Acute Respiratory Distress Syndrome - PowerPoint PPT Presentation


Title: Acute Respiratory Distress Syndrome


1
Acute Respiratory Distress Syndrome
  • Allen H. Roberts II, M.D.
  • Associate Professor of Medicine
  • Georgetown University HospitalMarch 2009

2
Case 1
  • 66 yo male admitted to ICU with dyspnea, O2
    desaturation. Has unilateral ureteral
    obstruction and bacteremia. CXR shows patchy
    bilateral infiltrates
  • After removal of a ureteral stone and institution
    of antibiotics, his oxygenation improved and the
    infiltrates resolved.

3
Case 2
  • 55 yo male admitted to SICU ESLD secondary to
    EtOH presented with LLL pneumonia 3 days prior.
    Developed hypoxemic respiratory failure requiring
    mechanical ventilation. Progressive airway
    pressure elevation and refractory hypoxemia on AC
    mode.
  • Transitioned to APRV
  • Progressive hypotension
  • Barotrauma
  • Multisystem failure
  • Death

4
(No Transcript)
5
Acute Lung Injury/ARDS
  • Definitions
  • Clinical settings / Presentation
  • Pathophysiology / Natural History
  • Ventilator Strategies Problems
  • Non-Ventilator Management

6
Acute Lung Injury/ARDS Definitions
  • Acute Lung Injury acute lung inflammation with
    increased vascular permeability- - bilateral
    widespread infiltrates - PaO2/FiO2 lt 300 mmHg -
    PAWP lt 18 mmHg (if measured)
  • ARDS - PaO2/FiO2 lt 200 mmHgBernard et al
    AJRCCM 1994 American-European Consensus
    Conference on ARDS

7
ARDS Incidence
  • Age adjusted incidence 86 per
    100,000 person-years
  • In-hospital mortality 38.5 - (60 in patients
    gt 85 y.o.)
  • 191,000 annual cases in US

  • Rubenfeld et al NEJM 2005 3531685-93

8
ARDS Clinical Settings
9
ARDS Clinical Features
  • Pts at risk
  • Onset of dyspnea, gas exchange abnormality within
    12-48 h of inciting event
  • S/S of underlying disorder may predominate early
  • Course can be variable not all require vent
  • Generally resp failure is HYPOXEMIC

10
ARDS in ICU
  • Patient at risk
  • Several days into unit stay primary process
    may be resolving
  • Increasing FiO2 requirementShunt physiology
  • Need to add PEEP to oxygenate or to down-titrate
    FiO2
  • CXR evolving diffuse infiltrates

11
(No Transcript)
12
ARDS Radiographic
  • Early, CXR may be normal transient!
  • Patchy or homogeneous diffuse, bilateral
    infiltrates
  • Patchy areas may coalesce white out
  • Diffuse alveolar infiltrates may clear somewhat
    leaving interstitial, then fibrotic
    patternor..CXR will clear with minimal
    residual
  • Findings of barotrauma pneumothorax,
    pneumomediastinum, etc.

13
ARDS CXR - Differential Diagnosis
  • Acute Lung Injury
  • Diffuse pneumonia (eg pneumococcal, Legionella)
  • Acute interstitial pneumonia (AIP)
  • Acute eosinophilic pneumonia
  • Cardiogenic Pulmonary edema
  • Diffuse alveolar hemorrhage
  • ARDS can coexist with other processes!

