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Definition
1a
Digitally signed by Dr.Sherif Badrawy
DN: cn=Dr.Sherif Badrawy, o=KKUH,
ou=Critical Care,
email=sherif_badra...
Acute hypoxaemic respiratory failure due
to bilateral and diffuse alveolar damage
1b
New Berlin Definition (JAMA 2012):
2a
◆ acute: within 1 week of insult or respiratory ⇊
◆ Bilateral opacities
◆ Respiratory failure not fully explained by HF or...
Issues é the Berlin definition
3a
◔ ability to predict mortality is still poor, but slightly better
◔ doesn't include underlying aetiology & lacks a direct ...
Old Criteria:(Old Definition)
4a
☆ Acute
☆ PaO2/FiO2 < 300 (ALI) or < 200 (ARDS)
☆ CXR: B/L infiltrates ➜ pulmonary oedema sparing
costophrenic angles
☆ PA...
Direct causes of ARDS (ie alveolar
insult):
5a
☆ Pneumonia (46%), aspiration(29%),
lung contusion
(34%), fat embolism, near drowning,
inhalational injury, reperfusion in...
Indirect causes of ARDS(ie capillary
insult):
6a
☆ non-pulmonary sepsis (25%), multiple
trauma (41%), massive transfusion
(34%), pancreatitis (25%),
cardiopulmonary bypass...
X-ray in ARDS
7a
☆ depending on the stage of the disease
☆ MC findings are bilateral, predominantly peripheral, asymmetrical
consolidation ...
CT in ARDS
8a
☆ dorsal dependent ↑lung density
☆ reverses with a shift from supine to prone
☆ Groundglass appearance ➜ fibrosis
☆ 2nd we...
Long term outcomes
9a
☆ Exercise tolerance dt critical illness
neuropathy and myopathy
☆ Depression, anxiety and PTSD
☆ cognitive impairments dt...
Pathogenesis of ARDS
10a
☆ Injury
☆ Exudative: alveolar capillary membrane disruption +
inflammatory cell infiltrate
☆ Proliferative: Type 2 alveol...
Effects of ARDS
11a
♙ hypoxaemia (V/Q mismatch, impaired hypoxic pulmonary
vasoconstriction)
♙ ↑in dependent densities (surfactant dysfunction...
Neutrophils in ALI:
12a
☆ Most abundant cell type in early ALI
☆ release reactive O2 ➜ tissue damage
☆ However, ALI occurs in neutropenic patients...
Biological markers
13a
➜ Stiff lungs (↓compliance) ➜ trauma with ventilation,
impaired ventilation (↑CO2) and V/Q mismatch
Changes are not unifor...
Mortality in ARDS is up to 40% is due to:
14a
Multiorgan failure
Severe hypoxaemia: alveoli perfused
but not ventilated (shunt)
Some argue ARDS is largely a hospital
ac...
Mechanisms of Ventilator Associated
Lung Injury
15a
✩ Volutrauma
✩ Barotrauma
✩ Biotrauma
✩ Atelectrauma
✩ Shearing injury
✩ Oxygen toxicity
15b
Definition of Volutrauma
16a
✩ dt over-distension of normal alveoli to
transpulmonary pressures ≥ 30 cm
✩ Non-homogenous lung injury
✩ disruption of th...
Causes of Volutrauma
17a
Alveolar rupture ➜ interstitial
emphysema, mediastinal emphysema,
pneumothorax, pneumoperitoneum and
SC emphysema ➜ HD & r...
Rx of Volutrauma
18a
Lung protective strategies: ↓Vt,↓RR,
↓mean Aw P (by ↓PEEP), avoid auto-
PEEP
Drain collections of gas
Double lumen tubes (...
Barotrauma
19a
↑trans-pulmonary pressures > 50 cm ➜
disruption of BM ➜ gross air leaks
19b
Biotrauma
20a
tissue disruption ➜ ↑chemokines &
cytokines ➜ WBC activation ➜
pulmonary & systemic inflammatory
response
20b
Atelectrauma
21a
Recruitment/de-recruitment injury: the
weight of oedematous lung ➜ collapse of
the dependant portions of the lung ➜
repeat...
