Expert answer:Use of ECMO in Adults , difference between VV VA E

Solved by verified expert:Does the hospital you work at actively participate in the use of ECMO as a way of treating adult patients?What is the difference between VV & VA ECMO?What recommendations do the authors provide as a way to mechanically ventilate ECMO patients? What is the rationale behind these recommendations, do you agree or disagree?Create your own question based upon the readings that you would like to pose to your fellow classmates which demonstrates you did more than simply skim the articles provided.Read the articles attatch Thank you
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Schmidt et al. Critical Care 2014, 18:203
http://ccforum.com/content/18/1/203
REVIEW
Mechanical ventilation during extracorporeal
membrane oxygenation
Matthieu Schmidt1*, Vincent Pellegrino2, Alain Combes3, Carlos Scheinkestel2, D Jamie Cooper1,2 and
Carol Hodgson1,2
Abstract
The timing of extracorporeal membrane oxygenation (ECMO) initiation and its outcome in the management of
respiratory and cardiac failure have received considerable attention, but very little attention has been given to
mechanical ventilation during ECMO. Mechanical ventilation settings in non-ECMO studies have been shown to have an
effect on survival and may also have contributed to a treatment effect in ECMO trials. Protective lung ventilation
strategies established for non-ECMO-supported respiratory failure patients may not be optimal for more severe forms of
respiratory failure requiring ECMO support. The influence of positive end-expiratory pressure on the reduction of the
left ventricular compliance may be a matter of concern for patients receiving ECMO support for cardiac failure. The
objectives of this review were to describe potential mechanisms for lung injury during ECMO for respiratory or cardiac
failure, to assess the possible benefits from the use of ultra-protective lung ventilation strategies and to review
published guidelines and expert opinions available on mechanical ventilation-specific management of patients
requiring ECMO, including mode and ventilator settings. Articles were identified through a detailed search of
PubMed, Ovid, Cochrane databases and Google Scholar. Additional references were retrieved from the selected
studies. Growing evidence suggests that mechanical ventilation settings are important in ECMO patients to
minimize further lung damage and improve outcomes. An ultra-protective ventilation strategy may be optimal for
mechanical ventilation during ECMO for respiratory failure. The effects of airway pressure on right and left ventricular afterload should be considered during venoarterial ECMO support of cardiac failure. Future studies are needed
to better understand the potential impact of invasive mechanical ventilation modes and settings on outcomes.
Review
Introduction
Over the past decade, the use of two distinct modalities
of extracorporeal membrane oxygenation (ECMO) for
respiratory and cardiac support in adults has increased.
Venovenous (VV)-ECMO may be initiated as a treatment strategy for patients with severe acute respiratory
failure, including adult respiratory distress syndrome
(ARDS) [1-5], as a salvage therapy for patients with profound gas-exchange abnormalities despite positivepressure ventilation. Additionally, partial extracorporeal
support systems have been suggested for less severe
* Correspondence: matthieuschmidt@yahoo.fr
1
The Australian & New Zealand Intensive Care Research Centre, Department
of Epidemiology and Preventive Medicine, School of Public Health and
Preventive Medicine, Level 6, The Alfred Centre, Commercial Road,
Melbourne, Victoria 3004, Australia
Full list of author information is available at the end of the article
respiratory failure as an adjunct to invasive mechanical
ventilation (MV) for patients who have excessively high
inspiratory airway pressures or who are unable to tolerate
volume-limited and pressure-limited strategies. These
devices predominately remove carbon dioxide (CO2) from
the blood and provide limited oxygenation [6-8]. Such
systems are often classified as extracorporeal carbon dioxide removal (ECCO2R) systems and cannot provide
complete respiratory support. VV-ECMO and ECCO2R
may now be considered management options for chronic
end-stage respiratory failure where MV is contraindicated
or undesirable; for example, as a bridge to lung transplantation in patients with cystic fibrosis who need to perform
airway clearance techniques for sputum retention [9,10].
ECCO2R has also been described for chronic obstructive
pulmonary disease patients with prolonged weaning of
invasive MV [11]. Venoarterial (VA)-ECMO is a rapidly
deployable treatment option for temporary circulatory
© 2014 Schmidt et al.; licensee BioMed Central Ltd. The licensee has exclusive rights to distribute this article, in any medium,
for 12 months following its publication. After this time, the article is available under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Schmidt et al. Critical Care 2014, 18:203
http://ccforum.com/content/18/1/203
assistance in patients with cardiogenic shock or refractory
cardiac arrest [12-14] secondary to a large number of
acute and chronic cardiac illnesses.
