Open Journal of Nursing, 2012, 2, 301-306 OJN Published Online November 2012 (
ARDS and ECMO, an update on critical care nursing
Audrey Courtin, Lucienne Sanchez, Jean-Claude Sinquet, Philippe Gaudard, Jacob Eliet,
Frédéric Barge, Pascal Colson
Department of Intensive Care, Hopital Arnaud de Villeneuve, Montpellier, France
Received 18 September 2012; revised 20 October 2012; accepted 2 November 2012
The acute respiratory distress syndrome (ARDS) is a
very serious pathology caused by inflammation of the
lung, usually infectious or traumatic. The alveoli are
filled with inflammatory fluid, impairing gas ex-
change. Mechanical ventilation is the inevitable treat-
ment, but it must ensure specific levels of alveolar
pressure, tidal volume, and positive end-expiratory
pressure (PEEP) not to exacerbate inflammation and
ARDS. This is called protective ventilation but it does
not always guarantee satisfactory blood gases, only
the extra-corporeal membrane oxygenation (ECMO)
can provide. Management of ARDS patient under
ECMO is complex because it combines the care rela-
ted to intensive care patient, very restrictive mecha-
nical ventilation and ECMO. Intensive care nurse re-
quires a very good knowledge of lung disease and re-
spiratory assistance constraints, whether ventilatory
or extra-corporeal.
Keywords: Acute Respiratory Distress Syndro me;
The acute respiratory distress syndrome (ARDS) seri-
ously attacks the pulmonary function and threatens life
because lungs become incompetent and severe hypoxia
develops [1,2]. Without respiratory suppor t, the patient is
unlikely to survive [3]. Howev er, mechanical ventilation,
which is “contra-physiological”, can be deleterious in
maintaining lun g inflammation that characterizes the dis-
ease [4]. Yet, it is essential to ensure oxy-genation and
CO2 removal of blood. So, strict ventilator settings
should be respected to make it “protective”. If haema-
tosis is not provided in these conditions, extra-corporeal
oxygenation (ECMO) takes over, allowing the lungs to
recover. These techniques require nurses a thorough
knowledge of the pathology and treatment issues: pro-
tecting the lung and ensuring haematosis until recovery.
This knowledge has substantially evolved over the last
20 years [5,6].
ARDS is a very serious condition with a high mortality
(20% - 40%) [3]. It is caused by inflammation of the
lung developing quite rapidly (less than 72 hours), cha-
racterized by bilateral opacities visible on chest X-ray
without signs of heart failure (pulmonary edema) [1,7].
Severe hypoxia refractory to high oxygen supply deve-
lops (PaO2/FiO2 < 200 mmHg). The inflammation is
usually reversible, but pulmonary fibrosis scarring may
occur, responsible for severe sequelae with definitive re-
spiratory disability [8].
2.1. ARDS Clinical Presentation
The ARDS is defined as an acute respiratory failure,
cyanosis refractory to oxygen therapy, and diffuse in-
filtrates evident on the chest radiograph. It is often pro-
gressive, characterized by distinct stages with different
clinical and radiographic manifestations. The acute, or
exudative, phase is manifested by the rapid onset of
respiratory failure. Arterial hypoxemia that is refractory
to treatment with supplemental oxygen is a ch aracteristic
feature. Radiographically, the findings are indistinguish-
able from those of cardiogenic pulmonary edema with
alveolar infiltrates. Bilateral infiltrates may be patchy or
asymmetric and may include pleural effusions. Com-
puted tomographic scanning has demonstrated that al-
veolar filling consolidation, and atelectasis occur predo-
minantly in dependent lung zones, while other areas may
be relatively spared. However, bronchoalveolar lavage
studies indicate that even radiographically spared, non-
dependent areas may have substantial inflammation.
