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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]

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]

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]

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]

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. [ABSTRACT FROM AUTHOR]

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]

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]

To study effects of vasopressin on hemodynamic, clinical, and laboratory variables in children with advanced vasodilatory shock. Retrospective study in a multidisciplinary tertiary pediatric critical care unit. Patients ( n = 117; 32 noncardiac, 85 postcardiac surgery) requiring intravenous vasopressin infusion longer than 60 min for advanced shock (January 2004 to December 2005). Vasopressin infusion ( n = 157). Both cardiac and noncardiac patients showed a significant decrease in inotrope requirement without change in central venous saturation or lactate during infusion. Both groups had increased urea and creatinine and decreased urine output with longer duration/higher cumulative dose of vasopressin. There was a significant increase in conjugated bilirubin level in the noncardiac group during vasopressin infusion; noncardiac patients showed higher AST levels with higher cumulative dose or longer duration of infusion. Postcardiac surgical patients showed a trend towards normal INR values which persisted after vasopressin infusion. Platelet counts were significantly lower during infusion in both groups. Vasopressin infusion improved the hemodynamic state in advanced shock without compromising cardiac function. Urine output and creatinine levels were adversely affected but were reversible. This effect was more pronounced with higher dose or duration of infusion. There was no major effect on liver function but a significant reduction in platelet counts. These data suggest that vasopressin is useful in states of vasodilatory shock with limitations regarding to its adverse renal effects and on platelet counts. [ABSTRACT FROM AUTHOR]

An estimated 700,000 cases of sepsis occur each year in the United States alone, over half of which will develop renal failure. Of those that develop renal failure, 70% will die. This article will examine how the use of vasopressin in sepsis may improve some aspects of renal function. The effects of vasopressin on the renal system in vasodilatory shock. [ABSTRACT FROM AUTHOR]

This is the case report of a 13-year-old mule who developed vasopressor-resistant hypotension after cardiac surgery for endocarditis. As norepinephrine resulted in aggravation of the preexisting ventricular arrhythmia, vasopressin was used to maintain blood pressure. The vasopressin continuous infusion was started at 0.00002 units/kg/min and titrated up to 0.0003 U/kg/min. This low dose led to resolution of hypotension without causing side effects. As the appropriate indication and dose of vasopressin is not established, the cautious use of vasopressin in children is recommended. [ABSTRACT FROM AUTHOR]

Arginine vasopressin is a peptide produced in the posteri- or pituitary whose primary physiologic role is fluid homeostasis. Recent investigations have demonstrated a therapeutic role for arginine vasopressin in adult cardiac arrest as well as adult and pediatric vasodilatory shock. We review the physiology of arginine vasopressin and examine the supporting data behind the developing clinical applications of this naturally produced peptide. [ABSTRACT FROM AUTHOR]

Summary: A 2-month-old female infant presented with septic shock, refractory to high doses of catecholamines. Continuous infusion of terlipressin at a rate of 10mcg/kgh produced a significant increase in the mean arterial pressure that was evident within half and hour, so allowing a reduction in the rate of catecholamine infusion. However, 18h later, the blood pressure fell again and finally the patient died. This case shows the potential value of terlipressin infusion to restore normal mean arterial pressure in children with vasodilatory shock and hypotension refractory to catecholamines. [Copyright &y& Elsevier]