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Bicarb In Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis.

Bicarbonate Therapy In Severe Metabolic Acidosis.

1. J Am Soc Nephrol. 2009 Apr;20(4):692-5. doi: 10.1681/ASN.2007121329. Epub 2008Mar 5. Bicarbonate therapy in severe metabolic acidosis. (1)Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. The utility of bicarbonate administration to patients with severe metabolicacidosis remains controversial. Chronic bicarbonate replacement is obviouslyindicated for patients who continue to lose bicarbonate in the ambulatorysetting, particularly patients with renal tubular acidosis syndromes or diarrhea.In patients with acute lactic acidosis and ketoacidosis, lactate and ketonebodies can be converted back to bicarbonate if the clinical situation improves.For these patients, therapy must be individualized. In general, bicarbonateshould be given at an arterial blood pH of < or =7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to apatient with severe acidemia is apt to be all but irresistible. Interventionshould be restrained, however, unless the clinical situation clearly suggestsbenefit. Here we discuss the pros and cons of bicarbonate therapy for patientswith severe metabolic acidosis. 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 Deficit Calc

Sodium Bicarbonate Deficit Calc

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 severe lactic acidosis the administration of sodium bicarbonate does not decrease mortality even when the acidosis is severe. In sum, sodium bicarbonate should be reserved for severe cases of acidosis only (pH <7.2 and serum bicarbonate levels <10-12 meq/L). This can be accomplished by adding 1 to 3 ampoules of sodium bicarb to D5W or 1/2NS. IV-push administration should be reserved for cardiac life support and not metabolic acidosis. Sodium bicarbonate administration: It is recommended that 50% of total deficit be given over 3 to 4 hours, and the remainder replaced over 8-24 hours. The usual initial target ((desired HCO3- concentration): 10 - 12 mEq/L, which should bring the blood pH to ~7.20. The subsequent goal is to increase the bicarbonate level to 15 meq/L over the next 24 hours. Replace 50% over 3 to 4 hours and the reminder over 24 hours. Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than 4 to 8 mEq/L over 6 to 12 hours to avoid the risks of over-alkalinization (paradoxical CNS acidosis; decr 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 >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany 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. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

OVERVIEW a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate CAUSES pathophysiological mechanism: (i) A gain of strong acid (ii) A loss of base the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). CLASSIFICATION high anion gap Lactate Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents Ketones Renal Normal anion gap Chloride Acetazolamide and Addisons GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Extras – RTA MAINTENANCE the disorder is maintained as long as the primary cause persists. in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute. EFFECTS Respiratory Effects hyperventilation (Kussmaul respirations) – this is the compensatory response shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Cardiovascular Effects depression of myocardial contractility sympathetic overactivity resistance to the effects of catecholamines peripheral arteriolar vasodilatation venoconstriction of peripheral veins vasoconstriction of pulmonary arteries (increased Continue reading >>

Sodium Bicarbonate Dosage

Sodium Bicarbonate Dosage

If acid-base status is available, dosages should be calculated as follows: 0.2 x weight (kg) x base deficit. HCO3 (mEq) required = 0.5 x weight (kg) x [24 - serum HCO3 (mEq/L)]. Moderate metabolic acidosis: 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. Severe metabolic acidosis: 90 to 180 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour during the first hour. If acid-base status is not available, dosages should be calculated as follows: 2 to 5 mEq/kg IV infusion over 4 to 8 hours; subsequent doses should be based on patient's acid-base status. Moderate metabolic acidosis: 325 to 2000 mg orally 1 to 4 times a day. One gram provides 11.9 mEq (mmoL) each of sodium and bicarbonate. Usual Adult Dose for Diabetic Ketoacidosis Although sodium bicarbonate is approved for the treatment of metabolic acidosis, data have shown that the use of this drug may be harmful in certain clinical settings such as lactic acidosis, acidosis with tissue hypoxia, uremia, severe cardiac dysfunction or arrest, and diabetic ketoacidosis. Most experts only allow for its use when tissue perfusion and ventilation are maximized and the arterial pH is 7.1 or lower. If sodium bicarbonate is used to treat diabetic ketoacidosis, the initial dosage is 50 mEq sodium bicarbonate in 1 L of appropriate IV solution to be given once. Insulin therapy may obviate the need for bicarbonate therapy since it will promote glucose utilization and decrease the production of ketoacids. Usual Adult Dose for Urinary Alkalinization 50 to 150 mEq sodium bicarbonate diluted in 1 L of D5W to be intravenously infused at a rate of 1 to 1.5 L/hour. 325 to 2000 mg orally 1 to 4 times a day. O Continue reading >>

Sodium Bicarbonate - Journal Of Emergency Medical Services

Sodium Bicarbonate - Journal Of Emergency Medical Services

Your paramedic crew responds to a cardiac arrest in a large shopping complex. Fortunately, the patient has all the links in the chain of survival in place. Bystander CPR has been initiated, and an automated external defibrillator (AED) was in place in the shopping complex and deployed, the 9-1-1 system was accessed, and your unit arrived rapidlywithin six minutes from the time of call. As you approach, you assess the situation, interview bystanders and begin the final linkearly advanced care. For patients in cardiac arrest, the American Heart Association (AHA) has determined this provides the best opportunity for someone to survive cardiac arrest in the prehospital environment. The patient remains in ventricular fibrillation (v fib) despite several AED shocks. You gain IV access and begin pharmacological therapy. After administering epinephrine and amiodarone, you consider sodium bicarbonate as directed by protocol. You recognize that over the past several years AHA has deemphasized the use of sodium bicarbonate. But what is the controversy? When is it appropriate to give sodium bicarbonate, and are paramedics using it to its fullest advantage? Seasoned paramedics will recall giving multiple ampules of sodium bicarbonate during a cardiac arrest, but today it appears to be an afterthought. Sodium bicarbonate (NaHCO3) is used primarily to combat acidosis, although its the treatment of choice in certain cases of overdose. It works by mixing with lactic acid that forms in low perfusion states and in periods of inadequate oxygenation, such as shock and cardiac arrest. It is then converted to a form of carbonic acid that turns into carbon dioxide, and in turn, is expelled through the lungs during ventilation. Primarily, NaHCO3 works as a buffer by mixing with acids within th 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 >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Sodium Bicarbonate In Severe Metabolic Acidosis

