Pulmonary Atelectasis: A Pathogenic Perioperative Entity

REVIEW ARTICLE
David C. Warltier, M.D., Ph.D., Editor

Anesthesiology 2005; 102:83854 2005 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.
Pulmonary Atelectasis
A Pathogenic Perioperative Entity
Michelle Duggan, M.B.,* Brian P. Kavanagh, M.B.
This article has been selected for the Anesthesiology
CME Program. After reading the article, go to http://
www.asahq.org/journal-cme to take the test and apply for
Category 1 credit. Complete instructions may be found in
the CME section at the back of this issue.
Atelectasis occurs in the dependent parts of the lungs of most
patients who are anesthetized. Development of atelectasis is
associated with decreased lung compliance, impairment of ox-
ygenation, increased pulmonary vascular resistance, and devel-
opment of lung injury. The adverse effects of atelectasis persist
into the postoperative period and can impact patient recovery.
This review article focuses on the causes, nature, and diagnosis
of atelectasis. The authors discuss the effects and implications
of atelectasis in the perioperative period and illustrate how
preventive measures may impact outcome. In addition, they
examine the impact of atelectasis and its prevention in acute
lung injury.
IT has been known for decades that in patients with
previously normal lungs, general anesthesia is associated
with impaired oxygenation.
1
Pulmonary atelectasis was
suspected as the major cause, based on the observation
of a successive decrease in lung compliance and the
partial pressure of arterial oxygen (PaO
2
), both of which
returned toward normal after deep inations of the
lung.
2
Bendixen et al.
2
thus demonstrated their concept
of a progressive alveolar collapse during general anes-
thesia with mechanical ventilation. It is now known that
atelectasis occurs in the most dependent parts of the
lung of 90% of patients who are anesthetized and plays
an important role in gas exchange abnormalities and
reduced static compliance associated with acute lung
injury (ALI).
3
This article reviews the causes, nature, and
consequences of atelectasis, focusing on the role of
atelectasis in development of perioperative morbidity,
and illustrates how preventive measures could impact
perioperative health. In addition, we discuss the impact
of atelectasis and of its prevention in ALI.
Etiology and Pathogenesis of Atelectasis
Three sets of mechanisms have been proposed that
may cause or contribute to the development of atelecta-
sis,
4
including compression of lung tissue, absorption of
alveolar air, and impairment of surfactant function. This
section describes these three underlying physiologic
causes of atelectasis; clinical factors that can modulate
the development of atelectasis are described in a subse-
quent section.
Compression Atelectasis
Compression atelectasis occurs when the transmural
pressure distending the alveolus is reduced to a level that
allows the alveolus to collapse. The diaphragm normally
separates the intrathoracic and abdominal cavities and,
when stimulated, permits differential pressures in the
abdomen and chest. After induction of anesthesia, the
diaphragm is relaxed and displaced cephalad and is
therefore less effective in maintaining distinct pressures
in the two cavities. Specically, the pleural pressure
increases to the greatest extent in the dependent lung
regions (g. 1) and can compress the adjacent lung
tissue. This is termed compression atelectasis.
5
Several lines of evidence support a role of the dia-
phragm in this setting. Froese and Bryan
6
used cinera-
diography to demonstrate a cephalad shift of the dia-
phragm during anesthesia and spontaneous breathing,
which did not progress after muscle relaxation. How-
ever, a difference in the pattern of diaphragmatic move-
ment was noted. In supine patients, during spontaneous
breathing, the lower, dependent portion of the dia-
phragm moved the most, whereas with muscle paralysis,
the upper, nondependent part showed the largest dis-
placement. Two distinctly different patterns of diaphrag-
matic displacement were seen from the same new func-
* Clinical Research Fellow, Associate Professor, Departments of Anesthesia
and Critical Care Medicine and the Lung Biology Program, Hospital for Sick
Children. Department of Anesthesia and the Interdepartmental Division of Crit-
ical Care Medicine, University of Toronto.
Received from the Departments of Anesthesia and Critical Care Medicine and
the Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada,
and the Department of Anesthesia and the Interdepartmental Division of Critical
Care Medicine, University of Toronto, Toronto, Ontario, Canada. Submitted for
publication December 30, 2003. Accepted for publication August 20, 2004.
Supported by the Canadian Institutes of Health Research, Ottawa, Ontario,
Canada, and a Premiers Research Excellence Award from the Ontario Ministry of
Science and Technology, Toronto, Ontario, Canada.
Address reprint requests to Dr. Kavanagh: Department of Critical Care Medi-
cine, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Can-
ada M5G 1X8. Address electronic mail to: [email protected].
Anesthesiology, V 102, No 4, Apr 2005 838
tional residual capacity (FRC) position. In an
anesthetized patient breathing spontaneously, the active
tension in the diaphragm is capable of overcoming the
weight of the abdominal contents, and the diaphragm
moves the most in the lower, dependent portion (be-
cause the lower or posterior diaphragm is stretched
higher into the chest, it has the smallest radius of curva-
ture and therefore contracts most effectively). In addi-
tion, the diaphragm is thicker posteriorly than anteriorly,
and this may account for the disproportionate move-
ment.
7
During paralysis and positive-pressure ventila-
tion, the passive diaphragm is displaced by the positive
pressure preferentially in the upper, nondependent por-
tion (where there is least impedance to diaphragmatic
movement). Subsequent studies conrmed these nd-
ings and, in addition, documented a reduction in the
transverse area of the chest.
8
Using an advanced com-
puted tomography (CT) scanner, Krayer et al.
9
demon-
strated a reduced thoracic cross-sectional area in anes-
thetized subjects but had more variable results regarding
shape and position of the diaphragm; some subjects
showed a cranial shift of the diaphragm, but in other
subjects, part of the diaphragm was unaffected or even
moved caudally. Other investigators have also shown
results inconsistent with the classic model of regional
ventilation
10
; nevertheless, it can be concluded that FRC
is reduced in the anesthetized subject, whether caused
by loss of traction of the chest wall or compression of
the lung. Loss of intercostal muscle function may also
contribute to reduced FRC during anesthesia. Inhalation
Fig. 1. (A and B) In normal lungs (A), the
alveolar ination and vascular perfusion
are associated with low stress and are not
injurious. Two separate barriers form the
alveolarcapillary barrier, the microvas-
cular endothelium, and the alveolar epi-
thelium. In contrast, with atelectasis (B),
alveolar ination and deation may be
heterogeneous, and the resulting airway
stress causes epithelial injury. Because
the blood vessels are compressed, perfu-
sion may be traumatic because of ow-
induced disruption of the microvascular
endothelium. Both epithelial and endo-
thelial injury may initiate or propagate
lung injury. This gure depicts the ad-
vanced stage of lung injury caused by at-
electasis. The initial injury is simple col-
lapse of alveoli. However, with time, this
leads to an inammatory reaction. As the
derecruited lungs cause epithelial injury
and loss of epithelial integrity, both type
I and type II alveolar cells are damaged.
Injury to type II cells disrupts normal
epithelial uid transport, impairing the
removal of edema uid from the alveolar
space. In addition to collapse, dere-
cruited lungs also become uid lled.
Neutrophils adhere to the injured capil-
lary endothelium and migrate through
the interstitium into the alveolar air-
space. In the airspace, alveolar macro-
phages secrete cytokines, interleukin
(IL)-1, -6, -8, and -10, and tumor necrosis
factor (TNF)-, which act locally to stim-
ulate chemotaxis and activate neutro-
phils. IL-1 can also stimulate the produc-
tion of extracellular matrix by
broblasts. Neutrophils can release oxi-
dants, proteases, leukotrienes, and other
proinammatory molecules, such as
platelet-activating factor (PAF). MIF
macrophage inhibitory factor.
839 ATELECTASIS AND LUNG INJURY
Anesthesiology, V 102, No 4, Apr 2005
agents decrease intercostal muscle activity, particularly
in children.
11
Hedenstierna et al.
8
also noted an additional source of
lung compression in that there was a net shift of central
blood volume from the thorax, which seemed to pool in
the abdomen, resulting in additional dependent pressure
arising from the abdomen and acting on the diaphragm.
