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

tension.3 The reversible pulmonary vascular re- nale (ACP) diagnosed by echocardiography was
modeling which usually occurs has many differ- associated with mortality in patients ventilated
ent mediators.4 The hemodynamic consequences with a plateau pressure (Pplat) of 27 cmH2O or
of such remodeling have forced physicians to pay more.7
attention to the right ventricle. Many studies In this review, we describe how and why the
have now demonstrated the deleterious impact right ventricle should be protected in patients
of pulmonary hypertension and of right ven- with ARDS, leading to a different approach for
tricular (RV) dysfunction on prognosis. In a re- 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 Figure 1.—Magnetic resonance imaging of heart chambers.
Dotted arrow represents the axis of the RV filling chamber and
axis. The filling chamber is in a posterior-ante- solid arrow represents axis of the RV outflow chamber. RV:
rior axis and has a triangular shape. The outflow right ventricle, LV: left ventricle, PA: pulmonary artery
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 minus pleural pressure). This mainly occurs if the
and high-compliance system, which explains why, tidal volume is excessive and/or if lung compliance
unlike the left ventricle, its isovolumetric contrac- is severely decreased, two conditions where the
tion pressure is very low and its isovolumetric re- pulmonary capillaries may be crushed by alveoli.15
laxation is insignificant.8 In other words, the right
ventricle nearly acts as a passive conduit. This is How to diagnose RV function impairment in
why its systolic function is very sensitive to any critically-ill patients ventilated for an ARDS
slight increase in pulmonary vascular resistance,
which will easily exceed its capacity of adapta- As explained above, uncoupling between the
tion, leading to systolic overload and dysfunction. right ventricle and the pulmonary circulation
However, thanks to its low diastolic elastance, the may lead to a pattern of ACP. Testa gave the first
right ventricle is able to adapt to a certain degree clinical description of ACP in 1831.16 Currently,
by dilating:9 its diastolic function is tolerant. ACP is optimally diagnosed using echocardiog-
raphy, even though some surrogates may be de-
RV function and ventilation 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 Many studies have evaluated RV function
pleural pressure 10 and RV afterload is limited and the pulmonary circulation in ARDS us-
because of a low transpulmonary pressure.11 ing the pulmonary artery catheter (PAC). RV
The situation is quite different during positive systolic dysfunction was historically defined by
pressure ventilation,12 especially in patients with a a CVP>PAOP in patients with RV myocardial
lung injury with decreased compliance. Decrease infarction.17, 18 In ARDS, this was proposed by
or other proprietary information of the Publisher.

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

942 MINERVA ANESTESIOLOGICA August 2012


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means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS REPESSÉ


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were measurements of pressure.20 De Monte et to evaluate the effects of lung injury and of posi-
al. demonstrated similar results in 36 patients.21 tive pressure ventilation on RV function, so as
Fast-response thermodilution may also be used to adapt ventilatory strategy, as explained below.
to calculate RV ejection fraction. ACP combines RV dilatation (RV diastolic over-
The pulmonary circulation may also be evaluat- load) and paradoxical septal motion at end-systole
ed in ARDS patients by an invasive approach. Pul- (RV systolic overload). Figure 3 depicts the pattern
monary vascular resistance (PVR) is probably not of ACP recorded by TTE and TEE. RV size is eval-
accurate in this very special situation where any uated using a four-chamber view by a transthoracic
change in cardiac output leads to change in PVR.3 or a transesophageal approach. When dilated, the
This reflects the flow-dependent competition be- right ventricle loses the triangular shape of its fill-
tween alveoli (and their distending pressure) and ing chamber. We defined RV dilatation as moder-
pulmonary capillaries. More interestingly, 30 years ate when the ratio between right and left ventricu-
ago, Marland and Glauser assessed the gradient lar end-diastolic areas is >0.6 and as severe for a
between diastolic pulmonary artery pressure and ratio >1.23 In the latter situation, simple qualita-
PAOP to evaluate the effects of PEEP22 (Figure 2). tive detection is sufficient. RV dilatation is usually
More recently, Bull et al. used the transpulmonary associated with right atrial and inferior vena caval
pressure gradient as the difference between mean dilatation and tricuspid regurgitation, easily visual-
pulmonary artery pressure and PAOP.5 In close to ized using the color Doppler mode.24
500 ARDS patients, they found that 73% of pa- Paradoxical septal motion is well-visualized on
tients had an elevated gradient (≥12 mmHg).5 a short-axis view of the left ventricle, ideally at the
RV outflow track. It is related to an inverted pres-
Echocardiography, the cornerstone of the diagnosis sure gradient between right and left ventricles, oc-
curring at end-systole,25, 26 and reflecting RV ejec-
In ARDS, echocardiography can easily be tion obstruction. Usually, detection of paradoxical
performed by a transthoracic (TTE) or a trans- septal motion is qualitative: there is or there is not.
esophageal (TEE) approach. We routinely prefer In some situations, as clinical research, LV systo-
the latter, as we consider it to be less operator-de- lic eccentricity index can be calculated to evaluate
pendent and more reproducible, providing pa- the degree of RV systolic overload.27
tients are intubated and ventilated. We consider Briefly, Doppler analysis of the pulmonary ar-
that RV evaluation in this field should mainly be tery flow can also be helpful and very informative
qualitative, using a focused and simple approach, on the (in)ability of the right ventricle to overcome
mainly based on the four-chamber, short-axis its afterload. It may be obtained from the great
view and the great vessel views. The main goal is vessel view. Figures 4, 5 report the two parameters

