DOCSLIB.ORG

Rational Treatment of Acid-Base Disorders

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Rational Treatment of Acid-Base Disorders Practical Therapeutics Drugs 39 (6): 841-855, 1990 0012-6667/90/0006-0841/$07.50/0 © ADlS Press Limited All rights reserved. DRUG03353 Rational Treatment of Acid-Base Disorders Margaret L. McLaughlin and Jerome P. Kassirer Nephrology Division, Department of Medicine, New England Medical Center, and Department of Med icine, Tufts Un iversity School of Medi cine, Boston , Massachusetts, USA Contents Summary , ,.., , ,.., ,.., ,..,.. 842 I. Metabolic Acidosis 843 1.1 Clinical Manifestations 843 1.2 Causes of Metabolic Acidosis 843 1.3 Treatment of Metabolic Acidosis 844 1.3.1 General Remarks 844 1.3.2 Loss of Alkaline Gastrointestinal Fluids 845 1.3.3 Carbonic Anhydrase Inhibitors 845 1.3.4 Urinary Diversion , 845 1.3.5 Lactic Acidosis 845 1.3.6 Diabetic Ketoacidosis 846 1.3.7 Alcoholic Ketoacidosis 846 1.3.8 Renal Tubular Acidosis ll47 1.3.9 Renal Acidosis (Uraemic Acidosis) 848 2. Metabolic Alkalosis , 848 2.1 Clinical Manifestations 848 2.2 Causes of Metabolic Alkalosis 848 2.3 Treatment of Metabolic Alkalosis 849 2.3.1 Milk-Alkali Syndrome 850 2.3.2 Combined Therapy with Nonabsorbabl e Alkali and Exchange Resins 850 2.3.3 Acute Alkali Loading 850 2.3.4 Gastric Fluid Losses 850 2.3.5 Diuretic Therapy , 851 2.3.6 Posthypercapnic Alkalosis 851 2.3.7 Primary Aldosteron ism 851 2.3.8 Bartter's Syndrom e 85I 2.3.9 Cushing's Syndrome 852 3. Respiratory Acidosis 852 3.1 Clinical Manifestations 852 3.2 Causes of Respiratory Acidosis , 852 3.3 Treatment of Respiratory Acidosis , 852 4. Respiratory Alkalosis 852 842 Drugs 39 (6) 1990 4.1 Clinical Manifestations 853 4.2 Causes of Respiratory Alkalosis 853 4.3 Treatment of Respiratory Alkalosis 853 5. Mixed Acid-Base Disturbances 853 5.1 Metabolic and Respiratory Acidosis 853 5.2 Metabolic and Respiratory Alkalosis 853 5.3 Metabolic Acidosis and Respiratory Alkalosis 854 5.4 Metabolic Alkalosis and Respiratory Acidosis 854 6. Conclusions 854 Summary Acid-base derangements are encountered frequently in clinical practice and many have life-threatening implications. Treatment is dependent on correctly identifying the acid­ base disorder and , whenever possible, repairing the underlying causal process. Bicarb­ onate is the agent of choice for the treatment of acute metabolic acidosis. Controversy surrounds the use of alkali therapy in lactic acidosis and diabetic ketoacidosis, but bi­ carbonate should clearly be administered for severe acidos is. In most patients with mild to moderate chloride-responsive metabolic alkalosis, providing an adequate amount of a chloride salt will restore acid-base balance to normal over a matter of days. In contrast, therapy of the chloride-resistant metabolic alkaloses is best directed at the underlying disease . When alkalaemia is severe, administering hydrochloric acid or a hydrochloric acid precursor may be necessary. Treatment of respiratory acidosis should be targeted at restoring ventilation; alkali should be administered only for superimposed metabolic acidosis . The therapy of res­ piratory alkalosis is centred on reversal of the root cause; short of this goal, there is no effective treatment of primary hypocapnia. The coexistence of more than one acid-base disorder (i.e. a mixed disorder) is not uncommon. When plasma bicarbonate concentration and arterial carbon dioxide tension (paCOl) are altered in opposite directions, extreme shifts in pH may occur. In such cases, it is imperative that the nature of the disturbance is identified early and therapy directed at both disorders. Disturbances of acid-base balance are wide­ ical reactions rapidly achieve equilibrium condi­ spread in practice and many pose serious threats tions, allowing a simple expression of their rela­ to the well-being of patients. A rational approach tionship (Henderson 1908): to the treatment of acid-base disorders is depend­ (Eq. I) ent on an understanding of the basic pathophys­ iological mechanisms that give rise to them. Cor­ Thus, hydrogen ion concentration is a function rect identification of the underlying disturbance of the ratio of the arterial carbon dioxide tension may suggest new diagnostic avenues, as well as (paC02) to the bicarbonate concentration. It fol­ provide a guide to specific, and often life-saving, lows that changes in hydrogen ion concentration therapy. and, consequently, all acid-base disorders, result The carbonic acid-bicarbonate buffer system from