Advanced Mechanical

Ventilation

John J. Marini
Alain F. Broccard

University of Minnesota
Regions Hospital
Minneapolis / St. Paul
USA
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
 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.
 Partitioning of Alveolar Pressure is a Function of Lung
and Chest Wall Compliances

Lungs are smaller and

pleural pressures are
higher when the chest
wall is stiff.
 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
 Hemodynamic Effects of Lung Inflation

With Low Lung Compliance, High Levels of

PEEP are Generally Well Tolerated.
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.
 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

Gas Extravasation
Barotrauma
Diseased Lungs Do
Not Fully Collapse,
Despite Tension Pneumothorax

…and

They cannot always

be fully “opened”

Dimensions of a fully
Collapsed Normal Lung
Tension Cysts
Tidally Phasic Systemic Gas Embolism

End-Expiration End-Inspiration
 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.
Recognized Mechanisms of Airspace Injury

Airway Trauma

“Stretch”

“Shear”
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.
 End-Expiration Pathways to VILI

Extreme Stress/Strain Tidal Forces Moderate Stress/Strain

(Transpulmonary and
Microvascular Pressures)

Rupture Signaling

Mechano signaling via

integrins, cytoskeleton, ion channels

inflammatory cascade

Cellular Infiltration and Inflammation

Marini / Gattinoni CCM 2004

 Microvascular Fracture in ARDS

A Portal for
Gas & Bacteria?

1µ
Hotchkiss et al
Crit Care Med 2002;
 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.
 Spectrum of Regional Opening Pressures
(Supine Position)
Opening
Pressure
Superimposed
Pressure Inflated 0

Small Airway 10-20 cmH2O

Collapse

Alveolar Collapse
(Reabsorption) 20-60 cmH2O

Consolidation ∞
= Lung Units at Risk for Tidal
Opening & Closure
(from Gattinoni)
 Different lung regions may be overstretched or underinflated, even as
measures of total lung mechanics appear within normal limits.

UPPER LUNG

TOTAL LUNG
Lung Volume

Alveolar Pressure

LOWER LUNG
 Recruitment Parallels Volume As A
Function of Airway Pressure

Recruitment and
Inflation (%)

Frequency
Distribution of
Opening Pressures
(%)

Airway Pressure (cmH2O)

Opening and Closing Pressures in ARDS
High pressures may be needed to open some lung units, but once open, many
units stay open at lower pressure.
50
40
Opening
30 pressure
Closing
%

20 pressure
From Crotti et al
10 AJRCCM 2001.

0
0 5 10 15 20 25 30 35 40 45 50
Paw
[cmH2O]
Zone of
↑ Risk
Dependent to Non-dependent
Progression of Injury
Histopathology of VILI

Belperio et al, J Clin Invest Dec 2002; 110(11):1703-1716

Links Between VILI and MSOF

Biotrauma and Mediator

De-compartmentalization

Slutsky, Chest 116(1):9S-16S

Airway Orientation in Supine Position
Prone Positioning Evens The Distribution of
Pleural & Transpulmonary Pressures
 Prone Positioning Relieves Lung
Compression by the Heart

Supine

Prone
Proning May Benefit the Most Seriously Ill
ARDS Subset
0.5 Supine
Mortality Rate
Prone
0.4
* p<0.05 vs
0.3 Supine
*
0.2

0.1

0.0
> 49 40- 49 31- 40 0 - 31
SAPS
Quartiles II II
of SAPS
Proning Helped Most in High VT Subgroup At
Risk For VILI
0.5
Mortality Rate Supine
0.4 Prone
* p<0.05 vs
0.3 Supine

0.2 *

0.1

0.0
< 8.2 8.2- 9.79.7- 12 > 12
V /Kg
Quartiles of VT /Predicted
T
body weight
 How Much Collapse Is Dangerous
Depends on the Plateau

Total Lung Capacity [%]

100 Less Extensive
Collapse But
Greater PPLAT R = 100%
R = 93%
More Extensive R = 81% Some potentially
60 Collapse But recruitable units
Lower PPLAT open only at
high pressure
R = 59%
From Pelosi et al
20 AJRCCM 2001
R = 22%
0
0 20 40 60
R = 0% Pressure [cmH2O]
 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 .
 Theoretical Effect of Sustained Inflation on Tidal Cycling

Benefit from a recruiting

maneuver is usually transient
VOLUME if PEEP remains unchanged
(% TLC) afterward.

