ARDS_Presentation.pptx acute respiratory disease syndrome

this slide is explore about acute respiratory disease syndrome

1. Acute Respiratory Distress Syndrome (ARDS) Madam rozila ibrahim May session 2024

2. LEARNING OUTCOME At the end of the session, learner’s would be able to; explain the pathophysiology of Acute Respiratory Disease Syndrome (ARDS) Discuss the specific management of patient with ARDS 7/2/2024 2

3. Definition Acute respiratory distress syndrome (ARDS) is a sudden and severe, life-threatening condition characterized by rapid onset of widespread lung inflammation in the lungs in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia and diffuse pulmonary infiltration. It result in impaired gas exchange leading to respiratory failure. ARDS is usually a complication of other serious conditions/ ill and is treated in hospital. On a microscopic level, the disorder is associated with capillary endothelial injury and diffuse alveolar damage. 7/2/2024 3

4. BERLIN DEFINITION NORMAL FI02 = 400-500 MMHG 7/2/2024 4

5. Etiology 1. Direct lung injury: Pneumonia aspiration of gastric contents near drowning toxic inhalation 2. Indirect lung injury: sepsis, severe trauma, pancreatitis, massive blood transfusion, drug overdose. In the United States, about 190,000 Americans are diagnosed with ARDS each year. 7/2/2024 5

6. PATHOPHYSIOLOGY Injury to alveolar /capillary membrane  cascade of cellular /enzyme biochem release (body autoregulatory response) trigger immune cells (neutrophil, macrophage, , monocytces  produce cytokinase ; produce inflammatory mediators/increase permeability - interstitial edema Normal alveolar INTERSTITIAL OEDEMA ALVEOLAR EODEMA 7/2/2024 6

7. CONT.. SUMMARY PATHOPHYSIOLOGY Injury phase: Injury to alveolar - capillary membrane leading to increase permeability, resulting in fluid accumulation in the alveoli. Exudative phase: inflammatory response causing alveolar and interstitial oedema. Proliferative phase: lung repair and remodelling begins. (autoregulatory body response) Fibrotic phase: reduced lung compliance and long-term respiratory issues due to the fibrotic changes. The fluid keeps your lungs from filling with enough air, which means less oxygen reaches your bloodstream. This deprives your organs of the oxygen they need to function. 7/2/2024 7

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9. Sign & symptoms Rapid onset of severe dyspnea Hypoxemia refractory to oxygen therapy Bilateral infiltrates on chest imaging Reduced lung compliance Difficulty with routine activities such as dressing, taking a shower, and climbing stairs, due to extreme tiredness. Shortness of breath or feeling like you cannot get enough air (called air hunger) Drowsiness. A bluish color on your fingers, toes, and lips. Symptoms include shortness of breath or feeling like you can't get enough air, extreme tiredness, an inability to exercise as you did before, and sleepiness. Tachypnoea, difficulty breathing, stridor, wheezing and use of accessory muscle, inability to speak, agitation or lethargy. Impending respiratory failure: ✓ Altered mental status or ALOC ✓ 2-3-word sentences ✓ Severe dyspnea ✓ Cyanosis ✓ Low RR or other signs of fatigue ✓ History of intubation for the same 7/2/2024 9

10. Investigation for Diagnosis Berlin definition: Timing: within 1 week of clinical insult or new/worsening respiratory symptoms. Chest imaging: Bilateral opacities not fully explained by effusion, lobar/lung collapse, or nodules. Origin of edema: Respiratory failure not fully explained by cardiac failure or fluid overload: Oxygenation: Pao2/Fio2 ratio ≤300 mm Hgwith PEEP or CPAP ≥5 cm H20. 7/2/2024 10

11. Bilateral diffusion infiltrations, white out (haze) 7/2/2024 11

12. Management 1 . Mechanical ventilation: Low tidal volume (4-6 ml/kg) to prevent volutrauma High peep strategy to maintain alveolar recruitment Prone positioning: improves oxygenation and outcomes in severe ARDS. Fluid management: conservative fluid strategy to minimize pulmonary oedema. Pharmacological treatment: Neuromuscular blocking agents in the early ARDS to improve oxygenation Corticosteroids (controversial), but may be considered in late-phase ARDS. 7/2/2024 12

13. Cont.. management identify patients at risk for acute respiratory failure monitor closely for any signs of deconditioning. maintaining the airway and applying oxygen is a priority. patients may require mechanical ventilation along with the treatment of the underlying condition do procedure insertion of under water seal drainage into the lungs might to remove or drain any fluids or embolism or blood inside the lungs. Positioning the patient – Prone, lateral rotation, prop up ; better lung expansion and improve oxygenation 7/2/2024 13

14. Treatment (5 p’s) oxygen therapy Positioning medicines : anti-inflammatory, antibiotic, vasodilator, bronchodilator procedures to help your lungs rest and heal. Chronic respiratory failure can often be treated at home. If you have serious chronic respiratory failure, you may need treatment in a long-term care center. 7/2/2024 14

15. Nursing diagnosis Ineffective airway patency due to disease process evidence by patient show difficulty in breathing. Assessment patient effort to breath, pattern Vital sign- spo2 (91%) patient status, bp Give o2 - nasal prone 3-4 /venti mask  Positive pressure ventilation (PPV) PEEP, CIPAP, BIPAP, ; Good ventilation system ; reduce number of visitors Reduce stress on patient Suction to clear airway Stand by emergency trolly Positioning- prop up, modified high fowlers Moral support; deep breathing exercise 7/2/2024 15

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