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REVIEW

Right ventricular failure in acute lung injury

and acute respiratory distress syndrome
X. REPESSÉ 1, 2 , C. CHARRON 1, A. VIEILLARD-BARON 1, 2

1Assistance Publique-Hôpitaux de Paris, University Hospital Ambroise Paré, Intensive Care Unit, Section Thorax-

Vascular Disease-Abdomen-Metabolism, Boulogne-Billancourt, France; 2Faculty of Medicine Paris Ile-de-France Ouest,

University of Versailles Saint-Quentin en Yvelines, Saint-Quentin en Yvelines, France

ABSTRACT
Acute respiratory distress syndrome (ARDS) is a clinical entity involving not only alveolar lesions but also capil-
lary lesions, both of which have deleterious effects on the pulmonary circulation, leading to constant pulmonary
hypertension and to acute cor pulmonale (ACP) in 20-25% of patients ventilated with a limited plateau pressure
(Pplat). Considering the poor prognosis of patients suffering from such acute right ventricular (RV) dysfunction,
RV protection by appropriate ventilatory settings has become a crucial issue in ARDS management. The goal of this
review is to emphasize the importance of analyzing RV function in ARDS, using echocardiography, in order to limit
RV afterload. Any observed acute RV dysfunction should lead physicians to consider a strategy for RV protection,
including strict limitation of Pplat, diminution of positive end-expiratory pressure (PEEP) and control of hypercap-
nia, all goals achieved by prone positioning. (Minerva Anestesiol 2012;78:941-8)
Key words: Respiratory distress syndrome, adult - Heart ventricles - Pulmonary heart disease - Echocardiography,

T he mortality of acute respiratory distress

syndrome (ARDS) remains significant 1, 2
despite improved knowledge of its pathophysi-
ology and routine application of protective me-
chanical ventilation. One of the crucial issues in
management of patients suffering from ARDS is
to compensate and to limit pulmonary vascular
dysfunction. It has been well known since the
1970s that ARDS is a clinical entity that involves
not only alveolar lesions but also pulmonary
capillary lesions, leading to pulmonary hyper-
or other proprietary information of the Publisher.
cent study using the pulmonary artery catheter,
Bull et al. reported that the degree of pulmonary
vascular dysfunction, according to the transpul-
monary gradient (mean pulmonary artery pres-
sure minus pulmonary artery occlusion pres-
sure, PAOP), was independently associated with
prognosis.5 Osman et al. using the same invasive
approach demonstrated that central venous pres-
sure (CVP) higher than PAOP was a strong and
independent predictor of mortality.6 Finally, we
suggested in a large series that acute cor pulmo-

tension.3 The reversible pulmonary vascular re-
modeling which usually occurs has many differ-
ent mediators.4 The hemodynamic consequences
of such remodeling have forced physicians to pay
attention to the right ventricle. Many studies
have now demonstrated the deleterious impact
of pulmonary hypertension and of right ven-
tricular (RV) dysfunction on prognosis. In a re-
nale (ACP) diagnosed by echocardiography was
associated with mortality in patients ventilated
with a plateau pressure (Pplat) of 27 cmH2O or
more.7
In this review, we describe how and why the
right ventricle should be protected in patients
with ARDS, leading to a different approach for
ventilation called the “RV protective approach”.

Vol. 78 - No. 8 MINERVA ANESTESIOLOGICA 941

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REPESSÉ RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS

This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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For this purpose, we briefly discuss the physiolo-

gy and the pathophysiology of the right ventricle
in normal conditions and during ARDS, before
demonstrating the crucial role of echocardiogra-
phy in the diagnosis of right heart failure.

