2025+SIECVI共识声明：脓毒性心肌病的超声检查

Abstract

Septec cardiomyopathy(SCM) is an acute, reversible myocardial dysfunction occurring in the context of sepsis, independent of ischemic heart disease. Despite its frequent occurrence in critically ill patients, SCM remains poorly defined and underdiagnosed. This article provides clinicians with a practical guide for the recognition and management of SCM, with particular attention to the role of bedside echocardiography.Echocardiography is emphasized as both a diagnostic and hemodynamic monitoring tool to optimize treatment strategies in patients with sepsis and septic shock. Advanced techniques such as speckle-tracking echocardiography enhance sensitivity for detecting subclinical myocardial impairment and support differential diagnosis. Real-time echocardiographic assessment allows tailored therapy and may improve patient outcomes. Key elements include the recognition of characteristic echocardiographic patterns, integration of global longitudinal strain analysis,and the use of echocardiographic findings to guide hemodynamic management decisions.

Keywords: Echocardiography, monitoring, myocardial dysfunction, myocardial strain, physiologic, sepsis, septic, shock

INTRODUCTION

Sepsis and septic shock are major causes of morbidity and mortality in intensive care unit(ICU) worldwide.[1] Among the several complications of sepsis, cardiac dysfunction plays a crucial role in determining patient outcomes. In 1921, E.Romberg first described septic cardiomyopathy(SCM) as“septic acute myocarditis.”[2] In 1967, McLean et al. described diagnostic criteria for detecting heart failure as part of sepsis included a low cardiac index.[3] In 1984, Parker et al.,using radionuclide angiography, defined SCM as reversible myocardial depression due to sepsis and septic shock, defined as a reduced left ventricular ejection fraction(LVEF<40%)and an increase in mean end-diastolic volume, excluding acute coronary events, that reversed to normal within two weeks.[4]Prevalence rates vary widely,from 20% to over 50%,depending

Videos available on: https://journals.lww.com/JCEG

|Access this article online|| |---|---| |Quick Response Code|Website: https://journals.lww.com/JCEG| |Quick Response Code||

on the diagnostic criteria used and timing of assessment.[5-7]The risk factors that stand out are male gender, age, high lactate levels at admission, and pre-existing heart diseases.[8]In addition, SCM has been associated with increased mortality,especially when not promptly identified and managed.[2,9]

# DEFINITION AND DIAGNOSIS

SCM is generally defined as a reversible cardiac dysfunction occurring during sepsis, characterized by ventricular dilation

Address for correspondence: Dr. Annalisa Piccolo,Department of Anesthesiology and Intensive Care, Grande Ospedeale Metropolitan of Athenalico"BMM", Reggio Di Calabria, Italy.E-mail: annalisa.piccolo@ospedalerc.it

This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix,tweaks,and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

For reprints contact: WKHLR PMedknow_reprints@wolterskluwer.com

Submitted: 13-Sep-2025 Accepted: 15-Sep-2025

Published: 29-Sep-2025

How to cite this article: Tescione M, Piccolo A, Vadala EG, Posteraro AG,Franzutzti C, Macheda I, et al. How to do echo inseptic cardiomyopathy:A consensus statement of the Italian Society of Echocardiography and Cardiovascular Imaging. J Cardiovasc Echography 2025;35:307-13.

Tescione,et al::A consensus statement of the SIECVI

with increased ventricular compliance and normal to low filling pressures, in contrast to the pattern of cardiogenic shock,where ventricular pressures are elevated. SCM has also been described as a systolic and/or diastolic impairment of the left and/or right ventricle, in the absence of pre-existing cardiac disease. This condition is usually transient, with recovery observed within 7 to 10 days.[10]

Concerning its diagnosis, serum biomarker dosage is advised.Indeed,N-terminal pro-B-type natriuretic peptide(NT-proBNP)and cardiac Troponin are elevated in 97.4% and 84.5% of patients, respectively, and this increase correlates with a greater degree of LV dysfunction, disease severity, and mortality.[11]Echocardiography has emerged as a cornerstone as both a diagnostic and therapeutic monitoring tool, enabling tailored hemodynamic support.[12,13] Cardiac magnetic resonance imaging(MRI) is also a very useful technique since it shows changes suggestive myocardial edema and inflammation without the presence of focal fibrosis on late gadolinium sequences that are the leading features of SCM.[7] Nonetheless,the leading limiting factor for the application of cardiac MRI in daily practice is the duration of the examination, especially when dealing with hemodynamically unstable patients. In contrast, echocardiography provides several possibilities for the diagnosis of SCM. The method is simple, available,cheap,easily repeatable, and it can be performed“at the bedside” even in critically ill patients.

