Abstract
Background
Persistent tachycardia in septic shock is associated with adverse outcomes, yet optimal management remains uncertain. Esmolol, a short-acting β1-selective blocker, has been investigated as a strategy to control heart rate and attenuate excessive sympathetic activation. This systematic review and meta-analysis evaluated the efficacy of esmolol in adult patients with septic shock.
Methods
A comprehensive search of PubMed/MEDLINE, Cochrane Central, and Google Scholar was conducted from database inception to March 28, 2025. Reference lists and clinical trial registries were also screened. Randomized controlled trials comparing esmolol plus standard care with standard care alone in adults with septic shock were included. The primary outcome was 28-day mortality. Secondary outcomes included heart rate, mean arterial pressure (MAP), and lactate.
Results
Three randomized controlled trials involving 314 patients were included. Esmolol was associated with a significant reduction in 28-day mortality (OR 0.33, 95% CI 0.20–0.53; I2 = 0%). Heart rate was significantly reduced at both 24 h (day 1) (MD − 8.50 bpm, 95% CI − 10.82 to − 6.17) and 48 h (day 2) (MD − 16.60 bpm, 95% CI − 20.03 to − 13.17). No statistically significant difference in MAP was observed between groups (MD 0.10 mmHg, 95% CI − 3.46 to 3.66; I2 = 53%). Although the included studies did not report clinically meaningful differences in lactate levels, differences in outcome reporting precluded quantitative synthesis.
Conclusions
Esmolol therapy may improve heart rate control and reduce 28-day mortality in carefully selected patients with septic shock without adversely affecting MAP. However, these findings should be interpreted cautiously because they are based on a limited number of randomized trials and are subject to clinical heterogeneity and potential risk of bias. Larger, high-quality randomized controlled trials are needed to confirm these findings and define the optimal use of esmolol in septic shock.
Systematic review registration
The review protocol was registered with PROSPERO (CRD42024584599).
Supplementary Information
The online version contains supplementary material available at https://doi.org/10.1186/s13643-026-03260-4.
Keywords: Esmolol, Septic shock, Mortality, Mean arterial pressure, β-Blockers, Tachycardia
Introduction
Septic shock remains a major cause of morbidity and mortality in critically ill patients, despite advances in early recognition and management. A dysregulated immune response to infection can lead to septic shock, a life-threatening condition associated with mortality rates ranging from 15% in sepsis without shock to up to 56% in patients with septic shock [1, 2]. Current management strategies focus on early antimicrobial therapy, fluid resuscitation, and vasopressor support to maintain adequate perfusion. However, persistent tachycardia following initial resuscitation is frequently observed and has been associated with worse clinical outcomes.
The pathophysiology of septic shock involves activation of the sympathetic nervous system and increased catecholamine release, which stimulates β-adrenergic receptors in the heart, leading to increased heart rate, cardiac output, and myocardial oxygen demand [3, 4]. While this response is initially compensatory, excessive and prolonged β-adrenergic stimulation may contribute to septic myocardial dysfunction, arrhythmias, and cardiovascular instability. This excessive stimulation of β-adrenergic receptors driven by β-adrenergic agonists may contribute to cardiovascular collapse, organ dysfunction, and mortality in patients with sepsis and septic shock [3–6].
There is conflicting evidence regarding the role of β-blockers in this setting. On one hand, β-blockers may mitigate harmful sympathetic overactivation by reducing heart rate, improving diastolic filling, and decreasing myocardial oxygen consumption. Esmolol, a short-acting and selective β1-adrenergic blocker, has been proposed as a potentially advantageous agent due to its rapid onset and titratability, allowing for precise heart rate control with minimal impact on blood pressure [4, 7]. Additionally, β-adrenergic blockade has been associated with modulation of inflammatory cytokine production and may contribute to improved hemodynamic stability and clinical outcomes [8–10].
On the other hand, concerns remain regarding the safety of β-blocker use in septic shock, particularly the risk of hypotension and impaired tissue perfusion in hemodynamically unstable patients [11]. These competing physiological effects contribute to ongoing uncertainty regarding the clinical role of β-blockers in septic shock.
