Cytokine Cascade

Inflammation becomes a cardiovascular emergency when immune signalling shifts from a local response to a self-amplifying systemic process. Vasodilation lowers systemic vascular resistance, endothelial leak moves fluid into tissues, and myocardial dysfunction can reduce cardiac output. Together, these effects can produce distributive shock, pulmonary capillary leak, tissue hypoperfusion, and multiorgan injury [1,2]. The trigger changes the bedside question. Infection points toward sepsis and source control; recent chimeric antigen receptor T-cell therapy or another T-cell-engaging treatment raises concern for cytokine release syndrome (CRS). Chronic low-grade signalling within an atherosclerotic plaque is a different clinical problem and belongs to cardiovascular risk reduction rather than acute shock management [2,6]. In every acutely unwell patient, assess for concurrent infection and alternative causes of shock rather than attributing all findings to a cytokine cascade.