The document discusses advanced mechanical ventilation techniques, focusing on the consequences of elevated alveolar pressure and the implications for lung mechanics and patient management. It emphasizes the importance of avoiding ventilator-induced lung injury (VILI) through lung protective strategies and highlights the challenges posed by heterogeneous lung inflation, particularly in acute lung injury and severe airflow obstruction cases. It also covers the effects of various ventilation modes and management approaches such as prone positioning and recruitment maneuvers to optimize outcomes in mechanically ventilated patients.

1. John J. Marini
John J. Marini
Alain F. Broccard
Alain F. Broccard
University of Minnesota
University of Minnesota
Regions Hospital
Regions Hospital
Minneapolis / St. Paul
Minneapolis / St. Paul
USA
USA
Advanced Mechanical
Advanced Mechanical
Ventilation
Ventilation

2. Advanced Mechanical Ventilation Outline
Advanced Mechanical Ventilation Outline
Consequences of Elevated Alveolar Pressure
Implications of Heterogeneous Lung Unit Inflation
Adjuncts to Ventilation
• Prone Positioning
• Recruitment Maneuvers
Difficult Management Problems
• Acute Lung Injury
• Severe Airflow Obstruction
• An Approach to Withdrawing Ventilator Support
Advanced Modes for Implementing Ventilation
Case Scenarios

3. Consequences of Elevated Alveolar Pressure--1
Consequences of Elevated Alveolar Pressure--1
Mechanical ventilation expands the lungs and chest wall by pressurizing the
airway during inflation. The stretched lungs and chest wall develop recoil
tension that drives expiration.
Positive pressure developed in the pleural space may have adverse effects
on venous return, cardiac output and dead space creation.
Stretching the lung refreshes the alveolar gas, but excessive stretch subjects
the tissue to tensile stresses which may exceed the structural tolerance limits
of this delicate membrane.
Disrupted alveolar membranes allow gas to seep into the interstitial
compartment, where it collects, and migrates toward regions with lower tissue
pressures.
Interstitial, mediastinal, and subcutaneous emphysema are frequently the
consequences. Less commonly, pneumoperitoneum, pneumothorax, and
tension cysts may form.
Rarely, a communication between the high pressure gas pocket and the
pulmonary veins generates systemic gas emboli.

4. Partitioning of Alveolar Pressure is a Function of Lung
Partitioning of Alveolar Pressure is a Function of Lung
and Chest Wall Compliances
and Chest Wall Compliances
Lungs are smaller and
pleural pressures are
higher when the chest
wall is stiff.

5. Hemodynamic Effects of Lung Inflation
Hemodynamic Effects of Lung Inflation
Lung inflation by positive pressure causes
• Increased pleural pressure and impeded venous return
• Increased pulmonary vascular resistance
• Compression of the inferior vena cava
• Retardation of heart rate increases
These effects are much less obvious in the presence of
• Adequate circulating volume
• Adequate vascular tone
• Spontaneous breathing efforts
• Preserved adrenergic responsiveness

6. Hemodynamic Effects of Lung Inflation
Hemodynamic Effects of Lung Inflation
With Low Lung Compliance, High Levels of
PEEP are Generally Well Tolerated.

7. Effect of lung expansion on pulmonary vasculature. Capillaries that
are embedded in the alveolar walls undergo compression even as interstitial
vessels dilate. The net result is usually an increase in pulmonary vascular
resistance, unless recruitment of collapsed units occurs.

8. Conflicting Actions of Higher Airway Pressure
Conflicting Actions of Higher Airway Pressure
Lung Unit Recruitment and Maintenance of Aerated Volume
• Gas exchange
• Improved Oxygenation
• Distribution of Ventilation
• Lung protection
• Parenchymal Damage
• Airway trauma
Increased Lung Distention
• Impaired Hemodynamics
• Increased Dead Space
• Potential to Increase Tissue Stress
…Only If Plateau Pressure Rises

9. Gas Extravasation
Barotrauma

10. Diseased Lungs Do
Not Fully Collapse,
Despite Tension Pneumothorax
…and
They cannot always
be fully “opened”
Dimensions of a fully
Collapsed Normal Lung

