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Lactic Acidosis Nejm

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 >>

Delta Gap And Delta Ratio - Deranged Physiology

Delta Gap And Delta Ratio - Deranged Physiology

The delta gap and delta ratio, advantages and disadvantages . Once one has calculated the anion gap and finds it raised, one is almost obliged to figure out whether those anions have been solely responsible for the acidosis, or whether another (non-anion-gap) cause is lurking in the background. A brief review of this can be found in the "Required Reading" section hidden among the CICM Fellowship Exam preparation material.For actual education, the exam candidates are directed to the LITFL delta ratio page , and to the excellent online works of Kerry Brandis. The delta gap is a straight-out difference between the change in anion gap and the change in bicarbonate. Delta gap = (change in anion gap) - (change in bicarbonate) (The normal anion gap is assumed to be 12, and the normal HCO3is assumed to be 24.) A simplified equation which does not require a bicarbonate value is also available: -6 = Mixed high and normal anion gap acidosis -6 to 6 = Only ahigh anion gap acidosis exists over 6 = Mixed high anion gap acidosis and metabolic alkalosis Delta gap is essentially a tool to determine whether or not there is also a normal anion gap metabolic acidosis present.The normal value for delta gap is zero, and it should remain zero as anion gap and bicarbonate changetogether (mole for mole, in opposite directions). If the bicarbonate is changing significantlyless than the anion gap, the delta gap will become more and more positive, reflecting the fact that an alkalosis is present. If the change in bicarbonateis significantly greater than the change in anion gap, there is clearly some acidosis present which is unrelated to the anion gap rise, and thedelta gap will be very negative. Why -6 and +6?Keith Wrenn established these parameters in 1990 , using the normal values supplied to Continue reading >>

Metformin Induced Lactic Acidosis Nejm

Metformin Induced Lactic Acidosis Nejm

by : incidence, management and prevention. Drug Saf 2010;33(9):727-40. 3. Kalantar-Zadeh K, Uppot RN, Lewandrowski KB. Case records of the Massachusetts General Hospital (Case 23-2013). A 54-year-old woman with abdominal pain, vomiting, and confusion. N Engl J Med 2013;Jan 22, 1998 Correspondence from The New England Journal of Medicine in Patients with Diabetes Treated with . Prepare to become a physician, build your knowledge, lead a health care organization, and advance your career with Group information and services. Dec 11, 2014 Using dialysis to provide bicarbonate can prevent a decrease in ionized calcium, prevent volume overload and hyperosmolality (potential complications of bicarbonate infusion), and remove substances associated with , such as . Through an alkalinizing effect, base administration,Aug 31, 1995 Such a mechanism of action might diminish the removal of lactate from plasma and present a risk of . .. On the other hand, if the - increase in the sensitivity of muscle to insulin included an anticatabolic effect of insulin on protein metabolism, one would expect no change inJan 2, 2003 is a toxic effect of linezolid whose mechanism is unknown. Other drugs, including and nucleoside reverse-transcriptase inhibitors, have been associated with . In the case of nucleoside reverse-transcriptase inhibitors, is thought to involve mitochondrialJul 26, 2013 Q: What are the characteristics of -? A: overdose or accumulation as the cause of is highly likely in any patient who has most or all of the following five criteria in the absence of a high level: a history of administration (e.g., in aMeSH terms. , /chemically *; Aged; Diabetes Mellitus/drug therapy; Female; Humans; Hypoglycemic Agents/adverse effects*; Male; /adverse effects*; Risk FactorsDec 14, 2017 cause Continue reading >>

