Current Anaesthesia & Critical Care 21 (2010) 244e249

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Current Anaesthesia & Critical Care

journal homepage: www.elsevier.com/locate/cacc

FOCUS ON: MECHANICAL VENTILATION IN THE OR

Treatment of anesthesia-induced lung collapse with lung recruitment maneuvers

Gerardo Tusman a, *, Javier F. Belda b
a
Department of Anesthesiology, Hospital Privado de Comunidad, 7600 Mar del Plata, Argentina
b
Department of Anesthesiology, Hospital Universitario, Valencia, Spain

s u m m a r y
Keywords: General anesthesia causes atelectasis and airway closure in dependent areas of the lung. Both kinds of
Atelectasis collapse induce a deterioration of gas exchange characterized by a decrease in arterial oxygenation and
Lung recruitment
an increase in dead space. The severity of this lung dysfunction is proportional to the amount of collapsed
Oxygenation
Dead space
tissue that depends on anesthesia, surgical and patient’s factors.
Airway closure Lung collapse can be partially prevented by decreasing FiO2 and/or by applying CPAP during the
induction of anesthesia. However, only lung recruitment maneuvers can resolve atelectasis completely.
These recruitment maneuvers are ventilatory strategies aimed to restore the normal aeration of the
lungs. The maneuvers consist in a brief and controlled increase in airway pressure to open up those
pulmonary areas with collapse. Afterward, the lungs are ventilated with a protective strategy setting
keeping the lungs open in time with enough positive-end expiratory pressure and low driving pressure.
This article describes the physiological and clinical background of lung recruitment maneuvers applied
during the intra-operative period.
Ó 2010 Elsevier Ltd. All rights reserved.

1. Introduction
Anesthesia-induced lung collapse is a well known entity
observed in approximately 90% of patients undergoing general
anesthesia. This collapse begins at the induction of anesthesia and
persists several hours after the end of the surgery. Such lung
collapse is not related to age, gender, anesthetic agents or muscle
relaxant drugs.1e3 Lung collapse can affect the whole acini (atel-
ectasis), the respiratory bronchioli (airway closure) and/or the
pulmonary capillaries.1e3 The functional lose of lung units makes
ventilation and perfusion more heterogeneously distributed within
the pulmonary parenchyma.4 The obvious consequence is an
impairment in gas exchange due to local dysfunction of the alve-
olar-capillary membrane. The ventilation/perfusion (V/Q) mis-
match observed is due to a mix of shunt and increasing numbers of
low V/Q units in dependent zones of the lungs, and dead space and
an increasing number of high V/Q units in the more ventral zones.
The mechanism of lung collapse can be multi-factorial. It can be
related to the loss of respiratory muscle tone induced by a central
effect of anesthetic drugs, to a displacement of blood outside the
thorax, to surfactant inactivation by anesthetics or to a change in
the shape of the thorax among many other factors.5e7 There is
* Corresponding author. Tel.: þ54 223 4990074; fax: þ54 223 4990099.
E-mail address: gtusman@hotmail.com (G. Tusman).
a strong evidence that the key factor involved in origin of the lung
collapse is the diaphragmatic dysfunction observed during anes-
thesia.5 It has been postulated that abdominal pressure is trans-
mitted into the thoracic cage through this dysfunctional diaphragm
and compresses the pulmonary parenchyma in the more depen-
dent areas. These are the lung zones with the lowest trans-
pulmonary pressure (Ptp) and thus, are predisposed to collapse at
the end of expiration. This kind of lung collapse is called
compressive atelectasis.1e3
Other important factors related to lung collapse are the high
FiO2 used during the anesthesia induction.8 High FiO2 induces
atelectasis by reabsorption of O2 in pulmonary areas with low V/Q;
because the rate of O2 diffusion into capillary blood is greater than
the amount of ventilation of those poorly ventilated units. The
consequence is a progressive loss of volume within these pulmo-
nary units until a complete collapse takes place. Reabsorption
atelectasis mainly develops in patients with a certain amount of
low V/Q areas like smokers or the elderly.9 However, as anesthesia
reduces functional residual capacity (FRC) and impairs ventilation
in some dependent zones of the lung in almost all patients, reab-
sorption atelectasis can be observed even in young patients with
healthy lungs.10.