Physiology and pathophysiology

of the right ventricle

RV characteristics
The right ventricle is composed of two cham-
bers wrapping the left ventricle around its short
axis. The filling chamber is in a posterior-ante-
rior axis and has a triangular shape. The outflow
chamber looks like a crescent in an inferior-su-
perior axis (Figure 1). In normal conditions, the
right ventricle ejects blood into a low-resistance
and high-compliance system, which explains why,
unlike the left ventricle, its isovolumetric contrac-
tion pressure is very low and its isovolumetric re-
laxation is insignificant.8 In other words, the right
ventricle nearly acts as a passive conduit. This is
why its systolic function is very sensitive to any
slight increase in pulmonary vascular resistance,
which will easily exceed its capacity of adapta-
tion, leading to systolic overload and dysfunction.
However, thanks to its low diastolic elastance, the
right ventricle is able to adapt to a certain degree
by dilating:9 its diastolic function is tolerant.
RV function and ventilation
Figure 1.—Magnetic resonance imaging of heart chambers.
Dotted arrow represents the axis of the RV filling chamber and
solid arrow represents axis of the RV outflow chamber. RV:
right ventricle, LV: left ventricle, PA: pulmonary artery
minus pleural pressure). This mainly occurs if the
tidal volume is excessive and/or if lung compliance
is severely decreased, two conditions where the
pulmonary capillaries may be crushed by alveoli.15
How to diagnose RV function impairment in
critically-ill patients ventilated for an ARDS
As explained above, uncoupling between the
right ventricle and the pulmonary circulation
may lead to a pattern of ACP. Testa gave the first
clinical description of ACP in 1831.16 Currently,
ACP is optimally diagnosed using echocardiog-
raphy, even though some surrogates may be de-
tected using invasive devices.

During spontaneous breathing, the right ven- Invasive approach

tricle is acting in the best conditions. Venous
return is optimal thanks a continuous negative
pleural pressure 10 and RV afterload is limited
because of a low transpulmonary pressure.11
The situation is quite different during positive
pressure ventilation,12 especially in patients with a
lung injury with decreased compliance. Decrease
or other proprietary information of the Publisher.
Many studies have evaluated RV function
and the pulmonary circulation in ARDS us-
ing the pulmonary artery catheter (PAC). RV
systolic dysfunction was historically defined by
a CVP>PAOP in patients with RV myocardial
infarction.17, 18 In ARDS, this was proposed by

in systemic venous return results from a less nega-
tive, even positive, pleural pressure.10 It could also
be related to a partial or complete collapse of the
thoracic part of the superior vena cava.13 Effect
on venous return is increased by application of
positive end-expiratory pressure (PEEP).14
Increase in RV afterload is related to an eleva-
tion in transpulmonary pressure (alveolar pressure
Monchi et al.19 and recently by Osman et al. in a
series of patients undergoing protective mechan-
ical ventilation.6 In the latter study, RV failure
was distinguished from RV dysfunction by an
RV stroke index below 30 mL/m-2.6 Using fast-
response thermodilution, Jardin et al. showed
in 18 ARDS patients that RV volume estima-
tion was a better indicator of RV preload than

942 MINERVA ANESTESIOLOGICA August 2012

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RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS REPESSÉ
This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies
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were measurements of pressure.20 De Monte et
al. demonstrated similar results in 36 patients.21
Fast-response thermodilution may also be used
to calculate RV ejection fraction.
The pulmonary circulation may also be evaluat-
ed in ARDS patients by an invasive approach. Pul-
monary vascular resistance (PVR) is probably not
accurate in this very special situation where any
change in cardiac output leads to change in PVR.3
This reflects the flow-dependent competition be-
tween alveoli (and their distending pressure) and
pulmonary capillaries. More interestingly, 30 years
ago, Marland and Glauser assessed the gradient
between diastolic pulmonary artery pressure and
PAOP to evaluate the effects of PEEP22 (Figure 2).
More recently, Bull et al. used the transpulmonary
pressure gradient as the difference between mean
pulmonary artery pressure and PAOP.5 In close to
500 ARDS patients, they found that 73% of pa-
tients had an elevated gradient (≥12 mmHg).5
Echocardiography, the cornerstone of the diagnosis
In ARDS, echocardiography can easily be
performed by a transthoracic (TTE) or a trans-
esophageal (TEE) approach. We routinely prefer
the latter, as we consider it to be less operator-de-
pendent and more reproducible, providing pa-
tients are intubated and ventilated. We consider
that RV evaluation in this field should mainly be
qualitative, using a focused and simple approach,
mainly based on the four-chamber, short-axis
view and the great vessel views. The main goal is
PAP
or other proprietary information of the Publisher.
2O
PCWP
mmHg
O
PEEP 0 cm H20
Figure 2.—Pressure gradient between diastolic pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure (PCWP)
induced by application of a high PEEP.
Vol. 78 - No. 8 MINERVA ANESTESIOLOGICA 943
to evaluate the effects of lung injury and of posi-
tive pressure ventilation on RV function, so as
to adapt ventilatory strategy, as explained below.
ACP combines RV dilatation (RV diastolic over-
load) and paradoxical septal motion at end-systole
(RV systolic overload). Figure 3 depicts the pattern
of ACP recorded by TTE and TEE. RV size is eval-
uated using a four-chamber view by a transthoracic
or a transesophageal approach. When dilated, the
right ventricle loses the triangular shape of its fill-
ing chamber. We defined RV dilatation as moder-
ate when the ratio between right and left ventricu-
lar end-diastolic areas is >0.6 and as severe for a
ratio >1.23 In the latter situation, simple qualita-
tive detection is sufficient. RV dilatation is usually
associated with right atrial and inferior vena caval
dilatation and tricuspid regurgitation, easily visual-
ized using the color Doppler mode.24
Paradoxical septal motion is well-visualized on
a short-axis view of the left ventricle, ideally at the
RV outflow track. It is related to an inverted pres-
sure gradient between right and left ventricles, oc-
curring at end-systole,25, 26 and reflecting RV ejec-
tion obstruction. Usually, detection of paradoxical
septal motion is qualitative: there is or there is not.
In some situations, as clinical research, LV systo-
lic eccentricity index can be calculated to evaluate
the degree of RV systolic overload.27
Briefly, Doppler analysis of the pulmonary ar-
tery flow can also be helpful and very informative
on the (in)ability of the right ventricle to overcome
its afterload. It may be obtained from the great
vessel view. Figures 4, 5 report the two parameters
PAP
PCWP
PEEP 20 cm H20
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REPESSÉ RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS

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Figure 3.—Acute cor pulmonale in a patient ventilated for severe ARDS, visualized by transthoracic (left side) and transesophageal
(right side) echocardiography on the same day. Top: Four-chamber view, showing the severely dilated right ventricle. Bottom:
short-axis view of the left ventricle, showing paradoxical septal motion at end-systole (arrow) with the “D-shape” of the left ven-
tricle. RV: right ventricle LV: left ventricle, RA: right atrium, LA: left atrium

that we usually look for, i.e. respiratory variation
of pulmonary flow and a biphasic flow pattern.24
Incidence of ACP and impact
of respiratory settings
Incidence of ACP may be considered before
and after implementation of protective mechani-
cal ventilation. Before, Jardin et al. used TTE to
characterize RV function in a small series of 25
patients with ARDS ventilated with high airway
pressure.28 They reported an incidence as high as
or other proprietary information of the Publisher.
in a large series of more than 200 patients where
incidence was 22%.30 In another study, we re-
ported a much higher incidence, i.e. 50%, but the
population was selected and consisted of patients
with particularly severe ARDS and a PaO2/FIO2
below 100 mmHg after 2 days of ventilation.31
This demonstrates something easily understanda-
ble, that the incidence of RV dysfunction increases
as we go from acute lung injury to ARDS and to
severe ARDS, according to alterations in respira-
tory mechanics. Interestingly, a recent TTE study
performed in 21 patients with H1N1 influenza-

60% of ACP and all patients with a severely di-
lated right ventricle died.28 After, most studies are
summarized in Table I. In particular, we reported
in 75 patients ventilated with a Pplat <30 cmH2O
and a PEEP of 7 cmH2O an incidence of ACP of
25% after 2 days of mechanical ventilation.29 This
was recently confirmed by Mekontso-Dessap et al.
related ALI/ARDS found that 83% exhibited RV
dilatation and 30% had ACP.32
Many studies in acute lung injury have clearly
demonstrated that respiratory settings and ventila-
tory strategy may significantly affect RV function.
First, using TEE we recently emphasized that the
impact of positive pressure ventilation on the right

944 MINERVA ANESTESIOLOGICA August 2012

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RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS REPESSÉ

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(either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other

Figure 4.—Pulmonary artery flow recorded by pulsed wave Doppler by a transesophageal approach in a patient ventilated for
severe ARDS. After 2 days on mechanical ventilation (panel A), plateau pressure was elevated and pulmonary artery flow had a
biphasic pattern (arrow), reflecting a huge obstruction of the ejection. After 3 sessions of prone positioning (panel B), plateau
pressure significantly decreased and the pulmonary flow was completely normalized. Vt: tidal volume, Pplat: plateau pressure.

