ARDS

1
ARDS
?"? ????? ???? MSMSICU
2
????? (????...)
ARDS

• First described in 1967 as Adult Respiratory
  Distress Syndrome
• ???? (100/100,000 ???? ???), ???, ????!
• American-European Consensus Conference Committee
  (AECC 1994) criteria
• Acute onset
• Bilateral infiltrates in chest radiography
• Pulmonary-artery wedge pressurelt18 mmHg
• Acute lung injury PaO2/FiO2lt300
• Acute respiratory distress syndrome PaO2/FiO2lt200

3
(No Transcript)
4
(No Transcript)
5
Piantadosi, Annals Int Med 2004 141460-470
6
(No Transcript)
7
(No Transcript)
8
First Berlin definition
9
Second Berlin fefinition

• ????????? ????? ??????MILD 27, MOD 35,
  SEVERE 45

10
(No Transcript)
11
(No Transcript)
12
(No Transcript)
13
ARDS Causes
14
(No Transcript)
15
ARDSEpidemiology

• Incidence 80 per 100,000
• Outcomes
• Traditionally 40-60 mortality
• Majority of deaths due to MSOF
• Low tidal volume ventilation decreases mortality
• Other critical care improvements may be involved
• Predictive factors for death CLD, non pulmonary
  organ dysfunction, sepsis and advance age
• Survivors Most of them will have normal
  pulmonary function within a year

16
ARDSPathogenesis

• ARDS is the manifestation of SIRS in the lungs
• Influx of protein rich edema into the air spaces
  due to increased permeability of the
  alveolar-capillary barrier
• Endothelial damage pathophysiology is similar to
  that of SIRS/SEPSIS

17
ARDSPathogenesis

• 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

18
(No Transcript)
19
ARDS Exudative Phase

• The definition applies for the acute exudative
  phase
• Rapid onset
• Hypoxemia refractory to supplemental oxygen
• CXR similar to pulmonary edema
• CT Scan Alveolar filling, consolidation and
  atelectasis in the dependent lung zones
• Pathologic findings
• diffuse alveolar damage with capillary injury and
  disruption of the alveolar epithelium
• hyaline membranes
• protein rich fluid edema with neutrophils and
  macrophages

20
ARDSPathogenesis
21
ARDS Exudative Phase

• CT Scan During Acute Phase

22
ARDS Fibroproliferative phase

• Some patients progress to fibrosing alveolitis
  with persistent hypoxemia, increase alveolar
  dead space and further decrease in pulmonary
  compliance
• The process may start as early as 5-7 days
• The alveolar space becomes filled with
  mesenchymal cells and their products as well as
  new blood vessels

23
ARDSPathogenesis
24
ARDS Fibroproliferative phase

• CT Scan during fibroproliferative phase.
• Diffuse interstitial opacities and bullae

25
(No Transcript)
26
DD

• Infectious causes
• Bacteria - Gm neg pos , mycobacteriae,
  mycoplasma, rickettsia, chlamydia
• Viruses- CMV, RSV, hanta virus, adeno virus,
  influenza virus
• Fungi- H.capsulatum, C.immitis
• parasites- pneumocytis carinii, toxoplasma gondii

27
DD

• Non infectious causes
• CCF
• Drugs toxins (paraquat, aspirin, heroin,
  narcotics, toxic gas, tricyclic anti depressants,
  acute radiation pneumonitis)
• Idiopathic (esinophilic pneumonia, Acute
  interstitial pneumonitis, BOOP, sarcoidosis,
  rapidly involving idiopathic pulmonary fibrosis)
• Immunologic (acute lupus pneumonitis, Good
  Pastures syndrome, hypersensitivity pneumonitis)
• Metabolic (alveolar proteinosis)
• Miscellaneous (fat embolism, neuro/high altitude
  pulmonary oedema)
• Neoplastic (leukemic infiltration, lymphoma)

28
ARDSTreatment

• Recent decrease of mortality
• Treatment of underlying cause
• Better supportive ICU Care
• Prevention of infections
• Appropriate nutrition
• GI prophylaxis
• Thromboembolism prophylaxis

29
(No Transcript)
30
(No Transcript)
31
ARDS Treatment

• Protective ventilation
• Smaller tidal volumes
• Avoid overdistention
• Tolerate permissive hypercarbia
• Open lung ventilation
• Avoid alveolar collapse and reopening

32
(No Transcript)
33
Ventilation with Lower Tidal Volumes as Compared
with Traditional Tidal Volumes for Acute Lung
Injury and the Acute Respiratory Distress
Syndrome The Acute Respiratory Distress
Syndrome Network N Engl J Med 20003421301-8

• Study stopped after 2nd interim analysis
• Reduction of mortality by 22

34
NIH/ARDS Network

• PROTOCOL
• Volume assist control
• lt 6mL/Kg body weight
• lt30 cm H2O
• 6-35/min adjusted for pH of 7.30 if possible
• Adjust to 11-13
• PaO2gt55 and or SpO2gt88
• Combinations
• PS wean when FiO2/PEEPlt.40/8

