Coronary Spasm During Postoperative Sedation With Dexmedetomidine

Abstract

This is a case report of an 81-year-old woman who underwent tracheostomy, bilateral cervical dissection, partial tongue resection, radial forearm free flap reconstruction, and split-thickness skin grafting under general anesthesia. After successful surgery, she was moderately sedated postoperatively with intravenous dexmedetomidine (DEX) and fentanyl. The fentanyl was discontinued 5 hours postoperatively. Eight hours after the operation, an atrioventricular junctional rhythm, a 2-mm elevation of the ST segment, and biphasic T waves were detected in lead II that lasted approximately 3 minutes. Hypotension and bradycardia were observed simultaneously with the abnormal electrocardiogram. The next day, a cardiologist examined the patient and suggested that coronary spasm had occurred based on those findings. The transient coronary spasm was likely caused by a combination of various factors including surgical stress and altered autonomic function. However, it is possible that stimulation of α-2 adrenergic receptors induced by DEX may also be linked to the coronary vasospasm that occurred.

The α-2 adrenergic agonist dexmedetomidine (DEX) continues to become more widely used for sedation and general anesthesia due to its sedative and analgesic effects primarily attributed to its actions on the locus coeruleus in the brainstem and suppressed pain signal transmission in the spinal cord, respectively. Sedation with DEX mimics physiological sleep and triggers less respiratory depression.^1,2 DEX is also frequently used in elderly patients as it may help prevent postoperative delirium.³ However, DEX suppresses the sympathetic response by acting on the reticular formation of the medulla oblongata, lowers blood pressure and heart rate, and acts on vascular smooth muscle to cause vasoconstriction. In this case report, we describe transient ST-segment elevation and hypotension during sedation with DEX after oral and maxillofacial reconstruction surgery in an elderly patient. Although there are reports of vasospasm occurring during DEX infusion, this is the first case of vasospasm during postoperative sedation with DEX.^3,4

CASE PRESENTATION

An 81-year-old woman (height 151 cm; weight 43 kg; body mass index 18.8 kg/m²) with a tongue malignancy was scheduled for tracheostomy, bilateral cervical dissection, partial tongue resection, reconstruction with radial forearm free flap, and split-thickness skin grafting under general anesthesia. The patient was otherwise healthy, had a functional capacity of >4 metabolic equivalents, and denied taking any medications. No abnormalities were found during the routine preoperative examination, which included a complete blood count, blood chemistry, posteroanterior chest radiograph, and pulmonary spirometry. The preoperative electrocardiogram (ECG) demonstrated sinus bradycardia (rate ∼35 bpm) and voltage criteria consistent with left ventricular hypertrophy (RV5 + SV1 = 4.190 mV; Figure 1). Echocardiography revealed moderate tricuspid regurgitation, a left ventricular ejection fraction of 72%, but no wall motion abnormalities. Since the patient had no cardiac history and was bradycardic on a previous ECG, that finding was considered normal for her.

Figure 1.

Preoperative 12-lead ECG. The patient's routine preoperative 12-lead ECG demonstrated severe sinus bradycardia (rate ∼35 bpm) and voltage criteria consistent with left ventricular hypertrophy.

The day of surgery, general anesthesia was induced by continuous intravenous infusion of remifentanil 0.3 μg/kg/min, a bolus of propofol 60 mg, and rocuronium 30 mg following placement of standard anesthesia monitors. The patient was intubated to secure the airway before the tracheostomy was performed. Anesthesia was maintained using sevoflurane 1%–2% with air and oxygen (FiO₂ of 40%) and continuous infusion of remifentanil 0.1–0.2 μg/kg/min. Although bradycardia (rate ∼40–50 bpm) was observed during surgery, no ST segment abnormalities were observed. Approximately 1 hour prior to the end of the surgery, infusions of DEX 0.46 μg/kg/h and fentanyl 100 μg/h were started for postoperative sedation and analgesia. The total surgical time was 9 hours 35 minutes, and the total anesthesia time was 11 hours 41 minutes.

After an uneventful operation, continuous blood pressure, ECG, and pulse oximetry monitoring was conducted on the patient in the regular patient ward. She maintained spontaneous breathing with the DEX and fentanyl infusions. Fentanyl was stopped 5 hours postoperatively to avoid oversedation. At 8 hours after the operation, an atrioventricular (AV) junctional rhythm without P waves, a 2-mm ST segment elevation, and biphasic T waves were detected in lead II that lasted ∼3 minutes (Figure 2a). The patient's systolic blood pressure decreased from 120 mm Hg to 78 mm Hg, and her heart rate slightly decreased to 31 bpm. However, her ECG returned to normal without any treatment (Figure 2b). During this time period, nursing staff noted that the patient was alert, oriented, and did not complain of any chest discomfort. Since these findings were transient, the nurse did not report to the on-call doctor. The DEX infusion was continued until 10 hours after the operation.

Figure 2.

Postop transient coronary spasm. While sedated 8 hours postoperatively with DEX, an AV junctional rhythm, 2 mm ST elevation, and biphasic T waves were detected in lead II, which lasted for 3 minutes before returning to normal sinus rhythm.

