7. DIRECT LUNG INJURY
• Pneumonia
• Aspiratia continutului
gastric
• Contuzia pulmonara
• Inhalatie de toxice
• Inecul
INDIRECT LUNG INJURY
• Sepsis
• Traumatism nou toracic
sever
• Bypass CP
• Pancreatita acuta
• Arsuri
• TRALI
cea mai frecventa
cauza
extraspitaliceasca
cea mai frecventa
cauza
11. Figure: Schema representation of sponge model. In ARDS the “tissue”, likely edema in
the early phase, is almost doubled in each lung level compared with normal,
indicating the nongravitational distribution of edema. The increased mass, however,
causes an increased superimposed pressure (SP), which in turn, leads to a “gas
squeezing” from the most dependent lung regions. Superimposed pressure in
expressed as cm H2O. The values indicated in the figures are taken from Pelosi and
cowerkers.
14. ARDS = Heterogenitate
• Intre pacienti
• In timp, la acelasi pacient
• In acelasi plaman
Faza precoce
(0-3 zile)
Faza tardiva
(>7 zile)
Colagen
structural
puternic degradat
Atelectazie ++++ ++
Edem ++++ ++
Mecanica heterogena mai putin heterogena
VILI edem si
hemoragie
pneumotorax
pneumatocele
-Regiuni inflate – mult, putin, mediu
-Regiuni consolidate (sticky atelect) –
deja proces de fibrinoformare
-Regiuni atelecto-colabate(loose atelect)-
mecanism presional
15. Factori determinanti ai presiunii de deschidere:
1. Absenta surfactantului
2. Ppl, SP mai crescute in partea dependenta
3. Reducerea compliantei toracice
4. Fibrinoformare
5. Marimea alveolei(T=Δ pr/2h)
16. •
• EL > N ĺ TPĹĺ VILI / VALI
• EW > N ĺ TPĻĺ PplĹĺ Alterare hemodinamica
17.
18. Mecanica heterogena
• Deschiderea plamanului are loc la p > decat colabarea
• Deschiderea unor unitati poate presupune hiperinflatia altora
19.
20. Mecanica respiratorie
ARDS pulmonar vs. ARDS extrapulmonar
• Consolidare ↑
• EL ↑↑ ↑
• Raspunde la manevre de
reĐrutare↓
• Nu raspunde la pozitia prona
• R ~
• ERS ~
• Sticky atelectasis
• Risc de barotrauma
• IAP normal
• Ground-glass
• EW ↑↑, EL ↑
• Raspunde la manevre de
reĐrutare ↑
• Raspunde la pozitia prona
• R ~
• ERS ~
• IAP ↑↑ ;~ EWͿ
• Edem interstitial
• Loose atelectasis
• Risc de alterare
hemodinamica
21. Figure: Changes of static
elastances of the respiratory
system (Est,rs), lung (Est,L), and
chest wall (Est,w) as a function of
PEEP in pacients with ARDS
caused by pulmonary disease
(Group 1, top panel) with in
ARDS caused by extrapulmonary
disease (Group 2, bottom panel).
Comparison within each group:
*p<0.05 versus PEEP O cm H2O;
**p<0.01 versus PEEP O cm
H2O. Comparison between the
two groups; ^p<0.05 versus
Group 1; ^^p<0.01 versus Group 1.
22.
23.
24. VILI / VALI
Def:
“Acute lung injury that develops during
mechanical ventilation is termed VALI if one
cannot prove beyond any doubt a causative
relationship.
VILI – a causative relationship can be proven.”
26. BAROTRAUMA
Odata principala cauza de VILI
Astazi “doar” un accident mecanic
Cauzata de: Include:
• MAwP ↑
• PP ↑
• PEEP ↑
• Emfizem interstitial
• Pneumomediastin
• Pneumotorax
• Embolism gazos
27. VOLUTRAUMA (supradistensia alveolara)
• Volumele tidal mari produc ALI
• 2 studii pe animale demonstreaza ca volumele
tidal mari, nu presiunile, produc ALI
• In realitate presiunea TP explica ambele fenomene
si:
-- presiunile mari nu produc tot timpul
barotrauma (Cw Ļ)
-- volumele mici pot produce ALI (CL Ļ)
28. Extravascular lung water (Qwl), dry lung weight, and albumin space are indicative of the
development of lung injury. These abnormalities were induced in rats ventilated with
high pressure and high tidal volume (HiP-HiV), low pressure and high volume (LoP-HiV),
but not in those ventilated with high pressure and low volume (HiP-LoV).