Currently, five echocardiographic patterns of different hemodynamic phenotypes of SCM can be identified, and they have similar prevalence.[14]

● Cluster 1: Absence of cardiac dysfunction(16.9%)

● Cluster 2: Left ventricular systolic dysfunction(17.7%)

● Cluster 3: Hyperkinetic profile with preserved or supernormal LV systolic function with elevated aortic blood flow velocities(23.3%)

● Cluster 4: Right ventricular(RV) failure(22.5%)

● Cluster 5: Persistent hypovolemia(19.4%).

The highest mortality was recorded in cluster 4(34% in the intensive care unit, and 22% of 7-day mortality). ${}^{[15]}$

Understanding differences between cardiac responses to sepsis and how to best treat them may help inform a more individualized hemodynamic resuscitation. For instance,limiting fluids in patients with LV systolic dysfunction and RV dysfunction, using inotropes only for those patients with systolic dysfunction, prioritizing vasopressin in RV dysfunction, and using beta blockers and ensuring adequate fluid resuscitation for hyperdynamic function and left ventricular outflow tract obstruction(LVOTO), are all theoretical ways to optimize cardiac function in sepsis, but more data are needed.

Recent literature proposes different ways of phenotyping cardiovascular presentations in septic shock, aiming to guide personalized management. Messina and Vieillard-Baron suggest three profiles(“good,”“bad,” and“ugly”).[16] Other

studies describe up to four hemodynamic profiles that can be referred to sepsis and septic shock.[17] These classifications overlap in many aspects, highlighting both similarities and nuanced distinctions.

● The“Good” profile aligns with the hyperkinetic profile(“Profile 1”), where left ventricular(LV) function is preserved and CO is maintained or elevated despite reduced systemic vascular resistance. Both groups correspond to the“classic” septic shock phenotype,usually requiring careful titration of fluids, vasopressors,and antibiotics

•The“Bad” profile encompasses patients with either acute LV systolic dysfunction or marked hyperkinesia. This partially overlaps with:

● Profile 2(Isolated LV systolic dysfunction), where new-onset SCM leads to decreased cardiac output and elevated LV filling pressures, with high risk of cardiogenic shock

● Some cases of Profile 1(Hyperkinetic), when profound vasoplegia persists despite vasopressors,representing fluid-refractory shock with poor prognosis.

● The“Ugly” profile corresponds broadly to Profile 3 (Septic shock with pre-existing cardiac dysfunction),where patients have chronic cardiac disease and may experience overlapping acute and chronic abnormalities. In both schemes, the challenge lies in distinguishing baseline dysfunction from sepsis-induced changes

•Primary cardiogenic shock with superimposed sepsis(Profile 4). This pattern involves primary cardiogenic shock that is subsequently complicated by an infectious process leading to septic shock.Pathophysiology and outcomes of patients in this group can differ significantly.

The“good-bad-ugly” model offers a pragmatic,echocardiography-driven bedside approach, whereas the four-pattern classification of Sato provides a higher level of detail, especially in distinguishing SCM and primary cardiogenic shock syndromes. Combining both frameworks may improve diagnostic precision, clarify therapeutic priorities(fluids, vasopressors, inotropes, and mechanical support), and ultimately enhance personalization of care in septic shock with cardiovascular involvement.

By integrating the conceptual framework proposed by Messina et al., with the clinical patterns outlined by Sato et al., we developed a summary table that combines echocardiographic features, pathophysiological mechanisms, and therapeutic implications of the main cardiovascular profiles observed frequently in septic shock. This integrated approach aims to provide clinicians with an immediate and practical tool to support early recognition of hemodynamic phenotypes and guide the initial management of critically ill patients,when timely and tailored decisions are crucial for improving outcomes[Table 1].

