Journal of Acute Care
Volume 2 | Issue 3 | Year 2023

Echocardiography in the Assessment of Shock

Shayan Arshed1, Pradeep R Madhivathanan2, Ashraf Roshdy3

1,2Department of Anaesthesia and Critical Care, Royal Papworth Hospital NHS Foundation Trust, Cambridge, Cambridgeshire, United Kingdom

3Department of Critical Care, North Middlesex University Hospital NHS Trust, London, United Kingdom; Department of Critical Care Medicine, Alexandria University, 21131, Alexandria, Egypt

Corresponding Author: Ashraf Roshdy, Department of Critical Care, North Middlesex University Hospital NHS Trust, London, United Kingdom; Department of Critical Care Medicine, Alexandria University, 21131, Alexandria, Egypt, Phone: +44 20 8887 2000, e-mail:

Received: 30 January 2023; Accepted: 27 February 2023; Published on: 19 February 2024


The use of point-of-care ultrasound (POCUS), including echocardiography in acute settings, has markedly expanded in recent years. Hemodynamic assessment using echocardiography in a Shock state is the most known one. It is gradually becoming unreplaceable due to its benefits, low costs, and negligible adverse effects. Serial exams following a structured approach are advisable. It provides insight into the cause and type of shock as well as the underlying hemodynamic derangement. Recent innovations mean echocardiography is easier to conduct and provides more informative data. Skilled acute physicians are better placed for such individualized management. In this review, we summarize the current application of echocardiography in shock and revisit some promising future modalities.

How to cite this article: Arshed S, Madhivathanan PR, Roshdy A. Echocardiography in the Assessment of Shock. J Acute Care 2023;2(3):136–143.

Source of support: Nil

Conflict of interest: None

Keywords: Critical Care, Echocardiography, Hemodynamic, Shock.


The evolution of echocardiography in acute settings was widely driven by the need for a rapid informative hemodynamic assessment.1 The objective evolved from searching for a culprit cardiac pathology to a holistic but focused assessment of the entire circulatory system.2 It differs from conventional exams by its urgency and the need for serial studies, so more conveniently provided by the primary clinician. The target is to secure organ perfusion rather than just assess the cardiac structure and function. Exams are questions focused, and the data are immediately interpreted and implemented representing an example of individualized care. As machines are becoming smaller, smarter, and increasingly available, POCUS has increasingly been recognized as a fundamental skill for most acute physicians.

In this review, we aim to summarize how the point of care echocardiography can serve shock management and then explore some recent advances and future trends.


It is good practice to start by recording patient details and saving clips, preferably on a central server. Documentation should include any intervention which can affect heart dynamics (e.g., vasoactive medications, mechanical ventilation, and sedation). This helps serial studies to be compared and tracked over time, especially in the case of different operators or machines. Phased array transducers with frequencies typically between 1.5 and 7.5 MHz are used for transthoracic cardiac ultrasound imaging.

Positioning can be a major challenge in acute settings (e.g., proning).3 The patient is best positioned in the left lateral decubitus position except for the subcostal view; he is kept in a supine position. When patients are sedated, turning them in during the study can be difficult and time-consuming.

The same windows as in conventional studies are used (supplementary videos 1-6); however, some may prove more useful (e.g., subcostal), some seldom used (e.g., suprasternal), while it can be very helpful to integrate imaging of other organs (see below).4


The skills, training, and approach can differ from one place to another, but it is generally recommended to follow a unique systematic approach in the same setting due to the usual need for serial studies by different operators.

The study can be focused or comprehensive. A systemic approach makes it easier to reveal the shock etiology and spot the hemodynamic parameter in need of correction (e.g., flow obstruction, volume responsiveness, inotropes, and vasoconstrictors). It is important to note that several mechanisms can interplay and hence the need for a comprehensive approach.

Based on our experience, we describe below our stepwise approach (Fig. 1):

Fig. 1: Echocardiography in the assessment of shock

Step 1: Confirm Shock State

This is usually a clinical diagnosis combined with biomarkers (e.g., mottling, capillary refill time, low urine output, lactate, and central venous oxygen saturation). However, some novel POCUS modalities can offer early and highly sensitive data and hence be integrated into the studies (please see the future section).

