Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Local Anesthetics: Adverse Effects01:12

Local Anesthetics: Adverse Effects

While local anesthetics are generally safe and well-tolerated, they can occasionally cause adverse effects that vary in severity. Local anesthetics can induce toxicity at two distinct levels. They can either produce local effects through direct contact with the neural elements or be absorbed into the bloodstream from the injection site, leading to systemic effects.
Once absorbed into the systemic circulation, local anesthetics can affect the organs that depend on the functioning of sodium...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...
Drug Toxicity: Overview01:00

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...
Drug toxicity: Idiosyncratic Reactions01:16

Drug toxicity: Idiosyncratic Reactions

Idiosyncratic drug reactions represent abnormal chemical responses that vary significantly among individuals, ranging from extreme sensitivity to low doses to insensitivity to high doses. These reactions often occur due to the drug's covalent binding with serum proteins, forming a foreign hapten that triggers an immunotoxicological response. The variability in drug reactions has a strong pharmacogenetic foundation, with genetic differences crucial in how individuals metabolize drugs. For...
Local Anesthetics: Mechanism of Action01:23

Local Anesthetics: Mechanism of Action

Local anesthetics (LAs) block sensory and motor impulses by inhibiting the sodium channels on the nerve cell membranes. This induces temporary loss of sensation, relieving pain in a specific body area.
Local anesthetics are amphiphilic molecules consisting of a hydrophobic aromatic part linked to a hydrophilic group by an ester or amide linkage. They are weak bases and are usually available as salts, which increases their solubility and stability. Once administered, LAs exist in the body either...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

I Shake Hands with Helen Taussig: Epiphanies in the Emergency Department.

The Journal of emergency medicine·2026
Same author

Martha: A Prose Poem Remembrance.

The Journal of emergency medicine·2025
Same author

Drowning incidents precipitated by unusual causes (DIPUCs): A narrative review of their diagnoses, evaluation and management.

Resuscitation plus·2024
Same author

When You Have a Dream That It's Time to Retire, It's Time to Retire.

The American journal of medicine·2023
Same author

Lethal Bradycardia.

The Journal of emergency medicine·2022
Same author

They Also Serve Who Only Sit and Answer COVID-19 Hotline Telephones.

The Journal of emergency medicine·2022

Related Experiment Video

Updated: Jun 17, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Lidocaine toxicity misinterpreted as a stroke.

Benjamin Bursell1, Richard M Ratzan, Alan J Smally

  • 1University of Connecticut School of Medicine, Division of Emergency Medicine, Hartford, CT.

The Western Journal of Emergency Medicine
|January 5, 2010
PubMed
Summary

Lidocaine toxicity can cause stroke, especially in elderly patients with liver or heart issues. This case highlights the importance of monitoring lidocaine levels to prevent adverse neurological events.

More Related Videos

Simultaneous Photothrombosis and Fiber Photometry to Induce and Monitor Ischemic Stroke in Behaving Mice
07:49

Simultaneous Photothrombosis and Fiber Photometry to Induce and Monitor Ischemic Stroke in Behaving Mice

Published on: November 14, 2025

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Related Experiment Videos

Last Updated: Jun 17, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
05:26

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction

Published on: May 28, 2019

Simultaneous Photothrombosis and Fiber Photometry to Induce and Monitor Ischemic Stroke in Behaving Mice
07:49

Simultaneous Photothrombosis and Fiber Photometry to Induce and Monitor Ischemic Stroke in Behaving Mice

Published on: November 14, 2025

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
06:01

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Published on: August 18, 2015

Area of Science:

  • Cardiology
  • Neurology
  • Clinical Pharmacology

Background:

  • Lidocaine is a common antiarrhythmic drug used for over 50 years.
  • Ventricular arrhythmias require effective treatment to prevent serious complications.

Purpose of the Study:

  • To report a case of acute neurologic dysfunction secondary to lidocaine toxicity.
  • To discuss risk factors associated with developing lidocaine toxicity.

Main Methods:

  • Case report of an 87-year-old female patient.
  • Administration of lidocaine and amiodarone infusions for ventricular tachycardia.
  • Diagnosis based on clinical presentation and serum lidocaine levels.

Main Results:

  • The patient experienced acute neurologic dysfunction, diagnosed as a stroke.
  • Serum lidocaine level was significantly elevated at 7.9 mg/L.
  • Risk factors identified included advanced age and co-administration of other drugs.

Conclusions:

  • Lidocaine toxicity can manifest as severe neurologic dysfunction, including stroke.
  • Hepatic dysfunction, cardiac dysfunction, advanced age, and polypharmacy are key risk factors.
  • Careful patient selection and monitoring are crucial when administering lidocaine.