Tescione,et al::A consensus statement of the SIECVI

Table 1: Echocardiographic profiles and management strategies in septic shock and SCM

|Integrated echocardiographic profiles and management strategies in septic shock and SCM|||| |---|---|---|---| |Profile|Key echo/ hemodynamic features|Pathophysiology|Primary bedside therapy| |Hyperdynamic vasoplegic septic shock(“Good” $\leftrightarrow$ Profile 1)|Preserved LV systolic function; CO normal/ high; low SVR|Normal systolic function preserved contractility, EF normal; CO may still be inadequate due to vasoplegia|Antibiotics Vasopressors Cautious fluids with small boluses and reassessment. Antibiotics Vasopressors| |Hyperkinetic with vasoplegia|LV hyperkinesia; vasoplegia persists; LV end-diastolic size normal|LV hyperdynamic function hypercontractility, ↓LVESV,CO $\uparrow$ if preload normal; pseudohypertrophy; may reflect vasoplegia|Antibiotics Vasopressors Stop fluids| |Low transesis(“bad”)|Hyperkinesia with small LVED size(±LVOT obstruction)|LV hyperdynamic with LVOT obstruction: anterior mitral motion, outflow obstruction, severely↓CO despite↑EF|Antibiotics Vasopressors as needed.| |SCM(“Bad” depressed LV $\leftrightarrow$ Profile 2)|New/worsened LV dysfunction; ↓CI;↑filling pressures; high lactate|LV systolic dysfunction $\downarrow$ [ATV loss, $\downarrow$ CO; EF may appear normal if low afterload; LV dilation possible|Antibiotics Vasopressors in low CI persistarsearly echo +PAC.| |LV diastolic dysfunction in sepsis(may overlap with all patterns)|Impaired relaxation, reduced LV filling|LV diastolic dysfunction $\downarrow$ relaxation,↓LEVED,↓CO|Antibiotics Vasopressors Avoid fluid overload(CCE to guide preload).| |Septic shock with pre- existing LV dysfunction (“Ugly” or Profile 3)|Chronic cardiomyopathy/ Valvular disease; acute versus chronic overlap|Mix of chronic LV systolic/diastolic dysfunction EF often reduced, variable CO|Antibiotics Variability Vasopressors Restrictive fluids with congestion monitoring| |RV dysfunction in sepsis (may overlap with all patterns)|↓RV contractility, 1RVESV,RV dilation; ↓LV filling by ventricular interdependence|RV dysfunction $\downarrow$ contractility,RV dilation,↓LEVED,↓CO|Antibiotics Vasopressors Vasopressors in thecridity RV preload/afterload| |Primary cardiogenic shock + superimposed sepsis (Profile 4)|Primary pump failure + infection|As per LV systolic $\pm$ RV dysfunction, often severe|Optimize RV preload/afterload in severe.Pusovressors/inotropes Consider pulmonary vasodilators if severe.|

LV=Left ventricular, RV=Right ventricular, CCE-Critical care echocardiography, LVED=LV end-diastolic cavity, LVEDV=LV end-diastolic volume, LVESV=LV end-systolic volume, MCS=Mechanical circulatory support, PAC=Pulmonary artery catheter, RVESV=RV end-systolic volume, SVR=Systemic vascular resistance,EF=Ejection fraction

What Key Features to LOOK FOR?

Echocardiography plays a central role in identifying SCM.[18,19][Figure 1]. Most recent studies use echocardiography to evaluate LV systolic function, using<40%-50% as a definition for decreased LVEF. Studies have yielded mixed results with respect to the relationship between LVEF value and outcomes.A 2013 meta-analysis showed no difference in survival based on presence of low LVEF or LV dilation.[20] A challenge with using LVEF is its dependence on preload and afterload conditions.A patient with significant contractile dysfunction can appear to have a normal LVEF in a setting of hypovolemia or low mean arterial pressure, as is often the case in sepsis. LVEF can change rapidly and significantly depending on arterial pressure and volume status, without reflecting the change in true contractility of the myocardium.[21] Thus, it is not surprising that studies based on LVEF have shown such variability in prognostication.

Reduced S' on tissue Doppler imaging(TDI) is suggestive of systolic dysfunction. It can be abnormal even when EF is preserved; therefore, this parameter helps to detect early or subclinical dysfunction.

