Acid-Base and Electrolyte Handbook for Veterinary Technicians E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Acid-Base and Electrolyte Handbook for Veterinary Technicians provides an easy to understand yet comprehensive approach to acid-base and electrolyte balance. * Covers the physiology of fluids and their effect on acid-base and electrolyte balance * Offers detailed information on managing acid-base and electrolyte derangements in disease * Includes access to a companion website with case studies and multiple choice questions
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Veröffentlichungsjahr: 2016
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Table of Contents
Cover
Title Page
List of Contributors
Foreword
About the Companion Website
CHAPTER 1: Introduction to Acid‐Base and Electrolytes
Introduction to acid‐base
What is acidity?
Introduction to electrolytes
Osmolality and osmolarity
The anion gap
Conclusion
References
CHAPTER 2: Disorders of Sodium
Physiology
Clinical assessment of sodium derangements
Hyponatremia
Hypernatremia
References
CHAPTER 3: Disorders of Chloride
Physiology of chloride
Hyperchloremia
Hypochloremia
References
CHAPTER 4: Disorders of Potassium
Regulation of potassium
Hypokalemia
Hyperkalemia
Acid‐/Base disturbances and potassium
Summary
References
Further reading
CHAPTER 5: Disorders of Magnesium
Disorders of magnesium
Hypomagnesemia
Hypermagnesemia
References
CHAPTER 6: Disorders of Phosphorus
Disorders of phosphorus
Regulation of phosphorus
Measurement of phosphorus
Hypophosphatemia
Hyperphosphatemia
Hypoparathyroidism
References
CHAPTER 7: Disorders of Calcium
Physiology of calcium
Hypocalcemia
Hypercalcemia
References
CHAPTER 8: Traditional Acid‐Base Physiology and Approach to Blood Gas
Introduction
Overview of acid‐base
Buffer systems
Respiratory acidosis
Respiratory alkalosis
The anion gap
Base excess
Tips and tricks for acid‐base
Summary
References
CHAPTER 9: Metabolic Blood Gas Disorders
Acid‐base review pertaining to metabolic blood gas disorders
Simple versus mixed acid‐base disorders
Compensatory responses
Metabolic alkalosis
Metabolic acidosis
Prognosis of metabolic acid‐base derangements
References
CHAPTER 10: Respiratory Acid‐Base Disorders
The respiratory system
Disorders of oxygenation
References
CHAPTER 11: Mixed Acid‐Base Disorders
Review and overview of mixed disorders (Figure 11.1)
Compensation (Table 11.1)
Compensatory responses of respiratory disorders
Compensatory responses of metabolic disorders
The anion gap and chloride’s role (Box 11.1)
Steps in evaluating for mixed acid‐base disorders
Effects of mixed disorders on pH
Specific diseases known to cause mixed disorders (Box 11.2)
Treatment
Sampling errors
Conclusion
References
CHAPTER 12: Strong Ion Approach to Acid‐Base
Henderson–Hasselbalch: Overview of traditional approach to acid‐base
Stewart’s strong ion approach to acid‐base
Strong ion difference [SID]
Affects of [A
TOT
]
Carbon dioxide and strong ion approach
Compensation
Simplified approaches to strong ion?
Strong ion gap (SIG)
References
CHAPTER 13: Companion Exotic Animal Electrolyte and Acid‐Base
Sample collection methods
Sample collection storage
Basic blood gas analysis of exotic species
Alternatives to blood gas analysis
Exotic small mammals
Birds
Reptiles
Amphibians
Fish
Conclusion
References
Index
End User License Agreement
List of Tables
Chapter 01
Table 1.1 Common electrolytes and their charges
Table 1.2 Average intracellular/extracellular electrolyte concentrations
Table 1.3 Units of measurement of electrolytes
Chapter 02
Table 2.1 Distribution of sodium and potassium in the intra‐extracellular fluid
Table 2.2 Treatment recommendations for hyponatremia based on clinical signs
Chapter 04
Table 4.1 Recommended potassium supplementation
Chapter 05
Table 5.1 Normal magnesium levels in dogs and cats
Table 5.2 Causes of magnesium deficit
Chapter 06
Table 6.1 Causes of hypophosphatemia
Chapter 07
Table 7.1 Factors affecting calcium analysis when sampling
Table 7.2 Common cancers and incidence of hypercalcemia
Chapter 08
Table 8.1 Percentages of buffering provided by each buffer type
Table 8.2 Normal arterial and venous acid‐base values for cats and dogs
Chapter 09
Table 9.1 Laboratory characteristics of metabolic alkalosis
Table 9.2 Laboratory characteristics of metabolic acidosis
Chapter 10
Table 10.1 Pros and cons of oxygen therapy techniques
Chapter 11
Table 11.1 Expected compensatory response to acid‐base disorders
Table 11.2 Example cases
Chapter 12
Table 12.1 SID and effect on acid‐base status
Table 12.2 List of major cations and anions
Table 12.3 Strong ion effect on SID and acid‐base status
Chapter 13
Table 13.1 Catheterization sites for common exotic animals
Table 13.2 The relationship between pCO
2
and pH when various metabolic disturbances are present
Table 13.3 Normal electrolyte ranges for common exotic animal
Table 13.4 Common causes of electrolyte abnormalities
List of Illustrations
Chapter 01
Figure 1.1 Arterial blood gases chart.
Figure 1.2 Effective and ineffective osmoles.
