THE ABC’S OF

ABG’S™
 THE ABC’S OF
ABG’S™
A Cyclopedic Dictionary
of the Testing Terms Used
in Critical Care

ROBERT F. MORAN, phd, fccm, facb

TIMOTHY N. LIESCHING, md, fccp
The ABC’s of ABG’s™: A Cyclopedic Dictionary of the Testing Terms Used
in Critical Care

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 Abstract

When a patient is brought into a trauma center in extremis, or becomes that

way during a hospital stay, the intervention mantra is airway, breathing
and circulation—the ABC’s. We provide the nonspecialist physician, and
those in the participating and supporting professions, a quick overview of
the meaning of the testing terms in this environment. Many tests, added
singly or in small groups over time as clinical and measurement technol-
ogy evolved, but whose rationale may have become less clear, are defined
and explained. Our format is simple—a brief overview of the physiologic
environment and then the encyclopedic dictionary of the terminology. We
include common terms as well as some of the confusing uses of terms
besides lesser known facts influencing their clinical use on the basis of the
analytical, medical, and managerial experience of the authors. Keep it in
your lab coat pocket—you’ll find it useful in understanding and teaching!

KEYWORDS

BGA, blood Gas, carbon dioxide, carboxyhemoglobin, CO oximetry,

cyanide poisoning, dyshemoglobin, eBGA, electrolytes, enhanced BGA,
flow-volume loop, fractional oxyhemoglobin, laboratory, methemoglobin,
oxygen, percent hemoglobin saturation, peripheral oximetry, plasma
­water, POCT, point-of-care, potassium, pulmonary function testing, satu-
ration, sodium, whole blood testing
 Contents

Foreword xi
Acknowledgments xiii
Chapter 1 In the Beginning . . . 1
Cyclopedic Dictionary of Acid–Base Homeostasis
and Oxygenation 27
Bibliography 185
About the Author 189
Index 191
 Foreword

The intent in this work is to provide the nonspecialist physician and those
in the participating and supporting professions a quick overview of the
meaning of the testing terms performed in this environment. Since many
of the tests have been added singly or in small groups over the years as the
clinical and measurement technology evolved, the rationale for the tests
may have become less clear, especially to the nonspecialist physician and
to professionals in different parts of the support team.
A common thread among the critical tests which include the blood
gases is the central laboratory and the pulmonary testing laboratory and
the professionals in both those areas. While blood gas testing itself was
originally performed in the central laboratory by clinical chemists or
­physicians such as Otto van Slyke or Sam Natelson, and more recently by
medical technologists, the more direct caregivers (respiratory ­therapists
and pulmonary function specialists) applied the information in patient
intervention guided by physicians and assisted by registered nurses.
­
­Simplified operation of the once-difficult-to-operate analytical systems
has brought on the use of laboratory analysis by nonlaboratory specialists.
By this work, we would hope to help bridge any gaps in understanding
among the terms used.
Since this is a “cyclopedic” dictionary of the testing terms used or
associated with these critical and immediately required measurements,
we don’t limit our definitions to a “Webster’s” approach, but expand
with ­personal vignettes, historical notes, and detailed insight whenever
­possible. We hope you find this work enjoyable and useful.
This is a living work, so we would like to hear from you with your
suggestions, comments, corrections, and additions.
 Acknowledgments

To all those who have helped along the way. From Messrs. Galvin and
Downing at Taunton, MA High School, to Dr. Maryalice Moore and
­
Fr.  Francis Hurley, PhD, CSC at Stonehill College and to all the experts
and mentors over the years including John Severinghaus, MD, Ole Siggaard-­
Anderson, MD, Freeman Bradley, Antonius van Kessell, and Steve Peltzman.
Professionally, I would like to thank the several organizations in
which I have worked or volunteered for the opportunity they have given
me to participate in and to learn.

• The Clinical and Laboratory Standards Institute [CLSI;

formerly the National Committee for Clinical L
­ ­ aboratory
­Standards (NCCLS)]: The activities of the blood gas and ­electrolytes
subcommittees and the interactions with many ­colleague-volunteers
in the process of bringing many related standards from concept to
approved document were invaluable in learning how to a­ ccurately
define terms and to compromise to get ultimately the best r­esult.
Many definitions here were influenced by my volunteer efforts with
CLSI/NCCLS. Additionally, the o­ pportunity to serve as m
­ ember and
chair of the National Reference System for the C­ linical ­Laboratory
(NRSCL), during the time when a consolidation of t­erminology
for all its subcommittees was in process, was a terrific one to see
how terminology morphed from one specialty area to another and
how to best harmonize the terminology without compromising the
meaning in the specialty.
• ASTM International: formerly the American Society for ­Testing
and Materials on which I served as member for the blood gas
­standard committee.
• The International Union of Pure and Applied Chemistry
(IUPAC), on which I served as a titular member for blood gases.
• The American Association for Clinical Chemistry: Especially,
the Blood Gas Committee (now the Point of Care Committee) and
its many members from around the world!
xiv  •  Acknowledgments

But especially my wife of more than 50 years, Marianne, a chemist

and mathematician in her own right as well as the Massachusetts Teacher
of the Year (2001), who has put up with my obsession to define everything
as unambiguously as possible.

Couldn’t have done it without you, Mairze!

 CHAPTER 1

In the Beginning . . .

When a patient is brought into a trauma center in extremis or becomes crit-

ical for whatever reason, the intervention mantra is Airway, B ­ reathing, and
Circulation—the motivation for the title of this book. The limited over-
view that follows should serve to focus the reader on the main content of
this book—the cyclopedic dictionary of the related terminology.
Nearly simultaneously with the initial diagnosis and treatment is the
need to assess patient status or the results of treatment with m
­ easurements—
blood gases and ventilatory status, renal function, acid–base assessment,
and other directly related tests such as electrolytes and glucose.
We begin our overview with a brief discussion of the systems and
measurements involved, including a brief general description of lung
­disease, followed by pulmonary function testing (PFT). While not directly
a part of “critical” assessment by measurement, the results of PFT are
­often an important part of the whole patient picture.

Airway: The assessment of the airway is primarily clinical—nothing

but patient deterioration can occur if the airway remains blocked!
So, we’ll leave that to the clinical texts.
Breathing: Is a process we are all familiar with but generally ignore
until it’s significantly impaired, since it occurs automatically and is
unconsciously carried out in response to biochemical and neurologic
homeostatic systems. Breathing or “external respiration” has as its
primary function the introduction of air (oxygen-O2) and removal of
carbon dioxide (CO2).1 In subjects with normally functioning lungs
and other airways, the variables include environment, activity levels,
and a complex interplay of nerves, muscles, and physiology.

1
There’s a great explanation of this entire process in Wikipedia under “Breathing.”
2  •   THE ABC’S OF ABG’S™

The effectiveness of breathing in getting oxygen to the blood and

carbon dioxide out of the blood can be determined by the physiologic
functioning of the pulmonary tree (nose/mouth, trachea, bronchi, and
­ultimately to the alveoli of the lungs).
Generally, lung dysfunction may be categorized as airway-based,
tissue-based, or blood-circulation-based disease.

Airway-based diseases affect the tubes (airways) that carry oxygen and
other gases into and out of the lungs causing narrowing or obstruc-
tion of the air passages. Both asthma and chronic obstructive pul-
monary disease (COPD) are in this category.
Tissue-based diseases may affect the structure of the lung tissue or
surrounding tissues. Scarring and/or inflammation of the tissue
­
reduces the ability of the lungs to fully expand (restrictive lung
­disease). Pulmonary fibrosis would be an example of a tissue-based
restrictive disease. Neuromuscular disease affecting the d­ iaphragm
or thoracic cage can also be the cause of restrictive disease,
­exemplified by myasthenia gravis.
Blood-circulation-based diseases affect the blood vessels in the lungs
and could be caused by inflammation and scarring of the pulmo-
nary blood vessels where gas exchange (oxygen and carbon diox-
ide) occurs. The consequences are many, including impairment of
gas exchange, fluid retention, and certain cardiovascular effects.
­Pulmonary hypertension is an example of this sort of disorder.
­Specific pulmonary diseases can have a mixture of characteristics.
Disease entities. Most common among lung diseases are asthma,
­collapse of all or part of the lung (e.g., pneumothorax or a­ telectasis),
bronchitis (swelling and inflammation of airways), COPD, lung
­cancer, pneumonia, and pulmonary edema.

So, as clinical evaluation warrants, various tests and measurements

as well as specific PFTs can be performed, frequently in conjunction with
certain cardiovascular tests, to confirm or quantify clinical impressions.

PULMONARY FUNCTION TESTING

With respect to the “breathing” part of the ABCs, first and foremost are tests to
measure volumes and flow of the air in different parts of the a­ irways/lungs as
well as the ability of the lungs to allow passage of gases between the ­airways
and the circulating blood. Many results can be o­ btained by a few simple p­ atient
 IN THE BEGINNING . . .  •   3

maneuvers in a controlled environment—some even in the physician’s office

(albeit a bit less precisely than in a fully equipped PFT laboratory).

Spirometry testing is the most basic of the tests—it simply measures

the volume of gas (air) as a function of time, as the gas moves in and
out of the lungs in a specified maneuver, a combination of normal
(tidal) breathing at rest, followed by a forced, complete inhalation
and exhalation. From this one can obtain the volumes referred to
as forced vital capacity (FVC), forced vital capacity at one second
(FVC1), as well as other quantities.

A more specialized device, but based on a similar patient maneuver,

results in the automatic calculation of air flow as well as volume, simul-
taneously, and presents a graphical representation of the results (as well
as a table of values) and a comparison of predicted values (from large
population studies). Since the major differentiation of pulmonary func-
tion is obstructive vs. restrictive disease or a combination, the flow vol-
ume display effectively displays a characteristic pattern compared to the
­“Normal.” (The two loops shown are a part of the process, to ensure that
patient results are reproducible.) The dots show predicted values.

