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The classification of cardiogenic shock (CS) has evolved from a singular cold-and wet-hemodynamic profile. Data from registries and clinical trials have contributed to a broader recognition that although all patients with CS have insufficient cardiac output leading to end organ hypoperfusion, there is considerable variability in CS acuity, underlying etiologies, volume status, and systemic vascular resistance. Mixed CS can be broadly categorized as CS with at least 1 additional shock state. Mixed CS states are now the second leading cause of shock in contemporary coronary intensive care units, but there is little high-quality evidence to guide routine care, and there are no standardized classification frameworks or well-established hemodynamic definitions. This primer summarizes the current epidemiology and proposes a classification framework and invasive hemodynamic parameters to guide categorization that could be applied to help better phenotype patients captured in registries and trials, as well as guide management of mixed CS states. [ABSTRACT FROM AUTHOR]

Vasoplegic syndrome (VS) is a common occurrence during heart transplantation (HT). It currently lacks a uniform definition between transplant centers, and its pathophysiology and treatment remain enigmatic. This systematic review summarizes the available published clinical data regarding VS during HT. We searched databases for all published reports on VS during HT. Data collected included the incidence of VS in the HT population, patient and intraoperative characteristics, and postoperative outcomes. Twenty-two publications were included in this review. The prevalence of VS during HT was 28.72% (95% confidence interval: 27.37%, 30.10%). Factors associated with VS included male sex, higher body mass index, hypothyroidism, pre-HT left ventricular assist device or venoarterial extracorporeal membrane oxygenation (VA-ECMO), pre-HT calcium channel blocker or amiodarone usage, longer cardiopulmonary bypass time, and higher blood product transfusion requirement. Patients who developed VS were more likely to require postoperative VA-ECMO support, renal replacement therapy, reoperation for bleeding, longer mechanical ventilation, and a greater 30-day and 1-year mortality. The results of our systematic review are an initial step for providing clinicians with data that can help identify high-risk patients and avenues for potential risk mitigation. Establishing guidelines that officially define VS will aid in the precise diagnosis of these patients during HT and guide treatment. Future studies of treatment strategies for refractory VS are needed in this high-risk patient population. [ABSTRACT FROM AUTHOR]

Study design: Retrospective cohort study Objectives: Vasoplegia is a life-threatening form of distributive or vasodilatory shock that is characterized by reduced systemic vascular resistance with resultant hypotension and normal to elevated cardiac output affecting morbidity and mortality. Vasoplegia in the context of Spine Surgery has not been described previously. The purpose of this case series is to determine incidence, risk factors, complications and postoperative outcome in patients with vasoplegia after complex multi-level thoraco-lumbar spine surgery. Methods: A retrospective review of the electronic medical records at our institution was conducted between January 2014 and June 2018. All patients undergoing multi-level spine surgery (>6 levels) were screened for intraoperative hypotension. Patient demographics, surgical characteristics, neurological status, blood loss, risk factors, medical treatment, complications, hospital course and mortality were collected. All patients included in this study had a minimum follow-up period of 3 months. Results: Out of 8521 surgically treated patients, 994 patients with multi-level thoraco-lumbar spine surgery were identified. A total of 41 patients had intraoperative hypotensive events. Of those, 5 patients with vasoplegia could be identified after elimination of all other potential contributing factors. Vasoplegia did not influence the neurological outcome. One major and three minor complications occurred. All patients showed full recovery. The risk factors identified for vasoplegia include prolonged surgery with osteotomies. Conclusions: Vasoplegia is a rare condition with an incidence of.6%. Patients experiencing vasoplegia did not appear to experience worse surgical outcomes. The use of special intraoperative hemodynamic monitoring should be considered in selected cases. [ABSTRACT FROM AUTHOR]

This review of the use of vasopressin aims to be comprehensive and highly practical, based on the available scientific evidence and our extensive clinical experience with the drug. It summarizes controversies about vasopressin use in septic shock and other vasodilatory states. Vasopressin is a natural hormone with powerful vasoconstrictive effects and is responsible for the regulation of plasma osmolality by maintaining fluid homeostasis. Septic shock is defined by the need for vasopressors to correct hypotension and lactic acidosis secondary to infection, with a high mortality rate. The Surviving Sepsis Campaign guidelines recommend vasopressin as a second-line vasopressor, added to norepinephrine. However, these guidelines do not address specific debates surrounding the use of vasopressin in real-world clinical practice. [ABSTRACT FROM AUTHOR]

BackgroundIn patients with vasodilatory shock, plasma concentrations of angiotensin I (ANG I) and II (ANG II) and their ratio may reflect differences in the response to severe vasodilation, provide novel insights into its biology, and predict clinical outcomes. The objective of these protocol prespecified and subsequent post hoc analyses was to assess the epidemiology and outcome associations of plasma ANG I and ANG II levels and their ratio in patients with catecholamine-resistant vasodilatory shock (CRVS) enrolled in the Angiotensin II for the Treatment of High-Output Shock (ATHOS-3) study.MethodsWe measured ANG I and ANG II levels at baseline, calculated their ratio, and compared these results to values from healthy volunteers (controls). We dichotomized patients according to the median ANG I/II ratio (1.63) and compared demographics, clinical characteristics, and clinical outcomes. We constructed a Cox proportional hazards model to test the independent association of ANG I, ANG II, and their ratio with clinical outcomes.ResultsMedian baseline ANG I level (253 pg/mL [interquartile range (IQR) 72.30-676.00 pg/mL] vs 42 pg/mL [IQR 30.46-87.34 pg/mL] in controls; P

Bambang Pujo Semedi,1,2 Nancy Margarita Rehatta,2 Jusak Nugraha,3 Soetjipto4 1Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, Indonesia; 2Department of Anesthesiology and Reanimation, Faculty of Medicine, Universitas Airlangga, Dr. Soetomo General Academic Hospital, Surabaya, East Java, 60132, Indonesia; 3Department of Clinical Pathology, Faculty of Medicine, Universitas Airlangga, Dr. Soetomo General Academic Hospital, Surabaya, East Java, 60132, Indonesia; 4Department of Medical Biochemistry, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, 60132, IndonesiaCorrespondence: Nancy Margarita Rehatta, Department of Anesthesiology and Reanimation, Faculty of Medicine, University Airlangga, Dr. Soetomo General Academic Hospital, Surabaya, 60132, East Java, Indonesia, Tel +62315020251, Email rita@fk.unair.ac.idPurpose: We aimed to evaluate the antioxidant role in critically ill patients with vasodilatory shock as it relates to severity of tissue hypoxia and organ failure.Patients and Methods: An observational and prospective study was conducted in critically ill patients with vasodilatory shock. Glutathione peroxidase (GPx) levels as antioxidants were measured based on their levels in the patient’s serum. Tissue hypoxia as micro-hemodynamic status was represented by lactate levels, the macro-hemodynamic status was represented by vasoactive inotropic score (VIS) and mean arterial pressure (MAP), while organ dysfunction severity was represented by the shock index (SI), the sequential organ failure assessment (SOFA) score, and the acute physiology and chronic health evaluation (APACHE) II score.Results: Thirty-four critically ill patients with vasodilatory shock met the eligibility criteria. The mortality rate was 41.2%. Glutathione peroxidase levels did not show a significant difference between survivors and non-survivors at baseline or after 24 hours. At the initial measurement, there was a correlation between GPx and lactate levels, GPx and SOFA scores. The macrohemodynamic status was represented by VIS and MAP, which were correlated with SI.Conclusion: Glutathione peroxidase as antioxidant is related to severity of tissue hypoxia and organ failure in critically ill patients with vasodilatory shock.Keywords: glutathione peroxidase, severity, mortality, vasodilatory shock, critically ill