Advanced techniques, over TDI, such as speckle tracking echocardiography(STE), further enhance sensitivity for detecting myocardial impairment since it is less dependent on loading conditions and is potentially more reflective of intrinsic myocardial function.[7] STE is an advanced echocardiographic technique that analyzes the motion of natural acoustic markers, called“speckles”within the myocardium on standard 2D gray-scale images. These speckles, which represent unique interference patterns created by ultrasound scattering, are tracked frame-by-frame throughout the cardiac cycle to assess myocardial deformation in multiple directions: longitudinal, radial, and circumferential.[22,23]

Global longitudinal strain(GLS) is the most commonly used parameter.[24] Normal GLS for LV is more than-18% and for RV,more than-22%.GLS assessment is certainly desirable in subclinical, early assessment of myocardial damage as part of sepsis; the main disadvantage of such a sophisticated method is the difficult availability in the ICU. GLS demonstrated its efficacy in the early identification of cardiac injury, even in patients with mild-to-moderate COVID-19, despite preserved LVEF.[25] Moreover, studies have shown that worse GLS(less negative) is associated with higher mortality in patients with

Tescione, et al.: A consensus statement of the SIECVI

sepsis, and the same relationship was not established between mortality and LVEF.[26] A specific finding in some patients with hyperdynamic cardiac function is dynamic LVOTO,where blood rapidly flowing through an underfilled ventricle causes anterior motion of the mitral valve and obstruction of flow through the outflow tract, similar to the obstruction seen in hypertrophic obstructive cardiomyopathy. LVOTO is observed in 22%-30% of septic shock patients and can occur due to high catecholamine states, inotrope administration, and hypovolemia, and typically indicates fluid responsiveness;studies show an association between LVOTO and mortality.[26]

The assessment of diastolic function is another important issue in the context of SCM to have an indirect estimation of LV filling pressure(increased E/E'). Moreover, E' may be reduced due to inflammation and myocardial stiffness. However, since these are patients who are mechanically ventilated, it has been demonstrated that the influence of ventilation on echocardiographic parameters of systolic and diastolic function. Moreover, the failure of weaning from mechanical ventilation is associated with worse diastolic function and increased LV filling pressure.[27]

Finally, it is estimated that RV dysfunction is present in 50-55%of cases, whereas isolated RV dysfunction is present in 47% of cases.[28] RV dysfunction is defined according to the values of tricuspid annular plane systolic excursion(TAPSE), tricuspid lateral annular systolic velocity(TDIS' wave), and RV fractional area change(FAC).[29] Lanspa et al. have shown in their research that half of patients with sepsis have RV dysfunction, and it is associated with three times higher 28-day mortality.[30]

Overall, echocardiographic hallmarks of SCM include:

● Left ventricular dilatation with normal or low filling pressures

● Depressed LV and RVEF(not necessarily indicating poor prognosis). Generally, it is a reversible condition

• Absence of regional wall motion abnormalities(RWMAs),differentiating SCM from takosubro syndrome(TTS)

 Figure 1: Practical echocardiographic algorithm for suspected septic cardiomyopathy, outlining indications for echocardiography, essential transthoracic views, and characteristic diagnostic features, including left ventricular(LV) ejection fraction, LV and right ventricular function, and GLS thresholds for early detection of subclinical dysfunction

•Global systolic dysfunction rather than focal changes

● Increased end-diastolic volume suggesting elevated ventricular compliance

RV dysfunction may also be seen, particularly in patients with ARDS or sepsis-induced pulmonary hypertension● LVOT obstruction(in hyperkinetic profile).

The methodological approach for performing bedside echocardiography, together with the key diagnostic features to be identified and their corresponding cut-off values, is listed in Table 2.

How to INTERPRET THE FINDINGS AND HOW THESE FindINGS CAN GUIDE THE RATERapeutic DECISIONS?

In all patients with septic shock, an early bedside echocardiogram should be performed to evaluate biventricular function, filling pressures, and volume status.If echocardiography suggests cardiac dysfunction, further

Table 2: Standardized protocol and diagnostic thresholds for bedside echocardiographic assessment

