Monitoring of central venous pressure and stroke volume variation in a case with a ruptured brain arteriovenous malformation and Fontan circulation

Abstract Background Patients with complex congenital heart disease increasingly undergo noncardiac surgeries because of advancements in surgical techniques and medical management. In Fontan circulation, maintaining an adequate transpulmonary gradient is essential for preserving both pulmonary blood flow and cardiac output. However, intraoperative circulatory monitoring of Fontan patients has not been established. Case presentation A 17-year-old girl required an emergency craniotomy for ruptured arteriovenous malformation. She had a surgical history of bidirectional Glenn operation and Fontan palliation for her congenital hypoplastic left heart syndrome and double outlet right ventricle. We performed general anesthesia with continuous monitoring of central venous pressure (CVP) and stroke volume variation (SVV). Transesophageal echocardiography was not conducted because of difficulty in manipulating the probe due to the patient’s position and surgical setting. After incision of the dura, approximately 1700 ml of rapid blood loss from the arteriovenous malformation was observed in 30 min. In this period, CVP decreased from 15 to 5 mmHg or less. In contrast, there was only a slight rise in SVV from 5 to 8%. We rapidly administered fluid and then transfused blood, and CVP gradually recovered to 10–15 mmHg. During the surgery, circulatory collapse was not observed. The patient was transferred to the intensive care unit under sedation and controlled ventilation. Conclusions CVP decreased sharply, whereas SVV rose only slightly during acute bleeding in the present case. CVP monitoring may have been useful for the management of an acute bleeding case with a Fontan circulation but SVV may not have been reliable. As more patients with a Fontan circulation undergo noncardiac surgeries, appropriate circulatory monitoring in these patients should be further investigated

Safety and immunogenicity of a Herpes Zoster subunit vaccine in Japanese population aged ≥50 years when administered subcutaneously vs. intramuscularly

The impact of alternate routes of vaccine administration, subcutaneous (SC) or intramuscular (IM), on the safety and immunogenicity of herpes zoster subunit candidate vaccine (HZ/su) was assessed in Japanese adults aged ≥ 50 y. During this phase III open-label study, 60 subjects were randomized (1:1) to receive HZ/su through SC or IM routes in a 0, 2 month schedule. Vaccine response rates (VRRs) and geometric mean concentrations (GMCs) of varicella zoster virus glycoprotein E (gE)-specific antibodies were determined by ELISA. Solicited and unsolicited symptoms were recorded for 7 and 30 d after each vaccination and graded 1–3 in severity. Serious adverse events (SAEs) were recorded throughout the study. At one month post-dose 2, VRRs were 100% (95% Confidence Interval (CI): 88.1–100) in both groups; anti-gE antibody GMCs were 44126.1 mIU/ml (95% CI: 36326.1–53601.0) and 45521.5 mIU/ml (95% CI; 37549.5–55185.9) in the SC and IM groups, respectively. Injection site reactions (pain, swelling and redness) were common, and observed more frequently following SC administration. Grade 3 redness and swelling were more frequently observed after SC administration. Fatigue and headache were the most frequently reported general symptoms for both routes of administration. Ten and 7 unsolicited AEs were reported in the SC and IM group, respectively. Two unsolicited AEs (1 in SC; 1 in IM) were considered related to vaccination by the investigator. Three non-fatal SAEs considered unrelated to vaccination were reported during the study. Administration of the HZ/su vaccine candidate resulted in a substantial immune response that was comparable between SC and IM subjects, but local reactogenicity may be greater for SC

Vasodilatory effect of arginine vasopressin is mediated by nitric oxide in human forearm vessels.

Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of AVP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (< or = 0.1 ng/kg per min) increased, whereas the higher doses of AVP (> or = 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 mumol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms