LOW COMPLIANT LUNG
VENTILATOR STRATEGIES
By: Maria Lopez & Rebecca Lentz
DEFINITIONS
Compliance is defined as the relative ease with which a structure
distends.
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Elastance is defined as the tendency of a structure to return to its
original form after being stretched or acted on by an outside force.
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In terms of the lungs the compliance is the ability of the lungs to
expand and accept an increased volume of gases, where elastance is the
ability to recoil to the original/smaller shape and results in a decreased
volume. These changes in the lung shape allow for changes in volume that
will result in the ability to move gasses in and out of the lungs –
ventilation. A decrease in either of these critical lung mechanics will affect
the patient’s ability to exchange gas and thus will reduce their ability to
maintain a normal pH, acid base balance and/or oxygenation.
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CONDITIONS RESULTING IN ↓ COMPLIANCE
ARDS decreases compliance as the lung parenchyma is often times replaced with
fibrotic tissue making the lung less able to accept volume or less compliant. The stiffness
associated with ARDS is a result of this fibrotic scar tissue and not only reduces compliance
and ventilation but also reduces the tissue participating in gas exchange.
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VILI or ALI are disease processes that are initiated by damage resulting from mechanical
ventilation and are considered indistinguishable from ARDS.
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Pneumoconiosis like ARDS will result in replaced lung parenchyma with fibrotic scar
tissue that is much less compliant than healthy lung tissue. Additionally the replacement
with fibrotic tissue will also result in less tissue participating in gas exchange.
Pneumoconiosis is different from ARDS as it is a result of exposure to dust particles that
cause the encapsulation of the dusts and thus causes scar tissue.
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Kyphoscoliosis decreases lung compliance but by way of reduced thoracic compliance
as the thoracic cage is restricted by the spinal position resulting in smaller overall volume
changes in the lungs. The lungs will likely have good characteristics – however their
reduced function is completely related to the decreased complicate of the thoracic cage.
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DECREASED COMPLIANCE
WHAT IS OVERDISTENTION
Over distention is the overstretching of alveoli as a
result of excessive pressure being delivered during
mechanical ventilation which can be a result of
therapist neglect or decreased lung compliance.
 When a patients lung compliance decreases as a
result of a disease process, such as ARDS, then
the pressures are quickly increased inside the
alveoli when a patient is on VC.
 Overdistention can also cause a disease process
within the lung parenchyma indistinguishable from
ARDS and is known as ALI or VILI.
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WHAT ARE THE PHYSIOLOGICAL EFFECTS OF
OVERDISTENTION?
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Mechanical ventilation over distention can cause
biochemical injury which will release cytokines,
complement, prostanoids, leukotrienes, reactive oxygen
species, proteases due to the biophysical injury of over
distention, cyclic stretch and increased intrathoracic
pressures which cause the release of bacteria in the
distal organs at the level of the tissue injury secondary
to inflammatory mediators cells, which can impair O2
delivery and cause bacteremia resulting to MODS.
WHAT ARE THE PHYSIOLOGICAL EFFECTS OF
OVERDISTENTION?
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Destruction of type 1 cells (alveolar) epithelial cells leads to detachment of
the underlying basement membrane which results in impairment of the
normal anatomic barrier
Which leads to increased permeability
Resultant influx of protein rich edema fluid in the interstitium and alv space.
In patients with persistent over distention causing lung injury (3-7 days)
after initial lung injury, the disease processes to a stage at which the
basement membrane is replaced with a more fibrotic material enhanced by
proliferation of alveolar type II cells;
The fibrosis contributes to the poor compliance of the lung, which can
contribute to loss of alveolar capillary interface. In addition to the
destruction of the vasculature in the alveoli is caused by fibrosis and
thrombosis which can lead to pulmonary hypertension.
In comparison of protein concentration in pulmonary edema fluid to the
protein concentration in plasma soon after initiation mechanical ventilation
for resp failure has shown a higher ratio in pts with permeability pulm
edema (ALI AND ARDS) than in pts with hydrostatic pulm edema (left heart
failure)
WHAT ARE THE PHYSIOLOGICAL EFFECTS OF
OVERDISTENTION?
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Over distention causes ALI & ARDS and is characterized by:
Acute alveolar inflammation
Neutrophil activation
Surfactant deficiencies
Damage to alveolar capillary membrane (increase permeability
neutrophil and bacterial migration)
Development of proteinaceous pulmonary edema and alveolar
collapse.
