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RESPIRATORY FAILURE and ARDS

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RESPIRATORY FAILURE and ARDS

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  1. RESPIRATORY FAILUREand ARDS By Laurie Dickson

  2. Respiration • Exchange of O2 and CO2 • gas exchange • Respiratory Failure • the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

  3. Hypoxemic Respiratory Failure-(Affects the pO2) • Causes- 4 Physiologic Mechanisms • 1. V/Q Mismatch • 2. Shunt • 3. Diffusion Limitation • 4. Alveolar Hypoventilation- CO2 and PO2

  4. VentilationPerfusion Mismatch (V/Q) • Normal V/Q =1 (1ml air/ 1ml of blood) • Ventilation=lungs • Perfusion or Q=perfusion

  5. Pulmonary Embolus • Pulmonary Embolus- • (VQ scan)

  6. Shunt Anatomic Intrapulmonary • blood passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect • blood flows through pulmonary capillaries without participating in gas exchange ex: alveoli filled with fluid * Patients with shunts are more hypoxemic than those with VQ mismatch and they may require mechanical ventilators

  7. Diffusion Limitation Gas exchange is compromised by a process that thickens or destroys the membrane Pulmonary fibrosis 2. ARDS * A classic sign of diffusion limitation is hypoxemia during exercise but not at rest

  8. Alveolar Hypoventilation • Mainly due to hypercapnic respiratory failure but can cause hypoxemia • Increased pCO2 with decreased PO2 • Restrictive lung disease • CNS diseases • Chest wall dysfunction • Neuromuscular diseases

  9. Hypercapnic Respiratory FailureFailure of Ventilation PaCO2>45 mmHg in combination with acidemia (arterial pH< 7.35) • Caused by conditions that keep the air in

  10. Hypercapnic Respiratory Failure • Abnormalities of the: • Airways and Alveoli-air flow obstruction and air trapping • Asthma, COPD, and cystic fibrosis • CNS-suppresses drive to breathe • drug OD, narcotics, head injury, spinal cord injury • Chest wall-Restrict chest movement • Flail chest, morbid obesity, kyphoscoliosis Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis

  11. Tissue Oxygen needs • Tissue O2 delivery is determined by: • Amount of O2 in hemoglobin • Cardiac output • *Respiratory failure places patient at more risk if cardiac problems or anemia

  12. Signs and Symptoms of Respiratory Failure • hypoxemia • pO2<50-60 • May be hypercapnia • pCO2>45-50 • only one cause- hypoventilation *In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02

  13. Specific Clinical Manifestations • Respirations- depth and rate • Patient position- tripod position • Pursed lip breathing • Orthopnea • Inspiratory to expiratory ratio (normal 1:2) • Retractions and use of accessory muscles • Breath sounds

  14. Hypoxemia • Tachycardia and Hypertension to comp. • Dyspnea and tachypnea to comp. • Cyanosis • Restlessness and apprehension • Confusion and impaired judgment • Later dysrhythmias and metabolic acidosis, decreased B/P and CO.

  15. Hypercapnia • Dyspnea to respiratory depression- if too high CO2 narcosis • Headache-vasodilation • Papilledema • Tachycardia and inc. B/P • Drowsiness and coma • Respiratory acidosis • **Administering O2 may eliminate drive to breathe especially with COPD patients

  16. Diagnosis • Physical Assessment • Pulse oximetry • ABG • CXR • CBC • Electrolytes • EKG • Sputum and blood cultures, UA • V/Q scan if ?pulmonary embolus • Pulmonary function tests

  17. Treatment • Goal- to correct Hypoxia • O2 therapy • Mobilization of secretions • Positive pressure ventilation(PPV) • Noninvasively( NIPPV) through mask • Invasively through oro or nasotracheal intubation

  18. O2 Therapy • If secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by mask • If secondary to intrapulmonary shunt- positive pressure ventilation-PPV • May be via ET tube • Tight fitting mask • Goal is PaO2 of 55-60 with SaO2 at 90% or more at lowest O2 concentration possible • O2 at high concentrations for longer than 48 hours causes O2 toxicity

  19. Mobilization of secretions • Effective coughing • quad cough, huff cough, staged cough • Positioning- • HOB 45 degrees or recliner chair or bed • “Good lung down” • Hydration – • fluid intake 2-3 L/day • Humidification- • aerosol treatments- mucolytic agents • Chest PT- • postural drainage, percussion and vibration • Airway suctioning

  20. Positive Pressure Ventilation • Noninvasive ( NIPPV) through mask • Used for acute and chronic resp failure • BiPAP- different levels of pressure for inspiration and expiration- (IPAP) higher for inspiration,(EPAP) lower for expiration • CPAP- for sleep apnea • Used best in chronic resp failure in patients with chest wall and neuromuscular disease, also with HF and COPD. NPPV

  21. Endotracheal Tube Endotracheal intubation Fig. 66-17

  22. Tracheostomy • Surgical procedure • Used when need for artificial airway is expected to be long term • Research shows benefit to early trach