changes in one or other of these 2 variables. plays a central role in acid-base balance because of Acid-base disturbances are classified into 4 pri­ its prevalence and its relation to physiological reg­ mary disorders - metabolic acidosis, metabolic al­ ulatory mechanisms. The hydration of dissolved kalosis, respiratory acidosis and respiratory alka­ C02 forms carbonic acid which then dissociates to losis - and various combinations of these disorders yield bicarbonate and hydrogen ions. These chem- categorised as mixed disturbances. Treatment of Acid-Base Disorders 843 1. Metabolic Acidosis duced capacity of the kidneys to excrete acid (see table I). Metabolic acidosis is initiated by a reduction in Loss of bicarbonate-rich fluid results in deple­ plasma bicarbonate concentration. The most im­ tion of extracellular fluid volume and a reduction mediate consequence of a fall in bicarbonate con­ in bicarbonate concentration. At the same time, centration is an increase in plasma acidity. Cor­ chloride concentration rises as the remaining responding changes in cerebral hydrogen ion chloride is confined to a smaller volume of distri­ concentration are sensed by central chemorecep­ bution. Such a hyperchloraemic metabolic acidosis tors, giving rise to reflex hyperventilation, a fall in results from diarrhoea (Darrow et al. 1949), pan­ paC02, and a consequent attenuation in the degree creatic or biliary drainage, administration of car­ of acidification. bonic anhydrase inhibitors, and certain forms of urinary diversion . Administration of hydrochloric 1.1 Clinical Manifestations acid and substances which give rise to hydrochloric The clinical manifestations of metabolic acid­ acid when metabolised (e.g. ammonium chloride, osis include effects on the cardiovascular and pul­ monary systems, the circulation, oxygen transport, Table I. Causes of metabolic acidosis (from Kassirer et al. 1989. and potassium metabolism (Mitchell et al. 1972; with permission) Relman 1972). Hyperventilation, or Kussmaul res­ Normal anion gap pirations, is one of the most readily apparent Loss of bicarbonate manifestations of severe acidosis. Myocardial dys­ Diarrhoea function due to acidosis and a reduced threshold Small bowel losses for ventricular fibrillation also occur. Acidosis has Carbonic anhydrase inhibitors several effects on vascular tone, producing direct Ureterosigmoidostomy Ileal loop bladder arterial vasodilatation, indirect sympathetic-me­ Dilutional acidosis diated vasoconstriction, and direct venous vaso­ Addition of hydrochloric acid constriction. In addition, acute acidaemia shifts the Ammonium chloride haemoglobin dissociation curve to the right, but Arginine-HCI acidosis-induced depletion in cellular 2,3-diphos­ Lysine-HCI Total parenteral nutrition phoglycerate shifts the curve back in a matter of Disproportionate failure of renal tubular function hours (Mitchell et al. 1972). Hyperkalaemia is a Renal tubular acidosis frequent accompaniment of acute metabolic acid­ Mild renal failure osis and has been attributed to transcellular shifts Hyporeninaemic hypoaldosteronism Adrenal insufficiency ofpotassium in response to acidosis. However, cer­ tain types of metabolic acidosis due to organic acids Increased anion gap (e.g, lactic acid and acetoacetic acid) have little or Overproduction of organic acids no direct effect on serum potassium concentration Lactic acidosis (Fulop 1979). When hyperkalaemia does occur in Diabetic ketoacidosis Starvation ketosis these kinds of acidosis, decreased renal function or Alcoholic ketoacidosis insulin deficiency is probably more important in Methyl alcohol ingestion its genesis. Ethylene glycol ingestion Paraldehyde ingestion 1.2 Causes of Metabolic Acidosis Salicylate intoxication Infantile organic acidosis Three distinct pathological processes work alone Severe renal failure or in concert to produce metabolic acidosis: (a) loss Acute Chronic of bicarbonate; (b) addition of acid; and (c) re- 844 Drugs 39 (6) 1990 lysine-HC1, and arginine-HCl) also produce hy­ small additional decrement in bicarbonate concen­ perchloraemic acidosis. The normal kidney re­ tration or increase in paC02. In normal individ­ sponds to the reduction in plasma bicarbonate by uals, administered bicarbonate distributes through augmenting net acid excretion, resulting in the con­ a space of approximately 40 to 50%of bodyweight, servation of sodium with newly generated bicarb­ but the space of distribution may be more than onate and in the excretion of chloride and hydro­ twice that large when plasma bicarbonate is ex­ gen ion. tremely low (Garella et al. 1973). In addition , there Overproduction of organic acids results in a fall is often no way to assess the magnitude of organic in plasma bicarbonate concentration and an in­ acid production or on-going alkali loss. Conse­ crease in the plasma concentration of the anion of quently, estimates of bicarbonate space to predict that acid. In contrast to the pattern seen with direct a desired increment in plasma bicarbonate must be loss of bicarbonate or administration of substances considered a first approximation only. Given the that yield hydrochloric acid, the acidosis