WHAT ARE THE PHYSIOLOGICAL EFFECTS OF
OVERDISTENTION?
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Over distention can lead to VILI and result to ARDS resulting to biotrauma
which is the migration of bacteria, neutrophils and pro inflammatory
mediators from the lungs through the porous alveolar capillary membrane.
Addition to this neutrophils are adhering to the injured capillary endothelium
and marginating through the interstitium into the airspace, which is protein
rich edema fluid. In the airspace art alveolar macrophage is secreting
cytokines, interleukin 1,6,8 and 10, tnf alpha (tumor necrosis factor alpha),
which act to stimulate chemotaxis and activate neutrophils. Macrophages
also secrete other cytokines Interleukin 1, 6, and 10. Interleukin 1 can also
stimulate the production of extracellular matrix and fibroblasts. Neutrophils
will release oxidants, proteases, leukotrienes, and other proinflammatory
molecules such as PHF (platelet activating factor). There is also a number of
anti inflammatory mediators also present in alveolar milieu, including
interleukin 1receptor antagonist, soluble tumor necrosis factor receptor,
auto antibodies against interleukin 8 and cytokines such as IL 10 and IL 11.
In addition to this, the influx of protein rich edema fluid into the alveolus has
led to the inactivation of surfactant.
ASSESSMENT TO DETERMINE THE DEGREE OF
LUNG DAMAGE
 Lung injury can be measured by the lung injury
score developed by Murray, which:
 It
incorporates the level of PEEP
 the Pa02/Fi02 ratio
 a chest radiographed score
 lung compliance into a summary score that can be
used to describe how severe of the lung injury is.
ASSESSMENTS TO DETERMINE OVERDISTENTION
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The best determination form overdistention is to look at
the Pressure/Volume loop.
If there is a beaked shape present then this will
indicate that the patient is experiencing overdistention
as a result of decreased lung compliance or a Vt too
high for their current lung mechanics.
ASSESSMENTS TO DETERMINE OVERDISTENTION
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Always thoroughly assess the patients Plateau Pressure
and compare it with previous values - as an increase in
this pressure can be indicative of overdistention.
It is important to insure that this pressure remains
under 30cmH2O to avoid all the potential risks
associated with overdistention.
ASSESSMENTS TO DETERMINE VENT SETTINGS TO
AVOID OVERDISTENTION AND ATELECTRAUMA
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Esophageal pressure (Pes) can be measured to have an
estimate of Transpulmonary Pressure (PL) and its effect on
Pleural Pressure (Ppl) to be able to estimate the impedance
on the lungs resulting from pressures exerted by the chest
wall.
Although this technique is not commonly used, it has been
shown in research studies to be beneficial in treating
patients with decreased compliance and improving the final
outcome for these mechanically ventilated patients. The use
of a ballooned catheter placed inside the esophagus is able
to obtain this information.
Having a good estimate of Ppl will allow for optimal ventilator
settings to be used – such as:
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Optimal Vt to avoid overdistention
Optimal PEEP to avoid atelectrauma from repetitive opening and
collapse of compromised alveoli.
VENTILATOR STRATEGIES TO TREAT LOW LUNG
COMPLIANCE
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Mode Choices:
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Assist Control (AC) is the most likely choice for a patient
experiencing severe respiratory failure.
SIMV may also be used if there is persistent asynchrony with the
patient and ventilator. However it is likely that the patient would
be sedated in order to achieve desired ventilation with AC prior to
moving to this mode.
Breath type Choices:
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Volume Control (VC) is the most commonly used breath type as it
allows for more precise control of Minute Ventilation (Ve) and CO2
clearance.
Pressure Control (PC) may also be used as a strategy to reduce
risk of overdistention as it will not allow for excessive pressures to
be reached and the Vt will be reduced to insure safe pressures.
VENTILATOR STRATEGIES TO TREAT LOW LUNG
COMPLIANCE
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VC
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It is important to remember that low Vt be used with VC
when treating a patient with low lung compliance. The Vt
should be set at 5-8ml/kg (IBW)
Increasing the RR to offset the difference in Vt will allow for
an adequate Ve to be reached. Set at 12-20 bpm
PC
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When using PC it would be worth noting that the pressures
will likely be at the higher end of the acceptable range (2025cmH2O)to insure an sufficient Vt when treating a patient
with low lung compliance.
