Lidocaine is a local anesthetic that numbs tissues by preventing nerves from sending pain signals to the brain. Whether it increases heart rate is complex, as its effects on the cardiovascular system depend on its administration, dosage, and the medical context. While it can cause an increased heart rate under certain conditions, its primary therapeutic action on the heart is to slow and stabilize abnormal rhythms.
Lidocaine’s Primary Mechanism of Action
Lidocaine’s principal effect is achieved by blocking sodium channels, which are microscopic pores on the surface of nerve and muscle cells. These channels are responsible for the rapid influx of sodium ions that creates an electrical impulse, known as an action potential. In local anesthesia, lidocaine attaches to these channels in nerve cells, which stops them from opening and prevents the transmission of pain signals to the brain.
This same mechanism is central to its effects on the cardiovascular system. Heart muscle cells and the heart’s specialized conduction tissue also rely on sodium channels to initiate the electrical signals that cause the heart to contract. By interfering with these channels, lidocaine can alter the heart’s electrical excitability and the speed at which signals travel through it. This dual action forms the basis for its use as both a local anesthetic and a cardiac medication.
The drug’s chemical structure allows it to diffuse quickly through tissues to reach its target channels. Its impact is most pronounced in tissues that are firing rapidly. This characteristic is relevant in both over-stimulated pain nerves and certain types of rapid heart rhythms, allowing it to control specific issues without depressing overall heart function at therapeutic doses.
The Intended Effect of Lidocaine on the Heart
When administered intravenously in a controlled medical setting, lidocaine acts as a cardiac depressant. It is classified as a Class Ib antiarrhythmic drug, used for treating life-threatening ventricular arrhythmias—rapid heartbeats originating in the heart’s lower chambers. These conditions are often associated with damaged and electrically unstable tissue, such as during a heart attack.
Lidocaine is effective because it preferentially targets sodium channels in heart cells that are firing too frequently, a state they enter after just being used. By binding to and stabilizing these channels, it raises the threshold required to generate another electrical signal. This makes the heart muscle less likely to conduct the premature or rapid impulses causing the arrhythmia.
This action effectively slows the chaotic electrical activity in the ventricles. It can terminate dangerous rhythms caused by a “re-entrant” mechanism, where an electrical signal gets caught in a loop and repeatedly stimulates heart muscle. By interrupting this loop, lidocaine helps restore a normal rhythm and is used to decrease, not increase, an abnormally fast heart rate.
Scenarios Causing an Increased Heart Rate
Despite its function as a cardiac depressant, a racing heart is often reported after a lidocaine injection, particularly in dental or minor surgical settings. This effect is usually caused by epinephrine (adrenaline), a vasoconstrictor frequently combined with lidocaine. Epinephrine is added to constrict blood vessels at the injection site, which reduces bleeding and slows the rate at which lidocaine is absorbed, prolonging its numbing effect. However, epinephrine also stimulates the body’s “fight or flight” response, directly causing an increased heart rate and palpitations.
Patient anxiety is another significant factor that can increase heart rate. The stress associated with receiving an injection or undergoing a procedure can trigger the body’s natural release of adrenaline. This physiological response can cause a fast heart rate independent of the medication administered, and its effects can be difficult to distinguish from those of epinephrine.
In rare instances, an increased heart rate can be an early sign of lidocaine toxicity. If lidocaine is absorbed into the bloodstream too quickly or in too high a dose, it can cause initial central nervous system (CNS) stimulation. This can manifest as agitation and nervousness, which may indirectly lead to a temporary increase in heart rate before more severe signs appear.
Signs of Systemic Lidocaine Toxicity
If lidocaine enters the bloodstream in excessive amounts, it can cause local anesthetic systemic toxicity (LAST), a serious and progressive condition. Recognizing the early signs is important for preventing severe outcomes. The initial symptoms often involve the central nervous system and are typically subtle, including:
- Numbness or tingling around the mouth (perioral numbness)
- A metallic taste in the mouth
- Ringing in the ears (tinnitus)
- Visual disturbances like difficulty focusing
As blood concentrations rise, CNS symptoms can become more pronounced, progressing from disorientation and drowsiness to more severe effects. Muscle twitching is a common sign that may escalate into seizures, which are a hallmark of significant CNS toxicity. Following this excitatory phase, CNS depression can occur, leading to unconsciousness and respiratory arrest if not treated.
Cardiovascular signs of toxicity usually appear after the initial CNS symptoms and at higher concentrations. While an initial brief period of hypertension and a fast heart rate can occur, the more characteristic and dangerous cardiac effects are depressant. These include a slowing heart rate (bradycardia), a drop in blood pressure (hypotension), and significant changes in the heart’s electrical rhythm, which can lead to cardiac collapse and arrest.