1. T RANSPULMONARY -G UIDED V ENTILATION Thom Petty BS RRT Lead Ventilation Solutions Specialist – Eastern & Midwestern U.S CareFusion Respiratory Technologies - Ventilation

2. Objectives  Review the hazards associated with positive pressure ventilation and the sequelae of Ventilator-Induced Lung Injury.  Identify the limitations of current Respiratory Mechanics.  Discuss the role of chest wall, pleura and abdominal pressures during positive pressure ventilation  Introduce the measurement of Transpulmonary Pressure as a valuable ventilation management tool.  Review two Case Studies highlighting the use of transpulmonary pressures in the management of ventilator settings.

3. Disclaimer

4. So, what’s so bad about

5. The Hazard that is Mechanical Ventilation 5

6. Just What is Positive-Pressure Ventilation? What is it that is actually delivered by the ventilator to the patients’ lungs?  Volume  Flow  Pressure

7. The Alveolar Structure  Adjacent alveoli and terminal bronchioles share common walls  Interdependence -  Interdependence - forces acting upon transmitted to those around it Uniform  During Uniform lung expansion - all lung units subjected to similar transpulmonary pressures. Non-Uniform  During Non-Uniform lung expansion – transpulmonary pressures vary considerably.

8. The Alveoli – Not Grapes on a Straw

9. Dynamic Alveolar Mechanics  Healthy alveoli  Healthy alveoli:  Small changes in alveolar size  Ventilation primarily from changes in the size of the alveolar duct or conformational changes as a result of alveolar folding  Alveoli in Acute Lung Injury:  Large changes in alveolar size  Widespread alveolar recruitment/derecruitment.  Significant shear stress-induced lung injury  Gross tearing of the alveolar wall  Injury to the cell membrane  Ultrastructural injury Wilson, J Appl Physiol, 2001 Carney, CCM, 2005 Steinberg, AJRCCM, 2004

10. Alveolar Interdependence  When an alveolus collapses, the traction forces that are exerted on its walls by adjacent expanded lung units increase as they are applied to a smaller surface area.  These forces will promote re-expansion at the expense of greatly increased and potentially harmful stress at the interface between collapsed and expanded lung units  At a transpulmonary pressure of 30 cmH2O it has been calculated that re-expansion pressures could reach 140 cmH2O.

11. The Problems with Positive-Pressure Ventilation  Departs radically from the physiology of breathing spontaneously.  Positive  Positive intrathoracic pressures are created during inhalation  Flow is not homogenously distributed throughout the lung:  Effectively distributed through compliant lung  Attenuated in low-compliant areas  Overdistension of compliant “healthy” lung and underdistension of non- compliant “injured” lung

12. Basic Ventilator Mechanics

13. Mechanics 101: Motion of Air Equation P AO = ( V L / C RS ) + ( F x R AW ) P AO P AO = Pressure at the Airway Opening V L V L = Volume in the Lung C RS C RS = Compliance of the Respiratory System (Lung + Pleura) F F = Flow Rate of Gas in L/s R AW R AW = Resistance of the Airway and ETT (  pressure /  flow)

14. L UNG -P ROTECTIVE V ENTILATION Safer Flow-Blowing

15. Early LPV Theory macroscopic  The macroscopic side-effects of positive-pressure ventilation were easily recognized and understood.  Lungs exposed to excessive pressures had more frequent PTX arotrauma  Early LPV – focus was prevention of Barotrauma  Lungs ventilated to high pressures have a propensity for air leaks  Keep PIP’s “safe”

16. Current LPV Theory microscopic  Recent (and some not-so-recent) research reveals significant microscopic side-effects  Increased permeability of the alveolar/capillary membrane  Increased production of pro-inflammatory mediators within the lung  Current Lung-Protective Ventilation strategies are directed primarily towards preventing/reducing this microscopic damage

17. Seminal LPV Research  Release of “ALI Lung Flooding” factors in rodents ventilated with three modes:  HiP/HiV  High Pressure (45 cmH2O)  High Volume  LoP/HiV  Low Pressure (neg.pres.vent)  High Volume  HiP/LoV  High Pressure (45 cmH2O)  Low Volume (chest bound) Dreyfuss,D ARRD 1988;137:1159

