Metabolic Acidosis
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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. -
Severe Metabolic Acidosis in a Patient with an Extreme Hyperglycaemic Hyperosmolar State: How to Manage? Marloes B
Clinical Case Reports and Reviews Case Study ISSN: 2059-0393 Severe metabolic acidosis in a patient with an extreme hyperglycaemic hyperosmolar state: how to manage? Marloes B. Haak, Susanne van Santen and Johannes G. van der Hoeven* Department of Intensive Care Medicine, Radboud University Medical Center, Nijmegen, the Netherlands Abstract Hyperglycaemic hyperosmolar state (HHS) and diabetic ketoacidosis (DKA) are often accompanied by severe metabolic and electrolyte disorders. Analysis and treatment of these disorders can be challenging for clinicians. In this paper, we aimed to discuss the most important steps and pitfalls in analyzing and treating a case with extreme metabolic disarrangements as a consequence of an HHS. Electrolyte disturbances due to fluid shifts and water deficits may result in potentially dangerous hypernatriema and hyperosmolality. In addition, acid-base disorders often co-occur and several approaches have been advocated to assess the acid-base disorder by integration of the principles of mass balance and electroneutrality. Based on the case vignette, four explanatory methods are discussed: the traditional bicarbonate-centered method of Henderson-Hasselbalch, the strong ion model of Stewart, and its modifications ‘Stewart at the bedside’ by Magder and the simplified Fencl-Stewart approach. The four methods were compared and tested for their bedside usefulness. All approaches gave good insight in the metabolic disarrangements of the presented case. However, we found the traditional method of Henderson-Hasselbalch and ‘Stewart at the bedside’ by Magder most explanatory and practical to guide treatment of the electrolyte disturbances and in exploring the acid-base disorder of the presented case. Introduction This is accompanied by changes in pCO2 and bicarbonate (HCO₃ ) levels, depending on the cause of the acid-base disorder. -
Problem-Based Review: a Patient with Metabolic Acidosis
Acute Medicine 2012 11(4): 251-256 251 Trainee Section Problem-Based Review: A patient 251 with metabolic acidosis saf R Allan & C Foster Abstract Metabolic acidosis is a common metabolic derangement present in the acute medical patient. A thorough and structured investigative approach is required as there are many causes and management is reliant on identifying these. In particular calculation of the anion gap with correction for albumin level and use of the delta ratio can be helpful in complex cases especially in patients where a combination of metabolic derangements may be present. Keywords metabolic acidosis, anion gap, delta ratio, renal tubular acidosis, bicarbonate Key points • Calculation of the anion gap is crucial in identifying the cause of metabolic acidosis. • Metabolic acidosis is often multi-factorial and the delta ratio calculation can be useful in identifying situations where a normal gap acidosis coexists with a raised anion gap cause. • Identification of the specific cause(s) of metabolic acidosis is vital as this will usually guide treatment. • Bicarbonate treatment has a role in some cases but adverse effects should be considered. Case Vignette Although the anion gap calculation will narrow A 37 year old male with no past medical history presents our differential (Table 2), many possible explanations to the acute medical unit (AMU) with a history of general for the acidosis remain, especially when the gap is deterioration in health over the last 8 months. He has lost 10 high. The mnemonic MUDPILERS (Methanol, kg of weight and has severe fatigue. More recently he describes a Uraemia, Diabetic Ketoacidosis or other causes Table 1. -
PHAR 503 Exam 2
PHAR 503 Exam 2 Rho Chi Acid-Base Disorders Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Which medication would most likely NOT lead to a metabolic alkalosis? A. Loop Diuretic B. Thiazide Diuretic C. Desmopressin D. Citrate Diuretics increase loss of H+, vomiting, hypokalemia, citrate is metabolized to HCO3- A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis A patient suffering from an acute panic attack might be at risk for developing: A. Respiratory alkalosis B. Metabolic alkalosis C. Respiratory Acidosis D. Metabolic Acidosis Hyperventilating -> blowing off CO2 (acid) If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 If you have a patient who is experiencing a respiratory acidosis, which of the following sets of labs would most likely match the patient? A. pH: 7.41, HCO3-: 20 B. pH: 7.35, CO2: 52 C. pH: 7.35, HCO3-: 20 D. pH: 7.45, CO2: 32 Metabolic: HCO3- abnormalities, respiratory: PaCO2 What is the normal range for PaCO2? What is the normal range for HCO3-? What is the normal range for PaCO2? 35-45 (40!) What is the normal range for HCO3-? 22-26 (24!) ROME Respiratory Opposite: PaCo2 and pH go in opposite directions Metabolic Equal: HCO3- and pH go in the same direction Which of the following would NOT cause a metabolic acidosis? A. -