How to perform bedside echocardiography

|Parameters|Cut- off| |---|---| |Patient position|Supine or 30° semi-recumbent position| |Probe|Use low-frequency phased array probe(2-5 MHz)| |Views to acquire|PLAX| |LV systolic function|Subcostal 4 Chamber(if other views are difficult)| |LV systolic function|IVC View (Subcostal Long Axis of IVC)| |LV systolic function|Visual EF(“eyeballing”)| |LV systolic function|EPSS>7 mm=↓EF[31]| |LV systolic function|Fractional shortening:<25% may indicate| |LV systolic function|systolic dysfunction,>45% is rare and could| |LV systolic function|reflect hyperdynamic states(e.g., early sepsis,| |anemia, thyrotoxicosis) [32]|| |Reduced S'(<6 cm/s)|| |GLS less negative than-18%(e.g.,-14%,-12%)|| |Left atrium volume(>34 mL/m2)|| |Tricuspid regurgitation velocity>2.8 m/s|| |TDI E' velocity<10 cm/s in the lateral annulus and<7 cm/s in the septal annulus|| |E/e' ratio>13 in the lateral annulus and>15 in|| |the septal annulus.[6]|| |RV function[34]|TAPSE<16 mm| |RV FAC<35%|RV FAC<35%| |RV data status|RV:LV ratio(>1=RV dilatation)| |(Preload), IVC dia/|(TDI S' wave)<15 cm/s| |collapse|>2.1 cm and<50% collapse=high RA pressure| |Pericardial|Echo free space around heart| |effusion|| |LVOT VTI[35,36]|LVOT- VTI< 14 c is suggestive of low cardiac output|

Tescione,et al::A consensus statement of the SIECVI

evaluation should exclude acute coronary syndrome and stress cardiomyopathy. Serial echocardiograms should be used to monitor response to therapy and adjust treatment dynamically.[37][Figure 2].

Tailored hemodynamic support depending on the echocardiographic profile

● LV systolic dysfunction: Consider inotropes if hypoperfusion persists despite adequate volume resuscitation. There is an important clinical implication, as catecholamine administration typically worsens the obstruction,resulting in unintended worsening of hemodynamic status.Vasopressin instead of adrenergic agents could be used in these patients. Beta-blockers are also a plausible treatment for this patient group, as they are recommended for the treatment of LVOTO in other conditions

RV dysfunction: Optimize preload and avoid excessive fluid administration; consider pulmonary vasodilators in selected cases

Normal systolic function with vasoplegia: Prioritize vasopressor support and limit inotropes.

Interpret and integrate data

In addition to guiding therapy, echocardiographic findings should be interpreted in the context of the differential diagnosis:

● Exclude ischemia: RWMAs confined to a coronary artery territory, in a patient with cardiovascular risk factors and/or typical symptoms, supported by electrocardiogram changes and elevated troponin, suggest ischemic cardiomyopathy(ICM)rather than SCM. In this setting, segmental impairment of strain parameters, with non-uniform reduction of GLS,reinforces the suspicion of ischemia[38,39]

● Exclude TTS: Stress-induced cardiomyopathy should be considered when RWMAs extend beyond a single coronary distribution, typically with apical ballooning and relative basal hyperkinesis. On strain analysis,GLS shows marked apical dysfunction with preserved basal segments, distinguishing TTS from the globally depressed strain pattern seen in SCM[40,41]

•Assess volume status to guide resuscitation

● Tailor therapy according to the dominant pathophysiological profile.

Repeat scans

● Perform follow-up echocardiograms whenever clinical status changes

● Document reversibility, typically within 7-10 days, which is a hallmark of SCM and TTS, but less characteristic of ischemic injury[34,42]

● Track response to therapy and adjust hemodynamic support accordingly.

How to Deal with DiAGNOSTIC UNCERTAINTY IN SEptic CARDIOMYOPATHY?

In patients with sepsis, bedside echocardiography is an essential tool for differentiating SCM, stress-induced

cardiomyopathy, or TTS, and ICM. Although all these conditions may present with acute left ventricular dysfunction,their echocardiographic patterns and clinical implications differ significantly.

Echocardiography-Guided Management Algorithm

Initial Assessment

Early bedside echo should be performed to evaluate biventricular function, filling pressures, volume status. If echo suggest cardiac dysfunction, further evaluation should exclude acute coronary syndrome.

Tailored Hemodynamic Support

LV systolic disfunction: If hypoperfusion persists despite adequate volume resuscitation, consider inotropes.

RV dysfunction: optimize preload and avoid excessive fluid administration; consider pulmonary vasodilators in selected cases.

Normal systolic function with vasoplegia:prioritize vasopressor support and limit inotropes.

Serial Monitoring

Serial echocardiograms should be used to monitor response to therapy and adjust treatment dynamically.