18. More LPV Research  Six RCT’s evaluating the effect of lung-protective ventilation vs conventional approaches 1988 Amato et al Brazil 29 pts: Vt < 6ml/kg, Pplat < 20cmH2O 24 pts: Vt = 12ml/kg, PaCO2 35-38 mmHg 38% Mortality 71% Mortality 1998 Stewart et al Canada 60 pts: Vt < 8ml/kg, Ppeak < 30cmH2O 60 pts: Vt 10-15ml/kg, Ppeak < 50cmH2O 50% Mortality at disch 47% Mortality at disch 1998 Brochard et al Multinational 58 pts: Vt 6-10ml/kg, Pplat < 25-30 cmH2O 58 pts: Vt 10-15ml/kg, PaCO2 38-42 mmHg 47% Mortality at 60 days 38% Mortality at 60 days 1999 Brower et al USA 26 pts: Vt 5-8ml/kg, Pplat <30 cmH2O 26 pts: Vt 10-12ml/kg, Pplat < 45-55 cmH2O 50% Mortality at disch 46% Mortality at disch 2000ARDSnetworkUSA 432 pts: Vt 6ml/kg, Pplat < 30 cmH2O 429 pts: Vt 12ml/kg, Pplat < 50 cmH2O 31% Mortality at disch/180 d 40% Mortality at disch/180 d 2006 Villar et al Spain 50 pts: Vt 5-8ml/kg, PEEP @ LIP + 2cmH2O 53 pts: Vt 9-11ml/kg, PEEP >5 cmH2O 32% Mortality in ICU 53% Mortality in ICU

19. Current Presumed Mechanism for VILI Mechanical Disruption of Pulmonary Epithelium Mechanotransduction Cell & Tissue Disruption Upregulation & release of Cytokines &, Chemokines Subsequent leucocyte attraction and activation Upregulation & release of Cytokines &, Chemokines Subsequent leucocyte attraction and activation Pulmonary Inflammation: VILI Systemic Spillover: SIRS / MODS Systemic Spillover: SIRS / MODS MECHANOTRANSDUCTION – Conversion of Mechanical Stimiuls into Chemical Reaction SIRS – systemic inflammatory Response Syndrome MODS – Multi Organ Dysfunction syndrome

20. Take Home Points - Volutrauma End-Inspiratory Volumes  Caused by excessive End-Inspiratory Volumes  Indicated by elevated end-inspiratory (Plateau) pressures  May result from a combination of “Safe” Vt + PEEP  Mechanical and Biochemical in nature  Even “safe” Vt’s may severely over-inflate normal alveoli due to heterogenicity of airflow within the lung  QUESTION: How can a clinician determine if elevated Airway Plateau Pressures accurately indicate end-inspiratory volutrauma

21. Take Home Points - Atelectrauma  Caused by repeated closing & re-opening of alveoli during ventilatory phasing  Worsens surfactant dysfunction  Release of inflammatory mediators into alveolar spaces and into the systemic circulation  QUESTION: How can the clinician determine what PEEP is truly necessary to keep the alveoli recruited at end-exhalation

22. An RT’s Working Definition of Lung-Protective Ventilation

23. Lung-Protective Controversies  The common denominator of the intervention sides of these trials is the use of lower Vt and limited Plateau Pressures.  Many attempts have been made to understand the differences in the survival outcomes of these six RCT’s as well as to clarify whether a low Vt strategy benefits patients with ALI/ARDS.  A 2002 meta-analysis by Eichacher of the trials revealed:  The control arms of the “non-beneficial” RCT’s actually had lower Pplat’s (a surrogate for end-inspiratory alveolar pressure) than in the two beneficial arms  Could the survival benefit of the two “non-beneficial” RCT’s be related to the larger-than-routine Vt’s in the control arms?  Could the differences be related to Pplat rather than Vt? Eichacker PQ, Am J Resp Crit Care Med 2002

24. A PPLYING L UNG -P ROTECTIVE V ENTILATION D RIVING V ENTS B ETTER

25. The Handful of Ventilator Settings Tidal Volume Accurately measured Respiratory Rate Accurately measured FiO2 PEEP Measured but not accurate Plateau Pressure Measured but not accurate

