Lipid Emulsion Improves Recovery from Bupivacaine-Induced Cardiac Arrest, but Not from Ropivacaine- or Mepivacaine-Induced Cardiac Arrest

Zausig, York; Zink, Wolfgang; Keil, Meike; Sinner, Barbara; Barwing, Jürgen; Wiese, C.H.R.; Graf, Bernhard M.

doi:10.1213/ane.0b013e3181af7fb3

Cited by 77 publications

(60 citation statements)

References 17 publications

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“…In the first, administration of intravenous lipid emulsion serves to create an expanded intravascular lipid phase into which toxins of high lipophilicity are sequested away from pharmacological sites of action [3][4][5]. Consistent with this thesis, a maximal response to lipid emulsion has been observed with toxins of highest lipophilicity for both local anaesthetics [27,28] and beta adrenergic blocking agents [17,29]. Augmented carriage of toxin to non-vital lipidrich tissues may additionally speed redistribution from pharmacological sites of action [6].…”

Section: Discussionmentioning

confidence: 84%

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Cave

Harvey²,

Prince

et al. 2010

Anaesthesia

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SummaryIntravenous lipid emulsion is established therapy for bupivacaine induced cardiotoxicity. The benefit of combined hypertonic saline and lipid treatment is unexplored. In this experiment, sedated rabbits were resuscitated from bupivacaine‐induced asystole with intravenous lipid according to the Association of Anaesthetists of Great Britain and Ireland’s guideline, or by identical lipid dosing with hypertonic saline: 6 mEq.kg−1 21% sodium chloride. Early electrocardiography QRS prolongation was less with lipid plus hypertonic saline (mean (SD) QRS 0.19 (0.07) s lipid only vs 0.09 (0.01) s lipid plus hypertonic saline; p = 0.003) at 9 min though not different from the lipid only group at 20 min. No difference was observed in rates of circulatory return (7/10 lipid only and 9/10 lipid plus hypertonic saline; p = 0.58) or survival (5/10 lipid only and 6/10 lipid plus hypertonic saline; p = 1.00). Some benefit to cardiac conduction may be afforded by hypertonic saline co‐administered with lipid emulsion in bupivacaine‐induced cardiotoxicity.

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Section: Discussionmentioning

confidence: 84%

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Cave

Harvey²,

Prince

et al. 2010

Anaesthesia

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“…Zausig et al could show in an animal study that the lipid emulsion had no influence on the recovery time from local anaesthetics induced cardiac arrest to the return of first signs of cardiac activity. However, after the return of heart rhythm, lipid emulsions significantly decreased the recovery time for heart rate and RPP (RPP = (left ventricular systolic pressure − left ventricular diastolic pressure) × heart rate) in bupivacaine-induced cardiac toxicity, but not in mepivacaine-or ropivacaine-induced cardiac toxicity [22]. So in conclusion intravenous lipid emulsions may show an effect on neurological results of mepivacaine overdose, but their effect in the treatment of cardiac symptoms is not clear.…”

Section: Discussionmentioning

confidence: 93%

Is Extracorporeal Membrane Oxygenation Necessary for Community Hospitals?

Yoo

2014

Korean J Crit Care Med

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Mepivacaine is a potent local anaesthetic and used for infiltration and regional anaesthesia in adults and pediatric patients. Intoxications with mepivacaine affect mainly the CNS and the cardiovascular system. We present a case of accidental intravenous mepivacaine application and intoxication of an infant resulting in seizure, broad complex bradyarrhythmia, arterial hypotension and finally cardiac arrest. The patient could be rescued by prolonged resuscitations and a rapid initiation of ECMO and survived without neurological damage. The management strategies of this rare complication including promising other treatment options with lipid emulsions are discussed.

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“…In regard to local anesthetics, bupivacaine is highly lipophilic (LogP, 3.6; LogD, 2.7 at pH 7.4) and the associated toxicity is responsive to LRT, whereas less lipophilic local anesthetics like ropivacaine (LogP, 2.9) and mepivacaine (LogP, 2.0) are also clinically responsive but LRT may not produce as robust a recovery in experimental models of overdose. 59,60 Meta-analysis confirms this discrepancy as ILE produced a robust and homogenous benefit for bupivacaine toxicity, but ILE for mepivacaine was an outlier in 1 study based on funnel-plot analysis. 8 The logP-dependent benefit extends to animal models of β-blocker toxicity, where overdose with the most lipophilic β-blocker, propranolol (LogP, 3.1), responds to treatment with lipid emulsion 61 whereas overdoses of less lipophilic β-blockers metoprolol 62 (LogP, 1.79) and atenolol 63 (LogP, 0.1) are less responsive.…”

Section: Bindingmentioning

confidence: 96%

The Mechanisms Underlying Lipid Resuscitation Therapy

Fettiplace

Weinberg

2018

Regional Anesthesia and Pain Medicine

111

104

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The experimental use of lipid emulsion for local anesthetic toxicity was originally identified in 1998. It was then translated to clinical practice in 2006 and expanded to drugs other than local anesthetics in 2008. Our understanding of lipid resuscitation therapy has progressed considerably since the previous update from the American Society of Regional Anesthesia and Pain Medicine, and the scientific evidence has coalesced around specific discrete mechanisms. Intravenous lipid emulsion therapy provides a multimodal resuscitation benefit that includes both scavenging (eg, the lipid shuttle) and nonscavenging components. The intravascular lipid compartment scavenges drug from organs susceptible to toxicity and accelerates redistribution to organs where drug (eg, bupivacaine) is stored, detoxified, and later excreted. In addition, lipid exerts nonscavenging effects that include postconditioning (via activation of prosurvival kinases) along with cardiotonic and vasoconstrictive benefits. These effects protect tissue from ischemic damage and increase tissue perfusion during recovery from toxicity. Other mechanisms have diminished in favor based on lack of evidence; these include direct effects on channel currents (eg, calcium) and mass-effect overpowering a block in mitochondrial metabolism. In this narrative review, we discuss these proposed mechanisms and address questions left to answer in the field. Further work is needed, but the field has made considerable strides towards understanding the mechanisms.

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Lipid Emulsion Improves Recovery from Bupivacaine-Induced Cardiac Arrest, but Not from Ropivacaine- or Mepivacaine-Induced Cardiac Arrest

Abstract: These data show that the effects of lipid infusion on LA-induced cardiac arrest are strongly dependent on the administered LAs itself. We conclude that lipophilicity of LAs has a marked impact on the efficacy of lipid infusions to treat cardiac arrest induced by these drugs.

Cited by 77 publications

References 17 publications

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Is Extracorporeal Membrane Oxygenation Necessary for Community Hospitals?

The Mechanisms Underlying Lipid Resuscitation Therapy

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