Vasoplegia: Mechanism and Management Following Cardiopulmonary Bypass

Abstract

Vasoplegia is defined by hypotension and low systemic vascular resistance despite the normal or elevated cardiac index, a complication frequently following cardiac surgery, carrying high morbidity and mortality rate. Vasoplegia is related with a profound systemic inflammatory response and is mainly mediated by cellular hyperpolarization, a relative vasopressin deficiency, and high levels of inducible nitric oxide, following cardiopulmonary bypass. Cardiopulmonary bypass is a distinct precipitant of vasoplegia, generally due to its association with nitric oxide production and severe vasopressin depletion. Postoperative vasoplegia is usually managed with vasopressors, of which catecholamines are the traditional agents of choice. Recent studies promote the use of non-catecholamine vasopressor (vasopressin) in restoring systemic vascular resistance. Alternative agents are also able to restore vascular tone and improve vasoplegia, including methylene blue, angiotensin II, hydroxocobalamin, and ascorbic acid; however, their effect on patient outcomes is still unclear .

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.

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.