11. Tension Cysts

12. Tidally Phasic Systemic Gas Embolism
Tidally Phasic Systemic Gas Embolism
End-Expiration End-Inspiration

13. Consequences of Elevated Alveolar Pressure--2
Consequences of Elevated Alveolar Pressure--2
In recent years there has been intense interest in another and perhaps
common consequence of excessive inflation pressure--Ventilator-Induced
Lung Injury (VILI).
VILI appears to develop either as a result of structural breakdown of the
tissue by mechanical forces or by mechano-signaling of inflammation due
to repeated application of excessive tensile forces.
Although still controversial, it is generally agreed that damage can result
from overstretching of lung units that are already open or from shearing
forces generated at the junction of open and collapsed tissue.
Tidally recurrent opening and closure of small airways under high
pressure is thought to be important in the generation of VILI.
Prevention of VILI is among the highest priorities of the ICU clinician
caring for the ventilated patient and is the purpose motivating adoption of
“Lung Protective” ventilation strategies.
Translocation of inflammatory products, bacteria, and even gas may
contribute to remote damage in systemic organs and help explain why
lung protective strategies are associated with lower risk for morbidity and
death.

14. Recognized Mechanisms of Airspace Injury
Recognized Mechanisms of Airspace Injury
“Stretch”
“Shear”
Airway Trauma

15. Mechanisms of Ventilator-Induced Lung Injury (VILI)
Mechanisms of Ventilator-Induced Lung Injury (VILI)
High airway pressures may injure the lungs by repeated overstretching
of open alveoli, by exposing delicate terminal airways to high pressure,
or by generating shearing forces that tear fragile tissues.
These latter shearing forces tend to occur as small lung units open and
close with each tidal cycle and are amplified when the unit opens only
after high pressures are reached.
To avoid VILI, end-inspiratory lung pressure (“plateau”) should be kept
from rising too high, and when high plateau pressures are required,
sufficient PEEP should be applied to keep unstable lung units from
opening and closing with each tidal cycle.
Independent of opening and closure, tissue strain is dramatically
amplified at the junctions of open and closed lung units when high
alveolar pressures are reached.
Extremely high tissue strains may rip the alveolar gas-blood interface.
Repeated application of more moderate strains incite inflammation.
Such factors as breath frequency, micro-vascular pressure,
temperature, and body position modify VILI expression.

16. End-Expiration
Tidal Forces
(Transpulmonary and
Microvascular Pressures)
Extreme Stress/Strain Moderate Stress/Strain
Mechano signaling via
integrins, cytoskeleton, ion channels
inflammatory cascade
Cellular Infiltration and Inflammation
Rupture Signaling
Marini / Gattinoni CCM 2004
Pathways to VILI

17. Microvascular Fracture in ARDS
Microvascular Fracture in ARDS
A Portal for
Gas & Bacteria?
Hotchkiss et al
Crit Care Med 2002;
1
1 


18. The Problem of Heterogeneity
The Problem of Heterogeneity
The heterogeneous nature of regional mechanical properties presents major
difficulty for the clinician, who must apply only a single pressure or flow
profile to the airway opening.
Heterogeneity means that some lung units may be overstretched while
others remain airless at the same measured airway pressure.
Finding just the right balance of tidal volume and PEEP to keep the lung as
open as possible without generating excessive regional tissue stresses is a
major goal of modern practice.
Prone positioning tends to reduce the regional gradients of pleural and
trans-pulmonary pressure.

19. Spectrum of Regional Opening Pressures
Spectrum of Regional Opening Pressures
(Supine Position)
(Supine Position)
Superimposed
Pressure Inflated 0
Alveolar Collapse
(Reabsorption) 20-60 cmH2O
Small Airway
Collapse
10-20 cmH2O
Consolidation 
(from Gattinoni)
)
Lung Units at Risk for Tidal
Opening & Closure
=
Opening
Pressure

20. Different lung regions may be overstretched or underinflated, even as
measures of total lung mechanics appear within normal limits.
Alveolar Pressure
Lung
Volume
UPPER LUNG
TOTAL LUNG
LOWER LUNG

21. Recruitment Parallels Volume As A
Recruitment Parallels Volume As A
Function of Airway Pressure
Function of Airway Pressure
Recruitment and
Inflation (%)
Frequency
Distribution of
Opening Pressures
(%)
Airway Pressure (cmH2O)

22. %
Opening and Closing Pressures in ARDS
50
Paw [cmH2O]
0 5 10 15 20 25 30 35 40 45 50
0
10
20
30
40
Opening
pressure
Closing
pressure
From Crotti et al
AJRCCM 2001.
High pressures may be needed to open some lung units, but once open, many
units stay open at lower pressure.

