ARDS (acute respiratory distress syndrome) ppt SlideShare

Acute respiratory distress syndrome (ARDS) occurs when fluid builds up in the tiny, elastic air sacs (alveoli) in your lungs. 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.

1. ACUTE RESPIRATORY DISTRESS SYNDROME Submitted by: Sonam

2. ANATOMY AND PHYSIOLOGY The respiratory system is comprised of the upper and the lower respiratory tracts. The primary purpose of the respiratory system is gas exchange. This involves the transfer of the oxygen and carbon dioxide between the atmosphere and the blood.

3. ARDS It is characterized by a severe inflammatory process causing diffuse alveolar damage that results in sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia unresponsive to oxygen supplementation regardless of the amount of PEEP, and the absence of an elevated left atrial pressure Patients often demonstrate reduced lung compliance.

4. EPIDEMIOLOGY Overall, 10% to 15% of patients admitted to the intensive care unit. ARDS has been associated with a mortality rate ranging from 26% to 58%. The major cause of death in ARDS is non pulmonary MODS, often with sepsis. In India, nearly 30% of the cases of ARDS are due to pneumonia.

5. . The annual rate of ARDS is generally 13–23 people per 100,000 in the general population.  It is more common in people who are  mechanically ventilated  with acute lung injury (ALI) occurring 16% of ventilated people. Rates increased in 2020 due to COVID-19 with some cases also appearing similar to HAPE (high altitude pulmonary edema)

6. RISK FACTORS Direct causes: Aspiration Localized infection Toxic inhalation injury Trauma, flail chest Major surgery Fat or air embolism

7. . Indirect causes : Shock Metabolic disorders Sepsis and Anaphylaxis Idiopathic Pregnancy induced HTN Hematologic disorders Multisystem trauma

8. PHASES Exudative stage : accumulation of excessive fluid Hypoxemia is usually most severe during this phase I njury to the endothelium and epithelium Leads to loss of the normally tight alveolar barrier to fluids and macromolecules Edema fluid that is rich in protein accumulates in the interstitial and alveolar spaces

9. . Proliferative (or fibroproliferative) stage : 7 to 10 days Connective tissue and other structural elements in the lungs proliferate in response to the initial injury, including development of fibroblasts The term stiff lung and shock lung frequently used to characterize this stage. Abnormally enlarged air spaces and fibrotic tissue(scarring) are increasingly apparent.

10. . Fibrotic stage:> 10-14 days Inflammation resolves. Oxygenation improves and extubation becomes possible. Lung function may continue to improve for as long as 6 to 12 months after onset of respiratory failure, depending on the precipitating condition and severity of the initial injury.

11. CLINICAL MANIFESTATIONS Early sign and symptoms : Dyspnea Cough fever Restlessness

12. . Mood swings Confusion Disorientation Change in LOC Low Bp Extreme tiredness

13. . Late sign and symptoms: Severe difficulty in breathing Shortness of breath Tachycardia Thick frothy sputum

14. . Metabolic acidosis Cyanosis Decreased paO2 Abnormal breath sound, like crackles Decreased paCO2 with respiratory alkalosis

15. Characteristic feature Arterial hypoxemia that does not respond to supplemental oxygen

16. ASSESSMENT AND DIAGNOSTIC FINDINGS History : history of present illness history of past illness medical and surgical history family history current lifestyle and habits sleep and rest cognition and perception

17. PHYSICAL EXAMINATION Vital Signs T emperature:  hyperpyrexia or hypothermia B lood pressure: inappropriately low, with a low mean arterial pressure H eart rate: rapid (tachycardia > 100 beats/minute), or bradycardia R espiratory rate:  tachypnea or bradypnea  Peripheral capillary oxygen saturation (SpO 2 ): low (< 90%)

18. . Skin C yanosis due to poor oxygenation P allor due to poor perfusion Lungs Dyspnea, tachypnea I ntercostal retractions, wheezing and crackles may be present as the fluid begins to leak into the alveolar interstitial space. Coarse breath sounds, rhonchi, or decreased breath sounds

