ARDS

Liliana Mirea
Clinica ATI, Sp. Clinic de Urgenta Bucuresti
Forme clinice

ALI
(Acute Lung Injury)

ARDS
(Acute Respiratory distress syndrome)

Acute hypoxemic respiratory failure

Insuficienta respiratorie acuta
hipoxemica
 Hipoxemie rezistenta la
suplimentarea de O2

 Sunt intrapulmonar dreapta-stanga

(alveole perfuzate, dar neventilate)
Date epidemiologice
 50.000-150.000/an in SUA

 Mortalitate 25-50%
Cuprins
 Definitia, cauzele precipitante ale
ARDS
 Elemente de fiziopatologie
 Dg. diferential ALI-ARDS si alte cauze
de insuficienta respiratorie
 Tratament – ARDS Clinical Trials
Network (ARDS Net)
Criterii de diagnostic
1. Debut
2. Hipoxemie – paO2/FiO2
3. Aspect radiografic
4. Excluderea cauzelor cardiace
Criterii de diagnostic
Variabila ALI ARDS

Debut Acut Acut

Hipoxemie 200<paO2/FiO2 paO2/FiO2 200

300
Rx pulmonar Infiltrate bilaterale Infiltrate bilaterale

Cauza noncardiaca Fara hipertensiune Fara hipertensiune

in AS sau in AS sau
PAP  18 mmHg PAP  18 mmHg
Cauze precipitante
Directe Indirecte

Aspiratia continutului gastric Pancreatita acuta

Pneumonie bacteriana Transfuzie masiva (TRALI)

Trauma toracica/contuzie By-pass cardio-pulmonar

pulmonara Sepsis sever/soc septic

Inhalatie de toxice (smog, Politraumatism cu fracturi
cocaina) multiple (micro/embolii
Pneumonie virala grasoase)
Ingestie de toxice
Factori de risc
 Varsta 
 Presiune de platou  (complianta)
  pO2,  FiO2
 Infiltrate pulmonare extensive
 Alte disfunctii de organ asociate
Cauza preciptantaprognostic
 ALI/ARDS postraumatic – cel mai bun
prognostic

 Cea mai mica rata de deces – VM cu

volum mic/presiune de platou
Fiziopatologie
 Faza precoce (exudativa) (S1)
 Edem (diffuse alveolar damage)
 Formarea membranelor hialine
 Faza tardiva (proliferativa) (> 7-10
zile)
 Inflamatie interstitiala
 Fibroza
Fiziopatologie – faza precoce
(exudativa)
 Edem interstitial si alveolar
 Congestie capilara
 Hemoragii alveolare
 Membrane hialine (fibrina, proteine
plasmatice)
 Activarea intraalveolara a coagularii
 Exudat inflamator la niv MAC
 Necroza extensiva a celulelor
alveolare tip I
Faza tardiva
 “vindecare dezordonata”
 Fibroza pulmonara extensiva
 Proliferare de celulel alveolare tip II,
fibroblasti
 Miofibroblasti

 Spatiu mort, necesar MV,

hipertensiune pulmonara progresiva,
compliantei, efect redus al PEEP
Factori fiziopatologici – faza precoce
 Citokine inflamatorii
 RLO
 Activarea coagularii
 Activarea complementului
 Activarea trombocitelor
 Activarea celulelor imune
 Proteaze
 Leucotriene, eicosanoizi etc
Factori fiziopatologici – faza tardiva
 Apoptoza celulara
 Fibroza
 Rezolutia edemului
Citokinele proinflamatorii
 TNF- si IL-1
1. Recruteaza macrofagele in parenchimul pulmonar,
stimuleaza amplificarea si diferentierea acestora
2. Stimuleaza eliberarea altor citokine proinflamatorii
(IL-6, IL-8)
3. Stimuleaza aderenta neutrofilelor la endoteliu

 BAL – nivele crescute de TNF- si IL-1 la p cu

ARDS
 Nivele persistent crescute in plasma, BAL – risc
crescut de deces
IL-6
 Macrofage alveolare
 Factor pro-inflamator
 Proprietati antiinflamatorii
 Nivele serice persistent crescute – risc
crescut de deces

 La p ventilati cu volume mici – nivele serice

mult reduse de IL-6, comparativ cu grupul
ventilat conventional, dupa primele 72 h
IL-10
 Produsa de monocite, LfT, Lf B
 Proprietati antiinflamatorii
 Puternic infibitor al TNF- si IL-1

 Nivele serice scazute de IL-10 (BAL)

