Author + information
- Received January 25, 2018
- Revision received May 25, 2018
- Accepted June 19, 2018
- Published online November 5, 2018.
- Eugenio Picano, MD, PhDa,∗ (, )
- Maria Chiara Scali, MD, PhDb,
- Quirino Ciampi, MD, PhDc and
- Daniel Lichtenstein, MDd
- aCNR Institute of Clinical Physiology, Pisa, Italy
- bCardiology Department, Nottola Hospital, Siena, Italy
- cCardiology Division, Fatebenefratelli Hospital, Benevento, Italy
- dMedical Intensive Care Unit, Ambroise-Paré Hospital, Paris-West University, Boulogne, France
- ↵∗Address for correspondence:
Dr. Eugenio Picano, Institute of Clinical Physiology, Italian National Research Council, Via Moruzzi 1, 56124 Pisa, Italy.
For a cardiologist, lung ultrasound is an add-on to transthoracic echocardiography, just as lung auscultation is part of a cardiac physical examination. A cardiac 3.5- to 5.0-MHz transducer is generally suitable because the small footprint makes it ideal for scanning intercostal spaces. The image quality is often adequate, and the lung acoustic window is always patent. The cumulative increase in imaging time is <1 min for the 2 main applications targeted on pleural water (pleural effusion) and lung water (pulmonary congestion as multiple B-lines). In these settings, lung ultrasound outperforms the diagnostic accuracy of the chest radiograph, with a low-cost, portable, real-time, radiation-free method. A “wet lung” detected by lung ultrasound predicts impending acute heart failure decompensation and may trigger lung decongestion therapy. The doctors of tomorrow may still listen with a stethoscope to their patient’s lung, but they will certainly be seeing it with ultrasound.
Lung Ultrasound in Cardiology: Historical Background
Two hundred years after Laennec (1), who first introduced mediated lung auscultation as part of the physical examination of the heart in 1819, the transducer follows the same pathway as the stethoscope, from the cardiac area to lung fields, with several diagnostic benefits in the same examination. This may seem obvious now, but for our generation of cardiologists it took 50 years of transthoracic echocardiography (TTE) practice before we shifted the transducer by a few centimeters from the cardiac acoustic window to gain a view of the amazing new diagnostic world of lung ultrasound.
In the 1990s, lung ultrasound was first proposed with pioneering applications in the critically ill in a range of clinical conditions (2), including the detection of hemodynamic acute pulmonary edema (APE). It was only in 2004 that TTE was combined with lung ultrasound to detect pulmonary congestion in patients with heart failure who were admitted to a cardiology ward (3).
In retrospect, the technological and cultural gap between TTE and lung ultrasound was very narrow and did not require an intuitive mind to bridge it. The 2 techniques share the same equipment, with neighboring or superimposed scanning fields on the left anterior hemithorax. The diagnostic information provided by lung ultrasound is of obvious clinical interest to the cardiologist, who is well aware of the prognostic and therapeutic relevance of extravascular lung water, and how a real-time assessment of lung water may provide information complementary to conventional methods based on physical examination and chest radiographs to detect pulmonary congestion. In addition, intensivists and cardiologists often work on the same patients, and there is usually a close spatial proximity between the intensive care and coronary units. This logistic setting should theoretically facilitate the spread of innovative practices. However, TTE and lung ultrasound remained divided for decades by an invisible but impenetrable cultural wall. Standard textbook knowledge told us that the lung is filled with air (>90%), and air stops the ultrasound signal because of the very high impedance mismatch with chest tissues. The clinical corollary was that “ultrasound imaging is not useful for evaluation of pulmonary parenchyma” (4). In reality, the lung acoustic window is always open, even when the cardiac acoustic window for TTE is shut (5). Although only a limited portion of lung parenchyma can be visualized, this minute portion is critically important because most acute life-threatening disorders abut the pleural line: pleural effusions, pneumothorax, and acute interstitial syndrome in 100% of cases; and lung consolidation in 98.5% of cases.