23. Zone of
↑ Risk

24. Dependent to Non-dependent
Dependent to Non-dependent
Progression of Injury
Progression of Injury

25. Histopathology of VILI
Histopathology of VILI
Belperio et al, J Clin Invest Dec 2002; 110(11):1703-1716

26. Links Between VILI and MSOF
Links Between VILI and MSOF
Biotrauma and Mediator
De-compartmentalization
Slutsky, Chest 116(1):9S-16S

27. Airway Orientation in Supine Position
Airway Orientation in Supine Position

29. Prone Positioning Evens The Distribution of
Prone Positioning Evens The Distribution of
Pleural & Transpulmonary Pressures
Pleural & Transpulmonary Pressures

30. Prone Positioning Relieves Lung
Prone Positioning Relieves Lung
Compression by the Heart
Compression by the Heart
Supine
Prone

31. Proning May Benefit the Most Seriously Ill
Proning May Benefit the Most Seriously Ill
ARDS Subset
ARDS Subset
SAPS II
Mortality
Rate
> 49 40- 49 31- 40 0 - 31
0.0
0.1
0.2
0.3
0.4
0.5 Supine
* p<0.05 vs
Supine
Prone
*
Quartiles of SAPS II

32. Proning Helped Most in High V
Proning Helped Most in High VT
T Subgroup At
Subgroup At
Risk For VILI
Risk For VILI
VT/Kg
< 8.2 8.2- 9.7 9.7- 12 > 12
0.0
0.1
0.2
0.3
0.4
0.5
Supine
Mortality
Rate
Quartiles of VT /Predicted body weight
* p<0.05 vs
Supine
Prone
*

33. How Much Collapse Is Dangerous
How Much Collapse Is Dangerous
Depends on the Plateau
Depends on the Plateau
R = 100%
20
60
100
Pressure [cmH2O]
20 40 60
Total
Lung
Capacity
[%]
R = 22%
R = 81%
R = 93%
0
0
R = 0%
R = 59%
From Pelosi et al
AJRCCM 2001
Some potentially
recruitable units
open only at
high pressure
More Extensive
Collapse But
Lower PPLAT
Less Extensive
Collapse But
Greater PPLAT

34. Recruiting Maneuvers in ARDS
Recruiting Maneuvers in ARDS
The purpose of a recruiting maneuver is to open collapsed
lung tissue so it can remain open during tidal ventilation with
lower pressures and PEEP, thereby improving gas exchange
and helping to eliminate high stress interfaces.
Although applying high pressure is fundamental to
recruitment, sustaining high pressure is also important.
Methods of performing a recruiting maneuver include single
sustained inflations and ventilation with high PEEP .

35. Theoretical
Theoretical Effect of Sustained Inflation on Tidal Cycling
Effect of Sustained Inflation on Tidal Cycling
Rimensberger ICM 2000
VOLUME
(% TLC)
Benefit from a recruiting
maneuver is usually transient
if PEEP remains unchanged
afterward.

36. Three Types of Recruitment Maneuvers
Three Types of Recruitment Maneuvers
S-C Lim, et al
Crit Care Med 2004

37. How is the Injured Lung Best Recruited?
How is the Injured Lung Best Recruited?
Prone positioning
Adequate PEEP
Adequate tidal volume (and/or intermittent ‘sighs’?)
Recruiting maneuvers
Minimize edema (?)
Lowest acceptable FiO2 (?)
Spontaneous breathing efforts (?)

38. Severe Airflow Obstruction
Severe Airflow Obstruction
A major objective of ventilating patients with severe airflow obstruction
is to relieve the work of breathing and to minimize auto-PEEP.
Reducing minute ventilation requirements will help impressively in
reducing gas trapping.
When auto-PEEP is present, it has important consequences for
hemodynamics, triggering effort and work of breathing.
In patients whose expiratory flows are flow limited during tidal
breathing, offsetting auto-PEEP with external PEEP may even the gas
distribution and reduce breathing effort.

39. Auto-PEEP Adds To the Breathing Workload
Auto-PEEP Adds To the Breathing Workload
The pressure-volume areas
correspond to the inspiratory
mechanical workloads of auto-PEEP (AP)
flow resistance and tidal elastance.

