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8.4 Sodium Bicarbonate Intracellular Acidosis

Bicarbonate Therapy And Intracellular Acidosis.

Bicarbonate Therapy And Intracellular Acidosis.

1. Clin Sci (Lond). 1997 Dec;93(6):593-8. Bicarbonate therapy and intracellular acidosis. (1)Renal Laboratory, St Thomas' Hospital, London, U.K. 1. The correction of metabolic acidosis with sodium bicarbonate remainscontroversial. Experiments in vitro have suggested possible deleterious effectsafter alkalinization of the extracellular fluid. Disequilibrium of carbon dioxideand bicarbonate across cell membranes after alkali administration, leading to thephenomenon of 'paradoxical' intracellular acidosis, has been held responsible forsome of these adverse effects. 2. Changes in intracellular pH in suspensions ofleucocytes from healthy volunteers were monitored using a fluorescentintracellular dye. The effect in vitro of increasing extracellular pH with sodiumbicarbonate was studied at different sodium bicarbonate concentrations. Lacticacid and propionic acid were added to the extracellular buffer to mimicconditions of metabolic acidosis. 3. The addition of a large bolus of sodiumbicarbonate caused intracellular acidification as has been observed previously.The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate wasadded as a series of small boluses the reduction in intracellular pH was small.Under conditions of initial acidosis this was rapidly followed by intracellularalkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect isminimal when the conditions approximate those seen in clinical practice. Wesuggest that the observed small and transient lowering of intracellular pH isinsufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. 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 >>

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 >>

Acid Base In The Critically Ill - Part V - Enough With The Bicarb Already

Acid Base In The Critically Ill - Part V - Enough With The Bicarb Already

Today's topic comes from a debate I have been having with Steve Smith of the amazing EKG Blog . The main thrust of the debate started with this question Does Bicarb Fix pH if You Can't Increase Minute Ventilation? When you can adjust PaCO2 to maintain a certain value (i.e. you increase minute ventilation), bicarb will raise pH as evidenced by this animal study (Crit Care Med 1996; 24:827-834). However, if you can't blow off the CO2 then the effects on pH will not be there (J Pediatr 1977;91(2):287). In this study, NaBicarb did not correct the pH, while CarbiCarb did (Carbicarb: an effective substitute for NaHCO3 for the treatment of acidosis. (Surgery 102:835839). This review article recommends against bicarb for permissive hypercapnia (Intensive Care Med (2004) 30:347356). This study furthers the idea that NaBicarb is not all that great in closed systems (J Pediatr 1972;80(4):671) and then this discussion explores all of the biochemical reasons why administering bicarbonate as a rapid push in a closed system is a bad idea ( J Pediatr. 1972 Apr;80(4):681-2 .). Here is a quote from another review article (Anesthesiology 1990;72(6):1064): The key concept in the equation [above] is that pH is not related to the absolute value of either bicarbonate concentration nor PCo2, but rather to their ratio. When exogenous bicarbonate is administered during acidemia, bicarbonate reacts with hydrogen ions to form carbonic acid. Physicochemical equilibrium is shifted, favoring dissociation of carbonic acid to C02 and water. C02 partial pressure increases. The degree of alkaliniza- tion resulting from increased [HC03] is limited by the rise in Pco2* In (open) systems where increases in PCo2 are prevented (by ventilation) alkalination occurs. When CO2 cannot be eliminated, the pH of the Continue reading >>

