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 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 | 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 >>
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 >>
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 >>
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 . 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 >>
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 >>
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 >>
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 >>
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 >>
Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia 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 >>
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 >>
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 >>
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 >>