Research And Reviews In The Fastlane 066

Research And Reviews In The Fastlane 066

Welcome to the66th editionof Research and Reviews in the Fastlane . R&R in the Fastlane is a free resource that harnesses the power of social media to allow some of the best and brightest emergency medicine and critical care clinicians from all over the world tell us what they think is worth reading from the published literature. This edition contains6 recommended reads. The R&R Editorial Team includes Jeremy Fried, Nudrat Rashid, Soren Rudolph, Anand Swaminathan and, of course, Chris Nickson. Find more R&R in the Fastlane reviews in the R&R Archive , read more about the R&R project or check out the full list of R&R contributors Sandroni C et al. Prognostication in comatose survivors of cardiac arrest: an advisory statement from the European Resuscitation Council and the European Society of Intensive Care Medicine. Intensive Care Med 2014; 40(12):1816-31. PMID: 25398304 (FREE OPEN ACCESS ARTICLE) This is a question that plagues most Critical Care Doctors. Unfortunately the quality of evidence remains poor. The authors suggest a multimodal prognostication approach in all patients. The most robust predictors remain bilateral absence of either pupillary and corneal reflexes or N20 wave of short-latency somatosensory evoked potentials in patients who are comatose with absent or extensor motor response at 72 h from arrest, either treated or not treated with controlled temperature. Vaillancourt S et al. Repeated Emergency Department Visits Among Children Admitted With Meningitis or Septicemia: A Population-Based Study. Ann Emerg Med 2014. PMID: 25458981 This is a retrospective cohort study looking at all kids within a database who were identified as having bacteremia or meningitis. The authors sought to look at whether there was a difference in outcomes between patients who Continue reading >>

Distrbios Cido Bsicos Reviso Nejm 2014-1

Distrbios Cido Bsicos Reviso Nejm 2014-1

Descubra todo lo que Scribd tiene para ofrecer, incluyendo libros y audiolibros de importantes editoriales. Distrbios cido Bsicos Reviso NEJM 2014-1 hacer clic para expandir la informacin del documento guardarGuardar Distrbios cido Bsicos Reviso NEJM 2014-1 para ms tarde Distrbios cido Bsicos Reviso NEJM 2014-1 guardarGuardar Distrbios cido Bsicos Reviso NEJM 2014-1 para ms tarde The n e w e ng l a n d j o u r na l of m e dic i n e Kenrick Berend, M.D., Ph.D., Aiko P.J. de Vries, M.D., Ph.D., From the Department of Internal Medi nternal acidbase homeostasis is fundamental for maintaining cine, St. Elisabeth Hospital, Willemstad, life. Accurate and timely interpretation of an acidbase disorder can be lifesav- phrology, Department of Medicine, Leiden ing, but the establishment of a correct diagnosis may be challenging.1 The three University Med ical Center, and Leiden major methods of quantifying acidbase disorders are the physiological approach, University, Leiden (A.P.J.V.), and the De the base-excess approach, and the physicochemical approach (also called the Stew- partment of Internal Medicine, University of Groningen, University Medical Center art method).2 This article reviews a stepwise method for the physiological approach. Groningen, Groningen (R.O.B.G.) The physiological approach uses the carbonic acidbicarbonate buffer system. both in the Netherlands. Address reprint Based on the isohydric principle, this system characterizes acids as hydrogen-ion of Internal Medicine, St. Elisabeth Hospi donors and bases as hydrogen-ion acceptors. The carbonic acidbicarbonate sys- tal, Breedestraat 193, Willemstad, Curaao, tem is important in maintaining homeostatic control. In the physiological ap- or at [email protected] proach, a primary change in the partial pressure of car Continue reading >>

