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Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
Management of persistent hypoxemic respiratory failure in the icu   garpestad
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Management of persistent hypoxemic respiratory failure in the icu garpestad

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  • Figure 1. Radiographic and Computed Tomographic (CT) Findings in the Acute, or Exudative, Phase (Panels A and C) and the Fibrosing-Alveolitis Phase (Panels B and D) of Acute Lung Injury and the Acute Respiratory Distress Syndrome. Panel A shows an anteroposterior chest radiograph from a 42-year-old man with the acute respiratory distress syndrome associated with gram-negative sepsis who was receiving mechanical ventilation. The pulmonary-artery wedge pressure, measured with a pulmonary-artery catheter, was 4 mm Hg. There are diffuse bilateral alveolar opacities consistent with the presence of pulmonary edema. Panel B shows an anteroposterior chest radiograph from a 60-year-old man with acute lung injury and the acute respiratory distress syndrome who had been receiving mechanical ventilation for seven days. Reticular opacities are present throughout both lung fields, a finding suggestive of the development of fibrosing alveolitis. Panel C shows a CT scan of the chest obtained during the acute phase. The bilateral alveolar opacities are denser in the dependent, posterior lung zones, with sparing of the anterior lung fields. The arrows indicate thickened interlobular septa, consistent with the presence of pulmonary edema. The bilateral pleural effusions are a common finding.1415 Panel D shows a CT scan of the chest obtained during the fibrosing-alveolitis phase. There are reticular opacities and diffuse ground-glass opacities throughout both lung fields, and a large bulla is present in the left anterior hemithorax. Panels C and D are reprinted from Goodman16 with the permission of the publisher.
  • Figure 2. Lung Injury Caused by Mechanical Ventilation in a 31-Year-Old Woman with the Acute Respiratory Distress Syndrome Due to Amniotic-Fluid Embolism. The patient had undergone mechanical ventilation for eight weeks with tidal volumes of 12 to 15 ml per kilogram of body weight, peak airway pressures of 50 to 70 cm of water, positive end-expiratory pressures of 10 to 15 cm of water, and a fractional inspired oxygen concentration of 0.80 to 1.00 in order to achieve a partial pressure of carbon dioxide that was less than 50 mm Hg and a partial pressure of oxygen that was 80 mm Hg or higher. Computed tomography (CT) performed two days before the patient died revealed a paramediastinal pneumatocele in the right lung (Panel A, arrowheads) and numerous intraparenchymal pseudocysts in the left lung (Panel B, black arrow, open circle, and asterisk). At autopsy, both lungs were removed and fixed by intrabronchial infusion of formalin, alcohol, and polyethylene glycol at an insufflation pressure of 30 cm of water. Panel C shows the paramediastinal pneumatocele in the right lung (arrowheads); the horizontal broken line is the level of the CT section. Panel D shows a 1-cm-thick section of the left lung, corresponding to the CT section. Small pseudocysts are present (arrow), and two large pseudocysts (asterisk and open circle) have compressed and partially destroyed the parenchyma. The development of these lesions in a patient without a history of chronic lung disease indicates the harm that may result with the use of high tidal volumes and airway pressures. The photographs were kindly provided by Dr. Jean-Jacques Rouby, Hopital de la Pitie-Salpetriere, Paris.
  • Figure 3. Respiratory Pressure-Volume Curve and the Effects of Traditional as Compared with Protective Ventilation in a 70-kg Patient with the Acute Respiratory Distress Syndrome. The lower and upper inflection points of the inspiratory pressure-volume curve (center panel) are at 14 and 26 cm of water, respectively. With conventional ventilation at a tidal volume of 12 ml per kilogram of body weight and zero end-expiratory pressure (left-hand panel), alveoli collapse at the end of expiration. The generation of shear forces during the subsequent mechanical inflation may tear the alveolar lining, and attaining an end-inspiratory volume higher than the upper inflection point causes alveolar overdistention. With protective ventilation at a tidal volume of 6 ml per kilogram (right-hand panel), the end-inspiratory volume remains below the upper inflection point; the addition of positive end-expiratory pressure at 2 cm of water above the lower inflection point may prevent alveolar collapse at the end of expiration and provide protection against the development of shear forces during mechanical inflation.
