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Tham Lactic Acidosis

Your Patient In Extremis: Tham To The Rescue?

Your Patient In Extremis: Tham To The Rescue?

Your Patient In Extremis: THAM To The Rescue? By: Prathap Sooriyakumaran, MD and Curtis Geier, PharmD One of the final common denominators dictating the success or failure of any resuscitative effort, be it a trauma or medical code, is the patients acid-base status. In the presence of acidosis, many of the tools at your disposal, including vasopressors, become impotent and the patients ability to strike a balance between bleeding and clotting or mounting an appropriate inflammatory response become deranged.16 So what are the options to tilt the acid-base status in our favor? One thing is clear, sodium bicarbonate is not the hero we have been searching for. Unfortunately, the buffer we all know and want to love is ineffective in producing any significant change that will alter outcomes in the setting of the acutely acidemic patient.7,8 Why? Well to understand this, well have to do a brief dive (a wade) into the relevant human biochemistry. So if you give sodium bicarbonate in an attempt to scavenge your troublemaking protons, youll get carbonic acid which dissociates into carbon dioxide and water, which can freely diffuse across the cell membrane creating an intracellular acidosis.9 If you can get rid of carbon dioxide (blow it off), you will force the equation to the right and get rid of your protons. However, patients in extremis may not be able to compensate for the increased carbon dioxide with increased respiratory drive further exacerbating intracellular acidemia. THAM (trometanol; tris-hydroxymethyl aminomethane) is an inert amino alcohol which is theoretically amore effective buffer than bicarbonate in the physiological range of blood pH because it has a pKa of 7.8 at normal body temperatures (compared to a pKa of 6.1 for sodium bicarbonate). Why may it be more Continue reading >>

[therapeutic Effect Of Tham On Lactic Acidosis Of Severe Brain Injury].

[therapeutic Effect Of Tham On Lactic Acidosis Of Severe Brain Injury].

1. Zhonghua Wai Ke Za Zhi. 1996 Jun;34(6):364-7. [Therapeutic effect of THAM on lactic acidosis of severe brain injury]. (1)Department of Neurosurgery, Affiliated of Tianjin Medical College. The presence of lactic acidosis in the cerebral spinal fluid of 50 patients with severe head injury was studied. The GCS scores of these patients were < or = 8.The patients were divided into two groups. We treated 25 patients with a dose of 4 to 5 ml/kg of THAM infused intravenously 2 to 3 times for daily administration.Other 25 patients who were not treated with THAM served as a control group. Ineach case, a ventricular pressure monitoring device was installed. The ICP wasthe contineously recorded. In addition, laboratory study, including lactate, pH, HCO-3 and BE in CSF was performed. THAM infusion was associated with improvedsurvival, decreased ICP as compared to that in the control group. We believe thatTHAM treatment may significantly improve the prognosis of presence of lacticacidosis as a result of severe head injury. Continue reading >>

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-Associated Lactic Acidosis following Intentional Overdose Successfully Treated with Tris-Hydroxymethyl Aminomethane and Renal Replacement Therapy Ngan Lam ,1,2 Gurbir Sekhon ,3and Andrew A. House 1,3 1Division of Nephrology, Department of Medicine, Western University, London, ON, Canada N6A 3K7 2London Health Sciences Centre, Kidney Clinical Research Unit, Victoria Hospital, Westminster Tower 800 Commissioners Road East, London, ON, Canada N6A 4G5 3Department of Medicine, Western University, London, ON, Canada N6A 3K7 Received 19 February 2012; Accepted 6 May 2012 Academic Editors: Y.Fujigaki, D.Packham, A.Papagianni, and H.Schiffl Copyright 2012 Ngan Lam et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 43-year-old woman was brought to the hospital with severe metabolic acidosis (pH 6.56, bicarbonate 3 mmol/L, and lactate 18.4 mmol/L) and a serum creatinine of 162 mol/L with a serum potassium of 7.8 mmol/L. A delayed diagnosis of metformin-associated lactic acidosis was made, and she was treated with tris-hydroxymethyl aminomethane (THAM) and renal replacement therapy (RRT). Following a complete recovery, she admitted to ingesting 180 tablets (90 grams) of metformin. Her peak serum metformin concentration was 170 g/mL (therapeutic range 1-2 g/mL). Our case demonstrates an intentional metformin overdose resulting in lactic acidosis in a nondiabetic patient who was successfully treated with THAM and RRT. Metformin is an oral antihyperglycemic agent that is the first-line therapy for noninsulin-dependent diabetes mellitus [ 1 ]. Although the adverse event rate is 2030%, the majority of the Continue reading >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man

