Sepsis echocardiography or ultrasound
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Sepsis echocardiography or ultrasound On the Web |
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American Roentgen Ray Society Images of Sepsis echocardiography or ultrasound |
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Risk calculators and risk factors for Sepsis echocardiography or ultrasound |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2] Jason Le, B.S.[3]
Synonyms and keywords: sepsis syndrome; septic shock; septicemia
Overview
Focused cardiac ultrasound (FoCUS) and point-of-care ultrasound (POCUS) are core bedside tools in sepsis, used to characterize hemodynamic phenotype, detect sepsis-induced cardiomyopathy, and guide fluid resuscitation, in addition to identifying an infectious source. Echocardiography is the first-line modality for working up circulatory failure in sepsis.[1][2]
POCUS should be interpreted together with the clinical examination, arterial pressure, perfusion findings, laboratory data, and the trajectory of the patient. Its principal role in this microchapter is hemodynamic assessment; ultrasound used primarily to identify the infectious source is addressed in the Other imaging and Laboratory findings microchapters.
Focused cardiac ultrasound and hemodynamic phenotyping
FoCUS is a focused examination intended to answer specific bedside cardiovascular questions rather than provide a comprehensive echocardiographic study. Standard views include parasternal long-axis and short-axis views, subcostal views, and apical 4-chamber and 5-chamber views, including assessment of the left ventricular outflow tract (LVOT) when feasible.[1]
In patients with sepsis or septic shock, FoCUS/POCUS can assess left and right ventricular systolic function, ventricular size and interaction, gross valvular abnormalities, pericardial effusion, inferior vena cava (IVC) respiratory variation, and Doppler-derived measures of stroke volume and cardiac output. Comprehensive echocardiography is required when detailed structural, valvular, diastolic, or quantitative assessment is necessary.[1]
POCUS combined with clinical assessment can help distinguish distributive shock from cardiogenic, hypovolemic, and obstructive shock. In the JAMA review, this approach identified distributive shock with approximately 99.7-100% specificity and 63.6-75% sensitivity, supporting its value particularly for ruling in alternative shock phenotypes when the clinical picture is uncertain.[1]
Five clinically useful hemodynamic phenotypes can be recognized at the bedside:
| Phenotype | Typical echocardiographic/POCUS features | Clinical implication |
|---|---|---|
| Distributive/vasoplegic | Hyperdynamic or apparently normal LV systolic function, small or underfilled ventricles in some patients, variable RV function, and evidence of low systemic vascular tone | Supports vasodilatory shock; ventricular function and fluid responsiveness should still be assessed rather than assuming fluid responsiveness from phenotype alone |
| LV systolic dysfunction | Reduced LV systolic function, potentially with reduced stroke volume | Suggests sepsis-induced myocardial dysfunction and may alter the interpretation of hypotension and fluid responsiveness |
| LV diastolic dysfunction | Abnormal relaxation or filling patterns with impaired diastolic function | May coexist with systolic dysfunction or preserved LVEF and can contribute to impaired filling and congestion |
| RV dysfunction | RV dilation and/or reduced RV systolic function, with possible RV pressure overload | May limit tolerance of further fluid administration and requires assessment of pulmonary vascular load and ventricular interaction |
| Normalized/post-resuscitation profile | No major residual ventricular abnormality after initial resuscitation | Represents a post-resuscitation state rather than a specific therapeutic target; interpretation should remain linked to the patient's current perfusion and volume status |
These phenotypes may coexist or evolve over time. A single echocardiographic examination therefore represents a time point rather than a fixed classification of the patient's shock state.[2]
Sepsis-induced cardiomyopathy
