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Metabolic Acidosis And Vasopressors

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 >>

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild Metabolic Acidosis Impairs The -adrenergic Response In Isolated Human Failing Myocardium

Mild metabolic acidosis impairs the -adrenergic response in isolated human failing myocardium Schotola et al.; licensee BioMed Central Ltd.2012 Pronounced extracellular acidosis reduces both cardiac contractility and the -adrenergic response. In the past, this was shown in some studies using animal models. However, few data exist regarding how the human end-stage failing myocardium, in which compensatory mechanisms are exhausted, reacts to acute mild metabolic acidosis. The aim of this study was to investigate the effect of mild metabolic acidosis on contractility and the -adrenergic response of isolated trabeculae from human end-stage failing hearts. Intact isometrically twitching trabeculae isolated from patients with end-stage heart failure were exposed to mild metabolic acidosis (pH 7.20). Trabeculae were stimulated at increasing frequencies and finally exposed to increasing concentrations of isoproterenol (0 to 1 10-6 M). A mild metabolic acidosis caused a depression in twitch-force amplitude of 26% (12.1 1.9 to 9.0 1.5 mN/mm2; n = 12; P < 0.01) as compared with pH 7.40. Force-frequency relation measurements yielded no further significant differences of twitch force. At the maximal isoproterenol concentration, the force amplitude was comparable in each of the two groups (pH 7.40 versus pH 7.20). However, the half-maximal effective concentration (EC50) was significantly increased in the acidosis group, with an EC50 of 5.834 10-8 M (confidence interval (CI), 3.48 10-8 to 9.779 10-8; n = 9), compared with the control group, which had an EC50 of 1.056 10-8 M (CI, 2.626 10-9 to 4.243 10-8; n = 10; P < 0.05), indicating an impaired -adrenergic force response. Our data show that mild metabolic acidosis reduces cardiac contractility and significantly impairs the -adrenerg Continue reading >>

Approach To Hemodynamic Shock And Vasopressors

Approach To Hemodynamic Shock And Vasopressors

Approach to Hemodynamic Shock and Vasopressors Departments of *Nephrology and General, Visceral and Transplant Surgery, University Hospital, University Duisburg-Essen, Essen, Germany; and Critical Care Medicine and Nephrology, George Washington University Medical Center, Washington, DC Dr. Stefan Herget-Rosenthal, Klinik fr Nieren- und Hochdruckkrankheiten, Universittsklinikum Essen, Universitt Duisburg-Essen, Hufelandstrasse 55, D-45122 Essen, Germany. Phone: +49-201-723-2552; Fax: +49-201-723-5633; E-mail: stefan.herget-rosenthal{at}uni-due.de Hemodynamic shock (HS) is a clinical syndrome that is commonly observed in hospitalized patients. Prompt recognition and intervention are the cornerstones of mitigating the dire consequences of HS. Untreated HS usually leads to death. Unlike other types of clinical syndromes (e.g., chest pain), for which a clinical diagnosis is made before treatment is initiated in earnest, the treatment of shock often occurs concurrently or ahead of the diagnostic process. The maintenance of end-organ perfusion is critical to prevent irreversible organ injury and failure, and this frequently requires the use of fluid resuscitation and vasopressors. A complete review of all of the signs and symptoms, diagnosis, and treatment of HS has been reviewed in detail elsewhere ( 1 ). This article provides a concise summary of how to approach the patient in HS, diagnostic and therapeutic decision making, and the use of vasopressors. In addition, the effects of vasopressors on end organs with particular focus on renal hemodynamics is reviewed. Clinical Manifestations and Recognition of Hemodynamic Shock HS is classically described as an acute clinical syndrome initiated by ineffective perfusion, resulting in severe dysfunction of organs vital to survival Continue reading >>