Step 2: Exclude Obstructive Shock

Examples are acute core pulmonale (ACP) [e.g., pulmonary embolism (PE)], right or left ventricular outflow obstruction (RVOT, LVOT), native or prosthetic valve obstruction, cardiac tamponade, and tension pneumothorax (needs lung ultrasound). In some cases, they are not the sole pathology but contribute to the hemodynamic instability (e.g., LVOT obstruction due to high catecholamine dose in septic shock or pericardial effusion compressing the right atrium (RA), reducing the venous return).

If spotted, they usually require immediate action, sometimes even before completing the focused exam. Examples are:

  • Thrombolysis in case of PE.
  • Drainage of cardiac tamponade.
  • Drainage of tension pneumothorax.
  • Fluid infusion and reducing catecholamines in case of LVOT obstruction.

Echocardiography remains the gold standard for the diagnosis of cardiac tamponade and is recommended as a guide for emergency pericardiocentesis. The European Society of Cardiology recommended a three-step scoring system, where a score of ≥6 indicates the need for urgent pericardiocentesis.5

Diastolic right ventricle (RV) collapse, RA collapse (more than a third of the cardiac cycle), and dilated inferior vena cava (IVC) with <50% inspiratory collapse are indicative of cardiac tamponade.5 Respiratory variability of the mitral and tricuspid diastolic inflow velocity or maximum E velocity (by >25 and 40%, respectively) may be less evident in mechanically ventilated than spontaneously breathing patients.6

Right ventricle (RV) dilatation is the most common sign of ACP, which is identified by measuring RV size and correlating it to the left ventricle (LV) size, usually in apical four chamber view.7 On the parasternal short axis view shifting of the interventricular septum (IVS) causing a D-shaped LV is another sign. If the IVS shift is marked in both diastole and systole, it is due to pressure overload, whereas if the IVS shift is maximum at end-diastole, it is due to RV volume overload (e.g., tricuspid regurgitation (TR).8 The velocity of the TR jet helps quantify the pulmonary artery systolic pressures (PASP). The caveat in massive PE is that PASP may not truly represent the severity of PE as the decrease in pulmonary blood flow and increase in pulmonary vascular resistance (PVR) offset each other (pressure = flow × resistance). Measurement of PVR may be more helpful but beyond the scope of focused studies. Detailed assessment of RV is further down the stepwise assessment.

Left ventricle (LV) hypertrophy, hypovolemia, and high inotropic support can predispose to an acquired left ventricular outflow tract obstruction (LVOTO) presenting as low cardiac output (CO) state refractory to inotropes. The systolic anterior motion of the mitral valve identified in 2D (two-dimensional) or M-mode parasternal long-axis view (PLAX) view contributes to LVOTO.

Obstruction can also be caused by stenotic valvular lesions (such as critical AS) or prosthetic valve dysfunction, which may require a surgical intervention.9

Step 3: CO Estimation

Warm vs cold shock (i.e., high vs low CO shock) can be differentiated by accurately quantifying CO and stroke volume (SV) or their indexed values.

Cardiac output (CO) = SV × heart rate

Stroke volume (SV) is calculated by measuring the LVOT cross-sectional area (PLAX) and the LVOT velocity-time integral (VTI) using pulsed wave Doppler (PWD) (apical five-chamber) (Fig. 2). The SV is then calculated by:

Fig. 2: Measuring left ventricular outflow tract velocity time integral in apical five-chamber view in a normal heart

SV = LVOT VTI × LVOT cross-sectional area

Using PWD in the apical five chamber view helps measure the VTI, also known as the stroke distance, which is the distance the column of blood travels through the LVOT during systole. Normal value for LVOT VTI is >18 cm. As measuring the LVOT cross-sectional area can be a major source of error, it was suggested that serial VTI measurements could be enough for following the trends.10 Although thermodilution via a pulmonary artery catheter remains the gold standard for measuring CO/SV, frequent serial measurements of VTI can be a surrogate for the trend of SV and used to track dynamic change and the effectiveness of therapy in critical illness.

Distributive shock presents with high CO with hypoperfusion warranting initiation of vasoconstrictors such as noradrenaline. On the other hand, in case of low output, the options are either to increase venous return (fluid responsiveness) or the initiation of inotropic support (impaired right or left ventricular contractility). It is not rare, in many cases, to combine all three interventions as guided by hemodynamic monitoring.