Once the cultural wall of impedance bias surrounding ultrasound evaluation of the chest had fallen, cardiologists learned quickly what intensivists had known for decades. Lung ultrasound (also called thoracic ultrasound or chest sonography, but these labels may include mediastinum and the heart) provides a highly versatile and valuable diagnostic tool in many conditions that cardiologists encounter every day in their practice, from heart failure to pulmonary embolism. The information on lung water can be easily obtained at baseline and by serially following interventions for tracking dynamic changes in pulmonary congestion and decongestion (6). With comprehensive, limited, or focused examinations, lung ultrasound is now ready to be embedded in the standard TTE, from full functionality platforms performed by certified echocardiographers up to pocket devices used by nonechocardiographers. It is difficult to find so much diagnostic gain with so little investment in terms of technology, training, and time in other areas of cardiology (7). This review is primarily aimed at those caring for cardiology patients (cardiologists, emergency room physicians, cardiac ultrasonographers).
For the cardiologist, a lung ultrasound study is an add-on to a TTE study, and it must be focused, fast, and factual without becoming an extra examination requiring excessive additional time, separate reporting, and supplementary billing. The average time of a comprehensive TTE cardiac scan is 40 to 45 min, and we can easily add 1 min more to scan the lung for pleural effusion or pulmonary edema. The methodology of a heart-driven lung ultrasound examination can be summarized as follows, regarding the basic requirements: training, transducer, technology, technique, and targets of examination (Table 1).
The American College of Chest Physicians has defined the knowledge and technical elements required for competence in lung ultrasound (8). In our own experience, 1 morning hands-on experience or even a standardized Internet-based module of 2 h is sufficient to achieve excellent reproducibility in identification and quantification of B-lines, even among lung ultrasound–naive sonographers. They are among the easiest and most reproducible signs to recognize in cardiovascular ultrasound, considered to be “kindergarten” in the echocardiography cursus studiorum, whereas the identification of regional wall motion abnormalities is the more challenging “university” (7).
The probe is applied perpendicular to the chest wall, in a sublongitudinal view following rib obliquity. The small footprint of a cardiac transducer makes it especially suitable for scanning spaces between ribs, and a 3.5- to 5.0-MHz frequency allows adequate visualization of subpleural structures, although with limited resolution to locate the pleural line with confidence. Critical care physicians increasingly use 5-MHz microconvex probes that give a better view of the whole lung, superficial and deep, and allow simple emergency TTE, as well as venous, abdominal, and whole body urgent approaches (9).
No Doppler, second harmonic, or contrast medium is needed (7), and lung ultrasound is performed at best using simple equipment.
The acoustic window for lung ultrasound is always patent, even when TTE is not feasible. On the left side of the chest, the lung ultrasound window is close to TTE apical and parasternal windows and corresponds to the popular BLUE points in intensivists’ approach (10), where BLUE stands for bedside lung ultrasonography in emergency (11). There are 3 symmetrical regions per lung: 2 anterior points (upper BLUE point, lower BLUE point); and 1 posterolateral point, at or behind the posterior axillary line, at the level of the lower BLUE point, called the PLAPS point, where PLAPS stands for posterolateral alveolar and/or pleural syndrome (Figure 1). The anterior BLUE points are sought for the diagnosis of pneumothorax and pulmonary edema and are the elective site for detection of pulmonary congestion at rest. With stress, there is an additional but important focus on the third intercostal space in the 2 regions between the posterior axillary and anterior axillary lines and the anterior axillary and the midclavicular lines (12), the “wet spots” where lung water accumulates most during semisupine exercise (Figure 2). The PLAPS point allows for immediately diagnosis of most pleural effusions (13) and posterior alveolar syndromes (14) with >90% sensitivity. The PLAPS point is accessible in all patients, including ventilated, supine, bariatric patients, by using a probe that can be inserted between this posterolateral part of the chest and the bed; the most posterior is the best, but sometimes this is not easy to access, so the most possible lateral part makes the best compromise for detecting PLAPS. Once a pleural effusion is detected, the positive diagnosis is made, and the operator is free to assess the volume of the effusion by moving the probe; if no effusion is found, however, time is spared. Using this simplified approach, lung scanning can be achieved in far <2 min. For serial examinations, the position (sitting or supine) must be consistent because pleural and pulmonary lung water changes with posture. Lung ultrasound remains feasible and reliable under all hemodynamic and ventilatory conditions, unlike TTE information, which can deteriorate in acute conditions because of hyperventilation and tachycardia, which make imaging and interpretation of some parameters (e.g., regional wall motion, diastolic filling) more challenging.
