Hypoxia During Thoracic Surgery:

Practical Advice for the Anesthesiologist

J avier H. Campos, MD
Professor
Director of Cardiothoracic Anesthesia
Vice Chair for Clinical Affairs
Executive Medical Director Operating Rooms
University of Iowa Health Care

2

Introduction

Lung separation with the use of a double-lumen tube (DLT) or bronchial blocker (BB) is used to provide one-lung
ventilation (OLV) in patients undergoing thoracic, mediastinal, cardiac, vascular or esophageal procedures. [1-2]
During OLV, an intrapulmonary shunt, related in part to collapse of the non-dependent lung and increased
atelectatic areas in the dependent lung, results in hypoxemia. [3] Hypoxemia by definition is a decrease in arterial
oxygen saturation (SpO
2
) to less than 90% [4], or a PaO
2
<60 mmHg when the patient is being ventilated with a
FiO
2
1.0. [5]

The incidence of hypoxemia during OLV has been reported to be 1-10%. This is partially related to advances with
routine use of a fiberoptic bronchoscope for optimal placement of lung isolation devices, as well as with the
introduction of newer volatile anesthetics that cause less inhibition of hypoxic pulmonary vasoconstriction (HPV)
and less shunting during OLV. [6-8]

This review focuses on the predictors of hypoxia during OLV, the pathophysiology of HPV, protective ventilation
maneuvers to restore or improve arterial oxygenation, the effects of anesthetics on hypoxia and inflammation, and
cerebral desaturation episodes and hypoxia during OLV.


Patients at Risk of Developing Hypoxia During OLV

Slinger, et al [9], using regression analysis in 80 patients undergoing OLV, showed that the three most significant
predictors for PaO
2
were: right-sided operation [because the right lung is larger than the left lung, oxygenation is
better during left thoracotomy (i.e. when the larger right lung is the dependent and ventilated lung)], preoperative
FEV
1
% and intraoperative PaO
2
during two lung ventilation. Others [10-11] have shown better oxygenation during
left-sided thoracic surgery as compared to right-sided surgeries when FiO
2
of 1.0 is used.
Morbidly obese patients (BMI >30 Kg-m
2
) undergoing thoracic surgical procedures under OLV have been shown to
develop intraoperative hypoxemia and an increase in alveolar arterial oxygen difference. [12] In a study by
Schwarzkopf, et al [10], they found that patients undergoing lobectomy and pneumonectomy had better oxygenation
during OLV than patients undergoing video thoracoscopic metastasectomy. Lung perfusion studies in these patients
showed that perfusion of the non-ventilated lung was more impaired in patients presenting for lobectomy and
pneumonectomy than in patients presenting for metastasectomy. Patients with previous lobectomy requiring
another surgery in the contralateral lung may be at risk of developing hypoxemia during total lung collapse.


Effects on Arterial Oxygen Tension (PaO
2
) in Supine or Lateral Decubitus Position in Thoracic Surgery

In general, for thoracic surgical patients undergoing OLV, the most common practice is to operate in a lateral
decubitus position. Therefore, gravity is a major determinant of shunt fraction and perfusion. [13] Recent studies
[14-15] have examined the changes in arterial oxygen tension (PaO
2
) during procedures requiring OLV. In the
Watanabe, et al study [14], patients were ventilated with a FiO
2
of 1.0 and divided into three groups. One group
was supine, another group was positioned in a left semi-lateral decubitus position and the third group was placed in
left fulllateral position. In the supine position group, 9 out of 11 patients had arterial oxyhemoglobin saturation
<90%; in the other two groups (semi lateral and full lateral), only one patient in each group developed hypoxemia.
The study by Bardoczky, et al [15], compared the positional effects and the inspired fraction of oxygen during OLV.
The patients, randomly assigned, received FiO
2
of 0.4, 0.6 or 1.0 during two lung ventilation and thereafter OLV in
the supine and lateral position. PaO
2
decreased more during OLV compared to two lung ventilation regardless of
the position. However, in all three groups, PaO
2
was significantly higher during OLV in the lateral than the supine
position. These studies clearly demonstrated that during OLV in a lateral decubitus position, the gravitational effect
augments the redistribution of perfusion to the ventilated (dependent) lung, improving V/Q match. Therefore, in
patients requiring OLV who are placed in supine position, it is possible to experience more transient episodes of
hypoxemia.


