prepared by tintu varghese icu department n.
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  3. GENERAL ASSESSMENT • The patient is 25 years of age, male, approximately weighs 80kg • He is unconscious with ET tube with ventilator support and patient is sedated. GCS3/15,with the following vital signs. • BP=130/80, PR=70bpm, RR=24mts • Temp= 38.2, • SPO2= 93%

  4. Fair complexionWarmNo palpable mass or lesions, with good turgor.Nail beds cyanosis SKIN

  5. Maxillary, frontal sinuses are not tender.No palpable masses and lesionNo areas of deformity HEAD

  6. LEVEL OF CONCIOUSNESS • Patient unconscious • On fully sedation • On ventilator

  7. Pink conjunctiva and no drynessPupils equally round and reactive to light EYES

  8. No unusual discharges noted EARS

  9. NOSE • No unusual discharge • No tenderness in sinus

  10. Pink and moist oral mucosa and free of swelling and lesions.ET tube present. MOUTH

  11. No palpable lymph nodesNo masses and lesions seen NECK AND THROAT

  12. Equal chest expansionDecreased air entryBilateral wheezing sound presentBilateral crept present CHEST AND LUNGS

  13. Regular rhythm HEART

  14. Soft abdomenBowel sound present ABDOMEN

  15. Foleys catheter present. GENITALS

  16. EXTRIMITIES • Pulse full and equal • No lesions noted

  17. PAST MEDICAL HISTORY • No past medical history

  18. PRESENT MEDICAL HISTORY • 25yres male patient came in ER with complaints of tachypnea, agitated, SOB, fever, productive cough which was started one week ago and became worse. From • ER patient was confused, SPO2 was low 85%,CXR showed patchy opacities are seen in the middle and lower zone of both lung . Hilar shadows and vascular markings are prominent in both lungs. Mild to moderate pleural effusion in both lungs

  19. Patient was shifted to surgery ward, patient was desaturated and developed tachypnea and shifted to ICU for further treatment and observation. Patient was intubated and on ventilator and fully sedated .patient developed hypotension and started inotropic support for two days. After all management patient was extubated and fully conscious and oriented. Patient shifted to surgery ward.



  22. X-RAY CHEST ( CHEST AP VIEW) • Patchy ( air space) opacities are seen in the middle and lower zone of the both lungs. • Hilar shadows and vascular markings are prominent in both lungs. • Mild to moderate plural effusion in both lungs.

  23. ULTRASOUND CHEST • BIilateralpleral effusion ( large amount)with opacity is seen in lower area of both lungs

  24. INTRODUCTION • A distinct type of hypoxemic respiratory failure characterized by acute abnormality of both lungs was first recognized during the 1960s. Military clinicians working in surgical hospitals in Vietnam called it shock. Then referred to it as adult respiratory distress syndrome . Subsequent recognition that individuals of any age could be afflicted led to the current term, acute respiratory distress syndrome (ARDS).

  25. ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue . Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage (ie, alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes).

  26. DEFINITION • Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of acute respiratory failure in which the alveolar capillary membrane becomes damaged and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia and diffuse pulmonary infiltrates.


  28. lobes: • superior lobe • inferior lobe


  30. ETIOLOGY AND RISK FACTORS • Direct Lung Injury • Common causes • Aspiration of gastric contents or other substances. • Viral/bacterial pneumonia

  31. Less common causes • Chest trauma • Embolism: fat, air, amniotic fluid • Inhalation of toxic substances • Near-drowning • O2 toxicity • Radiation pneumonitis

  32. Indirect lung injury • Common causes • Sepsis • Severe traumatic injury

  33. Less common causes • Less common causes • Acute pancreatitis • Anaphylaxis • Prolonged Cardiopulmonary bypass surgery • Disseminated intravascular coagulation • Multiple blood transfusions • Narcotic drug overdose (e.g., heroin) • Non pulmonary systemic diseases

  34. EARLY SIGNS AND SYMPTOMS • restlessness • Dyspnea • Low blood pressure • Confusion • Extreme tiredness • Change in patient’s behavior • Mood swing • Disorientation • Change in LOC • If pneumonia is causing ARDS then client may have • Cough • Fever

  35. LATE SIGNS AND SYMPTOMS • Shortness of breath. • Tachycardia • Cyanosis (blue skin, lips and nails) • Think frothy sputum • Metabolic acidosis • Abnormal breath sounds, like crackles • Increased PaCo2 with respiratory alkalosis. • Severe difficulty in breathing i.e., labored, rapid breathing. • Decreased PaO2