American Thoracic Society - Liver Dysfunction And Severe Lactic Acidosis In A Previously Healthy Man

Liver dysfunction and severe lactic acidosis in a previously healthy man A man in his eighth decade presented to his primary doctor three weeks prior to admission with easy bruising. A complete blood count revealed low counts in all three major cell lines and a subsequent bone marrow biopsy demonstrated B-cell follicular lymphoma. Other biochemical parameters, including tests of liver transaminases and bilirubin, were normal. Two weeks later he developed a cough and shortness of breath and he received a diagnosis of acute bronchitis, for which he was prescribed azithromycin along with an inhaler of salmeterol and fluticasone. His cough and dyspnea did not improve and he was admitted to another hospital for further evaluation. A diagnosis of liver failure was made based on elevated liver function tests (aspartate aminotransferase=995 U/L, alanine aminotransferase=552 U/L, total bilirubin=7.2 mg/dL, direct bilirubin=5.5 mg/dL); worsening pancytopenia was noted. Evaluation of the acute liver failure did not reveal an etiology, and he was transferred to a tertiary care hospital for further evaluation and care. Thyroid cancer, s/p partial thyroidectomy Denies excessive alcohol and illicit drug use 40 pack-year cigarette smoking history, stopped in 2004 Laboratory investigation did not reveal occult infectious hepatitis or autoimmune disease. Diagnostic imaging of the liver revealed a large intra-hepatic mass and trans-jugular liver biopsy showed extensive hepatic infiltration by lymphoma. His respiratory status became increasingly tenuous and his trachea was intubated and positive-pressure mechanical ventilation was initiated. He was transferred to the ICU but suffered the rapid onset of shock despite infusions of sodium bicarbonate and norepinephrine. After a conversation Continue reading >>

Lactic Acidosis - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

Tham - Fda Prescribing Information, Side Effects And Uses

Tham - Fda Prescribing Information, Side Effects And Uses

For the Prevention and Correction of Severe Metabolic Acidosis Tham Solution (tromeThamine injection) is a sterile, non-pyrogenic 0.3 M solution of tromeThamine, adjusted to a pH of approximately 8.6 with glacial acetic acid. It is administered by intravenous injection, by addition to ACD blood for priming cardiac bypass equipment and by injection into the ventricular cavity during cardiac arrest. Each 100 mL contains tromeThamine 3.6 g (30 mEq) in water for injection. The solution is hypertonic 389 mOsmol/L (calc.). pH 8.6 (8.4-8.7). The solution contains no bacteriostat, antimicrobial agent or added buffer (except acetic acid for pH adjustment) and is intended only for use as a single-dose injection. When smaller doses are required the unused portion should be discarded. Tham solution is a parenteral systemic alkalizer and fluid replenisher. TromeThamine, USP (sometimes called tris or tris buffer) is chemically designated 2-amino-2-(hydroxymethyl)-1, 3-propanediol, a solid readily soluble in water, also classified as an organic amine buffer. It has the following structural formula: Water for Injection, USP is chemically designated H20. Amyotrophic Lateral Sclerosis (ALS): Evolving Science For a Fatal Disease When administered intravenously as a 0.3 M solution, tromeThamine act as a proton acceptor and prevents or corrects acidosis by actively binding hydrogen ions (H+). It binds not only cations of fixed or metabolic acids, but also hydrogen ions of carbonic acid, thus increasing bicarbonate anion (HCO3). TromeThamine also acts as an osmotic diuretic, increasing urine flow, urinary pH, and excretion of fixed acids, carbon dioxide and electrolytes. A significant fraction of tromeThamine (30% at pH 7.40) is not ionized and therefore is capable of reaching equilibrium i Continue reading >>

