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Acid-Base disorders
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123
Clinical Evaluation
and Management
Alluru S. Reddi
Acid-Base Disorders
Acid-Base Disorders
Alluru S. Reddi
Acid-Base Disorders
Clinical Evaluation and Management
ISBN 978-3-030-28894-5 ISBN 978-3-030-28895-2 (eBook)
https://doi.org/10.1007/978-3-030-28895-2
© Springer Nature Switzerland AG 2020
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of
the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation,
broadcasting, reproduction on microfilms or in any other physical way, and transmission or information
storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology
now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication
does not imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and information in this book
are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the
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claims in published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Alluru S. Reddi
Professor of Medicine, Department of Medicine, Chief, Division of
Nephrology and Hypertension
Rutgers New Jersey Medical School
Newark, NJ, USA
v
Preface
Acid-base physiology is a difficult topic in medicine because of its complexity. The
purpose of writing this book is to present a clear and concise understanding of the
fundamentals of acid-base physiology and its associated disorders that are frequently encountered in clinical practice. Each clinical acid-base disorder begins
with pathophysiology followed by case studies and questions with explanations. I
believe that this kind of approach will increase the knowledge of a physician in
managing acid-base disturbances.
This book would not have been possible without the help of many students,
house staff, and colleagues who made me understand acid-base disorders and manage patients appropriately. I am grateful to all of them. I am extremely thankful and
grateful to my family for their immense support and patience. I extend my thanks to
Andy Kwan and Gregory Sutorius, Springer, New York, for their continued support,
help, and advice. Constructive critique for improvement of the book is gratefully
acknowledged.
Newark, NJ, USA Alluru S. Reddi
vii
Contents
1 Introduction to Acid–Base . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
2 Basic Acid–Base Chemistry and Physiology . . . . . . . . . . . . . . . . . . . . . 7
3 Methods to Assess Acid–Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . 21
4 Acid–Base Disorders: General Considerations and Evaluation . . . . . 39
5 Lactic Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
6 Ketoacidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
7 Toxin-Induced Acid-Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
8 Renal Tubular Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
9 Acid–Base Disorders in Gastrointestinal Diseases . . . . . . . . . . . . . . . . 157
10 Acid–Base Disorders in Kidney Disease . . . . . . . . . . . . . . . . . . . . . . . . 171
11 Metabolic Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
12 Respiratory Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
13 Respiratory Alkalosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
14 Mixed Acid–Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243
15 Drug-Induced Acid-Base Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257
16 Acid–Base Disorders in Critically Ill Patients . . . . . . . . . . . . . . . . . . . 263
17 Acid-Base Disorders in Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 281
18 Acid-Base Disorders in Total Parenteral Nutrition . . . . . . . . . . . . . . . 293
19 Acid-Base Disorders in Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299
20 Acid-Base Disorders in Surgical Patients . . . . . . . . . . . . . . . . . . . . . . . 305
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
© Springer Nature Switzerland AG 2020 1
A. S. Reddi, Acid-Base Disorders, https://doi.org/10.1007/978-3-030-28895-2_1
Chapter 1
Introduction to Acid–Base
The arterial blood gas (ABG) determination is an important laboratory test in the
evaluation of oxygenation and acid–base status of the body. This ABG test is most
frequently done in the emergency department and critical care units. Also, this test
is a valuable tool during operative procedures. When an ABG is ordered, four
important values are reported: pH, partial pressure of oxygen (pO2), partial pressure
of carbon dioxide (pCO2), and bicarbonate (HCO3
−). Base excess (BE) is also
reported (see Chap. 3), which is used by some clinicians. The percent saturation of
hemoglobin with oxygen in the arterial blood (SaO2) is done by either direct measurement using CO-oximetry or estimated from pO2. Only some blood gas analyzers
are equipped with CO-oximeter for measurement of SaO2 directly, and other laboratories report calculated value. Mean SaO2 is 98%.
Technique of ABG Measurement
After collection of either arterial or venous blood, it is introduced into the blood gas
analyzer (BGA). The BGA aspirates the blood into a measuring chamber which
contains ion-specific electrodes for pH, pO2, and pCO2. The pH is measured by two
electrodes: a pH-measuring electrode and a reference electrode. The reference electrode contains a saturated solution of KCl, and the current flow compares the voltage of the unknown blood with a reference voltage, and the difference in voltage is
displayed on a voltmeter calibrated in pH units.
pO2 is measured with Clark electrode or polarographic electrode. O2 diffuses
across polypropylene membrane through the electrode immersed in phosphate buffer. O2 then reacts with water in the buffer and generates voltage (current) that is
proportional to the number of O2 molecules in the solution. The current is measured
and expressed as pO2.