Chapter 02
Figure 2.1 Distribution of water by total bodyweight.
Figure 2.2 Transport of sodium across the luminal membrane of the renal tubule through the use of membrane co‐transporter proteins.
Figure 2.3 Renin‐angiotensin‐aldosterone system (RAAS).
Chapter 03
Figure 3.1 Corrected chloride.
Figure 3.2 Chloride gap.
Figure 3.3 Sodium chloride ratio.
Chapter 04
Figure 4.1 The Na
+
/K
+
‐ATPase pump.
Figure 4.2 ECG changes due to hyperkalemia, tall, spiked T‐waves.
Figure 4.3 ECG changes related to increasing hyperkalemia.
Chapter 05
Figure 5.1 Patient with tetanus receiving a constant rate infusion of intravenous magnesium.
Chapter 07
Figure 7.1 Body systems responsible for calcium regulation.
Figure 7.2 Initial response to hypocalcemia.
Chapter 08
Figure 8.1 Process of acid‐base balance in relation to pCO
2
and pH changes.
Figure 8.2 Acid‐base balance in the kidneys.
Figure 8.3 The anion gap.
Figure 8.4 Arterial blood gases chart.
Figure 8.5 Tic‐tac‐toe method of determining acid‐base imbalance.
Figure 8.6 How to use the tic‐tac‐toe method to determine acid‐base imbalance.
Chapter 09
Figure 9.1 Bicarbonate ion (
).
Figure 9.2 Flowchart indicating normal versus compensated acid‐base disturbances and alkalemia versus acidemia.
Figure 9.3 Flowchart indicating when primary and compensatory alkalosis or acidosis is not present.
Figure 9.4 Abaxis I‐Stat point‐of‐care blood gas analyzer and a CG8+ cartridge, which is a common device for obtaining quick and reliable blood gas values.
Figure 9.5 Calcium oxalate crystals form as a result of glycolic acid formation from ingesting ethylene glycol.
Figure 9.6 Image of an 8.4% sodium bicarbonate (
) injectable solution bottle.
Chapter 10
Figure 10.1 Alveoli pulmonary cross‐section.
Figure 10.2 Oxygen hemoglobin disassociation curve.
Figure 10.3 Dyspneic cat.
Figure 10.4 Respiratory bulldog.
Figure 10.5 Nasal cannula.
Figure 10.6 Dyspneic cat with oxygen hood.
Figure 10.7 Nasal prongs.
Chapter 11
Figure 11.1 Mixed acid‐base disorder with a high anion gap acidosis and inappropriate compensation as shown on a cage side chemistry analyzer.
Chapter 12
Figure 12.1 Variables in A‐B evaluation.
Chapter 13
Figure 13.1 The pinna of the rabbit is quite vascular. The blue arrow is pointing to the marginal auricular vein while the black arrow is pointing to the auricular artery.
Figure 13.2 The auricular artery is used for blood gas sampling in exotic mammals such as rabbits. The artery is numbed prior to sampling by applying a thin layer of local anesthetic cream to the surface and then covering it with a semi‐occlusive bandage.
Figure 13.3 Venipuncture in small rodents can be difficult. To help keep the vessel from collapsing, a small‐gauge needle can be inserted into the vessel and blood can be collected using several hematocrit tubes.
Figure 13.4 The femoral vein and artery can be used to obtain larger samples of blood from small rodents. A 27‐ or 25‐gauge needle attached to a 1 cc syringe works well for sample collection.
Figure 13.5 The black arrow is pointing to the medial metatarsal vein in an avian patient. The person restraining the bird holds off the vessel by placing a finger or thumb across the leg similar to what is done in a canine or feline patient. The syringe and needle size used will be based on the size of the patient. In general a 1 or 3 cc syringe attached to a 27‐ or 25‐gauge needle is used for sample collection.
Figure 13.6 The jugular vein can be used for sample collection in most species of birds. The right jugular vein is often larger than the left, but either vessel can be cannulated.
Figure 13.7 The syringe and needle size used will be based on the size of the patient. In general a 1 or 3 cc syringe attached to a 27‐ or 25‐gauge needle is used for sample collection.
Figure 13.8 Collecting blood via the jugular vein in chelonians.
Figure 13.9 Using the subcarapacial venous sinus when the jugular venipuncture is not an option.
Figure 13.10 Cardiocentesis is commonly used for blood collection in the snake.
Figure 13.11 Fish are anesthetized for basic physical examinations and diagnostic procedures including blood collection. The most common anesthetic used is tricaine methanesulfonate (MS‐222).
Figure 13.12 Blood collection in fish is very similar to that in the lizard.
Guide
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Table of Contents
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Acid‐Base and Electrolyte Handbook for Veterinary Technicians
EDITED BY
Angela Randels‐Thorp
Team Director1st Pet Veterinary CentersArizona
David Liss
Program Director‐Veterinary TechnologyPlatt CollegeLos Angeles
This edition first published 2017 © 2017 by John Wiley & Sons, Inc
Editorial Offices1606 Golden Aspen Drive, Suites 103 and 104, Ames, Iowa 50010, USAThe Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK9600 Garsington Road, Oxford, OX4 2DQ, UK
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Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book.
The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by health science practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.