Pathological findings include diffuse alveolar damage,
with neutrophils, macrophages, erythrocytes, hyaline mem-
branes, and protein rich edema fluid in the alveolar space,
capillary injury, and disruption of the alveolar epithe-
Although the ARDS may resolve completely in some
patients after the acute phase, in others it progresses to
fibrosing alveolitis with persistent hypoxemia, increased
A. Courtin et al. / Open Journal of Nursing 2 (2012) 301-306
alveolar dead space, and a further decrease in pulmonary
The recovery phase is characterized by the gradual
resolution of hypoxemia and improved lung compliance.
Typically, the radiographic abnormalities resolve com-
pletely. The degree of histologic resolution of fibrosis
has not been well characterized, although in many pati-
ents pulmonary function returns to normal [2].
2.2. ARDS Pathogenesis
Two separate barriers form the alveolar-capillary barrier,
the microvascular endothelium and the alveolar epithe-
lium. The acute phase of acute lung injury and the ARDS
is characterized by the influx of protein-rich edema fluid
into the air spaces as a consequence of increased per-
meability of the alveolar-capillary barrier [2].
The inflammatory pulmonary edema is due to direct
(infection, inhalation, trauma...) or indirect (systemic in-
flammation, polytransfusion, extracorporeal circulation
for cardiac surgery...) injury of the lung [1,2,7].
The alveoli are filled with inflammatory fluid, causing
gas exchange impairment. These soaked alveoli com-
press healthy adjacent areas, favoring alveolar collapse,
creating non-ventilated zones (derecruitment). In addi-
tion, the degradation of surfactant, which lines the walls
of the alveoli usually, preventing their closure during
expiration, may increase this phenomenon [1,2,7].
The inflammatory infiltration increases weight of the
lung. It loses its elastic properties and becomes difficult
to inflate; its compliance falls.
The surface of the alveoli available for gas exchange
in the lungs is decreased in some areas, and then be-
comes insufficient to ensure complete haematosis, cau-
sing hypoxemia. Similarly, the CO2 is difficult to remove,
resulting in hypercapnia and respiratory acidosis. To main-
tain satisfactory oxygenation and normocapnia, physiol-
ogical ventilation is strongly stimulated, but is ineffective
or quickly exhaus ting. Relay with mechanical ventilation
is unavoidable, ev en though it carries a risk of worsening
The cornerstone of the management of ARDS is treat-
ment of the precipitating illness (infection treatment for
instance), and application of a low-volume, low-pressure
ventilation strategy. The use of a conservative fluid-ma-
nagement strategy is also recommended and the admini-
stration of neuromuscular blocking agents may be as-
sociated with decreased mortality when they are used
early in the course of severe ARDS [9,10].
In patients with refractory gas-exchange abnormalities
despite these measures, other so-called unproven thera-
pies should be considered. These include glucocorticoids,
inhaled vasodilators (N0), lung recruitment maneuvers,
high levels of PEEP, prone positioning, and high-fre-
quency oscillatory ventilation.
The decision to use such therapies, including ECMO,
and the order in which they are used, depend on the
clinician’s preference and the availability of resources,
including access to referral centers, since evidence-based
algorithms are not available yet.
3.1. Mechanical Ventilation Can Worsen ARDS
Mechanical ventilation is essential in severe ARDS but
Physiological ventilation is intend ed to carry air to the
alveoli through a bronchial increasingly ramified circuit.
During inhalation, the diaphragm moves down, creating
a vacuum in the lungs which sucks the air inside the
bronchial tree to the alveoli. The rib cage expands and
the lungs, secured to the chest wall by the pleura, fill
with air. The expiration is passive. The thorax returns to
its initial position by releasing the elastic diaphragm and
chest. Pressure becomes positive, the air is expelled. It is
therefore a respiratory cycle at very low pulmonary pres-
sures (Figure 1).