Normal       Restrictive      Obstructive

The restrictive pattern shows a smaller size of the normal and the
o­bstructive shows a pronounced “coving” effect on the downslope of
the exhalation, with the mixed defect (not shown) having a combination
­pattern. More detailed evaluation of this pattern is beyond the scope of this
work, but greater differentiation is achieved by measurement of flow and
volume in different ­segments of the loop (e.g., FEV1 or FEV25–75). ­Various
physical and therapeutic–diagnostic maneuvers coupled with c­ linical judg-
ments and with cardiovascular evaluations and other technologies may be
required for the full picture.
4  •   THE ABC’S OF ABG’S™

One of the diagnostic tools available in many pulmonary f­unction

laboratories is the “body box” (plethysmograph), for whole-body plethys-
mography. The processes available with this device enable more diagnos-
tic detail of the flow–volume loop (as referred to earlier), as well as being
able to measure the residual volume of the lungs.
The measurement of the gas diffusion across the parenchyma of
the lung into the circulating blood is probably the best measure of the
extent of a fibrotic disease. It may be done as part of the use of the
­plethysmograph or as a separate test procedure. The diffusion test (DLCO)
mimics gas d­ iffusion through the lung tissue into the blood by using
small amounts of carbon monoxide (CO). Carbon monoxide is chosen
since it has a similar molecular size in comparison to both oxygen and
carbon dioxide and is not typically found in the blood, so interference in
the test is near zero.
Once gas exchange occurs at the alveolar–circulatory interface, the
biochemistry really begins.

Circulation: Within the organism, several processes are linked to gas

transport into and out of the lungs. Oxygen from the external envi-
ronment ultimately powers the energy production–storage–utili-
zation process and carbon dioxide is the immediate waste product
controlled by the lung’s function.

Internally, the acquisition of oxygen to facilitate energy production

and the maintenance of a balance between acids, bases, and electrolytes in
the human organism has evolved over millions of years. Our ­premammalian
ancestors were living in an oxygen-poor, carbon dioxide-containing ocean.
High bicarbonate levels in rainwater came about as that water passed
through the limestone deposits and the bicarbonate/carbon dioxide pairing
was ­captured inside the cell when the development of cell membranes
occurred.
The primitive base to acid ratio has not only survived inside many
species, but has become critical for the proper functioning of the whole
organism. This is especially reflected in the key role that hydrogen ion
concentration plays in many metabolic systems including the process of
extraction of energy from food, the maintenance of cell and tissue ­integrity,
and oxygen transport and delivery.
 IN THE BEGINNING . . .  •   5

All these phenomena are reflective of the triad of integrally ­related

homeostatic systems that are critical for both the near and long-term
maintenance of life, acid–base balance, gas transport/exchange, and
­
­electrolyte/osmotic pressure. While in various texts each system is ­typically
discussed on an individual basis for the sake of conceptual u­ nderstanding,
they are all fundamentally related as shown in the figure.
Since the primary objective of this work is to enable the p­ rofessionals
involved in the diagnosis and treatment of the critically ill to recognize
the relationship among the terminology of testing, patient diagnosis,
­expected results, and obtained results, we won’t go into the intricacies
of the ­interrelationships of acid–base electrolytes and oxygen transport
and delivery. However, it is important historically as well as biochemically
to understand that these interrelationships exist and to a certain extent
the context. For a comprehensive but brief overview, the authors would
suggest the monograph by John Toffaletti, Blood Gases and Electrolytes.2

ACID–BASE: HYDROGEN ION (pH), BICARBONATE

(HYDROGEN CARBONATE), AND CARBONIC ACID

The human body continually produces acid as it produces energy. Much

of this acid is in the form of carbon dioxide, the end-product of a­ erobic
metabolism which is akin to combustion—the burning metabolically of

2
J.D. Toffaletti. 2009. Blood Gases and Electrolytes, 2nd ed. (Washington, D.C.: AACC
Press), ISBN-13: 978-1-59425-097-2 and ISBN-10: 1-59425-097-9
6  •   THE ABC’S OF ABG’S™

carbohydrates and related compounds resulting in CO2 and water. The

­carbon dioxide is eliminated by the lungs at an approximate rate of almost
300 liters per day.3
In addition to carbon dioxide, a typical “Western” mixed diet produces
metabolic acids such as phosphoric and sulfuric acids. These acids are re-
ferred to as “fixed” acids as they cannot be converted to CO2 and “blown off ”
in the lungs. While the bases found in the diet and produced ­metabolically
neutralize some of these acids, the remainder of the acids must be neutral-
ized by systems in the body so that acid–base homeostasis is maintained.
Acids produced as a part of aerobic metabolism are, in general, ­either
carbonic acid (resulting from the direct metabolism of glucose (carbohy-
drates) in the presence of insulin) or ketoacids (acetoacetate, hydroxybu-
tyrate) which form when insulin levels are insufficient. The c­ arbonic acid
formed results from dissociation of the dissolved CO2 into its components,
hydrogen ion and bicarbonate ion. Ketoacids, on the other hand, dissociate
directly into hydrogen ions and the corresponding anions. The result is the
dynamic equilibrium between the various anions and the hydrogen ions.
The key concept is that the sources of specific hydrogen ions are indistin-
guishable and the hydrogen ion status can usually be assessed by an under-
standing of the carbonic acid/bicarbonate system alone.

INCREASING HYDROGEN IONS = METABOLIC CHANGES

Hydrogen ions produced by metabolic action will cause a decrease in

blood pH if “buffering” systems are not in place and functioning. Because
changes in pH in either direction can alter the hydrogen ion impact on
enzyme-catalyzed equilibria, various enzyme systems can be significantly
impacted such as enzymes that maintain cellular osmotic integrity.
The dynamic equilibria established between hemoglobin and ­oxygen
is also influenced by pH. As the patient becomes more acidotic, for
­example, the oxyhemoglobin tends to release oxygen more readily to
the tissues, which is good, but, conversely, oxygen is not bound to the
­hemoglobin as readily in the pulmonary circulation.
Further, in situations involving tissue hypoxia, more acid is produced
(e.g., lactic acid), which puts the organism at a further disadvantage. In
multiple organ failure (MOF), this acid production is carried to an ­extreme,
and a stepwise cataclysmic series of events can occur, resulting in death.

That’s about 12.8 moles per day per person times 7.4 × 109 people, which is equivalent to
3

more than 45 aircraft carriers of mass—just think of the global warming going on as a result.
Do your part and please stop respiring so much.
 IN THE BEGINNING . . .  •   7

With these several examples in mind, all of which can be occurring

in any one patient, it is simple to see just how critical the u­ nderstanding
and ­ assessment of acid–base status are to both the physician and
the ­laboratorian. The remainder of the monograph is devoted to an
­understanding of the “basics” of the acid–base homeostatic process and a
simple interpretive plan.

ACID–BASE HOMEOSTASIS

Buffers are utilized by the human body to maintain the hydrogen ion l­ evels/
pH within a necessary range for effective functioning of the many meta-
bolic processes. The pulmonary and renal organ systems are two o­ rgans
that “buffer” changes in pH as one of their important physiologic functions.
However, the two organs (discussed further below) are not true “chemical
buffers.” Rather, they are “buffering systems.” Because the chemical defini-
tion of a buffer is a substance that minimizes changes in the pH of a solution
when strong acids or bases are added, buffers are found in pairs consisting
of a weak acid and its salt or a weak base and its corresponding salt.
There are several biologically important chemical buffer pairs. Of
major importance is the carbonic acid/bicarbonate pair, not only because
it is quantitatively the largest at more than 50 percent of the total, but also
because the bicarbonate system is integrally related to the pulmonary and
renal systems and can be readily measured in the blood.
While the chemical buffers present in the tissues and intracellular
­fluids react immediately to neutralize any acid produced by m ­ etabolic
­processes, because of the normal, continuous production of acid, these
buffers will in time be overwhelmed. Consequently, two secondary
­mechanisms for “buffering” play major roles in maintaining acid–base
homeostasis—the pulmonary system, which has an immediate to interme-
diate time frame of action (minutes to hours), and the renal system, which
is intermediate or longer term in its time frame of activity (hours to days).

