Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrinein Human Distal Mammary Artery.
1. J Thorac Cardiovasc Surg. 2014 May;147(5):1698-705. doi:10.1016/j.jtcvs.2013.11.013. Epub 2013 Dec 9. Effect of severe acidosis on vasoactive effects of epinephrine and norepinephrinein human distal mammary artery. Vidal C(1), Grassin-Delyle S(2), Devillier P(2), Naline E(2), Lansac E(3),Mnasch P(4), Faisy C(5). (1)Research Unit UPRES EA220, Versailles Saint-Quentin-en-Yvelines University, Hpital Foch, Suresnes, France; Medical Intensive Care Unit, Hpital Europen Georges Pompidou, Assistance Publique-Hpitaux de Paris, University Paris Descartes, Sorbonne Paris Cit, Paris, France. (2)Research Unit UPRES EA220, Versailles Saint-Quentin-en-Yvelines University, Hpital Foch, Suresnes, France. (3)Department of Cardiovascular Surgery, Institut Mutualiste Montsouris, Paris, France. (4)Department of Cardiovascular Surgery, Hpital Europen Georges Pompidou, Assistance Publique-Hpitaux de Paris, Universit Paris Descartes, Sorbonne Paris Cit, Paris, France. (5)Research Unit UPRES EA220, Versailles Saint-Quentin-en-Yvelines University, Hpital Foch, Suresnes, France; Medical Intensive Care Unit, Hpital Europen Georges Pompidou, Assistance Publique-Hpitaux de Paris, University Paris Descartes, Sorbonne Paris Cit, Paris, France. Electronic address: [email protected]. OBJECTIVE: Acidosis is a very common pathologic process in perioperativemanagement. However, how to correct severe acidosis to improve the efficacy ofvasoconstrictors in hemodynamically unstable patients is still debated. Thepresent study investigated whether severe extracellular acidosis influences thevasoactive properties of vasoconstrictors on human isolated arteries.METHODS: Segments of intact distal internal mammary arteries were removed from 41patients undergoing artery bypass grafting. The arterial rin Continue reading >>
Lactate And Lactic Acidosis
The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>
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The Role Of Catecholamines In Metabolic Acidosis
The role of glucagon in regulating plasma lipid concentrations (nonesterified fatty acids, ketone bodies, and triglycerides) is reviewed. The effects of glucagon-induced insulin secretion upon this lipid regulation are discussed that may resolve conflicting reports in the literature are resolved. In addition, the unresolved problem concerning the pharmacologic versus physiologic effects of glucagon is stressed. Glucagon's role in stimulating lipolysis at the adipocyte serves two important functions. First, it provides plasma nonesterified fatty acids for energy metabolism and secondly, it ensures substrate for hepatic ketogenesis. In vitro, glucagon's lipolytic activity has been consistently observed, but in vivo, this activity has sometimes been obscured by the effects of glucagon-induced insulin secretion. Frequently, a biphasic response has been reported in which a direct lipolytic response is followed by a glucagon-induced insulin suppression of plasma nonesterified fatty acid concentration. When the glucagon-induced insulin secretion has been controlled by various in vivo techniques, glucagon's lipolytic activity in vivo has frequently been demonstrable. In the 1960s, in vitro liver perfusion experiments demonstrated that glucagon enhanced hepatic ketogenesis independent of glucagon's lipolytic activity. However, this direct effect of glucagon on the hepatocyte was not universally accepted because of conflicting reports in the literature. Failure to observe an in vitro ketogenic effect of the hormone in some studies may have been due to suboptimal experimental conditions. Certain factors are now known to influence the ketogenic response, such as the concentration of fatty acids in the media and the nutritional status of the animal. Under optimal in vitro condition Continue reading >>
Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass.