• VARIABLES
• Ventilator mode
• Tidal Volume
• Plateau Pressure
• Ventilation rate/pH goal
• Inspiration flow, IE
• Oxygenation goal
• FIO2/PEEP
• Weaning

35
ARDSPermissive Hypercapnia

• Hypercarbic acidosis
• Hypoxemia
• Respiratory failure and arrest
• Decrease myocardial contractility
• Cerebral vasodilatation
• Decrease seizure threshold
• Hyperkalemia

• Permissive hypercapnia
• Supplemental oxygen overcomes CO2 induced hypoxia
• No evolution to respiratory arrest
• Lack of significant deleterious effects
• Is hypercarbia beneficial?

36
Optimal PEEP

• Positive end-expiratory pressure should be high
  enough to shift the end-expiratory pressure above
  the lower inflection point by 2-3 cm H2O
  (usually 12-15 cm H2O)
• Allows maximal alveolar recruitment
• Decreases injury by repeated opening and closing
  of small airways

37
ARDS Treatment

• Recruiting maneuvers
• NO
• Prone positioning
• Steroids
• APRV
• ECMO
• Volume cycle vs. pressure cycle
• Inverse-Ratio Ventilation
• Non invasive Positive Pressure Ventilation
• High-Frequency Ventilation
• Tracheal Gas Insufflation
• Extracorporeal gas exchange
• Fluorocarbon Liquid Gas Exchange

38
APRV

• It uses a release of airway pressure from an
  elevated baseline to simulate expiration.
• The elevated baseline facilitates oxygenation
  avoids collapsing of alveoli and the timed
  releases aid in carbon dioxide removal.
• Potential advantages of APRV include lower airway
  pressures, lower minute ventilation, minimal
  adverse effects on cardio-circulatory function.
• Airway pressure release ventilation is consistent
  with lung protection strategies that strive to
  limit lung injury associated with mechanical
  ventilation, particularly recruitment/derecruitmen
  t
• More (larger) studies are needed to define its
  role in ALI/ARDS

39
(No Transcript)
40
ARDSTreatment

• Inhaled nitric oxide and other vasodilators
• Most ARDS/ALI patient may have mild to moderate
  pulmonary HTN
• Improvement in oxygenation was small and not
  sustained
• No change on mortality or duration of mechanical
  ventilation
• May be used as rescue therapy
• Surfactant
• Successful in neonatal respiratory distress
  syndrome

41
Recruitment maneuvers

• Lung recruitment in patients with ARDS Gattinoni
  NEJM 20063541175-86
• Sixty eight patients with ALI/ARDS underwent
  whole lung CT Scan during breath holding session
  at airway pressures of 5, 15 and 45 cm of water
• The percentage of potentially recruitable lung
  was defined as the proportion of lung tissue in
  which aeration was restored (Recruited)

42
Recruitment

• Knowing the of recruitable lung might be the
  key to the effects of PEEP
• PEEP in patients with limited recruitable areas
  might be of little benefit or harmful
• Overdistention
• Worsening of Shunt
• Authors suggest PEEP of 15 for those recruitables
  and 10 for those who are not

43
ARDS Treatment

• Gattinoni et al, NEJM 2001345568-573
• 304 patients with ARDS
• Prone group at least six hours/day for ten days
• Better oxygenation in the prone patients
• Similar incidence of complications
• No improvement in survival
• However patient only prone for 7 hours a day and
  up to 10 days

44
ARDS Treatment

• Fluid and hemodynamic management
• Optimal fluid management is controversial
• There is data supporting fluid restriction as a
  mean to minimize lung edema
• However maintenance and preservation of oxygen
  delivery may require fluid administration
• Euvolemia, judicious use of vasopressors
• Effects of ventilation in circulation
• To Swan or not to Swan

45
ARDS Treatment

• Glucocorticoids
• No benefits in acute phase
• Some evidence of improvement during
  proliferative phase (Meduri et al JAMA
  1998280159-165)
• Methylprednisolone 2mg/kg initially for 32 days
• Improvement in Lung injury scores, MOSD scores
  and mortality
• Benefits may be noticed by day 3
• High risk of infection
• ? May consider a short course of high dose as
  rescue therapy

46
ARDS Treatment

• Omega-3 (immunonutrition)
• Prostacyclines
• Surfactant
• NMA
• Ketoconazole
• Pentoxifylline
• Antioxidants, NAC

47
Swan and ARDS

• PAC versus CVP to guide treatment of ALI NEJM
  2006 354 2213-2224
• 1000 patients
• Mortality at 60 days was similar between groups,
  as well as the ventilator free days and days not
  spent in the ICU
• Fluid balances were similar among the groups
• PAC had double complications mainly arrhythmias

48
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