  • Table 1. Summary of Ventilator Procedures.
  • Table 4. Main Outcome Variables.
  • Figure 1. Probability of Survival and of Being Discharged Home and Breathing without Assistance during the First 180 Days after Randomization in Patients with Acute Lung Injury and the Acute Respiratory Distress Syndrome. The status at 180 days or at the end of the study was known for all but nine patients. Data on these 9 patients and on 22 additional patients who were hospitalized at the time of the fourth interim analysis were censored.
  • Figure 1. Actuarial 28-Day Survival among 53 Patients with the Acute Respiratory Distress Syndrome Assigned to Protective or Conventional Mechanical Ventilation. The data are based on an intention-to-treat analysis. The P value indicates the effect of ventilatory treatment as estimated by the Cox regression model, with the risk of death associated with the adjusted base-line score on APACHE II included as a covariate.
  • Table 1. Summary of Ventilator Procedures in the Lower- and Higher-PEEP Groups.
  • Figure 1. Probabilities of Survival and of Discharge Home While Breathing without Assistance, from the Day of Randomization (Day 0) to Day 60 among Patients with Acute Lung Injury and ARDS, According to Whether Patients Received Lower or Higher Levels of PEEP.
  • Table 4. Main Outcome Variables.
  • Figure 1. Computed Tomographic Images Obtained at the End-Expiratory Pause in a Patient with Pneumocystosis and the Acute Respiratory Distress Syndrome. The images were obtained under different ventilatory conditions: a positive end-expiratory pressure (PEEP) of 5 cm of water and a plateau pressure of 20 cm of water (Panel A), a PEEP of 17 cm of water and a plateau pressure of 40 cm of water (Panel B, similar to the strategy used by Gattinoni et al.), a PEEP of 25 cm of water and a plateau pressure of 40 cm of water (Panel C), and a PEEP of 25 cm of water and a plateau pressure of 60 cm of water (Panel D). The corresponding potential for recruitment (relative to the conditions in Panel A) was 35 percent for the conditions in Panel B, 67 percent for the conditions in Panel C, and 87 percent for the conditions in Panel D. At the same plateau pressures (Panels B and C), the application of a higher PEEP (25 cm of water in Panel C) improved the efficacy of the maneuver. A further increase in inspiratory plateau pressure (Panel D) revealed the full potential for recruitment.
  • Figure 1. Enrollment and Study Protocol. In the study group, a recruitment maneuver was performed immediately before application of each PEEP level. In the comparison groups, patients with bilateral pneumonia were excluded from the analysis to limit the possible confounding factors caused by the partial overlapping between patients with less severe acute lung injury or ARDS and patients with bilateral pneumonia (see the Supplementary Appendix for further details). Therefore, only patients with unilateral pneumonia, who by definition did not meet the inclusion criteria for acute lung injury or ARDS, were included. The group with a lower percentage of potentially recruitable lung includes patients with potentially recruitable lung values at or below the overall median of 9 percent, and the group with a higher percentage of potentially recruitable lung includes patients with values above the median.
  • Figure 2. Frequency Distribution of Patients According to the Percentage of Potentially Recruitable Lung (Panel A) and CT Images at Airway Pressures of 5 and 45 cm of Water from Patients with a Lower Percentage of Potentially Recruitable Lung (Panel B) and Those with a Higher Percentage of Potentially Recruitable Lung (Panel C). Panel A shows the frequency distribution of the 68 patients in the overall study group according to the percentage of potentially recruitable lung, expressed as the percentage of total lung weight. Acute lung injury without ARDS was defined by a PaO2:FIO2 of less than 300 but not less than 200, and ARDS was defined by a PaO2:FIO2 of less than 200. The percentage of potentially recruitable lung was defined as the proportion of lung tissue in which aeration is restored at airway pressures between 5 and 45 cm of water. Panel B shows representative CT slices of the lung obtained 2 cm above the diaphragm dome at airway pressures of 5 cm of water (left) and 45 cm of water (right) from a patient with a lower percentage of potentially recruitable lung (at or below the median value of 9 percent of total lung weight). Lung injury developed in the patient after an episode of severe acute pancreatitis (PaO2:FIO2, 296 at an airway pressure of 5 cm of water; PaCO2, 34 mm Hg; and respiratory-system compliance, 44 ml per centimeter of water). The percentage of potentially recruitable lung was 4 percent, and the proportion of consolidated lung tissue was 33 percent of the total lung weight. Panel C shows representative CT slices of the lung obtained 2 cm above the diaphragm dome at airway pressures of 5 cm of water (left) and 45 cm of water (right) from a patient in the group with a higher percentage of potentially recruitable lung. Lung injury developed in the patient after an episode of severe pneumonia (PaO2:FIO2, 106 at a PEEP of 5 cm of water; PaCO2,58 mm Hg; and respiratory-system compliance, 25 ml per cm of water). The percentage of potentially recruitable lung was 37 percent, and the proportion of consolidated lung tissue was 27 percent of the total lung weight.