Sodium Bicarbonate - Clinical Pharmacology

Sodium Bicarbonate - Clinical Pharmacology

FOR THE CORRECTION OF METABOLIC ACIDOSIS AND OTHER CONDITIONS REQUIRING SYSTEMIC ALKALINIZATION Sodium Bicarbonate Injection, USP is a sterile, nonpyrogenic, hypertonic solution of Sodium Bicarbonate (NaHCO3) in water for injection for administration by the intravenous route as an electrolyte replenisher and systemic alkalizer. Solution is offered in 8.4% concentration. See table in HOW SUPPLIED section for contents and characteristics. The solution has an approximate pH of 8.0 (7.5 to 8.5). Carbon dioxide may have been added to adjust the pH of the solution to approximately 8.0. The solution contains no bacteriostat, antimicrobial agent or added buffer and is intended only for use as a single-dose injection. When smaller doses are required, the unused portion should be discarded with the entire unit. Sodium Bicarbonate, 84 mg is equal to one milliequivalent each of Na+ and HCO3 . Sodium Bicarbonate, USP is chemically designated NaHCO3, a white crystalline powder soluble in water. Water for Injection, USP is chemically designated H2O. 7 First Aid Kit Must Haves For Your Medicine Cabinet Sodium Bicarbonate - Clinical Pharmacology Intravenous Sodium Bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis. Sodium Bicarbonate in water dissociates to provide sodium (Na+) and bicarbonate (HCO3 ) ions. Sodium (Na+) is the principal cation of the extracellular fluid and plays a large part in the therapy of fluid and electrolyte disturbances. Bicarbonate (HCO3 ) is a normal constituent of body fluids and the normal plasma level ranges from 24 to 31 mEq/liter. Plasma concentration is regulated by the kidney through acidification of the urine when there is a deficit or by alk Continue reading >>

Md51 - Anaesthesia_mcq

Md51 - Anaesthesia_mcq

MD51 [Jul01] An intravenous infusion of 8.4% sodium bicarbonate to a healthy adult maycause:A. HypotonicityB. Intracellular AcidosisC. Ionized HypercalcaemiaD.?Respiratory AlkalosisE. Rebound Metabolic AcidosisMD51b [Feb04] BicarbonateA. Complications include intracellular acidosisB. 100ml of 8.4% NaCO3 has 200 milliosmolesC.? Aug15 108. Side effect 8.4% NaHCO3 administration A. Intracellular acidosisB. Rebound metabolic acidosisC. ... Other options were easy to rule out =============================================================================================================== Brandis p38 - almost word for word (is that allowed?) 8.4% NaHCO3 is a one molar solution because the molecular weight of NaHCO3 is 84 = 84g/L = 8.4g/100mls.But each molecule of NaHCO3 dissociates into 2 particles in solution so the osmolality is double the molality. ie 2 osmoles/kg = 2000mOsm/kg = about 7 times the plasma osmolality. 100mls of the solution would then have 200 mOsm. The ECF HCO3 will cause decrease in H+ concentration. I think this then causes H+ to move out of the cells and K+ to move in. If this is true, B would also be incorrect. Don't know about C,D,E can some smart person help me? Rebound alkalosis is a complication so E would be incorrect. Also read somewhere that hypocalcaemia is a complication (but could be a trick q - ionised or total?) The dissociation of HCO3 would form CO2, which then diffuses into cell to cause intracellular acidosis (from P Kam's lecture notes). This intracellular acidosis has been mentioned before. Keeping in mind that the "neutral pH" intracellularly is thought to be anywhere from 6.8-7.0 where [H+]=[OH-]. See off-the-record discussions at queensland part one course. Lots of sources mention a paradoxical intracellular acidosis occuring followi Continue reading >>

Sodium Bicarbonate - Intravenous (iv) Dilution

Sodium Bicarbonate - Intravenous (iv) Dilution

The authors make no claims of the accuracy of the information contained herein; and these suggested doses and/or guidelines are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this document shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material. PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. Standard Dilutions [Amount of drug] [Infusion volume] [Infusion rate] May add ordered dose to empty viaflex bag or dilute in 50-1000ml. Monitor ABG's q2-3 hours to assess response. Administer IV either undiluted or diluted in other IV fluid (50-1000ml) depending on fluid status. Osmolarity: 2Na + gluc/18 + BUN/2.8 (nml: 280-295). **Note: treat hypokalemia or hypocalcemia first if present. In all cases, the primary goal in treating metabolic acidosis is to focus on reversal of the underlying process causing the acidosis. Examples: (1) Renal failure: dialysis if needed. (2) Alcoholic ketoacidosis: fluids, electrolytes, thiamine, folic acid. (3) Sepsis/shock: volume resuscitation, vasopressors, etc. (4) Salicylate intoxication: IV fluids, alkalinization of the urine, .... If there is a severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) correct with sodium bicarbonate. Sodium bicarb is also useful if the acidosis is due to inorganic acids (especially if renal disease is present). However, when the acidosis results from organic acids (lactic acid, acetoacetic acid, etc) the role of bicarbonate is controversial. In most cases of DKA or sever lactic acidosis the administration of sodium bicarbonat Continue reading >>