Epinephrine-induced lactic acidosis following cardiopulmonary bypass. Department of Intensive Care, Royal North Shore Hospital, St. Leonards, NSW, Australia. To determine if lactic acidosis occurring after cardiopulmonary bypass could be attributed to the metabolic or other effects of epinephrine administration. Postsurgical cardiothoracic intensive therapy unit. Thirty-six adult patients, without acidosis, requiring vasoconstrictors for the management of hypotension after cardiopulmonary bypass. Randomized administration of either epinephrine or norepinephrine by infusion. Hemodynamic and metabolic data were collected before commencement of vasoconstrictor therapy (time 0) and then 1 hr (time 1), 6 to 10 hrs (time 2), and 22 to 30 hrs (time 3) later. Six of the 19 patients who received epinephrine developed lactic acidosis. None of the 17 patients receiving norepinephrine developed lactic acidosis. In the epinephrine group, but not in the norepinephrine group, lactate concentration increased significantly at times 1 and 2 (p = .01), while pH and base excess decreased (p < or = .01). Blood glucose concentration was higher in the epinephrine group at time 2 (p = .02), while the cardiac index (p < .03) and the mixed venous Po2 (p = .04) were higher at time 1. compared with the norepinephrine group, the patients receiving epinephrine had higher femoral venous lactate concentrations (p = .03), increased lower limb blood flow (p = .05), and increased femoral venous oxygen saturations (p = .04). The use of epinephrine after cardiopulmonary bypass precipitates the development of lactic acidosis in some patients. This phenomenon is presumably a beta-mediated effect, and is associated with an increase in whole-body and lower limb blood flow and a decrease in whole-body and tran Continue reading >>
Bench-to-bedside Review: Is There A Place For Epinephrine In Septic Shock?
Bench-to-bedside review: Is there a place for epinephrine in septic shock? The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established. EpinephrineSeptic ShockMean Arterial PressureDobutamineAerobic Glycolysis Early goal directed therapy [ 1 ] is now considered as a gold standard in the early phase of septic shock. Fluid therapy and vasoactive therapy may be immediately required in order to maintain acceptable blood pressure levels. Invasive or non-invasive assessment of hemodynamic status, although essential to Continue reading >>
Influence Of Respiratory And Metabolic Acidosis On Epinephrine-inotropic Effect In Isolated Guinea Pig Atria
, Volume 347, Issue4 , pp 297307 | Cite as Influence of respiratory and metabolic acidosis on epinephrine-inotropic effect in isolated guinea pig atria The inotropic effect of calcium and of epinephrine was examined in an isolated guinea pig atrial preparation during a simulated respiratory and metabolic acidosis. Special care was taken to avoid alterations in ionized calcium which usually accompany most forms of acidosis. In acidosis the inotropic response to epinephrine is depressed to a greater extent than the response to calcium, independent of respiratory or metabolic origin. It is concluded that the overall depression of the inotropic response to epinephrine is produced by two mechanisms: firstly, by an unspecific depression of contractility caused by a direct action of hydrogen ions on the heart, and secondly, by a specific depression of the inotropic epinephrine-effector mechanism. The dose-ratios for production of identical epinephrine-specific responses as compared with those at pH 7.5 were calculated. At a pH of 6.9, the doseratio was 1.5 to 2.5; at a pH of 6.6, it was in the range of 4 to 4.6. In conclusion these observations are in accordance with a concept that acute acidosis affects myocardial function in intact animals bydirect andindirect effects in at least four ways: by a depression of contractility, by a diminished responsiveness of the epinephrineinotropic response mechanism, by an increase in the concentration of ionized calcium, and by a release of catecholamines. AcidosispHCardiac ContractilityEpinephrineCalcium This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Andersen, M. N., Border, J. R., Mouritzen, Ch. V.: Acidosis, catecholamines and cardiovascular dynamics: When does acidosi Continue reading >>
The Role Of Catecholamines In Metabolic Acidosis.
