hello this is Eric strong again from the
Palo Alto Veterans Hospital and Stanford
University this is the ninth lecture in
this series on mechanical ventilation
and today's topic is long protective
ventilation the learning objectives of
this lecture are as follows first to be
familiar with the general types of
ventilator associated lung injury next
to understand the basic principles of
and protocol for long protective
ventilation to be familiar with the
consequences of and contraindications
for permissive hypercapnia and finally
to be familiar with the term open lung
ventilation ventilator associated lung
injury can occur in virtually any lung
disease but most frequently complicates
acute lung injury and a RDS or adult
respiratory distress syndrome four basic
forms of ventilator associated lung
injury have been described
first is Barrow trauma which is a
collection of pathologic processes
caused by excessively high airway
pressures and which is the most
obviously recognizable class of injury
the second class of injury is known as
value trauma in which damage to the lung
occurs as a consequence of excessive
tidal volumes and not from excessive
airway pressures next is a phenomenon
known as bio trauma and finally is
cyclic atelectasis which is occasionally
referred to as italic trauma which
refers to injury occurring as a
consequence of alveoli continuously
collapsing and re expanding over and
over again some authorities do not
include bio trauma under the heading of
ventilator associated lung injury
although I personally find this
distinction to be kind of semantics and
which may not even make sense as baro
trauma and volume and of the same
pathologic phenomenon a somewhat
distinct form of ventilator associated
lung injury is oxygen toxicity this is
when excessive levels of oxygen can lead
to a variety of pathologic
processes in the lungs however these are
generally not clinically significant
until the fraction of inspired oxygen
exceeds 60% which is rarely necessary
the one notable exception is in patients
who are concurrently treated with the
chemotherapeutic bleomycin used in the
treatment of cancers such as Hodgkin's
lymphoma pulmonary oxygen toxicity may
develop at much lower levels of oxygen
in this circumstance I won't discuss
oxygen toxicity any more detail here but
this may be a subject of a future
lecture the most common manifestation of
Barrow trauma is a pneumothorax where
gas leaking from a ruptured alveolus
enters the pleural space where it can
hinder ventilation in severe cases known
as a tension pneumothorax the increased
intrapleural pressure becomes severe
enough to impair venous return and can
precipitate hypotension and even a peña
arrest other less common manifestations
of baro trauma include pneumomediastinum
and subcutaneous emphysema both of which
I will show images of in a moment one
can also get a systemic gas embolism
when the intra alveolar pressure exceeds
pulmonary venous pressure and finally
one can develop cystic lesions in the
lung parenchyma as a relatively
contained form of Barrow trauma here is
an example of a tension pneumothorax on
plain x-ray you can immediately note the
hyper lucency
and absence of lung markings on the left
along with a rightward shift of the
cardiac silhouette trachea and other
mediastinal structures this patient was
likely severely hypotensive here is the
more subtle pneumomediastinum if you
look very closely you can see an outline
of hyper lucency adjacent to the right
mediastinal border the extension of the
hyper lucency
being adjacent to both our borders is
suggestive that this patient has also
developed pneumopericardium these
conditions can be surprisingly
asymptomatic or lead to chest pain
hypotension can theoretically complicate
pneumopericardium though
I have personally never seen this occur
and here is the very dramatic
subcutaneous emphysema positive pressure
through a ruptured alveolus or airway
has forced air to dissect out into the
subcutaneous tissues this can usually be
readily detected on physical exam by the
presence of crepitus when gently pushing
down on the affected area although I
have never specifically read about
complications from examining for
crepitus I can't imagine that pushing
down on the skin to force the trapped
air to further dissect is particularly
good for the patient thus I would advise
against asking every medical student on
the ward to come over to the affected
patient and try to elicit crepitus
themselves although this can certainly
be tempting from time to time the most
significant risk factor for the
development of bio trauma is high
plateau pressure
some sources quote in excessive risk
with pressure above thirty five
centimeters of water while others quote
a threshold of 30 other risk factors
include high minute ventilation a
non-homogenous parenchymal disease such
as a RDS necrotizing lung pathology and
secretion retention even when alveolar
rupture doesn't occur excessive regional
volumes are believed to be damaging to
the lung parenchyma even in the absence
of excessive airway pressures the first
significant evidence that
ventilator-associated lung injury had
mechanisms aside from gross Barrow
trauma came in the 1980s when
researchers conducted rad experiments in
which rats were mechanically ventilated
with their chest walls bound
this allowed relatively independent
control of tidal volumes and airway
pressures the outcome was seen that the
