Current concepts in resuscitation of patients with local anesthetic cardiac toxicity

Weinberg, Guy

doi:10.1053/rapm.2002.37126

Cited by 48 publications

(34 citation statements)

References 92 publications

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“…[19][20][21][22] In addition, it has been experimantally demonstrated that lipid emulsion pretreatment diminishes bupivacaine associated cardiotoxicity. [23] Though intralipids are used for resuscitations, there are studies demonstrating propofol can be useful for preventive or protective treatment.…”

Section: Ağrimentioning

confidence: 99%

Sudden developing convulsion during interscalene block: Does propofol anesthesia diminish plasma bupivacaine level ?

Güngör

Akbaş

Kaya

et al. 2015

Agri

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Section: Ağrimentioning

confidence: 99%

Sudden developing convulsion during interscalene block: Does propofol anesthesia diminish plasma bupivacaine level ?

Güngör

Akbaş

Kaya

et al. 2015

Agri

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“…durch Lipidinfusionen signifikant attenuiert werden können [38, 255,256]. Inwieweit all diese experimentellen Befunde zur Therapie einer kardiovaskulären Intoxikation auf den menschlichen Organismus übertragen werden können, bleibt mit Spannung abzuwarten [76].…”

Section: Therapieoptionen Bei Systemischer Intoxikationunclassified

Toxikologie der Lokalan�sthetika

Zink

Graf

2003

Der Anaesthesist

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Regardless of their specific physico-chemical properties and chemical structures, all local anaesthetic agents block neuronal voltage-gated sodium channels, and thus suppress conduction in peripheral nerves. Since these ion channels ubiquitously appear in excitable membranes, systemic accumulation of local anaesthetic agents may affect the functional integrity of these structures. Clinically, local anaesthetic-induced systemic toxicity results in central nervous and cardiovascular malfunction. With regard to CNS toxicity, symptoms which are largely drug-independent appear in a characteristic biphasic sequence. Nevertheless, the plasma levels necessary to provoke these symptoms are to a large extent agent-specific. Initially, these toxic mechanisms are due to a selective blockade of cortical inhibitory neurons, which enables the formation of seizure potentials within subcortical structures. With high cerebral drug levels, however, excitatory neurons are also increasingly blocked, resulting in coma, apnoeic episodes and circulatory failure. Direct cardiac effects of local anaesthetics can be divided into (i) stereospecific inhibition of intracardial conduction and (ii) unspecific inhibition of myocardial energy supply and ion channels. The corresponding spectrum of symptoms is not uniform and may range from extreme bradycardia, (malignant) ventricular arrhythmia to refractory cardiac arrest. Local tissue toxicity has to be strictly delimited from systemic toxicity and allergies, respectively, which are mainly caused by aminoester agents. Local anaesthetics may cause neuronal and striated muscle injury at the site of injection. With regard to (central) neurotoxicity, "transient neurologic symptoms" and "cauda equina syndrome" have been increasingly recognised. However, the clinical relevance of local anaesthetic-induced myotoxicity is still controversly discussed. In order to avoid systemic accumulation of local anaesthetic agents, several safety procedures have to be considered during the application of these drugs. The treatment of systemic toxicity is strictly dependent on the expression of symptoms. However, hypoxia and acidotic episodes must be avoided and must be treated aggressively.

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“…7,10 Local Anesthetic Toxicity Local anesthetics are amphiphilic, having both lipophilic and hydrophilic properties. 11 This property allows local anesthetics to enter many cellular compartments, including the heart, brain, and skeletal muscle tissue. In certain body tissues, such as skeletal or heart muscle, local drug-induced interruptions in normal cellular metabolism in the areas of cell signaling and particular energy pathways can result in wider consequences.…”

Section: Introductionmentioning

confidence: 99%

“…In certain body tissues, such as skeletal or heart muscle, local drug-induced interruptions in normal cellular metabolism in the areas of cell signaling and particular energy pathways can result in wider consequences. 11 Administration of toxic doses of local anesthetics increases disruptions of cellular mechanisms, thus interfering with inotropic function, pathways that regulate Na 1 , K 1 , and Cl 2 ion flow, modulation of the autonomic nervous system, and enzymatic processes for adenosine triphosphate formation. Various studies of the hearts of rabbits, guinea pigs, and rats demonstrated the cardiotoxicity potential of local anesthetics.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, reentrant ventricular dysrhythmias were reported in all animal models, and hyperkalemia enhanced the cardiotoxicity potential of these agents. 11 One known risk during regional anesthesia is direct intravascular injection of local anesthetic into nearby arterial or venous vessels. 12 Intra-arterial injections may be more likely in the case of block administration in the upper extremity, and onset of toxic neurological signs and symptoms may occur within minutes because of proximity of the cerebral circulation, including the carotid artery.…”

Section: Introductionmentioning

confidence: 99%

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