14
(No Transcript)
15
ARDS Pathophysiology
  • Insult! Cytokines!!
  • PMN infiltration predominate in BAL
    profilePathology Exudative
    Fibroproliferative
    Fibrotic
  • Type II Pneumocyte damage decreased surfactant
    atelectasis
  • Loss of compliance
  • Shunt, VQ mismatch, Diffusion abnormality
    HYPOXEMIA

16

Piantadosi, Annals of Int Med 2004,141460-470
17
(No Transcript)
18
Piantadosi, Annals Int Med 2004 141460-470
19
Piantadosi, Annals of Int Med 2004,141460-470
20
ARDS Cytokines
  • ProinflammatoryTNF, IL-1, Il-6, IL-8 -
    elevated in plasma and BAL fluid of pts at risk
    for and with ARDS - predictive of mortality
    (ARDSNET) Frank et al
    Chest 2006 1301906-1914

21
Cytokines in ALI/ARDS
  • 44 patients randomized to - control
    (traditional) vent targeted to normalize PaCO2
    vs - study (lung protective) low Tidal
    Volume VT titrated based on pressure volume
    curve with strategy to minimize overinflation
    high airway pressures

  • Ranieri et al JAMA 282(1) July 1999

22
Cytokines in ALI/ARDS
  • ControlVT 11.1 cc/kgPEEP 6.5
  • StudyVT 7.6 cc/kgPEEP 14.8

  • Ranieri et al JAMA 282(1) July 1999

23
Cytokines, continued
  • In study group (low VT, lung protective), lower
    levels of TNF, IL1, IL6 were found in BAL (plt.05)
  • Mechanical ventilation induces a cytokine
    response which is minimized by lung protective
    strategies. Ranieri et al JAMA
    282(1) July 1999

24
(No Transcript)
25
(No Transcript)
26
(No Transcript)
27
(No Transcript)
28
(No Transcript)
29
(No Transcript)
30
(No Transcript)
31
ARDS Off to the Unit
  • Impaired Gas Exchange initially, respiratory
    alkalosis with widened A-a gradientinvariably
    progresses to frank hypoxemia.
  • Shunt, diffusion, and VQ mismatch physiology
  • Decreased Lung Compliance edema surfactant
    loss, atelectasishyaline membranes increased
    work of breathing
  • Pulmonary Hypertension hypoxic vasoconstriction
    (early)diffuse lung remodeling (late)

32
Ventilation General Approach
  • Can attempt noninvasive (dont count on it)
  • Intubate early if the clinical trajectory is
    clear
  • Prepare for hemodynamic consequences of
    intubation positive pressure ventilation
  • Goal Adequate Oxygenation with Avoidance of
    Complications

33
ARDS The Old Days
  • Start with Volume Cycled, Assist Control
  • As compliance decreases and airway pressures
    rise, - transition to Pressure Control set a
    maximum airway pressure tidal volume
    dependent variable minute ventilation (VE)
    not stable extremely uncomfortable for
    patient heavy sedation, neuromuscular
    blockade

34
Mechanical Ventilation in ARDSCurrent Theory
  • Closed lung strategy - ARDSNET protocol low
    tidal volume, lung protective
    vs
  • Open lung strategy - Airway Pressure Release
    Ventilation (APRV)
  • - AC with recruiting maneuvers

35
Volume-Cycled Ventilation Assist Control
(ACCMV)
  • Conventional, familiar start with this
  • Set Vt, rate (Vt x rate Ve)therefore
    guaranteed Ve ( minute ventilation)
  • Problem non-compliant lung set Vt gives high
    airway pressures barotrauma

36
ARDSNET
  • 831 patients randomized to conventional VT 12
    cc/kg vs study VT 6cc/kg
  • Enrollment stopped because of mid-study analysis
    showing improved survival in lower VT
    group(mortality 40 vs 31)ARDSNET, NEJM
    3421301-1308, 2000

37
NEJM 3421301-1308, 2000 The ARDSNET Study
38
What about patients without ARDS?
  • Retrospective review of 332 patients without ARDS
    at admission to ICU
  • 80 developed ARDS
  • Multivariate analysis ARDS associated with -
    large VT (OR 1.3 for each cc/kg above 6) - blood
    products - acidemia - h/o restrictive lung
    diseaseGajic et al Critical Care Medicine
    200432(9)1817-1824

