Ards ali

Lesão pulmonar aguda

Sindrome do Desconforto Respiratório Agudo

Antonio [email protected]édico coordenadorUnidade de Medicina Intensiva PediátricaUnidade de Medicina Intensiva Neonatal Hospital Padre Albino

Professor de Pediatria nível II Faculdades Integradas Padre AlbinoCatanduva / SP

Acute lung injury is characterized bycompromised gas exchange following

macrophage activation, surfactantdysfunction, and epithelial destruction.

Lewis JF, Am Rev Respir Dis 1993; 147:218–233

Lesão pulmonar

Mediadores inflamatórios

Pulmonar Extrapulmonar

Pneumonia SIRS

Aspiração Sepse

Inalação de fumaça Transfusão maciça

Afogamento pancreatite

Contusão Múltiplas fraturas

Pós PCR

Hipotensão

Pneumonia

SIRS - sepse

AMERICAN JOURNAL OF RESPIRATORY ANDCRITICAL CARE MEDICINE VOL 171 2005

Early events in ALI/ARDS

A variety of “direct” and “indirect” insults lead to ALI.

Inflammatory injury to the alveolar–capillarymembrane as a central pathogenetic

mechanism.

The key effector cells, molecules, and mechanisms that lead to dysregulation of inflammatory and hemostatic pathways in ALI/ARDS remain incompletely defined.

Zimmerman GA, 2003.

LesãoLesãoinicialinicialDireta/indiretaDireta/indireta

CascataCascatainflamatinflamat óóriariaComplementComplement

Cytokines (TNF, ILCytokines (TNF, IL --1, IL1, IL --8)8)ArachidonicArachidonic Acid MetabolitesAcid Metabolites

Coagulation CascadeCoagulation CascadePlatelet Activating FactorPlatelet Activating Factor

NeutrNeutróófilosfilos

LiberaLibera ççãoão de de citocinascitocinasProteasesProteases

Oxygen RadicalsOxygen RadicalsCationic ProteinsCationic Proteins

LesãoLesãodada paredeparedealveolaralveolarLesãoLesão endotelialendotelialLesãoLesãoepitelialepitelial

InativaInativa ççãoão do do surfactantesurfactanteEdema Edema pulmonarpulmonar

LesãoLesãoalveolar alveolar difusadifusa

Activated macrophages release a myriad ofcytokines, reactive oxygen and nitrogen species, and proteolytic enzymes that, in turn, disruptendothelial function.

Together, these events lead to the key clinicalmanifestations of this condition, pulmonaryedema, cellular infiltration, atelectasis, and, finally, complete respiratory failure.

Pittet JF, Am J Respir Crit Care Med 1997; 155:1187–1205

Ware LB, NEngl J Med 2000;342:1334–1349.

A low -power light micrograph of a lung biopsy specimencollected 2 d after the onset of ALI/ARDS secondary to gram -negative sepsis demonstrates key features of diffusealveolar damage, including hyaline membranes, inflammation, intraalveolar red cells and neutrophils, andthickening of the alveolar–capillary membrane.

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005

Hyaline membrane and diffusealveolar inflammation.

Polymorphonuclear leukocytesare imbedded in the

proteinaceous hyalinemembrane structure (black

arrows). The white arrow pointsto the edge of an adjacent

alveolus, which contains myeloidleukocytes


Reduced production or neutralization of surfactant by theplasma proteins and fibrin that extravasate into the alveoli

Ashbaugh DG, Lancet 1967;2:319–323

A decrease in functional surfactant would contribute to alveolar instability and arterial hypoxemia, potentially increaselung edema formation

Albert RK, J Clin Invest 1979;63:1015–1018.

Hepatização pulmonar

FaseFaseexsudativaexsudativa(7 Days)(7 Days)

FaseFaseproliferativaproliferativa(14 Days)(14 Days)

FaseFasefibrfibr óóticatica(21 Days)(21 Days)

Alveolar Wall DamageAlveolar Wall DamageWith FloodingWith Flooding

Type II Alveolar Cell HyperplasiaType II Alveolar Cell HyperplasiaMyofibroblastMyofibroblast Infiltration Infiltration

Resolution of EdemaResolution of Edema

Extensive FibrosisExtensive FibrosisWith Loss of Normal LungWith Loss of Normal Lung

ArchitectureArchitecture

↓↓↓↓ Pa0Pa022↓↓ ComplianceCompliance

Bilateral InfiltratesBilateral Infiltrates

↓↓ Pa0Pa022↓↓ ComplianceCompliance

Bilateral InfiltratesBilateral Infiltrates↑↑ VD/VTVD/VT

↓↓ Pa0Pa022↓↓ ComplianceCompliance

Infiltrates Infiltrates ±± BullaeBullae↑↑ VD/VTVD/VT

Fibrose intersticial

Crit Care Med 2003; 31[Suppl.]:S285–S295

The lung in ARDS has three components:

• Diseased lung that is not recruitable

• Diseased lung that is recruitable

• Normal lung

Joseph E. Previtera, RRTRespiratory Care Department

Beth Israel Deaconess Medical CenterBoston, MA

Impaired Oxygenation:Impaired Oxygenation:V/Q MismatchV/Q Mismatch

ShuntingShunting

Diffuse InfiltratesDiffuse InfiltratesRegionalRegional

Alveolar Wall Injury:Alveolar Wall Injury:

Surfactant InactivationSurfactant InactivationPulmonary EdemaPulmonary Edema

Normal PCWPNormal PCWPReduced ComplianceReduced Compliance

ARDS causes severe acute respiratory failurewith dynamic impairment in oxygen and carbondioxide transfer, with the need for high levels ofsupplementary oxygen and a high minute ventilation

Falke KJ, J Clin Invest 1972;51:2315–2323.