Finally, the displacement of the diaphragm has been
studied under dynamic conditions, whereby increases in
diaphragm tension through phrenic nerve stimulation
have been shown to reduce the amount of atelectasis at
isovolumic conditions in anesthetized patients.
12
Therefore, compression atelectasis occurs during gen-
eral anesthesia and is caused by chest geometry, overall
cephalad diaphragm displacement, differential regional
diaphragmatic changes, shift of thoracic central vascular
blood into the abdomen, and altered diaphragmatic
dynamics.
Gas Resorption
Resorption atelectasissometimes called gas atelecta-
sis
4
can occur by two mechanisms. After complete
airway occlusion, a pocket of trapped gas is created in
the lung unit distal to the obstruction. Because gas up-
take by the blood continues and gas inow is prevented
by blocked airways, the gas pocket collapses.
13
Under
these conditions, the rate of absorption of gas from an
unventilated lung area increases with elevation of the
fraction of inspired oxygen (FIO
2
).
14
A somewhat different mechanism explains absorption
atelectasis in the absence of airway occlusion. In this
context, lung zones that have low ventilation relative to
perfusion (low ventilation/perfusion [V
A
/Q] ratio) have a
low partial pressure of alveolar oxygen (PAO
2
) when air
is breathed. When the FIO
2
is increased, PAO
2
increases,
causing the rate at which oxygen moves from the alve-
olar gas to the capillary blood to increase greatly. The
oxygen ux may increase so much that the net ow of
gas into the blood exceeds the inspired ow of gas, and
the lung unit becomes progressively smaller. Collapse is
most likely to occur when the FIO
2
(and duration of
exposure) is high or where the V
A
/Q ratio (and mixed
venous oxygen content) is low.
15,16
Surfactant Impairment
Pulmonary surfactant that covers the large alveolar
surface is composed of phospholipids (mostly phos-
phatidylcholine), neutral lipids, and surfactant-specic
apoproteins (termed surfactant proteins A, B, C, and D).
By reducing alveolar surface tension, pulmonary surfac-
tant stabilizes the alveoli and prevents alveolar collapse.
This stabilizing function of surfactant may be depressed
by anesthesia, and such an effect has been conrmed in
vitro by Woo et al.
17
The authors evaluated the effect of
anesthetic agents on surfactant function using deation
pressurevolume curves in excised dog lungs. They
found that the reduction in percent maximum lung
volume was proportional to the concentration of both
chloroform and halothane.
17
Wollmer et al.
18
also used
pulmonary clearance of technetium-labeled diethylene-
triamine pentaacetic acid to demonstrate that halothane
anesthesia, in combination with high oxygen concentra-
tion, caused increased permeability of the alveolarcap-
illary barrier in rabbit lungs. The authors postulated that
the increased rate of pulmonary clearance of techne-
tium-labeled diethylenetriamine pentaacetic acid during
anesthesia with halothane was likely to be caused by
combined effects on the pulmonary surfactant or the
alveolar epithelium or both.
18
In addition, it is known
that the content of alveolar surfactant in isolated lungs is
modied by mechanical factors. Hyperventilation by in-
creased tidal volume,
19
sequential air inations to total
lung capacity,
20
or even a single cycle of increased tidal
volume
19
all cause release of surfactant in isolated animal
lungs. In rabbits, maintained increases in tidal volume
increased the amount of total phospholipids recovered
from bronchoalveolar lavages.
21,22
Supporting this is the
report that the spontaneous occurrence of large gasping
respirations increases the proportion of active forms of
alveolar surfactant (phospholipids). Oyarzun et al.
23
ex-
amined the ventilatory variables of cats breathing spon-
taneously during anesthesia for 4 h. They found that the
frequency of large gasps is directly correlated with the
concentration of phospholipids in bronchoalveolar la-
vage uid.
23
All three mechanismscompression, gas resorption,
and surfactant impairmentmay contribute to atelecta-
sis formation during general anesthesia (g. 2). How-
ever, given the surfactant reserve and the 14-h surfactant
turnover time, it may be that primary changes in surface
forces are less important; it is not known whether a
collapsed alveolus can denature surfactant, and so the
14-h turnover time may not be relevant. Nonetheless,
absorption and compression are considered to be the
two mechanisms most implicated in perioperative atel-
ectasis formation.
24
Fig. 2. This schematic outlines the probable pathogenic mech-
anisms underlying the development of atelectasis. FIO
2
frac-
tion of inspired oxygen; IV intravenous; V
A
/Q ventilation/
perfusion ratio.
840 M. DUGGAN AND B. P. KAVANAGH
Nature of Atelectasis
The following section reviews the characteristics of
atelectasis in several clinical contexts and then reviews
contemporary concepts regarding the nature of
atelectasis.
Atelectasis due to Anesthesia. Anesthesia-induced
atelectasis is traditionally thought of as collapse of alve-
oli. Brismar et al.
5
showed that within 5 min after induc-
tion of anesthesia, areas of increased density appeared in
the dependent regions of both lungs on CT. The dense
areas had an attenuation factor that corresponds to
blood and connective tissue and indicates the absence of
air. Injection of radiocontrast in the pleural space
showed that the densities were located above the pleura,
i.e., within the lung.
25
Hedenstierna et al.
26
also found
these densities in anesthetized sheep and conrmed his-
tologically that the densities were collapsed lung regions
and not uid accumulation.
Methods to restore normal FRC and various reexpan-
sion maneuvers have been suggested. The application of
positive end-expiratory pressure (PEEP) has been tested
in several studies. Arterial oxygenation does not usually
improve markedly, and atelectasis may persist.
27,28
Re-
opened units recollapse rapidly after discontinuation of
PEEP. However, Rothen et al.
29,30
demonstrated in vol-
unteers that peak inspiratory pressures of at least 40 cm
H
2
O were needed to fully reverse anesthesia-induced col-
lapse of healthy lungs, and most of the reexpanded atelec-
tatic lung tissue remains inated for at least 40 min.
Direct Visualization of Atelectasis. Using a unique
in vivo microscopic technique, Halter et al.
31
viewed
alveoli in the living animal in real time during mechanical
ventilation. In a surfactant deactivation model of acute
respiratory distress syndrome (ARDS), they measured
alveolar number and stability before, during, and after a
recruitment maneuver with ventilation with either de-
creased or increased PEEP. They demonstrated that a
recruitment maneuver opens atelectatic alveoli and that
without adequate PEEP, alveoli are unstable and suscep-
tible to derecruitment. Although associated with sam-
pling limitations,
32
this elegant study was the rst to
directly demonstrate visual evidence of collapse of indi-
vidual alveoli reecting atelectasis and stabilization re-
ecting recruitment.
32
Cyclic Lung Recruitment. Mechanical ventilation of
areas of lung that are atelectatic is associated with repet-
itive collapse and reexpansion with each breath, often
called cyclic recruitment. A conventional view of the
effects of atelectasis on gas exchange conveys an image
of mixed venous blood perfusing nonventilated or col-
lapsed alveoli, resulting in a consistent and stable pro-
portion of the pulmonary venous return that derives
from deoxygenated blood.
33
This notional contribution
(i.e., deoxygenated blood added to oxygenated blood) is
seen as the sum of two constant ow rates, resulting in
a shunt fraction (Q
s
/Q
t
%)
7
that can be mathematically
calculated.
However, we now know that the oxygen content of
pulmonary venous blood varies signicantly throughout
the respiratory cycle as the shunt fraction changes with
every breath. Baumgardner et al.
34
tested the hypothesis
that cyclic collapse of alveoli in dependent lung regions
with every breath should lead to large oscillations in
PaO
2
as shunt varies with the respiratory cycle. They
placed a partial pressure of oxygen (PO
2
) probe in the
brachiocephalic artery of rabbits after saline lavage. They
found a signicant effect of respiratory rate on the mag-
nitude of oscillations; as the respiratory rate increased,
the amplitude of oscillations became progressively small-
er.
