Title: ACUTE RESPIRATORY DISTRESS SYNDROME
1 ACUTE RESPIRATORY DISTRESS SYNDROME
University College of Medical Sciences GTB
Hospital, Delhi
2ARDS
- Definition
- Diagnosis
- Risk factors
- Pathophysiology
- Clinical features
- Management
3ARDS
- Severe, acute lung injury involving diffuse
alveolar damage, increased microvascular
permeability and non cardiogenic pulmonary edema - First defined by Ashbaugh and colleagues in 1967.
- Milder form of ARDS is Acute lung injury (ALI).
4American European Consensus Conference Criteria
for ALI ARDS
Clinical Variable ALI ARDS
Onset Acute Acute
Hypoxemia PaO2/FiO2 300 PaO2/FiO2200
Chest X-ray B/L infiltrates Consistent with pul. Edema B/L infiltrates Consistent with pul. Edema
Non-cardiac cause No clinical e/o left atrial HTN or pulm artery occlusion pressure 18 mmHg No clinical e/o left atrial HTN or pulm artery occlusion pressure 18 mmHg
5CARDIOGENIC VS NON-CARDIOGENIC EDEMA
Cardiogenic
Non-cardiogenic
1. Prior h/o cardiac disease
Absence of heart disease
2. Third heart sound
No third heart sound
3. Cardiomegaly
Normal sized heart
4. InfiltratesCentral distribution
Peripheral distribution
5. Widening of vascular pedicle
(? width of mediastinum)
Normal width of vascular pedicle
6. ? PA wedge pressure
N or ? PA wedge pressure
7. Positive fluid balance
Negative fluid balance
6ARDS
7ARDS exudative and fibrotic phases
Exudative (acute) phase
Fibrotic phase
8Murray Mathay Lung Injury Score
- Chest X film findings
- Alveolar consolidation Score
- One quadrant 1
- Two quadrant 2
- Three quadrant 3
- Four quadrant 4
- Oxygenation status (Hypoxemia Score)
- PaO2 / FiO2 Score
- gt 300 mmHg 0
- 225-299 mmHg 1
- 175-224 mmHg 2
- 100-174 mmHg 3
- lt 100 mmHg 4
9- Pulmonary compliance
- Compliance (ml/cmH2O) Score
- gt 80 0
- 60-79 1
- 40-59 2
- 20-39 3
- lt 19 4
- PEEP settings
- PEEP (cmH2O) Score
- lt 5 0
- 6-8 1
- 9-11 2
- 12-14 3
- gt 15 4
10- Acute lung injuries are assessed by dividing sum
of above points by 4, if - 0 points No pulmonary injury
- 1-2.5 points Mild to moderate
- gt 2.5 points Severe (ARDS)
11RISK FACTORS
Direct Lung Injury
- Aspiration of gastric contents
- Reperfusion pulmonary oedema - post lung
transplantation or pulmonary embolectomy
(N.Engl J Med 2000)
12RISK FACTORS
Indirect lung injury
13ARDS MECHANISM OF LUNG INJURY
- Activation of inflammatory mediators and cellular
components resulting in damage to capillary
endothelial and alveolar epithelial cells - Increased permeability of alveolar capillary
membrane - Influx of protein rich edema fluid and
inflammatory cells into air spaces - Dysfunction of surfactant
14HISTOPATHOLOGY
- Exudative phase (1st week)
- Alveolar and interstitial edema
- Capillary congestion
- Destruction of Type I alveolar cells
- Early hyaline membrane formation
- Proliferative Phase (2nd to 4th week)
- Increased type II alveolar cells
- Cellular infiltration of alveolar septum
- Organisation of hyaline membranes
- Fibrosis Phase (gt3 to 4 weeks)
- Fibrosis of hyaline membranes and alveolar septum
- Alveolar duct fibrosis
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16- INFLAMMATORY MEDIATORS IN ARDS
- IL-1, IL-6, IL-8
- MIP -1a
- Endothelin 1
- VWF
- Endotoxin
- Fas ligand
17PATHOPHYSIOLOGY
- Refractory hypoxemia shunting, dead space
ventilation - Alveolar collapse surfactant dysfunction, fluid
filled alveoli. - Decreased lung compliance
18CLINICAL FINDINGS IN ARDS
- Phase 1 Acute Injury
- Normal physical examination and chest X- Ray
- Tachycardia, Tachypnea, Respiratory alkalosis
- Phase 2 Latent Period
