pituitrin and Shock

Vasopressors and fluids are the cornerstones for the treatment of shock. The current international guidelines on shock recommend norepinephrine as the first-line vasopressor and vasopressin as the second-line vasopressor. In clinical practice, due to drug availability, local practice variations, special settings, and ongoing research, several alternative vasoconstrictors and adjuncts are used in the absence of precise equivalent doses. Norepinephrine equivalence (NEE) is frequently used in clinical trials to overcome this heterogeneity and describe vasopressor support in a standardized manner. NEE quantifies the total amount of vasopressors, considering the potency of each such agent, which typically includes catecholamines, derivatives, and vasopressin. Intensive care studies use NEE as an eligibility criterion and also an outcome measure. On the other hand, NEE has several pitfalls which clinicians should know, important the lack of conversion of novel vasopressors such as angiotensin II and also adjuncts such as methylene blue, including a lack of high-quality data to support the equation and validate its predictive performance in all types of critical care practice. This review describes the history of NEE and suggests an updated formula incorporating novel vasopressors and adjuncts.

Topics: Critical Care; Humans; Norepinephrine; Shock; Shock, Septic; Vasoconstrictor Agents; Vasopressins

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.

Topics: Angiotensin II; Ascorbic Acid; Cardiotonic Agents; Catecholamines; Cytomegalovirus Infections; Dobutamine; Humans; Hydroxocobalamin; Methylene Blue; Milrinone; Shock; Shock, Septic; Thiamine; Vasoconstrictor Agents; Vasopressins

Hemodynamic management of adults with distributive shock often includes the use of catecholamine-based vasoconstricting medications. It is unclear whether adding vasopressin or vasopressin analogues to catecholamine therapy is beneficial in the management of patients with distributive shock. The purpose of this guideline was to develop an evidence-based recommendation regarding the addition of vasopressin to catecholamine vasopressors in the management of adults with distributive shock.. We summarized the evidence informing this recommendation by updating a recently published meta-analysis. Then, a multidisciplinary panel from the Canadian Critical Care Society developed the recommendation using Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology.. The updated systematic review identified 25 randomized controlled trials including a total of 3,737 patients with distributive shock. Compared with catecholamine therapy alone, the addition of vasopressin or its analogues was associated with a reduced risk of mortality (relative risk [RR], 0.91; 95% confidence interval [CI], 0.85 to 0.99; low certainty), reduced risk of atrial fibrillation (RR, 0.77; 95% CI, 0.67 to 0.88; high certainty), and increased risk of digital ischemia (RR, 2.56; 95% CI, 1.24 to 5.25; moderate certainty).. After considering certainty in the evidence, values and preferences, cost, and other factors, the expert guideline panel suggests using vasopressin or vasopressin analogues in addition to catecholamines over catecholamine vasopressors alone for the management of distributive shock (conditional recommendation, low certainty evidence).

Topics: Adult; Canada; Critical Care; Critical Illness; Humans; Shock; Vasopressins

Vasodilatory shock is the most common type of shock. Catecholamine vasopressors are the cornerstone of hemodynamic therapy but carry risks. Angiotensin II (AT. Systematic review of controlled trials.. Numerous databases were searched using terms related to. 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.

Topics: Adult; Angiotensin II; Arterial Pressure; Female; Humans; Male; Middle Aged; Randomized Controlled Trials as Topic; Shock; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Vasopressors are administered to critically ill patients with vasodilatory shock not responsive to volume resuscitation, and less often in cardiogenic shock, and hypovolemic shock.. The objectives are to review safety and efficacy of vasopressors, pathophysiology, agents that decrease vasopressor dose, predictive biomarkers, β1-blockers, and directions for research.. The quality of evidence was evaluated using Grading of Recommendations Assessment, Development, and Evaluation (GRADE).. Vasopressors bind adrenergic: α1, α2, β1, β2; vasopressin: AVPR1a, AVPR1B, AVPR2; angiotensin II: AG1, AG2; and dopamine: DA1, DA2 receptors inducing vasoconstriction. Vasopressor choice and dose vary because of patients and physician practice. Adverse effects include excessive vasoconstriction, organ ischemia, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. No randomized controlled trials of vasopressors showed a significant difference in 28-day mortality rate. Norepinephrine is the first-choice vasopressor in vasodilatory shock after adequate volume resuscitation. Some strategies that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality while corticosteroids have decreased 28-day mortality significantly in some (two large trials) but not all trials. In norepinephrine-refractory patients, vasopressin or epinephrine may be added. A new vasopressor, angiotensin II, may be useful in profoundly hypotensive patients. Dobutamine may be added because vasopressors may decrease ventricular contractility. Dopamine is recommended only in bradycardic patients. There are potent vasopressors with limited evidence (e.g. methylene blue, metaraminol) and novel vasopressors in development (selepressin).. Norepinephrine is first choice followed by vasopressin or epinephrine. Angiotensin II and dopamine have limited indications. In future, predictive biomarkers may guide vasopressor selection and novel vasopressors may emerge.

Topics: Angiotensin II; Critical Illness; Dopamine; Epinephrine; Humans; Methylene Blue; Norepinephrine; Phenylephrine; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

To systematically review the literature and synthesize evidence concerning the effects of vasopressin and its analogs compared with other vasopressors in distributive shock, focusing on renal outcomes.. We performed a systematic review in MEDLINE, Embase, Cochrane Central, and Clinicaltrials.gov databases.. Randomized clinical trials that compared vasopressin and its analogs with other vasopressors and reported renal outcomes in adult patients with distributive shock.. Paired reviewers independently screened citations, conducted data extraction and assessed risk of bias. Three prespecified subgroup analyses were conducted. Three main outcomes related to acute renal failure were analyzed: the need for renal replacement therapy, acute kidney injury incidence, and acute kidney injury-free days. I test was used to evaluate heterogeneity between studies. Substantial heterogeneity was defined as I greater than 50%. A random-effects model with Mantel-Haenszel weighting was used for all analyses. Heterogeneity was explored using subgroup analysis. The quality of evidence for intervention effects was summarized using Grading of Recommendations Assessment, Development, and Evaluation methodology. This study was registered in the PROSPERO database (CRD42017054324).. Three-thousand twenty-six potentially relevant studies were identified, and 30 articles were reviewed in full. Seventeen studies met the inclusion criteria, including a total of 2,833 individuals. Of these, 11 studies (2,691 individuals) were suitable for quantitative meta-analysis. Overall, the evidence was of low to moderate quality. Patients who received vasopressin and its analogs had a reduced need for renal replacement therapy (odds ratio, 0.59 [0.37-0.92]; p = 0.02; I = 49%) and a lower acute kidney injury incidence (odds ratio, 0.58 [0.37-0.92]; p = 0.02; I = 63%). These results should be interpreted with caution, due to excessive heterogeneity. Acute kidney injury-free data was not pooled, since the small number of studies and extreme heterogeneity.. In patients with distributive shock, vasopressin and its analogs use is associated with a reduced need for renal replacement therapy and lower acute kidney injury incidence. These results are supported by high risk of bias evidence.

Topics: Acute Kidney Injury; Humans; Incidence; Randomized Controlled Trials as Topic; Renal Replacement Therapy; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

There is a distinct lack of age-appropriate cardiotonic drugs, and adult derived formulations continue to be administered, without evidence-based knowledge on their dosing, safety, efficacy, and long-term effects. Dopamine remains the most commonly studied and prescribed cardiotonic drug in the neonatal intensive care unit (NICU), but evidence of its effect on endorgan perfusion still remains. Unlike adult and pediatric critical care, there are significant gaps in our knowledge on the use of various cardiotonic drugs in various forms of circulatory failure in the NICU.

Topics: Adrenal Cortex Hormones; Asphyxia Neonatorum; Cardiotonic Agents; Dobutamine; Dopamine; Heart Defects, Congenital; Humans; Hypotension; Infant, Newborn; Intensive Care Units, Neonatal; Milrinone; Neonatal Sepsis; Norepinephrine; Persistent Fetal Circulation Syndrome; Shock; Simendan; Vasoconstrictor Agents; Vasopressins

Vasodilatory shock is a life-threatening syndrome in critically ill patients and is characterized by severe hypotension and resultant tissue hypoperfusion. This shock state requires the use of vasopressor agents to restore adequate vascular tone. Norepinephrine is still recommended as first-line vasopressor in the management of critically ill patients suffering from severe vasodilation. In the recent time, catecholaminergic vasopressor drugs have been associated with possible side effects at higher dosages. This so-called catecholamine toxicity has focused on alternative noncatecholaminergic vasopressors or the use of moderate doses of multiple vasopressors with complementary mechanisms of action. Besides vasopressin and terlipressin, angiotensin II may be a promising drug for the management of vasodilatory shock. In addition, adjunctive drugs, such as hydrocortisone, methylene blue or ascorbic acid can be added to conventional vasopressor therapy. The objective of this review is to give an overview of the current available vasopressor agents used in vasodilatory shock. A thorough search of PubMed was conducted in order to identify the majority of studies related to the subject. Data on the outcome of several drugs and future perspective of possible management strategies for the therapy of vasodilatory shock are discussed.

Topics: Angiotensin II; Catecholamines; Humans; Norepinephrine; Shock; Terlipressin; Vasoconstrictor Agents; Vasodilation; Vasopressins

Refractory shock is a lethal manifestation of cardiovascular failure defined by an inadequate hemodynamic response to high doses of vasopressor medications. Approximately 7% of critically ill patients will develop refractory shock, with short-term mortality exceeding 50%. Refractory vasodilatory shock develops from uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms. Standard approaches to the initial management of shock include fluid resuscitation and initiation of norepinephrine. When these measures are inadequate to restore BP, vasopressin or epinephrine can be added. Few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to this standard approach. Adjunctive therapies, such as hydrocortisone, thiamine, and ascorbic acid, may increase BP in severe shock and should be considered when combination vasopressor therapy is needed. Novel vasopressor agents, such as synthetic human angiotensin II, can increase BP and reduce the need for high doses of catecholamine vasopressors in severe or refractory vasodilatory shock. Few effective rescue therapies exist for established refractory shock, which emphasizes the importance of aggressive intervention before refractory shock develops, including the earlier initiation of rational combination vasopressor therapy. The present review discusses the diagnosis and management of refractory shock to offer guidance for management of this important clinical problem and to provide a framework for future research.

Topics: Drug Therapy, Combination; Hemodynamics; Humans; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

Vasopressin is an alternative to catecholamine vasopressors for patients with distributive shock-a condition due to excessive vasodilation, most frequently from severe infection. Blood pressure support with a noncatecholamine vasopressor may reduce stimulation of adrenergic receptors and decrease myocardial oxygen demand. Atrial fibrillation is common with catecholamines and is associated with adverse events, including mortality and increased length of stay (LOS).. To determine whether treatment with vasopressin + catecholamine vasopressors compared with catecholamine vasopressors alone was associated with reductions in the risk of adverse events.. MEDLINE, EMBASE, and CENTRAL were searched from inception to February 2018. Experts were asked and meta-registries searched to identify ongoing trials.. Pairs of reviewers identified randomized clinical trials comparing vasopressin in combination with catecholamine vasopressors to catecholamines alone for patients with distributive shock.. Two reviewers abstracted data independently. A random-effects model was used to combine data.. The primary outcome was atrial fibrillation. Other outcomes included mortality, requirement for renal replacement therapy (RRT), myocardial injury, ventricular arrhythmia, stroke, and LOS in the intensive care unit and hospital. Measures of association are reported as risk ratios (RRs) for clinical outcomes and mean differences for LOS.. Twenty-three randomized clinical trials were identified (3088 patients; mean age, 61.1 years [14.2]; women, 45.3%). High-quality evidence supported a lower risk of atrial fibrillation associated with vasopressin treatment (RR, 0.77 [95% CI, 0.67 to 0.88]; risk difference [RD], -0.06 [95% CI, -0.13 to 0.01]). For mortality, the overall RR estimate was 0.89 (95% CI, 0.82 to 0.97; RD, -0.04 [95% CI, -0.07 to 0.00]); however, when limited to trials at low risk of bias, the RR estimate was 0.96 (95% CI, 0.84 to 1.11). The overall RR estimate for RRT was 0.74 (95% CI, 0.51 to 1.08; RD, -0.07 [95% CI, -0.12 to -0.01]). However, in an analysis limited to trials at low risk of bias, RR was 0.70 (95% CI, 0.53 to 0.92, P for interaction = .77). There were no significant differences in the pooled risks for other outcomes.. In this systematic review and meta-analysis, the addition of vasopressin to catecholamine vasopressors compared with catecholamines alone was associated with a lower risk of atrial fibrillation. Findings for secondary outcomes varied.

Topics: Atrial Fibrillation; Catecholamines; Drug Therapy, Combination; Female; Humans; Length of Stay; Male; Publication Bias; Shock; Vasoconstrictor Agents; Vasopressins

Circulatory shock is a medical emergency that requires rapid intervention to optimize patient outcomes. Although catecholamine vasopressors are considered life-sustaining therapy, they are associated with adverse reactions, and vasopressin and angiotensin II may be used to minimize these adverse effects. However, vasopressin and angiotensin II are also associated with adverse reactions that must be known to the clinician to mitigate risk for patients. This review focuses on the known adverse drug effects of vasopressin and angiotensin II while offering potential solutions to minimize harm with these agents. Future directions with vasoactive medication safety including optimization of the electronic medical record, clinical decision support, prediction analytics, and precision medicine for patients with circulatory shock are also discussed.

Topics: Angiotensin II; Drug-Related Side Effects and Adverse Reactions; Humans; Shock; Vasoconstrictor Agents; Vasopressins

Vasopressin (AVP) and terlipressin (TP) have been used as last-line therapy in refractory shock in children. However, the efficacy and safety profiles of AVP and TP have not been determined in pediatric refractory shock of different origins. We aimed to assess the efficacy and safety of the addition of AVP/TP therapy in pediatric refractory shock of all causes compared to conventional therapy with fluid resuscitation and vasopressor and inotropic therapy.. We conducted a systematic review, meta-analysis, and trial sequential analysis (TSA) comparing AVP and TP to conventional therapy. MEDLINE, EMBASE, Cochrane Library, and ClinicalTrials.gov were searched up to February 2016. The systematic review included all reports of AVP/TP use in the pediatric population. Reports of clinical trials were pooled using random-effects models and TSA. Main outcomes were mortality and tissue ischemia.. Three randomized controlled trials and five "before-and-after clinical" trials (without comparator) met the inclusion criteria. Among 224 neonates and children (aged 0 to 18 years) with refractory shock, 152 received therapy with AVP or TP. Pooled analyses showed no association between AVP/TP treatment and mortality (relative risk (RR),1.19; 95% confidence interval (CI), 0.71-2.00), length of stay in the pediatric intensive care unit (PICU) (mean difference (MD), -3.58 days; 95% CI, -9.05 to 1.83), and tissue ischemia (RR, 1.48; 95% CI, 0.47-4.62). In TSA, no significant effect on mortality and risk for developing tissue ischemia was observed with AVP/TP therapy.. Our results emphasize the lack of observed benefit for AVP/TP in terms of mortality and length of stay in the PICU, and suggest an increased risk for ischemic events. Our TSA suggests that further large studies are necessary to demonstrate and establish benefits of AVP/TP in children. PROSPERO registry: CRD42016035872.

