Acute Lung Injury and ARDS - PowerPoint PPT Presentation

Loading...

PPT – Acute Lung Injury and ARDS PowerPoint presentation | free to download - id: 4c0651-NGUyN



Loading


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation
Title:

Acute Lung Injury and ARDS

Description:

Acute Lung Injury and ARDS Andreas Crede Emergency Medicine Registrar Overview Introduction Definition Pathophysiology Treatment New Stuff References Introduction 1st ... – PowerPoint PPT presentation

Number of Views:623
Avg rating:3.0/5.0
Slides: 48
Provided by: andreas151
Category:

less

Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Acute Lung Injury and ARDS


1
Acute Lung Injury and ARDS
  • Andreas Crede
  • Emergency Medicine Registrar

2
Overview
  • Introduction
  • Definition
  • Pathophysiology
  • Treatment
  • New Stuff
  • References

3
Introduction
  • 1st described 1967 (Ashbaugh et al)
  • Incidence 1.5 -7.5/ 100000 population
  • 28 day mortality 25 301
  • Diagnosis clinical

4
Definition
  • Acute onset (lt7days) respiratory failure/distress
  • Diffuse, bilateral infiltrates on CXR
  • Absent left atrial hypertension (PAOP 18mmHg)
  • Or absent clinical evidence of left atrial
    hypertension
  • PaO2/ FiO2 lt300mmHg (ALI)
  • PaO2/ FiO2 lt200mmHg (ARDS)2

5
(No Transcript)
6
Risk Factors
  • Alcoholism
  • Genetic predisposition

7
Causes
  • Direct Injury1
  • Pneumonia
  • Aspiration
  • Drowning
  • Amniotic fluid and fat embolism
  • Alveolar haemorrhage
  • Smoke, toxic gas inhalation
  • Reperfusion (incl rapid drainage pleural
    effusion)
  • Unilateral lung re-implantation

8
Causes
  • Indirect Injury1
  • Severe Sepsis
  • Massive transfusion
  • Shock
  • Pancreatitis
  • Salicylate/ narcotic overdose
  • Anaphylaxis
  • Cardiopulmonary bypass

9
Differential
  • LVF
  • Fluid overload
  • Mitral stenosis
  • Lymphangitis carcinomatosis
  • Interstitial lung disease1

10
(No Transcript)
11
(No Transcript)
12
(No Transcript)
13
(No Transcript)
14
Respiratory Failure
15
(No Transcript)
16
Histologically
  • Exudative Phase3
  • Neutrophilic Infiltrate
  • Alveolar Haemorrhage
  • Proteinaceous Pulmonary Oedema
  • Cytokines (TNF, IL1,8)
  • ? Inflammation
  • ? Oxidative Stress and Protease Activity
  • ? Surfactant Activity
  • Atelectasis

17
Histologically
  • Elastase- induced capillary and alveolar damage3
  • ? Alveolar flooding
  • ? Fluid clearance
  • Capillary thrombosis
  • ? Anticoagulant proteins
  • ? Procoagulant proteins (Tissue Factor)
  • ? Anti- fibrinolytic Protein (Plasminogen
    Activator Inhibitor)

18
Post Acute Phase
  • Fibroproliferative Phase3
  • Variable time period
  • Fibrosis
  • Chronic Inflammation
  • Neovascularisation
  • Resolution3
  • Improvement of hypoxaemia
  • Improved dead space and lung compliance
  • Resolution radiographic abnormalities
  • Can take up to 1 year
  • Residual restrictive or obstructive picture

19
Long Term
  • Chronic Respiratory Disease
  • Muscle Fatigue
  • Muscle Wasting
  • Weakness

20
Treatment
  • Ventilation
  • Fluid Management
  • Steroids
  • Other Stuff

21
Ventilation
  • Tidal Volumes
  • PEEP
  • Positioning
  • Weaning Protocols

22
Tidal Volume
  • Recommended 4-6ml/kg4
  • High tidal volumes4
  • Overdistention of alveoli
  • Local inflammatory response resulting in systemic
    inflammation
  • TNF, IL6, IL10,

23
Tidal Volume4
  • Low tidal volume ventilation
  • Weight
  • Predicted not actual
  • Plateau Pressure
  • 30cm H2O
  • Resp Rate
  • Titrated to pH 7.3-7.45
  • PEEP and FiO2
  • Adjusted to maintain saturation
  • Low tidal volume may result in hypercarbia
  • ARMA (Respiratory Management in ALI/ARDS Trial)
  • NaHCO3 infusions/ hyperventilation to maintain pH

24
Tidal Volumes
  • Same sedation strategies
  • No ? duration of ventilation
  • High frequency oscillatory ventilation shown no
    benefit over low tidal volume ventilation
  • 30 day mortality not statistically significant
    (37 vs 52, p0.10)
  • Earlier recovery from hypoxia
  • Only ventilation strategy shown to reduce
    mortality (40 - 31)4

25
PEEP
  • Recommendation lowest PEEP/ FiO2 to maintain
    saturation
  • Recruits collapsed alveoli
  • In dependant regions
  • Over-distends in non-dependant regions
  • ? Repetitive opening/ closing of alveoli ?
    airway damage
  • Endothelial/ epithelial stretch injury with
    subsequent capillary injury
  • Similar cytokine response as ?tidal volume