- Lasts approximately 6-48 hrs. after injury
- Patient appears clinically stable
- Hyperventilation and hypocapnia persists
- Mild increase in work of breathing
- Widening of alveolar-arterial oxygen gradient
- Minor abnormalities on physical examination and
chest x-ray
19- Phase 3 Acute Respiratory Failure
- Marked tachypnea and dyspnea
- Crepts
- Decreased Lung Compliance
- Diffuse infiltrates on chest x-ray
- Phase 4 Severe Abnormalities
- Severe Hypoxemia unresponsive to therapy
- Metabolic and respiratory acidosis
20MANAGEMENT OF ARDS
- Control of the causative factor
- Analgesia, antibiotics, sedation
- Nutritional support
- Optimization of hemodynamics
- Mechanical ventilation
- Adjuncts to low tidal volume ventilation
- Restrictive (dry) fluid management
- Permissive hypercapnia
- Prone positioning
- Recruitment maneuvers
21- MANAGEMENT OF ARDS
- Salvage intervention for patients with severe
hypoxemia with ARDS - Tracheal gas insufflation
- Inverse ratio ventilation
- ECMO
- HFOV
- Inhaled (NO, prostacyclin)
- corticosteroid
22VENTILATORY STRATEGY IN ARDS PATIENTS
- Traditional approach
- Open lung approach
- Lung protective ventilatory approach
- NIH NHLBI ARDS Clinical Network
23OPEN LUNG APPROACH
- On Static Pressure Volume curve of lung
- Lower Inflection Point (Pflex) most recruitable
alveoli opened, below which alveolar closure is
hypothesized to occur - Upper Inflection Point (UIP) beyond which
overdistention of alveolar units occurs, - PEEP set 2 cm H2O above Pflex
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25OPEN LUNG APPROACH
- Maintaining inflation deflation between 2
inflection points during entire respiratory cycle
is called Open Lung Ventilation - Ventilatory setting where PEEP gtPflex T.V is
reduced so that Pplat lt UIP is basis for lung
protective strategies - Advantages - avoids repetitive opening
closing of alveoli (AELECTRAUMA) - Traditional PEEP vs High PEEP study ALVEOLI
Trial -
26VILI
27ARDSnet protocol
- Calculated predicted body weight (PBW)
- Male 502.3height(inches)-60
- Female 45.52.3height(inches)-60
- Mode Volume assist-control
- Change rate to adjust minute ventilation
(notgt35/min) - pH goal 7.30-7.45
- Plateau presslt30cm H20
- PaO2 goal 55-80mmhg or SpO2 88-95
- FiO2/PEEP combination to achieve oxygenation goal
28ARDSnet protocol
- PEEP/FiO2 relationship to maintain adequate
PaO2/SpO2 - PaO2 goal 55-80mmHg or SpO2 88-95 use FiO2/PEEP
combination to achieve oxygenation goal
0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
5 5 8 8 10 10 10 12 14 14 14 16 18 20-24
FIO2
PEEP
29Mechanical ventilation in ARDSARDS network study
2000
Variable Setting
Ventilator mode Volume assist control
Tidal volume (ml/kg) 6 (adjusted acc. plateau press)
Plateau pressure (cm H2O) lt30
Rate 6-35
IE ratio 11 13
Oxygenation target
PaO2 (mmHg) 55 80
SpO2 () 88 95
PEEP FiO2 5-24 cmH2O lt0.6
30PERMISSIVE HYPERCAPNIA
- Strategy to minimize VILI
- Low tidal volume low peak airway pressures
- CO2 retention occurs
- Role of alkali ?
- Contraindications raised ICP
- acute CVA
- myocardial
ischemia - pulmonary
hypertension - uncorrected
severe metabolic acidosis - sickle cell
anemia - pregnancy
- ,
-
-
31INVERSE RATIO VENTILATION
- IE ratio gt 1
- Improvement in oxygenation by increases mean
airway pressure, auto PEEP, decreased deadspace
ventilation, improved V/Q mismatch, reduced
intrapulmonary shunting. - Advantages - lower peak alv press, ? FRC, ?ed
dead space ventilation, easily given through
modern ventilators. - Disadvantages barotrauma, sedation/muscle
paralysis required, worsening pulmonary edema.