Talk:lactic Acidosis

Talk:lactic Acidosis

This article is within the scope of WikiProject Physiology , a collaborative effort to improve the coverage of Physiology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks. This article has been classified as relating to the kidneys and renal physiology . This article is within the scope of WikiProject Medicine , which recommends that medicine-related articles follow the Manual of Style for medicine-related articles and that biomedical information in any article use high-quality medical sources . Please visit the project page for details or ask questions at Wikipedia talk:WikiProject Medicine . This article has been rated as Mid-importance on the project's importance scale . Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles . Here are links to possibly useful sources of information about Lactic acidosis. Other potential sources include: Centre for Reviews and Dissemination and CDC Acidosis is not due to lactic acid[ edit ] As I have mentioned on the talk pages of Anaerobic Respiration and Lactic Acid , relatively recent research has clearly established that lactate production in anaerobic respiration does not cause acidosis. The reference I cited there is . Lim Wei Quan ( talk ) 06:44, 30 October 2008 (UTC) Personally until proven otherwise, I think it warrants staying placed on the wiki to keep a 'warning' as the prevailing ideology behind the article vs leaving it otherwise. Preceding unsigned comment added by 71.61.125.253 ( talk ) 07:34, 3 January 2009 (UTC) In humans, perhaps, but lactic acid buildup can cause such extreme acidosis in large reptiles (particularly croc Continue reading >>

Metformin-associated Lactic Acidosis Reexamined

Metformin-associated Lactic Acidosis Reexamined

Metformin-Associated Lactic Acidosis Reexamined Allan S. Brett, MD reviewing Bodmer M et al. Diabetes Care 2008 Nov In this study, lactic acidosis was not more common with metformin than with sulfonylurea. The prescribing information for metformin carries strong warnings about risk for lactic acidosis, particularly in patients with renal insufficiency or heart failure. In this analysis drawn from the U.K. General Practice Research Database, investigators determined the incidence of lactic acidosis among 50,000 patients with type 2 diabetes who were prescribed any oral antidiabetic agent between 1994 and 2005. Six cases of lactic acidosis were identified among current users of oral antidiabetic drugs. One patient took metformin only, one took a sulfonylurea only, and four took metformin plus another drug (sulfonylurea or pioglitazone). The crude incidence of lactic acidosis was 3.3 per 100,000 person-years in metformin users and 4.8 per 100,000 person-years in sulfonylurea users. In contrast, 73 patients suffered severe hypoglycemia (resulting in hospitalization or death); 22 of them used sulfonylurea only, 3 used metformin only, and most others used oral drug combinations or insulin. In this study, lactic acidosis was not more common with metformin than with sulfonylurea. Moreover, severe hypoglycemia was much more common than was lactic acidosis and was usually associated with sulfonylurea or insulin but not with metformin. These observations lead the authors to imply (but not directly state) that clinicians should have more latitude in prescribing metformin. However, the authors do not discuss the possibility that judicious prescribing of metformin could have been the very reason that lactic acidosis was so rare in this cohort. Bodmer M et al. Metformin, sulfonylurea Continue reading >>

Lactic Acidosis | Trauma Anesthesia

Lactic Acidosis | Trauma Anesthesia

Key points for the trauma anesthesiologist The diagnosis of lactic acidosis is best made by the serum lactate level. Anion gap and decline in the serum HCO3 levels, although suggestive of lactic acidosis are non-specific and can be causedby other acid-base disorders. Cardiogenic or hypovolemic shock, advanced heart failure, sepsis, and severe trauma account for the majority of lactic acidosis. Treatment consists of restoring tissue perfusion with crystalloid,colloid, vasopressors, and inotropes, improving the microcirculation, initiating cause-specific measures (see the article), and base administration. Vasopressors and inotropes are best avoided in trauma. They can lead to a false sense that bleeding has been controlled and that resuscitation is adequate whenthey are not. In my opinion, colloids are best avoided. If a colloid is given, it should be albumin. Normal salineisbest avoided because itcan generate or exacerbate metabolic acidosis whereas balanced salt solutions do not. PlasmaLyte is compatible with banked blood, lactated Ringer is not. Dobutamine, acetylcholine, and nitroglycerin improve microvascular perfusion. NaHCO3 administration is not benign. The CO2 produced/accumulated causes intracellular acidosis and the elevated pH causes a decrease in ionized calcium, which modulates cardiac contractility. THAM, another buffer, is approved for clinical use. Goals of therapy include normal hemodynamics, HGB 7-10, pH > 7.2, O2 sat > 92, declining lactate. Continue reading >>