26. The Problem with Airway Pressures

27. As the Lung Inflates A IRWAY P RESSURE (P AW )  Measured at the circuit wye or ventilator outlet  Reflects both lung and pleural pressures P ERI - PULMONARY /P LEURAL P RESSURE (P ES )  Pressure imposed upon the lungs by the Chest Wall and Abdomen  Can be approximated by measuring pressures within the Esophagus T RANSPULMONARY P RESSURE (P TP )  The true pressure within the lung  P TP = P AW – P ES Paw Pes Ptp

28. PEEP Measured but not accurate Plateau Pressure Measured but not accurate The Two Settings we Estimate: PEEP

29. volume (FRC or EELV)  PEEP – the pressure that is being exerted by the volume of gas that is remaining in the lungs at the end of exhalation (FRC or EELV)  Optimal Lung-Protective PEEP remains undetermined.  PEEP > “traditional” values of 5-12 cmH2O minimize cyclical alveolar collapse and the corresponding shearing injury.  Potential adverse consequences including circulatory depression and lung overdistension may outweigh the benefits of higher PEEP’s  Use of PEEP < 10cmH 2 O leads to an increase in mortality Amato M., 8 th World Congress, Sydney, Australia Dreyfuss, Crit Care Med, 1998 Gattinoni, NEJM, 2006 Muscedere, Am J Respir Crit Care Med. 1994

30. The Two Settings we Estimate: PEEP Research  Three RCT’s comparing high PEEP vs Low PEEP in ARDS:  2010 – Briele Meta-Analysis  Differences in hospital mortality not statically significant  Significant reduction of death in the ICU in the High PEEP group 2004ARDSNetALVEOLIUSA 276 pts: Mean PEEP = 14.7cmH2O 273 pts: Mean PEEP = 8.9cmH2O 25% Mortality at disch 27.5% Mortality at disch 2008MeadeLOVSMultinational 508 pts: Mean PEEP = 15.6cmH2O 475 pts: Mean PEEP = 10.1cmH2O 36% Mortality at disch 40% Mortality at disch 2008MercatEXPRESSFrance 382 pts: Mean PEEP = 14.6cmH2O 385 pts: Mean PEEP = 7.1cmH2O 35% Mortality at 60 days 39% Mortality at 60 days

31. Low PEEP/High FiO2 Protocol FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 PEEP 5 5 8 8 10 10 10 12 14 14 14 16 16 18-24 High PEEP/Low FiO2 Protocol FiO2 0.3 0.3 0.3 0.3 0.3 0.4 0.4 0.5 0.5 0.5-0.8 0.8 0.9 1.0 PEEP 5 8 10 12 14 14 16 16 18 20 22 22 22-24 The Two Settings we Estimate: The High PEEP vs Low PEEP Controversy

32. The Two Settings we Estimate: Tools for Determining Optimal PEEP Ideal PEEP is defined as: High enough to induce alveolar recruitment, keeping the lung more aerated at end-exhalation, while not distending “good” alveoli Low enough to prevent hemodynamic impairment & overdistension PEEP T ABLE Table of FiO2 & PEEP combinations to achieve PaO2 or SpO2 in target range M AXIMAL PEEP WITHOUT OVERDISTENSION Use of highest PEEP while maintaining Pplat < 30 cmH2O G AS E XCHANGE Lowest shunt (highest PaO2), lowest deadspace (lowest PaCO2), best oxygen delivery (CaO2 x C.O.) C OMPLIANCE Use of the highest PEEP that results in the highest respiratory-system compliance S TRESS I NDEX Observe the Pressure/Time Curve during constant flow inhalation for signs of tidal recruitment and overdistension P RESSURE /V OLUME C URVE Set PEEP slightly higher than Lower Inflection Point I MAGING Computed tomography, Electrical impedence tomography, Ultrasound E SOPHAGEAL P RESSURE M ONITORING Estimate the intra-pleural pressure with the measurement of Esophageal Pressure then determine optimal PEEP

33. The Two Settings we Estimate: Alveolar Recruitability in ARDS patients with higher lung recruitabilityBriele – benefits of high PEEP in ARDS patients with higher lung recruitability low potential for recruitmentARDS patients with low potential for recruitment, the resulting over- distension associated with PEEP increases was harmful How To Quickly Determine Lung Recruitability: Non-RecruitableNon-Recruitable – If PEEP is  and Plateau Pressure then  in an equal or greater increment. RecruitableRecruitable – If PEEP is  and Plateau Pressure then  in a lesser increment

