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Vasoplegia occurs in up to 16% of patients who undergo heart transplantation (HT) and is associated with significant morbidity and mortality. We present a case of a 61-year-old man with ischemic cardiomyopathy receiving sacubitril/valsartan (Entresto; Novartis, Cambridge, MA) who developed profound hypotension after HT. He was treated with intravenous methylene blue and high-dose vasopressors, but developed acute kidney injury requiring dialysis and a prolonged stay in the intensive care unit. This case supports a potent vasodilatory effect of sacubitril/valsartan, and if confirmed by other studies, might warrant consideration for withholding treatment while awaiting HT, particularly in patients with risk factors for vasoplegia., (Copyright © 2017 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Background: Vasoplegia is characterized as a severe vasodilatory shock after cardiac surgery, and can be associated with substantial morbidity. Increased systemic inflammation and endothelial dysfunction, often related to prolonged cardiopulmonary bypass times, anesthesia, or mechanical circulatory support have been shown to be associated with the development of vasoplegia. We sought to identify risk factors and the impact of various degrees of vasoplegia after heart transplantation., Methods: A retrospective review was conducted of 244 consecutive patients who underwent heart transplantation over a 3-year period. Patients were divided into three groups: no vasoplegia, mild vasoplegia (requiring one vasopressor), and moderate/severe vasoplegia (more than two vasopressors). One-year survival, freedom from rejection, and postoperative complication rates were assessed. Risk factors for vasoplegia subgroups were retrospectively identified., Results: Vasoplegia syndrome was observed in 34.3% of patients after heart transplantation (mild, 74.1%; moderate/severe, 25.9%). Cardiopulmonary bypass time was significantly longer and pretransplant creatinine was significantly higher in the moderate/severe vasoplegia group. There was a strong trend toward greater use of mechanical circulatory support among moderate/severe vasoplegia patients compared with mild and no vasoplegia patients. After heart transplantation, 1-year survival, freedom from rejection, and need for hemodialysis were not significantly different between groups., Conclusions: Vasoplegia syndrome is common after heart transplantation. Risk factors for increased severity include longer cardiopulmonary bypass times and elevated preoperative creatinine. Although higher rates of mortality or graft rejection were not detected, vasoplegia was associated with prolonged intubation, greater blood product usage, and lengthened hospital stay. Further studies involving larger cohorts are warranted., (Copyright © 2018 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Vasoplegic syndrome (VS) is increasingly recognized as an important clinical entity in perioperative medicine. VS is characterized by significant arterial hypotension, normal or high cardiac output, low systemic vascular resistance, and increased requirements for intravenous volume and vasopressors. Tremendous variations exist regarding incidence reported in the literature and management at different institutions; and the incidence of VS is likely significantly higher than many anesthesiologists believe. Thus the aims of this article are to review the pertinent aspects related to VS and alert clinical anesthesiologists to this under-recognized yet very challenging clinical condition. The potential risk factors include blood transfusion, cardiopulmonary bypass, organ transplantation, trauma and sepsis, and use of specific medications such as angiotensin-converting enzyme inhibitors, Angiotensin-II antagonist, heparin, amiodarone, aprotinin, and protamine. The pathogenesis of VS may have several mechanistic pathways, overproduction of inducible nitric oxide, activation of ATP-dependent K channels, vasopressin V1A-receptor down-regulation, and nuclear factor-κB activation. Current management strategies include intravenous administration of volume and catecholamines, vasopressin, methylene blue and high dose hydroxocobalamin. Other treatment could include ATP-sensitive K channel blocker, nuclear factor-κB inhibitor, indigo carmine, and hyperbaric oxygen therapy. VS is still associated with significantly increased perioperative morbidity and mortality., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The vasomotor tone is an essential determinant of blood pressure. Vascular resistance is the result of a calculation including vasomotor tone, blood flow and blood viscosity. The vascular tone is modulated by the sympathetic system and the direct actions of drugs (patient's pathology, anaesthesia). The pressure and flow allow the vascular tone apprehension. A decrease in vasomotor tone lowers the mean arterial pressure and may cause an intense vasoplegia with arterial vascular resistance below than 800 dyn/s/cm(5) leading to a lack of tissue oxygenation. Vasomotor paralysis can be caused by the patient medications or an intense inflammatory reaction starting at the extracorporeal circulation onset. Monitoring parameters of extracorporeal circulation such as pressure, flow, arterial and venous oxygen saturation, blood level in the venous reservoir, and extensively blood gases, haemoglobin, CO(2) partial pressure level of the oxygenator vent, bispectral index, and oxygen saturation of cerebral tissue are reviewed. They will know the vasoplegia consequences and bear an indication of adequate tissue oxygenation. It may be obtained by using vasopressors (ephedrine, norepinephrine, terbutalin and vasopressin) methylene blue, increasing blood viscosity (erythrocytes) and blood flow, even by inducing hypothermia., (Copyright © 2012 Elsevier Masson SAS. All rights reserved.)