Topics: Adolescent; Advanced Cardiac Life Support; Child; Child, Preschool; Humans; Infant; Infant, Newborn; Length of Stay; Lypressin; Pediatrics; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Hypotensive state is frequently observed in several critical conditions. If an adequate mean arterial pressure is not promptly restored, insufficient tissue perfusion and organ dysfunction may develop. Fluids and catecholamines are the cornerstone of critical hypotensive states management. Catecholamines side effects such as increased myocardial oxygen consumption and development of arrhythmias are well known. Thus, in recent years, interest in catecholamine-sparing agents such as vasopressin, terlipressin and methylene blue has increased; however, few randomized trials, mostly with small sample sizes, have been performed. We therefore conducted a meta-analysis of randomized trials to investigate the effect of non-catecholaminergic vasopressors on mortality.. PubMed, BioMed Central and Embase were searched (update December 31st, 2014) by two independent investigators. Inclusion criteria were: random allocation to treatment, at least one group receiving a non-catecholaminergic vasopressor, patients with or at risk for vasodilatory shock. Exclusion criteria were: crossover studies, pediatric population, non-human studies, studies published as abstract only, lack of data on mortality. Studied drugs were vasopressin, terlipressin and methylene blue. Primary endpoint was mortality at the longest follow-up available.. A total of 1,608 patients from 20 studies were included in our analysis. The studied settings were sepsis (10/20 studies [50%]), cardiac surgery (7/20 [35%]), vasodilatory shock due to any cause (2/20 [19%]), and acute traumatic injury (1/20 [5%]). Overall, pooled estimates showed that treatment with non-catecholaminergic agents improves survival (278/810 [34.3%] versus 309/798 [38.7%], risk ratio = 0.88, 95% confidence interval = 0.79 to 0.98, p = 0.02). None of the drugs was associated with significant reduction in mortality when analyzed independently. Results were not confirmed when analyzing studies with a low risk of bias.. Catecholamine-sparing agents in patients with or at risk for vasodilatory shock may improve survival. Further researches on this topic are needed to confirm the finding.

Topics: Databases, Factual; Humans; Lypressin; Methylene Blue; Randomized Controlled Trials as Topic; Sepsis; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Topics: Antidiuretic Agents; Diagnosis, Differential; Dobutamine; Dopamine; Extracorporeal Membrane Oxygenation; Hemodynamics; Humans; Intra-Aortic Balloon Pumping; Monitoring, Physiologic; Norepinephrine; Practice Guidelines as Topic; Shock; Vasopressins

To examine the benefits and risks of vasopressin or its analog terlipressin for patients with vasodilatory shock.. 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.. We identified 10 randomized trials (1,134 patients). Six studies were considered for the main analysis on mortality in adults.. 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(2) = 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(2) = 26%). Metaregression analysis showed negative correlation between vasopressin dose and norepinephrine dose (P = 0.03).. 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.

Topics: Adolescent; Humans; Shock; Treatment Outcome; Vasoconstrictor Agents; Vasodilation; Vasopressins

A solid understanding of the mechanisms of action of cardiovascular medications used in clinical practice along with efforts to develop comprehensive hemodynamic monitoring systems to improve the ability to accurately identify the underlying pathophysiology of cardiovascular compromise are essential in the management of neonates with shock. This article reviews the mechanisms of action of the most frequently used cardiovascular medications in neonates. Because of paucity of data from controlled clinical trials, evidence-based recommendations for the clinical use of these medications could not be made. Careful titration of the given medication with close monitoring of the cardiovascular response might improve the effectiveness and decrease the risks associated with administration of these medications.

Topics: Cardiotonic Agents; Cardiovascular System; Dobutamine; Dopamine; Epinephrine; Hemodynamics; Humans; Hydrazones; Infant, Newborn; Infant, Premature; Intensive Care Units, Neonatal; Milrinone; Pyridazines; Shock; Simendan; Vasoconstrictor Agents; Vasopressins

Reports of successful use of vasopressin in various shock states and cardiac arrest has lead to the emergence of vasopressin therapy as a potentially major advancement in the management of critically ill children.. To provide an overview of physiology of vasopressin, rationale of its use and dose schedule in different disease states with special focus on recent advances in the therapeutic applications of vasopressin.. MEDLINE search (1966-September 2011) using terms vasopressin, terlipressin, arginine-vasopressin, shock, septic shock, vasodilatory shock, cardiac arrest, and resuscitation for reports on vasopressin/terlipressin use in children and manual review of article bibliographies. Search was restricted to human studies. Randomized controlled trials, cohort studies, evaluation studies, case series, and case reports on vasopressin/terlipressin use in children (preterm neonates to 21 years of age) were included. Outcome measures were analysed using following clinical questions: indication, dose and duration of vasopressin/terlipressin use, main effects especially on systemic blood pressure, catecholamine requirement, urine output, serum lactate, adverse effects, and mortality.. 51 reports on vasopressin (30 reports) and terlipressin (21 reports) use in pediatric population were identified. A total of 602 patients received vasopressin/terlipressin as vasopressors in various catecholamine-resistant states (septic - 176, post-cardiotomy - 136, other vasodilatory/mixed shock - 199, and cardiac arrest - 101). Commonly reported responses include rapid improvement in systemic blood pressure, decline in concurrent catecholamine requirement, and increase in urine output; despite these effects, the mortality rates remained high.. In view of the limited clinical experience, and paucity of randomized controlled trials evaluating these drugs in pediatric population, currently no definitive recommendations on vasopressin/terlipressin use can be laid down. Nevertheless, available clinical data supports the use of vasopressin in critically ill children as a rescue therapy in refractory shock and cardiac arrest.

Topics: Adolescent; Child; Child, Preschool; Heart Arrest; Humans; Infant; Infant, Newborn; Shock; Vasoconstrictor Agents; Vasopressins; Young Adult

The vasoconstrictive and antidiuretic physiologic properties of vasopressin (antidiuretic hormone) have long been known. Until recently however, vasopressin was mostly used for diabetes insipidus and noctournal enuresis. This review summarizes the growing body of evidence regarding the perioperative use of vasopressin and its analogues in the management of certain forms of cardiovascular collapse. Physiologically, vasopressin is involved in regulating osmotic, volemic, and cardiovascular homeostasis. It acts via several specific vasopressin receptors that are variably distributed in the heart, kidneys and vasculature etc. Under normal conditions, its antidiuretic effect predominates and vasopressin only induces vasoconstriction at high concentrations. Regarding catecholamine-resistant vasodilatory shock, current evidence suggests that with adequate volume resuscitation, exogenous vasopressin in low "physiologic" doses (0.01-0.04 units/min) safely supports mean arterial pressure without adversely affecting myocardial function and splanchnic circulation. One possible explanation is that metabolic acidosis impairs the function of alpha-adrenergic (but not vasopressin) receptors, thus diminishing the response to catecholamines. Although there is yet no clear cut mortality benefit, vasopressin is now recommended as a second-line agent in septic shock for its catecholamine-sparing effect and as an alternative to epinephrine in cardiopulmonary resuscitation. It has also demonstrated efficacy in ameliorating vasoplegia after cardiopulmonary bypass as well as perioperative hypotension in patients on renin-angiotensin system antagionists preoperatively. In summary, accumulating clinical experience and formal studies indicate that vasopressin has a role in restoring vascular tone in refractory vasodilatory shock states with minimal adverse effects provided that euvolemia is assured.

Topics: Anesthesia; Animals; Antidiuretic Agents; Critical Care; Heart Arrest; Hemodynamics; Humans; Perioperative Care; Shock; Shock, Septic; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Catecholamines are the most used vasopressors in vasodilatory shock. However, the development of adrenergic hyposensitivity and the subsequent loss of catecholamine pressor activity necessitate the search for other options. Our aim was to evaluate the effects of vasopressin and its analog terlipressin compared with catecholamine infusion alone in vasodilatory shock.. A systematic review and meta-analysis of publications between 1966 and 2011 was performed. The Medline and CENTRAL databases were searched for studies on vasopressin and terlipressin in critically ill patients. The meta-analysis was limited to randomized controlled trials evaluating the use of vasopressin and/or terlipressin compared with catecholamine in adult patients with vasodilatory shock. The assessed outcomes were: overall survival, changes in the hemodynamic and biochemical variables, a decrease of catecholamine requirements, and adverse events.. Nine trials covering 998 participants were included. A meta-analysis using a fixed-effect model showed a reduction in norepinephrine requirement among patients receiving terlipressin or vasopressin infusion compared with control (standardized mean difference, -1.58 (95% confidence interval, -1.73 to -1.44); P < 0.0001). Overall, vasopressin and terlipressin, as compared with norepinephrine, reduced mortality (relative risk (RR), 0.87 (0.77 to 0.99); P = 0.04). Vasopressin compared with norepinephrine decreased mortality in adult patients (RR, 0.87 (0.76 to 1.00); P = 0.05) and in patients with septic shock (42.5% vs. 49.2%, respectively; RR, 0.87 (0.75 to 1.00); P = 0.05; number needed to treat, 1 to 15). There was no difference in adverse events between the vasopressin and control groups (RR, 0.98 (0.65 to 1.47); P = 0.92).. Vasopressin use in vasodilatory shock is safe, associated with reduced mortality, and facilitates weaning of catecholamines. In patients with septic shock, use of vasopressin compared with norepinephrine may also decrease mortality.

Topics: Adult; Drug Therapy, Combination; Hemodynamics; Humans; Lypressin; Norepinephrine; Randomized Controlled Trials as Topic; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Shock occurs when failure of the cardiovascular system compromises tissue perfusion. When fluid administration fails to restore adequate arterial pressure and organ perfusion in patients with shock, therapy with vasoactive agents should be initiated. The key to selecting among vasoactive agents is to make the choice in the context of the goals of therapy. The ultimate goals of hemodynamic therapy in shock are to restore effective tissue perfusion and to normalize cellular metabolism. The clinician needs to consider ways of achieving those goals and the mechanisms of action of potential therapies. Armed with this knowledge, it becomes easier to match the mechanism of action of a particular agent to the goals of therapy. When this is done, differences among various agents are seen primarily as differences in mechanisms of action, and discussions about which agent is "best" are transformed into consideration of which agent is best suited to implement the therapeutic strategy that has been selected in a given clinical context. Despite the complex pathophysiology of shock, use of vasoactive agents for hemodynamic support of patients with shock can be guided by an underlying approach in which clinicians define specific goals and end points, titrate therapies to those end points, and evaluate the results of their interventions on an ongoing basis.

Topics: Cardiotonic Agents; Critical Care; Dopamine; Female; Hemodynamics; Humans; Intensive Care Units; Male; Norepinephrine; Prognosis; Randomized Controlled Trials as Topic; Risk Assessment; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Survival Analysis; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

During the last 5 years, new randomized trials in critically ill patients have challenged a number of traditional treatment strategies in intensive care. The authors review eight studies that helped change their medical practices.

Topics: Adrenal Cortex Hormones; Clinical Trials as Topic; Critical Care; Humans; Insulin; Phenylpropanolamine; Respiration, Artificial; Respiratory Distress Syndrome; Shock; Vasopressins

To discuss 3 potential mechanisms for loss of peripheral vasomotor tone during vasodilatory shock; review vasopressin physiology; review the available animal experimental and human clinical studies of vasopressin in vasodilatory shock and cardiopulmonary arrest; and make recommendations based on review of the data for the use of vasopressin in vasodilatory shock and cardiopulmonary arrest.. Human clinical studies, veterinary experimental studies, forum proceedings, book chapters, and American Heart Association guidelines. HUMAN AND VETERINARY DATA SYNTHESIS: Septic shock is the most common form of vasodilatory shock. The exogenous administration of vasopressin in animal models of fluid-resuscitated septic and hemorrhagic shock significantly increases mean arterial pressure and improves survival. The effect of vasopressin on return to spontaneous circulation, initial cardiac rhythm, and survival compared with epinephrine is mixed. Improved survival in human patients with ventricular fibrillation, pulseless ventricular tachycardia, and nonspecific cardiopulmonary arrest has been observed in 4 small studies of vasopressin versus epinephrine. Three large studies, though, did not find a significant difference between vasopressin and epinephrine in patients with cardiopulmonary arrest regardless of initial cardiac rhythm. No veterinary clinical trials have been performed using vasopressin in cardiopulmonary arrest.. Vasopressin (0.01-0.04 U/min, IV) should be considered in small animal veterinary patients with vasodilatory shock that is unresponsive to fluid resuscitation and catecholamine (dobutamine, dopamine, and norepinephrine) administration. Vasopressin (0.2-0.8 U/kg, IV once) administration during cardiopulmonary resuscitation in small animal veterinary patients with pulseless electrical activity or ventricular asystole may be beneficial for myocardial and cerebral blood flow.

Topics: Animals; Animals, Domestic; Heart Arrest; Humans; Shock; Vasoconstrictor Agents; Vasopressins

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.

Topics: Animals; Chemical and Drug Induced Liver Injury; Humans; Ischemia; Kidney Diseases; Lypressin; Shock; Skin; Terlipressin; Thrombosis; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Vasopressin is a 9-amino acid peptide synthesized by magnocellular neurons of the hypothalamus and released from posterior pituitary gland. The primary physiological role of vasopressin is the maintenance of fluid homeostasis. In this review, the classification of vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary, oxytocin receptors, and purinergic receptors, and the effects of vasopressin on vascular smooth muscles, the heart, and the kidneys are discussed. Mortality rates of vasodilatory (or distributive), for example septic shock, are high. The use of vasopressin is an alternative therapy for vasodilatory shock with better outcome. Vasopressin is effective in resuscitation of adults after ventricular fibrillation or pulseless tachycardia, when epinephrine is not effective.

Topics: Adult; Clinical Trials as Topic; Dilatation, Pathologic; Heart; Heart Arrest; Homeostasis; Humans; Intensive Care Units; Kidney; Muscle, Smooth, Vascular; Receptors, Vasopressin; Resuscitation; Shock; Shock, Septic; Survival Analysis; Tachycardia; Time Factors; Treatment Outcome; Vasoconstrictor Agents; Vasodilation; Vasopressins; Ventricular Fibrillation

To review the physiology and the published literature on the role of vasopressin in shock in children.. We searched MEDLINE (1966-2007), EMBASE (1980-2007), and the Cochrane Library, using the terms vasopressin, terlipressin, and shock and synonyms or related terms for relevant studies in pediatrics. We searched the online ISRCTN-Current Controlled Trials registry for ongoing trials. We reviewed the reference lists of all identified studies and reviews as well as personal files to identify other published studies.. Beneficial effects have been reported in vasodilatory shock and asystolic cardiac arrest in adults. Solid evidence for vasopressin use in children is scant. Observational studies have reported an improvement in blood pressure and rapid weaning off catecholamines during administration of low-dose vasopressin. Dosing in children is extrapolated from adult studies.. Vasopressin offers promise in shock and cardiac arrest in children. However, in view of the limited experience with vasopressin, it should be used with caution. Results of a double-blind, randomized controlled trial in children with vasodilatory shock will be available soon.

Topics: Animals; Cardiopulmonary Resuscitation; Child; Clinical Trials as Topic; Critical Illness; Heart Arrest; Humans; Shock; Vasoconstrictor Agents; Vasopressins

Vasopressin is critical for blood pressure regulation when cardiovascular homeostasis is threatened and some patients with shock have inappropriately low levels of hormone in plasma. The present review focuses on recent work that addresses the role of endogenous vasopressin in the pathogenesis of shock and the potential therapeutic indications and secondary effects of exogenous hormone in patients with shock.. Examples of types of shock resistant to catecholamine pressors in which exogenous vasopressin was effective in restoring arterial pressure continued to accumulate. Widespread determinations of plasma vasopressin in patients with shock suggest that endogenous vasopressin deficiency may be more frequent than previously thought. The generation of mice with deletion of vasopressin's V1a receptor highlighted the important role of the hormone on cardiovascular homeostasis.. Vasopressin administration is very effective in restoring arterial pressure in many forms of shock and this appears to be due, at least in part, to deficiency of endogenous hormone. Generation of mice lacking vasopressin V1a receptor open new and exciting avenues of inquiry to clarify the role of the hormone in cardiovascular homeostasis.

