Ards ali
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Transcript of 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
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005
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
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