Hemodynamic response to β-blockers in severe sepsis and septic shock: A review of current literature

Loon, Lex M. van; Hoeven, Johannes G. van der; Lemson, Joris

doi:10.1016/j.jcrc.2018.12.003

Cited by 18 publications

(13 citation statements)

References 64 publications

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“…Excessive catecholamine levels may also play an important role in sepsis-related cardiac dysfunction by causing cardiomyopathy and cardiomyocyte necrosis [5, 7]. β-adrenergic blockade could reduce the amount of exogenous catecholamines used by restoring sepsis-induced downregulation of β-adrenergic receptors [12, 30]. Four of the included studies in this systematic review, however, found that premorbid β-blocker exposure was not associated with a significant difference in vasopressor requirements during sepsis.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, some studies have suggested a benefit of premorbid β-blocker exposure on sepsis outcomes [10, 11]. Multiple systematic reviews have since concluded that there is limited preliminary evidence for the use of β-blockers during sepsis [12–14], while others are skeptical [15]. However, to date, no published systematic review exists on the effects of premorbid β-blocker exposure on sepsis outcomes, including mortality.…”

Section: Introductionmentioning

confidence: 99%

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The association between premorbid beta blocker exposure and mortality in sepsis—a systematic review

et al. 2019

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Background The effect of premorbid β-blocker exposure on clinical outcomes in patients with sepsis is not well characterized. We aimed to examine the association between premorbid β-blocker exposure and mortality in sepsis. Methods EMBase, MEDLINE, and Cochrane databases were searched for all studies of premorbid β-blocker and sepsis. The search was last updated on 22 June 2019. Two reviewers independently assessed, selected, and abstracted data from studies reporting chronic β-blocker use prior to sepsis and mortality. Main data extracted were premorbid β-blocker exposure, mortality, study design, and patient data. Two reviewers independently assessed the risk of bias and quality of evidence. Results In total, nine studies comprising 56,414 patients with sepsis including 6576 patients with premorbid exposure to β-blockers were eligible. For the primary outcome of mortality, two retrospective studies reported adjusted odds ratios showing a reduction in mortality with premorbid β-blocker exposure. One study showed that premorbid β-blocker exposure decreases mortality in patients with septic shock. Another study showed that continued β-blockade during sepsis is associated with decreased mortality. Conclusion This systematic review suggests that β-blocker exposure prior to sepsis is associated with reduced mortality. There was insufficient data to conduct a bona fide meta-analysis. Whether the apparent reduction in mortality may be attributed to the mitigation of catecholamine excess is unclear. Trial registration PROSPERO, CRD42019130558 registered June 12, 2019. Electronic supplementary material The online version of this article (10.1186/s13054-019-2562-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The association between premorbid beta blocker exposure and mortality in sepsis—a systematic review

et al. 2019

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“…Outside the heart, they improve vascular tone, enhance metabolic efficiency, and have anti-inflammatory effects and anti-thrombotic activity.The first use of beta-blockade in sepsis goes back nearly 50 years with successful use in some patients in refractory shock. In the last decade an increasing number of observational studies and a few single-centre randomised controlled trials have shown both safety and improved outcomes 5 . These reflect findings in animal models of sepsis where various mechanisms were demonstrated including protective effects on the heart, anti-inflammatory actions and preservation of the gut barrier 5 .Clearly, the patient needs to be adequately fluid-resuscitated and stabilised before commencing beta-blockers.…”

mentioning

confidence: 99%

“…In the last decade an increasing number of observational studies and a few single-centre randomised controlled trials have shown both safety and improved outcomes 5 . These reflect findings in animal models of sepsis where various mechanisms were demonstrated including protective effects on the heart, anti-inflammatory actions and preservation of the gut barrier 5 .Clearly, the patient needs to be adequately fluid-resuscitated and stabilised before commencing beta-blockers. Ideally, the use of a short-acting agent such as esmolol or landiolol allows easy titration, or cessation, of the infusion should hypotension or excess bradycardia occur with the unwanted effects wearing off within minutes.…”