Pathophys

Hypoxemi
(V/Q) gas
dependent
atelectatic
through the
compliance
The determ
(P
50
), oxyg
(PaCO
2
), b
last two fac

In a lateral
distributed
(more perf
(more vent
arterial oxy
resistance
redistributi
Figure 1B
vasoconstr

Figure 1:











Figure 1A.
approxima
approxima







Figure 1B
to the depe
(this is the
siology of Hyp
a during OLV
exchanging un
lung also caus
areas of the lun
e weight of the
e of the chest w
minants of arter
gen consumptio
blood flow thro
ctors are often
l decubitus pos
d as follows: th
fusion); in cont
tilation). When
ygen tension d
diverts blood f
ion of the pulm
displays the at
riction response
. The lungs of a
ately 60% of th
ately 40% of th
. A non-depen
endent lung. In
amount of blo
poxia During O
is caused by v
nits. During OL
ses a venous ad
ng seen with g
e mediastinum,
wall in the depe
rial oxygen con
on, total cardia
ough the unven
associated tog
sition when bot
e dependent (o
trast, the ventil
n OLV is institu
ecreases; there
flow away to ar
monary blood fl
telectatic non-v
e.
a patient positi
e total pulmon
e total PBF.
dent (collapsed
n general, the Q
ood not being o
One-Lung Ven
venous admixtu
LV, the collaps
dmixture throug
general anesthe
, abdominal org
endent position
ntent include:
ac output, inspi
ntilated lung an
gether as shunt
th lungs are bei
or down) lung r
lated (or non-d
uted, the non-d
e is a response t
reas with bette
flow on a latera
ventilated lung
ioned in the lat
nary blood flow
d) lung. This le
Qs/Qt fraction s
oxygenated).
3
ntilation
ure through shu
sed non-depen
gh shunt and ar
sia and is perh
gans, retractors
n.[16]
hemoglobin co
red oxygen fra
nd unventilated
(Q) or shunt fr
ing ventilated,
receives approx
ependent) lung
dependent lung
to hypoxia, HP
er perfusion tow
al decubitus po
along with the
teral decubitus
w (PBF). The n
eads to a 50% r
seen during gen
unts and areas o
ndent lung is an
areas of low V/
haps increased w
s, excessive pa
oncentration, h
action (FiO
2
), a
d or low V/Q ar
raction (Qs/Qt)
the proportion
ximately 60%
g receives 40%
g becomes atele
PV, in which th
wards the depe
osition while bo
e percentage of
position. The
non-dependent
response of HP
neral anesthesi
of low ventilat
n obligate shun
/Q. This is prim
with the latera
acking of the th
hemoglobin dis
arterial carbon
reas of the ven
). [17]
n of the pulmon
of the pulmona
% of the total pu
ectatic. Becau
he increase in p
endent lung. Fig
oth lungs are b
f hypoxic pulm
dependent, or
but ventilated
PV as blood flo
ia and OLV ran
tion-perfusion
nt while the
marily through
al decubitus pos
horax and low
ssociation curv
dioxide level
ntilated lungs. T
nary blood flow
ary blood flow
ulmonary blood
use the alveolar
pulmonary vas
gure 1A displa
eing ventilated
monary
down, lung rec
lung receives
ow is being div
nges from 15 to
ratio
h
sition
ve
The
w is
w
d flow
r
scular
ays the
d.
ceives
verted
o 40%
4

Effects of Hypoxia on Inflammatory Response and Cytokine Release During One-Lung Ventilation

