Consensus Statement | Open | Published:

Expert consensus document

Echocardiography and lung ultrasonography for the assessment and management of acute heart failure

  •  & for the Acute Heart Failure Study Group of the European Society of Cardiology Acute Cardiovascular Care Association

Nature Reviews Cardiology volume 14, pages 427440 (2017) | Download Citation


Echocardiography is increasingly recommended for the diagnosis and assessment of patients with severe cardiac disease, including acute heart failure. Although previously considered to be within the realm of cardiologists, the development of ultrasonography technology has led to the adoption of echocardiography by acute care clinicians across a range of specialties. Data from echocardiography and lung ultrasonography can be used to improve diagnostic accuracy, guide and monitor the response to interventions, and communicate important prognostic information in patients with acute heart failure. However, without the appropriate skills and a good understanding of ultrasonography, its wider application to the most acutely unwell patients can have substantial pitfalls. This Consensus Statement, prepared by the Acute Heart Failure Study Group of the ESC Acute Cardiovascular Care Association, reviews the existing and potential roles of echocardiography and lung ultrasonography in the assessment and management of patients with acute heart failure, highlighting the differences from established practice where relevant.

Key points

  • Over-reliance of traditional clinical findings and symptoms can potentially delay diagnosis of acute heart failure (AHF), prolonging the time to appropriate therapy

  • The use of echocardiography and lung ultrasonography can help to improve diagnostic accuracy and monitor responses to interventions in patients with AHF

  • Lung ultrasonography allows for rapid assessment of numerous conditions, including pulmonary oedema, pleural effusion, and pneumothorax

  • Use of echocardiography has extended beyond the traditional application in stable patients to become widespread in the acute and emergency settings

  • In the setting of AHF, echocardiography can be used to assess pericardial effusion, right ventricular dilatation, left ventricular systolic function, gross valvular abnormality, and potentially the presence of intracardiac masses

  • Echocardiography can also be used to monitor treatment in patients with cardiogenic shock


Heart failure is the primary cause of hospital admission in >1 million patients per year in the USA, with 25% of patients being readmitted within 1 month, and 10–20% mortality at 6 months after discharge1,2. Acute heart failure (AHF) — either a new diagnosis in patients with no history of cardiac disease, or as a result of acute decompensation in patients with known heart failure — is the leading cause of hospital admission in individuals aged >65 years in the UK3. According to data from Europe, approximately 50% of these patients will be readmitted within 12 months, and 30% will be deceased at the 1-year follow-up4. Despite numerous clinical trials to assess optimal treatment and management strategies for patients with AHF, little improvement has been made in AHF outcomes in the past 30 years1,4,5, with management decisions largely based on expert consensus rather than robust evidence. The burden of AHF is therefore substantial, both to individual patients and to society6,7. The successful management of patients with any acute condition involves early diagnosis, the identification of underlying reversible causes, and the implementation of effective therapies in a timely manner, all while avoiding harm; all these factors are associated with better in-hospital and short-term prognosis8. This Consensus Statement, prepared by the Acute Heart Failure Study Group of the ESC Acute Cardiovascular Care Association, reviews the existing and potential roles of echocardiography and lung ultrasonography (LUS) in the assessment and management of patients with AHF.

AHF: a diagnostic and management challenge

AHF is a syndrome rather than a diagnosis per se, caused by a wide array of pathologies that result in a spectrum of disease severity ranging from breathlessness to cardiogenic shock or cardiac arrest. AHF is a highly lethal condition, and studies have shown that minimizing the 'time to appropriate therapy' — the initiation of treatment as soon as possible, including in the prehospital setting — is potentially beneficial in improving outcomes9,10. AHF is variably defined as the rapid onset or acute worsening of symptoms and signs of heart failure that is associated with elevated plasma levels of natriuretic peptides4,11. However, substantial diagnostic uncertainty is inevitable when relying only on traditional clinical findings, and currently a lack of specificity exists in routine investigations for this condition. Indeed, although patients often present with a suggestive history, clinical features (such as shock, and pulmonary or peripheral congestion), and/or symptoms related to the underlying potential cause, these traditional clinical features are frequently absent; over-reliance on these factors might delay diagnosis and implementation of appropriate therapy, or contribute to a missed diagnosis in up to 20% of patients12,13. Furthermore, patients' clinical features might vary according to the site of initial medical contact and the management strategies employed14,15.

The majority of patients with AHF present to emergency departments; however, many patient are also assessed and managed in other acute care settings such as in intensive care and inpatient cardiology units. Patients with AHF usually present with symptoms of congestion and breathlessness rather than cardiac arrest or shock16. Symptoms of breathlessness account for 3–5% of emergency department attendances in Europe and the USA, and the major causes of breathlessness and their prevalence include AHF (50%), pneumonia or bronchitis (20%), exacerbation of chronic obstructive pulmonary disease or asthma (20%), and pulmonary embolism (5–10%)16,17. Current guidelines recommend that clinical examination and investigations should be integrated to form the diagnosis, including the use of electrocardiogram (ECG), chest radiograph, and biomarkers such as natriuretic peptides, troponin, and D-dimer as indicated16,18,19. Unfortunately, these data can be challenging to interpret, in particular in the 10–15% of patients in whom two concomitant diagnoses exist1,4,20. Specifically, although included in the current definition of AHF, levels of natriuretic peptides can be elevated in respiratory disease and other acute conditions such as pulmonary embolism, sepsis, and anaemia21,22,23,24.

Any acute condition can be further complicated by the external factors present in emergency settings, such as high ambient noise and restrictive space, limiting a clinician's ability to position the patient optimally for examination. Furthermore, the frequently atypical features of very severe pathology (in particular valvular disease), and the time pressures imposed by an acutely deteriorating patient can contribute to poor outcomes. These factors are further confounded by the presence of concomitant pathologies in the increasingly ageing patient population25.

Echocardiography and LUS are readily available and widely validated techniques that can be used to reveal anatomical and physiological abnormalities in patients with AHF, which when correctly applied in the acute setting, can improve patient assessment, management, and outcomes (Figs 1,2)26. Unlike other biomarkers used in AHF, echocardiography and LUS can be used to identify not only inadequate cardiac output and/or the presence of congestion, but also the underlying cause, allowing the most appropriate, individualized interventions to be delivered immediately to the patient27. Furthermore, these imaging modalities can be used to monitor the effects of treatment (either beneficial or detrimental), as well as to guide patient disposition and interventions as indicated28. Pocket-sized echocardiography devices are practical for screening, and provide information to clinicians in addition to that gathered from auscultation by a stethoscope alone. When AHF is suspected, an integrative approach is recommended, including determination of cardiopulmonary instability and evaluation of congestion (pulmonary and peripheral) using a combination of techniques4. When image quality is inadequate, either transoesophageal echocardiography or the use of contrast should be considered.

Figure 1: Lung and pleural ultrasonography.
Figure 1

a | Normal lung with pleural line, and ribs (*) with shadowing. b | Pulmonary oedema with multiple vertical B-lines (arrows) arising from the pleural line. c | Diaphragmatic view with spine ending at the level of the diaphragm, with no pleural effusion. d | Pleural effusion seen as anechoic (echo-free) space above the diaphragm with atelectatic lung. Spine can be visualized beyond the diaphragm owing to the effusion.

