20 Echocardiography and thoracic ultrasound

For the emergency management of cardiovascular disorders, echocardiography and thoracic ultrasound are indispensable imaging techniques at the bedside. In the intensive care environment, crucial questions, such as left and right ventricular function, valvular heart disease, volume status, aortic disease, cardiac infection, pleural effusion, pulmonary oedema, pneumothorax, and many others, can be sufficiently and reliably answered by using these techniques; in fact, it is almost impossible to manage patients with acute severe haemodynamic impairment reasonably well without a prompt and repeated access to echocardiography. This is confirmed by the prominent place that echocardiography has in the guideline-based diagnosis and treatment of all major cardiovascular emergencies, from acute heart failure to the acute coronary syndrome to pulmonary embolism, etc. Moreover, it is the ideal tool to follow the patient, since repeat examinations pose no risk to the patient and demand relatively little logistics and resources. To benefit from the wealth of information that echocardiography and thoracic ultrasound can provide, modern equipment (including a transoesophageal probe) and systematic training of echocardiographers must be ensured. The availability of prompt and experienced echocardiography and thoracic ultrasound services at all times is fundamental for sound contemporary cardiovascular intensive care.

The intensive care environment poses specific and rigorous demands on the availability, speed, versatility, and accuracy of cardiac imaging. Echocardiography is by far the technique which best matches these demands in the vast majority of cases and thus is clearly—as in cardiology in general—the ‘first-line’ imaging technique in intensive care. Prompt availability of echocardiography is indispensable to any intensive care unit (ICU) and, of course, central to cardiac care units. In this chapter, the basic knowledge of echocardiographic techniques and examination procedures is assumed; strengths, weaknesses, pitfalls, and particularities of echocardiography in specific situations are discussed. New techniques are briefly presented, but the main emphasis rests on the most appropriate use of standard armamentarium, corresponding to the typical needs of intensive care management. The text has been arranged according to clinical scenarios.

While echocardiography has always been a relatively small, portable, and deployable technique at the bedside, in contrast to other imaging modalities, technical progress in recent years has led to further reductions in size, even of state-of-the-art machines, making them well usable in an intensive care setting. Technical considerations in the selection of the best ultrasound machine for your coronary care unit (CCU) are provided in Fig. 20.11. Besides, the industry has produced miniaturized echocardiography machines which have begun to differentiate into two main lines. The first line of products comprises laptop-type devices which essentially have all the capabilities of larger machines, including full digital storage and transoesophageal imaging. These devices typically still need a power supply or additional battery package and, although eminently mobile, a table or similar support platform. The other line of products is further miniaturized to allow effortless portability (‘ultrasound stethoscope’), with a minimal weight of <1 kg; they can be carried in a coat pocket or around the physician’s neck (see Figure 20.1). These devices have quite limited options, if any, e.g. for Doppler interrogation and storage, and cannot be used for transoesophageal imaging [1, 2]. They still provide reasonable 2D quality sufficient to identify, for example, impaired LV function or a pericardial effusion.

The selection of an ultrasound machine for an ICU should consider the following fundamental issues:

In the intensive care setting, the maintenance of echocardiography equipment is a constant headache, often because no clear responsibilities exist. This relates to equipment maintenance, cleaning, proper disinfection of transoesophageal probes, housekeeping of reports and other documentation, management of digital storage, including protection against loss of data, regular software updates, providing sufficient space, and other issues.

Minimal training requirements are provided in the online data supplement. The ICU is often the first place where a cardiology or internal medicine fellow in training operates an echocardiography machine, usually under informal supervision of a more experienced colleague. Because of the frequent direct impact of the echocardiographic diagnosis on management, this is a particularly impressive and enlightening situation to learn echocardiography. However, this must be accompanied or followed by systematic training, in particular because the time pressures of the intensive care setting often lead to incomplete and hurried examinations. Also, crucial competencies, such as eyeballing LV pump function or assessing valvular regurgitation, are not acquired sufficiently without systematic training and comparison to other techniques. In a study of the diagnostic accuracy of ‘point-of-care’ echocardiography with portable devices, the diagnosis of impaired LV function agreed in only 75% of cases between fellows with limited training and fully trained echocardiographers [1]. Therefore, the training recommendations of the European Association of Cardiovascular Imaging [3] (see Table 20.1) or national societies should be followed, and it should be ensured that definitive reports are reviewed beforehand by a trained echocardiographer. For a fully trained cardiologist subspecializing in intensive cardiac care, the curriculum of the Acute Cardiac Care Association (ACCA) requests the ability to fully and independently perform trans thoracic echocardiography (TTE) and TOE (level III competence, including performance of at least 350 transthoracic and 50 transoesophageal studies).