Many things change during mechanical ventilation. It
is contra physiological, since the respiratory cycle is in
positive pressure, either during insufflation and expira-
tion. Moreover, mechanical ventilation may induce lung
injury, by excess of volume inflated (volotrauma) or by
excessive pressure (barotrauma) [10,11]. It has been
shown experimentally that in a few minutes, mechanical
ventilation may cause inflammatory destruction of the
alveoli [12]. These lesions are favored by their over-
distention and deflation. Especially, the sequence of both
activates the inflammatory process and alters the surfac-
tant. The overdistention can be avoided by reducing the
volume inflated (tidal volume) and intra alveolar pres-
sure. Maintaining a positive pressure at the end of expi-
ration (PEEP) prevents deflation and therefore alveolar
collapse, which causes loss of functional alveoli (dere-
cruitment) [13].
Alveoli affected by inflammation are excluded from
ventilation; normal tidal volume (8 to 10 ml/Kg) can
generate very high pressures in areas where alveoli are
healthy or mildly affected. To avoid this complication,
special attention shou ld be paid to the plateau pressure at
the end of insufflation, which represents the alveolar
pressure (Figure 2). The goal of mechanical ventilation
is to ensure haematosis, limiting the risks of trauma with
appropriate ventilator settings.
3.2. Is There a Protective Mechanical
This concept was originally introduced in the context of
ARDS, because the extremely serious pulmonary damage
Copyright © 2012 SciRes. OPEN ACCESS
A. Courtin et al. / Open Journal of Nursing 2 (2012) 301-306
Copyright © 2012 SciRes.
Figure 1. Changes in intrathoracic pressure during spontaneous breathing and mechanical
Table 1. Criteria for protective mechanical ventilation.
ventilation only Mechanical
ventilation and ECMO
Tidal volume 6 to 8 ml/kg* <6 ml/kg*
Plateau pressure<30 cm H2O <28 cm H2O
PEEP 8 - 15 cm H2O 8 - 15 cm H2O
*Ideal weight or predicted. Rating: Male: height in cm-100, Female: height
in cm-110.
barotrauma. The earliness of its implantation can be de-
cisive for the vital prognosis [16-18].
Figure 2. Respiratory cycle during mechanical
of this disease imposes drastic respiratory conditions as
not to aggravate the inflammation, but it tends to extend
to any mode of ventilation [12,13 ].
ECMO circuit includes a blood pump, a membrane lung,
and conduit tubing. Depending on the application addi-
tional components may include a heat exchanger, moni-
tors and alarms (Figure 3) [19].
The principle of this is to protect alveoli and avoid the
derecruitment. The membrane mimics and replaces the pulmonary
alveolar membrane. It thus allows oxygenating the blood
and purifying it of CO2. The most common technique is
the veno-venous ECMO where an extracorporeal circuit
is connected in parallel to the patient's circulation on the
venous return with two main options, femoral-femoral,
or jugular-femoral (more difficult to implant).
We are talking about protective ventilation when to
limit intra alveolar pressure (plateau pressure < 30 cm
H2O), tidal volume is reduced to a minimum (6 - 8 ml/kg)
(Table 1).
Sometimes, this leads to ventilator regime having to
tolerate acceptable hypercapnia if the acidosis is mode-
rate (pH 7.20). The alveolar derecruitment is avoided
by maintaining a high PEEP (8 to 15 cm H2O) [13-15]. 4.1. ECMO Circuit
If despite these conditions of mechanical ventilation,
possibly associated with adjuvant techniques (sedation,
muscle relaxation, prone position, NO inhalation), the
blood gases are not good enough (SpO2 < 90%, hyper-
capnia with pH < 7.20), the use of extracorporeal mem-
brane oxygenation (ECMO) is considered because in-
creasing tidal volume or plateau pressure would be to the
detriment of healthy areas that would suffer volo or
The pump should be able to provide full blood flow for
the patient, i.e. blood flow 3 L/m2/min (neonates 100
cc/kg/min; pediatrics 80 cc/kg/min; adults 60 cc/kg/min.)