19. . Heart T achycardia or bradycardia on heart auscultation Extremities C yanosis C ool extremities  Reduced peripheral pulses due to poor perfusion

20. COMMON DIAGNOSTIC TEST ABG & Blood test Chest x ray & Chest CT scan Bronchoscopy Sputum culture and analysis Echocardiogram plasma brain natriuretic peptide (BNP) levels

21. DIAGNOSTIC CRITERIA Diagnostic criteria for ALI(Acute Lung Injury) Time : acute onset Oxygenation : PaO2/FiO2 <300 mmHg(regardless of PEEP level used) Chest X- ray : bilateral infiltrates demonstrated at frontal view of X-ray Pulmonary capillary pressure : < 18 mmHg when measured or no clinical evidence of left atrial hypertension Diagnostic criteria for ARDS(Acute respiratory distress syndrome) The same as acute lung injury criteria except for Oxygenation : PaO2/FiO2 < 200 mmHg (regardless of PEEP level used )

22. TYPES OF ARDS MILD ARDS PaO2/FiO2 – 200 to 300 mmHg MODERATE ARDS PaO2/FiO2- 100 to 200 mmHg SEVERE ARDS PaO2/FiO2- < 100 mmHg

23. MEDICAL MANAGEMENT Antibiotics Anti-inflammatory drug Diuretics : to promote diuresis, Lasix 40 mg iv BD, spironolactone. Antianxiety : escitalopram, benzodiazepine like carbamezipine . Inhaled drugs (bronchodilators, Supplemental oxygen)

24. . Muscle relaxants : baclofen, methocarbamol, and tizanidine Drugs to raise blood pressure : pain medication, antianxiety, anti depressants,etc Mechanical ventilation : the aim is to increase paO2 while minimizing the risk of further lung injury

25. . indications are : Inadequate oxygenation (paO2 < 60 with FiO2> 0.6) Rising or elevated paCO2 >50 mmHg Clinical signs of incipient respiratory failure PEEP usually improves oxygenation , but it does not influence the natural history of the syndrome. By using PEEP, a lower FiO2, may be required. The goal is à PaO2, greater than 60 mm Hg or an oxygen saturation level of greater than 90% at the lowest possible FiO2 .

26. . VAP prevention/ bundle : O ral care with chlorhexidine Peptic ulcer prophylaxis Deep vein thrombosis prophylaxis Head end elevation Daily sedation assessment & spontaneous breathing trials DVT prophylaxis : medical treatment to prevent the development of DVT in a patient at risk of this condition. In patients with DVT, a  blood clot  forms in the deep veins of the arm or leg, occluding blood flow and potentially leading to complications. The most serious complication is a pulmonary  embolism  (PE). e.g. enoxaparin, heparin

27. . Nutritional therapy : require 35 to 45 kcal/kg/day to meet caloric requirements. Enteral feeding is the first consideration; however, parenteral nutrition also may be required. Inhaled nitric oxide (an endogenous vasodilator) may help to reduce V/Q mismatch and improve oxygenation ECMO: I t is an extracorporeal technique of providing prolonged cardiac and respiratory support to persons whose heart and lungs are unable to provide an adequate amount of gas exchange or perfusion to sustain life . nebulizer therapy : with budesonide, salbutamol, duolin . Chest physiotherapy : to loosen the secretions

28. . Position change : Prone position : improves oxygenation, Increases functional residual capacity Change in regional diaphragmatic motion Perfusion redistribution Improved clearance of secretion Lateral : to stimulate postural drainage and help mobilizes secretion Hypovolemia must be carefully treated without causing further overload. Inotropic or vasopressor agents may be required.

