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Bicarbonate In Lactic Acidosis

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use of Bicarbonate in Metabolic Acidosis Metabolic acidosis causes adverse metabolic effects (see Section 5.4 ). In particular the adverse effects on the cardiovascular system may cause serious clinical problems. Bicarbonate is an anion and cannot be given alone. Its therapeutic use is as a solution of sodium bicarbonate. An 8.4% solution is a molar solution (ie it contains 1mmol of HCO3- per ml) and is the concentration clinically available in Australia. This solution is very hypertonic (osmolality is 2,000 mOsm/kg). The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis (esp the adverse cardiovascular effects). Other reasons for use of bicarbonate in some cases of acidosis are: to promote alkaline diuresis (eg to hasten salicylate excretion) 8.7.2 Undesirable effects of bicarbonate administration In general, the severity of these effects are related to the amount of bicarbonate used. These undesirable effects include: 8.7.3 Important points about bicarbonate 1. Ventilation must be adequate to eliminate the CO2 produced from bicarbonate Bicarbonate decreases H+ by reacting with it to to produce CO2 and water. For this reaction to continue the product (CO2) must be removed. So bicarbonate therapy can increase extracellular pH only if ventilation is adequate to remove the CO2. Indeed if hypercapnia occurs then as CO2 crosses cell membranes easily, intracellular pH may decrease even further with further deterioration of cellular function. 2. Bicarbonate may cause clinical deterioration if tissue hypoxia is present If tissue hypoxia is present, then the use of bicarbonate may be particularly disadvantageous due to increased lactate production (removal of acidotic i Continue reading >>

Sodium Bicarbonate For The Treatment Of Lactic Acidosis - Sciencedirect

Sodium Bicarbonate For The Treatment Of Lactic Acidosis - Sciencedirect

Volume 117, Issue 1 , January 2000, Pages 260-267 Sodium Bicarbonate for the Treatment of Lactic Acidosis Author links open overlay panel Sean M.ForsytheMDa Gregory A.SchmidtMD, FCCPb Get rights and content Lactic acidosis often challenges the intensivist and is associatedwith a strikingly high mortality. Treatment involves discerning andcorrecting its underlying cause, ensuring adequate oxygen delivery totissues, reducing oxygen demand through sedation and mechanicalventilation, and (most controversially) attempting to alkalinize theblood with IV sodium bicarbonate. Here we review the literature toanswer the following questions: Is a low pH bad? Can sodium bicarbonateraise the pH in vivo? Does increasing the blood pH withsodium bicarbonate have any salutary effects? Does sodium bicarbonatehave negative side effects? We find that the oft-cited rationale forbicarbonate use, that it might ameliorate the hemodynamic depression ofmetabolic acidemia, has been disproved convincingly. Further, given thelack of evidence supporting its use, we cannot condone bicarbonateadministration for patients with lactic acidosis, regardless of thedegree of acidemia. 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 >>

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 >>

Q & A - Using Bicarbonate To Buffer Lactic Acid In Athletes

Q & A - Using Bicarbonate To Buffer Lactic Acid In Athletes

Home Resources Fitness Articles Coaching Corner Q & A - Using Bicarbonate To Buffer Lactic Acid In Athletes Q & A - Using Bicarbonate To Buffer Lactic Acid In Athletes Before I answer this question, lets examine a few basics of human physiology and exercise performance. When you exercise by jogging, cycling, lifting weights, or playing any sport, your muscles produce waste and breakdown products. These products build up in your muscles, and one of the biggest waste products of exercise is lactic acid. Lactic acid build up in your muscles is what makes your muscles burn during sprints or when trying to complete that last repetition on the bench press. The type of exercise you perform also affects how quickly this lactic acid accumulates in your muscles. The more anaerobic the exercise, the faster the lactic acid levels climb in your muscles. A maximum effort weight training session or a 40 yard sprint workout tends to make lactic acid levels soar much faster than a slow five mile jog since the first two are much more anaerobic. The body does have its own buffer system to prevent muscle pH from rising lactic acid and the muscle tissue becoming acidic. However, as a workout continues your bodys natural buffering system becomes unable to keep up with the acid levels. There are three main substances that buffer muscle cell tissue from rising pH levels and hydrogen ions: carnosine, phosphate, and bicarbonate (1). Interestingly, bicarbonate only accounts for less than ten percent of the bodys buffering potential. The bodys primary buffer in muscle tissue is carnosine with phosphate the secondary buffer (1). Where sodium bicarbonate becomes more important to athletes in terms of buffering potential is in the blood. Exercise not only increases the acidity in your muscles but al Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Is There A Role For Sodium Bicarbonate In Treating Lactic Acidosis From Shock?