Data storage, preferably digital, and written reporting of echocardiographic findings are of critical importance in the intensive care setting, not only for patient management, but also for medicolegal reasons. Understandably, there is a tendency to neglect these tasks in the context of life-threatening scenarios, which nevertheless should be counteracted. (See also Chapter 2).

Echocardiography is extremely valuable in acute coronary syndrome (ACS), and therefore an echocardiographic examination should be performed at the earliest possible point in time [4, 5]. The echocardiographic hallmark of ACS is the wall motion abnormality as a marker of ongoing or recent myocardial ischaemia (see Figure 20.2). Wall motion abnormalities result from impaired systolic wall thickening and reduced systolic endocardial inward motion. They range in degrees, from hypokinesia (reduced thickening and inward motion) through akinesia to dyskinesia (systolic outward movement and thinning) and aneurysm (systolic and diastolic outward bulging and thinning), and in extent by the number of wall segments affected, which most conveniently are described by the standard 16- or 17-segment schemes [6]. The wall motion score is a semi-quantitative way to express this; each segment receives a score from 1 (normokinetic) to 4 (dyskinetic), and the sum of all scores divided by the number of segments, called the ‘wall motion score index’, is a dimensionless semi-quantitative parameter of wall motion impairment, 1 being for a normal ventricle and increasing in value with increasing wall motion abnormalities. The pattern of affected segments may indicate which coronary artery is affected. The degree and extent of wall motion abnormalities depend on the severity of ischaemia, which, in turn, depends mainly on the location of the occlusive thrombus and the duration of ischaemia. However, it is frequently not possible to decide whether a wall motion abnormality is new or old, although myocardial thinning or increased echogenicity implying fibrosis are signs of an older scar. Also, whether a new wall motion abnormality is reversible by an acute intervention (myocardial hibernation) is not immediately possible to decide, although some newer techniques, like left heart contrast echocardiography or deformation imaging, may be helpful. Although echocardiography is quite good at detecting acute myocardial ischaemia, wall motion abnormalities may be missed, depending on the image quality, and therefore echocardiography is not 100% sensitive for ACS. However, a good-quality echocardiography without any wall motion abnormalities makes acute myocardial ischaemia highly unlikely. On the other hand, the extent and severity of a detected, and presumably new, wall motion abnormality is important for global LV function and also predicts the prognosis and likelihood of post-infarction remodelling.

A second crucial piece of information is global LV pump function, usually expressed as ejection fraction (EF), with well-known prognostic and management implications (see Figure 20.2). EF can be eyeballed by experienced (!) observers and can be measured by 2D and three-dimensional (3D) methods with sufficient image quality. A useful surrogate parameter for EF in patients difficult to image is the excursion of the mitral annulus (mitral annular plane systolic excursion, MAPSE) or the peak systolic longitudinal (apico-basal) tissue velocity at the base of the LV, e.g. the basal septal segment in the four-chamber view. Besides this information, echocardiography is able to provide evidence for increased filling pressures, e.g. restrictive transmitral filling pattern, which carries considerable prognostic weight, independently of the EF [7]; for more detail, the reader is referred to the literature [8, 9].

Finally, complications of an acute myocardial infarction (AMI) can be quickly detected in the acute phase of an ACS:

In the subacute phase and before release from hospital, it is important to provide a baseline study of wall motion and ventricular function for later follow-up. Regional and global function may still undergo changes in this phase, both in the direction of improvement if there is still myocardial stunning or of deterioration due to LV post-infarction remodelling. Other concerns are the presence of inducible ischaemia from coronary territories other than the culprit one and the question of myocardial viability in areas of wall motion abnormality; these questions can also be addressed by (stress) echocardiography. (See also Chapters 43 and 46.)

