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Ards PDF
Ards PDF
Ards PDF
• It is characterized by
▫ acute onset of severe hypoxemia
▫ signs of respiratory distress (dyspnoea, tachypnoea)
▫ diffuse bilateral infiltrates in the CXR
▫ no evidence of left atrial hypertension (PAWP<18mm
Hg).
Incidence
Four components:
1. Chest radiograph
2. PEEP score
3. Hypoxemia score
4. Respiratory system compliance score
Lung injury score
Chest radiograph
No alveolar consolidation 0
Alveolar consolidation confined to 1 quadrant 1
Score
No lung injury 0
• Advanced age
• Comorbid diseases
• Sepsis
• Liver dysfunction/ cirrhosis
• Non-pulmonary organ dysfunction
• Organ transplantation
• HIV infection
• Active malignancy
• Chronic alcoholism
• Mechanism of lung injury
Pathophysiology
3 phases –
1. Exudative/ Inflammatory
2. Proliferative
3. Fibrotic
1. Exudative Phase
Alveolar macrophages release
pro-inflammatory cytokines
(TNF-α, IL-1, IL-6, IL-8)
• 7-14 days
• Proliferation of inflammatory cells and fibroblasts
Obliteration of airspaces, atelectatic alveoli & poorly
compliant lung leads to
▫ persistent hypoxemia
▫ development of hypercarbia
▫ fibrosing alveolitis
▫ pulmonary hypertension
3. Fibrotic phase
• >14 days
6. Pulmonary compliance-
<30ml/ cm H2O
Easily measured in mechanically ventilated patients
7. Full bacteriological screen –
Blood , urine and tracheal aspirate cultures
Culture of other body secretions and discharges
Culture of bronchoalveolar lavage fluid.
8. Bronchoalveolar Lavage –
Very reliable & underutilized
In normal subjects, less than 5% of cells are neutrophils. In patients
with ARDS, upto 80% cells are neutrophils.
Lavage fluid is rich in protein in patients of ARDS as the
inflammatory exudates are rich in protein.
Hydrostatic edema: Lavage protein/ Plasma protein < 0.5
ARDS : Lavage protein/ Plasma protein > 0.7
Presence of a marker of pulmonary fibrosis called
procollagen peptide III (PCPIII) correlates with mortality.
Ventilatory management in ARDS
• In the early stages of ARDS, the hypoxia may be
corrected by 40 to 60% inspired oxygen with CPAP.
If all above criteria are met for at least 12 hours, initiate a trial of upto 120
minutes of spontaneous breathing with FiO2 < 0.5 and PEEP < 5:
1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with PS < 5
2. Assess for tolerance as below for up to two hours
a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg
b. Spontaneous VT ≥ 4 ml/kg PBW
c. RR ≤ 35/min
d. pH ≥ 7.3
e. No respiratory distress (distress= 2 or more)
1. HR > 120% of baseline
2. Marked accessory muscle use
3. Abdominal paradox
4. Diaphoresis
5. Marked dyspnoea
3. If tolerated for at least 30 minutes, consider extubation
4. If not tolerated resume pre-weaning settings.
Consequences of low tidal Contraindications of
volume ventilation : low tidal volume
ventilation:
Reduction in CO2 elimination via Increased intracranial
lungs – hypercapnia , respiratory pressure
acidosis , increased cardiac output. Stroke
Increased cerebral blood flow, Acute or chronic myocardial
cerebral edema, intracranial ischemia
hemorrhage Severe pulmonary
Leads to brainstem stimulation- hypertension
hyperventilation Right ventricular failure
Severe metabolic acidosis
Sickle cell anemia
TCA overdose
Beta blockers
Pregnancy
A strategy employing higher PEEP along with low tidal volume ventilation should be
considered for patients receiving mechanical ventilation for ARDS. This suggestion is
based on a 2010 meta-analysis of 3 randomized trials (n=2,229) testing higher vs.
lower PEEP in patients with acute lung injury or ARDS, in which ARDS patients
receiving higher PEEP had a strong trend toward improved survival.
Role of PEEP in ARDS
• PEEP avoids repetitive opening and collapse of atelectatic lung
units – could protect against VILI
• Improves arterial oxygenation
• Lung is kept open by using PEEP to avoid end expiratory
collapse
▫ Preserves inspiratory recruitment
▫ Re-establish end expiratory lung volume
▫ Prevent surfactant loss in airway
▫ Decreases intrapulmonary shunt
• Optimal /Best PEEP:
It is the minimum PEEP necessary to maintain adequate
PaO2 at non toxic FIO2 .
• It is required for optimization of arterial oxygenation without
introducing risk for oxygen toxicity and VILI, with least effect
on haemodynamics, oxygen delivery and airway pressures.
Adverse effects of PEEP
1. Decreased cardiac output
2. Increased pulmonary edema formation
3. Increased dead space & increased resistance of the bronchial
circulation
4. Increased lung volume and stretch during inspiration
lung injury or barotrauma.
• Permissive hypercapnia
• Fluid and hemodynamic management
• Inhaled nitric oxide
• Prone position ventilation
• Tracheal gas insufflation
• Steroids
• Nutritional support
• Other drug therapies
1.Permissive hypercapnia
• Result – improved lung function, improved central nervous system function, less
sedation, mechanical ventilation , less complications
• Avoiding a positive fluid balance in ARDS patients reduces the time on mechanical
ventilation and also mortality.
3. Haemodynamic management
Inotropes
Dobutamine is preferred- because vasodilators increase
intrapulmonary shunt
Dopamine – constricts pulmonary veins , rise in pulmonary capillary
hydrostatic pressure
4. Prone ventilation
• Mechanism –
Increased FRC
Change in regional diaphragmatic motion
Perfusion redistribution – better oxygenation
Improved clearance of secretions
• Limitations:
Need extra care- prevent pressure necrosis
Secure ET
Dislodgement of line or chest tube
Hemodynamic instability
GATTINONI AND COLLEAGUES – multicentre prospective
randomized trial ( 2001 )-No survival advantage, salvage
therapy
Prone position
Risks-
Tracheal erosion
Oxygen toxicity due to increased Fio2
Hemodynamic compromise
Barotraumas
Salvage therapy
7. Steroids
• Goals-
▫ Provision of adequate nutrition
▫ Prevention and treatment of deficiencies
• Diagnosis- Echocardiography