Abstract This study presents a numerical simulation of blood flow and oxygen transport in the human circulatory system under cardiac arrest conditions. During cardiac arrest, the effective pumping of the heart ceases, drastically reducing blood velocity and altering the balance between convective and diffusive transport mechanisms. The model couples the incompressible Navier–Stokes equations with an advection-diffusion-reaction equation to simulate the distribution of oxygen in blood vessels, incorporating different forms of tissue oxygen consumption. The effect of key dimensionless parameters, including the Reynolds number (Re), Péclet number (Pe), and the oxygen uptake rate R∗(C∗) are analyzed to understand their influence on flow dynamics and oxygen availability. Results show that under low-Re and low-Pe conditions, characteristic of cardiac arrest, flow becomes viscous-dominated and diffusion-driven, leading to rapid oxygen depletion and hypoxia in downstream tissues. Nonlinear tissue consumption models such as Michaelis-Menten kinetics further reveal how metabolic demand adapts to reduced oxygen availability. The study emphasizes the importance of restoring flow through resuscitative efforts to re-establish effective oxygen delivery and provides insights into physiological responses during critical ischemic events. These findings have implications for improving the modeling of tissue viability and guiding clinical interventions in cardiac arrest scenarios.