Topics: Blood Pressure; Humans; Shock; United States; Vasopressins

Infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac index and systemic oxygen transport. Whether or not such a vasoconstriction impedes regional blood flow and thus visceral organ function, even when low AVP is used, is still a matter of debate. Krejci and colleagues now report, in this issue of Critical Care, that infusing 'low-dose' AVP during early, short-term, normotensive and normodynamic fecal peritonitis-induced porcine septicemia markedly reduced both renal and portal blood flow, and consequently total hepatic blood flow, whereas hepatic arterial flow was not affected. This macrocirculatory response was concomitant with reduced kidney microcirculatory perfusion, whereas liver micro-circulation remained unchanged. From these findings the authors conclude that the use of AVP to treat hypotension should be cautioned against in patients with septic shock. Undoubtedly, given its powerful vasoconstrictor properties, which are not accompanied by positive inotropic qualities (in contrast with most of the equally potent standard care 'competitors', namely catecholamines), the safety of AVP is still a matter of concern. Nevertheless, the findings reported by Krejci and colleagues need to be discussed in the context of the model design, the timing and dosing of AVP as well as the complex interaction between visceral organ perfusion and function.

Topics: Animals; Humans; Kidney; Liver; Liver Circulation; Renal Circulation; Shock; Vasodilation; Vasopressins

In critical care medicine, catecholamines are most widely used to reverse circulatory dysfunction and thus to restore tissue perfusion. However, catecholamines not only influence systemic and regional hemodynamics, but also exert a variety of significant metabolic, endocrine, and immunologic effects. Arginine vasopressin is a vasomodulatory hormone with potency to restore vascular tone in vasodilatory hypotension. Although the evidence supporting the use of low doses of vasopressin or its analogs in vasodilatory shock is increasing, lack of data regarding mortality and morbidity prevent their implementation in critical care protocols.

Topics: Catecholamines; Critical Illness; Hemodynamics; Humans; Immune System; Neurosecretory Systems; Receptors, Vasopressin; Regional Blood Flow; Shock; Shock, Septic; Splanchnic Circulation; Stress, Physiological; Vasodilation; Vasopressins

Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time.

Topics: Animals; Cardiopulmonary Resuscitation; Clinical Trials as Topic; Combined Modality Therapy; Humans; Lypressin; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Ionotropic agents are frequently used in vasodilatory shock like conditions of septic or nonseptic origin. Conventional catecholamines such as norepinephrine are used at a very high dose with possibility of adverse effects in many patients. One often encounters refractoriness to these drugs. Infusion of vasopressin (VP) which is detectable at inappropriately low level in advanced phase of septic shock might allow withdrawal of catecholamines, as it maintains adequate mean arterial pressure (MAP), improves urine output and leaves perfusion of vital organs unhindered. Vasopressin has been found to be superior to epinephrine in animal models and some human trials, especially in patients with resistant ventricular fibrillation (VF) while doing cardiopulmonary resuscitation (CPR). Analogues of VP have also been used for diuresis in patients of hepatorenal syndrome.

Topics: Cardiopulmonary Resuscitation; Hepatorenal Syndrome; Humans; Shock; Vasoconstrictor Agents; Vasopressins

Vasopressin is a nonapeptide synthesised in the hypothalamus and released upon stimulations such as hyperosmolality, hypotension and hypovolaemia. In acute shock states serum vasopressin levels increase rapidly and decrease in prolonged septic shock. The administration of vasopressin in healthy subjects has little effect, whereas in vasodilatory shock it increases the mean arterial pressure through V1 receptors and decreases the cardiac output. Vasopressin stimulates the V2 receptors in the kidney leading to reabsorption of water through aquaporin 2. However, in vasodilatory shock the antidiuretic effects are overcome by the effect vasopressin has on the kidneys: improvement of renal blood flow leading to water excretion. Twenty-four studies on the use of vasopressin in patients with vasodilatory shock are reviewed. They show that vasopressin potentiates norepinephrine effects, increases blood pressure significantly in patients with vasodilatory shock and may improve renal function. Side effects ranging from ischaemic skin lesions to possible intestinal ischaemia should not be underestimated. Above a dose of 0.04 U/min it may lead to cardiac arrest. Effects on mortality cannot be interpreted from these studies. Broad clinical use should await controlled trials to clarify its effects on clinical outcomes such as organ failure and mortality.

Topics: Animals; Hemodynamics; Humans; Kidney; Norepinephrine; Shock; Shock, Septic; Vasodilation; Vasopressins; Water-Electrolyte Balance

Vasoactive drugs are the mainstay of hemodynamic management of vasodilatory shock when fluids fail to restore tissue perfusion. In this review, studies published during the past year that increase our understanding of the use of vasoactive drugs in the intensive care unit are discussed.. In septic shock, there is no benefit in increasing mean arterial pressure from 65 to 85 mmHg. Norepinephrine did not worsen renal function. Epinephrine induced visceral hypoperfusion and hyperlactatemia, and worsened organ function and survival compared with norepinephrine and vasopressin. There are a number of reports of the safety and efficacy of vasopressin but it is not currently recommended as first line therapy, and if used, should be given as a continuous low dose infusion. Terlipressin is showing promise but decreases cardiac output. Metaraminol is being investigated as an alternative to norepinephrine. Dopamine may improve splanchnic flow mainly by increasing cardiac output. Dobutamine improves oxygen delivery and may improve mesenteric blood flow.. Over the last 40 years, there have been few controlled clinical trials to guide clinicians on the use of vasoactive drugs of treating shock states. It is not known whether the currently favored combination of norepinephrine and dobutamine is superior to traditional therapy with dopamine. Epinephrine is not recommended as the first-line therapy. The role of vasopressin and terlipressin remains unknown. Three large ongoing clinical trials will be completed soon and the results should clarify the role of these various agents.

Topics: Dobutamine; Drug Therapy, Combination; Epinephrine; Hemodynamics; Humans; Intensive Care Units; Lypressin; Metaraminol; Norepinephrine; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Topics: Anaphylaxis; Child; Crystalloid Solutions; Fluid Therapy; Hemodynamics; Humans; Isotonic Solutions; Shock; Shock, Cardiogenic; Shock, Septic; Vasopressins

The preclinical diagnosis of shock is still based on the patient's history, the physical examination, the injury pattern and a few hemodynamic parameters available in the emergency set-up. The clinical picture is characterised by hypotension and tachycardia, tachypnoe and dyspnoea as well as cerebral impairment. Results from recent clinical trials indicate, that a adapted and specific therapeutic approach for the various shock forms is necessary. In case of traumatic hypovolemic-hemorrhagic shock it is of particular relevance if penetrating trauma and/or uncontrolled bleeding exists. Under these conditions an immediate definite surgical treatment is required ("scoop and run") and a moderate hypotension should be tolerated. ("treat and run"). Fluid substitution and therapy with catecholamines should be used conservatively. In all other forms of shock the treatment approach can and should be more aggressive in order to improve microvascular perfusion as early as possible. Besides adequate fluid resuscitation in a combination of crystalloid and colloid solutions catecholamines and-under specific circumstances-also vasopressin should be used. Of utmost importance in the pre-clinical management of patients in shock is the optimal selection of the centre that the patient is referred to in order to establish the fastest and best possible definite treatment for the patient.

Topics: Catecholamines; Combined Modality Therapy; Emergency Medical Services; Fluid Therapy; Humans; Monitoring, Physiologic; Prognosis; Resuscitation; Shock; Shock, Hemorrhagic; Shock, Traumatic; Trauma Centers; Vasopressins

Hemodynamic support during the circulatory failure with vasodilation, most frequently during the septic shock, is based on volume recovery and administration of inotropic drugs. If such therapy is not sufficient, vasoconstriction drugs are subsequently or parallel added to maintain the perfusion pressure. As a standard therapy, norepinephrine or other catecholamines with alpha-adrenergic effect are used in rising doses. Some patients do not respond to such therapy with desired hemodynamic changes--they develop catecholamine resistant shock. Because of serious side effects of high doses of catecholamines, alternative vasopressors are necessary. Vasopressin, antidiuretic hormone, has in physiological conditions only minimal effect of the vascular tone. During hypovolemia its concentration rises and it may significantly contribute to the maintenance of arterial pressure by vasoconstriction. Contrary to it, during septic shock the levels of vasopressine are very low and vasodilation clinically dominates. At the same time, the septic shock is accompanied by an increased sensitivity to vasopressin administration. In a critical shock a serious deficit of endogenous vasopressin is expected. At present several pilot studies with vasopressine administration in septic shock exist in literature describing beneficial effect of vasopressin on hemodynamic parameters. Such comparatively low doses have no side effects on perfusion and function of body organs. Terlipressin, which is available in Czech Republic, is a synthetic analogue of vasopressin with extended effect. Its intermittent administration is used for the treatment of portal hypertension complications. Terlipressin in animal model of septic shock has similarly beneficial effects as vasopressin. High doses of Terlipressin have, similarly to vasopressin, adverse effects on pulmonary circulation and other systems. Till present, only casuistic experience has been published with low doses of Terlipressin in the treatment of septic shock resistant to catecholamines, which has shown similar effects to vasopressin. In shock states with the deficit of endogenous vasopressin, which are resistant to high doses of catecholamines, administration of vasopressin analogues represents a new perspective therapy. The treatment should be studied from the point of morbidity and mortality. A careful approach has to be used in septic patients with pre-existing obliterative vassal disease.

Topics: Animals; Humans; Lypressin; Shock; Shock, Septic; Terlipressin; Vasoconstrictor Agents; Vasodilation; Vasopressins

Vasopressin and its analogue, terlipressin, are potent vasopressors that may be useful therapeutic agents in the treatment of cardiac arrest, septic and catecholamine-resistant shock and oesophageal variceal haemorrhage. The aim of this article is to review the physiology and pharmacology of vasopressin and summarise its efficacy and safety in clinical trials and its subsequent therapeutic use. Recent studies indicate that the use of vasopressin during cardiopulmonary resuscitation may improve the survival of patients with asystolic cardiac arrest. Vasopressin deficiency can contribute to refractory shock states associated with sepsis, cardiogenic shock and cardiac arrest. Low doses of vasopressin and 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 reducing bleeding and mortality associated with oesophageal variceal haemorrhage. The long-term outcome of the use of these drugs is not known.

Topics: Animals; Esophageal and Gastric Varices; Heart Arrest; Humans; Lypressin; Shock; Terlipressin; Vasoconstrictor Agents; Vasopressins

Vasopressin is an endogenous peptide hormone with the antidiuretic and vasoactive action. Its mechanisms of action on vasal smooth muscles and kidney collective tubules are well known. This hormone also plays a role in the central nervous system and influences smooth muscles of the gastrointestinal tract. The recent research results indicated much more extensive effects of endogenous vasopressin action on the circulation than appeared from the water-electrolyte balance regulation only. The use of this hormone is actually an alternative for catecholamine in treatment of the shock. This paper presents short review of vasopressin action, actual clinical use and perspectives in use of vasopressin antagonists in the heart failure.

Topics: Central Nervous System; Gastrointestinal Tract; Heart Failure; Humans; Muscle, Smooth; Shock; Vasopressins

Topics: Humans; Muscle, Smooth, Vascular; Shock; Syndrome; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Humans; Infusions, Intravenous; Ischemia; Prevalence; Shock; Skin; Vasoconstrictor Agents; Vasopressins

Vasopressin is a potent endogenous vasoconstrictor that increases blood pressure and systemic vascular resistance. The administration of exogenous vasopressin during closed and open cardiopulmonary resuscitation in humans was shown to be more effective than optimal doses of epinephrine in several clinical studies. We summarize here the recent experimental and clinical data on the use of vasopressin in cardiopulmonary resuscitation and septic shock. As the use of vasopressin in human resuscitation is now in its early stages, it is expected that accumulated future experience will shed more light regarding the risk-benefit aspects of its use.

Topics: Animals; Heart Arrest; Humans; Shock; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Epinephrine; Heart Arrest; Humans; Randomized Controlled Trials as Topic; Shock; Vasoconstrictor Agents; Vasopressins

The antidiuretic hormone (ADH) vasopressin is a simple peptide hormone with a number of complex, essential physiological actions. It is becoming clear that this hormone is developing an important therapeutic role in a number of different conditions. These include vasodilatory shock due to sepsis or cardiac surgery, cardiac arrest, and prolonged/excessive bleeding caused by, for example, variceal haemorrhage. This article reviews the physiology of ADH relevant to these actions and scrutinises the evidence for its therapeutic applications.

Topics: Heart Arrest; Hemorrhage; Hemostatics; Humans; Renal Agents; Shock; Thoracic Surgery; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Humans; Hypotension; Muscle, Smooth, Vascular; Nitric Oxide; Potassium Channels; Shock; Vasoconstriction; Vasodilation; Vasopressins

Vasopressin (antidiuretic hormone) is emerging as a potentially major advance in the treatment of a variety of shock states. Increasing interest in the clinical use of vasopressin has resulted from the recognition of its importance in the endogenous response to shock and from advances in understanding of its mechanism of action. From animal models of shock, vasopressin has been shown to produce greater blood flow diversion from non-vital to vital organ beds (particularly the brain) than does adrenaline. Although vasopressin has similar direct actions to the catecholamines, it may uniquely also inhibit some of the pathologic vasodilator processes that occur in shock states. There is current interest in the use of vasopressin in the treatment of shock due to ventricular fibrillation, hypovolaemia, sepsis and cardiopulmonary bypass. This article reviews the physiology and pharmacology of vasopressin and all of the relevant animal and human clinical literature on its use in the treatment of shock following a MEDLINE (1966-2000) search.

Topics: Advanced Cardiac Life Support; Animals; Cardiopulmonary Bypass; Humans; Shock; Shock, Septic; Vasopressins

To review the role of vasopressin in the treatment of vasodilatory shock.. A MEDLINE search on published reports (1966-April 1999) was conducted.. English-language studies and case reports were selected and evaluated based on quality of review of vasopressin in the treatment of vasodilatory shock.. In patients with end-stage vasodilatory shock, baroreceptor reflex is impaired and vasopressin stores are depleted. Persistent elevation of catecholamines may lead to down-regulation of beta-adrenergic receptors and reduces smooth-muscle response to catecholamines, leading to inability of maintaining organ perfusion. Small-scale studies and case reports have demonstrated vasopressin's efficacy in maintaining blood pressure in patients with septic shock, cardiac arrest, and end-stage heart failure, refractory to other vasopressor therapies.. Vasopressin may be a reasonable alternative for patients in vasodilatory shock. However, larger-scale controlled dinical trials are warranted before its routine use can be recommended.

Topics: Humans; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

The vasovagal response is the development of inappropriate cardiac slowing and arteriolar dilatation. Vasovagal responses reflect autonomic neural changes: bradycardia results from sudden augmentation of efferent vagal activity, and hypotension results from sudden reduction or cessation of sympathetic activity and relaxation of arterial resistance vessels. Two different neural pathways are thought to be involved, one originating in the hypothalamus, the other in the heart. Direct hypothalamic activation of the medullary cardiovascular centres triggered by emotional stress or pain causes a vasovagal response (central type). The combination of a reduced central blood volume secondary to venous pooling or blood loss, and an increased inotropic state of the heart, may stimulate ventricular mechanoreceptors and provoke vasodilatation and bradycardia (peripheral type). Cardiovascular afferents originating from stretch receptors in various parts of the vascular tree sometimes induce opposite reflexes when compared with those from ventricular afferents. The depressor reflex involved in the peripheral type of vasovagal response originates in the heart itself and overrides normal baroreflex circulatory control; an antagonism between the control of volume and pressure on the filling side of the heart and the control system of arterial pressure becomes apparent. Vasovagal responses are not necessarily abnormal; the neural pathways involved in the vasovagal response are probably present in all healthy subjects who individually mainly differ in susceptibility.