Figure 2: Echocardiography-guided management pathway for septic cardiomyopathy, emphasizing early evaluation of biventricular function,individualized hemodynamic interventions according to systolic dysfunction or vasoplejia, and repeated echocardiographic monitoring to adapt therapy over time

 Figure 3: Takotsubo syndrome: typical apical ballooning

  Figure 4: Left ventricular dysfunction in septic cardiomyopathy

Tescione, et al.: A consensus statement of the SIECVI

Takotsubo Syndrome Ischemic Cardiomyopathy Pico Strain Si Pico Costrain Si ANT SEPT ANT SEPT-14-14 ANT SEPT-15-15 ANT SEPT-13-15-15-15-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16-15-16

Figure 5: The global longitudinal strain bull's eyes show the typical circumferential pattern of left ventricular strain in takotsubo syndrome(right). This pattern is markedly different from the recognized pattern in anterior AMI(center) where strain alterations reflect site of coronary occlusion and from septic cardiomyopathy(left) showing diffuse reduction of longitudinal strain

Classical echocardiographic hallmarks of takotsubo syndrome

● Presence of RWMAS that extend beyond a single coronary artery territory, most commonly manifesting as apical ballooning[Figure 3 and Video 1]

• Akinesis or hypokinesis of the mid-to-apical segments of the left ventricle with preserved of hypercontractile basal segment[41] whereas in SCM ventricular function is globally depressed[Figure 4 and Video 2]

•RV function is often preserved in TTS, distinguishing it from SCM, where biventricular dysfunction is more frequent.[43]

Even in this clinical scenario, STE adds diagnostic value. In TTS, GLS typically reveals a distinctive reduction in apical strain with relative preservation of basal function, unlike the globally depressed strain seen in SCM.[40,41] SCM is characterized by diffuse, reversible myocardial dysfunction with impairment of GLS across all segments, without respect for coronary distributions.[42] ICM is usually associated with RWMs confined to a coronary artery territory, and segmental strain values reflect the distribution of ischemia.GLS is reduced in a non-uniform manner, mirroring regional involvement, whereas in SCM the impairment is global and homogeneous.[38,39] This distinction is crucial, as ischemic injury implies underlying coronary pathology requiring specific therapeutic interventions, whereas SCM and TTS are generally transient and reversible conditions[Figure 5].

CONCLUSION

SCM remains a challenging and often underrecognized complication of sepsis. Echocardiography, particularly at the bedside, plays a central role in identifying SCM and guiding hemodynamic management, permitting a targeted therapy.Its noninvasive nature, ease of use, and ability to guide hemodynamic management(e.g. fluid response, inotropes)make it a first-line modality. Transthoracic echocardiography is not only a reliable snapshot tool but also effective in monitoring cardiac output trends over time in critically ill patients, especially valuable when pulmonary artery catheter

<EndOfPara>placement is contradicated or not feasible. Standardized use of echocardiographic algorithms may enhance diagnostic accuracy,enable individualized therapy,improving outcomes in this critically ill population.

Financial support and sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.

REFERENCES

1.Evans L, Rhodes A, Alzazhan W, Antonelli M, Coopersmith CM,French C, et al. Surviving sepsis campaign: International guidelines for management of sepsis and septic shock 2021. Intensive Care Med 2021;47:1181-247.

2.Carbone F, Liberale L, Preda A, Schindler TH, Montecucco F. Septic cardiomyopathy: From pathophysiology to the clinical setting. Cells 2022;11:2833.

3.MacLean LD, Mulligan WG, McLean AP, Duff JH. Patterns of septic shock in man- A detailed study of 56 patients. Ann Surg 1967;166:543-62.

4.Parker MM, Shelhamer JH, Bacharach SL, Green MV, Natanson C,Frederick TM, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med 1984;100:483-90.

5.Sato R,Kuriyama A,Takada T, Nasu M, Luthe SK. Prevalence and risk factors of sepsis-induced cardiomyopathy: A retrospective cohort study.Medicine (Baltimore) 2016;95:e5031.

6.Zakynthinos GE, Giamouzis G, Xanthopoulos A, Oikonomou E,Kalogeras K, Karavidas N, et al. Septic cardiomyopathy: Difficult definition, challenging diagnosis, unclear treatment. J Clin Med 2025;14:986.

7. Lima MR, Silva D. Septic cardiomyopathy: A narrative review. Rev Port Cardiol 2023;42:471-81.

8. Lukie I, Mihie D, Varziic SC, Relatiic KS, Zibar L, Loinjak D, et al.Septic cardiomyopathy: From cardiomyopathy: Rev Cardiovasc Med 2024;25:23.

