Pulling lung out of VILI vortex.pdf

MATHEMATICS OF VENTILATOR INDUCED LUNG INJURY
Pulling Lung Out Of VILI Vortex
Dr. Ubaidur Rahaman
MBBS, M.D. (General Medicine), EDIC
Senior Consultant Critical Care Medicine and Toxicology
Meenakshi Mission Hospital and Research Center, Madurai, Tamilnadu
https://learningcriticalcaremedicine.blogspot.com

“Ventilator Induced Lung Injury is the collateral damage
suffered by the bystander functional baby lung,
caught in the crossfire
between mechanical ventilator and diseased lung.
The effect of this collateral damage can only be attenuated,
not eliminated in acute respiratory distress syndrome”

FRACTRUCTED
BONE
•
STABILIZE
• ALIGNING ENDS
CASTING
• TILL BONE HEALS
ARDS
•
STABILIZE
• ??
MECHANICAL
VENTILATION
• TILL LUNG HEALS
ARDS- dynamic pathophysiology- exudative phase- proliferative phase- fibrotic phase
Mechanical ventilation induces VILI- indistinguishable from ARDS

HOW TO STABILIZE LUNG AND KEEP IT STABILIZED ?
UNDERSTAND Mechanical force of Mechanical Ventilator-
Stress/ Strain
ARDS Pathophysiology
VILI Pathophysiology

MECHANICAL FORCE OF MECHAICAL VENTILATION
STRESS AND STRAIN

PPLAT-PPL CL= VT/ (PPLAT -PPL)
PL
TRANSPULMONARY PRESSURE

STRESS AND STRAIN
FORCE
STRESS
FORCE/AREA
FORCE
STRAIN
∆L/LI
Stress- Transpulmonary Pressure
Strain- tidal volume

Viscoelastic Polyurethane
(memory foam)
Elastic rubber band
Viscous Paint
ELASTIC: : Stress = Y * strain
VISCOUS: Stress= ή * Strain rate
VISCOELASTIC: Stress = Y * strain + ή * strain rate
VISCOELASTIC LUNG
VISCOELASTICITY

Stress (PL)= K * strain (VT/ FRC)
K is specific lung elastance, proportionality constant equivalent in pulmonary physiology
STRESS-STRAIN
Assume VT = FRC
strain (VT/ FRC)= 1
Stress= K
K is animal species specific
In humans K= 13.5
Stress (PL ) of 13.5 cmH2O will inflate lung with tidal volume equal to FRC
Stress (PL ) of 13.5 cmH2O doubles the lung volume,
irrespective of baseline lung volume
Stress = Y * strain

SAFE LIMIT OF STRESS-STRAIN
Lung inflated from FRC to TLC
Strain (VT/ FRC) = (80-35/ 35)= 45/35= 1.3
Stress (PL)= 13.5 * 1.3 = 17
Strain of 1.3 will inflate lung to TLC from FRC
PL of 17 cmH2O (13.5* 1.3) will increase lung volume to TLC
from FRC
Human lung FRC= 35 ml/kg , TLC= 80 ml/kg
PL = 13.5* (VT / FRC)

1.3K
(17
cmH
2
O)
17=13.5*1.3
SAFE LIMIT OF STRESS-STRAIN
AN STRAIN OF 1.3 AND STRESS
OF 17 cmH2O
inflate alveoli to complete
unfolding of collagen fibers: risk
of rupture: VILI
STRAIN OF 1.3
VT 1.3 times FRC
STRESS of 17
PL of 17 cmH2O
Irrespective of
lung volume

1.3K
(17
cmH
2
O)
17= 13.5*1.3
TLC=complete unfolding of collagen fibers=
structural damage of alveolar epi-end
basement membrane (blood-gas
membrane)
SAFE LIMIT OF STRESS- PL 17 cmH2O

