UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl)
UvA-DARE (Digital Academic Repository)
Lung-protective perioperative mechanical ventilation
Hemmes, S.N.T.
Publication date
2015
Document Version
Final published version
Link to publication
Citation for published version (APA):
Hemmes, S. N. T. (2015). Lung-protective perioperative mechanical ventilation.
General rights
It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s)
and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open
content license (like Creative Commons).
Disclaimer/Complaints regulations
If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please
let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material
inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter
to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You
will be contacted as soon as possible.
General introduction and
outline of the thesis
10
Prevention of postoperative pulmonary complications
Mechanical ventilation is frequently considered a simple but foremost harmless intervention
in patients under general anaesthesia for surgery. Recent investigations, however, suggest
that intraoperative ventilation has a strong potential to cause so called ventilator-associated
lung injury.
1Of all patients undergoing ventilation during general anaesthesia for surgery, 5%
will develop one or more postoperative pulmonary complications, that are associated with
high morbidity and mortality.
2, 3There are several mechanisms through which intraoperative
ventilation could cause ventilator–associated lung injury, as such contributing to development of
postoperative pulmonary complications (fig. 1). First, positive pressure ventilation can overstretch
patent alveoli causing damage in those parts of the lung that are aerated during the whole
breath cycle (fig. 1A & 1C).
4, 5Second, repeated opening and closing of alveoli that collapse
at the end of expiration is associated with increased shear stress, known to cause epithelial
destruction (fig. 1B & 1D).
6-8Third, hyperoxia can result in absorption atelectasis, and cause injury
of cellular structures through increased production of reactive oxygen species (ROS) (fig. 1E).
9All these harmful effects are suggested to be preventable through the use of lung–protective
ventilator settings, using low tidal volumes for prevention of overdistension,
10,11use of positive
end–expiratory pressure (PEEP)
12, 13with or without so–called recruitment manoeuvres to prevent
repeated opening and closing,
14, 15and low oxygen fractions (FiO2) preventing atelectasis and
ROS production.
16These insights have led to a paradigm shift from supranormal intraoperative
ventilation, with large tidal volumes to prevent atelectasis and high levels of FiO2 to maximize
oxygenation, to safer ventilation, using lower levels of tidal volumes, higher levels of PEEP and
lower arterial oxygen thresholds.
Tidal volumes
Low tidal volumes in animal studies
The harmful effects of high tidal volumes were first recognized in animal studies of ventilation.
17In these preclinical studies lungs of animals were either challenged with injurious ventilation
strategies using different tidal volumes alone, or in combination with other challenges such as
intratracheal instillation of lipopolysaccharide or live bacteria.
18More or less they all showed
that the extent of alveolar damage and pulmonary oedema depends on the size of tidal volumes
used.
17, 18Low tidal volumes in patients with ARDS
Traditionally patients were ventilated with large tidal volumes of 10 to 15 mL/kg predicted
body weight (PBW). These volumes far exceeded the range of normal tidal volumes in healthy
subjects in rest (7 to 8 mL/kg PBW). The rationale was to prevent atelectasis, as such optimizing
oxygenation and ventilation.
19Randomized controlled clinical trials in critically ill patients with
the acute respiratory distress syndrome (ARDS), however, showed large tidal volumes to be
harmful.
20-24Two metaanalyses convincingly confirmed that ventilation with low tidal volumes in
patients with ARDS is associated with improved survival.
25, 26Consequently, nowadays ventilation
Ch
apt
er
1
11
Low tidal volumes in critically ill patients without ARDS
The finding that ventilation with low tidal volumes benefits patients with ARDS evoked interest
in lung–protective ventilation in critically ill patients who need ventilation for other reasons than
ARDS, for example comatose patients with neurologic damage and patients after major cardiac
surgery. One randomized controlled trial comparing ventilation with low tidal volumes (6 mL/kg
PBW) to ventilation with high tidal volumes (10 mL/kg PBW) indeed suggested benefit from low
tidal volumes, as it seemed to reduce the incidence of ARDS.29 These findings were confirmed
in a series of metaanalyses.18, 30, 31 In addition, these analyses revealed that ventilation with
low tidal volumes was associated with earlier liberation from the ventilator. Even though a
substantial reduction in tidal volume size is seen in recent years,27, 28 lung–protective ventilation
using low tidal volumes is not yet considered standard of care for critically ill patients who need
ventilatory support for reasons other than ARDS.
Low tidal volumes during intraoperative ventilation
Several small clinical trials of intraoperative ventilation suggested that tidal volume reduction
could reduce local production of inflammatory mediators and possibly improve pulmonary
mechanics.
32-34A large retrospective trial showed that pressure- and volume–limited ventilation
during general surgery decreases the development of postoperative respiratory complications.
35Recently, three randomized controlled trials provided more robust evidence for benefit from this
ventilation strategy.
36-38An Italian single–centre trial showed that a ventilation strategy using tidal
volumes of 7 mL/kg PBW compared to ventilation with tidal volumes of 9 mL/kg PBW during
abdominal surgery was associated with superior postoperative pulmonary function.
36A French
multicentre trial found that in patients undergoing abdominal surgery a ventilation strategy
with reduced tidal volumes of 6 mL/kg PBW compared to tidal volumes of 12 mL/kg PBW was
associated with a decreased incidence of postoperative complications by almost 65%.
37One
Chinese trial in patients undergoing spinal fusion reported an even more impressive benefit of
tidal volume reduction from 12 to 6 mL/kg PBW on postoperative pulmonary complications.
