Lung ultrasound in acute and chronic heart failure: a clinical consensus statement of the European Association of Cardiovascular Imaging (EACVI)

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Lung ultrasound (LUS) was introduced to intensive care units and emergency departments more than 20 years ago, primarily as a tool for the assessment of patients with acute dyspnoea.1,2 Since then, it has gained popularity as a quick point-of-care examination enabling clinicians to answer crucial clinical questions. Over the last decade, the cardiology community has acknowledged the potential of LUS and expanded its use further, to assist with the diagnosis and management of patients with heart failure (HF).3–5 The importance of recognizing and treating pulmonary congestion is a cornerstone in the management of patients with HF.6 LUS is a versatile, high sensitivity point-of-care examination to detect pulmonary deaeration due to increased extravascular lung water. It has many advantages to the extent that an integrated cardiopulmonary ultrasound exam is likely to become the reference standard in HF care. This approach allows the aetiology of HF to be defined, through the assessment of cardiac structure and function by echocardiography, at the same time as the assessment of pulmonary congestion provided by LUS. In addition, it facilitates the exclusion of other highly prevalent conditions that may mimic/overlap with HF (e.g. pneumonia, acute lung injury/acute respiratory distress syndrome [ALI/ARDS], and pneumothorax). In a fully aerated lung, the only anatomical structure that can be visualized is the pleura, which appears as a smooth, hyperechoic horizontal line that moves synchronously with respiration. This line is called ‘pleural line’ and its movement is the ‘lung sliding’, providing visual assessment of lung excursion during ventilation. The sonographic pattern of the aerated lung also includes parallel, hyperechoic, horizontal lines that can be seen at regular intervals from the pleural line (A-lines, Figure 1, Supplementary data online, Video S1).7 When the air content in the lung decreases and lung density increases, vertical reverberation artefacts appear (B-lines, Figure 2, Supplementary data online, Video S2). B-lines originate from the pleural line and move synchronously with respiration, are laser-like in shape and extend towards the bottom of the US sector as displayed on the screen.8 B-lines are present in patients with HF and pulmonary oedema9 where an increasing number of visualized B-lines are associated with a decreasing air/water content ratio.10–12 B-lines are not specific for cardiogenic pulmonary oedema and can be detected in patients with non-cardiogenic pulmonary oedema, including those with end stage renal disease and in ALI/ARDS,13 but also in pulmonary fibrosis (interstitial lung disease)14 and interstitial pneumonia. Some sonographic characteristics can help differentiate these various causes of B-lines5 (Table 1). The sonographic pattern of a normally aerated lung with the pleural line (upper dotted yellow line) and A-lines (lower dotted orange lines). B-lines indicated by dotted white lines. Different LUS features in different conditions where multiple B-lines are present Different LUS features in different conditions where multiple B-lines are present Pleural effusion can be easily detected by LUS, placing the phased-array transducer on the surface of the chest wall in an intercostal space, and is displayed as an anechoic space above the diaphragm. Pleural effusion is advised to be sought at first in the dependent zones, i.e. lateral and posterior chest wall (e.g. posterior axillary line) at the level of costophrenic angles (Figure 3 and Supplementary data online, Video S3), which also allows other causes of chest X-ray radio-opacity, such as consolidation, mass, or an elevated hemidiaphragm to be ruled out (Figure 4 and Supplementary data online, Video S4). LUS is more sensitive than chest X-ray in detecting pleural effusions, when using computed tomography as the reference standard,15,16 and can determine the volume of pleural effusion and monitor its evolution. LUS can also provide information on its likely nature by differentiating between simple and complex effusions, and can help guide the optimal site for needle thoracentesis. The left costophrenic angle with pleural effusion. Pleural effusion with compression atelectasis. The pathophysiology of congestion in HF includes the different stages of haemodynamic, pulmonary, and systemic congestion,17 which can be all assessed by ultrasound. Traditional echocardiography provides indicators of haemodynamic congestion, including a dilated left atrium, a high E/e′, elevated pulmonary artery systolic pressure, and dilated inferior vena cava (IVC). B-lines on LUS are a sign of pulmonary congestion (increased extravascular lung water) due to left-sided HF, independent of—yet closely related with haemodynamic congestion. Chronically elevated left-sided filling pressures eventually result in a rise in right atrial pressures and IVC distension. An IVC smaller than 21 mm that collapses >50% during inspiration suggests normal right atrial pressures,18 although this measurement should be interpreted in the context of the overall patient’s underlying pathophysiological and haemodynamic status and integrated with other echocardiographic findings; an increased IVC diameter can identify intravascular volume expansion prior to changes in symptoms or body weight, and predicts a high risk of rehospitalization for HF or death in patients with acute or chronic HF.19,20 Using a high-frequency linear transducer, the internal jugular vein (IJV) diameter can be measured. When congestion is severe, IJV distensibility, provoked by Valsalva manoeuvre, is markedly reduced, indicating a poor prognosis.21 Congestion in other organs can be also assessed by ultrasound, such as the kidneys. A comprehensive review of these novel techniques and their potential clinical utility can be found elsewhere.22 Recently, the venous excess ultrasound (VExUS) score, including Doppler evaluation of the IVC, hepatic veins, portal vein, and renal venous flow, has been proposed to assess presence and severity of venous congestion.23 Whereas systemic venous congestion (as assessed by IVC, IJV, hepatic veins, portal veins, and renal veins) can be present in both right- and left-sided HF, LUS B-lines indicate pulmonary congestion due to left-sided HF. When the pulmonary air content is completely dissipated in areas of pulmonary consolidation, the lung parenchyma can be directly visualized (Figure 5 and Supplementary data online, Video S5) with a hypoechoic or tissue-like pattern. Different aetiologies of consolidations may have also different sonographic appearance (Figure 5). Compression atelectasis is frequent in patients with HF; here, a large cardiogenic pleural effusion causes direct compression of the pulmonary parenchyma.4 Different patterns of consolidation at LUS: A) pneumonia; B) pulmonary infarction; C) compression atelectasis; D) obstructive atelectasis. On occasion, a focal interstitial syndrome (i.e. multiple B-lines localized only in a single area of the chest) can suggest pneumonia. These are thought to represent either the very early phases of pneumonia with the partial deaeration LUS pattern (B-lines) preceding the total deaeration LUS pattern (consolidation), or the focal oedema surrounding any consolidation. Whenever possible, it is advised to perform LUS exams with a standardized approach, to facilitate interpretation and monitoring, as well as reproducibility.24 Several LUS protocols have been described, with a variable number of examination areas of the chest (‘zones’) to be examined, ranging from 4 to 2825–27 (Figure 6). Currently, the eight-zone scanning protocol is the most widely used, balancing the need for a simplified, rapid protocol, and good accuracy;8 with studies suggesting it the most appropriate approach across multiple settings, including the diagnosis of HF (with the 8-zone C-index non-inferior to the 28-zone C-index),28 and for risk stratification.29 Different LUS scanning protoc

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.