Figure 2: Echocardiographic methods to estimate left atrial pressure.
Figure 2

The upper panels show the echocardiographic scan of a patient aged 45 years admitted to hospital with dyspnoea owing to severe acute respiratory failure. a | Transthoracic echocardiogram (TTE) of the mitral inflow pattern showing a normal early (E) and late (A) transmitral flow pattern. b | Tissue Doppler imaging (TDI) of the lateral mitral valve annulus from the same patient; S is systolic annular velocity, E′ is early annular diastolic velocity, and A′ is late annular diastolic velocity (related to atrial contraction). c | Pulmonary venous Doppler (transesophageal echocardiography) demonstrating a dominant systolic wave (S) and smaller diastolic wave (D), with a normal deceleration time. The E/A ratio is >1 and the E/E′ is <8 cm/s with a dominant S wave on pulmonary vein, consistent with a normal left atrial pressure. The lower panels show the echocardiographic scan of a female patient aged 59 years admitted with dyspnoea owing to severe left ventricular dysfunction with pulmonary oedema. d | TTE of the mitral inflow pattern showing a dominant E wave with E/A ratio >2. e | TDI of the septal mitral valve annulus with a very low early diastolic velocity (E′), and f | pulmonary venous Doppler (transoesophageal echocardiography) showing a blunted systolic wave (S) and dominant diastolic wave (D). The E/E′ is 16.3 cm/s, and dominant D wave on pulmonary venous Doppler with D deceleration time <150 ms are consistent with an elevated left atrial pressure.

Lung ultrasonography

Based on the interpretation of a number of artefacts, specific ultrasonography appearances, and their distribution (Fig. 1), LUS allows for a rapid point-of-care evaluation of a number of conditions, including pulmonary oedema, lung consolidation, pleural effusion, and pneumothorax29. High intra-rater and inter-rater reproducibility, ease of learning, short exam duration (<5 min), and the noninvasive nature of this technique makes it an advantageous point-of-care tool30,31,32. LUS is increasingly used in the acute care setting, and has improved diagnostic accuracy compared with clinical assessment and chest radiography for the identification of a cardiac aetiology in patients presenting to the emergency department with undifferentiated dyspnoea33.

Interstitial fluid and pulmonary oedema

Quantification of B-lines (vertical artefacts that result from an increase in interstitial density; Fig. 1b) has been shown to be useful for the diagnosis, monitoring, and risk assessment of patients with known or suspected AHF34,35,36. Either curvilinear or phased array transducers can be used, typically at an imaging depth of 18 cm. Although the assessment of eight or more anterior and lateral thoracic zones (four on each hemithorax) has been recommended in a consensus statement29, a subsequent study demonstrated high diagnostic accuracy with examination of only six thoracic regions33. The visualization of three or more B-lines in two or more intercostal spaces bilaterally should be considered diagnostic for pulmonary oedema, with sensitivity of 94% (95% CI 81–98%) and specificity of 92% (95% CI 84–96%)33,37. By contrast, physical examination and chest radiography have a sensitivity of only 62% (95% CI 61–64%) and 57% (95% CI 55–59%), and a specificity of 68% (95% CI 67–69%) and 89% (95% CI 88–90%) for a diagnosis of pulmonary oedema, respectively38. The presence of multiple bilateral B-lines in AHF has been well-correlated with natriuretic peptide levels, and only variably correlated with pulmonary capillary wedge pressure and measures of extravascular lung water30,33,35,39,40,41. Given that studies to assess the incremental diagnostic value of LUS compared with natriuretic peptides for the identification of AHF in patients with dyspnoea reported variable results in different cohorts, this topic warrants further investigation31,33,42. The number of B-lines is thought to decrease with treatment for AHF and, therefore, this technique is potentially useful in the monitoring of pulmonary oedema in response to therapy35,36. For serial assessments, patient positioning (sitting versus supine) should be kept consistent43. Importantly, a higher number of B-lines on LUS at the time of discharge from hospital might help to identify patients with heart failure who have a worse prognosis36.

Pleural effusion

Similarly to B-lines, the presence of pleural effusions can be assessed using curvilinear or phased array transducers in the posterior–axillary line34 (Fig. 1d). Current data regarding the diagnostic utility of pleural effusions identified on ultrasonography in patients with AHF are less robust, but have been reported with sensitivities of 79–84% and specificities of 83–98% in small studies of patients with dyspnoea44,45.


LUS can be used to exclude pneumothorax in the area scanned with higher sensitivity than supine chest radiography by recognizing lung sliding, a slight horizontal movement of the pleural line with respiration; see Supplementary information S1 (video)46. In the setting of a pneumothorax, lung sliding is absent in the affected area of the chest. At the border of a pneumothorax, a transition point between normal lung surface (with lung sliding) and pneumothorax (without lung sliding) can sometimes be identified47. This so-called 'lung point' confirms the diagnosis. Lung sliding might be absent in several other pathological conditions (such as pleural adhesions or selective mainstem intubation) and, therefore, should not be used in isolation to make the diagnosis of pneumothorax, but rather in conjunction with the full range of sonographic features46.

Differential diagnosis and potential pitfalls

The major questions when using LUS for the assessment of patients with possible AHF include whether there is evidence of pulmonary oedema (such as multiple bilateral B-lines), whether there are other findings suggestive of AHF (such as pleural effusion), and finally, whether there are findings of alternate or concurrent conditions (such as pulmonary consolidation or pneumothorax). Despite its apparent simplicity, a number of caveats exist for the use of LUS. First, B-lines can resolve rapidly in response to treatment, and, therefore, LUS data must be interpreted in the context of previous interventions35. Second, B-lines can be seen in a number of pulmonary conditions, including pulmonary fibrosis or interstitial lung disease, acute respiratory distress syndrome, and pneumonitis29. The observation of B-lines together with other LUS abnormalities might indicate that two pathologies coexist, or that the B-lines are an expression of pathology other than AHF (for example, acute respiratory distress syndrome, or pulmonary oedema in patients receiving haemodialysis)48. Third, large pleural effusions might interfere with B-line quantification in the affected thoracic zones and induce lung consolidation (Fig. 1d). Together, these considerations outline why LUS should not be used in isolation, but rather integrated into clinical and laboratory assessment33,49,50.

Echocardiography in AHF

Driven by progressive advances in ultrasonography technology and an expanding evidence base, the use of echocardiography has extended beyond the traditional application in stable patients to become widespread in the acute and emergency settings51,52. Mirroring the concept of critical care, echocardiography is increasingly used as a tool to guide management of the most acutely unwell patients wherever they present along the management pathway. Pocket-sized devices have been recommended in the emergency department, intensive care unit, and coronary units for fast initial qualitative screening of ventricular and valvular function, pericardial and pleural effusion, or extravascular lung water. However, owing to the known limitations of this technique, they are not intended as a substitution for comprehensive echocardiography26,53. Remote expert review of images is now a possibility, and in the future, telemedicine will probably have an important role in guiding the assessment and management of these acutely unwell patients.

Echocardiography is used in AHF to help to confirm diagnosis, delineate potential underlying causes, identify associated pathophysiology, and monitor the response to therapy28,54. Echocardiography can also be used to guide specialist interventions in the catheter laboratory or operating room55,56,57. Furthermore, echocardiography can address several major questions, including whether a patient has a cardiac cause for their symptoms and signs, the severity of the cardiac impairment and its physiological effect, whether there is an underlying reversible cause, what the most appropriate initial treatment is, and how the patient responds to treatment.