  • Figure 2. Kaplan-Meier Estimates of the Probability of Survival and of Survival without the Need for Assisted Ventilation during the First 60 Days after Randomization.
  • Figure 3. Probability of Survival to Hospital Discharge and of Breathing without Assistance during the First 60 Days after Randomization.
  • Transcript

    • 1. Management of Persistent Hypoxemic Respiratory Failure in the ICU Erik Garpestad, M.D. Director, MICU Tufts Medical Center
    • 2. Case Presentation <ul><li>73 yo male underwent elective laporscopic surgery for lyses of abdominal adhesions. </li></ul><ul><li>Surgery went well, pt extubated post-op without difficulty. </li></ul><ul><li>POD# 1 pt developed abdominal pain, fever, hypotension requiring reoperation for peritonitis related to bowel perforation </li></ul>
    • 3. Case: persistent hypoxia <ul><li>For septic shock, pt started on EGDT, 3 pressor agents, VC ventilation with 6 ml/kg of IBW, PEEP 10 cm H20, FiO2 of 100% </li></ul><ul><li>ABG 7.10/46/53 </li></ul><ul><li>RR increase, PEEP increased 15-18 cm H20 but ABG with minimal improvement </li></ul>
    • 4.  
    • 5.  
    • 6. Persistent Hypoxemia <ul><li>What are your options? </li></ul><ul><li>How do you balance need to improve oxygen exchange and optimize oxygen delivery vs lung protective strategy </li></ul><ul><li>These goals are not mutually exclusive </li></ul>
    • 7. Persistent Hypoxemia <ul><li>Increase FiO2, increase PEEP </li></ul><ul><li>Recruitment maneuvers </li></ul><ul><li>Prone positioning </li></ul><ul><li>NO </li></ul><ul><li>Ventilator strategies: Lung protective and Open lung approach </li></ul><ul><li>APRV </li></ul><ul><li>HFOV </li></ul>
    • 8. Benefits of Mechanical Ventilation <ul><li>Improved oxygenation </li></ul><ul><li>Decreased work of breathing </li></ul>
    • 9. Risks of Mechanical Ventilation <ul><li>Barotrauma </li></ul><ul><li>Biotrauma </li></ul><ul><li>Baby lung </li></ul><ul><li>Cyclic atelectasis </li></ul>
    • 10. Minimizing MV Risks <ul><li>What pressures to measure? </li></ul><ul><li>What modality to use? </li></ul><ul><li>Is there a safe PIP? </li></ul><ul><li>Is there a safe plateau pressure? </li></ul><ul><li>How do you set optimal PEEP? </li></ul>
    • 11. Ventilator Strategy <ul><li>Low tidal volume strategy </li></ul><ul><li>Open lung strategy </li></ul>
    • 12. Other Ventilator Strategies <ul><li>APRV </li></ul><ul><li>HFOV </li></ul><ul><li>TGI </li></ul><ul><li>ECMO </li></ul>
    • 13. Discussion <ul><li>What do you do to decrease risks? </li></ul>
    • 14. Ware, L. B. et al. N Engl J Med 2000;342:1334-1349 Radiographic and Computed Tomographic (CT) Findings in the Acute, or Exudative, Phase (Panels A and C) and the Fibrosing-Alveolitis Phase (Panels B and D) of Acute Lung Injury and the Acute Respiratory Distress Syndrome
    • 15. ARDS: Mechanical Ventilation <ul><li>Traditional approach: </li></ul><ul><ul><li>Normalize blood gases </li></ul></ul><ul><ul><li>High minute ventilation </li></ul></ul><ul><ul><li>High tidal volumes </li></ul></ul><ul><ul><li>High inflation pressures </li></ul></ul>
    • 16. ARDS: Mechanical Ventilation <ul><li>Maintain adequate oxygenation (PaO2 of 55-80 mmHg or SaO2 of 88-95% </li></ul><ul><li>Avoid oxygen toxicity </li></ul><ul><li>Employ PEEP </li></ul><ul><li>Prevent ventilator induce lung injury </li></ul><ul><li>Minimize barotrauma and volutrauma </li></ul>
