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Advanced Ventilator Management Transpulmonary Guided Ventilation

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1 Advanced Ventilator Management Transpulmonary Guided Ventilation
Esophageal Balloonary Thom Petty BS RRT Lead Clinical Specialist – East CareFusion Critical Care Ventilation

2 Objectives Identify the limitations that current Respiratory Mechanics impose upon the management of mechanical ventilation. Review the hazards associated with positive pressure ventilation and the sequelae of Ventilator-Induced Lung Injury. 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 a Case Study regarding the use of transpulmonary pressures in the management of ventilator settings.

3 Basic Ventilator Mechanics
Esophageal Balloonary

4 Mechanics 101: Motion of Air Equation
PAO = ( VL / CRS) ( F x RAW ) PAO = Pressure at the Airway Opening VL = Volume in the Lung CRS = Compliance of the Respiratory System (Lung + Pleura) F = Flow Rate of Gas in L/s RAW = Resistance of the Airway and ETT ( pressure /  flow)

5 As the Lung Inflates Pressure in the Airway (Paw)
Measured at the circuit wye Not the actual pressure in the lungs but the pressure of the entire respiratory system Reflects both lung and pleural pressures Peri-pulmonary/Pleural Pressure (Pes) Pressure that is imposed upon the lungs by the Chest Wall and Abdomen Can be approximated by measuring pressures within the Esophagus Pressure within the Alveoli (Ptp) The TRUE pressure within the lung Ptp = Paw – Pes Paw Pes Ptp

6 Our Current Respiratory Mechanics Toolbox
Inspiratory Hold Measures the Plateau Pressure of the entire Respiratory System Indicator of end-inspiratory lung distension Static Compliance Reflects the compliance of the entire Respiratory System Expiratory Hold Measures the amount of intrinsic PEEP of the entire Respiratory System

7 Mechanical Ventilation?
What’s so bad about Mechanical Ventilation?

8 The Hazard that is Mechanical Ventilation
mechanical ventilation can no longer be seen merely as a supportive therapy in ali and ards, but as a treatment modality capable of significantly influencing the course of pulmonary disease and clinical outcome. Viana M, Jornal de Pediatria, 2004

9 Just What is Positive-Pressure Ventilation?
Just what is it that is delivered by the ventilator to the patients’ lungs? Volume Flow Pressure

10 The Alveoli – Not Grapes on a Straw
It’s important to remember that alveoli are not the “cluster of grapes at the end of a straw” like we envisioned in school. They are more like a sponge sharing common walls and full of holes.

11 The Alveolar Structure
Adjacent alveoli and terminal bronchioles share common walls Forces acting on one lung unit are transmitted to those around it (interdependence) Under conditions of uniform expansion, all lung units will be subject to a similar transpulmonary pressure. However, if the lung is unevenly expanded, such forces may vary considerably.

12 Dynamic Alveolar Mechanics in the Uninjured Lung
Healthy alveoli: Undergo relatively small changes in size during ventilation unless they totally collapse or re-expand. Ventilation may occur primarily with changes in the size of the alveolar duct or conformational changes as a result of alveolar folding Alveoli in ALI: Undergo large changes in alveolar size Widespread alveolar recruitment/derecruitment predominate. Can cause 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

13 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.

14 The Problems with Positive-Pressure Ventilation
Positive-pressure ventilation departs radically from the physiology of breathing spontaneously. During inhalation positive intrathoracic pressures are created. These inspiratory-phase pressures are not homogenously distributed throughout the lung: Effectively distributed through compliant lung Flow is attenuated in low-compliant areas This heterogenocity can result in overdistension of compliant “healthy” lung and underdistension of non-compliant “injured” lung

15 The Problems with Positive-Pressure Ventilation
Early on in the history of positive-pressure ventilation it was recognized that lungs that were ventilated to high pressures have a propensity to develop air leaks. Thus began the early focus on barotrauma However, further research has revealed that alveoli that do not overdistend were unlikely to experience injury. Excessive lung volume (volutrauma) rather than excessive airway pressures produced lung injury. At the other end of the spectrum, ventilation using low end expiratory volumes that allowed repetitive alveolar opening and collapse (atelectrauma) was also identified as injurious. Whitehead, Thorax, 2002 Diaz, Crit Care Med 2010

