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Refractory vasodilatory shock, or vasoplegia, is a pathophysiologic state observed in the intensive care unit and operating room in patients with a variety of primary diagnoses. Definitions of vasoplegia vary by source but are qualitatively defined clinically as a normal or high cardiac index and low systemic vascular resistance causing hypotension despite high-dose vasopressors in the setting of euvolemia. This definition can be difficult to apply to patients undergoing mechanical circulatory support (MCS). A large body of mostly retrospective literature exists on vasoplegia in the non-MCS population, but the increased use of temporary MCS justifies an examination of vasoplegia in this population. MCS, particularly extracorporeal membrane oxygenation, adds complexity to the diagnosis and management of vasoplegia due to challenges in determining cardiac output (or total blood flow), lack of clarity on appropriate dosing of noncatecholamine interventions, increased thrombosis risk, the difficulty in determining the endpoints of adequate volume resuscitation, and the unclear effects of rescue agents (methylene blue, hydroxocobalamin, and angiotensin II) on MCS device monitoring and function. Care teams must combine data from invasive and noninvasive sources to diagnose vasoplegia in this population. In this narrative review, the available literature is surveyed to provide guidance on the diagnosis and management of vasoplegia in the temporary MCS population, with a focus on noncatecholamine treatments and special considerations for patients supported by extracorporeal membrane oxygenation, transvalvular heart pumps, and other ventricular assist devices., Competing Interests: Declaration of competing interest J.O. has received honoraria from La Jolla Pharmaceutical Company., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Vasoplegic syndrome occurs relatively frequently in cardiac surgery, liver transplant, major noncardiac surgery, in post-return of spontaneous circulation situations, and in pateints with sepsis. It is paramount for the anesthesiologist to understand both the pathophysiology of vasoplegia and the different treatment strategies available for rescuing a patient from life-threatening hypotension., Competing Interests: Disclosure The authors have nothing to disclose., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Vasoplegic syndrome is a state of vasopressor resistant systemic vasodilation in the presence of a normal cardiac output. Its definition, pathophysiology, risk factors, diagnosis and therapeutic approach will be reviewed in this paper. It occurs frequently during cardiac surgery and is associated with high morbidity and mortality. A search in the LILACS, MEDLINE, and GOOGLE SCHOLAR databases was conducted to find the most relevant papers during the last 18 years. Prompt identification and diagnosis of patients at risk must be undertaken in order to implement an optimal therapeutic approach. This latter includes early treatment with vasopressors with different mechanisms of action., (Copyright © 2019 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.)

Vasoplegic syndrome, characterized by low systemic vascular resistance and hypotension in the presence of normal or supranormal cardiac function, is a frequent complication of cardiovascular surgery. It is associated with a diffuse systemic inflammatory response and is mediated largely through cellular hyperpolarization, high levels of inducible nitric oxide, and a relative vasopressin deficiency. Cardiopulmonary bypass is a particularly strong precipitant of the vasoplegic syndrome, largely due to its association with nitric oxide production and severe vasopressin deficiency. Postoperative vasoplegic shock generally is managed with vasopressors, of which catecholamines are the traditional agents of choice. Norepinephrine is considered to be the first-line agent and may have a mortality benefit over other drugs. Recent investigations support the use of noncatecholamine vasopressors, vasopressin in particular, to restore vascular tone. Alternative agents, including methylene blue, hydroxocobalamin, corticosteroids, and angiotensin II, also are capable of restoring vascular tone and improving vasoplegia, but their effect on patient outcomes is unclear., (Copyright © 2017 Elsevier Inc. All rights reserved.)

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.)

Methylene blue (MB) has been used for additional blood pressure support in patients who develop severe, refractory vasoplegia; however, MB can induce serotonin syndrome, especially when used in conjunction with other serotonergic agents. We describe a case of serotonin syndrome in a patient who received MB for vasoplegic syndrome after left ventricular assist device implantation and discuss its presentation and management., (© 2016 Wiley Periodicals, Inc.)