Step 4: Fluid Responsiveness and Tolerability

The next step is an assessment of fluid responsiveness and volume status. Studies have shown that fluid therapy is given unguided in 40% of cases carrying a risk of fluid overload in critical illness.11 Fluid responsiveness is defined as a 10–15% rise in SV/CO/VTI after a fluid challenge (or passive leg raise).12 It is worth mentioning that fluid responsiveness requires both ventricles to function at the slope of the Frank-Starling curve. The fluid administration increases the end-diastolic volume causing myocardial stretch and hence improved output. The change is measured within minutes of fluid administration, requiring the echo operator to be ready with the probe. SV variation is the percentage change in SV after a fluid challenge administration or passive leg raise; this variation can be easily inferred from the variation in LVOT VTI itself without the need for repeating the calculation of LVOT cross-sectional area.

Fluid resuscitation should continue until (1) the shock resolves, (2) patients become fluid unresponsive, or (3) fluid intolerability.

Fluid status can further be assessed transthoracic by IVC collapsibility or rarely superior vena cava (SVC) collapsibility which requires a transesophageal approach. IVC collapsibility is better validated in ventilated patients, with less evidence in spontaneously breathing patients. A threshold of 12–18% variation in the diameter of IVC (two methodologies—maximum diameter–minimum diameter divided either by mean or minimum diameter) is widely accepted for predicting fluid responsiveness.13 However, IVC respiratory variability can be less affected by many conditions making it less accurate (e.g., abdominal hypertension, low tidal volume).14 The cutoff for SVC collapsibility using transesophageal echo is 35%.15 Another dynamic parameter is the maximal velocity through the LVOT, which can be measured using continuous wave Doppler with high sensitivity.

It is important to mention the superiority of using IVC respiratory variability by echocardiography in case of cardiac arrhythmias over pulse contour analysis used by other hemodynamic tools (e.g., pulse contour cardiac output). Also, spotting RV dysfunction can indicate the inaccuracy of pulse pressure variation.

There is an increased interest in fluid tolerability, as over-resuscitation can worsen outcomes. Venous congestion leads to new organ dysfunction (e.g., respiratory failure) and, when it happens in encapsulated organs, increases their interstitial pressure and impairs blood flow and oxygen diffusion, counteracting any improved CO/SV, the main endpoint of hemodynamic management; as such venous congestion should be looked at in a continuum with the assessment of the cardiac and arterial part of the circulation. Sound hemodynamic management should aim to maintain organ perfusion without increasing venous congestion.

Classically, pulmonary congestion was considered a limit for fluid resuscitation. B-lines on lung ultrasound indicate pulmonary congestion, semi-quantitively reflect extravascular lung water, and can be used to monitor the tolerance to fluids.16,17 More recently, combining IVC assessment with Doppler studies of the portal, hepatic, and renal venous system was integrated into the venous excess ultrasound (VExUS) Score.18 The approach uses a curvilinear probe (sometimes phase-array) with pulsed wave Doppler capability in abdominal ultrasound settings. It interrogates venous congestion through 4 steps—IVC, liver, gut, and kidneys. Signs of congestion are as follows:

  • IVC diameter > 2 cm.
  • Prominent hepatic vein diastolic wave followed by systolic wave reversal.
  • Portal vein pulsatility (pulsatility index = (Vmax − Vmin)/Vmax).
  • Intrarenal venous Doppler findings: Gradual disappearance of the systolic component (e.g., the progress of monophasic flow (normal) into a biphasic (systolic and diastolic) phase, then ultimately only the diastolic phase).

Each component is scored and then summed into four grades (0–3); grade 3 represents severe congestion. VExUS score was able to predict acute kidney injury (AKI) postcardiac surgery, delineating its clinical significance.

Step 5: Intrinsic Cardiac and Valvular Assessment

Left Ventricle (LV)

Historically, LV ejection fraction (LVEF) has been the most sought data in echo reports as a parameter for LV systolic function. LVEF may be eyeballed or measured using various methods. The modified Simpson method, also called the biplane method of disks, is recommended by the American Society of Echocardiography. It uses 2D tracing of the LV endocardial border, at the end, diastole, and end-systole in the apical four chambers and two chamber views. The modified Quinones method uses linear ventricular measurements of either 2D or M-mode at the end diastole and end systole, making assumptions about the shape of the LV cavity. The Simpson differs from the modified Quinones methods in that lesser LV geometric assumptions also take into account the longitudinal contraction of LV.

The formula used for LVEF calculation is:


Where LVEF% is LVEF in percentage, LVEDV is left ventricular end-diastolic volume, and LVESV is left ventricular end-systolic volume.

The British Society of Echocardiography considers LVEF ≥ 55% as normal while ≤35% as severely impaired LV.