Topics: Arterioles; Blood Pressure; Heart Rate; Hemodynamics; Humans; Male; Neural Pathways; Reflex; Shock; Stress, Psychological; Syncope; Vagus Nerve; Vasodilation; Vasopressins

Animal experiments have shown that severe haemorrhage often is characterized by an initial general increase in sympathetic activity leading to an increase in heart rate and a subsequent vagally mediated, reversible decrease in heart rate. It is likely that the decrease in heart rate is triggered by mechanoreceptors situated in the left ventricle. The receptors are supposed to be activated by a reduction in end-systolic volume occurring as a result of a decrease in venous return concomitant with the initial increase in heart rate. SA vago-vagal reflex elicited from and returning to the heart is thereby activated, resulting in a slowing of the heart. It has been hypothesized that the left ventricular receptors are activated when the ventricle contracts around an almost bloodless chamber. The decrease in heart rate may allow for an increased filling of the heart and an improved coronary perfusion. However, these experimental observations are in clear contradiction to the general description of the regulatory mechanisms operating during haemorrhagic shock in man as presented by authoritative medical, surgical and anesthesiological textbooks. Until now the (over-simplified) notion has been, that progressive haemorrhage results in an increased activation of the sympathetic nervous system leading to an increase in heart rate and that the occurrence of bradycardia was a sign of irreversible shock. The present systematic measurements in patients in haemorrhagic shock showed that the heart rate during severe haemorrhage often was normal (mean value 73 beats/min, range 46-98 beats/min). Simultaneous measurements of plasma concentrations of pancreatic polypeptide (an index of vagal activity) indicated that organs other than the heart also were exposed to increased vagal activity. A marked increase in the plasma concentration of vasopressin was not a constant finding as it was during the experimental-induced hypotensive central hypovolemia. This difference may be due to a decline in the release of vasopressin during prolonged haemorrhage. In order to elucidate essential regulatory mechanisms behind the clinical observations, central hypovolemia was induced experimentally by "head-up tilt", "lower-body negative pressure", "venous tourniquets of the thighs plus haemorrhage", and by epidural anesthesia. The initial stage of central hypovolemia was characterized by an increase in sympathetic nervous activity resulting in an increase in heart rate. Activation of the renin-

Topics: Aldosterone; Angiotensin II; Animals; Atropine; beta-Endorphin; Blood Pressure; Blood Volume; Endocrine Glands; Heart Rate; Humans; Myocardium; Pressoreceptors; Renin; Shock; Shock, Hemorrhagic; Vasopressins

Topics: Animals; Cattle; Endocrine Glands; Humans; Hypotension; Hypothalamus; Neurophysins; Oxytocin; Rats; Shock; Stress, Physiological; Vasopressins

In the present review, an attempt has been made to describe the modern concept of circulatory shock (Part I). The shock inducing insults (low circulatory volume/vascular capacity equation, heart failure, or disturbance of cellular metabolism induce physiological defense mechanisms, which result in peripheral vasoconstriction in order to maintain adequate blood pressure and perfusion of vital organs (compensatory phase). However, when the insult is too aggressive or too prolonged, deterioration of the cardiovascular system and cellular function ensues as a result of anaerobic metabolism, loss of vascular tone, reperfusion injury, depression of the reticuloendothelial system, disseminated intravascular coagulation, and myocardial failure (decompensatory phase). This leads to widespread cellular destruction, autodigestion, and finally death of the patient. Recent features of shock therapy will be discussed in part II of this review.

Topics: Animals; Carbohydrate Metabolism; Cardiomyopathy, Dilated; Disseminated Intravascular Coagulation; Energy Metabolism; Hemodynamics; Lipid Metabolism; Mononuclear Phagocyte System; Neurotransmitter Agents; Oxygen Consumption; Proteins; Shock; Shock, Septic; Vasopressins

Topics: Angiotensin II; Animals; Blood Pressure; Bradykinin; Endorphins; Hypertension; Nerve Tissue Proteins; Neurotensin; Rats; Rats, Inbred Strains; Shock; Substance P; Vasopressins

Topics: Angiotensin II; Animals; Aorta; Arterioles; Blood Pressure; Catecholamines; Diabetes Insipidus; Female; Homeostasis; Male; Microcirculation; Mononuclear Phagocyte System; Muscle Contraction; Muscle, Smooth, Vascular; Oxytocin; Phagocytosis; Rats; Rats, Brattleboro; Rats, Inbred Strains; Rats, Mutant Strains; Shock; Vasopressins; Wounds and Injuries

Topics: Animals; Ergot Alkaloids; Glucocorticoids; Histamine Antagonists; Humans; Mice; Mononuclear Phagocyte System; Phagocytosis; Rats; Shock; Shock, Hemorrhagic; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Angiotensins; Catecholamines; Diabetes Mellitus; Hemorrhage; Hormones; Humans; Liver; Obesity; Phosphorylases; Shock; Vasopressins

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Animals; Blood Circulation; Catecholamines; Dopamine; Epinephrine; Homeostasis; Humans; Isoproterenol; Microcirculation; Muscle, Smooth; Norepinephrine; Peptides; Shock; Structure-Activity Relationship; Sympathomimetics; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Animals; Digitalis Glycosides; Heart Diseases; Humans; Infusions, Parenteral; Injections, Intravenous; Shock; Vasodilator Agents; Vasopressins

Topics: Adrenal Cortex Hormones; Analgesics; Angiotensin II; Animals; Anti-Bacterial Agents; Buffers; Cardiac Glycosides; Catecholamines; Diuretics; Electrolytes; Fibrinolytic Agents; Humans; Plasma Substitutes; Rabbits; Rats; Shock; Sympatholytics; Transfusion Reaction; Vasopressins

Topics: Adrenal Glands; Adrenal Medulla; Edema; Endocrine Glands; Heart; Heart Failure; Humans; Hyperaldosteronism; Shock; Thyroxine; Vasopressins

Topics: Angiotensins; Arginine Vasopressin; Blood Circulation; Bradykinin; Classification; Heparin; Histamine; Infections; Serotonin; Shock; Vasomotor System; Vasopressins

Although dopamine and norepinephrine are recommended as first-line agents in the treatment of shock, it is unclear which is the optimal vasoactive inotropic agent (VIA) to manage postcardiotomy circulatory shock. This single-center, randomized clinical trial aimed to investigate the efficacy and safety of dopamine versus norepinephrine in postcardiotomy circulatory shock.. We randomly assigned the patients with postcardiotomy circulatory shock to receive either dopamine or norepinephrine. When shock persisted despite the dose of 20 μg/kg/min of dopamine or the dose of 0.2 μg/kg/min of norepinephrine, epinephrine or vasopressin could be added. The primary endpoint was new-onset tachyarrhythmic event during drug infusion. Secondary endpoints included requirement of additional VIAs, postoperative complications, and all-cause mortality within 30 days of drug initiation.. At the planned interim analysis of 100 patients, the boundary for the benefit of norepinephrine has been crossed, and the study was stopped early. Excluding two patients withdrawing a consent, 48 patients were assigned to dopamine and 50 patients to norepinephrine. New-onset tachyarrhythmic event occurred in 12 (25%) patients in the dopamine and one (2%) patient in the norepinephrine group (p = .009). The requirement for additional VIAs was more common in the dopamine group (p < .001). Other secondary endpoints were similar between groups.. Despite the limited study subjects with early determination, in patients with postcardiotomy circulatory shock, dopamine as a first-line vasopressor was associated with higher tachyarrhythmic events and greater need for additional VIAs compared with norepinephrine.

Topics: Cardiac Surgical Procedures; Dopamine; Humans; Norepinephrine; Shock; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Although the use of vasopressin has become commonplace in pediatric patients with vasodilatory shock after cardiac surgery, its efficacy and hemodynamic effects have not been systematically documented. Furthermore, previous studies were mainly limited patients with left heart anomalies. To date, the use of vasopressin in patients with right heart anomalies has not yet been reported. To clarify the hemodynamic effects of vasopressin on pediatric patients with vasodilatory shock after cardiopulmonary bypass, 70 consecutive patients, most of whom with right heart anomalies, were retrospectively analyzed in Fuwai Hospital from October 2013 to September 2015. Vasopressin was administered continuously at a dose of 0.0002 to 0.002 u/kg/min. Hemodynamics, urine output, and catecholamine vasopressor doses were compared before and after vasopressin initiation. Results showed that besides the significant increase in blood pressure at 2 h after vasopressin administration, the systemic vascular resistance index also prominently elevated from 894.3 ± 190.8 dyn/s to 1138.2 ± 161.4 dyn/s per cm per m, while the heart rate, right atrial pressure, pulmonary artery pressure had a trend of decline. Subsequently, the fluid requirement, the catecholamine vasopressor requirement both decreased and urine output increased. Lactate concentration showed a later remarkable decline at 12 h since vasopressin administration. All the 70 patients survived to hospital discharge. In conclusion, low dose of vasopressin administration was associated with great and timely hemodynamic improvement for pediatric patients with vasodilatory shock after cardiac surgery without any significant adverse effects.

Topics: Adolescent; Blood Pressure; Cardiopulmonary Bypass; Child; Child, Preschool; Female; Heart Defects, Congenital; Hemodynamics; Humans; Infant; Infant, Newborn; Lactic Acid; Male; Postoperative Complications; Shock; Vasopressins

Vasoplegic syndrome is a common complication after cardiac surgery and impacts negatively on patient outcomes. The objective of this study was to evaluate whether vasopressin is superior to norepinephrine in reducing postoperative complications in patients with vasoplegic syndrome.. This prospective, randomized, double-blind trial was conducted at the Heart Institute, University of Sao Paulo, Sao Paulo, Brazil, between January 2012 and March 2014. Patients with vasoplegic shock (defined as mean arterial pressure less than 65 mmHg resistant to fluid challenge and cardiac index greater than 2.2 l · min · m) after cardiac surgery were randomized to receive vasopressin (0.01 to 0.06 U/min) or norepinephrine (10 to 60 μg/min) to maintain arterial pressure. The primary endpoint was a composite of mortality or severe complications (stroke, requirement for mechanical ventilation for longer than 48 h, deep sternal wound infection, reoperation, or acute renal failure) within 30 days.. A total of 330 patients were randomized, and 300 were infused with one of the study drugs (vasopressin, 149; norepinephrine, 151). The primary outcome occurred in 32% of the vasopressin patients and in 49% of the norepinephrine patients (unadjusted hazard ratio, 0.55; 95% CI, 0.38 to 0.80; P = 0.0014). Regarding adverse events, the authors found a lower occurrence of atrial fibrillation in the vasopressin group (63.8% vs. 82.1%; P = 0.0004) and no difference between groups in the rates of digital ischemia, mesenteric ischemia, hyponatremia, and myocardial infarction.. The authors' results suggest that vasopressin can be used as a first-line vasopressor agent in postcardiac surgery vasoplegic shock and improves clinical outcomes.

Topics: Brazil; Cardiac Surgical Procedures; Double-Blind Method; Female; Humans; Male; Middle Aged; Norepinephrine; Postoperative Complications; Prospective Studies; Shock; Treatment Outcome; Vasoconstrictor Agents; Vasoplegia; Vasopressins

Circulatory failure during brain death organ donor resuscitation is a problem that compromises recovery of organs. Combined administration of steroid, thyroxine and vasopressin has been proposed to optimize the management of brain deceased donors before recovery of organs. However the single administration of hydrocortisone has not been rigorously evaluated in any trial.. In this prospective multicenter cluster study, 259 subjects were included. Administration of low-dose steroids composed the steroid group (n = 102).. Although there were more patients in the steroid group who received norepinephrine before brain death (80% vs. 66%: P = 0.03), mean dose of vasopressor administered after brain death was significantly lower than in the control group (1.18 ± 0.92 mg/H vs. 1.49 ± 1.29 mg/H: P = 0.03), duration of vasopressor support use was shorter (874 min vs. 1160 min: P < 0.0001) and norepinephrine weaning before aortic clamping was more frequent (33.8% vs. 9.5%: P < 0.0001). Using a survival approach, probability of norepinephrine weaning was significantly different between the two groups (P < 0.0001) with a probability of weaning 4.67 times higher in the steroid group than in the control group (95% CI: 2.30 - 9.49).. Despite no observed benefits of the steroid administration on primary function recovery of transplanted grafts, administration of glucocorticoids should be a part of the resuscitation management of deceased donors with hemodynamic instability.

Topics: Aged; Anti-Inflammatory Agents; Brain Death; Female; France; Hemodynamics; Humans; Hydrocortisone; Kaplan-Meier Estimate; Logistic Models; Male; Middle Aged; Nordefrin; Prospective Studies; Resuscitation; Shock; Statistics, Nonparametric; Tissue and Organ Procurement; Tissue Donors; Vasoconstrictor Agents; Vasopressins

Among patients with cardiac arrest, preliminary data have shown improved return of spontaneous circulation and survival to hospital discharge with the vasopressin-steroids-epinephrine (VSE) combination.. To determine whether combined vasopressin-epinephrine during cardiopulmonary resuscitation (CPR) and corticosteroid supplementation during and after CPR improve survival to hospital discharge with a Cerebral Performance Category (CPC) score of 1 or 2 in vasopressor-requiring, in-hospital cardiac arrest.. Randomized, double-blind, placebo-controlled, parallel-group trial performed from September 1, 2008, to October 1, 2010, in 3 Greek tertiary care centers (2400 beds) with 268 consecutive patients with cardiac arrest requiring epinephrine according to resuscitation guidelines (from 364 patients assessed for eligibility).. Patients received either vasopressin (20 IU/CPR cycle) plus epinephrine (1 mg/CPR cycle; cycle duration approximately 3 minutes) (VSE group, n = 130) or saline placebo plus epinephrine (1 mg/CPR cycle; cycle duration approximately 3 minutes) (control group, n = 138) for the first 5 CPR cycles after randomization, followed by additional epinephrine if needed. During the first CPR cycle after randomization, patients in the VSE group received methylprednisolone (40 mg) and patients in the control group received saline placebo. Shock after resuscitation was treated with stress-dose hydrocortisone (300 mg daily for 7 days maximum and gradual taper) (VSE group, n = 76) or saline placebo (control group, n = 73).. Return of spontaneous circulation (ROSC) for 20 minutes or longer and survival to hospital discharge with a CPC score of 1 or 2.. Follow-up was completed in all resuscitated patients. Patients in the VSE group vs patients in the control group had higher probability for ROSC of 20 minutes or longer (109/130 [83.9%] vs 91/138 [65.9%]; odds ratio [OR], 2.98; 95% CI, 1.39-6.40; P = .005) and survival to hospital discharge with CPC score of 1 or 2 (18/130 [13.9%] vs 7/138 [5.1%]; OR, 3.28; 95% CI, 1.17-9.20; P = .02). Patients in the VSE group with postresuscitation shock vs corresponding patients in the control group had higher probability for survival to hospital discharge with CPC scores of 1 or 2 (16/76 [21.1%] vs 6/73 [8.2%]; OR, 3.74; 95% CI, 1.20-11.62; P = .02), improved hemodynamics and central venous oxygen saturation, and less organ dysfunction. Adverse event rates were similar in the 2 groups.. Among patients with cardiac arrest requiring vasopressors, combined vasopressin-epinephrine and methylprednisolone during CPR and stress-dose hydrocortisone in postresuscitation shock, compared with epinephrine/saline placebo, resulted in improved survival to hospital discharge with favorable neurological status.. clinicaltrials.gov Identifier: NCT00729794.

Topics: Adrenergic beta-Agonists; Aged; Aged, 80 and over; Brain; Cardiopulmonary Resuscitation; Double-Blind Method; Drug Therapy, Combination; Epinephrine; Female; Glasgow Outcome Scale; Heart Arrest; Hemostatics; Humans; Hydrocortisone; Inpatients; Male; Methylprednisolone; Middle Aged; Neuroprotective Agents; Patient Discharge; Shock; Survival Analysis; Treatment Outcome; Vasopressins

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.