Redrawn from Dreyfuss, D,Soler, P,Bassett, G, Saumon, Am Rev Respir Dis 1988
29. The effect of limited intrathoracic expansion by means of a body cast on ventilator-induced
lung injury in rabbits. Rabbits were ventilated with 15, 30, and 45 cmH20 peak inspiratory
pressure for one hour. Redrawn from Hernandez, LA, Peevy, Kj, Moise, AA, Parker, JC,
J Appl Physiol 1989.
32. Popping open of lung units under high pressure might be the answer
33.
34.
35.
36.
37. • “cyclic stress “ endotelial
• Zona 2 intermitenta
• Forte de sens opus la nivelul lumenului ce uneste cele doua tipuri de vase
38.
39. Toxicitatea oxigenului
• Form rad. liberi
- superoxid
- hidrogen peroxid
- ion hidroxil
• Atelectazie de resorbtie
• Studii pe animale cu FiO2=1
DECES IN 48-72 h (ALI/ARDS)
• Voluntari umani respirand FiO2=1
• Target: FiO2 ≤ 0,6
• Target: PaO2 = 55-80
SpO2 = 88-95%
Importanta hipoxemiei depaseste pe cea a
toxicitatii O2
RASP INFLAMATOR IN 24 h
40. BIOTRAUMA
• Rasunet celular al unui pattern ventilator inadecvat
• Presupune mecanotransductie
• Producere excesiva si import inadecvat de mediatori
inflamatori si antiinflamatori
• Raspunsul inflamator este intra si extracompartimental
(decompartimentalizare)
• Predispune la SIRS si MODS
• Alterarea patternului de crestere bacteriana si
imunosupresie
43. Lung protective ventilation
Conventional “Lung
protective”
Large tidal volume Small tidal volume
Minimum PEEP “Sufficient PEEP”
Normalize PaCO2 Permissive
hypercapnia
Unrestrained
airway pressure
Pressure limitation
1. Open Lung Ventilation
“Open up the lung and keep
the lung open”
(1992, Lachmann)
2. ARDS net
44. Open Lung Ventilation(1)
• Volume tidal mici (4-8 ml/kgc) (˜ ARDS net)
• Pplateau ≤ 25-30 cm H2O (˜ ARDS net)
• Manevre de recrutare
• PEEP optimizat
• RR ≤ 35/min (˜ ARDS net)
• Compromis:
HCO2, hO2 (˜ ARDS net)
45. Open Lung Ventilation(2)
• Nu exista un protocol universal
• Mare variabilitate
• Optimizarea PEEP-ului, manevra de recrutare,
potential de recrutare – puncte de interes
• Abordare fiziopatologica
• Permite individualizarea ventilatiei
• Presupune cunoastere aprofundata a mecanicii
respiratorii
46. Model clasic de Open Lung Ventilation (Lachmann)
Action (1) Data Comments
Pacient at day 2: volume
controlled ventilation with tidal
volumes of 6 ml/kg
FiO2=70%; PEEP=11cm H2O
RR=32; I:E=1:2;
SaO2=92% ; PAWP=26cmH2O ;
TV=6 ml/kg=480 ml;
PaO2=72mmHg; PaCO2=48 mmHg
Switch to pressure controlled
ventilation
FiO2 set to 100%
I:E=1:1; RR:40
PAW 26 cm H2O
PEEP 20
SaO2=100%
PaO2=140 mmHg
PaCO2=39 mmHg
Increase PAWP to 45 cmH2O for
three breaths (5 seconds), then
back to 30
PaO2=265 mmHg
1 min after stabilization increase
PAWP to 50 for 5 sec, then back
to 30
PaO2=350 mmHg
1 min after stabilization increase
PAWP to 55 for 5 sec, then back
to 30
PaO2=530 mmHg
PaCO2=28 mmHg
47. Model clasic de Open Lung Ventilation (Lachmann)
Action (2) Data Comments
1 min after stabilization increase
PaO2=531 mmHg
PAWP to 60 for 5 sec, then back
PaCO2=28 mmHg
to 30
PaO2 does no further increase.
