RT Article

February/March 2001

Lung-Protective Strategies

Combining ventilator strategies and compliance-improving techniques will help

clinicians keep patients ventilated at safe pressures

Patrick Yorio, RRT

Protecting the lung from potential damage is not a new concept.

Complications of positive-pressure ventilation are described as
barotrauma and are accompanied by a decrease in cardiac
output.1 The damage done through barotrauma is considered
catastrophic in that pneumo-

search: thorax can become tension pneumothorax (which is life threatening). The precaution
undertaken to protect patients from this damage has typically been to vent off
occasional high delivery pressures. The pressure buildup is usually due to a volume
.
ventilator’s attempt to deliver the mandatory breath in the presence of an obstruction.
. Recent studies,2,3 however, point to the need to limit the amount of pressure used to
deliver given tidal volumes. Continued studies4,5 on ventilator-induced lung injury
(VILI) pointed to overdistention caused by excessive volume delivery as responsible
for injury. With volutrauma, there is the possibility of causing damage to the lung
parenchyma through injuries related to overinflation (stretch) or opening and closing
(stress).4 Growing concern regarding VILI has prompted RCPs to consider substitutes
for traditional ventilation methods. Overdistention of the lungs is the cause of airway
remodeling,6 and increased permeability of the epithelial cells in the lung
parenchyma, which leads to edema. Oxygen radicals are released, along with toxins
causing inflammation and, eventually, fibrosis and death.5,7,8 If mechanical
ventilation is the cause of this damage,1 then it is necessary to examine

● • how much volume is needed to trigger this phenomenon4;

● • how this trigger can be measured7;
● • what can be done to prevent this5;
● • whether the treatment outweighs the risk.

The movement favoring protective lung ventilation has not been accepted by all who
practice mechanical ventilation. The early 1970s yielded groups focusing on pressure
or volume in the ventilation of infants and children. At that time, adult ventilation was

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uncontroversial. The adult respiratory distress syndrome (ARDS) was still being
defined as progressive pulmonary consolidation,9 and the only argument surrounding
pressure limits was that super positive end-expiratory pressure (PEEP) should be
limited to 44 cm H2O.10 The concern for pressure regulation has since entered adult
intensive care, and the conventional approach to adult ventilation has been questioned
for more than a decade.

Conventional Ventilation
Conventional ventilation can be defined as volume-focused (at 12 to 15 mL/kg),
pressure-variable support. The associated complications include pneumothorax,
pneumomediastinum, and cardiac-output impairment. Literature11 continues to appear
suggesting that lung overdistention (measured as airway pressure) causes damage.
Conventional ventilation methods cause nonphysiologic pressure buildup by using
excessive tidal volumes.

This awareness triggered the development of alternative ventilation methods. Most

suggestions for alternatives were nonphysiologic, such as placing the inspiratory and
expiratory (I:E) times in an inverse relationship or allowing hypercapnia and acidosis
to develop. Neuromuscular blocking agents are recommended with inverse I:E ratios
because the patient is subjected to intolerable circumstances. Hoyt12 notes that 38%
of patients using strategies such as pressure-controlled ventilation with inverse-ratio
ventilation needed neuromuscular blockade agents, while they were required by only
22% of the group using standard ventilation practices. The use of neuromuscular
blockade agents is cited by Hoyt as increasing persistent paralysis when used in large
doses for more than a week, even with hourly monitoring. Hoyt notes that the methods
of Kirby et al7 called for using the level of PEEP needed to correct hypoxia and
reduce shunting to 15% to 20%. Peak airway pressures reached the level necessary to
deliver the desired tidal volume and correct shunting. The risks involved must be
considered in weighing the value of protective lung strategies against the prolonged
use of neuromuscular blockade.

Comparing Children to Adults

Pediatric and adult ventilation are not the same. Heulitt and Bohn13 wrote that
children “differ both anatomically and developmentally from adults.” They also
pointed out that the higher chest-wall compliance of infants and small children
provides less protection against iatrogenic lung injury. While the infant-ventilation
controversies of the 1970s were unresolved, today’s ability to measure small tidal
volumes, even with constant-flow ventilators, enables the pressure-conscious group to
gain an appreciation for volume ventilation. Likewise, the volume-oriented group has
gained an appreciation of pressure limitations.