34. The Two Settings We Estimate PEEP Measured but not accurate Plateau Pressure Measured but not accurate

35. The Two We Estimate: Plateau Pressure  Plateau Pressure is the pressure exerted by the volume of gas in the lungs at end-inhalation.  Indicator of “lung fullness”  Goal: Keep P PLAT < 30 cmH2O

36. The Two We Estimate: Plateau Pressure and after each change in PEEP or V T  Check P PLAT (with a minimum 0.5 second inspiratory pause) at least q 4h and after each change in PEEP or V T  If P PLAT >30 cmH2O:   V T by 1ml/kg to minimum of 4 ml/kg.  If P PLAT < 25 cmH2O and V T < 6 ml/kg:   V T by 1 ml/kg until P PLAT > 25 cmH2O or V T = 6 ml/kg.  If P PLAT < 30 but patient/ventilator dys-synchrony is evident:   V T by 1ml/kg to a V T of 7-8 ml/kg keepng P PLAT < 30 cm

37. T RANSPULMONARY G UIDED V ENTILATION U SING THE P ROPER T OOLS

38. A Brief History of the Study of Advanced Respiratory Mechanics  150 AD  150 AD - Galen (Greek Physician): Postulated that lungs were expanded by the outward movement of the thorax.  1817  1817 – Carson: Attached a water manometer to the trachea of a recently-killed animal and noted an increase in tracheal pressure when the chest was opened. This he attributed to the elastic recoil of the lung.  1847  1847 – Ludwig: First to measure pleural pressure in an animal.  1900  1900 – Aron: Measured pleural pressure in a human with a chest tube.  1960’s  1960’s – Applicability of Esophageal Pressures to measure pleural pressures discovered.

39. Solving The Airway Pressure Problem do not reflect pressures within the lung  REMEMBER: Airway pressures do not reflect pressures within the lung but pressures of the entire Respiratory System Lung Pressure  To know true Lung Pressure (Transpulmonary Pressure) you must account for the pressures outside of the lung (Pleural or Peripulmonary Pressures)  Difficult to directly measure pressure in the pleura  A number of studies have demonstrated reasonable correlation between Esophageal Pressures and Pleural Pressures  Pleural pressures adjacent to the esophagus transmitted to esophagus.  Pressure within the pleural space is not uniform  Pressure in the dependent & basal regions is greater than in the upper regions of the thoracic cage

40. Solving The Airway Pressure Problem  Patients on mechanical ventilation are usually supine or semi-recumbent  Important to account for the effect that mediastinal structures such as the heart have on esophageal pressures.  Washko (2006) and Talmor (2008)  Approximately 2-5 cmH2O be subtracted from the esophageal pressure to more accurately reflect pleural pressures.

41. Stiff Lung or Stiff Abdomen? 30 = 15 + 15 30 = 25 + 5 P PLAT = P TP + P ES Gattinoni, Crit Care, Oct 2004; P PLAT = P TP + P ES

42. How Common are Increased Intra-Abdominal Pressures? Malbrain et al, Intensive Care Med (2004) 30:822–829 13 ICU’s, 6 countries, 97 patients

43. Can High Intra-abdominal Pressures Really Affect Ventilation? Rigid Abdomen in ACS S/P Decompressive Laparotomy

44. Transpulmonary-Guided Ventilation 3 Basic Concepts  For alveolar recruitment a transpulmonary pressure greater than the opening pressure of the lung must be applied to the lung.  To avoid alveolar collapse after recruitment, a PEEP that is greater than the compressive forces operating on the lung and alveolar ventilation that is sufficient to prevent absorption atelectasis must be provided.  Avoidance of stretch (by maintaining a low plateau pressure) and prevention of cyclic collapse and reopening (by maintaining adequate PEEP and alveolar ventilation) are the physiologic cornerstones of mechanical ventilation in ARDS..) Gattinoni et al,CritCareMed2003Vol.31,No.4(Suppl.)