Topics: Aged; Cardiac Surgical Procedures; Cardiopulmonary Bypass; Drug Therapy, Combination; Female; Glycopeptides; Humans; Male; Postoperative Complications; Prospective Studies; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Humans; Prospective Studies; Shock; Shock, Septic; Vasopressins

Topics: Biomarkers; Cardiac Surgical Procedures; Humans; Shock; Vasoconstrictor Agents; Vasopressins

After fluid administration for vasodilatory shock, vasopressors are commonly infused. Causes of vasodilatory shock include septic shock, post-cardiovascular surgery, post-acute myocardial infarction, postsurgery, other causes of an intense systemic inflammatory response, and drug -associated anaphylaxis. Therapeutic vasopressors are hormones that activate receptors-adrenergic: α1, α2, β1, β2; angiotensin II: AG1, AG2; vasopressin: AVPR1a, AVPR1B, AVPR2; dopamine: DA1, DA2. Vasopressor choice and dose vary widely because of patient and physician practice heterogeneity. Vasopressor adverse effects are excessive vasoconstriction causing organ ischemia/infarction, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias. To date, no randomized controlled trial (RCT) of vasopressors has shown a decreased 28-day mortality rate. There is a need for evidence regarding alternative vasopressors as first-line vasopressors. We emphasize that vasopressors should be administered simultaneously with fluid replacement to prevent and decrease duration of hypotension in shock with vasodilation. Norepinephrine is the first-choice vasopressor in septic and vasodilatory shock. Interventions that decrease norepinephrine dose (vasopressin, angiotensin II) have not decreased 28-day mortality significantly. In patients not responsive to norepinephrine, vasopressin or epinephrine may be added. Angiotensin II may be useful for rapid resuscitation of profoundly hypotensive patients. Inotropic agent(s) (e.g., dobutamine) may be needed if vasopressors decrease ventricular contractility. Dopamine has fallen to almost no-use recommendation because of adverse effects; angiotensin II is available clinically; there are potent vasopressors with scant literature (e.g., methylene blue); and the novel V1a agonist selepressin missed on its pivotal RCT primary outcome. In pediatric septic shock, vasopressors, epinephrine, and norepinephrine are recommended equally because there is no clear evidence that supports the use of one vasoactive agent. Dopamine is recommended when epinephrine or norepinephrine is not available. New strategies include perhaps patients will be

Topics: Angiotensin II; Dopamine; Epinephrine; Humans; Intensive Care Units; Norepinephrine; Shock; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Hemodynamic conditions with reduced systemic vascular resistance commonly are observed in patients undergoing cardiac surgery and may range from moderate reductions in vascular tone, as a side effect of general anesthetics, to a profound vasodilatory syndrome, often referred to as vasoplegic shock. Therapy with vasopressors is an important pillar in the treatment of these conditions. There is limited guidance on the appropriate choice of vasopressors to restore and optimize systemic vascular tone in patients undergoing cardiac surgery. A panel of experts in the field convened to develop statements and evidence-based recommendations on clinically relevant questions on the use of vasopressors in cardiac surgical patients, using a critical appraisal of the literature following the GRADE system and a modified Delphi process. The authors unanimously and strongly recommend the use of norepinephrine and/or vasopressin for restoration and maintenance of systemic perfusion pressure in cardiac surgical patients; despite that, the authors cannot recommend either of these drugs with respect to the risk of ischemic complications. The authors unanimously and strongly recommend against using dopamine for treating post-cardiac surgery vasoplegic shock and against using methylene blue for purposes other than a rescue therapy. The authors unanimously and weakly recommend that clinicians consider early addition of a second vasopressor (norepinephrine or vasopressin) if adequate vascular tone cannot be restored by a monotherapy with either norepinephrine or vasopressin and to consider using vasopressin as a first-line vasopressor or to add vasopressin to norepinephrine in cardiac surgical patients with pulmonary hypertension or right-sided heart dysfunction.

Topics: Cardiac Surgical Procedures; Consensus; Humans; Norepinephrine; Shock; Vasoconstrictor Agents; Vasopressins

The use of vasoactive agents like arginine vasopressin (AVP) and terlipressin to treat hypotension or persistent pulmonary hypertension in critically ill preterm neonates is increasing. Therefore, a systematic review of the available data on dosing, efficacy and safety of AVP and terlipressin in this patient population appears beneficial.. We will conduct a systematic review of the available evidence on the use of AVP and terlipressin for the treatment of hypotension or persistent pulmonary hypertension in preterm neonates. We will search Ovid MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, Web of Science and Google Scholar from inception to March 2021. Two reviewers will independently screen titles and abstracts, review the full text of eligible studies, extract data, assess the risk of bias and judge the certainty of the evidence. Our primary outcome will be an (1) improvement of end-organ perfusion after initiation of AVP or terlipressin and (2) mortality prior to discharge. Our secondary outcomes will include (1) major neurosensory abnormality and (2) the occurrence of adverse events.. The currently available evidence on the efficacy and safety of AVP and terlipressin in preterm neonates is limited. Yet, evidence on the pharmacology of these drugs and the pathophysiology of vasoplegic shock support the biological plausibility for their clinical effectiveness in this population. Therefore, we aim to address this gap concerning the use of vasopressin and terlipressin among critically ill preterm neonates.. This protocol has been submitted for registration to the international database of prospectively registered systematic reviews (PROSPERO, awaiting registration number).

Topics: Humans; Infant, Newborn; Lypressin; Shock; Systematic Reviews as Topic; Terlipressin; Vasoconstrictor Agents; Vasopressins

Topics: Angiotensin II; Humans; Shock; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Vasopressin has achieved common usage for the treatment of catecholamine-requiring and catecholamine-resistant shock. Diabetes insipidus is a syndrome characterized by excretion of abnormally large volumes of dilute urine. To date, very few reports of diabetes insipidus after discontinuation of vasopressin infusion have been published; the majority of previous reports describe neurosurgical patients. The purpose of the present study was to investigate the occurrence rate of diabetes insipidus after discontinuation of vasopressin infusion among patients treated with vasopressin infusion for shock.. Retrospective analysis of electronic health records of patients receiving continuous vasopressin infusion for the treatment of shock within a 5-year period (2012-2016).. Medical, surgical, and cardiothoracic ICUs within one academic medical center.. One-thousand eight-hundred ninety-six patients received vasopressin infusion for the treatment of shock.. None.. The occurrence rate of diabetes insipidus after discontinuation of vasopressin infusion was 1.53% among all patients. Sixteen of 29 patients with diabetes insipidus after discontinuation of vasopressin infusion had undergone cardiothoracic intervention, such as coronary artery bypass graft and valve replacement surgery, extracorporeal membrane oxygenation, and placement of ventricular assist devices. No neurosurgical patients were identified in our cohort. In a control group of patients receiving norepinephrine but not vasopressin infusion for treatment of shock, criteria for diabetes insipidus were observed in two of 1,320 subjects (0.15%).. Despite a paucity of published reports, diabetes insipidus after discontinuation of vasopressin infusion appears not to be a rare phenomenon, and is likely to be encountered by intensivists who regularly employ vasopressin for the treatment of vasoplegic shock. Previous reports consisted predominantly of neurosurgical patients. Our findings demonstrate the occurrence of diabetes insipidus after discontinuation of vasopressin infusion among patients with septic shock as well as vasoplegic shock after cardiothoracic intervention. The mechanism of diabetes insipidus after discontinuation of vasopressin infusion remains to be elucidated but may involve transient downregulation of V2 receptors induced by exposure to supraphysiological doses of vasopressin.

Topics: Adult; Child, Preschool; Diabetes Insipidus; Female; Humans; Infusions, Intravenous; Male; Middle Aged; Retrospective Studies; Shock; Vasopressins; Withholding Treatment; Young Adult

Despite international guidelines, regional differences in treatment of vasodilatory shock remain. We characterized these differences using data from Angiotensin II in High Output Shock (ATHOS-3) trial.. The 321 patients treated in the ATHOS-3 trial were included. Baseline and hour-48 data were analyzed for differences in demographics, clinical characteristics, and treatment patterns, and grouped into four geographical areas: United States, Canada, Europe, and Australasia. Differences were analyzed by Kruskal-Wallis tests for continuous, and chi-square tests for categorical data. Temporal analysis compared changes in the treatment of shock during the treatment period.. Differences in baseline characteristics across geographic areas were noted in BMI, albumin, CVP, MELD score, APACHE II score, and total SOFA score. Baseline norepinephrine and norepinephrine equivalent doses (NED) were higher (p < .0001 and p = .0494, respectively), and vasopressin use was lower (p < .0001) in Europe. Baseline steroids were utilized more in the US and Canada (p = .0011).. Management of vasodilatory shock differs globally with respect to utilization of steroids and vasopressors. This practice heterogeneity may influence shock trials interpretation and patient outcomes, though more definitive evidence would require larger prospective intervention data.

Topics: Adult; Aged; Aged, 80 and over; Albumins; Angiotensin II; Australia; Canada; Chi-Square Distribution; Europe; Female; Humans; Male; Middle Aged; Neurophysins; Norepinephrine; Prospective Studies; Protein Precursors; Retrospective Studies; Shock; Shock, Septic; United States; Vasoconstrictor Agents; Vasopressins; Young Adult

Topics: Humans; Norepinephrine; Shock; Shock, Septic; Vasoconstrictor Agents; Vasopressins

RCTs in septic shock negative for mortality may show organ dysfunction benefits. We hypothesized that RCTs in septic shock show significant differences between treatment groups in organ support despite no mortality differences.. RCTs of epinephrine vs. norepinephrine plus dobutamine, norepinephrine vs. dopamine and vasopressin vs. norepinephrine reported days alive and free ("DAF") of vasopressors, ventilation and RRT, by subtracting days with support from the lesser of 28 or days to death. We also assigned zero DAF to non-survivors ("DAF and Mortality") and calculated the composite "DAF vasopressors, ventilation and RRT".. Using "DAF", norepinephrine was better than dopamine for vasopressors. In contrast, using "DAF and Mortality", norepinephrine was better than dopamine for vasopressors, ventilation and RRT; norepinephrine + dobutamine was better than epinephrine for ventilation. Using the novel composite "DAF vasopressors, ventilation and RRT", norepinephrine + dobutamine was better than epinephrine (p = 0.033), norepinephrine better than dopamine (p = 0.03), and vasopressin better than norepinephrine in less severe shock (p = 0.03).. Differences between treatment groups in organ dysfunction in RCTs in septic shock occur despite lack of mortality differences depending on calculation method. If standardized and validated further, DAF could become the primary endpoint of RCTs in septic shock.

Topics: Clinical Trials as Topic; Dobutamine; Dopamine; Epinephrine; Humans; Neurophysins; Norepinephrine; Protein Precursors; Randomized Controlled Trials as Topic; Shock; Shock, Septic; Time Factors; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Topics: Arginine Vasopressin; Humans; Norepinephrine; Shock; Shock, Septic; Vasoconstrictor Agents; Vasodilation; Vasopressins

Shock, defined as the state where oxygen delivery to tissues is inadequate for the demand, is a common condition in veterinary patients and has a high mortality rate if left untreated. The key to a successful outcome for any patient in shock involves having a clear understanding of the pathophysiology and compensatory mechanisms associated with shock. This understanding allows more efficient identification of patients in shock based on clinical signs and timely initiation of appropriate therapies based on the type and stage of shock identified.

Topics: Angiotensin II; Animals; Blood Circulation; Catecholamines; Hydrocortisone; Shock; Vasopressins

Topics: Humans; Lypressin; Shock; Vasoconstrictor Agents; Vasopressins

Estrogen receptors are located in important brain areas that integrate cardiovascular and hydroelectrolytic responses, including the subfornical organ (SFO) and supraoptic (SON) and paraventricular (PVN) nuclei. The aim of this study was to evaluate the influence of estradiol on cardiovascular and neuroendocrine changes induced by hemorrhagic shock in ovariectomized rats. Female Wistar rats (220-280 g) were ovariectomized and treated for 7 days with vehicle or estradiol cypionate (EC, 10 or 40 μg/kg, sc). On the 8th day, animals were subjected to hemorrhage (1.5 ml/100 g for 1 min). Hemorrhage induced acute hypotension and bradycardia in the ovariectomized-oil group, but EC treatment inhibited these responses. We observed increases in plasma angiotensin II concentrations and decreases in plasma atrial natriuretic peptide levels after hemorrhage; EC treatment produced no effects on these responses. There were also increases in plasma vasopressin (AVP), oxytocin (OT), and prolactin levels after the induction of hemorrhage in all groups, and these responses were potentiated by EC administration. SFO neurons and parvocellular and magnocellular AVP and OT neurons in the PVN and SON were activated by hemorrhagic shock. EC treatment enhanced the activation of SFO neurons and AVP and OT magnocellular neurons in the PVN and SON and AVP neurons in the medial parvocellular region of the PVN. These results suggest that estradiol modulates the cardiovascular responses induced by hemorrhage, and this effect is likely mediated by an enhancement of AVP and OT neuron activity in the SON and PVN.

Topics: Angiotensin II; Animals; Atrial Natriuretic Factor; Cardiovascular System; Estradiol; Female; Hypothalamus; Models, Animal; Neurons; Ovariectomy; Oxytocin; Paraventricular Hypothalamic Nucleus; Prolactin; Rats; Rats, Wistar; Shock; Supraoptic Nucleus; Vasopressins

Topics: Africa, Eastern; Albumins; Anemia; Child; Coma; Critical Illness; Developing Countries; Dose-Response Relationship, Drug; Drug Administration Schedule; Fever; Fluid Therapy; Humans; Meningitis, Bacterial; Pneumonia; Randomized Controlled Trials as Topic; Resuscitation; Shock; Sodium Chloride; Vasopressins

To determine whether vasopressin is detectable in the continuous venovenous hemodialysis (CVVHD) effluent of patients receiving exogenous arginine vasopressin, and to determine whether treatment-specific factors are associated with vasopressin levels in CVVHD effluent. DESIGN. Prospective observational study. SETTING. Intensive care units of a tertiary care academic medical center. PATIENTS. Twenty-seven adults with vasodilatory shock who received a stable-dose continuous intravenous infusion of arginine vasopressin with concomitant uninterrupted CVVHD for at least 4 hours between September 2008 and May 2010. MEASUREMENTS AND MAIN RESULTS. Vasopressin levels in CVVHD effluent were assessed by radioimmunoassay. Statistical analysis was performed with analysis of variance and Pearson correlation. A multivariate linear regression was used to assess for independent factors associated with vasopressin levels in CVVHD effluent. The CVVHD effluent of all patients was assessed for vasopressin levels. The median exogenous arginine vasopressin dose was 0.03 unit/minute (range 0.02-0.18 unit/min), whereas the median CVVHD effluent flow rate was 22.6 ml/kg/hour (interquartile range [IQR] 21.5-26.8 ml/kg/hr). Vasopressin was detectable in all effluent samples (median 88.8 pg/ml, IQR 36.4-113.7 pg/ml). There were no significant differences in CVVHD effluent vasopressin levels among CVVHD filter types (p=0.39). The CVVHD effluent vasopressin levels correlated with exogenous arginine vasopressin dose (r2=0.49, p<0.001). After adjustment for CVVHD effluent flow rate and administration of corticosteroids, with multivariate linear regression, only exogenous arginine vasopressin dose was independently associated with CVVHD effluent vasopressin level. CONCLUSION. Vasopressin is detectable in CVVHD effluent, suggesting that it is removed by CVVHD. In addition, exogenous arginine vasopressin infusion dose is independently associated with CVVHD effluent vasopressin level.

Topics: Adult; Aged; Aged, 80 and over; Arginine Vasopressin; Dose-Response Relationship, Drug; Female; Hemodialysis Solutions; Humans; Male; Middle Aged; Pilot Projects; Prospective Studies; Renal Dialysis; Shock; Vasodilation; Vasopressins

As vasopressin is a small peptide, its sieving coefficient (SC) and clearance (CL) during continuous renal replacement therapy may be intermediate to those for urea and β2 microglobulin (commonly used markers for small- and middle-molecular weight solutes, respectively).. A prospective, minimal-risk study was undertaken of the SC and CL of vasopressin in critically ill children on the first day of continuous renal replacement therapy using AN69 membrane filters and prefilter replacement fluid. All prefilter plasma (vasopressin) samples were drawn from the arterial port after predilution.. Nine patients with fluid overload, renal failure, or both were recruited (median age, 14 years) during the first day of either continuous venovenous hemofiltration (n = 3) or hemodiafiltration (n = 6). Multiorgan dysfunction syndrome was present in 8 patients, and 3 were in shock (2 were receiving a vasopressin infusion). Median prefilter plasma (vasopressin) was 1.7 pg/mL, although data points were skewed: 5 patients had a low prefilter plasma (vasopressin) (<2 pg/mL), and 4 patients (including 2 receiving a continuous vasopressin infusion) had a prefilter plasma (vasopressin) between 4.2 and 56.4 pg/mL. All those with low prefilter plasma (vasopressin) had an effluent (vasopressin) less than the detection limit (0.6 pg/mL). The median SC was 1 in the 4 patients with a measurable effluent (vasopressin), and their median filter CL was 48 mL/min or 39 mL/(min 1.73 m(2)).. The SC and CL of vasopressin by continuous venovenous hemofiltration or hemodiafiltration in these critically ill children were similar to values for urea.