    • 17. Ventilator Induced Lung Injury <ul><li>Volutrauma: </li></ul><ul><ul><li>Overdistention, physical injury </li></ul></ul><ul><ul><li>Biotrauma </li></ul></ul><ul><li>Atelectrauma: </li></ul><ul><ul><li>Repetitive opening/closing </li></ul></ul><ul><ul><li>Shear forces at open/collapse lung interface </li></ul></ul>
    • 18. Barotrauma
    • 19. Tobin, M. J. N Engl J Med 2001;344:1986-1996 Lung Injury Caused by Mechanical Ventilation in a 31-Year-Old Woman with the Acute Respiratory Distress Syndrome Due to Amniotic-Fluid Embolism
    • 20.  
    • 21. Tobin, M. J. N Engl J Med 2001;344:1986-1996 Respiratory Pressure-Volume Curve and the Effects of Traditional as Compared with Protective Ventilation in a 70-kg Patient with the Acute Respiratory Distress Syndrome
    • 22. ARDS: ARDS Network Trial <ul><li>Largest randomized trial to date </li></ul><ul><li>Compared traditional mechanical ventilation (15 ml/kg, plateau < 50 cm H2O) to lower tidal volume (6 ml/kg, plateau < 30 cm H20) </li></ul><ul><li>Trial stopped after 861 pts because mortality was lower in low Vt pts, 31% vs 39.8%, p=0.007 (NEJM 2000;342:1301) </li></ul>
    • 23. The Acute Respiratory Distress Syndrome Network, N Engl J Med 2000;342:1301-1308 Summary of Ventilator Procedures
    • 24. The Acute Respiratory Distress Syndrome Network, N Engl J Med 2000;342:1301-1308 Main Outcome Variables
    • 25. The Acute Respiratory Distress Syndrome Network, N Engl J Med 2000;342:1301-1308 Probability of Survival and of Being Discharged Home and Breathing without Assistance during the First 180 Days after Randomization in Patients with Acute Lung Injury and the Acute Respiratory Distress Syndrome
    • 26. ARDS: Mechanical Ventilation <ul><li>What mode of ventilation to use? </li></ul><ul><ul><li>Either volume cycled ventilation or pressure cycled ventilation can be used </li></ul></ul><ul><ul><li>Choosing appropriate goals for mechanical ventilation is more important than mode </li></ul></ul><ul><ul><li>Target Vt of 6 ml/kg and plateau pressure less than 30 cm H2O </li></ul></ul>
    • 27. ARDS: Mechanical Ventilation <ul><li>After starting at Vt of 6 ml/kg and keeping plateau pressures < 30 cm H2O: </li></ul><ul><ul><li>adjust PEEP. Can use ARDSNet protocol </li></ul></ul><ul><ul><li>if FiO2 > 0.6, lengthen inspiratory time or consider IRV </li></ul></ul><ul><ul><li>adequate sedation if permissive hypercapnea is a consequence of ventilatory strategy </li></ul></ul>
    • 28. ARDS: Mechanical Ventilation <ul><li>ARDSnet established the benefit of small tidal volumes (4-8 ml/kg predicted ideal body weight) ventilation on ALI/ARDS mortality </li></ul><ul><li>Active debate continues over level of PEEP and the use of recruitment maneuvers </li></ul>
    • 29. ARDS: PEEP <ul><li>Improves oxygenation </li></ul><ul><li>Recruits atelectatic lung and prevents alveolar collapse </li></ul><ul><li>Increases FRC </li></ul><ul><li>Improves lung compliance </li></ul><ul><li>Assists in minimizing VILI </li></ul>
    • 30. Pressure Volume Curve in ARDS LIP Volume Pressure UIP 1 2 3 1 2 3 1 2 3 1 2 3 Too much VT Too little PEEP
    • 31. PEEP 5 PEEP 10 PEEP 15 PEEP 5 By keeping intrathoracic pressure positive throughout the respiratory cycle atelectatic lung can be re-expanded or recruited. Shunt decreases and PaO2 increases. PaO2 = 60 PaO2 = 100 PaO2 = 220