ZEEP PEEP 6 cm H2O PEEP 13 cm H2O

Figure 5.—Pulsed Doppler analysis of pulmonary artery flow obtained by a transesophageal approach during PEEP titration (0, 6
and 13 cmH2O). Note the drop in pulmonary artery blood flow, at end-inspiration and also end-expiration, when PEEP increases.

ventricle is directly related to tidal volume.33 Simi-
larly, in a large series of more than 350 patients,
we reported that incidence of ACP was strongly
related to Pplat:7 10% for a Pplat between 18 and
26 cmH2O, >30% for a Pplat between 27 and
35 cmH2O and finally 60% for a Pplat >35 cm-
or other proprietary information of the Publisher.
hypercarbia, which is a strong vasoconstrictor of
the pulmonary circulation, and right ventricular
overload has been demonstrated in humans.36
A different ventilatory strategy:
the RV protective approach

H2O.7 Second, PEEP may also overload the right

ventricle at both inspiration and expiration.34 We
recently demonstrated in severe ARDS patients
that a ventilatory strategy promoting “high” PEEP
was deleterious for the right ventricle despite a
strict limitation of Pplat.35 Finally, hypercapnia
may worsen the effect of mechanical ventilation
on RV afterload, since a direct relation between
The concept of this approach can be summa-
rized in few words: “what is good for the right
ventricle is good for the lung”.
The first goal of the RV protective approach
(Table II) is to limit Pplat. In the case of RV
dysfunction with hemodynamic consequences,

Vol. 78 - No. 8 MINERVA ANESTESIOLOGICA 945

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REPESSÉ RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS

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Table I.—Incidence of right ventricular dysfunction in ALI/ARDS in patients undergoing protective mechanical ventilation.
Review of the literature.
Number of Population Reported parameter of RV
Tool Incidence
patients characteristics dysfunction
Vieillard-Baron et al. 200129 75 ARDS Ultrasound (TEE) ACP 25%
Page et al. 200345 110 ARDS Ultrasound (TEE) ACP 24.5%
Vieillard-Baron et al. 200731 42 ARDS Ultrasound (TEE) ACP 50%*
Osman et al. 20096 145 ARDS PAC CVP > PAOP 27%
Mahjoub et al. 200946 35 ALI/ARDS Ultrasound (TTE) RV dilatation, low TAPSE 34%
Fougères et al. 201047 21 ARDS Ultrasound (TEE) ACP 14%
Bull et al. 20105 475 ALI/ARDS PAC TPG ≥ 12 mmHg 73%
Brown et al. 201132 48 ALI/ARDS Ultrasound (TTE) ACP 30%
Mekontso et al. 201130 203 ARDS Ultrasound (TEE) ACP 22%
TEE: transesophageal echocardiography; TTE: transthoracic echocardiography, PAC: pulmonary artery catheter; ACP: acute cor pulmonale; CVP:
central venous pressure; PAOP: pulmonary artery occlusion pressure; TAPSE: tricuspid annular plane systolic excursion (parameter of RV systolic
function); TPG: transpulmonary gradient (mean pulmonary artery pressure minus PAOP).
*Highly selected patients with severe ARDS and a PaO /FIO <100 mmHg after 2 days on
2 2
mechanical ventilation.

Table II.—Right ventricular protective ventilation: the step-by-step strategy.

Goal Methods Mechanisms of RV unloading
1 Plateau pressure <28 cmH2O 1- Decrease tidal volume Limit overdistension (decrease lung stress)
2- Limit PEEP
2 Lung recruitment Adapt PEEP according to beneficial Improve oxygenation (limit hypoxic
(recruitment) and deleterious (RV pulmonary vasoconstriction), improve
overload) effects. lung compliance (decrease lung stress)
3 Controlled hypercapnia 1- Remove HME Limit pulmonary vasoconstriction
(PaCO2<55-60 mmHg) 2- Increase respiratory rate without
generating intrinsic PEEP
4* Improve lung mechanics and pulmonary Consider prone positioning Improve lung compliance and decrease
circulation alveolar dead space (decrease lung stress),
limit pulmonary vasoconstriction related
to hypoxia and hypercapnia
PEEP: positive expiratory end-pressure, HME: heat and moisture exchanger
*For patients with
1) persistent PaO2/FiO2< 100, 24-hour optimization of mechanical ventilation
2) persistent acute cor pulmonale despite steps 1, 2 and 3