Usually centrifugal pump are preferred. Inlet and outlet
line caliber should be selected to avoid either excessive
suction or infusion pressure to avoid hemolysis.
The gas exchange material in membrane lung may be
A. Courtin et al. / Open Journal of Nursing 2 (2012) 301-306
Figure 3. Schematic ECMO circuit.
solid silicone rubber, a microporous hollow-fibre (poly-
propylene), or a solid hollow-fibre (PMP, polymethyl
pentene) membrane. Membrane surface area and mixing
in the blood path determine the maximum oxygenation
capacity (the rated flow) [19].
In venovenous mode, recirculation of infused blood
may occur, raising the inlet saturation well above 75%.
In this situation the outlet-inlet O2 difference per unit of
blood flow is decreased, and higher blood flow, cannula
repositioning, increased patient volume or higher hema-
tocrit are required to provide the desired amount of O2
For most applications, the sweep gas will be 100%
oxygen or carbogen (5% CO2, 95% O2) at a flow rate
equal to the blood flow rate (1:1). Increasing the sweep
flow will increase CO2 clearance but will not affect
oxygenation. Water vapor can condense in the membrane
lung and may be cleared by intermittently increasing
sweep gas flow to a hi g her flow.
Air or oxygen bubbles can pass through the membrane
into the blood if the sweep gas pressure exceeds the
blood pressure, or if the blood pressure is subatmos-
pheric (this occurs when there is no blood flow or blood
pressure, and blood drains from the membrane lung into
the tubing by gravity, entraining air through the mem-
brane lung). This is a specific problem with microporous
hollow fibre devices but can also occur with Silicone or
polymethyl-pentene lungs are due to minor defects which
can allow air entrainment. Prevention is achieved by
maintaining the blood side pressure higher than the gas
side pressure. This is accomplished by including a pres-
sure pop off valve or pressure servo regulatio n control in
the sweep gas supply, and by keeping the membrane lung
below the level of the patient, so that if the pump stops
the risk of entraining air from the room will be mi-
nimized. Even with silicon e and PMP lungs it is safest to
maintain the membrane lung below the level of the
patient [19].
4.2. Running ECMO
Ideally, the oxygenated blood would be closer to the
right atrium. Thanks to a centrifugal pump, the blood is
collected and fed to a membrane oxygenator. As for the
lungs, the blood oxygenation (and removing CO2) de-
pends on both the flow rate of blood there through (the
circuit has a blood flow calculator that is displayed on a
console) and also flow of oxygen-enriched air which
sweeps the surface of the membrane. The blood is then
reheated before being reinjected into the venous system
Then assistance provides haematosis and ventilation
may become even more protective (Ta b l e 1). Thus tidal
volume delivered by the ventilator can be decreased
below 6 ml/kg (down to 1 to 2 ml/kg!) respecting a
plateau pressure of less than 28 cm H2O, while main-
taining a high PEEP (10 to 15 cm H2O). These settings
will protect healthy areas pending recovery of those
affected by the inflammation. The auto worsening vici-
ous circle of mechanical ventilation is thus broken.
ECMO is left in place the necessary time to get suf-
ficient pulmonary function recovery. The theoretical dur-
ation of its use is ten days beyond which the membrane
can be altered and becomes less effective. But the mem-
brane can be changed by the perfusionist (extracorporeal
circulation specialist nurse) if assistance should be con-
Blood gas improvement, radiological and mechanical
ventilation (evidenced by an increase in compliance) sign
the beginning of normalization of pulmonary function.
ECMO withdrawal is considered if the blood gas can be
re-assured by the lungs while remaining in a profile of
ultra protective mechanical ventilation settings. It takes
place gradually with reduced flow rates to test the
effectiveness of the single mechanical ventilation on
oxygenatio n an d pu ri fi cat i o n of CO2.
The patient care with ARDS under ECMO combines
nursing related to heavy intensiv e treatment (immobility,
sedation, enteral and paren teral nutrition), acute monitor-
ing of very restrictive mechanical ventilation and ECMO.