2
The pCO2 electrode is a modified pH electrode with a silicone or Teflon rubber
CO2 semipermeable membrane covering the tip of the electrode. The electrode is
bathed in a solution containing NaHCO3. The CO2 diffuses from the blood across
the semipermeable membrane, and the reaction between CO2 and water generates
free H+ in proportion to the pCO2
A brief description of each of these components of ABG is described below.
pH
pH is measured by a specific pH electrode, and it indicates either acidity or alkalinity of blood. Actually the pH is an indirect measurement of hydrogen ion concentration (abbreviated as [H+]).The normal [H+] in the extracellular fluid is about
40 nmol/L or 40 nEq/L (range 38–42 nmol/L), which is precisely regulated by an
interplay between body buffers, lungs, and kidneys. Since many functions of the
cell are dependent on the optimum [H+], it is extremely important to maintain [H+]
in blood ~40 nmol/L. Any deviation from this [H+] results either in acidemia
([H+] >40 nmol/L) or alkalemia ([H+] <40 nmol/L). The [H+] in blood is so low that
it is not measured routinely. However, the [H+] is measured as pH, which is
expressed as:
pH = - éHë ù
û
+ log (1.1)
Thus, pH is defined as the negative logarithm of the [H+]. An inverse relationship
exists between pH and [H+]. In other words, as the pH increases, the [H+] decreases
and vice versa (Table 1.1). Cells cannot function at a pH below 6.8 and above 7.8.
The normal arterial pH ranges from 7.38 to 7.42, which translates to a [H+] of
38–42 nmol/L. Mean pH is 7.40.
pH (Units) [H+] (nmol/L)
7.90
7.80
7.70
7.60
7.50
7.40
7.30
7.20
7.10
7.00
6.90
6.80
6.70
6.60
13
16
20
25
32
40
50
63
79
100
126
159
199
251
Table 1.1 Relationship between
pH and [H+]
1 Introduction to Acid–Base
3
pO2
pO2 refers to the partial pressure of oxygen (tension) dissolved in blood. As mentioned,
it is measured specifically by a pO2 electrode. The mean value of pO2 in a normal
young man is approximately 97 mmHg at sea level. Various formulas have been developed to predict approximate values of pO2 in individuals of varying ages. Clinically,
however, it is cumbersome to use these formulas on daily basis. One suggested way of
estimating approximate pO2 is to assume 100 mmHg in a 10-year-old child and a
decrease of 5 mmHg for every 10 years up to 90 years of age. For example, a 20-yearold man will have a pO2 of 95 mmHg, and it is 60 mmHg for a 90-year-old man.
pCO2
pCO2 indicates the partial pressure of carbon dioxide (tension) dissolved in blood.
It reflects alveolar ventilation and represents respiratory component of ABG. The
normal values range from 35 to 46 mmHg with a mean value of 40 mmHg.
HCO3
−
HCO3
− represents the bicarbonate concentration ([HCO3
−]) of the blood sample that
is sent for the analysis of ABG. It is not a measured value but calculated from
Henderson–Hasselbalch equation (see Chap. 2). This calculated [HCO3
−] is lower
by 1–2 mEq/L than the [HCO3
−] from chemistry panel, which is measured as total
CO2. Total CO2 comprises three components: HCO3
−, dissolved CO2, and carbonic
acid. For this reason, total CO2 concentration is higher than the calculated HCO3−.
Total CO2, calculated HCO3
−, and base excess (see Chap. 3) are indicators of metabolic components of ABG.
Normal ABG Values
Mean and range values of normal ABG are shown in Table 1.2.