Severe hypotension, shock, and cardiac arrest all call for immediate echocardiographic support. When performing such emergency echocardiography, it is useful to have a list of the most important echocardiographic features in mind to search for (see Table 20.2). The imaging conditions are almost always suboptimal, with many individuals surrounding the patient, frequently in cramped conditions of an invasive laboratory, with simultaneous procedures such as establishing intravenous (IV) access or frank resuscitation going on in parallel. Obviously, portable echocardiographic machines are beneficial in these circumstances. Contrary to the typical protocol of echocardiography that begins with parasternal imaging, often only apical or subcostal windows are usable and should be quickly sought. In the ventilated patient, TOE, if quickly available, is very helpful. In the patient in cardiac arrest undergoing resuscitation, or shortly thereafter, it is typical to see diffusely hypokinetic, dilated ventricles. This per se does not establish a cause for the cardiac arrest. However, the presence of a pericardial effusion or a disproportionately large RV points to tamponade (see Chapter 27) or PE (see Chapter 64) as the most likely causes of arrest, and these two conditions can be detected or excluded by echocardiography within seconds, even in very unfavourable circumstances, and may lead to lifesaving treatment.

Most aetiologies of an acute drop in blood pressure (BP) are discussed in more detail in the pertinent sections of this chapter. Volume depletion, which is a frequent cause of hypotension, does not have specific echocardiographic signs; typically, the RV is relatively small (underfilled), and the inferior caval vein collapses with inspiration. The value of echocardiography in this scenario lies mainly in the exclusion of cardiac pathology. See Assessment of cardiac output and volume status section for more detail. (See also Chapter 49.)

See also Chapter 51.

Echocardiography provides crucial information on the mechanisms, severity, and therapeutic options in congestive heart failure [10]. Global LV function is typically categorized into systolic or pump function, which assesses the ability of LV to create an adequate stroke volume, and diastolic function, which relates to the ability of the LV to fill adequately at low diastolic pressures. The evaluation of global LV systolic function consists of:

See Table 20.3 for normal values.

Practically all patients with impaired global systolic function also have elevated LV filling pressures, and hence impaired diastolic function. Echocardiography provides an estimate of elevated filling pressures and is able to detect markers of impaired prognosis such as the restrictive transmitral filling pressure [8, 9]. On the other hand, there is a large group of patients suffering from symptoms of heart failure, although the EF is preserved, especially in the presence of hypertension and LV hypertrophy. This has been termed ‘heart failure with normal EF’ or ‘diastolic heart failure’. The following signs and parameters should be systematically used to evaluate diastolic LV filling pressures:

Further important information in patients with heart failure gleaned from echocardiography includes:

Echocardiography also plays a critical role in identifying candidates for therapies and procedures which may improve heart failure or its prognosis [10]. The most important issues are:

Knowledge of cardiac output and of intravascular volume status is crucial in intensive care. These parameters can be estimated, to a degree, from echocardiography. Cardiac output is most easily calculated by measuring LV outflow tract (LVOT) diameter (D) and the time velocity integral of LVOT flow by pulsed-wave Doppler (VTI), taking care to align the Doppler beam as well as possible with the long axis of the outflow tract ( Figure 20.15) (see Chapter 66). Provided there is no aortic regurgitation (AR), the systemic stroke volume (SV) is (assuming a circular outflow tract cross-section) approximated as:

A similar calculation can be made at the pulmonary valve level to calculate the pulmonary stroke volume. The product of the stroke volume and heart rate is the cardiac output. The calculation is far from precise but will give a reasonable estimate of the cardiac output.

The estimation of the intravascular volume status, specifically of central venous pressure (CVP) and of pulmonary capillary pressure, relies on indirect signs and is more complex.

A chapter on TTE is available in the online data supplement.

See Chapter 59.