Guidelines recommend immediate echocardiographic assessment for patients with suspected AHF with haemodynamic instability1,4; however, interpretation of echocardiographic data in these acutely unwell patients can be extremely complex (Table 1). First, the finding of a structurally or functionally abnormal heart does not necessarily mean the cause of dyspnoea is cardiac-related. Second, patients might be misdiagnosed as having primary respiratory disease, even in the presence of very severe cardiac pathology27,58. Third, substantial cardiac and respiratory disease might coexist, and determining the degree of cardiac contribution is frequently challenging in this setting59. These considerations are further compounded by the relative paucity of high-quality evidence to support the use of echocardiography techniques in the acute arena, as they have been predominantly validated in the outpatient clinic.

Table 1: Challenges in using echocardiography to determine the underlying cause of AHF

Left-sided disease and elevated LAP

Dyspnoea resulting from left-sided cardiac disease is likely to be associated with elevated left atrial pressure (LAP) and pulmonary oedema. Historically, pulmonary capillary wedge pressure has been measured using a pulmonary artery catheter as a substitute for LAP measurement60,61,62. The use of the pulmonary artery catheter has greatly declined over the past decade, owing to a number of studies that showed potential harm or no improved outcomes in the perioperative and critical care settings63. Although absolute pressure values cannot be measured using echocardiography, a drive has occurred to find an echocardiography-derived parameter that can be used to estimate the LAP noninvasively. Indices that have been proposed include interrogation of the transmitral left ventricular (LV) filling pattern (E/A ratio, E wave deceleration time, and the isovolumic relaxation time), pulmonary venous Doppler diastolic deceleration time (Fig. 2), M-mode colour Doppler propagation velocities, the time interval between the onset of early diastolic mitral inflow (E) and annular early diastolic velocity (e′) by tissue Doppler imaging, and the E/e′ ratio64,65,66,67,68,69. None of these measures has been well-validated in the context of emergency medicine70,71; they all present technical challenges that must be carefully considered for accurate interpretation, and provide only estimates of a potential range of corresponding LAP values. Even when used in combination (as proposed in critical care), they can at best only indicate that the LAP is probably very high or normal.

LV ejection fraction has been the main parameter used for the diagnosis, treatment, and stratification of patients with heart failure. However, this parameter has several limitations that are particularly relevant in the acute setting, such as load-dependency and inotropy-dependency72,73. Even in the absence of high-quality 2D images, Doppler abnormalities in transmitral filling might provide an early indicator of important pathology72,74,75,76.

Unlike LUS, echocardiography might be challenging to perform well and interpret accurately, as a number of considerations add to the complexity of its application in the acute setting. First, in all parameters described for LAP estimation, the confounding factors imposed by critical illness (changes in heart rate, cardiac output, LV compliance, and volume and ventilatory status) have not been fully evaluated. Second, not only might patients with a relatively normal LAP have radiographic and sonographic evidence of pulmonary oedema, but conversely, patients with chronically elevated LAP might have no evidence of pulmonary oedema. Similarly to LUS, however, the echocardiographic findings should be integrated with those from clinical examination, laboratory investigations, and lung imaging data (radiographic and/or sonographic), and be assessed within the clinical context. The main value of echocardiography in this setting is to diagnose or exclude an underlying cardiac cause for dyspnoea and guide subsequent interventions.

Right-sided disease: pulmonary embolism

The diagnosis of pulmonary embolism can be challenging, because symptoms and signs are nonspecific. The transthoracic echocardiogram is normal in approximately 50% of unselected patients with acute pulmonary embolism, and has a sensitivity of 50–60% and specificity of 80–90%77. Therefore, other investigations are used to confirm the diagnosis, with echocardiography used as a complementary imaging technique19. The principal indirect echocardiographic findings are nonspecific, and include right heart dilatation, right ventricular (RV) hypokinesis (with or without apical sparing), abnormal septal motion, and inferior vena cava dilatation78 (Fig. 3a). Secondary tricuspid regurgitation might be present, allowing estimation of pulmonary arterial systolic pressure using the simplified Bernoulli equation79 (Fig. 3b). Given that the right ventricle can generate a pulmonary artery systolic pressure of only ≤60 mmHg acutely, a higher pressure suggests a more chronic process (either multiple repeated episodes or chronic pulmonary parenchymal disease, with or without pulmonary embolism)80. Although the peak tricuspid regurgitation gradient is the most commonly used parameter to assess pulmonary artery systolic pressure in clinical practice, difficulties in the detection of good tricuspid regurgitation envelope might occur. Pulsed Doppler recordings of pulmonary valve flow acceleration time, pre-ejection period, and ejection time at the RV outflow tract can also be used to estimate pulmonary artery pressure and resistance81,82.

Figure 3: Echocardiographic features in patients presenting with severe haemodynamic impairment.
Figure 3

a | Transthoracic echocardiography in a patient with acute-on-chronic pulmonary embolism from an apical four-chamber view showing a severely dilated right ventricle (RV), and b | increased pulmonary systolic pressure estimated by applying the simplified Bernoulli equation using the measured tricuspid regurgitation peak velocity (50 mmHg; asterisk). c | Parasternal short axis view showing RV and left ventricle (LV) surrounded by a circumferential pericardial effusion (asterisk) that induced tamponade. d | Transoesophageal echocardiography (transgastric short-axis view) of a patient aged 42 years admitted with cardiogenic shock presenting with ST-segment elevation in the anterolateral electrocardiogram leads. Coronary angiography showed critical three-vessel coronary artery disease. The LV is severely dilated, and there is evidence of previous myocardial infarction, shown by the presence of thinned and akinetic myocardium (dotted red line). LA, left atrium; RA, right atrium.

Pericardial collection and tamponade

Echocardiography is pivotal for recognition of the haemodynamic consequences of a pericardial collection (Fig. 3c), allowing demonstration of features of tamponade including right atrial and/or RV diastolic collapse, in addition to guiding pericardiocentesis83. A number of potential pitfalls exist when interpreting the echocardiographic features of tamponade in the acute setting. These pitfalls include the effects of positive pressure ventilation (reversal of changes in transvalvular flows) and localized collections, in particular after cardiac surgery when substantial haemodynamic compromise might be present, even in the absence of echocardiographic features of tamponade84.

Monitoring of therapy

Echocardiography is not recommended for the monitoring of therapy in patients with AHF in the absence of cardiogenic shock4,9,11, given the complexity of LAP estimation using echocardiography, its lack of association with pulmonary congestion and symptoms, and superiority of natriuretic peptide levels in monitoring response to therapy. An emerging area in which echocardiography might be of use is in risk stratification before discharge from hospital. In patients with AHF with dyspnoea, persistent pulmonary congestion before discharge (demonstrated on LUS) has been shown to be an independent predictor of rehospitalization for AHF at 6 months after discharge36.

Cardiogenic shock

Cardiogenic shock is the most severe manifestation of AHF. Although relatively uncommon, the published prevalence (5% of patients with AHF) varies according to the point of initial contact and management (1–2% of patients with AHF in the prehospital or emergency setting versus 29% in intensive care)4,9,10,16. Precise definitions of cardiogenic shock can vary; however, the syndrome generally results from inadequate cardiac output for peripheral organ requirements85,86. Cardiogenic shock can manifest as hypotension despite adequate filling (with or without vasopressors), altered mentation, cool peripheries, oliguria, hyperlactataemia, metabolic acidaemia, and low mixed venous oxygen saturation86. In addition to standard evaluation of critically ill patients in parallel with resuscitation, echocardiography is mandated immediately in patients with cardiogenic shock, because without identification and treatment of the underlying cause, the outcome is usually fatal9,85 (Fig. 3d). Additional information that should be obtained from echocardiography includes estimation of stroke volume and cardiac output levels, because these data can provide guidance on how to maximize the cardiac output at the lowest filling pressures (see Supplementary information S2 (table)). These measurements should be taken during the echocardiogram, and should be performed repeatedly to monitor the response to therapeutic interventions and minimize potentially injurious treatment. Every study must be interpreted in the context of the level of inotropic and ventilatory support, as well as metabolic and arterial blood gas status, because these variables might have profound effects on echocardiographic findings.