Load more

Recommended publications
  • Acid-Base Abnormalities in Dogs with Diabetic Ketoacidosis: a Prospective Study of 60 Cases
    325 Acid-base abnormalities in dogs with diabetic ketoacidosis: a prospective study of 60 cases Distúrbios ácido-base em cães com cetoacidose diabética: estudo prospectivo de 60 casos Ricardo DUARTE1; Denise Maria Nunes SIMÕES1; Khadine Kazue KANAYAMA1; Márcia Mery KOGIKA1 1School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo-SP, Brazil Abstract Diabetic ketoacidosis (DKA) is considered a typical high anion gap metabolic acidosis due to the retention of ketoanions. The objective of this study was to describe the acid-base disturbances of dogs with DKA and further characterize them, according to their frequency, adequacy of the secondary physiologic response, and occurrence of mixed disturbances. Sixty dogs with DKA were enrolled in the study. Arterial blood pH and gas tensions, plasma electrolytes, serum b-hydroxybutyrate (b-OHB), glucose, albumin and urea concentrations were determined for all dogs included in the study. All dogs were evaluated individually and systematically by the traditional approach to the diagnosis of acid- base disorders. Most of the dogs had a high anion gap acidosis, with appropriated respiratory response (n = 18; 30%) or concurrent respiratory alkalosis (n = 14; 23%). Hyperchloremic acidosis with moderated to marked increases in b-OHB was observed in 18 dogs (30%) and 7 of these patients had concurrent respiratory alkalosis. Hyperchloremic acidosis with mild increase in b-OHB was observed in 6 dogs (10%). Four dogs (7%) had a high anion gap acidosis with mild increase in b-OHB and respiratory alkalosis. Most of dogs with DKA had a high anion gap acidosis, but mixed acid-base disorders were common, chiefly high anion gap acidosis and concurrent respiratory alkalosis, and hyperchloremic acidosis with moderated to marked increases in serum b-OHB.
    [Show full text]
  • Pathophysiology of Acid Base Balance: the Theory Practice Relationship
    Intensive and Critical Care Nursing (2008) 24, 28—40 ORIGINAL ARTICLE Pathophysiology of acid base balance: The theory practice relationship Sharon L. Edwards ∗ Buckinghamshire Chilterns University College, Chalfont Campus, Newland Park, Gorelands Lane, Chalfont St. Giles, Buckinghamshire HP8 4AD, United Kingdom Accepted 13 May 2007 KEYWORDS Summary There are many disorders/diseases that lead to changes in acid base Acid base balance; balance. These conditions are not rare or uncommon in clinical practice, but every- Arterial blood gases; day occurrences on the ward or in critical care. Conditions such as asthma, chronic Acidosis; obstructive pulmonary disease (bronchitis or emphasaemia), diabetic ketoacidosis, Alkalosis renal disease or failure, any type of shock (sepsis, anaphylaxsis, neurogenic, cardio- genic, hypovolaemia), stress or anxiety which can lead to hyperventilation, and some drugs (sedatives, opoids) leading to reduced ventilation. In addition, some symptoms of disease can cause vomiting and diarrhoea, which effects acid base balance. It is imperative that critical care nurses are aware of changes that occur in relation to altered physiology, leading to an understanding of the changes in patients’ condition that are observed, and why the administration of some immediate therapies such as oxygen is imperative. © 2007 Elsevier Ltd. All rights reserved. Introduction the essential concepts of acid base physiology is necessary so that quick and correct diagnosis can The implications for practice with regards to be determined and appropriate treatment imple- acid base physiology are separated into respi- mented. ratory acidosis and alkalosis, metabolic acidosis The homeostatic imbalances of acid base are and alkalosis, observed in patients with differing examined as the body attempts to maintain pH bal- aetiologies.