Viscoelastic Polyurethane
(memory foam)
Elastic rubber band
Viscous Paint
VISCOELASTIC: Stress = E * strain + ή * strain rate
Strain= (VT/FRC), Strain rate = (VT/ FRC)/ TI
Stress = E * (VT/FRC) + ή * (VT/ FRC)/ TI
Strain is function of VT , Strain rate is function of VT and Ti
VISCOELASTIC LUNG
VISCOELASTICITY

Strain rate = (VT/ FRC)/ TI
Ti , RR, Fi are related to each other for a given VT
Strain rate is a function of VT, Ti , RR and Fi
higher VT , lower Ti , higher RR/ FI --- higher strain rate---- higher stress
lower VT , higher Ti , lower RR/ FI -----lower strain rate---- lower Stress
STRAIN RATE VISCOELASTIC LUNG Stress = E * strain + ή * strain rate

Stress = E * strain + ή * strain rate
STRAIN
RATE
DYNAMIC
STRAIN
Clinical Equivalent

strainSTAT = VPEEP/ FRC
strainDYN = VT/ FRC
DYNAMIC VS STATIC STRAIN
strainSTAT
strainDYN

strainDYN
strainSTAT
DYNAMIC VS STATIC STRAIN
DYNAMIC STRAIN EXERTED WITH EACH INSPIRATION
STATIC STRAIN IS EXERTED THROUGHOUT RESPIRATORY CYCLE
DYNAMIC STRAIN IS A FUNCTION OF STRAIN AS WELL AS STRAIN RATE
STATIC STRAIN IS A FUNCTION OF STRAIN ONLY
DYNAMIC STRAIN GENERATES HIGHER STRESS THAN STATIC STRAIN

(low dynamic strain + high static
strain) = low strain rate
(low tidal volume + high PEEP)=
low strain rate
Less stress
(Low PL )
Stress is higher during dynamic strain than in static strain
Therefore for a given lung volume

(low tidal volume + high PEEP)= low strain rate
Less stress
(Low PL )
(high tidal volume + low PEEP)= high strain rate
high stress
(high PL )

(low tidal volume + high PEEP + Low RR /high Ti)= low
strain rate
Less stress
(Low PL )
strain rate is function of VT, Ti , RR and FI
Strain rate = strain/ time= VT/Fi
Stress will increase with high VT,, RR /FI and low Ti
(high tidal volume + low PEEP + high RR/ low Ti)= high
strain rate
high stress
(high PL )
DYNAMIC STRAIN

Stress ( transpulmonary pressure- PL ) is surrogate for VILI
Stress (PL ) of 17 cmH2O increases lung volume from FRC to TLC (safety limit of collagen fibers),
irrespective of lung volume
Mechanical ventilator exerts static strain (PEEP induced) and dynamic strain (PL induced)
Dynamic strain is a function of strain (VT ), and strain rate (RR/ FI/ TI)
Dynamic strain generates more stress than static strain
High tidal volume, low PEEP, high RR, low inspiratory time will generate high stress (transpulmonary
pressure)
Low tidal volume, high PEEP, low RR, high inspiratory time will generate low stress (transpulmonary
pressure)
REMEMBER

Transpulmonary pressure (PL ) of 17 cmH2O increases lung volume from FRC to TLC
(safety limit of collagen fibers), irrespective of lung volume
High tidal volume, low PEEP, high RR, low inspiratory time will generate high
transpulmonary pressure
Low tidal volume, high PEEP, low RR, high inspiratory time will generate low
REMEMBER

ARDS PATHOPHYSIOLOGY
ARDS
Alveolar-
endothelial
leakage
Alveolar
edema
Surfactant
deactivation

ARDS PATHOPHYIOLOLY
COLLAPSED/ NON RECRUITEABLE DISEASED LUNG
not participating in ventilation/ gas exchange
RECRUITABLE LUNG
healthy lung+ recruitable diseased lung
(BABY LUNG)
participating in ventilation/ gas exchange
BABY LUNG
Small volume
Alveolar
heterogeneity
Alveoli of different
size and shape

