Computational Modeling of Oxygen Delivery in Norwood Physiology: Differential Effects of Systemic and Pulmonary Vasodilator Conditions.

BACKGROUND

After the Norwood operation, systemic and pulmonary circulations are supplied in parallel by a single right ventricle. Pulmonary blood flow depends on both native pulmonary vascular resistance and shunt/conduit resistance; therefore, balanced Qp:Qs can occur despite low native pulmonary resistance. Changes in systemic, pulmonary, or shunt/conduit resistance may alter flow distribution, systemic venous saturation, and oxygen delivery.

OBJECTIVE

To evaluate the predicted hemodynamic and oxygen delivery effects of systemic and pulmonary vasodilator conditions in a computational Norwood circulation model, and to assess the robustness of these effects using Monte Carlo simulation, dose-response analysis, nonlinear shunt modeling, afterload-responsive flow, and Rp/R-shunt sensitivity analysis.

METHODS

A lumped-parameter Norwood circulation model was used with a balanced baseline state: Qs = Qp = 1.0 L/min, total right ventricular flow = 2.0 L/min, and Qp:Qs = 1:1. The primary steady-state fixed-flow model was supplemented with sensitivity analyses incorporating afterload-responsive ventricular output, nonlinear shunt/conduit resistance, dose-response simulations, and a two-parameter Rp/R-shunt oxygen delivery surface.

RESULTS

In the fixed-flow model, nicardipine increased systemic flow and improved oxygen delivery, whereas pulmonary vasodilators shifted flow toward the pulmonary circulation and could reduce systemic flow. In the extended sensitivity analyses, predicted drug effects varied with ventricular flow reserve and the relationship between native pulmonary resistance and shunt/conduit resistance.

CONCLUSIONS

In this Norwood circulation model, oxygen delivery depended primarily on systemic flow, ventricular response to afterload reduction, and the Rp/R-shunt relationship. Pulmonary vasodilators may improve modeled saturation but can reduce oxygen delivery when pulmonary runoff occurs without a compensatory increase in ventricular output.