Buffer Therapies: Sodium Bicarbonate, Carbicarb And Tham - Deranged Physiology

Buffer Therapies: Sodium Bicarbonate, Carbicarb And Tham - Deranged Physiology

Buffer Therapies: Sodium Bicarbonate, Carbicarb and THAM This has only come up once in the exam. Question 27 from the first paper of 2009 asked the candidates to compare and contrast the pharmacology of carbicarb, sodium bicarbonate and THAM. The unusual feature was of course the fact that carbicarb is not available in Australia, and THAM is so rarely used that our local supply consists of imported ampoules with labels exclusively in German. The answer to Question 27 works best as a table; it is reproduced below to simplify revision. As far as literature references go, the majority are from the 1980s and 90s (back when buffer therapy was still considered a viable option in cardiac arrest, for example). One potentially relevant article is a 1998 paper by Bar-Joseph et al , which compared THAM, Carbicarb and sodium bicarbonate in a canine cardiac arrest model. An 8.4% (1mol/L) solution of NaHCO3which offers 1000mmol/L of HCO3-and Na+ions. An equimolar (300mmol/L) solution of Na2CO3and NaHCO3which offers 666mmol/L of HCO3-ions, and 1000mmol/L of Na+ions An organic amine buffer, otherwise known as tris-hydroxymethyl-aminomethane, or tromethamine. Eliminated renally, as well as being converted to CO2and exhaled (in process of buffering reactions). These two substances differ mainly in the amount of bicarbonate anion they add. Rapidly eliminated by the kidney; 75% is excreted in the urine after 8 hours. Sodium bicarbonate contributes HCO3-which is a natural buffer, thus replenishing the buffer systems of the body in a state of acidosis. The sodium carbonate component is supposed to act as a bicarbonae precursor, regenerating HCO3-buffers without increasing the PaCO2. THAM is a "third buffer" to complement the buffering capacity of endogenous HCO3-and body protein. At pH of 7 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 >>

Use Of Tris-hydroxymethyl Aminomethane In Severe Lactic Acidosis Due To Highlyactive Antiretroviral Therapy: A Case Report.

Use Of Tris-hydroxymethyl Aminomethane In Severe Lactic Acidosis Due To Highlyactive Antiretroviral Therapy: A Case Report.

1. J Clin Pharm Ther. 2009 Feb;34(1):119-23. doi: 10.1111/j.1365-2710.2008.00977.x. Use of Tris-hydroxymethyl aminomethane in severe lactic acidosis due to highlyactive antiretroviral therapy: a case report. Marfo K(1), Garala M, Kvetan V, Gasperino J. (1)Department of Pharmacy Montefiore Medical Center, Bronx, NY, USA. BACKGROUND: Lactic acidosis is a rare, yet life-threatening adverse drug effectof highly active antiretroviral therapy (HAART), specifically stavudine andlamivudine. These nucleoside analogue reverse transcriptase inhibitors (NRTIs)are commonly used to treat patients infected with the human immunodeficiencyvirus (HIV).CASE: We report the use of Tris-hydroxymethyl aminomethane (THAM) to treat severelactic acidosis due to HAART in a 50-year-old African-American woman. NRTIs cancause hyperlactinaemia by interfering with mitochondrial oxidativephosphorylation function, which normally removes H(+) generated by the hydrolysisof adenosine triphosphate. This side-effect is associated with a high mortalityin patients infected with HIV. One explanation for this high mortality is thatlactic acidosis is typically refractory to treatment with commonly used bufferingagents.CONCLUSION: THAM generates serum bicarbonate, and reduces the level of carbondioxide in arterial blood. Both of these qualities appear to make THAM an idealagent for treating lactic acidosis caused by HAART. Antiretroviral Therapy, Highly Active/adverse effects* Continue reading >>

Buffers

Buffers

(Version 1.0 3/1/2001 - 7/30/2007) Acidosis is a frequent problem in critically-ill neonates. Buffers may be used as part of the treatment strategy of a metabolic acidosis. The etiology of a low pH must be understood to treat infants appropriately. Respiratory acidosis (increased CO2 on a blood gas) can only be treated by improving ventilation. Buffers will not help in this case, and may make the situation worse. The etiology of a metabolic acidosis (highly negative base deficit on a blood gas) must also be taken into account to determine the need to treat and appropriate measures to take. In all cases, giving buffer will only partially and transiently remedy the situation; the underlying problem generating the acidosis must be addressed. Although many different illnesses can cause a metabolic acidosis, the two most common etiologies seen in the NICU are lactic acidosis from impaired perfusion and non-anion gap hyperchloremic acidosis due to renal bicarbonate wastage. Lactic acidosis heralds a significant underlying problem; possibilities include hypovolemic shock, inadequate cardiac output, and sepsis. Hyperchloremic non-anion gap acidosis is a much less critical problem but is extremely common in < 1000g micropremies. The etiology of the acidosis also determines the threshold at which you would administer buffer to a patient. Buffers are administered because acidosis impairs cardiac performance at a pH < 7.2 7.25. Therefore, in patients with congenital heart disease, cardiologists often treat lactic acidosis at a base deficit of > -4 to improve organ perfusion. However, in micropremies with hyperchloremia, the risk-benefit ratio differs. Hyperchloremic acidosis is better tolerated and pharmacologic buffers are hypersosmolar and associated with an increased risk of IV Continue reading >>

