Pulmonary Vascular Dysfunction Is Associated with Poor Outcomes in Patients with Acute Lung Injury

Bull, Todd; Clark, Brendan; McFann, Kim; Moss, Marc

doi:10.1164/rccm.201002-0250oc

Cited by 186 publications

(151 citation statements)

References 41 publications

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“…In ARDS, pulmonary arterial pressure has been investigated, mainly invasively, with pulmonary arterial catheterization [Squara et al 1998;Ryan et al 2014;Beiderlinden et al 2006;Osman et al 2009;Bull et al 2010], and only a few reports assessed pulmonary systolic arterial pressure with echocardiography in patients with ALI with or without ARDS [Jardin et al 1985;Boissier et al 2013;Vieillard-Baron et al 2001;Cepkova et al 2007;Mekontso-Dessap et al 2010] (Table 1). Clinical interpretation of these data is challenging, since definition of ARDS has changed over time [Murray et al 1988;Bernard et al 1994;Force et al 2012], as well as the standard of care in ARDS with the introduction of lung-protective ventilation [The Acute Respiratory Distress Syndrome Network, 2000] and conservative fluid management [Wiedemann et al 2006].…”

Section: Pulmonary Systolic Arterial Hypertensionmentioning

confidence: 99%

The potential role and limitations of echocardiography in acute respiratory distress syndrome

Lazzeri

Cianchi

Bonizzoli

et al. 2015

Ther Adv Respir Dis

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Bedside use of Doppler echocardiography is being featured as a promising, clinically useful tool in assessing the pulmonary circulation in patients with acute respiratory distress syndrome (ARDS). The present review is aimed at summarizing the available evidence obtained with echocardiography on right ventricle (RV) function and pulmonary circulation in ARDS and to highlight the potential of this technique in clinical practice (only articles in English language were considered). According to the available evidence on echocardiographic findings, the following conclusions can be drawn: (a) echocardiography (transthoracic and transesophageal) has a growing role in the management ARDS patients mainly because of the strict interactions between the lung (and ventilation) and the RV and pulmonary circulation; (b) there may be a continuum of alterations in RV size and function and pulmonary circulation which may end in the development of acute cor pulmonale, probably paralleling ARDS disease severity; and (c) the detection of acute cor pulmonale should prompt intensivists to tailor their ventilatory strategy to the individual patient depending on the echocardiography findings. Bearing in mind the clinical role and growing importance of echocardiography in ARDS and the available evidence on this topic, we present a flow chart including the parameters to be measured and the timing of echo exams in ARDS patients. Despite the important progress that echocardiography has gained in the evaluation of patients with ARDS, several open questions remain and echocardiography still appears to be underused in these patients. A more systematic use of echocardiography (mainly through shared protocols) in ARDS could help intensivists to tailor the optimal treatment in individual patients as well as highlighting the limits and potential of this methodology in patients with ALI.

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Section: Pulmonary Systolic Arterial Hypertensionmentioning

confidence: 99%

The potential role and limitations of echocardiography in acute respiratory distress syndrome

Lazzeri

Cianchi

Bonizzoli

et al. 2015

Ther Adv Respir Dis

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“…Fifth, hypoxic pulmonary vasoconstriction can further increase PVR. All these of mechanisms can contribute to an elevation in PVR that can occur within 48 h after the onset of ARDS, as demonstrated many years ago [3] and also more recently [4,5]. The elevation in PVR may also be exacerbated by hypercapnia and acidosis.…”

mentioning

confidence: 92%

Acute cor pulmonale and the acute respiratory distress syndrome

Guérin

Matthay

2016

Intensive Care Med

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Acute respiratory distress syndrome (ARDS) is characterized by arterial hypoxemia secondary to protein-rich pulmonary edema associated with acute inflammation and loss of aerated lung volume [1,2]. ARDS also involves injury to the pulmonary circulation that is associated with pulmonary hypertension and an elevation in pulmonary dead space [1,2]. The pulmonary circulation is involved at different stages of ARDS with progression of the clinical syndrome. First, injury to the lung microcirculation causes an increase in lung vascular permeability which initiates the accumulation of pulmonary edema. Second, intravascular microthrombi can develop from an imbalance between procoagulant and fibrinolytic activity in the presence of acute inflammation and endothelial injury. Third, the marked reduction in functional residual capacity (FRC) can increase pulmonary vascular resistance (PVR). Fourth, positive pressure ventilation can induce high lung volume in some lung regions and compress alveolar vessels, resulting in increased PVR. The resulting higher regional FRC can also increase PVR. Fifth, hypoxic pulmonary vasoconstriction can further increase PVR. All these of mechanisms can contribute to an elevation in PVR that can occur within 48 h after the onset of ARDS, as demonstrated many years ago [3] and also more recently [4,5]. The elevation in PVR may also be exacerbated by hypercapnia and acidosis. These mechanisms are summarized in Fig. 1.An elevation in PVR has long been recognized as a predictor of poor prognosis in ARDS. Under normal conditions, the right ventricle (RV) pumps against a low resistance pulmonary circulation, but in the presence of an acute increase in afterload from a rise in PVR, the RV attempts to compensate by increasing end-systolic and end-diastolic volumes. If the increase in afterload is substantial, impairment of RV systolic function and interventricular septal kinetics results in a reduction in cardiac output and acute core pulmonale (ACP) with RV failure and shock. Before the era of lung protective ventilation, the incidence of ACP from elevated PVR in ARDS was as high as 60 % [6].In a recent article in Intensive Care Medicine, Mekontso-Dessap and colleagues [7] report the results of a study of 752 moderate to severe ARDS patients (ratio of partial pressure arterial oxygen and fraction of inspired oxygen: PaO 2 /FiO 2 \200 mmHg) designed (1) to determine the incidence of ACP, (2) to test a clinical score to predict the presence of ACP and (3) to determine the association of ACP with mortality. The diagnosis of ACP was determined by transesophageal echocardiography (TEE) and defined by septal dyskinesia with a dilated RV, end-diastolic RV/left ventricle area ratio of [0.6, and a score of [1 for severe ACP. Overall, ACP developed in Intensive Care Med (2016) 42:934-936