Table 1.2 Mean and range
values of normal ABG
Component Mean Range
pH 7.40 7.36–7.44
[H+] (nnol/L) 40 36–44
pO2 (mmHg) 97 80–100
pCO2 (mmHg) 40 36–44
[HCO3
−] (mEq/L) 24 22–26
BE (mEq/L) 0 0 ± 2
SaO2 (%) 97 97–98
BE base excess, SaO2 saturation of hemoglobin with oxygen
Normal ABG Values
4
Arterial vs. Venous Blood Sample for ABG
Arterial blood is used most of the time to evaluate an acid–base disorder. However,
venous blood samples can be used because there is insignificant difference in ABG
values between these two samples (Table 1.3).
Although there is not much difference between the two samples in normal individuals, significant difference can be observed in pathological conditions. For
example, large arteriovenous difference can be found in a patient with decreased
cardiac output and on mechanical ventilation. In such a patient, the arterial pCO2
remains normal, but central venous pCO2 may be extremely elevated, as more CO2
is added to the perfusing tissue. In low cardiac output states, an arterial ABG is useful in assessing pulmonary gas exchange, and central venous ABG is useful in
assessing pH and tissue oxygenation.
Primary Acid–Base Disorders
As stated above, a change in plasma [HCO3
−] results in a metabolic acid–base disturbance, whereas a change in arterial pCO2 results in a respiratory acid–base disorder. Clinically, four primary acid–base disorders can be recognized: (1) metabolic
acidosis, (2) metabolic alkalosis, (3) respiratory acidosis, and (4) respiratory alkalosis. Changes in pH, HCO3
−, and pCO2 for each primary acid–base disorder are
shown in Table 1.4. In addition, the respiratory acid–base disorders are classified
into either acute or chronic based on the buffering mechanism. Buffering for acute
disorder is complete in minutes to few hours, whereas for chronic disorder complete
buffering takes a few days (see Chap. 2). Systemic disorders cause primary acid–
base disorders, and the resultant pH changes are minimized by appropriate secondary physiologic response, as shown in Table 1.5.
Table 1.3 Differences
between arterial and venous
blood samples
ABG value Arterial blood Venous blood
pH 7.40 7.36
[H+] (nmol/L) 40 44
pCO2 (mmHg) 40 48
[HCO3
−] (mEq/L) 24 26
pO2 (mmHg) ~97 ~50
Table 1.4 Primary acid–base
disturbances
Acid–base disorder pH Primary change
Metabolic acidosis <7.40 ↓ HCO3
−
Metabolic alkalosis >7.40 ↑ HCO3
−
Respiratory acidosis <7.40 ↑ pCO2
Respiratory alkalosis >7.40 ↓ pCO2
↑ increase ↓ decrease
1 Introduction to Acid–Base
5
Secondary Physiologic Response (or Compensation)
It is a physiologic process that minimizes changes in pH or [H+] brought about by a
primary change. In clinical practice, the term compensation rather than secondary
physiologic response is usually used. Two types of compensatory responses (secondary physiologic responses) are involved: respiratory and renal. In a metabolic
acid–base disorder, the compensatory response is respiratory. For example, in metabolic acidosis, the primary change is a decrease in plasma [HCO3
−] and an increase
in [H+]. The compensatory response is a decrease in pCO2 due to hyperventilation.
This decrease in pCO2 limits the rise in [H+], and thus the pH is returned to normal.
The observed hyperventilation represents the normal physiologic response to an
increase in [H+]. Conversely, hypoventilation is an appropriate physiological
response to metabolic alkalosis. In a respiratory acid–base disorder, the compensatory response is renal. In respiratory acidosis, the primary change is an increase in
pCO2 and a decrease in pH or an increase in [H+]. The renal compensation increases
the plasma [HCO3
−] with a resultant increase in pH close to normal. Six “rules of
thumb” were introduced to calculate the extent of compensatory response to the
primary acid–base disorder (see Table 1.5).
Factors Influencing ABG
Factors such as collection of blood, time to collection of blood and its transportation
to the laboratory, and temperature will influence the ABG results. Arterial blood
should be collected under anaerobic conditions without air bubbles. Air bubbles
give high pO2, and the blood samples should be placed in ice immediately. At 4 °C,
ABG values remain stable for 2–4 h. Another reason for immediate determination
of ABG is to prevent continuous metabolism occurring in white blood cells (WBCs)
and reticulocytes. During metabolism, O2 is consumed and CO2 is generated. As a
result, a decrease in pO2 and an increase in pCO2 up to 5 mmHg can occur. Because
of an increase in pCO2, blood pH may be lower by 0.05 units. ABG should be determined immediately in patients with high WBC count (>12,000) because of high
consumption of O2 during metabolism in these cells.