38Contrasting to these results, one retrospective study showed that use of low tidal volume
ventilation (6 to 8 mL/kg PBW) is associated with increased postoperative mortality, though
the authors claim this to be caused by insufficient levels of PEEP.
39Despite the suggestion that
low tidal volume ventilation in surgery patients is increasingly accepted,
40, 41recent studies show
imperfect implementation of this strategy in the operation room.
42-45Positive end–expiratory pressure
Positive end–expiratory pressure in animal studies
Several studies in animals with lung injury have shown that ventilation with PEEP compared to
ventilation without PEEP improves oxygenation and lung mechanics, and prevents formation of
lung edema.
5, 17, 46Similar results came from studies in animals without lung injury. Ventilation
with PEEP in combination with low tidal volumes attenuated local production of inflammatory
mediators,
47-52lung edema,
48, 51and cell injury.
47-52One important shortcoming of PEEP, however,
is that it could cause overdistension of the lung parts that remain aerated during the complete
breath cycle.
53In addition, use of higher levels of PEEP could compromise the circulation.
5412
Figure 1. Mechanisms through which intraoperative ventilation could cause ventilator–
associated lung injury
A) Ventilation at high lung volumes result in overdistention of the lung and hyperinflation may cause gross barotrauma (air leaks), but can also cause an increase in pulmonary oedema; B) ventilation at low lung volumes causes repeated opening and closing of alveoli that collapse at the end of expiration, resulting in increased shear stress and lung injury (atelectrauma). Collapse of large regions of the lung during ventilation at low lung volumes cause lung inhomogeneity; C) ventilation at too high levels of PEEP can aggravate overdistention of lung tissue at end-expiration; D) ventilation at low levels of PEEP increases formation of atelectasis and lung inhomogeneity; E) high levels of fractional inspired oxygen (FiO2) can increase
the production of reactive oxygen species (ROS), which have a direct toxic effect on lung cells. Too high levels of FiO2 also
increases the risk of resorption atelectasis; F) these mechanical and chemical stressors cause structural and biological changes in the alveoli. Inflammatory mediators are released in the lung and recruit neutrophils. They also cause changes that promote pulmonary fibrosis. The increase in alveolar-capillary permeability causes an increase in pulmonary oedema, but also facilitate translocation of mediators and bacteria to the systemic circulation; G) these structural and biological changes result in lung injury, which can cause an increase in postoperative pulmonary complications and worse clinical outcome with increased length of hospital stay and higher incidence of mortality (H)
Positive end–expiratory pressure in patients with ARDS
Three randomized controlled trials in patients with ARDS failed to show an effect of higher levels
of PEEP on survival.
55-57One metaanalysis using the individual patient data of these three trials,
however, showed survival benefit in patients with more severe ARDS.
58Consequently, nowadays
most clinicians use higher levels of PEEP (10 cm H2O and higher) in patients with moderate or
severe ARDS.
27Ch
apt
er
1
13
Positive end–expiratory pressure in critically ill patients without ARDS
In critical care patients without ARDS, there is limited evidence for benefit of PEEP.
59, 60One
randomized controlled trial in patients at risk for ARDS showed no difference between a strategy
using PEEP (5 to 8 cm H2O) and a strategy using a minimal levels of PEEP for adequate oxygenation
with regard to later development of ARDS or mortality.
59This was confirmed in another trial in
patients without ARDS, but in this trial use of higher levels of PEEP was associated with a lower
incidence of ventilator–associated pneumonia.
60In the randomized controlled trial comparing low
and high tidal volumes (6 ml/kg PBW versus 10 ml/kg PBW) in patients without ARDS mentioned
above,
29an independent association between higher levels of PEEP and development of ARDS
was found. In the postoperative phase there is also no clear evidence for benefit from PEEP.
Indeed, while PEEP improves pulmonary compliance and arterial oxygenation, these effects only
last in the first hours after surgery.
61This is also true for the prevention of atelectasis.
62In one
trial in patients after cardiac surgery in which PEEP was titrated on the best achievable PaO2
level no sustained benefit was found.
63In general, intensive care unit clinicians now use PEEP
levels between 4 and 7 cm H2O in critically ill patients who need ventilation for other reasons
than ARDS,
28though the best level of PEEP for these patients remains unclear.
Positive end–expiratory pressure during intraoperative ventilation
Induction of anaesthesia induces atelectasis,
64increasing ventilation–perfusion mismatch and
suboptimal oxygenation.
65Intraoperative use of PEEP, with or without recruitment manoeuvres,
is suggested to prevent atelectasis and repeated opening and closing of lung tissue.
6514Indeed,
use of higher levels of PEEP seems to improve oxygenation and respiratory mechanics in a wide
range of patient populations and surgical settings.
15, 66-74However, in most trials of intraoperative
PEEP, recruitment of lung tissue was not maintained in the postoperative period at the post
anaesthesia care unit (PACU).
72, 73Benefit of higher levels of PEEP on postoperative outcome was suggested in the three randomized
controlled trials of lung–protective intraoperative ventilation mentioned above, where use of low
tidal volumes was actually combined with higher levels of PEEP with recruitment maneuvers.
36-38It is difficult, if not impossible to conclude what prevented postoperative complications: the
use of low tidal volumes or the high levels of PEEP, or recruitment manoeuvres, or altogether.
Despite this, both low tidal volumes and high levels of PEEP with recruitment manoeuvres are
suggested to be beneficial.