  36. Lung injury Release of Vasoactive substances (serotonin, histamine, bradykinin) Damaged Type II alveolar cell Surfactant production Alveolocapillary membrane permeability Vascular narrowing & obstruction Alveolar Compliance and recoil Bronchoconstriction Outward migration of blood cells & fluids from capillaries Atelectasis Hyaline membrane formation Pulmonary Edema Lung compliance Impairment in gas exchange Pulmonary hypertension ARDS PATHOPHYSIOLOGY

  37. NURSING INTERVENTION • 24 hours vital signs observed will be monitored and documented. • Monitor for exhaustion and signs of reduced lung compliance eg: use of accessory muscles for respiration. • Evaluate effectiveness of respiratory function like rate, rhythm and depth. • Suction airway hourly or as necessary to remove secretion. • Administer prescribed inhalations or bronchodilators mucolytic as ordered. • Institute safety of the patient. • Fall prevention. • Side rails up • low bed position. • Prevent infection and potential complication. • Provide patient and family education about treatment and recovery of the patient.

  38. Medical management • Persons with ARDS are hospitalized and require treatment in an intensive care unit. • No specific therapy for ARDS exists. • Supportive measures : • Supplemental oxygen • Mechanical respirator • Positioning strategies .

  39. Fluid therapy • –Fluid Administration – The patient should be aggressively fluid resuscitated for any signs /symptoms of shock in order to optimize end organ perfusion. Once hemodynamic stability is achieved, fluid administration should be minimized to decrease the alveolar-capillary leak and pulmonary edema. Aggressive diuresis should also be considered once hemodynamic stability is achieved. Nutritional support should be initiated as early as possible.–

  40. Prone position

  41. .Prone Positioning – Has been used since mid 1970’s in an effort to improve lung perfusion and oxygenation. Prone position or bed that provides continuous lateral position helps mobilize pulmonary secretions and improve ventilation/ perfusion matching. In prone position patient face down improves ventilation in posterior lung, where edema settles when patient in supine position . Risks are mainly logistical, i.e. dislodgement of endotracheal tube or vascular lines, increased intra-abdominal pressure, feeding intolerance, and edema (facial). The greatest effects are achieved when patients are maintained prone for 12 hours or longer and oxygenation improves in 60-70% of patients.

  42. MEDICATIONS • Antibiotics • Anti-inflammatory drugs; such as corticosteroids • Diuretics • Drugs to raise blood pressure • Anti-anxiety • Muscle relaxers • Inhaled drugs (Bronchodilators)

  43. VENTILATOR SETTINGS • RECRUITMENT MANEUVER • Patients with ARDS require support with mechanical ventilator. • Utilizing a CPAP mode and providing PEEP 35 to 40 for 40 second. • In ventilator PEEP used to prevent alveolar de-recruitment at end-expiration. In patients with ARDS, PEEP is used primarily to improve arterial oxygenation. Increased end-expiratory pressure increases mean airway and intra thoracic pressure. When applied correctly, this prevents alveolar collapse, increasing the volume of aerated lung by preventing alveolar de-recruitment at end-expiration

  44. The beneficial effects of PEEP include improved total lung compliance, and decrease in the work of breathing for spontaneously breathing patients, and improved gas exchange through a reduction in intrapulmonary shunting and improved ventilation–perfusion matching. Improved gas exchange may allow for reduction in the fraction of inspired oxygen (FiO2) and oxygen toxicity. Furthermore, studies have suggested that PEEP can reduce the release of bioactive mediators by the lung and may reduce the incidence of secondary infections in the lungs

  45. COMPLICATION • Common complications are; • Nosocomial pneumonia: • Barotrauma • Renal failure • Other complications are : • O2 toxicity, • stress ulcers, • Tracheal ulceration, • Blood clots leading to deep vein thrombosis & • pulmonary embolism.

  46. NURSING DIAGNOSIS • Ineffective breathing pattern related to decreased lung compliance, decreased energy as characterized by dyspnea, abnormal ABGs, cyanosis & use of accessory muscles • Impaired gas exchange related to diffusion defect as characterized by hypoxia, & cyanosis. • Risk for decreased Cardiac output related to positive pressure ventilation. • Impaired physical mobility related to monitoring devices, mechanical ventilation & medications as characterized by imposed restrictions of movement, decreased muscle strength & limited range of motion.