When considering the effects of ventilation on arterial oxygenation during OLV, it is better to consider the blood
flow through the unventilated lung (V/Q =O) separately from the ventilation of the low V/Q areas of the ventilated
lung. In general, the Qs/Qt fraction seen during anesthesia and OLV ranges from 15-40%.
During OLV, the non-dependent (operated) lung remains atelectatic and hypoperfused because of hypoxic
pulmonary vasoconstriction (HPV). Thus, the HPV in the non-dependent lung ameliorates the pulmonary
ventilation/perfusion relationship, preserving the systemic oxygenation by constricting pulmonary vessels in poorly
ventilated or atelectatic hypoxic lung regions to divert the pulmonary blood flow to better aerated areas.[18]
Although HPV decreases the shunt fraction and attempts to resolve hypoxemia[19], it is a serious aggravating factor
when ventilation is restored because pulmonary re-expansion promotes the re-entry of oxygen through the airways,
causing the release of excessive oxidative radicals.[20] The re-expansion of a previously collapsed lung is
accompanied by an ischemia/reperfusion like response resulting in the release of cytokines from the collapsed lung
and the contralateral lung. Through this mechanism, OLV increases the risk of developing acute lung injury (ALI).
[21]
During OLV, inflammatory response reactions can be produced by multiple factors such as mechanical damage due
to surgical manipulation, OLV induced atelectasis and re-expansion, atelectasis, and damage by high oxygen tension
or by the use of high peak inspiratory pressure during mechanical ventilation. [22-25] Inflammatory cytokines,
tumor necrosis factor, interleukin (IL) IB, IL-6 and IL-8 are important chemoattractants that affect the recruitment
of neutrophils and alveolar macrophages. Alveolar macrophages secrete biologically active products and thereby
play a significant role in regulating pulmonary inflammatory reactions. An increase in these inflammatory cytokines
can be clinically relevant to pulmonary complications and impairment of oxygenation during or following thoracic
surgery.
One study [25] has shown that the epithelial lining fluid contained significantly increased levels of interleukins in
the dependent or ventilated lung and the non-dependent lung at the end of thoracic surgery. The inflammatory
response was even greater in the dependent lung. The peak inspiratory pressures used in this study were below 30
cmH
2
O, tidal volume of 6 ml/Kg and FiO
2
of 0.6-1.0. Misthos, et al [26], has shown that patients with non-small cell
lung cancer have a higher production level of oxygen free radicals than the normal population; mechanical
ventilation and surgical trauma are weak free radical generators. Manipulated lung tissue is also a source of free
radicals in the intra or postoperative period and lung re-expansion provoked severe oxidative stress. Interestingly,
this study also showed that the degree of generated oxygen free radicals was associated with the duration of OLV.
Oxygen toxicity is a well-recognized consequence of prolonged exposure to high FiO
2
characterized by
histopathologic changes similar to ALI. Oxygen toxicity occurs during OLV and involves ischemia-reperfusion
injury and oxidative stress. [27] Collapse of the operative lung and surgical manipulation result in relative organ
ischemia and reperfusion at the time of lung expansion, which leads to the production of radical oxygen species.
Increasing the duration of OLV and the presence of tumor also increases the markers of oxidative stress. Lung re-
expansion should likely occur at a lower FiO
2
as hypoxemic reperfusion has been shown to attenuate reperfusion
syndrome.



Influence of Protective Ventilation, Continuous Positive Airway Pressure (CPAP), Positive End Expiratory
Pressure (PEEP) and Selective Lobar Ventilation in the Management of Hypoxia During OLV

Malposition of lung isolation devices is a common cause of hypoxemia. A study by Inoue, et al [5], has shown that
patients who experience DLT malposition after turning the patient into lateral decubitus position had more
malpositions during OLV and more hypoxemia. Also, this study showed that after correction of the malposition, the
patients required more interventions (i.e. CPAP or apneic oxygen insufflation) to treat the hypoxemia.
If during OLV the patient experiences hypoxemia, the first step is to ventilate the patients lung with FiO
2
1.0 and
restore two lung ventilation. Once oxygenation improves, reassessment of the lung isolation device takes
precedence (expands the non-ventilated lung and re-assesses the position of the DLT or a bronchial blocker with the

flexible fib
addition, it
alteration o
present, de
interfere w
bronchosco
An alternat
during OLV
seconds at
oxygenatio
Use of CPA
dependent
volume bre
CPAP. If n
Figure 2