Too much anticoagulant such as heparin may lower pH, pO2, and pCO2. Citrate
may decrease pH.
Table 1.5 Primary acid–base disturbances and their secondary response
Acid–base disorder pH
Primary
change
Secondary
change
Mechanism of secondary
change
Metabolic acidosis <7.40 ↓ HCO3
− ↓ pCO2 Hyperventilation
Metabolic alkalosis >7.40 ↑ HCO3
− ↑ pCO2 Hypoventilation
Respiratory acidosis <7.40 ↑ pCO2 ↑ HCO3
− ↑ HCO3
− reabsorption
Respiratory alkalosis >7.40 ↓ pCO2 ↓ HCO3
− ↓ HCO3
− reabsorption
Factors Influencing ABG
6
Changes in body temperature affect ABG results. In the ABG analyzer, the samples are read at a temperature of 370
C. Deviations from this temperature, either
decrease or increase, result in changes in pH, pO2, and pCO2. Table 1.6 shows
temperature-corrected values for a normal ABG.
Suggested Reading
Adrogué HJ, Madias NE. Measurement of acid-base status. In: Gennari FJ, Adrogué HJ, Galla JH,
Madias NE, editors. Acid-base disorders and their treatment. Boca Raton: Taylor & Francis;
2005. p. 775–88.
Ashwood ER, Kost G, Kenny M. Temperature correction of blood-gas and pH measurements. Clin
Chem. 1983;29:1877–85.
Byrne AL, Bennett M, Chatterji R, et al. Peripheral venous and arterial blood gas analysis in adults:
are they comparable? A systemic review and meta-analysis. Respirology. 2014;19:168–75.
Hasan A. Handbook of blood gas/acid-base interpretation. London: Springer; 2013.
Kelly A-M. Review article: can venous blood gas analysis replace arterial in emergency medical
care. Emerg Med Australia. 2010;22:493–8.
Malley WJ. Clinical blood gases. Application and noninvasive alternatives. Philadelphia: WB
Saunders; 1990.
Neufeld O, Smith JR, Goldman SL. Arterial oxygen tension in relation to age in hospitalized
patients. J Am Geriatr Soc. 1973;XXI:4–9.
Table 1.6 Effect of temperature on ABG
Temperature (C) pH pO2 (mmHg) pCO2 (mmHg)
37 7.40 80 40
30 7.50 51 30
35 7.43 70 37
39 7.37 91 44
1 Introduction to Acid–Base
© Springer Nature Switzerland AG 2020 7
A. S. Reddi, Acid-Base Disorders, https://doi.org/10.1007/978-3-030-28895-2_2
Chapter 2
Basic Acid–Base Chemistry and Physiology
As discussed in Chap. 1, the acid–base physiology deals with the maintenance of
normal hydrogen ion concentration ([H+]) and pH in body fluids and is precisely
regulated by an interplay between body buffers, lungs, and kidneys. In everyday
life, the blood pH is under constant threat by endogenous acid and base loads. If not
removed, these loads can cause severe disturbances in blood pH and thus impair
cellular function. However, three important regulatory systems prevent changes in
pH and thus maintain blood pH in the normal range. These protective systems, as
stated, are buffers, lungs, and kidneys.
Production of Endogenous Acids and Bases
An acid is a proton donor, whereas a base is a proton acceptor. Under physiological
conditions, the diet is a major contributor to endogenous acid and base
production.
Endogenous Acids
The oxidation of dietary carbohydrates, fats, and amino acids yields CO2. About
15,000 mmol of CO2 are produced by cellular metabolism daily. This CO2 combines
with water in the blood to form carbonic acid (H2CO3):
CO H O H CO H HCO CA
2 2 + « 2 3 « + 3
+ - . (2.1)
This reaction is catalyzed by carbonic anhydrase (CA), an enzyme present in tissues and red blood cells but absent in plasma. When H2CO3 dissociates into CO2 and
8
H2O (a process called dehydration), the CO2 is eliminated by the lungs. For this
reason, H2CO3 is called a volatile acid. In addition to volatile acid, the body also
generates nonvolatile (fixed) acids from cellular metabolism. These nonvolatile
acids are produced from sulfur-containing amino acids (i.e., cysteine and methionine) and phosphoproteins. The acids produced are sulfuric acid and phosphoric
acid, respectively. Other sources of endogenous nonvolatile acids include glucose,
which yields lactic and pyruvic acids; triglycerides, which yield acetoacetic and
β-hydroxybutyric acids (ketoacids); and nucleoproteins, which yield uric acid.