Use Of 1.27% And 1.4% Sodium Bicarbonate As Initial Fluid Therapy In Acute Resuscitation | Bja: British Journal Of Anaesthesia | Oxford Academic

Use Of 1.27% And 1.4% Sodium Bicarbonate As Initial Fluid Therapy In Acute Resuscitation | Bja: British Journal Of Anaesthesia | Oxford Academic

Adequate restoration of intravascular volume remains an important goal in the management of both surgical, medical and intensive care patients. Interest is now focusing on organ perfusion and function, as keyparameters by which adequate fluid replacement can be assessed. There has long been a debate over which is the ideal intravenous fluid for volume replacement, and controversy still exists in the literature as to whether colloid or crystalloid is most beneficial. 0.9% saline is the mainstay for volume depleted patients especially in the accident and emergency setting, although it is associated with potentially detrimental physiological effects. Many studies have shown that volume replacement with 0.9% saline can result in hyperchloremic acidosis1 2 3 thus exacerbating the existing acidosis due to tissue and organ hypo-perfusion. Although, Brill et al showed this base deficit to beassociated with a lower mortality compared to other causes of acidosis,4 concern is still voiced over the clinical significance of hyperchloremic acidosis. As chloride ions are present for electrochemical balance of the cations present and not specifically required, this problem could potentially be avoided by the used of a non-chloride containing solution. Sodium bicarbonate 8.4% used during resuscitation to correct acidaemia is a hypertonic solution containing 1000mmol of both sodium and bicarbonate per litre, and associated with several unfavourable effects. The significant osmotic sodium load may potentiate large fluid shifts, circulatory overload and pulmonary oedema. Hypernatraemia with dilution ofother serum electrolytes and rapid changes in HCO3/CO2 concentrations cause sudden electrical and pH shifts which contribute to cell damage and dysfunction. Corresponding abrupt increases in Continue reading >>

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

Nw Newborn Drug Protocol - Sodium Bicarbonate Pharmacology

0.25-0.50 mmol/kg/hour. Continuous IV infusion. Doses needs to be individualised and titrated according to response and to adverse effects (e.g. hypernatraemia) Not recommended for hypercapnia or hypernatraemic states. Caution in infants with renal impairment. Caution in preterm infants. Rapid infusion of hypertonic NaHCO3 has been incriminated in the pathogenesis of intraventricular haemorrhage in preterm infants. Sodium bicarbonate is the alkali most frequently employed for correction of metabolic acidosis. The drug is well absorbed from the gastrointestinal tract. Between 20-50% of an orally administered dose can be recovered in the form of expired carbon dioxide. The apparent bicarbonate space has been estimated to be 74% of body weight (range of 37-134%). Thus calculations of bicarbonate dosage are based on an apparent volume of distribution of 0.3 to 0.6 L/kg. Bicarbonate is rapidly metabolised to carbonic acid which rapidly dissociates into water and carbon dioxide. The carbon dioxide is excreted via the lungs. Venous irritation, soft tissue injury at the site of IV injection. Increased vascular volume, serum osmolarity, serum sodium. Continue reading >>

Sodium Bicarbonate

Sodium Bicarbonate

Treat acidosis with ventilation and perfusion Bicarbonate has not been shown to improve survival Bicarbonate may transiently depress CV parameters Bicarbonate 4.2% (0.5 meq/ml in 10 ml ampule) Bicarbonate 8.4% (1 meq/ml in 50 ml prefilled syringe) Equivalents of Sodium Bicarbonate (NaHCO3) Standard bicarb ampule is 50 meq in 50 ml Equivalent to 8.4 grams/dl or 4.2 grams/50 ml One ampule = 50 meq = 4.2 grams = 50 mmoles Do not use 8.4% in child under 3 months old Bicarbonate 8.4% is hyperosmolar (2000 mosm/L) Intraventricular bleeding risk in Preterm Infant Use in Child over 3 months old and adults Sodium Bicarbonate 8.4%: 1 amp (50 meq or 50 mmol) Base actual dosing on standard pharmacology texts IV infusion must be slow even in emergency Initial Dose: 1 meq/kg IV or IO over 1-2 minutes Additional Dose: 0.5 meq/kg IV or IO every 10 minutes Base repeat dosages on Arterial Blood Gas Continuous Infusion: 5% bicarbonate (297.5 meq/500ml) VI. Dosing: Adults for Urine Alkalinization Irrigate IV or IO tubing with Normal Saline Irrigate before and after bicarbonate infusion Intracranial Hemorrhage in newborns (hyperosmolality) Use only 4.2% bicarbonate in under age 3 months Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Sodium Bicarbonate." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window FPnotebook.com is a rapid access, point-of-care medical reference for primary care and emergency clinicians. Started in 1995, this collection now contains 6552 interlinked topic pages divided into a tree of 31 specialty books and 722 chapters. Content is updated monthly with systematic literatu Continue reading >>

