ARDS

ARDS
ACUTE RESPIRATORY
DISTRESS SYNDROME
Pathophysiology of ARDS -Apr 2018
DEFINITION
• Berlin definition of ARDS (2012)

ETIOLOG
Y
PATHOPHYSIOLOGY/ Pathogenesis
• Direct injury - regional consolidation , alveolar damage
• Indirect injury - pulmonary vascular congestion, interstitial edema, and less
severe alveolar involvement .
• Damage to capillary endothelium & alveolar epithelium → disruption of

normal epithelial fluid transport, impaired reabsorption of edema fluid.
• Damage to Type I & Type II pneumatocytes → Impaired surfactant production,
re epithelization & repair of damaged alveoli.
PATHOPHYSIOLOGY/ Pathogenesis
• Cytokine related inflammation
• Activated macrophages→ chemotaxis & activated neutrophils
• VILI – increased pulmonary edema in uninjured & injured lung → MOD
• Fibrotic stage (after 5-7 days) → Fibrosing alveolitis

• - Initiated by IL 1, TNF &other Cytokines
• Alveoli filled with mesenchymal cells, collagen, new blood vessels,
• Resolution stage
– Removal of Soluble proteins : by diffusion in between epithelial cells & interstitium,
Insoluble proteins : by endocytosis & phagocytosis by macrophages.
• Type II cells – initiate re epithelization & repair of alveoli.

Phases of ARDS
Acute- Exudative inflammatory ( 0-3 Days )
• characterized by the acute development of decreased pulmonary compliance and arterial
hypoxemia.
Subacute – Proliferative ( 4-10 days)
• increased alveolar dead space and refractory pulmonary hypertension may develop
• as a result of chronic inflammation and scarring of the alveolar-capillary unit.
Chronic- Fibrotic phase fibrosing alveolitis ( >10 days )

MANIFESTATIONS
SYMPTOMS
• Dyspnoea
• Increased work of breathing
• anxiety, agitation
SIGNS
• Diminished breath sounds
• Crepitations
• Hypoxemia refractory to supplemental O2
• Hypercarbia
• Acidosis.
•
Xray – B/l infiltrates – patchy, asymmetric, may associated pleural effusion
In progressive fibrosing alveolitis

• persistent hypoxemia, decreasing compliance
• Pulmonary HT
• Rt ventricular failure
DIFFERENTIAL DIAGNOSIS
1. Congestive Cardiac Failure
2. Interstitial Lung Disease
3. Connective tissue diseases (Polymyositis)
4. Endobronchial Tuberculosis
5. Diffuse alveolar hemorrhage (vasculitis)

INVESTIGATIONS
1. ABG:
Arterial blood gases reveal hypoxemia
which is often accompanied by acute respiratory alkalosis
High concentrations of supplemental oxygen are generally required
2. CXR will reveal b/l Patchy infiltrates
3. CT scan
will reveal patchy distribution of disease
with areas of atelectasis and
MANAGEMENT
MAIN GOALS
❑Treatment of Underlying disorder
❑Provide adequate oxygenation and ventilation without causing iatrogenic harm
❑Support multiple organs system showing dysfunction

MANAGEMENT
Control of underlying disease/infection – Antibiotics
Respiratory support :
• Basic ventilation strategies : Goal – maintain adequate oxygenation, minimize
VILI,
Lung protective strategies –

1. Avoid regional overinflation (Baby lung concept)
2. Avoid repeated opening/closing of alveoli (Open lung strategy)
3. Permissive hypercapnia
4. Permissive Hypoxemia
Intubation and Mechanical Ventilation
• effective way of optimizing oxygenation and ventilation in patients of ARDS
• emphasis has shifted from achieving near normal blood gas values of PaO2 &
PCO2 to providing sufficient oxygenation & ventilation while ensuring lung
protection & avoiding ventilator induced lung injury
• This has led to use of so-called Lung Protective Settings
Lung Protective Settings

▪ Lower FiO2
▪ Limiting Plateau Pressures to < 30 cm H20
▪ Low Tidal Volume : 6-8 ml/kg
▪ Target PaO2 : 60-80 mmHg
▪ Target pH : > 7.25
INITIAL VENTILATOR SETTINGS
• TV : <6ml/kg (adjusted acc to Pplat)
• Pplat <30 cm H2O
• Rate : 15 to 35
• I:E – 1:1 to 1:3
• PEEP & FiO2 is set acc to predetermined combinations (PEEP 5-24 ) FiO2 < 60%
• Oxygenation target : PaO2 : 55-80 mm Hg, SpO2 88-95%
• However in severe ARDS – SPO2 (85%) and PaO2 upto 60% is acceptable
• Maintain Hb at least 10g/dl
• Selection of PEEP :
• Higher PEEP & low FiO2 preferred
• Titration of PEEP and FiO2 according to lung recruitability
BABY LUNG CONCEPT
• In most patients of ARDS, normally aerated tissue has dimension of 5-6 year old child (300-500gm
aerated tissue)
• Compliance is linearly related to baby lung quality i.e ARDS lung is not only stiff but also small
with nearly normal intrinsic elasticity in early phases
• This concept provides rationale for gentle ventilation d/t risk of VILI (at TV >8 ml/kg)
OPEN LUNG STRATEGY