TISSUE/BLOOD/PULMONARY ACID–BASE
INTERACTIONS

Carbon dioxide is a major end-product of aerobic metabolism. Dissolved

in an aqueous solution, it forms carbonic acid, which further dissociates
into hydrogen ions and bicarbonate ions. These are in equilibrium with
other components within the aqueous system. Since the net result of the
formation of carbon dioxide is the formation of hydrogen ions, it’s easy
8  •   THE ABC’S OF ABG’S™

to understand why release of carbon dioxide from the body can cause a
reduction in the total number of hydrogen ions present.
Carbon dioxide formed in the tissues diffuses through cellular
and ­capillary membranes to dissolve in the circulating blood plasma
­intracellular and other fluids. The reaction to form carbonic acid from
­dissolved carbon dioxide is very slow in the plasma, such that the ­ratio
of concentrations at the dynamic equilibrium present in the blood is
about 1000:1. The ­actual amount of carbon dioxide transported in the
plasma ­represents about 5  percent of the total. Carbon dioxide in the
plasma ­diffuses through the red cell membrane and establishes a dynamic
­equilibrium between that dissolved in the plasma and that dissolved in
the red blood cell. The enzyme carbonic anhydrase found in red blood
cells ­enhances the formation of carbonic acid from carbon dioxide and
­results in the subsequent formation of hydrogen ions and bicarbonate
ions in the red cell. Approximately two-thirds of the carbon dioxide of the
blood is transported as bicarbonate in this manner by the red blood cells.
The remaining carbon dioxide is transported as a carbamino complex with
­nitrogen atoms of the hemoglobin found in the red blood cell.
The result of these three systems (plasma, red blood cell, and
carbamino complex) is an effective mechanism for transporting the
­
­carbon dioxide produced in the tissues to both the pulmonary and renal
­circulation, where other mechanisms shift the equilibria causing carbon
dioxide to be exhaled and bicarbonate to be reabsorbed, respectively, with
the consequent elimination of hydrogen ions.
As venous blood circulates from the tissues where it has taken on
­carbon dioxide and hydrogen ions, it returns to the pulmonary ­circulation.
The carbon dioxide tension in mixed venous blood (the venous blood
­returning from various sites in the body and measured in the right atrium
or pulmonary artery) is approximately 46 mmHg (6.1 kPa), while the
­alveolar carbon dioxide tension is approximately 40 mmHg (5.3 kPa). This
small pressure or tension differential causes a diffusion of carbon dioxide
from the blood in the pulmonary circulation to the alveolar gas and release
to the air by the process of expiration.
Within the pulmonary circulation, this diffusion from the blood into
the alveoli starts a chain of events based on the chemical principles of the
Law of Mass Action.4 As dissolved carbon dioxide leaves the plasma, the
equilibrium shifts ions drawing carbon dioxide out of the red cell and, in
turn, out of its association as carbamino hemoglobin. The net result is de-
creased total amount of carbon dioxide and free hydrogen ions in the blood.

4
The Law of Mass Action characterizes the relationship among the quantities in a ­chemical
reaction (see our dictionary section). Henderson and Hasselbalch applied the negative
­logarithm to the equation to relate it to pH.
 IN THE BEGINNING . . .  •   9

RENAL ACID–BASE CONTROL

The carbonic acid/bicarbonate system is also a key component in re-

nal acid–base control. Renal cells, as with red cells, contain the enzyme
­carbonic anhydrase. As the carbon dioxide in the blood diffuses from the
blood during its transit through the renal circulation, the action of c­ arbonic
anhydrase results in the formation of bicarbonate and ­hydrogen ions. A pri-
mary reaction establishes the relationship such that the e­ quilibrium b­ etween
carbon dioxide and water and between bicarbonate and ­hydrogen ions ex-
ists in the blood, the renal cell, and urine. The bicarbonate formed in the
renal cells diffuses back into the blood, thus bringing back a­ dditional buff-
ering capacity to the blood. At the same time, the hydrogen ions diffuse into
the renal filtrate, and subsequently are excreted through the urinary tract.
Hydrogen ions formed in the kidney also can combine with p­ hosphates
and ammonia so that those protonated forms can be excreted in the urine.
Simultaneously, the bicarbonate formed renal cell diffuses back into the
blood, thus being available for buffering of more hydrogen ions.

SIGNIFICANCE OF THE CARBONIC

ACID–BICARBONATE BUFFER SYSTEM

When the carbon dioxide produced in the tissues during metabolism ­dissolves
in the aqueous intra/extracellular fluids and by diffusion ­dissolves in the blood,
it forms an equilibrium according to the basic c­ hemical Law of Mass Action
as shown in the figure. The amount of ­carbonic acid formed equals the prod-
uct of the solubility/unit conversion constant KS and the CO2 partial pressure.
10  •   THE ABC’S OF ABG’S™

As may be seen in the preceding chart, Henderson–Hasselbalch

r­elationship enables the evaluation of the acid–base data (pH) from a
blood gas report with respect to both primary acid–base disorder and
­compensating responses.
By calculating the negative logarithm of the mathematical r­ elationship
derived for the chemical equation for dissolved carbon dioxide, ­Henderson
and Hasselbalch, nearly a century ago, derived an equation still ­useful
­today. This equation shows the relationship between hydrogen ion concen-
tration (as pH), the equilibrium constant of an acid/salt pair (pKa), and the
concentrations of the components of that pair.
The effectiveness of a buffer pair depends on two factors, the first
of which is the “chemical” strength of the pair represented by the pKa
of the buffering system and the pH of the environment in which it exits.
(A buffer is more effective when the pKa of the buffer is closest to the pH
of the environment.) The second factor is the amount of base relative to
the amount of acid present in the system, which can be thought of as the
“physiological” strength.
The carbonic acid–bicarbonate buffering system in human blood
has a normal pH of 7.4. Since the negative logarithm of the d­ issociation
­constant, pKa, is 6.1, with a pKa more than 1.0 unit lower than the ­normal
pH, the chemical strength of carbonic acid–bicarbonate is ­considered
weak. However, what the system lacks in chemical strength is made
up for by the physiologic strength as represented by the 20:1 ratio of
salt (­bicarbonate) to acid (carbonic acid). The pulmonary/­ respiratory
component of the equation is directly related to ventilation and
­
alveolar/arterial PCO2 (therefore, pH), while renal function affects the
­hydrogen carbonate (bicarbonate) concentration.
Clinical Implications of Blood Gas Measurands. The amount of
hydrogen ion (measured pH) in the blood is key to the ­interpretation
of a blood gas report since it answers the basic question of whether
the ­condition is acidosis or alkalosis. Changes in the measured PCO2
­leading to changes in pH come next. Increases in PCO2 result from
­hypoventilation, with a subsequent increase in carbonic acid and h­ ydrogen
ions (decrease in pH). Thus, a decrease in pH due to an increase in PCO2
­(hypoventilation) is classified as a pulmonary or respiratory acidosis.
The reverse, a d­ ecrease in PCO2 due to hyperventilation, results in a
­respiratory or respiratory ­alkalosis because of the decreased carbonic
acid and subsequent increase in pH.
When disease processes alter the hydrogen ion concentration, v­ arious
control mechanisms attempt to return hydrogen ion concentration to ­normal
values. This phenomenon, known as compensation, can occur in response
to the primary disorder over a period of a few seconds to hours or days.
 IN THE BEGINNING . . .  •   11

Carbonic acid in turn is in a dynamic equilibrium with hydrogen ions

and bicarbonate, defined by the equilibrium constant Ka. A decrease in
bicarbonate (a base) results in an increase in hydrogen ion concentration
(decrease in pH), thus a renal or “metabolic” acidemia (decreased blood
pH) can result from either a true increase in hydrogen ions or a decrease
in the bicarbonate or base. Conversely, a renal or metabolic (increased pH)
alkalemia is reflected by an increase in the bicarbonate ion.

ACIDOSIS–ALKALOSIS CATEGORIES AND

MEASURED VALUES

The following chart can serve to summarize acid–base status based on the
measured values from a blood gas system—the quantities known with
greatest certainty.

CLINICAL DESCRIPTION AND IMPLICATIONS

RESPIRATORY ACIDOSIS/VENTILATORY FAILURE

The overall etiology of respiratory acidosis is impairment in respiration.

The primary change and the one, in fact, that defines respiratory acido-
sis is the increase in PCO2 that results from alveolar hypoventilation.
12  •   THE ABC’S OF ABG’S™

This retention of CO2 can be the result of having one of several conditions

but the result is that the ratio of bicarbonate to carbonic acid is less than
the 20:1 value that results in the normal pH of 7.4. Additionally, there is
the concomitant H+ formation and pH drop.
Compensation for this disorder generally is renal, provided there is
no correction for the underlying cause. The kidneys in their compensa-
tory approach retain the bicarbonate base and excrete acid salts. Addi-
tionally, there is the likelihood of increased formation of ­ammonia ions.
Respiratory Acidosis (Hypoventilation) Etiology. What follows is a
brief listing of some of the causes of ventilatory failure.

• Airway Obstruction: Foreign Body, pneumonia, emphysema,

­laryngospasm, chronic bronchitis
• CNS Depression: Narcotics, anesthetics, injury, tumor
• Thoracic Injury: Pneumothorax, flail chest, tracheal tear
• Mechanical Ventilation: Inadequate rate and/or tidal volume,
­increased dead space.
• Chest Wall Disease (Musculoskeletal and Neuromuscular
­dysfunction): Kyphoscoliosis, post-polio syndrome, myopathy
• Miscellaneous: Congestive heart failure, severe obesity

RESPIRATORY ALKALOSIS/HYPERVENTILATION

The converse of respiratory acidosis is respiratory alkalosis. The

­primary etiology of this disorder is inappropriate excess ventilation or
­hyperventilation. It is important to distinguish hyperventilation, which
means too much ventilation for the carbon dioxide produced, vs. i­ ncreased
ventilation, which may be an appropriate response to conditions. A clear
example of an increase in ventilation is that due to exertion which r­ equires
more energy and produces more carbon dioxide. The increased ­ventilation
rids the body of the excess carbon dioxide produced and keeps the pH
within the acceptable range. This is not hyperventilation, but rather
­increased ventilation.
Respiratory Alkalosis (Hyperventilation) Etiology. Again a few
causes of hyperventilation follow.

• CNS Disorders: Injury, tumor, stroke, anxiety

• Hypoxia: ARDS, pulmonary emboli, atelectasis, anemia
(low hemoglobin)
• Mechanical ventilation: Excess tidal volume and/or rate
 IN THE BEGINNING . . .  •   13

• Hypermetabolism: Fever, injury, sepsis

• Miscellaneous: Congestive heart failure, salicylate intoxication,
cirrhosis

Hyperventilation is characterized by a decrease in carbon dioxide

t­ension below acceptable limits, while the bicarbonate to carbonic acid
­ratio is increased above the normal 20:1 ratio. The consequent change in
pH is toward an increased value. Changes in other analytes (particularly
bicarbonate) depend on the extent and severity of the primary disorder.
Renal compensation occurs, resulting in excretion of alkaline and bicar-
bonate salts and retention of acid salts. In addition, ammonium ion is
formed to a lesser extent.
A common cause of respiratory alkalosis is a patient apprehensive
about the potential pain caused by an arterial puncture. Another common
cause is excess mechanical ventilation. This can be either inadvertent, due
to changing patient conditions or missetting of the ventilator, or a conse-
quence of trying to improve the amount of oxygen available to the patient.