Recent randomized trials and meta-analyses have explored the use of β-blockers in septic shock, with some suggesting a potential mortality benefit, particularly with esmolol [12–18]. However, these studies vary in terms of patient populations, timing of initiation, and outcome definitions. Furthermore, several recent meta-analyses included heterogeneous β-blocker agents or relied heavily on studies conducted in China and published in non-English languages, which may limit the generalizability of the findings to the septic shock population in other geographic regions, given variation in demographics and clinical practice.
Therefore, an updated and focused synthesis of randomized controlled trials evaluating esmolol specifically is warranted. This systematic review and meta-analysis aim to evaluate the efficacy of esmolol in reducing 28-day mortality and improving hemodynamic parameters in patients with septic shock, while addressing inconsistencies in the current literature and providing a clinically relevant interpretation of the available evidence.
Methods
This meta-analysis was conducted following the recommendations and checklist of the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) statement [19]. The protocol was registered with PROSPERO (registration number CRD42024584599). The completed PRISMA checklist is available in Supplementary Table S1 (Appendix 1).
Search strategy
We searched PubMed/MEDLINE and Cochrane from inception to 28 March 2025. The search was conducted without language restrictions; however, only English-language studies were included in the final analysis due to feasibility constraints. We also searched Google Scholar, the International Clinical Trials Registry Platform (ICTRP), the US Clinical Trials Registry, the Australian New Zealand Clinical Trials Registry (ANZCTR), the Clinical Trial Registry in Japan, the International Standard Randomized Controlled Trial Number Registry (ISRCTN registry), EU Clinical Trials, Nederland’s Trial Register, and the bibliographies of the included studies and recent review articles to identify any additional relevant studies. The keywords used for the search included esmolol, sepsis, septic shock, and β-blockers; further details on the search strategies are available in the Supplementary Materials (Appendix 2).
Eligibility criteria
Studies were eligible for inclusion if they met the following criteria: (1) enrolled adult patients with septic shock and tachycardia; (2) evaluated esmolol administration; (3) included a comparator group receiving standard therapy without esmolol; (4) reported the primary outcome of 28-day mortality and/or secondary outcomes including heart rate, mean arterial pressure (MAP), or lactate levels; and (5) were randomized controlled trials (RCTs).
Studies were excluded if they: (1) did not involve patients with septic shock; (2) compared esmolol with another β-blocker or active pharmacologic intervention rather than standard therapy; (3) did not provide sufficient data for extraction and quantitative synthesis of the predefined outcomes, including studies in which outcome data were unavailable, incompletely reported, or not extractable from the published report; or (4) were non-randomized studies, observational studies, duplicate publications, conference abstracts without sufficient data, or other non-full-text publications.
Data extraction and quality assessment
Two reviewers independently screened the titles and abstracts, followed by a full-text review of potentially eligible studies. Data were extracted using a standardized form that included study characteristics, participant demographics, intervention details, and outcome measures.
Risk of bias was assessed using the Cochrane Risk of Bias 2 (RoB 2) tool [20], specifically for the primary outcome of 28-day mortality. Five domains were evaluated, including bias arising from the randomization process, deviations from intended interventions, missing outcome data, outcome measurement, and selection of the reported result. Domain-level assessments and supporting justifications are provided in Supplementary Table S2 (Appendix 2).
Data synthesis
The meta-analysis was conducted using Review Manager (RevMan) version 5.4.1. Dichotomous outcomes were analyzed using the Mantel–Haenszel method and reported as odds ratios (ORs) with 95% confidence intervals (CIs), whereas continuous outcomes were analyzed using the inverse-variance method and reported as mean differences (MDs) with 95% CIs. When outcomes were reported at multiple time points, the most consistently reported time point across studies was selected for each outcome. For MAP analyses, approximately 48-h (day 2) measurements were preferentially selected. For lactate, the same time point was prespecified; however, quantitative synthesis was only performed when comparable data were available. Heart rate was analyzed separately at 24 h (day 1) and 48 h (day 2) when sufficient data were available. Statistical heterogeneity was assessed using the I2 statistic, with values of 25%, 50%, and 75% considered indicative of low, moderate, and substantial heterogeneity, respectively. A fixed-effect model was used when heterogeneity was low, whereas a random-effects model was applied in the presence of substantial heterogeneity.