What is the volume needed to induce lung injury? Is the 12 to 15 mL/kg of

conventional ventilation excessive? Johnson et al14 assessed hyperinflation using
radiographic measurements and mechanical ventilation. Of the 102 patients studied,
radiographically recognizable hyperinflation occurred in 18%. Patients with
hyperinflation had been ventilated at higher tidal volumes (11 mL/kg versus 9.4 mL/
kg; P=.0081). Peak airway pressures, plateau pressures, and PEEP were similar. This
study was based on the subjective conclusions of three independent radiologists using
objective measurements. It would be difficult to determine the presence of ventilator-
induced hyperinflation based on a bedside chest radiograph. Overdistention of the
lung is a result of transpulmonary pressure,2 not airway pressure, yet the difficulty of
measuring transpulmonary pressure is such that airway pressure is relied on as an

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indicator of volutrauma. Webb and Tierney3 demonstrated that, while no lung

abnormality developed in rats ventilated at a pressure of 14 cm H2O, pulmonary
edema developed at 45 cm H2O. A similar rat study7 revealed that prolonged
exposure to high-pressure ventilation alone (without hyperoxia) promotes
overdistention of lung tissues, airway remodeling, and airway hyperreactivity. The rats
were ventilated at 32 to 35 cm H2O for 3.5 to 4 hours per day for 6 days.

The literature is flooded by work on the effects of volutrauma, yet volume is not the
parameter being measured. The most recent human trial15 compared traditional tidal-
volume ventilation at 10 to 15 mL/kg and 6 mL/kg. A 0.5-second pressure plateau was
used as an indicator to keep the higher volume at a pressure of 50 cm H2O or less and
the lower volume at less than 30 cm H2O. With the larger tidal volumes and higher
pressures, mortality increased.

The Acute Respiratory Distress Syndrome Network limited plateau pressure to 30 cm

H2O. In a consensus conference2 on mechanical ventilation, however, it was
recommended that plateau pressures be kept below 35 cm H2O. Peak airway pressures
are dynamic and incorporate the pressure needed to overcome airway resistance and
lung compliance. Experimental studies rarely use plateau pressures; most have been
based on peak pressures during mechanical positive-pressure breathing. If ventilator-
induced injury is caused by volume, then it would be more appropriate to use plateau
pressure as an indicator of lung stretching.

In the general mechanically ventilated population, plateau pressures of 30 to 35 cm

H2O are not much of a problem. High pressure becomes a problem when the
compliance of the lungs is decreased. The RCP must find a balance that keeps the
patient ventilated, with pressure held in check.

Providing Adequate Ventilation

Avoiding high plateau pressures while providing adequate ventilation is a dynamic
process that can be accomplished only with a thorough understanding of physiological
and mechanical interactions. The approach to ventilation with minimal pressures is
two-pronged: clinicians must reduce the amount of force used to push air into
noncompliant lungs or increase the compliance of the lungs so that less force is
needed. Much effort has been expended in the effort to avoid volutrauma.

Avoiding VILI is the RCP’s ultimate challenge. It may call for a combination of
techniques, and it should be understood that no single technique or combination will
work on every patient all the time. It is more likely that RCPs will find themselves
shifting techniques to keep ventilation adequate and safe. Ventilation-perfusion
abnormalities are dynamic, and RCPs must be ready to respond to changes (even if it
means using a technique that did not work a day earlier). Diseased lungs make blood
flow and ventilation unstable, so monitoring must become more focused as the lungs
become more diseased.

Monitoring
The easier it is to provide ventilation, the less monitoring is needed. Certain triggers
indicate a need to move to the next monitoring level. A step-up monitoring system
(Table 1, page 32) should be considered as a guide; this also allows earlier
intervention through the use of lung-protection strategies. As a patient’s condition
worsens, monitoring can become labor intensive, so consideration should be given to
respiratory care staffing levels.

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Level 1 Monitored Level 2 Monitored Level 3 Monitored

Parameters Parameters Parameters
(to be used when peak (to be used in the
• Tidal volume exhaled airway pressures exceed presence of plateau
• Minute ventilation 35 to 40 cm H2O) pressures that are
• Peak inspiratory pressure continuously above 30 to
• Inspired oxygen • Level 1 parameters 35 cm H2O)
• Electrocardiogram • Plateau pressure
• Blood pressure • End-tidal carbon dioxide • Parameters for levels 1
• Pulse oximetry • Mean airway pressure and 2
• Inspiratory to expiratory • Shunting
ratio • Dead space
• Static compliance • Serial compliance
• Waveforms for pressure, • Alveolar-arterial gradient
volume, and flow or Pao2/Fio2 (P/F ratio)
• Alveolar tidal volume
If plateau pressure • Carbon dioxide production
remains within • Cardiac output
predetermined safe limits,
the cause of increased
resistance should be
found and treated (for
example, bronchospasm
should be treated using a
bronchodilator), with
monitoring at level 2 to
continue until the problem
is resolved
Table 1. Severity-based steps in monitoring mechanically ventilated patients.

