Lidocaine CRI · Antiarrhythmic

Class IB antiarrhythmic. Blocks voltage-gated sodium channels in cardiac tissue, preferentially during depolarization (use-dependent block). Suppresses ectopic ventricular activity and raises ventricular fibrillation threshold. Particularly effective for ventricular arrhythmias arising from myocardial ischemia, increased automaticity, and reperfusion. Onset 1–2 minutes IV; duration 10–20 minutes after stopping. Hepatic metabolism via CYP1A2 and CYP3A4. Clearance is reduced in hepatic dysfunction, severe heart failure (reduced hepatic blood flow), and on prolonged infusions. Cats: dramatically impaired clearance compared to dogs, with toxicity at much lower CRI rates.

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Clinical background

Lidocaine in its antiarrhythmic role is the first-line CRI for ventricular tachyarrhythmia in dogs and a high-caution adjunct in cats. It is a class IB sodium-channel blocker with use-dependent kinetics, which means it preferentially binds open and inactivated sodium channels and dissociates rapidly during diastole. This pharmacology produces strong suppression of abnormal ventricular automaticity and re-entry while leaving normal sinus and atrial activity relatively unaffected. The clinical pivot is species asymmetry: dogs tolerate the standard antiarrhythmic dose range well, while cats are markedly more sensitive to both CNS and cardiovascular toxicity at any given mg/kg dose, with a loading-dose ceiling roughly four times lower than the dog ceiling. This article covers the antiarrhythmic indication. The analgesic CRI use of lidocaine is at /lidocaine.

Pharmacology

Class IB antiarrhythmic. The molecular action is voltage-gated sodium channel blockade with rapid on-off kinetics:

• Preferential binding to open and inactivated channels means lidocaine has more effect during rapid pacing (where channels spend more time in the open state) than during normal sinus rhythm. The clinical translation is selective suppression of ectopic ventricular activity with little effect on normal cardiac conduction.
• Rapid dissociation during diastole means the QRS does not widen significantly at therapeutic doses, in contrast to class IA agents.
• Reduces ventricular automaticity by shortening phase 4 depolarization in ectopic foci.
• Raises ventricular fibrillation threshold in ischemic and reperfusion settings, which is the rationale for post-cardioversion VF prophylaxis.
• No effect on AV-nodal conduction or atrial tissue at therapeutic doses. Lidocaine does not slow ventricular response in atrial fibrillation (that is the diltiazem and esmolol role).

Onset is within 1–2 minutes of IV administration. Duration after a single bolus is 10–20 minutes. Hepatic metabolism via CYP1A2 and CYP3A4 produces active metabolites (MEGX and GX) that contribute to both efficacy and toxicity at higher plasma concentrations. The pharmacokinetic relevance of this metabolism is two-fold: hepatic dysfunction prolongs the parent drug’s clinical effect, and prolonged infusions accumulate metabolites that account for the late-CRI toxicity that is not present with shorter use.

Cats have dramatically reduced hepatic clearance of lidocaine relative to dogs. The mechanism is incompletely characterized but includes reduced CYP activity for some lidocaine metabolic pathways and reduced glucuronidation capacity for downstream metabolites. The clinical consequence is that the dose that produces therapeutic plasma levels in a dog produces toxic levels in a cat.

Indications

Primary use cases:

• Sustained ventricular tachycardia with hemodynamic compromise. The first-line agent in dogs; the loading bolus plus CRI maintenance is the standard approach. Most dogs respond within minutes of an adequate loading dose.
• Hemodynamically significant ventricular premature complexes (VPCs) when frequency or coupling pattern (R-on-T, multifocal, bigeminal/trigeminal patterns) compromises forward flow. Often seen in canine gastric dilatation-volvulus, hemoabdomen, sepsis, and following any abdominal surgery.
• VF prophylaxis after cardioversion or in the setting of acute myocardial ischemia, where the increased ventricular fibrillation threshold reduces the risk of redegeneration.
• Reperfusion arrhythmia following splenectomy for hemoabdomen, gastric derotation, or ischemic limb reperfusion. Pre-emptive CRI through the reperfusion window is a common protocol.