NON-RESPIRATORY/“METABOLIC” ACIDOSIS:
NORMAL ANION GAP

Non-respiratory or “metabolic” acidosis can result from either an ­excess

production or ingestion of acids or a decrease in the base present. A
­primary metabolic acidosis is represented by a drop in the pH, while the
PCO2 remains normal. Non-respiratory acidosis has as its root causes
­either a fixed acid retention or a base loss. As with respiratory acidosis the
bicarbonate to carbonic acid ration of 20:1 is decreased but in contrast to
respiratory acidosis the non-respiratory primary disorder is compensated
by a pulmonary mechanism in that there is an increase rate and depth of
breathing. With compensation, the PCO2 decreases.
Non-respiratory/“Metabolic” Acidosis Etiology. Several common
causes of acidosis have non-respiratory origins:

• Diarrhea, small bowel fistula, ureterosigmoidostomy (CO2 loss)

• Proximal renal tubular acidosis (Decreased H2CO3−)
• Distal renal tubular acidosis (Decreased acid excretion)
• Acid administration (HCl, NH4Cl) (Increased load)
• “Dilutional” acidosis (Volume expansion with bicarbonate free
fluids)
14  •   THE ABC’S OF ABG’S™

Base loss, depending on its cause, may be compensated for by

r­enal mechanism if they are not at the root cause of the problem. R ­ enal
­compensation would be retention of bicarbonate, excretion of the acid
salts, and increased formation of ammonia ions.
The anion gap or the difference between the total measured c­ ations
and the measured anions serves to differentiate metabolic acidosis of
different etiology. Most common in this category are problems and
­
changes ­associated with bicarbonate loss, either relative or absolute.

NON-RESPIRATORY OR “METABOLIC” ACIDOSIS:

ELEVATED ANION GAP

A typical cause of metabolic acidosis with an increased anion gap is

diabetic ketoacidosis (DKA), resulting from impaired metabolism of
­
glucose or a lactic acidosis resulting from anaerobic metabolism. In both
cases the “gap” is increased. The latter can occur if oxygen availability
is decreased by any one of several mechanisms including the temporary
lactic acidosis seen after vigorous exercise.
A less common cause would be a decrease in the fraction of inspired
oxygen. In fact, any condition impairing oxygen delivery to the tissues
could result in a non-respiratory or “metabolic” acidosis. In addition,
­uremia and some poisons can add to the hydrogen ion and atypical anion
loads on the acid–base homeostatic system.

NON-RESPIRATORY/“METABOLIC” ALKALOSIS

The final category of primary acid–base disorder is non-respiratory or

“metabolic” alkalosis. In this case, the cause can be one or a combination
of fixed acid loss, base gain, or potassium depletion. As with respiratory
alkalosis the bicarbonate to carbonic acid ratio is increased. Pulmonary
compensation for this non-respiratory disorder is typically a decreased
rate and depth of ventilation. This is clearly not a complete and sufficient
­compensatory mechanism, however, since the drive by the body to supply
itself with adequate oxygen takes precedence over the need to maintain
acid–base balance using the pulmonary mechanism.
As with the respiratory alkalosis the renal compensatory mechanism
is the same if that mechanism itself is not involved in the primary cause
of the disorder. Thus, we would find excretion of bicarbonate, retention
of acid salt, and decreased ammonia ion formation as a part of the overall
compensatory response.
 IN THE BEGINNING . . .  •   15

A common cause within the hospital setting is bicarbonate adminis-

tration. The use of (excess) amounts of over-the-counter antacids has also
been implicated.

ACID–BASE STATUS INTERPRETATION

The interpretation of acid–base results is a conceptually simple sequel

to the understanding of the basic physiology and clinical conditions just
­outlined. This interpretation is important to assess the validity of blood gas
data in terms of what is known about the patient. If the data “make sense,”
the analyst has added confidence in the reporting of results. While for
many tests performed in the clinical laboratory, the evaluation of the data
obtained in relationship to the clinical state of the patient is interesting, in
blood gas measurement, it is a critical part of total quality assurance. There
is only one opportunity to get the right results for that specimen/patient.
The dynamic nature of pH and blood gases in the patient, the turnaround
time requirements, and the labile nature of the analytes themselves in the
specimen collected preclude obtaining meaningful results by reanalysis.
The most common sequence in the interpretation of the data is: (1) to
make note of the pH or hydrogen ion concentration to determine if any
significant acid–base disorder exists, (2) to check the arterial PCO2 to
­determine if any acid–base disorder results from, or is compensated by
a ventilatory change, and (3) to observe the change in pH or ­bicarbonate
with respect to the change resulting from changes in carbon dioxide tension
alone. By understanding the relationship among the measured values and
observable patient status in the context of an analysis of the Henderson–
Hasselbalch equation, the quality of measured results can be improved.

OXYGENATION ASSESSMENT IN BLOOD

GAS ANALYSIS

Complete laboratory evaluation of oxygenation often requires much more

than simple blood gas measurements. Nevertheless, many patients can
be evaluated and treated successfully using blood gases alone if clinical
­observations and patient history are considered.
The oxygen partial pressure or tension of arterial blood, PO2(aB) or
PaO2, an indicator of the oxygen diffusion into the pulmonary ­circulation,
is the driving force in moving oxygen from one compartment of the body
to another (e.g., alveoli of the lungs to the pulmonary capillaries). A ­typical
level for PO2(aB) in young, healthy adults is generally considered to be
16  •   THE ABC’S OF ABG’S™

>95 mmHg (12.7 kPa). Nevertheless, action due to hypoxemia is usually

not taken unless the PO2 is <80 mmHg (10.7 kPa) (10). The PO2(aB) may
be decreased in cases of impaired lung function (COPD) when there is a
low inspired oxygen tension (e.g., at high altitudes or in the presence of
other gases) and with age when the PO2(aB) lowers by about 1 mmHg or
0.13 kPa for each year of age beyond 60. Measures to improve PO2(aB)
include optimizing the mechanical ventilation and otherwise increasing
the inspired oxygen tension such as by increases in FIO2. Along with the
total hemoglobin, the PO2 of arterial blood is the primary indication of
oxygenation status for most patients.
Evaluating the blood gases alone, for example, in a healthy young
adult living near sea level, the laboratory reference value for PO2 is u­ sually
about 95 mmHg (12.7 kPa). As with PCO2 and pH, however, a wider range
of values may occur before any therapeutic action is ­indicated. ­Generally, a
PO2 of 80 mmHg (10.7 kPa) signals therapeutically s­ ignificant ­hypoxemia
(low blood oxygen). Above this value there is very little change in o­ xygen
saturation5 or oxygen content with changes in oxygen tension, but ­below
80 mmHg changes in saturation can occur rapidly. ­Exceptions to this
limit are newborns, who have an acceptable range of 40 to 70 mmHg
(5.3–9.3  kPa), and adults over 60 years. Normal deterioration of lung
­function with ­increasing age causes a decrease in expected PO2 ­values of
­approximately 1 mmHg (0.13 kPa) per year.
Hypoxemia is commonly defined based on a patient’s PO2 while
breathing room air. Estimates of hypoxemia can be made, however, even
if the patient’s ventilation is being supported. It is unnecessary, and ­indeed
potentially dangerous, to withhold oxygen therapy from symptomatic
­patients while awaiting the drawing of a sample of blood gas analysis.
An estimate of the expected PO2(aB) used by many clinicians for
­patients receiving oxygen therapy is based on multiplying the fraction of
oxygen in inspired air (FIO2) by 5 (for mmHg). If measurements are in
kPa (SI), the FIO2 should be multiplied by two-thirds (0.67). If a patient’s
measured value is lower than the estimated, hypoxemia on room air may be
assumed, or a collection/measurement error may be suspected.
Clinically, if cardiac output and peripheral perfusion are deemed
­adequate, then one or more of the following are probably involved in
the decreased tissue oxygenation: oxygen saturation (gas exchange/­
shunting), oxyhemoglobin fraction, and total oxygen content of the blood

5
Saturation (oxygen saturation) is always in reference to available hemoglobin, so take care
when other hemoglobins (dyshemoglobins) are present. Carbon monoxide poisoning and
treatment, for example, can result in a saturation of >95 percent but a hypoxic patient!
 IN THE BEGINNING . . .  •   17

(gas  ­ exchange and functioning hemoglobin/dyshemoglobins) or P50

­(tendency to take up and release oxygen from the blood hemoglobin.
Oxygen “saturation” is a common means of assessing oxygenation
status, especially with the widespread use of peripheral or “pulse” oximetry.
There are two significant caveats in application of oxygen ­“saturation”
values used for diagnosis or treatment: one holds true for “saturation” de-
termined by any modality, the other applies in outpatient or emergency/
trauma settings where patients may have been exposed to various toxic
agents.
The first concerns the PO2—oxygen saturation relationship itself—
the oxyhemoglobin dissociation curve (ODC) and its sigmoid or s-shape.
As can be seen in the figure, there is a steep drop off in the value for
­oxygen partial pressure below saturation levels of 90 percent. A change
of ­saturation of but a few percentage points can correspond to a change
in o­ xygen tension of 30 mmHg (4 kPa), a difference which is highly
­significant, but might not be recognized as such if merely monitoring the
saturation.