39
  • Gajic et al Critical Care Medicine
    200432(9)1817-1824

40
(No Transcript)
41
(No Transcript)
42
Piantadosi Annals 2004
43
(No Transcript)
44
PEEP
  • ARDSNET Patients
  • Randomized 549 pts to receive low PEEP
    (8.9/-3.5 cm) vshigh PEEP (14.7 /-
    3.5 cm)ARDSNET NEJM 351(4) 327-336 2004

45
ARDSNET PEEP NEJM 2004, 351(4)327-36
46
(No Transcript)
47
ARDSNET Published Conclusions 2000-2006
  • Low VT associated with improved survival
  • Optimal PEEP not definedhigher PEEP had no
    survival advantage

48
Steroids for ARDS?
  • Meduri et al, early 1990s subgroup of patients
    with ARDS had clinical radiographic improvement
    on 1-2 mg/kg methylprednisolone during the
    fibroproliferative phase.
  • Infection sought pretreatment with BAL, some OLBx

49
Steroids ARDSNET
  • 180 pts randomized to methylprednisolone vs
    placebo
  • Primary endpoint - 60 day mortality
  • Secondary endpoints vent-free
    organ-failure-free days complications
  • NEJM 2006 3541671-84

50
Steroids ARDSNET
  • 60 day mortality - 28.6 (placebo) vs 29.2
    (ns) - higher mortality with steroids if
    enrolled gt14 days after ARDS onset
  • Greater incidence of neuromuscular weakness
  • No increase in rate of infectious complications
    NEJM
    2006 3541671-84

51
ARDSNET 2006 354(16) 1671-1684
52
ARDSNET 2006354(16) 1671-83
53
ARDSNET Published Conclusions 2000-2006
  • Low VT associated with improved survival
  • Optimal PEEP not definedhigher PEEP had no
    survival advantage
  • Steroid treatment showed no benefit and some
    potential adverse effects - in general NOT
    recommended

54
Steroids, continued
  • 91 patients w/ARDS randomized to continuous
    low-dose methylprednisolone vs placebo
  • Treated patients had - earlier reduction in
    lung injury score - reduced time on vent p.002
    - reduced ICU stay p .007 - reduced ICU
    mortality (21 vs 43) p.03 - lower rate of ICU
    infections p .0002
  • Attributed to steroid-induced down-regulation of
    systemic inflammation
  • Meduri et al Chest 2007 131954
    - 963

55
No Survival Advantage
  • Prone position
  • Nitric oxide
  • Liquid ventilation with fluorocarbons
  • Intratracheal instillation of recombinant
    surfactant
  • Use of Pulmonary Artery Catheter to help guide
    treatment

56
Alternatives to ARDSNET
  • Pressure control- inverse ratio
    ventilation(PC-IRV)
  • Airway pressure release ventilation (APRV)
  • High frequency oscillatory ventilationAll modes
    may improve oxygenation because of sustained
    recruitment, but to date none is known to offer a
    survival advantage.

57
APRV
Habashi, N. CCM 33(3)S228-240, 2005
58
ARDS Outcome
  • Mortality 60 down to 30 1983 1996.Felt
    largely due to improved CCM capabilities rather
    than ARDS-specific therapy.
  • Survivors have pulmonary restriction early after
    dischargeimproved PFTs plateau by 1 year.Many
    return to nl spirometry /- reduced DLCO.
  • Significant neuropsychiatric issues may persist

59
Rubenfeld et al NEJM 2005 353(16)1685-93
60
ARDS- Survival Follow-up
  • One year post discharge, 49 of survivors had
    returned to work, most to prior positions
  • Those not returning - persistent weakness
    fatigue - job stress - poor mobility - poor
    functional statusHerridge et al NEJM 2003
    348(8)683-93

61
Herridge et al NEJM 2003, 348(8) 683-93
62
ARDS Conclusion
  • Index of suspicion in pts at risk who develop
    resp sx or infiltrates
  • Intubate early when it appears inevitable
  • Low tidal volume
  • Titrate FiO2 and PEEP
  • Transition to APRV as rescue
  • Steroids party line vs bottom line
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Acute Respiratory Distress Syndrome