In cats, lidocaine is used cautiously for the same indications when alternatives are unavailable, but many feline cardiologists prefer sotalol (where time allows the oral route) or magnesium (for refractory cases) over lidocaine CRI specifically because of the sensitivity profile.

Lidocaine is not appropriate for atrial fibrillation rate control (it does not slow AV-nodal conduction). It is also not appropriate for VPCs that are infrequent and hemodynamically inconsequential; the decision to treat is itself a clinical judgment, and treating every VPC in every patient overtreats.

Dosing

• Dogs, antiarrhythmic CRI: 25–80 µg/kg/min, titrated against rhythm response.
• Cats, antiarrhythmic CRI: 10–40 µg/kg/min. Note the lower range.
• Initial CRI rate (dogs): 25–50 µg/kg/min after the loading bolus.
• Initial CRI rate (cats): 10 µg/kg/min. Do not start at the top of the published range in a cat.
• Caution above (dogs): 75 µg/kg/min. CNS toxicity (tremors, twitches, ataxia, seizures) and cardiovascular toxicity (hypotension, AV block, negative inotropy) become more likely.
• Caution above (cats): 20 µg/kg/min. The cat toxicity margin is much narrower; some cardiologists treat 20 µg/kg/min as a practical ceiling rather than 40.

Loading dose, dogs: 2 mg/kg IV slowly over 1–2 minutes. May repeat 1–2 mg/kg every 5–10 minutes to a cumulative loading dose of 8 mg/kg if arrhythmia persists. Watch for CNS signs during repeat boluses; if tremors or twitches appear, the patient is at the toxicity threshold and the next bolus should be deferred.

Loading dose, cats: 0.25–0.75 mg/kg IV slowly over 1–2 minutes. The four-fold reduction from the dog loading dose is real and is not a typo. Cats given the dog loading dose of 2 mg/kg can seize and arrest. Give the bolus very slowly, reassess in 5 minutes before considering repeat dosing, and have flumazenil and an anticonvulsant prepared in case of CNS signs.

Continue the CRI for 24–48 hours after rhythm stabilization, then taper. Patients with structural heart disease may need longer courses, transitioning to oral mexiletine or amiodarone for sustained suppression.

Cat-specific cautions

Cats have markedly impaired hepatic clearance of lidocaine compared to dogs. The toxicity threshold for both CNS and cardiovascular adverse effects is reached at much lower CRI rates and total doses than in dogs.

Practical implications:

• Start at the lower end of the cat range (10 µg/kg/min) and titrate cautiously upward, watching for any CNS sign (tremors, ataxia, twitching of facial musculature, vocalization, hyperalgesia).
• Reassess every 30–60 minutes during the first few hours of CRI. A cat that is tolerating the rate well initially may decompensate as plasma levels rise toward steady state.
• Cumulative loading dose in cats should not exceed 0.75 mg/kg in the first hour. Repeated boluses on top of CRI escalate plasma levels rapidly.
• Consider alternatives. Sotalol (oral, when the patient can tolerate oral medication), magnesium CRI (for adjunct effect), or simply tolerating an arrhythmia with minor hemodynamic impact are all reasonable alternatives in cats. Lidocaine CRI is not the only or always the best answer in this species.
• Pause immediately if any CNS sign appears. The effect dissipates over 10–20 minutes once the infusion stops; supportive care (oxygen, anticonvulsant if seizing) carries the patient through.

Administration

Use preservative-free 2% lidocaine (20 mg/mL), the “plain” formulation. Do not use lidocaine with epinephrine, which is intended for local infiltration only; the epinephrine in those products produces unwanted systemic catecholamine effects on IV administration.

Stock is 20 mg/mL in 20 mL multi-dose vials (400 mg per vial). For CRI delivery, the InfusionFox calculator preselects three weight-banded preparations (20, 10, or 4 mg/mL). Larger dogs can run the 2% stock directly through a syringe pump without dilution; cats and small patients need progressive dilution to keep the pump rate in the precision range.

Diluent: 0.9% sodium chloride or 5% dextrose, both compatible.

Compatibility is broad. Avoid mixing in the same line with sodium bicarbonate (precipitation risk at higher lidocaine concentrations).

