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Review
. 2020 Feb 4;24(1):36.
doi: 10.1186/s13054-020-2743-8.

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

Laurence W Busse  1   2 , Nicholas Barker  3 , Christopher Petersen  4
Affiliations
Review

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

Laurence W Busse et al. Crit Care. .

Abstract

Vasoplegic syndrome is a common occurrence following cardiothoracic surgery and is characterized as a high-output shock state with poor systemic vascular resistance. The pathophysiology is complex and includes dysregulation of vasodilatory and vasoconstrictive properties of smooth vascular muscle cells. Specific bypass machine and patient factors play key roles in occurrence. Research into treatment of this syndrome is limited and extrapolated primarily from that pertaining to septic shock, but is evolving with the expanded use of catecholamine-sparing agents. Recent reports demonstrate potential benefit in novel treatment options, but large clinical trials are needed to confirm.

Keywords: Angiotensin II; Cardiopulmonary bypass; De-catecholaminization; Hydroxocobalamin; Shock; Vasoplegic syndrome.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
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
Fig. 2
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
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References

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