Rimensberger ICM 2000

Three Types of Recruitment Maneuvers

S-C Lim, et al
Crit Care Med 2004
 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 (?)
 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.
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.
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
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.
 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
Inhalation Lung Scans in the Lateral Decubitus Position for a
Normal Subject and COPD Patient

No PEEP PEEP10

Normal

Addition of 10 cm H2O PEEP

re-opens dependent airways
in COPD

COPD
Flow Limitation “Waterfall”

PEEP
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.
Adding PEEP Lessens the Heterogeneity of End-expiratory Alveolar
Pressures and Even the Distribution of Subsequent Inspiratory Flow.
 PEEP may offset
COPD ASTHMA (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

 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.
Positive Airway Pressure Can Be Either Pressure or
Flow Controlled—But Not Both Simultaneously

Dependent
Variable
Set Variable

Set Variable
Dependent
Variable
Decelerating flow profile is an option in flow controlled
ventilation but a dependent variable in pressure control.
Peak pressure is a function of flow;
plateau pressure is not

Decelerating Flow Pressure Control

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

Residual Flows
Paw Reflects Effort and Dys-Synchrony During
Constant Flow Ventilation
Deformed Airway Pressure Waveforms
 High Pressure Alarm

Variable Tidal Volume or Pressure Limit Alarm During Pressure Control

What to Do When the Patent and Ventilator are
“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.
 Advanced Interactive Modes of
Mechanical Ventilation

Airway pressure release/BiPAP/Bi-Level

Combination or “Dual control” modes
Proportional assist ventilation
Adaptive support ventilation
Automatic ET tube compensation
 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
 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)
 Pressure Regulated Volume Control
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
Compliance Changes During Pressure
Controlled Ventilation
PRVC Automatically Adjusts To
Compliance Changes
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.
Airway Pressure Release and Bi-Level
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.
Inverse Ratio Airway Pressure Release
(APRV), and Bi-Level (Bi-PAP)
 Bi-Pap &Airway Pressure Release
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
 Unlike PCV, BiPAP Allows Spontaneous
Breathing During Both Phases of Machine’s Cycle
Bi-Level Ventilation
 Bi-Level Ventilation
With Pressure Support
Modes That Vary Their Output to Maintain
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
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.
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).
Goals of Adaptive Support Ventilation

Reduce Dead-space Ventilation

Avoid Auto-PEEP
Discourage Rapid Shallow Breathing
Mirror Changing Patient Activity
 Adaptive Lung Ventilation
Synchronized Intermittent Pressure Control
Rate
Inspiratory Pressure
PSV cycling characteristics

Physician Settings
Ideal body weight
% Minute Volume
Maximal Allowed Pressure
 Neural Control of Ventilatory Assist
(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.
Neural Control of Ventilatory Assist (NAVA)

Ideal
Central Nervous System
Neuro-Ventilatory Coupling

Technology
↓
Phrenic Nerve
↓ New
Diaphragm Excitation Ventilator
↓ Technology Unit
Diaphragm Contraction
↓
Chest Wall and Lung Expansion
↓
Current
Airway Pressure, Flow and
Technology
Volume
Electrode Array in Neurally Adjusted
Ventilatory Assist (NAVA)

Sinderby et al, Nature Medicine; 5(12):1433-1436

NAVA Provides Flexible Response to Effort

Volume

PAW

DGM
EMG

Sinderby et al, Nature Medicine; 5(12):1433-1436

 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.
External and Tracheal Pressures Differ
Because of Tube Resistance

ATC offsets a fraction of tube

resistance
Valve Control Maintains Tracheal Pressure
During ATC

Pressure Support Pressure Support

ATC ATC

Fabry et al, ICM 1997;23:545-552

ATC Adjusts Inspiratory Pressure to Need

Postop
Critically Ill
 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
Preparation: Factors Affecting
Ventilatory Demand
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.
Integrative Indices Predicting Success
Measured Indices Must Be Combined With
Clinical Observations
 Three Methods for Gradually
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.
 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