    • 32. ARDS: What is optimal level of PEEP? <ul><li>Amato et al (NEJM 1998) used an “open-lung” strategy. PEEP (1st 36 hrs) in conventional ventilation was 8.7 and in protective ventilation was 16.4 cm H2O. </li></ul><ul><li>Mortality difference 72% vs 38% </li></ul><ul><li>However, patients who received higher PEEP levels also received lower Vt. </li></ul>
    • 33. Amato M et al. N Engl J Med 1998;338:347-354 Actuarial 28-Day Survival among 53 Patients with the Acute Respiratory Distress Syndrome Assigned to Protective or Conventional Mechanical Ventilation
    • 34. ARDS: What is optimal level of PEEP? <ul><li>NIH ARDS Clinical Trials Network looked at Higher vs Lower PEEP in ARDS patients </li></ul><ul><li>549 pts with ALI or ARDS randomly assigned to low PEEP (mean on day 1-4 was 8.3 + 3.2 cm H2O) vs high PEEP (mean 13.2 + 3.5 cm H2O) </li></ul><ul><li>No significant difference in mortality, vent free days, ICU-free days or Organ failure. </li></ul>
    • 35. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. N Engl J Med 2004;351:327-336 Summary of Ventilator Procedures in the Lower- and Higher-PEEP Groups
    • 36. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. N Engl J Med 2004;351:327-336 Probabilities of Survival and of Discharge Home While Breathing without Assistance, from the Day of Randomization (Day 0) to Day 60 among Patients with Acute Lung Injury and ARDS, According to Whether Patients Received Lower or Higher Levels of PEEP
    • 37. The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network. N Engl J Med 2004;351:327-336 Main Outcome Variables
    • 38. ARDSnet High/Low PEEP trial <ul><li>Potential Concerns: </li></ul><ul><li>Plateau pressures in both groups not dangerously high and importance of PEEP is likely to depend on plateau pressure </li></ul><ul><li>Baseline imbalances in age at randomization </li></ul><ul><li>Recruitment maneuvers not used </li></ul>
    • 39. ARDS: Recruitment maneuvers <ul><li>Strategy of using a sustained, high pressure breath to recruit or open atelectatic lung </li></ul><ul><li>No standard method. For example: Sustain single inflation at CPAP of 35 cm H2O for 60 seconds. Monitor SaO2 and BP </li></ul><ul><li>Need to use higher PEEP after maneuver: go to 20 cm H2O and then decrease sequentially by 2.5 cm until dec SaO2 </li></ul>
    • 40. Borges J et al. N Engl J Med 2006;355:319-322 Computed Tomographic Images Obtained at the End-Expiratory Pause in a Patient with Pneumocystosis and the Acute Respiratory Distress Syndrome
    • 41. Gattinoni L et al. N Engl J Med 2006;354:1775-1786 Enrollment and Study Protocol
    • 42. Gattinoni L et al. N Engl J Med 2006;354:1775-1786 Frequency Distribution of Patients According to the Percentage of Potentially Recruitable Lung (Panel A) and CT Images at Airway Pressures of 5 and 45 cm of Water from Patients with a Lower Percentage of Potentially Recruitable Lung (Panel B) and Those with a Higher Percentage of Potentially Recruitable Lung (Panel C)
    • 43. ARDS: Open Lung Approach <ul><li>To determine if the use of lung recruitment maneuvers and a decremental PEEP trial along with small Vt results in lower mortality in severe established ARDS than the original ARDSnet protocol </li></ul>
    • 44. ARDS: Open Lung Approach <ul><li>Intubated, ventilated, ARDS criteria met </li></ul><ul><li>Initial 12-36 hrs, pts will be ventilated per ARDSnet protocol </li></ul><ul><li>Reassessment of oxygenation, PaO2/FiO2 still <200 for pt to be randomized </li></ul><ul><li>Pts randomized to ARDSnet protocol and Open Lung Approach </li></ul>