26
PEEP
27
PEEP
  • ALVEOLI Trial4
  • Higher PEEP improved oxygenation
  • In hospital mortality equal btw high and low PEEP
  • Time on ventilator similar
  • Duration non- pulmonary organ failure equal

28
PEEP
  • Adverse effects of PEEP
  • ? Cardiac output
  • Volutrauma
  • ? Lung water
  • ? High VA/Q
  • ? Dead space
  • ? Endothelial permeability
  • ? Epithelial permeability
  • ? Bronchial blood flow

29
Fessler, ARRD 1993
30
PEEP Lung Perfusion
Permutt, JAP 1961
31
PEEP
  • Some Endpoints
  • Best PaO2
  • Lowest Shunt
  • Best O2 delivery
  • Best lung perfusion
  • Plateau Pressure 30cm H2O
  • Optimise aeration on CT
  • Pressure/ volume curve becomes concave

32
Positioning
  • Prone positioning1,4
  • Redistribution of blood ventilation to least
    affected areas of lung
  • Secretion clearance
  • Shifts mediastinum anteriorly assists
    recruitment of atelectatic areas
  • ? reduce lung injury
  • Reduced lung compression by abdominal contents

33
Supine Ventilation
  • 40 lung volume under lung, especially patients
    with large hearts

34
Prone Ventilation
35
Effect of Blood Flow in Prone Positioning7
50
25
Percent Flow
0
Dorsal
Ventral
Supine
36
Positioning
  • Prone position4
  • Transient improvement PaO2/FiO2
  • No improvement survival/ time on ventilator/
    time in ICU
  • Role
  • High FiO2
  • High plateau pressures

37
Weaning Protocols
  • Reduce duration of mechanical ventilation vs
    patients managed by IMV protocol4
  • Daily spontaneous breathing trial4
  • 30-120 mins unassisted ventilation
  • 4 Criteria before commencement
  • Some reversal of underlying cause
  • PEEP 8cm H2O/ FiO2 50
  • Haemodynamic stability
  • Ability to initiate inspiratory effort

38
Fluid Management
39
Fluid Management
  • Fluid movement regulated by
  • Starling equation
  • Vessel wall
  • Ability to filter fluid
  • Selective permeability to proteins

40
Fluid Management
41
Fluid Management
  • Study of conservative vs liberal fluid
    management5
  • 60 day mortality 25.5 vs 28.4 p0.30
  • 1st 28 days ventilator free 14.6 vs 12.1 plt0.001
  • 1st 28 days ICU free 13.4 vs 11.2 plt0.001
  • Difference in organ failure and need for dialysis
    not statistically significant
  • No specific mention of CVP/ PAOP levels which to
    aim for
  • Conservative 4mmHg Liberal 10-14mmHg CVP

42
Steroids
  • Theoretical use to ?inflammatory response
    associated with ARDS6
  • 2006 study6
  • No ?60 day mortality (28.6 vs 29.2 p 0.10)
  • Use of steroids 14 days post onset ? mortality
  • ? need for vasopressors
  • ? ventilator and shock free days
  • ? neuromuscular weakness
  • Short term improvement in oxygenation

43
Other stuff
  • Extracorporeal membrane oxygenation
  • Improvement in oygenation
  • No ? long term survival
  • Vasodilators
  • Improved oygenation
  • No ? long term survival
  • Ketoconazole
  • Pentoxyfilline
  • Nutritional modification
  • Antioxidants
  • Surfactant
  • B2 stimulants1

44
Emergency Department Summary
  • PREVENT!
  • Low tidal volume ventilation
  • Restrict PEEP
  • Restrict Fluids (if possible)
  • Initiate Weaning Protocol
  • Supine Ventilation

45
Conclusion
  • Many theoretical therapies
  • Only proven strategy to improve survival is low
    tidal volume ventilation
  • Therapies to reduce number of days needing scarce
    resources valuable in our setting

46
Thank You
47
References
  • 1. Wheeler, A.P. and Bernard, G.R. 2007,Acute
    Lung Injury and the Acute Respiratory Distress
    Syndrome A Clinical Review. Lancet 369 155365
  • 2. The Acute Respiratory Distress Syndrome
    Network. 2000, Ventilation With Lower Tidal
    Volumes as Compared with Traditional Tidal
    Volumes for Acute Lung Injury and the Acute
    Respiratory Distress Syndrome. N Engl J Med
    3421301-08
  • 3 Plantadosi, C.A and Schwartz, D.A. 2004, The
    Acute Respiratory Distress Syndrome. Ann Intern
    Med 141460-470.
  • 4. Girard, TgtDgt and Bernard,G.R. 2007, Mechanical
    Ventilation in ARDS A State-of-the-Art Review.
    Chest 131921-929
  • 5. The National Heart, Lung and Blood Institue
    Acute Respiratory Distress Syndrome Clinical
    Trials Network. 2006, Comparison of Two
    Fluid-Management Strategies in Acute Lung Injury.
    N Engl J Med 3542564-75
  • 6. The National Heart, Lung and Blood Institue
    Acute Respiratory Distress Syndrome Clinical
    Trials Network. 2006, Efficacy and Safety of
    Corticosteroids for Persistent Acute Respiratory
    Distress Syndrome. N Engl J Med 3541671-84
  • 7. www.slideshare.net
About PowerShow.com