Hydrochloric acid is also formed from the metabolism of cationic amino acids (i.e.,
lysine, arginine, and histidine). Sulfuric acid accounts for 50% of all acids produced. A typical North American diet produces 1 mmol/kg/day of endogenous nonvolatile acid. Under certain conditions, acids are produced from sources other than
the diet. For example, starvation produces ketoacids, which can accumulate in the
blood. Similarly, strenuous exercise generates lactic acid. Drugs such as corticosteroids cause endogenous acid production by enhancing catabolism of muscle
proteins.
Endogenous Bases
Endogenous base (HCO3
−) is generated from anionic amino acids (glutamate and
aspartate) in the diet. Also, citrate or lactate generated during metabolism of
carbohydrate yields HCO3
−. Vegetarian diets contain high amounts of anionic
amino acids and small amounts of sulfur and phosphate-containing proteins.
Therefore, these diets generate more base than acid. In general, the production of
acid exceeds that of base in a person ingesting a typical North American diet.
Table 2.1 summarizes endogenous sources of acids and bases in normal
individuals.
Table 2.1 Sources of acid and alkali production
Source Acid produced
Alkali
produced
Sulfur-containing amino acids (cysteine,
cystine, methionine)
Sulfuric acid (H2SO4)
Phosphoproteins, phospholipids Phosphoric acid (H2PO4)
Glucose Lactic acid, pyruvic acid
Triglycerides Acetoacetic acid,
β-hydroxybutyric acid
Nucleoproteins Uric acid
Organic cations HCl
Diet with anionic amino acids (glutamate,
aspartate)
HCO3
−
Citrate, lactate HCO3
−
2 Basic Acid–Base Chemistry and Physiology
9
Maintenance of Normal pH
Buffers
All acids that are produced must be removed from the body in order to maintain
normal blood pH. Although the kidneys eliminate most of these acids, it takes hours
to days to complete the process. Buffers (both cellular and extracellular) are the first
line of defense against wide fluctuations in pH. The most important buffer in blood
is bicarbonate/carbon dioxide (HCO3
−/CO2). Other buffer systems are disodium
phosphate/monosodium phosphate (Na2HPO4
2−/NaH2PO4
−) and plasma proteins. In
addition, erythrocytes contain the important hemoglobin (Hb) system, reduced Hb
(HHb−) and oxyhemoglobin (HbO2
2−). Bones also participate in buffering. The
HCO3
−/CO2 system provides the first line of defense in protecting pH. Its role as a
buffer can be described by incorporating this system into the Henderson–Hasselbalch
equation as follows:
pH pKa
HCO
H CO
= +
é
ë ù
û
[ ]
-
log . 3
2 3
(2.2)
Although H2CO3 cannot be measured directly, its concentration can be estimated
from the partial pressure of CO2 (pCO2) and the solubility coefficient (α) of CO2 at
known temperature and pH. At normal temperature of 37 °C and pH of 7.4, the
pCO2 is 40 mmHg, α is 0.03, and pKa is 6.1. The Henderson–Hasselbalch equation
can be appropriately written as:
pH
HCO
pCO
= +
é
ë ù
û
+
-
6 1
0 03
3
2
. log . . (2.3)
Normal plasma [HCO3
−] is 24 mEq/L. Therefore,
pH
pH
pH
= + ´
= + = +
= + =
6 1 24
0 03 40
6 1 24
1 2
6 1 20
1
6 1 1 3 7
. log .
. log . . log
. . .40
(2.4)
It should be noted from the Henderson–Hasselbalch equation that the pH of a solution is determined by the pKa and the ratio of [HCO3
−] to pCO2, and not by their
absolute values. Thus, because the kidneys regulate the [HCO3
−] and the lungs
pCO2, the kidneys and lungs determine the pH of extracellular fluids.
Phosphate buffers are effective in regulating intracellular pH more efficiently
than extracellular pH. Their increased effectiveness intracellularly is due to their
Maintenance of Normal pH