Assessment of volume status. The physiological basis of providing 'optimal' filling in cardiogenic shock is that a critical decrease in intravascular-stressed volume reduces the difference between mean systemic venous and right atrial pressure, thereby limiting stroke volume. Although frequently used, invasive static pressure monitoring is not helpful for determining whether an individual patient is volume-responsive87,88. Static echocardiographic parameters are widely used to predict volume responsiveness in critically ill patients (Fig. 4); however, their use requires that a number of strict criteria (relating to the patient, their underlying pathology, and medical interventions) are met, otherwise the investigation becomes invalid (see Supplementary information S3 (table)). Similarly, although thought to be superior, dynamic echocardiographic parameters to predict volume responsiveness are valid only in fully mechanically ventilated patients in sinus rhythm and without chronic heart disease89. In the presence of cardiac disease (either left-sided and/or right-sided), these measurements can be misleading and should not be used. Conversely, tolerance to volume loading among different patients is variable. The conventional teaching to increase volume in RV failure has not been upheld by findings published in the past 3 years90,91. Physiological models suggest that in some patients, progressive fluid loading leads to a plateauing of cardiac output, with a progressive increase in pulmonary artery occlusion pressure. In addition, higher volume is associated with worse outcome in critically ill patients92,93,94.

Figure 4: Static 2D echocardiography parameters are used to evaluate potential volume responsiveness.
Figure 4

The upper panels show a patient who is severely hypovolaemic, and responded to volume loading with an increase in stroke volume. a | Short-axis view of the left ventricle (LV) is shown, where the left ventricular end-diastolic area (dotted red circle) is small. b | From a subcostal view, an obliterated inferior vena cava (IVC) at end-expiration (<1 cm) can be observed. The lower panels show a patient who, according to static 2D echocardiography parameters, would not be predicted to respond to volume loading by increasing stroke volume. c | Short-axis view of the LV with a normal left ventricular end-diastolic area (dotted red circle). d | Dilated IVC at end-expiration.

Inotropes and vasoactive agents. Although inotropes and vasopressors are commonly used to improve cardiac output and blood pressure in patients with cardiogenic shock, there is currently insufficient evidence to support the use of any particular agent in this context9,95,96. Dobutamine is generally the first-line inotrope of choice in the clinic9,95,96. The detrimental effects of positive inotropic agents have been extensively described in the literature97,98, and their use should, therefore, be restricted to the shortest possible duration and the lowest dose, both individualized to the patient. Although little guidance exists on how inotrope treatment should be individualized, echocardiography might be helpful in certain scenarios.

First, not all patients with cardiac disease respond to escalating doses of dobutamine by increasing their stroke volume; in some patients, dobutamine can result in an increase in the total isovolumic time (tIVT)99. Echocardiographic identification of an abnormally prolonged tIVT with dobutamine use, or an increase in tIVT in response to escalating inotropic support might indicate that inotropes are directly impairing myocardial performance, thereby prompting a reduction in dose or a change in treatment strategy99,100,101 (Fig. 5). Second, the combination of LV end-diastolic pressure (LVEDP) and low aortic root pressure might result in a mismatch of coronary perfusion and myocardial oxygen demand. If untreated, this mismatch can result in type 2 myocardial infarction102 (Fig. 3d). Echocardiographic demonstration of a dominant or isolated A wave on transmitral Doppler in combination with postejection shortening can also be diagnostic (Fig. 6a,b), and indicates that aortic root pressure should be increased and/or LVEDP reduced103,104. Third, physiological studies have demonstrated that the combination of RV ischaemia and increased RV afterload is particularly injurious to RV performance, resulting in a fall in systemic blood pressure and cardiac output levels105. Echocardiography can be used to estimate pulmonary artery systolic pressure and pulmonary vascular resistance, as well as measure RV dimensions and performance106. Echocardiographic identification of high pulmonary vascular resistance with or without pulmonary hypertension in combination with RV dysfunction in cardiogenic shock might necessitate the introduction of a pressor agent plus treatment to reduce RV afterload90,107 (Fig. 6c,d). Finally, in a patient with falling cardiac output levels despite escalating inotropic support, echocardiography can help to diagnose LV outflow tract obstruction (with or without associated mitral regurgitation)27,108. Treatment in this context involves reduction or cessation of positive inotropic agents, in combination with volume and pressor support.

Figure 5: Echocardiography-guided cardiac output optimization using pulsed-wave Doppler imaging.
Figure 5

a,b | Transmitral and transaortic pulsed-wave Doppler imaging at 90 bpm. c,d | Transmitral and transaortic pulsed-wave Doppler imaging at 100 bpm. The filling time (FT) is measured from the start to the end of transmitral filling, and the ejection time (ET) from the start to the end of aortic ejection. The total ejection (t–ET) and filling (t–FT) periods are then derived as the product of the corresponding time interval and heart rate, and expressed in s/min. t–IVT (also in s/min) is calculated as 60–(t–FT + t–ET). A heart rate reduction of 10 bpm resulted in a reduction of t–IVT from 16.8 s/min to 10.0 s/min, and a corresponding increase in cardiac output from 3.6 l/min to 5.6 l/min.

Figure 6: The haemodynamic effects of thrombosis (coronary and pulmonary) as demonstrated by echocardiography.
Figure 6

a | Early features of myocardial ischaemia can be demonstrated by the presence of prolonged long-axis shortening, measured by M-mode echocardiography across the base of the left ventricle (post-ejection shortening; arrow). b | Prolonged left ventricular wall tension suppresses early transmitral filling, resulting in an isolated late-diastolic transmitral A wave. c | Increased right ventricular afterload leads to a reduction in right ventricular systolic function, as demonstrated by tricuspid annular plane systolic excursion on M-mode echocardiography across the tricuspid annulus. d | A substantial increase in pulmonary vascular resistance might be associated with a midsystolic notch (arrows) on pulmonary valve pulsed-wave Doppler ejection wave and a short pulmonary valve acceleration time (78 ms; red lines).

Cardiac arrest. The most extreme presentation of cardiogenic shock is cardiac arrest. International evidence- based guidelines recommend the use of echocardiography to diagnose or exclude some of the causes of arrest109. However, echocardiography should not affect the delivery of high-quality cardiopulmonary resuscitation, and specific training in advanced cardiovascular life support is required, even for experienced practitioners. As images are obtained and recorded only during the pulse/rhythm check, studies performed during cardiac arrest are strictly time-limited, and therefore are dissimilar to comprehensive studies that use only focused 2D imaging aimed at diagnosis or exclusion of potentially reversible causes in a simple, binary manner. The pathology leading to arrest is likely to be extreme (tamponade, massive pulmonary embolism, severe LV and/or RV dysfunction, myocardial infarction/ischaemia, hypovolaemia, or tension pneumothorax) and fairly easy to diagnose without more sophisticated echocardiographic techniques. Whether the use of echocardiography in cardiac arrest (and as part of care after resuscitation) can improve outcomes is unknown, but its application in the prehospital setting has been found to change management strategies in up to 60% of patients110,111.