MV management during VV-ECMO and VA-ECMO
has received scant attention to date despite high-level
evidence to support low-tidal-volume ventilation strategies
to improve survival [15,16]. The design of randomized
controlled trials of ECMO in ARDS did not use standardized protective ventilation in the interventional arm [8,17]
or in the control arm [3], which could have jeopardized
the success of the ECMO treatment in these trials. MV settings may have important implications in both modes of
ECMO (that is, VV-ECMO and VA-ECMO). Patients with
the most severe forms of lung injury are likely to be particularly susceptible to ventilator-associated lung injury.
Limiting stress and strain with a volume-limited and
pressure-limited protective ventilation strategy beyond that
recommended for patients with ARDS could provide additional benefit during ECMO support [4,18,19]. For patients
with severe cardiac failure supported with VA-ECMO, pulmonary artery blood flow may be severely reduced and the
maintenance of normal alveolar ventilation might lead to
severe over-ventilation of the lungs [20]. Positive airway
pressure settings will also affect right and left ventricular
load in both VV-ECMO and VA-ECMO [21].
Brief guidelines for the use of ECMO [22] and expert
points of views [3,23] have been published, mostly during the recent influenza A(H1N1) pandemic [24]. These
publications are based on clinician preference, experience of centers with high case volumes, previous randomized trials [3] and local resource availability.
While there are extensive reviews on ECMO management [23,25-29], there is a significant knowledge gap in
understanding the benefits and risks of MV during
ECMO. Unlike previous reviews on ECMO [23,27,29],
this review will focus on MV during ECMO. The purpose is to highlight the interactions between MV, ECMO
and the pathophysiology of severe acute respiratory and
cardiac failure. A second purpose is to provide evidence
of the risks associated with MV during ECMO. Additionally, this review will summarize current guidelines,
describe new strategies advocated for MV, provide
evidence-based criteria that can be used for MV during
ECMO and discuss what future studies are needed to
address the evidence gap in this area.
Physiological considerations and possible
mechanisms for harm and benefit of mechanical
ventilation during venovenous extracorporeal
membrane oxygenation
Nonpulmonary gas exchange: how much gas exchange
can extracorporeal membrane oxygenation provide?
The extent of nonpulmonary gas exchange required
during ECMO is directly related to the limitation of
Page 2 of 10
pulmonary gas exchange. The amount of oxygen supplied to the patient by the ECMO circuit is limited by
the maximal oxygen delivery of the membrane (that is,
membrane outlet–inlet oxygen content). The current
generation of ECMO membranes can deliver up to
450 ml oxygen/minute [30]. Actual patient oxygen delivery from an ECMO circuit is affected by the rate of
circuit blood flow, the hemoglobin concentration and
the oxyhemoglobin saturation of the venous blood
(partly reflecting the level of recirculation). Of note,
with VV-ECMO the circuit blood flow is related to both
the inflow cannula diameter and the cardiac output
[31]. The CO2 content in blood is higher than the oxygen
content, and is rapidly diffusible. CO2 transfer provided by
current membranes may exceed 450 ml/minute depending on the ratio of gas to blood flow in the membrane and
the CO2 partial pressure. Higher sweep gas flow and
higher CO2 partial pressure in the oxygenator blood result
in greater CO2 clearance. CO2 removal is therefore easily
controlled with sweep gas flow settings [32].
Minimizing ventilator-induced lung injury
MV can activate inflammation and worsen the pulmonary
damage of the underlying disease, leading to ventilatorinduced lung injury (VILI) [33]. Three possible causal
mechanisms of VILI may be modifiable with the use of
ECMO.
First is the alveolar strain, which represents the amount
of aerated lung receiving ventilation [34,35]. In 2000,
the ARDS Network published a multicenter randomized clinical trial where a strategy aimed at maintaining
plateau pressure ≤30 cmH2O with an initial tidal volume
of ≈ 6 ml/kg predicted body weight (PBW) was compared
with traditional ventilation treatment that involved an
initial tidal volume of ≈ 12 ml/kg PBW [15]. The protective ventilation, which minimizes the alveolar strain
physiological concept, was associated with a decreased
mortality of 22%. Patients at many centers who have received ECMO for severe ARDS have a very low arterial
partial pressure of oxygen/fraction of inspired oxygen
ratio (≈50 mmHg) [1,4] and a very high acute injury
score [1,4]. In addition, these patients have a very small
area of normally aerated alveoli located in the nondependent lung, a large consolidated or nonaerated region
located in the dependent lung along the vertical axis
[36-38] and frequent infiltration of all of the four lung’s
quadrants on chest radiographs [1]. As the aerated
compartment receives the largest part of the tidal
volume [37,39], these severely unwell patients with a
large amount of collapsed lung may be exposed to VILI
despite low-tidal-volume ventilation strategies [40].
