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Acute Resp Failure.ppt

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  • Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.
  • Alveolar hypoventilation can cause both hypoxemia and hypercapnia. In trauma, we see this acutely when pts splint from painful rib fxs - tire out, need intubation. Maximum inspiratory pressure.
  • VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
  • VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
  • VCO2 is rate of CO2 production. Nl is 90 to 130 L/min/m2, which is 80% of VO2.
  • This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
  • This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
  • DO2 oxygen delivery; VO2 oxygen uptake. Imbalance can aggravate hypoxemia caused by abnl gas exchange in lungs.
  • * pulmonary oedema * normal vascular pedicle * no cardiomegaly or upper lobe blood diversion * when pulmonary vessels can be distinguished they are often constricted * septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema) * progressive lung destruction and transition from alveolar to interstitial opacities Chronic phase * fibrosis * focal emphysema
  • * pulmonary oedema * normal vascular pedicle * no cardiomegaly or upper lobe blood diversion * when pulmonary vessels can be distinguished they are often constricted * septal lines usually absent because capillary leak occurs directly into alveolar spaces (cf cardiogenic pulmonary oedema) * progressive lung destruction and transition from alveolar to interstitial opacities Chronic phase * fibrosis * focal emphysema
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant
  • Direct Lung Injury : a) PNA and aspiration of gastric contents or other causes of chemical pneumonitis b) pulmonary contusion, penetrating lung injury c) fat emboli d) near drowning e) inhalation injury f) reperfusion pulm edema after lung transplant Indirect lung injury a) sepsis b) severe trauma w/ shock hypoperfusion c) drug over dose d) cardiopulmonary bypass e) acute pancreatitis f) transfusion of multp blood products
  • Indirect lung injury a) sepsis b) severe trauma w/ shock hypoperfusion c) drug over dose d) cardiopulmonary bypass e) acute pancreatitis f) transfusion of multp blood products
  • patients with ALI/ARDS at 10 centers, 861 patients Patients randomized to tidal volumes of 12 mL /kg or 6 ml/kg(volume control, assist control, plat Press = 30 cm H2O) 22% reduction in mortality in patients receiving smaller tidal volume Number-needed to treat: 12 patients
  • Transcript

    • 1. Acute Respiratory Failure Cindy Kin Trauma Conference 6 August 2007 Stanford Surgery
    • 2. Acute Respiratory Failure
      • Failure in one or both gas exchange functions: oxygenation and carbon dioxide elimination
      • In practice:
      • PaO2<60mmHg or PaCO2>46mmHg
      • Derangements in ABGs and acid-base status
    • 3. Acute Respiratory Failure
      • Hypercapnic v Hypoxemic respiratory failure
      • ARDS and ALI
    • 4. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality  PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Problem  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
    • 5. The Case of Patient RV
      • 71M s/p L AKA revision.
      • PMH: CAD s/p CABG, COPD on home O2 and CPAP, DM, CVA, atrial fibrillation
      • PACU: L pleural effusion, hypotension, altered mental status. Sent to ICU for monitoring.
      • POD#1:  RR overnight, intermittently hypoxic.
      • BiPAP 40%: 7.34/65/63/35/+10
      • Preintubation: 7.28/91/81/43
    • 6. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality  PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Problem  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
    • 7. Hypercapnic Respiratory Failure Alveolar Hypoventilation Brainstem respiratory depression Drugs (opiates) Obesity-hypoventilation syndrome  PI max Central Hypoventilation Neuromuscular Disorder nl  PI max Critical illness polyneuropathy Critical illness myopathy Hypophosphatemia Magnesium depletion Myasthenia gravis Guillain-Barre syndrome
    • 8. Hypercapnic Respiratory Failure (PAO2 - PaO2) Alveolar Hypoventilation V/Q abnormality  PI max increased normal Nl VCO2 PaCO2 >46mmHg Not compensation for metabolic alkalosis Central Hypoventilation Neuromuscular Disorder  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
    • 9. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient Nl VCO2  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
    • 10. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient Nl VCO2  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
      • Increased dead space ventilation
        • advanced emphysema
        •  PaCO2 when Vd/Vt >0.5
      • Late feature of shunt-type
        • edema, infiltrates
    • 11. Hypercapnic Respiratory Failure V/Q abnormality Increased Aa gradient Nl VCO2  VCO2 V/Q Abnormality Hypermetabolism Overfeeding
      • VCO2 only an issue in pts with ltd ability to eliminate CO2
      • Overfeeding with carbohydrates generates more CO2
    • 12. Hypoxemic Respiratory Failure Is PaCO2 increased? Hypoventilation  (PAO2 - PaO2)? Hypoventilation alone  Respiratory drive Neuromuscular dz Hypovent plus another mechanism Shunt  Inspired PO2 High altitude  FIO2  (PAO2 - PaO2) No No Yes Yes Is low PO2 correctable with O2? V/Q mismatch No Yes
    • 13. The Case of Patient ES
      • 77F s/p MVC.