Infective endocarditis may necessitate intensive care for several reasons: sepsis, acute valvular regurgitation, and central or peripheral systemic embolism. The echocardiographic hallmark of infective endocarditis are new mobile mass lesions (vegetations) ( Figures 20.16 and 20.19) attached to valvular structures and valvular destruction, leading to regurgitation; in fact, echocardiographic evidence of infective endocarditis is a major diagnostic criterion. Mitral and aortic valves are affected with similar frequency. Tricuspid endocarditis occurs mainly in drug addicts and patients with long-standing disease necessitating the insertion of indwelling central catheters and ports. Vegetations may also be attached to cardiac foreign bodies, such as pacemaker electrodes, and, in rare cases, directly to the endocardium, e.g in the proximity of a VSD. Abscess formation in the perivalvular tissue may be observed, especially in aortic valve endocarditis ( Figure 20.17) and in prosthetic valves. Further sequelae of endocarditis are fistulae, perforations, or the formation of a mitral pseudoaneurysm. Valve endocarditis may induce regurgitation of all degrees by perforation or rupture of valvular structures. Transoesophageal examination, because of its higher spatial resolution and better image quality, is superior to TTE and should always be used if there is a substantial suspicion of infective endocarditis (e.g., positive blood cultures) and no definite diagnosis can be established by TTE. In the presence of prosthetic valves, the use of TOE is mandatory [11], since infective endocarditis is frequent, difficult to detect, and more prone to complications, especially ring abscesses, in the presence of prosthetic valves. (See also Chapter 59 and Figure 20.18.)

Acute severe MR occurs in several scenarios. Due to systolic regurgitation into the LA, there is acute volume overload, and consequently pressure overload of the LA, leading to increases in pulmonary capillary pressures and pulmonary oedema. Forward stroke volume is low, causing hypotension and ultimately CS. Key echocardiographic findings are [12, 13]:

Acute severe AR causes sudden LV volume overload and increased diastolic pressures, leading ultimately to pulmonary oedema, and, with reduced forward stroke volume, also leads to CS. Key echocardiographic findings are:

Prosthetic mitral or aortic valves may develop sudden severe regurgitation due to ring dehiscence (e.g. in the course of infective endocarditis, endocarditic destruction or degenerative rupture of bioprosthetic leaflets) or thrombotic fixation or embolization of a mechanical occluder ( Figure 20.22) (e.g. after strut fracture of a tilting disc prosthesis). (See also Chapter 59 and Table 20.7.)

Prosthetic valve thrombosis occurs almost exclusively in mechanical valves, leading to predominant stenosis, with or without regurgitation, depending on the dynamics of the prosthetic leaflet(s). Symptoms and clinical findings depend on how rapidly the prosthetic obstruction develops and on the severity of the obstruction [14, 15]. The incidence of prosthetic valve thrombosis is twice as high in the mitral as in the aortic position, and even higher in the tricuspid position, independently of the prosthesis type. Echocardiographic signs are increased transprosthetic Doppler gradients and, especially in mitral prostheses, absent motion of one or both occluders. TOE is mandatory and sometimes can distinguish obstruction by thrombus or by pannus. Fluoroscopy is very helpful and indispensable in aortic prosthetic thrombosis ( Figure 20.23). (See also Chapter 59.)

The two main pericardial pathologies important for cardiac intensive care are pericardial effusion, including tamponade, and constrictive pericarditis. Pericardial effusions occur in many circumstances, including infectious, immunological, and malignant diseases, as well as in perforation or rupture of coronary vessels or cardiac chambers and traumatic damage.

Cardiac tamponade is a life-threatening complication of pericardial effusion and can occur even with small, but acutely developing, effusions, e.g. after coronary artery perforation or rupture due to PCI (see also Chapter 27). Due to the limited intrapericardial space and low compliance of the pericardium, compression of cardiac chambers ensues, typically the right atrium (in late diastole and early systole) and RV (in early diastole) due to their relatively low inside pressures. This ‘collapse’, along with the effusion, can be seen directly on 2D echocardiography, especially in the four-chamber view and the subcostal view (see Figures 20.8 and 20.9). The duration of collapse during the cardiac cycle parallels the severity of haemodynamic compromise. While temporary inward displacement of the right atrial wall during the cardiac cycle is an early and sensitive sign of the haemodynamic significance of the pericardial effusion, its specificity for tamponade is low; on the other hand, RV collapse has lower sensitivity but higher specificity for haemodynamic compromise. In rare cases of localized pericardial effusions (e.g. post-operatively), the LA or LV may be primarily compressed; these localized effusions may be difficult to detect and may necessitate TOE, especially in the post-operative patient. The compression of the heart chambers leads to an exaggeration of the respiratory variation of inflow and outflow patterns of the ventricles; mitral inflow and aortic stroke volume decrease with inspiration, whereas tricuspid inflow increases. A >25 % decrease in peak transmitral E wave velocity with inspiration is considered a sign of haemodynamic compromise. A ‘paradoxical’ septal shift to the left in early diastole, created by the increase in transtricuspid flow, is also observed. In expiration, these changes are reversed. Furthermore, the inferior vena cava is usually distended and does not collapse with inspiration ( Table 20.8).

