5. ◆ 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
7. ◔ 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
9. ☆ 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
15. ☆ depending on the stage of the disease
☆ MC findings are bilateral, predominantly peripheral, asymmetrical
consolidation with air bronchograms
☆ ±Septal lines and pleural effusions 7b
25. ☆ 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
27. ➜ 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
29. 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
33. ✩ 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
37. Lung protective strategies: ↓Vt,↓RR,
↓mean Aw P (by ↓PEEP), avoid auto-
PEEP
Drain collections of gas
Double lumen tubes (differential lung
ventilation)
18b
45. 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
51. ↑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
53. 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
55. ✾ 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
57. ★ 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
59. ★ 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
61. 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
67. 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
69. ✯ 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
71. ✯ ↑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
73. ✾ ↓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
75. 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
77. 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
79. 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
81. 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
83. ✰ 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
85. 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
87. ↓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
93. ✪ "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
97. 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
99. 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
101. 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
103. 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
107. 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
108. Possible reasons for no positive trials of
Steroids in ARDS despite experimental
evidence:
54a
109. Given too late. need to be early to
↓inflammation ? Trials have often
started after ARDS established
SEs outweigh benefits
54b