Curr Opin Crit Care. 2008 Aug;14(4):379-83. doi: 10.1097/MCC.0b013e3283069d5c. Is there a role for sodium bicarbonate in treating lactic acidosis from shock? University of British Columbia, Critical Care Research Laboratories, Vancouver, British Columbia, Canada. Bicarbonate therapy for severe lactic acidosis remains a controversial therapy. The most recent 2008 Surviving Sepsis guidelines strongly recommend against the use of bicarbonate in patients with pH at least 7.15, while deferring judgment in more severe acidemia. We review the mechanisms causing lactic acidosis in the critically ill and the scientific rationale behind treatment with bicarbonate. There is little rationale or evidence for the use of bicarbonate therapy for lactic acidosis due to shock. We agree with the Surviving Sepsis guidelines recommendation against the use of bicarbonate for lactic acidosis for pH at least 7.15 and we further recommend a lower target pH of 7.00 or less. If bicarbonate is used, consideration must be given to slow infusion and a plan for clearing the CO2 that is produced and measuring and correcting ionized calcium as the resultant 10% drop may decrease cardiac and vascular contractility and responsiveness to catecholamines. When continuous renal replacement therapy is used during severe acidosis, we recommend bicarbonate-based replacement fluid over citrate as citrate may increase the strong ion gap. Effective therapy of lactic acidosis due to shock is to reverse the cause. Continue reading >>

Is Bicarbonate Therapy Beneficial In Lactic Acidosis.

Is Bicarbonate Therapy Beneficial In Lactic Acidosis.

IS BICARBONATE THERAPY BENEFICIAL IN LACTIC ACIDOSIS. ASB reviewing Cooper DJ et al. Ann Intern Med 1990 Apr 1. Critically ill patients with lactic acidosis usually receive sodium bicarbonate, in part to maintain cardiovascular sensitivity to circulating catecholamines. However, several side effects of bicarbonate, ... Critically ill patients with lactic acidosis usually receive sodium bicarbonate, in part to maintain cardiovascular sensitivity to circulating catecholamines. However, several side effects of bicarbonate, including hypercapnia and decreases in plasma ionized calcium, may depress myocardial contractility. This randomized crossover study compared the hemodynamic effects of sodium bicarbonate and a control solution (equimolar sodium chloride) in 14 patients. All patients had metabolic acidosis (serum bicarbonate less than 17 mmol/l) and increased lactate levels, and required mechanical ventilation; 11 patients had serious infections. Bicarbonate therapy produced a transient increase in arterial pH and serum bicarbonate levels, but its hemodynamic effects (transient increases in wedge pressure and cardiac output, and no change in blood pressure) were identical to those of sodium chloride. Moreover, plasma ionized calcium decreased and arterial PaCO2 increased after bicarbonate administration, possibly explaining the lack of hemodynamic improvement. Although it is conceivable that bicarbonate may provide benefits not measured in this study, those benefits do not seem to translate into improved hemodynamics in patients with severe lactic acidosis. Cooper DJ et al. Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis: a prospective, controlled clinical study. Ann Intern Med 1990 Apr 1 112 492498 Continue reading >>

