Understanding circulatory failure in sepsis

Excerpt

Septic shock or acute circulatory failure in sepsis causes a mismatch between tissue perfusion and metabolic demands. The heart, the vasculature and alterations in various tissue and cellular functions are involved in the pathophysiology. The clinical presentation can be highly variable, changes over time and is modified by preceding and concomitant treatment and comorbidities. The clinical hallmarks of septic shock are signs of tissue hypoperfusion, hypotension or need for vasopressors to prevent hypotension, despite adequate fluid resuscitation. Signs of tissue hypoperfusion vary and can include impaired capillary perfusion, oliguria, elevated blood lactate and altered mentation. The blood pressure level that is clinically relevant varies between patients, and “adequate” fluid resuscitation is highly subjective. Therefore, septic shock defies explicit, objective definitions, as shown by the current debate around attempts to define it [1, 2]. Nevertheless, increasing severity of circulatory failure is associated with increasing mortality [3]. Delayed treatment increases the severity of circulatory failure in sepsis, necessitates more support with fluids and vasoactive drugs, and increases mortality [4]. …