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Pancreatitis triggers a systemic inflammatory cascade that increases pulmonary capillary permeability, producing protein-rich edema and diffuse alveolar damage—central to ARDS physiology. The result is shunt and severe V/Q mismatch with refractory hypoxemia and reduced compliance; PaO₂/FiO₂ ≤300 supports ARDS (here moderate at 135). Hydrostatic edema (A) would correlate with elevated left-sided filling pressures and often improves with diuresis; echo indicates normal LV function. Massive PE (C) mainly increases alveolar dead space with abrupt hemodynamic compromise rather than diffuse opacities. Pure airway obstruction (D) yields hyperinflation and increased resistance, not the stiff, noncompliant lungs typical of ARDS. Transport priorities: lung-protective ventilation (VT 4–6 mL/kg PBW), plateau ≤30, adequate PEEP, permissive hypercapnia, consideration of prone positioning and short-course neuromuscular blockade for severe dyssynchrony. Avoid fluid overload; use ultrasound to guide volume and monitor for evolving effusions.