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Lactic Acidosis Treatment With Sodium Bicarbonate

Sodium Bicarbonate For The Treatment Of Lactic Acidosis.

Sodium Bicarbonate For The Treatment Of Lactic Acidosis.

Sodium bicarbonate for the treatment of lactic acidosis. Department of Medicine, University of Chicago School of Medicine, Chicago, IL, USA. Lactic acidosis often challenges the intensivist and is associated with a strikingly high mortality. Treatment involves discerning and correcting its underlying cause, ensuring adequate oxygen delivery to tissues, reducing oxygen demand through sedation and mechanical ventilation, and (most controversially) attempting to alkalinize the blood with IV sodium bicarbonate. Here we review the literature to answer the following questions: Is a low pH bad? Can sodium bicarbonate raise the pH in vivo? Does increasing the blood pH with sodium bicarbonate have any salutary effects? Does sodium bicarbonate have negative side effects? We find that the oft-cited rationale for bicarbonate use, that it might ameliorate the hemodynamic depression of metabolic acidemia, has been disproved convincingly. Further, given the lack of evidence supporting its use, we cannot condone bicarbonate administration for patients with lactic acidosis, regardless of the degree of acidemia. 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 >>

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 >>

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 >>

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment Of Metformin-associated Lactic Acidosis With Closed Recirculation Bicarbonate-buffered Hemodialysis

Treatment of Metformin-Associated Lactic Acidosis With Closed Recirculation Bicarbonate-Buffered Hemodialysis To the Editor. The use of massive amounts of intravenous (IV) sodium bicarbonate in the management of lactic acidosis seems necessary as soon as the acidosis becomes severe.1 However, some patients have an apparent resistance to this alkali therapy.2 In addition, intensive administration of sodium bicarbonate carries the combined risks of volume and sodium overload. Several authors tried hemodialysis (HD) or peritoneal dialysis (PD) but, most of the time, the precarious hemodynamic state of these patients limits the use of conventional HD.3,4 The new possibilities allowing the use of dialysate containing bicarbonate in HD have led us to try this method in the case of a metformin-treated diabetic with severe lactic acidosis.5 Report of a Case. A 64-year-old woman was admitted to the hospital in severe shock. Despite chronic renal failure (serum creatinine level of 300 moles/L, she was given 1,700 mg/day of metformin for six Continue reading >>

Acidosis

Acidosis

When your body fluids contain too much acid, it’s known as acidosis. Acidosis occurs when your kidneys and lungs can’t keep your body’s pH in balance. Many of the body’s processes produce acid. Your lungs and kidneys can usually compensate for slight pH imbalances, but problems with these organs can lead to excess acid accumulating in your body. The acidity of your blood is measured by determining its pH. A lower pH means that your blood is more acidic, while a higher pH means that your blood is more basic. The pH of your blood should be around 7.4. According to the American Association for Clinical Chemistry (AACC), acidosis is characterized by a pH of 7.35 or lower. Alkalosis is characterized by a pH level of 7.45 or higher. While seemingly slight, these numerical differences can be serious. Acidosis can lead to numerous health issues, and it can even be life-threatening. There are two types of acidosis, each with various causes. The type of acidosis is categorized as either respiratory acidosis or metabolic acidosis, depending on the primary cause of your acidosis. Respiratory acidosis Respiratory acidosis occurs when too much CO2 builds up in the body. Normally, the lungs remove CO2 while you breathe. However, sometimes your body can’t get rid of enough CO2. This may happen due to: chronic airway conditions, like asthma injury to the chest obesity, which can make breathing difficult sedative misuse deformed chest structure Metabolic acidosis Metabolic acidosis starts in the kidneys instead of the lungs. It occurs when they can’t eliminate enough acid or when they get rid of too much base. There are three major forms of metabolic acidosis: Diabetic acidosis occurs in people with diabetes that’s poorly controlled. If your body lacks enough insulin, keton 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 >>

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 >>

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium Bicarbonate In The Critically Ill Patient With Metabolic Acidosis

Sodium bicarbonate in the critically Ill patient with metabolic acidosis Uso de bicarbonato de sdio na acidose metablica do paciente gravemente enfermo Lactic acidosis is an acid-base imbalance frequently found in critically ill patients. It is associated with a poor prognosis. Despite the substantial body of evidence that critical levels of acidemia have several adverse effects on cell function, the use of sodium bicarbonate to treat lactic acidosis in critically ill patients remains highly controversial. This article aimed at: 1) analyzing the main differences between hyperchloremic and organic acidoses, with high anion gap; 2) comparing the risks associated with critical levels of acidemia with those associated with the use of sodium bicarbonate; 3) critically analyzing the literature evidence about the use of sodium bicarbonate for the treatment of lactic acidosis in critically ill patients, with an emphasis on randomized control trials in human beings; and 4) providing a rationale for the judicious use of sodium bicarbonate in that situation. Descriptors: lactic acidosis, diabetic ketoacidosis, sodium bicarbonate, septic shock. A acidose ltica um distrbio do equilbrio cido-base muito frequente em pacientes internados em unidades de terapia intensiva e est associado a um mau prognstico. Embora exista um acmulo substancial de evidncias de que nveis crticos de acidemia provocam inmeros efeitos adversos sobre o funcionamento celular, a utilizao de bicarbonato de sdio para o tratamento da acidose ltica em pacientes gravemente enfermos permanece alvo de controvrsias. Neste artigo, pretendemos: 1) analisar as principais diferenas entre as acidoses hiperclormicas e as acidoses orgnicas, com nion gap (AG) elevado, visando embasar a discusso sobre os fundamentos da terapia Continue reading >>

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 >>

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 >>

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 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 >>

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 >>

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 >>

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