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Sodium Bicarbonate Intracellular Acidosis

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 >>

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Volume 49, Issue 5 , May 1996, Pages 1262-1267 Effect of sodium bicarbonate on intracellular pH under different buffering conditions Author links open overlay panel JacquesLevrautDr. Effect of sodium bicarbonate on intracellular pH under different buffering conditions. Previous in vitro studies have reported a paradoxical exacerbation of intracellular acidosis following bicarbonate therapy due to the generated CO2 entering the cytoplasm. However, these studies were conducted in nonphysiological Hepes-buffered media. We compared the effect of a sodium bicarbonate load on the intracellular pH (pHi) of hepatocytes placed in nonbicarbonate (NBBS) or bicarbonate (BBS) buffering systems. The pHi of isolated rat hepatocytes was measured using the fluorescent pH sensitive dye BCECF and a single-cell imaging technique. Cells were placed in medium buffered with or Hepes. All media were adjusted to pH 7 with L-lactic acid or HCl. An acute 45mM sodium bicarbonate load was added to each medium and the changes in pHi were measured every three seconds for 90 seconds. The sodium bicarbonate load caused rapid cytoplasmic acidification of cells in NBBS (N = 50, P < 0.001). In contrast, hepatocytes in BBS underwent a marked increase in pHi (N = 50, P < 0.001) without any initial decrease in pHi. These differences were highly significant for the buffer (P < 0.01), but not for the acid used. We conclude that sodium bicarbonate exacerbates intracellular acidosis only in a NBBS. Hence, in vitro studies reporting a paradoxical intracellular acidosis following bicarbonate therapy cannot be extrapolated to the in vivo buffering conditions, and should not be used to argue against bicarbonate therapy. Continue reading >>

Buffer Therapies: Sodium Bicarbonate, Carbicarb And Tham - Deranged Physiology

Buffer Therapies: Sodium Bicarbonate, Carbicarb And Tham - Deranged Physiology

Buffer Therapies: Sodium Bicarbonate, Carbicarb and THAM This has only come up once in the exam. Question 27 from the first paper of 2009 asked the candidates to compare and contrast the pharmacology of carbicarb, sodium bicarbonate and THAM. The unusual feature was of course the fact that carbicarb is not available in Australia, and THAM is so rarely used that our local supply consists of imported ampoules with labels exclusively in German. The answer to Question 27 works best as a table; it is reproduced below to simplify revision. As far as literature references go, the majority are from the 1980s and 90s (back when buffer therapy was still considered a viable option in cardiac arrest, for example). One potentially relevant article is a 1998 paper by Bar-Joseph et al , which compared THAM, Carbicarb and sodium bicarbonate in a canine cardiac arrest model. An 8.4% (1mol/L) solution of NaHCO3which offers 1000mmol/L of HCO3-and Na+ions. An equimolar (300mmol/L) solution of Na2CO3and NaHCO3which offers 666mmol/L of HCO3-ions, and 1000mmol/L of Na+ions An organic amine buffer, otherwise known as tris-hydroxymethyl-aminomethane, or tromethamine. Eliminated renally, as well as being converted to CO2and exhaled (in process of buffering reactions). These two substances differ mainly in the amount of bicarbonate anion they add. Rapidly eliminated by the kidney; 75% is excreted in the urine after 8 hours. Sodium bicarbonate contributes HCO3-which is a natural buffer, thus replenishing the buffer systems of the body in a state of acidosis. The sodium carbonate component is supposed to act as a bicarbonae precursor, regenerating HCO3-buffers without increasing the PaCO2. THAM is a "third buffer" to complement the buffering capacity of endogenous HCO3-and body protein. At pH of 7 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 >>