    • 45. ARDS: Open Lung Approach <ul><li>Lung recruitment procedure: </li></ul><ul><ul><li>PEEP 25 cm H2O, PCV 15 cm H2O (Peak airway pressure 40 cm H2O) for 5 breaths </li></ul></ul><ul><ul><li>PEEP 25, PCV 20 for 5 breaths </li></ul></ul><ul><ul><li>PEEP 30, PCV 20 for final 20 breaths </li></ul></ul><ul><li>Decremental PEEP procedure: decrease in 2 cm H2O steps until the maximum compliance is identified </li></ul>
    • 46. ARDS: Permissive Hypercapnia <ul><li>Allowing respiratory acidosis improves our ability to use lower tidal volumes and airway pressures </li></ul><ul><li>May require sedation, or even paralysis </li></ul><ul><li>Contraindicated in pts with increased ICP </li></ul>
    • 47. ARDS: Inverse Ratio Ventilation <ul><li>Increase I:E ratio from 1:3 to 1:1 or more </li></ul><ul><li>Increasing inspiratory time improves oxygenation without increasing pressures </li></ul><ul><li>Watch for dynamic hyperinflation or worsening hemodynamics </li></ul>
    • 48. ARDS: Prone positioning <ul><li>Improves oxygenation but no change in mortality (NEJM 2001;345:568) </li></ul><ul><li>Not routinely recommended </li></ul><ul><li>Consider use early in course of ALI/ARDS in patients requiring high PEEP and FiO2. </li></ul><ul><li>Try recruitment maneuvers first </li></ul>
    • 49. Supine Prone Dependent Atelectasis
    • 50. ARDS: Supportive Care <ul><li>Fluid management </li></ul><ul><ul><li>maintain intravascular volume at lowest level that allows for adequate perfusion </li></ul></ul><ul><li>Nutrition </li></ul><ul><ul><li>enteral feedings when possible </li></ul></ul><ul><li>Prophylaxis </li></ul><ul><ul><li>for DVT and GI bleeding </li></ul></ul>
    • 51. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. N Engl J Med 2006;354:2213-2224 Kaplan-Meier Estimates of the Probability of Survival and of Survival without the Need for Assisted Ventilation during the First 60 Days after Randomization
    • 52. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. N Engl J Med 2006;354:2564-2575 Probability of Survival to Hospital Discharge and of Breathing without Assistance during the First 60 Days after Randomization
    • 53. ARDS: Pharmacological Therapy <ul><li>Antibiotics </li></ul><ul><li>Neuromuscular blockade </li></ul>
    • 54. ARDS: Pharmacological Therapy <ul><li>Corticosteroids </li></ul><ul><ul><li>No benefit early in course of ALI/ARDS </li></ul></ul><ul><ul><li>Have been used in fibrosing-alveolitis phase of ARDS </li></ul></ul><ul><ul><li>Consider short course in pts with severe disease that have prolonged course and not improving (Meduri, JAMA 1998;280:159) </li></ul></ul>
    • 55. ARDS: Pharmacological Therapy <ul><li>Inhaled nitric oxide </li></ul><ul><ul><li>may improve oxygenation and PVR, but only transiently. No improvement in outcome </li></ul></ul><ul><li>Inhaled surfactant </li></ul><ul><ul><li>no outcome improvement </li></ul></ul>
    • 56. ARDS <ul><li>Mechanical Ventilation of 6 ml/kg and maintain plateau < 30 cm H20 </li></ul><ul><li>Lowest FiO2 that maintains adequate oxygenation </li></ul><ul><li>Titrate PEEP </li></ul><ul><li>Supportive care </li></ul>
    • 57. Alternative Methods of Ventilatory Support <ul><li>Airway pressure release ventilation </li></ul><ul><li>High-Frequency Ventilation </li></ul>
