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Lactic Acidosis Treatment With Sodium Bicarbonate

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 >>

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 >>

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment of Acidosis: Sodium Bicarbonate and Other Drugs Lactic acidosis, defined as a lactate level > 5 mmol/1 and a pH 7.35, is far and away the most-important acidosis during critical illness and most of this discussion of acidosis treatment will focus on treatment of lactic acidosis. Even in the face of maximal supportive therapy, lactic acidosis is associated with a mortality of 60-90% [ 1 , 2 , 3 , 4 ], so physicians have long relied on treatments to lower the [H+], such as sodium bicarbonate. Less common than lactic acidosis, and much more amenable to conventional treatments, are ketoacidoses and respiratory acidosis, but these too occasionally prompt consideration of alkalinizing therapies. Lowering the [H+] in blood depends on manipulating the strong ion difference ([SID]), total concentration of non-volatile weak acid buffer (ATOT), or arterial CO2 tension (PaCO2), or raising the total concentration of weak bases, BTOT (normally sufficiently small that it can be ignored). Therefore, potential treatments include: 1. Raise [SID]: a) add strong cations: bicarbonate, carbicarb, dialysis b) remove strong anions: dichloroacetate (DCA), dialysis, thiamine, riboflavin, vasoactive drugs? 2. Lower the paCO2: raise VE or lower VD/VT or VCO2 3. Reduce ATOT: remove albumin, but very limited effect Acute Lung InjurySodium BicarbonateAcute Respiratory Distress SyndromeLactic AcidosisDiabetic Ketoacidosis These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Weil MH, Afifi AA (1970) Experimental and clinical studies on lactate and pyruvate as indicators of th Continue reading >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 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 >>

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 >>

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 >>

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 >>

Sodium Bicarbonate Use

Sodium Bicarbonate Use

metabolic acidosis leads to adverse cardiovascular effects bicarbonate must be administered in a solution as sodium bicarbonate 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000mOsm/kg) goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) Urinary alkalinisation (salicylate poisoning) Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8) Severe pulmonary hypertension with RVF to optimize RV function Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues POINTS TO REMEMBER WHEN USING BICARBONATE it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate ensure adequate ventilation to eliminate CO2 pro Continue reading >>

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