PAP
PAP
or other proprietary information of the Publisher.

PCWP
2O
PCWP

mmHg
O
PEEP 0 cm H20 PEEP 20 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


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

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

944 MINERVA ANESTESIOLOGICA August 2012


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COPYRIGHT© 2012 EDIZIONI MINERVA MEDICA
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

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- hypercarbia, which is a strong vasoconstrictor of
larly, in a large series of more than 350 patients, the pulmonary circulation, and right ventricular
we reported that incidence of ACP was strongly overload has been demonstrated in humans.36
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- A different ventilatory strategy:
the RV protective approach
or other proprietary information of the Publisher.

H2O.7 Second, PEEP may also overload the right


ventricle at both inspiration and expiration.34 We
recently demonstrated in severe ARDS patients The concept of this approach can be summa-
that a ventilatory strategy promoting “high” PEEP rized in few words: “what is good for the right
was deleterious for the right ventricle despite a ventricle is good for the lung”.
strict limitation of Pplat.35 Finally, hypercapnia The first goal of the RV protective approach
may worsen the effect of mechanical ventilation (Table II) is to limit Pplat. In the case of RV
on RV afterload, since a direct relation between 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 ing the respiratory rate, without inducing intrin-
cmH2O, a safe limit for the right ventricle.7 The sic PEEP, which also has deleterious effects on
second goal is to evaluate the effect of increasing the right ventricle.29
PEEP on lung recruitment and overdistension, In some patients, those with the most severe
but we lack tools to do this at the bedside. CT- ARDS, blood gas control, respiratory mechan-
scan is probably the most effective tool,37 but is ics and RV protection are difficult to combine.
currently unavailable in usual practice. However, Then, prone positioning should be proposed.
when overdistension is predominant, RV func- By recruiting the lung, thus decreasing airway
or other proprietary information of the Publisher.

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


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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Pharmacological approach to
RV failure management —— Respiratory settings significantly im-
pact its occurrence.
Hemodynamic management of shock-related —— ACP is clearly associated with poor
ACP in ARDS relies on few drugs. Nitric oxide prognosis.
(NO) inhalation has been shown to improve —— A right ventricular protective approach
RV systolic function in patients with ARDS,39 can be proposed, based on strict limitation of
even though no effect on mortality was found.40 plateau pressure, limitation of PEEP, control
In our practice, we reserve it for persistent of hypercapnia, and finally on prone position
shock related to ACP despite optimization of in the most severely ill patients.
respiratory settings. Norepinephrine has been
recognized to be the elective drug for improv-
ing RV performance by its ability to restore RV References
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Vol. 78 - No. 8 MINERVA ANESTESIOLOGICA 947


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COPYRIGHT© 2012 EDIZIONI MINERVA MEDICA
means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is

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
(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

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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
This article is freely available at www.minervamedica.it

948 MINERVA ANESTESIOLOGICA August 2012