16 The Problems with Positive-Pressure Ventilation
The immediate macroscopic physiological side-effects of positive-pressure ventilation are readily recognized and easily understood. However, there are significant microscopic physiological interactions which are less obvious, more insidious, and may only produce complications if ventilation is prolonged. Increased permeability of the alveolar/capillary membrane Increased production of pro-inflammatory mediators within the lung Lung-protective ventilation strategies are directed primarily towards volume and pressure limitation during the inspiratory phase and maintenance of alveolar recruitment during the expiratory phase.

17 Ventilator-Induced Lung Injury Volutrauma
Classic study applied excessive alveolar pressures to both volume-limited lungs (chests bound to prevent alveolar expansion) and volume-unlimited lungs (chests unbound with unchecked alveolar expansion) Less lung damage in the volume-limited lungs (alveoli with limited expansion) than in the volume-unlimited lungs (alveoli in the unbound chest).

18 Ventilator-Induced Lung Injury Volutrauma & Inflammation
Study investigating the release of “Lung Flooding” factors in Rodents ventilated with three modes: HiP/HiV High Pressure (45 cmH2O) High Volume LoP/HiV Low Pressure (neg.pres.vent) HiP/LoV Low Volume (chest bound) Dreyfuss,D ARRD 1988;137:1159

19 Ventilator-Induced Lung Injury Take-Home Points - Volutrauma
Mechanical and Biochemical in nature Caused by excessive End-Inspiratory Volumes Indicated by elevated end-inspiratory (Plateau) pressures May result from a combination of “Safe” Vt + PEEP 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 alveoli are over-distended at end-inspiration?

20 Ventilator-Induced Lung Injury Atelectrauma
Research has revealed that repeated cyclical collapse & re-expansion of alveoli results in a release of cytokines and the reinforcement and amplification of the local and systemic inflammatory response. Interleukin-6 Interleukin-11 Interleukin-γ Tissue Necrosis Factor-α

21 Ventilator-Induced Lung Injury Take-home Points - Atelectrauma
Associated with repeated opening and closing of alveoli during ventilatory phasing Associated with regional differences in ventilation Worsens surfactant dysfunction Release of inflammatory mediators into alveolar spaces and into the systemic circulation QUESTION: How can the clinician determine what PEEP is necessary to keep the alveoli open at end-exhalation

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

23 Lung-Protective Ventilation Safer Ventilator Management

24 Lung-Protective Ventilation Theory
Gattinoni’s CT studies of ALI/ARDS lungs revealed that ALI/ARDS lung is not a stiff organ made up of homogeneously stiff lung units with low static compliance but is a multi-compartmental heterogeneous structure in which there is a portion of aerated normal tissue with normal compliance (baby lung). Limiting VILI should be accomplished through an Lung Protective approach to ventilator management which includes: Volume & pressure limitation Modest PEEP & Plateau pressures The challenge is to maintain acceptable gas exchange while avoiding harmful mechanical ventilation practices. The need for potentially injurious pressures, volumes, and FiO2’s must be weighed against the benefits of gas exchange support.

25 Lung-Protective Ventilation Research
1988 Amato et al Brazil 29 pts: Vt < 6ml/kg, Pplat < 20cmH2O 24 pts: Vt = 12ml/kg, PaCO 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 Brochard et al Multinational 58 pts: Vt 6-10ml/kg, Pplat < cmH2O 58 pts: Vt 10-15ml/kg, PaCO 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 < cmH2O 46% Mortality at disch 2000 ARDSnetwork 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, LIP + 2cmH2O 53 pts: Vt 9-11ml/kg, PEEP >5 cmH2O 32% Mortality in ICU 53% Mortality in ICU There have been six randomized controlled trials evaluating the effect of lung-protective ventilation in comparison with conventional approaches:

26 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

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

28 The Problem with Airway Pressures
A key limitation to mechanical ventilators is that they report peak airway pressures without distinguishing compliance that reflects intrinsic lung mechanics or chest wall and abdominal pressures Piraino T, Respiratory Care, April 2011