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Title: Acute Respiratory Distress Syndrome


1
Acute Respiratory Distress Syndrome
  • Allen H. Roberts II, M.D.
  • Associate Professor of Medicine
  • Georgetown University HospitalMarch 2009

2
Case 1
  • 66 yo male admitted to ICU with dyspnea, O2
    desaturation. Has unilateral ureteral
    obstruction and bacteremia. CXR shows patchy
    bilateral infiltrates
  • After removal of a ureteral stone and institution
    of antibiotics, his oxygenation improved and the
    infiltrates resolved.

3
Case 2
  • 55 yo male admitted to SICU ESLD secondary to
    EtOH presented with LLL pneumonia 3 days prior.
    Developed hypoxemic respiratory failure requiring
    mechanical ventilation. Progressive airway
    pressure elevation and refractory hypoxemia on AC
    mode.
  • Transitioned to APRV
  • Progressive hypotension
  • Barotrauma
  • Multisystem failure
  • Death

4
(No Transcript)
5
Acute Lung Injury/ARDS
  • Definitions
  • Clinical settings / Presentation
  • Pathophysiology / Natural History
  • Ventilator Strategies Problems
  • Non-Ventilator Management

6
Acute Lung Injury/ARDS Definitions
  • Acute Lung Injury acute lung inflammation with
    increased vascular permeability- - bilateral
    widespread infiltrates - PaO2/FiO2 lt 300 mmHg -
    PAWP lt 18 mmHg (if measured)
  • ARDS - PaO2/FiO2 lt 200 mmHgBernard et al
    AJRCCM 1994 American-European Consensus
    Conference on ARDS

7
ARDS Incidence
  • Age adjusted incidence 86 per
    100,000 person-years
  • In-hospital mortality 38.5 - (60 in patients
    gt 85 y.o.)
  • 191,000 annual cases in US

  • Rubenfeld et al NEJM 2005 3531685-93

8
ARDS Clinical Settings
9
ARDS Clinical Features
  • Pts at risk
  • Onset of dyspnea, gas exchange abnormality within
    12-48 h of inciting event
  • S/S of underlying disorder may predominate early
  • Course can be variable not all require vent
  • Generally resp failure is HYPOXEMIC

10
ARDS in ICU
  • Patient at risk
  • Several days into unit stay primary process
    may be resolving
  • Increasing FiO2 requirementShunt physiology
  • Need to add PEEP to oxygenate or to down-titrate
    FiO2
  • CXR evolving diffuse infiltrates

11
(No Transcript)
12
ARDS Radiographic
  • Early, CXR may be normal transient!
  • Patchy or homogeneous diffuse, bilateral
    infiltrates
  • Patchy areas may coalesce white out
  • Diffuse alveolar infiltrates may clear somewhat
    leaving interstitial, then fibrotic
    patternor..CXR will clear with minimal
    residual
  • Findings of barotrauma pneumothorax,
    pneumomediastinum, etc.

13
ARDS CXR - Differential Diagnosis
  • Acute Lung Injury
  • Diffuse pneumonia (eg pneumococcal, Legionella)
  • Acute interstitial pneumonia (AIP)
  • Acute eosinophilic pneumonia
  • Cardiogenic Pulmonary edema
  • Diffuse alveolar hemorrhage
  • ARDS can coexist with other processes!

