diabetestalk.net

Epinephrine Lactic Acidosis Mechanism

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis And Insulin Resistance Associated With Epinephrine Administration In A Patient With Noninsulin-dependent Diabetes Mellitus

Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus Epinephrine raises plasma lactate concentrations when infused intravenously in normal subjects. We studied a patient with noninsulin-dependent diabetes mellitus who developed lactic acidosis and marked insulin resistance when treated with epinephrine after open heart surgery. Caruso M, Orszulak TA, Miles JM. Lactic Acidosis and Insulin Resistance Associated With Epinephrine Administration in a Patient With NonInsulin-Dependent Diabetes Mellitus. Arch Intern Med. 1987;147(8):14221424. doi:10.1001/archinte.1987.00370080058013 New! JAMA Network Open is now accepting submissions. Learn more. Customize your JAMA Network experience by selecting one or more topics from the list below. Challenges in Clinical Electrocardiography Clinical Implications of Basic Neuroscience Health Care Economics, Insurance, Payment Scientific Discovery and the Future of Medicine United States Preventive Services Task Force JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Facial Plastic Surgery JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA OtolaryngologyHead & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) AMA Manual of Style Art and Images in Psychiatry Breast Cancer Screening Guidelines Colorectal Screening Guidelines Declaration of Helsinki Depression Screening Guidelines Evidence-Based Medicine: An Oral History Fishbein Fellowship Genomics and Precision Health Health Disparities Hypertension Guidelines JAMA Network Audio JAMA Network Conferences Med Men Medical Education Opioid Management Guidelines Peer Review Congress Research Ethics Sepsis and Septic Shock Continue reading >>

Epinephrine-induced Lactic Acidosis In Orthognathic Surgery: A Report Of Two Cases

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 >>

Review. Perioperative Management Of Lactic Acidosis In End-stage Liver Disease Patient

Review. Perioperative Management Of Lactic Acidosis In End-stage Liver Disease Patient

Review. Perioperative Management of Lactic Acidosis in End-Stage Liver Disease Patient Review. Perioperative Management of Lactic Acidosis in End-Stage Liver Disease Patient Department of Anesthesiology & Pain Medicine University of Washington Medical Center, Department of Surgery, Transplant Surgery Division, P.O.Box 356540 1959 NE Pacific street, Seattle WA, 98195, United States of America University of Medicine and Pharmacy of Trgu Mure, Trgu Mure, Romania Carol Davila University of Medicine and Pharmacy, Anesthesiology and Intensive Care Department 3, Fundeni Clinical Institute, Bucharest, Romania Department of Anesthesiology & Pain, Medicine University of Washington Medical Center, Seattle WA, United States of America Published Online: 2017-05-11 | DOI: Lactic acidosis (LA) in end-stage liver disease (ESLD) patients has been recognized as one of the most complicated clinical problems and is associated with increased morbidity and mortality. Multiple-organ failure, associated with advanced stages of cirrhosis, exacerbates dysfunction of numerous parts of lactate metabolism cycle, which manifests as increased lactate production and impaired clearance, leading to severe LA-induced acidemia. These problems become especially prominent in ESLD patients, that undergo partial hepatectomy and, particularly, liver transplantation. Perioperative management of LA and associated severe acidemia is an inseparable part of anesthesia, post-operative and critical care for this category of patients, presenting a wide variety of challenges. In this review, lactic acidosis applied pathophysiology, clinical implications for ESLD patients, diagnosis, role of intraoperative factors, such as anesthesia- and surgery-related, vasoactive agents impact, and also current treatment options and Continue reading >>

Understanding Lactate In Sepsis & Using It To Our Advantage

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 >>

Causes Of Lactic Acidosis - Deranged Physiology

Causes Of Lactic Acidosis - Deranged Physiology

A discussion of the causes of a high anion gap metabolic acidosis are frequently required by the CICM SAQs, and lactate often comes up as a differential. Beyond that, there are a series of questions which ask specifically about the causes of lactic acidosis. These questions are numerous. There is practically one in every paper. Question 4.1 from the first paper of 2016 Question 3.3 from the second paper of 2015 Question 27 from the second paper of 2014 Question 23 from the second paper of 2013 Question 26.4 from the second paper of 2013 Question 28 from the second paper of 2012 Question 9.1 from the first paper of 2011 Question 15.3 from the second paper of 2009 Question 3.3 from the second paper of 2009 Many of these questions for some reason focus repetitively on the plight of a certain middle-aged diabetic with a history of alcohol abuse. A specific feature of these questions is the use of red cell transketolase as a test of thiamine deficiency, reminding the candidates that this is an important differential. Lactic acidosis is discussed at greater length in a series of chapters dedicated to acid-base disturbances in their various forms and permutations. In order to simplify revision, a tabulated list of aetiologies is offered below, organised according to an increasingly irrelevant classification system from the 1980s. The massively flawed Cohen-Woods classification Type A lactic acidosis: impaired tissue oxygenation Type B1 lactic acidosis, due to a disease state NRTIs (nucleoside reverse transcriptase inhibitors) Continue reading >>