The second issue is that devices measuring only oxygen ­saturation

(and possibly pulse rate) cannot measure the presence of depleted
­oxygenation resulting from dyshemoglobins (e.g., COHb and MetHb).
Use of a “saturation” calculated from a standard oxyhemoglobin curve
plus the measured PO2 and use of some estimating algorithm, as has been
done on some blood gas-only analyzers, may only be valid for healthy
people! Further, some quantities reported from “enhanced” blood gas
18  •   THE ABC’S OF ABG’S™

a­ nalyzers (i.e., blood gas + CO-oximetry, etc.) have given rise to some
confusion in terminology.6

INTRAPULMONARY SHUNT FRACTION, Qsp/Qt

The Intrapulmonary Shunt fraction (Qsp/Qt) is the fraction of total cardiac

output into the pulmonary circulation that is not oxygenated, usually due
to the lack of exposure to fully functioning alveoli. Shunts can either be
true cardiac shunts where blood flow from the right-sided cardiac cham-
bers to those on the left or pulmonary shunts in which the PO2 is less than
ideal, but still high enough to saturate hemoglobin.
With an increased FIO2, the shunt fraction can differentiate pulmo-
nary cardiac shunts. It is quantified using O2 content in the Qsp/Qt equation
though substituting a measured saturation (in the designated blood speci-
mens) is probably satisfactory. It should be recognized that the pulmonary
contribution estimates, for example, a/A and (A-a) PO2, correlate poorly
the more precise equation shown below the figure. Using the shunt frac-
tion equation, oxygen content is measured and applied to the calculation:
Shunt Fraction and the Shunt Equation

Qsp  ctO 2 ( c ) − ctO2 ( a ) 

= 
Qt  ctO 2 ( c ) − ctO2 ( v ) 

Reference range: 2 to 6 percent (0.02–0.06)

SUMMARY: GAS EXCHANGE, OXYGEN

QUANTITIES, AND ACID–BASE HOMEOSTASIS

The pH or hydrogen ion concentration affects several critical ­homeostatic

systems, including oxygen delivery to and utilization by the cells, and

6
Before photometric technology was introduced for blood analysis of hemoglobin moieties,
both total oxygen content and oxygen saturation were directly measured by a long and ­exacting
process of extracting the gases from the blood. It wasn’t necessary to i­ncorporate the t­otal
hemoglobin in the determination. In photometry, the relative amounts of each ­hemoglobin
moiety are measured and calibrated with a reference total hemoglobin. S ­ aturation is simply
the percent of oxyhemoglobin relative to the sum of the oxyhemoglobin plus the unbound
but available hemoglobin (oxyHb + deoxyHb). The fraction of oxyhemoglobin relative to the
total hemoglobin is necessary to determine oxygen content. This fractional oxyhemoglobin
and saturation are numerically identical for healthy people not exposed to toxins, and many
began to treat them similarly—though they are in many instances (especially in patients
presenting to the ED) both different and numerically different.
 IN THE BEGINNING . . .  •   19

the distribution of electrolytes in tissues and intracellular fluids. B ­ ecause

changes in pH of a relatively small amount can affect the function of
critical systems, the human body has compensatory and physiologic
­
­responses that attempt to control such fluctuations. Three “buffering”
­systems act in ­concert with each other: chemical buffers of the cells and
intracellular ­fluids, pulmonary buffering via expiration of CO2 that has
been transported to the pulmonary circulation via the blood, and ­excretion
of hydrogen ions by the kidneys. Net physiology results are to minimize
pH change and its effects on oxygen-energy production as well as to
­maintain appropriate pH-dependent metabolic activity.
Understanding these relationships and definitions relates to the
­laboratorian’s ability to assess the quality of results obtained before they
are recorded so the values obtained can be better evaluated and, if they
do not make sense, reanalysis or other consultation may be appropriate.
By understanding of the concepts involved and reviewing the data prior
to reporting the results, an overall improvement in the quality of these
most critical values can be obtained and delays and reanalysis will be
minimized.

BASIC OXYGENATION INTERPRETATION

Hypoxemia is commonly defined based on a patient’s PO2 while ­breathing

room air. Estimates of hypoxemia can be made, however, even if the
­patient’s ventilation is being supported. It is unnecessary, and indeed
­potentially dangerous, to withhold oxygen therapy from symptomatic
­patients while awaiting the drawing of a sample of blood gas analysis.
An estimate of the expected PO2(aB) used by many clinicians for
­patients receiving oxygen therapy is based on multiplying the fraction of
oxygen in inspired air (FIO2) by five (for mmHg). If measurements are in
kPa (SI), the FIO2 should be multiplied by two, then divided by three. If a
patient’s measured value is lower than the estimated, hypoxemia on room
air may be assumed, or a collection/measurement error may be suspected.
The table (hypoxemia decision criteria) gives criteria for defining
the probable existence and extent of hypoxemia, provided ventilatory and
acid–base status have been evaluated.
If cardiac output and peripheral perfusion are deemed adequate, then
one or more of the following are probably involved in the decreased ­tissue
oxygenation: oxygen saturation, oxyhemoglobin fraction, total oxygen
content, or P50. Measurements of COHb, MetHb, sulfhemoglobin, and
2,3-diphosphoglycerate can help determine which parameter is tied to the
decreased oxygenation.
20  •   THE ABC’S OF ABG’S™

ELECTROLYTES AND WATER: MEASUREMENT

AND CLINICAL OVERVIEW

Electrolytes as chemical entities are simply charged particles that get their
charge characteristics by dissolving in an aqueous medium. That charge,
either positive or negative, can be either the result of a complete or partial
dissociation of a molecule into positively and negatively charged compo-
nents. Each molecule that has the potential for dissociation is influenced
by its environment as well as its own characteristics and each influences
the other. Acids, bases, proteins, and salts and solids can be electrolytes
under a specific set of circumstances. The complexity of the human (mam-
malian) organism is such that all these aspects can play a role, but for sake
of convenience and brevity this brief discussion of electrolytes will take a
simple approach to a complex subject.
Electrolytes play several major roles in maintaining life. Key among
these are the maintenance of cellular integrity and transmission of electric
signals. Further, some are essential to enzyme action and energy produc-
tions when they act as cofactors in critical reactions.
Among the common electrolytes, sodium (Na) and potassium (K) are
the principal cations (positive ions) in the extracellular and intracellular
fluids, respectively. Jointly they help to maintain both electrical neutrality
and cellular integrity, along with their counterpart anions (negative ions),
chloride (Cl), and bicarbonate (HCO3−), the latter of which we discussed
under the acid–base overview. Calcium and magnesium (Ca and Mg) are
significant in bone structure and metabolism, but a small portion of each
as ions is critical to many functions in the organism. Finally, proteinate
(Pr−) anion is a contributor to cell integrity because of its osmotic pressure
along with the osmotic pressure of the other ions.
New Measurement Technology Affects Clinical Decisions: ­Clinical
evaluation in the acute care setting requires both testing of body fluids
for electrolyte levels and clinical diagnostic/therapeutic intervention
activities. Therefore, the point-of-care measurement capabilities must
­
be not only rapid but also as accurate as central laboratory testing. The
­enhanced blood gas analyzers (eBGAs) marketed by several m ­ anufacturers
meet that criteria, but in doing so raise some issues that generally may
not be fully appreciated by many caregivers or physicians, and the issues
can impact terminology as well as clinical practice and judgment. Without
­getting too much into the details in this overview, the most significant
­issue in this author’s view has already been alluded to. It is the fact that the
electrolyte-ions are active in aqueous (water) solution!
 IN THE BEGINNING . . .  •   21

That simple fact means that the organism’s homeostatic systems

d­epend on the concentration/activity of each and all the ions in the
­aqueous/water phase of the blood.
From the earliest days of measurement, laboratories were basing their
reports for electrolytes on the concentration in the liquid portion (mainly in
serum or plasma and in the very early days, lysed whole blood). The report
factitiously lowered values of the electrolytes, which didn’t really matter
if all patients had approximately the same protein levels. But as is well
known, protein abnormalities exist and they can affect the apparent elec-
trolyte results. There is a similar situation that can exist in situations of high
lipid levels—very low results can be reported using the older technology!
The new technology wins! The sensors in the eBGAs are of their very
nature selective for measurement of the concentration/activity of the elec-
trolytes in the water portion of the blood specimen. So even though the
specimen is whole blood (necessary for the blood gases), the electrolytes
in the cells are not measured—only the electrolytes in that aqueous phase
of the plasma! (we repeat this description in each electrolyte’s definition/
discussion, to ensure that it’s always considered). One added note to this is-
sue, the eBGAs are all designed to report the electrolytes with reference val-
ues based on normal plasma water, so despite the technology improvement,
no significant change in reference values for electrolytes was ever mani-
fested out of concern for potential confusion and issues with clinical care.7

THE ELECTROLYTE’S CLINICAL IMPLICATIONS

The two major ions in the extracellular fluid, especially in the blood
plasma which is measured, are sodium and chloride. These ions generally
track each other in health and abnormal conditions with a few notable
exceptions. Potassium is also present significantly in the plasma, but at
levels much lower than the other two.
Sodium’s typical values are between 135 and 148 mmol/L, a nar-
row range. Deviations outside of <120 or >155 mmol/L may be life
­threatening, but any deviations outside the reference range may cause
­clinical changes.

