Primary Causes & Pathophysiology
Microbe parts (germ fragments) trigger innate immunity (first-line defense). Massive cytokines (inflammatory signals) cause vasodilation (vessel widening) and capillary leak (fluid loss from vessels). Low vascular tone (vessel tightness) and relative hypovolemia (low effective blood volume) drop pressure. Myocardial depression (weakened heart pumping) and microthrombosis (tiny clots) impair perfusion (blood delivery). Mitochondrial dysfunction (energy factory failure) worsens cell injury. Together these sustain hypotension (low pressure) and lactate rise despite fluids.
Triggers systemic inflammation (body-wide immune response) and hypoxia (low oxygen) that progress to vasodilation and organ failure when antibiotics are delayed
Gram-negative bacteria (gut-type germs) release endotoxin (bacterial poison) that drives cytokine surge and vascular collapse
Polymicrobial contamination (many germs) with poor source control (failure to drain infection) sustains inflammation and hypotension
Toxin-producing bacteria (poison-making germs) cause tissue damage and cytokine storm (overwhelming inflammation) with capillary leak
Persistent bacteremia (bacteria in blood) seeds organs and maintains immune activation leading to refractory vasodilation
Allow higher pathogen load (germ burden) and dysregulated response (harmful immune overreaction) that tips sepsis into shock