Does Lidocaine Increase Your Heart Rate?

Lidocaine on its own does not typically increase heart rate, and at therapeutic doses it tends to either stabilize or slightly reduce it. The picture gets complicated, though, because most people encounter lidocaine in situations that also involve other heart-rate-altering factors: the epinephrine commonly mixed into dental injections, the anxiety of sitting in a procedure chair, or the stress response triggered by intubation during surgery. Untangling what lidocaine itself does to your pulse from what everything around it does is where the real answer lives.

What Lidocaine Actually Does to Your Heart

Lidocaine is a sodium channel blocker. It works by reducing the ability of sodium channels in heart cells to open, which slows down the electrical signals that drive each heartbeat. In laboratory studies on isolated heart tissue, lidocaine decreases the probability of cardiac sodium channels opening and shortens the time they stay open.¹ This blocking effect is dose-dependent and becomes stronger at higher concentrations.²

In a living heart, this translates to a dampening effect on electrical excitability. When researchers compared lidocaine with other local anesthetics in an animal model, lidocaine produced the smallest electrocardiographic and hemodynamic changes of the group.³ Among several local anesthetics tested on the heart’s natural pacemaker, all caused a dose-dependent decrease in heart rate, with lidocaine falling in the middle of the potency ranking.⁴

So if the drug’s direct cardiac effect is to slow things down, why do some people feel their heart racing after a lidocaine injection? The answer usually has little to do with lidocaine itself.

The Epinephrine Factor

Most lidocaine formulations used in dentistry and minor surgery contain epinephrine (adrenaline). Epinephrine is added because it constricts local blood vessels, which keeps the lidocaine concentrated at the injection site longer and reduces bleeding. But epinephrine is also a potent heart-rate booster, and some of it inevitably reaches the bloodstream.

A randomized trial comparing dental injections of plain lidocaine versus lidocaine with epinephrine found that plain lidocaine slightly reduced both blood pressure and heart rate compared to baseline, while lidocaine combined with epinephrine significantly increased both.⁵ Another study found that plain lidocaine caused no significant cardiovascular changes, while lidocaine with 80 micrograms of epinephrine raised heart rate by up to 13 beats per minute above baseline by the end of the observation period.⁶

The dose of epinephrine matters a lot here. A lower dose of 20 micrograms caused only about a 4-beat-per-minute increase, while 80 micrograms produced a more dramatic rise that kept climbing for 15 minutes. In practice, a standard dental cartridge contains somewhere in that range, and about two-thirds of patients in one study experienced a noticeable increase in heart rate after receiving lidocaine with epinephrine at a 1:100,000 concentration. In most of those patients, the rate settled back to near baseline within four minutes.⁷

If you’ve ever felt your heart pound after a dental injection, the epinephrine is almost certainly the culprit. This is worth knowing because epinephrine-free lidocaine formulations exist, and for patients with heart conditions or anxiety about heart-rate spikes, a dentist can sometimes use one of these alternatives.

Anxiety and the Stress Response

The other major contributor to a racing heart during lidocaine injections is anxiety, which releases your body’s own adrenaline. Researchers studying dental extractions found that patients with severe preoperative anxiety had significantly higher heart rates and blood pressure during administration of anesthetic compared to calmer patients.⁸ Pain on injection amplified the effect further.⁹

This means the very act of receiving an injection can drive your heart rate up before the drug has even had time to work. If you are already nervous, the needle sting sends a surge of endogenous adrenaline through your system that is chemically identical to the epinephrine in the syringe. A study of hypertensive patients undergoing tooth extractions confirmed that heart rate, pulse rate, and blood pressure all rose immediately after local anesthetic delivery, and that the increase was tied to severity of anxiety rather than to the drug’s pharmacology.¹⁰

For many people, the experience of “lidocaine made my heart race” is really “the stress of getting a shot made my heart race.” That does not make the experience any less real, but it changes what you might do about it. Relaxation techniques, slower injection speeds, and good communication with your provider can all help bring the stress component under control.