This explains why this nursing workload may require
nurse staffing adaptation, allowing one nurse per patient.
5.1. Monitoring Ventilation
A key challenge in the nurse management is monitoring
ventilation. To prevent baro-or-volo trauma, plateau pres-
sure is monitored continuously to alert if it rises beyond
28 cm of water. This data can also assess the recovery of
the lung: a decrease in the plateau pressure for a fixed
tidal volume indicates an improved compliance, then a
regression of inflammation, whatever the ventilator mode
Copyright © 2012 SciRes. OPEN ACCESS
A. Courtin et al. / Open Journal of Nursing 2 (2012) 301-306 305
(Table 2).
5.2. Avoiding Alveolar Derecruitment
Recovery m a y be delay e d by derecruitment episodes.
Some nursing expose to the fall of the PEEP like endo-
tracheal aspirations, or disconnections of the respiratory
circuit during aerosol delivery or mobilization of the
patient [20]. To limit the risk, arrangements can be made
(Table 3) as the installation of a closed aspiration system
on the respiratory circuit that will allow to make the
aspirations without disconnection [20]. For manipula-
tions that require disconnection of the circuit, the endo-
tracheal tube can be clamped few seconds; then PEEP
effect is not lost. Similarly, for a good seal of the circuit,
the tracheal balloon pressure should be checked several
times a day. Finally, verifying the proper humidification
of the circuit helps to protect lung as cold oxygen dries
respiratory secretions that may cause mucus plugs.
5.3. Monitoring ECMO
ECMO, compensating the lungs, ensures highly protec-
tive ventilation, provided its optimal functioning is
appropriately ensured by the nurse. Blood flow may be
variable and should be controlled continuously. The
effectiveness of extracorporeal membrane oxygenation
depends on the blood flow th at must be at least 2.5 liters/
minute. Below, the patient may not receive enough
oxygenated blood and is exposed to hypo xia. In addition
to adjusting the flow of the blood pump (tour/min), the
performance depends on the ECMO circuit integrity (the
lines are not to be bent or stuck in a fence!), and a suf-
ficient blood volume (risk of flow rate decrease if there
is not enough venous return to the pump). Finally, like
any extracorporeal circuit, there is a risk of thrombosis
Table 2. Ventilator modes, settings and monitoring.
Volume Controlled
ventilation Pressure Controlled
Settings Respiratory rate
Tidal volume
Respiratory rate
Monitoring Plateau pressure Tidal volume
*PEEP: Positive end expiratory pressure; **Insufflation pressure = Plateau
Table 3. Preventing the derecruitment risk.
Avoiding leakages
1) Closed aspiration system
2) Endotracheal tube clamping if circuit
disconnection (aerosols, mobilization)
3) Vigilance +++ in care
which would reduce the effectiveness of the membrane
oxygenator, and therefore alters the patient’s blood gas.
The blood is anticoagulated (heparin), which requires
close monitoring (ACT) (Table 4).
The performance of the combination of protective ven-
tilation and ECMO is assessed on haematosis, already
estimated by the nurse through cannula color: a dark red
line corresponds to venous blood, low oxygened then the
admission line. Conversely red line signs a well oxy-
genated blood, then the infusion line. Blood gas taken
regularly allows adapting the settings of ECMO. If the
blood flow rate is satisfactory, the FiO2 is increased (up
to 1 if necessary) in cases of hypoxia, and the sweep gas
rate is increased in case of hypercapnia [19].