Again – increasing the RR with PC will also help to meet an
adequate Ve to support CO2 clearance. Set at 12-20 bpm
VENTILATOR STRATEGIES TO TREAT LOW LUNG
COMPLIANCE
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Positive End Expiratory Pressure (PEEP) is used to recruit collapsed alveoli
and reduces the need for high pressure to do such and will prevent
overdistention in alveoli that are already open.
PEEP is able to maintain patency of newly recruited alveoli by preventing
their complete collapse
PEEP is able to transfer pressure to collapsed alveoli by maintaining a small
pressure over that of ambient pressure which will then have the ability to
open collapsed alveoli by passing through the Pores of Kohn and Canals of
Lambert.
PEEP is able to help reduce shear stress associated with the abrupt closing
and opening of the alveoli that often occurs with high pressures.
PEEP is set at a beginning pressure of up to 5cmH20 and may be set as
high as 25cmH20. PEEP Should be set just above the
lower inflection point on the pressure/volume loop to
insure that the alveoli remain patent.
VENTILATOR STRATEGIES TO TREAT LOW LUNG
COMPLIANCE
Oxygen / FiO2 should be maintained as low as
possible to support a PaO2 of >55mmHg and a
SpO2 of >88%.
 Using PEEP should reduce the overall need for
increased FiO2 and possible complications
associated with ROS as a result of long term
exposure to increased FiO2.
 Patients with ARDS will likely require higher FiO2
due to the lung parenchyma that has been
replaced with fibrotic tissue and no longer
participates in gas exchange.
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VENTILATOR STRATEGIES TO TREAT LOW LUNG
COMPLIANCE
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Surfactant replacement for patients with ARDS is being
studied at this time. Preliminary studies may indicate
that a formula different from that used with neonates
may be required to treat adult patients that have
reduced surfactant due to alveolar damage and
dysfunction in the late stages of ARDS.
Early stages of the disease processes related to
decreased lung compliance have been found to have
better responses to the current exogenous surfactant.
FUTURE VENTILATOR STRATEGIES BEING
RESEARCHED AT THIS TIME
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Surfactant Replacement
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Partial Liquid Ventilation
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Pulmonary vasodilator that may help with excessive oxygen
exposure
Extracorporeal Membrane Oxygenation Systems (ECMO)
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Oxygen soluble fluro carbon liquid is used to recruit compromised
alveoli
Nitric Oxide
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To help prevent atelectrauma
Reduces need for positive pressure ventilation
High Frequency Ventilation
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Helps with alveolar recruitment and avoid atelectrauma and
decreases risk of overdistention
WORK CITED
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Cairo, J., & Pilbeam, S. (2012). Pilbeam's mechanical ventilation: Physiological and clinical applications (5th ed.). St. Louis, Mo.: Elsevier Mosby.
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consulting ed.). St. Louis, Mo.: Mosby.
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Hess, D. (2012). Ventilatory Support Involves Trade-Offs. In Respiratory care: Principles and practice (2nd ed.). Sudbury, Mass.: Jones & Bartlett Learning.
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Kacmarek, R., & Dimas, S. (2005). ARDS, SARS and Sepsis. In The essentials of respiratory care (4th ed.). St. Louis, Mo.: Elsevier Mosby.
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Ludwig, M. (2007, September 1). Proteoglycand and Pathophysiology. Retrieved August 19, 2014.
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Mac Intyre, N. (1999, May 1). Mechanical Ventilation Strategies. Retrieved August 14, 2014.
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Piantadosi, C., & Schwartz, D. (2004, September 21). The Acute Respiratory Distress Syndrome. Retrieved August 18, 2014.
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Souza-Fernandes, A. (2006, November 10). Bench-to-bedside review: The role of glycosaminoglycans in respiratory disease. Retrieved August 18, 2014.
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Talmor, D. (2008, November 13). Mechanical Ventilation Guided by Esophageal Pressure in Acute Lung Injury — NEJM. Retrieved August 14, 2014.
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https://v.cdn.vine.co/r/videos/DA00277CC01101978909580591104_1f85d8dab91.3.2.mp4?versionId=SwmNvqVAn90ve4fB8qq5ls75.Jjx4cSV