Respiratory-system failure can be defined as inability to keep up with carbon dioxide

production. As long as alveolar minute ventilation keeps up with carbon dioxide
production, homeostasis is achieved. It is the inverse relationship of carbon dioxide
production and minute ventilation that results in respiratory failure. Normal carbon
dioxide production is approximately 2 mL/kg per minute.

Respiratory failure index (RFI) is the alveolar minute ventilation divided by the CO2
production. RFI accounts for three variables of CO2 elimination, which are CO2
production, dead-space ventilation, and minute ventilation. Using normal values of
CO2 production and alveolar minute ventilation, the RFI would be 30-40. Less than
30 would indicate respiratory failure.

The use of monitoring is an important guide in determining the effectiveness of lung-

protective strategies. Each patient who is mechanically ventilated, however, will not
need complete, intensive-care monitoring. Patient data-management tools can be
linked to share data with ventilators, respiratory monitors, and cardiac monitors in
order to provide real-time graphing of patient parameters. This, in turn, helps
clinicians pinpoint the results of their lung-protective techniques, whether these are
aimed at reducing pressure or at improving compliance.

Hybrid Technology
In the mandatory breath, the ventilator industry has made an effort to combine the
efficacy of controlling pressure and the power of volume delivery. Each ventilator

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model has its own way of regulating pressure, with volume guaranteed. Some
ventilators have automatically controlled pressures and use initial tidal volume to
deliver a dynamic breath (with an inflation hold). The resulting plateau pressure is
used as the controlling pressure for subsequent volume delivery. Other manufacturers
use operator-set pressure, flow, and volume. The mandatory breath is delivered at the
preset pressure. If the desired tidal volume is not reached within a specified time, or if
flow reduction is sensed during the mandatory breath, then the preset flow is used to
deliver the preset tidal volume. Thus, the machine becomes both a pressure ventilator
and a volume ventilator.

As pulmonary consolidation increases, it becomes very difficult to provide adequate

ventilation. Monitors that would alert clinicians to overdistention are needed.
Developing accurate, reliable pressure-volume loops might allow ventilation to be
delivered with lower inflection points (with less risk of excessive opening stress and
overdistention). The ventilator industry has made tremendous advances in providing
safer ventilation.

Conclusion
Controversy concerning ventilation strategies exists. The similarity of the lung injuries
seen in ARDS and VILI makes it difficult to distinguish between the two.2 Does this
make it equally difficult to distinguish between the outcomes of ventilator strategies
and the outcomes of the disease process? Stewart et al16 studied ARDS in two groups,
with one (in which hypercapnia was permitted) using limited volumes (8 mL/kg) and
low peak inspiratory pressures (<30 cm H2O)and the other using volumes of 10 to 15
mL/kg and pressures of 50 cm H2O. They found that “a strategy of mechanical
ventilation that limits tidal volume does not appear to reduce mortality and may
increase morbidity.” Dreyfuss and Saumon2 stated, “The possibility that mechanical
ventilation can actually worsen acute lung disease is widely accepted.” The
identification of VILI has promoted compromise in conventional ventilation, from 12
to 15 cc/kg to an often acceptable 10 cc/kg for tidal volume delivery.

No ventilator strategy or compliance-improving technique will provide sufficient lung

protection. It is the combination of several procedures that will help clinicians keep
the patient ventilated at safe pressures. Monitoring provides guidance in balancing
volume-pressure relationships. The RCP also monitors a very complicated set of
variables.

Clinicians must bear in mind the risks and benefits of sacrificing ventilation for
pressure (or vice versa). The respiratory community has made advances in both
providing and monitoring ventilation. More studies will clarify what clinicians need to
monitor in order to provide safer ventilation.

Patrick Yorio, RRT, is respiratory care coordinator, St Francis Medical Center,

Cranberry, Pa; chair of the Society for Critical Care Medicine’s respiratory care
section; and the 1999 American Association for Respiratory Care acute care therapist.

References
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Care: A Guideline to Clinical Practice. 2nd ed. Philadelphia: JB Lippincott; 1984:573-
575.
2. Dreyfuss D, Saumon G. Ventilator-induced lung injury. Am J Respir Crit Care
Med. 1998;157:294-323.

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3. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive
pressure ventilation with high inhalation pressures: protection by positive end
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Copyright © 2005 CurAnt Communications,

an MWC/Allied Healthcare Group Company. All rights reserved.

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