Diabetic Ketoalkalosis in Children and Adults
Original Article Diabetic Ketoalkalosis in Children and Adults Emily A. Huggins, MD, Shawn A. Chillag, MD, Ali A. Rizvi, MD, Robert R. Moran, PhD, and Martin W. Durkin, MD, MPH and DR are calculated because the pH and bicarbonate may be near Objectives: Diabetic ketoacidosis (DKA) with metabolic alkalosis normal or even elevated. In addition to having interesting biochemical (diabetic ketoalkalosis [DKALK]) in adults has been described in the features as a complex acid-base disorder, DKALK can pose diagnostic literature, but not in the pediatric population. The discordance in the and/or therapeutic challenges. change in the anion gap (AG) and the bicarbonate is depicted by an Key Words: delta ratio, diabetic ketoacidosis, diabetic ketoalkalosis, elevated delta ratio (DR; rise in AG/drop in bicarbonate), which is metabolic alkalosis normally approximately 1. The primary aim of this study was to de- termine whether DKALK occurs in the pediatric population, as has been seen previously in the adult population. The secondary aim was iabetic ketoacidosis (DKA), a common and serious dis- to determine the factors that may be associated with DKALK. Dorder that almost always results in hospitalization, is de- Methods: A retrospective analysis of adult and pediatric cases with a fined by the presence of hyperglycemia, reduced pH, metabolic 1 primary or secondary discharge diagnosis of DKA between May 2008 and acidosis, elevated anion gap (AG), and serum or urine ketones. August 2010 at a large urban hospital was performed. DKALK was as- In some situations, a metabolic alkalosis coexists with DKA sumedtobepresentiftheDRwas91.2 or in cases of elevated bicarbonate. -
Chapter 26: Fluid, Electrolyte, and Acid-Base Balance
Chapter 26: Fluid, Electrolyte, and Acid-Base Balance Chapter 26 is unusual because it doesn’t introduce much new material, but it reviews and integrates information from earlier chapters to cover 3 types of regulation: regulation of fluid volume, regulation of electrolyte (=ion) concentrations, and regulation of pH. • Outline of slides: • 1. Regulating fluid levels (blood/ECF) • Compartments of the body • Regulation of fluid intake and excretion • 2. Regulating ion concentrations (blood/ECF) • 3. Regulating pH (blood/ECF) • Chemical buffers • Physiological regulation • Respiratory • Renal 1 3 subsections to this chapter – we will cover the middle one only briefly. 1 Ch. 26: Test Question Templates • Q1. Given relevant plasma data, classify a patient’s possible acid-base disorder as a metabolic or respiratory acidosis or alkalosis that is or is not fully compensated. Or, if given such a disorder, give expected plasma pH and CO2 level (high, normal, or low). • Example A: Plasma pH is 7.32, CO2 levels in blood are low. What is this? • Example B: A patient’s plasma has a pH of 7.5. Explain how you could make an additional measurement to determine whether the cause of this unusual pH is metabolic or respiratory. • Example C: A patient’s plasma CO2 levels are very low, yet plasma pH is normal. How can this be? 2 Q1. Example A: (slight) metabolic acidosis. Example B: Measure the CO2 level in the plasma. If the high plasma pH is due to a respiratory problem, the CO2 concentration will be low. If the high pH is NOT due to a respiratory problem, the CO2 will not be low, and may be high if the person is undergoing respiratory compensation for a metabolic alkalosis. -
The Electro-Physiology-Feeedback Measures of Interstitial Fluids