    [Show full text]
  • Evaluation and Treatment of Alkalosis in Children
    Review Article 51 Evaluation and Treatment of Alkalosis in Children Matjaž Kopač1 1 Division of Pediatrics, Department of Nephrology, University Address for correspondence Matjaž Kopač, MD, DSc, Division of Medical Centre Ljubljana, Ljubljana, Slovenia Pediatrics, Department of Nephrology, University Medical Centre Ljubljana, Bohoričeva 20, 1000 Ljubljana, Slovenia J Pediatr Intensive Care 2019;8:51–56. (e-mail: [email protected]). Abstract Alkalosisisadisorderofacid–base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Keywords Respiratory alkalosis is a consequence of dysfunction of respiratory system’s control ► alkalosis center. There are no pathognomonic symptoms. History is important in the evaluation ► children of alkalosis and usually reveals the cause. It is important to evaluate volemia during ► chloride physical examination. Treatment must be causal and prognosis depends on a cause. Introduction hydrogen ion concentration and an alkalosis is a pathologic Alkalosis is a disorder of acid–base balance defined by process that causes a decrease in the hydrogen ion concentra- elevated pH of the arterial blood. According to the origin, it tion. Therefore, acidemia and alkalemia indicate the pH can be metabolic or respiratory. Metabolic alkalosis is char- abnormality while acidosis and alkalosis indicate the patho- acterized by primary elevation of the serum bicarbonate that logic process that is taking place.3 can result from several mechanisms. It is the most common Regulation of hydrogen ion balance is basically similar to form of acid–base balance disorders.
    [Show full text]
  • ./0) (Mm...)Conte H
    BRITISH 511 Auc,.Auo. 25,25, 19621962 CARBON-MONOXIDE POISONIN6 MEDICAL JOURNAL Br Med J: first published as 10.1136/bmj.2.5303.511 on 25 August 1962. Downloaded from Case Reports HYPERVENTILATION IN Case 1.-A woman aged 61 was found with her head in CARBON-MONOXIDE POISONING a gas-oven. On admission to hospital she was deeply unconscious, with a generalized increase of muscle tone. BY pulse rate 140 a minute, and blood-pressure 110/70 mm. Hg. G. L. LEATHART, M.D., M.R.C.P. There was marked hyperventilation suggesting the possibility of coincident aspirin poisoning. A stomach wash-out, how- Nuflield Department of Industrial Health, the Medical ever, revealed no tablets, and a sample of urine collected School, King's College, Newcastle upon Tyne a few hours later contained no detectable salicylate. In 24 hours she had recovered fully and was transferred to a The recent revival of interest in the use of 5% or 7% mental hospital. carbogen in the treatment of carbon-monoxide poisoning Case 2.-An accountant aged 40 was working late in his has prompted the description of four unusual cases in office and was seen to be well at 9.15 p.m. At 8.45 a.m. which gross hyperventilation occurred. The investiga- the following morning he was found in the office with the tion of these cases was not very thorough, but such cases gas turned on but unlit. He was deeply unconscious with are seen so seldom that it is felt that even this incomplete strikingly deep and rapid respiration suggesting a condition report may be of value in stimulating further research.