• Preventing repeated opening and closing of alveolar segments is believed to be more protective
for lungs
• Similarly preventing overstretching and overdistention of the alveoli is considered to be desirable
• This is achieved by using adequate PEEP in the range of 5-18 cm of H20
• High frequency Oscillatory (HFO) Ventilation is considered as ideal protective ventilation by
providing optimal recruitment of lungs
PRONE POSITIONING
• It has been used as an adjuvant therapy to the ventilator management
• Child is proned for at least 18 hours or more every day
ADVANTAGES :
• Physiologically, it improves V/Q matching
• Improves aeration to dorsal portion of lungs
• Helps in recruiting dependent alveoli
• increase lung volume and reduce the amount of atelectatic regions;
• facilitate the drainage of secretions; and
• reduce ventilator-associated lung injury
DISADVANTAGES :
• Accidental dislodgement of ET tube or vascular access
• Pressure related ulcers
PERMISSIVE HYPERCAPNIA
• As far as pH is maintained >7.15 ( PaCO2 is accepted upto 80mm Hg)
• But in septic patient , correct acidosis to improve outcome.
• Hypothesis – Hypercapneic acidosis is beneficial as it downregulates inflammatory cell activity
and xanthine oxidase activity thus reducing oxidative stress.
• C/I in Traumatic brain injury & Cardiac dysfunction
Stepwise treatment of Hypoxemia

• PIP/PEEP titration
• Prone position
• HFOV
• Surfactant
• Inhaled NO
• Corticosteroids
• ECMO
HFO Ventilation
• Introduced by Lunkenheimer 1972
• Expiration and Inspiration active process
• VT 1-3ml/kg ,freq 100 - 2400/min
• Prevents air trapping,over distension and CVS depression
• Applied for severe ARDS
• better oxygenation
• Early institution may be beneficial
• Considered in pts requiring high Pressures
• FiO2 req >60%
• Failure to improve oxygenation index within 24-48hrs
• Non responders to HFOV have high mortality.
Fluid management in ARDS
• Total body fluid overload seems to be associated with worsening pulmonary
compliance , hypoxemia & unfavorable outcomes
• Fluid restriction after initial shock resuscitation or diuresis often shows improved
oxygenation
Nutrition in ARDS
• Ensuring adequate nutrition despite fluid restriction is essential for healing of
lungs and for weaning from ventilator
• Enteral nutrition is possible in most children and chances of success of enteral
feeds are higher with transpyloric feeding
EXTRACORPOREAL MEMBRANE OXYGENATION
• It has been used as a rescue therapy for supporting oxygenation and ventilation when conventional treatment
has failed
• Lack of clear outcome benefits
• It also helps in reducing potential for ventilator induced lung injury by minimizing settings on conventional
ventilator
ECMO is of two types :

a) Venovenous
b) Venoarteial
Other treatment modalities

• Surfactant: -ARDS often leads to a secondary deficiency of surfactant due to destruction of Type II cells &
inflammatory exudates
-Roll of surfactant in ARDS remains controversial
• Inhaled Nitric Oxide

• Corticosteroids
• Muscle relaxants
Summary – Management strategy of ARDS
Summary – Management strategy of ARDS
Complications
• Multiple Organ System Failure

• AKI
• Renal Failure
• Barotrauma
• Air leaks : Pneumothorax , Pneumomediastinum, Subcutaneous emphysema
• Ventilator associated lung injury
• Secondary infections due to ET tube, IV lines , catheters
• Prolonged mech. Ventilation , need for tracheostomy
• Muscular weakness
Prognostic factors
Predictor of poor outcome :
o Severe hypoxemia (low PaO2/fiO2 ratios)
o Multiple organ system failure
o Pre-existing immunocompromised state

ARDS

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ARDS

• Berlin definition of ARDS (2012)

• Damage to capillary endothelium & alveolar epithelium → disruption of

• Fibrotic stage (after 5-7 days) → Fibrosing alveolitis

• Type II cells – initiate re epithelization & repair of alveoli.

Subacute – Proliferative ( 4-10 days)

Chronic- Fibrotic phase fibrosing alveolitis ( >10 days )

Xray – B/l infiltrates – patchy, asymmetric, may associated pleural effusion

In progressive fibrosing alveolitis

1. Congestive Cardiac Failure

2. Interstitial Lung Disease

3. Connective tissue diseases (Polymyositis)

5. Diffuse alveolar hemorrhage (vasculitis)

2. CXR will reveal b/l Patchy infiltrates

❑Treatment of Underlying disorder

❑Provide adequate oxygenation and ventilation without causing iatrogenic harm

❑Support multiple organs system showing dysfunction

Lung protective strategies –

Lung Protective Settings

OPEN LUNG STRATEGY

Stepwise treatment of Hypoxemia

ECMO is of two types :

Other treatment modalities

• Inhaled Nitric Oxide

• Multiple Organ System Failure

Predictor of poor outcome :

o Severe hypoxemia (low PaO2/fiO2 ratios)

o Multiple organ system failure

o Pre-existing immunocompromised state

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