Results
Description of the characteristics of the included articles
Our systematic search identified 268 records, including 205 from Google Scholar, 47 from the Cochrane Library, and 16 from PubMed. After removing 38 duplicate records, 230 records remained for title and abstract screening. Of these, 203 records were excluded because they did not meet the predefined eligibility criteria. The remaining 27 reports underwent full-text eligibility assessment, of which 24 were excluded for reasons outlined in the PRISMA flow diagram (Fig. 1), including inappropriate study design, lack of trial registration with published results, incorrect population, or incorrect intervention. Ultimately, three RCTs involving 314 participants were included in the systematic review and meta-analysis. The characteristics of the included studies are summarized in Table 1.
Fig. 1.
Flow diagram for selection of studies included in the systematic review and the meta-analysis. *Studies classified as “Outcome data unavailable or not extractable” included reports in which predefined outcomes were not reported in sufficient detail for quantitative synthesis
Table 1.
The characteristics of the included studies
| Study | Population | Number of participants | Intervention | Target heart rate | Key outcomes reported |
|---|---|---|---|---|---|
| Gadallah et al. 2020 [15] | Patients with sepsis/septic shock admitted to ICU | 60: 30 esmolol, 30 control | Standard sepsis care plus IV esmolol infusion, starting at 0.05–0.2 mg/kg/min and titrated every 20 min | Not clearly prespecified; esmolol held if HR < 55 bpm with hypotension | 28-day mortality, HR, MAP, CVP, ScvO2, lactate, SOFA score, ICU stay |
| Morelli et al. 2013 [7] | Patients with septic shock and persistent tachycardia requiring norepinephrine | 154: 77 esmolol, 77 control | Continuous IV esmolol infusion added to standard care | 80–94 bpm | 28-day mortality, HR, MAP, norepinephrine dose, lactate AUC, stroke volume index, cardiac index, adverse events |
| Wang et al. 2023 [14] | Patients with sepsis-induced cardiomyopathy and tachycardia | 100: 50 esmolol, 50 control | Standard care plus IV esmolol for septic cardiomyopathy | 80–100 bpm | 28-day and 90-day mortality, HR, MAP/MBP, lactate, GLS, LVEF, GEF, dP/dtmax, norepinephrine dose, ICU/hospital stay |
Bias evaluation
Three randomized controlled trials were included in this systematic review. Risk of bias for the primary outcome (28-day mortality) was assessed using the Cochrane RoB 2 tool. Two studies [7, 15] were judged to have some concerns regarding risk of bias primarily due to insufficient reporting of allocation concealment and limited information to fully assess certain RoB 2 domains. In particular the absence of publicly available study protocols or statistical analysis plans limited the assessment of bias in the selection of the reported result. Although [7] was an open-label study, 28-day mortality is an objective outcome and therefore unlikely to be substantially affected by detection bias. Nevertheless, the lack of blinding may have introduced performance bias through differences in concurrent clinical management or co-interventions.
Wang et al.’s trial was judged to be at low risk of bias across all RoB 2 domains, with adequate reporting of randomization procedures, outcome assessment, and analysis methods. In addition, although the included studies did not provide detailed participant flow diagrams or explicit information regarding loss to follow-up, all randomized participants appeared to be accounted for in the reported outcome analyses, suggesting a low likelihood of bias arising from missing outcome data.
A summary of the risk of bias assessment for the included randomized controlled trials is presented in Fig. 2, and detailed domain-level justifications are provided in Supplementary Table S2.
Fig. 2.
Risk of bias assessment for the primary outcome (28-day mortality) using the Cochrane RoB 2 tool
Primary outcome
28-day mortality
Three studies were included in the analysis of the primary outcome (28-day mortality) [7, 14, 15], with a total of 314 participants.
The pooled analysis demonstrated a reduction in 28-day mortality odds with esmolol treatment compared to the control group, with an overall effect of 0.33 (95% CI 0.20, 0.53) (Fig. 3). I2 = 0% indicates low heterogeneity between the studies included in the meta-analysis.
Fig. 3.
28-day mortality risk in the esmolol versus the control group
Secondary outcomes
Day 1 heart rate
Two studies were included in the analysis of heart rate at day 1 [7, 15], totaling 210 participants. The pooled analysis demonstrated a significant reduction in HR upon treatment with esmolol compared to the control group with an overall mean difference of − 8.50 (95% CI − 10.82, − 6.17) (Fig. 4). I2 = 0% demonstrates low heterogeneity between the studies included in the meta-analysis.