In critical care practice, LVEF reflects intrinsic LV function contribution into the SV/CO. It can suffer chronic preexistent or acute impairment and, in both cases, can contribute to hemodynamic derangement and impact clinical decisions (e.g., fluid resuscitation in chronic heart failure). If no previous echo studies are available, dilated LVs, and thin hyperechoic walls can raise the suspicion of chronic rather than acute pathology. Meanwhile, intensivists should be aware of its caveats.19

Firstly, preload and afterload can affect the LVEF significantly, so the clinical context of any resuscitation is important. Profound vasoplegia can mask an impaired LV systolic function when the afterload is significantly reduced. Obviously, inotropic agents have their effects. Secondly, LVEF is a marker of LV systolic function and does not reflect tissue perfusion, which is more related to CO. For example, mild to moderately impaired LVEF in a dilated heart with a bigger end-diastolic volume may be able to pump adequate SV, while an adequate LVEF in the context of severe mitral regurgitation (MR) can lead to low SV. Last, the heart rate is equally important as the SV in determining the CO and should be considered in the hemodynamic plan,

Regional wall motion abnormalities (RWMAs) are regional kinetic dysfunction of the ventricular wall that may contribute to overall systolic dysfunction. RWMAs can be classified by their severity and by region. It raises the suspicion of coronary artery disease if they correspond to a specific coronary territory. The presence of RWMA can lead to a wrong estimation or even calculation of LVEF in certain Echo windows.

Left ventricle (LV) diastolic function can affect the ventricular filling but generally plays less role in the determination of SV/CO. More importantly, its presence may predispose to less fluid tolerability and earlier pulmonary edema. Echocardiography can help to calculate the LV filling pressure by different methodologies and calculations, including mostly transmitral E/A and tissue Doppler imaging (TDI) E/e’.20,21 Acutely dilated RV can impair the septal motion and induces LV diastolic dysfunction adding to the hemodynamic compromise associated with ACP (ventricular interdependence). Interestingly, impaired diastolic function rather than LVEF was associated with mortality in septic patients.22

Right Ventricle (RV)

The RV has a thinner wall and lower elastance, making it sensitive to hemodynamic changes such as increased afterload. As described above, RV dilatation can be caused by ACP or any severe pulmonary disease, positive pressure ventilation, vasoactive drugs, or hypoxia/hypercapnia, all causing increased PVR leading to pressure overload on the RV. ACP is defined as:

Right ventricle (RV) dilatation with RVEDA/LVEDA ratio >0.6 and paradoxical IVS motion.

Where RVEDA is RV end diastolic area, LVEDA is LV end diastolic area, and IVS is IVS.

Most commonly, RV systolic function is assessed by two different measures. Tricuspid annular plane systolic excursion (TAPSE) is measured in M-mode in the apical 4-chamber windows by aligning the lateral tricuspid annulus with the ventricular apex and measuring its displacement. TAPSE is normally ≥16 mm. The second measure for RV systolic function is S’. This is measured by TDI as the peak velocity of the tricuspid annulus during systole, with a normal value of ≥9 cm/sec.23

It is important to differentiate acute from chronic RV impairment due to long-term pathology (e.g., chronic obstructive pulmonary disease, chronic thromboembolism). RV hypertrophy indicates a long-standing pressure overload and can be measured in the subcostal window at the end-diastole (hypertrophy > 5 mm).8 The 60/60 sign indicates a value of <60 for both the pressure gradient across the TV and pulmonary acceleration time (time from the start of pulmonary valve opening till the peak flow across the pulmonary valve in the PSAX RVOT view) and suggests a more acute process.24 Last, McConnell’s sign (RV free wall akinesia sparing the RV apex) is a 97% specific (but 22% sensitive) sign of acute PE.25,26

Recently, many intensive care studies started to integrate venous pressure (e.g., central venous pressure) into the definition of RV failure.27 This may reflect again a hemodynamic approach where the cardiac function is assessed in line with its consequence on other organs.

Not uncommonly, the impaired ventricular function during critical illness proves to be reversible, as in the case of septic cardiomyopathy, stress cardiomyopathy, or even sometimes acute myocarditis. As such, it is recommended, in case of de novo ventricular dysfunction, to repeat the study during recovery; otherwise, follow-up echocardiography may be needed.


Unfortunately, the role of valves in hemodynamic management is frequently overlooked. This may be due to the focused nature and skills of operators. However, in case of their presence, whether acute or chronic, they can considerably influence the data obtained from the echo and, subsequently, the hemodynamic management.

