Local Anaesthetic Toxicity Overview
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Questions and Answers

What is the primary reason for low blood pressure in cases of local anesthetic toxicity?

  • Vasodilation due to anesthetic properties
  • Low stroke volume (correct)
  • Increased heart rate
  • Hyperventilation causing acidosis

    • Which sign indicates severe local anesthetic toxicity?

  • Stable vital signs
  • Sinus bradycardia and conduction blocks (correct)
  • Slurred speech without agitation
  • Persistent hyperventilation

    • What immediate action should be taken upon suspicion of local anesthetic toxicity?

  • Stop injecting the local anesthetic (correct)
  • Administer fluids rapidly
  • Continue administering local anesthetic
  • Start CPR immediately

    • During management of local anesthetic toxicity, what is the recommended bolus dose of lipid emulsion for a 70 kg adult?

    <p>1.5 ml/kg</p> Signup and view all the answers

    What is the most important reason to avoid hypercarbia during the management of local anesthetic toxicity?

    <p>It decreases oxygenation</p> Signup and view all the answers

    Which therapy is indicated if no circulatory arrest occurs following local anesthetic toxicity?

    <p>Conventional therapies for arrhythmias</p> Signup and view all the answers

    What cardiovascular condition is associated with local anesthetic toxicity?

    <p>Ventricular tachyarrhythmias</p> Signup and view all the answers

    What is the recommended rate of lipid infusion after the initial bolus for management of local anesthetic toxicity?

    <p>15 ml/kg/hr</p> Signup and view all the answers

    What is an expected outcome of administering a small incremental dose of benzodiazepine for seizure control?

    <p>Decreasing seizure intensity</p> Signup and view all the answers

    Which enzyme's function is impaired due to local anesthetic toxicity leading to ATP depletion?

    <p>Adenosine triphosphatase</p> Signup and view all the answers

    What is the primary effect of local anaesthetic toxicity on the heart?

    <p>Interference with ion channels leading to possible cardiac arrest</p> Signup and view all the answers

    Which symptom is most indicative of severe local anaesthetic toxicity?

    <p>Loss of consciousness</p> Signup and view all the answers

    What is the mechanism by which local anaesthetics (LAs) produce toxicity?

    <p>Blocking sodium channels, affecting nerve signals</p> Signup and view all the answers

    How does the binding of local anaesthetics to plasma affect their duration?

    <p>It prolongs the duration by altering absorption rates</p> Signup and view all the answers

    What role does lipid emulsion therapy play in managing local anaesthetic toxicity?

    <p>It displaces sodium from tissues and fats</p> Signup and view all the answers

    Which of the following best describes the relationship between local anaesthetic dosage and its toxicity?

    <p>Toxicity depends on both dosage and the vascularity of the injection site</p> Signup and view all the answers

    Which process in the mitochondria is disrupted by local anaesthetic toxicity?

    <p>Oxidative phosphorylation leading to ATP generation</p> Signup and view all the answers

    What might signal the onset of seizures in a patient experiencing local anaesthetic toxicity?

    <p>Muscle fasciculation</p> Signup and view all the answers

    What physiological effect does local anaesthetic toxicity have on the plasma levels of electrolytes?

    <p>Depletes sodium levels leading to arrhythmias</p> Signup and view all the answers

    What is the primary mechanism contributing to prolonged skeletal muscle contraction in malignant hyperthermia?

    <p>Genetically altered RyR1 receptor release</p> Signup and view all the answers

    Which symptom is characterized by elevated levels of carbon dioxide in the blood due to excessive muscle contraction?

    <p>Hypercarbia</p> Signup and view all the answers

    What triggers hyperthermia in a patient experiencing malignant hyperthermia?

    <p>Rapid muscle contraction rate</p> Signup and view all the answers

    What is one of the treatment priorities in managing malignant hyperthermia?

    <p>Provide 100% FiO2</p> Signup and view all the answers

    During malignant hyperthermia, why might a patient develop metabolic acidosis?

    <p>Increased respiratory demand and CO2 retention</p> Signup and view all the answers

    What is a consequence of rhabdomyolysis in the context of malignant hyperthermia?

    <p>Myoglobinuric renal failure</p> Signup and view all the answers

    Which condition is not a typical symptom of malignant hyperthermia?

    <p>Bradycardia</p> Signup and view all the answers

    What is the primary reason for calling for help during a malignant hyperthermia crisis?

    <p>To gather additional staff for effective crisis management.</p> Signup and view all the answers

    What causes the excess release of potassium into the extracellular blood during malignant hyperthermia?

    <p>Cell membrane damage from rhabdomyolysis</p> Signup and view all the answers

    What is the role of dantrolene in the treatment of malignant hyperthermia?

    <p>Acts as a muscle relaxant by inhibiting calcium release</p> Signup and view all the answers

    Which vital sign change is most indicative of malignant hyperthermia?

    <p>Increased heart rate.</p> Signup and view all the answers

    What is a significant risk factor that may exacerbate malignant hyperthermia during surgical procedures?

    <p>Use of muscle relaxants such as succinylcholine</p> Signup and view all the answers

    What is the first step after recognizing malignant hyperthermia symptoms?

    <p>Call for help and inform the theatre team.</p> Signup and view all the answers

    What does hypermetabolism during malignant hyperthermia lead to?

    <p>Increased carbon dioxide production.</p> Signup and view all the answers

    What is the initial dosage for dantrolene in an adult patient during a malignant hyperthermia crisis?

    <p>2-3 mg/kg IV bolus.</p> Signup and view all the answers

    Which intervention is crucial for managing elevated ETCO2 levels in a malignant hyperthermia situation?

    <p>Hyperventilation and administering oxygen.</p> Signup and view all the answers

    During a malignant hyperthermia episode, which of the following is NOT a noted sign?

    <p>Stable body temperature.</p> Signup and view all the answers

    What is an appropriate measure to eliminate the trigger drug during a malignant hyperthermia crisis?

    <p>Remove the trigger drug from the workstation.</p> Signup and view all the answers

    What type of drug should be used for neuromuscular blockade in this crisis?

    <p>Non-depolarizing muscle relaxants.</p> Signup and view all the answers

    What type of monitoring is crucial during a malignant hyperthermia emergency?

    <p>Invasive BP, CVP, core and peripheral temperature monitoring.</p> Signup and view all the answers

    Study Notes

    Local Anaesthetic Toxicity (LA)

    • Life-threatening adverse event to LA
    • Can take place within 10 mins - 1 hr
    • Blocks pain receptors from sending signals to the brain

    Function

    • Various LAs have different dissolving rates (bupivacaine)
    • But these can cause fast LA toxicity
    • Target Na+ channel + carry risk of toxicity
    • Block Na+ channels which interferes with signals to brain
    • Na+ important to cardiac conduction (prevents early depolarization)
    • Na+ carries electrical charge (allows for muscle contraction + nerve transmission)
    • Without Na+ = arrhythmias (prevents regularly occurring depolarization between contractions)

    Pathophysiology

    • Toxicity occurs when LA reaches a level that affects heart/brain
    • Effects can be mild (progressive) to life-threatening cardiac arrest
    • Ultrasound given to reduce nerve block
    • Rate of absorption depends on how much circulated it is
    • Rate of absorption depends on how much circulated it is (how much iv given)
    • Bonds to plasma (water soluble)
    • Each LA binds differently / bupivacaine binds faster so duration is longer
    • Metabolism evaluated on enzymes in plasma dysfunction to enzymes with LA
    • Plasma becomes saturated / systemic circulation poisoned by toxins
    • It will reduce the metabolism/
    • Metabolism dependant on enzymes in plasma-dysfunction to enzymes with LA
    • Fast occurs when mitochondria cannot generate ATP - anaerobic metabolism (build-up of CO2)
    • Inhibits oxidative phosphorylation (in mitochondria)
    • No ATP: anaerobic metabolism (build up of CO2)
    • No ATP to displace H ions = metabolic acidosis
    • Reduction in SVR (which need to no ATP) = Vasopressors + inotropes ineffective

    Brain

    • LA drugs cross blood-brain barrier
    • Interferes with nerve impulses (blocks Na+)
    • Blockage directly in the brain (increased excitation around the mouth)
    • Muscle fasciculation can occur
    • Some heat seizures can happen

    Heart

    • Blocks ion channels = hypotension (affects contractility)
    • Might start with hyptertension (treat tries to compensate)
    • Tachycardia + arrhythmias (heart tries to compensate)
    • Severe hypotension + bradycardia = cardiac arrest
    • Progression to compensate

    Symptoms

    • Severe = loss of consciousness
    • Tingling
    • Tinnitus
    • slurred speech

    Treatment (Clinical Management)

    • Stop injection, use 20% lipid emulsion (IV bolus)
    • Catch for (airway)
    • Maintain airway
    • Increase max dose = 12ml/kg, or 840ml for 70kg
    • If CA = start CPR - use smaller adrenalin dose
    • Benzo for seizures

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    Description

    This quiz covers the critical aspects of local anaesthetic toxicity, including its life-threatening effects, mechanisms of action, and pathophysiology. Understand how different local anaesthetics can lead to severe cardiac complications and the importance of sodium channels in nerve transmission. Test your knowledge on the absorption rates and risk management strategies in clinical practice.

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