For the cardiologist, the main diseases targeted by lung ultrasound are characterized by a change in water in the pleural space (pleural effusion) or lung parenchyma (pulmonary congestion, at rest and during stress). In both conditions, lung ultrasound has obvious advantages of sensitivity and specificity compared with chest radiographs. The BLUE protocol has proposed a standardized approach to the most common causes of acute respiratory failure, which are in the scope of the cardiologist assessing undifferentiated dyspnea (by decreasing frequency): pneumonia, APE, chronic obstructive pulmonary disease, asthma, pulmonary embolism, and pneumothorax (11).
Main Signs of Lung Ultrasound in Physiology and Disease
With lung ultrasound, the lung surface has always a simple pattern wherever the probe is applied. The whole structure is dynamic and produces physiological variations in movement from end-inspiration to end-expiration through the respiratory cycle mirrored in the pleural movement. The main signs of cardiological interest involve the pleural line, the pleural space, lung motion, the lung interstitium, and the lung alveolar space.
The 2 separate anatomic structures of parietal and visceral pleura are apposed and, with low-frequency transducers, merge into a single pleural line, a 0.2- to 0.3-mm thick echogenic, horizontal, smooth specular echo (Figure 3). The reverberation or repetition artifacts behind the pleural line can be horizontal (A-lines) or vertical (B-lines) images with regular, straight, and geometric shapes more precisely converging to the head of the probe (the top of the screen) like parallels (A-lines) or meridians (B-lines).
In acute respiratory distress syndrome (ARDS) and pneumonia, the fluid exudated by inflammation is a glue (15), which sticks the lung to the parietal pleura, thereby abolishing lung sliding. The pleural line appears thickened and irregular, possibly because of a small subpleural alveolar syndrome (Figure 3). Usually, these static signs come together with a single critical dynamic sign, the abolition (or severe impairment) of lung sliding. This sign is helpful in the differential diagnosis of B-lines in ARDS or pneumonia versus cardiogenic APE (15). The thickening of the pleural line is the main and most sensitive sign of lung fibrosis, found, for instance, in rheumatologic disease, and it is best detected with a high-frequency probe.
The visceral pleura slides over the motionless parietal pleura during breathing. The “lung sliding” is a horizontal, to-and-fro movement, beginning at the pleural line, synchronous with respiration. There is an obvious vertical gradient in the amplitude of lung sliding, which is near zero at the apex and gradually increases up to a maximum near the diaphragm (15). In healthy subjects quietly breathing, the amplitude of lung sliding is roughly 10 to 15 mm on the anterior chest window at the bases (lower BLUE points).
When air separates the 2 pleural layers (pneumothorax), the movement disappears. When a sticky exudate glues the parietal and the visceral pleura (pneumonia, ARDS), the movement is reduced or abolished. When collagen bundles bridge the parietal and visceral pleura, the movement is also reduced, as in pleural adhesions.
The fluid-filled space between the 2 specular reflectors of parietal and visceral pleura is only a potential space under normal conditions because the 2 pleurae adhere to each other through the few milliliters of serous fluid, thus allowing smooth movement of the visceral pleura during the respiratory cycle (Figure 3).
The pleural effusion noted by ultrasound is characterized by the static sign of a space between the pleural line and the lung line (always regular, roughly parallel to pleural line, which shows the visceral pleura) (Figure 3). The dynamic sign is a variation of this interpleural space within the respiratory cycle, with the inspiratory displacement of the lung line toward the pleural line and maximal distance at end-expiration. The static sign is called the “quad sign,” and the dynamic sign is the “sinusoid sign” (15). Transudative effusions are anechoic (echo free). Exudates can be anechoic or echoic, the most severe cases being usually perfectly echoic (empyema, hemothorax).
The normal lung shows lung sliding with A-lines, which are artifactual horizontal reverberations, equidistant from one another below the pleura, at exact multiples of the transducer-pleural line (Figure 3). A-lines indicate that there is air below the pleural line, either 99.5% air (i.e., normal lung below, which contains trace amount of water) or 100% air (in pneumothorax) (14).