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

30 The Two Settings we Estimate: PEEP
Measured at the end of exhalation PEEP is the pressure that is exerted by the volume of gas that is remaining in the lungs (FRC) Although ventilation with Low Vt’s & Plateau Pressures is generally accepted by the critical-care community, the optimal level of PEEP at which to ventilate remains unclear. PEEP levels exceeding the “traditional” values of 5-12 cmH2O have been shown to minimize cyclical alveolar collapse and the corresponding shearing injury. However, potential adverse consequences including circulatory depression and lung overdistension may outweigh the benefits Use of PEEP < 10cmH2O leads to an increase in mortality Amato M., 8th World Congress, Sydney, Australia Dreyfuss, Crit Care Med, 1998 Gattinoni, NEJM, 2006 Muscedere , Am J Respir Crit Care Med. 1994

31 The Two we Estimate: PEEP Research
There have been three randomized controlled trials comparing higher versus lower levels of PEEP in ALI/ARDS: 2010 – Briele Meta-Analysis Differences in hospital mortality not statically significant Significant reduction of death in the ICU in the High PEEP group 2004 ARDSNet ALVEOLI USA 276 pts: Mean PEEP = 14.7cmH2O 273 pts: Mean PEEP = 8.9cmH2O 25% Mortality at disch 27.5% Mortality at disch 2008 Meade LOVS Multinational 508 pts: Mean PEEP = 15.6cmH2O 475 pts: Mean PEEP = 10.1cmH2O 36% Mortality at disch 40% Mortality at disch Mercat EXPRESS France 382 pts: Mean PEEP = 14.6cmH2O 385 pts: Mean PEEP = 7.1cmH2O 35% Mortality at 60 days 39% Mortality at 60 days

32 The Two we Estimate: The PEEP Controversy
Low PEEP/High FiO2 Protocol FiO PEEP High PEEP/Low FiO2 Protocol FiO PEEP

33 The Two we Estimate: Optimal PEEP
PEEP Table Table of FiO2 & PEEP combinations to achieve PaO2 or SpO2 in target range Maximal PEEP without overdistension Use of highest PEEP while maintaining Pplat < 30 cmH2O Gas Exchange Lowest shunt (highest PaO2), lowest deadspace (lowest PaCO2), best oxygen delivery (CaO2 x C.O.) Compliance Use of the highest PEEP that results in the highest respiratory-system compliance Stress Index Observe the Pressure/Time Curve during constant flow inhalation for signs of tidal recruitment and overdistension Pressure/Volume Curve Set PEEP slightly higher than Lower Inflection Point Imaging Computed tomography, Electrical impedence tomography, Ultrasound Esophageal Pressure Monitoring Estimate the intra-pleural pressure with the measurement of Esophageal Pressure then determine 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

34 The Two we Estimate: Alveolar Recruitability
Briele also suggests that the beneficial impact of reducing intra-tidal alveolar opening and closing by increasing PEEP prevailed over the effects of increasing alveolar distention in ALI/ARDS patients with higher lung recruitability In ALI/ARDS patients with low potential for recruitment, the resulting over-distension associated with PEEP increases was harmful How To Determine Lung Recruitability: Non-Recruitable – If PEEP is  and Plateau Pressure then  in an equal or greater increment. Recruitable – If PEEP is  and Plateau Pressure then  in a lesser increment

35 The Two We Estimate PEEP Plateau Pressure Measured but not accurate

36 The Two We Estimate: Plateau Pressure
Plateau Pressure is the pressure exerted by the volume of gas in the lungs after an inhalation. Indicator of “lung fullness” Plateau Pressure Goal: Keep < 30 cmH2O

37 The Two We Estimate: Plateau Pressure
Check PPLAT (with a minimum 0.5 second inspiratory pause) at least q 4h and after each change in PEEP or VT. If PPLAT >30 cmH2O: VT by 1ml/kg to minimum of 4 ml/kg. If PPLAT < 25 cmH2O and VT< 6 ml/kg:  VT by 1 ml/kg until PPLAT > 25 cmH2O or VT = 6 ml/kg. If PPLAT < 30 but patient/ventilator dysynchrony is evident:  VT by 1ml/kg to a VT of 7-8 ml/kg if PPLAT remains < 30 cm