Limitation of the alveolar strain is a major concern of
patients with ARDS receiving MV during ECMO.
Schmidt et al. Critical Care 2014, 18:203
http://ccforum.com/content/18/1/203
A second mechanism of VILI is due to repeated intratidal alveolar opening and closing (atelectrauma), defined
as the amount of collapsed lung tissue that is re-opened
during inspiration and re-collapsed during expiration
[41-43]. The challenge is to find the right ventilator settings to avoid intra-tidal alveolar opening and closing
while limiting the risk of alveolar overdistension or strain
[44]. Combining a low tidal volume with high levels of
positive end-expiratory pressures (PEEP) appears to be important. Caironi and colleagues showed similar alveolar
strain after application of 15 cmH2O PEEP in two distinct
groups of 34 ARDS/acute lung injury patients (that is,
higher vs. lower percentage of potentially recruitable lung
groups) [41], suggesting that the beneficial impact of reducing intra-tidal alveolar opening and closing by increasing
PEEP prevailed over the effects of increasing alveolar
strain. Of note, despite improving oxygenation [45,46] and
reducing the duration of MV [46], a strategy for setting
PEEP aimed at increasing alveolar recruitment while limiting hyperinflation did not significantly reduce mortality in
ARDS [45-47].
Finally, oxygen lung toxicity from a high fraction of
inspired oxygen in lung areas with a low ventilation–
perfusion ratio might alone cause reabsorption atelectasis [48-51]. Such areas are frequent in ARDS, and
Aboab and colleagues showed in mechanically ventilated patients with acute lung injury that the breathing
of pure oxygen leads to derecruitment, which is prevented by high PEEP [52]. The challenge of MV settings
with ECMO, particularly when lung function is severely
impaired, is to minimize these pitfalls.
Physiological considerations and possible
mechanisms for harm and benefit of mechanical
ventilation during venoarterial extracorporeal
membrane oxygenation
Patients with cardiac failure receiving VA-ECMO often
have abnormal lung function that may be associated
with ARDS. Considerations from the previous section
may also apply to this group. However, the major cardiovascular effect associated with PEEP is reduction in
cardiac output. Although the effect of PEEP on cardiac
output is complex, the decrease is caused predominantly
by decreasing the right ventricular preload and direct
heart–lung interaction [53]. By increasing the intrathoracic pressure, PEEP can increase pulmonary vascular
resistance, which may cause right ventricular overload and
reduced left ventricular compliance. Patients who have
received VA-ECMO with predominately right ventricular
failure can be adversely affected by high PEEP [54,55].
Conversely, patients with predominately left ventricular
failure supported with VA-ECMO may develop pulmonary
edema despite adequate systemic support and often benefit from the application of high PEEP [34].
Page 3 of 10
Additionally, VA-ECMO may dramatically reduce pulmonary blood flow as a result of pulmonary shunting. If
normal lung ventilation is maintained in this setting, severe local alkalosis might result. To date, this potential
deleterious effect has not been widely described and
clinical consequences are still unknown. However, some
authors have suggested that decreased lung perfusion
with VA-ECMO may accelerate pulmonary vascular
thrombosis in the presence of severe lung injury [17,20].
Evidence and current recommendations
To date, animal data, observational studies and previous
randomized trials may give a physiologic rationale to
promote ultra-protective ventilation during ECMO.
Mechanical ventilation settings: tidal volume and plateau
pressure limitation
The main objectives of MV during ECMO for patients
with severe acute respiratory failure are summarized in
Figure 1. However, multiple approaches to ventilation
could be acceptable [29]. By directly removing CO2 from
the blood, ECMO enables lung-protective ventilation.
Without ECMO, difficulty maintaining adequate alveolar
ventilation is one limitation to the use of a protective
ventilation strategy – exposing patients to potential side
effects of subsequent hypercapnia, such as intracranial
pressure elevation, pulmonary hypertension, depressed
myocardial contractility and a reduction in renal blood
flow [56,57].
