Vasovagal syncope (VVS) is mediated by orthostatic or emotional stress associated with hypotension and relative bradycardia. When VVS occurs, cardiac output (CO) and systemic vascular resistance (SVR) decrease. Previous studies… Click to show full abstract
Vasovagal syncope (VVS) is mediated by orthostatic or emotional stress associated with hypotension and relative bradycardia. When VVS occurs, cardiac output (CO) and systemic vascular resistance (SVR) decrease. Previous studies measuring cerebral oximetry with near-infrared-spectroscopy, a noninvasive technology monitoring regional tissue oxygen saturation, have demonstrated a significant decrease in absolute cerebral tissue oxygen saturation (SctO2) in VVS. 2 Although studies of hemodynamics and cerebral perfusion in vasovagal syncope have been increasing, reports of simultaneous monitoring of hemodynamics and SctO2 are rare, especially in children. We report four pediatric cases of VVS whose hemodynamics and SctO2 were simultaneously evaluated during head-up tilt test (HUTT). The patients were an 11-year-old girl (case 1), a 12-yearold girl (case 2), an 11-year-old boy (case 3), and an 8-yearold girl (case 4). The HUTT was performed to investigate the cause of multiple histories of syncope with no echocardiography, electrocardiography, electroencephalography, brain magnetic resonance imaging, or active standing test abnormalities. We measured heart rate (HR), beat-to-beat blood pressure (BP), CO, and SVR by establishing vascular access from radial artery to evaluate real-time hemodynamics. Heart rate and BP were measured with VISMO PVM-2701 (Nihon Kohden). Cardiac output and SVR were measured with FloTrac Sensor/ EV1000 Clinical Platform (Edwards Lifescience). SctO2 was measured using INVOS 5100C/ SOMASENSOR (Medtronic), which has two sensors to monitor bilateral brain. These parameters were measured simultaneously. The HUTT was performed as follows: supine pre-tilt phase (20 min), tilt phase (30 min), additional supine phase (20 min), and additional tilt phase with intravenous isoproterenol administration (15 min). Informed consent was obtained from the children’s parents. Changes in hemodynamics and SctO2 during HUTT are shown in Figure 1. Case 1, 3, and 4 fainted without drug provocation whereas case 2 fainted with isoproterenol administration. Before syncope, SctO2 decreased despite increased CO, suggesting that cerebral perfusion did not increase even if CO increased. Heart rate increase suggests the sympathetic overactivity before syncope. When syncope occurred, CO dropped sharply with the decrease of SctO2 and SVR. A previous report showed that BP falls by progressive cardiac afterload reduction in a majority of young VVS patients as in our cases. We speculate that the vagal nerve stimulation that occurred at the time of syncope to suppress sympathetic overactivity, which was relatively too strong, caused a decrease in CO and SVR, resulting in a BP drop. After syncope, CO did not increase whereas SctO2 and SVR increased, indicating that syncope improves not by increased CO due to increased venous return caused by tilt down but by the SVR increase mediated by sympathetic nerve activation. A previous report demonstrated that cerebral autoregulation deteriorates in VVS. Systemic vascular resistance and SctO2 changed in parallel in our cases, suggesting that SVR changes resulted in a decrease in cerebral perfusion in the presence of cerebral autoregulation deteriorated condition when syncope occurred. Although it has been reported that patients faint when SctO2 falls below 60%, 2 cases 2 and 3 fainted even though SctO2 was above 60%. In our cases, SctO2 dropped sharply from baseline levels when fainted. Syncope was considered to be caused by a rapid drop in SctO2, not the absolute values. Monitoring SctO2 was a useful method to diagnose syncope. It is unclear why VVS causes sympathetic overactivity before syncope. Emotions such as fear may cause VVS and catecholamine levels increase in a stressed condition. All three cases who fainted without isoproterenol administration were prone to nervousness, which may have induced endogenous catecholamines similar to isoproterenol administration. Prodromes such as nausea and blackout appeared before syncope (Fig. 1). Time from the appearance of prodromes to syncope was between 12 s and 9 min 39 s. Sitting or lying down when prodromes appear may prevent fainting. Simultaneous measurement of hemodynamics and SctO2 during HUTT led to accurate diagnosis of VVS. Both patients and their parents understood that countermeasures during prodromes may prevent the following syncope. This technique may be used for patient education. Correspondence: Yuji Maruo, MD, Department of Pediatrics, Obihiro-Kosei General Hospital, West 14 South 10, Obihiro 0800024, Japan. Email: [email protected] Received 2 June 2020; revised 8 July 2020; accepted 16 July 2020. doi: 10.1111/ped.14403
               
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