Mitral Regurgitation (MR)

Acute MR (e.g., rupture, mitral valve prolapse, endocarditis) can cause hemodynamic instability and even cardiac arrest.30 Patients are at risk of pulmonary edema, so cautious fluid resuscitation management with careful titration of vasopressors is needed as sudden increases in systemic vascular resistance (SVR) can worsen the MR. LVEF can overestimate the flow across the aortic valve and hence the CO (as a significant part can be flowing back to the left atrium).

Mitral Stenosis (MS)

Slow flow from the left atrium to LV means SV is dependent on diastolic time, so avoidance of tachycardia to maintain adequate ventricular filling and CO. It is not associated with atrial fibrillation, which again reduces LV filling by abolishing the LA contraction contribution. Similarly, to MR, these patients are at risk of pulmonary edema, so cautious fluid resuscitation is warranted.

Aortic Regurgitation

Raising SVR can worsen the regurgitation, so careful titration of vasopressors. SVR is not correctly reflected by the low diastolic blood pressure.

Aortic Stenosis (AS)

Be cautious of low flow and low gradient states in shock patients. It is a fixed CO state often associated with left ventricular hypertrophy and LV diastolic dysfunction, and significant hypotension can happen secondary to diuresis or vasodilators.

Tricuspid Regurgitation (TR)

This can occur due to raised RV afterload (increased PVR) and RV dilatation. This will increase right atrial pressure and central venous pressure and reduce venous return and thus reduce fluid responsiveness.

How can Other POCUS Modalities Help?

Point-of-care ultrasound (POCUS) modalities were used in shock states for a long time, even before the recognition of the role of echocardiography. One example is the focused assessment with sonography in trauma (FAST) scan in case of trauma. The utility can be divided into etiology diagnosis and hemodynamic assessment.

Etiology Diagnosis

  • Focused assessment with sonography in trauma (FAST) scan in case of trauma
  • Vascular: Detection of deep venous thrombosis, aortic dissection
  • Lungs: Tension pneumothorax

Hemodynamic Assessment

  • Contrast-enhanced ultrasound (CEUS)
  • Transcranial Doppler
  • Assessment of venous congestion:

Lung ultrasound

Venous excess Doppler ultrasound (VExUS)


Many protocols exist for the use of POCUS in shock states (e.g., rapid ultrasonography for shock and hypotension (RUSH), sonography in hypotension and cardiac arrest).28,29 While our stepwise approach has not been validated in prospective studies, this review provides a narrative of the combined use of POCUS and echocardiography in an updated integrated approach. Despite it remains based on a point-of-care approach, it requires a considerable level of skills and probably a longer study time. This is warranted in the more complex cases of shock where multiple hemodynamic mechanisms can interplay (e.g., septic cardiomyopathy, hypovolemia, and vasoplegia in case of septic shock; myocardial infarction leading to contractile dysfunction and acute valvulopathy in patients under positive pressure ventilation). The rising interest, technology breakthroughs, and affordable, user-friendly machines are boosting the applicability of POCUS, and one major recent advance is the integration of organ perfusion (e.g., CEUS) and congestion (e.g., VExUS) as a more relevant clinical endpoint than just the previously sought CO/SV. This demonstrates how POCUS in acute settings is drawing its defined role distinct from the cardiology and radiology traditional exams.


With the growing use and availability of POCUS machines, there is an increased risk of misinterpretation and misdiagnosis, leading to potential harm.19 Therefore, it is always useful to be aware of the pitfalls and limits of any imaging tool. They can be broadly divided in relation to image acquisition or interpretation.

In acute settings, Image acquisition is usually more challenging than during elective studies. Patients’ position (e.g., prone), cooperation (e.g., distressed or confused patients), concomitant pathology (e.g., lung hyperinflation), or interventions (e.g., mechanical ventilation, drains, dressings) are common barriers. In some cases, the subcostal window can prove very useful and overcome the limits posed by hyperinflation and mechanical ventilation. Despite continuous improvement, machines are most often smaller, possess fewer options, and have poorer image quality. While operators usually have less expertise, they carry the advantage of being aware of the clinical background and, subsequently, the ability to integrate data immediately into the clinical management (i.e., no delay or communication gaps). Urgency and time restraint lead to a general reliance on eyeballing rather than measurements which can be less accurate and less documentable. Some pathologies (e.g., small vegetations, prosthetic valve pathologies) can be beyond the expertise of many operators with basic (and sometimes even advanced) skills and necessitate the awareness of self-limits and expert escalation.