    [Show full text]
  • TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam
    TITLE: Acid-Base Disorders PRESENTER: Brenda Suh-Lailam Slide 1: Hello, my name is Brenda Suh-Lailam. I am an Assistant Director of Clinical Chemistry and Mass Spectrometry at Ann & Robert H. Lurie Children’s Hospital of Chicago, and an Assistant Professor of Pathology at Northwestern Feinberg School of Medicine. Welcome to this Pearl of Laboratory Medicine on “Acid-Base Disorders.” Slide 2: During metabolism, the body produces hydrogen ions which affect metabolic processes if concentration is not regulated. To maintain pH within physiologic limits, there are several buffer systems that help regulate hydrogen ion concentration. For example, bicarbonate, plasma proteins, and hemoglobin buffer systems. The bicarbonate buffer system is the major buffer system in the blood. Slide 3: In the bicarbonate buffer system, bicarbonate, which is the metabolic component, is controlled by the kidneys. Carbon dioxide is the respiratory component and is controlled by the lungs. Changes in the respiratory and metabolic components, as depicted here, can lead to a decrease in pH termed acidosis, or an increase in pH termed alkalosis. Slide 4: Because the bicarbonate buffer system is the major buffer system of blood, estimation of pH using the Henderson-Hasselbalch equation is usually performed, expressed as a ratio of bicarbonate and carbon dioxide. Where pKa is the pH at which the concentration of protonated and unprotonated species are equal, and 0.0307 is the solubility coefficient of carbon dioxide. Four variables are present in this equation; knowing three variables allows for calculation of the fourth. Since pKa is a constant, and pH and carbon dioxide are measured during blood gas analysis, bicarbonate can, therefore, be determined using this equation.
    [Show full text]
  • Package Insert Template for Oral Rehydration Salt (Ors)
    PACKAGE INSERT TEMPLATE FOR ORAL REHYDRATION SALT (ORS) Brand or Product Name [Product name] Powder for Oral Solution [Product name] Liquid in the form of solution/suspension Name and Strength of Active Substance(s) Sodium chloride ………………(12.683% w/v) Glucose, anhydrous…………...(65.854% w/v) Potassium chloride………...…...(7.317% w/v) Trisodium citrate, dihydrate ….(14.146% w/v) Product Description [Visual description of the appearance of the product (eg colour etc)] Eg:A white to off-white colour granules, when dissolved in water, forms an orange colour solution. Pharmacodynamics The reconstituted solution contains a mixture of sodium and potassium salts along with glucose, which facilitates the absorption of sodium and potassium from the intestine. Water is drawn from the bowel by the osmotic effect. As well as “drying up” the stools, the dehydration and loss of electrolytes caused by the diarrhoea is corrected by the water and electrolytes absorbed. Pharmacokinetics Glucose After oral administration glucose is completely absorbed by a sodium dependent uptake mechanism exhibiting saturation kinetics. Blood levels return to normal within two hours of ingestion. Potassium Chloride No specific control mechanisms limit absorption of potassium, which is usually complete. Potassium is excreted largely by the kidneys, though 10% is excreted by the colonic mucosa. Potassium excretion is reduced in patients with renal impairment and in the elderly, so extreme caution should be used in treating such patients with potassium salts. Sodium Bicarbonate Kinetics are determined by the physiological state of the patient at the time. Sodium Chloride Readily absorbed from the gastrointestinal tract. Gut absorption, particularly in the jejunum is enhanced by the addition of glucose.
    [Show full text]
  • Acid-Base Physiology & Anesthesia
    ACID-BASE PHYSIOLOGY & ANESTHESIA Lyon Lee DVM PhD DACVA Introductions • Abnormal acid-base changes are a result of a disease process. They are not the disease. • Abnormal acid base disorder predicts the outcome of the case but often is not a direct cause of the mortality, but rather is an epiphenomenon. • Disorders of acid base balance result from disorders of primary regulating organs (lungs or kidneys etc), exogenous drugs or fluids that change the ability to maintain normal acid base balance. • An acid is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. • A base is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. • Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. • When hydrochloric acid is dissolved in water all or almost all of the H in the acid is released as H+. • When lactic acid is dissolved in water a considerable quantity remains as lactic acid molecules. • Lactic acid is, therefore, said to be a weaker acid than hydrochloric acid, but the lactate ion possess a stronger conjugate base than hydrochlorate. • The stronger the acid, the weaker its conjugate base, that is, the less ability of the base to accept H+, therefore termed, ‘strong acid’ • Carbonic acid ionizes less than lactic acid and so is weaker than lactic acid, therefore termed, ‘weak acid’. • Thus lactic acid might be referred to as weak when considered in relation to hydrochloric acid but strong when compared to carbonic acid.