29. COMPLICATIONS Nosocomial pneumonia Barotrauma Renal failure VAP 

30. . Others: o2 toxicity Stress ulcers Tracheal ulcerations Blood clots leading to deep vein thrombosis Peumoperitoneum Pulmonary embolism Infection: catheter related, hospital acquired, sepsis Sleep deprivation PTSD

31. MANAGEMENT OF COMPLICATIONS Sterile techniques Prevent aspiration Control infection Elevate bed

32. PROGNOSIS Mortality ranges-26-44% Risk factors – advanced age, CKD, CLD, chronic immunosuppression, chronic alcohol abuse ARDS from direct lung injury has double mortality Prognosis with ARDS depends primarily on the underlying cause of lung injury. In an analysis of the ARDSNet database, survival to home discharge was lowest in patients with sepsis. intermediate in patients with pneumonia, and highest in patients with trauma and ARDS.

33. . In 2001, a 1-year follow-up study of patients with ARDS in the United States found that a significant percentage of deaths occurred between day 28 and 4 months, which raised the potential for longer monitoring in the evaluation of new interventions or therapies. On the basis of cumulative evidence, a patient surviving hospitalization for ARDS can be expected to return to a similar lifestyle over the course of a year, with some lingering physical and psychological challenges. Therefore, in the absence of significant comorbid conditions, the long-term outcome data are sufficient to warrant aggressive treatment for ARDS

34. NURSING MANAGEMENT Ineffective breathing pattern related to decreased lung compliance, decreased energy as characterized by dyspnea, abnormal ABG, cyanosis and use of accessory muscles Impaired gas exchange related to diffusion defect as characterized by hypoxia (restlessness, irritability and fear of suffocation), hypercapnia, tachycardia and cyanosis Risk for decreased cardiac output related to positive pressure ventilation

35. . Ineffective protection related to positive pressure ventilation, decreased pulmonary compliance and increased secretions as characterized by crepitus, altered chest excursion, abnormal ABG and restlessness. Impaired physical mobility related to monitoring devices, mechanical ventilation and medications as characterized by imposed restrictions of movement, decreased muscle strength and limited range of motion Risk for impaired skin integrity related to prolonged bed rest, prolonged intubation and immobility Knowledge deficit related to health condition, new equipment and hospitalization as characterized by increased frequency of questions posed by patient and significant others.

36. . Nursing Alert : Nursing assessment is essential to minimize the complications related to neuromuscular blockade. The patient may have discomfort or pain but cannot communicate these sensations. In addition, frequent oral care and suctioning may be needed.

37. CONCLUSION Consideration must be given to the sign and symptoms of the disease, so that early diagnosis and treatment can be done as ARDS is a sudden, progressive form of respiratory failure characterized by severe dyspnea, refractory hypoxemia and diffuse bilateral infiltrates. It is a life-threatening lung condition that prevents enough oxygen from getting into the blood. ARDS is a multisystem syndrome not a disease.

38. . Characterized by accumulation of excessive fluid in the lungs with resulting hypoxemia and ultimately some degree of fibrotic changes The most frequent causes of ARDS include sepsis, aspiration, pneumonia and sever trauma Treatment is primarily supportive and can non traditional type of ventilation and oxygenation strategies The best proven strategy to improve survival is low tidal volume ventilation

39. BIBLIOGRAPHY Brunner and Suddharths . textbook of medical and surgical nursing. 13th edition Vol. I. .New Delhi: Reed Elsevier India Pvt. Ltd.; 2014. Pg. No. 360- 395 Lewis. Medical Surgical Nursing. Assessment and Management of Clinical Problems. 2015. New Delhi. Elsevier Vol. I. Pg. No. 461-493 Joyce M. Black and Jane Hokanson ; medical surgical nursing; volume 2, 8 th edition, reed Elsevier, India pvt. Pg. no. https://docs.google.com/presentation/d/1qxclz7XrQR45ZUbC7PLBNxUgpxr3GgURd57tSuJ8cck/mobilepresent?slide=id.g81762d57bf_116_336

40. THANK YOU .