Drug interactions

• Cimetidine, propranolol, and beta-blockers reduce hepatic blood flow and slow lidocaine clearance. Plasma levels rise faster than expected at standard infusion rates; consider reducing the CRI when these are concurrent.
• Halogenated inhalant anesthetics may modestly potentiate lidocaine cardiotoxicity through additive negative inotropy. The risk is small at therapeutic plasma levels and significant only at high doses or in compromised patients.
• Other class I antiarrhythmics (procainamide, mexiletine) have additive effects on sodium-channel blockade and QRS widening. Concurrent IV use is generally avoided.
• Beta-blockers and calcium channel blockers have additive negative inotropy and AV-conduction effects. The combination is not contraindicated but warrants closer monitoring.
• Hepatic CYP inducers (phenobarbital, rifampin) accelerate lidocaine metabolism and shorten clinical duration. Less common interaction but relevant in chronic phenobarbital-treated seizure patients.

Adverse effects

CNS toxicity is the most common dose-limiting effect. The sequence as plasma levels rise: lip-smacking and facial twitching, then muscle tremors, then ataxia, then frank seizures. The early signs are subtle and easily missed; bedside attention every 30 minutes during the first few hours of CRI is the standard.

Cardiovascular toxicity appears at higher plasma levels: hypotension (negative inotropy and peripheral vasodilation), AV block (slowed conduction), and bradyarrhythmia. In severe overdose, asystole.

Other adverse effects:

• Methemoglobinemia at very high doses; uncommon at therapeutic plasma levels
• GI signs (nausea, vomiting) in dogs at higher CRI rates
• Worsening of underlying CHF through negative inotropy in patients with reduced ejection fraction
• Tachyphylaxis with prolonged infusion (uncommon at clinical doses but reported)
• Cat-specific: profound CNS depression, seizures, respiratory depression at doses that would be unremarkable in dogs

Monitoring

• Continuous ECG for rate, rhythm, QRS duration, and PR interval. The expected response is suppression of the targeted arrhythmia; widening QRS or new conduction block is a toxicity sign.
• Continuous or frequent BP, particularly during loading and at higher CRI rates. Hypotension is the most common acute hemodynamic problem.
• Mental status and neurologic exam every 30–60 minutes during the first few hours, then every 2–4 hours during the maintenance phase. CNS toxicity signs are subtle initially; lip-smacking, facial twitching, and minor ataxia are early warnings.
• Lidocaine plasma levels are available but rarely used in vet practice; the cost and turnaround time make clinical assessment the standard.
• Hepatic function at baseline and at intervals during prolonged infusion. Patients with hepatic dysfunction need lower CRI rates and may need to be switched to alternatives.

Weaning

For brief CRIs (less than 24 hours) treating reversible arrhythmia (post-operative VPCs that have stabilized), abrupt cessation is usually acceptable. The brief half-life means rebound is unlikely.

For prolonged CRIs in patients with structural heart disease, taper over 2–6 hours while observing rhythm. Transition to oral mexiletine (a class IB orally bioavailable agent) or amiodarone for sustained suppression. Watch for arrhythmia recurrence during the taper.

In cats, the threshold for stopping the infusion is much lower. Any sign of toxicity or any cumulative dose concern should prompt cessation rather than dose reduction; the safety margin does not support gradual taper at the toxicity threshold.

Sources

• Plumb’s Veterinary Drugs, lidocaine HCl (systemic) monograph (current edition).
• Côté E, MacDonald KA, Meurs KM, Sleeper MM, eds. Feline Cardiology. Wiley-Blackwell; 2011. (Cat-specific sensitivity, alternative agents for feline VT.)
• Kittleson MD, Côté E. Therapy of cardiac arrhythmias. In: Ettinger SJ, Feldman EC, Côté E, eds. Textbook of Veterinary Internal Medicine. 8th ed. Elsevier; 2017. (Lidocaine place in VT management algorithms.)
• Macintire DK, Drobatz KJ, Haskins SC, Saxon WD. Manual of Small Animal Emergency and Critical Care Medicine. 2nd ed. Wiley-Blackwell; 2012. (ICU antiarrhythmic protocols and loading dose conventions.)