Another al
the use of a
segment w
is approxim
be at risk o
improve ox
lung will in
non-depen


Should PE

In some pa
functional
value is titr
PEEP in th
during OLV
below their
external PE

Outcomes
factors that
beroptic bronch
t is important to
of these factors
espite the fact t
with surgical ex
ope has been sh
tive to improve
V. One study [
different interv
on rose from 67
AP has been tr
(collapsed) lun
eath. It is prud
necessary CPA
ternative to im
a selective loba
while the rest is
mately 24%. [3
of developing h
xygenation wit
nterfere with su
dent lung, it is
EEP be used R
atients, the app
residual capac
rated along the
he dependent lu
V. [37] Howev
r functional res
EEP to the dep
research studie
t is independen
hoscope). [28]
o maintain the
s will also cont
that tube positio
xposure, a selec
hown to impro
e oxygenation
[30] has shown
val periods imp
712 to 9920
raditionally use
ng. The applic
dent to start wit
AP can be easil
mprove oxygena
ar blockade. In
being ventilate
33] Patients wit
hypoxemia dur
th or without C
urgical exposu
advisable to o
Routinely in al
lication of PEE
city close to nor
e static complia
ung during OLV
ver, patients wi
sidual capacity
endent lung. [3
es performed in
ntly associated
After the corre
patient under
tribute to the de
on is optimal, d
ctive ipsilateral
ove oxygenatio
to the non-dep
n that slow infl
proves oxygen
mmHg during
ed to treat hypo
cation of CPAP
th 5 cmH
2
O of
ly applied to a D
ation and treatm
n some instanc
ed. [31-32] It i
th previous lob
ring total lung c
CPAP. [34] Hig
ure and may com
observe the dire
ll Patients Und
EP to the depen
rmal values. [3
ance curve. [36
V. Many patie
ith normal lung
y at the end-exp
37]
n patients unde
with acute lun
5
ect position is o
OLV normoca
evelopment of
during thorasc
l segmental ins
n without inter
pendent lung is
ation of 2 l/min
nation and satur
g OLV.
oxemia due to t
P has been sugg
f CPAP and pro
DLT or a bron
ment of hypox
ces, it will only
is estimated tha
bectomy requir
collapse. One a
gher levels of C
mpromise veno
ect distention o
dergoing OLV
ndent (ventilate
35] This ventila
6] However, no
ents, particular
g parenchyma
piration during
ergoing thoraci
ng injury is the
obtained, aspir
arbic, normoten
f hypoxemia. I
opic surgery w
sufflation of ox
rfering with su
s to use intermi
n of oxygen in
ration. In the 1
the obligatory
gested to be us
ogressively inc
nchial blocker.
emia in patient
y be necessary
at after a lobe r
ring another su
alternative is to
CPAP (i.e. >10
ous return. Al
of the collapsed
V
ed) lung is ben
atory maneuve
ot all patients w
rly those with e
or those with r
g OLV and may
ic surgical proc
high intraoper
ration of secret
nsive and norm
In cases where
where the appli
xygen with a fi
urgical exposur
ittent positive a
nto the non-dep
10 patients rep
shunt develope
sed in the defla
crease to no mo
See Figure 2
ts who have pr
to partially col
resection, the l
urgery in the co
o use selective
0 cmH
2
O) to th
lways, when ap
d lung.
neficial through
er will prevent
will tolerate the
emphysema, de
restrictive lung
y benefit from
cedures have s
rative ventilato
tions follows.
mothermic. A
hypoxemia is
cation of CPA
iberoptic
re. [29]
airway pressur
pendent lung fo
ported, the mea
ed by the non-
ation phase of a
ore than 10 cm
revious lobecto
llapse one lobe
oss of lung fun
ontralateral lun
lobar collapse
he non-depende
pplying CPAP
h the restoratio
atelectasis whe
e routine use o
evelop auto-PE
g disease tend t
the application
shown that one
ory pressure ind
In
Any
P can
e
or 2
an
a tidal
mH
2
O
omy is
e
nction
ng may
e to
ent
to the
on of
en its
f
EEP
to fall
n of
of the
dex.
6