Acute mechanical circulatory support. The indications for mechanical circulatory support (MCS) in the acute setting are constantly changing112,113. Intra-aortic balloon pumps are no longer routinely recommended for cardiogenic shock114. A range of new percutaneous ventricular assist devices are available, in addition to extracorporeal membrane oxygenation (ECMO). These techniques can be used as a bridge to recovery or for longer-term support, and differ not only in terms of their technical aspects, but the degree and type of support provided (LV and/or RV support, with or without the addition of respiratory support)115,116,117,118,119,120. Echocardiography is critical for successful implementation of acute MCS121,122 (Table 2). MCS is not a treatment per se, but instead a supportive therapy for patients awaiting treatment or resolution of the underlying pathological process. As in all cases of AHF, the most important role of echocardiography is to diagnose the underlying cardiac cause. When the decision to institute MCS is made, echocardiography is then used to corroborate the decision regarding the type and level of support required. Although clear echocardiography parameters have been used to guide longer-term MCS for both the left and right heart123,124, these parameters are not yet available for devices designed for short-term use. Furthermore, clear contraindications to MCS exist that can be diagnosed only using echocardiography. Echocardiography is used in the initiation of MCS, including the use of vascular ultrasonography to guide safe vessel cannulation and steer device or cannula placement. Echocardiography is subsequently used to monitor MCS by ensuring the goals of support are met, and for detecting complications and assessing tolerance to assistance121. Unfortunately, peripheral ECMO can paradoxically worsen cardiac function by increasing LV afterload. Although a number of echocardiographic parameters exist that might indicate this complication (including lack of aortic valve opening, biphasic retrograde flow across the mitral valve in diastole, and retrograde systolic pulmonary venous flow; Fig. 7), the inherent limitations of echocardiography in estimating LAP and LVEDP, especially when the heart is partially bypassed, makes this strategy particularly challenging122. Echocardiography can be used, however, to guide interventions to ensure that the heart is adequately offloaded. Finally, a number of echocardiographic parameters are used in conjunction with clinical and haemodynamic assessment to predict which patients might be successfully weaned off MCS125,126.

Table 2: Echocardiography for acute mechanical circulatory support
Figure 7: Echocardiographic features in patients receiving extracorporeal support.
Figure 7

Transthoracic echocardiography in a patient with severe respiratory failure receiving venovenous extracorporeal membrane oxygenation (ECMO). a | Parasternal long axis M-mode echocardiography across the mitral valve showing systolic anterior motion of the mitral valve leaflets (arrow). b | This motion was associated with substantial left ventricular intracavity gradient of 125 mmHg (asterisk). c | A complication of ST-segment elevation myocardial infarction requiring peripheral ECMO is revealed on M-mode echocardiography; papillary muscle rupture had resulted in a flail anterior mitral valve leaflet (white arrow) with associated torrential mitral regurgitation. The increase in left ventricular afterload from ECMO has resulted in failure of the left ventricle (LV) to eject, with a persistently closed aortic valve (AV; red arrow) and stasis of blood in the aortic root. d | Reversal of systolic pulmonary venous flow (arrows) in a patient receiving peripheral venovenous ECMO, suggesting inadequate offloading of the LV.

Other indications

Transoesophageal echocardiograpy can also be used in the acute setting in patients with dynamic mitral regurgitation (see Supplementary information S4 (figure)). Furthermore, features of infective endocarditis caused by aortic prostheses or a device can be demonstrated using transoesophageal echocardiography (see Supplementary information S5 (figure)).

Quality assurance

A detailed overview of the necessary organizational structure and processes for use of ultrasonography and echocardiography in the acute setting is beyond the scope of this Review, and has been published previously26,127,128,129,130. However, when used in routine clinical care, training, education, protocols, and ongoing certification of practitioners are required, which should all be performed within existing governance structures.


Echocardiography and LUS can assist in the rapid assessment of patients with acute dyspnoea and hypotension, and have the potential to transform the way in which clinicians assess and manage critically ill patients with AHF and cardiogenic shock (Table 3). The current AHF guidelines are cautious in recommendations for the widespread use of advanced echocardiography techniques in the acute care setting because robust applicability data are lacking, interpretation of findings requires highly specialized, in-depth knowledge of cardiac pathophysiology, and there is potential for harm by injudicious application in this patient population. The opportunities to improve diagnostic accuracy, reduce delays in treatment, and improve outcomes through the use of advanced echocardiography need to be further explored.

Table 3: Proposed initial focused cardiac and lung ultrasonography assessment for patients with suspected AHF in acute care setting

Publisher's note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.


  1. 1.

    et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. J. Am. Coll. Cardiol. 62, e147–e239 (2013).

  2. 2.

    Epidemiology of heart failure. Circ. Res. 113, 646–659 (2013).

  3. 3.

    , , , & Guideline Development Group of the National Institute for Health and Care Excellence. Diagnosing and managing acute heart failure in adults: summary of NICE guidance. BMJ 349, g5695 (2014).

  4. 4.

    et al. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur. Heart J. 37, 2129–2200 (2016).

  5. 5.

    Heart failure. JACC Heart Fail. 1, 1–20 (2013).

  6. 6.

    et al. The global health and economic burden of hospitalizations for heart failure: lessons learned from hospitalized heart failure registries. J. Am. Coll. Cardiol. 63, 1123–1133 (2014).

  7. 7.

    , , , & The annual global economic burden of heart failure. Int. J. Cardiol. 171, 368–376 (2014).

  8. 8.

    et al. Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis. Crit. Care 10, R82 (2006).

  9. 9.

    et al. Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. Intensive Care Med. 42, 147–163 (2016).

  10. 10.

    et al. Recommendations on pre-hospital and early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. Eur. J. Heart Fail. 17, 544–558 (2015).

  11. 11.

    et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Circulation 128, e240–e327 (2013).

  12. 12.

    et al. Timing of immunoreactive B-type natriuretic peptide levels and treatment delay in acute decompensated heart failure: an ADHERE (Acute Decompensated Heart Failure National Registry) analysis. J. Am. Coll. Cardiol. 52, 534–540 (2008).

  13. 13.

    et al. NT-proBNP testing for diagnosis and short-term prognosis in acute destabilized heart failure: an international pooled analysis of 1256 patients: the International Collaborative of NT-proBNP Study. Eur. Heart J. 27, 330–337 (2006).

  14. 14.

    et al. European Society of Cardiology — Acute Cardiovascular Care Association position paper on safe discharge of acute heart failure patients from the emergency department. Eur. Heart J. Acute Cardiovasc. Care (2016).

  15. 15.

    et al. European Society of Cardiology — Acute Cardiovascular Care Association position paper on acute heart failure: a call for interdisciplinary care. Eur. Heart J. Acute Cardiovasc. Care 6, 81–86 (2017).

  16. 16.

    et al. Recommendations on pre-hospital and early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine — short version. Eur. Heart J. 36, 1958–1966 (2015).

  17. 17.

    et al. Acute heart failure syndromes: emergency department presentation, treatment, and disposition: current approaches and future aims: a scientific statement from the American Heart Association. Circulation 122, 1975–1996 (2010).

  18. 18.

    , , , & Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 294, 1944–1956 (2005).

  19. 19.

    et al. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur. Heart J. 35, 3033–3069 (2014).

  20. 20.

    et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N. Engl. J. Med. 350, 647–654 (2004).

  21. 21.

    et al. NT-proBNP in chronic hypercapnic respiratory failure: a marker of disease severity, treatment effect and prognosis. Respir. Med. 101, 2003–2010 (2007).

  22. 22.

    et al. Prognostic utility of NT-proBNP in acute exacerbations of chronic pulmonary diseases. Eur. J. Intern. Med. 22, 167–171 (2011).