32PRONE POSITION VENTILATION
- The prone ventilation of patients with ARDS first
described in the 1970s - Large RCT by Gattinoni and colleagues
- Suggested mechanisms include
- Better ventilation perfusion matching from
alteration in regional blood flow - Increase in functional residual capacity
- Alteration in respiratory mechanics and the
creation of more uniform lung expansion. Change
in regional diaphragm motion - Recruitment of collapsed alveoli
- Better clearance of secretions
33PROBLEMS OF PRONE POSITION
- Facial edema
- Airway obstruction
- Difficulties with enteral feeding
- Vascular and nerve compression
- Loss of venous accesses and probes
- Loss of chest drain and catheters
- Accidental extubation
- Apical atelectasis
- Increased need for sedation
- Pressure sores
34CONTRAINDICATIONS OF PRONE POSITION VENTILATION
- Unstable spine
- Head injury with raised ICP
- Unstable Cardiac rhythm
- Severe abdominal and soft tissue infection
35LIQUID VENTILATION
- Perflurocarbons carry 50ml/100ml of O2
200ml/100ml of CO2 - FRC filled with warmed, oxygenated PFC pt
ventilated from conventional ventilator - Mechanism alveolar recruitment, promotes
oxygenation, anti inflammatory action, attenuates
VILI. - Disadvantage high density
36FLUID MANAGEMENT
- Controversy regarding type of fluid
- Acute Respiratory Distress Network Study 05
(ARDSNet 05) Fluid and Catheter Treatment Trial
(FACTT) - conservative strategy of fluid
management is associated with improved lung
function and shortened duration of mechanical
ventilation and intensive care without increasing
non pulmonary-organ failures. - (NEJM June 15, 2006 Vol 354, No. 24, pp
2564-75 NEJM May 25, 2006 Vol 354, No. 21, pp
2213-24)
37NITRIC OXIDE IN ARDS
- NO is a selective pulmonary vasodilator
- NO acts selectively on well ventilated alveoli
bypassing fluid filled or collapsed alveoli - Improve ventilation-perfusion mismatch
- NO immunomodulator
- Very costly
- C/I absolute methemoglobinemia, relative
bleeding diathesis, intracranial bleed, severe LVF
38- ROLE OF OTHER DRUGS
- Surfactant therapy
- Surfactant dysfunction exist in ARDS, surfactant
decreases alveolar surface tension and alveolar
edema - Anticytokine effect inhibition of IL-1, IL-6,
TNF - Steroids
- Routine use not advocated esp. in acute phase
- NSAIDs
- Inhibit prstaglandin pathways esp. indomethacin
and ibuprofen - Other agents
- Ketoconazole inhibit Tx synthesis
- Pentoxyphylline
39COMPLICATIONS ASSOCIATED WITH ARDS
- Pulmonary barotrauma (volutrauma), pulmonary
embolism, pulmonary fibrosis, ventilator-associate
d pneumonia (VAP), Oxygen Toxicity - Gastrointestinal haemorrhage (ulcer),
dysmotility, pneumoperitoneum, bacterial
translocation - Cardiac Arrhythmias, myocardial dysfunction
- Renal acute renal failure (ARF), Fluid retention
- Mechanical vascular injury, tracheal
injury/stenosis (result of intubation and/or
irritation by endotracheal tube) - Nutritional malnutrition, anaemia, electrolyte
deficiency - Hematologic DIC, thrombocytopenia, anemia
- Infection sepsis, nosocomial pneumonia
40REFERENCES
- Christie JD, Lanken PN. Acute lung injury and the
acute respiratory distress syndrome. Critical
Care Hall - Harrisons Principle of Internal Medicine, 16th
ed. - Foner BJ, Norwood SH, Taylor RW. Acute
respiratory distress syndrome. Critical Care, 3rd
ed. Civetta - Allen B. Gilman, Parsons E. Polly.acute
respiratory failure due to ARDS and pulmonary
edema. Critical care-Irwin Rippe, 6th edition. - Mechanical ventilation Chang, 2nd ed.
- NIH NHLBI ARDS Clinical Network - Mechanical
Ventilation Protocol Summary 2000 - Wiener-Kronish JP, et al. The adult respiratory
distress syndrome definition and prognosis,
pathogenesis and treatment. BJA 1990 65 107-129.
41Thank You