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Lidocaine cardiac arrest

Unlabeled uses In pediatric patients with cardiac arrest, less than 10% develop ventricular fibrillation, and others develop ventricular tachycardia the hemodynamically compromised child may develop ventricular couplets or frequent premature ventricular beats. In these cases, administer 1 mg/kg lidocaine by the IV, intraosseous, or endotracheal route. A second 1 mg/kg dose may be given in 10 to 15 minutes. Start a lidocaine infusion if the second dose is required a third bolus may be needed in 10 to 15 minutes to maintain therapeutic levels. [Pg.442]

Amide-type agents include articaine, lidocaine, bupivacaine, prilocaine, mepivacain and ropiva-caine. These are metabolized in the liver by microsomal enzymes with amidase activity. The amide group is preferred for parenteral and local use. If by accident rapidly administered intravascularly these agents, especially bupivacaine but also lidocaine, can produce serious and potentially lethal adverse effects including convulsions and cardiac arrest. They can more easily accumulate after multiple administrations. Intravenous lidocaine is sometimes used for regional anesthesia, for infiltration procedures, for the induction of nerve blockade and for epidural anesthesia. However, it is also used as an antiarrhythmic. Bupivacaine is a long-acting local anesthetic used for peripheral nerve blocks and epidural anesthesia. [Pg.363]

Although serious adverse reactions to lidocaine are uncommon, high dosage by any route may produce cardiovascular depression, bradycardia, hypotension, arrhythmias, heart block, cardiovascular collapse, and cardiac arrest,... [Pg.698]

Intravenous. A double cuff is applied to the arm, inflated above arterial pressure after elevating the limb to drain the venous system, and the veins filled with local anaesthetic, e.g. 0.5-1% lidocaine without adrenaline (epinephrine). The arm is anaesthetised in 6-8 min, and the effect lasts for up to 40 min if the cuff remains inflated. The cuff must not be deflated for at least 20 minutes. The technique is useful in providing anaesthesia for the treatment of injuries speedily and conveniently, and many patients can leave hospital soon after the procedure. The technique must be meticulously conducted, for if the full dose of local anaesthetic is accidentally suddenly released into the general circulation severe toxicity and even cardiac arrest may result. Bupivacaine is no longer used for intravenous regional anaesthesia as cardiac arrest caused by it is particularly resistant to treatment. Patients should be fasted and someone skilled in resuscitation must be present. [Pg.360]

Lidocaine can cause dysrhythmias and hypotension. The dysrhythmias that have been reported include sinus bradycardia, supraventricular tachycardia (11), and rarely torsade de pointes (12). There have also been rare reports of cardiac arrest (2) and worsening heart failure (13). Lidocaine can also cause an increased risk of asystole after repeated attempts at defibrillation (14). Lidocaine may increase mortality after acute myocardial infarction, and it should be used only in patients with specific so-called warning dysrhythmias (that is frequent or multifocal ventricular extra beats, or salvos) (15). [Pg.2052]

A 31-year-old woman had a cardiac arrest and was resuscitated to a wide-complex tachycardia, which was treated with intravenous lidocaine 100 mg. She immediately became asystohc but responded to calcium chloride. [Pg.2052]

A 32-year-old man, who had been in hospital for several months because of acute intermittent porphyria and chronic pancreatitis, had a seizure and an asystolic cardiac arrest. Resuscitation was unsuccessful. There was a suspicion of patient mistreatment by one of the attending nurses, and toxicological analyses showed high blood concentrations of lidocaine, diazepam, phenytoin, and promethazine. Diazepam and phenytoin... [Pg.2057]

Propofol dose-dependently reduced the threshold for lidocaine-induced convulsions in rats (82). Higher doses of propofol completely abolished convulsions. However, there was no difference in the dose of lidocaine that caused cardiac arrest and death, when it was given with three different propofol infusions and placebo. [Pg.2058]

Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb LA, Copass MK. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990 82(6) 2027-34. [Pg.2058]

For many years lidocaine has been used for the treatment of ventricular arrhythmias in the setting of acute myocardial infarction (AMI). The efficacy seen in cardiac arrest, however, has not mirrored that seen in AMI. In the only published case-control trial where patients were classified according to whether they received lidocaine, no significant... [Pg.178]

Chow MS, Ronfeld RA, Ruggett D, Fieldman A. Lidocaine pharmacokinetics during cardiac arrest and external cardiopulmonary resuscitation. AmHeartJ 1981 102 799-801. [Pg.183]

Hendrie J, O Callaghan CJ. Lidocaine pharmacokinetics after cardiac arrest and external cardiopulmonary resuscitation. Am J Cardiol 1996 78 1322-1323. [Pg.183]

Central nervous system changes are the most frequently observed systemic toxicities of lidocaine. The initial manifestations are restlessness, vertigo, tinnitus, slurred speech, and eventually, seizures. Subsequent manifestations include CNS depression with a cessation of convulsions and the onset of unconsciousness and respiratory depression or cardiac arrest. This biphasic effect occurs because local anesthetics initially block the inhibitory GABAergic pathways, resulting in stimulation, and eventually block both inhibitory and excitatory pathways... [Pg.683]

Lidocaine is bound to aj-acid glycoprotein, which varies in settings that lidocaine is commonly administered (e.g., cardiac arrest, myocardial infarction). [Pg.150]

