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Ards ali

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  • 1. Lesão pulmonar agudaSindrome do Desconforto Respiratório Agudo Antonio Souto acasouto@bol.com.br Médico coordenador Unidade de Medicina Intensiva Pediátrica Unidade de Medicina Intensiva Neonatal Hospital Padre Albino Professor de Pediatria nível II Faculdades Integradas Padre Albino Catanduva / SP
  • 2. 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
  • 3. Pneumonia SIRS - sepse Lesão pulmonar Mediadores inflamatóriosPulmonar ExtrapulmonarPneumonia SIRSAspiração SepseInalação de fumaça Transfusão maciçaAfogamento pancreatiteContusão Múltiplas fraturas Pós PCR Hipotensão
  • 4. AMERICAN JOURNAL OF RESPIRATORY ANDCRITICAL CARE MEDICINE VOL 171 2005
  • 5. Early events in ALI/ARDSA variety of “direct” and “indirect” insults lead to ALI. Inflammatory injury to the alveolar–capillary membrane as a central pathogenetic mechanism.The key effector cells, molecules, and mechanisms that leadto dysregulation of inflammatory and hemostatic pathways inALI/ARDS remain incompletely defined. Zimmerman GA, 2003.
  • 6. Cascata inflamatória Complement Lesão inicial Neutrófilos Cytokines (TNF, IL-1, IL-8)Direta/indireta Arachidonic Acid Metabolites Coagulation Cascade Platelet Activating Factor Lesão da parede alveolar Liberação de citocinas Lesão endotelial Proteases Lesão epitelial Oxygen Radicals Inativação do surfactante Cationic Proteins Edema pulmonarLesão alveolar difusa
  • 7. 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
  • 8. Ware LB, NEngl J Med 2000;342:1334– 1349.
  • 9. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005A low-power light micrograph of a lung biopsy specimencollected 2 d after the onset of ALI/ARDS secondary togram-negative sepsis demonstrates key features of diffusealveolar damage, including hyaline membranes,inflammation, intraalveolar red cells and neutrophils, andthickening of the alveolar–capillary membrane.
  • 10. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005 Hyaline membrane and diffuse alveolar inflammation. Polymorphonuclear leukocytes are imbedded in the proteinaceous hyaline membrane structure (black arrows). The white arrow points to the edge of an adjacentalveolus, which contains myeloid leukocytes
  • 11. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY VOL 33 2005
  • 12. Reduced production or neutralization of surfactant by theplasma proteins and fibrin that extravasate into the alveoli Ashbaugh DG, Lancet 1967;2:319–323A decrease in functional surfactant would contribute toalveolar instability and arterial hypoxemia, potentially increaselung edema formation Albert RK, J Clin Invest 1979;63:1015–1018.
  • 13. Hepatização pulmonar
  • 14. Fase exsudativa Fase proliferativa Fase fibrótica (7 Days) (14 Days) (21 Days)Alveolar Wall Damage Type II Alveolar Cell Hyperplasia Extensive Fibrosis With Flooding Myofibroblast Infiltration With Loss of Normal Lung Resolution of Edema Architecture ↓↓ Pa02 ↓ Pa02 ↓ Pa02 ↓ Compliance ↓ Compliance ↓ Compliance Bilateral Infiltrates Bilateral Infiltrates Infiltrates ± Bullae ↑ VD/VT ↑ VD/VT
  • 15. Fibrose intersticial
  • 16. Crit Care Med 2003; 31[Suppl.]:S285–S295
  • 17. The lung in ARDS has three components:• Diseased lung that is not recruitable• Diseased lung that is recruitable• Normal lung Joseph E. Previtera, RRT Respiratory Care Department Beth Israel Deaconess Medical Center Boston, MA
  • 18. Alveolar Wall Injury: Surfactant Inactivation Pulmonary EdemaImpaired Oxygenation: Diffuse Infiltrates Reduced Compliance Normal PCWP V/Q Mismatch Regional Shunting
  • 19. ARDS causes severe acute respiratory failurewith dynamic impairment in oxygen and carbondioxide transfer, with the need for high levels ofsupplementary oxygen and a high minuteventilation Falke KJ, J Clin Invest 1972;51:2315–2323. Nuckton TJ, NEngl JMed 2002;346:1281– 1286.