INTERNATIONAL MEDICAL UNIVERSITY The elecTro-Physiology-Feeedback Measures oF inTersTiTial Fluids BY PROFESSOR OF MEDICINE DESIRÉ DUBOUNET IMUNE PRESS 2008 Electro-Physiology -FeedBack Measures of Interstitial Fluids edited by Professor Emeritus Desire’ Dubounet, IMUNE ISBN 978-615-5169-03-8 1 CHAPTER 1 THE ELECTRO-PHYSIOLOGY-FEEDBACK MEASURES OF INTERSTITIAL FLUIDS The interstitial liquid constitutes the true interior volume that bathe the organs of the human body. It is by its presence that all the exchanges between plasma and the cells are performed. With the vascular, lymphatic and nervous systems, it seems to be the fourth communication way of information's between all the cells. No direct methods for sampling interstitial fluid are currently available. The composition of interstitial fluid, which constitutes the environment of the cells and is regulated by the electrical process of electrochemistry. This has previously been sampled by the suction blister or liquid paraffin techniques or by implantation of a perforated capsule or wick. The results have varied, depending on the sampling technique and animal species investigated. In one study, the ion distribution between vascular and interstitial compartments agreed with the Donnan equilibrium; in others, the concentrations of sodium and potassium were higher in interstitial fluid than in plasma. The concentration of protein in interstitial fluid is lower than in plasma, and the free ion activities theoretically differ from those of plasma because of the Donnan effect. In spite of these differences, and for practical reasons only, plasma is used clinically to monitor fluid and electrolytes. The relation between plasma and interstitial fluid is important in treating patients with abnormal plasma volume or homeostasis. -
ABG Analysis in Clinical Setting
CHAPTER ABG Analysis in Clinical Setting 117 Rajesh Mahajan, Suman Sethi INTRODUCTION defined by the ratio of PCO2 to HCO3 and not by absolute Acid-Base balance is an intricate concept which requires an value of either one alone.5,6 intimate and detailed knowledge of the body’s metabolic Overview of Fundamentals of Acid-Base Disorder pathways used to eliminate the H+ ion. Accurately Normal metabolism of proteins and nucleotides generates interpreting acid-base balance requires simultaneous about 100 mmol H+ per day in the form of sulphuric and measurements of arterial pH and plasma electrolytes, phosphoric acids. By comparison, hydration of CO2 to as well as knowledge of compensatory physiologic form H CO generates 12,500 mmol H+ per day. mechanisms. In this article, we’ll review normal acid-base 2 3 physiology, acid-base disturbances, and lab techniques Carbon dioxide transport and mathematical calculations used to identify the cause 1. Transport of carbon dioxide in the blood is of acid-base derangements. considerably more complex. A small portion of carbon dioxide, about 5 percent, remains BASIC PHYSIOLOGY unchanged and is transported dissolved in blood. Acid-base Chemistry 2. The remainder is found in reversible chemical pH combinations in red blood cells or plasma. Some The concept of pH was put forward by the Danish chemist, carbon dioxide binds to blood proteins, principally Soren Peter Sorensen in 1909 to refer to the negative hemoglobin, to form a compound known as logarithm of hydrogen ion (H+) concentration. An increase carbamate. in the pH indicates a proportionate decrease in the 3., About 88 percent of carbon dioxide in the blood is [H+] and a decrease in the pH indicates a proportionate in the form of bicarbonate ion. -
New Jersey Chapter American College of Physicians Resident
New Jersey Chapter American College of Physicians Resident Abstract Competition 2018 Submissions Category Name Additional Authors Program Abstract Title Abstract Clinical Vignette Ankit Bansal Ankit Bansal MD, Robert Atlanticare Rare Case of A 62‐year‐old male IV drug abuser with hepatitis C and diabetes presented to the emergency Lyman MS IV, Saraswati Regional Necrotizing department with progressively worsening right forearm pain and swelling for two days after injecting Racherla MD Medical Myositis leading to heroin. Vitals included temperature 98.8°F and heart rate 107 bmp. Physical examination showed Center Thoracic and erythematous skin with surrounding edema and abscess formation of the right biceps extending into (Dominik Abdominal the axilla, and tenderness to palpation of the right upper extremity (RUE). Labs were white blood cell Zampino) Compartment count 16.1 x103/uL with bands 26%, hemoglobin 12.4 g/dL, platelets 89 x103/uL and blood lactate 2.98 Syndrome mmol/L. Patient was admitted to telemetry for sepsis secondary to right arm cellulitis and abscess. Bedside incision and drainage was performed. Blood and wound cultures were drawn and patient was started on Vancomycin and Levofloxacin. On the third day of admission, patient became febrile, obtunded and had signs of systemic toxicity. Labs showed a worsening leukocytosis and lactic acidosis. CT RUE was consistent with complex fluid collection and with extensive gas tracking encircling the entire length of the right biceps brachii muscle. Surgical debridement was performed twice over the next few days. Blood cultures grew corynbacterium and coagulase negative staphylococcus; wound culture grew coagulase negative staphylococcus. Levofloxacin was switched to Aztreonam. -