Bambang Pujo Semedi,1,2 Nancy Margarita Rehatta,2 Soetjipto Soetjipto,3 Jusak Nugraha,4 Muhammad H Mahyuddin,5 Jannatin N Arnindita,5 Nabilah A P Wairooy5 1Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, East Java, 60132, Indonesia; 2Department of Anesthesiology and Reanimation, Medical Faculty of Medicine, Universitas Airlangga—Dr Soetomo General Hospital, Surabaya, East Java, 60132, Indonesia; 3Department of Medical Biochemistry, Medical Faculty of Universitas Airlangga, Surabaya, East Java, 60132, Indonesia; 4Department of Clinical Pathology, Medical Faculty of Universitas Airlangga, Surabaya, East Java, 60132, Indonesia; 5Medical Faculty Universitas Airlangga, Surabaya, East Java, 60132, IndonesiaCorrespondence: Nancy Margarita Rehatta, Email margaritarehatta@gmail.comBackground: Patients with severe vasodilation accompanied by refractory hypotension despite high doses of vasopressors were associated with a high mortality rate. The Ang-2 for the Treatment of High-Output Shock (ATHOS) 3 trial demonstrated that angiotensin 2 (Ang-2) could effectively increase MAP and blood pressure in vasodilatory shock patients. This systematic review aims to summarize the impact of Ang-2 for the treatment of vasodilatory shock on clinical outcomes, including length of stay, MAP level (before and after), and mortality also Ang-2 dose needed.Methods: A systematic search in PubMed, Sage, ScienceDirect, Scopus and Gray literature was conducted to obtain studies about the use of Ang-2 in vasodilatory shock patients.Results: In all of the studies that we obtained, there were different results regarding mortality in patients with vasodilatory shock with Ang-2. Mortality was significantly lower when Ang-2 was administered to patients with elevated renin. The initial dose of Ang-2 can be started at 10– 20 ng/kg/min, but there is no agreement on the maximum dose. Ang-2 may be considered a third-line vasopressor if the targeted MAP has not been achieved after administration of norepinephrine > 200 ng/kg/min for more than 6 hours. Although not statistically significant, the use of Ang-2 can reduce the length of stay in the ICU and in the hospital when compared to patients without Ang-2 therapy, in addition to reducing the dose of vasopressor.Conclusion: Overall, the use of Ang-2 has potential to be a regimen for patients with vasodilatory shock. Further study is needed to obtain more data.Keywords: angiotensin II, vasodilatory shock, vasopressor, mortality

Vasoplegia is a condition characterized by persistent low systemic vascular resistance despite a normal or high cardiac index, resulting in profound and uncontrolled vasodilation. Vasoplegia may occur due to various conditions, including cardiac failure, sepsis, and post-cardiac surgery. In the cardiac cohort, multiple risk factors for vasoplegia have been identified. Several factors contribute to the pathophysiology of this condition, and various mechanisms have been proposed, including nitric oxide, adenosine, prostanoids, endothelins, the renin-angiotensin-aldosterone system, and hydrogen sulfide. Early identification and prompt management of vasoplegia is crucial to prevent development of shock. This review expands upon the different vasopressors used in management of vasoplegia, including catecholamines such as norepinephrine, dopamine, epinephrine, phenylephrine, and other agents including vasopressin, methylene blue, angiotensin II, hydroxocobalamin, vitamin C, thiamine, and corticosteroids (ie, hydrocortisone). It also emphasizes the importance of conducting further research and making advancements in treatment regimens for vasoplegia. [ABSTRACT FROM AUTHOR]

Background: Patients supported on mechanical circulatory support devices experience vasodilatory hypotension due to high surface area exposure to nonbiological and non-endothelialized surfaces. Angiotensin II has been studied in general settings of vasodilatory shock, however concerns exist regarding the use of this vasopressor in patients with pre-existing cardiac failure. The objective of this study was to assess the systemic and central hemodynamic effects of angiotensin II in patients with primary cardiac or respiratory failure requiring treatment with mechanical circulatory support devices. Methods: Multicenter retrospective observational study of adults supported on a mechanical circulatory support device who received angiotensin II for vasodilatory shock. The primary outcome was the intraindividual change from baseline in mean arterial pressure (MAP) and vasopressor dosage after angiotensin II. Results: Fifty patients were included with mechanical circulatory devices that were primarily used for cardiac failure (n = 41) or respiratory failure (n = 9). At angiotensin II initiation, the norepinephrine equivalent vasopressor dosage was 0.44 (0.34, 0.64) and 0.47 (0.33, 0.73) mcg/kg/min in the cardiac and respiratory groups, respectively. In the cardiac group, MAP increased from 60 to 70 mmHg (intraindividual P <.001) in the 1 h after angiotensin II initiation and the vasopressor dosage declined by 0.04 mcg/kg/min (intraindividual P <.001). By 12 h, the vasopressor dosage declined by 0.16 mcg/kg/min (P =.001). There were no significant changes in cardiac index or mean pulmonary artery pressure throughout the 12 h following angiotensin II. In the respiratory group, similar but nonsignificant effects at 1 h on MAP (61-81 mmHg, P =.26) and vasopressor dosage (decline by 0.13 mcg/kg/min, P =.06) were observed. Conclusions: In patients requiring mechanical circulatory support for cardiac failure, angiotensin II produced beneficial systemic hemodynamic effects without negatively impacting cardiac function or pulmonary pressures. The systemic hemodynamic effects in those with respiratory failure were nonsignificant due to limited sample size. [ABSTRACT FROM AUTHOR]

Abstract Background Refractory vasodilatory shock is a state of uncontrolled vasodilation associated with underlying inflammation and endothelial dysregulation. Rescue therapy for vasoplegia refractory to catecholamines includes methylene blue (MB) which restores vascular tone. We hypothesized that (1) at least 40% of critically ill patients would respond positively to MB administration and (2) that those who responded to MB would have a survival benefit. Methods This study was a retrospective review that included all adult patients admitted to an intensive care unit treated with MB for the indication of refractory vasodilatory shock. Responders to MB were identified as those with a ≥ 10% increase in mean arterial pressure (MAP) within the first 1-2 hours after administration. We examined the association of mortality to the groups of responders versus non-responders to MB. A subgroup analysis in patients undergoing continuous renal replacement therapy (CRRT) was also performed. Statistical calculations were performed in Microsoft Excel® (Redmond, WA, USA). Where appropriate, the comparison of averages and standard deviations of demographics, dosing, MAP, and reductions in vasopressor dosing were performed via Chi squared, Fisher's exact test, or two-tailed t-test with a p-value < 0.05 being considered as statistically significant. After using the F-test to assess for differences in variance, the proper two tailed t-test was used to compare SOFA scores among responders versus non-responders. Results A total of 223 patients were included in the responder analysis; 88 (39.5%) had a ≥ 10% increase in MAP post-MB administration that was not associated with a significant change in norepinephrine requirements between responders versus non-responders (p=0.41). There was a non-statistically significant trend (21.6% vs 14.8%, p=0.19) toward improved survival to hospital discharge in the MB responder group compared to the non-responder group. In 70 patients undergoing CRRT, there were 33 responders who were more likely to survive than those who were not (p = 0.0111). Conclusions In patients with refractory shock receiving MB, there is a non-statistically significant trend toward improved outcomes in responders based on a MAP increase >10%. Patients supported with CRRT who were identified as responders had decreased ICU mortality compared to non-responders.