40. Gas Trapping in Severe Airflow Obstruction
Gas Trapping in Severe Airflow Obstruction
Disadvantages the respiratory muscles and increases the work
of tidal breathing
Often causes hemodynamic compromise, especially during
passive inflation
Raises plateau and mean airway pressures, predisposing to
barotrauma
Varies with body position and from site to site within the lung

42. Volume Losses in Recumbent Positions
Volume Losses in Recumbent Positions
Note that COPD patients lose
much less lung volume than
normals do, due to gas trapping
and need to keep the lungs more
inflated to minimize the severity of
obstruction. Orthopnea may result.

43. PEEP in Airflow Obstruction
PEEP in Airflow Obstruction
Effects Depend on Type and Severity of Airflow Obstruction
Generally Helpful if PEEP  Original Auto-PEEP
Potential Benefits
• Decreased Work of Breathing
• Increased VT During PSV or PCV
• (?) Improved Distribution of Ventilation
• (?) Decreased Dyspnea

44. Inhalation Lung Scans in the Lateral Decubitus Position for a
Inhalation Lung Scans in the Lateral Decubitus Position for a
Normal Subject and COPD Patient
Normal Subject and COPD Patient
Normal
COPD
No PEEP PEEP10
Addition of 10 cm H2O PEEP
re-opens dependent airways
in COPD

45. PEEP
Flow Limitation “Waterfall”

46. Adding PEEP that approximates auto-PEEP may reduce the difference
in pressure between alveolus (Palv) and airway opening, thereby
lowering the negative pleural (Pes) pressure needed to begin
inspiration and trigger ventilation.

47. Adding PEEP Lessens the Heterogeneity of End-expiratory Alveolar
Pressures and Even the Distribution of Subsequent Inspiratory Flow.

48. PEEP may offset
(COPD) or add to
auto-PEEP
(Asthma),
depending on flow
limitation.
Note that adding 8
cmH2O PEEP to 10
cmH2O of intrinsic
PEEP may either
reduce effort (Pes,
solid arrow) or
cause further
hyper-inflation
(dashed arrow).
Ranieri et al, Clinics in Chest Medicine 1996; 17(3):379-94
ASTHMA
COPD

49. Conventional Modes of Ventilatory Support
Conventional Modes of Ventilatory Support
The traditional modes of mechanical ventilation—Flow-regulated volume Assist Control
(“Volume Control”, AMV, AC)) or Pressure-Targeted Assist Control (“Pressure Control”),
Synchronized Intermittent Mandatory Ventilation (SIMV)—with flow or pressure targeted
mandatory cycles), Continuously Positive Airway Pressure (CPAP) and Pressure Support can
be used to manage virtually any patient when accompanied by adequate sedation and settings
well adjusted for the patient’s needs. Their properties are discussed in the “Basic Mechanical
Ventilation” unit of this series.

50. Positive Airway Pressure Can Be Either Pressure or
Positive Airway Pressure Can Be Either Pressure or
Flow Controlled—But Not Both Simultaneously
Flow Controlled—But Not Both Simultaneously
Dependent
Variable
Dependent
Variable
Set Variable
Set Variable

51. Decelerating flow profile is an option in flow controlled
ventilation but a dependent variable in pressure control.
Decelerating Flow Pressure Control
Peak pressure is a function of flow;
plateau pressure is not

52. Patient-Ventilator Interactions
Patient-Ventilator Interactions
Coordination of the patient’s needs for flow, power, and cycle timing with
outputs of the machine determine how well the ventilator simulates an
auxiliary muscle under the patient’s control.
Flow controlled, volume cycled ventilator modes offer almost unlimited
power but specify the cycle timing and flow profile.
Traditional pressure targeted modes (Pressure Control (PCV) and Pressure
support (PSV)) provide no greater power amplitude than that set by the
clinician but do not limit flow. PCV has a cycle time fixed by the clinician, and
in that sense is as inflexible as VCV.
Pressure Support (PSV) allows the patient to determine both flow and, within
certain limits, cycle length as well. Because flow is determined by respiratory
mechanics as well as by effort, adjustments may be needed to the
inspiratory flow offswitch criterion of PSV so as to coordinate with the
patient’s needs.
Modification of the rate at which the pressure target is reached at the
beginning of inspiration (the ramp or ‘attack’ rate) may be needed to help
ensure comfort

53. Pressure Support ‘off-switch’ is a set flow value or a set % of
peak inspiratory flow. The patient with airflow obstruction may need
to put on the brake with muscular effort to slow flow quickly enough
to satisfy his intrinsic neural timing.