  23. 23.

    et al. Cardiovascular history and adverse events in patients with acute exacerbation of COPD. COPD 12, 560–567 (2015).

  24. 24.

    & Biomarkers and diagnostics in heart failure. Biochim. Biophys. Acta 1832, 2442–2450 (2013).

  25. 25.

    , , & Considerations for initial therapy in the treatment of acute heart failure. Crit. Care 19, 399 (2015).

  26. 26.

    et al. The use of echocardiography in acute cardiovascular care: recommendations of the European Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association. Eur. Heart J. Acute Cardiovasc. Care 4, 3–5 (2015).

  27. 27.

    , , & Echocardiography in the critically ill: current and potential roles. Intensive Care Med. 32, 48–59 (2006).

  28. 28.

    et al. Guidelines for the use of echocardiography as a monitor for therapeutic intervention in adults: a report from the American Society of Echocardiography. J. Am. Soc. Echocardiogr. 28, 40–56 (2015).

  29. 29.

    et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 38, 577–591 (2012).

  30. 30.

    et al. Utility of lung ultrasound in predicting pulmonary and cardiac pressures. Eur. J. Heart Fail. 14, 1276–1284 (2012).

  31. 31.

    et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad. Emerg. Med. 16, 201–210 (2009).

  32. 32.

    et al. Inter-rater reliability of quantifying pleural B-lines using multiple counting methods. J. Ultrasound Med. 32, 115–120 (2013).

  33. 33.

    et al. Lung ultrasound-implemented diagnosis of acute decompensated heart failure in the ED: a SIMEU multicenter study. Chest 148, 202–210 (2015).

  34. 34.

    , , & Assessment and prevalence of pulmonary oedema in contemporary acute heart failure trials: a systematic review. Eur. J. Heart Fail. 17, 906–916 (2015).

  35. 35.

    et al. Bedside ultrasound of the lung for the monitoring of acute decompensated heart failure. Am. J. Emerg. Med. 26, 585–591 (2008).

  36. 36.

    et al. Persistent pulmonary congestion before discharge predicts rehospitalization in heart failure: a lung ultrasound study. Cardiovasc. Ultrasound 13, 40 (2015).

  37. 37.

    , , , & Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Acad. Emerg. Med. 21, 843–852 (2014).

  38. 38.

    et al. Diagnosing acute heart failure in the emergency department: a systematic review and meta-analysis. Acad. Emerg. Med. 23, 223–242 (2016).

  39. 39.

    et al. “Ultrasound comet-tail images”: a marker of pulmonary edema: a comparative study with wedge pressure and extravascular lung water. Chest 127, 1690–1695 (2005).

  40. 40.

    et al. Lung ultrasound for the evaluation of pulmonary congestion in outpatients: a comparison with clinical assessment, natriuretic peptides, and echocardiography. JACC Cardiovasc. Imaging 6, 1141–1151 (2013).

  41. 41.

    et al. Lung ultrasound predicts well extravascular lung water but is of limited usefulness in the prediction of wedge pressure. Anesthesiology 121, 320–327 (2014).

  42. 42.

    et al. Ultrasound lung comets for the differential diagnosis of acute cardiogenic dyspnoea: a comparison with natriuretic peptides. Eur. J. Heart Fail. 10, 70–77 (2008).

  43. 43.

    et al. Impact of patient positioning on lung ultrasound findings in acute heart failure. Eur. Heart J. Acute Cardiovasc. Care 4, 326–332 (2014).

  44. 44.

    et al. Diagnostic accuracy and reproducibility of pleural and lung ultrasound in discriminating cardiogenic causes of acute dyspnea in the emergency department. Intern. Emerg. Med. 7, 65–70 (2011).

  45. 45.

    et al. Diagnosing acute heart failure in patients with undifferentiated dyspnea: a lung and cardiac ultrasound (LuCUS) protocol. Acad. Emerg. Med. 22, 182–191 (2015).

  46. 46.

    Sonographic diagnosis of pneumothorax. Intensive Care Med. 37, 224–232 (2011).

  47. 47.

    , , & The “lung point”: an ultrasound sign specific to pneumothorax. Intensive Care Med. 26, 1434–1440 (2000).

  48. 48.

    et al. Pulmonary congestion predicts cardiac events and mortality in ESRD. J. Am. Soc. Nephrol. 24, 639–646 (2013).

  49. 49.

    Lung ultrasound: a new tool for the cardiologist. Cardiovasc. Ultrasound 9, 6 (2011).

  50. 50.

    et al. Integrated use of bedside lung ultrasound and echocardiography in acute respiratory failure: a prospective observational study in ICU. Chest 146, 1586–1593 (2014).

  51. 51.

    et al. Emergency echocardiography: the European Association of Cardiovascular Imaging recommendations. Eur. Heart J. Cardiovasc. Imaging 14, 1–11 (2013).

  52. 52.

    , & Echocardiography in the ICU: time for widespread use! Intensive Care Med. 32, 9–10 (2006).

  53. 53.

    et al. The use of pocket-size imaging devices: a position statement of the European Association of Echocardiography. Eur. J. Echocardiogr. 12, 85–87 (2011).

  54. 54.

    et al. Recommendations for transoesophageal echocardiography: EACVI update 2014. Eur. Heart J. Cardiovasc. Imaging 15, 353–365 (2014).

  55. 55.

    et al. Echocardiography-guided interventions. J. Am. Soc. Echocardiogr. 22, 213–231 (2009).

  56. 56.

    et al. EAE/ASE recommendations for the use of echocardiography in new transcatheter interventions for valvular heart disease. Eur. Heart J. 32, 2189–2214 (2011).

  57. 57.

    et al. Basic perioperative transesophageal echocardiography examination: a consensus statement of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J. Am. Soc. Echocardiogr. 26, 443–456 (2013).

  58. 58.

    et al. Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology. Eur. J. Heart Fail. 11, 130–139 (2009).

  59. 59.

    et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 38, 1573–1582 (2012).

  60. 60.

    Clinical significance of pulmonary artery occlusion pressure. Intensive Care Med. 29, 175–178 (2003).

  61. 61.

    , & Relationship of pulmonary artery-wedge pressure to left atrial pressure in man. Circ. Res. 11, 315–318 (1962).

  62. 62.

    et al. The pulmonary capillary wedge pressure accurately reflects both normal and elevated left atrial pressure. Am. Heart J. 167, 876–883 (2014).

  63. 63.

    The Swan–Ganz catheters: past, present, and future. A viewpoint. Circulation 119, 147–152 (2009).

  64. 64.

    , & Established and novel clinical applications of diastolic function assessment by echocardiography. Circ. Cardiovasc. Imaging 4, 444–455 (2011).

  65. 65.

    , , , & Doppler estimation of left ventricular filling pressures in patients with mitral valve disease. Circulation 111, 3281–3289 (2005).

  66. 66.

    Echocardiography as a noninvasive Swan–Ganz catheter. Circulation 111, 3192–3194 (2005).

  67. 67.

    , , , & Doppler echocardiography in advanced systolic heart failure: a noninvasive alternative to Swan–Ganz catheter. Circ. Heart Fail. 3, 387–394 (2010).

  68. 68.

    et al. Serial Doppler echocardiography and tissue Doppler imaging in the detection of elevated directly measured left atrial pressure in ambulant subjects with chronic heart failure. JACC Cardiovasc. Imaging 4, 927–934 (2011).

  69. 69.

    et al. Unlocking the mysteries of diastolic function: deciphering the Rosetta Stone 10 years later. J. Am. Coll. Cardiol. 51, 679–689 (2008).