Elevated hydrogen sulfide (H 2 S) contributes to vasodilatation and hypotension in septic shock, and traditional therapies do not target this pathophysiologic mechanism. High-dose IV hydroxocobalamin scavenges and prevents H 2 S formation, which may restore vascular tone and may accentuate recovery. No experimental human studies have tested high-dose IV hydroxocobalamin in adults with septic shock. In adults with septic shock, is comparing high-dose IV hydroxocobalamin with placebo feasible? We conducted a phase 2 single-center, double-blind, allocation-concealed, placebo-controlled, parallel-group pilot randomized controlled trial comparing high-dose IV hydroxocobalamin with placebo in critically ill adults with septic shock. Patients meeting Sepsis 3 criteria were randomized 1:1 to receive a single 5-g dose of high-dose IV hydroxocobalamin or equivalent volume 0.9% saline solution as placebo. The primary outcome was study feasibility (enrollment rate, clinical and laboratory compliance rate, and contamination rate). Secondary outcomes included between-group differences in plasma H 2 S concentrations and vasopressor dose before and after infusion. Twenty patients were enrolled over 19 months, establishing an enrollment rate of 1.05 patients per month. Protocol adherence rates were 100% with zero contamination. In the high-dose IV hydroxocobalamin group, compared to placebo, there was a greater reduction in vasopressor dose between randomization and postinfusion (-36% vs 4%, P <.001) and randomization and 3-h postinfusion (-28% vs 10%, P =.019). In the high-dose IV hydroxocobalamin group, the plasma H 2 S level was reduced over 45 mins by –0.80 ± 1.73 μM, as compared with –0.21 ± 0.64 μM in the placebo group (P =.3). This pilot trial established favorable feasibility metrics. Consistent with the proposed mechanism of benefit, high-dose IV hydroxocobalamin compared with placebo was associated with reduced vasopressor dose and H 2 S levels at all time points and without serious adverse events. These data provide the first proof of concept for feasibility of delivering high-dose IV hydroxocobalamin in septic shock. ClinicalTrials.gov; No.: NCT03783091; URL: www.clinicaltrials.gov [Display omitted] [ABSTRACT FROM AUTHOR]

Background: The initial trials on angiotensin II (AT II) administration indicated a high incidence of thrombocytopenia and thrombosis, as well as a positive correlation between hyperreninemia and response to the medication., Case Summary: We describe a case of a patient presenting with catecholamine resistant septic shock, thrombocytopenia, deep vein thrombosis, and normal renin concentration who responded immediately to AT II treatment. We observed no worsening of thrombocytopenia and no progression of thrombosis or additional thromboses during treatment., Conclusion: Our case underscores the need for individualized assessment of patients for potential therapy with AT II., Competing Interests: Conflict-of-interest statement: The authors declare that they have no conflict of interest to disclose., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Background: Off-pump coronary artery bypass grafting (OPCABG) is associated with hemodynamic fluctuations which usually require the use of various vasoactive drugs like norepinephrine and phenylephrine The aim of this study was to evaluate the effect of low dose vasopressin on hemodynamics in patients undergoing Off-pump Coronary Artery Bypass Graft Surgery (OPCABG). Methods: Sixty patients undergoing elective Off pump coronary artery bypass grafting (CABG) having triple vessel coronary artery disease (CAD). were randomly divided into two groups: group A (n=30), patients received Vasopressin 0.03 IU/min via infusion pump (diluted in 50 ml syringe) during the LIMA extraction and continued till the end of surgery; group B (n==30), patients received normal saline infusion pump during the LIMA extraction and continued till the end of surgery. The anesthetic technique was the same in both the groups. Hemodynamic parameters were recorded at various time intervals during the surgery. Results: HR, CO and CI were lower and MAP, SVR and SVRI were higher in vasopressin group. CVP was stable with no significant difference in SV and SVV. Conclusion: To achieve better intra operative hemodynamic stability during the triple vascular coronary anastomosis and to cope up with post-operative vasodilatory shock, low dose vasopressin infusion is a safe option.

BackgroundThe role of methylene blue (MB) in patients with vasodilatory shock is unclear. The purpose of this systematic review and meta-analysis was to evaluate the efficacy and safety of MB in patients with vasodilatory shock.MethodsWe searched MEDLINE at PubMed, Embase, Web of Science, Cochrane, CNKI, CBM and Wanfang Medical databases for all observational and intervention studies comparing the effect of MB vs. control in vasodilatory shock patients. This study was performed in accordance with the PRISMA statement. There were no language restrictions for inclusion.ResultsA total of 15 studies with 832 patients were included. Pooled data demonstrated that administration of MB along with vasopressors significantly reduced mortality [odds ratio (OR) 0.54, 95% confidence interval (CI) 0.34 to 0.85, P = 0.008; I2 = 7%]. This benefit in mortality rate was also seen in a subgroup analysis including randomized controlled trials and quasi-randomized controlled trials. In addition, the vasopressor requirement was reduced in the MB group [mean difference (MD) −0.77, 95%CI −1.26 to −0.28, P = 0.002; I2 = 80%]. Regarding hemodynamics, MB increased the mean arterial pressure, heart rate and peripheral vascular resistance. In respect to organ function, MB was associated with a lower incidence of renal failure, while in regards to oxygen metabolism, it was linked to reduced lactate levels. MB had no effect on the other outcomes and no serious side effects.ConclusionsConcomitant administration of MB and vasopressors improved hemodynamics, decreased vasopressor requirements, reduced lactate levels, and improved survival in patients with vasodilatory shock. However, further studies are required to confirm these findings.Systematic review registrationIdentifier: CRD42021281847.