Shearing injury:
22a
at the junction of the collapse lung and
ventilated lung, ➜ ventilate lung moving
against the relatively fixed collapsed l...
Oxygen toxicity
23a
✬ Lung toxicity:
◒ ↑FiO2 ➜ cellular damage (?by O2 free radicals over whelming scavenging systems)
➜ progressive ↓complian...
Ventilation measures in ARDS
24a
↓Tidal volume
Limit plateau pressure
Slow respiratory rate
FiO2, aim for < 60%
Optimise recruitment
Optimise blood flow to...
Optimise recruitment in ARDS
25a
↑PEEP: ↑surface area for gas
exchange, ↓atelectasis, ➜ redistribute lung
water
Lung recruitment
↑I:E ratio towards 1:1
Inv...
NIV in ARDS
26a
Role of NIV uncertain - > complications, delays
intubation. Current data do not support the routine
use of NIV in undiffer...
ARDS Network study (NEJM 2000)
27a
✾ P/F ratio < 300 in the first 36 hours ➜ Strict PEEP & FiO2
protocol ,
✾ AC mode to avoid excessive spontaneous Vt
✾ Aver...
Invasive Ventilation in ARDS
Tidal Volume: Avoidance of overstretch
28a
★ Vt need to be reduced in proportion to the
reduction in aerated lung otherwise aerated lung
will over stretch. It is lun...
measurement of transpulmonary
pressure
29a
★ Vt limitation > practical than PSV or
measurement of
transpulmonary P.
★ By oesophageal P. monitoring with an
oesophagea...
MV mode in ARDS
30a
PC has theoretical advantage that Ppk
~ Pplat but HD stability & mean Aw P ➜
no difference
Inverse ratio ventilation: smal...
HFOV in ARDS:
31a
early studies showed no benefit
31b
Heavy sedation +/- paralysis: in ARDS:
32a
ACURASYS Study ➜48- hour infusions of
cisatracurium ↓mortality & barotrauma, no
effect on ICU-acquired weakness
Minimise O...
Permissive Hypercapnea in ARDS
33a
pH > 7.1 (problematic in head injury & PHTN)
Low Vt ➜ ↑PaCO2 unless ↑rate ➜ > tidal
stretch & possibly alveolar injury ➜ ↑...
Should I ↑RR to ↓CO2 in ARDS ?
34a
✯ ARDS Net aimed at normocapnea with
RR up to 35 to minimize acidosis.
✯ ARDSNET tried to avoid hypercapnea
by ↑RR & givin...
Advantages of PEEP in ARDS
35a
✯ ↑O2 & ↓VILI (dt tidal opening & closing of
alveoli).
✯ ↑PaO2 by ↑FRC ➜ recruiting alveoli but may↓VR
✯ ARDSNet protocol ...
Disadvantages of PEEP in ARDS
36a
✾ ↓VR ➜ ↓COP even though O2 rises
✾ over-inflation of non-dependent alveoli
(+ recruitment of dependent alveoli).
✾ Less l...
Reasonable approach for Ideal PEEP ?
37a
Use a scale similar to the ARDS Network
protocol
Titrate PEEP to PaO2, ➜ a PEEP of ~15
cmH2O, levels up to 25 cm H20 in se...
Recruitment manoeuvres in ARDS
38a
Recruitment is not homogenous ➜ will preferentially distend
normal lung
Unclear whether they add anything to PEEP ➜ larges...
Oxygenation in ARDS
39a
Balance bw damage from ↑Aw P &
↑FiO2 is unknown - generally FiO2
regarded as less damaging
Start at FiO2 of 1 & titrate do...
Prone Position in ARDS
40a
For persisting severe hypoxia
Prone position ➜ ↓chest wall compliance. So in
PCV should have ↑recruitment at same levels o...
Evidence of Prone Position in ARDS
41a
✰ MRCT ➜ French ICUs proning, early in illness, 16
hours prone at a time vs supine, in PF ratio of < 150
persisting > 24 h...