To prepare for pericardial puncture, the subcostal view is useful to determine the location, angle, and depth of the puncture. If the subcostal approach is not feasible, echocardiography helps to select alternative sites for puncture, i.e. sites where the distance between the skin and pericardial fluid is minimal, e.g. the apex. After puncture, the location of the tip of the needle or of the catheter introduced in the pericardial space may be confirmed by injecting an agitated infusion solution, which will create a bright contrast echo in the pericardial space.

In constrictive pericarditis, a thickened (>5 mm) or calcified pericardium may be apparent but often is not. The ventricles are of normal size, whereas the atria are enlarged. Global LV and RV systolic functions are normal, but paradoxical septal motion is present. In clear-cut cases, there is an inspiratory decrease in transmitral flow and increase in transtricuspid flow, with opposite changes in expiration. Sometimes, however, this sign is blunted by massive diuretic therapy. The transmitral flow in the typical case is characterized by tall, short E waves, with short deceleration time (‘restrictive transmitral pattern’). (See also Chapters 27 and 58.)

A detailed discussion on traumatic cardiac and aortic injury is provided in Chapter 62. A focus on echocardiography is provided in the online data supplement.

Virtually all cardiac structures may be damaged by blunt trauma. The ventricles may develop intramyocardial haematoma, myocardial necrosis, or frank rupture, leading to usually a lethal tamponade, if a free wall is affected, or else to a VSD. The RV free wall is most often affected due to its anterior localization in the chest. The atria may also rupture. Coronary vessels may be lacerated, leading to haematopericardium and tamponade. Valvular structures may also be damaged, including leaflets and the support apparatus, most prominently papillary muscles or chordae. Tears of the pericardium, with or without other cardiac injury, may lead to herniation of other organs into the pericardial sac (e.g. intestinal herniation through an also ruptured diaphragm) or displacement of cardiac structures outside the pericardial sac.

The thoracic aorta is affected, especially by deceleration trauma (e.g. traffic accidents or falls) (see also Chapter 61). Traffic accidents typically cause aortic damage at the aortic isthmus, the junction of the aortic arch, and the descending aorta. Falls may lead to aortic damage at the level of the innominate artery. The damage to the aorta ranges from intramural haematoma to complete transection of the vessel.

Echocardiography, and especially TOE, is very helpful after blunt chest trauma. In a study, more than half of 117 patients with blunt chest trauma showed clearly pathological findings on TOE, ranging from RV wall motion abnormalities to pericardial effusions; the ECG was often normal in these patients [16, Table 20.3]. Penetrating trauma of the heart or large vessels is typically rapidly deadly, precluding echocardiographic examination.