  70. 70.

    et al. Echocardiographic assessment of pulmonary artery occlusion pressure in ventilated patients: a transoesophageal study. Crit. Care 12, R18 (2008).

  71. 71.

    Hemodynamic assessment of critically ill patients using echocardiography Doppler. Curr. Opin. Crit. Care 11, 227–234 (2005).

  72. 72.

    & Beyond ejection fraction: an integrative approach for assessment of cardiac structure and function in heart failure. Eur. Heart J. 37, 1642–1650 (2016).

  73. 73.

    et al. Validity of ejection fraction as a measure of myocardial functional state: impact of asynchrony. Eur. J. Echocardiogr. 10, 613–618 (2009).

  74. 74.

    , & Functional importance of the long axis dynamics of the human left ventricle. Br. Heart J. 63, 215–220 (1990).

  75. 75.

    & Long axis function in disease. Heart 81, 229–231 (1999).

  76. 76.

    , , & An 82-year-old woman with ongoing dyspnea. Chest 150, e9–e11 (2016).

  77. 77.

    , , , & Diagnostic accuracy of Doppler-echocardiography in unselected patients with suspected pulmonary embolism. Int. J. Cardiol. 65, 101–109 (1998).

  78. 78.

    , , & Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur. J. Echocardiogr. 6, 11–14 (2005).

  79. 79.

    et al. Addressing the controversy of estimating pulmonary arterial pressure by echocardiography. J. Am. Soc. Echocardiogr. 29, 93–102 (2016).

  80. 80.

    , & Comprehensive invasive and noninvasive approach to the right ventricle-pulmonary circulation unit: state of the art and clinical and research implications. Circulation 120, 992–1007 (2009).

  81. 81.

    , & Echocardiography in the assessment of right heart function. Eur. J. Echocardiogr. 9, 225–234 (2008).

  82. 82.

    et al. Echocardiography in pulmonary arterial hypertension: from diagnosis to prognosis. J. Am. Soc. Echocardiogr. 26, 1–14 (2013).

  83. 83.

    & Management of pericardial effusion. Eur. Heart J. 34, 1186–1197 (2013).

  84. 84.

    et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases: the task force for the diagnosis and management of pericardial diseases of the European Society of Cardiology (ESC). Endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS). Eur. Heart J. 36, 2921–2964 (2015).

  85. 85.

    , , , & Management of cardiogenic shock. Eur. Heart J. 36, 1223–1230 (2015).

  86. 86.

    & Cardiogenic shock: current concepts and improving outcomes. Circulation 117, 686–697 (2008).

  87. 87.

    & Assessment of volume responsiveness during mechanical ventilation: recent advances. Crit. Care 17, 217 (2013).

  88. 88.

    et al. The emerging role of biomarkers and bio-impedance in evaluating hydration status in patients with acute heart failure. Clin. Chem. Lab. Med. 50, 2093–2105 (2012).

  89. 89.

    , , & Echocardiographic measurement of fluid responsiveness. Curr. Opin. Crit. Care 12, 249–254 (2006).

  90. 90.

    , , & Acute right ventricular failure — from pathophysiology to new treatments. Intensive Care Med. 30, 185–196 (2004).

  91. 91.

    , , & The challenges in the management of right ventricular infarction. Eur. Heart J. Acute Cardiovasc. Care 2, 226–234 (2013).

  92. 92.

    & Fluid responsiveness in mechanically ventilated patients: a review of indices used in intensive care. Intensive Care Med. 29, 352–360 (2003).

  93. 93.

    My paper 20 years later: effect of positive end-expiratory pressure on right ventricular function in humans. Intensive Care Med. 40, 935–941 (2014).

  94. 94.

    , & Measurements of right ventricular volumes during fluid challenge. Chest 98, 1450–1454 (1990).

  95. 95.

    , & Inotropes. J. Am. Coll. Cardiol. 63, 2069–2078 (2014).

  96. 96.

    et al. Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome. Cochrane Database Syst. Rev. 1, CD009669 (2014).

  97. 97.

    , & Use of inotropes and vasopressor agents in critically ill patients. Br. J. Pharmacol. 165, 2015–2033 (2012).

  98. 98.

    Catecholamine treatment for shock — equally good or bad? Lancet 370, 636–637 (2007).

  99. 99.

    , , & Limitation of exercise tolerance in chronic heart failure: distinct effects of left bundle-branch block and coronary artery disease. J. Am. Coll. Cardiol. 43, 1524–1531 (2004).

  100. 100.

    , , & Electromechanical interrelations during dobutamine stress in normal subjects and patients with coronary artery disease: comparison of changes in activation and inotropic state. Heart 85, 411–416 (2001).

  101. 101.

    , , & Limitation of cardiac output by total isovolumic time during pharmacologic stress in patients with dilated cardiomyopathy: activation-mediated effects of left bundle branch block and coronary artery disease. J. Am. Coll. Cardiol. 41, 121–128 (2003).

  102. 102.

    et al. Third universal definition of myocardial infarction. Eur. Heart J. 33, 2551–2567 (2012).

  103. 103.

    & Clinical assessment of left ventricular diastolic function. Heart 89, 231–238 (2003).

  104. 104.

    & Suppression of left ventricular early diastolic filling by long axis asynchrony. Br. Heart J. 73, 151–157 (1995).

  105. 105.

    , , , & Performance of the right ventricle under stress: relation to right coronary flow. J. Clin. Invest. 50, 2176–2183 (1971).

  106. 106.

    et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J. Am. Soc. Echocardiogr. 23, 685–713 (2010).

  107. 107.

    & Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am. J. Respir. Crit. Care Med. 184, 1114–1124 (2011).

  108. 108.

    , , & Dynamic left ventricular outflow tract obstruction in acute myocardial infarction with shock: cause, effect, and coincidence. Circulation 116, e110–e113 (2007).

  109. 109.

    et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation 95, 100–147 (2015).

  110. 110.

    et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 1. Executive summary. Resuscitation 95, 1–80 (2015).

  111. 111.

    Bedside echocardiography in the assessment of the critically ill. Crit. Care Med. 35, S235–S249 (2007).

  112. 112.

    et al. Mechanical circulatory support devices in the ICU. Chest 146, 848–857 (2014).

  113. 113.

    & Mechanical circulatory support for advanced heart failure: patients and technology in evolution. Circulation 125, 1304–1315 (2012).

  114. 114.

    et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet 382, 1638–1645 (2013).

  115. 115.

    , , & Mechanical circulatory support in cardiogenic shock. Eur. Heart J. 35, 156–167 (2014).

  116. 116.

    & Spotlight on cardiogenic shock therapies in the era of mechanical circulatory support. Curr. Opin. Cardiol. 29, 241–243 (2014).

  117. 117.

    et al. Recommendations for the use of mechanical circulatory support: device strategies and patient selection: a scientific statement from the American Heart Association. Circulation 126, 2648–2667 (2012).

  118. 118.

    et al. Mechanical circulatory support for right ventricular failure. JACC Heart Fail. 1, 127–134 (2013).

  119. 119.

    , , & Short-term mechanical circulatory support for recovery from acute right ventricular failure: clinical outcomes. J. Heart Lung Transplant. 33, 794–799 (2014).

  120. 120.

    et al. Seventh INTERMACS annual report: 15,000 patients and counting. J. Heart Lung Transplant. 34, 1495–1504 (2015).

  121. 121.

    , , , & The role of echocardiography in the management of patients supported by extracorporeal membrane oxygenation. J. Am. Soc. Echocardiogr. 25, 131–141 (2012).