Septic and vasoplegic shock are common types of vasodilatory shock (VS) with high mortality. After fluid resuscitation and the use of catecholamine-mediated vasopressors (CMV), vasopressin, angiotensin II, methylene blue (MB), and hydroxocobalamin can be added to maintain blood pressure. VS treatment utilizes a phased approach with secondary vasopressors added to vasopressor agents to maintain an acceptable mean arterial pressure (MAP). This review covers additional vasopressors and adjunctive therapies used when fluid and catecholamine-mediated vasopressors fail to maintain target MAP. Evidence supporting additional vasopressor agents in catecholamine-resistant VS is limited to case reports, series, and a few randomized control trials (RCTs) to guide recommendations. Vasopressin is the most common agent added next when MAPs are not adequately supported with CMV. VS patients failing fluids and vasopressors with cardiomyopathy may have cardiotonic agents such as dobutamine or milrinone added before or after vasopressin. Angiotensin II, another class of vasopressor, is used in VS to maintain adequate MAP. MB and/or hydroxocobalamin, vitamin C, thiamine, and corticosteroids are adjunctive therapies used in refractory VS. More RCTs are needed to confirm the utility of these drugs, at what doses, which combinations and in what order they should be given. [ABSTRACT FROM AUTHOR]

Background: Refractory vasodilatory shock is a state of uncontrolled vasodilation associated with underlying inflammation and endothelial dysregulation. Rescue therapy for vasoplegia refractory to catecholamines includes methylene blue (MB) which restores vascular tone. We hypothesized that (1) at least 40% of critically ill patients would respond positively to MB administration and (2) that those who responded to MB would have a survival benefit. Methods: This study was a retrospective review that included all adult patients admitted to an intensive care unit treated with MB for the indication of refractory vasodilatory shock. Responders to MB were identified as those with a ≥ 10% increase in mean arterial pressure (MAP) within the first 1-2 hours after administration. We examined the association of mortality to the groups of responders versus non-responders to MB. A subgroup analysis in patients undergoing continuous renal replacement therapy (CRRT) was also performed. Statistical calculations were performed in Microsoft Excel® (Redmond, WA, USA). Where appropriate, the comparison of averages and standard deviations of demographics, dosing, MAP, and reductions in vasopressor dosing were performed via Chi squared, Fisher's exact test, or two-tailed t-test with a p-value < 0.05 being considered as statistically significant. After using the F-test to assess for differences in variance, the proper two tailed t-test was used to compare SOFA scores among responders versus non-responders. Results: A total of 223 patients were included in the responder analysis; 88 (39.5%) had a ≥ 10% increase in MAP post-MB administration that was not associated with a significant change in norepinephrine requirements between responders versus non-responders (p=0.41). There was a non-statistically significant trend (21.6% vs 14.8%, p=0.19) toward improved survival to hospital discharge in the MB responder group compared to the non-responder group. In 70 patients undergoing CRRT, there were 33 responders who were more likely to survive than those who were not (p = 0.0111). Conclusions: In patients with refractory shock receiving MB, there is a non-statistically significant trend toward improved outcomes in responders based on a MAP increase >10%. Patients supported with CRRT who were identified as responders had decreased ICU mortality compared to non-responders. [ABSTRACT FROM AUTHOR]

Abstract Background In patients with vasodilatory shock, plasma concentrations of angiotensin I (ANG I) and II (ANG II) and their ratio may reflect differences in the response to severe vasodilation, provide novel insights into its biology, and predict clinical outcomes. The objective of these protocol prespecified and subsequent post hoc analyses was to assess the epidemiology and outcome associations of plasma ANG I and ANG II levels and their ratio in patients with catecholamine-resistant vasodilatory shock (CRVS) enrolled in the Angiotensin II for the Treatment of High-Output Shock (ATHOS-3) study. Methods We measured ANG I and ANG II levels at baseline, calculated their ratio, and compared these results to values from healthy volunteers (controls). We dichotomized patients according to the median ANG I/II ratio (1.63) and compared demographics, clinical characteristics, and clinical outcomes. We constructed a Cox proportional hazards model to test the independent association of ANG I, ANG II, and their ratio with clinical outcomes. Results Median baseline ANG I level (253 pg/mL [interquartile range (IQR) 72.30–676.00 pg/mL] vs 42 pg/mL [IQR 30.46–87.34 pg/mL] in controls; P

Abstract Background Vasoplegia is a severe complication which may occur after cardiac surgery, particularly in patients with heart failure. It is a result of activation of vasodilator pathways, inactivation of vasoconstrictor pathways and the resistance to vasopressors. However, the precise etiology remains unclear. The aim of the Vasoresponsiveness in patients with heart failure (VASOR) study is to objectify and characterize the altered vasoresponsiveness in patients with heart failure, before, during and after heart failure surgery and to identify the etiological factors involved. Methods This is a prospective, observational study conducted at Leiden University Medical Center. Patients with and patients without heart failure undergoing cardiac surgery on cardiopulmonary bypass are enrolled. The study is divided in two inclusion phases. During phase 1, 18 patients with and 18 patients without heart failure are enrolled. The vascular reactivity in response to a vasoconstrictor (phenylephrine) and a vasodilator (nitroglycerin) is assessed in vivo on different timepoints. The response to phenylephrine is assessed on t1 (before induction), t2 (before induction, after start of cardiotropic drugs and/or vasopressors), t3 (after induction), t4 (15 min after cessation of cardiopulmonary bypass) and t5 (1 day post-operatively). The response to nitroglycerin is assessed on t1 and t5. Furthermore, a sample of pre-pericardial fat tissue, containing resistance arteries, is collected intraoperatively. The ex vivo vascular reactivity is assessed by constructing concentrations response curves to various vasoactive substances using isolated resistance arteries. Next, expression of signaling proteins and receptors is assessed using immunohistochemistry and mRNA analysis. Furthermore, the groups are compared with respect to levels of organic compounds that can influence the cardiovascular system (e.g. copeptin, (nor)epinephrine, ANP, BNP, NTproBNP, angiotensin II, cortisol, aldosterone, renin and VMA levels). During inclusion phase 2, only the ex vivo vascular reactivity test is performed in patients with (N = 12) and without heart failure (N = 12). Discussion Understanding the difference in vascular responsiveness between patients with and without heart failure in detail, might yield therapeutic options or development of preventive strategies for vasoplegia, leading to safer surgical interventions and improvement in outcome. Trial registration The Netherlands Trial Register (NTR), NTR5647. Registered 26 January 2016.

Vasodilatory shock is a serious medical condition that increases the morbidity and mortality of perioperative and critically ill patients. Norepinephrine is an established first-line therapy for this condition, but at high doses, it may lead to diminishing returns. Oftentimes, secondary noncatecholamine agents are required in those whose hypotension persists. Angiotensin II and vasopressin are both noncatecholamine agents available for the treatment of hypotension in vasodilatory shock. They have distinct modes of action and unique pharmacologic properties when compared to norepinephrine. Angiotensin II and vasopressin have shown promise in certain subsets of the population, such as those with acute kidney injury, high Acute Physiology and Chronic Health Evaluation II scores, or those receiving cardiac surgery. Any benefit from these drugs must be weighed against the risks, as overall mortality has not been shown to decrease mortality in the general population. The aims of this narrative review are to provide insight into the historical use of noncatecholamine vasopressors and to compare and contrast their unique modes of action, physiologic rationale for administration, efficacy, and safety profiles. [ABSTRACT FROM AUTHOR]