Lung collapse is associated with negative clinical consequences
and complications that influence patient’s outcome. It is not easy
to make a correlation between lung collapse and later respiratory
complications because the diagnosis of atelectasis at the bedside

0953-7112/$ e see front matter Ó 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cacc.2010.07.007
 G. Tusman, J.F. Belda / Current Anaesthesia & Critical Care 21 (2010) 244e249
is not simple. The gold-standard CT scan shows that approxi-
mately 90% of patients develop atelectasis during anesthesia,
which is invisible to simple chest X-ray.1 Therefore, due to the
complexity in diagnosis of lung collapse at the bedside with
standard technologies, the link between atelectasis, respiratory
complications and patient’s outcome is impossible to determine
with accuracy.
The most important consequences of lung collapse are those
associated with deterioration in gas exchange (hypoxemia and
hypercapnia)11 and the detrimental effect to arterial O2 content
and O2 delivery to body tissues. This is the reason why a FiO2
higher than 21% is needed during anesthesia and also in the
immediate post-operative period. The higher the venous
admixture induced by lung collapse, the higher the FiO2 should
be in the peri-operative period to avoid hypoxemia. In specific
groups of patients (morbidly obese or critically ill of any cause)
and surgery (cardiac, thoracic or laparoscopy) hypoxemia can be
observed even when using high FiO2. Increasing FiO2 is effective
for treating the “symptom” but not the patho-physiological
mechanisms behind hypoxemia and hypercapnia. Moreover,
increasing FiO2 promotes reabsorption atelectasis and can8,9,12
impair the V/Q ratio after surgery.
Beyond the known deleterious and dangerous effect of acute
hypoxemia and/or hypercapnia, the persistence of low arterial O2
content and delivery to the tissues is associated to organ failure
caused by a local dysequilibrium between O2 supplied and
demand. Low urine output rate and a predisposition to bacterial
translocation in the gut are both clinical examples that are said to
be associated with inappropriate delivery of O2 to body tissues. In
the post-operative period, a low delivery of O2 was associated to
wound infection, nausea/vomiting and acute13e15 myocardial
ischemia.
Another important complication of lung collapse is the lung
injury induced by mechanical ventilation (VILI).16 There is
increasing evidences showing that positive-pressure ventilation
induces pulmonary injury when lungs are partially17e20collapsed,
not only in sick but also in “healthy” lungs. Lung collapse induced
lung16,20injury can be due to two main mechanisms:
1) One of them is the strain and stress that normally aerated areas
suffer when they receive an excess of volume and positive-
pressure. As the collapsed areas cannot be totally recruited
using a standard ventilatory setting, the inspiratory flow goes
to normal ventilated areas. These are zones of the lungs placed
more ventrally related to the gravitational plane.
2) The other mechanism is the tidal recruitment; i.e. a cycling
inspiratory recruitment followed by an expiratory collapse of
some lung units induced by a mechanical breath. This kind of
mechanism takes place in those pulmonary zones where their
opening (plateau pressure) and closing (PEEP) pressures fall
within the tidal range. The involved parenchyma suffers
a stress with shearing forces on bronchiolar/alveolar walls
calculated as high as 100 cm H2O.21
Experimental and clinical studies revealed a progressive
pulmonary immune18e20dysfunction in healthy lungs during
anesthesia and surgery. An injurious ventilatory pattern with high
VT and low PEEP has been associated with increased cytokine
production which was19,22 observed in BAL samples. This relation
between the inflammatory response and the size of VT is related to
mortality in acute lung injury; where a decrement in VT to 6 mL/kg
is associated with an increase in survival rate.23 These conse-
quences and complications of lung collapse in “healthy” lungs call
for a solution beyond the cosmetic effect of increasing FiO2 in the
peri-operative period.