Abnormal interstitial pattern: multiple B-lines
The B line is defined according to 7 criteria: 3 constant and 4 almost constant. The B-line is constantly a comet-tail, vertical artifact. Constantly, it arises from the pleural line. Constantly, it moves in sync with lung sliding (when there is lung sliding). Quasi-constantly, the B-line is well defined and laser-like; long, extending to the bottom of the screen without fading; erasing A-lines; and hyperechoic. This precise definition allows universal recognition in all cases (Figure 3). B-line is now the preferred name, but these lines are also called ultrasound lung comets. More than 2 B-lines per intercostal space have been called lung rockets (15). In some locations, 1 or 2 B-lines are physiological, for instance, anteriorly corresponding to lung fissures or lung rockets at the bases (likely natural gravity). Ultrasound interstitial syndrome is defined by lung rockets. It can be diffuse at the whole chest wall or symmetrical and associated with conserved lung sliding in the case of cardiogenic APE. This very precise pattern is called the B profile in the BLUE protocol (11). It can be diffuse but associated with abolished or very decreased lung sliding and labeled the B′ profile (11) in some cases of pneumonia and/or ARDS. It can be localized, usually in infectious or inflammatory processes (pneumonia, ARDS), and labeled the A/B profile.
Ultrasound multiple B-lines are the equivalent of the radiological interstitial syndrome (Kerley lines and more). We see interstitial syndrome, in acute conditions, in 2 main diagnoses with opposed management: cardiogenic APE and pneumonia or ARDS. Cardiogenic APE is associated with normal lung sliding, which is often reduced or abolished in pneumonia or ARDS.
B-lines must not be mixed up with Z-lines, which are frequently observed as bundle-shaped reflections arising from the pleural line, but that—unlike true B-lines—do not erase A-lines, are ill-defined, are less echogenic than the pleural line, are short, and do not move in synchrony with respiration (15).
Abnormal alveolar pattern: lung consolidation
In some conditions, the extreme progression of the interstitial syndrome leads to the consolidation process with an echogenic lung, with a tissue texture similar to that of spleen or liver, the result of replacement of air in the alveolar space with material other than air, usually water, pus, or blood (15) (Figure 3). Lung consolidation can have a variety of causes, including alveolar cardiogenic APE, pneumonia, lung infarction, cancer, lung contusion, and obstructive atelectasis. In some etiologies, such as drowning or aspiration pneumonitis, the fluid comes directly to fill the alveoli first, and the initial presentation is lung consolidation, without the usual initial phase of interstitial syndrome. Lung consolidations may arise in any site, and, although only the peripheral part of the lungs can be visualized by ultrasound, 98.5% of consolidations touch the pleura, and 90% of cases locate at the PLAPS point (14).
Pleural Effusion in Heart Failure
Elevated left atrial pressure in left-sided heart failure may cause pleural effusion only after pulmonary edema has developed (16,17). Elevated right atrial pressure in right-sided heart failure can increase the pressure in the thoracic duct, thus limiting the volume of lymphatic drainage from the pleural space to the right atrium through the superior vena cava (16–19).
The main signs on physical examination are reduced air entry and dullness to percussion at lung bases (20). In up to 20% of patients with acute heart failure (AHF), the chest radiograph is nearly normal, and the sensitivity of the method is less than one-half compared with lung ultrasound, especially for mild to moderate pleural effusions (20).
Semiquantitative grading of the amount of pleural effusion is possible by measuring the maximal expiratory interpleural distance from the pleural line to the lung line on the posterior axillary line with the patient in the supine position (13) or the paravertebral, scapular, posterior axillary, or medial axillary lines in the sitting position (21). The amount of pleural effusion can be scored as trivial (<2 mm), small (2 to 15 mm, too small to tap), moderate (15 to 25 mm), or large (>25 mm) (Table 2).
Diagnostic, prognostic, and therapeutic implications
The prevalence of pleural effusion may range anywhere between 56% and 90% in AHF, 30% and 60% at pre-discharge, 10% and 70% in outpatients with chronic stable heart failure, or 25% in patients with isolated right-sided heart failure (10,21–31) (Table 3). The main TTE predictor of pleural effusion is the increased systolic pulmonary arterial pressure (31).