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“…Bull et al published data on 470 patients with ARDS demonstrating an increased 60-day mortality with elevated baseline transpulmonary gradient (TPG) >12 mm of Hg. Both pulmonary vascular resistance index and TPG were determined to be independent risk factors for increased 60-day mortality, number of ICU free days, ventilator free days on multivariate analysis in his study (18).…”

mentioning

confidence: 99%

“…It is difficult to objectively demonstrate pulmonary vascular dysfunction due to fact that most modern intensive care units have shied away from using pulmonary catheters. In one of the few studies that looked at pulmonary vascular dysfunction in ARDS, Bull et al (18) reported a greater than 70% incidence of pulmonary vascular dysfunction among those with acute lung injury. Right ventricular dysfunction and ACP occurs as downstream effects of pulmonary vascular dysfunction and elevation in pulmonary vascular resistance.…”

mentioning

confidence: 99%

Preventing the development of acute cor pulmonale in patients with acute respiratory distress syndrome: the first step

Biswas

2016

Ann. Transl. Med.

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Acute respiratory distress syndrome (ARDS) is a clinical condition characterized by acute hypoxemic respiratory failure that is associated with substantial mortality even 40 years since it was first described. Although hypoxemia appears to be the most conspicuous abnormality noticed with this condition, it isn't the most common cause of death. Conservative oxygen saturation targets of 88-92% have been recently reported to be as effective as targeting saturation above 96%, which indicates that the human body can survive relatively short periods of relative hypoxemia without any lingering effects (1). On the other hand, circulatory failure is frequently encountered and is reported to be one of the major causes of mortality (2). Systemic inflammation drives the shock state to a large extent. Nevertheless, another significant cause of circulatory failure is pulmonary vascular dysfunction and elevated pulmonary vascular resistance that is frequently observed in ARDS. These subsequently lead to failure of the right ventricle and refractory cardiogenic shock in addition to a component of distributive shock state which often coexists. Although hypothesized and agreed upon by many, the direct effect of pulmonary vascular dysfunction on mortality in ARDS has been difficult to demonstrate. Utilizing transesophageal echocardiogram probes (TEE), the demonstration of severe forms of right ventricular dysfunction and acute cor pulmonale (ACP) is relatively easier compared to quantifying pulmonary vascular dysfunction, which requires the use of a pulmonary artery catheter (PAC). Modern intensive care units around the world report the existence of right ventricular dysfunction in about 25-50% of patients with severe ARDS (3). Despite these numbers, current ARDS guidelines do not recommend searching for evidence of ACP or strategies directed at treating elevated right ventricular pressures as a part of managing ARDS. This is probably because of lack of any high quality evidence that clearly demonstrates the effect of ACP on mortality in ARDS.Several recent studies have demonstrated strategies that have improved survival rates in ARDS (4-6). Most of these involve advancements in ventilator strategies and measures to protect the lung while attempting to improve oxygenation. However, the pooled mortality rate in ARDS still stands at 40% in spite of best standards of care (7). This invites the question "Is there something else that can be offered to improve mortality in ARDS? Could the early identification and management of ACP associated with ARDS help us save more lives (8)?" Unfortunately, the answer is not entirely clear with the evidence available to us.As pointed out earlier, although the prevalence of ACP resulting from pulmonary vascular dysfunction has diminished with safer and more effective strategies of mechanical ventilation, it continues to occur in 25-50% of patients with ARDS (3,9-15). Pulmonary vascular dysfunction is a result of acute vascular inflammation that spills over from the alveoli to the microcirculation le...

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Pulmonary Vascular Dysfunction Is Associated with Poor Outcomes in Patients with Acute Lung Injury

Abstract: Pulmonary vascular dysfunction is common in ALI, and is independently associated with poor outcomes. Future trials targeting pulmonary vascular dysfunction may be indicated.

Cited by 186 publications

References 41 publications

The potential role and limitations of echocardiography in acute respiratory distress syndrome

The potential role and limitations of echocardiography in acute respiratory distress syndrome

Acute cor pulmonale and the acute respiratory distress syndrome

Preventing the development of acute cor pulmonale in patients with acute respiratory distress syndrome: the first step

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