Pplat must absolutely be decreased to a level <27
cmH2O, a safe limit for the right ventricle.7 The
second goal is to evaluate the effect of increasing
PEEP on lung recruitment and overdistension,
but we lack tools to do this at the bedside. CT-
scan is probably the most effective tool,37 but is
currently unavailable in usual practice. However,
when overdistension is predominant, RV func-
or other proprietary information of the Publisher.
ing the respiratory rate, without inducing intrin-
sic PEEP, which also has deleterious effects on
the right ventricle.29
In some patients, those with the most severe
ARDS, blood gas control, respiratory mechan-
ics and RV protection are difficult to combine.
Then, prone positioning should be proposed.
By recruiting the lung, thus decreasing airway

tion is impaired,35 a warning signal the response
to which must be to decrease PEEP. Studying RV
function may therefore help intensivists to assess
the balance between recruitment and overdisten-
sion. Finally, as emphasized above, hypercapnia
must be limited by reducing the instrumental
dead space (heat and moisture exchanger re-
placement by heated humidifier) and by increas-
pressure, and by increasing PaO2 and decreas-
ing PaCO2, thus decreasing pulmonary vaso-
constriction, it may significantly improve RV
function, as we demonstrated.31 In other words,
prone positioning reconciles the lung protective
approach with the RV protective approach. We
recently reported that such a strategy can be in-
cluded in a routine protocol.38

946 MINERVA ANESTESIOLOGICA August 2012

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RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS REPESSÉ
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Pharmacological approach to
RV failure management
Hemodynamic management of shock-related
ACP in ARDS relies on few drugs. Nitric oxide
(NO) inhalation has been shown to improve
RV systolic function in patients with ARDS,39
even though no effect on mortality was found.40
In our practice, we reserve it for persistent
shock related to ACP despite optimization of
respiratory settings. Norepinephrine has been
recognized to be the elective drug for improv-
ing RV performance by its ability to restore RV
perfusion pressure.41, 42 It was confirmed in an
experimental model of massive pulmonary em-
bolism.42 However, no clinical study has been
performed in ARDS. Finally, a calcium sensi-
tizer (levosimendan) has been described as su-
perior to dobutamine in isolated myocardial
infarction-related right heart failure.43 In the
context of ARDS, it was proposed by Morelli et
al. for its ability to dilate the pulmonary circu-
lation and to increase RV contractility.44
Conclusions
In ARDS, hemodynamic effects on the right
ventricle in pulmonary vascular remodeling,
combined with positive pressure ventilation,
are well characterized. It is now established that
pulmonary vascular dysfunction and RV systolic
overload are strongly associated with poor prog-
nosis. Many studies suggest that monitoring of
RV function is mandatory to optimize hemo-
dynamics but also, more interestingly, to opti-
mize respiratory settings. Echocardiography, by
a transthoracic or a transesophageal approach,
may help intensivists to apply a RV protective
approach, which should be prospectively evalu-
ated in the future in a large prospective study. In
this strategy, prone positioning has a key role in
the most seriously ill patients.
or other proprietary information of the Publisher.
Key messages
—— Incidence of ACP is high in ARDS
patients submitted to protective ventilation:
25%.
Vol. 78 - No. 8 MINERVA ANESTESIOLOGICA 947
—— Respiratory settings significantly im-
pact its occurrence.
—— ACP is clearly associated with poor
prognosis.
—— A right ventricular protective approach
can be proposed, based on strict limitation of
plateau pressure, limitation of PEEP, control
of hypercapnia, and finally on prone position
in the most severely ill patients.
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Jardin F. Influence of superior vena caval zone condition on
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14. Michard F, Chemla D, Richard C, Wysocki M, Pinsky MR,
Lecarpentier Y et al. Clinical use of respiratory changes in
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Funding.—Support was provided solely from institutional and/or departmental sources.
Received on April 18, 2012 - Accepted for publication on June 1, 2012.
Corresponding author: Prof. A. Vieillard-Baron, Intensive Care Unit, Section Thorax-Vascular Disease-Abdomen-Metabolism, University
Hospital Ambroise Paré, 9, avenue Charles-de-Gaulle 92100 Boulogne-Billancourt, France. E-mail: antoine.vieillard-baron@apr.aphp.fr
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