Despite all the above, interpretation remains the overlooked main noise.19 Hemodynamic derangement can affect heart dynamics, especially flow (i.e., Doppler studies). Furthermore, acute pathologies can evolve within a few hours necessitating serial exams subject to interoperator variabilities. Systemic inflammation causes vasodilation (reduced afterload), tachycardia, and hyperdynamic hearts (i.e., increased LVEF). Interventions also like mechanical ventilation, sedation, and vasoactive medications, which can affect cardiac contractility, vascular tone, and fluid responsiveness. It is sometimes challenging to differentiate acute Corpulmonale due to acute respiratory distress syndrome from PE. Not all focused protocols interrogate the valvular system overlooking its major impact on hemodynamics, especially if not known beforehand. An example is normal LVEF in the context of significant mitral regurgitation. In this case, CO may be reduced despite high LVEF, and excessive fluid therapy and vasopressors can worsen the condition (pulmonary edema and increased MR, respectively). Lastly, the shock state itself can impact the assessment of valvular lesions as in a low flow, low gradient state.

Compared to other hemodynamic monitors, POCUS/echocardiography are limited by not being continuous tools and being operator dependent, which usually requires trained personnel. However, it is noninvasive, and a first-focused study can be conducted faster than most other tools, which makes it very attractive in emergency settings. Also, the cost is negligible and hence the popularity in resource-limited settings. Lastly, it combines hemodynamic parameters with a diagnostic role due to the direct visualization of the right and left heart.

To mitigate those limits, it is advised to have a supervision plan in place, especially when studies are done by novice operators. Images should be stored and available for reinterpretation, especially in the case of serial exams. Trends can be more valuable than absolute values. Collaboration with imaging and cardiology services can help create a channel for escalation when needed.


It is increasingly recognized how other POCUS modalities can complement echocardiography. Ultrasound lungs, CEUS, and VExUS, are examples we strongly recommend integrating into the hemodynamic assessment.

Contrast-enhanced ultrasound (CEUS) uses microbubbles to directly visualize the microcirculation. It provides real-time visualization of deep organs (e.g., kidneys), an advantage over other microcirculatory tools, and clinical and biochemical markers (e.g., lactate, urine output), offering superficial and delayed data, respectively.31,32 When such data are integrated with Echo ones, it can be very valuable to precise the start and end of resuscitation. Sometimes, organ dysfunction decouples from perfusion (i.e., cellular/mitochondrial injury), and in those cases, CEUS may help to prevent over-resuscitation and direct toward other treatment modalities (e.g., renal replacement therapy in AKI). CEUS is still under investigation but represents a promising modality for future hemodynamic assessment.

Artificial intelligence (AI) is the ability of computers to perform smart human tasks. Imaging is one of the most promising applications supporting image optimization, measurements, and interpretation. This can be greatly helpful in acute settings where eyeballing, time restraints, and less experienced operators are commonplace.33,34 Despite promising, it still faces many obstacles and may need years to be fully applied in clinical practice.

Speckle tracking echocardiography (STE) is a novel modality allowing a more sensitive assessment of intrinsic myocardial function. It interrogates the behavior of myocardial pixels’ speckles’ to each other within the myocardium. It represents a more sensitive tool to spot subtle or early myocardial dysfunction.35 This may prealert clinicians and impact their plans. However, STE requires high image quality, which is sometimes difficult to obtain in acute settings. STE global longitudinal strain and not the LVEF was associated with mortality in severe sepsis and septic shock.36 Except few centers, STE is not widely available as an imaging modality in acute settings yet.

The divergence of operator skills (basic vs advanced) necessitates supervision, quality assurance, and escalation plans. In this context, telemedicine and cloud-based platforms can help with remote supervision and interpretation.37 This may be very useful in small hospitals where local expertise is not available.


Echocardiography, along with POCUS, is becoming fundamental for the individualized management of shock. The continuous improvement in both hardware and software will help the integration of POCUS as an unreplaceable. It is advisable to go through a structural approach while keeping a platform for supervision, follow-up, and quality control. Remote supervision of the studies and AI are of great help, especially for operators in training.