Acid-Base Disorders Made So Easy Even a Caveman Can Do It
ACID-BASE DISORDERS MADE SO EASY EVEN A CAVEMAN CAN DO IT Lorraine R Franzi, MS/HSM, RD, LDN, CNSD Nutrition Support Specialist University of Pittsburgh Medical Center Pittsburgh, PA I. LEARNING OBJECTIVES The clinician after participating in the roundtable will be able to: 1) Indicate whether the pH level indicates acidosis or alkalosis. 2) State whether the cause of the pH imbalance is respiratory or metabolic. 3) Identify if there is any compensation for the acid-base imbalance. II. INTRODUCTION Acid-Base balance is an intricate concept which requires an intimate and detailed knowledge of the body’s metabolic pathways used to eliminate the H+ ion. Clinicians may find it daunting to understand when first introduced to the subject. This roundtable session will demonstrate how to analyze blood gas levels in a very elementary manner so as to diagnose any acid-base disorder in a matter of minutes. The body is in a constant state of flux delicately stabilizing the pH so as to maintain its normalcy. In order to prevent untoward effects of alkalosis or acidosis the body has three major buffering systems that it uses to adjust the pH. They are: 1) Plasma protein (Prot-) 2) Plasma hemoglobin (Hb-) 3) Bicarbonate (HCO3-) The Bicarbonate-Carbonic acid system is the most dominate buffering system and controls the majority of the hydrogen ion (H+) equilibrium. Maintaining homeostasis when these acid-base shifts occur is vital to survival. Metabolic and respiratory processes work in unison to keep the H+ normal and static. II. ACID-BASE ABNORMALITIES The four principal acid-base imbalances are illustrated in Table 1. -
Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: a Pathophysiological Review
Hindawi Publishing Corporation Journal of Biomedicine and Biotechnology Volume 2012, Article ID 915150, 8 pages doi:10.1155/2012/915150 Review Article Acid-Base Disorders in Patients with Chronic Obstructive Pulmonary Disease: A Pathophysiological Review Cosimo Marcello Bruno and Maria Valenti Department of Internal Medicine and Systemic Diseases, University of Catania, 95100 Catania, Italy Correspondence should be addressed to Cosimo Marcello Bruno, [email protected] Received 29 September 2011; Accepted 26 October 2011 Academic Editor: Saulius Butenas Copyright © 2012 C. M. Bruno and M. Valenti. 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. The authors describe the pathophysiological mechanisms leading to development of acidosis in patients with chronic obstructive pulmonary disease and its deleterious effects on outcome and mortality rate. Renal compensatory adjustments consequent to acidosis are also described in detail with emphasis on differences between acute and chronic respiratory acidosis. Mixed acid-base disturbances due to comorbidity and side effects of some drugs in these patients are also examined, and practical considerations for a correct diagnosis are provided. 1. Introduction However, an alteration in respiratory exchanges, as occurs in advanced phase of COPD, results in retention of CO2. Chronic obstructive pulmonary disease (COPD) is a major Carbon dioxide is then hydrated with the formation of public health problem. Its prevalence varies according to carbonic acid that subsequently dissociates with release of country, age, and sex. On the basis of epidemiologic data, hydrogen ions (H+) in the body fluids according to the fol- the projection for 2020 indicates that COPD will be the lowing equation: third leading cause of death worldwide and the fifth leading − + cause of disability [1]. -
PGE2 EP1 Receptor Inhibits Vasopressin-Dependent Water
Laboratory Investigation (2018) 98, 360–370 © 2018 USCAP, Inc All rights reserved 0023-6837/18 PGE2 EP1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct Rania Nasrallah1, Joseph Zimpelmann1, David Eckert1, Jamie Ghossein1, Sean Geddes1, Jean-Claude Beique1, Jean-Francois Thibodeau1, Chris R J Kennedy1,2, Kevin D Burns1,2 and Richard L Hébert1 PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1 − / − mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1 − / − , Htn, HtnEP1 − / − . Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1 − / − , but sglt2 was increased in EP1 − / − mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1 − / − or HtnEP1 − / − mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.