32
The higher respiratory rate avoided cyclic recruit-
ment; i.e., the shorter expiratory time allowed expiration
without collapse. In practice, the benecial effect of
higher respiratory rates leading to improved oxygen-
ation can be seen when ventilating pediatric patients and
in particular neonates. This suggests that the dynamics of
mechanical events leading to recruitment and derecruit-
ment are important determinants of the amount of lung
that is cyclically recruited.
34
A previous study by Wil-
liams et al.
35
also showed within-breath arterial PO
2
os-
cillations in an animal model of ARDS and conrmed that
PaO
2
oscillations occur in the atelectatic lung. The au-
thors investigated the effect of PEEP on PaO
2
oscillations.
They found that as PEEP was increased, the amplitude of
the PaO
2
oscillation decreased and the mean PaO
2
in-
creased.
35
Several studies have evaluated the effects of
various inspiratory-to-expiratory ratios on gas exchange,
lung mechanics, and FRC; the inspiratory-to-expiratory
ratio per se was not found to be a signicant factor.
3638
Atelectasis: Volume Loss versus Fluid Filling.
More recently, it has been argued that the dependent
injured lung is derecruited, not because it is collapsed
but because it is lled with uid.
39
Work by Gattinoni et
al.
4042
had concluded that dependent portions of the
injured lung are exposed to a compressive pressure from
the increased weight of edematous lung and are col-
lapsed. Such a weight-of-the-lung hypothesis has been
studied, and it seems that the weight of the lung ac-
counts for only approximately 20% of the vertical gradi-
ent in pleural pressure and alveolar volume in normal
lungs.
4345
Hubmayr
39
suggests an alternative view of
the mechanics of injured lungs based on lung weight,
shape matching, interpretation of CT images of the lung,
and pressurevolume curves. For example, where
edema uid and foam ll dependent regions, high ina-
tion pressures are required to inate with air, as opposed
to low pressures required for ination with uid. The
pressurevolume characteristics of the former more
closely display the classic ndings associated with atel-
ectasis, including the prominent lower inection point
reecting opening pressure.
39
Evidence in support of
edema as the source of regional impedance in ARDS
include parenchymal marker studies in oleic acidin-
jured lungs.
46
The parenchymal marker technique de-
scribes the topographic distribution of regional volume
and ventilation in laboratory animals. The authors found
that oleic acid injury did not produce collapse of depen-
dent lung units in this model of ARDS.
46
They proposed
an alternative mechanism for the topographic variability
in regional impedances and lung expansion after injury,
which was liquid or foam in alveoli and conducting
airways.
46
Factors Modulating the Formation of Atelectasis
It is important for clinicians to understand how atel-
ectasis develops or worsens in the clinical context. Sev-
eral important clinical events act as modiers that inu-
ence the formation of atelectasis (g. 2).
Type of Anesthesia. Atelectasis develops with both
intravenous and inhalational anesthesia, regardless of
whether the patient is breathing spontaneously or is
paralyzed and mechanically ventilated.
4749
Ketamine is
the only anesthetic that does not produce atelectasis
when used alone, although in conjunction with neuro-
muscular blockade, it does result in atelectasis.
50
Ventilatory effects of regional anesthesia depend on
the type and extension of motor blockade.
4
Neuroaxial
blockade that has signicant cephalad extension reduces
inspiratory capacity by up to 20%, and expiratory reserve
volume approaches zero
51
; less extensive blockade af-
fects pulmonary gas exchange only minimally, and arte-
rial oxygenation and carbon dioxide elimination are well
maintained during most spinal and epidural anesthe-
sia.
52,53
Closing capacity and FRC remain unchanged.
54
Impact of Time. The maximum decrease in FRC
seems to occur within the rst few minutes of general
anesthesia.
5,55
During anesthesia for surgical operations
on the limb, FRC is not inuenced further by depth or
duration of anesthesia.
55,56
Don et al.
55
studied patients
undergoing peripheral limb surgery who were free of
cardiac and respiratory disease. Patients were divided
into two groups, those breathing halothane in 100%
oxygen and those breathing halothane in 30% oxygen in
nitrogen. The FRC decreased comparably in both groups
after induction of anesthesia, but this did not progress
with time. However, other studies have found that dur-
ing abdominal or thoracic surgery, pulmonary gas ex-
change deteriorates progressively during the course of
the operation
57,58
; these studies were unable to deter-
mine the independent impact of time on atelectasis as
opposed to surgical manipulation (e.g., surgical packing,
tissue retraction).
Effects of Position. In adults, changing from the
upright to the supine position results in a decrease of
0.5 l in FRC to 1.0 l, even in the awake state.
7
After
anesthesia, FRC is reduced by a further 0.5 l to 0.7 l.
49
The Trendelenburg position allows the abdominal con-
tents to push the diaphragm further cephalad, resulting
in a further decrease in FRC.
59
In the lateral decubitus
position, the dependent lung is predisposed to atelecta-
sis, whereas the nondependent lung may have an in-
creased FRC. The overall result is usually a slight increase
in total lung FRC, which, despite the differences in lung
size, is independent of whether the right or the left lung
is in the dependent position.
60
The prone position may
increase FRC slightly,
61
although this may not decrease
atelectasis. In fact, distribution of ventilation is more
uniform in anesthetized patients in the prone position,
in particular where the abdomen is not supported.
62
Prone positioning improves oxygenation in patients
with ARDS.
63
Animal models have also demonstrated the
benet of prone positioning after oleic acidinduced
lung injury as well as a model of lung injury induced
solely by mechanical forces.
64,65
Prone positioning
causes less extensive histologic injury and alters its
distribution.
64,65
Atelectasis is more prominent after cardiac surgery
with cardiopulmonary bypass (CPB) than after other
forms of surgery. Using a porcine model, Magnusson et
al.
66
found that atelectasis is produced to a much larger
extent after CPB than after anesthesia alone or with
sternotomy. Furthermore, the CPB-associated atelectasis
accounted for most of the marked post-CPB increase in
shunt and hypoxemia.
66
Clinical experience is consis-
tent with laboratory reports, and prominent atelectasis
has been noted in the dorsal lung regions on the rst
postoperative day in cardiac surgery patients.
67
Other
causes of gas exchange impairment after sternotomy and
CPB have been investigated, including pulmonary endo-
thelial permeability.
68
Macnaughton et al.
68
did not nd
any increase in pulmonary endothelial permeability, and
they hypothesized that the major component of the
deterioration in lung function was probably atelectasis
occurring during bypass. Numerous studies have shown
that a lung recruitment strategy and PEEP improves ox-
ygenation in patients after CPB.
69,70
In addition, the
application of PEEP of 10 cm H
2
O during CPB to main-
tain lung ination has been shown to be benecial.
71
Many anesthetists intentionally inate the patients lungs
before coming off CPB and directly visualize equal ex-
pansion of the lungs. This simple maneuver may detect
signicant obstruction from secretions or blood in the
endotracheal tube.
Inspired Oxygen. High oxygen concentration has
been associated with atelectasis formation, and this is
important because use of high FIO
2
(i.e., approaching
1.0) represents standard practice among many anesthe-
siologists.
72
Previous studies suggested that inspired ox-
ygen concentration may not be an important indepen-
dent predictor of anesthesia-associated atelectasis.
5,55
However, one of these studies used the helium-dilution
technique to measure FRC, which may not be as sensi-
tive as the CT that was used in later studies.
55,73
In the
absence of preoxygenation, atelectasis is not seen di-
rectly after induction of anesthesia; however, when FIO
2
is increased to 1.0 before intubation, development of
atelectasis is a consistent nding.
74,75
Concerns about
oxygen-induced atelectasis are not restricted to induc-
tion of anesthesia; increasing FIO
2
at the end of surgery to
1.0 before extubation also causes additional atelectasis,
which persists into the postoperative period.
76
How-
ever, the use of lower FIO
2
may increase the risk of
hypoxemia, should airway management subsequently
prove difcult and ventilation be threatened.
77
One
study investigated how different oxygen concentrations
may affect the formation of atelectasis and the decrease
in arterial oxygen saturation during apnea.
78
The authors
found that during routine induction of general anesthe-
sia, 80% oxygen caused minimal atelectasis, but the time
margin before desaturation occurred was signicantly
shortened compared with that of 100% oxygen.
