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 depression can reduce cardiac output. The combination produces distributive shock, pulmonary capillary leak, tissue hypoperfusion, and sometimes multiorgan failure. The trigger changes the bedside question. Infection points toward sepsis and source control; recent CAR-T or another T-cell-engaging therapy 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.