Patofiziologija vazoplegije po kirurškem posegu

Vasoplegia is characterised as persistently low systemic vascular resistance despite a normal or high cardiac output, resulting in low mean arterial pressure and end-organ hypoperfusion. It can arise in several clinical states (e.g., sepsis, burns, major surgery, trauma), yet there is currently no unifying definition of vasoplegia. Postoperative vasoplegia is predominantly seen after cardiac surgery, but it has also been described after liver transplantation and surgery with significant blood loss necessitating transfusion. Vasoplegia is associated with prolonged inpatient stay, increased risk of infection, and increased mortality. In the context of cardiac surgery, vasoplegia predominantly results from the release of inflammatory mediators and activation of the complement system. In turn, this generates a proinflammatory state featuring high levels of proinflammatory cytokines, nitrous oxide, hydrogen sulphide, prostaglandins, reactive oxygen species, and increased secretion of vaso-active mediators through sympathetic activation. Prolonged vasoplegia results in desensitisation of adrenergic and angiotensin receptors, reduced vasopressin levels, and reduced glucocorticoids, in turn leading to a vas-opressor-refractory state. The understanding of the pathophysiology of postoperative vasoplegia provides an opportunity for targeted therapeutic development to improve the clinical outcomesof this condition.