54. Tapered inspiratory
‘attack’ rate and a
higher percentage
of peak flow off
switch criterion are
often more
appropriate in
airflow obstruction
than are the default
values in PSV.
Airflow Obstruction

55. Although early flows
are adequate, mid-cycle
efforts may not be
matched by
Decelerating Flow
Control (VCV).
Pressure Controlled
breaths (PCV) do not
restrict flow.
Since the flow demands
of severely obstructed
patients may be nearly
unchanging in severe
airflow obstruction ,
decelerating VCV may
not be the best choice.

56. Interactions Between Pressure Controlled
Interactions Between Pressure Controlled
Ventilation and Lung Mechanics
Ventilation and Lung Mechanics
The gradient of pressure that determines tidal volume is the difference between
end-inspiratory (Plateau) and end-expiratory alveolar pressure (total PEEP).
In PCV, tidal volume can be reduced if the inspiratory time or the expiratory time
is too brief to allow the airway and alveolar pressures to equilibrate.
The development of auto-PEEP reduces the gradient for inspiratory flow and
curtails the potential tidal volume available with any given set inspiratory airway
pressure.
These conditions are most likely to arise in the setting of severe airflow
obstruction. Therefore, modifications of the breathing frequency and inspiratory
cycle period (‘duty cycle’) may powerfully impact ventilation efficiency.

57. Alveolar
Pressure
Airway
Pressure
Residual Flows

59. Deformed Airway Pressure Waveforms
P
Paw
aw Reflects Effort and Dys-Synchrony During
Reflects Effort and Dys-Synchrony During
Constant Flow Ventilation
Constant Flow Ventilation

60. High Pressure Alarm
Variable Tidal Volume or Pressure Limit Alarm During Pressure Control

61. What to Do When the Patent and Ventilator are
What to Do When the Patent and Ventilator are
“Out of Synch”?
“Out of Synch”?
Frequent pressure alarms during Volume Assist Control or Tidal Volume alarms
during Pressure Control both mean that the patient is not receiving the desired
tidal volume.
If not explained by an important underlying change in the circuit properties (e.g.,
disconnection or plug) or in the impedance of the respiratory system, this often
arises from a timing “collision” between the patient and ventilator’s cycling
rhythms.
To quickly regain smooth control without deep sedation, the patient must be
given back some degree of control over cycle timing.
This timing control is conferred by introducing flow off-switched cycles in the
form of high level pressure support. Pressure Support alone, or SIMV at a
relatively low mandated rate together with PSV, are the logical choices to
provide adequate power, achieve flow synchrony and yield cycle timing to the
patient. Pressure Controlled SIMV, where the inspiratory time of the PCV cycle
is set to be a bit shorter than the observed PSV cycle, is a good strategy for this
purpose.

62. Advanced Interactive Modes of
Advanced Interactive Modes of
Mechanical Ventilation
Mechanical Ventilation
Airway pressure release/BiPAP/Bi-Level
Combination or “Dual control” modes
Proportional assist ventilation
Adaptive support ventilation
Automatic ET tube compensation

63. Combination “Dual Control” Modes
Combination “Dual Control” Modes
Combination or “dual control” modes combine features
of pressure and volume targeting to accomplish
ventilatory objectives which might remain unmet by
either used independently.
Combination modes are pressure targeted
 Partial support is generally provided by pressure support
 Full support is provided by Pressure Control

64. Combination “Dual Control” Modes
Combination “Dual Control” Modes
Volume Assured Pressure Support
(Pressure Augmentation)
Volume Support
(Variable Pressure Support)
Pressure Regulated Volume Control
(Variable Pressure Control, or Autoflow)
Airway Pressure Release
(Bi-Level, Bi-PAP)

65. Pressure Regulated Volume Control
Pressure Regulated Volume Control
Characteristics
Characteristics
Guaranteed tidal volume using “pressure control”
waveform
Pressure target is adjusted to least value that satisfies
the targeted tidal volume minimum
Settings:
Minimum VE
Minimum Frequency
Inspiratory Time per Cycle