78
In
addition, evidence suggests that administration of sup-
plemental oxygen reduces the incidence of wound in-
fection and could be benecial during anesthesia and
recovery.
79,80
Another possible benet of supplemental
oxygen during anesthesia includes a reduced incidence
of postoperative nausea and vomiting after colorectal
surgery,
81
although this was not found in patients under-
going gynecologic laparoscopy.
82
The effects of nitrous oxide on lung volumes during
anesthesia have also been studied.
8385
There was no
difference in the incidence of postoperative atelectasis if
nitrous oxide in oxygen was used or if air in oxygen was
used as the inspired gas.
In treating patients for induction of general anesthesia,
anesthesiologists must trade off the very rare possibility
of acute hypoxemia in the event of difculty with airway
management versus the common and predictablebut
generally mildimpact of hyperoxia-induced atelectasis
on later intraoperative gas exchange. Therefore, the use
of a lower FIO
2
to replace preoxygenation has not been
recommended as a new standard in clinical practice.
78
Effects of Age. In adulthood, progressive age is not
associated with increased propensity for development of
atelectasis.
86
However, in young children (aged 13 yr)
atelectasis seems to develop more readily than in
adults,
87
possibly because of the far greater thoracic wall
compliance resulting in less outwardly directed lung
distension forces.
88
In infants, contraction of the dia-
phragm may cause paradoxical inward movement of the
highly deformable chest wall, resulting in loss of lung
traction. The resultant atelectasis could reduce ventila-
tory efciency, increase diaphragmatic fatigue, and
thereby further increase the tendency for atelectasis de-
velopment. In addition, type I and II muscle bers are
not fully developed in children who are younger than 2
yr. This makes them prone to respiratory failure and
fatigue when there is extra stress put on their respiratory
system, not only during general anesthesia
89
but also in
the presence of a respiratory tract infection, epiglottitis,
or airway obstruction.
Closing volume is also greater in young children in
whom the elastic supporting structure of the lung is
incompletely developed. This puts the infant at greater
risk for atelectasis because airway closure can occur
even during tidal breathing.
24
The closing volume plus
the residual volume constitutes the closing capacity. If
FRC is decreased relative to closing capacity, this con-
verts normal areas of lung to low V
A
/Q areas and com-
pounds the propensity for development of atelectasis.
90
Body Habitus. Obesity worsens arterial oxygenation
through multiple mechanisms,
91
of which development
of atelectasis is an important contributor. This is because
of a markedly reduced FRC promoting airway closure to
a greater extent than in healthy-weight subjects.
92
As the
weight of the torso and abdomen make diaphragmatic
excursions more difcultespecially when recumbent
or supinethe FRC decreases, and this is intensied in
the setting of diaphragmatic paralysis associated with
neuromuscular blockade. Don et al.
55
further claried
the effect of body size on gas exchange and showed that
an individual with an increased weight/height ratio (i.e.,
obese) would be at a particular disadvantage in the
supine position because closing volume is increased in
relation to FRC. Pelosi et al.
93
also investigated the ef-
fects of body mass index on FRC, respiratory mechanics,
and gas exchange during general anesthesia. They found
that with increasing body mass index (i.e., ratio of body
weight/surface area), FRC and lung compliance de-
creased, and the oxygenation index (PaO
2
/PAO
2
) de-
creased exponentially.
93
Prone positioning, although dif-
cult in obese patients, may improve oxygenation.
63
Consistent with the effects of obesity, the reduced FRC that
occurs during pregnancy also potentiates atelectasis.
94
Tidal Volume. The ARDSnet study recommends the
use of low tidal volume in patients with ARDS.
95
Lower
tidal volume reduces stretch-induced lung injury in pa-
tients with ARDS,
96
and this approach is translated into
improved patient survival.
95,97
However, extrapolation
of the low-tidal-volume approach to patients without
lung injury (or ARDS) requires caution for two principal
reasons. First, it has been long recognized that low tidal
volume increases the development of atelectasis in the
absence of lung injury.
2,98100
Therefore, generalized
adoption of low tidal volume in patients without preex-
isting lung injury (e.g., during general anesthesia) could
promote development of atelectasis. Second, in the pres-
ence of ARDS, the ARDSnet protocol is specic: The data
stipulate 6 ml/kg (vs. 12 ml/kg) in the context of a
precise ventilatory management protocol that stipulates
many ventilatory parameters, in addition to tidal vol-
ume.
95
A recent study has suggested that the specic
low-tidal-volume approach used in the ARDSnet
study
95
was actually associated with the development of
intrinsic PEEP,
97
raising the possibility that recruit-
mentnot simply low tidal stretchplayed a protective
role in these patients. Therefore, if a low tidal volume
strategy is used that does not result in the development
of intrinsic PEEP, the propensity for development of
atelectasis might be signicant. The use of low tidal
volume in the absence of recruitment or PEEP in anes-
thetized patients without lung injury may lead to atelec-
tasis and is not recommended.
Two practical points are important regarding mode of
ventilation during general anesthesia. In contrast to vol-
ume-controlled ventilation, pressure-controlled ventila-
tion results in smaller delivered tidal volumes when
respiratory system compliance is decreased (e.g., during
surgical retraction or in the presence of abdominal
packs). Smaller tidal volumes may lead to atelectasis and
may go undiagnosed because there is no change in the
peak airway pressure as pressure-controlled ventilation
is being used. In addition, fresh gas ow may have an
impact because with older volume-controlled ventila-
tors, increased fresh gas ow results in increased deliv-
ered tidal volume.
101
Preexisting Lung Disease. Smokers and patients
with lung disease show more pronounced gas exchange
impairment in the awake state than healthy subjects do,
and this difference also persists during anesthesia.
102
However, only a small shunt and almost no atelectasis
develops in these patients, but they may have severe
V
A
/Q mismatch. Hyperination of the lungs may make
them resist collapse.
103
The chronic hyperinated state
of the lungs in chronic bronchitis changes the mechan-
ical behavior of the lungs and the interaction with the
chest wall so that the tendency to collapse is reduced.
However, patients with chronic obstructive lung disease
may have large regions with low V
A
/Q ratios that can
result, over time, in resorption atelectasis.
4
Effects of Atelectasis
Development of atelectasis is associated with the de-
velopment of several pathophysiologic effects, including
decreased compliance, impairment of oxygenation, in-
creased pulmonary vascular resistance, and develop-
ment of lung injury.
Decreased Compliance. One of the rst articles ex-
amining the effects of atelectasis was by Mead and Col-
lier
99
in 1959. They noted that when anesthetized dogs
were allowed to breathe spontaneously or were para-
lyzed and ventilated at tidal volumes of approximately
12.5 ml/kg, pulmonary compliance decreased progres-
sively. They found that these changes were immediately
reversed after forced inations of the lungs, whereas
forced deations caused further compliance reductions.
The appearance of the lungs as well as measurement of
total and ventilatory lung volumes indicated that the
lungs were atelectatic.
99
These laboratory ndings were translated into the peri-
operative context with the article by Bendixen et al.,
2
which reported that atelectasis caused a decrease in
pulmonary compliance in surgical patients and was as-
sociated with a worsening in systemic oxygenation. The
decreased compliance is conventionally considered to
be due to a reduction in lung volume, such that inspira-
tionexpiration cycles commencing from a lower FRC
are completed on a less efcient section of the notional
pressurevolume curve.
104
Therefore, greater energy is
consumed because a given change in transpulmonary
pressure results in a lesser tidal volume because of the
sigmoid shape of the pressurevolume curve. An ana-
tomical basis has been suggested for such atelectasis-
associated decreased FRC in the context of general an-
esthesia (see Compression Atelectasis).
6
The pressurevolume characteristics of the lung deter-
mine the work of breathing, and ventilatory work may
be analyzed by plotting pressure against volume.
105
In
the presence of increased airway resistance or decreased
lung compliance, increased transpulmonary pressure is
required to achieve a given tidal volume with conse-
quent increase in the work of breathing.