BABY LUNG- SMALL VOLUME
BABY lung volume is a function of ARDS severity
Severe ARDS- baby lung volume may be 20-30% of normal lung
volume
Small baby lung exposed to 100% of mechanical force of mechanical
ventilation and participate in 100% of gas exchange

EVOLUTION OF BABY LUNG CONCEPT
Static anatomical
model- non
dependent location
static functional
model- sponge
lung
dynamic model-
VILI vortex

ALVEOLAR HETEROGENEITY
Alveoli in baby lung have different size/ shape - different mechanics (Compliance- C/ Resistance- R/
time constant- TC)- UNSTALBLE ALVEOLI

UNSTABLE ALVEOLI
STABLE ALVEOLI
homogenous size/ shape and mechanics (compliance-C/ resistance-R/ time constant-TC) resulting in alveoli
with homogenous inflation during inspiration which do not collapse during expiration
Uniform distribution of mechanical force in all alveoli, minimal repeated opening/ closing of alveoli
Structural/
functional
interdependence
non
diffusible
Nitrogen
surfactant
mechanical
support of
shared wall
- Remain open at end expiration (do not collapse at end expiration)

UNSTABLE ALVEOLI
Heterogenous alveolar
size and shape
Heterogenous alveolar
C/R/ TC
fast alveoli
Rapid filling/ emptying
slow alveoli
Slow filling/ emptying

UNSTABLE ALVEOLI
FAST ALVEOLI
Hyperinflation at end
inspiration
Collapse at end expiration
repeated opening and closing
bear more mechanical force
during inflation
SLOW ALVEOLI
Partial filling at end
inspiration
Partial emptying at end
expiration
Partial recruitment at end
inspiration
autoPEEP at end expiration

UNSTABLE ALVEOLI End
expiration
End
inspiration

In baby lung Recrutiment (R) takes long time because of slow alveoli
Derecrutiment (D) occurs rapidly because of fast alveoli
More severe ARDS- more heterogenous alveolar TC - more delayed R and more rapid D
R/D of baby lung is continuous process throughout the lung volume range- no safe level of PEEP at
which R/D is eliminated
UNSTABLE ALVEOLI

UNSTABLE ALVEOLI

REMEMBER
Baby lung is functional/ recruitable lung, venerable to VILI
Baby lung is small volume with heterogenous alveoli (different time constants)
Baby lung volume and heterogeneity is a function of severity of ARDS
Alveolar heterogeneity makes baby lung alveoli unstable, resulting in fast and slow alveoli
In Baby lung- Recruitment (R) takes long time because of slow alveoli
-Derecruitment (D) occurs rapidly because of fast alveoli
R/D of baby lung is continuous process throughout the lung volume range- no safe level of PEEP at which R/D is
eliminated

ALSO REMEMBER
Transpulmonary pressure (PL ) of 17 cmH2O increases lung volume from FRC to TLC
(safety limit of collagen fibers), irrespective of lung volume
High tidal volume, low PEEP, high RR, low inspiratory time will generate high
Low tidal volume, high PEEP, low RR, high inspiratory time will generate low

BABY LUNG
SMALL VOLUME WITH UNSTABLE ALVEOLI
BABY LUNG
Small volume
Normal Compliance:
Specific lung elastance is
normal- 13.5
Heterogenous alveoli-
different TC-
Unstable alveoli

BABY LUNG
SMALL VOLUME WITH UNSTABLE ALVEOLI
fast alveoli hyperinflate-
receive high stress/ strain
fast alveoli- rapid collapse-
repeated opening and
collapse cycle- receive high
dynamic strain= higher stress
STRESSED
BUT NOT
STRAINED
INCREASED
STRESS AND
STRAIN
Multiplied stress-
Stress riser effect
stress generated in fast
alveoli is more than applied
stress because of stress riser
effect

Stress =
4.5*PL
C1/10
N
Applied PL of 30 cmH2O
Generated stress of 132 cmH2O

BABY LUNG
SMALL VOLUME WITH UNSTABLE ALVEOLI Severity of ARDS
Smaller baby lung
More heterogenous
alveoli
More collapse are fast
alveoli
more are stress riser
higher dynamic strain