Lactic Acidosis | Md Nexus

Lactic Acidosis | Md Nexus

Cohen-Woods Classification of Lactic Acidosis Type A: due to decreased perfusion or oxygenation However, these may cause type A lactic acidosis in some cases Type B2: due to medication or intoxication Type B3: due to inborn error of metabolism Mitochondrial Encephalomyopathy + Lactic Acidosis + Stroke-Like Episodes (MELAS) Tumors May Benefit from Acidosis: acidic microenvironment is critical for tumorigenesis, angiogenesis, and metastasis Physiology: decreased lactate clearance (with severe liver metastases)+ increased glycolytic activity of tumor (Warburg Effect) + tissue tumor hypoxia Treatment: bicarbonate administration may increase lactic acid production Tumor Lysis Syndrome (see Tumor Lysis Syndrome , [[Tumor Lysis Syndrome]]) Anaphylaxis (see Anaphylaxis , [[Anaphylaxis]]) Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Congestive Heart Failure (CHF)/Cardiogenic Shock (see Congestive Heart Failure , [[Congestive Heart Failure]] and Cardiogenic Shock , [[Cardiogenic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hemorrhagic Shock (see Hemorrhagic Shock , [[Hemorrhagic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Hypovolemic Shock (see Hypovolemic Shock , [[Hypovolemic Shock]]): common etiology of lactic acidosis Physiology: decreased oxygen delivery to tissues + epinephrine-induced 2-adrenergic receptor stimulation Sepsis (see Sepsis , [[Sepsis]]): common etiology of lactic acidosis Physiology: decreased lactate clearance (likely due to inhibition of pyruvate dehydrogenase + epinephrine-induced 2-adrene Continue reading >>

Lactic Acidosis: Background, Etiology, Epidemiology

Lactic Acidosis: Background, Etiology, Epidemiology

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [ 1 , 2 ] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [ 3 ] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentationand Differe 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

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 >>

Epinephrine-induced Lactic Acidosis Following Cardiopulmonary Bypass.

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 >>

Lactic Acidosis - Now@nejm Now@nejm

Lactic Acidosis - [email protected] [email protected]

Posted by Carla Rothaus December 11th, 2014 When lactic acidosis accompanies low-flow states or sepsis, mortality rates increase sharply. A new review summarizes our current understanding of the pathophysiological aspects of lactic acidosis, as well as the approaches to its diagnosis andmanagement. Lactic acidosis results from the accumulation of lactate and protons in the body fluids and is often associated with poor clinical outcomes. The effect of lactic acidosis is governed by its severity and the clinical context. Mortality is increased by a factor of nearly three when lactic acidosis accompanies low-flow states or sepsis, and the higher the lactate level, the worse theoutcome. Hyperlactatemia occurs when lactate production exceeds lactate consumption. In tissue hypoxia, whether global or localized, lactate is overproduced and underutilized as a result of impaired mitochondrial oxidation. Even if systemic oxygen delivery is not low enough to cause generalized hypoxia, microcirculatory dysfunction can cause regional tissue hypoxia and hyperlactatemia. Hyperlactatemia can also result from aerobic glycolysis, a term denoting stimulated glycolysis that depends on factors other than tissue hypoxia. Activated in response to stress, aerobic glycolysis is an effective, albeit inefficient, mechanism for rapid generation of ATP. In the hyperdynamic stage of sepsis, epinephrine-dependent stimulation of the (beta)2-adrenoceptor augments the glycolytic flux both directly and through enhancement of the sarcolemmal Na+,K+-ATPase (which consumes large quantities of ATP). Other disorders associated with elevated epinephrine levels, such as severe asthma (especially with overuse of beta2-adrenergic agonists), extensive trauma, cardiogenic or hemorrhagic shock, and pheochromocytoma, Continue reading >>

Causes Of Lactic Acidosis

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 >>

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?

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 >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus.

Epinephrine-induced Lactic Acidosis In The Setting Of Status Asthmaticus.

Epinephrine-induced lactic acidosis in the setting of status asthmaticus. Murphy FT(1), Manown TJ, Knutson SW, Eliasson AH. (1)Department of Medicine, Walter Reed Army Medical Center, Washington, DC 20307-5000, USA. A relationship between intravenous epinephrine infusion and the development oflactic acidosis has been well described. We report a temporal association betweenthe administration of subcutaneous epinephrine and the development of lacticacidosis in the setting of status asthmaticus. A 20-year-old woman with a historyof asthma came to the emergency service in acute respiratory distress and wastreated with subcutaneous epinephrine. Six hours later, serial arterial blood gasstudies revealed the onset of a primary metabolic acidosis. Additional diagnosticstudies revealed a serum lactate level of 9.5 mumol/L. The lactic acidosisresolved within 15 hours. The patient never exhibited signs of hypotension,hypoxemia, or sepsis, and other potential etiologies for lactic acidosis wereexcluded. We believe the events of this case constitute a new observation andtheorize a mechanism of peripheral vasoconstriction and transient tissuehypoperfusion mediated by the subcutaneous epinephrine. Continue reading >>

Lactic Acidosis

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 >>

More in ketosis