Although the concept of altered compliance has been
well established in the setting of macroatelectasis (e.g.,
lobar or dependent atelectasis sufciently large to be
radiologically apparent), there are no data regarding
whether microatelectasis (e.g., after brief exposure to
increased FIO
2
during preoxygenation
75
) has comparable
effects on lung mechanics.
Impaired Oxygenation. In many situations, the most
striking effect of atelectasis is impairment of systemic
oxygenation. This was rst identied in the context of
general anesthesia
2
where the use of passive hyperina-
tions reversed the hypoxemia.
2
Others reported impair-
ment of oxygenation during prolonged constant-volume
ventilation using small tidal volumes in the absence of
intermittent hyperinations.
106108
Atelectasis can occur as a result of hyperoxia.
75,109
If
high FIO
2
is continued, the effects may not be noted by
observing pulse oximetry, but only if PaO
2
is measured.
In this situation, the impaired oxygenation can be ex-
pressed in terms of PaO
2
. The cause of the impaired
oxygenation has been shown, using the multiple inert
gas technique, to result from increased mismatch of
ventilation with perfusion.
75
Two approaches have been shown to mitigate against
the development of hypoxia. First, as demonstrated orig-
inally, intermittent hyperination maneuvers reverse the
effect on gas exchange.
2
Maintenance of lung volume
from the outset can prevent, as opposed to reverse,
development of intraoperative atelectasis.
28
Second, al-
though recognized as an issue for decades, the compo-
sition of the inspired gases used during induction of
general anesthesia has been shown to directly impact
the development of microatelectasis in healthy patients
undergoing general anesthesia,
75
as well as in patients
with lung injury.
110
Rothen et al.
75
found that very little
atelectasis occurred after the induction of general anes-
thesia in subjects whose lungs were ventilated with 30%
oxygen in nitrogen. Furthermore, the increase in the
amount of atelectasis was less rapid in the setting of 30%
oxygen (in nitrogen) compared with 100% oxygen. This
is consistent with the notion that a poorly absorbed gas
such as nitrogen might prevent the early formation of
atelectasis and, conversely, that use of a highly absorbed
gas (e.g., oxygen) would enhance the development of
atelectasis.
Pulmonary Vascular Resistance. Early studies sug-
gested that the pulmonary vascular resistance was min-
imal at FRC. Lung volume much above this notional
value resulted in alveolar compression due to lung
stretch, whereas lung volume falling below the FRC was
thought to result in compression of extraalveolar vessels.
Therefore, this notion explained the changes in pulmo-
nary vascular resistance on the basis of physical alter-
ation of the pulmonary blood vessels, either stretching
or narrowing caused by increased lung volume or com-
pression caused by decreased lung volume.
111113
How-
ever, regional hypoxia develops in atelectatic lungs, and
it has been shown that the mechanism of increased large
vessel pulmonary vascular resistance in the lungs is due
to hypoxic pulmonary vasoconstriction, due in turn to
decreased alveolar and mixed venous oxygen ten-
sion.
114116
Recent work by our group has demonstrated
that this signicant increase in vascular resistance can
occur in previously normal lungs in an experimental
setting, resulting in right ventricular dysfunction and
increased microvascular leakage.
117
Lung Injury. Extensive evidence has established the
importance of maintenance of lung volume in the pre-
vention of lung injury. The pivotal publication by Webb
and Tierney
118
demonstrated that application of PEEP
prevented the development of lung injury induced by
extremely high tidal volume. The specic degree of
atelectasis responsible for attenuation or prevention of
high tidal volumeinduced lung injury was explored by
Sandhar et al.
119
and Muscedere et al.
120
using different
experimental models over 5- and 2-h time periods, re-
spectively. In isolated, nonperfused lungs that are venti-
lated with no or low PEEP, reductions in compliance and
evidence of morphologically apparent lung injury occur.
Permitting such atelectasis in the presence of high tidal
volumes is associated with hyaline membrane formation,
along with regional inhomogeneity of atelectasis and
overdistension. Other articles have also demonstrated
that repetitive lung collapse or atelectasis leads to in-
creased neutrophil activation in previously injured
lungs.
121,122
In addition to lung injury induced by ex-
tremely high tidal volumes, ventilation at low lung vol-
umes worsens lung injury by repeated small airway clo-
sure.
123,124
The concept of permissive hypercapnia
developed to avoid lung injury caused by high tidal
volumes or high ination pressures. Higher end-tidal
carbon dioxide levels may be accepted to reduce vo-
lutrauma or barotrauma, particularly in pediatric
patients.
Potentiation of lung injury by atelectasis has additional
implications for inammatory effects in the lung. Trem-
blay et al.
125
examined the effect of ventilation strategy
on lung inammatory mediators in the presence and
absence of lung injury and demonstrated that in the
absence of PEEP, an impairment in lung compliance was
accompanied by increased cytokine concentrations (e.g.,
tumor necrosis factor , interleukin 1) that were great-
est in the groups pretreated with lipopolysaccharide.
125
These concepts were extended to the in vivo setting,
where it was reported that maximal serum cytokine
concentrations induced by high tidal volume occurred in
the context of zero PEEP. In addition, atelectasis wors-
ened the impairment of compliance induced by high
tidal volume.
126
Perhaps of greatest concern in that pub-
lication was the high mortality (in the absence of cyto-
kine alterations) observed in the in vivo combination of
low-tidal-volume ventilation in the presence of atelecta-
sis. These data suggest that in terms of the most mean-
ingful outcome (i.e., survival), the combination of low
tidal volume and atelectasis may be the most adverse
ventilation strategy and that the increased cytokines ob-
served in the high-tidal volume groups may be of less
importance.
126
Recent work by our group, wherein rats without lung
injury received ventilatory strategies with and without
PEEP and recruitment maneuvers, may place these nd-
ings into perspective.
117
We found decreased survival in
the zero-PEEP group and also demonstrated ultrastruc-
tural evidence of microvascular epithelial disruption in
those animals. In addition, we demonstrated that right
ventricular dysfunction, possibly secondary to increased
pulmonary vascular resistance, occurred in the presence
of reduced FRC.
117
Clinical Impact of Atelectasis beyond the Operat-
ing Room. Development of atelectasis intraoperatively
is associated with decreased lung compliance, impair-
ment of oxygenation, increased pulmonary vascular re-
sistance, and development of lung injury. The adverse
effects of atelectasis persist in the postoperative period
and can impact patient recovery. Atelectasis can persist
for 2 days after major surgery.
127
Often, the lung dys-
function is transient, and normal lung function resumes
soon after anesthesia and surgery. For example, atelec-
tasis resolves within 24 h after laparoscopy in nonobese
subjects.
128
Nevertheless, patients experience perioper-
ative respiratory complications that may be related to
reduction in FRC.
129,130
Some pulmonary complications occur during or imme-
diately after anesthesiamainly hypoxemia. In a large
study with more than 24,000 patients, 0.9% had a hy-
poxemic event in the postanesthesia care unit that ne-
cessitated a specic intervention other than only supple-
mental oxygen.
131
There is no clear evidence that
atelectasis is the cause of all of these postoperative
hypoxemic events; respiratory depression from residual
anesthetic may be more likely.
24
However, it seems
likely that preventing atelectasis formation during the
whole perioperative period would increase the pulmo-
nary oxygen reserve, potentially reducing the likelihood
of late postoperative complications.
The characteristic postoperative mechanical respira-
tory abnormality after abdominal or thoracic surgery is a
restrictive pattern with severely reduced inspiratory ca-
pacity, vital capacity, and FRC.
132134
Patients breathe
rapidly with small tidal volumes and are unwillingor
unableto inspire deeply. Patients in whom postopera-
tive pulmonary complications develop have a relatively
greater reduction of FRC, vital capacity, and PaO
2
than
those who do not.
132,134
The impact of postoperative
pain control in preventing postoperative atelectasis has
been the focus of much research effort. Although pain
and muscle splinting in response to pain are traditionally
assumed to be the principal causative factors, total relief
of pain after upper abdominal surgeryusing epidural
analgesiaresults in only partial restoration of vital ca-
pacity and has minimal effect on FRC.