Library of Congress Cataloging‐in‐Publication Data
Names: Randels‐Thorp, Angela, 1971– editor. | Liss, David, 1985– editor.Title: Acid‐base and electrolyte handbook for veterinary technicians / edited by Angela Randels‐Thorp, David Liss.Description: Ames, Iowa : John Wiley & Sons Inc., 2017. | Includes bibliographical references and index.Identifiers: LCCN 2016035702| ISBN 9781118646540 (pbk.) | ISBN 9781118922880 (Adobe PDF)Subjects: LCSH: Veterinary pathophysiology. | Acid‐base imbalances. | Water‐electrolyte imbalances. | MESH: Acid‐Base Imbalance–veterinary | Acid‐Base Equilibrium | Water‐Electrolyte Imbalance–veterinary | Water‐Electrolyte Balance | Animal TechniciansClassification: LCC SF910.W38 A25 2017 | NLM SF 910.W38 | DDC 636.089/607–dc23LC record available at https://lccn.loc.gov/2016035702
A catalogue record for this book is available from the British Library.
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.
List of Contributors
Brandee BeanAdobe Animal HospitalLos AltosCalifornia, USAAngela ChapmanHead Nurse Emergency and Critical Care University of Melbourne Veterinary Hospital Victoria, AustraliaStephen CitalDirector of Anaesthetic Nursing and TrainingUnited Veterinary Specialty and EmergencyInterventionalist, Surpass Inc.Relief Veterinary Technician, Oakland ZooOaklandCalifornia, USADave CowanVeterinary TechnicianVeterinary Emergency Centre of ManchesterManchester, UKMeri HallVeterinary Specialty Hospital of Palm Beach GardensPalm Beach GardensFlorida, USAKatherine HowiePrincipal Nurse ManagerVets Now‐EmergencyUKDavid LissProgram Director‐Veterinary TechnologyPlatt CollegeLos AngelesJody Nugent‐DealAnaesthesia Department SupervisorUniversity of California Davis andWilliam R. Pritchard Veterinary Medical Teaching HospitalInstructor for VSPN.org, VetMedTeam.comLouise O’DwyerClinical Support ManagerVets Now LtdUKPaula PlummerFeline Internal Medicine ServiceTexas A&M University Teaching HospitalTexas, USAAngela Randels‐ThorpTeam Director1st Pet Veterinary CentersArizonaJo WoodisonJo‐Pet Emergency and Specialty Center of MarinSan RafaelCalifornia, USAEric Zamora‐MoranSmall Animal Surgery Technologist SupervisorPurdue University Veterinary Teaching HospitalIndiana, USA
Foreword
It is gratifying for me to see Blackwell‐Wiley’s publication of this Acid‐Base and Electrolyte Handbook for Veterinary Technicians by Angela Randels‐Thorp and David Liss. This work clearly is more than a “handbook” in that the authors have taken care to explain the physiology and pathophysiology underlying disturbances in acid‐base and electrolyte homeostasis. Their love of the subject shows in their treatment of it. As I previously said in the preface to my own textbook, Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, a sound foundation in physiology and pathophysiology enables the clinician to best understand the abnormalities he or she encounters: “Thoughtful evaluation of laboratory results provides valuable insight into the fluid, electrolyte and acid base status of the animal and can only improve the veterinary care provided.” The same can be said for veterinary technicians. If they understand the basis for the abnormal laboratory findings, they will be better able to take an informed approach to care for their veterinary patients. This type of in‐depth understanding allows veterinarians and veterinary technicians to make the best decisions when treating their patients. A favorite example of mine is understanding why chloride is the critical electrolyte needed to restore acid base balance in a dog or cat with metabolic alkalosis caused by protracted vomiting of stomach contents (HINT: it involves the vital need of the kidneys to reabsorb sodium in the volume‐depleted patient). Understanding the pathophysiology allows the clinician to make the logical choice of 0.9% NaCl as the crystalloid fluid of choice in this situation.
Randels‐Thorp and Liss have taken an in‐depth approach in their book, and indicate that they hope they are “providing an easy to understand approach to this detailed material, while not neglecting to incorporate the advanced nature of the topic.” They have delivered on this promise in their book, which takes considerable care to explain the physiology behind the laboratory abnormalities. Their approach will be useful not only to veterinary technicians pursuing specialty certification but also to veterinary students and veterinarians too. Their book provides valuable information about disorders of sodium, chloride, potassium, calcium, magnesium, and phosphorus as well as acid base disorders. The authors have not shied away from complexity, and have included a chapter on mixed acid base disturbances as well as a chapter on the non‐traditional approach to acid base balance, along with case examples to illustrate the value of the non‐traditional approach in complicated cases. The final chapter (Companion Exotic Animal Electrolytes and Acid‐Base) provides in one place hard‐to‐find valuable information not only about exotic mammalian species but also about birds, reptiles, and fish. I hope the community of veterinary technicians welcomes the challenge the authors have given them and uses this book as a foundation for advanced studies and specialty certification.
Stephen P. DiBartola,DVM, ACVIM (internal medicine)Emeritus ProfessorDepartment of Veterinary Clinical SciencesCollege of Veterinary MedicineOhio State UniversityColumbus, OH 43210
About the Companion Website
This book is accompanied by a companion website:
www.wiley.com/go/liss/electrolytes
The website includes:
Interactive MCQs
Case studies
Figures
CHAPTER 1Introduction to Acid‐Base and Electrolytes
Angela Randels‐Thorp, CVT, VTS (ECC, SAIM) and David Liss, RVT, VTS (ECC, SAIM)
Understanding of acid‐base and electrolyte chemistry and physiology is both an important and valuable knowledge base for all veterinary technicians, and especially those in emergency and critical care or specialty practice. These very topics, however, are frequently thought of as boring at best or utterly confusing at worst. In actuality neither is true. These topics are often approached in a piecemeal or qualitative way, which lends itself to confusion. It is the goal of this text to provide a useful, easy‐to‐learn, and practical approach to the concepts regarding acid‐base and electrolytes.