The Use Of Sodium Bicarbonate In Patients With Severe Lactic Acidosis

The Use Of Sodium Bicarbonate In Patients With Severe Lactic Acidosis

Bicarbonate itself is not the only determinant of blood pH, as everyone knows. If you follow the physiochemical method of acid base disorders the pH is determined by subtracting strong cations (Na, K, Ca and Mg) from strong anions (Cl- and SO4). The SID increases due to bicarbonate administration because of an increase in sodium (bicarbonate is not a strong ion at all). However, bicarbonate drives Le Chateliers principle of chemical equilibrium: (HCO3 + H+ <==> H20 + CO2) which will drive CO2 production. Therefore if ventilation is fixed, or MAXED as in a patient with a Minute ventilation of 20L, excess CO2 production cannot be eliminated and a rise in CO2 negates any potentially beneficial effects of the bicarbonate itself. IF that gave you a migraine let me say it in another way. Sodium bicarb does increase the serum pH but it also increases CO2 production (think about ETCO2 jumping during a code when giving bicarb if you do this) and if you cannot blow off the CO2 with increased ventilation it has no net effect on the serum pH. *Another potentially MORE IMPORTANT problem with following the serum pH is that different compartments have different pHs (i.e; inner mitochondrial membrane, blood brain barrier etc) and CO2 readily crosses many of these membranes whereas bicarbonate itself does not. Therefore are we making the central veins for sampling more alkalemic at the cost of worsening intracellular and cerebral acidemia? Multiple studies have demonstrated that sodium bicarbonate will worsen acidosis in the brain and CSF (LP sampling and spectroscopy MRI). Several animal studies have shown that intracellular pH drops in RBCs, muscle, liver and lymphocytes. Conclusion: Yes bicarbonate can increase the serum pH, but its effects on intracellular pH are unknown, but likel Continue reading >>

Should Acidosis During Liver Transplantation Be Treated? | Anesthesiology | Asa Publications

Should Acidosis During Liver Transplantation Be Treated? | Anesthesiology | Asa Publications

Should Acidosis during Liver Transplantation Be Treated? David L. Bogdonoff, M.D., Assistant Professor of Anesthesiology and Surgery. Burkhard F. Spiekermann, M.D., Assistant Professor of Anesthesiology, Box 238, Department of Anesthesiology University of Virginia Health Sciences Center, Charlottesville, Virginia 22908. Should Acidosis during Liver Transplantation Be Treated? Anesthesiology 6 1995, Vol.82, 1540-1541.. doi: Anesthesiology 6 1995, Vol.82, 1540-1541.. doi: David L. Bogdonoff, Burkhard F. Spiekermann; Should Acidosis during Liver Transplantation Be Treated?. Anesthesiology 1995;82(6):1540-1541.. 2018 American Society of Anesthesiologists Should Acidosis during Liver Transplantation Be Treated? You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account To the Editor:--Shangraw et al. described the use of dichloroacetate during liver transplantation (OLTX). [1] Although we agree with the authors' concerns that too much NaHCO3is potentially problematic, we have taken a different approach to lactic acidosis during liver transplantation. There is conflicting evidence in the literature concerning the potential harm of acidosis. [2] Much evidence exists that there are no significant enhancements to myocardial performance and responsiveness to catecholamines as long as the pH is greater than 7.1. [3] Additionally, we believe that the acidosis in OLTX differs from most lactic acidoses in that it usually arises as a result of inadequate clearance by the diseased or excised liver rather than a situation where excessive production from tissue hypoperfusion or hypoxia overwhelms a normal liver. Although lactic acidosis during OLTX may result from tissue hypoperfusion, much of Continue reading >>

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy Of Lactic Acidosis: Alternatives To Sodium Bicarbonate

Therapy of Lactic Acidosis: Alternatives to Sodium Bicarbonate Part of the Clinical Physiology Series book series (CLINPHY) Lactic acidosis is the most common form of metabolic acidosis, and the current mortality from this condition is in excess of 50%. Because of its diverse pathophysiology, the clinical management of lactic acidosis is difficult. The mainstay of therapy has traditionally been the intravenous administration of sodium bicarbonate (NaHCO3), but recent clinical and experimental evidence strongly suggests that such therapy may in fact be detrimental. Lactic acidosis is generally defined as a metabolic acidosis due to the accumulation of lactic acid in the blood in excess of 5 mM, with an accompanying blood pH of less than 7.25. However, the mechanisms by which lactic acid accumulation occurs vary and include both the stimulation of lactate production and reductions of lactate metabolism. Clinically, the disorders of lactate metabolism are conveniently divided as either anaerobic (type A) or aerobic (type B) (16). The hallmark of type A lactic acidosis is tissue hypoxia, resulting in anaerobic lactic acid production. The most common causes of type A lactic acidosis are cardiopulmonary arrest and other states characterized by impaired cardiac performance, reduced tissue perfusion, and arterial hypoxemia. In these states, the hypoxia and circulatory insufficiency combine to reduce tissue oxygen availability, resulting in anaerobic metabolism and stimulation of lactic acid production. In type B lactic acidosis, on the other hand, tissue hypoxia appears not to be present, and lactic acid production is metabolically enhanced for other reasons in what is apparently an aerobic state. Examples of type B lactic acidosis include diabetes mellitus, certain malignanci Continue reading >>

