Accelerated Idioventricular Rhythm Following Intraoral Local Anesthetic Injection During General Anesthesia

An accelerated idioventricular rhythm (AIVR) is characterized by an ectopic regular ventricular rhythm with 3 or more consecutive ventricular complexes at a faster rate (50–100 beats per minute [bpm]),^1,2 compared with a ventricular escape beat/rhythm (20–40 bpm). Several drugs or anesthetic agents routinely administered during general anesthesia, including desflurane,^2,3 isoflurane,⁴ propofol,⁵ and epinephrine,⁶ have been reportedly associated with AIVR. There is also evidence that AIVR is associated with higher vagal tone and lower sympathetic activity,⁷ as well as a sympathetic nerve block during spinal anesthesia for cesarean section.⁸ Herein, we describe AIVR that was induced by vagal response to injection-related pain following infiltration of local anesthetic into the oral mucosa during general anesthesia.

CASE PRESENTATION

A 48-year-old woman (weight 50 kg; height 150 cm; body mass index 22.2 kg/m²) was scheduled to undergo extraction of a residual tooth root from the left maxillary sinus. She had no prior medical history and had not been prescribed any drugs. Her preoperative electrocardiogram (ECG) findings were within normal limits, demonstrating a normal sinus rhythm, 0.183-second PR interval (the period from the beginning of the P wave until the beginning of the QRS complex), 0.08-second QRS, and 0.469-second QT interval (Figure 1). All preoperative serum electrolyte levels were within normal ranges, and the patient had no known drug allergies. Atropine 0.2 mg and midazolam 3.0 mg were administered intravenously as premedications in the operating room (OR). General anesthesia was induced with propofol 100 mg, fentanyl 50 μg, and rocuronium 40 mg. After the patient was intubated, anesthesia was maintained with sevoflurane 1% to 1.5% in oxygen 40% and air 60%, combined with fentanyl 50 μg and a remifentanil infusion 0.2 μg/kg/min. The patient's hemodynamics were stable for the subsequent 30 minutes during preparation for the surgical procedure, with a heart rate of 50 to 60 bpm (Figure 2a), a blood pressure (BP) ranging from 80 to 98/38 to 50 mm Hg, an EtCO₂ of 37 to 38 mm Hg, and an SpO₂ of 100%. The bispectral index was 56 to 58. The patient's vital signs, ECG, EtCO₂, and SpO₂ were continuously monitored. A period of brief hypotension (ie, a BP of 80/38 mm Hg) was treated with intravenous fluids and rapidly normalized.

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Immediately before the administration of local anesthesia, the patient's heart rate was 50 bpm and BP was 88/50 mm Hg. The oral and maxillofacial surgeon rapidly infiltrated around the left maxillary molars with 8 mL of 1% lidocaine (80 mg) containing 1:100,000 epinephrine (80 μg) over a period of 20 seconds with a 23-gauge needle and firm pressure. Widened QRS complexes (≥120 ms) consistent with AIVR suddenly appeared on the ECG and continued for ∼60 seconds. At this time, the patient had a heart rate of 55 bpm (Figure 2b) and a BP of 106/55 mm Hg (mean 72 mm Hg). During observation of the ECG, the run of monomorphic ventricular complexes disappeared as an atrioventricular junctional rhythm (rate of 60 bpm) began and continued for ∼60 seconds. This was followed by the return of a normal sinus rhythm (rate of 60 bpm; Figures 2c–d).

Although we initially presumed that a small amount of local anesthetic had been injected intravascularly, immediate consultation with a cardiologist and a 12-lead ECG obtained in the OR revealed no major concerns; thus, the surgical procedure proceeded. The patient's hemodynamics were stable for the remainder of the surgery, which was successfully completed ∼30 minutes after the transient AIVR episode. The patient's plasma troponin I concentration measured at 3 hours postoperatively was within the normal range (0.0002 ng/mL). Postoperative Holter ECG on the day of surgery showed a normal sinus rhythm (51−96 bpm) and no prolonged R-R interval; the patient had no subjective symptoms during the Holter ECG recording.