Using tidal volume <4 ml/kg PBW is thus recommended with ECMO [29] and is often referred to imprecisely as lung rest or ultra-protective ventilation [3,7]. The concept of ultra-protective MV was suggested and investigated in animal studies [58]. Using a rat model of acid-induced lung injury, Frank and colleagues showed that a tidal volume reduction from 12 to 6 to 3 ml/kg, with the same level of PEEP (10 cmH2O), decreased pulmonary edema and lung injury, and increased protection of the alveolar epithelium [58]. In addition, post-hoc analysis of the ARDS Network data in a multivariable logistic regression model showed that lower tidal volume assignment and lower plateau pressure quartile were significant predictors of lower mortality [59]. Favorable outcome of patients with ARDS treated with a strong tidal volume reduction until 1.9 ml/kg PBW with ECMO [19] and with ECCO2R [18] have been reported. Terragni and colleagues used a system that predominately removed CO2 to reduce tidal volume <6 ml/kg PBW and observed a reduction of pulmonary cytokine concentration [60]. However, survival benefit from ultra-protective lung ventilation was not seen in a recent multicenter randomized controlled trial [6]. Bein and colleagues compared a very low tidal volume ventilation strategy (≈ 3 ml/kg PBW) combined with ECCO2R to lower tidal ventilation (≈ 6 ml/kg PBW) without the Schmidt et al. Critical Care 2014, 18:203 http://ccforum.com/content/18/1/203 Page 4 of 10 Figure 1 Specifications of mechanical ventilation with extracorporeal membrane oxygenation for patients with severe acute respiratory failure. ECMO, extracorporeal membrane oxygenation; FiO2, fraction of inspired oxygen; NAVA, neurally adjusted ventilator assist; PBW, predicted body weight; PEEP, positive end-expiratory pressure. extracorporeal device in 79 patients with ARDS. The number of ventilator-free days at day 60 and the mortality rates were not significantly different between the two study groups. However, promising results were found in patients with severe hypoxemia with a lower number of ventilatorfree days at 60 days in the control group [6]. In addition, Pham and colleagues recently showed, in a cohort of 123 patients with influenza A(H1N1)-induced ARDS, that a higher plateau pressure on the first day of VV-ECMO for acute respiratory failure was significantly associated with ICU death (odds ratio = 1.33, 95% confidence interval = 1.14 to 1.59, P <0.01) [4]. It is worth noting that the ultraprotective ventilation strategy was associated with the use of high PEEP levels in all cases [6,18,60]. Using a pressure control approach with tight limitation of the peak inspiratory pressure between 20 and 25 cmH2O has been suggested to be beneficial [3]. Depending on the severity of the lung disease, ultra-protective ventilation with plateau pressure limitation may lead to apneic ventilation (that is, no tidal volume) for several days. This may be particularly evident with pediatric patients [61,62], and in some cases the reduction of the tidal volume to achieve limited ventilation pressure strategy is considered so important that the result is insufficient ventilation to maintain adequate oxygen delivery. In this case, a third venous ECMO cannula to increase ECMO blood flow may be utilized rather than increasing the inspiratory pressure, which may negate the beneficial effect of the ECMO. Despite its feasibility reported on animal studies [63], pediatric studies [64] and in our daily adult practice, the long-term effect of apneic ventilation is unknown. A very low tidal volume results in dead space ventilation only. In our opinion, this must be combined with a high level of PEEP, to maintain convective ventilation for the elimination of alveolar nitrogen [63] and avoid alveolar collapse. Although there are no large randomized studies focused on MV settings during ECMO in severe acute respiratory failure, it is reasonable, at this time, to advise an ultraprotective ventilation strategy with ECMO, based on a tidal volume reduction (that is, <4 ml/kg PBW) and on a plateau pressure reduction (that is, ≤25 cmH2O), provided lung recruitment with PEEP is sufficient. For patients without ARDS treated by VA-ECMO, lung function is often abnormal. Cardiogenic pulmonary edema, postoperative lung damage and thoracic compliance reduction are frequently present after cardiac surgery, and these patients are at risk of developing ARDS. Targeting lower tidal volumes (6 to 8 ml/kg PBW) appears to decrease the incidence of adverse outcome, even without ARDS [65], and would appear to be reasonable in this population [22], as would a reduction in the respiratory rate during periods of minimal pulmonary artery blood flow. In addition, CO2 removal Schmidt et al. Critical Care 2014, 18:203 http://ccforum.com/content/18/1/203 by VA-ECMO might allow a better tolerance of low tidal volume with less discomfort and dyspnea, and therefore less sedation – but this is an area for further research. Mechanical ventilation settings: positive end-expiratory pressure It is important to be aware that, despite the use of ECMO, decreasing tidal volume <4 ml/kg PBW may increase atelectasis and result in severe ventilation/perfusion mismatch unless PEEP is appropriately increased [66]. Higher PEEP levels are essential [18,19,63] – probably higher than suggested by the Extracorporeal Life Support Organization (ELSO) guidelines, which suggest a modest PEEP of 10 cmH2O [22] – while taking into account ... Purchase answer to see full attachment

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