rats with lower tidal volumes and high
airway pressures developed less lung
injury the nose with high tidal volumes
irrespective of their airway pressures
thus the conclusion that it was actually
the high tidal volumes that were the
problem some authors have suggested
based on physiology that what was
commonly referred to as Barrow trauma
and as valued trauma are actually
manifestations of the same phenomenon
a discussion this is beyond the scope of
this talk but I would direct the
interested listener to examiner a review
paper by Gaston Oni and colleagues in
vol 38 of critical care medicine
entitled ventilator induced lung injury
the anatomic and physiological framework
the term bio trauma refers to the
release of pro-inflammatory cytokines in
response to Supra normal intra alveolar
pressures even in the absence of
physical damage to the lung architecture
that might be seen with gross baro
trauma the most clinically relevant
physiologic consequence is pulmonary and
interstitial edema from increased micro
vascular permeability
however systemic circulation of
pro-inflammatory mediators may
contribute to the multi organ failure
that frequently accompanies a RDS here
is a rather dramatic demonstration of
extreme bio trauma on the left our
normal rat lungs in the middle are rat
lungs that have been ventilated at high
airway pressures for five minutes
rare regional atelectasis has developed
and finally on the right are rat lungs
that have been ventilated at high airway
pressures for 20 minutes where the
extreme pulmonary edema is grossly
evident the final class of ventilator
associated lung injury is cyclic
atelectasis this somewhat unconcerned
for Hmong injury is thought to be the
result of non-uniform cyclic expansion
and collapse of alveoli where shear
forces may damage alveoli adjacent to
cyclic collapsing ones in addition a
published theoretical model has also
suggested that the intra alveolar
pressure during alveolar collapse may
increase as much as four times over the
measured airway pressures this has not
been experimentally confirmed however
and the overall importance or even
existence of an electron remains a
little unclear as a consequence of these
forms of ventilator associated lung
injury an approach to mechanical
ventilation generally known as long
protective ventilation has been
developed to help prevent it the
principal feature to all lung protective
protocols is low tidal volumes although
you can imagine patients with
respiratory failure from most causes
with benefits in practice it is used
almost solely in patients with a RDS as
they are the ones at greatest risk for
ventilator associated injury the first
significant trial showing possible
benefit to lung protective ventilation
came in 1998 where 53 patients were
randomized to either conventional
ventilation in which they were given
tidal volumes of 12 milliliters per
kilogram of ideal body weights and the
lowest peep that allowed acceptable
oxygenation or protective ventilation in
which they were given tidal volumes of 6
milliliters per kilogram of ideal body
weights and the peep was set to no less
than the lower inflection point on this
static pressure volume curve what this
amounted to was the conventional group
had high tidal volumes and low peep
while the protective group had low tidal
volumes and high peep here is their most
notable finding as is pretty apparent
the long protective strategy of low
tidal volumes and high peep
appears to have conferred significant
survival advantage though interestingly
there was not a statistically
significant difference in the chance
that any particular patient would
survive the hospital discharge
although these discrepant findings
initially seem counterintuitive it was
probably the result of small study size
and the fact that the patients involved
were extremely sick in addition to the
survival benefit at 28 days there is
also significantly less Barrow trauma
noted in the protective ventilation
group you may have noted that this trial
was not truly controlled in the sense
that two variables were changed between
the two groups subsequent trials have
investigated whether the benefits seen
here was due to the low tidal volumes or
the high peep
let's take a look at the most
historically important of these trials
in 2000 the ARDS net trial randomized
861 patients to a tidal volume of either
12 milliliters per kilogram or 6
milliliters per kilogram of ideal body
weights unlike the last trial the peep
in both groups was set according to
identical predefined tables
in other words only one variable was
being tested here is the primary outcome
the lower title volume group had higher
rates of survival and hospital discharge
here are some specific numbers in the
conventional ventilation group 60.2%
survived a discharged while 69% did so
in the lung protective ventilation group
the average number of ventilator three
days in the first four weeks was 10 in
the conventional group and twelve in the
protective group finally the number of
days without failure of a non pulmonary
organ was 12 in the conventional group
and a 15 in the protective group this
last result also highlights that a RDS
and the subsequent ventilator associated
lung injury is a systemic disorder with
consequences throughout the body on the
basis of the ARDS net trial lung
protective ventilation has become
standard of care for patients in a RDS
