Vasoplegic syndrome following cardiothoracic surgery—review of pathophysiology and update of treatment options

Figures

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  Fig. 1. Pathophysiology of vasoplegia. Physiologic contraction of vascular smooth muscle occurs in response to intracellular calcium, which cause myosin phosphorylation leading to myosin-actin filament crosslinking and vasoconstriction. Cytoplasmic calcium is increased through alpha-1 adrenergic receptor, vasopressin-1 receptor, and angiotensin type-1 receptor activation. Inflammatory mediators released during cardiopulmonary bypass can lead to adrenoreceptor desensitization, an immediate increase in vasoconstrictive mediators with subsequent depletion, and the production of nitric oxide (NO). NO leads to an increase in cGMP, which inhibits calcium into cells, leading to muscle relaxation. NO also activates ATP-sensitive potassium channels (KATP), leading to hyperpolarization and inhibited vasoconstriction

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  Fig. 2. An approach to the treatment of vasoplegia. Non-catecholamine agents should be started at low doses, followed by non-catecholamine agents, including vasopressin and methylene blue. Use of hydroxocobalamin and/or angiotensin II should be considered with increasing doses of catecholamines. Clinical judgment should guide avoidance of certain agents if there is undue risk of side effects. All agents can be associated with intolerance, and discontinuation of offending agent(s) should be made accordingly