After explantation, the nurse monitoring remains fo-
cused on mechanical ventilation with the same objec-
tives of protective ventilation. When the situation is nor-
malized, weaning from mechanical ventilation is started
with the usual steps, including relief sedation and spon-
taneous ventilation as soon as possible. Even in this
mode, lung protection criteria should be applied in par-
ticular to the tidal volume which must remain at a low
The emergence of serious diseases such as H1N1 that
cause ARDS, has lead medical teams designed to take
care of these patients to turn to alternative techniques of
respiratory support like ECMO. These techniques require
expertise developed through regular practice to be ex-
ploited optimally and safely. Indeed, a multidisciplinary
team of intensivists, surgeons and perfusionists is mo-
bilized during the implantation of the assistance. Logi-
cally, intensive care nurses taking care of these patients
afterwards should be educated in order to guarantee ap-
propriate monitoring and care. In addition to the usual
intensive care unit patient, the intensive care nurse will
have to integrate the operation of the machine, under-
standing ventilation requirements, to be able to provide
early warning if the patient develops signs of worsening
condition. So, naturally, the role of the nurse tends to
evolve with technological developments, its role being
close supervision of course, but also an ability to assess
Table 4. ECMO settings and monitoring.
Settings Monitoring
Blood flow Tours/min Flow L/min
Sweep gas Air/O2 mixture flow
Color of cannulas
Blood gas
State of the membrane
AnticoagualtionHeparin ACT
Copyright © 2012 SciRes. OPEN ACCESS
A. Courtin et al. / Open Journal of Nursing 2 (2012) 301-306
Copyright © 2012 SciRes.
the risks to which expert knowledge and a good under-
standing of the treatment plan are necessary.
[1] Bernard, G.R., Arti gas, A., Brigham, K. L., Carlet, J., Fa l-
ke, K., Hudson, L., Lamy, M., Legall, J.R., Morris, A.
and Spragg, R. (1994) The Amer ican European Consensus
Conference on ARDS. Definitions, mechanisms, relevant
outcomes, and clinical trial coordination. American Jour-
nal of Respiratory and Critical Care Medicine, 149, 818-
[2] Ware, L.B. and Matthay, M.A. (2000) The acute respira-
tory distress sy ndrome. The New England Journal of Me-
dicine, 342, 1334-1349.
[3] Brun-Buisson, C., Minelli, C., Brun-Buisson, C., Bertolini,
G., Brazzi, L., Pimentel, J., Lewandoski, K., Bion, J., Ro-
mand, J.A., Villar, J., Thorsteinsson, A., Damas, P., Ar-
maganidis, F. and the ALIVE Study group (2004) Epi-
demiology and outcome of acute lung injury in European
intensive care units. Results from the ALIVE study. In-
tensive Care Medicine, 30, 51-56.
[4] Webb, H.H. and Tierney, D.F. (1974) Experimental pul-
monary edema due to intermittent positive pressure ven-
tilation with high inflation pressures. American Review of
Respiratory Disease, 110, 556-565.
[5] Dirkes, S., Dickinson, S. and Valentine, J. (1992) Acute
respiratory failure and ECMO. Critical Care Nurse, 12,
[6] Combes, A., Bacchetta, M., Brodie, D., Müller, T. and Pel-
legrino, V. (2012) Extracorporeal membrane oxygenation
for respiratory failure in adults. Current Opinion in Cri-
tical Care, 18, 99-104.
[7] Crimi, E. and Slutsky, A.S. (2002) Inflammation and the
acute respiratory distress syndrome. Best Practice & Re-
search Clinical Anaesthesiology, 18, 477-492.
[8] Herridge, M.S., Tansey, C.M., Matté, A., Tomlinson, G.,
Diaz-Granados, N., Cooper, A., Guest, C.B., Mazer, C.D.,
Mehta, S., Stewart, T.E., Kudlow, P., Cook, D., Slutsky,
A.S. and Cheung, A.M. (2011) Functional disability 5
years after acute respiratory distress syndrome. The New
England Journal of Medicine, 364, 1293-1304.
[9] Brodie, D. and Bacchetta, M. (2011) Extracorporeal me m-
brane oxygenation for ARDS in Adults. The New Eng-
land Journal of Medicine, 365, 1905-1914.