In patients with heart failure, the presence of pleural effusion is associated with a higher rehospitalization rate (26) and clearly worse quality of life, which has improved after reduction of pleural effusion with medical therapy (30). In patients with AHF and pleural effusion, thoracentesis with fluid evacuation may be considered if feasible to alleviate dyspnea (20). For thoracentesis, a ≥15-mm interpleural inspiratory distance is required (13); the needle is inserted after careful check that 6 organs are not in the pathway of the needle: the diaphragm, of course, but also the heart, descending aorta, spleen, liver, and lung. The quantification is especially important for assessing variations in the same patient in natural history or following intervention. Lung ultrasound is ideal for guiding thoracentesis and draining effusions. The absence of a virtual space after the procedure (interpleural space >10 mm) reflects an incomplete procedure.
The sequence of events leading to APE during heart failure can be conceptualized as a cascade—the so-called lung water cascade—whose sequence was unveiled with the advent of lung ultrasound (32). The initiating events of the cascade are the increases in left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (hemodynamic congestion), eventually leading to the imbalance of Starling’s equilibrium in the alveolar capillary barrier, which is the pre-requisite for increased accumulation of lung water (Figure 4). In between hemodynamic and clinical pulmonary congestion, the intermediate event is interstitial pulmonary congestion detectable by lung ultrasound as multiple B-lines (33), linked biophysically to an increased water-to-air ratio per unit of lung volume tissue in the subpleural interlobular septa (7).
Pulmonary congestion is the key manifestation of impending AHF, but the clinical, auscultatory, and chest radiographic findings are all late, insensitive, and unspecific signs of pulmonary congestion (34). The reproducibility of the findings is poor for crackles and moderate for chest radiography, but high for B-lines (35). Quantification is easier and more effective for lung ultrasound, and it is based on the number of B-lines per space and spatial extension. Changes in B-lines are very quick to appear (for instance, during exercise or a volume challenge) and to disappear (for instance, with diuretics or dialysis), and therefore they must be interpreted in view of previous interventions (36). Multiple B-lines (lung rockets) are not designed for identifying a disease, but rather a syndrome: interstitial syndrome. From this basis, the physician knows that the patient can have cardiogenic APE, ARDS or pneumonia, or, rarely, any chronic interstitial disease. The physician will use the profiles of the BLUE protocol for refining the diagnosis: lung sliding associated, making at the anterior wall the B profile, highly accurate for cardiogenic APE; or lung sliding abolished, making the B′ profile, highly specific to pneumonia or ARDS. In spite of these caveats, the technique is now the best available for bedside detection of pulmonary congestion.
The comprehensive 28-site scan on the anterolateral chest was initially proposed in a cardiologic setting in 2004 (3) and adopted in research studies, but it was still too time-consuming for routine use in real-world laboratories, especially during stress echocardiography, when the time pressure is higher (7). Similar information can be obtained in much less time with a simplified 4-site scan, including only the “wet spots” with most B-lines (Figure 2). In this way lung ultrasound mapping does not interfere with electrocardiographic leads and takes only 20 s to be completed (10–12).
Diagnostic, prognostic, and therapeutic implications
AHF accounts for about 1 million emergency department visits in the United States, and even when cardiac peptides are incorporated into the clinical work-up of acute dyspnea, the misclassification rate remains at 14% to 29% (37). As shown by a recent meta-analysis recruiting 1,914 patients (37), the B profile identifies the cardiogenic origin of dyspnea with 85% sensitivity and 92% specificity (11,37–49), superior to pleural effusion and TTE (Table 4), and comparable to cardiac natriuretic peptides (37–41). The variability of reported specificities (ranging from 45% to 97%) likely reflects the selection criteria adopted in the different studies, with high pre-test probability of cardiogenic origin in critically ill patients admitted to intensive care units (11) and low to intermediate pre-test probability in clinically stable patients evaluated on admission to the emergency department (38).
The B profile is useful to track dynamic changes in pulmonary congestion in response to treatment (3,36), and its persistence at pre-discharge or in clinically stable outpatients with heart failure is predictive of heart failure hospitalization or death (22–30).
The key question is whether B profile can be used as a surrogate endpoint to guide interventions, such as increase in diuretic therapy in patients with heart failure or of dialysis rate in patients with advanced chronic kidney disease. Several large-scale randomized studies are in progress (NCT02310061, NCT03262571, NCT02959372, NCT03136198).
