Objective: To investigate how vasopressin preserves cardiac output in Fontan patients while increasing perfusing pressure. Phenylephrine was included as a comparator to clarify vasopressin’s specific hemodynamic effects in this circulation.
Methods:
Design: Placebo-controlled study using a physiologically based computational simulation of Fontan circulation.
Methods: A closed-loop, lumped-parameter model was developed to simulate Fontan physiology in a 3-year-old patient. Governing equations described pressure, flow, and oxygen saturation across systemic and pulmonary circuits. Vasopressin and phenylephrine were modeled using published hemodynamic data, representing their effects on systemic and pulmonary vascular resistances. Model outputs included cardiac output (CO), systemic and pulmonary flows and pressures, oxygen saturation, and oxygen extraction ratio (OER). Three cohorts of 100 virtual patients each received vasopressin, phenylephrine, or placebo using Monte Carlo simulations.
Results: Data from 300 reports were analyzed. Vasopressin significantly increased systemic vascular resistance (SVR) by 21.7% (p < 0.001) and modestly reduced pulmonary vascular resistance (PVR) by 9.8% (p = 0.122), while preserving CO (1.83 to 1.72, p = 0.068). It also increased systemic arterial and pulmonary venous pressures (p < 0.001), while pulmonary arterial pressure decreased (p < 0.001). OER increased from 25.7% to 28.4% (p = 0.0054). Phenylephrine significantly increased SVR and PVR by 21.7% (p < 0.001), and markedly reduced CO (1.83 to 1.44, p < 0.001). Systemic oxygen saturation fell from 73.5% to 65.9% (p < 0.001). OER rose from 25.7% to 33.5% (p < 0.001).
Conclusions: In a modeled Fontan circulation, vasopressin preserved cardiac output and oxygenation more effectively than phenylephrine, likely due to its pulmonary vasodilatory effects. These findings align with catheter-based studies and support vasopressin as the preferred agent when maintaining pulmonary blood flow and oxygen delivery is critical.