[10] Papazian, L., Forel, J.-M., Gacouin, A., Penot-Ragon, C.,
Perrin, G., Loundou, A., Jaber, S., Arnal, J.-M., Perez, D.,
Seghboyan, J.-M., Constantin, J.-M., Courant, P., Lefrant,
J.-Y., Guerin, C., Prat, G., Morange, S. and Roch, A. (2010)
Neuromuscular blockers in early acute respiratory dis-
tress syndrome. The New England Journal of Medicine,
363, 1107-1116. doi:10.1056/NEJMoa1005372
[11] Boussarsar, M., Thierry, G., Jaber, S., Roudot-Thoraval,
F., Lemaire, F. and Brochard, L. (2004) Relationship be-
tween ventilatory settings and barotrauma in the ARDS.
Intensive Care Medicine, 28, 406-413.
[12] Dreyfuss, D. and Saumon, G. (1998) Ventilator-induced
lung injury: Lessons from experimental studies. American
Journal of Respiratory and Critical Care Medicine, 157,
[13] Briel, M., Meade, M., Mercat, A., Brower, R.G., Talmor,
D., Walter, S.D., Slutsky, A.S., Pullenayegum, E., Zhou,
Q., Cook, D., Brochard, L., Richard, J.C., Lamontagne, F.,
Bhatnagar, N., Stewart, T.E. and Guyatt, G. (2010) Higher
vs lower positive end-expiratory pressure in patients with
acute lung injury and acute respiratory distress syndrome.
Systematic review and Meta-analysis. Journal of the
American Medical Association, 303, 865-873.
[14] Amato, M.B.P., Barbas, C.S.V., Medeiros, D.M., Magaldi,
R.B., Schettino, G.P.P., Lorenzi-Filho, G., Kairalla, R.A.,
Deheinzelin, D., Munoz, C., Oliveira, R., Takagaki, T.Y.
and Carvalho, C.R.R. (1998) Effect of a protective ventil-
ation strategy on mortality in the ARDS. The New Eng-
land Journal of Medicine, 338, 347-354.
[15] The Acute Respiratory Distre ss Syndrome Netwo rk (2000)
Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. The New England
Journal of Medicine, 342, 1301-1308.
[16] Peek, G.J., Mugford, M., Tiruvoipati, R., Wilson, A., Al-
len, E., Thalanany, M.M., Hibbert, C.L., Truesdale, A.,
Clemens, F., Cooper, N., Firmin, R.K. and Elbourne, D.
(2009) Efficacy and economic assessment of conven-
tional ventilatory support versus extracorporeal membrane
oxygenation for severe adult respiratory failure (CESAR):
A multicentre randomized controlled trial. Lancet, 374,
1351-1363. doi:10.1016/S0140-6736(09)61069-2
[17] The Australia and New Zealand Extracorporeal Mem-
brane Oxygenation (ANZ ECMO) Influenza Investigators
(2009) Extracorporeal membrane oxygenation for 2009
influenza A (H1N1) acute respiratory distress syndrome.
Journal of the American Medical Association, 302, 1888-
1895. doi:10.1001/jama.2009.1535
[18] Kopp, R., Henzler, D., Dembinski, R. and Kuhlen, R.
(2004) Extracorporeal membrane oxygenation by acute
respiratory distress syndrome. Anaesthesist, 53, 168-174.
[19] ELSO Guidelines for Cardiopulmonary Extracorporeal
Life Support Extracorporeal Life Support Organization,
Version 1:1. Ann Arbor, April 2009.
[20] Maggiore, S.M., Lellouche, F., Pigeot, J., Taille, S., Deye,
N., Durrmeyer, X., Richard, J.-C., Mancebo, J., Lemaire,
F. and Brochard, L. (2003) Prevention of endotracheal
suctioning-induced alveolar derecruitment in acute lung
injury. American Journal of Respiratory and Critical
Care Medicine, 167, 1215-1224.