Disadvantages of Prone Position in
ARDS
42a
potential for dislodgement of tube/lines,
problems with airway access, ➜ new
pressure sores, ↑ICP, ↓enteral feed
tolerance...
Advantages Pulmonary Vasodilators in
ARDS (iNO/ Inhaled Nitric oxide)
43a
↓shunt & ↓RV afterload (↑CO is unusual).
Delivered to well ventilated lung ➜ VD
pulmonary circulation & redistribute blood...
Disadvantages Pulmonary Vasodilators
in ARDS (iNO/ Inhaled Nitric oxide)
44a
Risk of opening circulation to poorly aerated
lung ➜ ↑shunt ➜ ↓PO2
Expensive ➜ $2,000 per day
Toxicity with NO2 ➜ Met Hb
C...
INDICATIONS of iNO/ Inhaled Nitric
oxide
45a
(1) controversial role in ARDS
(2) PHTN (adults & newborn)
(3) Rt HF (e.g. post-cardiac surgery ,
heart transplant)
45b
Evidence of iNO/ Inhaled Nitric oxide:
46a
✪ "Routine use should be discontinued",
at least until trials indicate any subgroup
that may benefit.
✪ RCTs in ARDS ➜ sho...
Mechanism of iNO/ Inhaled Nitric oxide
47a
✪ Smooth-muscle relaxant via cAMP ➜ local
pulmonary VD ➜ ±improving VQ mismatch &
↓PHTN, ± immuno-modulation (↓neutrophil
...
Monitoring of efficacy of iNO/ Inhaled
Nitric oxide
48a
PAP/PaO2 and/or Pulmonary Vascular
Resistance (via pulmonary artery catheter or
TEE)
↑PaO2 of 20% a positive response - co...
Requirements of iNO/ Inhaled Nitric
oxide
49a
Cylinders contain 800 ppm +
nitrogen. complex equipment to monitor
PO2, PAP, Met Hb & NO & nitrogen
dioxide
Delivery via m...
Inhaled prostaglandins/Inhaled
PGI2:(Iloprost)
50a
improves oxygenation as effectively as iNO.
Continuously jet nebulised dt short half life
May be better than iNO. in (PAH ...
Fluid management in ARDS
51a
Limit CVP to PEEP + 2 maximum. Consider
frusemide if CVP > PEEP + 5
ARDSNET, NEJM 2006, ➜ fluid, diuretics &
vasoactive in...
surfactant replacement therapy in ARDS
52a
theoretically good, improves O2 but no
improvement in
mortality, problems é distribution to
alveoli
52b
Steroids in ARDS:
53a
Menduri study: ↓Lung injury score, ↓LOS, ↓duration of
IPPV
ARDSNET 7 - 28 days to placebo vs methylprednisolone
(ie late i...
Possible reasons for no positive trials of
Steroids in ARDS despite experimental
evidence:
54a
Given too late. need to be early to
↓inflammation ? Trials have often
started after ARDS established
SEs outweigh benefits...
