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Metabolic Acidosis Correction Formula

Calculation Of Sodium Bicarbonate Requirement In Metabolic Acidosis - Sciencedirect

Calculation Of Sodium Bicarbonate Requirement In Metabolic Acidosis - Sciencedirect

Volume 283, Issue 1 , JanuaryFebruary 1982, Pages 18-22 Calculation of Sodium Bicarbonate Requirement in Metabolic Acidosis Author links open overlay panel Patrick B.HazardM.D. Get rights and content Despite the host of complications which may be associated with intravenous sodium bicarbonate infusion, the use of this agent is a frequent necessity in patients with metabolic acidosis. No satisfactory formula for calculating bicarbonate dose has previously been described, although such an approach might be expected to reduce the incidence of these complications. The authors have devised a simple formula for bedside calculation of bicarbonate requirement in metabolic acidosis, designed to elevate the pH to the region about 7.30, and report their experience with the use of this formula in 13 instances. In all but one, the post-infusion pH was between 7.25 and 7.37, with a mean of 7.300.04 and no instances of serious overtitration. It is concluded that the formula is useful as a pragmatic aid in the management of patients with metabolic acidosis. 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 >>

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 >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

Acid Base Calculation Made Easy !

Acid Base Calculation Made Easy !

Posted by Ash from IP 74.138.144.66 on October 12, 2006 at 17:50:13: 6 steps to ABG analysis, go step by step in the very same order:- 1.Chk whether the pt is academic or alkalemic,by looking at the arterial pH (NL = 7.38 7.42) 2. Chk whether the ABG abnormality is due to a primary repiratory or metabolic disorder by chking the PCo2 levels( NL 38-42) and HCO3 levels (NL 22-26) 3. Now if there is respiratory component identified,chk whether this is acute or chronic respiratory acidosis or alkalosis. 4. Now if u identify a metabolic component ,chk whether it is high anion or normal anion gap M.Acidosis 5. Chk wether the respiratory system is adequetly compensating for this primary metabolic disorder. 6. Now u identify a high anion gap M.A,chk the corrected HCO3 level,y we do this coz to know wether there was a intial primary disorder ,before this new metabolic disorder developed. VERY IMPO FORMULAS :- U have to learn the formulas byheart) In Metabolic acidosis pH and HCO3 (DECREASES) So to compensate for every 1 mmol/l of drop in HCO3 , 1.2mmhg of PCO2 shld decrease So to compensate for every 1 mmol/l of increase HCO3, 0.07 mmhg of pco2 will increase. In Resp .Acidosis (PH - DECREASED and PCO2 AND HCO3 INCREASED) Acute R.acidosis:- For every 10 mmhg increase in pco2 , 1 mmol/l Hco3 shld increase Chronic R acidosis:- for every 10 mmhg increase in pco2, Hco3 increases by 3.5mmol/l In Respiratory Alkalosis pH INCREASED, pco2 and Hco3 DECREASED Acute R.alkalosis :- for every 10 mmhg decrease in PCO2 , hco2 decreases by 2meq/l Chronic :- for very 10 mmhg decrease in PCO2 ,hco3 decreases by 10mmol/l Winters equation :- this equation helps u to determine ,what the expected PCO2 lloks like when there is a metabolic acidosis:- Anion GAP :- done always when the disorder is metabol Continue reading >>

Metabolic Acidosis And Alkalosis

Metabolic Acidosis And Alkalosis

Page Index Metabolic Acidosis. Metabolic Alkalosis Emergency Therapy Treating Metabolic Acidosis Calculating the Dose Use Half the Calculated Dose Reasons to Limit the Bicarbonate Dose: Injected into Plasma Volume Fizzes with Acid Causes Respiratory Acidosis Raises Intracellular PCO2 Subsequent Residual Changes Metabolic Acidosis. The following is a brief summary. For additional information visit: E-Medicine (Christie Thomas) or Wikepedia Etiology: There are many causes of primary metabolic acidosis and they are commonly classified by the anion gap: Metabolic Acidosis with a Normal Anion Gap: Longstanding diarrhea (bicarbonate loss) Uretero-sigmoidostomy Pancreatic fistula Renal Tubular Acidosis Intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants Renal failure Metabolic Acidosis with an Elevated Anion Gap: lactic acidosis ketoacidosis chronic renal failure (accumulation of sulfates, phosphates, uric acid) intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, INH, toluene, sulfates, metformin. rhabdomyolysis For further details visit: E-Medicine (Christie Thomas). Treating Severe Metabolic Acidosis. The ideal treatment for metabolic acidosis is correction of the underlying cause. When urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. The best measure of the level of metabolic acidosis is the Standard Base Excess (SBE) because it is independent of PCO2. If it is decided to administer bicarbonate, the SBE and the size of the treatable space are used to calculate the dose required: Metabolic Alkalosis Etiology: Primary Metabolic alkalosis may occur from various causes including: Loss of acid via the urine, stools, or vomiting Transfer of Continue reading >>