Topics: Adolescent; beta 2-Microglobulin; Child; Child, Preschool; Critical Care; Critical Illness; Hemodiafiltration; Hemofiltration; Humans; Infant; Metabolic Clearance Rate; Multiple Organ Failure; Prospective Studies; Renal Replacement Therapy; Shock; Urea; Vasopressins; Young Adult

The San Antonio Vasopressin Symposium reviewed substantial accumulated data concerning vasopressin in haemorrhagic, septic, and cardiac arrest shock conditions and found that there is considerable evidence to support the use of vasopressin in overcoming vasopressin deficiency or insufficiency. The value of vasopressin in the setting of trauma requires further investigation. It was concluded that a large, multicenter controlled trial of vasopressin is needed to assess the therapeutic benefit of vasopressin replacement in the setting of trauma with haemorrhagic shock that is prolonged and profound.

Topics: Brain Injuries; Evidence-Based Medicine; Heart Arrest; Humans; Shock; Texas; Vasopressins

Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery.. Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained.. The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin.. Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.

Topics: Aged; Carbon Dioxide; Cardiac Surgical Procedures; Female; Hemodynamics; Hemostatics; Humans; Intestinal Mucosa; Jejunum; Laser-Doppler Flowmetry; Male; Middle Aged; Oxygen Consumption; Postoperative Complications; Regional Blood Flow; Shock; Splanchnic Circulation; Vasodilation; Vasopressins

Topics: Acute Kidney Injury; Adolescent; Age Factors; Child, Preschool; Critical Care; Dose-Response Relationship, Drug; Female; Glomerular Filtration Rate; Humans; Infant, Newborn; Intensive Care Units, Pediatric; Kidney Function Tests; Male; Severity of Illness Index; Shock; Survival Rate; Treatment Outcome; Vasopressins

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.

Topics: Child; Child, Preschool; Female; Hemodynamics; Humans; Infant; Infusions, Intravenous; Intensive Care Units, Pediatric; Kidney; Kidney Function Tests; Liver; Liver Function Tests; Male; Medical Records Systems, Computerized; Retrospective Studies; Shock; Vasoconstrictor Agents; Vasopressins

Tachyphylaxis against catecholamines often complicates hemodynamic support in patients with septic shock. Recent experimental and clinical research suggests that the hemodynamic response to exogenous arginine vasopressin (AVP) infusion may also be blunted. The purpose of the present study was therefore to clarify whether the efficacy of a continuous AVP infusion (0.04 U x min(-1)) decreases over time in ovine endotoxemia. An additional objective was to determine whether the anticipated hyporesponsiveness can be counteracted by corticosteroids. Fourteen adult ewes (37 +/- 1 kg) were instrumented for chronic hemodynamic monitoring. All ewes received a continuous endotoxin infusion that contributed to a hypotensive-hyperdynamic circulation. After 16 h of endotoxemia, the sheep were randomized to receive either AVP (0.04 U x min(-1)) or the vehicle (normal saline; n = 7 each). After 6 h of AVP or placebo infusion, respectively, methylprednisolone (30 mg x kg(-1)) was injected. Arginine vasopressin infusion increased mean arterial pressure and systemic vascular resistance index at the expense of a reduced cardiac index (P < 0.05 each). Supraphysiologic AVP plasma levels in the treatment group (298 +/- 15 pg x mL(-1)) were associated with increased surrogate parameters of liver, mesenterial, and myocardial dysfunction. After 6 h of continuous AVP infusion, the vasopressor effect was significantly reduced. Interestingly, a bolus infusion of methylprednisolone (30 mg x kg(-1)) reestablished mean arterial pressure by increasing both cardiac index and systemic vascular resistance index. The present study demonstrates that in endotoxemia, (a) the vasopressor effect of AVP infusion may be reduced, (b) corticosteroids may potentially be useful to increase the efficacy of AVP infusion, and (c) even moderate AVP doses may potentially impair myocardial and hepatic function.

Topics: Adrenal Cortex Hormones; Animals; Arginine Vasopressin; Blood Pressure; Endotoxemia; Endotoxins; Female; Methylprednisolone; Oxygen; Pressure; Sepsis; Sheep; Shock; Time Factors; Vasopressins

A 27-year-old man with schizophrenia took an overdose of a psychotic agent. He became unconscious and had severe hypotension. Although he was diagnosed as having distributive shock caused by drug overdose and treated by hydration and catecholamine, the shock status was lasting. The use of vasopressin changed the situation dramatically. After the injection of vasopressin at maximum dose, 0.1 U/min, the dose of vasopressin could be tapered. He recovered from shock and was discharged on the third day without sequelae. There are an increasing number of reports that indicate that vasopressin is effective for distributive shock, especially catecholamine-resistant septic shock. It seems that the appropriate dose of vasopressin is under 0.04U/min considering the deterioration of cardiac function although the maximum dose of vasopressin was O.1U/min in this case. For that reason, monitoring by pulmonary artery catheter is recommended. The side effects of vasopressin should be discussed for appropriate use.

Topics: Adult; Antidiuretic Agents; Antipsychotic Agents; Catecholamines; Drug Overdose; Humans; Injections, Intravenous; Male; Schizophrenia; Shock; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Published guidelines suggest that vasopressin has a role in shock treatment, although its safety has not been adequately evaluated in a clinical setting. Vasopressin causes platelet aggregation and has been associated with the release of factor VIII coagulant and von Willebrand factor.. To compare the incidence of venous thromboembolism (VTE) in patients with a diagnosis of shock who received vasopressin with those who did not receive vasopressin for hemodynamic support.. A retrospective, single-center, cohort study was conducted at an academic, tertiary care center with 350 patients with a diagnosis of shock. Patients from the intensive care unit were randomly selected and separated into 2 groups for comparison of those receiving only catecholamines with those receiving vasopressin with or without catecholamines for hypotension. Patients with diabetes insipidus or variceal hemorrhage and those with any documented history of VTE were excluded. The primary outcome, VTE occurrence, was defined as a positive Doppler ultrasound, spiral computed tomography, or documented diagnosis in the discharge records. Frequency and type of risk factors for VTE were compared between the 2 study arms. A risk factor modeling approach was performed, using logistic regression to identify potential confounders and effect modifiers in the relationship between vasopressin and VTE.. There were 175 patients in each arm of the study. The crude incidence of VTE was 7.4% and 8% in the vasopressin and catecholamine groups, respectively (p = 0.84). No significant difference in the incidence of deep venous thrombosis (vasopressin 5.1%, control 7.4%; p = 0.51) or pulmonary embolism (vasopressin 2.3%, control 0.6%; p = 0.37) was found between groups. After adjusting for covariates, there was no statistically significant difference in the incidence of VTE between the 2 arms (p = 0.72).. This investigation provides initial evidence that vasopressin infusions do not increase the risk of VTE in patients with shock.

Topics: Adult; Aged; Aged, 80 and over; Catecholamines; Female; Hemostatics; Humans; Infusions, Intravenous; Intensive Care Units; Male; Middle Aged; Pulmonary Embolism; Risk Factors; Shock; Thromboembolism; Vasopressins; Venous Thrombosis

To measure arginine vasopressin (AVP) serum concentrations in critically ill patients.. Prospective study.. Twelve-bed general and surgical intensive care unit in a tertiary, university teaching hospital.. Two-hundred-thirty-nine mixed critically ill patients and 70 healthy volunteers.. None.. Demographic data, hemodynamic variables, vasopressor drug requirements, blood gases, AVP serum concentrations within 24 hrs after admission, multiple organ dysfunction score, and outcome were recorded. Twenty-four hours after admission, study patients had significantly higher AVP concentrations (11.9 +/- 20.6 pg/mL) than healthy controls (0.92 +/- 0.38 pg/mL; p < .001). Males had lower AVP concentrations than females (9.7 +/- 19.5 vs. 15.1 +/- 20.6 pg/mL; p = .014). Patients with hemodynamic dysfunction had higher AVP concentrations than patients without hemodynamic dysfunction (14.1 +/- 27.1 vs. 8.7 +/- 10.8 pg/mL; p = .042). Patients after cardiac surgery (n = 96) had significantly higher AVP concentrations when compared to patients admitted for other diagnoses (n = 143; p < .001). AVP concentrations were inversely correlated with length of stay in the intensive care unit (correlation coefficient, -0.222; p = .002). There was no correlation between serum AVP concentrations and the incidence of shock or specific hemodynamic parameters. Four (1.7%) of the 239 study patients met criteria for an absolute AVP deficiency (AVP, <0.83 pg/mL), and 32 (13.4%) met criteria for a relative AVP deficiency (AVP, <10 pg/mL, and mean arterial pressure, <70 mm Hg). In shock patients, relative AVP deficiency occurred in 22.2% (septic shock), 15.4% (postcardiotomy shock), and 10% (shock due to a severe systemic inflammatory response syndrome) (p = .316).. AVP serum concentrations 24 hrs after intensive care unit admission were significantly increased in this mixed critically ill patient population. The lack of a correlation between AVP serum concentrations and hemodynamic parameters suggests complex dysfunction of the vasopressinergic system in critical illness. Relative and absolute AVP deficiency may be infrequent entities during acute surgical critical illness, mostly remaining without significant effects on cardiovascular function.

Topics: Case-Control Studies; Critical Illness; Female; Hospital Mortality; Humans; Intensive Care Units; Male; Middle Aged; Sepsis; Shock; Vasopressins

Topics: Adenosine Triphosphate; Blood Pressure; Brain Ischemia; Calcium Channels; Hemostatics; Humans; Hypotension; Muscle, Smooth, Vascular; Shock; Shock, Cardiogenic; Shock, Septic; Vasoconstrictor Agents; Vasodilation; Vasopressins

To describe the utility of vasopressin in the treatment of acute distributive shock clinically compatible with the diagnosis of aprotinin anaphylaxis.. A 57-yr-old female patient underwent repeat cardiac surgery to treat prosthetic valve endocarditis. She had received aprotinin during her first surgery 60 days ago. Despite a negative test dose of i.v. aprotinin 20,000 KIU, when aprotinin loading was initiated during the repeat surgery, the patient developed bronchospasm and hypotension secondary to acute distributive shock. Bronchospasm responded to inhaled salbutamol and ipatropium. The hypotension was refractory to high doses of phenylephrine. Two doses of i.v. vasopressin 5 U reversed the vasodilation and reestablished normal blood pressure.. Vasopressin, in association with alpha-agonists, can reverse acute refractory distributive shock following aprotinin administration.

Topics: Aprotinin; Blood Pressure; Bronchial Spasm; Cardiac Output; Cardiac Surgical Procedures; Central Venous Pressure; Endocarditis; Female; Heart Rate; Heart Valve Prosthesis; Hemostatics; Humans; Hypotension; Middle Aged; Prosthesis Failure; Reoperation; Shock; Staphylococcal Infections; Vasoconstrictor Agents; Vasopressins

Topics: Adrenal Gland Neoplasms; Catecholamines; Humans; Male; Middle Aged; Pheochromocytoma; Shock; Vascular Diseases; Vascular Resistance; Vasopressins

Topics: Blood Pressure; Cardiopulmonary Bypass; Humans; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Cardiopulmonary Bypass; Humans; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Blood Pressure; Hemodynamics; Humans; Pulmonary Artery; Shock; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

Topics: Brain Death; Humans; Shock; Vasopressins

Topics: Adult; Age Factors; Child; Epinephrine; Evidence-Based Medicine; Heart Arrest; Humans; Infant; Resuscitation; Shock; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

A 54-year-old patient, admitted to the intensive care unit with a diagnosis of severe pancreatitis, developed circulatory shock that failed to respond to standard vasopressor treatment: epinephrine and norepinephrine. Addition of vasopressin helped reduce standard catecholamine need while maintaining adequate arterial blood pressure. Vasopressin appears to be a promising agent for maintaining arterial pressure during septic shock or systemic inflammatory response syndrome, but due to limited data and potential side effects, its use as first-line treatment for these indications is not recommended.

Topics: Blood Pressure; Fatal Outcome; Female; Humans; Middle Aged; Pancreatitis; Shock; Systemic Inflammatory Response Syndrome; Vasoconstrictor Agents; Vasopressins

We retrospectively investigated the effects of continuous arginine vasopressin (AVP) infusion on systemic hemodynamics, acid/base status, and laboratory variables in patients (mean age [mean +/- SD]= 66.3 +/- 10.1 yr) with catecholamine-resistant septic (n = 35) or postcardiotomy shock (n = 25). Hemodynamic and acid/base data were obtained before; 30 min after; and 1, 4, 12, 24, 48, and 72 h after the start of AVP infusion. Laboratory examinations were recorded before and 24, 48, and 72 h after the start of AVP infusion. For statistical analysis, a mixed-effects model was used. The overall intensive care unit mortality was 66.7%. AVP administration caused a significant increase in mean arterial pressure (+29%) and systemic vascular resistance (+56%), accompanied by a significant decrease in heart rate (-24%) and mean pulmonary arterial pressure (-11%) without any change in stroke volume index. Norepinephrine requirements could be reduced by 72% within 72 h. During AVP infusion, a significant increase in liver enzymes and total bilirubin concentration and a significant decrease in platelet count occurred. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.. In this retrospective analysis, the influence of a continuous infusion of an endogenous hormone (arginine vasopressin) on systemic hemodynamics and laboratory variables was assessed in patients with vasodilatory shock unresponsive to conventional therapy. Arginine vasopressin was effective in reversing systemic hypotension. However, adverse effects on gastrointestinal perfusion and coagulation cannot be excluded.

Topics: Acid-Base Equilibrium; Aged; Cardiac Surgical Procedures; Catecholamines; Critical Care; Drug Resistance; Female; Hemodynamics; Humans; Male; Models, Biological; Norepinephrine; Postoperative Complications; Retrospective Studies; Shock; Shock, Septic; Stroke Volume; Survivors; Vasoconstrictor Agents; Vasopressins

The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow.. Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow.. University hospital laboratory.. Fourteen pigs weighing 30 +/- 3 kg.. Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation.. Mean +/- sem bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 +/- 4.1 to 3.7 +/- 1.8 mL.100 g-1.min-1 in the vasopressin group and from 18.2 +/- 4.0 to 5.2 +/- 1.0 mL.100 g-1.min-1 in the epinephrine group (p =.025 in both groups). Five minutes after return of spontaneous circulation, mean +/- sem bone marrow blood flow was 3.4 +/- 1.1 mL.100 g-1.min-1 after vasopressin and 0.1 +/- 0.03 mL.100 g-1.min-1 after epinephrine (p =.004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p =.004) higher in the epinephrine group when compared with vasopressin (1455 +/- 392 vs. 43 +/- 19 mm Hg. mL-1.100 g.min, respectively).. Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resuscitation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.

Topics: Animals; Bone Marrow; Epinephrine; Female; Heart Arrest; Hemodynamics; Infusions, Intraosseous; Microspheres; Resuscitation; Shock; Swine; Vasoconstrictor Agents; Vasopressins

A patient with perforated appendicitis developed progressive vasodilatory shock which was complicated by perioperative acute myocardial infarction. Cardiovascular support included dopamine infusion, and later, intra-aortic balloon counterpulsation balloon pump and noradrenaline and dobutamine infusion. Vasopressin was introduced as a final attempt to reverse the refractory shock and was associated with recovery. The experience with this case suggests that vasopressin may be a valuable adjunct to the treatment of catecholamine-resistant vasodilatory shock.