Vasopressor Agentsinfluence Of Acidosis On Cardiac And Vascular Responsiveness

Vasopressor Agentsinfluence Of Acidosis On Cardiac And Vascular Responsiveness

VASOPRESSOR AGENTSInfluence of Acidosis on Cardiac and Vascular Responsiveness This article has been cited by other articles in PMC. Clinical observations have indicated that patients who are in shock and who have coexisting acidosis respond relatively poorly to sympathomimetic amines. In experiments with dogs, it was found that, in the presence of acidosis, the pressor action of epinephrine, norepinephrine and metaraminol was considerably reduced. The effect on cardiac rhythm was also considerably lessened after the pH value of the blood had been lowered. In view of these observations in animals, six human patients with profound shock and acidosis were studied. All had a considerably lessened pressor response to vasopressor agents; then, after elevation of the blood pH by intravenous infusion of a 1-molar solution of sodium lactate, responsiveness was restored. These observations emphasize the desirability of close observation of the acid-base status, and early treatment of acidosis, as an important aspect in the management of patients with shock. Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (662K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . Continue reading >>

Vascular Hyporesponsiveness To Vasopressors In Septic Shock: From Bench To Bedside

Vascular Hyporesponsiveness To Vasopressors In Septic Shock: From Bench To Bedside

Vascular hyporesponsiveness to vasopressors in septic shock: from bench to bedside Purpose: To delineate some of the characteristics of septic vascular hypotension, to assess the most commonly cited and reported underlying mechanisms of vascular hyporesponsiveness to vasoconstrictors in sepsis, and to briefly outline current therapeutic strategies and possible future approaches. Methods: Source data were obtained from a PubMed search of the medical literature with the following MeSH terms: Muscle, smooth, vascular/ physiopathology; hypotension/etiology; shock/physiopathology; vasodilation/physiology; shock/therapy; vasoconstrictor agents. Results: Nitric oxide (NO) and peroxynitrite are crucial components implicated in vasoplegia and vascular hyporeactivity. Vascular ATP-sensitive and calcium-activated potassium channels are activated during shock and participate in hypotension. In addition, shock state is characterized by inappropriately low plasma glucocorticoid and vasopressin concentrations, a dysfunction and desensitization of alpha-receptors, and an inactivation of catecholamines by oxidation. Numerous other mechanisms have been individualized in animal models, the great majority of which involve NO: MEK1/2ERK1/2 pathway, H2S, hyperglycemia, and cytoskeleton dysregulation associated with decreased actin expression. Conclusions: Many therapeutic approaches have proven their efficiency in animal models, especially therapies directed against one particular compound, but have otherwise failed when used in human shock. Nevertheless, high doses of catecholamines, vasopressin and terlipressin, hydrocortisone, activated protein C, and non-specific shock treatment have demonstrated a partial efficiency in reversing sepsis-induced hypotension. Septic shockVasopressorNitric Continue reading >>

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Lactic Acidosis Treatment & Management: Approach Considerations, Sodium Bicarbonate, Tromethamine

Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a septic focus, chemotherapy of malignant disorders, discontinuation of causative drugs, and dietary modification in certain types of congenital lactate acidosis. Cardiovascular collapse secondary to hypovolemia or sepsis should be treated with fluid replacement. Both crystalloids and colloids can restore intravascular volume, but hydroxyethyl starch solutions should be avoided owing to increased mortality. [ 21 ] Excessive normal saline administration can cause a nongap metabolic acidosis due to hyperchloremia, which has been associated with increased acute kidney injury. [ 32 ] Balanced salt solutions such as Ringer lactate and Plasma-Lyte will not cause a nongap metabolic acidosis and may reduce the need for renal replacement therapy; however, these can cause a metabolic alkalosis. [ 33 ] No randomized, controlled trial has yet established the safest and most effective crystalloid. If a colloid is indicated, albumin should be used. Despite appropriate fluid management, vasopressors or inotropes may still be required to augment oxygen delivery. Acidemia decreases the response to catecholamines, and higher doses may be needed. Conversely, high doses may exacerbate ischemia in critical tissue beds. Careful dose titration is needed to maximize benefit and reduce harm. Lactic acidosis causes a compensatory increase in minute ventilation. Patients may be tachypneic initially, but respiratory muscle fatigue can ensue rapidly a Continue reading >>

Lactate Clearance And Vasopressor Seem To Be Predictors For Mortality In Severe Sepsis Patients With Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis

Lactate Clearance And Vasopressor Seem To Be Predictors For Mortality In Severe Sepsis Patients With Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis

Lactate Clearance and Vasopressor Seem to Be Predictors for Mortality in Severe Sepsis Patients with Lactic Acidosis Supplementing Sodium Bicarbonate: A Retrospective Analysis Contributed equally to this work with: Su Mi Lee, Seong Eun Kim Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Contributed equally to this work with: Su Mi Lee, Seong Eun Kim Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliation: Department of Internal Medicine, Dong-A University, Busan, Korea Affiliations: Department of Internal Medicine, Dong-A University, Busan, Korea, Institute of Medical Science, Dong-A University College of Medicine, Busan, Korea Initial lactate level, lactate clearance, C-reactive protein, and procalcitonin in critically ill patients with sepsis are associated with hospital mortality. However, no study has yet discovered which factor is most important for mortality in severe sepsis patients with lactic acidosis. We sought to clarify this issue in patients with lactic acidosis who were supplementing with sodium bicarbonate. Data were collected from a single center between May 2011 and April 2014. One hundred nine patients with severe sepsis and lactic acidosis who were supplementing with sodium bicarbonate were included. The 7-day mortality rate was 71.6%. The survivors had higher albumin levels and lower SOFA, APACHE II scores, vasopressor use, and follow-up lactate levels at an elapsed time after their initial lactate levels were checked. In particular, a decrement in lactate clearance of at least 10% for the first 6 hours, 24 hours, and 48 hours of tre Continue reading >>

Use Of Bicarbonate In Lacticacidosis

Use Of Bicarbonate In Lacticacidosis

Five days post emergency colorectal surgery, an elderlywoman, following a brief period of chest pain a few hours earlier, developed progressive hypotension and tachycardia on the ward. She had a background of hypertension, type 2 diabetes and a chronic left foot ulcer. On examination she was found to be clammy, mottled and peripherally vasoconstricted with a GCS of 15/15. Her abdomen was soft and non-tender. Her initial ECG had showed no ischaemic changes and subsequent ECGs showed only a sinus tachycardia. Initial blood gas analysis showed a metabolic acidosis (pH 7.21 Lactate 2.8mmol/l, HCO3 11.1mmol/l with a pCO2 of 2.7kPa). A starting differential diagnosis of a cardiac event, a pulmonary embolism, critical ischaemia or sepsis related to a hip or foot ulcer were made. Urgent orthopaedic and vascular review were obtained, and it was deemed that neither the hip, ulcer or vascular insufficiency were a likely source for the deterioration. Initially it was planned to transfer her for a CTPA, however she became progressively unstable, was no longer fluid responsive, and was intubated on the ward and transferred to the intensive care unit (ICU) for stabilisation. On arrival on ICU she continued to deteriorate, and in addition to fluid resuscitation required a high dose noradrenaline infusion to maintain her blood pressure. Broad spectrum antibiotics were started, a bedside echocardiogram and blood tests performed and hydrocortisone started. Her metabolic acidosis continued to deteriorate, subsequent arterial blood gas showed a pH 6.91, Lactate of 13.7mmol/l, HCO3 7.7mmol/l, base excess -25mmol/l with a pCO2 of 5.4kPa. It was decided to correct this acidosis with a bicarbonate infusion and initially 200ml of 8.4% was given over an hour, based on correcting half the calcula 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 >>

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 >>

Effect Of Severe Acidosis On Vasoactive Effects Of Epinephrine And Norepinephrine In Human Distal Mammary Artery - Sciencedirect

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 >>

Levo And Ph | Allnurses

Levo And Ph | Allnurses

we had the most awful night last night starting at the beginning of the shift (1945). got a "code blue to c-section #2" page overhead so the sc and myself (the float/resource nurse) ran there and they're doing compressions on a lady who's not even closed up from her c-s yet! baby was good, but the mom ended up coming to us and it was basically an all night medical code with another official "code blue" called on her at around 0200. first time i've cried on the way home from work anyways, my question was about the levo not working for her bp. her ph was in the 7.2 range on the first abg and she got an amp of hco3. then on the next abg (maybe an hour later) it was down to 7.19. then, since the bp was dropping so fast, the pma in the unit said to just run it wide open, but it wasn't working. the primary nurse (who's very experienced, whereas i've barely been in the icu for 2 years) said that the levo wouldn't do anything for the bp while the ph was so low. can someone explain this? god, every night i work i seem to be overwhelmed with everything i don't know!!! Continue reading >>