Lung ultrasound is a useful adjunct to TTE during stress echocardiography (10,50,51), by providing information on a different pathophysiological target (alveolar-capillary barrier rather than physiologically critical epicardial artery stenosis), with a different sign (B-lines rather than regional wall motion abnormalities), and in a different time window (after rather than at peak stress). As a parameter, B-lines are more feasible, simpler to image and to measure, and inherently more quantitative than regional wall motion. The accumulation of lung water during exercise is correlated with more advanced functional forms of heart failure and worse prognosis in patients with heart failure with reduced ejection function (10), and it is found also in patients with heart failure and preserved ejection fraction (51) (Figure 5, Online Video 1).
Lung ultrasound usually shows normal anterior A-lines and lung sliding (i.e., A profile), often accompanied by posterior lung consolidation and pleural effusion (11). Venous ultrasonography (with compression in cases when thrombosis is not seen directly) shows deep vein thrombosis with good sensitivity (11). TTE may detect (with high specificity but low sensitivity) prognostically relevant right ventricular overload and, rarely, the pathognomonic sign of a mobile serpentine thrombus in the right side of the heart or the pulmonary artery. Triple ultrasound imaging of heart, lung, and veins may have a role as a first-line add-on to clinical probability scores and D-dimer testing (52).
Primary Pulmonary Diseases: Interstitial Lung Diseases, Pneumonia and ARDS, Pneumothorax
Different primary pulmonary diseases are present as comorbidities in heart failure or as causes of dyspnea suspected to be cardiac in origin. Lung ultrasound is helpful in recognizing these diseases.
Pulmonary interstitial fibrosis with lung rockets accompanied by a thickened or irregular pleural line can be found in 20% to 50% of patients with systemic sclerosis and, less frequently, in other rheumatologic diseases (53). Fibrotic (“dry”) B-lines are not increased by exercise or decreased by upright position or diuretic challenge (Table 5).
With lung ultrasound, pneumonia and ARDS appear, roughly, as a single entity (11,54). ARDS can be separated from cardiogenic APE on the basis of several lung ultrasound and TTE features, summarized in Table 6.
As opposed to what happens for water in pleural effusion, in pneumothorax air tends to accumulate according to antigravity laws in the least dependent part of the chest. The ultrasound diagnosis of pneumothorax is based on 2 sequential signs. The first is the anterior detection of abolished lung sliding with the complete absence of B-line (called A′ profile in the BLUE protocol). The second sequential sign, to be sought only in presence of an A′ profile, is the detection of the lung point, defined as the sudden replacement of the A′ profile by any other pattern, usually lung sliding or B-lines (11,55).
From Lung Ultrasound Signs to Specific Diseases
Different diseases can be identified by lung ultrasound on the basis of the main signs that may translate into specific diagnosis of disease (Table 7), obviously after integration with the clinical presentation, TTE, venous ultrasonography for deep vein thrombosis detection, and others.
Lung Ultrasound in Scientific Societies’ Recommendations
Ultrasound guidance has been “strongly recommended” since 2010 by the British Thoracic Society for all pleural procedures with pleural fluid because it is associated with a lower failure rate and rate of complications such as pneumothorax and bleeding (56). It is becoming increasingly difficult to justify performing these procedures without ultrasound guidance (57).
European Association of Cardiovascular Imaging recommendations for use of pocket-size devices explicitly list “semi-quantification of extra-vascular lung water” with B profile among the top 8 indications (58). In emergency echography, the absence of B profile excludes cardiogenic edema with a negative predictive value close to 100% (11,59). The 2016 guidelines on heart failure of the European Society of Cardiology recommend lung ultrasound among diagnostic tests in heart failure (Class IIb, Level of Evidence: C) as a test that may be considered in patients with AHF to confirm pulmonary congestion and pleural transudate (20). In patients with AHF, in 2015 lung ultrasound was recommended by the European Society of Cardiology as a first-line diagnostic test to assess pulmonary congestion in suspected AHF because “in reasonably expert hands it can be equally or more informative than chest X-ray allowing also an important time-saving” (60). The 2017 expert consensus of the AHF group of the European Society of Cardiology concluded that “TTE and lung ultrasound can assist in the rapid assessment of patients with acute dyspnea and hypotension and have the potential to transform the way in which the clinicians assess and manage critically ill patients with AHF and cardiogenic shock” (61).