Introduction to acid‐base
Assessment of acid‐base status provides insight into three physiologic processes: alveolar ventilation, acid‐base status, and oxygenation. Evaluating acid‐base status has become an integral part of the emergent/critical care patient workup and should be performed as a baseline on all emergent patients. Deviation from normal acid‐base balances is indicative of clinical disease processes and can aid the clinician in identifying underlying causes of illness in the patient. Venous samples can provide most of the information needed regarding acid‐base status and even alveolar ventilation. Arterial samples are required, however, in order to provide oxygenation status (Sorrell‐Raschi 2009). It is ever more important for the emergency and critical care (ECC) technician to be familiar in his/her understanding of acid‐base values and what they mean.
What is acidity?
In the simplest of terms, the acidity or alkalinity of a solution is based on how many hydrogen (H+) ions, or molecules of carbon dioxide (CO2), are present. Hydrogen ions are produced daily as a normal part of metabolism of protein and phospholipids, and are considered a fixed, non‐volatile acid. Carbon dioxide is a byproduct of the metabolism of fat and carbohydrates in the body, and is considered a volatile acid (volatile = readily vaporized). Gaseous CO2 is soluble in water. CO2 is considered an acid because it readily combines with H2O in the presence of carbonic anhydrase (enzyme/catalyst) to form carbonic acid (H2CO3). Without the catalyst, this change occurs very slowly. CO2 is continually removed by ventilation and thereby kept at a stable partial pressure (pCO2) in the body. The change in dissolved CO2 in body fluids is proportional to pCO2 in the gas phase. Elimination of these acids is dependent on the function of the lung, kidney, and liver.
Bronsted and Lowry state an acid is a proton donor (H+) and a base is a proton acceptor (A–) (DiBartola 2006: 229). The H+ concentration ([H+]) of body fluids must be kept at a constant level to prevent detrimental changes in enzyme function and cellular structure. Levels compatible with life are between 16 and 160 nEq/L. Excessive hydrogen ions in the blood result in acidemia. Decreased hydrogen ions in the blood result in alkalemia (Kovacic 2009). Hydrogen ions are not typically measured or tested in clinical practice. Therefore, Sorenson developed pH notation in order to provide simpler notation of the wide range of [H+] (DiBartola 2006: 229). There is an inverse relationship between pH and [H+] (Ex: ↑[H+] → ↓pH). Normal pH ranges between 7.35 and 7.45, approximately. The processes which lead to changes in production, retention, or excretion of acids or bases, which may or may not result in a change in pH, are called acidosis or alkalosis.
Buffering systems
The body contains several mechanisms in order to maintain the desired “normal” pH level, which is called buffering. A buffer is a compound that can accept or donate protons (H+) and minimize a change in pH. Buffers consist of a weak acid and its conjugate salt (Sorrell‐Raschi 2009). If a strong acid is added to a buffer, the protons from the acid dissociate to the salt of the buffer and the change of pH is therefore minimized. With these buffers the body is continually converting CO2, H2O, H+, and to maintain pH within normal ranges. The following equation represents this constant interaction:
There are several compounds that serve as buffers in the body. The primary buffer of extracellular fluid (ECF) is bicarbonate (). Non‐bicarbonate buffers consist of proteins and inorganic and organic phosphates, which are primarily intracellular fluid (ICF) buffers. Bone is a prominent source of buffer (calcium carbonate and calcium phosphate). Up to 40% of buffering can be done from resources found in bone. Upon treatment/administration of sodium bicarbonate (), carbonate that has been released to buffer can then be deposited back into the bone. In the blood, proteins, including hemoglobin and plasma, serve as buffers. Hemoglobin constitutes 80% of the buffering capacity of blood, whereas plasma proteins only account for 20% of buffering in the blood.
The body’s buffering system is considered an open buffering system, with both bicarbonate and carbonic acid systems. In a closed system the exchanges would have to occur in a reciprocal manner. Since the body eliminates the majority of CO2 through ventilation, keeping pCO2 constant, a reciprocal reaction does not have to occur, which allows the body’s buffering systems to be considered open. Both hydrogen ion excretion and bicarbonate regeneration are regulated by the kidneys.
Physiologic response system
The balance of acid‐base in the body is regulated by metabolic, respiratory, and renal pathways. In terms of acid‐base discussion, generally either a metabolic or a respiratory derangement occurs with the renal or respiratory system compensating for either/both.
When an excess of H+ ions occurs, this causes a decrease in pH. Within minutes of this imbalance, the hydrogen ions begin to titrate with bicarbonate ions in ECF and then titrate with ICF buffers in order to minimize changes in pH. Next, alveolar ventilation is stimulated in order to decrease CO2 until levels are below normal, thereby raising the pH back up to near normal. Within hours (2–3 days peak effect), the renal system begins to regenerate . As is increased, the body’s pH is increased. Alveolar ventilation no longer needs to be increased, so returns to normal rates, restoring pCO2 levels to normal.