Low VT ventilation mandates higher RR to excrete CO2
Higher RR increases Fi /decreases Ti
Higher strain rate
Higher dynamic strain

Severe ARDS
For a set VT , generated stress (PL) is much higher than expected

ALVEOLAR STRUCTURE
BLOOD GAS BARRIER and Skeletal Matrix
Thickness of 50-100 nm but can withstand a transpulmonary pressure upto 35 cmH2O,
Collagen: inextensible, acts as safety limit at TLC,
Elastin: stretchable causing elastic property of lung,
Proteoglycans: stabilizes fibrillar network, provides viscoelastic behavior to lung

Toshima et al. Arch Histol Cytol. 67(1):31-40 (2004)
COLLAGEN FIBERS NETWORK IN RAT LUNG
COLLAPSED INFLATED

INJURING BABY LUNG
STRESS FAILURE
MECHANICAL DISRUPTION
STRESS FAILURE
ALVEOLAR ODEMA,
INFLAMMATION, HEMORRHAGE

INCREASED STRESS (PL)
Higher dynamic strain
Higher RR/ Fi/ low Ti
STRESS FAILURE
Alveolar edema, inflammation,
hemorrhage
SHRINKING BABY LUNG
Smaller baby lung/ more alveolar
instability
VICIOUS CYCLE– SHRINKING BABY LUNG

Increased stress/ strain
stress failure
Alveolar unit drop
Progressive stress
loading
VILI VORTEX

VILI PATHOPHYSIOLOGY
Fast alveoli receive higher stress (PL ) because of rapid inflation during inspiration and rapid collapse
during expiration (higher strain rate- dynamic strain)
Generated stress is more than applied stress because of stress riser effect and strain rate (a high Fi/
RR/ low Ti )
When this stress (PL) exceeds the safety limit of collagen fibers (17 cmH2O), it results in mechanical
disruption of collage fibers, culminating in stress failure (alveolar inflammation/ edema/
hemorrhage)
Stress failure further increases alveolar inhomogeneity and deranges mechanics, which further
increases generated stress causing further stress failure, creating a vicious cycle of incremental
generated stress and stress failure perpetuating each other
Vicious cycle of stress and stress failure creates a vortex into which baby lung getting sucked into
diseased lung tornado.
VILI vortex transforms recruitable baby into non recruitable diseased lung

HOW TO STABILIZE ALVEOLI
UNSHRINKING BABY LUNG
PULLING OUT OF VILI VORTEX

PULLING BABY LUNG OUT OF VILI VORTEX
REDUCE ALVEOLAR HETEROGTENEITY
OPTIMIZE LUNG MECHANICS- Reduce Dynamic Stress
• Reduce strain and strain rate-
• achieve Recruitment (R) of max alveoli
• Prevent Decruitment (D) of max alveoli
• Low RR/ long Ti/ slow Fi
VENTILATE WITH VT OF BABY LUNG
• Limit stress (Transpulmonary pressure PL)

REDUCE ALVEOLAR HETEROGTENEITY
OPTIMIZE LUNG MECHANICS- Reduce Dynamic Stress
In baby lung R takes a long time but D occurs rapidly
More severe ARDS- more heterogenous alveolar TC - more delayed R and more rapid D

OPTIMIZE LUNG MECHANICS- REDUCE ALVEOLAR HETEROGTENEITY
Reduce Dynamic Stress

Optimal PEEP- Promote R max alveoli/ Prevent D of max alveoli
reduce dynamic strain and increase static strain
long Ti/ brief Te- Promote R max alveoli, prevent D of max alveoli
Slow Fi/ low RR/ long Ti- reduce strain rate (dynamic strain)
PRONE POSITION- Promote R o max alveoli, prevent D of max alveoli
strainDYN
strainSTAT

OLV- OPTIMAL PEEP- PEEP titration to best compliance/ optimal gas exchange/ best hemodynamics
INVERSE RATION VENTILATION- long Ti/ brief Te
low RR
PRONE POSITION- reduces heterogeneity of baby lung

