxygenation goal

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How to select vent settings

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 other ventilation strategies
 Recruitment maneuvers

 Prone

 Inhaled nitric oxide

 High frequency oscillation

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 Treatment
 Treatment strategy is one of low volume and high frequency
ventilation (ARDSNet protocol)
- Low TV(6ml/kg) to prevent over-distention
- increase respiratory rate to avoid very high level of
hypercapnia
- PaCO2 allowed to rise, usually well tolerated
- May be beneficial
- low CVPs
 Search for and treat the underlying cause; surgery if needed
 Ensure adequate nutrition and place on GI/DVT prophylaxis
 Prevent and treat nosocomial infection
 Consider short course of high dose steroids in patients w/
severe diagnosis that is not resolving.
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 References
1. Straight A’s I Pathophysiology, A Review Series. Lippincott Williams & Wilkins
2006.
2. The NHLBI ARDS Clinical Trials Network. Comparison of two fluid-management
strategies in acute lung injury. N Engl J Med. Jun 15 2006;354(24):2564-72
3. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal
volumes as compared with traditional tidal volumes for acute lung injury and the
acute respiratory distres syndrome. N Engl J Med. May 4 2000;342(18):1301-
4. Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz
M. Higher versus lower positive end-expiratory pressures in patients with the
acute respiratory distress syndrome. N Engl J Med. Jul 22 2004;351(4):327-36
5. Griffiths MJ, Evans TW. Inhaled nitric oxide therapy in ARDS. N Engl J Med. Dec
22 2005;353(25):2683-95.
6. Albert RK. The prone position in acute respiratory distress syndrome:
where we are, and where do we go from here. Critical Care
Med. Sep 1997;25(9):1453-4
7. Herridge MS, Cheung AM, Tansey CM. One-year outcomes in survivors of the
acute respiratory distress syndrome. N Engl J Med. Feb 20 2003;348(8):683-93

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THANK YOU!!!

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