In this case, stenosis of the left common carotid artery, bilateral vertebral artery, and bilateral subclavian artery was observed. Moreover, the patient had a history of treatment for coronary artery stenosis, and severe aortic regurgitation and pericardial effusion were observed. Therefore, we believed it was important to select the correct anesthetic method, to maintain perioperative cerebral blood flow, to maintain coronary artery blood flow, and to manage heart failure.
First, regarding the selection of anesthetic method, all the reports so far have reported on epidural anesthesia, spinal anesthesia, or a combination of both [3,4,5,6,7,8,9]. In previous reports, epidural anesthesia was selected to prevent sudden blood pressure deterioration [4,5,6]. In this case, the patient was under antiplatelet drug therapy. Therefore, general anesthesia was also an option because of concerns about bleeding complications associated with regional anesthesia. However, we selected regional anesthesia because of the possibility that airway edema was progressing due to pregnancy, heart failure, and severe tachycardia and hypertension due to insufficient depth of rapid sequence induction followed by myocardial oxygen supply-demand imbalance causing myocardial ischemia and exacerbation of heart failure. Furthermore, general anesthesia conceals neurological deficits, such as consciousness disturbance and paralysis due to cerebral ischemia. Epidural anesthesia is desirable to avoid sudden circulatory fluctuations, as per previous reports [4,5,6]. However, we selected spinal anesthesia because the patient was under aspirin therapy and the puncture needle was thinner than the epidural needle, and a sufficient anesthesia area could be obtained by a single puncture and drug administration and we could prepare effective vasopressors, even though epidural anesthesia is relatively safe without concern about spinal hematoma according to the guideline of regional anesthesia in patients receiving antithrombotic or thrombolytic therapy . When spinal anesthesia was performed, we ensured to prevent hemodynamic deterioration caused by a rapid decrease in blood pressure and aggravation of aortic regurgitation associated with bradycardia.
For the treatment of hypotension during cesarean section under spinal anesthesia, phenylephrine tends to cause maternal bradycardia, whereas noradrenaline is not likely to cause bradycardia [11, 12]. A continuous administration of noradrenaline can prevent hypotension after spinal anesthesia during cesarean section and phenylephrine-induced bradycardia and reactive hypertension . In contrast, noradrenaline increases myocardial contractility and heart rate by beta 1 receptor stimulation, which can lead to tachycardia . In this case, to maintain circulation with spinal anesthesia, bradycardia and increased cardiac afterload should be prevented considering severe aortic regurgitation; however, tachycardia should also be prevented considering coronary artery disease. Therefore, continuous administration of low-dose noradrenaline was selected to prevent an excessive decrease in systemic vascular resistance and to maintain heart rate. Until the onset of these effects, a single dose of noradrenaline, which may cause tachycardia, was not selected, and a single dose of phenylephrine (0.1 mg) was carefully and appropriately administered to maintain blood pressure. The sufficient effect of the continuous administration of noradrenaline, which led to stable and appropriate blood pressure and heart rate, appeared at the beginning of the surgery. A previous study reported that noradrenaline was effective for various maternal and fetal outcomes of cesarean section with regional anesthesia to prevent low blood pressure . Noradrenaline is not inferior to phenylephrine for fetal acidosis . In this case, noradrenaline was effective for maintaining blood pressure during surgery, and both arterial blood pH of the umbilical cord and the infant’s Apgar score were also acceptable. To maintain coronary blood flow, we maintained sufficient diastolic blood pressure and preload and administered a continuous infusion of nicorandil. Lee et al. used cardiac output measured by the FloTrac™ sensor to indicate adequate fluid volume. However, they reported that the reliability was low due to the presence of vascular lesions . In this case, we used the FloTrac™ sensor, and the cardiac index remained at greater than 3.5 L/min/m2; however, we recommend to carefully evaluate the result depending on which arterial was used for measurement.
Finally, there are several reports wherein invasive arterial blood pressure measurement and rSO2 monitoring were performed for patients with cervical vascular stenosis or obstruction and valvular disease as monitored in our case [4,5,6]. Lee et al. reported that rSO2 monitoring was useful for detecting transient decrease of cerebral perfusion in a patient who developed dysarthria, tinnitus, and stiff neck during cesarean section . In our case, temporal decrease in rSO2 was observed in accordance with a decrease of blood pressure immediately after spinal anesthesia. Although neurological abnormalities were not observed, rSO2 may be monitored for cerebral blood flow assessment in pregnant women with TA.