Fig. 4.
Forest plot comparing heart rate at day 1
Day 2 heart rate
Two studies were included in the analysis of heart rate at day 2 [14, 15], with a total of 160 participants. The pooled analysis demonstrated a significant reduction in heart rate upon treatment with esmolol compared to the control group, with an overall mean difference of − 16.60 (95% CI − 20.03, − 13.17) (Fig. 5). I2 = 0% demonstrates low heterogeneity between the studies included in the meta-analysis.
Fig. 5.
Forest plot comparing heart rate at day 2
Lactate level
Only one study (Gadallah et al.) reported extractable between-group mean ± SD data for lactate at the predefined day 2 (approximately 48-h) time point. Although the remaining studies evaluated lactate, the outcome was reported using different summary measures and reporting formats, precluding quantitative synthesis. Therefore, a meta-analysis of lactate was not performed, and the findings were summarized narratively. The available studies did not report clinically meaningful differences in lactate levels between the esmolol and control groups.
MAP
Two studies [15] and [14] involving 160 participants were included in the MAP analysis.Morelli et al. reported MAP graphically and did not provide directly extractable patient-level measures of variability at the predefined 48 -h time point; therefore, the study was not included in the quantitative MAP synthesis.
No statistically significant difference in MAP was observed between the esmolol and control groups (MD 0.10 mmHg, 95% CI − 3.46 to 3.66; Fig. 6). Moderate heterogeneity was observed across studies (I2 = 53%); therefore, a random-effects model was used. These findings suggest that esmolol therapy did not adversely affect MAP compared with standard care (Fig. 6).
Fig. 6.
Forest plot comparing MAP at 48 h (day 2) between the esmolol and control groups
Discussion
This systematic review and meta-analysis evaluated the efficacy of esmolol in patients with septic shock. Our findings suggest that esmolol administration may be associated with improved selected clinical outcomes, including reduced odds of 28-day mortality and effective heart rate control. Specifically, esmolol treatment was associated with significantly lower odds of 28-day mortality compared with standard care while achieving significant reductions in heart rate without evidence of adverse effects on MAP. Although the available studies reporting lactate did not suggest clinically meaningful differences between treatment groups, differences in outcome reporting precluded quantitative synthesis of this outcome. Given the limited number of included studies, relatively small sample size, and clinical heterogeneity across trials, these findings should be interpreted with caution and considered hypothesis-generating rather than definitive evidence of clinical benefit.
Several mechanisms may explain the observed benefits of esmolol in septic shock. Excessive sympathetic activation and persistent tachycardia are common features of septic shock and have been associated with increased myocardial oxygen consumption, impaired diastolic filling, myocardial dysfunction, and adverse clinical outcomes. By selectively blocking β1-adrenergic receptors, esmolol may attenuate harmful catecholamine-mediated effects while preserving adequate systemic perfusion. Consistent with this proposed mechanism, our analysis demonstrated significant reductions in heart rate without affecting MAP, suggesting that heart rate control may be achieved without compromising hemodynamic stability in appropriately selected patients. Although the included studies generally reported stable lactate concentrations during esmolol therapy, variability in outcome reporting prevented formal quantitative evaluation.
Our findings are generally consistent with previous systematic reviews and meta-analyses evaluating β-blockers in septic shock.Vásquez-Tirado et al. included nine randomized controlled trials involving 1121 patients and reported reduced overall mortality among patients receiving β-blockers, with the mortality benefit primarily driven by the esmolol subgroup rather than the landiolol subgroup [16]. Similarly, Huang et al. demonstrated that ultrashort-acting β-blockers reduced 28-day mortality in patients with persistent tachycardia after initial resuscitation, with the benefit observed predominantly among patients receiving esmolol [17]. Another esmolol-focused meta-analysis byHuang et al. also reported reduced 28 -day mortality but included a substantial number of non-English publications, most of which were conducted in China [18].
Compared with previous systematic reviews and meta-analyses, our study provides a more focused evaluation of esmolol by restricting inclusion to randomized controlled trials evaluating esmolol specifically and excluding studies involving other β-blockers with different pharmacologic properties. Previous reviews combined evidence from esmolol with other ultrashort-acting β-blockers, introducing additional clinical heterogeneity related to pharmacologic characteristics, treatment protocols, and patient populations. In contrast, our review synthesized only randomized evidence specific to esmolol, providing a treatment-specific assessment of its efficacy and safety in septic shock. By focusing on English-language randomized controlled trials, our review also provides an updated synthesis of the currently accessible evidence for international readers.