      • Injuries include multiple L rib fxs, L hemopneumothorax s/p chest tube placement, L iliac wing fx.
      • PMH: atrial arrhythmia, on coumadin. INR>2
      • HD#1
      • RR 30s and shallow. Pain a/w breathing deeply.
      • Placed on BiPAP overnight
      • PID#1
      • BiPAP 80%: 7.45/48/66/32/+10
    • 14. Hypoxemic Respiratory Failure Is PaCO2 increased? Hypoventilation  (PAO2 - PaO2)? Hypoventilation alone  Respiratory drive Neuromuscular dz Hypovent plus another mechanism Shunt  Inspired PO2 High altitude  FIO2  (PAO2 - PaO2) No No Yes Yes Is low PO2 correctable with O2? V/Q mismatch No Yes
    • 15. Hypoxemic Respiratory Failure V/Q mismatch V/Q mismatch DO2/VO2 Imbalance PvO2>40mmHg PvO2<40mmHg  DO2: anemia, low CO  VO2: hypermetabolism
    • 16. Hypoxemic Respiratory Failure V/Q mismatch SHUNT V/Q = 0 DEAD SPACE V/Q = ∞ Atelectasis Intraalveolar filling Pneumonia Pulmonary edema Pulmonary embolus Pulmonary vascular dz Airway dz (COPD, asthma) Intracardiac shunt Vascular shunt in lungs ARDS Interstitial lung dz Pulmonary contusion
    • 17. Hypoxemic Respiratory Failure V/Q mismatch SHUNT V/Q = 0 DEAD SPACE V/Q = ∞ Atelectasis Intraalveolar filling Pneumonia Pulmonary edema Pulmonary embolus Pulmonary vascular dz Airway dz (COPD, asthma) Intracardiac shunt Vascular shunt in lungs ARDS Interstitial lung dz Pulmonary contusion
    • 18. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • Severe ALI
      • B/L radiographic infiltrates
      • PaO2/FiO2 <200mmHg (ALI 201-300mmHg)
      • No e/o  L Atrial P; PCWP<18
    • 19. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • Develops ~4-48h
      • Persists days-wks
      • Diagnosis:
        • Distinguish from cardiogenic edema
        • History and risk factors
    • 20.  
    • 21. Inflammatory Alveolar Injury
    • 22. Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8)
    • 23. Inflammatory Alveolar Injury Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
    • 24. Inflammatory Alveolar Injury Fluid in interstitium and alveoli Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
    • 25. Inflammatory Alveolar Injury Fluid in interstitium and alveoli
      • Impaired gas exchange
      •  Compliance
      •  PAP
      Pro-inflmm cytokines (TNF, IL1,6,8) Neutrophils - ROIs and proteases damage capillary endothelium and alveolar epithelium
    • 26. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome Exudative phase Fibrotic phase Proliferative phase Diffuse alveolar damage
    • 27. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • Direct Lung Injury
      • Infectious pneumonia
      • Aspiration, chemical pneumonitis
      • Pulmonary contusion, penetrating lung injury
      • Fat emboli
      • Near-drowning
      • Inhalation injury
      • Reperfusion pulmonary edema s/p lung transplant
    • 28. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • Indirect Lung Injury
      • Sepsis
      • Severe trauma with shock/hypoperfusion
      • Burns
      • Massive blood transfusion
      • Drug overdose: ASA, cocaine, opioi ds, phenothiazines, TCAs.
      • Cardiopulmonary bypass
      • Acute pancreatitis
    • 29. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • Complications
      • Barotrauma
      • Nosocomial pneumonia
      • Sedation and paralysis  persistent MS depression and neuromuscular weakness
    • 30. Hypoxemic Respiratory Failure Acute Respiratory Distress Syndrome
      • 861 patients, 10 centers
      • Randomized
      • Tidal Vol 12mL/kg PDW, PlatP<50cmH2O
      • Tidal Vol 6mL/kg PDW, PlatP<30cmH2O
      • NNT 12
      • 31% mortality v 39.8%
      • 65.7% breathing without assistance by day 28 v 55%
      • Significantly more ventilator-free days
      • Significantly more days without failure of nonpulmonary organs/systems