    • 58. Case presentation <ul><li>73 yo male underwent elective laporscopic surgery for lysis of abdominal adhesions. </li></ul><ul><li>Surgery went well, pt extubated post-op without difficulty. </li></ul><ul><li>POD# 1 pt developed abdominal pain, fever, hypotension requiring reoperation for peritonitis related to bowel perforation </li></ul>
    • 59. Case: persistent hypoxia <ul><li>For septic shock, pt started on EGDT, 3 pressor agents, VC ventilation with 6 ml/kg IBW, PEEP 10 cm H20, FiO2 of 100% </li></ul><ul><li>ABG 7.10/46/53 </li></ul><ul><li>RR increase, PEEP increased 15-18 cm H20 but ABG with minimal improvement </li></ul>
    • 60. Case: Persistent hypoxemia <ul><li>Inhaled NO was started </li></ul><ul><li>APRV: Hi-PEEP 32, low-PEEP 15, FiO2 of 100%. ABG 7.24/32/63 </li></ul><ul><li>HFOV: Mean airway pressure 32, frequency 5 Hz, set oscillation pressure for “Movement of torso from clavicle to mid thigh”. ABG 7.23/31/65 </li></ul>
    • 61. What is APRV? <ul><li>An “open” ventilator strategy </li></ul><ul><li>Essentially = CPAP + Time Cycled Pressure Release </li></ul>Habashi NM, crit care med 2005: 33(3S)
    • 62. APRV Pressure/Flow Diagram
    • 63. Theoretical Advantages <ul><li>Spontaneous Breathing Allows: </li></ul><ul><ul><li>Improved Ventilation of Dependent Lung </li></ul></ul><ul><ul><li>Less Likely to have alveolar overdistention </li></ul></ul><ul><ul><li>Potentially less sedation </li></ul></ul><ul><li>Increased time at high pressures may improve recruitment </li></ul>
    • 64. Theoretical Advantages <ul><li>Pressure Release </li></ul><ul><ul><li>Improved TV for given Δ P, utilizes increased elastic recoil, expiratory limb of PV curve </li></ul></ul><ul><ul><li>Less chance of over distension given not “filling” lung but “emptying”. </li></ul></ul><ul><ul><li>Short release time does not allow significant dercruitment </li></ul></ul>
    • 65. APRV Settings <ul><li>P high = CPAP </li></ul><ul><li>P low = Release Pressure </li></ul><ul><li>T high = Time at P high </li></ul><ul><li>T low = Time at P low </li></ul><ul><li>Can supplement spontaneous breathing with pressure support </li></ul>
    • 66. APRV Settings <ul><li>P high </li></ul><ul><ul><li>Newly Intubated = Desired Pplat </li></ul></ul><ul><ul><li>From Conventional Vent = Current Pplat </li></ul></ul><ul><li>P low </li></ul><ul><ul><li>Suggested setting: 0 </li></ul></ul><ul><li>T high </li></ul><ul><ul><li>4-6 secs </li></ul></ul><ul><li>T low </li></ul><ul><ul><li>0.2-0.8 secs </li></ul></ul>Habashi NM, crit care med 2005: 33(3S)
    • 67. APRV Settings <ul><li>Oxygenation </li></ul><ul><ul><li>Decrease T low to ensure end-exhaled flow rate is >50% PEFR and < 75% PEFR </li></ul></ul><ul><ul><li>Increase P high and/or T high </li></ul></ul><ul><li>Ventilation </li></ul><ul><ul><li>Assess sedation </li></ul></ul><ul><ul><li>Increase P high and/or T high ( TV) </li></ul></ul><ul><ul><li>Decrease T high ( Ve) </li></ul></ul>Habashi NM, crit care med 2005: 33(3S)
    • 68. APRV Pressure/Flow Diagram
    • 69. High Frequency Ventilation Modes From UptoDate, Ostenholzer and Hyzy
    • 70. Physiology <ul><li>Oscillating pressure around a set mean airway pressure </li></ul><ul><li>Higher Mean Pressures increase oxygenation </li></ul><ul><li>Lower peak pressures and in theory small volumes result in no overdistension </li></ul>From Quissell et al
    • 71. Increased Mean Pressures = Improved oxygenation From Mehta et al Critical Care 2001
