Acute Hemodynamics in the Fontan Circulation: Open-Label Study of Vasopressin.
Journal
Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies
ISSN: 1529-7535
Titre abrégé: Pediatr Crit Care Med
Pays: United States
ID NLM: 100954653
Informations de publication
Date de publication:
01 11 2023
01 11 2023
Historique:
medline:
3
11
2023
pubmed:
18
7
2023
entrez:
18
7
2023
Statut:
ppublish
Résumé
To describe the acute hemodynamic effect of vasopressin on the Fontan circulation, including systemic and pulmonary pressures and resistances, left atrial pressure, and cardiac index. Prospective, open-label, nonrandomized study (NCT04463394). Cardiac catheterization laboratory at Lucile Packard Children's Hospital, Stanford. Patients 3-50 years old with a Fontan circulation who were referred to the cardiac catheterization laboratory for hemodynamic assessment and/or intervention. A 0.03 U/kg IV (maximum dose 1 unit) bolus of vasopressin was administered over 5 minutes, followed by a maintenance infusion of 0.3 mU/kg/min (maximum dose 0.03 U/min). Comprehensive cardiac catheterization measurements before and after vasopressin administration. Measurements included pulmonary artery, atrial, and systemic arterial pressures, oxygen saturations, and systemic and pulmonary flows and resistances. There were 28 patients studied. Median age was 13.5 (9.1, 17) years, and 16 (57%) patients had a single or dominant right ventricle. Following vasopressin administration, systolic blood pressure and systemic vascular resistance (SVR) increased by 17.5 (13.0, 22.8) mm Hg ( Z value -4.6, p < 0.001) and 3.8 (1.8, 7.5) Wood Units ( Z value -4.6, p < 0.001), respectively. The pulmonary vascular resistance (PVR) decreased by 0.4 ± 0.4 WU ( t statistic 6.2, p < 0.001), and the left atrial pressure increased by 1.0 (0.0, 2.0) mm Hg ( Z value -3.5, p < 0.001). The PVR:SVR decreased by 0.04 ± 0.03 ( t statistic 8.1, p < 0.001). Neither the pulmonary artery pressure (median difference 0.0 [-1.0, 1.0], Z value -0.4, p = 0.69) nor cardiac index (0.1 ± 0.3, t statistic -1.4, p = 0.18) changed significantly. There were no adverse events. In Fontan patients undergoing cardiac catheterization, vasopressin administration resulted in a significant increase in systolic blood pressure, SVR, and left atrial pressure, decrease in PVR, and no change in cardiac index or pulmonary artery pressure. These findings suggest that in Fontan patients vasopressin may be an option for treating systemic hypotension during sedation or general anesthesia.
Identifiants
pubmed: 37462430
doi: 10.1097/PCC.0000000000003326
pii: 00130478-990000000-00232
doi:
Substances chimiques
Vasopressins
11000-17-2
Banques de données
ClinicalTrials.gov
['NCT04463394']
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
952-960Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2023 by the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies.
Déclaration de conflit d'intérêts
The authors have disclosed that they do not have any potential conflicts of interest.
Références
Shekerdemian LS, Bush A, Shore DF, et al.: Cardiopulmonary interactions after Fontan operations: Augmentation of cardiac output using negative pressure ventilation. Circulation. 1997; 96:3934–3942
Rychik J, Atz AM, Celermajer DS, et al.: Evaluation and management of the child and adult with Fontan circulation: A scientific statement from the American Heart Association. Circulation. 2019; 140:E234–E284
Rehberg S, Yamamoto Y, Sousse L, et al.: Selective V(1a) agonism attenuates vascular dysfunction and fluid accumulation in ovine severe sepsis. Am J Physiol Heart Circ Physiol. 2012; 303:H1245–H1254
Russ RD, Walker BR: Role of nitric oxide in vasopressinergic pulmonary vasodilatation. Am J Physiol. 1992; 262:H743–H747
Evora PR, Pearson PJ, Schaff HV: Arginine vasopressin induces endothelium-dependent vasodilatation of the pulmonary artery. V1-receptor-mediated production of nitric oxide. Chest. 1993; 103:1241–1245
Wallace AW, Tunin CM, Shoukas AA: Effects of vasopressin on pulmonary and systemic vascular mechanics. Am J Physiol. 1989; 257:H1228–H1234
Tsuneyoshi I, Yamada H, Kakihana Y, et al.: Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock. Crit Care Med. 2001; 29:487–493
Siehr SL, Feinstein JA, Yang W, et al.: Hemodynamic effects of phenylephrine, vasopressin, and epinephrine in children with pulmonary hypertension: A pilot study. Pediatr Crit Care Med. 2016; 17:428–437
Farias JS, Villarreal EG, Flores S, et al.: Effects of vasopressin infusion after pediatric cardiac surgery: A meta-analysis. Pediatr Cardiol. 2021; 42:225–233
Loomba RS, Culichia C, Schulz K, et al.: Acute effects of vasopressin arginine infusion in children with congenital heart disease: Higher blood pressure does not equal improved systemic oxygen delivery. Pediatr Cardiol. 2021; 42:1792–1798
Bigelow AM, Ghanayem NS, Thompson NE, et al.: Safety and efficacy of vasopressin after Fontan completion: A randomized pilot study. Ann Thorac Surg. 2019; 108:1865–1874
Lopez L, Colan SD, Frommelt PC, et al.: Recommendations for quantification methods during the performance of a pediatric echocardiogram: A report from the Pediatric Measurements Writing Group of the American Society of Echocardiography Pediatric and Congenital Heart Disease Council. J Am Soc Echocardiogr. 2010; 23:465–95; quiz 576-467
Zoghbi WA, Adams D, Bonow RO, et al.: Recommendations for noninvasive evaluation of native valvular regurgitation: A report from the American Society of Echocardiography Developed in Collaboration with the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2017; 30:303–371
Sarkar J, Golden PJ, Kajiura LN, et al.: Vasopressin decreases pulmonary-to-systemic vascular resistance ratio in a porcine model of severe hemorrhagic shock. Shock. 2015; 43:475–482
Yimin H, Xiaoyu L, Yuping H, et al.: The effect of vasopressin on the hemodynamics in CABG patients. J Cardiothorac Surg. 2013; 8:49
Jolley M, Colan SD, Rhodes J, et al.: Fontan physiology revisited. Anesth Analg. 2015; 121:172–182
Gewillig M, Brown SC, Eyskens B, et al.: The Fontan circulation: Who controls cardiac output? Interact Cardiovasc Thorac Surg. 2010; 10:428–433
Senzaki H, Masutani S, Kobayashi J, et al.: Ventricular afterload and ventricular work in Fontan circulation: Comparison with normal two-ventricle circulation and single-ventricle circulation with Blalock-Taussig shunts. Circulation. 2002; 105:2885–2892