High Frequency Oscillatory Ventilation of the Large Patient

1. High Frequency Oscillatory Ventilation of the Large Patient William R. Howard MBA, RRT Director, Respiratory Care Programs

2. High Frequency Ventilation Defined by FDA as a ventilator that delivers more than 150 breaths/min. Delivers a small tidal volume, usually less than or equal to anatomical dead space volume. While HFV�s are frequently described by their delivery method, they are usually classified by their exhalation mechanism (active or passive).

3. Jet Ventilators

4. Adult High Frequency Jet Ventilation First reports 1977 (Klain and Smith) First Randomized Controlled Trial 1983 Carlon (Sloan Kettering Hospital, NY) 300 patients with ARDS Outcome reported no difference to CMV Methodology limitation was low mean airway pressure First commercially sponsored study 1993 APT1010 (Infrasonics 1010) Rescue of 90 patients with ARDS (non RCT) Improved survival as compared to historic controls

5. Piston - Diaphragm Oscillators

6. Mechanisms of HFOV Gas Exchange There are six mechanisms of gas exchange during HFOV Convective Ventilation Asymmetrical Velocity Profiles Taylor Dispersion Pendeluft Molecular Diffusion Cardiogenic Mixing

7. Proximal and Alveolar Pressures HFOV vs. CMV Gerstmann D.

8. Why High Frequency Oscillatory Ventilation?

9. ARDS Pulmonary Injury Sequence Phase 1 Early Exudative Process Endo/Epithelial Damage Type 1 Alveolar Cell Injury Capillary Congestion Interstitial/Alveolar Edema, Hemorrhage Protein Accumulation Surfactant Deactivation Atelectasis Hyaline Membrane Formation Inflammatory Cell Migration Volutrauma - Increased Protein Leak, Atelectasis, etc.

10. ARDS Pulmonary Injury Sequence Phase 2 Proliferative (Day 5-10) Proliferation of Type 2 Cells Fibroblast Migration Interstitial Collagen Formation Increased Dead Space Decreased Compliance Increased Pulmonary Vascular Resistance

11. ARDS Pulmonary Injury Sequence Phase 3 Fibrotic (Day 10-14) Lung Destruction Emphysematous Changes Fibrosis Pulmonary Vascular Obliteration Chronic Lung Disease

12. Ventilator Induced Lung Injury Rodents ventilated with three modes: High Pressure (45 cmH2O), High Volume Low Pressure (negative pressure ventilator), High Volume High Pressure (45 cmH2O), Low Volume (strapped chest and abdomen) Dreyfuss,D ARRD 1988;137:1159

13. Ventilator Induced Lung Injury Stretch Injury Alters capillary transmural pressures Relaxation changes in transmural pressure causes breaks in capillary endo and epithelium Increases leak of proteinacious material Promotes Atelectasis

14. Capillary Leak

15. Ventilator Induced Lung Injury Premature baboon model Coalson J. Univ Texas San Antonio

16. Ventilator Induced Lung Injury Premature baboon model Coalson J. Univ Texas San Antonio

17. Ventilator Induced Lung Injury ARDS Atelectasis Over-distended airways and alveoli Cellular accumulation Hyaline Membranes

18. Ventilator Induced Lung Injury ARDS late stage structural changes Enlarged air space Septal destruction Fibrotic lesions

19. Pediatric Randomized Controlled Trial

20. Pediatric Randomized Controlled Trial 3100A HFOV 29 patients 11 failures (82% died on CMV) 83% HFOV only survivors had normal lung function Conventional Ventilation 29 patients 19 failures (HFOV Saved 58%) 30% CMV only survivors had normal lung function

21. Pediatric Randomized Controlled Trial

22. 3100B Pilot Trial

23. 3100B Rescue Trial Fort P, et al. High-frequency oscillatory ventilation for adult respiratory distress syndrome-a pilot study. Crit Care Med 1997; 25:937-947 Seventeen patients failing inverse ratio ventilation recruited for rescue with HFOV (3100B) Projected mortality > 80 percent

24. 3100B Rescue Trial Fort P, Crit Care Med 1997; 25:937

25. 3100B Rescue Trial Fort P, Crit Care Med 1997; 25:937

26. 3100B Rescue Trial Oxygenation Index and P/F ratio in first 48 hours of HFOV Survivors versus non-survivors Fort P, Crit Care Med 1997; 25:937

27. 3100B Rescue Trial Fort P, Crit Care Med 1997; 25:937

28. 3100B Rescue Trial Summary Seventy-six percent (13/17) improved their oxygenation as indicated by improvements in P/F ratio (p<0.02), Oxygenation Index (p < 0.01) and change in FiO2 (p < 0.02). Forty-seven percent (8/17) weaned back to conventional ventilation. Thirty day mortality was 53%

29. 3100B Rescue Trial Summary Overall respiratory deaths were 33% There were no signs of change in cardiac output with use of high mean airway pressures More days of CMV prior to HFOV resulted in increased mortality (p < 0.009) Similar to the pediatric RCT, failure to respond to HFOV was highly specific for death

30. MOAT II

31. Multicenter Oscillator ARDS Trial(MOAT2) Prospective Randomized Controlled Trial of the SensorMedics 3100B High Frequency Oscillatory Ventilator for adults with ARDS Follow-up to MOAT Pilot Rescue Trial Early Entry, Non-Crossover Trial Eight Institutions, North American Study

32. Multicenter Oscillator ARDS Trial(MOAT2) Inclusions: Age 16 years and Weight 35 kg and P/F ratio < 200 (with PEEP 10 cm H2O or greater) on two consecutive ABG�s > 30 min. apart but <4 hrs apart with bilateral infiltrates and PA wedge < 18 mmHg or no evidence of LA hypertension and ability to gain Informed Consent (surrogate)