66. Compliance Changes During Pressure
Compliance Changes During Pressure
Controlled Ventilation
Controlled Ventilation

67. PRVC Automatically Adjusts To
PRVC Automatically Adjusts To
Compliance Changes
Compliance Changes

68. Several modes allow the physician to allow for variability in patient efforts while achieving a
targeted goal. Volume support monitors minute ventilation and tidal volume , changing the
level of pressure support to achieve a volume target. Volume assured pressure support
allows the patient to breathe with pressure support, supplementing the breath with constant
flow when needed to achieve the targeted tidal volume within an allocated time. Proportional
assist (see later) varies pressure output in direct relation to patient effort.

69. Airway Pressure Release and Bi-Level
Airway Pressure Release and Bi-Level
Airway Pressure
Airway Pressure
Over the past 20 years, modes of ventilation that move the airway pressure
baseline around which spontaneous breaths occur between two levels have
been employed in a variety of clinical settings.
Although the machine’s contribution to ventilation may resemble inverse ratio
ventilation, patient breathing cycles occur through an open (as opposed to
closed) circuit, so that airway pressure never exceeds that value desired by
the clinician.
Transpulmonary pressure—the pressure across the lung—can approach
dangerous levels, however, and mean airway pressure is relatively high.

70. Inverse Ratio Airway Pressure Release
Inverse Ratio Airway Pressure Release
(APRV), and Bi-Level (Bi-PAP)
(APRV), and Bi-Level (Bi-PAP)

71. Bi-Pap &Airway Pressure Release
Bi-Pap &Airway Pressure Release
Characteristics
Characteristics
Allow spontaneous breaths superimposed on a set
number of “pressure controlled” ventilator cycles
Reduce peak airway pressures
“Open” circuit / enhanced synchrony between patient
effort and machine response
Settings:
Pinsp and Pexp (Phigh and Plow)
Thigh and Tlow

72. Unlike PCV, BiPAP Allows Spontaneous
Unlike PCV, BiPAP Allows Spontaneous
Breathing During Both Phases of Machine’s Cycle
Breathing During Both Phases of Machine’s Cycle

73. Bi-Level Ventilation
Bi-Level Ventilation

74. Bi-Level Ventilation
Bi-Level Ventilation
With Pressure Support
With Pressure Support

75. Modes That Vary Their Output to Maintain
Modes That Vary Their Output to Maintain
Appropriate Physiology
Appropriate Physiology
Proportional Assist Ventilation
(Proportional Pressure Support)
- Support pressure parallels patient effort
Adaptive Support Ventilation
- Adjusts Pinsp and PC-SIMV rate to meet
“optimum” breathing pattern target
Neurally Adjusted Ventilatory Assist
- Ventilator output is keyed to neural signal

76. Proportional Assist Ventilation (PAV)
Proportional Assist Ventilation (PAV)
Proportional assist ventilation attempts to regulate the pressure output of
the ventilator moment by moment in accord with the patient’s demands for
flow and volume.
Thus, when the patient wants more, (s)he gets more help; when less, (s)he
gets less. The timing and power synchrony are therefore nearly optimal—at
least in concept.
To regulate pressure, PAV uses the monitored flow and a calculated
assessment of the mechanical properties of the respiratory system as
inputs into the equation of motion of the respiratory system.
More than with any other currently available mode, PAV acts as an auxiliary
muscle whose strength is regulated by the proportionality constant
determined by the clinician.
At present, PAV cannot account for auto-PEEP, and there is a small
chance for inappropriate support to be applied.

77. Proportional Assist Amplifies Muscular Effort
Proportional Assist Amplifies Muscular Effort
Muscular effort (Pmus) and
airway pressure assistance
(Paw) are better matched for
Proportional Assist (PAV)
than for Pressure Support
(PSV).

78. Goals of Adaptive Support Ventilation
Goals of Adaptive Support Ventilation
• Reduce Dead-space Ventilation
• Avoid Auto-PEEP
• Discourage Rapid Shallow Breathing
• Mirror Changing Patient Activity

79. Adaptive Lung Ventilation
Adaptive Lung Ventilation
Synchronized Intermittent Pressure Control
Rate
Inspiratory Pressure
PSV cycling characteristics
Physician Settings
Ideal body weight
% Minute Volume
Maximal Allowed Pressure

81. Neural Control of Ventilatory Assist
Neural Control of Ventilatory Assist
(NAVA)
(NAVA)
Although still in its development phase, the possibility of
controlling ventilator output by sensing the neural traffic flowing
to the diaphragm promises to further enhance synchrony.
NAVA senses the desired assist using an array of esophageal
EMG electrodes positioned to detect the diaphragm’s
contraction signal.
The reliability of neurally-controlled ventilator assistance needs
to be determined before its deployment in the clinical setting.