38 Transpulmonary Guided Ventilation

39 A Brief History of the Study of Advanced Respiratory Mechanics
150 AD - Galen (Greek Physician): Postulated that lungs were expanded by the outward movement of the thorax. 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 – Ludwig: First to measure pleural pressure in an animal. 1900 – Aron: Measured pleural pressure in a human with a chest tube. 1960’s – Applicability of Esophageal Pressures to measure pleural pressures discovered.

40 Solving The Problem with Airway Pressures
REMEMBER: Airway pressures displayed by ventilators do not reflect pressures within the lung but within the Entire Respiratory System To truly know the pressure within the lung (Transpulmonary Pressure) it is necessary to measure and account for the pressures outside of the lung (Peripulmonary Pressures) Very difficult to directly measure pressure in the pleura A number of historic studies have demonstrated reasonable correlation between Esophageal Pressures and Pleural Pressures Pressure in the pleura adjacent to the esophagus is transmitted to the 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

41 Solving The Problem with Airway Pressures
Patients on mechanical ventilation are usually supine or semi-recumbent so it is important to account for the effect that mediastinal structures such as the heart have on esophageal pressures. Washko (2006) and Talmor (2008) have recommended that approximately 2-5 cmH2O be subtracted from the esophageal pressure to more accurately reflect pleural pressures.

42 Stiff Lung or Stiff Chest Wall?
PAW = PTP + PES PAW = PTP + PES 30 = 30 = Gattinoni, Crit Care, Oct 2004;

43 How Common are Increased Intra-Abdominal Pressures?
Total Prevalence MICU Prevalence SICU Prevalence >12 mmHg 58.8% 54.4% 65% >15 mmHg 28.9% 29.8% 27.5% >20 mmHg 8.2% 10.5% 5.0% 13 ICU’s, 6 countries, 97 patients Malbrain et al, Intensive Care Med (2004) 30:822–829

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

45 Transpulmonary-Guided Ventilation 3 Basic Concepts
To exploit the potential for alveolar recruitment, a transpulmonary pressure that is 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 acute lung injury/acute respiratory distress syndrome. Gattinoni et al,CritCareMed2003Vol.31,No.4(Suppl.)

46 The Talmor/Ritz Study Survival of ALI/ARDS patients has improved in recent years with the advent of low Vt’s and the use PEEP Optimal level of PEEP is difficult to determine. Could the use of Transpulmonary Pressure Measurements (as estimated by 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 ALI/ARDS patients randomly assigned to one of two groups: CONTROL GROUP: PEEP adjusted as per ARDSNet recommendations PES-GUIDED GROUP: PEEP was adjusted to achieve a PTP PEEP of 0 to +10 cmH2O

47 The Results The 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. 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

48 Outcomes

49 A Sampling of What’s in the Journals
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. It is logical that estimating pleural pressures from PES and setting PEEP to achieve a target PTP may allow higher PEEP in many patients without overdistending lung regions that are already recruited.

50 A Sampling of What’s in the Journals
Systematic use of esophageal manometry has the potential to improve ventilator management in acute respiratory failure by providing more direct assessment of lung distending pressure.

51 A Sampling of What’s in the Journals
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. Thus PTP must be used to accurately set mechanical ventilation in the critically ill.

52 A Sampling of What’s in the Journals
Increases in peak airway pressure without a concomitant increase in alveolar distension are unlikely to cause damage. Critical variable is not PIP but PTP 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

53 A Sampling of What’s in the Journals
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.

54 One Hospital’s Protocol for Identification of Pes Candidates
Pplat > 25 cmH2O Static Lung Compliance < 40 ml/cmH2O P/F Ratio < 300 PEEP > 10 cmH2O to maintain SaO2 > 90% PaCO2 > 60 mmHg or pH < 7.2 attributable to respiratory acidosis Wolfson Medical Center, Holon, Israel

55 Esophageal Balloonary: The Catheter
Can utilize either a 5 or 7fr balloon-tipped catheter or a specialized NG/OG catheter that is inserted into the lower third of the esophagus, above the diaphragm. Pressures that are exerted on the balloon are measured by a transducer either integral in the ventilator or in a separate box 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.