ketoconazole in ARDS:
55a
antifungal that inhibits thromboxane
synthase & 5-lipooxygenase ➜ early data
but not confirmed
55b
ARDS 【A simplified evidence based approach】
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ARDS 【A simplified evidence based approach】

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Critical Care , Pulmonology, ICU, respiratory failure

contact me at (sherif_badrawy@yahoo.com)

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ARDS 【A simplified evidence based approach】

  1. 1. Definition 1a Digitally signed by Dr.Sherif Badrawy DN: cn=Dr.Sherif Badrawy, o=KKUH, ou=Critical Care, email=sherif_badrawy@yahoo.com, c=SA Date: 2015.02.25 18:17:25 +03'00'
  2. 2. Acute hypoxaemic respiratory failure due to bilateral and diffuse alveolar damage 1b
  3. 3. New Berlin Definition (JAMA 2012): 2a
  4. 4. ◆ acute: within 1 week of insult or respiratory ⇊ ◆ Bilateral opacities ◆ Respiratory failure not fully explained by HF or fluid overload (PAOP removed ➜ ↓use of PACs) ◆ Oxygenation: Mild: PaO2/FiO2 from 201 - 300 with PEEP or CPAP >= 5 (27% mortality) Moderate: 101 - 200 with PEEP >= 5 (32% mortality) Severe: <= 100 (45% mortality) ◆ The term acute lung injury (ALI) has been discarded ◆ 4 other variables ✫ compliance <= 40 ✫ PEEP >= 10 ✫ Expired minute volume > 10 ✫ Radiographic severity ◆ an "objective assessment" (e.g. echo) should be done if there is no clear cause such as trauma or sepsis 2b
  5. 5. Issues é the Berlin definition 3a
  6. 6. ◔ ability to predict mortality is still poor, but slightly better ◔ doesn't include underlying aetiology & lacks a direct measure of lung injury ◔ use of vasopressors at the time of Dx of ARDS is associated é a much higher mortality regardless of the PF ratio (not accounted for in the Berlin definition) ◔ Does not allow early identification of Pts who may be amenable to Rx before ARDS becomes established ◔ still allows CXR to be used for Dx, ῶ compared poorly é CT chest ῳ studied by Figueroa-Casa et al, 2013 ◔ Berlin definition has low sensitivity ῳ compared to autopsy findings. 3b
  7. 7. Old Criteria:(Old Definition) 4a
  8. 8. ☆ Acute ☆ PaO2/FiO2 < 300 (ALI) or < 200 (ARDS) ☆ CXR: B/L infiltrates ➜ pulmonary oedema sparing costophrenic angles ☆ PAOP: < 18 mmHg or no ↑LAP ◆ Weaknesses were: ◕ NO definition of acute, and the effect of PEEP ◕ variations in PiO2/FiO2 ratio ◕ Not specific about radiologic criteria 4b
  9. 9. Direct causes of ARDS (ie alveolar insult): 5a
  10. 10. ☆ Pneumonia (46%), aspiration(29%), lung contusion (34%), fat embolism, near drowning, inhalational injury, reperfusion injury 5b
  11. 11. Indirect causes of ARDS(ie capillary insult): 6a
  12. 12. ☆ non-pulmonary sepsis (25%), multiple trauma (41%), massive transfusion (34%), pancreatitis (25%), cardiopulmonary bypass 6b
  13. 13. X-ray in ARDS 7a
  14. 14. ☆ depending on the stage of the disease ☆ MC findings are bilateral, predominantly peripheral, asymmetrical consolidation with air bronchograms ☆ ±Septal lines and pleural effusions 7b
  15. 15. CT in ARDS 8a
  16. 16. ☆ dorsal dependent ↑lung density ☆ reverses with a shift from supine to prone ☆ Groundglass appearance ➜ fibrosis ☆ 2nd week ➜ cysts or pneumatoceles ☆ Abscess formation, empyema ☆ pneumothorax 8b
  17. 17. Long term outcomes 9a
  18. 18. ☆ Exercise tolerance dt critical illness neuropathy and myopathy ☆ Depression, anxiety and PTSD ☆ cognitive impairments dt desaturation < 90% (cautions against permissive hypoxaemia) 9b
  19. 19. Pathogenesis of ARDS 10a