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base Disturbances In Children, Acidosis, Alkalosis

Acid-base disturbances in children, Acidosis, Alkalosis Acid-base disturbances in children, Acidosis, Alkalosis The pH of the blood is controlled via three systems: chemical buffering, respiratory function, and renal function. Acidosis means a clinical disturbance in which there is an increase in plasma acidity, whether due to increased production by the tissues, loss of buffering ability or decreased clearance by the kidneys. A multitude of problems, congenital and acquired, can result in metabolic acidosis. The hallmark of a metabolic acidosis is a low serum HCO3 level. Metabolic alkalosis means the patient has an elevated HCO3, most typically seen with administration of loop diuretics. A respiratory acidosis means an increase in the partial pressure of carbon dioxide in the blood (PaCO2) due to inadequate respiration. Respiratory alkalosis typically occurs in response to a metabolic stimulus, such as hyperammonemia (seen in urea cycle defects) or diabetic ketoacidosis (DKA). Metabolic and respiratory mechanisms affect the acid-base state. The relationship between the pH and PaCO2 is dependent upon the plasma bicarbonate-plasma carbonic acid pool. To estimate the effect of pH change, for every 10 mmHg PaCO2, the pH will change by approximately 0.08; for example, if the PaCO2 rises to 50 from a normal 40 mmHg, then the expected pH will be approximately 7.32, or decreased by 0.08. Comparison of the base excess with the reference range assists in determining whether an acid-base disturbance is caused by a respiratory, metabolic or mixed metabolic/respiratory problem. While CO2 defines the respiratory component of acid-base balance, base excess defines the metabolic component. To generalize, a metabolic acidosis will have a low serum HCO3 and a respiratory acidosis will Continue reading >>

Morning Report Pearls 9/6/17 Lactic Acidosis

Morning Report Pearls 9/6/17 Lactic Acidosis

UCSF Internal Medicine Chief Resident Hub Thank you Courtney and Nancy for presenting a diagnostic mystery! This elderly woman presented to the ED after an episode of witnessed syncope with headstrike complicated by SDH and SAH, transferred from neurosurgery to medicine for a profound metabolic acidosis lactate of 21!! Syncope its all about the history! There are 4 main categories: cardiac arrhythmias, structural cardiopulmonary disease, neurogenic, and orthostatic hypotension. Lactate make you nervous? Not all lactates come from sepsis use an algorithm to help flesh out the other causes of elevated lactate. Remember that medications can affect all of these categories! Check out this previous post all about syncope and the associated Evernote ! Global: shock of any type! Distributive, cardiogenic, neurogenic, obstructive Local: mesenteric ischemia, compartment syndrome, seizure, etc. Decreased delivery of O2: severe anemia, severe hypoxemia, methemoglobinemia, carbon monoxide, cyanide Lack of required cofactor: thiamine deficiency Mitochondrial toxicity: EtOH, ARVs, Propofol, Salicylates, mitochondrial d/o Warburg effect conversion to anaerobic metabolism within a high-grade malignancy Decreased clearance of lactate from any cause: WAY less commonly D-lactic acidosis the D-isomer of lactate associated with small bowel overgrowth, short gut syndrome, unusual causes of sepsis. Of note, our lab at UCSF does NOT detect the d-lactate isomer, so if you have an elevated lactate here, its the L-lactate isomer. To read more, here is a link to a 2014 review article from the NEJM on Lactic Acidosis by Kraut and Madias: For more specifically about Type B lactic acidosis as a complication of lymphoma and leukemia, check out this case series and review by Friedenberg, Brandoff, and Continue reading >>