The supplementary videos 1 to 6 are available online on the website of

Video 1: Parasternal long-axis view (PLAX)

Video 2: Parasternal short-axis view (mitral valve level)

Video 3: Parasternal short axis view (papillary muscle level)

Video 4: Apical four-chamber view

Video 5: Apical five-chamber view

Video 6: Subcostal view


Ashraf Roshdy


1. Roshdy A, Francisco N, Rendon A, et al. Critical care echo rounds: haemodynamic instability. Echo Res Pract 2014;1(1):D1–D8. DOI: 10.1530/ERP-14-0008

2. Roshdy A. POCUS in the assessment of shock. In Point of care Ultrasound in Critical Care, Flower L and Pradeep Madhivathanan (eds.). Scion Publishing, Banbury, U.K. 2022, pp. 271–288.

3. Giustiniano E, Padua E, Negri K, et al. Echocardiography during prone-position mechanical ventilation in patients with COVID-19: a proposal for a new approach. J Am Soc Echocardiogr 2020;33(7):905–906. DOI:10.1016/j.echo.2020.04.027

4. Flower L, Madhivathanan PR, Andorka M, et al. Getting the most from the subcostal view: The rescue window for intensivists. J Crit Care 2021;63:202–210. DOI: 10.1016/j.jcrc.2020.09.003

5. Ristic AD, Imazio M, Adler Y, et al. Triage strategy for urgent management of cardiac tamponade: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J 2014;35(34):2279–2284. DOI:10.1093/eurheartj/ehu217

6. Faehnrich JA, Noone RB Jr, White WD, et al. Effects of positive-pressure ventilation, pericardial effusion, and cardiac tamponade on respiratory variation in transmitral flow velocities. J Cardiothorac Vasc Anesth 2003;17(1):45–50. DOI: 10.1053/jcan.2003.9

7. Vieillard-Baron A, Prin S, Chergui K, et al. Echo-Doppler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med 2002;166(10):1310–1319. DOI:10.1164/rccm.200202-146CC

8. Rudski LG, Lai WW, Afilalo J, 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 2010;23(7):685–713. DOI: 10.1016/j.echo.2010.05.010

9. Roshdy A, Karapanagiotidis GT, Sarsam MA, et al. Acute obstruction of a mechanical aortic valve in a young woman: case report and review of the literature. Echo Res Pract 2015;2(1):K1–K5. DOI:10.1530/ERP-14-0068

10. Mowat DH, Haites NE, Rawles JM. Aortic blood velocity measurement in healthy adults using a simple ultrasound technique. Cardiovasc Res 1983;17(2):75–80. DOI: 10.1093/cvr/17.2.75

11. Cecconi M, Hofer C, Teboul JL, et al. Fluid challenges in intensive care: the FENICE study: a global inception cohort study. Intensive Care Med 2015;41(9):1529–1537. DOI: 10.1007/s00134-015-3850-x.

12. Toscani L, Aya HD, Antonakaki D, et al. What is the impact of the fluid challenge technique on diagnosis of fluid responsiveness? A systematic review and meta-analysis. Crit Care 2017;21(1):207. DOI:10.1186/s13054-017-1796-9

13. Furtado S, Reis L. Inferior vena cava evaluation in fluid therapy decision making in intensive care: practical implications. Rev Bras Ter Intensiva 2019;31(2):240–247. DOI: 10.5935/0103-507X.20190039

14. Monnet X, Shi R, Teboul JL. Prediction of fluid responsiveness. What’s new? Ann Intensive Care 2022;12(1):46. DOI:10.1186/s13613-022-01022-8

15. Upadhyay V, Malviya D, Nath SS, et al. Comparison of superior vena cava and inferior vena cava diameter changes by echocardiography in predicting fluid responsiveness in mechanically ventilated patients. Anesth Essays Res 2020;14(3):441–447. DOI: 10.4103/aer.AER_1_21

16. Enghard P, Rademacher S, Nee J, et al. Simplified lung ultrasound protocol shows excellent prediction of extravascular lung water in ventilated intensive care patients. Crit Care 2015;19(1):36. DOI:10.1186/s13054-015-0756-5

17. Picano E, Pellikka PA. Ultrasound of extravascular lung water: a new standard for pulmonary congestion. Eur Heart J 2016;37(27):2097–2104. DOI: 10.1093/eurheartj/ehw164

18. Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J 2020;12(1):16. DOI: 10.1186/s13089-020-00163-w

19. Roshdy A. Echodynamics: interpretation, limitations, and clinical integration! J Intensive Care Med 2018;33(8):439–446. DOI:10.1177/0885066617734151

20. Boussuges A, Blanc P, Molenat F, et al. Evaluation of left ventricular filling pressure by transthoracic Doppler echocardiography in the intensive care unit. Crit Care Med 2002;30(2):362–367. DOI:10.1097/00003246-200202000-00016