  20. 20. ☆ Injury ☆ Exudative: alveolar capillary membrane disruption + inflammatory cell infiltrate ☆ Proliferative: Type 2 alveolar cells and inflammatory cells ☆ Fibrotic: infiltration with fibroblasts ☆ Resolution: slow and incomplete repair ☆ The alveolocapillary barrier ➜ damage é bidirectional flow (proteins & fluid in to alveoli, surfactant & alveolar cytokines into plasma) ☆ surfactant dysfunction ↓activity ➜ ↓in pulmonary compliance 10b
  21. 21. Effects of ARDS 11a
  22. 22. ♙ hypoxaemia (V/Q mismatch, impaired hypoxic pulmonary vasoconstriction) ♙ ↑in dependent densities (surfactant dysfunction, alveolar instabilities) ♙ ↓compliance (surfactant dysfunction, ↓lung volume, fibrosis) ♙ collapse/consolidation (↑compression of dependent lung) ♙ ↑minute ventilation (↑in alveolar dead space) ♙ ↑WOB (↑elastance, ↑minute volume requirement) pulmonary HTN (VC, microvascular thrombi, fibrosis, PEEP) 11b
  23. 23. Neutrophils in ALI: 12a
  24. 24. ☆ Most abundant cell type in early ALI ☆ release reactive O2 ➜ tissue damage ☆ However, ALI occurs in neutropenic patients Other cell types: Microvascular thrombosis ➜ PHTN Alveolar macrophages ➜ TGF α & PDGF 12b
  25. 25. Biological markers 13a
  26. 26. ➜ Stiff lungs (↓compliance) ➜ trauma with ventilation, impaired ventilation (↑CO2) and V/Q mismatch Changes are not uniform TNF-α, IL-1β, IL 6 and IL 8 most important. Measurement of cytokines is not predictive of ALI or mortality ferritin and serum surfactant protein B ➜ predictive Biopsy ➜ fibrosing alveolitis after 5 days. 13b
  27. 27. Mortality in ARDS is up to 40% is due to: 14a
  28. 28. Multiorgan failure Severe hypoxaemia: alveoli perfused but not ventilated (shunt) Some argue ARDS is largely a hospital acquired iatrogenic injury dt delayed Abs, ↑fluid and poor ventilation 14b
  29. 29. Mechanisms of Ventilator Associated Lung Injury 15a
  30. 30. ✩ Volutrauma ✩ Barotrauma ✩ Biotrauma ✩ Atelectrauma ✩ Shearing injury ✩ Oxygen toxicity 15b
  31. 31. Definition of Volutrauma 16a
  32. 32. ✩ dt over-distension of normal alveoli to transpulmonary pressures ≥ 30 cm ✩ Non-homogenous lung injury ✩ disruption of the lung architecture ✩ ↑alveolar-capillary permeability, ✩ activation or stretch responsive inflammatory pathways 16b
  33. 33. Causes of Volutrauma 17a
  34. 34. Alveolar rupture ➜ interstitial emphysema, mediastinal emphysema, pneumothorax, pneumoperitoneum and SC emphysema ➜ HD & respiratory compromise 17b
  35. 35. Rx of Volutrauma 18a
  36. 36. Lung protective strategies: ↓Vt,↓RR, ↓mean Aw P (by ↓PEEP), avoid auto- PEEP Drain collections of gas Double lumen tubes (differential lung ventilation) 18b
  37. 37. Barotrauma 19a
  38. 38. ↑trans-pulmonary pressures > 50 cm ➜ disruption of BM ➜ gross air leaks 19b
  39. 39. Biotrauma 20a
  40. 40. tissue disruption ➜ ↑chemokines & cytokines ➜ WBC activation ➜ pulmonary & systemic inflammatory response 20b
  41. 41. Atelectrauma 21a
  42. 42. Recruitment/de-recruitment injury: the weight of oedematous lung ➜ collapse of the dependant portions of the lung ➜ repeated opening and closing with Vt 21b
  43. 43. Shearing injury: 22a
  44. 44. at the junction of the collapse lung and ventilated lung, ➜ ventilate lung moving against the relatively fixed collapsed lung ➜ ↑shearing force and subsequent injury. 22b
  45. 45. Oxygen toxicity 23a