Sepsis-induced cardiomyopathy (SICM) is characterized by myocardial dysfunction occurring during sepsis and may involve the left ventricle, right ventricle, or both. Reported prevalence varies substantially according to definitions, patient populations, loading conditions, and echocardiographic methods.[2]
| Component | Reported prevalence | Important considerations |
|---|---|---|
| LV systolic dysfunction | ~5-32% | LVEF is strongly load-dependent and may appear normal or preserved in severe vasoplegia despite impaired myocardial contractility |
| LV diastolic dysfunction | ~20-57% | May occur with or without LV systolic dysfunction and can impair ventricular filling |
| RV dysfunction | ~18-79% | Particularly important when pulmonary vascular resistance is increased or RV afterload is elevated |
A normal LVEF does not exclude SICM because reduced systemic vascular resistance can increase measured ejection fraction despite impaired myocardial contractility. Global longitudinal strain (GLS) can detect subtle LV systolic dysfunction when LVEF remains preserved and may provide additional prognostic information. Assessment of RV-pulmonary artery (RV-PA) coupling can further characterize right-sided ventricular dysfunction and its interaction with pulmonary vascular load.[2][3]
SICM is often reversible, but its presence is associated with worse outcomes in observational studies. Interpretation should account for loading conditions, vasopressor therapy, mechanical ventilation, and changes over time rather than relying on LVEF alone.[2]
Assessment of fluid responsiveness
Fluid responsiveness refers to an increase in stroke volume or cardiac output after a preload-increasing maneuver. Approximately 57% of critically ill patients with sepsis are fluid responsive at baseline; however, fluid responsiveness alone is not an indication to administer fluid. Fluids should be considered when there is evidence of inadequate perfusion and a reasonable expectation that additional volume will improve the clinical state without causing unacceptable harm.[4]
Passive leg raise (PLR) combined with measurement of cardiac output or LVOT velocity-time integral (VTI) is among the most robust bedside approaches because PLR provides a reversible endogenous fluid challenge and can be used in patients with spontaneous breathing or arrhythmias. A change of approximately 10-15% in stroke volume, cardiac output, or LVOT VTI is commonly used to define a positive response. PLR combined with cardiac-output measurement has reported sensitivity of approximately 88%, specificity of approximately 92%, and a positive likelihood ratio of approximately 11.[4]
The Surviving Sepsis Campaign (SSC) 2021 and 2026 guidelines suggest using dynamic measures, including PLR or a fluid challenge assessed by stroke volume, stroke-volume variation (SVV), pulse-pressure variation (PPV), or echocardiography, rather than static parameters to guide fluid resuscitation.[5][6]
The 2026 SSC guideline reports that POCUS-guided resuscitation probably reduces 28-day mortality (RR 0.88, 95% CI 0.78-0.99). It also cautions that IVC diameter and collapsibility principally reflect central venous pressure and therefore inherit the limitations of static filling-pressure assessment.[6]
A multicenter randomized trial of PLR-guided resuscitation in sepsis-induced hypotension and shock (the FRESH trial) reported approximately 1.37 L lower net fluid balance, lower renal replacement therapy use (5.1% vs 17.5%), and lower mechanical ventilation use (17.7% vs 34.1%) in the dynamic-assessment group.[7]
These FRESH results are from a single randomized clinical trial and should not be conflated with the pooled estimates reported in the 2026 SSC guideline. In the guideline's pooled evidence for dynamic-measure-guided resuscitation, the estimated relative risk was 0.91 (95% CI 0.79-1.06) for mortality and 0.75 (95% CI 0.58-0.98) for renal replacement therapy.[6]
Dynamic ultrasound and hemodynamic indices
The diagnostic performance of dynamic measures varies according to the maneuver, patient characteristics, mechanical ventilation, spontaneous respiratory effort, cardiac rhythm, and the method used to measure the change in stroke volume or cardiac output.