135
However, a
recent meta-analysis suggested that postoperative epi-
dural opioids signicantly decrease the frequency of
atelectasis but not other pulmonary complications when
compared with systemic opioids.
136
Other studies have
found no difference in the incidence of pulmonary com-
plications. Manikian et al.
137
demonstrated that thoracic
epidural analgesia in 13 patients undergoing upper ab-
dominal surgery caused a signicant increase in forced
vital capacity, but the FRC remained unchanged. Spence
and Logan
138
reported no signicant impact of postop-
erative epidural analgesia on oxygenation when com-
pared with patients receiving systemic morphine, and
Jayr et al.
139
reported that although the epidural pro-
vided superior postoperative analgesia, it did not affect
the frequency of postoperative pulmonary complica-
tions, regardless of preoperative pulmonary status. Fi-
nally, a recent multicenter randomized trial of 915 high-
risk surgical patients reported a slight reduction in
postoperative pulmonary complicationsbut no impact
on mortality or major morbidityattributable to epi-
dural versus systemic analgesia, although this study may
have been underpowered to examine mortality.
140
Two particular aspects of pulmonary defense mecha-
nisms, coughing and removal of particulate matter, are
adversely affected by the changes in lung mechanics and
breathing pattern
135
; this may predispose to pulmonary
infection. A number of studies examined the effects of
halothane and thiopentone on mucociliary clearance
and found that these agents may be responsible for
reduced mucous clearance in the postoperative peri-
od.
141143
A more recent study demonstrated that total
intravenous anesthesia with propofol, alfentanil, and ve-
curonium depressed mucociliary ow in patients with
healthy lungs.
144
Cervin and Lindberg
145
examined the
effects of desurane on mucociliary activity in the rabbit
maxillary sinus in vivo. Desurane increased mucocili-
ary activity, and the authors concluded that desurane is
an airway irritating compound.
145
Atelectasis and pneu-
monia are often considered together because the
changes associated with atelectasis may predispose to
pneumonia.
146
Despite a direct lack of evidence of a
correlation between atelectasis and pneumonia, reduc-
ing or avoiding atelectasis may diminish postoperative
pulmonary complications
147
and thus improve outcome;
however, this remains to be proven.
In a series of adults undergoing elective abdominal
surgery, postoperative pulmonary complications oc-
curred in 9.6% of cases.
148
Atelectasis and infectious
complications account for the majority of reported pul-
monary complications,
149
and the consequences include
a signicant burden in terms of morbidity
149
and addi-
tional healthcare costs.
150
In some series, pulmonary
complications account for 24% of deaths within 6 days of
surgery,
130,149
although the precise relation to atelectasis
is unclear.
Experimental Evidence that Atelectasis Causes
Lung Injury. The majority of studies examining the
interactions of mechanical ventilation and nonventila-
tory lung injury have observed the effects of injurious
mechanical ventilation strategy on preinjured lungs.
However, several experimental studies have examined
the effect of preemptive recruitment on the effects of
subsequent lung injury.
Atelectasis Worsens Lung Injury Caused by Me-
chanical Stretch. Multiple studies have convincingly
demonstrated that recruitment provides effective protec-
tion against lung injury that is either induced
118,151,152
or
aggravated
120,125,153,154
by mechanical stretch. This may
assume increasing importance as the role of tidal volume
and plateau pressures in ARDS is debated.
95,155,156
Atelectasis Worsens Lung Injury Not Caused by
Mechanical Stretch. Most patients with severe lung
injury require supportive mechanical ventilation. It is
clear from multiple laboratory
157,158
and clinical
95,159
studies that stretch can cause or worsen lung injury.
However, there is a vast spectrum of causes of ALI, and
there are striking similaritiesand few differencesin
the pathogenesis, pathophysiologic dysfunction, and his-
tologic appearance of ALI or ARDS, whether caused by
stretch
158
or other etiologies.
160
Therefore, because re-
cruitment is effective in reducing stretch-induced injury
and because so many pathogenic and morphologic fea-
tures are shared between stretch-induced versus other
forms of injury, it may be that the protective effects of
recruitment could be applicable to lung injury that is not
caused by increased tidal stretch.
Additional specic lines of evidence exist. Ination of
a lung graft before reimplantation, as opposed to main-
tenance of the lung in a deated state, confers increased
viability.
161163
The importance of ination in lung pro-
tection has been conrmed in in vivo
162,163
and ex
vivo
161
models and may be mediated either via reduc-
tion in pulmonary vascular resistance
161
(potentially de-
creasing endovascular shear injury) or through preven-
tion of surfactant inactivation.
163
Finally, early
application of mechanical ventilation may, through
maintenance of lung volume (FRC), reduce mortality in
experimental porcine sepsis
164
and in experimental
hemorrhagic shock.
165
Detection of Atelectasis
Atelectasis is usually suspected when alterations in
lung physiology consistent with the development of
atelectasis (e.g., decreased compliance, impaired oxy-
genation) occur in a setting where atelectasis is likely.
However, conrmation of atelectasis is possible through
a variety of means.
Conventional Chest Radiography. Lobar or seg-
mental atelectasis is classically represented as opacica-
tion of the lobe or lobar segment in question. General
signs of atelectasis relate to volume loss. The most direct
and reliable sign is the displacement of the interlobar
ssure. Other signs of volume loss, such as increase of
the hemidiaphragm and mediastinal shift, are maximal
nearest the point of volume loss. Compensatory overin-
ation of the remaining aerated segments in the affected
lobe is present, and the collapsed portion of the lung is
of increased opacity and often triangular in at least one
projection.
166
For example, when atelectasis results
from proximal bronchial occlusion, an obstruction may
be identiable in the proximal bronchial tree, beyond
which the tree is not aerated. If atelectasis results from
absorption, the features are similar to consolidation,
where the atelectatic lung parenchyma is opacied, and
contrasts with the patent bronchial airway.
In addition to airway characteristics, other features of
atelectasis are important. The silhouette sign allows
identication of the lobe or segment of the lung that is
affected. It is based on the principle that apposition of
densely atelectatic lung with an additional contiguous
structure, such as the diaphragm or the heart, results in
obliteration of the boundary between the lung and the
adjacent structure. For example, opacication of part of
an atelectatic lung in conjunction with obliteration of
the ipsilateral hemidiaphragm suggests lower lobar atel-
ectasis; in contrast, preservation of the hemidiaphragm
indicates that the ipsilateral lower lobe is not atelectatic.
A cardinal characteristic of atelectasis is volume loss of
the affected lobe. This is associated with secondary
changes in adjacent structures, in an attempt to ll the
gap created by the loss of lung volume, and results in
alterations including shift of the mediastinum or the
hilum towards the affected area, elevation of the ipsilat-
eral hemidiaphragm, and secondary (or compensa-
tory) emphysema in the adjacent nonatelectatic lung.
There is no doubt that conventional chest radiographs
can reveal collapse in a segmental or lobar distribution.
However, the ability of chest radiographs to detect atel-
ectasis that occurs during general anesthesia or during
mechanical ventilation of recumbent critically ill patients
is less certain.
167
Computed Tomography. Computed tomography is
emerging as the preferred method for imaging the lung
because of the widespread availability, resolution, high
signal/noise ratio for lung tissue, and speed. From con-
ventional CT images, it is possible to measure whole and
regional lung volumes, distribution of lung aeration, and
recruitment behavior under various clinical conditions
and interventions.
168
In the 1980s, atelectasis was
shown by CT in anesthetized patients.
5,169
Since then, atelectasis has been studied extensively.
Atelectasis on a CT scan has been dened as pixels with
attenuation values of 100 to 100 Hounseld units.
3
Hounseld units quantify attenuation or density seen on
CT. In this study, Lundquist et al.
3
studied patients un-
dergoing elective abdominal surgery with CT of the
thorax during anesthesia. Attenuation values in histo-
grams of the lung and atelectasis were studied using two
methods of calculating the atelectatic area. On the basis
of the CT ndings, atelectasis occurs in the most depen-
dent parts of the lungs and occurs in almost 90% of
patients who are anesthetized. The extent of the atelec-
tasis in the dependent regions can be reduced by PEEP.