Opening presure=55 cmH2O.
Decrease PAWP to 28-24 No changes
Decrease PAWP to 23 PaO2=480 mmHg The lung is collapsing.
Minimum required upper
pressure limit = 24 cmH2O
Recruit the lung (PAWP to 55,
then 24)
Reach opening pressure and airway
pressure set back just above collapse
pressure
PAWP 24, decrease PEEP to 18 No changes
PEEP to 17 PaO2=541 mmHg
PEEP to 16 PaO2=470 mmHg Minimum required lower
pressure limit = 17 cm H2O
48. Model clasic de Open Lung Ventilation (Lachmann)
Action (3) Data Comments
Set PEEP to 17
PaO2=544mmHg
Increase PAWP to 55 for 5 sec
PaCO2=34 mmHg
(recruit) and back to 24
Optimal CO2 removal requires VCO2
of 430 ml/min;
Slight hyperventilation
Increase RR to 47
I:E=3:2
PaCO2=36mmHg
VCO2=435 ml/min
TV=395 ml=4,9
Smaller pressure amplitude due to
auto-PEEP and increased dead space
ventilation
Decrease FiO2 to 30% PaO2=114 mmHg
PaCO2=36 mmHg
Optimized patient ventilation at open
lung
49. Manevre de recrutare
• Nu exista “o cea mai buna”
• Cele mai folosite: 1 si 2
• 1:Cel mai mare impact
hemodinamic
• 3>1 daca presiuni mai mari
ca cele tolerate la 1 sunt
necesare
• 1>3 pentru ca recrutarea
depinde mult de MANP
50. Recrutam pas cu pas?
When collapse is prevalent (top), the overall
pleural pressure results very low and the local
transpulmonary pressures increase
significantly. The risk of overdistension is very
high at this condition, especially if one
considers a single step – high pressure
recruiting maneuver. Contrarily, we propose
the application of lower pressure at this
moment (top), increasing it progressively as
new units get recruited.
51. Facilitarea recrutarii
• Pozitie prona
• Presiune de inspir adecvata (40-45 cmH2O)
• PEEP adecvat
• Cel mai mic FiO2 acceptabil (in afara
momentului recrutarii – Lachmann)
• Respiratie spontana posibila
(BIPAP, Autoflow, APRV)
• Minimizeaza edemul interstitial
(repletie volemica adecvata,
monitorizare EVLW-PICCO,Vigileo,
TA invaziv - ΔdoǁŶ+Δup)
52. Factori determinanti ai eficientei recrutarii (1)
• Tipul de ARDS EP>Pulm
• Stadiul ARDS
• Punctul de pornire
• PEEP postrecrutare
• Tipul de manevra
• PaO2/FiO2 < 150 (at PEEP 5 cm H2O)
• RxCP – voalat
• LIP – pe curba PV, bratul inspirator
53. Factori determinanti ai eficientei recrutarii (2)
• Recrutezi doar ce este recrutabil
• ↑PEEP are seŶs peŶtru plaŵaŶul reĐrutaďil
• Cat de recrutabil este recrutabil?
ENGSTRÖM
> 9 % CT
54. Cel mai des derecrutezi prin:
• FiO2 ↑ (>0,6) pentru Δt ↑
• Aspiratie / Bronhoscopie
55. Care este PEEP-ul optim?
Maximum de recrutare cu minimum de distensie
Electric impedance tomography (EIT)
images are presented on the right,
whereas the corresponding CT images
(obtained at the same PEEP level) are
represented in the left side of the
figure. The EIT images represent the
ventilation map during tidal breaths.
Brighter areas indicate pixels with
larger impedance variations (larger
alveolar ventilation) during tidal
breaths. Excessive, as well as
insufficient PEEP levels, caused uneven
ventilation. Excessive PEEP caused
preferential ventilation in the
dependent lung zones (because of the
relative overdistention of non –
dependent lung zones). Insufficient
PEEP caused dependent collapse with
preferential ventilation towards the
patent airspaces at the non- dependent
“baby lung”.