| Dynamic measure | Diagnostic performance | Practical interpretation |
|---|---|---|
| Tidal-volume challenge (TVC) | AUC ~0.96 | Among the most accurate dynamic indices in mechanically ventilated patients |
| End-expiratory occlusion test (EEOT) | AUC ~0.95 | Highly accurate in appropriate mechanically ventilated patients |
| Passive leg raise (PLR) | AUC ~0.91 | Broadly applicable when stroke volume or cardiac output can be measured dynamically |
| Pulse-pressure variation (PPV) | AUC ~0.88 | Useful mainly in appropriately selected mechanically ventilated patients with regular rhythm and controlled ventilation |
| Stroke-volume variation (SVV) | AUC ~0.87 | Similar limitations to PPV; interpretation depends on ventilation and rhythm |
| Plethysmographic variability index (PVI) | AUC ~0.83 | Less reliable and should not be used in isolation |
| IVC respiratory variation (ΔIVC) | AUC ~0.82 | Less reliable than several dynamic measures and should not be used in isolation |
An umbrella review of 7 meta-analyses comprising 123 studies and approximately 10,300 patients ranked TVC and EEOT highest, followed by PLR, PPV/SVV, and PVI/ΔIVC.[8]
Inferior vena cava respiratory variation
A sepsis-specific meta-analysis of 21 studies involving 1207 patients found pooled sensitivity of 0.84 and specificity of 0.87 for respiratory changes in IVC diameter, with an area under the receiver operating characteristic curve of approximately 0.92. IVC collapsibility performed best in spontaneously breathing patients.[9]
In spontaneously breathing, non-intubated septic patients, an IVC collapsibility of approximately 48% during a standardized deep inspiration had reported sensitivity of 84% and specificity of 90% for predicting fluid responsiveness.[10]
IVC respiratory variation should therefore be interpreted in context rather than used as a standalone volume target. Mechanical ventilation, spontaneous inspiratory effort, intra-abdominal pressure, right-sided cardiac dysfunction, pulmonary hypertension, and other factors can alter IVC behavior independently of preload responsiveness.[9][6]
LVOT VTI and passive leg raise
When an adequate apical 5-chamber or equivalent Doppler window is available, LVOT VTI can provide a noninvasive surrogate for stroke volume. During PLR, a rise in LVOT VTI of approximately 10-15% supports preload responsiveness. This approach is particularly useful when respiratory-variation indices are unreliable, including spontaneous breathing and cardiac arrhythmias.[4]
Other ultrasound approaches, including measurement of aortic VTI during PLR, can be integrated with IVC assessment. These approaches may improve individualized assessment but should not be interpreted as interchangeable with outcome evidence from randomized trials.[6]
Other dynamic measures
PPV and SVV can be useful in selected mechanically ventilated patients but are affected by tidal volume, respiratory mechanics, arrhythmias, spontaneous respiratory effort, and right ventricular dysfunction. PVI and ΔIVC have lower diagnostic performance in the comparative umbrella review and should not be used in isolation.[8]
Pulse-pressure variation, stroke-volume variation, plethysmographic variability index, and IVC variation should therefore be viewed as components of a broader hemodynamic assessment rather than as independent triggers for fluid administration.[8]
Clinical outcomes and limitations of ultrasound-guided resuscitation
Dynamic assessment can reduce unnecessary fluid administration, but diagnostic evidence of fluid responsiveness should not be equated with a demonstrated survival benefit from administering fluid to every responsive patient.
The FRESH randomized clinical trial used stroke-volume changes during PLR to guide resuscitation and demonstrated lower net fluid balance, renal replacement therapy, and mechanical ventilation as described above.[7]
By contrast, a single-center randomized trial of 202 emergency-department patients with sepsis-induced hypoperfusion or septic shock found that ultrasound-guided, IVC-based fluid resuscitation reduced cumulative fluid administration but did not improve 30-day mortality (18.8% vs 19.8%).[11]
The 2026 SSC guideline's pooled estimates for dynamic-measure-guided resuscitation are therefore best understood as evidence concerning a broader strategy rather than proof that any individual ultrasound variable or algorithm improves survival in isolation.[6]
Role of ultrasound in source identification
POCUS can also identify findings compatible with common infectious sources, including pulmonary, biliary, cardiac, urinary, and intra-abdominal abnormalities. However, source-identification ultrasound is outside the primary scope of this hemodynamic assessment microchapter and is addressed in the relevant diagnostic and imaging microchapters.[12]