– risc crescut de deces
Chemokinele
 Polipeptide cu functie de modulare
locala a activitatii celulelor leucocitare
 IL8, implicata in chemotactismul
neutrofilelor
 Ac IL8 – atenuarea injuriei
pulmonare
Neutrofilele si stresul oxidativ
 Migrarea neutrofilelor in spatiu alveolar este
evidenta in special in faza precoce
 Alterarea apoptozei neutrofilelor si nivele GM-CSF
 Eliberare de RLO (superoxid, radicali
hidroxil,peroxinitrit)– stres oxidativ (leziuni ale
proteinelor, ADN, peroxidarea lipidelor)
Coagularea si fibrinoliza
 Depunere difuza de fibrina la nivelul
MAC
 TNF- si IL-1 induc un status
procoagulant prin activarea factorului
tisular, a trombomodulinei si PAI
Rezolutia edemului alveolar
 Transport activ de apa si Na prin
epiteliu pulmonar (canale epiteliale de
Na de la niv celulelor alveolare tipI,
activate de catecolamine)
 CFTR (factorul reglator al
conductactei transmembranare)
Fibroza pulmonara
 Se suprapune pe faza inflamatorie
 Acumulare de matrix si celule in sp. interstitial si
alveolar, cu alterarea arhitecturii alveolare
 PCP III (tip III de peptid procolagenic) – evolutie scurta
 TGF
 MMP
 Plasmina
 PAI1
 GAG…
Manifestari clinice
 Debut acut
 Dispnee cu tahipnee
 Raluri pulmonare de obicei lipsesc

 Hipoxemie severa, ce nu raspunde la

suplimentarea O2
 RX
 Infiltrate alveolare difuze, bilateral
EPAC
Dg. diferential
 EPAC
 Pneumonie de aspiratie bilaterala
 Atelectazie bilaterala
 Pierderea acuta a functiei ventilatorii
prin pneumotorax sever, revarsate
pleurale masive
 Hemoragie alveolara difuza (post-
transplant medular)
 Embolie pulmonara masiva
Principii de tratament
 !factor precipitant
 VM – “cu volume mici”
 Protocolul ARDS net (2008)
 Tratament suportiv
VM in ARDS
 Clasic
 Oxigenare - mentinerea SpO2>88-90%
 Ventilatia – mentinerea paCO2, pH in
limite normale
 VM protectiva
 Prioritatea principala – evitarea VILI
 Conceptia clasica – plamanul era privit ca
un singur compartiment, toate alveolele au
aceeasi complianta ()
 Modelul muticompartimental (CT scan)
 O mica parte din plaman are complianta relativ
normala – “baby lung” (Gattinoni, 2001)
 Risc de supradistensie
 Restul alveolelor sunt inundate sau colabate
(recrutate)
VM protectiva reduce mortalitate in
ARDS
 Amato M (1998) 38% vs 71%

 ARDS net (2000) 31 vs 39.8%

 Curba presiune volum

LIP – 14-15 cm H2O

UIP – 35 cmH2O

Limitarea VT – volutrauma (supradistensie)

PEEP suficient – recrutarea-derecrutarea ciclica a alveolelor (atelectrauma)
Protocol ARDS net
 PART I: VENTILATOR SETUP AND ADJUSTMENT

 1. Calculate predicted body weight (PBW)

 Males = 50 + 2.3 [height (inches) - 60]
 Females = 45.5 + 2.3 [height (inches) -60]

 2. Select any ventilator mode

 3. Set ventilator settings to achieve initial VT = 8 ml/kg PBW

 4. Reduce VT by 1 ml/kg at intervals ≤ 2 hours until VT = 6ml/kg PBW.

 5. Set initial rate to approximate baseline minute ventilation (not > 35

bpm).

 6. Adjust VT and RR to achieve pH and plateau pressure goals below

Protocolul ARDS net
 Part II OXYGENATION GOAL:
 PaO2 55-80 mmHg or SpO2 88-95%
 Use a minimum PEEP of 5 cm H2O. Consider use of
incremental FiO2/PEEP combinations such as shown
below (not required) to achieve goal.
 Lower PEEP/higher FiO2
 FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7
0.7
 PEEP 5 5 8 8 10 10 10 12

 FiO2 0.7 0.8 0.9 0.9 0.9 1.0

 PEEP 14 14 14 16 18 18-24
Protocol ARDS net
 Higher PEEP/lower FiO2
 FiO20.3 0.3 0.3 0.3 0.3 0.4 0.4
0.5


