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Lung Stress and Strain in
ARDS
2016, Toronto
Luciano Gattinoni, MD, FRCP
Georg-August-Universität Göttingen
Germany
Chest wall elastance
EtotEtot
cmH2O
StiffStiff
2525
LEEL
“Soft”“Soft”
EwEw
55
StiffStiff
1515
EwEw
“Soft”“Soft”
1515
LEEL
EtottotE
Clinical equivalents
Stress PL transpulmonary pressure
Strain VT / FRC
The linkage is the specific elastance
PL VT
FRC= *
Elspec
Barotrauma Volotrauma
FRCml
TLCml
Sp Ecm H2O
PL (TLC)
cm H2O
2.5 7.5 4 8
300 900 6 12
2000 6000 12 24
VT/kg (mL/kg)
6 8 10 12
Str
ain
0.20.40.60.81.01.21.41.61.82.02.22.42.62.83.0
ALI patients
ARDS patients
B
Chiumello et al. Am J Respir Crit Care Med. 2008 Aug 15;178(4):346-55.
PEEP 5 cmH2O
50 sbj
Strain vs VT/kg IBW
Airway plateau pressure (cmH2O)
0 10 20 30 40 50 60
0
10
20
30
40
50
60
Airway plateau pressure (cmH2O)
0 10 20 30 40 50 60
T
ran
spulm
on
ary
pla
teau
pre
ssue
(cm
H2O
)
0
10
20
30
40
50
60
A
Surgical control group
Medical control group ARDS patients
ALI patients
B
Chiumello et al, Am J Respir Crit Care Med. 2008
Slope PL/Paw = Ew/Etot [0.2 - 0.8]
Strain (dVgas/Vgas0)
0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0
Str
ess
(PL
, cm
H2
O)
0
5
10
15
20
25
30
35
40
45
50
55
Stress-strain curve of healthy pigs
Specific Lung
Elastance
5.8 cmH2O
Protti A. et al. Am J Respir Crit Care Med. 2011 Feb 4.
TLC
FRC
Lun
g V
olu
me
VT 100%
VPEEP 0%
VT 75%
VPEEP 25%
VT 50%
VPEEP 50%
VT 25%
VPEEP 75%
Protti et al. Crit Care Med. 2013 Feb 4.
Tidal Strain
P*ΔV = Energy Input
Dissipated Undissipated
Surface Tension
Sliding EM
Opening and ClosingElastic System
PEEP *ΔV = Energy Input = 0
Continuous Strain
Pressure
0 10 20 30 40 50 60
Volu
me
0
200
400
600
800
1000
1200
PE
EP
Pea
k
Pre
ssure
PEEP Volume
Total Inspiratory Volume
Pressure
0 10 20 30
Volu
me
0
200
400
600Z
EE
P
Pea
k
Pre
ssure
Total Inspiratory Volume
Pressure
0 10 20 30 40
Volu
me
0
200
400
600
800
1000
1200
PE
EP
Pea
k
Pre
ssure
PEEP Volume
Total Inspiratory Volume
EXAPLES OF ENERGY
COMPUTATIONS AT
DIFFERENT PRESSURES
ZEEP
LOW PEEP HIGH PEEP
Global stress able to damage healthy (or “baby”?) lung
in clinical practice is uncommon
However, when the lung starts to deteriorate the rate of
damage is impressively fast, why?
If global stress is so rare, how can we explain the
following slide?
ARR = absolute
risk reduction
Hager et al. Am J Respir Crit Care Med. 2005 Nov 15;172(10):1241-5.
min max
Stress distribution:
high stiffness zone
Mead J et al. J. Appl. Physiol. 28(5):596-608 1970
Healthy subject
Moderate ARDS
Severe ARDS
Average ratio in normal subjects : 1.37±0.15
Hypothesis
Lesions should first occur where
physiological stress risers are located
Before appearance first new densities
TIME 1: 5.7±6.5 hours
END EXPIRATION END INSPIRATION
Courtesy of dr. Cressoni M.
First CT scan with new densities
TIME 2: 8.4±6.3 hours
END EXPIRATION END INSPIRATION
Courtesy of dr. Cressoni M.
Last CT scan with distinguishable densities
TIME 3: 15±12 hours
END EXPIRATION END INSPIRATION
Courtesy of dr. Cressoni M.
First CT scan with one-field edema
TIME 4: 18±11 hours
END EXPIRATION END INSPIRATION
Courtesy of dr. Cressoni M.
First CT scan with all-field edema
TIME 5: 20±11 hours
END EXPIRATION END INSPIRATION
Courtesy of dr. Cressoni M.
Hours0 5 10 15 20 25
Sev
erit
y t
rend
CT scan only
+ Lung mechanics
+ Gas Exchange
T2
T3
T4-5
VILI cumulative time course
Courtesy of dr. Cressoni M.
PET
FDG UPTAKE
CT SCAN
INFLATION INHOMOGENEITY
LUNG IMAGING
Ki/lung inhomogeneity interaction and gas/tissue
composition
MILD
MODERATE
SEVERE
Lung protective strategy
Less energy
+
More homogeneous lung