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RESPIRATORY FAILURE and ARDS

RESPIRATORY FAILURE and ARDS

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RESPIRATORY FAILURE and ARDS

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  1. RESPIRATORY FAILUREand ARDS By Laurie Dickson with thanks to Nancy Jenkins

  2. Respiration • Exchange of O2 and CO2 • gas exchange • www.le.ac.uk/pathology/teach/va/anatomy/case2/lunganim.gif • Respiratory Failure • the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs

  3. Acute Respiratory Failure • Hypoxemia • Inadequate O2 transfer • PaO2 of 60 mmHg or less when patient receiving 60% or greater O2 • Hypercapnia • Insufficient CO2 removal • Increases PaCO2

  4. Hypoxemic Respiratory Failure-(Affects the pO2) • V/Q Mismatch • Shunt • Diffusion Limitation • Alveolar Hypoventilation- inc. CO2 and dec. PO2

  5. VentilationPerfusion Mismatch (V/Q) • Normal V/Q =1 (1ml air/ 1ml of blood) • Ventilation=lungs • Perfusion or Q=perfusion • Pulmonary Embolus- (VQ scan)

  6. Range of V/Q Relationships Fig. 68-4

  7. Pulmonary Embolus

  8. Shunt • 2 Types • Anatomic- blood passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect

  9. Shunt 2. Intrapulmonary - 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

  10. Diffusion Limitations • Gas exchange is compromised by a process that thickens or destroys the membrane • 1. Pulmonary fibrosis • 2. ARDS * A classic sign of diffusion limitation is hypoxemia during exercise but not at rest

  11. Diffusion Limitation Fig. 68-5

  12. 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

  13. Hypercapnic Respiratory FailureFailure of Ventilation • PaCO2>45 mmHg in combination with acidemia (arterial pH< 7.35)

  14. Hypercapnic Respiratory FailureVentilatory Failure- affects CO2 • 1. Abnormalities of the airways and alveoli- • air flow obstruction and air trapping • Asthma, COPD, and cystic fibrosis 2. Abnormalities of the CNS- suppresses drive to breathe drug OD, narcotics, head injury, spinal cord injury

  15. Hypercapnic Respiratory Failure • 3. Abnormalities of the chest wall • Restrict chest movement • Flail chest, morbid obesity, kyphoscoliosis 4. Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis

  16. 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

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

  18. 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

  19. 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.

  20. 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

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

  22. Treatment Goals • O2 therapy • Mobilization of secretions • Positive pressure ventilation(PPV)

  23. 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

  24. 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, prercussion and vibration • Airway suctioning

  25. Positive Pressure Ventilation • Invasively through oro or nasotracheal intubation • Noninvasively( 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.

  26. NPPV NPPV

  27. Endotracheal Tube endotrachael intubation Fig. 66-17

  28. Surgical Intervention: • Tracheotomy • Surgical procedure performed when need for an artificial airway is expected to be long term

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

  30. 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

  31. 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.

  32. Medical Supportive Treatment • Treat underlying cause • Maintain adequate cardiac output- monitor B/P and MAP. • Maintain adequate Hemoglobin concentration- need 9g/dl or greater • **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs

  33. Nutrition • During acute phase- enteral or parenteral nurtition • In a hypermetabolic state- need more calories • If retain CO2- avoid high carb diet

  34. 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

  35. 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

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

  37. 150,000 adults develop ARDS • About 50% survive • Patients with gram negative septic shock and ARDS have mortality rate of 70-90%

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

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

  40. ↓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

  41. 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

  42. What does surfactant do?

  43. 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

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