56 Esophageal Balloonary: Catheter Placement
Properly inserted the esophageal balloon will show simultaneous negative deflections in airway and esophageal pressures during an expiratory hold during a patient-initiated breath (Baydur Method). 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. PES should be similar (+ 10) to PGA (Bladder Pressure) Measurements should match the patients clinical presentation.

57 Esophageal Numerology: PTP PLAT
Transpulmonary Pressure at End-Inspiratory Plateau Increased abdominal pressure and/or decreased chest wall compliance is imposing a load on the lungs which is reflected in an increased pleural pressure during an inspiratory plateau. PAW PLAT = 39 cmH2O PTP PLAT = 9 cmH2O Keep PTP PLAT < 20 cmH2O

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

59 Esophageal Numerology: PTP PEEP
Transpulmonary Pressure at End-Expiratory Plateau Goal is to adjust PEEP to maintain PTP PEEP between cmH2O Negative PTP PEEP = pressure outside the lung is greater than pressure inside the lung. Positive PTP PEEP = pressure inside the lung is greater than pressure outside the lung May cause end-expiratory overdistension if too high

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

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

62 Case Study 1: Transpulmonary-Guided Ventilation in Increased Abdominal Pressures

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

64 Pump Up the PEEP Placed on PC/AC, RR-16, PIP-36, Ti-.70 & PEEP-20.
PTP PEEP now -3.7 cmH2O Some Heart Border & Diaphragm now visible

65 Which Plateau Pressure is Correct?
PAW Plateau 41 cmH2O PTP PLAT 21 cmH2O

66 Further PEEP Pumpage PEEP Increased to 25 cmH2O
Ptp PEEP now +2.4 cmH2O Lungs are remaining open at end-exhalation

67 Hey, Let’s Try APRV! PLOW of 0 PTP PEEP of -15 cmH2O
IMMEDIATE Derecruitment!

68 Now What? Returned to PC/AC with PEEP of 25 cmH20
PTP PEEP now +2.4 cmH2O No derecruitment! PAW PEAK of 46 cmH2O PTP PEAK of 27 cmH2O Physicians were hesitant to maintain PEEP of 25

69 Now What? CXR six day post PEEP adjustment using PES monitoring
PEEP 16cmH2O with FiO2 of .40 Heart border and diaphragms visible

70 Case Study 2: Transpulmonary-Guided Ventilation Identifying Post-Code Derecruitment

71 PTP Pre & Post Instillation of Oleic Acid
Pre-Instillation PTP PEEP = +2 cmH2O No Derecruitment Post-Instillation PTP PEEP = -2 cmH2O Derecruitment on PEEP of 4

72 PEEP Increased to 8 PEEP increased to 8 cmH2O
PTP PEEP increased to +1.2 cmH2O Delta PES should be less than 15cm. Anything more results in increased wob. The Ptp waveform is much more important than the Paw waveform in determining what’s truly going on inside of the lungs.

73 Changes Following Resuscitative-Fluid Bolus
Following multiple fluid boluses during resuscitation it was noticed that PES increased from 8 cmH2O to 12 cmH2O PTP PLAT increased to 27 cmH2O PEEP immediately increased to 10 cmH2O This kept PTP PEEP from dropping into negative No “Post-Code Derecruitment”

74 One Last Point

75 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 Before we determine what’s bad with mechanical ventilation we need to identify what is good about spontaneous ventilation. The problem is that we know very little about how the alveoli actually function during spontaneous ventilation.

76 We Need to Define Quality
Q = A x (O + S) W Q – Quality A – Appropriateness O – Outcomes S – Service W – Waste Before we determine what’s bad with mechanical ventilation we need to identify what is good about spontaneous ventilation. The problem is that we know very little about how the alveoli actually function during spontaneous ventilation.

77 Questions? Email:

78 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 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 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 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

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