56. Care este PEEP-ul optim?
1. Curba P-V brat inspirator (Engstrom
dynostatic curve – dynostatic algorithm,
constant low flow P-V loop pe Drager (VCV))
2. DO2
DO2>600 mlO2/min chiar cu
PEEP ↓ → ateleĐtrauŵa ↑
3. Evaluare PaO2,PaCO2
4. Monitorizarea compliantei tidal (CRS)
5. Indexul de stress
6. CRF, volum recrutat - Engstrom
58. Evaluare PaCO2, PaO2
A. Model Lachmann (PaO2)
B. PaCO2 -- necesita VCV (MV=const)
--la ↓ PEEP ;de la ϭ5 - 20):
1. PaCO2 ~ (overdist=recr)
Ϯ. PaCOϮ ↓ ;reĐr>oǀerdistͿ
ϯ. PaCOϮ ↑ ;dereĐrutareͿ
PEEP optim = cea mai mica PCO2
Dezavantaje redistributia sangelui intre teritorii cu V/Q
diferit
59. CRS
• Cea mai la indemana
• CRS d.p. cu recrutare/supradistensie
• Dezavantaje:
- CRS are Sb ↓ la Đei Đu Cǁ ↓
- ΔCRS suŶt ↓↓
60. Stress index
• Analiza in dinamica a curbei P-T (Paw)
• Ventilatie cu flux constant (VCV)
• Permite (teoretic) optimizarea ventilatiei
- setare PEEP optim
-setare VT optim
• Vede raportul recrutare/supradistensie
• Nu vede recrutarea sau distensia
• Pp. culegerea de semnale cu frecventa ↑
• Foarte controversata
• Odata efectuata optimizarea autoflow
66. Date statistice (1)
ARMA TRIAL (ARDS Network)
• Studiu prospectiv, randomizat, multicentric
• 861 pacienti cu ARDS
• 12 ml/kg (A) vs 6 ml/kg (B) volum tidal
• Grupul B: rata mortalitatii ↓ (31% vs 40%)
• Grupul B: zile fara ventilatie mecanica (12 vs 10)
67. Date statistice (2)
ALVEOLI TRIAL (ARDS NETWORK)
• Studiu prospectiv, randomizat, multicentric
• 768 pacienti cu ARDS ventilati conform ARMA
cu exceptia FiO2 / PEEP
• PEEP ↑ ǀs PEEP ↓
• PEEP mediu 13 vs 8
• Rata mortalitatii: scadere nesemnificativa statistic
• NB: Nu s-au efectuat MR
• NB: Grupul PEEP ↑ -pacienti cu varste mai ↑
- PaO2/FiO2 mai ↓
68. Date statistice (3)
(A) Open Lung Ventilation
MR PEEP optim/ ↑
(B) Conventional LPV
ARDS net
• Fara impact pe mortalitate
• A – incidenta mai mica a hO2
– recuperare mai rapida
• Majoritatea studiilor au limite
-- potentialul de recrutare este omis
-- + MR - ĹPEEP
-- + Ĺ PEEP - MR
-- heterogenitate dpdv al bolii de baza
-- randomizare defectuoasa (pacienti
mai varstnici cu PaO2/FiO2 mai Ļ in grupul A)
Recrutezi doar ce e recrutabil!
Castigi doar unde poti castiga!
69. PRO si CONTRA respiratie spontana in
managementul ventilator ALI/ARDS
PRO
• V/Q ↑in teritoriile
supradiafragmatice
• Efort inspirator
Ppl ↓
↑TP
↑ raspuŶsul la MR
• CO↑ DO2 ↑
CONTRA
• VO2 Ĺ
• VCO2 Ĺ
• ITBV Ĺ EVLW Ĺ
EDEM Ĺ
SP,Ppl Ĺ
ĻTP
Atelectazie
Efort exp ↑ Ppl↑
76. Hipercapnia permisiva
Are the effects of high PaCO2 deleterious or Protective?
