We read with interest the editorial by Bolliger et al.¹ on heparin resistance. We report a bedside dilemma in a child who experienced cardiopulmonary arrest from septic pulmonary embolism complicating ductal endarteritis and was supported on venoarterial extracorporeal membrane oxygenation (ECMO), in whom discordant laboratory indices raised concern for heparin resistance. An 11-year-old girl on venoarterial ECMO required progressive escalation of an unfractionated heparin (UFH) infusion from 4 to 45 U/kg/h over a period of 36 hours. The Celite activated clotting time (ACT) and activated partial thromboplastin time (aPTT) did not rise in tandem with the dosing adjustments. The ACT inexplicably fell to 136 seconds at the highest infusion rate, despite a consistently low thrombin time (Table 1). The only anti-Xa assay available was calibrated for low-molecular-weight heparin rather than UFH, and this limitation applied equally to every value in the series. The anti-Xa level remained between 0.10 and 0.19 IU/mL through most of the dose escalation, then abruptly rose to 1.50 IU/mL, coinciding with parallel prolongation of the ACT and aPTT. We could not be certain whether this pattern reflected true UFH resistance, pseudo-resistance, a delayed pharmacologic effect of the fixed infusion rate, or an assay artifact from the calibration mismatch because only a UFH-specific assay could have distinguished these possibilities. Fibrinogen rose steadily from 1.80 to 6.83 g/L, the platelet count fell from approximately 150 to 80 × 10⁹/L, C-reactive protein exceeded 30 mg/L, and D-dimer was grossly elevated. This constellation initially suggested heparin resistance in the context of sepsis.²