Background: Vasodilatory shock refractory to catecholamine vasopressors and arginine vasopressin is highly morbid and responsible for significant mortality. Synthetic angiotensin II is a potent vasoconstrictor that may be suitable for use in these patients.Research Question: What is the safety and effectiveness of angiotensin II and what variables are associated with a favorable hemodynamic response?Study Design and Methods: We performed a multicenter, retrospective study at five tertiary medical centers in the United States. The primary end point of hemodynamic responsiveness to angiotensin II was defined as attainment of mean arterial pressure (MAP) of ≥ 65 mm Hg with a stable or reduced total vasopressor dosage 3 h after drug initiation.Results: Of 270 included patients, 181 (67%) demonstrated hemodynamic responsiveness to angiotensin II. Responders showed a greater increase in MAP (+10.3 mm Hg vs +1.6 mm Hg, P < .001) and reduction in vasopressor dosage (-0.20 μg/kg/min vs +0.04 μg/kg/min; P < .001) compared with nonresponders at 3 h. Variables associated with favorable hemodynamic response included lower lactate concentration (OR 1.11; 95% CI, 1.05-1.17, P < .001) and receipt of vasopressin (OR, 6.05; 95% CI, 1.98-18.6; P = .002). In severity-adjusted multivariate analysis, hemodynamic responsiveness to angiotensin II was associated with reduced likelihood of 30-day mortality (hazard ratio, 0.50; 95% CI, 0.35-0.71; P < .001). Arrhythmias occurred in 28 patients (10%) and VTE was identified in 4 patients.Interpretation: In postmarketing use for vasopressor-refractory shock, 67% of angiotensin II recipients demonstrated a favorable hemodynamic response. Patients with lower lactate concentrations and those receiving vasopressin were more likely to respond to angiotensin II. Patients who responded to angiotensin II experienced reduced mortality. [ABSTRACT FROM AUTHOR]

Shock is an acute condition of circulatory failure resulting in life-threatening organ dysfunction, high morbidity and high mortality. Current management includes fluid and catecholamine therapy to maintain adequate mean arterial pressure and organ perfusion. Norepinephrine is recommended as first-line vasopressor, but other agents are available. Angiotensin II is an alternative potent vasoconstrictor without chronotropic or inotropic properties. Several studies, including a large randomized controlled trial have demonstrated its ability to increase blood pressure with catecholamine-sparing effects. Angiotensin II was consequently approved by the US FDA in 2017 and the EU in 2019 as an add-on vasopressor in vasodilatory shock. This review aims to discuss its basic pharmacology, clinical efficacy, safety and future perspectives. [ABSTRACT FROM AUTHOR]

This case describes the first reported use of human-derived synthetic angiotensin II (Ang-2) in a patient with decompensated cirrhosis and septic shock. The patient presented in vasodilatory shock from Enterobacter cloacae bacteremia with a Sequential Organ Failure Assessment Score of 14 and a Model for End-Stage Liver Disease score of 36. This case is significant because liver failure was an exclusion criterion in the Angiotensin II for the Treatment of Vasodilatory Shock (ATHOS-3) trial, but the liver produces angiotensinogen, which is key precursor to Ang-2 in the renin-angiotensin-aldosterone system. Resuscitation with Ang-2 is a potentially beneficial medication when conventional vasopressors have failed to control mean arterial pressure in this population. [ABSTRACT FROM AUTHOR]

Study Objective: Vasodilatory shock is the most common type of shock. Catecholamine vasopressors are the cornerstone of hemodynamic therapy but carry risks. Angiotensin II (AT2) was recently approved, and other novel agents (selepressin and terlipressin) are under investigation and used outside the United States (terlipressin). We performed a systematic review to summarize the efficacy and safety of these novel vasopressors and to offer guidance on their appropriate use. Design: Systematic review of controlled trials. Methods: Numerous databases were searched using terms related to angiotensin II, selepressin, terlipressin, vasopressor, and shock. Twenty-one citations, including 16 prospective comparative trials and 5 post hoc analyses reporting effects of AT2, selepressin, and terlipressin, were reviewed for data on outcomes related to hemodynamic measures, mortality, severity and duration of illness, concomitant vasopressor utilization, and adverse effects. Findings from eligible literature are described qualitatively using Cochrane methods. Results: Fourteen controlled trials were assessed after exclusion of 2 dated trials of a distinct AT2 formulation. Trials are limited for AT2 (n = 2) and selepressin (n = 1), while terlipressin was investigated in 11 small trials. Overall, the trials have an unclear risk of bias. Most report mean arterial pressure (MAP) as primary end point, and all indicate novel vasopressors increase MAP compared to placebo and to a similar degree as with catecholamine vasopressors. Mortality findings are preliminary, as they have been limited to specific subgroups in trials of terlipressin and post hoc analyses of one trial of AT2. Trials reported safety concerns for each agent including thromboembolism with AT2 and ischemia with terlipressin/selepressin. Conclusion: In this systematic review, controlled trials of novel vasopressors in treatment of vasodilatory shock were limited and of low quality. Angiotensin II, selepressin, and terlipressin appear to significantly increase MAP, but further study is required, particularly for selepressin, to determine their safety, efficacy, and role in treatment of vasodilatory shock. [ABSTRACT FROM AUTHOR]

Arginine vasopressin (AVP), also known as antidiuretic hormone, is a peptide endogenously secreted by the posterior pituitary in response to hyperosmolar plasma or systemic hypoperfusion states. When administered intravenously, it causes an intense peripheral vasoconstriction through stimulation of V1 receptors on the vascular smooth muscle. Patients in refractory shock associated with severe sepsis, cardiogenic or vasodilatory shock, or cardiopulmonary bypass have inappropriately low plasma levels of AVP (‘relative vasopressin deficiency’) and supersensitivity to exogenously-administered AVP. Low doses of AVP and its synthetic analog terlipressin can restore vasomotor tone in conditions that are resistant to catecholamines, with preservation of renal blood flow and urine output. They are also useful in the treatment of refractory arterial hypotension in patients chronically treated with renin-angiotensin system inhibitors, cardiac arrest, or bleeding esophageal varices. In the perioperative setting, they represent attractive adjunct vasopressors in advanced shock states that are unresponsive to conventional therapeutic strategies.

