Vasoplegia: Mechanism and Management Following Cardiopulmonary Bypass

Figure 1.. The cellular mechanism of vasodilatory shock. The smooth muscles of blood vessels contract when intracellular calcium levels rise and cause cross bonds between actin and myosin, which are phosphorylated. This process is triggered after vasoconstrictive mediators, such as angiotensin II or catecholamines, bind to surface receptors. Conversely, vasodilation occurs when molecules such as a nitric oxide or atrial natriuretic peptides produce an increase in intracellular cyclic guanosine monophosphate (cGMP) and deposition of myosin.2

Figure 2.. The mechanism of CPB-associated vasoplegia. Cardiopulmonary bypass triggers a severe inflammatory reaction that increases NO production, ATP depletion, and an increase in the vascular smooth muscle acidemia, which results in decreased myosin phosphorylation and vasodilation. Simultaneously, neuro-hypophyseal deposits from endogenous vasopressin are depleted rapidly, adding to the vasodilation effect and creating vasoplegia. ATP: adenosine triphosphate, cGMP: cyclic guanosine monophosphate, CPB: cardiopulmonary bypass; KATP: ATP-sensitive potassium channel.2