Acute Respiratory

Distress Syndrome
(ARDS)
 ARDS
An inflammatory disorder
that damages the alveolar
capillary membrane
throughout the lung
interfering with gas
exchange
Overview on breathing and gas
exchange
 Overview on Alveoli

• Approximately 500 million alveoli

• Located at most distal portion of the respiratory tract

• separated by alveolar septum; contains the pulmo capillaries

• Each alveoli consists of three types of cell

• Type I pneumocytes

• Type II pneumocytes

• Alveolar macrophages
 Alveolar structure
• Type I pneumocytes
• Facilitate gas exchange
• Communicate with type II pneumocytes to secrete surfactant in
response to stretch.
• Type II pneumocytes
• Produce & secrete pulmonary surfactant (reduces surface tension,
prevent alveoli from collapsing)
• Removes fluid from alveoli into interstitial space
• Regeneration of alveolar epithelium after injury
• Alveolar macrophages
• Trigger immune response by collecting inhaled particles
• facilitates the phagocytosis release inflammatory mediators to
enhance the local immune response
 ARDS
• non-cardiac pulmonary edema caused by ↑ increased
permeability of alveolar capillary membrane & diffused
alveolar injury
• Usually affects both lungs
• High morbidity and mortality rate
• Earlier, ARDS was considered a severe form of acute lung
injury (ALI)
• Categorized into mild (ALI) → moderate → severe
• The berlin Definition of ARDS (most recent, 2012) categorizes
the severity of ARDS
 Abbreviation List
• Partial Pressure of Oxygen (PaO2)
The pressure of the O2 found in the blood

• Fraction of Inspired Oxygen (FiO2)

Concentration of O2 in the gas mixture eg: FiO2 of RA is 21%

• Tidal Volume (VT)

Amount of air that moves in & out of the lung with each respiratory cycle

• Plateau pressure (Pplat)

Pressure applied to small airways & alveoli during +ve pressure MV, measured during

inspiratory pause

•
 Causes
Primary (direct damage to alveolar Secondary (cellular or humoral
membrane) injury to capillary endothelium
• Pneumonia • Sepsis
• Aspiration • Severe pancreatitis
• Pulmonary contusion • Embolism (air, fat)
• Near drowning • Massive blood transfusion
• Inhalation of smoke or toxic • Hypovolemic shock associated with
substance chest trauma/ sepsis
 Pathophysiology
Injury to Alveolar epithelium (type 1 & 2
pneumocytes) starts and inflammatory immune
response

Site of injury release inflammatory mediator

(cytokines, interleukins)
Initiation
Phase

Activates and accumulation of neutrophils,

macrophages, platelets in pulmonary capillaries
releasing chemical mediators like interleukins and
Cytokine

Activates humoral mediators which cause damage

to alveolar capillary membrane, ↑capillary
permeability
 Pathophysiology
Proteins, Blood cells, fibrin, activated cellular & humoral
mediators move out into pulmonary interstitium (interstitial
edema) eventually forcing in to alveoli (alveolar edema)

Alveolar edema cause swelling of type 1

Exudative

pneumocytes (poor gas exchange)

Phase

Protein, fibrin, cell debrides in edema fluid forms a

thick layer over the inflamed alveoli wall (Hyaline
membrane)

Eventually, type II pneumocytes are damage and the

remaining surfactant was washed off with edema
leading to alveolar collapse
ibroproliferative Pathophysiology

Disordered healing with cellular granulation

and collagen deposition with in alveolar
capillary membrane
Phase

Alveoli becomes enlarged, irregularly shaped

(fibrotic), pulmonary capillaries become
scarred

Lead to further stiffening of lungs,

↑pulmonary hypertension, continues
hypoxemia
 Pathophysiology

Structural & vascular remodeling takes place

over several weeks. Hyaline membrane is
cleared and alveolar fluid is transported out
Resolution

into interstitium
Phase

Type II Pneumocytes multiplies and form

Type 1 & Type II Pneumocytes

Alveolar macrophages removes cellular

debris
 Clinical Features of ARDS
Signs Symptoms
• Tachypnea (>40 breaths/min) • Dyspnea
• Tachycardia • Cough
• Cyanosis • Chest pain
• Use of accessory muscles • Anxiety
• Frothy sputum (white or Pink)
• Metabolic acidosis
• Abnormal chest sound
(crackles/ wheeze)
• Respiratory alkalosis
• Hypoxemia
 Quick Question!
What is the difference between Hypoxia and Hypoxemia?
• Hypoxemia: SUBnormal concentration of O2 in the blood vs to the
concentration of O2 being inhaled
• Hypoxia: an insufficient amount of O2 in the tissues
Example
A patient breathing an FiO2 of 50% O2 who has a PaO2 of 100 is
relatively hypoxemic as his PaO2 should be more than 100
with that FiO2. But he’s not hypoxic, since a PaO2 of 100
provides an adequate amount of O2 to his tissues
• Hypoxemia can progress to hypoxia if the patient’s condition
worsens
Criteria for ARDS: Berlin Definition
• Timing: Acute RF, S&S develops < 1 week of initial cause
• Work up on causal factors eg: septic screening
• Blood, Urine sputum c/s, Imaging of the abdomen for signs of infection