[38] Recent research has recommended the use of low tidal volumes during thoracic surgical procedures and during
OLV. One study [39] has shown that low tidal volume of 6 ml/kg during OLV with the use of FiO
2
=0.6-0.7 and
CPAP 5 cmH
2
O to the non-dependent lung lead to a higher PaO
2
(14182 vs 11249) mmHg when compared to low
tidal volumes and PEEP 5 cmH
2
O to the dependent lung.

Also, alveolar recruitment maneuvers have been recommended to improve oxygenation during OLV. Tusman, et al
[40], have shown the beneficial effects with an alveolar recruitment maneuver with pressure controlled ventilation.
They reported that PaO
2
values were similar to the ones obtained during two lung ventilation.

During OLV it is not uncommon to alternate from volume controlled ventilation to pressure controlled ventilation in
order to improve oxygenation. One study has demonstrated that a better oxygenation is achieved when pressure
controlled ventilation is used during OLV. [41] However, another study [42] in a crossover experiment involving
thoracic surgical patients requiring OLV showed that arterial oxygenation was similar in the groups that received
volume controlled ventilation when compared to pressure controlled ventilation. Also, this study observed a
decrease in peak plateau pressure in the patients that received pressure controlled ventilation. The use of pressure
controlled ventilation would be more beneficial in the morbidly obese patient undergoing OLV. (Personal report this
study is underway) to demonstrate the advantage of this mode of ventilation to maintain optimal oxygenation during
OLV.

Pharmacologic interventions have been studied to control pulmonary blood flow during OLV. [43-46] Some studies
have shown that the use of a respiratory stimulant, such as almitrine intravenously and with an infusion, improved
oxygenation during OLV, probably due to the molecular mechanisms of action on the pulmonary vessels combined
with direct stimulation of chemoreceptors and direct pulmonary vasoconstrictive action. [43] Also, others have
shown no effect on oxygenation when inhaled nitric oxide has been used in patients requiring OLV. [44] However,
the combination of inhaled nitric oxide with intravenous almitrine has shown promising results while improving
PaO
2
during OLV. [45-46] At the present time, I believe these drugs are in the experimental phase to recommend
routine use to improve oxygenation during OLV.


Influence of Anesthetics on Hypoxia During the Intraoperative Period and Potential Complications in the
Postoperative Period

In the 1980s, special attention was given to the effects of anesthetics and HPV during OLV. However, in the past
10 years more attention has been given to the effects on ventilation, and the inflammatory response and their
potential complications after OLV, which is the development of ALI. Some of the studies have included very
limited samples of studied patients. One study [24] has shown that the use of small tidal volumes (5 ml/kg) during
OLV had lower levels of interleukin (IL-8, 10, and TNF) when compared to high tidal volumes of 10 ml/kg. Others
have shown a protective effect in modulating the inflammatory response when inhalational agents are used during
OLV compared to pure total intravenous anesthesia. [47-49] Reduction of inflammatory mediators had significantly
better clinical outcomes defined by postoperative adverse events such as atelectasis or systemic inflammatory
response syndrome. [48] As part of the intervention to manage hypoxemia and inflammatory response during OLV,
I recommend the use of inhalational agents during the management of these patients.