The role of catecholamines in metabolic acidosis. Catecholamines (noradrenaline and adrenaline) are catabolic hormones secreted during stress. They initiate many metabolic processes including increased production of both ketoacids and lactic acid. Support for a direct participation of these hormones in the development and/or maintenance of ketoacidosis includes: (1) the high incidence of stress (approx. 70%) as a precipitating factor for ketoacidosis; (2) the elevated plasma levels of noradrenaline (norepinephrine) in patients with ketoacidosis; (3) the rise in plasma concentrations of ketone bodies during catecholamine infusion; and (4) the reduction in the incidence of ketoacidosis with beta-adrenergic pharmacological blockade. Support for a direct participation of catecholamines in the development and/or maintenance of lactic acidosis includes: (1) the common association of stress and lactic acidosis; (2) the rise in plasma lactate concentration during adrenaline (epinephrine) infusion; (3) the precipitation of lactic acidosis by adrenaline intoxication and phaeochromocytoma; and (4) the vasoconstrictor effects of catecholamines leading to tissue anoxia and lactic acid production. Thus, in susceptible patients, catecholamines may be principal determinants of whether ketoacidosis and/or lactic acidosis develops. Continue reading >>
Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect
Volume 147, Issue 5 , May 2014, Pages 1698-1705 Acidosis is a very common pathologic process in perioperative management. However, how to correct severe acidosis to improve the efficacy of vasoconstrictors in hemodynamically unstable patients is still debated. The present study investigated whether severe extracellular acidosis influences the vasoactive properties of vasoconstrictors on human isolated arteries. Segments of intact distal internal mammary arteries were removed from 41 patients undergoing artery bypass grafting. The arterial rings were washed in Krebs-Henseleit solution and suspended in an organ bath. The rings were set at a pretension equivalent of 100 mm Hg, and the relaxation response to 10 M acetylcholine was verified. Concentrationresponse curves for epinephrine, norepinephrine, methoxamine (1A/D-adrenoceptor agonist), phenylephrine (equipotent agonist of 1A/B-adrenoceptors), and clonidine (2-adrenoceptor agonist) were achieved under control conditions (pH 7.40) and under acidic conditions by substitution of the Krebs-Henseleit solution with a modified solution. Decreasing the pH from 7.40 to 7.20, 7.0, or 6.80 did not significantly alter the potency and efficacy of epinephrine and norepinephrine, although the standardized effect size was sometimes large. Severe acidosis (pH6.80) did not significantly change the potency and efficacy of phenylephrine and clonidine, although it increased the efficacy and potency of methoxamine (P<.001 and P=.04 vs paired control conditions, respectively). Extracellular acidosis did not impair the vasoactive properties of epinephrine and norepinephrine in human medium-size arteries until pH 6.80. The results of the present study also suggest that acidosis might potentiate arterial responsiveness to vasoconstrictors, mos Continue reading >>
Causes Of Lactic Acidosis
INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>
Adrenaline (epinephrine)
Hormone description: a catecholamine and belongs to the family of biogenic amines, synthesized in the neurones of the adrenal medulla and stored in the chromaffin granula. Biological functions: a natural antidote to the chemicals released during severe allergic reactions triggered by drug allergy, food allergy or insect allergy. Health benefits : used as sympathicomimeticum, broncholyticum and antiasthmaticum; prevents bleedings during surgery or in the case of inner organ bleeding. Side effects: contraindicated in patients with narrow-angle glaucoma, hypersensitivity to epinephrine, side effects include tremor, excitability, vomiting, hypertension , arrhythmias, hyperuricemia. Adrenal gland health is crucial for energy and stamina. Unfortunately, everyday stresses can have your adrenal glands working overtime, which can zap energy. ADRENergize supports the adrenal glands, which create adrenaline, a natural stimulant in your body This fast-acting formula is readily absorbed to replenish your body's natural stress defenses and promote healthy energy levels. Get daily energy and adrenal support with