CO2 concentrations are a balance of mitochondrial production and alveolar removal by ventilation. An excess of CO2 (in excess of ventilatory regulation) cannot be buffered directly by . CO2 is converted to carbonic acid by the mechanisms described above, which then allows H+ from carbonic acid to titrate with intracellular buffers (proteins/phosphates). The renal system also adapts by increasing reabsorption (2–5 days peak effect).
There is a variety of terms that can be used to describe acid‐base imbalances, including: acidosis, alkalosis, acidemia, and alkalemia. While it may seem overly technical, knowing the differences between the terminologies can be important. The terms acidosis/alkalosis refer to the pathophysiologic processes that cause the net accumulation of acid or alkali in the body. The terms acidemia/alkalemia refer to the actual change in pH of ECF. In cases of acidemia, the pH is lower than normal, or < 7.35 (↑[H+]). With alkalemia, the pH is higher than normal, or > 7.45 (↓[H+]). For example: a patient with chronic respiratory acidosis may have normal pH due to renal compensation. The patient has acidosis, but not acidemia. Mixed acid‐base disorders may also have an overall normal pH, due to one counter‐balancing the other (Murtaugh 2002). These concepts will be covered in more detail in subsequent chapters.
Primary acid‐base disturbances
There are four primary acid‐base disturbances that may occur in the body: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. When evaluating a patient’s acid‐base status, the following parameters are primarily needed: pH, (or TCO2), and pCO2 (Figure 1.1). If blood gases, or oxygenation, are being evaluated on an arterial blood sample, then PaO2 values are also provided. Simple acid‐base analysis may be done on either venous or arterial blood samples. Arterial samples are mandatory if one is attempting to assess the oxygenation status of a patient.
Figure 1.1 Arterial blood gases chart.
These imbalances will be discussed in greater detail throughout the chapters of this text, as well as practical approaches and applications for day‐to‐day practice.
Introduction to electrolytes
Just as fluid imbalances can affect the patient’s electrolyte balance, electrolyte imbalances can, in turn, result in fluid imbalances, as well as a host of other problems. Imbalances involving sodium, potassium, chloride, calcium, phosphorus, and magnesium can all result in potentially life‐threatening problems for animals. It is imperative for technicians to understand the role of electrolytes in the body and recognize the signs of imbalances in these electrolytes in order to aid in the quick recognition, diagnosis, and treatment of these problems. In this section we will introduce electrolyte physiology and regulation in the body, and specific and greater detail on each is covered in its respective chapter.
General electrolyte physiology (Table 1.1)
Table 1.1 Common electrolytes and their charges
Name
Chemical symbol
Charge
Anion/Cation
Role in the body
Sodium
Na
+
1
+
Cation
Nervous/cardiac impulse transmission Water balance
Chloride
Cl
–
1
–
Anion
Water balance Acid‐base balance
Potassium
K
+
1
+
Cation
Nervous/cardiac impulse transmission
Magnesium
Mg
2+
2
+
Cation
Co‐factor in enzymatic processes
Phosphorus/Phosphate
3
–
Anion
Acid‐base buffer Biochemical reactions
Bicarbonate
1
–
Anion
Acid‐base buffer
Calcium
Ca
2+
2
+
Cation
Skeletal/cardiac muscle contraction
Lactate
CH
3
CHCO
2
H
1
–
Anion
Byproduct of anaerobic metabolism
Electrolytes are substances that ionize when dissolved in ionizing solvents, such as water. An example would include salt, or sodium chloride (NaCl), which when dissolved in water ionizes to form Na+ and Cl– ions. A positively charged ion is called a cation (example Na+) and a negatively charged ion is called an anion (example Cl–). Electrolytes, in their ionic form, are extremely important in the body as they promote cardiac and neurologic impulse transmissions, regulate water balance, assist in skeletal muscle contraction, regulate acid‐base balance, maintain oncotic balance (albumin), and provide concentration gradients for glomerular filtration in the kidney, among many other functions (Table 1.2).
Table 1.2 Average intracellular/extracellular electrolyte concentrations
Electrolyte
Average serum concentration (mEq/L)
Average intracellular concentration (mEq/L)
Sodium
142
12
Potassium
4.3
140
Chloride
104
4
Bicarbonate
24
12
Magnesium
1.1
34
Phosphate
2.0
40
Calcium
2.5
4
Typically the body’s electrolytes are distributed intra‐ and extracellularly, and it is important to understand in which compartment they mostly reside. Sodium, the body’s primary and most abundant cation, resides extracellularly. In addition, sodium’s counterpart, chloride, and bicarbonate reside mainly extracellularly. The abundant intracellular electrolytes include: potassium, calcium, magnesium, and phosphorus/phosphate.