245
2. Mechanism of lung collapse and recruitment
Lung collapse as well as lung recruitment are pressure-dependent
phenomena because the main factor responsible for acini integrity
during mechanical ventilation is trans-pulmonary pressure (Ptp)
i.e. the pressure differences between airways and pleural space.
Gravity transforms pleural pressure from negative to positive in
dependent zones of the lungs due to the weight of pulmonary
tissue within the thorax. Assuming that the pressure in the airways
is homogeneously distributed within lungs, the vertical pressure
gradient into the pleural space makes Ptp lower in dependent
compared to the non-dependent lung areas. During anesthesia this
vertical gradient in pleural pressure is exaggerated because the
diaphragm becomes dysfunctional and it is displaced upward by
the abdominal pressure, compressing the lungs in the lowermost
zones.1,5
Each lung unit has a closing pressure or Ptp threshold when this
unit begins to collapse and an opening pressure or Ptp threshold
when the collapsed unit becomes aerated again. The closing pres-
sure is reached at the end of expiration because the Ptp is the
lowest airway pressure possible during this part of the mechanical
respiratory cycle. Contrarily, the opening pressure is reached at the
end of inspiration because this pressure is the highest.
YoungeLaplace equation explains why a semi-spherical shape-
like alveolus needs high pressure to open up but lower pressure to
keep it open, according to the expression:
P ¼ 2T=r
where P is the airway pressure, T is the surface tension and r the
radius of the lung unit. The P necessary to open up and to keep
a lung unit in the “open” state is inversely proportional to its radius.
This means that the radius of a collapsed unit is “short” and needs
high pressure during inspiration to open up. In an opposite fashion,
an open unit with a “large” radius (at normal FRC) needs a lower
airway pressure at the end of expiration to avoid its collapse.
In summary, we can say that lung recruitment is an inspiratory
process that is performed by the plateau pressure while lung
collapse is an expiratory one, which can be avoided by increasing
the end-expiratory pressure beyond the closing pressure of
dependent zones of the lungs.
3. Treatment of lung collapse
Lung collapse can be partially prevented by two main strategies:
one of them is to use continuous positive airway pressure (CPAP)
during the anesthesia induction.24 The main mechanism of CPAP is
to avoid the fall in FRC by keeping airway pressure higher than the
lung’s closing pressure. It has been demonstrated in patients that
the amount of atelectasis decreases when CPAP is applied during
induction of anesthesia. The problem is that CPAP is useless in
apneic patients when they fall sleep and that some atelectasis can
appear quickly when CPAP is discontinued during the laryngoscopy.
The second strategy to prevent atelectasis is to reduce FiO2
during induction.8,25,26 It is well known that low FiO2 decreases
reabsorption atelectasis in lungs with reduced FRC, but at the cost
of reducing the available safe time of apnea during laryngoscopy.
This is for surely a dangerous technique because difficult ventila-
tion and/or intubation cannot be predicted with accuracy in all
patients. Both of these “preventive” strategies could have a syner-
gistic, although partial effect on the genesis of lung collapse.
Lung recruitment maneuvers are ventilatory strategies in which
the main goal is to recover collapsed areas of the lungs. These
maneuvers are based in the premise described by Lachmann27
a few decades ago, taking into account the YoungeLaplace
246 G. Tusman, J.F. Belda / Current Anaesthesia & Critical Care 21 (2010) 244e249
equation: the lungs can be opened by applying high pressures in
the airways and then, keep them open in time by using enough
PEEP. There are basically two types of recruitment maneuvers:
, The CPAP maneuvers, which consist of the application of high
continuous positive-pressure in the airways for a few seconds
(10e40 s) in a breathless patient.28
, The cycling maneuvers, where airway pressure is increased in
a step-wise fashion during normal respiratory cycles.29
The alveolar recruitment strategy (ARS) is a kind of cycling
maneuver that was originally conceived to solve lung collapse in
the intra-operative period.29 The ARS consists of a controlled and
step-wise increment and decrement of airway pressures using
a fixed setting in pressure control ventilation mode (driving pres-
sure of 15 cm H2O, a respiratory rate between 10 and 15 bpm, I:E 1:1
and FiO2 of 1). The ARS is constituted by three well defined phases
(Fig. 1) that can be conducted by the algorithm described in Fig. 2.