Background: Noradrenaline and metaraminol are commonly used vasopressors in critically ill patients. However, little is known of their dose equivalence., Methods: We conducted a single centre retrospective cohort study of all ICU patients who transitioned from metaraminol to noradrenaline infusions between August 26, 2016 and December 31, 2020. Patients receiving additional vasoactive drug infusion were excluded. Dose equivalence was calculated based on the last hour metaraminol dose (in μg/min) and the first hour noradrenaline dose (in μg/min) with the closest matched mean arterial pressure (MAP). Sensitivity analyses were performed on patients with acute kidney injury (AKI), sepsis and mechanical ventilation., Results: We studied 195 patients. The median conversion ratio of metaraminol to noradrenaline was 12.5:1 (IQR 7.5-20.0) for the overall cohort. However, the coefficient of variation was 77% and standard deviation was 11.8. Conversion ratios were unaffected by sepsis or mechanical ventilation but increased (14:1) with AKI. One in five patients had a MAP decrease of >10 mmHg during the transition period from metaraminol to noradrenaline. Post-transition noradrenaline dose (p < 0.001) and AKI (p = 0.045) were independently associated with metaraminol dose. The proportion of variation in noradrenaline dose predicted from metaraminol dose was low (R 2  = 0.545)., Conclusions: The median dose equivalence for metaraminol and noradrenaline in this study was 12.5:1. However, there was significant variance in dose equivalence, only half the proportion of variation in noradrenaline infusion dose was predicted by metaraminol dose, and conversion-associated hypotension was common., Competing Interests: Declaration of Competing Interest The authors have disclosed that they do not have any conflicts of interest. There are no sources of funding to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

High-dose vitamin B 12 is a potential treatment for patients with vasodilatory shock that is refractory to other therapies. Vasodilatory shock is characterized by low blood pressure and low systemic vascular resistance. Nitric oxide and hydrogen sulfide, two potential targets of high-dose vitamin B 12 given as hydroxocobalamin, facilitate this syndrome. This review explores the relationship between high-dose vitamin B 12 and hemodynamic outcomes in adults with vasodilatory shock and provides an update on the literature since a 2019 review on this topic. A literature search of studies published in the past 5 years was conducted in the CINAHL, PubMed, Cochrane, and EMBASE databases in May 2023. After assessing for eligibility, eight studies met this review's inclusion criteria. Seven of the eight studies reported decreased vasopressor requirements for part or all of the study samples after receiving a hydroxocobalamin infusion. However, not all patients responded to hydroxocobalamin. These findings are limited by patient selection and differences in the timing of vasopressor requirement and blood pressure outcome assessments. The current evidence is promising as to whether vitamin B 12 , given as a hydroxocobalamin infusion, may improve hemodynamic outcomes in vasodilatory shock, but the evidence is of low quality. The use of hydroxocobalamin to treat refractory, vasodilatory shock remains investigative. Larger randomized controlled trials are required to elucidate the role of vitamin B 12 in treating refractory, vasodilatory shock, including in conjunction with other alternative therapies such as methylene blue and corticosteroids., (© 2023 American Society for Parenteral and Enteral Nutrition.)

Patients undergoing heart failure surgery are at risk for developing postoperative vasoplegia. The aim of this study was to determine the incidence, survival, and predictors of vasoplegia in heart failure patients undergoing mitral valve repair for functional mitral regurgitation and to evaluate the effect of ischemic versus non-ischemic etiology. Retrospective. University medical center, single institutional. Heart failure patients with functional mitral regurgitation who underwent restrictive mitral annuloplasty (2006-2015). One hundred twenty-two patients were included (48% ischemic etiology). The incidence of vasoplegia was 19% and was not influenced by mitral regurgitation etiology. Ninety-day survival rate was decreased in vasoplegic compared with non-vasoplegic patients (65% v 93%, p < 0.001). After adjusting for age, gender, and heart failure etiology, prior hypertension (odds ratio [OR] 0.28; 95% confidence interval [CI] 0.08-0.91; p = 0.034), higher creatinine clearance (OR 0.97; 95% CI 0.95-0.99; p = 0.009), and beta-blocker use (OR 0.25; 95% CI 0.09-0.73; p = 0.011) decreased the risk of vasoplegia. Anemia (OR 3.00; 95% CI 1.10-8.20; p = 0.032) and longer cross clamp (OR 1.03; 95% CI 1.01-1.04; p = 0.001), cardiopulmonary bypass (OR 1.01; 95% CI 1.00-1.02; p = 0.003), and procedure times (OR 1.01; 95% CI 1.00-1.02, p = 0.002) increased the risk of vasoplegia. Vasoplegia occurs in 19% of heart failure patients undergoing mitral valve repair for functional mitral regurgitation. It is associated with a poor early outcome. Prior hypertension, a higher creatinine clearance, and beta-blocker use were associated with a decreased risk of vasoplegia, whereas anemia and longer procedure times were associated with an increased risk of vasoplegia, independent of heart failure etiology. [ABSTRACT FROM AUTHOR]

Vasodilatory shock is a critical manifestation of cardiovascular failure. There is uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing the failure of physiologic vasoregulatory mechanisms. Unfortunately, only few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to the standard approach of managing vasodilatory shock. The present review offers the latest updates in management of this important clinical entity and a guidance framework for future research. [ABSTRACT FROM AUTHOR]

Vasodilatory shock in sepsis is caused by the failure of the vasculature to respond to vasopressors, which results in hypotension, multiorgan failure, and ultimately patient death. Recently, it was reported that CPI-17, a key player in the regulation of smooth muscle contraction, was downregulated by lipopolysaccharide (LPS) in mesenteric arteries concordant with vascular hypocontractilty. While Sp1 has been shown to activate CPI-17 transcription, it is unknown whether Sp1 is involved in LPS-induced smooth muscle CPI-17 downregulation. Here we report that tumor necrosis factor (TNF) was critical for LPS-induced smooth muscle CPI-17 downregulation. Mechanistically, we identified two GC boxes as a key TNF response element in the CPI-17 promoter and demonstrated that KLF4 was upregulated by TNF, competed with Sp1 for the binding to the GC boxes in the CPI-17 promoter, and repressed CPI-17 transcription through histone deacetylases (HDACs). Moreover, genetic deletion of TNF or pharmacological inhibition of HDACs protected mice from LPS-induced smooth muscle CPI-17 downregulation, vascular hypocontractility, hypotension, and mortality. In summary, these data provide a novel mechanism of the transcriptional control of CPI-17 in vascular smooth muscle cells under inflammatory conditions and suggest a new potential therapeutic strategy for the treatment of vasodilatory shock in sepsis. [ABSTRACT FROM AUTHOR]

Purpose: Angiotensin II is approved for catecholamine-refractory vasodilatory shock but the conversion dose ratio from norepinephrine to angiotensin II remains unclear., Methods: We conducted a post-hoc analysis of the Acute Renal effects of Angiotensin II Management in Shock (ARAMIS) trial involving patients with vasodilatory hypotension. We determined the norepinephrine equivalent dose immediately prior to angiotensin II initiation and calculated the conversion dose ratio between norepinephrine and angiotensin II. We performed subgroup analyses based on recent exposure to angiotensin receptor blockers (ARBs) and renin levels at baseline., Results: In 37 patients, the median conversion dose ratio between norepinephrine equivalent and angiotensin II was to 10:1 for norepinephrine bitartrate (5:1 for norepinephrine base). The conversion ratio was not affected by the baseline renin, with a median ratio of 10 (7-21) in the high renin group versus 12 (5-22) in the low renin group. Finally, exposure to ARBs prior admission appeared to diminish the conversion ratio with a median ratio of 7 (4-13) in ARB patients vs. 12 (7-22) in non-ARB patients., Conclusions: The norepinephrine to angiotensin II conversion dose ratio is 10:1 in a vasodilatory hypotension population. These findings can guide clinicians and researchers in the use, dosing, and study of angiotensin II in critical care., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Rinaldo Bellomo reports equipment, drugs, or supplies was provided by La Jolla Pharmaceutical Company. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