  122. 122.

    , , & Echocardiography for adult patients supported with extracorporeal membrane oxygenation. Crit. Care 19, 326 (2015).

  123. 123.

    et al. The ABCs of left ventricular assist device echocardiography: a systematic approach. Eur. Heart J. Cardiovasc. Imaging 13, 885–899 (2012).

  124. 124.

    et al. Echocardiography in the management of patients with left ventricular assist devices: recommendations from the American Society of Echocardiography. J. Am. Soc. Echocardiogr. 28, 853–909 (2015).

  125. 125.

    et al. Predictors of successful extracorporeal membrane oxygenation (ECMO) weaning after assistance for refractory cardiogenic shock. Intensive Care Med. 37, 1738–1745 (2011).

  126. 126.

    et al. Two-dimensional strain rate and Doppler tissue myocardial velocities: analysis by echocardiography of hemodynamic and functional changes of the failed left ventricle during different degrees of extracorporeal life support. J. Am. Soc. Echocardiogr. 25, 632–640 (2012).

  127. 127.

    et al. European Association of Echocardiography recommendations for standardization of performance, digital storage and reporting of echocardiographic studies. Eur. J. Echocardiogr. 9, 438–448 (2008).

  128. 128.

    et al. Echocardiography practice, training and accreditation in the intensive care: document for the World Interactive Network Focused on Critical Ultrasound (WINFOCUS). Cardiovasc. Ultrasound 6, 49 (2008).

  129. 129.

    et al. Focused cardiac ultrasound: recommendations from the American Society of Echocardiography. J. Am. Soc. Echocardiogr. 26, 567–581 (2013).

  130. 130.

    et al. Guidelines for the appropriate use of bedside general and cardiac ultrasonography in the evaluation of critically ill patients — part II: cardiac ultrasonography. Crit. Care Med. 44, 1206–1227 (2016).

  131. 131.

    et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J. Am. Soc. Echocardiogr. 23, 1225–1230 (2010).

  132. 132.

    et al. International evidence-based recommendations for focused cardiac ultrasound. J. Am. Soc. Echocardiogr. 27, e1–e33 (2014).

  133. 133.

    , & Focused training of emergency medicine residents in goal-directed echocardiography: a prospective study. Acad. Emerg. Med. 10, 1054–1058 (2003).

  134. 134.

    et al. Diagnostic accuracy of hospitalist-performed hand-carried ultrasound echocardiography after a brief training program. J. Hosp. Med. 6, 340–349 (2009).

  135. 135.

    et al. Rapid evaluation by lung-cardiac-inferior vena cava (LCI) integrated ultrasound for differentiating heart failure from pulmonary disease as the cause of acute dyspnea in the emergency setting. Cardiovasc. Ultrasound 10, 49 (2012).

  136. 136.

    , & Test characteristics of ultrasonography for the detection of pneumothorax: a systematic review and meta-analysis. Chest 141, 703–708 (2012).

Download references

Author information

Author notes

    • Susanna Price
    • , Elke Platz
    •  & Louise Cullen

    These authors contributed equally to this work.


  1. Royal Brompton & Harefield NHS Foundation Trust, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.

    • Susanna Price
  2. Department of Emergency Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA.

    • Elke Platz
  3. Department of Emergency Medicine, Royal Brisbane and Women's Hospital, Butterfield St & Bowen Bridge Road, Herston, Queensland 4029, Australia.

    • Louise Cullen
  4. University of Pavia Intensive Care Unit 1st Department, Fondazione Policlinico IRCCS San Matteo, Viale Camillo Golgi 19, 27100 Pavia, Italy.

    • Guido Tavazzi
  5. Department of Emergency and Critical Care Medicine, Klinikum Nürnberg, Prof.-Ernst-Nathan-Straße 1, 90419 Nürnberg, Germany.

    • Michael Christ
  6. Department of Cardiology, Imperial College London, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.

    • Martin R. Cowie
  7. Coronary Care Unit and Heart Failure Program, Veterans Affairs San Diego Healthcare System, 3350 La Jolla Village Drive, San Diego, California 92161, USA.

    • Alan S. Maisel
  8. Critical Care Department, Consorci Sanitari Integral, Hospital Sant Joan Despí Moisès Broggi and Hospital General de l'Hospitalet, University of Barcelona, Grand Via de las Corts Catalanes 585, 08007 Barcelona, Spain.

    • Josep Masip
  9. Emergency Department, Hospital Clínic de Barcelona, Carrer de Villarroel 170, 08036 Barcelona, Spain.

    • Oscar Miro
  10. BHF Cardiovascular Research Centre, University of Glasgow, 126 University Place, Glasgow G12 8TA, UK.

    • John J. McMurray
  11. Emergency Medicine, Baylor College of Medicine, Scurlock Tower, 1 Baylor Plaza, Houston, Texas 77030, USA.

    • W. Frank Peacock
  12. Emergency Department, Hospital Clinico San Carlos, Instituto de Investigacion Sanitaria del Hospital Clinico San Carlos, Calle del Prof Martín Lagos, 28040 Madrid, Spain.

    • F. Javier Martin-Sanchez
  13. Emergency Department, Sant'Andrea Hospital, Faculty of Medicine and Psychology, LaSapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy.

    • Salvatore Di Somma
  14. Centro Nacional de Investigaciones Cardiovasculares and Department of Cardiology, Hospital 12 de Octubre, Avenida de Córdoba, 28041 Madrid, Spain.

    • Hector Bueno
  15. Klinikum Ludwigshafen, Institut für Herzinfarktforschung Ludwigshafen, Bremserstraße 79, 67063 Ludwigshafen am Rhein, Germany.

    • Uwe Zeymer
  16. Department of Cardiology and Cardiovascular Research Institute Basel, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland.

    • Christian Mueller


  1. for the Acute Heart Failure Study Group of the European Society of Cardiology Acute Cardiovascular Care Association


  1. Search for Susanna Price in:

  2. Search for Elke Platz in:

  3. Search for Louise Cullen in:

  4. Search for Guido Tavazzi in:

  5. Search for Michael Christ in:

  6. Search for Martin R. Cowie in:

  7. Search for Alan S. Maisel in:

  8. Search for Josep Masip in:

  9. Search for Oscar Miro in:

  10. Search for John J. McMurray in:

  11. Search for W. Frank Peacock in:

  12. Search for F. Javier Martin-Sanchez in:

  13. Search for Salvatore Di Somma in:

  14. Search for Hector Bueno in:

  15. Search for Uwe Zeymer in:

  16. Search for Christian Mueller in:


S.P., L.C., and G.T. researched data for the article. S.P., E.P., and G.T. wrote the manuscript. S.P., L.C., E.P., J.M., and W.F.P. substantially contributed to the discussion of content. All the authors reviewed and edited the manuscript before submission.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Susanna Price.

Supplementary information


  1. 1.

    Normal lung sliding

    Normal lung sliding (back and forth movement with respiration along the pleural line) rules out a pneumothorax in the scanned area of the chest.

PDF files

  1. 1.

    Supplementary table 1

    Common challenges in filling pressure assessment in the acute setting

  2. 2.

    Supplementary table 2

    Common challenges in volume status assessment in the acute setting

  3. 3.

    Supplementary figure 1

    Transoesophageal echocardiography in a patient with dynamic mitral regurgitation.

  4. 4.

    Supplementary figure 2

    Echocardiographic features of infective endocarditis demonstrated using transoesophageal echocardiography.

About this article

Publication history



Further reading