ADRENergize! Click here for more information. Adrenaline is a catecholamine and belongs to the family of biogenic amines. Adrenaline is a natural stimulant made in the adrenal gland of the kidney. Its biological name is epinephrine, from the Greek nephros for kidney. Adrenaline is carried in the bloodstream and affects the autonomous nervous system, which controls functions such as the heart rate, dilation of the pupils, and secretion of sweat and saliva. L-adrenaline was the first hormone which could be crystallized. Adrenaline is synthesized in the neurones of the adrenal medulla and stored in the chromaffin granula. An activating signal, which can be induced through a low Continue reading >>
Epinephrine-induced Lactic Acidosis In Orthognathic Surgery: A Report Of Two Cases
Your browser does not support the NLM PubReader view. Go to this page to see a list of supporting browsers. Epinephrine-induced lactic acidosis in orthognathic surgery: a report of two cases J Korean Assoc Oral Maxillofac Surg. 2016 Oct;42(5):295-300. J Korean Assoc Oral Maxillofac Surg. 2016 Oct;42(5):295-300. English. Published online October 25, 2016. Copyright 2016 The Korean Association of Oral and Maxillofacial Surgeons. All rights reserved. Epinephrine-induced lactic acidosis in orthognathic surgery: a report of two cases 1Department of Anesthesiology and Pain Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. 2Department of Oral and Maxillofacial Surgery, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. Corresponding author: Jang-Ho Son. Department of Oral and Maxillofacial Surgery, Ulsan University Hospital, 877 Bangeojinsunhwan-doro, Dong-gu, Ulsan 44033, Korea. TEL: +82-52-250-7230, FAX: +82-52-250-7236, Email: [email protected] Received April 04, 2016; Revised July 22, 2016; Accepted August 17, 2016. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effects of epinephrine have been documented in numerous studies. However, its metabolic effects (especially during surgery) have been seldom recognized clinically. We report two cases of significant metabolic effects (including lactic acidosis and hyperglycemia) as well as hemodynami Continue reading >>
Understanding Lactate In Sepsis & Using It To Our Advantage
You are here: Home / PULMCrit / Understanding lactate in sepsis & Using it to our advantage Understanding lactate in sepsis & Using it to our advantage Once upon a time a 60-year-old man was transferred from the oncology ward to the ICU for treatment of neutropenic septic shock. Over the course of the morning he started rigoring and dropped his blood pressure from 140/70 to 70/40 within a few hours, refractory to four liters of crystalloid. In the ICU his blood pressure didn't improve with vasopressin and norepinephrine titrated to 40 mcg/min. His MAP remained in the high 40s, he was mottled up to the knees, and he wasn't making any urine. Echocardiography suggested a moderately reduced left ventricle ejection fraction, not terrible but perhaps inadequate for his current condition. Dobutamine has usually been our choice of inotrope in septic shock. However, this patient was so unstable that we chose epinephrine instead. On an epinephrine infusion titrated to 10 mcg/min his blood pressure improved immediately, his mottling disappeared, and he started having excellent urine output. However, his lactate level began to rise. He was improving clinically, so we suspected that the lactate was due to the epinephrine infusion. We continued the epinephrine, he continued to improve, and his lactate continued to rise. His lactate level increased as high as 15 mM, at which point the epinephrine infusion was being titrated off anyway. Once the epinephrine was stopped his lactate rapidly normalized. He continued to improve briskly. By the next morning he was off vasopressors and ready for transfer back to the ward. This was eye-opening. It seemed that the epinephrine infusion was the pivotal intervention which helped him stabilize. However, while clinically improving him, the epineph Continue reading >>
Risk Factors Of Post-operative Severe Hyperlactatemia And Lactic Acidosis Following Laparoscopic Resection For Pheochromocytoma