The rationale of each ARS phase is described in detail as follow.
3.1. Hemodynamic pre-conditioning phase
One main problem of positive-pressure ventilation is the
potential of hemodynamic instability in patients who are hypo-
volemic. High airway pressure decreases right and left ventricle
preload in hypovolemic patients without a direct effect on heart
contractility.30 The consequence is a decrease in cardiac output and
in systemic arterial pressure. These hemodynamic events are
treated by adequate preload replacement with i.v. fluids.
Patients with occult hypovolemia (i.e. an unsuspected hypo-
volemic condition) are a clinical challenge for anesthesiologists
because the application of PEEP can induce episodes of hemody-
namic instability in patients. For this reason, we include a simple
test at the beginning of the ARS called hemodynamic “pre-condi-
tioning” phase. This test is part of the ARS and checks the hemo-
dynamic response in presence of 10 and/or 15 cm H2O of PEEP
before the highest airway pressures are reached during the
recruitment phase. In our experience, these are adequate levels of
PEEP at which an occult hypovolemia starts to be clinically mani-
fest. The maneuver is interrupted if mean arterial pressure, heart
rate and cardiac output (if available) change more than 15e20%
from baseline or if mean arterial pressure fall below 55 mm Hg. If
these cut-off values are observed, PEEP is reduced to a known safer
level. Such occult hypovolemia is treated by i.v. infusion of crys-
talloids/colloids before the maneuver is reestablished. The amount
of volume expansion will depend on the degree of hypovolemia but
3e5 mL/kg of crystalloids/colloids should be enough in most cases.
Fig. 1. Scheme of the alveolar recruitment strategy. The ARS is performed in pressure control ventilation with a driving pressure (plateau e PEEP) of 15 cm H2O. Each rectangle
represents a tidal volume. PEEP is increased in steps of 5 cm H2O during the hemodynamic pre-conditioning phase. Then, PEEP and driving pressure are increasing to 20 cm H2O to
reach the opening pressure of the lungs. After 10 breaths a complete open lung state is achieved. The PEEP titration trial starts reducing driving pressure to 15 cm H2O and then
reducing PEEP in steps of 2 cm H2O, from 20 cm H2O until the closing pressure is found. Later on, a new recruitment maneuver is performed and the patient is then ventilated with
a protective setting (low VT) but at the established OL-PEEP.
The pre-conditioning phase is part of the 5 cm H2O step-wise
increment in PEEP, from 0 to 20 cm H2O (Fig. 1). Each PEEP step is
maintained for at least 5 breaths. Clinicians should spend a few
minutes at a PEEP of 10 and/or 15 cm H2O to test the hemodynamic
response described above. Then the maneuver can continue. The
rationale of this step-wise increment in airway pressure is to
achieve progressive recruitment with the plateau pressure keeping
these new recruited areas open with PEEP. This strategy decreases
the strain and stress on the lung parenchyma during the maneuver
because the increased pressure and volume are distributed over
a progressively larger tissue surface. In our experience this step-
wise increment in PEEP also gives time for hemodynamic adapta-
tion. The scenario is different for CPAP recruitment maneuvers,
which produce a large and abrupt airway pressure gradient during
the maneuver and also a high rate of hemodynamic instability.
3.2. Recruitment phase
It is important to stand out that the recruitment effect is
observed along the ascending limb of the PeV curve of the lungs.31
This is why a progressive (although incomplete) recruitment effect
is accomplished any time plateau pressure is increased by each
PEEP step during the hemodynamic pre-conditioning phase.