Lidocaine’s Parasympatholytic Effect

There is one scenario where lidocaine itself genuinely raises heart rate, and it involves the vagus nerve. One study measured heart rate in healthy volunteers, patients who had recently had a heart attack, and patients currently in the acute phase of a heart attack, all receiving intravenous lidocaine. In every group, mean heart rate increased: roughly 5.5% in healthy subjects, about 9.4% in the recent-heart-attack group, and around 8.1% in the acute-heart-attack group. At the same time, the power of respiratory-related heart-rate fluctuations dropped significantly, indicating that lidocaine was suppressing the parasympathetic (vagal) tone that normally acts as a brake on heart rate.¹¹

This parasympatholytic effect is consistent and statistically significant, but in absolute terms the increase is modest. A 5-6% rise on a resting rate of 70 beats per minute works out to about 4 extra beats a minute. Most people would not notice that without a heart rate monitor. Still, it is a real pharmacological action of lidocaine, distinct from epinephrine or anxiety, and it is worth knowing exists, especially for patients whose cardiac rhythm is already unstable.

Intravenous Lidocaine in Surgery

When anesthesiologists give lidocaine intravenously during general anesthesia, the goal is often the opposite of speeding the heart up. Intubation and extubation tend to trigger sharp spikes in heart rate and blood pressure, and IV lidocaine helps blunt those spikes. A systematic review and meta-analysis of patients undergoing thoracoscopic surgery found that perioperative IV lidocaine significantly attenuated both heart rate and blood pressure surges during intubation and extubation.¹²

A controlled trial comparing IV lidocaine to saline during general anesthesia found that the lidocaine group had significantly lower heart rates immediately after intubation and at several time points afterward. At one minute post-intubation, the lidocaine group averaged about 78 beats per minute compared to about 103 in the saline group.¹³ Another randomized trial found that lidocaine, used alone or with magnesium sulfate, produced significantly smaller fluctuations in heart rate during anesthesia induction and maintenance compared to controls.¹⁴

In the surgical context, lidocaine acts as a cardiovascular stabilizer. It does not drive heart rate down to dangerous levels; it prevents the sharp upward swings that the stress of surgery provokes. This stabilizing role has made IV lidocaine a common part of anesthetic protocols, alongside its well-documented benefits for pain management and reduced opioid use.

When Too Much Lidocaine Gets Into the Bloodstream

Local anesthetic systemic toxicity, or LAST, occurs when lidocaine blood levels climb too high, usually because of accidental intravascular injection or absorption of excessive doses from tissues. The cardiovascular effects of LAST are biphasic: the early phase features nervous system excitation along with tachycardia (a fast heart rate), while the late phase can produce severe hypotension, bradycardia (a dangerously slow rate), abnormal heart rhythms, and in the worst case, cardiac arrest.¹⁵

That early tachycardia phase is worth noting because it is one situation where lidocaine can genuinely cause a fast heart rate, but it is a warning sign that something has gone wrong rather than a normal response. Symptoms often include ringing in the ears, a metallic taste, dizziness, and agitation before the cardiovascular effects kick in. In animal studies, lidocaine-induced ventricular arrhythmias at toxic central nervous system doses did tend to revert to normal rhythm spontaneously, which is one reason lidocaine is considered less cardiotoxic than longer-acting local anesthetics like bupivacaine.¹⁶

When LAST does cause cardiac arrest, intravenous lipid emulsion therapy has emerged as a life-saving treatment. In one reported case, a patient who went into cardiac arrest after lidocaine received a bolus of 20% intralipid solution, and return of spontaneous circulation occurred within minutes.¹⁷ LAST is rare in properly dosed procedures, but awareness of it matters for anyone receiving large-volume lidocaine injections, such as during tumescent liposuction or extensive nerve blocks.

Higher Blood Levels and Cardiac Depression

Even short of full-blown toxicity, lidocaine blood levels at the higher end of the therapeutic range can depress heart function. When researchers measured hemodynamic effects after paravertebral blocks, patients whose blood lidocaine levels exceeded 3 micrograms per milliliter at the 15-minute mark showed significant reductions in blood pressure, cardiac output, and cardiac contractility compared to patients with lower levels.¹⁸ In dogs receiving continuous epidural lidocaine, heart rate, blood pressure, and cardiac output all decreased in a dose-dependent fashion as plasma levels rose.¹⁹

The clinical takeaway is that lidocaine’s direct effect on the heart is depressive, not stimulatory. As you absorb more of it, your heart rate and contractility tend to drop, not rise. This is consistent with its mechanism as a sodium channel blocker and is why dosing guidelines exist to keep blood levels in the therapeutic window. For patients with heart failure, dosing may need to be adjusted since both clearance of the drug and the heart’s tolerance for further depression are reduced.