5
The lung in ARDS is characterized by a marked in-
crease in lung tissue and a massive loss of aeration.
170
Gattinoni et al.
40,41,171,172
have extensively investigated
the distribution of tidal volume and recruitment in pa-
tients with ARDS using CT scans. They concluded that
PEEP makes the gas distribution more homogenous in
patients with ARDS, stretching the upper levels and
recruiting the lower ones, and thereby reduces the at-
electatic tissue in dependent regions. Rouby
173
has as-
sessed PEEP-induced lung overdistension using CT.
Rouby determined the threshold to differentiate PEEP-
induced alveolar recruitment from PEEP-induced lung
overdistension. The threshold of 900 Hounseld units
allows a reliable determination of PEEP-induced alveolar
overdistension. A number of human studies have clearly
reported the simultaneous onset of alveolar recruitment
and lung overination in patients receiving PEEP levels
of 10 and 20 cm H
2
O.
174177
These recent approaches
have important implications in the diagnosis as well as
the management of atelectasis because they point clearly
to the propensity for injurious regional overination
occurring as a result of efforts to reverse atelectasis (e.g.,
increased PEEP, recruitment maneuvers) in the setting of
ARDS.
Magnetic Resonance Imaging. Magnetic resonance
imaging allows three-dimensional imaging without the
use of ionizing radiation. Unfortunately, the lung is not
well suited to magnetic resonance imaging. On spin-
echo images in healthy subjects, little signal is obtained
from lung parenchyma. Areas of consolidation and
masses can be identied, but the degree to which they
can be differentiated has yet to be fully established. This
technique has been used in preterm neonates to study
pulmonary dysfunction.
178
The authors compared lung
water content and distribution between preterm and
term infants and concluded that lung water content is
higher in preterm infants, consistent with dependent
atelectasis.
178
Xenon-enhanced CT is a method for non-
invasive measurement of regional pulmonary ventilation,
determined from the wash-in and wash-out rates of the
radiodense, nonradioactive xenon gas, measured by se-
rial CT scans.
179
This may provide a valuable tool for
noninvasive measurement of regional lung function and
atelectasis in the future. Although magnetic resonance
has several advantages over CT (e.g., contrast material is
not necessary, possibility for multiple planar imaging), it
is not apparent that magnetic resonance offers any dis-
tinct advantages over CT in the evaluation of atelectasis
at the current time.
180
Ultrasonography. Although more commonly used in
assessment of pleural collections or in the context of
echocardiography, thoracic ultrasonography has been
used in assessment of lung parenchyma.
181
It has been
suggested as a useful aid to the rapid diagnosis of atel-
ectasis
182
and, in the context of ARDS, seems to be
useful for the assessment of regional consolidation.
183
Recently, use of a specic ultrasonographic detection of
the cardiac impulse, termed the lung pulse, has been
reported to be a highly sensitive early indicator of the
presence of atelectasis.
184
The use of ultrasonography
may offer signicant advantages for patients in the op-
erating room or in the intensive care unit in terms of
rapidity and ease of examination, without the disadvan-
tages of patient transport and radiation exposure. How-
ever, its role in clinical practice remains to be
determined.
185
Intravital Microscopy. Intravital microscopy applied
to the pleural surface enables experimental visualization
of atelectasis and examination of its role in the patho-
genesis of lung injury (see Direct Visualization of Atelec-
tasis).
31
In addition to access issues, there are limitations
to interpretation,
32
including the fact that visualization is
restricted to lung tissue that is immediately below the
pleural surface, with deeper parenchyma beyond the
range of the instrument.
Cytokine Prole. There are other methods of detect-
ing atelectasis in the preclinical setting, including lung
lavage levels of cytokines.
125
Tremblay et al.
125
exam-
ined the effect of ventilation strategy on lung inamma-
tory mediators in the presence and absence of lung
injury using an isolated rat model. Lung lavage cytokine
concentrations were greatest in the groups ventilated
without PEEP in both the control intravenous lipopo-
lysaccharidetreated groups. Zero PEEP in combination
with high volume ventilation had a synergistic effect on
cytokine concentrations. This nding that atelectasis
worsens stretch-induced lung injury resulting in in-
creased lung and systemic cytokine concentrations was
conrmed by Chiumello et al.
126
However, it is impor-
tant to note that experimental atelectasiseven when
lethalis not associated with increased cytokines in the
absence of high tidal volumes.
126
The measurement of
lung lavage levels of cytokines in the clinical situation is
impractical.
Prevention or Reversal of Atelectasis
The factors important in the prevention or reversal of
atelectasis differ considerably, depending on whether
the lungs are injured or uninjured. Because of the ad-
verse pathophysiology associated with the development
of atelectasis and the preclinical ndings that recruit-
ment of atelectatic lung may reduce the propensity to-
ward subsequent injury,
161163
it is important to exam-
ine how recruitment may be achieved.
Prevention or Reversal of Atelectasis in Healthy
Lungs. Progressive pulmonary atelectasis (and the asso-
ciated impairment of oxygenation) may occur during
constant ventilation whenever periodic hyperination is
lacking; it is reversible by passive hyperination (i.e.,
three successive inations: rst, with a pressure of 20 cm
H
2
O for 10 s; second, with a pressure of 30 cm H
2
O for
15 s; and third, with a pressure of 40 cm H
2
O sustained
for 15 s).
2
This was taken as evidence that atelectatic
alveoli are reopened by the deep breaths, and that con-
clusion was supported by the reduction in pulmonary
compliance occurring during ventilation and the return
of compliance to control values after hyperination.
Nunn et al.
107
examined arterial oxygenation in pa-
tients during routine anesthesia. They found that arterial
oxygenation increased when a pressure of 40 cm H
2
O
was maintained for 40 s; lower pressures, even with
modest levels of PEEP, were not effective.
107
A more
recent study by Tusman et al.
28
examined an alveolar
recruitment strategy in healthy lungs during general
anesthesia. The authors hypothesized that because atel-
ectasis occurs during general anesthesia, an initial in-
crease in pressure would be required to open collapsed
alveoli, and if this inspiratory recruitment was combined
with sufcient end-expiratory pressure, alveoli would
remain open. They allocated patients to one of three
groups: no PEEP; an initial control period without PEEP
followed by PEEP of 5 cm H
2
O; and PEEP of 15 cm H
2
O
with high tidal volume (18 ml/kg, or peak inspiratory
pressure 40 cm H
2
O) maintained for 10 breaths, fol-
lowed by stepwise reduction of PEEP and tidal volume.
The third group, receiving the alveolar recruitment strat-
egy, had a signicant increase in arterial oxygenation
during general anesthesia. Treatment with PEEP of 5 cm
H
2
O alone did not have the same effect on oxygenation.
The authors concluded that high initial pressures are
needed to overcome the anesthesia-induced collapse and
that PEEP of 5 cm or more is required to prevent the
newly recruited alveoli from collapsing. In addition,
there was no evidence of barotrauma or pulmonary
complications as a result of the high initial airway
pressures.
28
Prevention or Reversal of Atelectasis in Injured
Lungs. It has become evident that a number of ventila-
tory strategies can produce or worsen lung injury.
157
The use of large tidal volumes,
153
high peak airway
pressures,
186
and end-expiratory alveolar collapse with
cyclic reopening
120
have all been proposed as deleteri-
ous when ventilating injured lungs. Several studies have
shown that lung injury secondary to ventilation with
large tidal volume is attenuated if end-expiratory volume
is maintained by the use of PEEP.
118,126,152
In addition,
ventilation at low FRC worsens lung injury, possibly by
repeated small airway closure, and PEEP markedly atten-
uates this injury.
120,126
Therefore, recruitment of atelec-
tatic lung reduces the injurious effects of mechanical
ventilation with both low and high tidal volumes and
protects against development of ventilator-induced lung
injury.
The open-lung approach to ventilating patients with
ARDS consists of a recruitment maneuver with high
sustained airway pressures to open atelectatic alveoli
followed by application of PEEP to maintain alveolar
patency. This approach was among the interventions
performed in a study that showed an improvement in
oxygenation and reduced mortality in patients with
ARDS.