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 >>

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 >>

Buffers

Buffers

Metabolic acidosis: Assessment and Treatment Acidosis is a frequent problem in critically-ill neonates. Buffers, such as sodium bicarbonate, are often used to treat metabolic acidosis. However, evidence to support the use or efficacy of this therapy is lacking. The etiology of a low pH must be understood to treat infants appropriately. Respiratory acidosis (increased CO2 on a blood gas and normal or near normal serum bicarbonate concentration) can only be treated by improving ventilation. Buffers will not help in this case, and may make the situation worse because infusion of NaHCO3 results in the immediate formation of CO2. For every mole of proton neutralized by bicarbonate, an equimolar amount of CO2 is produced. The futility of using NaHCO3 in a situation where ventilation is inadequate can be appreciated by the Henderson-Hesselbalch equation: pH - pK1 + log [HCO3-]/[CO2] (pK1 = 6.1) When ventilation is impaired, use of NaHCO3 will move the pH toward the pK of the equation, which is 6.1. In order to achieve a pH of 7.4, the molar ratio of HCO3 to CO2 must be 20:1. Thus, correction of acidosis depends on the removal of CO2. CO2 elimination depends on minute ventilation and pulmonary blood flow. Infusion of NaHCO3 in a patient with inadequate minute ventilation will worsen acidosis from CO2 accumulation and shift of the Henderson-Hesselbalch equation to the left. Compared to bicarbonate, CO2 rapidly crosses cell membranes, leading to intracellular acidosis. The bicarbonate lags behind in the vascular space, causing an increase in arterial pH. The intracellular acidosis associated with the use of NaHCO3 may not be reflected in the arterial blood gases we follow so carefully in our patients. The etiology of a metabolic acidosis (low pH associated with low serum bicarbo 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 >>

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 >>

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 >>

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 >>

Sodium Bicarb For Treatment Of Acidosis?

Sodium Bicarb For Treatment Of Acidosis?

SDN members see fewer ads and full resolution images. Join our non-profit community! Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? except, when a sudden intolerable decrease in pH is expected (ie release of a clamp or tourniquet), or when all else is failing (ie during a code when i want the pressors to work long enough to gain a foothold - little evidence for this). Agreed. Bicarb is only masking the acidosis and it is better to treat the cause rather than correct the pH. However, if things are beginning to go south in a hurry and you can't correct the problem rapidly enough then bicarb can be a benefit. Mostly by increasing the effectiveness of your inotropes, as Slavin said. Remember, some of the criticism of bicarb came from codes where removal of CO2 was impaired. We don't usually have that issue so some say it won't harm anything to give bicarb. I disagree, CO2 will Continue reading >>

Sodium Bicarbonate - An Overview | Sciencedirect Topics

Sodium Bicarbonate - An Overview | Sciencedirect Topics

Jamie McElrath Schwartz, ... Donald H. Shaffner, in Smith's Anesthesia for Infants and Children (Eighth Edition) , 2011 Sodium bicarbonate causes an acid-base reaction in which bicarbonate combines with hydrogen ion to form water and carbon dioxide, resulting in an elevated blood pH: Because sodium bicarbonate generates CO2, adequate alveolar ventilation must be present before its administration. As respiratory failure is the leading cause of cardiac arrest in children, caution should be taken before sodium bicarbonate administration in the face of preexisting respiratory acidosis. Sodium bicarbonate use during CPR is one of the most controversial issues in the literature related to cardiac arrest. This stems from lack of evidence of benefit during CPR in animals and humans, as well as the potential adverse effects associated with sodium bicarbonate administration. Literature on sodium bicarbonate use in CPR dates back to the 1960s, but there are little data demonstrating a beneficial impact on human survival (Levy, 1998). In animal models of resuscitation from cardiac arrest, sodium bicarbonate has been associated with increased survival in few studies and with no difference in survival in many studies (Andersen et al., 1967; Redding and Pearson, 1968; Kirimli et al., 1969; Lathers et al., 1989; Bleske et al., 1992; Neumar et al., 1995; Vukmir et al., 1995). Administration of sodium bicarbonate to humans experiencing cardiopulmonary arrest has been associated with increased mortality in retrospective reviews and nonblinded prospective studies (Suljaga-Pechtel et al., 1984; Skovron et al., 1985; Delooz and Lewi, 1989). Several studies in both humans and animals document deleterious effects on physiologic endpoints such as myocardial performance, arterial blood pressure 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 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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