    [Show full text]
  • Mechanical Ventilation Bronchodilators
    A Neurosurgeon’s Guide to Pulmonary Critical Care for COVID-19 Alan Hoffer, M.D. Chair, Critical Care Committee AANS/CNS Joint Section on Neurotrauma and Critical Care Co-Director, Neurocritical Care Center Associate Professor of Neurosurgery and Neurology Rana Hejal, M.D. Medical Director, Medical Intensive Care Unit Associate Professor of Medicine University Hospitals of Cleveland Case Western Reserve University To learn more, visit our website at: www.neurotraumasection.org Introduction As the number of people infected with the novel coronavirus rapidly increases, some neurosurgeons are being asked to participate in the care of critically ill patients, even those without neurological involvement. This presentation is meant to be a basic guide to help neurosurgeons achieve this mission. Disclaimer • The protocols discussed in this presentation are from the Mission: Possible program at University Hospitals of Cleveland, based on guidelines and recommendations from several medical societies and the Centers for Disease Control (CDC). • Please check with your own hospital or institution to see if there is any variation from these protocols before implementing them in your own practice. Disclaimer The content provided on the AANS, CNS website, including any affiliated AANS/CNS section website (collectively, the “AANS/CNS Sites”), regarding or in any way related to COVID-19 is offered as an educational service. Any educational content published on the AANS/CNS Sites regarding COVID-19 does not constitute or imply its approval, endorsement, sponsorship or recommendation by the AANS/CNS. The content should not be considered inclusive of all proper treatments, methods of care, or as statements of the standard of care and is not continually updated and may not reflect the most current evidence.
    [Show full text]
  • Important Prescribing Information
    Important Prescribing Information Subject: Temporary importation of 8.4% Sodium Bicarbonate Injection to address drug shortage issues June 14, 2019 Dear Healthcare Professional, Due to the current critical shortage of Sodium Bicarbonate Injection, USP in the United States (US) market, Athenex Pharmaceutical Division, LLC (Athenex) is coordinating with the U.S. Food and Drug Administration (FDA) to increase the availability of Sodium Bicarbonate Injection. Athenex has initiated temporary importation of another manufacturer’s 8.4% Sodium Bicarbonate Injection (1 mEq/mL) into the U.S. market. This product is manufactured and marketed in Australia by Phebra Pty Ltd (Phebra). At this time, no other entity except Athenex Pharmaceutical Division, LLC is authorized by the FDA to import or distribute Phebra’s 8.4% Sodium Bicarbonate Injection, (1 mEq/mL), 10 mL vials, in the United States. FDA has not approved Phebra’s 8.4% Sodium Bicarbonate Injection but does not object to its importation into the United States. Effective immediately, and during this temporary period, Athenex will offer the following presentation of Sodium Bicarbonate Injection: Sodium Bicarbonate Injection, 8.4% (1mEq/mL), 10mL per vial, 10 vials per carton Ingredients: sodium bicarbonate, water for injection, disodium edetate and sodium hydroxide (pH adjustment) Marketing Authorization Number in Australia is: 131067 Phebra’s Sodium Bicarbonate Injection contains the same active ingredient, Sodium Bicarbonate, in the same strength and concentration, 8.4% (1 mEq/mL) as the U.S. registered Sodium Bicarbonate Injection, USP by Pfizer’s subsidiary, Hospira. However, it is important to note that Phebra’s Sodium Bicarbonate Injection (1 mEq/mL), is provided only in a Single Use 10 mL vials, whereas Hospira’s product is provided in 50 mL single-dose vials and syringes.
    [Show full text]
  • Parenteral Nutrition Primer: Balance Acid-Base, Fluid and Electrolytes
    Parenteral Nutrition Primer: Balancing Acid-Base, Fluids and Electrolytes Phil Ayers, PharmD, BCNSP, FASHP Todd W. Canada, PharmD, BCNSP, FASHP, FTSHP Michael Kraft, PharmD, BCNSP Gordon S. Sacks, Pharm.D., BCNSP, FCCP Disclosure . The program chair and presenters for this continuing education activity have reported no relevant financial relationships, except: . Phil Ayers - ASPEN: Board Member/Advisory Panel; B Braun: Consultant; Baxter: Consultant; Fresenius Kabi: Consultant; Janssen: Consultant; Mallinckrodt: Consultant . Todd Canada - Fresenius Kabi: Board Member/Advisory Panel, Consultant, Speaker's Bureau • Michael Kraft - Rockwell Medical: Consultant; Fresenius Kabi: Advisory Board; B. Braun: Advisory Board; Takeda Pharmaceuticals: Speaker’s Bureau (spouse) . Gordon Sacks - Grant Support: Fresenius Kabi Sodium Disorders and Fluid Balance Gordon S. Sacks, Pharm.D., BCNSP Professor and Department Head Department of Pharmacy Practice Harrison School of Pharmacy Auburn University Learning Objectives Upon completion of this session, the learner will be able to: 1. Differentiate between hypovolemic, euvolemic, and hypervolemic hyponatremia 2. Recommend appropriate changes in nutrition support formulations when hyponatremia occurs 3. Identify drug-induced causes of hypo- and hypernatremia No sodium for you! Presentation Outline . Overview of sodium and water . Dehydration vs. Volume Depletion . Water requirements & Equations . Hyponatremia • Hypotonic o Hypovolemic o Euvolemic o Hypervolemic . Hypernatremia • Hypovolemic • Euvolemic • Hypervolemic Sodium and Fluid Balance . Helpful hint: total body sodium determines volume status, not sodium status . Examples of this concept • Hypervolemic – too much volume • Hypovolemic – too little volume • Euvolemic – normal volume Water Distribution . Total body water content varies from 50-70% of body weight • Dependent on lean body mass: fat ratio o Fat water content is ~10% compared to ~75% for muscle mass .