VENTILATE WITH VT OF BABY LUNG- LIMIT PL PRESSURE
baby lung volume undetermined– how to set tidal volume
baby lung volume is function of severity of ARDS,
Setting VT as per PBW is inaccurate surrogate of baby lung strain and stress
targeting VT as primary variable and transpulmonary pressure as dependent variable
is not a safe strategy
limiting stress by making transpulmonary pressure (PL) as primary variable and tidal
volume as dependent variable is safe strategy to prevent VILI

VENTILATE WITH VT OF BABY LUNG- LIMIT PL PRESSURE
primary variable
Tidal Volume
dependent variable
Set transpulmonary pressure and accept generated tidal volume

LIMIT TRANSPULMONARY PRESSURE (PL )
PL of 17 cmH2O will inflate baby lung to limit of structural damage, irrespective
of volume
Set PL of 17 would be multiplied to more, by dynamic strain (stress risers/
Fi/RR/Ti)
Safe limit of PL is less than 17 cmH2O
SAFE LIMIT OF PL
LESS THAN 17 CMH2O
BUT HOW
MUCH

PPLAT-PPL
PPLAT
CL= VT/ (PPLAT -PPL)
PL
CRS= VT/PPLAT
TRANSPULMONARY PRESSURE (PL)- Distending pressure of lung
DRIVING PRESSURE (∆P)- Distending pressure of Respiratory system
∆P
PL MEASUREMENT
Requires pleural pressure (ppl ) measurement which is invasive and complicating

DRIVING PRESSURE (∆P)
∆P is the distending pressure of the respiratory system, which is
plateau pressure above PEEP (PPLAT- PEEP)
it is considered as a surrogate of pl , as easy and non invasive
measurement
Limiting ∆P, irrespective of severity of ARDS, would prevent dangerous
stress- strain and prevent VILI

DRIVING PRESSURE- ∆P
strainDYN
strainSTAT
DRVING
PRESSU
RE
Limiting ∆P mandates application of
optimal PEEP to prevent D of max alveoli
Limiting ∆P is akin to limiting dynamic
strain at the cost of static strain

DRIVING PRESSURE PRESUMES
Optima PEEP
P-V relationship on linear part
LIP
UIP
STRESS
INDES
≤1
STRESS INDEX ≥1
S
T
R
E
S
S
I
N
D
E
X
0
DRIVING PRESSURE- ∆P

LIMIT DRIVING PRESSURE (∆P)
∆P of 17 cmH2O will inflate baby lung to limit of structural damage, irrespective
of volume
Set ∆P of 17 would be multiplied to more, by dynamic strain (stress risers/
Fi/RR/Ti)
Safe limit of ∆P is less than 17 cmH2O
EVIDENE BASE MEDICINE
SAFE LIMIT OF ∆P
LESS THAN 14 CMH2O

SPONTANEOUS BREATHING IN MECHANICAL VENTILATION
DOUBLE EDGED SWORD
STRESS (PL ) = PLATEU PRESSURE – PLEURAL PRESSURE
VIDD
VENTILATOR INDUCED
DIAPHRAGMATIC
DYSFUNCTION
P-SILI
PATIENT SELF INDUCED
LUNG INJURY
PATIENT- VENTILATOR
ASYNCHRONY
PATIENT DISCOMFORT,
WORSENING PULMONARY MECHANICS,
INCREASED WOB,
HEMODYNAMIC INSTABILITY

OPTIMIZE PEEP– BEST COMPLIANCE/ OPTIMAL GAS EXCHANGE/ BEST HEMODYNAMICS
ADD 13 TO PEEP- SET PPLAT AT THIS LEVEL (KEEP ∆P <14, PPAT <30)
ACCEPT GENERATED VT
SET RR AT MINIMAL TO ACHIEVE PERMISSIVE HYPERCAPNIA (PH >7.20)
IRV I:E ratio >1:1
SET FI TO PATIENT’S COMFORT (NO FLOW ASYNCHRONY)
BLOOD GAS TARGET- PaO2 55-80 MMHG, SPO2 88-92%, PaCO2 TO PH >7.20 (permissive hypercapnia)