We report a case of vasoplegic syndrome (VS) after aortic valve replacement in a 65 year old male with aortic stenosis. The patient developed hypotension after separation from cardiopulmonary bypass (CPB). Transesophageal echocardiography revealed well-maintained cardiac function and normal prosthetic valve function. However, his cardiac index was 3.0 l x min(-1) x m(-2) and systemic vascular resistance index (SVRI) was 1100 dynes x sec(-1) x cm(-5) x m(-2). Diagnosing VS, norepinephrine administration was commenced. Since his respiratory status was good, the patient was extubated on the day of surgery. Two days after surgery, catecholamines were discontinued with the stabilization of his circulatory status. However, his respiratory status showed gradual deterioration, and he was re-intubated. Chest X-ray showed bilateral pleural effusion, which was treated by drainage and fluid restriction. With this, his oxygenation improved and he could be extubated 5 days after surgery. Vasoplegic syndrome is a potentially life-threatening complication following cardiac surgery. Hypotension at the time of separation from CPB can be due to multiple factors. Despite an incidence rate of 10%, little is known about VS. We hope that, in future, tailored therapeutic protocols for VS will be developed.

The care of the cardiac surgical patient postoperatively is fraught with several complications because of the nature of the surgical procedure itself and the common comorbidities of this patient population. Most complications occurring in the immediate postoperative period are categorized by organ system, and their pathophysiology is presented. Current diagnostic approaches and treatment options are offered. Preventive measures, where appropriate, are also included in the discussion., (Copyright © 2014 Elsevier Inc. All rights reserved.)

There has been considerable recent progress liver transplantation (LTX). The postreperfusion syndrome has clearly defined and typically responds to vasopressin and/or methylene blue when refractory to catecholamine therapy. Diastolic dysfunction and cirrhotic cardiomyopathy are prevalent and important in LTX recipients. The high cardiovascular risk and the increasing medical complexity of the current liver transplant recipient have stimulated the publication of guidelines for cardiovascular assessment before LTX. Cardiac surgery is increasingly more successful in patients with cirrhosis, including simultaneous heart-liver transplantation. Cardiopulmonary bypass in LTX is indicated for hemodynamic rescue and, at some centers, serves as the hemodynamic platform for liver implantation. Although acute renal injury is common after LTX, early diagnosis is now possible with novel biomarkers. Earlier detection of postoperative renal dysfunction may prompt intervention for renal rescue. The metabolic milieu in LTX remains critical. Regular insulin therapy may be more effective than infrequent large bolus therapy for potassium homeostasis. Careful titration of insulin therapy may improve freedom from severe hyperglycemia to decrease morbidity. Since the organization of dedicated anesthesia care teams for LTX improves perioperative outcome, this aspect of perioperative care is receiving systematic attention to optimize safety and quality. The specialty of LTX is likely to continue to flourish even more, given these pervasive advances., (Copyright © 2013 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.)

The hemodynamics of septic shock is characterized by a primary reduction of vascular tone, which defines vasoplegia. Septic vasoplegia is due to reduced endogenous production of vasopressin, as well as to the overproduction of vasodilating molecules (nitric oxide, prostacyclin, peroxynitrite and kynurenine) and the opening of ATP-sensitive potassium channels. Treatment is supportive and includes primarily alpha-adrenergic catecholamines. Vasopressin may also be useful, although its place is still controversial. Further agents can improve the vascular responsiveness to catecholamines, most notably low doses hydrocortisone, and, to a lesser extent, activated protein C. Further, innovative therapies, based on recent understanding of pathophysiological mechanisms, might become useful agents to treat septic vasoplegia in the future.

Vasoplegic syndrome (VS) is a recognized and relatively common complication of cardiopulmonary bypass (CPB), appearing with an incidence ranging between 5% and 25%. It is characterized by significant hypotension, high or normal cardiac outputs and low systemic vascular resistance (SVR), and increased requirements for fluids and vasopressors during or after CPB. Patients developing VS are at increased risk for death and other major complications following cardiac surgery. This review will focus on the pathophysiology and contemporary strategies of treating VS encountered after CPB., (Copyright © 2010 Elsevier Inc. All rights reserved.)