The Use Of Tris-hydroxymethyl Aminomethane In The Emergency Department

The Use Of Tris-hydroxymethyl Aminomethane In The Emergency Department

The use of tris-hydroxymethyl aminomethane in the emergency department Lu, Leibner, and Wright: The use of tris-hydroxymethyl aminomethane in the emergency department Christina Lu , Evan Leibner , Brian Wright Department of Emergency Medicine, Stony Brook University, Stony Brook, NY, USA Correspondence to: Brian Wright Department of Emergency Medicine, Stony Brook University, Hsc, Level 4, Room 080, Stony Brook, NY 11794, USA Received: July 20, 2016 Revised: August 22, 2016 Accepted: August 22, 2016 Copyright 2016 The Korean Society of Emergency Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ). Bicarbonate therapy is often not effective for alkalinizing the blood pH in critically ill patients because it requires patients to augment their already maxed respiratory drive. Tris-hydroxymethyl aminomethane is a little known amine buffer that works in a closed system independent of pulmonary function and may be an effective alternative to sodium bicarbonate. Treatment of critically ill patients is a multi-faceted problem. Often the physician is faced with multiple complex tasks that range from correctly diagnosing the underlying disease process to appropriately managing the hemodynamics and homeostasis. Critically ill patients commonly have acid-base abnormalities, especially acidosis. Critical care dogma teaches that treatment of the primary condition will lead to a correction of the acidosis. That acidosis, however, can be so severe that it needs to be addressed before the underlying medical condition can be reversed. This review will discuss tris-hydroxymethyl aminomethane (THAM). THAM is a rarely used buffer approved by the Food and Drug Administration for treatment of metabolic acidosis as Continue reading >>

Guidelines For The Treatment Of Acidaemia With Tham.

Guidelines For The Treatment Of Acidaemia With Tham.

Guidelines for the treatment of acidaemia with THAM. Nahas GG(1), Sutin KM, Fermon C, Streat S, Wiklund L, Wahlander S, Yellin P,Brasch H, Kanchuger M, Capan L, Manne J, Helwig H, Gaab M, Pfenninger E,Wetterberg T, Holmdahl M, Turndorf H. (1)Department of Anaesthesiology, New York University Medical Center, New York, USA. [email protected] THAM (trometamol; tris-hydroxymethyl aminomethane) is a biologically inert amino alcohol of low toxicity, which buffers carbon dioxide and acids in vitro and invivo. At 37 degrees C, the pK (the pH at which the weak conjugate acid or base inthe solution is 50% ionised) of THAM is 7.8, making it a more effective bufferthan bicarbonate in the physiological range of blood pH. THAM is a protonacceptor with a stoichiometric equivalence of titrating 1 proton per molecule. Invivo, THAM supplements the buffering capacity of the blood bicarbonate system,accepting a proton, generating bicarbonate and decreasing the partial pressure ofcarbon dioxide in arterial blood (paCO2). It rapidly distributes through theextracellular space and slowly penetrates the intracellular space, except forerythrocytes and hepatocytes, and it is excreted by the kidney in its protonated form at a rate that slightly exceeds creatinine clearance. Unlike bicarbonate,which requires an open system for carbon dioxide elimination in order to exertits buffering effect, THAM is effective in a closed or semiclosed system, andmaintains its buffering power in the presence of hypothermia. THAM rapidlyrestores pH and acid-base regulation in acidaemia caused by carbon dioxideretention or metabolic acid accumulation, which have the potential to impairorgan function. Tissue irritation and venous thrombosis at the site ofadministration occurs with THAM base (pH 10.4) admini Continue reading >>

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Kimmoun et al.; licensee BioMed Central.2015 The Erratum to this article has been published in Critical Care 2017 21:40 Lactic acidosis is a very common biological issue for shock patients. Experimental data clearly demonstrate that metabolic acidosis, including lactic acidosis, participates in the reduction of cardiac contractility and in the vascular hyporesponsiveness to vasopressors through various mechanisms. However, the contributions of each mechanism responsible for these deleterious effects have not been fully determined and their respective consequences on organ failure are still poorly defined, particularly in humans. Despite some convincing experimental data, no clinical trial has established the level at which pH becomes deleterious for hemodynamics. Consequently, the essential treatment for lactic acidosis in shock patients is to correct the cause. It is unknown, however, whether symptomatic pH correction is beneficial in shock patients. The latest Surviving Sepsis Campaign guidelines recommend against the use of buffer therapy with pH 7.15 and issue no recommendation for pH levels <7.15. Furthermore, based on strong experimental and clinical evidence, sodium bicarbonate infusion alone is not recommended for restoring pH. Indeed, bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. This review addresses the principal hemodynamic consequences of shock-associated lactic acidosis. Despite the lack of formal evidence, this review also highlights the various adapted supportive therapy options that could be putatively added to causal treatment in attempting to reverse the hemodynamic consequences of shock-associated lactic Continue reading >>

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic Shock From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Bra Continue reading >>

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