7
This was accomplished by a consensus process through the Clinical and Laboratory
­ tandards Institute (CLSI, formerly NCCLS) of Wayne, PA, the US’s National Institute of
S
Standards and Technology (NIST), and scientists of several manufacturers of systems having
this technology.
22  •   THE ABC’S OF ABG’S™

Note on Unit Used: The unit of concentration recommended by the

International Federation for Clinical Chemistry (IFCC) is mol/L or one of
its fractions in this case, mmol/L. However, it is common to find r­ eports
using mEq/L. The numeric value for all monovalent ions is the same
whichever unit is reported.
Specimen Required: Whole blood, collected in syringes, evacuated
tubes, or capillary tubes; identify source (arterial, venous, capillary) on
the requisition and collection device label; collection device must contain
standardized volumes of liquid heparin or very soluble dry/lyophilized
(“crystallized”) heparin. The heparin salt used must not interfere with
other measurements that may be required. In most instances, Li-heparin
is suitable.
Use of therapeutic heparin is likely to cause errors in analysis, due
to specimen dilution variation and/or electrolyte/pH effects from the
heparin.
Clinical Implications: Sodium is the major extracellular cation. As
such it controls the fluid space and balance and consequently osmotic
relationships.

Na-Related Disorders
Hypernatremia Hyponatremia8
Water loss Dilutional
• Diarrhea • CHF
• Excess sweating • Edema hypoalbuminemia
• Nephrotic syndrome
• Malabsorption
Low intake Nonrenal Na loss
• Coma • Vomiting
• Hypothalamic lesion • Diarrhea
Renal polyuria Renal Na loss
• High calcium • Enforced diuresis
• K+ depletion • Renal disease
• Interstitial nephritis
Polyuria
• Osmotic diuretics
• Diabetes: Insipidus and mellitus

8
Note that when using direct-measuring ISEs as described, there is no longer the risk of
­artifactually low sodium, since the measurement is in plasma water.
 IN THE BEGINNING . . .  •   23

The major extracellular anion, the element chlorine has an atomic

number of 17 and an atomic mass of 35.5 g/mol.
Chloride levels: Generally parallel to those of sodium (Na+).
Typical values for chloride are between 95 and 110 mmol/L. Again,
as with sodium the concentration may be reported as mEq/L, with no
­numeric difference.
Specimen collection is also identical to sodium.
Chloride Measurement: Early measurement technology relied on
reaction of the chloride ion present in the specimen with either silver to
form a precipitate of AgCl or with a chelating agent to form a colored
complex with subsequent titration of results. Most eBGAs are based on
ISEs, with the sensor containing a chloride-sensitive chromophore. The
key characteristic is the selectivity of the sensor for the chloride in the
water phase.
Diagnostics based on elevation or decrease of chloride include
­several primary conditions as well as those which are secondary to other
disorders.

Increased > 110 Decreased < 95

• Hyperchloremic metabolic • Metabolic alkalosis
acidosis • Overhydration
• Respiratory alkalosis/ • Congestive heart failure
hyperventilation • Burns
• Severe dehydration (diabetes) • Salt depletion
• IV saline • Addison’s disease
• Renal disease • Excess hypotonic IV fluids

Potassium (K+) in the blood plasma/serum is a minor cation with

­major impact. With typical values between 3.5 and 4.6 mmol/L, it is
­between 2 and 3 percent of the cationic load. However, as seen in the chart
below, relatively small changes have serious consequences.
Potassium has the same unit (mmol/L) and the same sample h­ andling
requirements as sodium and chloride and using eBGAs, it is m ­ easured in
plasma water as those ions. However, the fact that potassium is found
in high concentrations in intact cells leads to the need for special care
in c­ollecting specimens so that tissue potassium is not introduced to
the ­sample by excessive manipulation of the limb during collection.
­Additionally, hemolysis may be a factor in the values obtained.
Measurement Technology for potassium has evolved along with the
other electrolytes. Originally potassium was measured by techniques like
those for sodium. Today in the eBGAs measurements are based on ISEs, with
24  •   THE ABC’S OF ABG’S™

the sensor containing a potassium-sensitive chromophore rather than the

glass electrode used for sodium, but other than that the procedure is the same.
Clinical implications of differing potassium values are shown in the
table below.

Hyperkalemia Hypokalemia
Intracellular
Acidosis GI loss Urine loss movement
Renal failure Emesis/abuse Mg depletion DKA
Muscle necrosis NG suction Antibiotics Familial
hypokalemic
paralysis
IV Malabsorption Increased
administration mineralocorticoids
Transfusion of Diarrhea/ Renal tubular
older blood laxative acidosis Other
abuse
Adrenogenital Pyloric Licorice abuse Acute
syndrome obstruction myeloid
leukemia
Adrenal Dec K+ intake
insufficiency
Thrombocytosis

Hemolyzed
specimen

The anion gap (A.G.) is the difference between the “total” concentration
of cations and the measured number of anions and has been used as a diagnos-
tic tool to differentiate between causes of electrolyte and acid–base disorders.
Almost exclusively on eBGAs the cations used are sodium and
­potassium and the anions are the measured chloride and the calculated
bicarbonate (hydrogen carbonate), since all are readily available on the
same measurement platform:
Anion Gap = [Na+] + [K+] − [Cl−] − [HCO3−]

Typical values using this equation are between 11 and 20 mmol/L.

Make sure you know your testing lab’s protocol and expected range before
using any values to interpret patient status.
 IN THE BEGINNING . . .  •   25

Clinical Implications: The purpose of the anion gap calculation is

to aid in the assessment of non-respiratory/metabolic acidosis. A high
anion gap usually indicates the presence of some combination of the
unmeasured anions already mentioned, as well as SO4−2, acetoacetate,
-hydroxybutyrate, etc. Thus, sources of these anions that must be part
of the evaluation of an acidosis such as in DKA and alcohol abuse would
need to be considered due to its production of ketoacids. Toxins such as
methanol, glycols, iron, cyanide, aspirin, etc., or uremia/renal failure with
the decreased bicarbonate reabsorption, decreased acid excretion, accu-
mulation of sulfates, urates, and phosphates should also be considered.
Normal Anion Gap with acidosis can only be the result of decreased
bicarbonate. To maintain neutrality, chloride must increase as it is the only
major anion. Loss of bicarbonate may be caused by GI loss—diarrhea,
­renal loss—renal tubular acidosis, or ingestions—ammonium chloride,
total parenteral nutrition (TPN).
Low Anion Gap can result from loss of albumin resulting in increase
in chloride and bicarbonate to maintain neutrality.
Electrolytes and Overall Summary: The full scope of a discussion of
both the analytical and the clinical electrolytes deserves much more space
than we have here. But even in the brief paragraphs above it’s evident that
there is a dramatic clinical impact on overall well-being of the organism.
The clinician must consider not only whether there is a primary electrolyte
disturbance or one related to other therapeutic interventions. The electro-
lyte homeostatic systems are clearly related to the acid–base and all are
related to the pulmonary gas exchange, oxygen transport, and utilization.
Hopefully, the pages that follow will be of further help in your understand-
ing of the full range of diagnostic testing for all these related systems.
 Index
A Acronym, 34
A-a gradient. See Alveolar–arterial
oxygen gradient
A-aDO2. See Alveolar–arterial
oxygen gradient
a/A ratio (arterial/alveolar ratio),
29, 43–44
aB (arterial blood), 28
Acid, 30–31
Acid dissociation
constant (ka), 108
Acid–base, 5–6
balance, 31
chart, 31–32
disorders, 32
homeostasis, 7, 18–19
status interpretation, 15
Acid–base disorders, 32–33. See
also specific disorders
Acid–Base Status of the Blood,
The, 165
Acidemia, 33. See also Acidosis;
Acid–base disorders;
Alkalosis
Acidosis, 33–34. See also
Acidemia; Base excess of
extracellular fluid (B.E. (ecf))
categories and measured
values, 11
nonrespiratory. See
­Nonrespiratory acidosis
respiratory, 10, 11–12, 32,
154–156, 182
Adenosine triphosphate (ATP),
34–35, 45
Air sacs. See Alveolus
Airway assessment, 1
Airway-based diseases, 2
Airway obstruction, 12, 155
Airway resistance (RAW), 35
Albumin, low, correction of anion
gap for, 41
Alcohol abuse, DKA and, 41
Alkalemia, 35–36. See also
Alkalosis; Acid–base
disorders; Acidosis;
Acidemia
Alkalosis, 36. See also Alkalemia;
Acid–base disorders;
Acidosis; Acidemia; Base
excess of extracellular fluid
(B.E. (ecf))
categories and measured
values, 11
non-respiratory. See
­Nonrespiratory alkalosis
respiratory, 10, 12–13, 33,
106, 156
Allen test, 36–37
Alveolar air equation, 37
Alveolar dead space, 83
Alveolar gas (air) (A), 28. See also
End-tidal (end expiration)
air (et)
exchange, 37–38
192  •   INDEX
Alveolar oxygen partial pressure
(PO2(A)), 38
Alveolar ventilation, 38
Alveolar–arterial oxygen
gradient, 39
Alveolar–circulatory interface, 4
Alveolus, 39
Anatomic dead space, 83
Anesthesia, 60
Anion, 40
Anion gap (AG), 24–25, 40–41
low, 25, 41
normal, 25, 41
Anticoagulant, 41–42
in critical care testing, 42–43
ap (arterial plasma), 28
Arterial blood (aB), 28
Arterial blood gases (ABGs), 30
Arterial plasma (ap), 28
Arterial puncture, 43
Arterial/alveolar ratio (a/A ratio),
29, 43–44. See also Alveolar
air equation; Alveolar–arterial
oxygen gradient
Artery, 44
brachial, 44
femoral, 44–45
pulmonary, 45
radial, 45
ulnar, 45
Atmospheric pressure (P(Atm)/
p(Atm)), 138, 153
Atom, 45
ATP (adenosine triphosphate), 45
Average Volume Assured Pressure
Support (AVAPS), 46
Azotemia, 46
B (BUN)
Barometer, 46–47. See also Partial
pressure
Base excess (in vitro) (B.E. (vt)), 47
Base excess of blood (B.E. (B)), 47
Base excess of extracellular fluid
(B.E. (ecf)), 47–48
Base excess/deficit (B.E.), 48
Base units. 49, 163. See also SI units
Bases, 30, 47
Bedside testing, 49
BGA/BGs. See Blood gas analysis
(BGA/BGs)
Bicarbonate (hydrogen carbonate),
5–6, 49–51, 103
BiPAP (BIPAP), 51
Blood acid–base interactions, 7–8
Blood-circulation-based diseases, 2
Blood gas analysis (BGA/BGs),
49, 51–53. See also Enhanced
blood gas analysis (eBG/
eBGA)
oxygenation assessment, in blood
gas analysis, 15–18
Blood gas measurands, clinical
implications of, 10
Blood gas symbols, 53
Blood glucose, 183–184
Blood source (vt), 29
Blood testing, anticoagulant and, 42
Blood urea nitrogen (BUN),
54–56, 57. See also
Azotemia; Urea; Urea
nitrogen
Body Box (plethysmograph),
4, 56, 148
Boron (B), 46
BPM (breath rate), 56
Bradley, Freeman, 56
Breath rate (BPM), 56
Breathing process, 1–2
Bronchodilator, 56
Buffer system, carbonic
acid–bicarbonate, 9–11
BUN. See Blood urea nitrogen
Bunsen solubility coefficient, 57
C
Calcitonin, 57
Calcium, ionized (iCa, Ca++),
57–58