14
(No Transcript)
15
ARDS Pathophysiology
  • Insult! Cytokines!!
  • PMN infiltration predominate in BAL
    profilePathology Exudative
    Fibroproliferative
    Fibrotic
  • Type II Pneumocyte damage decreased surfactant
    atelectasis
  • Loss of compliance
  • Shunt, VQ mismatch, Diffusion abnormality
    HYPOXEMIA

16

Piantadosi, Annals of Int Med 2004,141460-470
17
(No Transcript)
18
Piantadosi, Annals Int Med 2004 141460-470
19
Piantadosi, Annals of Int Med 2004,141460-470
20
ARDS Cytokines
  • ProinflammatoryTNF, IL-1, Il-6, IL-8 -
    elevated in plasma and BAL fluid of pts at risk
    for and with ARDS - predictive of mortality
    (ARDSNET) Frank et al
    Chest 2006 1301906-1914

21
Cytokines in ALI/ARDS
  • 44 patients randomized to - control
    (traditional) vent targeted to normalize PaCO2
    vs - study (lung protective) low Tidal
    Volume VT titrated based on pressure volume
    curve with strategy to minimize overinflation
    high airway pressures

  • Ranieri et al JAMA 282(1) July 1999

22
Cytokines in ALI/ARDS
  • ControlVT 11.1 cc/kgPEEP 6.5
  • StudyVT 7.6 cc/kgPEEP 14.8

  • Ranieri et al JAMA 282(1) July 1999

23
Cytokines, continued
  • In study group (low VT, lung protective), lower
    levels of TNF, IL1, IL6 were found in BAL (plt.05)
  • Mechanical ventilation induces a cytokine
    response which is minimized by lung protective
    strategies. Ranieri et al JAMA
    282(1) July 1999

24
(No Transcript)
25
(No Transcript)
26
(No Transcript)
27
(No Transcript)
28
(No Transcript)
29
(No Transcript)
30
(No Transcript)
31
ARDS Off to the Unit
  • Impaired Gas Exchange initially, respiratory
    alkalosis with widened A-a gradientinvariably
    progresses to frank hypoxemia.
  • Shunt, diffusion, and VQ mismatch physiology
  • Decreased Lung Compliance edema surfactant
    loss, atelectasishyaline membranes increased
    work of breathing
  • Pulmonary Hypertension hypoxic vasoconstriction
    (early)diffuse lung remodeling (late)

32
Ventilation General Approach
  • Can attempt noninvasive (dont count on it)
  • Intubate early if the clinical trajectory is
    clear
  • Prepare for hemodynamic consequences of
    intubation positive pressure ventilation
  • Goal Adequate Oxygenation with Avoidance of
    Complications

33
ARDS The Old Days
  • Start with Volume Cycled, Assist Control
  • As compliance decreases and airway pressures
    rise, - transition to Pressure Control set a
    maximum airway pressure tidal volume
    dependent variable minute ventilation (VE)
    not stable extremely uncomfortable for
    patient heavy sedation, neuromuscular
    blockade

34
Mechanical Ventilation in ARDSCurrent Theory
  • Closed lung strategy - ARDSNET protocol low
    tidal volume, lung protective
    vs
  • Open lung strategy - Airway Pressure Release
    Ventilation (APRV)
  • - AC with recruiting maneuvers

35
Volume-Cycled Ventilation Assist Control
(ACCMV)
  • Conventional, familiar start with this
  • Set Vt, rate (Vt x rate Ve)therefore
    guaranteed Ve ( minute ventilation)
  • Problem non-compliant lung set Vt gives high
    airway pressures barotrauma

36
ARDSNET
  • 831 patients randomized to conventional VT 12
    cc/kg vs study VT 6cc/kg
  • Enrollment stopped because of mid-study analysis
    showing improved survival in lower VT
    group(mortality 40 vs 31)ARDSNET, NEJM
    3421301-1308, 2000

37
NEJM 3421301-1308, 2000 The ARDSNET Study
38
What about patients without ARDS?
  • Retrospective review of 332 patients without ARDS
    at admission to ICU
  • 80 developed ARDS
  • Multivariate analysis ARDS associated with -
    large VT (OR 1.3 for each cc/kg above 6) - blood
    products - acidemia - h/o restrictive lung
    diseaseGajic et al Critical Care Medicine
    200432(9)1817-1824

