Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored. Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this common, multifactorial condition.
Cardiac surgery produces an altered activation of the inflammatory response due to the combination of surgical trauma, cardiopulmonary bypass and ischemia-reperfusion injury [7]. Marked amplification of this process can result in SIRS. In CMML, some patients may progress to the acute phase of myeloid leukaemia, a complex and poorly understood response by the bone marrow to stress. In this patient, it appears that the inflammatory storm generated by cardiac surgery with CPB precipitated a dramatic myelomonocytic leukaemoid reaction, with a clinical picture of SIRS and MOD. The pathways responsible for this response are unknown.
cardiopulmonary bypass cambridge clinical guides.pdf
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Patients with CMML may benefit from a strategy aimed at decreasing their exposure to inflammatory stimuli. Off-pump coronary artery bypass (OPCAB) surgery avoids the need for CPB but still causes significant surgical trauma. Whilst recent studies suggest a decrease in the systemic inflammatory response in OPCAB surgery, there may not always be a direct correlation between measured inflammatory markers, pathophysiological consequences and clinical outcome [7]. The only report of OPCAB in a patient with CMML, performed via a median sternotomy, highlighted concerns over leukaemoid transformation and the assumed benefits of a reduction in cytokine release [6].
In conclusion, patients with CMML are at increased risk for cardiac surgery. The response to the inflammatory stimulus of surgery is difficult to predict. A leukaemoid reaction may prove rapidly fatal although the cause of disease acceleration and potential remitting factors remain obscure. With better understanding of the inflammatory response to surgery, cardiopulmonary bypass and bone marrow homeostasis in chronic leukaemic conditions, patient selection for surgery may be refined dependent on CMML subtype risk assessment. As these patients may represent a group in whom the lowering of inflammatory stress is particularly beneficial, OPCAB may have a specific role. Alternatively, cytokines such as interleukin-2 and interleukin-6 may present potential therapeutic targets for modulating the inflammatory response following cardiac surgery in patients at risk. 2ff7e9595c
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