Cerebral Desaturation During OLV

Another area that deserves special attention is the effect of hypoxia during OLV in relationship to a decrease in
regional cerebral oxygen saturation (SctO
2
) in thoracic surgical patients. There are different monitors that measure
SctO
2
such as the FORESIGHT

or the INVOS

[50, 51] monitor. These devices have been used in patients

undergoing OLV with mixed results. A study by Hemmerling et al [50] showed that an absolute value of SctO
2
of
80% was recorded while the patients were awake; during OLV this value decreased to an average of 63%, and
during extubation it rose to 71%. Overall in the 20 patients studied, cerebral desaturation >20% was recorded from
7

baseline values. Interesting in this study was the lack of correlation with SpO and PaO
2
. Also, no mini-mental state
examination (MMSE) test was performed to evaluate the cognitive function outcome of these patients. In another
study [51] involving 40 patients undergoing OLV, a SctO
2
monitor was used to measure cerebral desaturation in 28
patients; the minimum SctO
2
during OLV was lower than baseline value. The percentage of change was
significantly negatively correlated with preoperative respiratory function. Another study [52] showed that the
duration of cerebral desaturation time during OLV correlates with the MMSE; of the 69 patients studied only 17
developed desaturation (SctO
2
<80% of the baseline value) and MMSE scores decreased significantly in this group
of patients. Overall, although measuring SctO
2
values is interesting technology, further studies are needed to
demonstrate the changes in SctO
2
during OLV and the association with hypoxemic events measured by SpO
2
.


Restoration of Two-Lung Ventilation

During OLV, the non-dependent (collapsed) lung remains atelectatic and hypoperfused due to HPV. After expansion
of two-lung ventilation along with the re-entry of oxygen through the airways and alveoli, this produces a reactive
pulmonary vascular dilation due in part to the phenomenon of reperfusion as subsequent free oxygen radicals are
released. The re-oxygenation injury is the structural damage caused by the excessive production of free radicals.
The free radicals interact with cellular structural molecules, producing dysfunction to the endothelial cells. One
study [20] has shown that switching from OLV to two-lung ventilation induces a massive production of reactive
oxygen species in video-assisted thoracoscopic surgery with minimal lung injuries. In this study, extravascular lung
water index, intrathoracic blood volume, and permeability index were insignificantly changed after reassuming two-
lung ventilation. Also, this study showed that the amount of total antioxidants was adequate to counteract the
reactive oxygen species. However, these values may be different in patients with extensive lung tumors or
pulmonary trauma. Another study [53] showed that OLV >1 hour can be a potential cause for cardiovascular
complications (i.e., cardiac arrhythmias) through the generation of severe oxidative stress during re-expansion and
conversion to two-lung ventilation. However, further studies are needed to validate these results as a potential
cause/effect.


Summary

Hypoxemia during OLV is an infrequent finding, ventilatory maneuvers to optimize and improve oxygenation is
listed in table I. Inhalational agents appear to have a protective effect in controlling inflammatory response during
OLV. Low tidal volumes with PEEP in the dependent lung along with CPAP in the non-dependent lung appear to
be the most common intervention to treat hypoxemia [54].

Table 1: Treatment of Hypoxia During One-Lung Ventilation
Increase FiO
2
1.0 Adjust ventilation according to patient needs pressure
control vs volume control?
Re-expand the collapsed lung If a DLT is being used in video thoracoscopic
surgery, consider selective O
2
insufflation to the non-
ventilated lung with fiberoptic bronchoscope
Convert to two lung ventilation If a bronchial blocker is used, consider selective lobar
blockade in patients with previous contralateral
lobectomy
Confirm position with fiberoptic bronchoscope for
optimal position of lung isolation device
Intermittent O
2
insufflation with 2 l/min for short
intervals to the non-dependent lung
After SPO
2
>98%, convert to OLV and apply CPAP
5 cmH
2
O to non-dependent lung
Recruitment ventilatory maneuvers during OLV
Unless contraindicated (i.e. auto PEEP >10), use
PEEP 5 cm H
2
O routinely to the dependent lung
Clamping of pulmonary vessel during
pneumonectomy cases will reduce the shunt fraction

8

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