A dilated and hypokinetic RV is the typical echocardiographic finding in severe PE. Additionally, there is a variable increase in RV systolic pressure, as estimated by measuring peak tricuspid regurgitant velocity (see Figure 20.10). This is done by measuring peak tricuspid regurgitant velocity using continuous-wave Doppler, calculating the peak pressure difference between the RV and right atrium from the Bernoulli equation (Δp = 4 × v²) and adding an estimate of the mean right atrial pressure, e.g. 10 mmHg (for more detail on right atrial pressure estimation, see section on heart failure). Note, however, that, in the acutely failing RV associated with fulminant PE, this pressure may be deceptively normal or only minimally elevated. Very high peak pulmonary pressures (e.g. >80 mmHg) cannot be generated by a previously normally loaded RV and do not occur in response to an acute embolism, unless there is previous PH. A shift of the ventricular septum to the left, flattening the cross-section of the LV into a ‘D’ shape, instead of the normal circular shape, in short-axis views, and paradoxic septal motion are important signs of acute RV pressure overload. Tricuspid regurgitation is invariably present, and the inferior vena cava may be distended and lack inspiratory collapse. Thrombi may sometimes be seen directly in the pulmonary artery imaged in parasternal or subcostal views. If TOE is performed, the right pulmonary artery can also be evaluated quite well, and thrombotic material may be seen there. The acute pressure increase in the right atrium leads to a shift in position of the atrial septum to the left side and may create continuous right-to-left shunt through a patent foramen ovale. In the presence of severe PE, paradoxical embolism of thrombotic material through a patent foramen ovale is a recognized and devastating complication. On the other hand, small PEs are not detectable on echocardiography. The role of echocardiography therefore is not in the definitive exclusion of a (small) PE, but in the assessment of whether a haemodynamically significant embolism has taken place and whether RV compromise warrants thrombolytic therapy.

The echocardiographic differentiation of chronic and acute pulmonary pressure elevation is difficult. RV hypertrophy, with an end-diastolic free wall thickness >5 mm, supports chronic PH but does not exclude an additional acute pressure increase. Several signs that have been described as relatively specific (but not sensitive) for acute PE [17] are:

It should be clear, however, that these signs are far from being ideally predictive for an acute PE. (See also Chapter 66.)

The ascending aorta can be seen over its first few centimetres from the left and right parasternal echocardiographic windows, and the aortic arch is seen from the suprasternal window, which, however, is often obstructed in elderly or emphysematous individuals. A much better evaluation of the thoracic aorta is afforded by TOE where almost the entire course is visible, except for a ‘blind spot’ created by tracheal and left bronchial interposition at the distal ascending aorta and proximal arch. Dilatation and aneurysms, atheromatous disease, plaque-adherent thrombi, aortic dissection or intramural haematoma, and traumatic damage (see section on cardiac trauma) can be diagnosed by TOE. The following are important pathological features of the aorta [18, Table 20.4]:

Dissection and intramural haematoma are life-threatening diseases which require emergency surgery if they affect the ascending aorta [19]. The questions that an echocardiographic examination should quickly and decisively address are summarized in Additional online material. Importantly, non-classical forms of the acute aortic syndrome, such as an intramural haematoma or a penetrating ulcer, are often difficult to detect by echocardiography. CT or nuclear magnetic resonance should be liberally used in any cases of doubt. (See also Chapter 61.)

Echocardiography is the method of choice if a cardiovascular source of embolism is suspected [20]. TOE has a higher yield than TTE in identifying such sources and should be used if results may lead to a change in management. TOE is particularly valuable in assessing LA thrombi, endocarditic vegetations, tumours, and aortic atheromas. The presence of the following potential sources of embolism should be systematically sought:

Thoracic ultrasound (US) is a rapidly evolving method in assessing diseases of the lungs and pleura [1, 2]. It can be promptly applied at the bedside as a part of point of care testing (POCT) by a single clinician and minimal monitoring [2].

It is non-invasive, repeatable, relatively cheap, mobile, utilizes no radiation and has a short examination time that can augment physical examination with accurate and fast answers facilitating decision making in emergency conditions. [2, 3]. We will give an overview of the basic principles, technical aspects of thoracic US, cover clinical applications and conclude to current limitations.

In normal aerated lungs the ultrasound beam finds the lung air and no image is obtained, because US waves cannot be transmitted through air. The only visible structure is the pleura [1–4]. Thus the basic physical principle of lung US is that the less air in the lungs, the easier is the detection of lung abnormalities. When the air content decreases (e.g. pulmonary edema, pulmonary effusions) the acoustic mismatch needed to reflect the ultrasound beam is created, and some images appear. When the air content is further decreased, such as in lung consolidations, the acoustic window on the lung becomes completely open, and the lung may be directly visualized as a solid parenchyma, as the liver [5, 6].