• Chest Imaging: Bilateral Opacification “White outs”

• Chest xray, CT chest, Lung ultrasounds

• Oxygenation, low P/F ratio:

• Mild: P/F ratio 200-300mmHg & PEEP >5cmH2O
• Moderate: P/F ratio 100-200mmHg & PEEP >5cmH2O
• Severe: P/F ratio <100mmHg & PEEP >5cmH2O

• Origin of edema: non cardiogenic cause

Lets Calculate P/F Ratio

P/F ratio = PaO2 ÷ FiO2

Example
PaO2 = 100
FiO2 = 21%

P/F = 100 ÷ ( 21/100)

=100 ÷ 0.21
476mmHg
 Now, Can you do it?

PaO2 = 100 PaO2 = 100 PaO2 = 90

FiO2 = 40% FiO2 = 60% FiO2 = 100%

P/F = 100 ÷ P/F = 100 ÷ P/F = 90 ÷

(40/100) (60/100) (100/100)
=100 ÷ 0.40 =100 ÷ 0.60 =90 ÷ 1
P/F = 250mmHg P/F = 166mmHg P/F = 90mmHg

Mild ARDS Moderate ARDS Severe ARDS

 Medical Management
• Treatment strategy depends of the category of ARDS,
and hemodynamic stability of the patient
• Treatment Goal: support respiration, treat cause,
prevent complication
• Treat the underline cause throughout the treatment
process
 Mild ARDS Treatment strategy HFNC

Hemodynamically
NIPPV BIPAP
Mild ARDS stable
P/F ratio 200-
300mmHg Hemodynamically Mechanical
CPAP
unstable Ventilation

High Flow Nasal Cannula (HFNC) BIPAP & CPAP

• High flow air (50 to 60L of air) • Supportive pressure:
• Reduces dead space inspiratory (IPAP) and
expiratory airway pressure
• Little bit of PEEP (0-5cmH2O) (EPAP/ PEEP)
• Controlled FiO2 • Controlled FiO2
Moderate to Severe ARDS treatment strategies

Alternative
Lung
ventilator
protective
Mode (VC &
ventilation
PC)
Proning
Moderate to severe Makes
ARDS patient
Mechanical
Sedation and comfortable
P/F ratio Ventilation
paralysis and prevent
<200mmHg Vent
asynchrony
Inhaled
pulmonary Nitric oxide
vasodilators
 Lung Protective Ventilation

Tidal Volume PEEP FiO2 Plateau Driving

Pressure Pressure
(Pplat) (ΔP)
• TV 4 – 6 • ≥ 5cmH2O • Avoid • <30cm H2O • = Pplat –
ml/kg(IPBW) • Prevent alveoli hyperoxygenation • = degree of lung PEEP
• ↑ TV → Barotrauma/ from collapsing (oxygen toxicity) injury • <15cmH2O →
Volutrauma in ARDS • Target FiO2 ≤ 60%, • ≥30 ↑barotrauma ↓ Mortality
(overdistention of (↓surfactant) SPO2 85-95%, PaO2 • If ↑ then ↓ TV not rate
alveoli) • ↑PEEP = ↑ depending on the less than 4ml/kg.
• Low TV → ↑PaCO2 oxygenation patient • If TV is lowest ↓
(permissive • ↑FiO2 = ↑ PEEP
 Proning

Most dependent areas

of ventilation is in the
posterior lung field
Clinical Progression of ARDS

Hypotension &
↓cardiac output,
Further Ultimately Death
Hypoxemia to
Respiratory
Dyspnea & Acidosis
Hypoxemia to
Metabolic acidosis

Hyperventilation
to Respiratory
Alkalosis
Nursing Management: 5 P’s of ARDS therapy
Perfusion Positioning Protective lung Protocol Preventing
Ventilation weaning complicatio
ns
• Evaluate volume status • In mild ARDS • Assees respiratory • Follow hospital Assess for
(BP, RR variation, CVP, Kinetic therapy status (RR, adventitious protocol • DVT
urine output) Give (bilateral turning breath sound, ↓ SPO2 • Off sedation day • Pressure Ulcers
fluid if required of a patient 40 every 4 hourly or after time • Nutritional
• Inotropic support if degrees or more every change PEEP/ TV) • Spontaneous status
cardiac output ↓ per side) breathing trials • VAP
(assess vital signs, skin • Proning in severe
color, tolerance to ARDS
treatment)

(ANA, 2022)
Lets Recall!