AVOID SPONTANEOUS RESPIRATION AND PATIENT VENTILATOR ASYNCHRONY
Spontaneous respiration (negative pleural pressure) in mechanical ventilation (positive plateau pressure)
will increase transpulmonary pressure (Stress)
Transpulmonary pressure= Plateau pressure – Pleural pressure
• SEDATION/ NM BLOCKER
• CONTINUOUS MANDATORY VENTILATION (CMV)
BLOOD GAS TARGET- PaO2 55-80 MMHG, SPO2 88-92%, PaCO2 TO PH >7.15

ASSESS LUNG MECHANICS EVERY 6 HOURLY AND TIRTRATE PEEP
TITRATE RR BASED ON PERMISSIVE HYPERCAPNIA
INDIVIDUALIZE PPLAT AND ∆P TO BODY HABITUS
PRONE POSITION- REFRACTORY HYPOXIMIA- P/F < 150, BREAKING OF DRIVING PRESSURE/ Pplat BARRIER
TO ACHIEVE PERMISSIVE HYPERCAPNIA (pH <7.12)
AVOID ABRUPT TRANSITION OF SUPPORT/ CAUTIOUS WEANING ( ARDS LUNG WILL TAKE TIME TO HEAL
AND OPTIMIZE MECHANICS)

Optimize hemodynamics- optimal PEEP- DO2= CO*Hb*SaO2
Conservative fluid strategy
Reduce O2 demand (OER) and CO2 production
• Reduce WOB- intubation and sedation/ NM blocker
• Treat fever, pain, agitation, metabolic acidosis
Target Minimal acceptable oxygenation and permissive hypercapnia
OPTIMIZING OXYGENATION AND VENTILATION

Inhaled NITRIC OXIDE
In severe ARDS with severe RV dysfunction or refractory hypoxemia for short period while waiting for
ECMO
STEROIDS
Individualized according to steroid responsive pathology mimicking/ leading to ARDS-
Covid pneumonia, eosinophilic pneumonia, pneumocystis jeruvaci pneumonia
ECMO
Selected patients with severe ARDS- LIS >=3, severe ARDS, severe respiratory acidosis (pH < 7.2) despite
optimal PEEP, NM blocker, prone position
ECCO2R
OPTIMIZING OXYGENATION AND VENTILATION

Driving
Pressure <13
Platue
pressure <30

TOPIC Grade/ Recommendation Condition
Tidal volume/ Plateu pressure 1+/ Strong- should be done VT 6 ml/kg PBW, PPLAT <30
Driving pressure No recommendation More data needed
PEEP 2+/ optional- probably be done Moderate/ severe ARDS, high PEEP
Conservative fluid strategy
Prone position 1+/ Strong- should be done Moderate/ Severe ARDS (P/F <150), at least
16 hours a day
NM blocker 2+/ optional- probably be done Moderate/ Severe ARDS (P/F <150,
continuous infusion for <48 hours
Inhaled NO No recommendation Expert opinion- in Refractory hypoximia for
short time till ECMO initiated
ECMO 2+/ optional- probably be done P/F ration <80, PPLAT >30 despite optimal
PEEP, Nm Blocker and proning
ECCO2R No recommendation
Early spontaneous breathing Acute phase ARDS- no recommendation Post acute phase ARDS- may be allowed if VT
< 8 ml/kg PBW
GUIDELINE-FRENCH INTENSIVE CARE SOCIETY (SRLF)- 2019

GUIDELINE- INTENSIVE CARE SOCIETY UK 2019

“Before treating you must understand the mechanics
that lead to what you want to treat"
-Luciano Gattinoni
MINIMIZE IOTROGENIC HARM
THANK YOU
https://learningcriticalcaremedicine.blogspot.com

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