33. Multicenter Oscillator ARDS Trial(MOAT2) Exclusions: FiO2> 80% for 48 hrs Air Leak grade 3 or 4 Non-pulmonary terminal prognosis Intractable shock (see below) other experimental Rx for ARDS or Sepsis > 30 days Severe COPD or Asthma

34. Multicenter Oscillator ARDS Trial(MOAT2) Initial HFOV Strategy: mean Paw set 5 cmH2O > CMV setting set rate 5 Hz, 33% I-time set Amp. for adequate chest wiggle

35. Study Population

36. Study Population

37. Study Population

38. Study Population

39. Outcomes

40. Outcomes 30 Day Mortality

41. Predictors of CMV Outcomeby Tidal Volume � Ideal Body Weight Based on the NIH ARDSnet data, an analysis of mortality in the CMV group found that there appeared to be no relationship between tidal volume per kg ideal body weight in the control group and mortality and that other factors may have influenced the outcome.

42. Predictors of Outcome OI at 16 hours was the only significant predictor of mortality in a stepwise logistic regression analysis. Risk of death increases 2% for every OI increase of 1 at 16 hours e.g., Patients with OI of 25 have a 55% risk of death, for those with an OI of 15 its only 35%

43. MOAT2 Conclusions Based on a study of only 148 patients, use of HFOV for the treatment of severe ARDS has a 90% predictive value for reducing mortality (p < 0.1) by 29 percent This reduction trend in mortality is still recognizable (20 percent) at six months in this same population There may also be benefits related to chronic lung changes as reflected by the small but extended use of respiratory support in the conventional ventilation managed patients

44. Clinical Management

45. Managing Large Patients Special Considerations for Selecting Patients: Increased Airway Resistance Increased Physiologic Dead Space Mean Arterial Pressure < 55 mmhg Elevated ICP Passive Pulmonary Blood Flow Dependency

46. HFOV Strategy Initial mean Paw set 5 cmH2O > CMV setting set rate 5 Hz, 33% I-time set Amp. for adequate chest wiggle

47. Open Lung Ventilation

48. Oxygenation-Pressure Curve

49. Lung Inflation PatternsMulti-Scan CT (10 scans/sec)

50. Lung Inflation PatternsMulti-Scan CT (10 scans/sec)

55. HFOV Strategy If SO2<88% increase mean Paw (3-5 cm H2O incr.) (max. 45 cmH2O) If high pCO2 (pH < 7.15) increase Amp.(5- 10 cm H2O incr.) then decrease rate (1 Hz incr., to 3 Hz) then induce ETT cuff leak (maintain mean Paw)

57. Managing Large Patients Increase the amplitude in 5 cmH2O increments until the Delta-P is maximized. If ventilation does not improve, then decrease the frequency in increments of 1 Hz.

58. Frequency

59. HFOV Strategy Wean- FiO2 to 40%- 50%, if SO2> 90% then mean Paw to 20 (decr. 3 cmH2O Q 4-6 hrs) then switch to PCV (TV 6-10 ml/kg, 1:1 with PEEP 10)

60. Managing Large Patients Increasing the % I-Time may improve ventilation. Increasing the % I-Time will raise distal Paw to be closer to proximal values. If Paw limits have been reached at 33% I-Time, and more lung recruitment is required, increasing % I-Time may improve lung volume.

61. HFOV Strategy If CO2 retention persists, decreasing cuff pressure to allow gas to escape around the ET tube will move the fresh gas supply from the wye connector to the tip of the ET tube

62. Clinical Assessment Chest X-rays Obtain the first x-ray at the (1) hour mark to determine the lung volume at that time. Paw may need to be re-adjusted accordingly. Always obtain a CXR , if unsure as to whether the patient is hyper-inflated or has de-recruited the lung.

63. Clinical Assessment Chest X-rays Stopping the piston, or re-positioning the head to shoot an appropriate film is not necessary. Do not remove the patient from HFOV and manually ventilate to shoot the film. The purpose of the x-ray is to verify the lung volume that the HFOV is producing. A physician, nurse, or therapist should be at bedside to assure the patency of the airway and the patient�s position.

64. Clinical Assessment Chest Wiggle factor (CWF) must be evaluated upon initiation and followed closely after that. CWF absent or becomes diminished is a clinical sign that the airway or ET tube is obstructed. CWF present on one side only is an indication that the ET tube has slipped down a primary bronchus or a pneumothorax has occurred. Check the position of the ET tube or obtain a CXR. Reassess CWF following any position change.

65. Clinical Assessment Cardiac Function: Mean Arterial Pressure Pulse Pressure Heart rate Capillary re-fill CVP Swan-Ganz ECHO for cardiac function

66. Clinical Assessment Auscultation Breath sounds - identifying the normal �breath � sounds is difficult, since HFOV is not ventilation with a bulk flow of gas through the airway. Listen to the �intensity or sound� that the piston makes, it should be equal through out. If not the same sound, re-assess the patient to determine if a chest x-ray is necessary at this time.

67. Clinical Assessment Auscultation Heart Sounds - stop the piston, (the patient is now on CPAP); listen to the heart sounds quickly, and start the piston back up. Removing the patient from the ventilator may result in loss of lung volume.

68. Patient Care Issues Suctioning If using a closed suction catheter remember to: Remove the suction catheter all the way from the ET tube. Use both oximetry and TcCO2 to monitor the patient for potential disconnects. If the patient disconnects between the adapter and ET tube, there may be sufficient pressure to prevent the low pressure alarm from sounding.