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

60.  PES = PPEAK ES – PPEEP ES
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: thomas.petty@carefusion.com

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