DISCUSSION

In this report, we described a case of AIVR during general anesthesia associated with the rapid infiltration of local anesthetic into the oral mucosa involving a large gauge needle and firm pressure. The potential mechanism of AIVR in this case was presumed to involve excessive vagal response to injection-related pain. For dental treatment under general anesthesia, surgeons occasionally use a large needle and firm pressure to rapidly administer local anesthesia, while more conservative slower approaches are typically used when the patient is conscious. Immediately after surgery in the present case, the surgeon stated that he had infiltrated the local anesthetic using greater hand pressure than usual. During infiltration, we observed that the surgeon injected the local anesthetic into the oral mucosa with substantial force, which involved shaking in his right hand and shoulder.

In conscious patients, the dentist or oral maxillofacial surgeon generally administers local anesthetic gently into the oral tissues, typically using smaller needles (27- or 30-gauge) and slower injection speeds (1.8 mL over 30–60 seconds) to reduce injection pain. However, for patients under general anesthesia, surgeons may infiltrate using a larger needle (23-gauge), stronger pressure, and a more rapid injection speed (8 mL over 20 seconds in the present case) likely because they presume injection pain will be reduced.

Bradycardia and sinus arrest can occur as a result of surgical stimulation during a variety of surgical procedures, including neurosurgery, as well as general abdominal, laparoscopic, ophthalmic, and facial surgeries, and most instances are thought to involve vagally mediated reflexes.⁹ In oral and maxillofacial surgery, the trigeminocardiac reflex may manifest after stimulation of any of the trigeminal nerve branches and has been reported with procedures such as a Le Fort I osteotomy,¹⁰ midface fracture reduction,¹¹ zygomatic fracture elevation,¹² and temporomandibular joint insufflation.¹³ The oculocardiac reflex (a trigeminocardiac reflex subtype) can be caused by traction of the extraocular muscles or compression of the globe, leading to a rapid and often profound reduction in heart rate through the efferent limb of the vagus nerve from the cardiovascular center of the medulla to the heart.¹⁴

In the present case, the surgeon infiltrated local anesthetic into the area of the piriform aperture, nasal sidewall, and anterior maxillary sinus wall. When surgeons rapidly infiltrate local anesthetic into this area using a larger needle (ie, 23-gauge) and very firm pressure, an intense noxious stimulus directly related to peripheral nociceptor activation in response to the rapid infiltration may evoke the trigeminocardiac reflex and possibly lead to AIVR. General anesthesia can inhibit the sensory tract, cerebral cortex, and spinal neurotransmission; however, activation of peripheral nociceptors remains possible. Furthermore, severe bradycardia under general anesthesia has been reported following assisted mouth opening that involved the trigeminocardiac reflex triggered by stimulation from opening the patient's mouth.¹⁵ We previously reported that bradycardia was induced by an intense noxious stimulus following rapid infiltration of large volumes of local anesthetic into the oral submucosa facilitated by the use of a large gauge needle and strong hand pressure.¹⁶ Thus, the AIVR in our case was likely induced by the intense noxious stimulation caused by the rapid infiltration of local anesthetic, which activated the trigeminocardiac reflex.

Another possibility relates to the use of local anesthetic or general anesthetic agents. Oral and maxillofacial surgeons typically infiltrate local anesthetics with epinephrine to decrease surgical bleeding, reduce mucosal congestion, and maintain a clear surgical field. Local anesthetics containing epinephrine can induce arrhythmias when used in conjunction with inhaled anesthetics.¹⁷ As mentioned previously, surgeons may administer local anesthetics quite rapidly to patients under general anesthesia, which can increase systemic uptake particularly if inadvertent intravascular delivery occurs. For example, in our hospital, up to 10 mL of local anesthetic with epinephrine is commonly infiltrated into 1 side over 10−20 seconds for a sagittal split ramus osteotomy. In the present case, 8 mL of 1% lidocaine with 1:100,000 epinephrine was infiltrated over 20 seconds, which could have produced a rapid increase in systemic epinephrine levels. In contrast, for patients who are conscious, local anesthesia is typically administered in smaller volumes over a longer period (eg, 1.8 mL of local anesthetic administered slowly over 30–60 seconds). Assuming negative aspiration, slow administration considerably reduces the systemic uptake.