  46. 46. ✬ Lung toxicity: ◒ ↑FiO2 ➜ cellular damage (?by O2 free radicals over whelming scavenging systems) ➜ progressive ↓compliance + interstitial oedema ➜ fibrosis. The safe concentration /duration is unknown. "Safe" periods > 50% vary from 16 to 30 hours. ◒ ↑O2 ➜ ↑atelectasis & bronchoalveolar distension ➜ Absorption atelectasis at FiO2 as low as 0.3 - 0.5 ➜ ↑V/Q mismatch ◒ ↑PaO2 ➜ pulmonary vasoconstriction ➜ worse V/Q mismatch ➜ ↑dead space ventilation ➜ ↑PaCO2 ◒ Alters tracheal flora in favour of pseudomonas & Proteus ✬ ↑PaO2 ➜ ↓coronary artery blood flow ✬ CNS effects (incl seizures) with O2 > 3 atmospheres ✬ ↓innate immunity in lab studies ✬ Fire risk: turn off O2 when defibrillating - sparks cause fires 23b
  47. 47. Ventilation measures in ARDS 24a
  48. 48. ↓Tidal volume Limit plateau pressure Slow respiratory rate FiO2, aim for < 60% Optimise recruitment Optimise blood flow to ventilated alveoli: Inhaled NO or prostacyclin Permissive hypercapnea Spontaneous ventilation Transpulmonary pressure monitoring ▤ Last resorts: Decrease circuit dead space (lower CO2) HFOV ECMO 24b
  49. 49. Optimise recruitment in ARDS 25a
  50. 50. ↑PEEP: ↑surface area for gas exchange, ↓atelectasis, ➜ redistribute lung water Lung recruitment ↑I:E ratio towards 1:1 Inverse ratio ventilation: use autoPEEP to ↑FRC and area for gas exchange 25b
  51. 51. NIV in ARDS 26a
  52. 52. Role of NIV uncertain - > complications, delays intubation. Current data do not support the routine use of NIV in undifferentiated hypoxaemic ARF NIV vs intubation in haematological malignancy and ARDS. ➜ No difference in mortality bw NIV and intubated patients. 71% mortality overall 26b
  53. 53. ARDS Network study (NEJM 2000) 27a
  54. 54. ✾ P/F ratio < 300 in the first 36 hours ➜ Strict PEEP & FiO2 protocol , ✾ AC mode to avoid excessive spontaneous Vt ✾ Average RR ~ 30/min in low mortality group. ✾ Pplat target was < 30 ✾ Showed 6 ml/kg LBW (with plateau pressures < 30) better than 12 ml/kg LBW (with plateau pressures < 30) - mortality reduced by 22% show that over-distension is bad ✾ Meta-analysis showed Vt < 7.7 ml predicted body weight was protective. ✾ Now called "Lung Protective Ventilation" 27b
  55. 55. Invasive Ventilation in ARDS Tidal Volume: Avoidance of overstretch 28a
  56. 56. ★ Vt need to be reduced in proportion to the reduction in aerated lung otherwise aerated lung will over stretch. It is lung stretch, not Paw, that leads to volutrauma ★ Normal lung fully inflated at a transpulmonary pressure of ~30 cmH2O. Pplat, the elastic distending pressure, should not exceed 30 - 35. 28b
  57. 57. measurement of transpulmonary pressure 29a
  58. 58. ★ Vt limitation > practical than PSV or measurement of transpulmonary P. ★ By oesophageal P. monitoring with an oesophageal balloon ➜ exclude effect of the chest wall. ★ better when chest wall pressures are abnormal (↑obesity , chest wall trauma, etc.) 29b
  59. 59. MV mode in ARDS 30a
  60. 60. PC has theoretical advantage that Ppk ~ Pplat but HD stability & mean Aw P ➜ no difference Inverse ratio ventilation: small decrease in CO2 but ↑mean Aw P & ↑risk of HD consequences 30b
  61. 61. HFOV in ARDS: 31a
  62. 62. early studies showed no benefit 31b
  63. 63. Heavy sedation +/- paralysis: in ARDS: 32a
  64. 64. ACURASYS Study ➜48- hour infusions of cisatracurium ↓mortality & barotrauma, no effect on ICU-acquired weakness Minimise O2 consumption/CO2 production & eliminate dyssynchrony Improved ventilation/perfusion relationships 32b
  65. 65. Permissive Hypercapnea in ARDS 33a