  23. Exhaled C02 (ETC02) normal 35-45 Used when trying to wean patient from a ventilator

  24. Drug Therapy • Relief of bronchospasm- • Bronchodilators • metaproterenol (Alupent) and albuterol-(Ventolin, Proventil, Proventil-HFA, AccuNeb, Vospire, ProAir ) • Watch for what side effect? • Reduction of airway inflammation • corticosteroids by inhalation or IV or po • Reduction of pulmonary congestion- • diuretics and nitroglycerine with heart failure

  25. Drug Therapy • Treatment of pulmonary infections- • IV antibiotics- vancomycin and ceftriaxone (Rocephin) • Reduction of anxiety, pain and agitation • propofol (Diprivan), lorazepam (Ativan), midazolam (Versed), opioids • May need sedation or neuromuscular blocking agent if on ventilator • vecuronium (Norcuron), cisatracurium besylate (Nimbex ) • assess with peripheral nerve stim.

  26. Medical Supportive Treatment • Treat underlying cause • Maintain adequate cardiac output- • monitor B/P and MAP. • **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs • Maintain adequate Hemoglobin concentration- • need 9g/dl or greater • Nutrition- • During acute phase- enteral or parenteral nurtition • In a hypermetabolic state- need more calories • If retain CO2- avoid high carb diet

  27. Acute Respiratory FailureGerontologic Considerations • Physiologic aging results in • ↓ Ventilatory capacity • Alveolar dilation • Larger air spaces • Loss of surface area • Diminished elastic recoil • Decreased respiratory muscle strength • ↓ Chest wall compliance

  28. ARDSAlso known as DAD(diffuse alveolar disease)or ALI (acute lung injury) a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias

  29. Memory Jogger • Assault to the pulmonary system • Respiratory distress • Decreased lung compliance • Severe respiratory failure

  30. 150,000 adults develop ARDS • About 50% survive • Patients with gram negative septic shock and ARDS have mortality rate of 70-90%

  31. Direct Causes • Inflammatory process is involved • Pneumonia* • Aspiration of gastric contents* • Pulmonary contusion • Near drowning • Inhalation injury

  32. Indirect Causes • Inflammatory process is involved • Sepsis* (most common) gm - • Severe trauma with shock state that requires multiple blood transfusions* • Drug overdose • Acute pancreatitis

  33. ↓CO Metabolic acidosis ↑CO Interstitial & alveolar edema Severe & refractory hypoxemia *Causes (see notes) DIFFUSE lung injury (SIRS or MODS) Damage to alveolar capillary membrane Pulmonary capillary leak SHUNTING Stiff lungs Inactivation of surfactant Hyperventilation Hypocapnea Respiratory Alkalosis Alveolar atalectasis Hypoventilation Hypercapnea Respiratory Acidosis

  34. Pathophysiology of ARDS • Damage to alveolar-capillary membrane • Increased capillary hydrostatic pressure • Decreased colloidal osmotic pressure • Interstitial edema • Alveolar edema or pulmonary edema • Loss of surfactant

  35. Pathophysiologic Stages in ARDS • Injury or Exudative- 1-7 days • Interstitial and alveolar edema and atelectasis • Refractory hypoxemia and stiff lungs • Reparative or Proliferative-1-2 weeks after • Dense fibrous tissue, increased PVR and pulmonary hypertension occurs • Fibrotic-2-3 week after • Diffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension

  36. The essential disturbances of ARDS • Interstitial and alveolar edema and atelectasis • Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS

  37. Clinical Manifestations: Early • Dyspnea-(almost always present), tachypnea, cough, restlessness • Lung sounds-may be normal or reveal fine, scattered crackles • ABGs -Mild hypoxemia and respiratory alkalosis caused by hyperventilation • Chest x-ray -may be normal or show minimal scattered interstitial infiltrates • Edema -may not show until 30% increase in lung fluid content

  38. Clinical Manifestations: Late • Symptoms worsen with progression of fluid accumulation and decreased lung compliance • PFTs show decreased compliance and lung volume • Evident discomfort and increased WOB • Suprasternal retractions • Tachycardia, Diaphoresis • Changes in sensorium with decreased mentation, cyanosis, and pallor • Hypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 ( ex: 80/.8=100)

  39. Clinical Manifestations • As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation • Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs

  40. Clinical Manifestations • If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue

  41. Nursing Diagnoses • Ineffective airway clearance • Ineffective breathing pattern • Risk for fluid volume imbalance • Anxiety • Impaired gas exchange • Imbalanced nutrition

  42. Planning • Following recovery • PaO2 within normal limits or at baseline • SaO2 > 90% • Patent airway • Clear lungs or auscultation

  43. ARDS Diagnosis • Progressive hypoxemia due to shunting • Decreased lung compliance • Bilateral diffuse lung infiltrate

  44. Nursing Assessment • Lung sounds • ABG’s • CXR • Capillary refill • Neuro assessment • Vital signs • O2 sats • Hemodynamic monitoring values • The Auscultation Assistant - Breath Sounds

  45. Diagnostic Tests • ABG • CXR • Pulmonary Function Tests • Hemodynamic Monitoring • ABG review • RealNurseEd (Education for Real Nurses by a Real Nurse)

  46. ARDS Severe ARDS