9.Lin YM, Lee MC, Toh HS, Chang WT, Chen SY, Kuo FH, et al.Association of sepsis-induced cardiomyopathy and mortality:A systematic review and meta-analysis.Ann Intensive Care 2022;12:112.

10. Sato R, Nasu M. A review of sepsis-induced cardiomyopathy. J Intensive Care 2015;3:48.

11.Ehrman RR, Sullivan AN, Favot MJ, Sherwin RL, Reynolds CA,Abidov A, et al. Pathophysiology, echocardiographic evaluation,biomarker findings, and prognostic implications of septic cardiomyopathy: A review of the literature. Crit Care 2018;22:112.

12. Mercado P, Maizel J, Beyls C, Titeca-Beauport D, Joris M, Kontar L,et al. Transthoracic echocardiography: An accurate and precise method

Tescione, et al.: A consensus statement of the SIECVI

for estimating cardiac output in the critically ill patient. Crit Care 2017;21:136.

13. Porter TR, Shillcutt SK, Adams MS, Desjardins G, Glas KE, Olson JJ,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 2015;28:40-56.

14. Geri G, Vignon P, Aubry A, Fedou AL, Charron C, Silva S, et al.Cardiovascular clusters in septic shock combining clinical and echocardiographic parameters: A post hoc analysis. Intensive Care Med 2019;45:657-67.

15. Aneman A, Vieillard-Baron A. Cardiac dysfunction in sepsis. Intensive Care Med 2016;42:2073-6.

16. Messina A, Vieillard-Baron A. How we could use critical care echocardiography in the assessment of and management of cardiovascular phenotypes in septic shock: The good, the bad, and the ugly profiles. Intensive Care Med 2025;51:397-400.

17. Sato R, Hasegawa D, Guo S, Nuqali AE, Moreno JE. Sepsis-induced cardiogenic shock: Controversies and evidence gaps in diagnosis and management. J Intensive Care 2025;13:1.

18. Burkhoff D, Mirsky I, Suga H. Assessment of systolic and diastolic ventricular properties via pressure-volume analysis: A guide for clinical,translational, and basic researchers. Am J Physiol Heart Circ Physiol 2005;289:H501-12.

19. Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C,et al. Consensus on circulatory shock and hemodynamic monitoring.Task force of the European Society of Intensive Care Medicine.Intensive Care Med 2014;40:1795-815.

20. Huang SJ, Naol M, McLean AS. Is early ventricular dysfunction or dilatation associated with lower mortality rate in adult severe sepsis and septic shock? A meta-analysis. Criti Care 2013;17:896.

21. Weng L, Liu YT, Du B, Zhou JF, Guo XX, Peng JM, et al. The prognostic value of left ventricular systolic function measured by tissue Doppler imaging in septic shock. Crit Care 2012;16:R71.

22. Collier P, Phelan D, Klein A. A test in context: Myocardial strain measured by speckle-tracking echocardiography. J Am Coll Cardiol 2017;69:1043-56.

23. Fujikura K, Makiya M, Farooq M, Xing Y, Humphrey W,Mustehsan MH, et al. Speckle-tracking echocardiography with novel imaging technique of higher frame rate. J Clin Med 2021;10:2095

24 El Mokadem M, El Maraghi S, El Hosseiny R, Moawad A, Yassin A.The usefulness of strain echocardiography as diagnostic and prognostic index of cardiac dysfunction in septic patients in correlation with cardiac biomarkers. J Cardiovasc Echogr 2024;34:114-9.

25. Mansour H, Abdelhady AO, Reheim WA, William V. Can global longitudinal strain assess asymptomatic subtle left ventricular dysfunction in recovered COVID-19 patients? J Cardiovasc Echogr 2023;33:183-8.

26. Elhadidy S. Dynamic left intraventricular obstruction in patients with septic shock: Pathogenic role and prognostic implications. Res Opin Anesth Intensive Care 2019;6:424-8.

23. Sanfilippo F, Di Falco D, Noto A, Santonocito C, Morelli A, Bignami E,et al. Association of weaning failure from mechanical ventilation with transformacic echocardiography parameters: A systematic review and meta-analysis. Br J Anaesth 2021;126:319-30.

28. Vallabajosyula S, Kumar M, Pandompatam G, Sakhuja A, Kashyap R,Kashani K, et al. Prognostic impact of isolated right ventricular dysfunction in sepsis and septic shock: An 8-year historical cohort study. Ann Intensive Care 2017;7:94.

29. Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD,Chandrasekaran K, 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;23:685-713.

30. Lanspa MJ, Cirulis MM, Wiley BM, Olsen TD, Wilson EL, Beesley SJ,et al. Right ventricular dysfunction in early sepsis and septic shock.Chest 2021;159:1055-63.

31. McKaigney CJ, Krandt MJ, La Rocque CL, Hurst ND, Buchanan MS,Kendall JL. E-point septal separation: A bedside tool for emergency physician assessment of left ventricular ejection fraction. Am J Emerg Med 2014;32:493-7.

23. Johansson Blipt, Chew MS, Ahman R, de Geer L, Blomqvist L,Astrm Aneq M, et al. Left ventricular longitudinal wall fractional shortening accurately predicts longitudinal strain in critically ill patients with septic shock. Ann Intensive Care 2021;11:52.

33. Nagueh SF, Smiseth OA, Appleton CP, Byrd BF 3rd, Dokainish H,Edrwards T, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2016;17:1321-60.

34. L'Heureux M, Sternberg M, Brath L, Turlington J, Kashiouris MG.Sepsis-induced cardiomyopathy: A comprehensive review. Curr Cardiol Rep 2020;22:35.

35. Wang J, Zhou D, Gao Y, Wu Z, Wang X, Lv C. Effect of VTILVOT variation rate on the assessment of fluid responsiveness in septic shock patients. Medicine(Baltimore) 2020;99:e22702.

36. Sasidharan P, Kaaley N, Sharma P, Jain G, Shankar T, Jayachandran S,et al. The left ventricular outflow tract velocity time integral as a predictor of fluid responsiveness in patients with sepsis-related acute circulatory failure. Cureus 2025;17:e77353.

37. Sweeney DA, Wiley BM. Integrated multiorgan bedside ultrasound for the diagnosis and management of sepsis and septic shock. Semin Respir Crit Care Med 2021;42:641-9.

38.Mohamed MA,Abd-elmelon Mohamed A, Hammoda MA, Sabry AM.Role of Speckle Tracking Echocardiography in Differentiating between Ischemic and Non-ischemic Cardiomyopathy. Int J Cardiovasc Acad 2024;10:1-6.[doi:10.4274/ijca.2023.18209].

39. Smiseth OA, Rider O, Cvijic M, Valkovic L, Remme EW, Voigt JU Myocardial strain imaging: Theory, current practice, and the future.JACC Cardiovasc Imaging 2025;18:340-81.

40. Sanfilippo F, Corredor C, Fletcher N, Tritapepe L, Lorini FL,Arcardiapane A, 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;22:183.

41. Omar T, Inci K, Olfu Y, Dilek M, Celik ZB, Kina S, et al. The predictive value of left ventricular global longitudinal strain in normotensive critically ill septic patients. Crit Care Sci 2023;35:187-95.

42. Fu X,Lin X,Seery S,Zhao LN,Zhu HD,Xu J,et al. Speckle-tracking echocardiography for detecting myocardial dysfunction in sepsis and septic shock patients: A single emergency department study. World J Emerg Med 2022;13:175-81.

43. Hiraiwa H, Kasugai D, Okumura T, Murohara T. Clinical implications of septic cardiomyopathy: A narrative review. Medicine(Baltimore)2024;103:e37940.

相关指南

• 2026 AHA科学声明：儿童心肌病的体育活动-运动健康 · 心血管内科 2026
• 2025 HFA／EAPC 临床共识声明：癌症患者和幸 存者与癌症治疗相关的心功能障碍和心力衰竭的预防 · 心血管内科 2025
• 2024 HFSA科学声明：心力衰竭的器械治疗（更新版） · 心血管内科 2024
• 2024 ACC专家共识决策路径：心肌炎诊断和管理的策略与标准 · 心血管内科 2024
• AHA／ACC／AMSSM／HRS／PACES／SCMR：肥厚型心肌病的管理指南2024 · 心血管内科 2024
• 2025 HFA／H FAI科学声明：SG LT2抑制 剂用于预防 和治疗心力衰竭 · 心血管内科 2025
• 2024 AHA科学声明：晚期心力衰竭患者肾功能不全的评估和管理 · 心血管内科 2024
• 2025 EMN共识声明：功能性高危多发性骨髓瘤 · 血液内科 2025