Units of measure
Electrolytes are typically measured in mEq/L, or milliequivalent weight per liter, but can also be expressed as mg/dL or milligrams per deciliter. The milliequivalent weight (or mEq/L) represents the atomic, molecular, or formula weight of a substance divided by its valence. The valence number of a substance refers to the net number of charges it accumulates when it ionizes. For example, calcium, as Ca2+, would have a valence of 2; chloride, as Cl–, would have a valence of 1. Using sodium as an example, since it has a 1+ charge its valence number is 1. That means each millimole of sodium provides 1 mEq of sodium, because we are dividing the ionic weight by 1. Atomic, molecular, and formula weights and other units of measure are summarized in Table 1.3. In the case of magnesium, because its valence number is 2, each millimole would contribute in reality 0.5 mEq because we would divide by a valence of 2. This simply provides a reasonable unit of measure when dealing with substances that exist in very large quantities in the body. As some electrolytes are typically measured or reported in concentrations (such as mg/dL) these units can be converted back and forth. Phosphorus has an approximately normal plasma concentration of 4 mg/dL. Its average valence, because it exists in several forms, is 1.8. The molecular weight of phosphorus is 31. The equation to convert mg/dL to mEq/L is:
Table 1.3 Units of measurement of electrolytes
Unit of measure
Definition
Atomic mass Example:
12
C = 12.000
Unitless measure of weight which is an average of all the isotopic weights of a substance. It is typically reported in the periodic table of the elements. For example, C is typically reported as
12
C and weighs 12.000
Molecular mass Example: H
2O
= 18
The weight of a molecule (combination of atoms) represented by the addition of their combined atomic weights. For example: H
2
O has a molecular mass of 18 because O has an atomic mass of 16 and H has an atomic mass of 1 (which is doubled by the presence of two H molecules)
Formula weight Example: CaCl
2
= 111
This is similar to molecular mass but typically is discussed in the case of ions. Since ions dissociate in a solvent, this term is used. Example: calcium chloride is CaCl
2
and has a formula weight of 111. This comes from calcium’s weight of 40 + 2× chloride’s weight of 35.5
Mole
A unit of measure for a large number of particles. 6.02 × 10
23
particles of a substance = 1 mole of that substance
Molar mass
This term refers to the weight in grams of 1 mole of a substance. For example, 1 mole of sodium (which is 6.02 × 10
23
sodium ions) weighs 23 grams
Millimole/milligram
This represents one‐thousandth (10
–3
) of a mole or a gram
Valence Example: Ca
2+
= valence of 2
A number representing the number of charges an ion has. Example: Ca
2+
has a valence of 2; Cl
–
has a valence of 1
Milliequivalent (mEq)
This is a measure of an ion’s millimolecular weight divided by its valence
So our equation becomes:
Although not terribly important to commit to memory, a basic understanding of the units used to report electrolytes is essential in forming a foundation for interpreting them clinically.
Osmolality and osmolarity
A fundamental concept in electrolyte physiology is understanding how electrolytes affect fluid movement across membranes (tissue, cellular, etc.). This is described in the concept of osmolality. Osmolality describes the number of osmoles per kilogram of solvent, and osmolarity represents the number of osmoles per liter of solvent. An osmole is a measure of the solutes in a solution that exert an osmotic effect and typically is represented as 1 Osm is equal to 1 gram of molecular weight, which also indicates 6.02 × 1023 particles from the definition of a mol. This would be the case of a molecule that does not dissociate in the solution. In the case of NaCl, which dissociates into Na+ and Cl–, a millimole of NaCl would contribute 2 mOsm (milliosmole) (1 mOsm of Na+ and 1 mOsm of Cl–). In biologic fluids osmolarity and osmolality are used interchangeably and for the sake of uniformity osmolality will be used going forward in this chapter.
The total osmolarity of a solution represents the number of osmoles present in a solution. This can be measured in serum in a clinical patient and is typically between 300 and 310 mOsm/kg in the dog and cat. Hyper‐ and hypo‐osmolar conditions can arise and are beyond the scope of this chapter but will be discussed in future chapters in this textbook.
Since osmoles exert an osmotic effect, they can affect fluid balance and movement in a solution with a membrane. Osmosis is defined as a spontaneous movement of a solvent (fluid) across a semi‐permeable membrane from a region of lower solute concentration (solid) to a region of higher solute concentration. This movement will cause an equilibrium in the concentrations of solutes on either side. For example, imagine a beaker with a thin membrane dividing it into two halves. One each side there is a solvent (liquid) of equal volume, and one adds sodium chloride (salt) to the right side. Now on the right side there is much solute compared to the left side and this means it is highly concentrated on the right and dilute (low concentration) on the left. Thus, the water will move from the diluted left side (with more solvent than solute) to the more concentrated right side (with more solute than solvent) creating an equilibrium of solute:solvent on each side. This is depicted in the upper portion of Figure 1.2.
Figure 1.2 Effective and ineffective osmoles.
This concept is extremely important in physiology, as the body has several of these membranes. Of note are the cellular membrane and the capillary membrane. For a thorough discussion of the anatomy of these, the reader is directed to a physiology textbook, but water and fluid must remain outside of a cell, inside of a cell, outside of a capillary (in tissue) and inside a capillary (blood volume) in appropriate proportions or disease ensues.
Also, not all osmoles are created equal. Some, although called osmoles, can traverse a physiologic membrane and thus do not exert an osmotic effect. These are called ineffective osmoles and lie in contrast to effective osmoles that will pull the solvent across the membrane. An example of an ineffective osmoles is urea: where urea could exert an osmotic effect in the laboratory, in the body urea can pass through the pores of a semi‐permeable cellular membrane thereby creating an equilibrium of solute, causing no net movement of solvent across the membrane. This is demonstrated in the lower portion of Figure 1.2. Effective osmoles have a special name for their measure in bodily fluids. This is referred to as the tonicity. The tonicity of a solution is the measure of the effective osmolarity. So in a solution with tonicity fluid will move across the semi‐permeable membrane when an effective osmole is added. One such example is sodium. Sodium is an effective osmole in the body, and solutions where there is more sodium relative to the concentration of solvent are referred to as hypertonic, and solutions where the solute (sodium) concentration is less than the solvent are called hypotonic. When solvent:solute concentrations are equal that is called an isotonic solution.