Capnography, 59–60
Carbamino complex, 8
Carbon, 60
Carbon dioxide (CO2), 6, 7–8, 65
electrode, 62–63. See also
Severinghaus electrode
solubility, 65
Carbon dioxide content (ctCO2/
TCO2), 60–62
Carbon monoxide (CO), 4,
66–67, 75
Carbonic acid (H2CO3), 5–6, 67
Carbonic acid–bicarbonate buffer
system, 9–11, 67
Carboxy-hemoglobinemia, 70.
See also Carboxyhemoglobin
(COHb)
Carboxyhemoglobin (COHb),
68–69, 159
Cardiac output (CO, Q, Qc), 57,
70–71, 153. See also Fick
equation
Cation, 71. See also Anion
Cellular metabolic pathways,
71–72
Centers for Disease Control and
Prevention, 80–81
Centimeters of H2O (Water)
(cmH2O), 72
Chest wall disease, 12
Chloride (Cl−), 23, 72–74
Clark electrode, 74, 129, 149.
See also Oxygen electrode;
Polarographic electrode
Clark, Leland C, 74–75
Clinical and Laboratory Standards
Institute (CLSI), 75
CNS depression, 12, 155
CNS disorders, 12, 156
CO. See Carbon monoxide (CO);
Cardiac output (CO, Q, Qc)
CO-oximeter, 75–76
CO2. See Carbon dioxide (CO2)
Coefficient, 76–77. See also
Matrix algebra coefficient
INDEX  •   193
COHb (carboxyhemoglobin),
68–69, 159
Compensation (for acid–base
production), 10, 77–78
Compliance, 77–78
Continuous positive airway
pressure (CPAP), 78–79
CPAP (continuous positive airway
pressure), 78–79
Creatinine, 79–80. See Blood urea
nitrogen (BUN); Azotemia
Creatinine clearance. See
Glomerular filtration rate
(GFR/eGFR)
Crit/’crit/crit. See Hematocrit
Critical care testing, anticoagulant
in, 42–43
ctO2 (oxygen content), 128
Cyanide (CN-), 80–81
poisoning, 80–81
Cyanocobalamin, 81–82. See also
Hydroxocobalamin
CyanoKit, 82
D
Dead space (Vd), 83–84, 181
ventilation, 83
Dead space equation (Vd/Vt), 83
Deoxyhemoglobin (HHb), 84, 159
Deoxyribose, 84. See also
Adenosine Triphosphate;
Ribose
Derived units, 84–85, 164–165.
See also SI units
Dextrose. See Glucose
Diabetic ketoacidosis (DKA), 14
and alcohol abuse, 41
Diaphragm, 85
Dichloromethane (methylene
chloride), 118
Diffusion Capacity, Lung, CO
(DLCO), 4, 86, 87
Diffusion test (DLCO). See
Diffusion Capacity, Lung, CO
(DLCO)
194  •   INDEX
Disease entities, 2
Dissolved oxygen, 86
DLCO (Diffusion Capacity, Lung,
CO), 4, 86, 87
DO2 (oxygen delivery), 87, 128
Duplicates/duplicate
measurement, 87
Dyshemoglobin (dysHb), 44, 87
E Forced expiratory flow
EBG/eBGA (enhanced blood gas
analysis), 88, 89
ecf (extracellular fluid), 28
Electrochemical sensor, 88. See
also Clark electrode; pH
(hydrogen ion), electrode;
Severinghaus electrode
Electrolyte
clinical implications of, 21–25
and water, 20–21
Electron, 88
Elevated anion gap, 14, 123–124
End-tidal (end expiration)
air (et), 29
End-tidal CO2 (ETCO2/PCO2(et)),
88–89
Enhanced blood gas analysis
(eBG/eBGA), 88, 89
Equivalent (Eq) weight, 89. See
also Normal
et (end-tidal (end expiration)
air), 29
ETCO2 (end-tidal CO2), 88–89
Expiratory flow, volume
(timed), 90
Extracellular fluid (ecf), 28
Extracellular fluid source (vv), 29
Extrainstitutional care, 60
F Gas exchange, 18–19
FCOHb (fractional
carboxyhemoglobin), 90, 93
FHHb (fractional
deoxyhemoglobin), 90, 93
Fick equation, 90
Flow–volume loop, 90–91
FMetHb (fractional
methemoglobin), 91, 93
FO2 (fraction of oxygen in gas
specimen), 91
FO2(I)/FIO2 (fraction of oxygen in
inspired gas), 90, 91
FO2Hb (fractional
oxyhemoglobin), 92, 94
(midrange), 92
Forced inspiratory flow
midrange, 92
volume (timed), 92
Forced vital capacity, 92–93
1 second, 93
25–75 percent, 93
Fraction of oxygen in gas
specimen (FO2), 91
Fraction of oxygen in inspired gas
(FO2(I)/FIO2), 90, 91
Fractional carboxyhemoglobin
(FCOHb), 90, 93
Fractional deoxyhemoglobin
(FHHb), 90, 93
Fractional methemoglobin
(FMetHb), 91, 93
Fractional oxyhemoglobin
(FO2Hb), 92, 94
Fractional sulfhemoglobin
(FSHb), 94
Fractional “xx” hemoglobin,
93–94
FSHb (fractional
sulfhemoglobin), 94
G
Gas (g), 94
Gas diffusion, measurement of, 4
Gas transfer test. See Diffusion
Capacity, Lung, CO (DLCO)
Glomerular filtration rate (GFR/
eGFR), 88, 94–95
Glucose, 95–96

H Hypoxemia, 107
H-H equation
(Henderson–Hasselbalch
equation), 97, 99–101, 181
H2CO3 (carbonic acid), 5–6, 67
Hasselbalch, Karl Albert, 97
Hct. See Hematocrit
Heart rate (HR), 96
Helium Dilution Method, 176
Hematocrit (Hct, PCV, ’crit),
97–98
Hemiglobin (Hi), 98
Hemoximeter, 75–76
Henderson, Lawrence Joseph, 99
Henderson–Hasselbalch equation
(H-H equation), 97,
99–101, 181
Heparin, liquid, 42–43
HHb (deoxyhemoglobin),
84, 159
Homeostasis, 7, 18–19
Homeostatic systems, 4–5
Homeotherms, 101
HR (heart rate), 96
Hüfner, 101–102
Hüfner’s factor, 102
Hydrogen carbonate (bicarbonate),
5–6, 49–51, 103
Hydrogen ion (pH). See pH
(hydrogen ion)
Hydrogen ion loss, 125
Hydronium ions, 103–104
Hydroxocobalamin, 104–105
Hypercapnia, 105
Hyperkalemia, 24, 151
Hypermetabolism, 12, 156
Hypernatremia, 22, 169
Hyperoxia, 105–106
Hyperventilation. See Respiratory
alkalosis
Hypocapnia, 106
Hypokalemia, 24, 151
Hyponatremia, 22, 169
Hypoventilation. See Respiratory
acidosis
INDEX  •   195
decision criteria, 107
defined, 16, 19
refractory, 108
Hypoxemic hypoxia, 108
Hypoxia, 12, 156
hypoxemic, 108
I
Ig/I (inspired air/inspired gas), 29
In vitro, 41
In vivo, 41
Initialism, 34, 108
Inspired air/inspired gas (Ig/I), 29
Intrapulmonary Shunt fraction
(Qsp/Qt). See Shunt fraction
(Qsp/Qt)
Invasive ventilation, 182. See also
Ventilation support
Ionized calcium (iCa, Ca++), 57–58
Isopleth, 108
J
Junction potentials, 28
K
Ka (acid dissociation
constant), 108
Kalium (K), 108. See also
Potassium
Ketoacid, 6, 108–109
Ketoacidosis, 109
KiloPascal (kPa), 109, 138
Kind of quantity, 109
kPa (KiloPascal), 109, 138
Kreb’s cycle, 71, 109
Krebs, Hans, 109–110
L
Lactate (lactic acid), 110–112
Lactic acid (lactate), 110–112
Large population study, 112
Larynx (Voice box), 112
Law of Mass Action, 8, 112–114
Li-heparin, 42–43
Liquid-(l), 113
196  •   INDEX
Low anion gap, 41
Lung volumes, 113
M Laboratory Standards
Magnesium (Mg, Mg++), 113–114
Mass concentration, 114
Matrix, 115
Matrix algebra coefficient, 115–116
Matter, 116
Measurand, 116
Mechanical ventilation, 12, 116,
155, 156
Metabolic acidosis. See
Nonrespiratory acidosis
Metabolic alkalosis. See
Nonrespiratory alkalosis
Methemoglobin (MetHb), 117, 159
Methylene chloride
(dichloromethane), 118
Metric unit, 118
Milliequivalent (mEq). See
Equivalent (Eq) weight
Millimeters of mercury (mmHg),
118, 119. See also Barometer;
cmH2O; kPa
Mitochondria, 127
Mitochondrion (pl.-mitochondria),
119
mmHg (millimeters of mercury),
118, 119. See also Barometer;
cmH2O; kPa
Molar concentration (M), 119
Molarity, 119
Mole, 119–120
Momentum, 164
Multiple organ failure (MOF), 6
Multiplier, 120. See also SI Unit
multiplier/prefix
N See also Point-of-Care (POC)
Na-related disorders, 22, 169
Natelson microgasometer,
120–121
Natelson, Samuel, 121
National Institutes of Health, 81
Natural spontaneous
ventilation, 182
NCCLS. See Clinical and
Institute (CLSI)
Near Patient testing (NPT), 126.
See also Point-of-Care (POC)
Negative logarithm of apparent
acid dissociation constant
(pKa), 143
Neuromuscular system disorder,
12, 155
Nithiodote, 121–122
Nitrogen (N/N2), 120, 122
NIV (noninvasive ventilation),
122, 123. See also
Noninvasive positive pressure
ventilation (NPPV)
Nomogram. See Acid–base, chart
Noninvasive positive pressure
ventilation (NPPV), 122, 126
Noninvasive ventilation (NIV),
122, 123, 182. See also
Noninvasive positive pressure
ventilation (NPPV)
Nonrespiratory acidosis, 33
assessment of, 40
differentiation decision tree, 124
elevated anion gap, 14
general etiology, 123–124
normal anion gap, 13–14
Nonrespiratory alkalosis, 14–15,
33, 125
differential diagnosis chart, 125
Normal, 126
Normal anion gap, 13–14, 41, 123
NPPV (noninvasive positive
pressure ventilation), 122, 126
NPT (near patient testing), 126.
Nucleoside, 126
O
O, O2 (oxygen), 135
O2Hb (oxyhemoglobin), 137, 159