  66. 66. pH > 7.1 (problematic in head injury & PHTN) Low Vt ➜ ↑PaCO2 unless ↑rate ➜ > tidal stretch & possibly alveolar injury ➜ ↑PCO2 may not be that harmful as - if it occurs slowly‫ز‬ ↑ CO2 may ➜ ↓inflammatory response (↓neutrophil function, ↓proinflammatory cytokines). 33b
  67. 67. Should I ↑RR to ↓CO2 in ARDS ? 34a
  68. 68. ✯ ARDS Net aimed at normocapnea with RR up to 35 to minimize acidosis. ✯ ARDSNET tried to avoid hypercapnea by ↑RR & giving NaHCO3 ✯ Augmenting RR to combat rises in CO2 may augment mechanical & bio- trauma to the lung 34b
  69. 69. Advantages of PEEP in ARDS 35a
  70. 70. ✯ ↑O2 & ↓VILI (dt tidal opening & closing of alveoli). ✯ ↑PaO2 by ↑FRC ➜ recruiting alveoli but may↓VR ✯ ARDSNet protocol titrates PEEP to PaO2/FiO2 ➜ tidal over-inflation in 1/3. ✯ Lower inflection point of a volume-pressure curve used to set PEEP as it was thought this reflected recruitment 35b
  71. 71. Disadvantages of PEEP in ARDS 36a
  72. 72. ✾ ↓VR ➜ ↓COP even though O2 rises ✾ over-inflation of non-dependent alveoli (+ recruitment of dependent alveoli). ✾ Less likely if alveolar distending pressure is < 30 - 35 cmH2O, or change in driving pressure is < 2cmH2O when Vt is constant 36b
  73. 73. Reasonable approach for Ideal PEEP ? 37a
  74. 74. Use a scale similar to the ARDS Network protocol Titrate PEEP to PaO2, ➜ a PEEP of ~15 cmH2O, levels up to 25 cm H20 in severe ARDS the delta-PEEP technique indirectly assesses excess stress as PEEP is ↑at a constant Vt 37b
  75. 75. Recruitment manoeuvres in ARDS 38a
  76. 76. Recruitment is not homogenous ➜ will preferentially distend normal lung Unclear whether they add anything to PEEP ➜ largest trial showed no effect. ?Only effective in early ARDS when lower levels of baseline PEEP used Apply 30 - 40 cm CPAP in an apnoeic patient for 30 - 40 seconds May lead to improved oxygenation. May also cause hypotension in an under-filled patient Stretch above resting Vt powerful stimulus for surfactant release 38b
  77. 77. Oxygenation in ARDS 39a
  78. 78. Balance bw damage from ↑Aw P & ↑FiO2 is unknown - generally FiO2 regarded as less damaging Start at FiO2 of 1 & titrate down to < 0.6 SaO2 > 90% & PaO2 > 60 reasonable targets 39b
  79. 79. Prone Position in ARDS 40a
  80. 80. For persisting severe hypoxia Prone position ➜ ↓chest wall compliance. So in PCV should have ↑recruitment at same levels of pressure Theoretically ↑secretion drainage (dorsal ventral orientation of large airways) Debate over who should be proned, when in their course, duration of proning, how many days to persist 40b
  81. 81. Evidence of Prone Position in ARDS 41a
  82. 82. ✰ MRCT ➜ French ICUs proning, early in illness, 16 hours prone at a time vs supine, in PF ratio of < 150 persisting > 24 hours. 28 day morality 16% vs 32%. Complications the same. Guerin et al, NEJM 2013. Very dramatic result - is it true? Influenced by number of H1N1 patients? ✰ MRCT comparing supine with prone for 6 h per day. ↑PaO2 in 70% No improvement in mortality - but ↑in the most hypoxic ➜ use as a rescue therapy. 41b
  83. 83. Disadvantages of Prone Position in ARDS 42a
  84. 84. potential for dislodgement of tube/lines, problems with airway access, ➜ new pressure sores, ↑ICP, ↓enteral feed tolerance, difficult or CI in spinal trauma/abdo surgery /pelvic fractures/pregnancy. 42b
  85. 85. Advantages Pulmonary Vasodilators in ARDS (iNO/ Inhaled Nitric oxide) 43a
  86. 86. ↓shunt & ↓RV afterload (↑CO is unusual). Delivered to well ventilated lung ➜ VD pulmonary circulation & redistribute blood away from poorly ventilated lung Bind Hb inactivates NO so systemic complications modest Technically easier than proning & HFVO For temporary rescue only 43b