39
  • Gajic et al Critical Care Medicine
    200432(9)1817-1824

40
(No Transcript)
41
(No Transcript)
42
Piantadosi Annals 2004
43
(No Transcript)
44
PEEP
  • ARDSNET Patients
  • Randomized 549 pts to receive low PEEP
    (8.9/-3.5 cm) vshigh PEEP (14.7 /-
    3.5 cm)ARDSNET NEJM 351(4) 327-336 2004

45
ARDSNET PEEP NEJM 2004, 351(4)327-36
46
(No Transcript)
47
ARDSNET Published Conclusions 2000-2006
  • Low VT associated with improved survival
  • Optimal PEEP not definedhigher PEEP had no
    survival advantage

48
Steroids for ARDS?
  • Meduri et al, early 1990s subgroup of patients
    with ARDS had clinical radiographic improvement
    on 1-2 mg/kg methylprednisolone during the
    fibroproliferative phase.
  • Infection sought pretreatment with BAL, some OLBx

49
Steroids ARDSNET
  • 180 pts randomized to methylprednisolone vs
    placebo
  • Primary endpoint - 60 day mortality
  • Secondary endpoints vent-free
    organ-failure-free days complications
  • NEJM 2006 3541671-84

50
Steroids ARDSNET
  • 60 day mortality - 28.6 (placebo) vs 29.2
    (ns) - higher mortality with steroids if
    enrolled gt14 days after ARDS onset
  • Greater incidence of neuromuscular weakness
  • No increase in rate of infectious complications
    NEJM
    2006 3541671-84

51
ARDSNET 2006 354(16) 1671-1684
52
ARDSNET 2006354(16) 1671-83
53
ARDSNET Published Conclusions 2000-2006
  • Low VT associated with improved survival
  • Optimal PEEP not definedhigher PEEP had no
    survival advantage
  • Steroid treatment showed no benefit and some
    potential adverse effects - in general NOT
    recommended

54
Steroids, continued
  • 91 patients w/ARDS randomized to continuous
    low-dose methylprednisolone vs placebo
  • Treated patients had - earlier reduction in
    lung injury score - reduced time on vent p.002
    - reduced ICU stay p .007 - reduced ICU
    mortality (21 vs 43) p.03 - lower rate of ICU
    infections p .0002
  • Attributed to steroid-induced down-regulation of
    systemic inflammation
  • Meduri et al Chest 2007 131954
    - 963

55
No Survival Advantage
  • Prone position
  • Nitric oxide
  • Liquid ventilation with fluorocarbons
  • Intratracheal instillation of recombinant
    surfactant
  • Use of Pulmonary Artery Catheter to help guide
    treatment

56
Alternatives to ARDSNET
  • Pressure control- inverse ratio
    ventilation(PC-IRV)
  • Airway pressure release ventilation (APRV)
  • High frequency oscillatory ventilationAll modes
    may improve oxygenation because of sustained
    recruitment, but to date none is known to offer a
    survival advantage.

57
APRV
Habashi, N. CCM 33(3)S228-240, 2005
58
ARDS Outcome
  • Mortality 60 down to 30 1983 1996.Felt
    largely due to improved CCM capabilities rather
    than ARDS-specific therapy.
  • Survivors have pulmonary restriction early after
    dischargeimproved PFTs plateau by 1 year.Many
    return to nl spirometry /- reduced DLCO.
  • Significant neuropsychiatric issues may persist

59
Rubenfeld et al NEJM 2005 353(16)1685-93
60
ARDS- Survival Follow-up
  • One year post discharge, 49 of survivors had
    returned to work, most to prior positions
  • Those not returning - persistent weakness
    fatigue - job stress - poor mobility - poor
    functional statusHerridge et al NEJM 2003
    348(8)683-93

61
Herridge et al NEJM 2003, 348(8) 683-93
62
ARDS Conclusion
  • Index of suspicion in pts at risk who develop
    resp sx or infiltrates
  • Intubate early when it appears inevitable
  • Low tidal volume
  • Titrate FiO2 and PEEP
  • Transition to APRV as rescue
  • Steroids party line vs bottom line
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