Response To 100mmol Of Sodium Bicarbonate

Response To 100mmol Of Sodium Bicarbonate

Response to 100mmol of Sodium Bicarbonate These are the physiological effects of infusing 100mmol of concentrated (8.4%) sodium bicarbonate into a patient. A 1 molar solution of sodium bicarbonate is what you are giving. The osmolality is 2000mosm/L. Let us unfocus from the movements of water and sodium, as they are predictable, and their patterns already well rehearsed. Let us instead observe the traffic of the HCO3- anion. Let us pretend that suddenly 100mmol of this anion is dumped into the extracellular fluid (and being easily water soluble, it frolics merrily through the extracellular fluid compartments, distributing evenly among them). This means 25mmol of HCO3- is now in the vascular compartment and 75 mmol is in the interstitial fluid. The extracellular concentration of bicarbonate pre-infusion in our model is 24mmol/L, which gives us 336 mmol overall. A sudden increase by 100mmol (to a total content of 436 mmol) would cause the concentration to rise to 31.1mmol/L. The change in extracellular bicarbonate concentration following a bicarbonate infusion From the above calculations, it would seem that the volume of distribution for bicarbonate is the same as the extracellular fluid, 14L or about 0.2L/Kg. Experimental findings demonstrate that this is not the case. Simplistic fluid-filled cylinder models of distribution do not do justice to the complexity of bicarbonate distribution. The major source of complexity, is the tendency of the bicarbonate to buffer hydrogen ions and become "lost" in the process, converting to water and carbon dioxide. This tendency, as one might imagine, is dependent on the presence of acidosis or alkalosis. An excellent article has examined this relationship, and I will clumsily paraphrase Figure 5 from it below. The figure describes the Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

Sodium Bicarbonate Injection

Sodium Bicarbonate Injection

Sodium bicarbonate is a systemic alkalinizing agent. It most often is administered IV in the treatment of metabolic and respiratory acidosis. Sodium bicarbonate is also used in the acute treatment of hyperkalemia, although it should be kept in mind that this represents palliative treatment for this condition. Sodium bicarbonate is sometimes used for urinary alkalinization. Despite being a highly effective antacid, sodium bicarbonate is rarely used for the chronic treatment of peptic ulcer disease because it can be absorbed and can affect systemic acid-base balance. Sodium bicarbonate was in use prior to 1938 and approved by the FDA at its inception. Mechanism of Action: After oral administration, sodium bicarbonate neutralizes hydrochloric acid in the stomach, forming sodium chloride, carbon dioxide, and water. Excess bicarbonate ions are absorbed in the small intestine. Thus, all of a dose of exogenous sodium bicarbonate eventually reaches the extracellular fluid, and a mild alkalosis can result. This usually is corrected quickly by the renal system in patients with normal renal function. After IV administration, sodium bicarbonate dissociates to bicarbonate ions, which constitute the conjugate base portion of the body's extracellular buffer system (bicarbonate/carbonic acid buffer). Administration of sodium bicarbonate will restore acid-base balance in patients with metabolic or respiratory acidosis; however, metabolic alkalosis can result from the use of sodium bicarbonate. Excess bicarbonate ions that result from the administration of sodium bicarbonate are excreted in the urine, alkalizing the urine. This alkalization decreases renal absorption and increases the clearance of certain drugs, intoxicants, weak acids, and blood pigments. Pharmacokinetics: Sodium bicar 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 >>

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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