Vasoplegic shock after cardiac surgery is characterized by hypotension, a high cardiac output, and vasodilation. Much of the understanding of this pathologic state is informed by the understanding of septic shock. Adverse outcomes and mortality are increased with vasoplegic shock. Early recognition and a systematic approach to its management are critical. The need for vasopressors to sustain an adequate blood pressure as well as pharmacologic adjuncts to mitigate the inflammatory inciting process are necessary. The rationale behind vasopressor escalation and consideration of adjuncts are discussed., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Objective To summarize the results of randomized controlled trials on the use of vasopressin as a vasopressor agent in cardiac surgery. Design Meta-analysis. Participants Six-hundred-twenty-five adult patients undergoing elective or emergency cardiac surgery. Interventions Arginine vasopressin infusion (n = 313) or control/standard therapy (n = 312). Measurements and Main Results The rates of perioperative complications and postoperative mortality were used as primary and secondary endpoints, respectively. Fixed and/or random effects models were used to compare pooled odds ratios. Arginine vasopressin reduced the pooled odds ratio (OR) of perioperative complications (OR, 0.33; 95% confidence interval [CI], 0.2-0.54; p < 0.0001). A sensitivity analysis excluding the largest trial showed an unchanged reduction in perioperative complications (OR, 0.35; 95% CI, 0.18-0.69; p = 0.002). When analyzing each perioperative complication separately, vasopressin reduced the pooled OR of vasodilatory shock (OR, 0.4; 95% CI, 0.16-0.97; p = 0.04) and new-onset atrial fibrillation (OR, 0.42; 95% CI, 0.21-0.82; p = 0.01). The pooled OR of postoperative death was not different between patients treated with arginine vasopressin and those receiving standard therapy or placebo (OR, 0.83; 95% CI, 0.45-1.53; p = 0.55). The funnel plot for the primary endpoint suggested a relevant publication bias. All included trials suffered from a high risk of bias. Conclusion Our meta-analysis suggests that arginine vasopressin may reduce the rate of perioperative complications in patients undergoing elective or emergency cardiac surgery. No difference in postoperative mortality was observed. An adequately powered multicenter trial is required for reliable estimation of the effects of arginine vasopressin on perioperative complication rates and mortality in cardiac surgical patients. [ABSTRACT FROM AUTHOR]

Vasodilatory shock can be caused by septic shock, neurogenic shock, anaphylaxis, drugs, and toxins. Vasopressin is commonly used for the restoration of vasomotor tone in vasodilatory shock due to sepsis. This agent exerts its vasoconstrictive effect via smooth muscle V1 receptors and has antidiuretic activity via kidney V2 receptors. Stimulation of V2 receptors results in the integration of aquaporin 2 channels into the apical membrane of collecting ducts leading to free water reabsorption. This antidiuretic action of vasopressin predisposes to hyponatremia. Yet, the development of hyponatremia with the use of vasopressin in critically ill patients with sepsis is rare. A 75-year-old female presented after a suicidal attempt by ingestion of amlodipine and lisinopril. Despite adequate intravenous fluids administration, she remained hypotensive, requiring the initiation of vasopressors. She developed hyponatremia after initiation of vasopressin due to the absence of endotoxemia, and her serum sodium normalized once vasopressin was discontinued. We recommend monitoring for hyponatremia as a complication of vasopressin, especially in patients without sepsis., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Rasheed et al.)

With more than 2000 ventricular assist devices (VAD) placed annually in the United States, understanding postoperative management is important. One of the most common postoperative morbidities encountered with VAD implantation is vasodilatory shock. The mechanisms for this phenomenon are numerous and include cellular and hormonal aberrancies unique to the VAD recipient. Management of vasodilatory shock in VAD patients needs to be undertaken with an understanding of the side effects associated with each treatment, especially the effects on the right ventricle and pulmonary vasculature. This article focuses on the incidence, the pathogenesis, the consequences, and the management of vasodilatory shock in the postoperative VAD patient. [ABSTRACT FROM AUTHOR]

Vasopressin has gained wide support as an adjunct vasopressor in patients with septic shock. This agent exerts its vasoconstriction effects through smooth muscle V1 receptors and also has antidiuretic activity via renal V2 receptors. This interaction with the renal V2 receptors results in the integration of aquaporin 2 channels in the apical membrane of the renal collecting duct leading to free water reabsorption. Thus, water intoxication with subsequent hyponatremia, although rare, is a potentially serious side effect of exogenous vasopressin administration. We present 2 patients who developed hyponatremia within hours of initiation of vasopressin infusion. Extensive diuresis followed its discontinuation with subsequent normalization of serum sodium. One of the patients required the use of hypertonic saline for more rapid normalization of serum sodium due to concerns for potential seizure activity. A review of the literature relevant to the incidence of vasopressin-induced hyponatremia is provided as well as discussion on additional factors relevant to septic shock that should be considered when determining the relative risk of hyponatremia in patients receiving vasopressin. [ABSTRACT FROM AUTHOR]

The perioperative management of pheochromocytomas requires meticulous anesthetic care. There has been considerable progress in its management, recently 3 agents that may be particularly advantageous to the anesthetic team have been identified. Magnesium sulfate is readily available, cheap, safe, and effective for hemodynamic control before tumor resection. It has demonstrated efficacy in adults, children, and in rarer scenarios, such as pheochromocytoma resection in pregnancy and in pheochromocytoma crises. Although only recently entering clinical practice, clevidipine exhibits a pharmacologic profile of great interest, showing efficacy in the management of hypertensive crisis and providing rapid titration and precise hemodynamic control. Its application in the perioperative management of pheochromocytoma before tumor resection recently has been described and likely will expand in the near future. Vasopressin has demonstrated utility in the management of catecholamine-resistant shock after tumor resection. A familiarity with these 3 agents offers anesthesia providers further effective pharmacologic options for managing the hemodynamic challenges inherent to this population before and after tumor resection. [ABSTRACT FROM AUTHOR]

Objective: To assess the efficacy of arginine vasopressin (AVP) as a rescue therapy in children with catecholamine refractory vasodilatory shock and its effect on various hemodynamic, clinical, and laboratory variables. Methods: This prospective hospital based study was conducted from January 2008 through July 2008 at a tertiary pediatric cardiac critical care unit. Twelve post cardiac surgery patients with advanced vasodilatory shock requiring intravenous vasopressin infusion longer than 60 min were included and continuous vasopressin infusion was given. The primary outcome measures were restoration of Mean arterial blood pressure (MAP) after starting AVP infusion and decrease in other concurrent catecholamines requirement. The secondary outcome measures were survival to hospital discharge, adverse effects, and laboratory variables. Results: Vasopressin was infused in the dose range of 0.0005 to 0.003units/kg/min for a mean duration of 55.6 h. MAP improved from 41.08 ± 6.15 mmHg at baseline to 48.92 ± 10.05 mmHg after 1 h ( P < 0.05), to 57.01 ± 8.30 mmHg after 4 h of AVP infusion ( P < 0.001), and to 62.33 ± 8.55 mmHg after 12 h ( P < 0.001), which further increased to 71.75 ± 9.55 mmHg after 24 h ( P < 0.001). Inotrope score and requirement of other concurrent inotropes declined significantly in all patients after starting AVP infusion ( P < 0.001). Lactate levels also declined significantly ( P < 0.0001). No significant adverse effect due to end organ ischemia was observed. Only one patient expired while on vasopressin infusion due to refractory hypotension. Conclusions: Concurrent addition of vasopressin at an appropriate stage help improving MAP significantly with decreased dependence on high dose catecholamines without any significant adverse effects. [ABSTRACT FROM AUTHOR]