Acid-base

Acid-base

Normal anion gap = 3-11 mEq/L. (8-16 if K is included in equation). Made upof unmeasured anions. Consist of proteins, mainly albumin. As a result areduction of albumin can reduce the baseline anion gap so that ahypoalbuminaemic patient may not have a high anion gap even in the presence of adisorder which usually produces an increased anion gap. Anion gap is reduced byapprox 2.5 mEq/L for every 10g/L fall in albumin. Alternatively a correctedvalue for a a normal anion gap (assuming K is included in calculation of aniongap) can be otained from: Corrected normal anion gap = 0.2[albumin] x 1.5[phosphate] where albumin is in g/L and phosphate in mmol/L - with hypokalaemia: classic distal (type 1) RTA - with hyperkalaemia: hyperkalaemic distal RTA , hypoaldosteronism (type 4) RTA Metabolic acidosis and respiratory alkalosis stimulation of respiratory centre by acidaemia causes a fall in PCO2 that in uncomplicated metabolic acidosis can be estimated from: lower than expected PCO2 indicates a superimposed respiratory alkalosis whereas a higher PCO2 indicates a respiratory acidosis. Equation only useful if plasma bicarbonate <20 mmol/L alternatively: a decrease in PCO2 of 0.16 kPa can be expected for a decrease in bicarbonate of 1 mmol/L. Ideally use nomogram complete respiratory compensation for primary metabolic acidosis does not occur respiratory compensation for acute acidosis tends to be somewhat greater than for chronic metabolic acidosis. Minimum level of PCO2 that can usually be attained is approx 1.3 kPa. Levels <2-2.7 kPa rarely maintained in chronic metabolic acidosis - combined hepatic and renal insufficiency (cirrhosis often associated with chronic respiratory alkalosis) - recent alcohol binge (alcoholic ketoacidosis + hyperventilation due to DTs) Metabolic acidosi 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 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 >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Metabolic Madness -- Mixed Disorders Sometimes patients have a combination of metabolic disorders. For example, a diabetic with ketoacidosis (anion gap metabolic acidosis) could also be vomiting and losing gastric acid (metabolic alkalosis). In the setting of an anion gap metabolic acidosis, calculation of the "corrected serum bicarbonate" (sometimes called the "gap-gap") can help you find an additional non-gap metabolic acidosis or metabolic alkalosis. Where AG = anion gap and the normal anion gap = 12. Remember, metabolic disturbances alter the serum HCO3. With an anion gap acidosis each "extra added acid" is reflected as one less bicarbonate. Therefore if you ingest 5 mEq/L of acid, the serum bicarbonate will be decreased by 5 mEq/L (24 - 5 = 19 mEq/L). In other words, 5 mEq/L of bicarbonate is consumed to neutralize the extra acid and the measured HCO3 would be decreased to 19 mEq/L. For example, if the calculated anion gap is 20 and the normal anion gap is 12, then there are 8 "extra acids" that are being consumed by bicarbonate. The measured serum bicarbonate would then be approximately 16 mEq/L (24 - 8). In other words, for a pure anion gap acidosis, when you add the amount of unmeasured acid/lost bicarbonate (Measured AG - Normal AG) to the Measured HCO3, the "Corrected HCO3" should equal a normal serum HCO3 (22-26 mEq/L). If the "corrected HCO3" is above normal (> 26 mEq/L), then you also have a metabolic alkalosis because there are extra bicarbonates. If the "corrected HCO3" is below normal (< 22 mEq/L), then you also have an non-anion gap acidosis bec Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid 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 >>

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 >>

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 >>

[calculation Of The Dose Of Sodium Bicarbonate For Correcting Metabolic Acidosis In Surgery With Circulation Arrest And Deep Hypothermia].

[calculation Of The Dose Of Sodium Bicarbonate For Correcting Metabolic Acidosis In Surgery With Circulation Arrest And Deep Hypothermia].

Anesteziol Reanimatol. 1997 Nov-Dec;(6):23-6. [Calculation of the dose of sodium bicarbonate for correcting metabolic acidosis in surgery with circulation arrest and deep hypothermia]. Dement'eva II , Rotman EV , Maba EN , Charnaia MA , Zolicheva NIu , Bogorad IV . The study was aimed at detecting the factors which determine the amount of 7% sodium bicarbonate solution needed to correct metabolic acidosis in patients subjected to repair surgery on the aorta involving long arrest of circulation under conditions of deep hypothermia. The total dose of 7% sodium bicarbonate solution was calculated as the sum of volumes of this solution needed to neutralize certain concentrations of underoxidized metabolites and BE. Accumulation of acid metabolites in tissues is caused by ineffective compensation of energy expenditure during warming of a patient after circulation arrest and deep hypothermia. After reperfusion injury to tissues, the release of these metabolites into the blood and further neutralization are appreciably slower during such operations than during other cardiovascular bypass interventions. That is why the routine method for calculating the dose of 7% sodium bicarbonate solution for correcting metabolic acidosis is not adequate in cases with abnormal body temperature. Estimation of the dose with consideration for venous blood temperature and pO2 is more correct. An algorithm of calculation is proposed. Continue reading >>

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