CO2
Activation of
signal
transduction
pathways
Decreased
alveolar
fluid Cl
Decreased
inflamatory
response
Decreased
VILI/VALI
77. Hipercapnia permisiva – Contraindicatii
(absolute si relative)
• ICP ↑ ;trauŵa, tuŵora, HTA seǀeraͿ
• Acidoza metabolica severa
• B. coronariana, IC, aritmii
• Tratament cu beta blocante
• HTP, IC dreapta
• Hipovolemie
• Sangerari GI
• Siclemie
• ATC – supradozaj
• SarĐiŶa risĐ de FBF ↓ priŶ sdr. de furt datorat VD
79. Hipercapnia permisiva
• PRO pH≥7,15
• PRO pH=7,3-7,45
• CONCLUZIE:
1. Nu corectezi acidemia (pH-ul) ci acidoza
2. Acidoza este un raspuns individual la acidemie
(ex – instab. hemod)
Corectarea se va face individual (vezi CI)
iar pH-ulĻ este UN semnal de alarma si
NU indicator al corectarii
Cand
?
-Relativ bine tolerata cand PaCO2a Ĺ treptat
- Ļ VALI independent de VT Ļ
- pH fiziologic
80. Hipercapnia permisiva
Cu ce?
Cum?
1. Setarea parametrilor ventilatori (RR, VT) a.i. sa ramai in intervalul de LPV
2. Adm subst alcalinizante
-- NaHCO3 – folosit in protocolul ARDS net
-- THAM (trishidroximetilaminometan – R – NH2)
-- Carbicarb- amestec echimolar CO3/HCO3
NaHCO3+H+ H2CO3 CO2Ĺ ĹPaCO2
ĹCO2icel ↓pH icel
Obs: ĹPaCO2 este temporara
Ļ pH icel este temporara VA=const – PaCO2 dp FACO2=
Adm NaHCO3 treptata are impact minim pe PaCO2, pHicel
81. Interventii de salvare in managementul ventilator
1. Ventilatia in pozitie prona
2. TGI (tracheal gas insufflation)
3. ECMO (extracorporeal membrane oxygenation)
4. EC CO2R (extracorporeal CO2 removal)
5. LPPPV – EC CO2 R (low frequency positive pressure vent + EC
CO2 R)
6. HFV (high frequency ventilation)
7. LV (liquid ventilation)
8. ILV (independent lung ventilation)
9. PC – IRV (pressure controlled inverted ratio ventilation) clasic,
APRV (airway pressure release ventilation) modern
10. Surfactant inhalator
11. Redistribuirea din teritorii de sunt inspre teritorii ventilate: NO
inhalator, Almitrina iv, prostanoizi inhalator (epoprostenol,
iloprost)
85. Ventilatia prona
SUMMARY AND RECOMMENDATIONS
• Prone positioning appears to improve the oxygenation of most
patients with ALI or ARDS; however, a mortality benefit has not been
established.
• Post-hoc analyses of multiple studies suggest that the greatest benefit of
prone positioning occurs in the sickest patients if used early after the
diagnosis of ALI or ARDS.
• Duration: The optimal duration of prone positioning is unknown. While
many studies have used repeated sessions lasting approximately six to
eight hours per day, impressive and persistent improvements in
oxygenation have been noted with prone positioning of longer duration
• Routine prone positioning of all patients with ALI or ARDS is not
recommended because there is substantial inconvenience associated with
its use and there is insufficient data demonstrating improvement of patient-important
outcomes.
• In our clinical practice, however, we implement prone positioning early in
selected patients with ALI or ARDS. Specifically, we initiate prone
positioning if our goals of lung-protective ventilation are not being met, or
if there is persistent respiratory acidosis or tissue hypoxia despite standard
ventilation in the supine position. This reflects our belief that the risks of
prone positioning are minimal when properly performed and that the
physiologic rationale for its use is sound.
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86. Insuflatia traheala (TGI)
• Concept vechi (1969)
• Mapleson D.
• Flux secundar de O2/aer la niv
carinei
• Necesar doar spre sfarsitul
expirului
• Cateterul TGI spre carina sau
spre circuitul ventilator (Ĺ
PEEP)
• TGI flow 4-15 l / min
• Eficienta Ĺpentru Vda/Vdf ĺ1
• Pentru siguranta trebuie sa
“comunice” cu ventilatorul
TGE (Tracheal Gas Exsufflation)
Sistem coaxial (5mm+8mm)
88. HFV - Indicatii
• There are no universally accepted indications for HFV. Its use has also been
described in a variety of clinical situations. HFV should be avoided in patients with
obstructive lung disease. .