Risk factors of post-operative severe hyperlactatemia and lactic acidosis following laparoscopic resection for pheochromocytoma Scientific Reportsvolume7, Articlenumber:403 (2017) Severe hyperlactatemia (SH)/lactic acidosis (LA) after laparoscopic resection of pheochromocytoma is an infrequently reported complication. The study aims to investigate the incidence of this complication and to determine the clinical risk factors. Patients who underwent laparoscopic resection for pheochromocytoma between 2011 and 2014 at Peking Union Medical College Hospital were enrolled. LA was defined as pH < 7.35, bicarbonate <20 mmol/L, and serum lactate 5 mmol/L; SH as lactate 5 mmol/L; and moderate hyperlactatemia (MH) as lactate 2.55.0 mmol/L without evidence of acidosis (pH > 7.35 and/or bicarbonate >20 mmol/L). Data concerning patient demographics, clinical history, and laboratory results were collected and statistical analyses were performed. Out of 145 patients, 59 (40.7%) developed post-operative hyperlactatemia. The incidences of MH and SH/LA were 25.5% and 15.2%, respectively. Multivariate analysis demonstrated that body mass index (BMI) (odds ratio [OR], 1.204; 95% confidence interval [CI], 1.0161.426), 24-hour urine epinephrine concentration (OR, 1.012; 95% CI, 1.0021.022), and tumor size (OR, 1.571; 95% CI, 1.1022.240) were independent predictors of post-operative SH/LA. The data show that post-operative SH/LA is not a rare complication after pheochromocytoma resection and may be closely associated with higher BMI, larger tumor size, and higher levels of urine epinephrine. Pheochromocytoma is a rare, catecholamine-producing neuroendocrine tumor originating from chromaffin cells of the adrenal medulla 1 . Cardinal manifestations of pheochromocytoma include episodic hypertens Continue reading >>
Lactic Acidosis In Pheochromocytoma
MICHAEL BORNEMANN, M.D.; SUSAN C. HILL, M.D.; GERALD S. KIDD II, M.D. Article, Author, and Disclosure Information Author, Article, and Disclosure Information Requests for reprints should be addressed to COL Michael Bornemann, MC; Box 700, Tripler Army Medical Center; Honolulu, HI 96859-5000. Lactic acidosis is not generally recognized as a complication of pheochromocytoma. We review three prior case reports of lactic acidosis in patients with pheochromocytoma and one report of lactic acidosis following epinephrine poisoning and describe an additional case report of a patient with lactic acidosis in whom an unsuspected pheochromocytoma was discovered at autopsy. The pathophysiology of lactic acidosis in pheochromocytoma is related to the effect of catecholamines on intermediary metabolism and the peripheral circulation. Although the possible development of lactic acidosis in persons with pheochromocytoma is underappreciated, the differential diagnosis of lactic acidosis should include this tumor. Continue reading >>
Lactic Acidosis
hyperlactaemia: a level from 2 to 5 mmol/L normal production is 20 mmols/kg/day, enters the circulation and undergoes hepatic and renal metabolism (Cori cycle) all tissues can produce lactate under anaerobic conditions lactic acid has a pK value of about 4 so it is fully dissociated into lactate and H+ at body pH (i.e. it is a strong ion) during heavy exercise, the skeletal muscles contribute most of the much increased circulating lactate during pregnancy, the placenta is an important producer of lactate (can pass to fetus as well) major source in sepsis and ARDS is the lung lactate is metabolised predominantly in the liver (60%) and kidney (30%) the heart can also use lactate for ATP production 50% is converted into glucose (gluconeogenesis) and 50% into CO2 and water (citric acid cycle) this results in no net acid accumulation but requires aerobic metabolism the small amount of lactate that is renally filtered (180mmol/day) is fully reabsorbed (ii) impaired hepatic metabolism of lactate (large capacity to clear) clinically there is often a combination of the above to produce a persistent lactic acidosis anaerobic muscular activity (sprinting, generalised convulsions) tissue hypoperfusion (shock, cardiac arrest, regional hypoperfusion -> mesenteric ischaemia) reduced tissue oxygen delivery (hypoxaemia, anaemia) or utilisation (CO poisoning) Type B No Evidence of Inadequate Tissue Oxygen Delivery once documented the cause must be found and treated appropriately D lactate is isomer of lactate produced by intestinal bacterial and not by humans it is not detected on standard lactate assays a bed side test may be able to be developed to help with diagnosis of mesenteric ischaemia venous samples are equivalent to arterial in clinical practice do not need to take off tourniq Continue reading >>