Fluid movement across bodily compartments/membranes
In order to fully understand disorders of sodium and chloride, the veterinary technician needs to comprehend the idea of fluid movement across membranes that reside in the body. Fluid is maintained in several different compartments, including the ICF compartment and the ECF compartment. The ECF compartment is then divided into interstitial fluid (ISF) and intravascular fluid (IVF) compartments. The cell membrane divides the ICF and the ECF compartments and the capillary membrane divides the IVF from the ISF compartments. Osmotically active particles will largely determine the fluid balance across the cell membrane which maintains the balance between the ICF and ECF compartments. In this case, these effective osmoles are not easily or at all permeable to the cell membrane and thus exert the concentration effect drawing fluid either in or out of the cell across the membrane. Sodium, potassium, chloride, bicarbonate, glucose, and to some extent urea can all affect osmolality and fluid balance. Gain or loss of these osmoles from the extracellular or intracellular space, or gain or loss of fluid on either side, will create a ripple effect, causing net movement of fluid in or out of the cell across the cell membrane. Further descriptions of these effects are found later in this textbook.
Movement of fluid across the capillary membrane is quite different. Although not fully understood, the idea of Starling’s forces remains the major theory to describe net fluid movement from the interstitial space into or out of the capillary or into and out of the tissue space. Starling’s equation is:
While seemingly daunting at first, this equation simply describes how fluid moves across the capillary membrane. The net filtration, if positive, means fluid extravasates out of the capillary and if negative means fluid moves into the capillary.
Kf = Filtration coefficient, describes the permeability of the capillary wall
Pcap = The hydrostatic pressure inside the capillary (fluid pressure), will tend to drive fluid out of the capillary if elevated
Pif = The hydrostatic pressure of the tissues, will tend to drive fluid into the capillary if elevated
πcap = The oncotic pressure in the capillary. This is the pressure generated by plasma proteins (negatively charged) attracting water toward them and thus tending to draw water into the capillary and keeping it there.
πif = Represents the oncotic pressure in the tissues. This tends to exert a pressure maintaining water inside the tissue (interstitial) space.
Disturbances in Starling’s law demonstrate why fluid would move out of the capillary space, causing edema, or potentially into the capillary space, causing hypervolemia. If the capillary hydrostatic pressure increases, as caused by congestive heart failure in pulmonary capillaries, water will tend to move out of the capillary and into the interstitial space, thus causing pulmonary edema. If plasma protein concentration drops, such as in hypoproteinemia or hypoalbuminemia, the capillary oncotic pressure drops as well. As this pressure tends to maintain water within the capillary space, when it is not present water will tend to leak out of the capillary and into the tissue bed, also causing edema.
The anion gap
The anion gap is a concept that will be discussed in later chapters in reference to acid‐base. As electrolytes have charges and affect fluid balance, disturbances in them can be responsible for causing acid‐base conditions. The anion gap can help identify if certain electrolytes are responsible for the acid‐base condition, or illuminate other causes. The body exists in a state of electroneutrality, meaning all electrolyte charges sum to zero. All cation charges (positive) when added to all anion charges (negative) are equal and thus maintain a 0 net charge in the body. However, routine analyzers don’t measure all known anions and cations. So trying to identify total concentrations of all electrolytes becomes challenging. For example, only sodium and potassium, and chloride and bicarbonate, are routinely measured. Even if phosphorus, magnesium, and lactate are measured, there are still ions that are unaccounted for. Due to limits of technology, analyzers tend to analyze more cations than anions, meaning more anions are not measured in clinical assays. This leads to an overabundance of anion charges/measures that are not accounted for routinely. If unmeasured anions (UAs) and unmeasured cations (UCs) are represented in a total neutrality equation, one can develop an equation accounting for these unmeasured, yet biologically active, ions.
Total cations should equal total anions: Na
+
+ K
+
+ UC = Cl
–
+
+ UA
Rearranging: Measured cations – measured anions = UA – UC = anion gap
Final: (Na
+
+ K
+
) – (Cl
–
+
) = UA – UC
The result of the third equation will yield a number representing how many more UAs there are than UCs. For example, if lactate (typically a UA) is high, it will make the UA value in the third equation much higher, yielding an elevated anion gap. More on this in later chapters.
Fluid maintenance and loss basics
Although mainly about electrolytes and acid‐base, this textbook will cover some measure of discussion on fluids, fluid balance, and gain or loss in the presence of disease. As electrolytes affect fluid balance across compartments, as discussed above, alterations in gain or loss of fluid will also exert osmotic and fluid‐moving effects.
Typically, the body exists in a state of equilibrium of fluid movement, called homeostasis. Fluid is lost and gained in equal proportions to maintain hydration and blood volume. All gains and losses end up totaling to zero, meaning no net gain or loss. A gain of fluid is called a positive fluid balance and a loss of fluid is called a negative fluid balance. These can occur in disease states.
Fluid or water loss is described as sensible or insensible. Sensible losses are those that can be measured or quantified easily, and insensible losses are those that must be estimated. Water lost in urine, feces, or saliva is typically called sensible loss and can be measured. Insensible losses include sweating and evaporative losses from the skin and respiratory tract.