Appropriate probe depends on the location of the pathology and the patients’ BMI [2]. Any modern 2-D black-and-white scanner unit is appropriate having a high frequency (7.5 – 10 MHz) linear transducer for surface structures (e.g. pleura), and a lower frequency (3.5 MHz) convex transducer for the evaluation of deeper lesions. Suitable modes are real-time B-mode to evaluate and scan organs in real-time, providing anatomic and functional information and time motion (M-mode) to image moving structures [1, 2, 3].

The patient is scanned in the supine and sitting position, and if possible in lateral decubitus position [7, 8]. Patients are usually scanned using an intercostal approach from the 2^nd to the 4^th (left) or 5^th (right) intercostal space of the anterior and the lateral chest using parasternal, mid-clavicular, anterior axillary, and mid-axillary lines as anatomical landmarks (Volpicelli’s zones) [9, 10].

The transducer is moved longitudinally and transversely to visualize the lung surface through the intercostal spaces avoiding the acoustic restriction of the ribs. An abdominal window is used with a linear-convex probe for the sonographic imaging of caudal parts of the lungs, passing through the liver and diaphragm on the right and through the spleen and diaphragm on the left. A water-soluble US transmission gel is used to the skin as coupling medium and disinfection measures of the transducer and personnel hands are applied.

Various US lung signs and lines can be recognized related to the normal lung and pleura. see Figure 20.27 ONLINE Localization of the pleura constitutes the basic anatomic landmark for the examination of the lung described as an intense hyper-echoic line that is created by the surface of visceral pleura against that of air-filled lung moving synchronously with respiration [4]. The thoracic wall is recognized by the characteristic posterior shadowing of the ribs. The intercostal muscles extend between the ribs, creating a useful intercostal monographic window. Due to the varying thickness of the subcutaneous tissues, the ribs constitute the most suitable anatomical landmark for recognition of the pleura, which can be found 0.5–1 cm in depth from the hyper echoic surface of the ribs. Lung signs, points, lines and patterns are shown in Table 20.9 (ONLINE) and include ‘Lung sliding’ (see Figure 20.28, Video 1), ‘A’ lines (see Figure 20.29), Seashore sign (see Figure 20.30), ‘B’ lines (see Figure 20.31), Lung point (see Figure 20.32), Lung pulse, Air bronchogram (see Figure 20.33) (all ONLINE) [6, 11–16].

The most informative lung US sign for the cardiologist is the sum of B-lines denoting the extent of extravascular lung water (EVLW) [4]. In each scan, B-lines may range from zero to ten. A total score of severity is calculated ranging from 0 (≤ 5 B-lines, No sign), 1 (6 – 15 B-lines, Mild degree), 2 (16 - 30 B-lines, Moderate degree), 3 (> 30 B-lines, Severe degree) indicating the amount of EVLW [7].

Clinical applications of lung ultrasound in the ICU are shown in Table 20.10 (ONLINE).

In this condition there is an increase in interstitial fluids characterized by the presence of B-lines [3, 4, 6]. B-lines cannot differentiate cardiogenic edema and acute respiratory distress syndrome (ARDS) but several findings are suggestive of ARDS: alterations of the pleura (subpleural consolidations); “spared areas”, defined as areas of normal sonographic lung appearance surrounded by areas of multiple B-lines; and large consolidations of various sizes [17, 18].

B-lines are present in patients with cardiogenic edema, but not in patients with exacerbation of chronic obstructive pulmonary disease (COPD) [19]. They are also reliable in predicting the cardiogenic origin of dyspnea, with accuracy comparable to natriuretic peptides [20]. In acute dyspnea, multiple B-lines associated to subpleural consolidations are highly suggestive of non-cardiogenic pulmonary edema.

B-lines are related to radiographic Kerley B-lines and lung water score on chest X-ray [9], to EVLW accumulation and pulmonary congestion [9, 20], and to the severity of diastolic dysfunction [21]. The number of B-lines increases with worsening New York Heart Association (NYHA) functional class [21] and allow monitoring of pulmonary congestion by observing its clearance [20, 22, 23].

B-line pattern facilitates the differential diagnosis of acute respiratory failure because respiratory, contrary to cardiogenic causes, show a non-interstitial pattern [9, 24–27].