75A recent large retrospective study confirms this suggestion, showing
that both low tidal volumes (< 10 mL/kg) and higher PEEP levels (≥ 5 cmH2O) are independently
associated with a decreased risk of postoperative respiratory complications.
35The lack of sufficient evidence for benefit of higher levels of PEEP during surgery is mirrored in
the remarkable variation in use of intraoperative PEEP varying from 17% to as high as 82% of
recently reported series.
40-42, 44, 4514
Oxygen fractions
Oxygen fractions in animal studies
The potentially toxic effects of high fractions of inspired oxygen (FiO2) have long been known
from animal studies. Mice exposed to hyperoxia develop a condition similar to ARDS, which
is at least in part dependent on an increased production of reactive oxygen species (ROS) by
mitochondria.
76, 77Hyperoxia could further cause atelectasis, tracheobronchitis, interstitial fibrosis,
protein leakage and neutrophil infiltration.
78-80In spontaneous breathing rodents with pneumonia,
hyperoxia has been shown to contribute to bacterial spread beyond the lungs,
81lung injury and
even lethality.
82More cytokine production and increased lung injury was found in experiments
in ventilated rodents with hyperoxia during injurious ventilation (tidal volume > 20 mL/kg).
83-85Oxygen fractions in patients with ARDS
In human lungs high FiO2 can also accelerate the production of ROS, which overwhelms natural
anti–oxidant defences and injures cellular structures in the lung.
9,16,86,87Furthermore, hyperoxia
can cause derecruitment of lung tissue by resorption atelectasis.
88Critically ill patients with lung
injury are possibly more prone to the harmful pulmonary effects of oxygen toxicity, which can
coincide with the primary pulmonary injury (e.g., ARDS, pneumonia) and ventilator–associated
lung injury.
77,89,90One small trial found that 100% compared to 60% FiO2 increased development of
atelectasis in patients with ARDS, which was prevented by application of higher levels of PEEP.
91However, clinical trials examining the effect of hyperoxia on the development of lung injury in
patients with ARDS are lacking.
Oxygen fractions in critically ill patients without ARDS
In critical care patients who need ventilatory support for reasons other than ARDS, an association
between hyperoxia and mortality was found in ventilated patients,
89patients after cardiac arrest,
92and patients with traumatic brain injury,
93or stroke.
94However, other studies did not reveal such
associations.
90, 95-97For example, two recent metaanalyses investigating the effect of high FiO2
in critical care patients on survival showed mixed results.
98, 99One metaanalysis did not find a
significant association in the general ICU,
98while another metaanalysis of pooled data from all
critically ill patients suggested arterial hyperoxia to increase the risk of mortality.
99In subset
analyses, hyperoxia was associated with decreased survival in patients after cardiac arrest,
traumatic brain injury, and stroke.
98In patients after cardiac arrest a dose–dependent association
between hyperoxia and patient outcome was found.
99,100Notably, arterial hyperoxia decreases
coronary blood flow and cardiac output, increases systemic vascular resistance, and contributes
to reperfusion injury in patients with myocardial infarction.
101-104A recent randomized controlled
trial in patients with myocardial infarction indeed clearly showed that supplemental oxygen
increased myocardial injury.
105Research on the effect of FiO2 on the development of lung injury
in patients ventilated for other reasons than ARDS, however, is currently unavailable. Despite
the lack of evidence, current guidelines in critically ill patients aim at PaO2 levels around 55–80
mm Hg.
55,106Oxygen fractions during intraoperative ventilation
Anaesthesiologists use high FiO2 during pre–oxygenation and denitrogenation to prolong the
apnoea tolerance time
107and during intraoperative ventilation to correct for arterial hypoxemia
Ch
apt
er
1
15
induced by ventilation–perfusion mismatches caused by alveolar collapse.
64High FiO2 (> 80%)
increases the incidence of resorption atelectasis, which not only augments atelectasis formation
after induction,
107,108but also directly before emergence from anaesthesia in the post–oxygenation
phase, annulling the open lung created during intraoperative ventilation.
109At the same time,
there is a risk of hyperoxia–induced injury to the lungs. The available trials and metaanalyses on
perioperative hyperoxia focused on the beneficial effect of high FiO2 on postoperative nausea
and vomiting
110-112and postoperative wound infections.
113-118A large trial on postoperative
wound infections investigated the effect of 80% compared to 30% oxygen during surgery on
development of postoperative pulmonary complications as secondary endpoint and found no
difference in incidence of atelectasis, pneumonia, and respiratory failure.
117A clinical trial in
obese patients showed worse postoperative lung function in patients receiving FiO2 during
ventilation.
119One metaanalysis found no difference in presence or absence of atelectasis or
postoperative gas exchange during intraoperative ventilation with either high or low FiO2.
120A
large recent metaanalysis, however, suggested that hyperoxia was not associated with increased
30–day mortality.
121Sufficiently powered clinical trials on lung injury and postoperative pulmonary
complications due to high FiO2 are lacking.
Aims of this thesis
This thesis is a collection of investigations that focused on several aspects of perioperative
ventilation, specifically ventilation practice and the associations between ventilator settings and
the effects on postoperative pulmonary complications and outcome. The main interest was on
PEEP. We hypothesized that the use of higher PEEP and recruitment manoeuvres would protect
against development of postoperative pulmonary complications during intraoperative ventilation.
The specific aims of this thesis were:
1.
To investigate the effect of intraoperative use of PEEP and recruitment manoeuvres on
occurrence of postoperative pulmonary complications during low tidal volume ventilation
during open abdominal surgery.
2.