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Aged; Appendicitis; Cardiotonic Agents; Dobutamine; Dopamine; Humans; Infusions, Intravenous; Intestinal Perforation; Intra-Aortic Balloon Pumping; Intraoperative Complications; Male; Myocardial Infarction; Norepinephrine; Recovery of Function; Shock; Vasoconstrictor Agents; Vasodilation; Vasopressins

Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital organ perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), and 2 (0-48) mL. 100 g(-1). min(-1), respectively; and after vasopressin 96 (12-161), and 44 (16-105) mL. 100 g(-1). min(-1), respectively (P: <.01 between groups). Epinephrine animals developed a profound metabolic acidosis by 15 min after return of spontaneous circulation (mean arterial pH, 7.11 +/- 0.01), and by 60 min all epinephrine-treated animals had died. The vasopressin pigs had (P: = 0.015) less acidosis (pH = 7.26+/-0. 04) at corresponding time points, and all survived > or =55 min (P: < 0. 01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted.. The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion and prolonged survival in an animal model of suspended infusion therapy.

Topics: Animals; Blood Gas Analysis; Blood Pressure; Cardiopulmonary Resuscitation; Coronary Circulation; Female; Heart Arrest; Microspheres; Regional Blood Flow; Shock; Survival Analysis; Swine; Vasopressins

The aim of this study was to investigate the roles of prostaglandins (PGs) in the anteroventral third ventricular region (AV 3V), a cerebral site for cardiovascular homeostasis, in hypovolemia-induced vasopressin (AVP) secretion.. We infused meclofenamate (78. 3 nmol in 1 microl), a PG synthesis inhibitor, or PGE2 (7.1 nmol in 0.5 microl) into the AV 3V of conscious rats, examining their effects on plasma AVP and other variables in the presence or absence of hemorrhages. The hemorrhages (about 14% of blood volume) were conducted successively by taking femoral arterial blood over a 30-s period at 10-min intervals.. The first hemorrhage increased plasma AVP in blood samples obtained 10 min later, without affecting plasma angiotensin II (ANG II), arterial pressure and heart rate. The second hemorrhage after 10 min raised plasma AVP further and, remarkably, augmented plasma ANG II, and reduced arterial pressure. The AVP responses to both the first and second hemorrhages were attenuated by meclofenamate infusion into the AV 3V performed 35 min before the first hemorrhage. The meclofenamate infusion did not alter the response of ANG II, while that of arterial pressure was potentiated and heart rate was decreased after the second hemorrhage. These effects of meclofenamate on plasma AVP and the cardiovascular parameters were not found when the drug was infused into the nucleus accumbens, the region slightly distant from the AV 3V, or the lateral cerebral ventricle. In the normovolemic state, meclofenamate administered into the three brain regions did not affect any of the variables monitored. In contrast, application of PGE2 into the AV 3V enhanced plasma AVP, heart rate and arterial pressure after 5 and 15 min. Histological examination indicated that infusion sites of meclofenamate in the AV 3V were close to those of PGE2 in several cases and included areas such as the organum vasculosum of the lamina terminalis, periventricular hypothalamic nucleus, and the median and medial preoptic nuclei.. These results suggest that PGs synthesized in and/or near the AV 3V may be involved in the regulation of AVP release and cardiovascular function in the hypovolemic state.

Topics: Animals; Blood Pressure; Cerebral Ventricles; Consciousness; Cyclooxygenase Inhibitors; Dinoprostone; Heart Rate; Male; Meclofenamic Acid; Nucleus Accumbens; Prostaglandins; Rats; Rats, Wistar; Shock; Vasopressins

1. The release of vasopressin from the neurohypophysial terminals of hypothalamic magnocellular neurosecretory neurons is subject to regulation by peripheral baroreceptors, cardiopulmonary volume receptors and circulating angiotensin II. Information from these sources is transmitted through different pathways to achieve different influences on the excitability of the vasopressin-secreting cells. 2. A brief increase in arterial pressure, sufficient to activate baroreceptors, is associated with a transient and selective GABAergic inhibition of these neurosecretory neurons, achieved through a multisynaptic pathway that involves ascending catecholaminergic fibres and neurons in the diagonal band of Broca. A decrease in arterial pressure activates peripheral low volume receptors and initiating neural inputs that result in an increase in the excitability of vasopressin-secreting neurons, achieved via pathways that include direct projections from caudal ventrolateral medulla A1 neurons. 3. Hypotension also releases renal renin and leads to the formation of angiotensin II; binding of this hormone to AT1 receptors on subfornical organ neurons promotes activation of a central angiotensinergic input that evokes a predominantly excitatory effect on vasopressin neurons.

Topics: Angiotensin II; Blood Pressure; Cardiovascular Physiological Phenomena; Hypotension; Hypothalamus; Neurosecretory Systems; Pressoreceptors; Shock; Subfornical Organ; Vasopressins

Pinealectomy has been shown to alter daily rhythms of neurohypophysial hormone release, with plasma hormone concentrations being elevated in the morning, as compared to intact rats. To determine whether pineal removal also altered the response to known stimuli of hormone release, vasopressin concentrations were measured in control, sham-operated, and pinealectomized animals during extracellular fluid hypertonicity produced by an intraperitoneal (i.p.) injection of hypertonic saline or hypovolaemia produced by an i.p. injections of polyethylene glycol. In the combined sham-operated and unoperated groups, injection of hypertonic saline produced a marked increase in plasma vasopressin concentrations from 2.18 +/- 0.28 to 7.2 +/- 1.24 pmol/liter, but the response was attenuated in pinealectomized animals, concentrations increasing to only 3.4 +/- 1.2 pmol/liter. Similarly, following infusion of hypertonic saline, the increase in plasma vasopressin per unit increase in plasma sodium was lower in pinealectomized animals than the pineal intact controls. The response to hypovolaemia was also attenuated, plasma hormone concentrations following reduction in blood volume of approximately 10% increasing to only 3.6 +/- 0.6 pmol/liter as compared to 7.3 +/- 2.2 pmol/liter in the control groups. There were no significant differences in pituitary vasopressin content in any of the groups studied. Thus, the pineal may influence the vasopressin response to physiological stimuli.

Topics: Animals; Blood Volume; Male; Osmolar Concentration; Pineal Gland; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Shock; Vasopressins

Subcutaneous injection of the potent, nonselective opioid antagonist diprenorphine inhibits the vasopressin response to acute hypovolemia. To determine if this inhibition is due to antagonism of opioid receptors in brain pathways that mediate volume control, we determined the vasopressin response to different stimuli when diprenorphine or other opiates were injected into the cerebral ventricles, the nucleus tractus solitarius (NTS), or the lateral parabrachial nucleus (PBN) of rats. We found that the vasopressin response to hypovolemia was inhibited by injection of diprenorphine into the cerebral ventricles at a dose too low to be effective when given subcutaneously. This response also was inhibited when a 20-fold lower dose of diprenorphine was injected into the PBN but not when it was injected into the NTS. The inhibitory effect of diprenorphine in the PBN was not attributable to a decrease in osmotic or hypovolemic stimulation and did not occur with osmotic or hypotensive stimuli. Injecting the PBN with equimolar doses of the mu antagonist naloxone, the delta antagonist ICI-154,129 or the kappa-1 agonist U-50,488H had no effect on basal or volume-stimulated vasopressin. We conclude that the inhibition of vasopressin by diprenorphine is due partially to action at a novel class of opioid receptors that transmit volume stimuli through the PBN.

Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Acute Disease; Animals; Antihypertensive Agents; Brain; Cerebral Ventricles; Diprenorphine; Enkephalin, Leucine; Hemodynamics; Male; Naloxone; Narcotic Antagonists; Pyrrolidines; Rats; Rats, Sprague-Dawley; Shock; Solitary Nucleus; Stimulation, Chemical; Vasopressins

Conscious rats were given i. p. polyethylene glycol (PEG) or dextran injections to compare their efficacy in inducing moderate hypovolaemia. Dextran was found unsuitable, producing large variability in the plasma vasopressin (AVP) concentrations. Putative neurotransmitters involved in the AVP response to hypovolaemia and in basal release were examined using opioid, and beta-adrenoceptor and dopamine receptor-blocking agents. A dose of PEG was chosen to produce a decrease in blood volume of approx 14.5% giving plasma AVP concentrations of 19.0 +/- 4.6 pmol/l. Naloxone and phenoxybenzamine failed to influence AVP release under both hypovolaemic and basal conditions. Prazosin also failed to influence the AVP response. In contrast propranolol elevated the plasma AVP concentrations in both conditions. Haloperidol enhanced basal AVP release but did not influence release during hypovolaemia. Guanethidine pretreatment partially blocked the response to hypovolaemia, but did not affect basal plasma AVP. Thus it appears that aminergic pathways have an inhibitory influence on AVP release under hypovolaemic and basal conditions. However, endogenous opioids do not appear to contribute significantly to the hypovolaemic response.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Amines; Animals; Blood Pressure; Catecholamines; Consciousness; Dopamine Antagonists; Endorphins; Male; Narcotic Antagonists; Polyethylene Glycols; Rats; Rats, Inbred Strains; Shock; Vasopressins

Interactions between emotional stress due to fear and hypovolemic stimuli on vasopressin secretion were studied in rats. Intraperitoneally injected dextran did not significantly change plasma osmolality and arterial blood pressure but increased blood hemoglobin and plasma vasopressin level. An i.v. infused physiological solution reversed these changes. Emotional stress due to fear acquired by learning suppressed plasma vasopressin level in dextran-injected rats. Emotional stress due to fear produced by low-frequency footshocks also suppressed the increased plasma vasopressin level. These results suggest that emotional stress due to fear interacts with afferent neural signals originating from cardio-vascular volume receptors in the control of vasopressin secretion.

Topics: Animals; Blood Pressure; Dextrans; Electroshock; Fear; Learning; Male; Oxytocin; Rats; Rats, Inbred Strains; Shock; Stress, Psychological; Vasopressins

Heart rate (HR), mean arterial pressure (MAP), indices of sympathetic and parasympathetic activity (plasma concentrations of adrenaline, noradrenaline and pancreatic polypeptide, PP), vasopressin (VP) and aldosterone (ALDO) were measured in six pigs during continuous bleeding resulting in hypovolaemic shock, from which five survived. Three stages of haemorrhage could be defined. Stage I. Resting MAP was 85 +/- 6 mmHg and increased to 96 +/- 5 mmHg with a blood loss of 275 (range 250-300) (10 (9-12)% of the estimated blood volume) concomitant with an increase in HR from 105 +/- 5 to 113 +/- 6 beats min-1 (P less than 0.05). Stage II. After a blood loss of 375 (300-500) ml (15 (13-16)%) MAP fell to 62 +/- 9 mmHg and HR to 95 +/- 5 beats min-1 (P less than 0.05). Stage III. A blood loss of 1113 (825-1450) ml (44 (30-52)%) resulted in a MAP of 50 +/- 4 mmHg and an increase in HR to 206 +/- 3 beats min-1 (P less than 0.05). Adrenaline increased from 0.3 +/- 0.1 to 0.8 +/- 0.3 (stage II) and 3.6 +/- 1.1 nmol l-1 (stage III) (P less than 0.05); noradrenaline from 0.4 +/- 0.1 to 1.5 +/- 0.4 (stage II) and 5.9 +/- 1.7 nmol l-1 (stage III) (P less than 0.05); PP from 6.2 +/- 1.6 to 13.3 +/- 2.3 (stage II) and 20.9 +/- 7.8 pmol l-1 (stage III) (P less than 0.05). VP changed only marginally, but ALDO increased from 496 +/- 54 to 623 +/- 76 pmol l-1 (stage III) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldosterone; Animals; Blood Pressure; Blood Transfusion, Autologous; Blood Volume; Endocrine Glands; Epinephrine; Heart Rate; Norepinephrine; Pancreatic Polypeptide; Shock; Swine; Vasopressins

The aim of this paper was to study plasma atrial natriuretic factor, renin activity, aldosterone and antidiuretic hormone in low-output heart failure syndromes such as cardiogenic shock, hypovolemic shock and hypotension with bradycardia syndrome. A total of 30 patients were investigated: 10 with cardiogenic shock due to acute myocardial infarction of the anterior wall (systolic and diastolic blood pressure 56.0 +/- 3.7/40.5 +/- 2.0 mmHg; heart rate 119.7 +/- 1.2 beats/min; central venous pressure 16.2 +/- 0.6 cmH2O) (I group), 10 with hypovolemic shock induced by melena in peptic ulcer (systolic and diastolic blood pressure 74.5 +/- 1.5/57.5 +/- 1.7 mmHg; heart rate 111.0 +/- 1.4; central venous pressure 6.3 +/- 0.5 cmH2O) (II group), 10 with hypotension with bradycardia syndrome which occurred in patients during acute myocardial infarction of the inferior wall (systolic and diastolic blood pressure 71.9 +/- 2.0/58.0 +/- 2.6 mmHg; heart rate 52.0 +/- 2.2 beats/min; central venous pressure 4.6 +/- 0.4 cmH2O) (III group). Plasma atrial natriuretic factor values were measured using radioimmunoassay after chromatographic pre-extraction; plasma renin activity, aldosterone and antidiuretic hormone values were calculated using radioimmunoassay. Circulating atrial natriuretic factor was significantly (p less than 0.01) higher in patients with cardiogenic shock (102.4 +/- 7.4 pg/ml) than in healthy volunteers (8.4 +/- 0.3 pg/ml). In the former there was a positive correlation between atrial natriuretic factor and central venous pressure values. Atrial natriuretic factor and central venous pressure values in the IInd and IIIrd groups of patients were in the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Bradycardia; Cardiac Output, Low; Female; Hemodynamics; Humans; Hypotension; Male; Middle Aged; Myocardial Infarction; Renin; Shock; Shock, Cardiogenic; Vasopressins

Topics: Esophageal and Gastric Varices; Esophagoscopes; Gastrointestinal Hemorrhage; Humans; Laser Therapy; Recurrence; Sclerosing Solutions; Shock; Vasopressins

The pituitaries and adrenals of 30 patients died from extensive fresh myocardial infarction and of 25 patients died from other diseases were studied. In myocardial infarction the mean weight of the above glands was significantly higher than in other diseases. In most cases an increase in number of pituitary ACTH-cells was observed with the immunoperoxidase method. In non-cardiogenic shock (another 9 cases) gland weight was also increased but without a significant increase in the number of ACTH-cells. Hyperactivity of the anterior pituitary-adrenal system is due to a number of known factors. It may be assumed that patients who have infarction are either exposed to an extraordinary amount of stress stimuli or are more susceptible to stress than normal subjects. The findings may indicate the morphological basis of this situation. Of the shock phenomena, incomplete necrosis and haemorrhage of the adrenal cortex are frequent. In the pituitary neural lobe the neurosecretory material, which proved to be vasopressin with the PAP-method, was found to be increased more frequently in myocardial infarction than after other diseases.

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Female; Humans; Immunoenzyme Techniques; Male; Middle Aged; Myocardial Infarction; Organ Size; Pituitary Gland, Anterior; Shock; Shock, Cardiogenic; Vasopressins

Topics: Adult; Aged; Aldosterone; Angiotensin II; Animals; Blood Circulation; Blood Pressure; Female; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Pancreatic Polypeptide; Posture; Shock; Vasopressins

Topics: Animals; Diprenorphine; Hematocrit; Hypotension; Male; Morphinans; Naloxone; Nitroprusside; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Shock; Vasopressins

Ten piglets were bled to a mean BP of 60 mm Hg, after which vasopressin was infused for 30 minutes (2.75 mU/kg/min.). Twenty minutes after completion of the vasopressin infusion, the shed blood was retransfused. Small bowel and liver tissue pO2 and pCO2 were continuously monitored. Systemic arterial and portal blood gas analyses and plasma lactate were studied every 30 minutes. Tissue pO2 in both the small bowel and the liver decreased significantly during hypovolaemic shock; a further non-significant decline was noted during vasopressin infusion. Small bowel pCO2 increased, but liver pCO2 remained unchanged. Plasma lactate increased significantly during hypovolaemia, and vasopressin caused a further increase to a level three times the rest period level. These findings indicate that vasopressin infused during hypovolaemia may increase the risk of hypoxic intestinal lesions and impair liver function.