Bicarbonate For Lactic Acidosis?

Bicarbonate For Lactic Acidosis?

After reading some recent posts on emcrit.org and doing some research on quantitative acid-base analysis, I decided to write a simple post on a related subject: the controversy of administering sodium bicarbonate (or simply, bicarb) in the setting of lactic acidosis. With severe sepsis commonly causing lactic acidosis, its worth exploring. At first cursory glance, how could this not work? Bicarb is a base and the problem with lactic acidosis is acid. So, one would assume adding a base to an acid would neutralize things. However, addingNaHCO3to a patient with lactic acidosis is not a good idea. We are going to distill some review articles on the subject so us juniors can remember the basics and maybe learn a thing or two about current truth. To simplify this presentation of complex ideas, Ive organized this into two parts: the good and the bad. The good part will detail the intuitive and advantageous aspects of using NaHCO3in lactic acidosis. The bad part will go into why its not so great or intuitive. I. NaHCO3will make solution more basic/raise the pH. II. Despiteraising arterial pH,NaHCO3does not raise the intracellular pH nor the CSF pH. III. NaHCO3 did not improve hemodynamics or catecholamine responsiveness. Continue on for the more detailed explanations. I. NaHCO3will make solution basic. Simply put, sodium bicarb will affect acid-base status towards alkalemia. But, not because of the bicarb. Rather, it is due to the sodium. NaHCO3s pH raising effects are from the Na+strong cation. The HCO3-trivially affects pH because itgets blown off as CO2. This is crucial; if the minute ventilation cannot be increased (i.e. CO2cannot be blown off), then the bicarb will not have a strong alkalinizing effect. Increased sodium increases the strong ion difference (SID). Increased Continue reading >>

Lactic Acidosis

Lactic Acidosis

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

Lactic Acidosis Treatment & Management

Lactic Acidosis Treatment & Management

Approach Considerations 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 and mechanical ventilation may be necessary. Alkali therapy remains controversial Continue reading >>

Payperview: Rapid Correction Of Severe Lactic Acidosis With Massive Isotonic Bicarbonate Infusion And Simultaneous Ultrafiltration - Karger Publishers

Payperview: Rapid Correction Of Severe Lactic Acidosis With Massive Isotonic Bicarbonate Infusion And Simultaneous Ultrafiltration - Karger Publishers

Rapid Correction of Severe Lactic Acidosis with Massive Isotonic Bicarbonate Infusion and Simultaneous Ultrafiltration Gudis S.M. Mangi S. Feinroth M. Rubin J.E. Friedman E.A. Berlyne G.M. I have read the Karger Terms and Conditions and agree. Patients with severe lactic acidosis and oliguria who receive large amounts of sodium bicarbonate may develop fluid overload and hyperosmolarity. We infused massive amounts of isotonic sodium bicarbonate and simultaneously removed the excess sodium and water with ultrafiltration if 2 patients with lactic acidosis. The first patient received 1,125 mmol of bicarbonate over 4.5 h with a rise in pH from 7.00 to 7.36 and in HCO3 from 3.5 to 15.7 mmol/l. The second received 968 mmol of bicarbonate over 5.25 h with a rise in pH from 7.00 to 7.27 and in HCO3 from 5.3 to 14 mmol/l. Blood pressure remained stable or rose, electrolytes normalized, excess fluid was removed, and a higher pH was maintained. Isotonic bicarbonate infusion with simultaneous ultrafiltration is a safe and rapid method of correcting the metabolic status of patients with severe lactic acidosis who have not responded to standard therapy. Continue reading >>

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