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ACUTE RESPIRATORY DISTRESS SYNDROME

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ACUTE RESPIRATORY DISTRESS SYNDROME Dr. Poonam Patel University College of Medical Sciences & GTB Hospital, Delhi CONTRAINDICATIONS OF PRONE POSITION VENTILATION ... – PowerPoint PPT presentation

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Title: ACUTE RESPIRATORY DISTRESS SYNDROME


1
ACUTE RESPIRATORY DISTRESS SYNDROME
  • Dr. Poonam Patel

University College of Medical Sciences GTB
Hospital, Delhi
2
ARDS
  • Definition
  • Diagnosis
  • Risk factors
  • Pathophysiology
  • Clinical features
  • Management

3
ARDS
  • 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).

4
American 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
5
CARDIOGENIC 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
6
ARDS
7
ARDS exudative and fibrotic phases
Exudative (acute) phase
Fibrotic phase
8
Murray 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)

11
RISK FACTORS
Direct Lung Injury
  • Pneumonia
  • Aspiration of gastric contents
  • Toxic inhalation
  • Near drowning
  • Pulmonary contusion
  • Fat embolism
  • Reperfusion pulmonary oedema - post lung
    transplantation or pulmonary embolectomy

(N.Engl J Med 2000)
12
RISK FACTORS
Indirect lung injury
  • Sepsis
  • Severe trauma
  • Acute pancreatitis
  • Cardiopulmonary bypass
  • Massive transfusions
  • Drug over dose

13
ARDS 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

14
HISTOPATHOLOGY
  • 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

15
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16
  • INFLAMMATORY MEDIATORS IN ARDS
  • IL-1, IL-6, IL-8
  • MIP -1a
  • Endothelin 1
  • VWF
  • Endotoxin
  • Fas ligand

17
PATHOPHYSIOLOGY
  • Refractory hypoxemia shunting, dead space
    ventilation
  • Alveolar collapse surfactant dysfunction, fluid
    filled alveoli.
  • Decreased lung compliance

18
CLINICAL 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

20
MANAGEMENT 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

22
VENTILATORY STRATEGY IN ARDS PATIENTS
  • Traditional approach
  • Open lung approach
  • Lung protective ventilatory approach
  • NIH NHLBI ARDS Clinical Network

23
OPEN 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

24
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25
OPEN 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

26
VILI
27
ARDSnet 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

28
ARDSnet 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
29
Mechanical 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
30
PERMISSIVE 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
  • ,


31
INVERSE 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.

32
PRONE 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

33
PROBLEMS 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

34
CONTRAINDICATIONS OF PRONE POSITION VENTILATION
  • Unstable spine
  • Head injury with raised ICP
  • Unstable Cardiac rhythm
  • Severe abdominal and soft tissue infection

35
LIQUID 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

36
FLUID 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)

37
NITRIC 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

39
COMPLICATIONS 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

40
REFERENCES
  • 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.

41
Thank You
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