To determine the association between intraoperative use of high tidal volumes, PEEP and
recruitment manoeuvres, and the occurrence of postoperative pulmonary complications.
3.
To investigate the effects of development of postoperative lung injury on postoperative
clinical course and mortality.
4.
To examine the effects of different levels of PEEP during postoperative ventilation after
coronary artery bypass grafting on the duration to extubation.
16
Outline of this thesis
The following chapters in this thesis report on observational studies, clinical trials and
metaanalyses that reported on several aspects of lung–protective perioperative ventilation,
including effects of tidal volume size and level of PEEP.
Chapter 2 provides the results of a metaanalysis of eight clinical trials examining the effects of
intraoperative ventilator settings on postoperative outcome of non–cardiac surgery patients.
We hypothesized that use of low tidal volumes and/or PEEP with or without recruitment
manoeuvres could prevent postoperative pulmonary complications, and as such improving
postoperative outcome. In this metaanalysis we tried to separate the effects of tidal volume
and PEEP manipulations.
Chapter 3 constitutes a comprehensive review of the literature on predictive models of
postoperative pulmonary complications, the pathophysiology of ventilation–induced lung injury,
and protective ventilation strategies, including the respective roles of tidal volume size, the level
of PEEP and the use of recruitment manoeuvres. In this review we propose an algorithm for
protective intraoperative mechanical ventilation.
In Chapter 4 and chapter 5 we describe the design and the results, respectively, of the ‘Local
Assessment of Ventilatory Management during General Anaesthesia for Surgery’–study (LAS
VEGAS), a prospective observational cohort study designed to assess intraoperative ventilation
practice in Europe and the America’s, and to test the hypothesis that certain ventilator settings,
especially high tidal volumes and low PEEP levels, are associated with the occurrence of
postoperative pulmonary complications.
In Chapter 6 we show the results of a metaanalysis using individual patient data from 15
randomized controlled trials of intraoperative ventilation. We hypothesized that intraoperative
ventilation with lower tidal volumes protects against postoperative pulmonary complications,
and that use of higher levels of PEEP adds to the beneficial effects of lower tidal volumes.
Chapter 7 and chapter 8 constitute the design and results of the PROVHILO trial (High versus
low positive end-expiratory pressure during general anaesthesia for open abdominal surgery),
a randomized controlled trial of intraoperative ventilation for open abdominal surgery. In
chapter 9 entails letters with comments on PROVHILO written by peers, as well as our Author’s
reply. In this trial patients were randomized to ventilation with high levels of PEEP (12 cm
H2O) with recruitment manoeuvres or low levels of PEEP (0 to 2 cm H2O) without recruitment
manoeuvres. We hypothesized that a ventilation strategy with high levels of PEEP and recruitment
manoeuvres would protect against development of postoperative pulmonary complications.
In Chapter 10 we describe the results of another metaanalysis, using individual patient data from
12 clinical investigations of intraoperative ventilation. We hypothesized that the occurrence of
postoperative lung injury was associated with a worse outcome, and that postoperative outcome
would depend on intraoperative ventilation settings.
Ch
apt
er
1
17
In Chapter 11 we present the results of a secondary analysis of two randomized controlled trials
of postoperative ventilation in patients undergoing cardiac surgery, in which we determined the
effects of PEEP manipulations on pulmonary compliance and gas exchange in the first hours
of weaning from mechanical ventilation and time on the ventilator.
122, 123We hypothesized that
higher levels of PEEP would improve pulmonary function, but not to be associated with a shorter
duration of postoperative ventilation.
This thesis ends with a summary of the abovementioned studies and a general discussion in
18
References
1. Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from the bench to the bedside. Intensive care medicine 2006; 32(1): 24-33
2. Canet J, Gallart L, Gomar C, et al. Prediction of Postoperative Pulmonary Complications in a Population-based Surgical Cohort. Anesthesiology 2010; 113(6): 1338-50
3. Mazo V, Sabate S, Canet J, et al. Prospective external validation of a predictive score for postoperative pulmonary complications. Anesthesiology 2014; 121(2): 219-31
4. Chiumello D, Carlesso E, Cadringher P, et al. Lung stress and strain during mechanical ventilation for acute respiratory distress syndrome. American journal of respiratory and critical care medicine 2008; 178(4): 346-55
5. Dreyfuss D, Saumon G. Ventilator-induced lung injury: lessons from experimental studies. American journal of respiratory
and critical care medicine 1998; 157(1): 294-323
6. Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol 1970; 28(5): 596-608
7. Chu EK, Whitehead T, Slutsky AS. Effects of cyclic opening and closing at low- and high-volume ventilation on bronchoalveolar lavage cytokines. Critical Care Medicine 2004; 32(1): 168-74
8. Albert RK. The role of ventilation-induced surfactant dysfunction and atelectasis in causing acute respiratory distress syndrome. American journal of respiratory and critical care medicine 2012; 185(7): 702-8
9. Kallet RH, Matthay MA. Hyperoxic acute lung injury. Respiratory Care 2013; 58(1): 123-41
10. Plataki M, Hubmayr RD. The physical basis of ventilator-induced lung injury. Expert Rev Respir Med 2010; 4(3): 373-85 11. Rocco PR, Dos Santos C, Pelosi P. Pathophysiology of ventilator-associated lung injury. Current Opinion in Anaesthesiology