45. The Talmor/Ritz Study  ARDS survival has improved in recent years with low Vt’s and the use PEEP but the Optimal level of PEEP remains difficult to determine.  Could the use of Esophageal Pressure measurements enable the clinician to determine a PEEP value that would maintain oxygenation while preventing lung injury due to repeated alveolar collapse and/or overdistention?  Mechanically-ventilated ARDS patients randomly assigned to groups:  CONTROL GROUP:  PEEP adjusted as per ARDSNet recommendations  PES-GUIDED GROUP: P TP PEEP  PEEP adjusted to achieve a P TP PEEP of 0 to+10 cmH2O

46. The Results Primary end point of the study was improvement in oxygenation. Secondary end points - respiratory-system compliance & pt outcomes. The study reached its stopping criterion and was terminated after 61 patients had been enrolled. PaO2/FiO288 mmHg higher The PaO2/FiO2 ratio at 72 hours was 88 mmHg higher in the Pes-group than in the control group This effect was persistent through the 24, 48 & 72 hour follow-up time. Respiratory-system compliance was also significantly improved at 24, 48, and 72 hours in the Pes-guided group

47. Outcomes

48. maximum allowable airway plateau pressure large portions of the lung under-inflated at risk of VILI  Basing ventilator settings on a maximum allowable airway plateau pressure may leave large portions of the lung under-inflated and at risk of VILI from repeated airway opening and closing. pleural pressures from PES may allow higher PEEP without overdistending lung regions  Estimating pleural pressures from PES and setting PEEP to achieve a target P TP may allow higher PEEP in many patients without overdistending lung regions that are already recruited. A Sampling of What’s in the Journals

49.  Systematic use of Pes more direct assessment of lung distending pressure.  Systematic use of Pes has the potential to improve ventilator management in ARF by providing more direct assessment of lung distending pressure. A Sampling of What’s in the Journals

50. airway Plateau Pressures may under-ventilate patients overdistend  The use of airway Plateau Pressures to set ventilation may under-ventilate patients with intra-abdominal hypertension and overdistend the lungs of patients with atelectasis. P TP must be used to accurately set mechanical ventilation  Thus P TP must be used to accurately set mechanical ventilation in the critically ill. A Sampling of What’s in the Journals

51.  Increases in peak airway pressure unlikely to cause damage.  Increases in peak airway pressure without a concomitant increase in alveolar distension are unlikely to cause damage.  Critical variable is not PIP but P TP patients with a stiff chest non-pulmonary ARDS Plateau Pressures may exceed 35 cmH2O without causing alveolar distension  In patients with a stiff chest wall from non-pulmonary ARDS that may have elevated pleural pressures airway Plateau Pressures may exceed 35 cmH2O without causing alveolar distension A Sampling of What’s in the Journals

52. meaningful information, otherwise unavailable, in critically ill patients  Pes can be used to estimate transpulmonary pressures that are consistent with known physiology, and can provide meaningful information, otherwise unavailable, in critically ill patients. A Sampling of What’s in the Journals

53.  P PLAT > 25 CM H2O  S TATIC L UNG C OMPLIANCE < 40 ML / CM H2O  P/F R ATIO < 300  PEEP > 10 CM H2O TO MAINTAIN S A O2 > 90%  P A CO2 > 60 MM H G OR P H 60 MM H G OR P H < 7.2 ATTRIBUTABLE TO RESPIRATORY ACIDOSIS Wolfson Medical Center, Holon, Israel One Hospital’s Protocol for Identification of Pes Candidates

54.  5fr or 7fr balloon-tipped catheter or a specialized NG/OG catheter with balloon tip  Inserted into the lower third of the esophagus, above the diaphragm.  An approximation of proper placement can be made by measuring the distance from the tip of the nose to the bottom of the earlobe and then from the earlobe to the distal tip of the xiphoid process of the sternum. Esophageal Balloonary: The Catheter

55. Baydur Maneuver  Properly inserted balloon will show simultaneous negative Paw & Pes deflections with a patient-initiated breath during an expiratory hold (Baydur Maneuver).  If balloon is inserted too far into the esophagus Pes will deflect positively during a spontaneous inspiration.  PES tracing may show small cardiac oscillations reflective of cardiac activity.  P ES should be similar (+ 10) to P GA (Bladder Pressure)  Measurements should match the patients clinical presentation. Esophageal Balloonary: Determining Proper Catheter Placement

56.  Properly inserted an inflated balloon may show small cardiac oscillations reflective of cardiac activity. Esophageal Balloonary: Determining Proper Catheter Placement