159
The researchers calculated the inection point
from a pressurevolume curve (corresponding to an
upward shift in the slope of the curve), and PEEP was
preset at 2 cm H
2
O above the inection point in the
protective ventilation group. If the inection point could
not be determined on the pressurevolume curve, PEEP
of 16 cm H
2
O was used. Recruiting maneuvers were
frequently used and consisted of continuous positive
airway pressures of 3540 cm H
2
O for 40 s followed by
a return to previous PEEP levels.
159
Gattinoni et al.
40
also showed that with increasing
PEEP from 0 to 20 cm H
2
O, gas distribution became
more homogenous in sedated and paralyzed patients
with ARDS and reduced the reopeningcollapsing tis-
sue. Suter et al.
187
suggested that the optimum end-
expiratory pressure in patients with acute respiratory
failure was the PEEP level that resulted in the greatest
total static compliance. This maximum compliance pro-
duced by PEEP resulted in optimum overall cardiopul-
monary interaction to ensure maximal global oxygen
delivery. In patients with low FRC values at zero end-
expiratory pressure, maximum oxygen transport was
achieved at higher levels of PEEP than in patients with
normal or high FRC values.
The timing of recruitment maneuvers was examined
by Grasso et al.
188
in patients with ARDS who were
ventilated with a lung-protective ventilatory strategy
(low tidal volumes of 6 ml/kg). They dened a recruiting
maneuver as continuous positive airway pressure of
40 cm H
2
O for 40 s. Measurements of PaO
2
/FIO
2
ratio,
volumepressure curve, and respiratory mechanics were
obtained 2 and 20 min after application of a recruiting
maneuver. The authors classied the patients as respond-
ers and nonresponders. Recruitment maneuvers in-
creased the PaO
2
/FIO
2
ratio signicantly more in respond-
erswho had been ventilated for a longer period of
timethan in nonresponders. The authors concluded
that application of recruiting maneuvers improves oxy-
genation only in patients with early ARDS who do not
have impairment of chest wall mechanics and with a
large potential for recruitment.
188
Treating Atelectasis in the Postoperative Period.
Postoperative pulmonary complications are increasingly
recognized as an important perianesthetic issue.
146
De-
termination of the frequency and clinical impact of post-
operative pulmonary complications is hampered by the
lack of a uniform denition of a postoperative pulmo-
nary complication among studies. Included in the de-
nition are pneumonia, severe respiratory failure (usually
dened as the need for mechanical ventilation), bron-
chospasm, and atelectasis (often not dened). Most stud-
ies referring to postoperative atelectasis do not directly
measure FRC.
Reversing or preventing atelectasis is possible in many
patients in the perioperative period
146,189
and is of
proven benet in preventing pulmonary complica-
tions.
146
Techniques or devices that either encourage or
force patients to inspire deeply are of most clinical
importance.
190192
The aim is to produce a large and
sustained increase in transpulmonary pressure distend-
ing the lung and reexpanding collapsed lung units. Sev-
eral methods have been studied, including intermittent
positive-pressure breathing, deep-breathing exercises,
incentive spirometry, and chest physiotherapy. A meta-
analysis suggests that all regimens studied are equally
efcacious in reducing the frequency of postoperative
pulmonary complications after upper abdominal
surgery.
193
The benecial effect on gas exchange of a simple
posture change from supine to seated has been demon-
strated, both in healthy subjects
90
and after upper ab-
dominal surgery.
91
Identication of FRC as the single
most important lung volume in postoperative patients
provides a specic goal of therapy.
189
FRC can be mea-
sured by a number of techniques. Gas dilution tech-
niques (e.g., helium equilibration, nitrogen washout)
have been used.
93,194
One disadvantage of these meth-
ods is that the tracer gas may not mix with all gas in the
lungs because of occluded airways; this source of error
can be overcome by using body plethysmography.
Finally, early work reported the use of thoracic or
sternal traction
195,196
as well as the use of intravenous
aminophylline
197
as successful treatments of atelectasis
in a number of case reports, but given the impracticali-
ties and adverse effects of these therapies, they have no
clinical application today.
Recruitment of Atelectatic Lung Is Easier to
Achieve in the Absence of Injury. Although the pres-
surevolume relation in ARDSand the ability to recruit
lungmay depend on the etiology,
171
it is always easier
to recruit lung when injury is absent or mild, compared
with when signicant injury is established.
42,188,198
This
is because the uninjured lung is highly compliant, and its
inection point (opening pressure) on the ination pres-
surevolume curve is either low or not detectable. In
contrast, the inection point is signicantly greater
when injury has been established; in fact, elevation of
the inection point increases in proportion to the extent
of injury.
194
Such impaired compliance (and difculty
with recruitment) has a pathophysiologic basis in estab-
lished injury. The causes include surfactant dysfunction
due to impairment of large aggregate formation,
199
di-
rect inhibition by plasma proteins that have exudated
into the air space,
200202
and the progression of cellular
inltration and edema in the pulmonary interstitium and
alveoli.
203,204
Increases in pulmonary vascular resis-
tance, which characteristically parallel the progression
of the lung injury,
205
may decrease lung compliance
further.
206
Finally, when recruitment has been achieved,
less airway pressure is required to prevent derecruit-
ment than is required to achieve recruitment.
207
Summary and Future Implications
In the future, clinicians may be able to predict the
subsequent development of ALI. In an optimal setting,
this would be after recognition of the identiable etiol-
ogy and before its initiation (e.g., before major surgery or
before reperfusion during transplantation surgery). Alter-
natively, early institution of prophylactic recruitment
after identication of an etiologic event, particularly
when associated with a worrisome predictive stratica-
tion (e.g., pancreatitis with elevated cytokine prole),
would be ideal. The eventual prospect of predicting (or
early detection of) ALI and ARDS makes prophylactic
lung recruitment (to maintain or recover normal resting
lung volume) increasingly tenable, and if validated by
clinical studies, this could become integrated into the
perioperative care of patients who are at risk of devel-
oping critical illness.
Atelectasis occurs in almost all patients undergoing
general anesthesia. We have reviewed the causes, ef-
fects, nature, identication, and prevention of atelectasis
in the perioperative period. Unless restoration of FRC
takes place, atelectasis can have detrimental conse-
quences. Current literature indicates that intraoperative
and postoperative lung recruitment improves intermedi-
ate physiologic outcomes (e.g., oxygenation, work of
breathing); however, the benets might have more sig-
nicant implications for lung injury and ARDS. Low
stretch ventilation can achieve, at best, attenuation of
stretch-induced injury; at worst, it can cause loss of lung
volume, potentially contributing to or worsening injury.
Prophylactic recruitment however, could reduce or pre-
vent lung injury that results from a variety of primary
etiologies, as well as reducing injury resulting from me-
chanical stretch. If proven in the clinical setting, this
approach could reduce the development of critical ill-
ness in many general medical and surgical patient
populations.
Note Added in Proof
Since acceptance of this manuscript, Squadrone et al.
have demonstrated that reversing atelectasis with non-
invasive continuous positive airway pressure in high-risk
postoperative patients who are hypoxic results in re-
duced need for reintubation and a lower incidence of
pneumonia and sepsis (Squadrone V, Coha M, Cerutti E,
Schellino MM, Biolino P, Occella P, Belloni G, Vilianis G,
Fiore G, Cavallo F, Ranieri VM; Piedmont Intensive Care
Units Network [PICUN]: Continuous positive airway
pressure for treatment of postoperative hypoxemia: A
randomized controlled trial. JAMA 2005; 293:58995).
The authors thank Steven Deem, M.D. (Associate Professor, Departments of
Anesthesiology and Medicine, University of Washington, Seattle, Washington),
Rolf Hubmayr, M.D. (Professor, Department of Medicine, Mayo Clinic, Rochester,
Minnesota), and John Laffey, M.D. (Consultant Anesthetist, University Hospital
and National University of Ireland, Galway, Ireland), for their expert comments
on the manuscript; and Theresa Sakno (Sakno Media, Toronto, Ontario, Canada)
for the artwork.
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