  • 20. Hipertensão pulmonar Microtrombos Embolia pulmonar Vasoconstrição hipóxica Edema intersticial Ventilação pulmonar mecânica
  • 21. Figure 1. FACTORS AFFECTING OXYGEN DELIVERY Hgb CaO2 Hipoxêmica A-a gradient DPG Acid-Base Balance Influenced By Blockers Oxygenation Competitors Temperature DO2 Drugs Influenced By Conduction SystemHipóxia HR CVP CO EDV Venous Volume Venous Tone Metabolic Milieu SV Ventricular Ions Compliance Acid Base Temperature Influenced By Drugs ESV Contractility Toxins Afterload Blockers Influenced By Temperature Competitors Drugs Autonomic Tone
  • 22. Quadro clínico Inespecíficos Severidade Disfunção de múltiplos órgãos e Lesão direta e/ou Sistemas indireta pulmonar Taquicardia CIVD, Hemorragia digestiva Respiratórias Disfunção hepática, IRA Hipotensão Cardiocirculatórias DMOS Infecção Choque
  • 23. Tratamento Severidade da doença Função dos diferentes orgãos e sistemas
  • 24. Figure 1. FACTORS AFFECTING OXYGEN DELIVERY Hgb 10 g/dl CaO2 A-a gradient DPG Acid-Base Balance Influenced By Blockers Oxygenation Competitors Temperature DO2 Choque Drugs Influenced By Conduction System HR CVP CO EDV Venous Volume Venous Tone Metabolic Milieu SV Ventricular Ions Compliance Acid Base Temperature Influenced By Drugs ESV Contractility Toxins Afterload Blockers Influenced By Temperature Competitors Drugs Autonomic Tone
  • 25. Oxigenação
  • 26. Pediatr Crit Care Med 2006; 7:562–570
  • 27. Pediatr Crit Care Med 2006; 7:562–570
  • 28. #@&*^%$#>? !!+#$
  • 29. Lesão aguda pulmonar induzida pela ventilação mecânica (LPAIV)O2PressãoFR
  • 30. (LPAIV)Pressão normal Pressão + Alta Pressão + Alta + PEEP Hiperdistensão Recrutamento- derecrutamento
  • 31. Median Number of Ventilator Free Days 14 12 10 Time (Days) 8 6 4 2 0 6cc/kg 12cc/kg Treatment Groups
  • 32. Mortality at the Time of Hospital Discharge 45 40 35 Mortality (%) 30 25 20 15 10 5 P=0.0054 0 6cc/kg 12cc/kg Treatment groups
  • 33. Estratégia ventilatória protetora pulmonar PEEP VcPinsp <35mL/kg6 cmH2O
  • 34. Prone Positioning Reduced Atelectasis Anterior Prone Anterior Atelectasis Improved Low V/Q and Shunt + Decreased AtelectasisAlveolar Flooding Redistribution of Blood Flow
  • 35. From The Cochrane Library, Issue 2, 2005. Chichester, UK: John Wiley &Sons, Ltd. All rights reserved. Pharmacologic therapies for adults with acute lung injury and acute respiratory distress syndrome (Cochrane Review) Adhikari N, Burns KEA, Meade MO ABSTRACTObjectives: Our objective was to determine the effects of pharmacologic treatments on clinical outcomes in adults with ALI or ARDS.
  • 36. From The Cochrane Library, Issue 2, 2005. Chichester, UK: John Wiley &Sons, Ltd. All rights reserved. Pharmacologic therapies for adults with acute lung injury and acute respiratory distress syndrome (Cochrane Review) Adhikari N, Burns KEA, Meade MO ABSTRACTAuthors conclusions: Effective pharmacotherapyfor ALI and ARDS is extremely limited, withinsufficient evidence to support any specific intervention.
  • 37. Diminuir VO2RepousoSedação e analgesiaControle da T0C