Despite the observed mortality benefit, the clinical applicability of esmolol in septic shock remains uncertain. Persistent tachycardia may represent either a maladaptive consequence of excessive sympathetic activation or a compensatory mechanism required to maintain adequate cardiac output. Accordingly, the optimal timing of initiation, target heart rate, therapy duration, and patient selection remain incompletely defined.
Important clinical differences existed among the included studies. Wang et al. enrolled patients with sepsis-induced cardiomyopathy, whereas the remaining studies included broader populations with septic shock and persistent tachycardia. Furthermore, esmolol dosing regimens, titration strategies, therapeutic heart-rate targets, and outcome reporting varied across studies. These differences may have contributed to clinical heterogeneity and should be considered when interpreting the pooled estimates.
Several limitations should be acknowledged. First, only three randomized controlled trials involving 314 participants were included, limiting the precision and certainty of the pooled estimates. Second, our review was restricted to English-language publications, thereby excluding several studies conducted predominantly in China, where esmolol has been more extensively investigated. Third, although all included studies reported hemodynamic parameters such as cardiac index (CI) and stroke volume index (SVI), these outcomes were not prespecified in our registered protocol and were therefore not quantitatively synthesized. Additionally, variability in measurement methods, outcome definitions, and reporting time points prevented meaningful pooling of several secondary outcomes, including lactate. Fourth, selective outcome reporting cannot be ruled out, as some clinically relevant outcomes were incompletely reported. Finally, differences in concomitant therapies, including vasopressor administration, fluid resuscitation strategies, and other aspects of septic shock management, may have influenced patient outcomes and could not be fully accounted for.
The risk of bias should also be considered when interpreting these findings. Two studies were judged to have some concerns regarding risk of bias, primarily because of insufficient reporting of allocation concealment and the absence of publicly available study protocols or statistical analysis plans, limiting assessment of selective reporting. One study was judged to be at low risk of bias across all domains. Although 28-day mortality is an objective outcome and therefore less susceptible to detection bias, performance bias related to differences in co-interventions and clinical management cannot be excluded. Consequently, confidence in the pooled estimates remains limited.
From a clinical perspective, esmolol may be considered in carefully selected patients with septic shock and persistent tachycardia following adequate fluid resuscitation and hemodynamic stabilization. However, the current evidence is insufficient to support its routine use in all patients with septic shock.
Larger, adequately powered randomized controlled trials are needed to better define the optimal patient population, the timing of initiation, the target heart rate, the duration of therapy, and the impact on clinically meaningful outcomes. Future studies should also adopt standardized definitions, measurement methods, and reporting of hemodynamic outcomes to facilitate more comprehensive and reliable evidence synthesis.
Conclusion
This systematic review and meta-analysis suggest that esmolol may be associated with improved selected clinical outcomes in patients with septic shock, including a potential reduction in 28-day mortality and effective heart rate control without evidence of adverse effects on MAP. Although the available studies reporting lactate did not suggest clinically meaningful differences between treatment groups, heterogeneity in outcome reporting precluded quantitative synthesis of this outcome.
These findings should be interpreted with caution because they are based on only three RCTs involving 314 participants and are subject to clinical heterogeneity and potential risk of bias. Furthermore, the optimal timing of initiation, target heart rate, duration of therapy, and patient selection for esmolol remain uncertain.
Additional large, high-quality randomized controlled trials are needed to confirm these findings, establish optimal treatment strategies, and standardize the measurement and reporting of hemodynamic outcomes to facilitate more robust evidence synthesis.
Supplementary Information
Acknowledgements
Not applicable.
Registration
The review protocol was registered with PROSPERO (CRD42024584599).
Authors’ contributions
All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Funding
The preparation of this study was not supported by any external funding.
Data availability
The data supporting the findings of this review will be made available by the corresponding author upon request.
Declarations
Ethics approval and consent to participate
Not applicable.
Competing interests
The authors declare no conflicts of interest.
Footnotes
Publisher's Note
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The data supporting the findings of this review will be made available by the corresponding author upon request.