Sodium Bicarbonate In Severe Metabolic Acidosis

Sodium Bicarbonate in Severe Metabolic Acidosis Sodium Bicarbonate in Severe Metabolic Acidosis Aka: Sodium Bicarbonate in Severe Metabolic Acidosis No evidence that Sodium Bicarbonate improves outcomes Treat acidosis with ventilation and perfusion Documented severe Metabolic Acidosis associated with: Diabetic Ketoacidosis with Arterial pH <6.9 Adequate ventilation and perfusion are critical V. Dosing: Adults (if arterial pH <6.9 to 7.0) Sodium Bicarbonate 1 amp (50 meq or 100 mmol) Dose full bag or 400 cc of 50 meq if pH <6.9 Dose half bag or 200 cc of 25 meq if pH 6.9 - 7.0 If arterial pH <6.9 on recheck in 2 hours Solution should contain <0.5 meq/ml bicarbonate Sodium should be <155 meq/L (NS concentration) Every bicarb ampule contains 2000 meq/L Sodium Limit infusion rate to <1 meq/kg/hour bicarbonate Example: 20 kg child with arterial pH <6.9 Maximum replacement is 40 meq bicarbonate Contains 40 meq Na + 38 meq Na = 78 meq Na Sodium concentration is 156 meq/L (same as NS) Limit this 20 kg child's rate to 20 meq/hour Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Sodium Bicarbonate in Severe Metabolic Acidosis." 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 Continue reading >>

Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?

Metabolic Acidosis And Kidney Disease: Does Bicarbonate Therapy Slow The Progression Of Ckd?

Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD? Correspondence and offprint requests to: Csaba P. Kovesdy; E-mail: [email protected] Search for other works by this author on: Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Csaba P. Kovesdy; Metabolic acidosis and kidney disease: does bicarbonate therapy slow the progression of CKD?, Nephrology Dialysis Transplantation, Volume 27, Issue 8, 1 August 2012, Pages 30563062, Metabolic acidosis is a common complication associated with progressive loss of kidney function. The diminishing ability of the kidneys to maintain acidbase homeostasis results in acid accumulation, leading to various complications such as impairment in nutritional status, worsened uremic bone disease and an association with increased mortality. In addition to these adverse effects which are related to acid retention, metabolic acidosis may also cause kidney damage, possibly through the stimulation of adaptive mechanisms aimed at maintaining acidbase homeostasis in the face of decreasing kidney function. Recent clinical trials have suggested that correction or prevention of metabolic acidosis by alkali administration is able to attenuate kidney damage and to slow progression of chronic kidney disease (CKD), and may hence offer an effective, safe and affordable renoprotective strategy. We review the physiology and pathophysiology of acidbase homeostasis in CKD, the mechanisms whereby metabolic acidosis may be deleterious to kidney function, and the results of clinical trials suggesting a benefit of alkali therapy, with special attention to details related to the practical implementation of the results of these trials. bicarbonate , chronic kidney disease , metabolic ac Continue reading >>

Use Of Bicarbonate In Patients With Metabolic Acidosis

Use Of Bicarbonate In Patients With Metabolic Acidosis

Use of Bicarbonate in Patients With Metabolic Acidosis Myra F. Ellis is a clinical nurse in the cardiothoracic intensive care unit at Duke University Hospital in Durham, North Carolina. Corresponding author: Myra F. Ellis, rn, msn, ccrn-csc, Duke Medical Pavilion 7 West (CTICU), Duke University Hospital, Box 100302, Durham, NC 27710 (e-mail: myra.ellis{at}duke.edu). Q: Please elaborate on why bicarbonate is not used unless the ph is 7.2 or less. Many nurses, particularly cardiovascular nurses, have difficulty understanding this when the patients blood pressure is low and the patient is acidotic with large negative base excesses. Please explain the physiological basis for the decision and clarify why it doesnt work or it is not beneficial. A: Myra F. Ellis, RN, MSN, CCRN-CSC, replies: Bicarbonate therapy is sometimes prescribed to treat acute metabolic acidosis, an acid-base disorder that is characterized by a primary decrease in the concentration of bicarbonate ions (HCO3), a compensatory decrease in the partial pressure of carbon dioxide (PaCO2), and a decrease in serum pH. 1 Acidosis is considered severe when the pH is less than 7.20. Assuming an appropriate ventilatory response, this blood pH would be associated with a serum HCO3 concentration of less than 10 mEq/L. 2 Two general mechanisms cause metabolic acidosis: a true HCO3 deficit (such as renal or gastrointestinal losses) or a net addition of strong acids (such as toxins, diabetic ketoacidosis, or lactic acid production). 1 , 3 Bicarbonate replacement is beneficial for patients with true bicarbonate deficits, but not in patients with metabolic acidosis caused by an increase in acid production. 1 , 3 Most experts currently recommend reserving bicarbonate replacement for patients with severe acidemia (pH < 7.1) 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 >>

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 s Continue reading >>

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