However, the opening pressure of the entire lungs is around
40 cm H2O of alveolar pressure according to the findings of Rothen
et al.28 Such alveolar pressure is the one that will open the “last”
collapsed areas placed in the very dependent lung. This is the
reason why we called this part of the ARS “recruitment phase”
despite a considerable amount of pulmonary tissue become nor-
mally aerated during the previous phase. Once patient’s hemody-
namics have been tested and stabilized, the recruitment phase
consists in an increment in both, driving pressure to 20 cm H2O and
PEEP to 20 cm H2O to reach the opening pressure at 40 cm H2O of
plateau pressure (Fig. 1). A driving pressure of 20 cm H2O is
commonly related to a safe tidal volume (VT) 8 mL/kg. In those
patients with high respiratory compliance (Crs), driving pressure
should keep at 15 cm H2O to avoid larger VT. In this case, PEEP
should be increased to 25 cm H2O with the intention to reach the
same target opening pressure while keeping VT within a normal
range. Ten breaths maintaining this setting are enough to open up
the whole lung in healthy patients.
3.3. Decremental PEEP titration phase
From an academic point of view, this phase would identify the
lung’s closing pressure or the PEEP value at which lungs start to
collapse again in dependent zones. Thus, the PEEP titration phase
 G. Tusman, J.F. Belda / Current Anaesthesia & Critical Care 21 (2010) 244e249
Fig. 2. Algorithm for the alveolar recruitment strategy.
consists in a progressive decrease of PEEP in steps of 2 cm H2O
every few minutes. This closing pressure can be determined by
observing atelectasis in lung images (CT scan, MRI, electrical
impedance tomography), by a sudden fall in PaO2, by a sudden
increase in dead space or by obtaining non-invasive32,37 informa-
tion from Crs or expired CO2 kinetics (see below).32e36 Once this
pressure has been determined, another recruitment phase is
applied to recover any lung tissue that might have collapsed during
the PEEP titration process. Baseline ventilation is then reassumed
with a protective strategy (low VT) but setting a PEEP value a few
cm H2O above the closing pressure. This level of PEEP that keeps the
lung open in time after the recruitment phase is called the “open-
lung” PEEP (OL-PEEP).36
The setting of OL-PEEP is a hot topic in mechanical ventilation
because the methods used to detect such level of PEEP are invasive
or technically impossible for use at the bedside. In the operating
room we commonly apply pre-defined values not only for closing
but also for opening pressures. These target values were derived
from physiologic studies performed in anesthetized patients. The
opening pressure of normal lungs was assumed to be around
40 cm H2O while the closing pressure was expected to be
247
somewhere between 5 and 15 cm H2O depending on the clinical
circumstances.28,37
In theory, the closing pressure (PEEP) must be determined in
each patient at the bedside in order to personalize the recruitment
maneuver; avoiding excessive or deficient airway pressure. To solve
the problem, our group has described a non-invasive method for
monitoring the OL-PEEP that can be easily applied at the bedside.
This kind of monitoring has been validated in an experimental
model of acute lung injury32 and works very well in anesthetized
patients (personal unpublished data). The method consists in the
analysis of the behavior of dynamic compliance Crs and airway
resistance (Raw) and CO2 elimination per breath (VTCO2,br) during
the PEEP titration phase (Fig. 3). The “open-lung” condition is found
immediately before the highest Crs was reached in an animal
model of ALI.32 In our experience in the operating room, the OL-
PEEP coincides with the highest Crs value and the lowest Raw
during the PEEP titration trial. These findings make sense from the
physiological point of view taking into account the relationship of
Crs and Raw to lung volume: Crs is highest and Raw is lowest at
normal FRC and the opposite is found at total lung capacity and at
volumes close to the residual volume (Fig. 3).
248 G. Tusman, J.F. Belda / Current Anaesthesia & Critical Care 21 (2010) 244e249
Fig. 3. Determination of OL-PEEP during the PEEP titration phase of the ARS. The PEEP
titration phase in an anesthetized patient is shown. Each level of PEEP was maintained
for 2 min and the studied variables are presented as mean  SD (n ¼ 30 breaths per
each PEEP step). Dynamic respiratory compliance (Crs), airway resistance (Raw) and
the elimination of CO2 per breath (VTCO2,br) were recorded non-invasively and on-line
with proper sensors placed at the airway opening. The open lung PEEP (OL-PEEP) and
the lung’s closing pressure are marked by arrows. The grey area shows the safest range
of PEEP in this particular patient without causing lung overdistension or collapse.
