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COPYRIGHT© 2012 EDIZIONI MINERVA MEDICA
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 ThoraxVascular 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 capillary 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 hypercapnia, 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 pathophysiology and routine application of protective mechanical 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 hypertension.3 The reversible pulmonary vascular remodeling which usually occurs has many different 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 ventricular (RV) dysfunction on prognosis. In a re-
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cent study using the pulmonary artery catheter, Bull et al. reported that the degree of pulmonary vascular dysfunction, according to the transpulmonary gradient (mean pulmonary artery pressure minus pulmonary artery occlusion pressure, PAOP), was independently associated with prognosis.5 Osman et al. using the same invasive approach demonstrated that central venous pressure (CVP) higher than PAOP was a strong and independent predictor of mortality.6 Finally, we suggested in a large series that acute cor pulmonale (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”.
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RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS
For this purpose, we briefly discuss the physiology and the pathophysiology of the right ventricle in normal conditions and during ARDS, before demonstrating the crucial role of echocardiography in the diagnosis of right heart failure. Physiology and pathophysiology of the right ventricle RV characteristics The right ventricle is composed of two chambers wrapping the left ventricle around its short axis. The filling chamber is in a posterior-anterior axis and has a triangular shape. The outflow chamber looks like a crescent in an inferior-superior 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 contraction pressure is very low and its isovolumetric relaxation 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 adaptation, 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 During spontaneous breathing, the right ventricle 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 in systemic venous return results from a less negative, 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 elevation in transpulmonary pressure (alveolar pressure
942
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 echocardiography, even though some surrogates may be detected using invasive devices. Invasive approach Many studies have evaluated RV function and the pulmonary circulation in ARDS using 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 Monchi et al.19 and recently by Osman et al. in a series of patients undergoing protective mechanical 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 fastresponse thermodilution, Jardin et al. showed in 18 ARDS patients that RV volume estimation was a better indicator of RV preload than
MINERVA ANESTESIOLOGICA
August 2012
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 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 not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.
COPYRIGHT© 2012 EDIZIONI MINERVA MEDICA RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS
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 evaluated in ARDS patients by an invasive approach. Pulmonary 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 between 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 patients 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 transesophageal (TEE) approach. We routinely prefer the latter, as we consider it to be less operator-dependent and more reproducible, providing patients 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
REPESSÉ
to evaluate the effects of lung injury and of positive pressure ventilation on RV function, so as to adapt ventilatory strategy, as explained below. ACP combines RV dilatation (RV diastolic overload) 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 evaluated using a four-chamber view by a transthoracic or a transesophageal approach. When dilated, the right ventricle loses the triangular shape of its filling chamber. We defined RV dilatation as moderate when the ratio between right and left ventricular end-diastolic areas is >0.6 and as severe for a ratio >1.23 In the latter situation, simple qualitative detection is sufficient. RV dilatation is usually associated with right atrial and inferior vena caval dilatation and tricuspid regurgitation, easily visualized 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 pressure gradient between right and left ventricles, occurring at end-systole,25, 26 and reflecting RV ejection obstruction. Usually, detection of paradoxical septal motion is qualitative: there is or there is not. In some situations, as clinical research, LV systolic eccentricity index can be calculated to evaluate the degree of RV systolic overload.27 Briefly, Doppler analysis of the pulmonary artery 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 PAP
2O
PCWP
PCWP
mmHg PEEP 0 cm H20
O
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.
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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 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 not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.
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RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS
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 ventricle. 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 mechanical 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 60% of ACP and all patients with a severely dilated right ventricle died.28 After, most studies are summarized in Table I. In particular, we reported in 75 patients ventilated with a Pplat 30% for a Pplat between 27 and 35 cmH2O and finally 60% for a Pplat >35 cmH2O.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
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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 The concept of this approach can be summarized 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,
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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 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 not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.
COPYRIGHT© 2012 EDIZIONI MINERVA MEDICA REPESSÉ
RIGHT VENTRICULAR FAILURE IN ACUTE LUNG INJURY AND ARDS
Table I.—Incidence of right ventricular dysfunction in ALI/ARDS in patients undergoing protective mechanical ventilation. Review of the literature. Number of patients
Population characteristics
Tool
Reported parameter of RV dysfunction
Incidence
75 110 42 145 35 21 475 48 203
ARDS ARDS ARDS ARDS ALI/ARDS ARDS ALI/ARDS ALI/ARDS ARDS
Ultrasound (TEE) Ultrasound (TEE) Ultrasound (TEE) PAC Ultrasound (TTE) Ultrasound (TEE) PAC Ultrasound (TTE) Ultrasound (TEE)
ACP ACP ACP CVP > PAOP RV dilatation, low TAPSE ACP TPG ≥ 12 mmHg ACP ACP
25% 24.5% 50%* 27% 34% 14% 73% 30% 22%
Vieillard-Baron et al. 200129 Page et al. 200345 Vieillard-Baron et al. 200731 Osman et al. 20096 Mahjoub et al. 200946 Fougères et al. 201047 Bull et al. 20105 Brown et al. 201132 Mekontso et al. 201130
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