    [Show full text]
  • Tissue and Renal Response to Chronic Respiratory Acidosis
    TISSUE AND RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS Norman W. Carter, … , Donald W. Seldin, H. C. Teng J Clin Invest. 1959;38(6):949-960. https://doi.org/10.1172/JCI103878. Research Article Find the latest version: https://jci.me/103878/pdf TISSUE AND RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS * By NORMAN W. CARTER,t DONALD W. SELDIN AND H. C. TENG (From the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas) (Submitted for publication October 27, 1958; accepted February 26, 1959) The elevation of pCO2 which occurs during to enter during respiratory acidosis is the red cell respiratory acidosis is accompanied by a rise in (1, 3, 9). The role of renal losses in the produc- the concentration of bicarbonate and a fall in the tion of hypochloremia is less certain. In short concentration of chloride in serum (1). The term human experiments, chloruresis has not increased bicarbonate concentration results from been observed during respiratory acidosis (5, both cellular and renal responses. The cellular 10). However, in the rat, Epstein, Branscome response is characterized by the exchange of ex- and Levitin observed increased chloride excre- tracellular hydrogen ions for intracellular cations, tion during the first 24 hours of an imposed re- thereby contributing to the elevation of the ex- spiratory acidosis (11). tracellular concentration of bicarbonate (2, 3). The present study in the rat was undertaken in The renal factors responsible for the elevated an attempt to delineate the pattern of renal and bicarbonate concentration may be divided into extrarenal responses to respiratory acidosis.
    [Show full text]
  • Observations Compensatory Hypochloraemic Alkalosis In
    Letters 871 tended to the DQ-LTR13 integration, where we also find a con- 2. Pascual M, Martin J, Nieto A et al. (2001) Distribution of tribution of DQ-LTR13 to RA susceptibility in DQ8-positive HERV-LTR elements in the 5′-flanking region of HLA- individuals. Furthermore we recently published that patients DQB1 and association with autoimmunity. Immunogenetics with Addison’s disease—another HLA DQ8-associated autoim- 53:114–118 mune disease of the adrenals which may occur in combination 3. Donner H, Tonjes RR, Bontrop RE et al. (1999) Intronic se- with Type 1 diabetes as part of the autoimmune pluriglandular quence motifs of HLA-DQB1 are shared between humans, syndrome Type 2—have more often the DQ8-DQ-LTR13 com- apes and Old World monkeys, but a retroviral LTR element bination in contrast to the DQ-LTR3 insertion. Although both (DQLTR3) is human specific. Tissue Antigens 53:551–558 DQ-LTR3 and DQ-LTR13 are linked to DQ8, DQ-LTR13 en- 4. Donner H, Tonjes RR, Van der Auwera B et al. (1999) The hances the risk for Addison’s disease [7]. presence or absence of a retroviral long terminal repeat Whether DQ-LTR13 has a functional significance or not is influences the genetic risk for type 1 diabetes conferred by currently under investigation. Preliminary data indicate that human leukocyte antigen DQ haplotypes. J Clin Endocrinol DQ-LTR13 harbours regulatory capacity and shows functional Metab 84:1404–1408 activity of an upstream element as revealed by analyses of nu- 5. Seidl C, Donner H, Petershofen E et al.
    [Show full text]