AIVR has reportedly been induced by epinephrine following the infiltration of local anesthetic containing epinephrine into the oral mucosa during general anesthesia.⁶ The electrophysiologic characteristics of AIVR suggest a mechanism involving abnormal automaticity, such as enhanced phase 4 depolarization of ventricular muscle fibers.³ Epinephrine typically increases the rate of phase 4 depolarization, which can induce arrhythmias like AIVR.^2,3 Although it was unclear whether AIVR in this case was induced by a rapid increase in systemic epinephrine levels, we felt it unlikely based on the patient's vital signs. Our findings suggest that surgeons should consider the potential risk of cardiovascular complications when rapidly administering local anesthetics with vasoconstrictors.

Nevertheless, the potential influences of general anesthetic agents (eg, atropine, midazolam, propofol, fentanyl, rocuronium, sevoflurane, and remifentanil) on AIVR remain unclear. Some anesthetics are presumably associated with AIVR because of their toxicity.¹⁸ In our case, atropine and midazolam were administered as premedication before induction. Low-dose atropine (≤0.2 mg) can reportedly induce paradoxical bradycardia through stimulation of vagal nuclei in the medulla oblongata.¹⁹ Midazolam influences autonomic neurocardiac regulation in a biphasic manner, which causes the reduction of central vagal tone and may directly decrease cardiac pacemaker activity.²⁰ Propofol suppresses sympathetic and parasympathetic tones, although sympathetic suppression is greater than parasympathetic.²¹ Rocuronium administered alone has shown no effect on heart rate at clinically relevant concentrations. However, when administered at high concentrations (>2 mg/kg) and combined with IV acetylcholine, rocuronium partially inhibits vagally mediated cardiac activity.²³ Sevoflurane does not induce arrythmias by stimulation of the sympathetic nervous system but has been shown to sensitize the heart and reduce the epinephrine concentration at which arrhythmias can be induced.² Remifentanil depresses sinus node function and most parameters of atrioventricular nodal function²⁴ while enhancing vagal tone.²⁵ Although these anesthetic agents influence aspects such as ion channel activity, sinoatrial and atrioventricular nodal functions, and the balance of sympathetic versus parasympathetic activity, it is unlikely these anesthetic agents alone induced AIVR in our case. However, they may have influenced the onset of AIVR in combination with stimulation from the local anesthetic injection, which activated the trigeminocardiac reflex.

Most instances of AIVR do not require specific treatment and resolve spontaneously.¹⁸ AIVR may occur upon either slowing of an atrial pacemaker or accelerated ventricular pacemaker automaticity.²⁶ Generally, AIVR disappears gradually after 30 beats² but may persist for up to 5 minutes. Additionally, causative drugs may be discontinued or therapeutic agents may be administered.^2–4,6,18 Recurrent AIVR was reportedly observed in some instances when treatment with a causative drug was continued or restarted.^2–4,6,18 Patients with AIVR often undergo close monitoring (eg, hourly vital sign assessment and continuous ECG) and observation until the recovery of a normal sinus rhythm, generally within 3 hours. This approach is used in our hospital in accordance with the published literature.² Enhancement of the sinoatrial node depolarization rate is the recommended treatment for AIVR and typically involves administration of atropine and/or atrial pacing rhythm management.^2,18,27,28 Ephedrine is controversial because it can potentially increase AIVR duration.⁸ Lidocaine has been administered to patients with AIVR to successfully restore a normal sinus rhythm.⁶ In the present case, conservative management comprising close monitoring was performed, and our patient exhibited stable hemodynamics with no obvious symptoms during postoperative recovery.

CONCLUSION

The AIVR that occurred during general anesthesia in this case was attributed to pain-induced activation of the trigeminocardiac reflex associated with the rapid infiltration of local anesthetic facilitated using a large gauge needle and firm pressure. To minimize excessive pressure and stimulation that may trigger the trigeminocardiac reflex and lead to AIVR, local anesthetic administration should be performed cautiously in a controlled manner, particularly when using a large gauge needle.