Drug Interactions That Shift the Balance

Certain medications can change how quickly your body clears lidocaine, which in turn affects how high blood levels climb and how pronounced the cardiovascular effects become. Beta-blockers like metoprolol and propranolol significantly reduce lidocaine elimination from the body.²⁰ If you are on a beta-blocker and receive lidocaine, the drug hangs around longer, making higher-than-expected blood levels more likely. Interestingly, the same study found no direct correlation between the heart-rate-lowering effect of the beta-blocker and the change in lidocaine clearance, meaning slower elimination happens regardless of how much the beta-blocker has slowed your pulse.

This interaction matters in practice because the same patients most likely to be on beta-blockers (those with heart disease or high blood pressure) are also the patients for whom lidocaine blood levels drifting upward poses the greatest risk. If you are taking a beta-blocker and are scheduled for a procedure involving substantial amounts of lidocaine, your provider should be aware and may adjust the dose accordingly.

Lidocaine’s Original Claim to Fame as an Antiarrhythmic

Lidocaine was first synthesized as a local anesthetic in 1943, but its antiarrhythmic properties were not recognized until the late 1950s when anesthesiologists noticed it could stop dangerous heart rhythms during open-heart surgery.²¹ By the 1960s, lidocaine had become a cornerstone drug in the newly developed coronary care units for treating and preventing ventricular arrhythmias in heart attack patients. Its whole clinical purpose in cardiology is to suppress abnormally fast or chaotic electrical activity, not to speed the heart up.

Today, lidocaine remains in use for acute ventricular arrhythmias in intensive care settings, though it has been partially displaced by newer drugs like amiodarone. A recent study of ICU patients with ventricular arrhythmias and heart failure found that standard maintenance dosing kept lidocaine within the therapeutic range about two-thirds of the time.²² The fact that a meaningful fraction of patients drifted outside the therapeutic window underscores how carefully this drug needs to be dosed, especially in people with compromised hearts.

Lidocaine and Fetal Heart Rate

Pregnant patients receiving epidural lidocaine for cesarean sections understandably want to know whether the drug will affect their baby’s heart rate. The evidence here is reassuring. A study comparing epidural lidocaine to bupivacaine for elective cesarean delivery found no changes in fetal heart rate after anesthesia and no significant differences between the two drugs in baseline fetal heart rate, variability, or the occurrence of accelerations or decelerations.²³

An earlier study did observe temporary changes in fetal heart rate variability in about half of patients after lumbar epidural lidocaine, with or without epinephrine. The changes appeared within minutes of drug injection and resolved within 4 to 18 minutes. The researchers concluded that these transient shifts in variability did not indicate fetal distress.²⁴ The short-lived nature of the changes fits with what we know about lidocaine’s pharmacokinetics: it is metabolized relatively quickly, and the small amounts that cross the placenta do not accumulate in the fetus.

Sorting Out What You Actually Felt

If you noticed your heart beating faster after a lidocaine injection, here is a rough guide to figuring out why, listed from most likely to least:

Epinephrine: If the formulation contained epinephrine (most dental cartridges do), that is by far the most common explanation. The spike typically resolves within a few minutes.
Anxiety or pain: Your body’s own adrenaline response to the needle, the procedure, or the pain of injection can raise heart rate substantially, especially if you were already nervous.
Vagal suppression: Lidocaine’s parasympatholytic effect can produce a modest increase, usually around 4 to 6 extra beats per minute, though you are unlikely to feel this without other factors amplifying it.
Early toxicity: If the dose was large or some was accidentally injected into a blood vessel, early systemic toxicity can include tachycardia alongside neurological symptoms like ringing ears or dizziness. This is uncommon but worth being aware of.

For most people undergoing a routine dental or dermatological procedure, the heart-rate increase is brief, benign, and driven primarily by the epinephrine additive or by the stress of the moment. Lidocaine’s own pharmacological fingerprint on the heart leans toward slowing things down, not speeding them up.