    • 72. Ventilation <ul><li>Occurs through multiple proposed mechanisms </li></ul><ul><ul><li>Direct Conductive </li></ul></ul><ul><ul><li>Longitudinal dispersion from turbulence </li></ul></ul><ul><ul><li>Pendeluft flow due to varying time constants </li></ul></ul><ul><ul><li>Venturi Effect </li></ul></ul><ul><ul><li>Diffusion </li></ul></ul>
    • 73. Gas Transport in HFOV From UptoDate, Ostenholzer and Hyzy
    • 74. Case Presentation <ul><li>Pt is a 38 year-old man who presents with severe pneumonia and ARDS. The pt is started on conventional ventilation by ARDSnet protocol. Yet despite increasing PEEP to 18, the PaO2 is still 55 on an FiO2 of 1.0 </li></ul><ul><ul><li>You are asked to initiate HFOV. What are your initial settings? </li></ul></ul>
    • 75. Initial Settings <ul><li>Set Mean Pressure at Mean pressure of Conventional Ventilation </li></ul><ul><li>Set Frequency 3-5 Hz </li></ul><ul><li>Set oscillation pressure for “Movement of torso from clavicle to mid thigh” </li></ul>
    • 76. Case Presentation <ul><li>The pt is sedated/paralyzed and placed on HFOV. Mean pressure: 25cmH2O,Frequency 3Hz and FiO2 = 1.0 Initial ABG: </li></ul><ul><ul><li>pH = 7.22 </li></ul></ul><ul><ul><li>PaCO2 = 60 </li></ul></ul><ul><ul><li>PaO2 = 65 </li></ul></ul><ul><ul><li>What adjustments would you make to your settings? </li></ul></ul>
    • 77. Adjustments <ul><li>Oxygenation </li></ul><ul><ul><li>Mean Pressure </li></ul></ul><ul><ul><li>FiO2 </li></ul></ul><ul><li>Ventilation (CO2) </li></ul><ul><ul><li>Frequency </li></ul></ul><ul><ul><li>Oscillation pressure amplitude </li></ul></ul><ul><ul><li>Intentional cuff leak </li></ul></ul>
    • 78. Case <ul><li>The frequency is increased to 5Hz and Mean pressure increased to 28cmH2O </li></ul><ul><li>ABG: pH = 7.30 PaCO2 = 50 PaO2 = 105 </li></ul><ul><li>What complications are associated with HFOV? </li></ul>
    • 79. Complications <ul><li>Similar to conventional ventilation </li></ul><ul><li>Higher Mean Airway Pressures may have more hemodynamic effects </li></ul><ul><li>90% + pts require paralysis – no rates of post-paralytic syndrome reported in clinical trials </li></ul>
    • 80. Literature <ul><li>Neonates: associated with improved gas exchange and decreased barotrauma. No change in mortality </li></ul><ul><li>Adults: Improved early oxygenation but no other outcome improved </li></ul><ul><li>Can be combined with other modalities to improve oxygenation: Prone, NO </li></ul>
    • 81. Randomized Trials <ul><li>Derdak et al, AJRCCM 2002: Primary outcome safety; No difference in safety c/w conventional ventilation </li></ul><ul><ul><li>Mortality secondary outcome </li></ul></ul><ul><ul><ul><li>37%(HFOV) vs 52% (conv) p=0.10 </li></ul></ul></ul><ul><ul><ul><li>Prior to ARDSnet protocol </li></ul></ul></ul><ul><li>Bollen et al; Crit Care 2005: No mortality difference [28% vs 32%] </li></ul>
    • 82. Preventing Derecruitment after Proning Demory et al Crit Care Med 2007
    • 83. Management of Hypoxic Respiratory Failure: Conclusions <ul><li>Initially employ a lung protective strategy with low tidal volumes with adequate PEEP and monitoring of plateau pressures </li></ul><ul><li>Routine use of Open lung approach, high PEEP, recruitment maneuvers, APRV and HFOV continue to be investigated. Select these interventions on case by case basis </li></ul>

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