Clinically useful summary
| Clinical question | Preferred bedside approach | Key limitation |
|---|---|---|
| Is shock distributive or another phenotype? | Integrate clinical assessment with FoCUS/POCUS, including LV/RV function, ventricular size, and signs of obstruction | POCUS is an adjunct to clinical assessment and does not replace comprehensive echocardiography when detailed structural assessment is required |
| Is the patient fluid responsive? | PLR with LVOT VTI or another direct cardiac-output/stroke-volume measurement | Responsiveness does not by itself indicate that fluid should be administered |
| Can respiratory variation help assess responsiveness? | PPV/SVV in appropriately selected mechanically ventilated patients; IVC variation in selected patients | Performance depends strongly on ventilation, rhythm, respiratory effort, and right-heart conditions |
| Is SICM present? | Assess LV systolic and diastolic function, RV function, GLS when available, and RV-PA coupling when appropriate | LVEF is load-dependent and a normal LVEF does not exclude myocardial dysfunction |
| Should IVC variation be used alone? | No; integrate with clinical perfusion and other dynamic measures | IVC diameter and collapsibility principally reflect CVP and inherit the limitations of static filling-pressure assessment |
| Has ultrasound-guided resuscitation been shown to improve outcomes? | Dynamic, individualized assessment can reduce fluid exposure and may improve selected outcomes | Individual ultrasound variables and IVC-guided algorithms have not established a universal mortality benefit |
References
- ↑ 1.0 1.1 1.2 1.3 Kaselitz, TB; Seymour, CW (2025). "Point-of-Care Ultrasound in Sepsis and Septic Shock". JAMA. 333 (19): 1720–1721. doi:10.1001/jama.2025.1983. PMID 40094635 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 2.3 2.4 Sato, R; Sanfilippo, F; Lanspa, M; Duggal, A; Dugar, S (2025). "Sepsis-Induced Cardiomyopathy: Mechanism, Prevalence, Assessment, Prognosis, and Management". Chest. doi:10.1016/j.chest.2025.08.013. PMID 40912296 Check
|pmid=value (help). - ↑ Zakynthinos, GE; Giamouzis, G; Xanthopoulos, A (2025). "Septic Cardiomyopathy: Difficult Definition, Challenging Diagnosis, Unclear Treatment". Journal of Clinical Medicine. 14 (3): 986. doi:10.3390/jcm14030986. PMID 39941657 Check
|pmid=value (help). - ↑ 4.0 4.1 4.2 Zampieri, FG; Bagshaw, SM; Semler, MW (2023). "Fluid Therapy for Critically Ill Adults With Sepsis: A Review". JAMA. 329 (22): 1967–1980. doi:10.1001/jama.2023.7560.
- ↑ Evans, L; Rhodes, A; Alhazzani, W (2021). "Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021". Critical Care Medicine. 49 (11): e1063–e1143. doi:10.1097/CCM.0000000000005337.
- ↑ 6.0 6.1 6.2 6.3 6.4 6.5 Prescott, HC; Antonelli, M; Alhazzani, W (2026). "Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026". Critical Care Medicine. 54 (4): 725–812. doi:10.1097/CCM.0000000000007075.
- ↑ 7.0 7.1 Douglas, IS; Alapat, PM; Corl, KA (2020). "Fluid Response Evaluation in Sepsis Hypotension and Shock: A Randomized Clinical Trial". Chest. 158 (4): 1431–1445. doi:10.1016/j.chest.2020.04.025. PMID 32353418 Check
|pmid=value (help). - ↑ 8.0 8.1 8.2 Meco, M; Giustiniano, E; Nisi, F; Zulli, P; Agosteo, E (2026). "Predicting Fluid Responsiveness in Mechanically Ventilated Adults: An Umbrella Review of Diagnostic Accuracy Meta-Analyses". Anesthesia and Analgesia. doi:10.1213/ANE.0000000000008215. PMID 42461688 Check
|pmid=value (help). - ↑ 9.0 9.1 Zhang, H; Jiang, J; Dai, M; Liang, Y; Li, N; Gao, Y (2025). "Predictive accuracy of changes in the inferior vena cava diameter for predicting fluid responsiveness in patients with sepsis: A systematic review and meta-analysis". PLOS One. 20 (5): e0310462. doi:10.1371/journal.pone.0310462. PMID 40344560 Check
|pmid=value (help). - ↑ Preau, S; Bortolotti, P; Colling, D (2017). "Diagnostic Accuracy of the Inferior Vena Cava Collapsibility to Predict Fluid Responsiveness in Spontaneously Breathing Patients With Sepsis and Acute Circulatory Failure". Critical Care Medicine. 45 (3): e290–e297. doi:10.1097/CCM.0000000000002090. PMID 27749318.
- ↑ Musikatavorn, K; Plitawanon, P; Lumlertgul, S (2021). "Randomized Controlled Trial of Ultrasound-Guided Fluid Resuscitation of Sepsis-Induced Hypoperfusion and Septic Shock". The Western Journal of Emergency Medicine. 22 (2): 369–378. doi:10.5811/westjem.2020.11.48571. PMID 33856325 Check
|pmid=value (help). - ↑ Torres-Arrese, M; García-Casasola, G; Blancas, R (2026). "Role of Point-of-Care Ultrasound in Septic Shock". Medicina Clinica. 166 (1): 107269. doi:10.1016/j.medcli.2025.107269. PMID 41505938 Check
|pmid=value (help).