ARDS Overview

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  • 1.Acute RespiratoryDistress Syndrome (ARDS)Presented by Melinda C. Jordan

2. Acute RespiratoryDistress Syndrome Sudden, progressive form of acute respiratory failure Characterised by: Severe dyspnea Hypoxaemia Lung compliance Diffuse pulmonary infiltrates 3. Clinical Conditions Associated withthe development of ARDS Sepsis Severe Trauma Pulmonary contusion Pneumonia Near drowning Massive transfusion Fat embolism 4. Aetiology and Pathophysiology Develop from a variety of direct orindirect lung injuriesExact cause for damage to alveolar- alveolar-capillary membrane not knownPathophysiologic changes of ARDSthought to be due to stimulation ofinflammatory and immune systems 5. Pathophysiology of ARDS Fig. 66-9 6. Aetiology and PathophysiologyPhases:ExudativeProliferativeFibrotic 7. Aetiology and Pathophysiology Exudative phase 1-7 days after direct lung injury or host 1-7 insult Neutrophils adhere to pulmonary microcirculation Damage to vascular endothelium Increased capillary permeability Results in leakage of H2O Protein Inflammatory chemical 8. Oedema Formation in Acute Respiratory Distress SyndromeA, Normal alveolus andpulmonary capillary B, Interstitial oedema occurswith increased flow of fluidinto the interstitial space C, Alveolar oedema occurswhen the fluid crosses theblood-gas barrierFig. 66-8 9. Aetiology and PathophysiologyAlveolar cells type 1 and 2 are damagedSurfactant dysfunction atelectasisHyaline membranes line alveoliContribute to atelectasis and fibrosisLungs become less compliant 10. Aetiology and Pathophysiology WOB RR Tidal volumeProduces respiratory alkalosis from increase inCO2 removal 2 CO and tissue perfusion 11. Aetiology and PathophysiologyProliferative phase 1-2 weeks after initial lung injury 1-2 Influx of neutrophils, monocytes, and lymphocytes Fibroblast proliferation Lung becomes dense and fibrous Lung compliance continues to decrease 12. Aetiology and PathophysiologyHypoxaemia worsens Thickened alveolar membraneCauses diffusion limitation and shunting If reparative phase persists, widespread fibrosis results If phase is arrested, fibrosis resolves 13. Aetiology and Pathophysiology Fibrotic phase 2-3 weeks after initial lung injury 2-3 Lung is completely remodeled by sparsely collagenous and fibrous tissues Lung compliance Reduced area for gas exchange Pulmonary hypertension Results from pulmonary vascular destruction and fibrosis 14. Clinical ProgressionSome persons survive acute phase of lung injury Pulmonary oedema resolves Complete recovery 15. Clinical Progression Survival chances are poor for those who enter fibrotic phase Requires long-term mechanical ventilationlong-term 16. Clinical Manifestations Initial presentation often insidious May only exhibit dyspnea, tachypnea, cough, and restlessness Auscultation may be normal or have fine, scattered crackles Mild hypoxaemia Chest x-ray may be normalx-ray Oedema may not show until 30% increase in lung fluid content 17. Clinical ManifestationsSymptoms worsen with progression of fluid accumulation and decreased lung compliance Evident discomfort and WOB Pulmonary function tests reveal decreased compliance and lung volume 18. Clinical Manifestations As ARDS progressesIncreasing Tachypnea Diaphoresis Cyanosis Pallor Decreases in sensorium Chest x-ray termed whiteout or white lungx-ray due to consolidation 19. Clinical ManifestationsIf prompt therapy not initiated, severe hypoxaemia, hypercapnea, and hypoxaemia, metabolic acidosis may ensue Mechanical Ventilation may be required to prevent profound hypoxaemia 20. ComplicationsNosocomial pneumoniaStrategies for preventionInfection control measuresElevating HOB 45 degrees or more to preventaspiration 21. ComplicationsBarotraumaRupture of overdistended alveoli duringmechanical ventilationTo avoid, ventilate with smaller tidalvolumesResults in higher PaCO22Permissive hypercapniaPermissive hypercapnia 22. Complications Volu-pressure trauma Volu-pressure Occurs when large tidal volumes used to ventilate noncompliant lungs Alveolar fractures and movement of fluids and proteins into alveolar spaces Avoid by using smaller tidal volumes or pressure ventilation 23. ComplicationsStress ulcers Bleeding from stress ulcer occurs in 30% of patients with ARDS on PPV Management strategies include correction of predisposing conditions, prophylactic antiulcer agents, and early initiation of enteral nutrition 24. ComplicationsRenal failure Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia May also be caused by nephrotoxic drugs used for infections associated with ARDS 25. Nursing Assessment History of lung disease, Smoking Restlessness Agitation Pale, cool, clammy or warm, flushed skin Shallow breathing with increased respiratory rate Use of accessory muscles 26. Nursing AssessmentTachycardia progressing to bradycardia Extra heart sounds Abnormal breath sounds Hypertension progressing to hypotension 27. Nursing AssessmentSomnolence, confusion, delirium Changes in pH, PaCO2, PaO2, SaO2 Decreased tidal volume, FVC Abnormal x-rayx-ray 28. PlanningPatient with at least 60 mmHg and adequate lung ventilation to maintain normal pH following recovery will have PaO2 within normal limits 2 SaO2 >90% 2 Patent airway Clear lungs on auscultation 29. TreatmentOxygenHigh flow systems used to maximize O2 2deliverySaO2 continuously monitored 2Give lowest concentration that results inPaO2 60 mmHg or greater 2Risk for O2 toxicity increases when FIO22 2exceeds 60% for more than 48 hours 30. TreatmentMechanical ventilation May still be necessary to maintain FIO2 at 2 60% or greater to maintain PaO2 at 60 2 mmHg or greater PEEP at 5 cm H2O2 Opens collapsed alveoli 31. TreatmentPositioning strategies Turn from prone to supine position May be sufficient to reduce inspired O2 or PEEP 2 Fluid pools in dependent regions of lung Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone position 32. Medical Supportive TherapyMaintenance of cardiac output and tissue perfusion Continuous hemodynamic monitoring Arterial catheter 33. Medical Supportive TherapyUse of inotropic drugs may be necessary Hemoglobin usually kept at levels >9 or 10 with SaO2 >90% >90% Packed RBCs Maintenance of fluid balance 34. Evaluation No abnormal breath sounds Effective cough and expectoration Normal respiratory rate, rhythm, and depth Synchronous thoracoabdominal movement Appropriate use of accessory muscles 35. EvaluationPaO2 and PaCO2 within normal ranges Maintenance of weight or weight gain Serum albumin and protein within normal ranges