57.  Increased abdominal pressure and/or decreased chest wall compliance is skewing P AW PLAT  P AW PLAT = 39 cmH2O  P TP PLAT = 9 cmH2O  Keep P TP PLAT < 20 cmH2O Esophageal Numerology: P TP PLAT Transpulmonary Pressure at End-Inspiratory Plateau

58. P AW PEEP = 5 cmH2O P ES = 15 cmH2O P TP PEEP = -10 cmH2O 15 5 10 -10 15 15 Esophageal Numerology: P TP PEEP Transpulmonary Pressure at End-Expiratory Plateau

59. Esophageal Numerology: P TP PEEP Transpulmonary Pressure at End-Expiratory Plateau  Goal is to adjust PEEP to maintain P TP PEEP 0 - +2-5 cmH2O  Negative P TP PEEP  Negative P TP PEEP = pressure outside the lung is greater than pressure inside the lung.  Positive P TP PEEP  Positive P TP PEEP = pressure inside the lung is greater than pressure outside the lung  May cause end-expiratory overdistension if excessive

60. Visualizing P TP PEEP

61.  Good indicator of Work of Breathing  Values <15 cmH2O may indicate patient is a good candidate for weaning.  The difference between PEAK esophageal pressure (P PEAK ES ) and BASELINE esophageal pressure (PEEP ES )  P ES = P PEAK ES – P PEEP ES  Adult Normal:10 – 15 cm H2O  Pediatric Normal: 7 – 19 cm H2O Esophageal Numerology:  P ES Delta Esophageal Pressure

62.  Analyzing the shape of the esophageal pressure tracing may provide information regarding lung compliance.  Stiff lung  Stiff lung – airway pressures only partially transmitted to pleura  Compliant lung  Compliant lung – airway pressures readily transmitted to pleura  Clear differences between end-expiratory and end-inspiratory Interpreting the Pes Tracing Sorosky A, Crit Care Research and Practice

63. CASE STUDY 1: TRANSPULMONARY- GUIDED VENTILATION IN INCREASED ABDOMINAL PRESSURES

64. Typical Ventilator Patient HPX: Morbidly Obese 24 yo Female with PancreatitisSettings: PRVC-AC, RR-24, Vt-340, PEEP-7, FiO2-.45, Ti-.7ABG: pH-7.36, PaCO2-50, PaO2-57, SaO2-93% CXR on current vent settings: Any heart silhouette? Any diaphragms? Any aeration? Esophageal Balloon inserted Initial P TP PEEP = -12.3 cmH2O A negative P TP PEEP indicates the lung is being derecruited from elevated external (pleural and/or abdominal) pressures.A negative P TP PEEP indicates the lung is being derecruited from elevated external (pleural and/or abdominal) pressures.

65.  Placed onto:  PC/AC  RR-16  PIP-36  PEEP-20.  P TP PEEP now -3.7 cmH2O Some Heart Border & Diaphragm now visible First Thought - Pump Up the PEEP

66. P AW PLATP AW PLAT 41 cmH2O41 cmH2O P TP PLATP TP PLAT 21 cmH2O21 cmH2O Which Plateau Pressure is Correct?

67. 25 cmH2OPEEP Increased to 25 cmH2O Ptp PEEP now +2.4 cmH2OPtp PEEP now +2.4 cmH2O Lungs are remaining open at end-exhalation Further PEEP Pumpage

68. Hey, Let’s Try APRV! P LOW of 0 P TP PEEP of -15 cmH2O IMMEDIATE Derecruitment!IMMEDIATE Derecruitment!

69. Now What?  Returned to PC/AC with PEEP of 25  P TP PEEP now +2.4 cmH2O  No derecruitment!  P AW PEAK of 46 cmH2O  P TP PEAK of 27 cmH2O  Physicians were hesitant to maintain PEEP of 25

70. So, then what? CXR six-day post PEEP adjustment using PES monitoring PEEP -16cmH2O with FiO2 of.40 Heart border & diaphragms visible

71. CASE STUDY 2: T RANSPULMONARY -G UIDED V ENTILATION I DENTIFYING P OST -C ODE D ERECRUITMENT

72. P TP Pre & Post Instillation of Oleic Acid Pre-InstillationPre-Instillation PTP PEEP = +2 cmH2O No Derecruitment Post-Instillation Post-Instillation PTP PEEP = -2 cmH2O Derecruitment on PEEP of 4

