Type 2 myocardial infarction is defined by myocardial necrosis from supply-demand mismatch in the absence of acute atherothrombosis. It remains a heterogeneous entity without dedicated clinical guidelines or a validated management pathway. This challenge is particularly relevant in patients with cardiorenal vulnerability, including heart failure with reduced ejection fraction and chronic kidney disease, in whom limited physiological reserve may increase susceptibility to acute hemodynamic or metabolic stress. This narrative review explores how the cardiorenal substrate may contribute to type 2 myocardial infarction risk, with attention to possible roles of uremic myocardial toxicity, hypoalbuminemia, and catecholamine-mediated arrhythmic stress. We also review diagnostic challenges in this population, including troponin interpretation, electrocardiographic confounders, and the decision to pursue coronary angiography during active sepsis. A 5-step clinical pathway is proposed as a hypothesis-generating framework to support structured bedside reasoning in the absence of formal guidelines. Emerging biomarkers and recent guideline considerations are discussed as areas requiring further validation before clinical adoption.