2012; 25(2): 123-30
12. Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta
Anaesthesiologica Scandinavica 1999; 43(3): 295-301
13. Rusca M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during induction of general anesthesia.
Anesthesia and Analgesia 2003; 97(6): 1835-9
14. Lachmann B. Open up the lung and keep the lung open. Intensive Care Medicine 1992; 18(6): 319-21
15. Reinius H, Jonsson L, Gustafsson S, et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis: a computerized tomography study. Anesthesiology 2009; 111(5): 979-87
16. Bhandari V, Elias JA. Cytokines in tolerance to hyperoxia-induced injury in the developing and adult lung. Free radical
biology & medicine 2006; 41(1): 4-18
17. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Respective effects of high airway pressure, high tidal volume, and positive end-expiratory pressure. The American review of respiratory disease 1988; 137(5): 1159-64
18. Serpa Neto A, Nagtzaam L, Schultz MJ. Ventilation with lower tidal volumes for critically ill patients without the acute respiratory distress syndrome: a systematic translational review and metaanalysis. Current opinion in critical care 2014; 20(1): 25-32
19. Marini JJ. Evolving concepts in the ventilatory management of acute respiratory distress syndrome. Clinics in chest
medicine 1996; 17(3): 555-75
20. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. NEJM 1998; 338(6): 347-54
21. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trail Group on Tidal Volume reduction in ARDS. American
journal of respiratory and critical care medicine 1998; 158(6): 1831-8
22. Stewart TE, Meade MO, Cook DJ, et al. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. Pressure- and Volume-Limited Ventilation Strategy Group. NEJM 1998; 338(6): 355-61
23. Brower RG, Shanholtz CB, Fessler HE, et al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Critical care medicine 1999; 27(8): 1492-8
24. ARDSnet. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. NEJM 2000; 342(18): 1301-8
25. Putensen C, Theuerkauf N, Zinserling J, Wrigge H, Pelosi P. Metaanalysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury. Ann Intern Med 2009; 151(8): 566-76
Ch
apt
er
1
19
patients with acute lung injury: a systematic review and metaanalysis. PLoS One 2011; 6(1): e14623
27. Needham DM, Colantuoni E, Mendez-Tellez PA, et al. Lung protective mechanical ventilation and two year survival in patients with acute lung injury: prospective cohort study. BMJ 2012; 344: e2124
28. Esteban A, Frutos-Vivar F, Muriel A, et al. Evolution of mortality over time in patients receiving mechanical ventilation.
American journal of respiratory and critical care medicine 2013; 188(2): 220-30
29. Determann RM, Royakkers A, Wolthuis EK, et al. Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: a preventive randomized controlled trial. Critical Care 2010; 14(1): R1 30. Serpa Neto A, Simonis FD, Barbas CS, et al. Association between tidal volume size, duration of ventilation, and sedation
needs in patients without acute respiratory distress syndrome: an individual patient data metaanalysis. Intensive Care
Medicine 2014; 40(7): 950-7
31. Serpa Neto A, Cardoso SO, Manetta JA, et al. Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a metaanalysis. JAMA 2012; 308(16): 1651-9
32. Zupancich E, Paparella D, Turani F, et al. Mechanical ventilation affects inflammatory mediators in patients undergoing cardiopulmonary bypass for cardiac surgery: a randomized clinical trial. The Journal of thoracic and cardiovascular
surgery 2005; 130(2): 378-83
33. Chaney MA, Nikolov MP, Blakeman BP, Bakhos M. Protective ventilation attenuates postoperative pulmonary dysfunction in patients undergoing cardiopulmonary bypass. Journal of cardiothoracic and vascular anesthesia 2000; 14(5): 514-8 34. Michelet P, D’Journo XB, Roch A, et al. Protective ventilation influences systemic inflammation after esophagectomy:
a randomized controlled study. Anesthesiology 2006; 105(5): 911-9
35. Ladha K, Vidal Melo MF, McLean DJ, et al. Intraoperative protective mechanical ventilation and risk of postoperative respiratory complications: hospital based registry study. BMJ 2015; 351: h3646
36. Severgnini P, Selmo G, Lanza C, et al. Protective mechanical ventilation during general anesthesia for open abdominal surgery improves postoperative pulmonary function. Anesthesiology 2013; 118(6): 1307-21
37. Futier E, Constantin JM, Paugam-Burtz C, et al. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. NEJM 2013; 369(5): 428-37
38. Ge Y, Yuan L, Jiang X, Wang X, Xu R, Ma W. [Effect of lung protection mechanical ventilation on respiratory function in the elderly undergoing spinal fusion]. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2013; 38(1): 81-5
39. Levin MA, McCormick PJ, Lin HM, Hosseinian L, Fischer GW. Low intraoperative tidal volume ventilation with minimal PEEP is associated with increased mortality. British journal of anaesthesia 2014; 113(1): 97-108
40. Treschan TA, Schaefer MS, Subasi L, Kaisers W, Schultz MJ, Beiderlinden M. Evolution of ventilator settings during general anaesthesia for neurosurgery: An observational study in a German centre over 15 years. European journal of
anaesthesiology 2015; Jan 13 [Epub ahead of print]