PEEP 5 8 10 12 14 14 16 16

 FiO2 0.5 0.5-0.8 0.8 0.9 1.0 1.0


PEEP 18 20 22 22 22 24
Protocol ARDS net
 Part III
 PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
Plateau pressure
Protocol ARDS net
 Part III
 PLATEAU PRESSURE GOAL: ≤ 30 cm H2O
 Check Pplat (0.5 second inspiratory pause), at least q
4h and after each change in PEEP or VT.
 If Pplat > 30 cm H2O: decrease VT by 1ml/kg steps
(minimum = 4 ml/kg).
 If Pplat < 25 cm H2O and VT< 6 ml/kg, increase
VT by 1 ml/kg until Pplat > 25 cm H2O or VT = 6
ml/kg.
 If Pplat < 30 and breath stacking or dys-
synchrony occurs: may increase VT in 1ml/kg
increments to 7 or 8 ml/kg if Pplat remains < 30
cmH20
Protocol ARDS
 Part IV pH GOAL: 7.30-7.45
 Acidosis Management: (pH < 7.30)
 If pH 7.15-7.30: Increase RR until pH > 7.30 or PaCO2 <
25 (Maximum set RR = 35).
 .
 If pH < 7.15: Increase RR to 35.
 If pH remains < 7.15, VT may be increased in 1 ml/kg steps
until pH > 7.15 (Pplat target of 30 may be exceeded).
 May give NaHCO3
 Alkalosis Management: (pH > 7.45) Decrease vent rate
if possible.
 ________________________________________________
______
 I: E RATIO GOAL: Recommend that duration of inspiration
be < duration of expiration.
Protocol ARDS net
 WEANING

 A. Conduct a SPONTANEOUS BREATHING TRIAL daily

when:

 1. FiO2 ≤ 0.40 and PEEP ≤ 8 OR FiO2 < 0.50 and PEEP < 5.

 2. PEEP and FiO2 ≤ values of previous day.

 3. Patient has acceptable spontaneous breathing efforts. (May

decrease vent rate by 50% for 5 minutes to detect effort.)

 4. Systolic BP ≥ 90 mmHg without vasopressor support.

 5. No neuromuscular blocking agents or blockade

Protocol ARDS net

 SPONTANEOUS BREATHING TRIAL (SBT):

 If all above criteria are met and subject has been in the study for at
least 12 hours, initiate a trial of UP TO 120 minutes of spontaneous
breathing with FiO2 < 0.5 and PEEP < 5:
1. Place on T-piece, trach collar, or CPAP ≤ 5 cm H2O with PS < 5
Protocol ARDS net
 2. Assess for tolerance as below for up to two hours.

 a. SpO2 ≥ 90: and/or PaO2 ≥ 60 mmHg

 b. Spontaneous VT ≥ 4 ml/kg PBW

 c. RR ≤ 35/min

 d. pH ≥ 7.3

 e. No respiratory distress (distress= 2 or more)

Protocol ARDS net

 􀂾 HR > 120% of baseline

 􀂾 Marked accessory muscle use

 􀂾 Abdominal paradox

 􀂾 Diaphoresis

 􀂾 Marked dyspnea

 3. If tolerated for at least 30 minutes, consider extubation.

 4. If not tolerated resume pre-weaning settings.

Terapii adjuvante
 Aport restrictiv de fluide
 Crestere CO sau DO2 la nivele
supranormale
 Hipercapnia permisiva
 Pozitia prona
 Manevrele de recrutare
Hipercapnia permisiva
 Disfunctie celulara metabolica
 Depresia contractilitatii miocardice
 Coronarodilatatie
 Vasodilatatie sistemica
 Vasoconstrictie pulmonara
 Vasodilatatie cerebrala, cresterea PIC
 Vasoconstrictie renala

 Este bine tolerata la pacientii sedati

(mecanisme compensatorii celulare)
Hipercapnia permisiva si acidoza
respiratorie - contraindicatii
 PIC
 AVC acut
 Ischemie miocardica
 Hipertensiune pulmonara severa
 Insuficienta ventriculara dreapta
 Acidoza metabolica severe, necontrolata
 Siclemie
 Intoxicatii (ATC)
 Tratament -blocant

Sarcina
Prone-position
1.  FRC
2. Modificari ale miscarilor
diafragmatice
3. Redistributia perfuziei
4. Clearance mai bun al secretiilor
 Se foloseste la pacientii cu hipoxemie
severa, refractara
 Se combina cu VM protectiva
Manevrele/ terapia de salvare

 Tracheal gas insufflation

 NO inhalator
 Prostaciclina inhalator
 Corticosteroizi
 Invers-ratio ventilation
 Oxigenare/indepartare de CO2 extracorporeala
 Surfactant exogen
 Partial liquid ventilation
Mersi!

ARDS Rover Rose