Approximately 70% of lidocaine is bound to plasma proteins (70% aj-acid glycoprotein, 30% albumin). Therefore, conditions that increase aj-acid glycoprotein (e.g., myocardial infarction, trauma, cardiac arrest) may dramatically alter the unbound fraction. This poses a clinical challenge as lidocaine is often administered... [Pg.150]

Cardiovascular Cardiac arrest has been reported after nasal infiltration with lidocaine and adrenaline in a patient with a hypophysoma and a previously undiagnosed hypertrophic cardiomyopathy [26 ]. This emphasizes that absorbed adjuncts, such as adrenaline, can be hazardous and should be considered in the differential diagnosis if hemodynamic instability occurs after infiltration of a local anesthetic with adrenaline. [Pg.212]

Most of the adverse events related to lidocaine are associated with sermn toxicity, with various symptoms presenting at different sermn levels. Symptoms such as lightheadedness, perioral numbness, tinnitus, nausea, or metallic taste in the mouth may occur when plasma lidocaine concentrations are 1-5 pg/mL. Dysarthria, local muscle twitches, hallucinations, or nystagmus may present at plasma concentrations from 5 to 8 pg/ mL. Seizmes may occur at 8-12 pg/mL, followed by respiratory depression or coma at levels higher than 20 pg/mL. Hypotension, bradycardia, cardiac arrest, and arrhythmias may also occm at serum levels greater than 20 pg/mL. IntraUpid remains the only available treatment for adverse events related to serum toxicity. [Pg.282]

Cardiovascular Ingested lidocaine meant for gargling before direct laryngoscopy led to cardiac arrest [54 ]. [Pg.288]

A 50-year-old woman received 20 ml of lidocaine 5% as a gargling solution before direct laryngoscopy and accidently swallowed the solution 20 minutes later she had a cardiac arrest and was successfully resuscitated. Plasma lidocaine concentrations were not measured. [Pg.288]

Doumiri M, Moussaoui A, Maazouzi W. Cardiac arrest after gargling and oral ingestion of 5% lidocaine. Can J Anaesth 2008 55(12) 882-3. [Pg.296]

Cardiac arrest occurred after 20 minutes a 52-year-old woman gargled and accidentally swallowed 20 ml of a 5% lidocaine solution before laryngoscopy [71 ]. She developed somnolence, bradypnea, hypotension, and eventual cardiac arrest, which necessitated external cardiac massage, intubation, and adrenaline infusion. Recovery was uneventful. [Pg.388]

This agent is used for the small venous malformations. Polidocanol is effective by altering the vascular wall. The emulsion of aetoxisclerol would allow for the visualization of the draining veins, thanks to the bubbles accordingly, this emulsion could direct the compression to the involved veins, sparing then the normal adjacent veins. Injection Some authors used it mixed with a lidocaine solution to minimize pain after injection. Dose The quantity is Icc per cavity [25] up to a total of 6 cc of polidocanol with 0,2-l,0 cc of 1% lidocaine solution. Complications Skin necrosis, sciatic neurolysis, and infections were reported in 6-8% of cases [25,27[. One cardiac arrest was also reported [28[. [Pg.29]

The earliest signs of CNS toxicity are circumoral and tongue numbness, tinnitus, tremor, and dizziness. These appear at plasma lidocaine (lignocaine) concentrations of about 5 pg-mL-1. The value for prilocaine is similar to lidocaine but bupivacaine toxicity appears at about half those of lidocaine. Further progression is evidenced by drowsiness, visual disturbances, or muscle twitching (plasma lidocaine of 5-10 pg-mL-1). Over 10 p-mL-1 grand mal convulsions, coma and respiratory arrest are likely. Serious CNS toxicity is indicative of imminent and potentially fatal cardiac toxicity since lidocaine is associated with direct cardiac depression at plasma concentrations in excess of 20 pg-mL-1. [Pg.102]

A death due to ventricular fibrillation after 50 mg and another due to sinus arrest after 100 mg have been reported (SED-12, 255) (17). Two cases of ventricular fibrillation and cardiopulmonary arrest occurred after local infiltration of lidocaine for cardiac catheterization (SEDA-21,136). [Pg.2052]

An elderly man with long standing brady-tachycardia was successfully treated for atrial flutter firstly with a temporary pacemaker (later withdrawn) and 600 mg amiodarone daily. Ten days later, and 25 minutes after a permanent pacemaker was inserted under local anaesthesia with 15 mL of 2% lidocaine, severe sinus bradycardia and long sinoatrial arrest developed. He was effectively treated with atropine plus isoprenaline, and cardiac massage. ... [Pg.262]


See other pages where Lidocaine cardiac arrest is mentioned: [Pg.16]    [Pg.128]    [Pg.9]    [Pg.7]    [Pg.19]    [Pg.434]    [Pg.165]    [Pg.320]    [Pg.717]    [Pg.116]    [Pg.263]    [Pg.177]    [Pg.178]    [Pg.183]    [Pg.183]    [Pg.350]    [Pg.64]    [Pg.19]    [Pg.848]    [Pg.377]    [Pg.82]    [Pg.82]    [Pg.1525]    [Pg.377]    [Pg.82]   
See also in sourсe #XX -- [ Pg.16 ]

See also in sourсe #XX -- [ Pg.388 ]




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