Water lost through the kidney (sensible urinary water loss) can take two forms: water with solute (called obligatory water loss), which helps maintain solute balance in the kidney and body, and water without solute (simply H2O, also called free water loss) which is generated through the action of vasopressin/antidiuretic hormone (ADH) on the kidney. Remember the examples of sodium and water in a beaker with a membrane? The loss of water through the kidney can effectively change sodium or water concentrations in the body. If water and sodium are lost in equal proportions through the kidney (obligatory water loss), all concentrations remain the same. But if free water (simply H2O) is lost, a concentration gradient is established because the water on one side of the membrane (in this case outside of the cell) is depleted of water but still has sodium. This becomes a hypertonic solution. The same situation could occur if water was lost in great amounts through respiratory or evaporative means. This will cause disease in the body and will be discussed in more detail in later chapters.
Conclusion
Understanding these general concepts of acid‐base balance and electrolyte/fluid physiology in the body are essential to move on to later chapters in this text. The veterinary technician cannot understand hypertonic fluid loss in the presence of hypernatremia, or hyperosmolar states or triple acid‐base disorders without first mastering the basic physiologic concepts discussed here. Once these concepts are fully understood, alterations in electrolyte or acid‐base balance will make sense and allow the veterinary technician to fully comprehend the complex physiologic alterations occurring during the disease conditions. Although confusing and sometimes frustrating, having a strong foundation in electrolyte and acid‐base conditions is essential for the veterinary technician working with sick and injured patients. Electrolyte and acid‐base abnormalities affect all species, ages, breeds, and disease conditions and can cause life‐threatening alterations in heart rate, cardiac conduction, blood pressure, and nervous transmission. The veterinary technician must be ready to quickly identify abnormalities, alert the attending veterinarian, and apply rapid treatment to stabilize the critically ill veterinary patient.
References
DiBartola, S. (2006). Introduction to acid‐base disorders. In: S. DiBartola (ed.),
Fluid, Electrolytes, and Acid‐Base Disorders in Small Animal Practice
, 3rd ed. St Louis, MO: Saunders Elsevier.
Kovacic, J. (2009). Acid‐base disturbances. In: D. C. Silverstein & K. Hopper (eds),
Small Animal Critical Care Medicine
. St Louis, MO: Saunders Elsevier: 249–54.
Murtaugh, R. (2002).
Quick Look Series in Veterinary Medicine‐Critical Care
. Jackson, WY: Teton New Media, Chapter 14.
Sorrell‐Raschi, L. (2009). Blood gas and oximetry monitoring. In: D. C. Silverstein & K. Hopper (eds),
Small Animal Critical Care Medicine
. St Louis, MO: Saunders Elsevier: 878–82.
CHAPTER 2Disorders of Sodium
Angela Chapman, BSc (Hons), RVN, Dip HE CVN, Dip AVN, VTS (ECC)
Sodium is an extremely important electrolyte in the body and is routinely measured in both baseline testing and ongoing monitoring of sick patients. It is easily measured using a wide range of point of care or laboratory analyzers and is expressed as milliequivalents or millimoles per liter of plasma (mEq/L or mmol/L respectively). Normal extracellular fluid (ECF) levels of sodium are approximately 140 mEq/L, whereas sodium levels in the intracellular fluid (ICF) are only about 10 mEq/L. As the body’s major extracellular cation (positively charged ion), sodium has several key functions, including:
maintaining water homeostasis, including volume and distribution of water within the body;
contributing to impulse transmission in nerve and muscle fibers;
maintaining cellular electroneutrality.
Disorders of sodium can be relatively common in critically ill animals and severe derangements can lead to the development of neurologic issues. Treatment is not always easy, or straightforward, and if not initiated carefully can lead to development or worsening of existing neurologic signs, and in some cases death. Therefore, a thorough knowledge of the complex factors influencing the physiologic causes of sodium derangements and how these impact treatment are imperative to the successful management of these patients.
Physiology
Sodium balance is closely linked to water homeostasis. Though sodium and water are regulated by different mechanisms, the result has an impact on both, and therefore it is important to understand both processes in order to appreciate the role and balance of sodium in the body.
Approximately 60% of normal adult bodyweight is water. Two‐thirds (40% of bodyweight) of this water is found in the cells of the body and is referred to as the ICF compartment. The remaining third (20% of bodyweight) is found in the ECF compartment and distributed between the interstitial fluid (75% of ECF, 15% of bodyweight) that bathes the cells, and plasma (25% of ECF, 5% of bodyweight) (Wellman, DiBartola, & Kohn 2012; Figure 2.1). Water moves relatively easily between these compartments, and its distribution is established and maintained by the osmolality of plasma, which, in large part, is due to sodium concentration.
Figure 2.1 Distribution of water by total bodyweight.
Osmoles are particles dissolved in a solution that contribute to the pull of water across a cell membrane, a process known as osmosis. Osmolality is a measure of the number of osmoles per kilogram of solvent. This measurement does not take into account the weight, charge, or size of the osmoles, merely the quantity. Water will flow along a concentration gradient from an area of low osmolality (few particles) to an area of high osmolality (many particles) until the concentration of osmoles is equal. This is also known as osmotic pressure. Osmoles can be categorized as effective or ineffective