73. PEEP Increased to 8 PEEP increased to 8 cmH2O P TP PEEP increased to +1.2 cmH2O

74. Changes Following Resuscitative Fluid Bolus Following multiple fluid boluses during resuscitation it was noticed that P ES increased from 8 cmH2O to 12 cmH2O P TP PLAT increased to 27 cmH 2 O PEEP immediately increased to 10 cmH 2 O This kept P TP PEEP from dropping into negative No “Post-Code Derecruitment ”

75. ONE LAST POINT

76. Quality Requires Standardization The most meaningful cost reduction strategies will involve standardization of clinical care and elimination of variation in patient procedures. May 9, 2012

77. We Need to Define Quality Q = A x (O + S) W Q – Quality A – Appropriateness O – Outcomes S – Service W – Waste

78. QUESTIONS? Email: thomas.petty@carefusion.com

79. References  Mechanical Ventilation Guided by Esophageal Pressure in Acute Lung Injury, Talmor D, NEJM 2008  Should Mechanical Ventilation be Guided by Esophageal Pressure Measurements?, Plataki M, Curr Op in Crit Care 2011  Are Esophageal Pressure Measurements Important in Clinical Decision-Making in Mechanically Ventilated Patients?. Talmor D, Resp Care 2010  Transpulmonary Pressure as a Surrogate of Plateau Pressure for Lung Protective Strategy: Not Perfect but more Physiologic, Richard JC, Int Care Med 2012  Abdominal Compartment Syndrome in Patients with Isolated Extraperitoneal Injuries, Kopelman T, J Trauma 2000 79

80. References  Esophageal and Gastric Pressure Measurement, Benditt J, Resp Care 2005  Esophageal Pressure in Acute Lung Injury: do they Represent Artifact of Useful Informatinon about Transpulmonary Pressure, Chest Wall Mechanics and Lung Stress, Loring S, J Appl Physiol 2010  Maintaining End-Expiratory Transpulmonary Pressure Prevents Worsening of Ventilator-Induced Lung Injury Caused by Chest Wall Constriction in Surfactant-Depleted Rate, Loring S, Crit Care Med 2010  Medical Effectiveness of Esophageal Balloon Pressure Manometry in Weaning Patients from Mechanical Ventilation, Gluck E, Crit Care Med 1991  Optimal PEEP Guided by Esophageal Balloon, Piraino T, AARC Open Forum Abstract  Plateau and Transpulmonary Pressure with Elevated Intra-Abdominal Pressure or Atelectasis, Kubiak B, J Surg Res 2009 80

81. References  Esophageal and Transpulmonary Pressures in Acute Respiratory Failure, Talmor D, Crit Care Med 2000  Effect of Intra-Abdominal Pressure on Respiratory Mechanics, Pelois P, Acta Clinica Belgica 2007  What is Normal Intra-Abdomial Pressure and how is it Affected by Positioning, Body Mass and Positive End-Expiratory Pressure?, DeKeulenaer B, Int Care Med 2009  Targeting Tranpsulmonhary Pressure to Prevent Ventilator Induced Lung Injury, Talmor D, Min Anest 2009  BiCor Directed Weaning Reduces Ventilator Days, ICU Stay, Length of Hospitalization, and Cost of Care, Rouben L, Chest 1996  Effects of Positive End-Expiratory Pressure on Respiratory Function and Hemodynamics in patients with Acute Respiratory Failre with and without Intra-Abdominal Hypertension: a Pilot Study, Krebs J, Crit Care 2009 81

82. References  Refocusing on Transpulmonary Pressure, Marini, Focus Journal 2010  Respiratory Restriction and Elevated Pleural and Esophageal Pressures in Morbid Obesity, Behazin N, J Appl Physiol 2010  Weaning Prediction: Esophageal Pressure Monitoring Compliments Readiness Testing, Jubran A, Am J Respir Crit Care Med 2005  The use of Transpulmonary Pressure to Set Optimal Positive End-Expiratory Pressure: A Case Report, Piraino T, Can J Resp Ther 2010  Goal-Directed Mechanical Ventilation: Are We Aiming at the Right Goals? A Proposal for an Alternative Approach Aiming at Optimal Lung Compliance, Guided by Esophageal Pressure in ARDS, Sorosky A, Critical Care Research and Practice 2012 82