21. Dokainish H, Zoghbi WA, Lakkis NM, et al. Optimal noninvasive assessment of left ventricular filling pressures: a comparison of tissue Doppler echocardiography and B-type natriuretic peptide in patients with pulmonary artery catheters. Circulation 2004;109(20):2432–2439. DOI: 10.1161/01.CIR.0000127882.58426.7A

22. Sanfilippo F, Corredor C, Fletcher N, et al. Diastolic dysfunction and mortality in septic patients: a systematic review and meta-analysis. Intensive Care Med 2015;41(6):1004–1013. DOI:10.1007/s00134-015-3748-7

23. Harkness A, Ring L, Augustine DX, et al. Education Committee of the British Society of Echocardiography. Normal reference intervals for cardiac dimensions and function for use in echocardiographic practice: a guideline from the British Society of Echocardiography. Echo Res Pract 2020;7(1):X1. DOI: 10.1530/ERP-19-0050

24. Kurzyna M, Torbicki A, Pruszczyk P, et al. Disturbed right ventricular ejection pattern as a new Doppler echocardiographic sign of acute pulmonary embolism. Am J Cardiol 2002;90(5):507–511. DOI:10.1016/s0002-9149(02)02523-7

25. McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996;78(4):469–473. DOI:10.1016/s0002-9149(96)00339-6

26. Fields JM, Davis J, Girson L, et al. Transthoracic echocardiography for diagnosing pulmonary embolism: a systematic review and meta-analysis. J Am Soc Echocardiogr 2017;30(7):714–723.e4. DOI:10.1016/j.echo.2017.03.004

27. Flower L, Parulekar P, Roshdy A. The challenges of defining right ventricular dysfunction in critical illness. Anaesthesia 2022;77(11):1307–1308. DOI: 10.1111/anae.15794.

28. Perera P, Mailhot T, Riley D, et al. The RUSH exam 2012: rapid ultrasound in shock in the evaluation of the critically ill patient. Emerg Med Clin North Am 2010;28(1):29–56. DOI: 10.1016/j.emc.2009.09.010

29. Atkinson P, Bowra J, Milne J, et al. International Federation for Emergency Medicine consensus statement: sonography in hypotension and cardiac arrest (SHoC): an international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest. CJEM 2017;19(6):459–470. DOI: 10.1017/cem.2016.394

30. Ahmed M, Roshdy A, Sharma R, et al. Sudden cardiac arrest and coexisting mitral valve prolapse: a case report and literature review. Echo Res Pract 2016;3(1):D1–D8. DOI: 10.1530/ERP-15-0020

31. Wu J, Chen DC. Contrast-enhanced ultrasonography: a promising method for blood flow and perfusion evaluation in critically ill patients. Chin Med J (Engl) 2018;131(10):1135–1137. DOI:10.4103/0366-6999.231527.

32. Emanuel AL, Meijer RI, van Poelgeest E, et al. Contrast-enhanced ultrasound for quantification of tissue perfusion in humans. Microcirculation 2020;27(1):e12588. DOI: 10.1111/micc.12588

33. Alsharqi M, Woodward WJ, Mumith JA, et al. Artificial intelligence and echocardiography. Echo Res Pract 2018;5(4):R115–R125. DOI:10.1530/ERP-18-0056

34. Knackstedt C, Bekkers SC, Schummers G, et al. Fully automated versus standard tracking of left ventricular ejection fraction and longitudinal strain: the FAST-EFs multicenter study. J Am Coll Cardiol 2015;66(13):1456–1466. DOI: 10.1016/j.jacc.2015.07.052

35. Ehrman RR, Bredell BX, Harrison NE, et al. Increasing illness severity is associated with global myocardial dysfunction in the first 24 hours of sepsis admission. Ultrasound J 2022;14(1):32. DOI:10.1186/s13089-022-00282-6.

36. Sanfilippo F, Corredor C, Fletcher N, et al. Left ventricular systolic function evaluated by strain echocardiography and relationship with mortality in patients with severe sepsis or septic shock: a systematic review and meta-analysis. Crit Care 2018;22(1):183. DOI:10.1186/s13054-018-2113-y

37. Butnar A, Wong A, Ho S, Malbrain M. The Future of Critical Care Ultrasound. ICU Management & Practice 2019/2020. as accessed 21 January 2023.

© The Author(s). 2023 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.