Resident Report Internal Medicine Residency Program | Boston University

Resident Report Internal Medicine Residency Program | Boston University

61 yo F with HTN, DM brought in by daughter for acute onset of a single acuteepisode of visual hallucinations. She saw a girl (non existent) run across her living room and then saw lasagna (non existent) all over herself. Daughter was with her at this time and called 911. Medical and neurologicalproblems were ruled out with MRI/MRA, labs, complete neurological exam. On further asking she says that her visual acuity has declined over past few months. She had possibly Charles Bonnet syndrome. Charles Bonnet syndrome is a benign condition where patients with decreased visual acuity have vivid visual hallucinations as a release phenomenon. Reassurance and treatment of the underlying visual disorder is the treatment of this disorder. 32 yo M brought in by sister and mother for sitting in a water-filled bathtub for three whole days. He sat in the tub all dressed and did not eat/drink for the whole time but ketp reading the bible stating that he had to save mankind by reading the bible. When brought in to the ED, other than being agitated, hyper-religiousand needing restraints, he also displayed autonomic instability. DDx included Neuroleptic Malignant Syndrome,acute psychosis, malignant catatonia,CNS/ systemic infectious process. He had elevated CK and leucocytosis with tachycardia, fever and was admitted to MICU for monitoring. Concluding diagnosis was malignant catatonia. Stimulating discussion at Intern Report of a case of classic Graves hyperthyroidism. 21 yo F presenting with 40 lbs weight loss, palpitation, SOB/DOE, neck swelling, diarrhea, irregular mensesfor 6 months. On further evaluation was found to be hyperthyroid per labs and diagnosed with Graves disease (TSI/ thyroid stimulating immunoglobulins-elevated). She was also found to have an anterior mediastinal mass Continue reading >>

Welcome To Osmolality.com | Presented By Advanced Instruments, Inc.

Welcome To Osmolality.com | Presented By Advanced Instruments, Inc.

Bhagat, C.I., Garcia-Webb, P., Fletcher, E., Beilby, J.P. Calculated versus Measured Plasma Osmolalities Revisited. Clinical Chemistry, 30(10):1703 1984 Boyd, D.R., Mansberger, A.R., Serum Water and Osmolal Changes in Hemorrhagic Shock: An Experimental and Clinical Study, Am Surgeon, 34: 744 (1968) Dorwart, W.V., Chalmers, L., Comparison of Methods for Calculating Serum Osmolality from Chemical Concentrations, and the Prognostic Value of Such Computations, Clinical Chemistry, 21: 190 (1975) Eskew, L., Speicher, C.E., Using Anion and Osmolal Gaps to Diagnose the Cause of Intoxication, Diagnostic Medicine, p. 6 February 1985 Evans, J.R., Osmolal Gaps in Urine, Clinical Chemistry, 32(7): 1415 (1986) Evans, J.R., Yet More on Osmolal Gaps in Urine, Clinical Chemistry, 33(5): 736 (1987) Garg, A.K., Nanji, A.A., Osmolar Gap, Diagnostic Medicine, p. 38 Mar/Apr 1982 Neary, R.H., More on Osmolal Gaps in Urine, Clinical Chemistry, 32(12): 2225 (1986) Osterloh, J.D., Discrepancies in osmolal gaps and calculated alcohol concentrations -see comments-. Archives of Pathology Laboratory Medicine 1996; 120: 637-41. Soloway, H.B., What is an osmotic gap, and how is it used in diagnosis?, Diagnostic Medicine, p. 20 Nov/Dec 1983 Speicher, C.E., Anion and Osmolal Gaps, Consultation Casebook, Pathologist, 2: 117 (1984) Walker, J.A., Missing gap: pitfall in the diagnosis of alcohol intoxication by osmometry. Archives of Internal Medicine 1986; 146: 1843-4. Weisberg, H.F., Osmolality: Calculated, "Delta" and More Formulas. Clinical Chemistry, 21: 1182 (1975) 1. Bekeris, L., Baker, C., Fenton, J., Kimball, D., et al. Propylene Glycol as a Cause of Elevated Serum Osmolality. Am. Journal of Clinical Pathology, 72 (4): 633, October 1979. 2. Cate, J.C., Propylene Glycol Intoxication and Lactic Acid Continue reading >>