Nuckton TJ, NEngl JMed 2002;346:1281– 1286.

Hipertensão pulmonar

Microtrombos

Embolia pulmonar

Vasoconstrição hipóxica

Edema intersticial

Ventilação pulmonar mecânica

Figure 1. FACTORS AFFECTING OXYGEN DELIVERY

DO2

CaO2

CO

SV

HR

Oxygenation

Hgb

A-a gradient DPG

Acid-Base Balance Blockers

Competitors Temperature

Drugs Conduction System

Ventricular Compliance

EDV

ESV Contractility

CVP Venous Volume Venous Tone

Afterload Blockers Temperature Competitors Drugs Autonomic Tone

Metabolic Milieu Ions

Acid Base Temperature

Drugs Toxins

Influenced By

Influenced By

Influenced By

Influenced By

Hipóxia

Hipoxêmica

Quadro clínico

� Inespecíficos

� Severidade

� Lesão direta e/ouindireta pulmonar

� Respiratórias

� Cardiocirculatórias

� DMOS

Disfunção de múltiplos órgãos e

Sistemas

CIVD, Hemorragia digestiva

Disfunção hepática, IRA

Infecção

Taquicardia

Hipotensão

Choque

Tratamento

� Severidade da doença

� Função dos diferentes orgãos e sistemas

Figure 1. FACTORS AFFECTING OXYGEN DELIVERY

DO2

CaO2

CO

SV

HR

Oxygenation

Hgb

A-a gradient DPG

Acid-Base Balance Blockers

Competitors Temperature

Drugs Conduction System

Ventricular Compliance

EDV

ESV Contractility

CVP Venous Volume Venous Tone

Afterload Blockers Temperature Competitors Drugs Autonomic Tone

Metabolic Milieu Ions

Acid Base Temperature

Drugs Toxins

Influenced By

Influenced By

Influenced By

Influenced By

10 g/dl

Choque

Oxigenação

Pediatr Crit Care Med 2006; 7:562–570

#@&*^%$#>?!!+#$

Lesão aguda pulmonarinduzida pela ventilação mecânica(LPAIV)

O2

Pressão

FR

Pressão normal Pressão + Alta Pressão + Alta

+ PEEP

(LPAIV)

Hiperdistensão Recrutamento-

derecrutamento

Median Number of Ventilator Free DaysMedian Number of Ventilator Free Days

Treatment GroupsTreatment Groups

00

22

44

66

88

1010

1212

1414

6cc/kg6cc/kg 12cc/kg12cc/kg

Tim

e (D

ays)

Tim

e (D

ays)

Mortality at the Time of Hospital DischargeMortality at the Time of Hospital Discharge

Treatment groupsTreatment groups

00

55

1010

1515

2020

2525

3030

3535

4040

4545

6cc/kg6cc/kg 12cc/kg12cc/kg

Mor

talit

y (%

)M

orta

lity

(%)

P=0.0054P=0.0054

Estratégia ventilatóriaprotetora pulmonar

PEEP

Vc

6 mL/kg

Pinsp <

35 cmH2O

Prone PositioningProne Positioning

ProneProne

AnteriorAnterior

AnteriorAnterior

Reduced Reduced AtelectasisAtelectasis

Improved Low V/Q and ShuntImproved Low V/Q and Shunt

Decreased Decreased AtelectasisAtelectasisRedistribution of Blood FlowRedistribution of Blood Flow

AtelectasisAtelectasis++

Alveolar FloodingAlveolar Flooding

From The Cochrane Library, Issue 2, 2005. Chichester, UK: John Wiley &

Sons, Ltd. All rights reserved. Pharmacologic therapies for adultswith acute lung injury and acute respiratory distress

syndrome (Cochrane Review)

Adhikari N, Burns KEA, Meade MO

ABSTRACT

Objectives: Our objective was to determine theeffects of pharmacologic treatments on clinical

outcomes in adults with ALI or ARDS.

From The Cochrane Library, Issue 2, 2005. Chichester, UK: John Wiley &

Sons, Ltd. All rights reserved. Pharmacologic therapies for adultswith acute lung injury and acute respiratory distress

syndrome (Cochrane Review)

Adhikari N, Burns KEA, Meade MO

ABSTRACT

Authors' conclusions: Effective pharmacotherapyfor ALI and ARDS is extremely limited, withinsufficient evidence to support any specific

intervention.

Diminuir VO2

� Repouso

� Sedação e analgesia

� Controle da T0C

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