According to the 2016 joint European Association of Cardiovascular Imaging and American Society of Echocardiography recommendations, during exercise stress echocardiography the acute increase in B-lines detected by lung ultrasound is a feasible way for demonstrating that the symptom “dyspnea when exercising” is related to pulmonary congestion secondary to backward heart failure (62).
Severe subcutaneous emphysema can be an absolute hindrance. Dressings should be limited for favoring ultrasound studies. Morbid obesity is not a limitation for several areas of lung ultrasound, mainly detection of A profile, A′ profile, B profile, and B′ profile (15).
Lung rockets reflect the presence of an interstitial syndrome that can be caused by water, inflammation, or fibrosis, but integration with clinical presentation, systematic application of lung ultrasound with the BLUE protocol, and association with TTE allow the clinician to identify the underlying etiologic factors and to answer the clinical question most of the time (11).
Lung ultrasound is currently used by many different medical disciplines, from cardiology to intensive care, from pneumology to nephrology, from rheumatology to sports medicine. This range adds appeal to the technique, but it may pose communication difficulties related to heterogeneity of terminology, execution, and reporting, and better harmonization is needed (7). For the past 3 decades, standardized labels for lung ultrasound have been refined for maximal efficiency in a field made free of any confusion (11,15).
Lung ultrasound can reduce medicolegal risk by shortening the time to diagnosis in patients with life-threatening conditions. The best defense against litigation is to follow training strictly. Malpractice lawsuits have been filed for not performing the examination in a timely manner (63).
The image texture is, at least in principle, suitable for treatment with video-densitometric analysis, and lung water software is already included in some commercially available instruments to provide quantitative support to B-line reading. This option is attractive, but as in any field, and especially in imaging, checking the quantitative, machine-generated findings using experience, prudence, and clinical wisdom is always necessary.
Large scale, prospective, international, multicenter, effectiveness studies are currently ongoing with rest and stress B-lines in known or suspected heart failure and coronary artery disease in the Stress Echo 2020 study, which is planning to recruit 10,000 patients within the year 2020 with the new standard of dual imaging, including regional wall motion and B-lines (64).
Randomized outcome studies are needed to assess the value of lung ultrasound are needed to reduce mortality in patients with either chronic heart failure or acute circulatory failure.
After opening the acoustic window on lung parenchyma, the cardiologist discovers unique information that will soon induce a durable mutation in the structure of cardiac ultrasound examination, destined to become a cardiopulmonary (TTE-lung ultrasound) study. Now is the appropriate time for professional cardiology and echocardiography societies to incorporate lung ultrasound into the mainstream of core teaching, certification, and reporting in TTE. Lung ultrasound can provide unique information in the cardiology ward, intensive care unit, emergency room, echocardiography laboratory, stress testing laboratory, outpatient clinic, and perhaps especially in home care with handheld devices in patients with heart failure (Central Illustration). The use of lung ultrasound will reduce the use of techniques based on ionizing radiation, such as chest radiography or computed tomography, thereby contributing to minimize the cumulative burden of unwanted effects of radiation exposure, especially relevant in cardiology patients (65). A “wet lung” detected as B profile by lung ultrasound, at rest or after stress, in a stable patient with chronic heart failure predicts impending AHF decompensation and may trigger lung decongestion therapy. No cardiologist would evaluate a patient with heart failure without listening to lung fields for crackles or a pleural effusion. In the same way, today no comprehensive, limited, or focused TTE examination will be considered complete without a short but efficient assessment of the lung.
All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- acute heart failure
- acute pulmonary edema
- acute respiratory distress syndrome
- bedside lung ultrasonography in emergency
- posterolateral alveolar and/or pleural syndrome
- transthoracic echocardiography
- Received January 25, 2018.
- Revision received May 25, 2018.
- Accepted June 19, 2018.
- 2018 American College of Cardiology Foundation
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- et al.
- Picano E.,
- Vano E.,
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- et al.
- Central Illustration
- Lung Ultrasound in Cardiology: Historical Background
- Current Methodology
- Main Signs of Lung Ultrasound in Physiology and Disease
- Pleural Effusion in Heart Failure
- Pulmonary Congestion
- Pulmonary Embolism
- Primary Pulmonary Diseases: Interstitial Lung Diseases, Pneumonia and ARDS, Pneumothorax
- From Lung Ultrasound Signs to Specific Diseases
- Lung Ultrasound in Scientific Societies’ Recommendations
- Current Limitations