Topics: Animals; Blood Pressure; Carbon Dioxide; Hydrogen-Ion Concentration; Infusions, Parenteral; Intestine, Small; Lactates; Liver; Oxygen; Shock; Swine; Vasopressins

Many factors may contribute to producing a shock state within the surgical environment. The classic causes of shock--hypovolemia, cardiac failure, and sepsis--occur commonly in the operating room. Additionally, concurrent surgery and anesthesia may contribute to produce clinical shock. Surgery may produce hypovolemia from "third space" loss and/or from blood loss. Some anesthetic drugs, by inhibiting the autonomic nervous system, impair the body's ability to compensate for hypovolemia, cardiac failure, or sepsis. Other entities such as tension pneumothorax, drug allergy, or mechanical factors produced by surgical exposure may contribute to hemodynamic compromise of the patient. Shock that occurs outside the surgical suite may also be produced by a variety of insults. One or more factors may contribute to inadequate tissue perfusion, thus making diagnosis of the cause(s) of shock a clinical challenge. Presented in this review is an anesthesiologist's approach to shock on a macrocirculatory level. Two important concepts are vital to this approach. First, one must act immediately to restore adequate perfusion to the brain and heart when confronted with a patient in shock. This is possible without knowing the specific cause(s) of the poor perfusion. Second, a rapid, accurate diagnosis of the cause(s) must be made if the patient is slow to respond to the initial therapy. Through the use of pulmonary artery catheterization, the factors producing any given shock state may be identified, and appropriate therapy may be instituted and monitored.

Topics: Anesthesia, General; Anesthetics; Emergencies; Fluid Therapy; Heart; Hemodynamics; Humans; Intraoperative Complications; Male; Middle Aged; Shock; Vasopressins

The relationship between gastric blood flow and acid secretion has been studied by using a number of secretory stimulants and inhibitors and different techniques that measure gastric blood flow. Although there are conflicting data, there appears to be a consensus regarding the main aspects of this relationship. Agents that stimulate gastric acid secretion such as histamine, gastrin, cholinergic agents, and vagal stimulators also increase gastric blood flow. Other agents such as isoproterenol, epinephrine, and prostaglandins, which at low doses increase gastric blood flow, reduce gastric acid secretion at higher doses. Norepinephrine, vasopressin, and shock reduce gastric blood flow and thereby cause a decrease in secretion. Histamine H2-receptor antagonists reduce stimulated acid secretion and gastric blood flow. Histamine, gastrin, and acetylcholine have been shown to stimulate acid secretion in vitro. Therefore, these observations suggest that although blood flow is not a prerequisite for initiation of stimulated acid secretion, it can become rate-limiting at higher rates of secretion. Although the literature is replete with studies that attempt to characterize the relationship between gastric blood flow and acid secretion, conclusions have varied. Much of the difficulty has arisen because of the differences in technique used to measure gastric blood flow and the differences between anesthetized and unanesthetized animal preparations. Under some specific conditions, the different blood flow techniques give comparable results and this relationship can be defined.

Topics: Animals; Blood Flow Velocity; Dogs; Epinephrine; Gastric Juice; Gastrins; Histamine; Histamine H2 Antagonists; Norepinephrine; Parasympathomimetics; Prostaglandins; Regional Blood Flow; Shock; Stomach; Vagus Nerve; Vasopressins

Topics: Blood Transfusion; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Resuscitation; Shock; Vasopressins

The influence of GABA and of drugs, known to alter GABA-metabolism, on the hypovolaemia-provoked vasopressin release was investigated in rats. Blood volume was decreased without altering plasma osmolality or arterial blood pressure by i.p. injection of polyethylene glycol and the resulting plasma vasopressin concentration was measured using a radioimmunoassay. I.c.v. injections of GABA (0.4-2 mg) markedly suppressed the hypovolaemia-induced vasopressin release. The central inhibitory effect of GABA could not be related to appropriate changes in peripheral parameters believed to regulate vasopressin release (arterial blood pressure, renin-angiotensin system). Aminooxyacetic acid (9-81 mg kg-1, i.m.) and gamma-vinyl-GABA (1.5 g kg-1, i.p.), two potent inhibitors of GABA aminotransferase and known to increase brain GABA content, reduced vasopressin release to a comparable degree as did GABA (i.c.v.). On the other hand, 3-mercaptopropionic acid (10-90 mg kg-1, i.p.), an inhibitor of the GABA synthetizing enzyme glutamic acid decarboxylase, promoted the release of vasopressin when the rats were killed prior to the onset of convulsions. These results, on the whole, intimate the existence of a GABA-mediated inhibition in the central control of vasopressin release.

Topics: 3-Mercaptopropionic Acid; Aminooxyacetic Acid; Animals; gamma-Aminobutyric Acid; Male; Polyethylene Glycols; Rats; Shock; Vasopressins

The administration of a vasopressor in the presence of hypovolemia results in a severe acidosis which may be fatal if continued.

Topics: Acidosis; Adult; Blood Volume; Female; Humans; Lactates; Male; Middle Aged; Shock; Vasoconstrictor Agents; Vasopressins

Experiments performed on male Wistar, Long Evans and Brattleboro rats indicate that the latter strain of animals, lacking vasopressin in their posterior pituitaries, are extremely sensitive to hemorrhagic and bowel ischemic shock. Mild forms of both hemorrhagic and bowel ischemic shock, as produced in Wistar or Long Evans rats, results in marked hypotension, hemoconcentration and blockade of the reticuloendothelial system (RES) in Brattleboro animals of similar sex, age and weight. These direct findings indicate that release of endogenous vasopressin in shock syndromes may be critical in maintenance of circulatory homeostasis and RES function.

Topics: Animals; Blood Pressure; Hematocrit; Hemorrhage; Intestines; Ischemia; Male; Mononuclear Phagocyte System; Phagocytosis; Rats; Shock; Species Specificity; Vasopressins

Rational intraoperative fluid therapy is based on an understanding of the pathophysiology of severe trauma and surgery. Fluids of suitable compositions are administered in sufficient quantities to form part of the daily maintenance requirement and also to replace blood and ECF lost during surgery.

Topics: Acute Kidney Injury; Adrenal Cortex Hormones; Blood Transfusion; Extracellular Space; Humans; Infusions, Parenteral; Kallikreins; Kidney; Oliguria; Postoperative Complications; Renin; Shock; Sodium; Surgical Procedures, Operative; Vasopressins; Water-Electrolyte Balance

The present study indicates that: (a) local administration of low concentrations of an analog of vasopressin, 1-deamino-[2-phenylalanine, 8-arginine]-vasopressin (DPAVP), constricts venules in the rat splanchnic terminal vascular bed of normal animals, unlike that seen for catecholamines; (b) maximal concentrations of DPAVP narrow but do not occlude both arterioles and venules: (c) microscopic muscular venules (31-39 mu i.d.) do not narrow more than 20% in response to the vasopressin analog DPAVP; and (d) terminal arterioles (17-23 mu i.d.) do not narrow more than 50% in response to DPAVP. Systemic administration of DPAVP to rats subjected to hemorrhage or bowel ischemia shock more than doubles survival rates over control rats receiving Ringer solution. Infusion of DPAVP produces a dose-dependent effect on arterial blood pressure, microscopic capacitance vessels, large arterioles and small arteries. In addition, i.v. administration of DPAVP: (a) returns arterial hematocrit towards normal after shock; and (b) regenerates and sustains vasomotion and venular tone, decreases microvascular hyperreactivity characteristic of shock syndromes, restores constricted arteriolar lumen sizes towards normal, predisposes to a splanchnic microbed virtually free of stasis, petechiae and leukocytic sticking, and restores capillary perfusion and outflow to near-normal. Further, DPAVP effectively restores the early reticuloendothelial system (RES) phagocytic depression, characteristic of shock syndromes, to normal; the latter eventuating in RES hyper-phagocytic activity. These findings indicate it is possible to synthesize vasoactive molecules which: (a) exert selective microvascular and RES phagocytic effects; and (b) are highly beneficial in the therapy of low-flow states, at least in rats.

Topics: Animals; Blood Pressure; Female; Intestines; Ischemia; Microcirculation; Mononuclear Phagocyte System; Phagocytes; Rats; Shock; Shock, Hemorrhagic; Vasopressins

During the past decade the diagnostic use of blood volume determinations has declined as a result of the generation of largely inaccurate results and inappropriate normalization and interpretation. After historical development of more than 50 years, current methodology employs 125I-labeled human serum albumin and 51Cr-labeled red blood cells to determine plasma volume and red cell volume, respectively. Accurate blood volume determinations require (1) abandoning the use of the mean body hematocrit:venous hematocrit ratio and using simultaneous independent measurements of both volumes; (2) delaying multiple postinjection patient samples until complete mixing and equilibration are complete; (3) backextrapolation of plasma concentrations of 125I to account for albumin loss from the plasma, and, rarely, back-extrapolation of red cell concentrations to account for dilution by red cells transfused during the procedure; (4) normalization of volumes by adjusting patient weight to normal correspondence with lean tissue mass, whenever necessary. A rapid, routine method that fulfills these four requirements is presented. A number of surgical and medical conditions in which blood volume determinations are very useful in diagnosis and therapy are discussed. Recently developed techniques for blood volume measurements include neutron acativation analysis and fluorescent excitation analysis. Correct normalization of accurate blood volume measurements will provide a valuable service to the entire medical community.

Topics: Aged; Blood Volume Determination; Body Constitution; Carbon Monoxide; Central Venous Pressure; Chromium Radioisotopes; Diagnostic Errors; Erythrocytes; Hematocrit; Hormones, Ectopic; Humans; Hyperaldosteronism; Hypertension; Indium; Iron Radioisotopes; Male; Phosphorus Radioisotopes; Plasma Volume; Polycythemia; Postoperative Complications; Potassium Radioisotopes; Radioisotope Dilution Technique; Serum Albumin, Radio-Iodinated; Shock; Technetium; Time Factors; Transferrin; Vasopressins

Topics: Animals; Aorta, Thoracic; Blood Vessels; Digestive System; Dose-Response Relationship, Drug; Epinephrine; Hemodynamics; Hydrocortisone; In Vitro Techniques; Ischemia; Male; Methylprednisolone; Microcirculation; Mononuclear Phagocyte System; Muscle, Smooth; Norepinephrine; Phagocytosis; Rats; Serotonin; Shock; Shock, Hemorrhagic; Time Factors; Vasopressins

Topics: Acetylcholine; Animals; Blood Circulation; Cardiovascular System; Endocrine Glands; Humans; Lysine; Nervous System; Seizures; Shock; Vasopressins

Topics: Adaptation, Physiological; Angiotensin II; Animals; Blood Pressure; Catheterization; Female; Intestine, Large; Ischemia; Mononuclear Phagocyte System; Norepinephrine; Phagocytes; Phagocytosis; Rats; Shock; Shock, Hemorrhagic; Shock, Traumatic; Vasopressins

Topics: Adult; Blood Pressure; Cardiac Output; Diuresis; Female; Hemodynamics; Humans; Injections, Intravenous; Male; Middle Aged; Ornithine; Plethysmography; Shock; Skin; Vasopressins

Topics: Adolescent; Adult; Aged; Animals; Blood Circulation; Blood Pressure; Child; Female; Humans; Male; Microcirculation; Middle Aged; Ornithine; Rats; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Vasopressins

Topics: Acid-Base Equilibrium; Blood Coagulation Disorders; Body Temperature; Capillaries; Cardiac Output; Digitalis Glycosides; Glucocorticoids; Heart; Humans; Liver; Lung; Oxygen; Pulmonary Circulation; Shock; Vasopressins

Topics: Adrenal Cortex Hormones; Blood Circulation; Cardiac Output; Humans; Microcirculation; Shock; Shock, Cardiogenic; Time Factors; Vasopressins

Topics: Adrenal Cortex Hormones; Blood Circulation; Cardiac Output; Humans; Microcirculation; Shock; Shock, Cardiogenic; Time Factors; Vasopressins

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Aldosterone; Animals; Cricetinae; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Lymphoid Tissue; Pituitary-Adrenal System; Rats; Shock; Stress, Physiological; Vasopressins

Topics: Animals; Arteriovenous Anastomosis; Dogs; Epinephrine; Hemodynamics; Humans; Shock; Sympatholytics; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Dogs; Epinephrine; Hepatic Artery; Histamine; Liver Circulation; Norepinephrine; Portal Vein; Serotonin; Shock; Vasopressins

Topics: Angiotensins; Blood Pressure Determination; Central Nervous System Stimulants; Heart Arrest; Heart Failure; Humans; Hypotension; Pharmacology; Postoperative Care; Postoperative Complications; Shock; Sympathomimetics; Toxicology; Vascular Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Blood Pressure; Blood Pressure Determination; Pharmacology; Rats; Research; Shock; Shock, Hemorrhagic; Vasopressins

Topics: Adrenal Cortex Hormones; Allergy and Immunology; Angiotensins; Antibodies; Biochemical Phenomena; Biochemistry; Blood; Blood Coagulation Disorders; Bradykinin; Catecholamines; Complement System Proteins; Endotoxins; Ferritins; Histamine; Humans; Intercellular Signaling Peptides and Proteins; Kallikreins; Mononuclear Phagocyte System; Peptides; Properdin; Serotonin; Shock; Vasopressins

Topics: Angina Pectoris; Coronary Disease; Digoxin; Electrocardiography; Hydrochlorothiazide; Hypercholesterolemia; Hypertension; Metaraminol; Nitroglycerin; Shock; Shock, Cardiogenic; Vasopressins; Warfarin

Topics: Adrenal Cortex; Adrenal Glands; Animals; Arginine Vasopressin; Cats; Dogs; Epinephrine; Kallikreins; Niacin; Norepinephrine; Octopamine; Research; Shock; Shock, Hemorrhagic; Theophylline; Vasopressins

Topics: Abdomen; Anemia; Angiotensins; Antihypertensive Agents; Blood Circulation; Bradykinin; Coronary Vessels; Ganglionic Blockers; Heart Diseases; Hypertension; Hyperthyroidism; Hypothyroidism; Liver Circulation; Niacin; Pharmacology; Polycythemia; Serotonin; Shock; Vasopressins; Xanthines

Topics: Electrocardiography; Heart; Pharmacology; Shock; Shock, Surgical; Surgical Procedures, Operative; Toxicology; Urology; Vasopressins

Hemodynamic studies have demonstrated that the fall of blood pressure in shock caused by endotoxin in dogs does not result primarily from dilatation or "vasomotor collapse." Indeed, vasoconstriction is increased and may be excessive. Progression of shock has recently been blamed on such excessive vasoconstriction. For this reason the use of sympathomimetic drugs as vasopressor agents has been challenged and sympatholytic or adrenolytic agents have been recommended. In the present study, vasopressor and vasodilator drugs were used for the treatment of shock in dogs caused by endotoxin. Vasodilator drugs, when used after the onset of shock, hastened a fatal outcome but vasopressor agents were not detrimental when used in moderate doses. The effectiveness of the vasopressor agent is not necessarily due to a primary vasoconstrictor action on arteries and arterioles, as previously assumed.

Topics: Animals; Antitoxins; Arginine Vasopressin; Arterioles; Blood Pressure; Dogs; Hemodynamics; Shock; Shock, Septic; Toxins, Biological; Vasoconstriction; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

Topics: Adrenocorticotropic Hormone; Arginine Vasopressin; Chlorpromazine; Norepinephrine; Shock; Vasoconstrictor Agents; Vasopressins

Topics: Arginine Vasopressin; Kidney; Shock; Vasopressins