41. Wanderer JP, Ehrenfeld JM, Epstein RH, et al. Temporal trends and current practice patterns for intraoperative ventilation at U.S. academic medical centers: a retrospective study. BMC Anesthesiology 2015; 15: 40
42. Jaber S, Coisel Y, Chanques G, et al. A multicentre observational study of intra-operative ventilatory management during general anaesthesia: tidal volumes and relation to body weight. Anaesthesia 2012; 67(9): 999-1008 43. Lellouche F, Dionne S, Simard S, Bussieres J, Dagenais F. High tidal volumes in mechanically ventilated patients increase
organ dysfunction after cardiac surgery. Anesthesiology 2012; 116(5): 1072-82
44. Hess DR, Kondili D, Burns E, Bittner EA, Schmidt UH. A 5-year observational study of lung-protective ventilation in the operating room: a single-center experience. J Crit Care 2013; 28(4): 533 e9-15
45. Karalapillai D, Weinberg L, Galtieri J, et al. Current ventilation practice during general anaesthesia: a prospective audit in Melbourne, Australia. BMC Anesthesiology 2014; 14: 85
46. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high inflation pressures. Protection by positive end-expiratory pressure. The American review of respiratory disease 1974; 110(5): 556-65
47. Vobruba V, Klimenko OV, Kobr J, et al. Effects of high tidal volume mechanical ventilation on production of cytokines, iNOS, and MIP-1beta proteins in pigs. Experimental lung research 2013; 39(1): 1-8
48. Hegeman MA, Hemmes SN, Kuipers MT, et al. The extent of ventilator-induced lung injury in mice partly depends on duration of mechanical ventilation. Critical care research and practice 2013; 2013: 435236
49. Theroux MC, Fisher AO, Horner LM, et al. Protective ventilation to reduce inflammatory injury from one lung ventilation in a piglet model. Paediatric anaesthesia 2010; 20(4): 356-64
50. Wilson MR, Choudhury S, Goddard ME, O’Dea KP, Nicholson AG, Takata M. High tidal volume upregulates intrapulmonary cytokines in an in vivo mouse model of ventilator-induced lung injury. Journal of applied physiology 2003; 95(4): 1385-93 51. Ota S, Nakamura K, Yazawa T, et al. High tidal volume ventilation induces lung injury after hepatic ischemia-reperfusion.
20
American journal of physiology Lung cellular and molecular physiology 2007; 292(3): L625-31
52. Fanelli V, Mascia L, Puntorieri V, et al. Pulmonary atelectasis during low stretch ventilation: “open lung” versus “lung rest” strategy. Critical care medicine 2009; 37(3):
1046-53. Bellardine Black CL, Hoffman AM, Tsai LW, et al. Relationship between dynamic respiratory mechanics and disease heterogeneity in sheep lavage injury. Critical care medicine 2007; 35(3): 870-8
54. Luce JM. The cardiovascular effects of mechanical ventilation and positive end-expiratory pressure. Jama 1984; 252(6): 807-11
55. Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome. The New England journal of medicine 2004; 351(4): 327-36
56. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299(6): 637-45
57. Mercat A, Richard JC, Vielle B, et al. Positive end-expiratory pressure setting in adults with acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2008; 299(6): 646-55
58. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and metaanalysis. JAMA 2010; 303(9): 865-73 59. Pepe PE, Hudson LD, Carrico CJ. Early application of positive end-expiratory pressure in patients at risk for the adult
respiratory-distress syndrome. NEJM 1984; 311(5): 281-6
60. Manzano F, Fernandez-Mondejar E, Colmenero M, et al. Positive-end expiratory pressure reduces incidence of ventilator-associated pneumonia in nonhypoxemic patients. Critical Care Medicine 2008; 36(8): 2225-31
61. Ranieri VM, Vitale N, Grasso S, et al. Time-course of impairment of respiratory mechanics after cardiac surgery and cardiopulmonary bypass. Critical Care Medicine 1999; 27(8): 1454-60
62. Marvel SL, Elliott CG, Tocino I, Greenway LW, Metcalf SM, Chapman RH. Positive end-expiratory pressure following coronary artery bypass grafting. Chest 1986; 90(4): 537-41
63. Celebi S, Koner O, Menda F, Korkut K, Suzer K, Cakar N. The pulmonary and hemodynamic effects of two different recruitment maneuvers after cardiac surgery. Anesthesia and Analgesia 2007; 104(2): 384-90
64. Hedenstierna G, Edmark L. Mechanisms of atelectasis in the perioperative period. Best practice & research Clinical
anaesthesiology 2010; 24(2): 157-69
65. Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005; 102(4): 838-54 66. Yoshino J, Akata T, Takahashi S. Intraoperative changes in arterial oxygenation during volume-controlled mechanical ventilation in modestly obese patients undergoing laparotomies with general anesthesia. Acta Anaesthesiologica
Scandinavica 2003; 47(6): 742-50
67. Valenza F, Vagginelli F, Tiby A, et al. Effects of the beach chair position, positive end-expiratory pressure, and pneumoperitoneum on respiratory function in morbidly obese patients during anesthesia and paralysis. Anesthesiology 2007; 107(5): 725-32
68. Hedenstierna G, Santesson J. Studies on intra-pulmonary gas distribution in the extremely obese. Influence of anaesthesia and artificial ventilation with and without positive end-expiratory pressure. Acta anaesthesiologica
Scandinavica 1977; 21(4): 257-65
69. Perilli V, Sollazzi L, Modesti C, et al. Comparison of positive end-expiratory pressure with reverse Trendelenburg position in morbidly obese patients undergoing bariatric surgery: effects on hemodynamics and pulmonary gas exchange.