In this condition there is increase in alveolar fluids leading to lung consolidation even with complete air loss. When no aerated lung is interposed between consolidation and the probe, consolidation can be visualized on US as a hypoechoic region or a tissue-like echo pattern, which differs from the surrounding aerated pattern [28, 29].

Analysis of the shape, margin, distribution, vascularization, and some peculiar characteristics such as air and fluid bronchograms often allows for a differential diagnosis between different types of consolidation (i.e., pneumonia, infarctions in pulmonary embolism, contusions, and obstructive and compressive atelectasis) [17]. Ultrasound monitoring of these patients may show reaeration of the consolidated area from alveolar pattern to the interstitial pattern and finally normal aeration [17, 30].

It should be mentioned that both alveolar and interstitial pattern may coexist according to different degrees of the affected lung aeration.

A conventional application of thoracic US is the diagnosis and quantification of pleural fluid see Figure 20.34 ONLINE [31–33] and subcutaneous emphysema see Figure 20.35, Video 2 ONLINE.

Lung US is useful for the diagnosis of pneumothorax which is visible on US. The diagnostic hallmark of pneumothorax is the “lung point” with specificity of 100%, and sensitivity of about 65%. It corresponds to the point where visceral and parietal pleura regain contact with each other. M-mode performed at the lung point, shows a clear change from one pattern (seashore sign) to the other (stratosphere sign) indicating air in the pleural space [14]. (see Figure 20.32)

A simple algorithm by the International recommendations for POC lung US has been proposed for the exclusion of pneumothorax. Pneumothorax is present if “lung point” is present and there is no lung pulse sign [34]. However, absent lung sliding does not always mean pneumothorax. Pneumothorax is excluded if there is lung sliding, lung pulse or even a single B-line with negative predictive value of 100% [11, 35, 36].

US is superior to chest radiograph for the determination of the optimal site for thoracentesis having a success rate of up to 97% [37, 38]. US detect pleural fluid septations with greater sensitivity than CT scanning and also minimize the risk of visceral puncture [38, 39] and pneumothorax following aspirations independently of the size of the effusion [39].

US is ideal and strongly recommended for identifying the optimal site for safe and effective intercostal fluid drainage [39, 40]. This is particularly relevant in patients with loculated parapneumonic effusions, where thickened parietal pleura, adhesions or loculations often complicate insertion [37]. Depending on operator experience, US may also guide further decisions regarding the need for intrapleural fibrinolytics, thoracoscopy or for surgical intervention [41].

Lung US is much easier than echocardiography and minimal teaching and image recognition skill sessions are needed [42]. The learning curve for B-lines evaluation and grading is very short [43]. The addition of lung US to echocardiography provides insights on the eventual pulmonary involvement and requires only a few minutes.

Presence of multiple, diffuse, bilateral B-lines associated to left ventricular systolic and/or diastolic dysfunction or valvular heart disease is highly indicative of cardiogenic pulmonary congestion. Presence of multiple, diffuse, bilateral B-lines, associated to a normal heart, indicates a non-cardiac cause of pulmonary edema, such as ARDS, pneumonias, or pulmonary fibrosis.

It is important to distinguish the multiple, diffuse, bilateral B-lines pattern from focal multiple B-lines that can be present in normal lungs or may be seen around many pathologic conditions, as lobar pneumonia, pulmonary contusion, pulmonary infarction, pleural disease, and neoplasia.

Lung US limitations are essentially patient and operator dependent. Obese patients are frequently difficult to examine because of the thickness of their ribcage and soft tissues. The presence of subcutaneous emphysema or large thoracic dressings is a significant limitation. The main limitation of B-lines is the lack of specificity for cardiogenic pulmonary edema. We should have in mind that all imaging data should be evaluated within the clinical context and integrated with patient’s history, clinical presentation and other laboratory data.

Lung US is a simple, fast, low-cost, reliable and repeatable examination for the evaluation of respiratory status contributing to the bedside diagnosis of lung and pleural disorders. Also, estimates EVLW through B-lines assessment representing a new, helpful tool for the cardiologist, for the management of HF patients. A combination of lung US with echocardiography may help to differentiate the main causes of acute dyspnea and life-threatening conditions in critically ill hypoxic patients.