82. Neural Control of Ventilatory Assist (NAVA)
Neural Control of Ventilatory Assist (NAVA)
Neuro-Ventilatory
Coupling
Central Nervous System

Phrenic Nerve

Diaphragm Excitation

Diaphragm Contraction

Chest Wall and Lung Expansion

Airway Pressure, Flow and
Volume
New
Technology
Ideal
Technology
Current
Technology
Ventilator
Unit

83. Electrode Array in Neurally Adjusted
Electrode Array in Neurally Adjusted
Ventilatory Assist (NAVA)
Ventilatory Assist (NAVA)
Sinderby et al, Nature Medicine; 5(12):1433-1436

84. NAVA Provides Flexible Response to Effort
NAVA Provides Flexible Response to Effort
Volume
PAW
DGM
EMG
Sinderby et al, Nature Medicine; 5(12):1433-1436

85. Automatic Tube Compensation
Automatic Tube Compensation
The endotracheal tube offers resistance to ventilation both on
inspiration and on expiration.
A low level of pressure support can help overcome this pressure
cost, but its effect varies with flow rate.
Automatic tube compensation (ATC) adjusts its pressure output
in accordance with flow, theoretically giving an appropriate
amount of pressure support as needed as the cycle proceeds
and flow demands vary within and between subsequent breaths.
Some variants of ATC drop airway pressure in the early portion
of expiration to help speed expiration.
Supplemental pressure support can be provided to assist in tidal
breath delivery.

86. External and Tracheal Pressures Differ
External and Tracheal Pressures Differ
Because of Tube Resistance
Because of Tube Resistance
ATC offsets a fraction of tube
resistance

87. Valve Control Maintains
Valve Control Maintains Tracheal
Tracheal Pressure
Pressure
During ATC
During ATC
Pressure Support Pressure Support
ATC ATC
Fabry et al, ICM 1997;23:545-552

88. ATC Adjusts Inspiratory Pressure to Need
ATC Adjusts Inspiratory Pressure to Need
Postop
Critically Ill

89. Discontinuation of Mechanical Ventilation
Discontinuation of Mechanical Ventilation
To discontinue mechanical ventilation requires:
 Patient preparation
 Assessment of readiness
For independent breathing
For extubation
 A brief trial of minimally assisted breathing
An assessment of probable upper airway patency after extubation
 Either abrupt or gradual withdrawal of positive pressure,
depending on the patient’s readiness

90. Preparation: Factors Affecting
Preparation: Factors Affecting
Ventilatory Demand
Ventilatory Demand

92. The frequency to tidal volume ratio (or rapid shallow breathing index, RSBI) is a simple and
useful integrative indicator of the balance between power supply and power demand. A
rapid shallow breathing index < 100 generally indicates adequate power reserve. In this
instance, the RSBI indicated that spontaneous breathing without pressure support was not
tolerable, likely due in part to the development of gas trapping.
Even when the mechanical requirements of the respiratory system can be met by
adequate ventilation reserve, congestive heart failure, arrhythmia or ischemia may cause
failure of spontaneous breathing.

93. Integrative Indices Predicting Success
Integrative Indices Predicting Success

94. Measured Indices Must Be Combined With
Measured Indices Must Be Combined With
Clinical Observations
Clinical Observations

95. Three Methods for Gradually
Three Methods for Gradually
Withdrawing Ventilator Support
Withdrawing Ventilator Support
Although the majority of patients do not require gradual withdrawal of ventilation, those
that do tend to do better with graded pressure supported weaning than with abrupt
transitions from Assist/Control to CPAP or with SIMV used with only minimal pressure
support.

96. Extubation Criteria
Extubation Criteria
Ability to protect upper airway
 Effective cough
 Alertness
Improving clinical condition
Adequate lumen of trachea and larynx
 “Leak test” during airway pressurization with the
cuff deflated