Obesity surgery 2003; 13(4): 605-9
70. Gander S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Positive end-expiratory pressure during induction of general anesthesia increases duration of nonhypoxic apnea in morbidly obese patients. Anesthesia and Analgesia 2005; 100(2): 580-4
71. Coussa M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesthesia and Analgesia 2004; 98(5): 1491-5
72. Wetterslev J, Hansen EG, Roikjaer O, Kanstrup IL, Heslet L. Optimizing peroperative compliance with PEEP during upper abdominal surgery: effects on perioperative oxygenation and complications in patients without preoperative cardiopulmonary dysfunction. European journal of anaesthesiology 2001; 18(6): 358-65
73. Weingarten TN, Whalen FX, Warner DO, et al. Comparison of two ventilatory strategies in elderly patients undergoing major abdominal surgery. British journal of anaesthesia 2010; 104(1): 16-22
74. Wirth S, Baur M, Spaeth J, Guttmann J, Schumann S. Intraoperative positive end-expiratory pressure evaluation using the intratidal compliance-volume profile. British journal of anaesthesia 2015; 114(3): 483-90
75. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. NEJM 2014; 370(10): 980
76. Clark JM, Lambertsen CJ. Pulmonary oxygen toxicity: a review. Pharmacological reviews 1971; 23(2): 37-133 77. Morse D, Otterbein LE, Watkins S, et al. Deficiency in the c-Jun NH2-terminal kinase signaling pathway confers
susceptibility to hyperoxic lung injury in mice. American journal of physiology Lung cellular and molecular physiology 2003; 285(1): L250-7
Ch
apt
er
1
21
78. Crapo JD. Morphologic changes in pulmonary oxygen toxicity. Annual review of physiology 1986; 48: 721-31 79. Crapo JD, Barry BE, Foscue HA, Shelburne J. Structural and biochemical changes in rat lungs occurring during exposures
to lethal and adaptive doses of oxygen. The American review of respiratory disease 1980; 122(1): 123-43
80. Fracica PJ, Knapp MJ, Piantadosi CA, et al. Responses of baboons to prolonged hyperoxia: physiology and qualitative pathology. Journal of applied physiology 1991; 71(6): 2352-62
81. Kikuchi Y, Tateda K, Fuse ET, et al. Hyperoxia exaggerates bacterial dissemination and lethality in Pseudomonas aeruginosa pneumonia. Pulmonary pharmacology & therapeutics 2009; 22(4): 333-9
82. Tateda K, Deng JC, Moore TA, et al. Hyperoxia mediates acute lung injury and increased lethality in murine Legionella pneumonia: the role of apoptosis. Journal of immunology 2003; 170(8): 4209-16
83. Li LF, Liao SK, Ko YS, Lee CH, Quinn DA. Hyperoxia increases ventilator-induced lung injury via mitogen-activated protein kinases: a prospective, controlled animal experiment. Critical care 2007; 11(1): R25
84. Makena PS, Luellen CL, Balazs L, et al. Preexposure to hyperoxia causes increased lung injury and epithelial apoptosis in mice ventilated with high tidal volumes. American journal of physiology Lung cellular and molecular physiology 2010; 299(5): L711-9
85. Quinn DA, Moufarrej RK, Volokhov A, Hales CA. Interactions of lung stretch, hyperoxia, and MIP-2 production in ventilator-induced lung injury. Journal of applied physiology 2002; 93(2): 517-25.
86. Aggarwal NR, Brower RG. Targeting normoxemia in acute respiratory distress syndrome may cause worse short-term outcomes because of oxygen toxicity. Annals of the American Thoracic Society 2014; 11(9): 1449-53
87. Barazzone C, White CW. Mechanisms of cell injury and death in hyperoxia: role of cytokines and Bcl-2 family proteins.
American journal of respiratory cell and molecular biology 2000; 22(5): 517-9
88. Edmark L, Auner U, Enlund M, Ostberg E, Hedenstierna G. Oxygen concentration and characteristics of progressive atelectasis formation during anaesthesia. Acta Anaesthesiologica Scandinavica 2011; 55(1): 75-81
89. de Jonge E, Peelen L, Keijzers PJ, et al. Association between administered oxygen, arterial partial oxygen pressure and mortality in mechanically ventilated intensive care unit patients. Critical Care 2008; 12(6): R156