Objective: To examine the benefits and risks of vasopressin or its analog terlipressin for patients with vasodilatory shock. Data source: We searched the CENTRAL, MEDLINE, EMBASE, and LILACS databases (up to March 2011) as well as reference lists of articles and proceedings of major meetings; we also contacted trial authors. We considered randomized and quasirandomized trials of vasopressin or terlipressin versus placebo or supportive treatment in adult and pediatric patients with vasodilatory shock. The primary outcome for this review was short-term all-cause mortality. Study selection: We identified 10 randomized trials (1,134 patients). Six studies were considered for the main analysis on mortality in adults. Data extraction and synthesis: The crude short-term mortality was 206 of 512 (40.2%) in vasopressin/terlipressin-treated patients and 198 of 461 (42.9%) in controls [six trials, risk ratio (RR) = 0.91; 95% confidence interval (CI) 0.79-1.05; P = 0.21; I = 0%]. There were 49 of 463 (10.6%) patients with serious adverse events in the vasopressin/terlipressin arm and 51 of 431 (11.8%) in the control arm (four trials, RR = 0.90; 95% CI 0.49-1.67; P = 0.75; I = 26%). Metaregression analysis showed negative correlation between vasopressin dose and norepinephrine dose ( P = 0.03). Conclusions: Overall, use of vasopressin or terlipressin did not produce any survival benefit in the short term in patients with vasodilatory shock. Physicians may value the sparing effects of vasopressin/terlipressin on norepinephrine requirement given its apparent safe profile. [ABSTRACT FROM AUTHOR]

Septic shock is a major cause of morbidity and mortality in the intensive care unit, and effective therapies are limited. Methylene blue is a selective inhibitor of guanylate cyclase, a second messenger involved in nitric oxide-mediated vasodilation. The use of methylene blue in the treatment of septic shock has been repeatedly evaluated over the past 20 years, but data remain scarce. To evaluate the safety and efficacy of methylene blue for the treatment of septic shock, we conducted a literature search of the EMBASE (1974-June 2009), MEDLINE (1966-June 2009), and International Pharmaceutical Abstracts (1970-June 2009) databases. All available studies published in English were reviewed. Observational studies with methylene blue have demonstrated beneficial effects on hemodynamic parameters and oxygen delivery, but use of methylene blue may be limited by adverse pulmonary effects. Methylene blue administration is associated with increases in mean arterial pressure while reducing catecholamine requirements in patients experiencing septic shock; however, its effects on morbidity and mortality remain unknown. Well-designed, prospective evaluations are needed to define the role of methylene blue as treatment of septic shock. [ABSTRACT FROM AUTHOR]

Purpose: To compare the effects of two arginine vasopressin (AVP) dose regimens on the hemodynamic response, catecholamine requirements, AVP plasma concentrations, organ function and adverse events in advanced vasodilatory shock. Methods: In this prospective, controlled, open-label trial, patients with vasodilatory shock due to sepsis, systemic inflammatory response syndrome or after cardiac surgery requiring norepinephrine >0.6 μg/kg/min were randomized to receive a supplementary AVP infusion either at 0.033 IU/min ( n = 25) or 0.067 IU/min ( n = 25). The hemodynamic response, catecholamine doses, laboratory and organ function variables as well as adverse events (decrease in cardiac index or platelet count, increase in liver enzymes or bilirubin) were recorded before, 1, 12, 24 and 48 h after randomization. A linear mixed effects model was used for statistical analysis in order to account for drop-outs during the observation period. Results: Heart rate and norepinephrine requirements decreased while MAP increased in both groups. Patients receiving AVP at 0.067 IU/min required less norepinephrine ( P = 0.006) than those infused with AVP at 0.033 IU/min. Arterial lactate and base deficit decreased while arterial pH increased in both groups. During the observation period, AVP plasma levels increased in both groups (both P < 0.001), but were higher in the 0.067 IU/min group ( P < 0.001) and in patients on concomitant hydrocortisone. The rate of adverse events and intensive care unit mortality was comparable between groups (0.033 IU/min, 52%; 0.067 IU/min, 52%; P = 1). Conclusions: A supplementary AVP infusion of 0.067 IU/min restores cardiovascular function in patients with advanced vasodilatory shock more effectively than AVP at 0.033 IU/min. [ABSTRACT FROM AUTHOR]

Objective To realize the characteristics of the diagnosis and treatment of vasodilatory shock(VS) in the patient with severe burns. Methods The report with VS happened in a patient with severe burns displayed possible cause,characteristic of symptoms and signs,management and prevent of VS. Results The patient with VS associated severe burns was salvaged successfully. Conclusion Persistent hypotension with tachycardia, normal cardiac output,and decreased systemic vascular resistance, and poorly responsive or unresponsive to volume increase with fluid infusion in a patients with severe burns should be considered as VS. Risen blood pressure through pressors including norepinephrine and vasopressin is the key to burned patients with VS,beside routine therapy including administration of volume,maintenance of aspiratory way and adequate urinary quantity, and prevention of volume overload. [ABSTRACT FROM AUTHOR]

To evaluate arginine vasopressin (AVP) and copeptin plasma concentrations in patients with vasodilatory shock after cardiac surgery. Prospective, controlled, clinical study. Surgical intensive care unit and cardiac surgery ward in a tertiary university teaching hospital. Thirty-three critically ill patients with vasodilatory shock after cardiac surgery and ten control patients undergoing uncomplicated aorto-coronary bypass surgery. Hemodynamic, laboratory and clinical data were recorded daily in all patients during the first 7 days after cardiac surgery. At the same time, points blood was withdrawn to determine plasma concentrations of AVP (radioimmunoassay) and copeptin (immunoluminometric assy). Standard tests, a mixed effects model and regression analyses were used for statistical analysis. The course of AVP was significantly different between groups ( P < 0.001). While AVP concentrations were lower in the study group on the first postoperative day, they were higher than that in the control group from postoperative day 3 on. There was no difference in the postoperative AVP response between study patients with or without chronic angiotensin-converting enzyme inhibitor therapy. Except during continuous veno-venous hemofiltration, AVP and copeptin correlated significantly with each other ( P < 0.001; r = 0.749). The AVP response to cardiac surgery is significantly different between patients with vasodilatory shock and patients undergoing uncomplicated aorto-coronary bypass surgery. Although no causative relationship between AVP concentrations and cardiovascular instability can be drawn from these results, our data support the hypothesis that inadequately low AVP plasma levels contribute to the failure to restore vascular tone in vasodilatory shock after cardiac surgery. [ABSTRACT FROM AUTHOR]