Postoperative atrial fibrillation (POAF) affects up to 30% of cardiac surgery patients and peaks two to four days post-operatively, coinciding with the acute peri-operative inflammatory response. Although elevated cytokines are consistently associated with POAF onset, the electrophysiological contributions of individual mediators, and their combined action on overlapping ion-channel targets, remain poorly understood. We integrated experimentally observed ion-channel modulation by IL-1β, IL-6, TNF-α, and TGF-β1 into the Courtemanche-Ramirez-Nattel human atrial cardiomyocyte model. Patch-clamp and dose-response data from the literature were translated into concentration-dependent Hill-type scaling functions for each affected conductance, and a dominant-effect ceiling rule was applied where multiple cytokines target the same channel. Single-cell simulations in openCARP were pre-paced at a basic-cycle-length of 500 ms for 400 beats, and each cytokine concentration was swept from 10% to 100% of its experimental calibration value, individually and in combination. IL-6 emerged as the dominant modifier, prolonging APD90 by +30% through synergistic IKr inhibition, ICaL upregulation, and SERCA suppression, consistent with the clinical primacy of IL-6 as a POAF predictor. IL-1β shortened APD90 by -20% via ICaL suppression, and TNF-α produced -8% shortening. TGF-β1 displayed qualitatively distinct behaviour: a loss of spike-and-notch morphology, suppressed upstroke, and an abrupt period-2 alternans above 90% of its calibration concentration with beat-to-beat APD90 swings of ≈40%. The combined sweep was non-linear: Ca²⁺ transient amplitude collapsed, diastolic Ca²⁺ rose, and upstroke velocity fell from ≈145 to ≈40 mV/ms at high inflammatory loads. These results identify IL-6 as the primary driver of inflammation-induced APD prolongation and TGF-β1-induced alternans as an atrial-specific pro-arrhythmic mechanism, providing a mechanistic basis for the POAF substrate.