90. Eastwood G, Bellomo R, Bailey M, et al. Arterial oxygen tension and mortality in mechanically ventilated patients.
Intensive Care Medicine 2012; 38(1): 91-8
91. Aboab J, Jonson B, Kouatchet A, Taille S, Niklason L, Brochard L. Effect of inspired oxygen fraction on alveolar derecruitment in acute respiratory distress syndrome. Intensive Care Medicine 2006; 32(12): 1979-86
92. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. Jama 2010; 303(21): 2165-71
93. Brenner M, Stein D, Hu P, Kufera J, Wooford M, Scalea T. Association between early hyperoxia and worse outcomes after traumatic brain injury. Archives of surgery 2012; 147(11): 1042-6
94. Rincon F, Kang J, Maltenfort M, et al. Association between hyperoxia and mortality after stroke: a multicenter cohort study. Critical Care Medicine 2014; 42(2): 387-96
95. Bellomo R, Bailey M, Eastwood GM, et al. Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest. Critical care 2011; 15(2): R90
96. Young P, Beasley R, Bailey M, et al. The association between early arterial oxygenation and mortality in ventilated patients with acute ischaemic stroke. Critical care and resuscitation : journal of the Australasian Academy of Critical
Care Medicine 2012; 14(1): 14-9
97. Raj R, Bendel S, Reinikainen M, et al. Hyperoxemia and long-term outcome after traumatic brain injury. Critical Care 2013; 17(4): R177
98. Damiani E, Adrario E, Girardis M, et al. Arterial hyperoxia and mortality in critically ill patients: a systematic review and metaanalysis. Critical care 2014; 18(6): 711
99. Helmerhorst HJ, Roos-Blom MJ, van Westerloo DJ, de Jonge E. Association Between Arterial Hyperoxia and Outcome in Subsets of Critical Illness: A Systematic Review, Metaanalysis, and Meta-Regression of Cohort Studies. Critical Care
Medicine 2015
100. Wang CH, Chang WT, Huang CH, et al. The effect of hyperoxia on survival following adult cardiac arrest: a systematic review and metaanalysis of observational studies. Resuscitation 2014; 85(9): 1142-8
101. Farquhar H, Weatherall M, Wijesinghe M, et al. Systematic review of studies of the effect of hyperoxia on coronary blood flow. American heart journal 2009; 158(3): 371-7
102. Kenmure AC, Murdoch WR, Beattie AD, Marshall JC, Cameron AJ. Circulatory and metabolic effects of oxygen in myocardial infarction. British medical journal 1968; 4(5627): 360-4
103. McNulty PH, Robertson BJ, Tulli MA, et al. Effect of hyperoxia and vitamin C on coronary blood flow in patients with ischemic heart disease. Journal of applied physiology 2007; 102(5): 2040-5
104. Mak S, Azevedo ER, Liu PP, Newton GE. Effect of hyperoxia on left ventricular function and filling pressures in patients with and without congestive heart failure. Chest 2001; 120(2): 467-73
105. Stub D, Smith K, Bernard S, et al. Air Versus Oxygen in ST-Segment-Elevation Myocardial Infarction. Circulation 2015; 131(24): 2143-50
22
106. Patroniti N IG. Mechanical ventilation—Skills and techniques. Patient-centered Acute Care Training (PACT) Module— European Society of Intensive Care Medicine 2015
107. Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003; 98(1): 28-33
108. Hedenstierna G. Oxygen and anesthesia: what lung do we deliver to the post-operative ward? Acta Anaesthesiologica
Scandinavica 2012; 56(6): 675-85
109. Benoit Z, Wicky S, Fischer JF, et al. The effect of increased FiO2 before tracheal extubation on postoperative atelectasis.
Anesthesia and Analgesia 2002; 95(6): 1777-81, table of contents
110. Greif R, Laciny S, Rapf B, Hickle RS, Sessler DI. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology 1999; 91(5): 1246-52
111. Orhan-Sungur M, Kranke P, Sessler D, Apfel CC. Does supplemental oxygen reduce postoperative nausea and vomiting? A metaanalysis of randomized controlled trials. Anesthesia and analgesia 2008; 106(6): 1733-8
112. Simurina T, Mraovic B, Mikulandra S, et al. Effects of high intraoperative inspired oxygen on postoperative nausea and vomiting in gynecologic laparoscopic surgery. Journal of clinical anesthesia 2010; 22(7): 492-8
113. Scifres CM, Leighton BL, Fogertey PJ, Macones GA, Stamilio DM. Supplemental oxygen for the prevention of postcesarean infectious morbidity: a randomized controlled trial. American journal of obstetrics and gynecology 2011; 205(3): 267 e1-9 114. Greif R, Akca O, Horn EP, Kurz A, Sessler DI. Supplemental perioperative oxygen to reduce the incidence of
surgical-wound infection. NEJM 2000; 342(3): 161-7
115. Qadan M, Akca O, Mahid SS, Hornung CA, Polk HC, Jr. Perioperative supplemental oxygen therapy and surgical site infection: a metaanalysis of randomized controlled trials. Archives of surgery 2009; 144(4): 359-66
116. Pryor KO, Fahey TJ, 3rd, Lien CA, Goldstein PA. Surgical site infection and the routine use of perioperative hyperoxia in a general surgical population: a randomized controlled trial. JAMA 2004; 291(1): 79-87
117. Meyhoff CS, Wetterslev J, Jorgensen LN, et al. Effect of high perioperative oxygen fraction on surgical site infection and pulmonary complications after abdominal surgery: the PROXI randomized clinical trial. JAMA 2009; 302(14): 1543-50 118. Bustamante J, Tamayo E, Alvarez FJ, et al. Intraoperative PaO2 is not related to the development of surgical site
infections after major cardiac surgery. Journal of cardiothoracic surgery 2011; 6: 4
119. Zoremba M, Dette F, Hunecke T, Braunecker S, Wulf H. The influence of perioperative oxygen concentration on postoperative lung function in moderately obese adults. European journal of anaesthesiology 2010; 27(6): 501-7 120. Hovaguimian F, Lysakowski C, Elia N, Tramer MR. Effect of intraoperative high inspired oxygen fraction on surgical
site infection, postoperative nausea and vomiting, and pulmonary function: systematic review and metaanalysis of randomized controlled trials. Anesthesiology 2013; 119(2): 303-16
121. Wetterslev J, Meyhoff CS, Jorgensen LN, Gluud C, Lindschou J, Rasmussen LS. The effects of high perioperative inspiratory oxygen fraction for adult surgical patients. The Cochrane Database of Systematic Reviews 2015; 6: CD008884 122. Dongelmans DA, Veelo DP, Paulus F, et al. Weaning automation with adaptive support ventilation: a randomized
controlled trial in cardiothoracic surgery patients. Anesthesia and Analgesia 2009; 108(2): 565-71
123. Dongelmans DA, Veelo DP, Binnekade JM, et al. Adaptive support ventilation with protocolized de-escalation and escalation does not accelerate tracheal extubation of patients after nonfast-track cardiothoracic surgery. Anesthesia