  87. 87. Disadvantages Pulmonary Vasodilators in ARDS (iNO/ Inhaled Nitric oxide) 44a
  88. 88. Risk of opening circulation to poorly aerated lung ➜ ↑shunt ➜ ↓PO2 Expensive ➜ $2,000 per day Toxicity with NO2 ➜ Met Hb Coagulopathy ➜ Risk of pulmonary Hge dt platelet inhibition & ↑bleeding time rebound PAH & hypoxia with discontinuation ↑renal failure & nosocomial infection 44b
  89. 89. INDICATIONS of iNO/ Inhaled Nitric oxide 45a
  90. 90. (1) controversial role in ARDS (2) PHTN (adults & newborn) (3) Rt HF (e.g. post-cardiac surgery , heart transplant) 45b
  91. 91. Evidence of iNO/ Inhaled Nitric oxide: 46a
  92. 92. ✪ "Routine use should be discontinued", at least until trials indicate any subgroup that may benefit. ✪ RCTs in ARDS ➜ short term oxygenation benefits up to 72 hours, ➜ no change in length of ventilation or mortality 46b
  93. 93. Mechanism of iNO/ Inhaled Nitric oxide 47a
  94. 94. ✪ Smooth-muscle relaxant via cAMP ➜ local pulmonary VD ➜ ±improving VQ mismatch & ↓PHTN, ± immuno-modulation (↓neutrophil adhesion & platelet aggregation) ✪ Physiological improvement in PHTN & heart transplant but no longer term benefits 47b
  95. 95. Monitoring of efficacy of iNO/ Inhaled Nitric oxide 48a
  96. 96. PAP/PaO2 and/or Pulmonary Vascular Resistance (via pulmonary artery catheter or TEE) ↑PaO2 of 20% a positive response - continue iNO at the minimum effective dose May be no fall in PA pressure (though PVR has fallen). Positive response may be seen in CO,SvO2 and/or CVP 48b
  97. 97. Requirements of iNO/ Inhaled Nitric oxide 49a
  98. 98. Cylinders contain 800 ppm + nitrogen. complex equipment to monitor PO2, PAP, Met Hb & NO & nitrogen dioxide Delivery via mixed NO/N2 - measure inspiratory concentrations of each Commonly used doses are 1 - 60 ppm 49b
  99. 99. Inhaled prostaglandins/Inhaled PGI2:(Iloprost) 50a
  100. 100. improves oxygenation as effectively as iNO. Continuously jet nebulised dt short half life May be better than iNO. in (PAH & RV function) Given via ultrasonic nebuliser. Doesn't cause systemic hypotension that IV would. Neither has been shown to improve outcomes. 50b
  101. 101. Fluid management in ARDS 51a
  102. 102. Limit CVP to PEEP + 2 maximum. Consider frusemide if CVP > PEEP + 5 ARDSNET, NEJM 2006, ➜ fluid, diuretics & vasoactive infusions to achieve CVP of 10 - 14 mmHg or < 4. ➜ No difference in 60 day mortality. ?reduced duration of ventilation in dry/conservative group. 51b
  103. 103. surfactant replacement therapy in ARDS 52a
  104. 104. theoretically good, improves O2 but no improvement in mortality, problems é distribution to alveoli 52b
  105. 105. Steroids in ARDS: 53a
  106. 106. Menduri study: ↓Lung injury score, ↓LOS, ↓duration of IPPV ARDSNET 7 - 28 days to placebo vs methylprednisolone (ie late in the disease process). ➜ no change in 60 day mortality but ↑O2, ↑ventilator free days & shock free days, offset by neuromuscular complications & ↑reintubation Another study ➜ initiation after 2 weeks ➜ ↑mortality Overall, not recommended 53b
  107. 107. Possible reasons for no positive trials of Steroids in ARDS despite experimental evidence: 54a
  108. 108. Given too late. need to be early to ↓inflammation ? Trials have often started after ARDS established SEs outweigh benefits 54b
  109. 109. ketoconazole in ARDS: 55a
  110. 110. antifungal that inhibits thromboxane synthase & 5-lipooxygenase ➜ early data but not confirmed 55b

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