unfortunately there is not yet a single
standardized protocol for delivering
lung protective ventilation one of the
more variable aspects of these protocols
is the method for selecting peep peep
can t be selected using a published
table of fio2 and peep combinations to
achieve an arterial oxygen tension or
peripheral Oh to saturation within the
target range this was what was done in
the arch net trial peep can also be set
at the highest value that allows the
plateau pressure to remain under 30 the
peep can be adjusted to provide the
highest possible respiratory system
compliance and finally peep can be set
slightly higher than the lower
inflection point on the pressure-volume
curve there are probably additional
methods with which I'm unfamiliar and
the theories behind each of these four
options are beyond the scope of this
lecture series in practice use of a
published table is probably the most
common method employed here is what such
a table looks like this is the specific
one taken from the ARDS net paper for
example if a patient requires an fio2 of
80% in order to maintain an oxygenation
above an arbitrary target of 92% the
collision would set the peep to 10
centimeters of water one concept which
is integral to lung protective
ventilation is that of permissive
hypercapnia the first thing to realize
about this is that permissive
hypercapnia is itself not a strategy or
goal per se but rather a common
consequence of alveolar ventilation in
patients receiving lung protective
ventilation the arterial co2 is allowed
to climb with the resulting drop in
arterial pH there are no universal or
well-defined thresholds which the
patient's P co2 and pH should be
prohibited from exceeding there are a
number of important contraindications to
permissive hypercapnia hypercapnia
induces three valve a zone
intracranial pressure hypercapnia can
induce systemic basal dilation which may
worsen hypotension it may increase
pulmonary vascular resistance further
worsening right ventricular dysfunction
and finally a combined respiratory
acidosis and severe metabolic acidosis
may lead to an unacceptably low arterial
ph which can inhibit numerous processes
at the cellular level you may come
across the term open lung ventilation
while in the ICU so it's important to
know what this is referring to in the
most general sense open lung ventilation
is a modification of lung protective
ventilation that combines low tidal
volumes to protect against value trauma
and high peep to protect against cyclic
atelectasis it may or may not also
utilize recruitment maneuvers
unfortunately trials to date that have
shown potential benefit have had serious
methodological flaws and therefore this
is not currently considered standard
practice for any group of patients
however I suspect that in another 5 or
10 years the evidence will be sufficient
to recommend this strategy for a subset
of patients with a RDS specifically
those with refractory hypoxia
I'm going to end this lecture by running
through one protocol offer ventilating
patients in a RDS that utilizes the
basic principles of lung protective
ventilation as mentioned before there is
no one standardized protocol but they
are all mostly quite similar this
particular one was taken from a 2011
article on respiratory care for those
interested the specific citation is
there at the bottom step 1 choose the
ventilation mode typically either assist
control or simv step 2 start with a
total volume of 6 milliliters per
kilogram of ideal body weights
step 3 start with peep at greater than
or equal to 8 centimeters of water step
4
set the ite ratio at 1 to 2 step 5
measure and record the plateau pressure
every 4 hours and after any changes in
tidal volume or peep if the plateau
pressure is greater than 30 lower the
tidal volume in 1 milliliter per
kilogram increments until either the
plateau pressure is equal to or less
than 30 or until a minimum of 4
milliliters per kilogram of ideal body
weight is reached if the total volume is
less than 6 milliliters per kilogram and
the plateau pressure is less than 25
increase the total volume by 1 bolita
per kilogram increments to a maximum of
6 adjust the respiratory rate or tidal
volume according to pH goals if the pH
is less than 7 point 3-0 consider
increasing the respiratory rate to as
high as 35 breaths per minute while
monitoring for the development of
auto-peep if the pH is less than 7 point
1 5 and the respiratory rate is greater
than or equal to 35 breaths per minute
consider increasing the tidal volume and
suspending the plateau pressure limit
step 7 adjust the IDE ratio to avoid
auto-peep and diss synchrony both
auto-peep in the synchrony will be
discussed at a future lecture
step 8 adjust the peep to maximize
alveolar recruitment
while avoiding over distension by
increasing or decreasing peep in
increments of 2 to 3 centimeters of
water to a goal either that gives the
best overall respiratory system
compliance or according to tables a
preferred peep for a particular fio2
such as that shown earlier in this
lecture
finally step 9 adjust the fio2 to
achieve an o2 set of 88 to 95 percent on
arterial oxygen tension of 55 to 80
millimeters of mercury with some room to
adjust those goals depending upon the
clinical situation I hope you found this
lecture on long protective ventilation
to be both interesting and useful please
continue to lecture 10 on the
physiologic consequences of mechanical
ventilation
you