Acid-base Balance Understanding Is Critical To Treat Patients

Acid-base Balance Understanding Is Critical To Treat Patients

Acid-Base Balance Understanding is Critical to Treat Patients By James Tanis, MD, NRP dvxxtrvscafftzcatwdtzeytyyc , Joseph E. DiCorpo, BSC, MMSc, PA , Daniel Friedman, DO, EMT-P , Mark Merlin, DO, EMT-P, FACEP Every critically ill patient we encounter in the field will have an acid-base derangement; therefore, an understanding of acid-base balance is critical to properly treat patients. First, its important you appreciate that every chemical reaction that occurs in the human body is regulated or substantially influenced by the hydrogen ion (H+) concentration in the surrounding tissue, from the way hemoglobin picks up and delivers oxygen to the tissues to the way that sugar, protein and fat are metabolized by the body. The regulation of hydrogen ions, which we measure as pH, is what acid-base balance refers to. The bodys concentration of hydrogen ions must be maintained within a strict range for optimal cellular function, and even a small deviation can significantly affect a patient.1Its a complex balancing act that you can affect based upon your assessment of the patients vital signs. An acid has a pH below 7.0 and an increased concentration of hydrogen ions, while an alkaline has a pH above 7.0 and a decreased concentration of hydrogen ions. The body maintains a slightly alkaline pH range of 7.35 to 7.45. Therefore, a pH higher than this range is in a state of alkalosis and a pH below this range is considered to be acidosis. A pH of 6.9 on the acid side and 7.8 on the alkaline side are considered non-compatible with life.1(See Table 1, above) An excess of acid is usually produced during the normal process of metabolism, so the body must rid itself of this excess acid to maintain the acid-base balance and keep a normal hydrogen ion concentration. Three defense mechanis 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 Antoine Kimmoun , Emmanuel Novy , Thomas Auchet , Nicolas Ducrocq , and Bruno Levy CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital de Brabois, Vandoeuvre-les-Nancy, 54511 France Universit de Lorraine, Nancy, 54000 France INSERM U1116, Groupe Choc, Facult de Mdecine, Vandoeuvre-les-Nancy, 54511 France Antoine Kimmoun, Email: [email protected] . Author information Copyright and License information Disclaimer Copyright Kimmoun et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution Continue reading >>

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

The Use Of Sodium Bicarbonate In The Treatment Of Acidosis In Sepsis: A Literature Update On A Long Term Debate

Volume2015(2015), Article ID605830, 7 pages The Use of Sodium Bicarbonate in the Treatment of Acidosis in Sepsis: A Literature Update on a Long Term Debate 1Internal Medicine Department, University Hospital of Patras, 26500 Rion, Greece 2University of Patras School of Medicine, 26500 Rion, Greece 3Intensive Care Department, Brugmann University Hospital, 1030 Brussels, Belgium 4Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA Received 22 March 2015; Revised 29 June 2015; Accepted 1 July 2015 Copyright 2015 Dimitrios Velissaris 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. Introduction. Sepsis and its consequences such as metabolic acidosis are resulting in increased mortality. Although correction of metabolic acidosis with sodium bicarbonate seems a reasonable approach, there is ongoing debate regarding the role of bicarbonates as a therapeutic option. Methods. We conducted a PubMed literature search in order to identify published literature related to the effects of sodium bicarbonate treatment on metabolic acidosis due to sepsis. The search included all articles published in English in the last 35 years. Results. There is ongoing debate regarding the use of bicarbonates for the treatment of acidosis in sepsis, but there is a trend towards not using bicarbonate in sepsis patients with arterial blood gas . Conclusions. Routine use of bicarbonate for treatment of severe acidemia and lactic acidosis due to sepsis is subject of controversy, and current opinion does not favor routine use of bicarbonates. However, available evidence is inconclusive, and Continue reading >>

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