mentioning

confidence: 99%

“…The first use of beta-blockade in sepsis goes back nearly 50 years with successful use in some patients in refractory shock. In the last decade an increasing number of observational studies and a few single-centre randomised controlled trials have shown both safety and improved outcomes 5 . These reflect findings in animal models of sepsis where various mechanisms were demonstrated including protective effects on the heart, anti-inflammatory actions and preservation of the gut barrier 5 .…”

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confidence: 99%

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Beta-blockers in sepsis

Singer

2020

Qatar Medical Journal

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Catecholamines are an integral component of the host stress response and usually increase appropriately at times of need. Unfortunately, in severe and prolonged critical illness, they can contribute to significant harm with unwanted biological effects on cardiac function, inflammatory, immune, metabolic, and coagulation pathways1. A good example is Takotsubo (‘stress’) cardiomyopathy where heart failure ensues after an emotional stress resulting in extremely high levels of circulating catecholamines, considerably above that seen in a significant myocardial infarction2.Unwittingly, we are likely contributing to catecholamine toxicity in our management of the critically ill septic patient through use of exogenous catecholamine therapies which carry the same detrimental effects as endogenous catecholamines1,3. Catecholamines are currently recommended first-line agents for septic shock, and are used in an attempt to overcome the vascular hyporeactivity and myocardial depression associated with sepsis. Use of higher doses of catecholamines is however associated with worse outcomes4. This is usually ascribed to the patient's underlying illness severity and an iatrogenic contribution is not considered – but perhaps should be.Beta-blockers have multiple actions, on cardiac function and beyond. They reduce cardiac work through negative inotropic and chronotropic effects. Importantly, through slowing an excessive heart rate, both systolic and diastolic ventricular function are improved. They also act on adrenergic receptor responsiveness, enhancing the activity of catecholamines and allowing reductions in dose to achieve the same haemodynamic effect. Outside the heart, they improve vascular tone, enhance metabolic efficiency, and have anti-inflammatory effects and anti-thrombotic activity.The first use of beta-blockade in sepsis goes back nearly 50 years with successful use in some patients in refractory shock. In the last decade an increasing number of observational studies and a few single-centre randomised controlled trials have shown both safety and improved outcomes5. These reflect findings in animal models of sepsis where various mechanisms were demonstrated including protective effects on the heart, anti-inflammatory actions and preservation of the gut barrier5.Clearly, the patient needs to be adequately fluid-resuscitated and stabilised before commencing beta-blockers. Ideally, the use of a short-acting agent such as esmolol or landiolol allows easy titration, or cessation, of the infusion should hypotension or excess bradycardia occur with the unwanted effects wearing off within minutes. The largest study to date by Morelli et al., randomised 154 septic shock patients to receive either placebo or esmolol to reduce heart rate to 80-95 bpm. This was successfully achieved with no increase in complication rates compared to placebo. Importantly, there were also benefits in terms of earlier recovery of renal function, cessation of norepinephrine infusion, lower troponin levels (indicative of less cardiac damage), and imp...

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Lactoferrin and Metoprolol Supplementation Increase Mouse Survival in an Experimental LPS-Induced Sepsis Model

Martínez-García

Canizalez-Román

Angulo-Zamudio

et al. 2022

Int J Pept Res Ther

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Hemodynamic response to β-blockers in severe sepsis and septic shock: A review of current literature

Cited by 18 publications

References 64 publications

The association between premorbid beta blocker exposure and mortality in sepsis—a systematic review

The association between premorbid beta blocker exposure and mortality in sepsis—a systematic review

Beta-blockers in sepsis

Lactoferrin and Metoprolol Supplementation Increase Mouse Survival in an Experimental LPS-Induced Sepsis Model

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