On the basis of these findings, we suspected that hypotension occurred due to transient coronary spasm. On postoperative day (POD) 1, a cardiologist was consulted and a 12-lead ECG was obtained. However, the ECG did not suggest any ischemic changes or cardiac disease. Moreover, the serum biomarkers used as predominant indicators of acute myocardial infarction (eg, cardiac troponin-T, creatine kinase, and aspartate transaminase) did not show any significant increase. The cardiologist concluded that transient hypotension was caused by coronary spasm. Other tests to investigate cardiac functions were not performed as the cardiologist felt them unnecessary. The patient did not complain of chest pain or other cardiac symptoms during her hospitalization and was discharged on POD 30 as is customary in our hospital system.

Approximately 3 months after the operation, another 12-lead ECG was performed. Although bradycardia (rate ∼37 bpm) with an AV junctional rhythm without P waves was observed, no specific ST segment abnormalities were noted (Figure 3). Nitroglycerin for chest pain, which was prescribed by the cardiologist, has never been used to date.

Figure 3.

Repeat 12-lead ECG 3 months later. Another 12-lead ECG performed 3 months later demonstrated bradycardia (rate ∼37 bpm), an AV junctional rhythm, but no ST segment abnormalities.

DISCUSSION

Here, we report a case of a transient AV junctional rhythm, 2 mm ST elevation, biphasic T waves, and hypotension observed during postoperative sedation with DEX, which was diagnosed as coronary spasm. The patient did not complain of any symptoms indicative of coronary spasm. In fact, the incidence of silent myocardial ischemia caused by coronary spasm has been reported to be more than twice that of symptomatic ischemia or angina pectoris.⁶ In some elderly patients, however, ischemic heart disease might not be noticed due to a lack of subjective symptoms. In this case, the symptoms were thought to be obscured by sedation.

It has been suggested that the use of DEX during cardiac surgery is effective for reducing the incidence of postoperative complications, reducing postoperative mortality, and improving the outcome of postoperative patients.^5,7,8 However, some reports have suggested a correlation with DEX and coronary spastic angina that may warrant further investigation. Kundra et al³ reported coronary angiography after administration of DEX resulted in significant right coronary artery stenosis in patients without coronary artery disease, with bradycardia and hypotension occurring at the same time.³ Furui et al⁴ reported a case where an ablation was performed under sedation with propofol and was completed without any problems. During a second treatment to prevent recurrence, however, the sedation was performed using a high-dose loading of DEX (4 μg/kg/h) when an ST-segment elevation developed in the inferior leads and the diagnosis of coronary vasospasm was made by urgent coronary angiography. Additionally, the presence of α-adrenergic coronary artery stenosis in humans has been established by catheterization or studies using PET.¹⁰ Since it has been shown that α-2 adrenoreceptor-mediated vasoconstriction can involve the coronary circulation, it is possible that stimulation of α-2 adrenergic receptors induced by DEX could have contributed to the coronary vasospasm.^4,9

Although Furui et al⁴ reported that coronary spasm can occur during early high-dose loading of DEX, the coronary spasm in this case occurred long after the DEX was initiated. However, the high-dose intravenous administration of DEX has been reported to cause moderate local coronary vasoconstriction at the same time as a marked vasoconstrictor reaction in young domestic pigs, and a similar phenomenon may occur in humans.¹¹ There is also a report that Japanese people have a higher frequency of coronary spasm than other races.¹² Therefore, it seems that Japanese people need to be especially careful, as based on these reports, it may be possible for coronary spasm to occur when DEX is used.

Since coronary spasm can be induced by variation in parasympathetic activity, angina occurs most often during rest throughout the night until early morning.^13,14 This suggests that an imbalance in autonomic activity has been implicated in the genesis of coronary artery spasm, although coronary spasm can be induced by a variety of stimuli acting on different vascular smooth muscle receptors. Kaneko et al¹⁵ reported that the pharmacologic actions of sedatives can cause abnormalities in autonomic nervous system function due to suppression of sympathetic activity and increased parasympathetic tone. In this case as well, abnormalities in autonomic function due to the stress of long-term surgery likely occurred, and the direct action by the release of vasoconstrictors like noradrenaline coupled with predominant parasympathetic tone due to postoperative sedation were likely major contributors to the coronary spasm.¹⁵

In this case, the report from the nurse who noticed the transient abnormal ECG was late, as the symptoms appeared late at night and the patient did not report any symptoms. When we were informed about the abnormal ECG episode in the morning the next day, we immediately consulted the cardiologist. Fortunately, the patient suffered no long-term sequelae from this incident. As coronary spasm plays an important role in the pathogenesis of ischemic heart disease, including angina pectoris, myocardial infarction, and sudden death, early detection and prompt treatment of coronary spasm is very important in the prognosis of patients.

CONCLUSION

The patient in this case report experienced transient coronary spasm with ST elevation and hypotension in the postoperative ward while sedated with DEX. Often used in the elderly population, DEX causes less respiratory depression and has sedative effects that mimic physiological sleep, but it can also cause hypotension and bradycardia. The combination of various factors in this case such as surgical stress and altered autonomic function likely led to the coronary spasm. However, it is also possible that stimulation of α-2 adrenergic receptors induced by dexmedetomidine also may have contributed. Considering the other reports of coronary spasm occurring concurrently with DEX, further studies are needed.