• There is evidence that HFOV and HFPV improve oxygenation, although neither has
been shown to improve clinical outcomes (eg, mortality, duration of mechanical
ventilation, or length of ICU stay).
• HFV is not risk free. Potential harms include intrinsic positive end-expiratory
pressure (auto-PEEP), dynamic hyperinflation, and related sequelae (eg, pulmonary
barotrauma, hemodynamic instability). In addition, there are specific risks associated
with each type of HFV.
• Bronchopleural fistula — HFJV is approved by the United States Food
and Drug Administration for ventilating patients in whom a large and persistent
bronchopleural fistula exists. However, the likelihood that HFJV will allow the
bronchopleural fistula to close is unpredictable. While HFJV may promote fistula
closure by limiting alveolar distension, this may be outweighed in some patients by
increased plateau airway pressure (alveolar pressure), decreased oxygenation, or
worse hypercapnia.
• ALI/ARDS — The theoretical benefit of using HFV in patients with ALI/ARDS
relates to the small tidal volumes. A strategy of low tidal volume ventilation has been
proven in randomized trials to improve mortality, possibly due to decreased alveolar
distension and ventilator-associated lung injury. Although the trials did not use HFV,
many clinicians suspect that HFV confers a similar benefit. Until this is proven, HFV
should not be considered routine care for patients with ALI/ARDS. HFV is
used by some clinicians when there is persistent hypoxemia during the first three
days of mechanical ventilation despite maximal conventional therapy, although the
data to support this are limited
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91. LV (TLV+PLV)
• Ventilatie cu perfluorocarbon (Ex perflubron – C,H, fluor, brom-radioopac)
• Carrier inert de oxigen si CO2(O2=15 x plasma)
• Nontoxic, abs sistemica minima, stabil chimic
• Incolor, inodor, limpede
• PFG abs e metabolizat de macrofage
• Eliminare I prin volatilizare
Avantaje:
1. Ļ TS
2. Rezervor de oxigen
3. Deschide si mentine deschise alveolele prin presiune hidraulica (Ļ riscul
de barotrauma)
4. Δ Q minima
5. V/Q mismatch Ļ (PFG sunt grele si “merg” in zonele dependente)
6. Favorizeaza lavajul
7. Efect antiinflamator
In theory, LV may be of benefit for numerous neonatal and adult
diseases. Clinical trials, however, have shown little improvement in
important clinical outcomes. As a result, LV cannot be recommended in
routine clinical care. (www.UpToDate.org)
93. Indicator of the Severity of Lung
Injury and a Predictor of Mortality
•For every 0.05 increase in
dead space fraction, the
odds of death increased by
45%.
•Other observational studies
suggest that a value of 0.60
or higher may be
associated with more
severe lung injury.
94. Indicator of the Severity of Lung
Injury and a Predictor of Mortality
95. Indicator of Lung Overdistension
During PEEP Titration
• Optimum End Expiratory Airway Pressure in
Patients with Acute Pulmonary Failure
• Suter PM, Fairley HB, Isenberg MD. NEJM 1975
• Best PEEP corresponds
to the lowest dead space
fraction and the highest
compliance
96. Anatomic Vd
Alveolar Vd
Components of
Physiologic Dead Space = Anatomic + Alveolar
20 – 40 %
15 – 25 %
5 – 15 %
98. Dead Space Fraction Measurements
on the Dräger Ventilator
Uses Fowler Method to Calculate
Anatomic Dead Space Fraction
and Volume
Vds / Vt
Vds (mL)
Integrated Mainstream
CO2 Sensor
99. Dead Space Fraction Measurements
on the Dräger Ventilator
VCO2
Minute Ventilation
VCO2 = FēCO2
MV
FēCO2 x (760 – 47) = PēCO2
VDphys = PaCO2 - PēCO2
VT PaCO2
100. Dead Space Fraction Measurements
on the Dräger Ventilator
• Requires manually averaging
VCO2 and MV over a 5 – 10
minutes especially with large
variations.
• Validation study is not
complete.
• Requires commitment by
Dräger to implement software
revision.