Expired CO2 elimination per breath (VTCO2,br) is measured in
real time and on a breath-by-breath basis using volumetric cap-
nography. VTCO2,br reaches the maximum value when the lungs are
open because in this condition V/Q is optimal and this way gas
exchange area is the largest for a particular pulmonary condition. If
the lungs become overdistended, VTCO2,br decreases because high
alveolar pressure compresses a considerable amount of pulmonary
capillaries. If the lungs become collapsed, VTCO2,br also decreases
because the CO2 exchange area is reduced by atelectasis and/or
airway closure (Fig. 3).
Fig. 3 shows an example of the PEEP titration phase in a patient
undergoing a laparoscopic prostatectomy in Trendelemburg posi-
tioning. The OL-PEEP was found at 14 cm H2O according to the
highest Crs and VTCO2,br and the lowest Raw. The closing pressure
was found at 10 cm H2O of PEEP when those variables change for
more than 10% of their local maximum (Crs and VTCO2,br) or
minimum (Raw) values. Therefore, the safest range of PEEP was
between 10 and 16 cm H2O (although the best pulmonary condition
was found at the OL-PEEP). Values of PEEP outside this range would
make the lungs prone to unnecessary collapse or overdistension.
4. Clinical results, indications and contraindications of lung
recruitment maneuvers
Lung recruitment maneuvers during the intra-operative period
were tested extensively over the last few years. They have been
applied successfully in patients of different ages9,29,33,34,37e42 and in
different types of surgery. The main clinical response to recruit-
ment maneuvers is related to the improvement in lung function as
observed through better gas exchange and ventilatory efficacy.
These results are the consequence of the treatment of low venti-
lated zones (airway closure) and shunt areas (atelectasis) by
applying the maneuver. These clinical studies, and also experi-
mental data, have demonstrated that recruitment maneuvers are
safe for patients.43
As the respiratory compliance and airway resistance are
improved after recruitment, the likelihood of overdistending
normal lung areas is lowered because ventilation is distributed
more homogeneously within the pulmonary parenchyma. This
effect is supported by the decrease in dead space observed after
recruitment maneuvers, which is telling us that pulmonary capil-
laries are not compressed by alveolar pressure.38,39
As 90% of patients undergoing general anesthesia develop lung
collapse,1 lung recruitment can be applied in almost all anes-
thetized patient. The remaining 10% are day-case and/or minor
surgery in young, healthy and slim patients in which there is a small
amount (if any) of lung collapse. In these few patients, recruitment
maneuvers would not be indicated. In contrast, moderate or major
surgery in patients ASA  2 will improve their clinical condition
with lung recruitment maneuvers.
The ARS should be performed once after the induction of the
anesthesia to get the clinical benefit during the entire period of the
surgery. Whenever the airway is opened to the atmosphere (i.e.
disconnection of the endotracheal tube from the anesthetic circuit)
a new recruitment maneuver should be performed because lung
collapse takes place in seconds. Thus, it is imperative to avoid
circuit disconnection during surgery until patients are extubated at
the end of the anesthesia.
Recruitment maneuvers are contraindicated in those patients in
which airway are not sealed by a cuffed endotracheal tube (laryngeal
or facial mask). In hemodynamically unstable patients of any origin,
especially those who are hypovolemic, lung recruitment maneuvers
are contraindicated until a stable state is reached following adequate
treatment. Patients with bronchospasm, bronchial fistula, pneu-
mothorax or high intracranial pressure are also unsuitable.
5. Conclusions
Lung collapse during general anesthesia is a well described
entity that explains the impairment in lung function and some of
the respiratory complications observed in the peri-operative
period. Such collapse can be easily resolved by a lung recruitment
maneuvers. These maneuvers normalize lung function which is
proven by showing an increment in arterial oxygenation and
respiratory compliance and by a decrease in dead space. Ventilator
induced lung injury is theoretically minimized or avoided by lung
recruitment maneuvers because a protective ventilatory setting can
be applied in a normal FRC lungs, far away from the stress and
strain that mechanical ventilation causes in collapsed lungs.
Conflict of interest statement
None.
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