Lactic Acidosis In An Infant Receiving Hiv Prophylaxis

Lactic Acidosis In An Infant Receiving Hiv Prophylaxis

Lactic Acidosis in an Infant Receiving HIV Prophylaxis The rate of vertical transmission of human immunodeficiency virus (HIV) has dramatically decreased with the administration of antiretroviral treatments (ART) to HIV-infected mothers and their infants. The Pediatric AIDS Clinical Trials Group 076 (PACTG 076) originally showed zidovudine, a nucleoside analogue reverse transcriptase inhibitor (NRTI), to be a safe and effective therapy in preventing vertical transmission when administered to both mother and child.1 Guidelines currently recommend zidovudine for HIV prophylaxis for 4-6 weeks for neonates exposed to HIV in utero.2 Despite the overall safety findings of zidovudine from PACTG 076, rare, but serious, side effects have been observed. Although data are conflicting, NRTIs have been linked to mitochondrial toxicity that leads to lactic acidosis, cardiac abnormalities, neurologic delays, and death.3-5 We present a case of presumed mitochondrial toxicity and lactic acidosis in an infant exposed to zidovudine for HIV prophylaxis. A 5-week-old female born to an HIV-positive mother presented to a referring hospital for excessive vomiting of 2 days duration. Emesis was reported to occur after each feed and was non-bloody, non-bilious, and non-projectile. She had been afebrile with no sick contacts. She did have a history of reflux and would have small spit-ups after each feed. Diet consisted of infant formula 2-4 oz every 2-4 hours, mixed appropriately. Prenatal history was notable for maternal HIV diagnosed 16 years prior to the pregnancy; the mother, however, did not start HAART until pregnancy was confirmed. Treatment was initiated with elvitegravir/cobicistat/emtricitabine/tenofovir 6 months prior to her giving birth. She received IV zidovudine intrapartum, and th 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 >>

Lactic Acidosis (pdf Download Available)

Lactic Acidosis (pdf Download Available)

hypoxemia (e.g., summiting Mount Everest), lac- tate levels are either normal or only minimally elevated. Lactate is a major biofuel used for intra- cellular, intercellular, and interorgan shuttles, processes that appear to increase bioenergetic efficiency. It is doubtful that lactic acidosis is due to the release of protons from ATP hydrolysis, since no ATP depletion can be shown on mag- netic resonance spectroscopy, even in severe septic (although similarly unproven) lies with the Stewart, or strong ion, approach to acidbase physiology. Lactate is an anion that decreases the strong-ion difference and increases the dissociation of water Australian and New Zealand Intensive Care Research Centre No potential conflict of interest relevant to this letter was re- 1. Kraut JA, Madias NE. Lactic acidosis. N Engl J Med 2. Garcia-Alvarez M, Marik P, Bellomo R. Sepsis-associated hy- 3. Garcia-Alvarez M, Marik P, Bellomo R. Stress hyperlactate- mia: present understanding and controversy. Lancet Diabetes 4. May CN, Ishikawa K, Wan L, et al. Renal bioenergetics dur- ing early gram-negative mammalian sepsis and angiotensin II infusion. Intensive Care Med 2012;38:886-93. 5. Kellum JA. Disorders of acid-base balance. Crit Care Med To the Editor: Kraut and Madias provide an ex- cellent overview of lactic acidosis. But the asser- tion that it remains unproven that the therapeu- tic administration of sodium bicarbonate may improve hemodynamics is inaccurate. Two pro- spective, randomized, blinded, crossover studies specifically examined the effects of sodium bi- carbonate or isovolemic aliquots of normal sa- line on hemodynamics in critically ill patients with lactic acidemia who required vasoactive sup- Mathieu et al. concluded that sodium bicarbon- ate did not improve hemodynamic vari Continue reading >>

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