O2SAT, 126–127
Obstructive lung disease, 127
ODC (oxyhemoglobin dissociation
curve), 17, 127, 136
Oxidative phosphorylation
(OXPHOS), 34, 127
OXPHOS (oxidative
phosphorylation), 34, 127
Oxygen (O, O2), 135
Oxygen consumption (VO2),
127, 183
Oxygen content (ctO2), 128
Oxygen delivery (DO2), 87, 128
Oxygen electrode, 129
Oxygen quantities, 18–19
Oxygen saturation (sO2/SO2),
17, 131–132, 167. See also
Saturation, vs. fractional
oxyhemoglobin
in venous blood SO2 (vB), SvO2, 167
Oxygen solubility, 135
Oxygenation assessment, in blood
gas analysis, 15–18
Oxygenation interpretation, 19
Oxyhemoglobin (O2Hb), 137, 159
Oxyhemoglobin dissociation curve
(ODC), 17, 127, 136
P Plasma, 8, 51, 58, 61, 73, 97, 111,
P(A-a) O2. See Alveolar–arterial
oxygen gradient
P vs. p, 138
Pa (Pascal), 138
Packed cell volume (PCV), 138.
See also Hematocrit
Partial pressure of carbon dioxide
(PCO2), 10, 63–64, 138
Partial pressure of inspired oxygen
(PO2(I)), 148
Partial pressure of nitrogen
(PN2), 148
Partial pressure of oxygen (PO2),
130–131, 148
Partial pressure of water (PH2O),
138, 142
INDEX  •   197
Pascal (Pa), 138
PCO2 (partial pressure of carbon
dioxide), 10, 63–64, 138
PCO2(et) (end-tidal CO2), 88–89
PCV (packed cell volume), 138.
See also Hematocrit
Peak expiratory flow, 138
Peak inspiratory pressure (PIP),
139, 142
PEEP (positive end expiratory
pressure), 139, 149
Percent predicted (value), 139
Periodic table (PTE), 139
Peripheral-pulse-oximetry, 106
pH (hydrogen ion), 5–6, 10,
103–104, 140–141, 182
electrode, 141–142
metabolic changes, 6–7
and ventilatory state, 141
PH2O (partial pressure of water),
138, 142
Photometry, 142
Physicochemical properties, 142
PIP (peak inspiratory pressure),
139, 142
pKa (negative logarithm of the
apparent acid dissociation
constant), 143
143–147, 150, 168
Plasma water, 51, 58, 61, 73, 97,
111, 143–147, 150, 168
Plethysmograph (Body Box), 4,
56, 148
PN2 (partial pressure of nitrogen),
148
PO2 (partial pressure of oxygen),
130–131, 148
PO2(I) (partial pressure of inspired
oxygen), 148
PO2 (vB), PvO2 (partial pressure of
O2 in venous blood), 148
PO2 electrode. See Oxygen
electrode; Polarographic
electrode
198  •   INDEX
PO2(A)–PO2(aB). See Alveolar–
arterial oxygen gradient
Point-of-Care (POC), 148
Polarographic electrode, 129,
148–149. See also Oxygen
electrode
Positive end expiratory pressure
(PEEP), 139, 149
Postrenal, 46
Potassium (K/K+) (Kalium),
23–25, 149
Power of hydrogen, 151. See also
pH (hydrogen ion)
Predicted (value), 152
Prefix, 152. See also SI unit
multiplier/prefix
Prefix/unit modifier, 152. See also
SI unit multiplier/prefix
Prerenal, 46
Pressure, 152
atmospheric P(Atm)/p(Atm),
138, 153
conversion, 153
Primary renal, 46
Proton, 153
PTE (periodic table), 139
Pulmonary acid–base interactions,
7–8
Pulmonary function testing
(PFT), 2–4
Q Sean (S), 158
Q, Qc (cardiac output), 57, 70–71,
153
Qsp/Qt (shunt fraction), 18, 153,
161–162
Quantity, 153
R SI unit multiplier/prefix, 164–165
Red blood cell, 8
Reduced hemoglobin, 154
Reference electrode, 154
Refractory hypoxemia. See
Hypoxemia
Renal, 156
Renal acid–base control, 9
Residual volume, 154
Respiratory acidosis, 10, 11–12,
32, 106–107, 154–156
Respiratory alkalosis, 10, 12–13,
106, 156
Respiratory quotient (RQ), 157
Respiratory rate (RR), 157
Respiratory system, 157
Restrictive lung disease, 158
Ribose, 158
S
Sample source symbol
for alveolar gas (air), 28
for arterial blood, 28
for arterial plasma, 28
for blood source, 29
defined, 27
for end-tidal (end expiration)
air, 29
for extracellular fluid, 28
for extracellular fluid source, 29
for inspired air or inspired
gas, 29
for venous blood, 29
Saturation, 158. See also Oxygen
saturation (sO2/SO2)
vs. fractional oxyhemoglobin,
158–160
Scientific notation, 160
Severinghaus, John, 161
Severinghaus electrode. See
Carbon dioxide, electrode
Shunt. See Shunt fraction (Qsp/Qt)
Shunt fraction (Qsp/Qt), 18, 153,
161–162
SI units, 163–164
Siggaard-Andersen, Ole, 165
Simultaneous equation(s), 166
Simultaneous multicomponent
assay, 166
Single-breath diffusion (test), 167

Smoke inhalation, 81
Sodium (Na/Na+) (Natrium L.),
21–22, 167–169
Solubility, 169
Solubility coefficient/constant,
169. See also Bunsen
solubility coefficient
Sørensen, S.P.L., 170
Specimen source symbol, 170
Spectrophotometer, 171
Spirogram, 171. See also Lung
volumes; Flow–volume loop;
Spirometry
Spirometry, 3, 172. See Forced
vital capacity
Spun crit, 172. See also
Hematocrit
Standard base excess (SBE), 173
Standard deviation (SD, σ), 173
Standard deviation of duplicates
(SDdupe), 173
Standard temperature, pressure
(STP/STPD), 173–174
State (physical) of matter, 174
Stomach acid (HCl), 140
STP/STPD (standard temperature,
pressure), 173–174
Stroke volume (S.V./SV), 159, 174
Supported ventilation, 174, 182
S.V./SV (stroke volume), 159, 174
Symbols, 174
T equation, 181
TAT (turn-around time), 175,
177–178
Temperature “correction”, 175
Tension, 176
Therapeutic response test, 176
Thoracic injury, 12, 155
Tidal volume, 176
Tissue acid–base interactions,
7–8
Tissue-based disease, 2
Torr, 46
Torricelli, 46
INDEX  •   199
Total carbon dioxide—tCO2/TCO2.
See Carbon dioxide content
(ctCO2/TCO2)
Total hemoglobin, 159
Total lung capacity, 176
Trachea, 176–177
Tracheostomy, 177
Transducer, 177
Tricarboxylic cycle. See Kreb’s
cycle
Turn-around time (TAT), 175,
177–178
U
Unit conversion, 178–179
Unit multiplier/prefixes. See SI
unit multiplier/prefix
Units, 178, 179. See also SI Units
Uranium (U), 178
Urea, 179. See also Blood urea
nitrogen (BUN); Urea
nitrogen
Urea clearance, 179. See also
Glomerular filtration rate
Urea nitrogen, 179–180. See also
Blood urea nitrogen (BUN);
Urea
Uremia/renal failure, 41
V
Van Slyke, Donald, 181
apparatus, 180
Vanadium (V), 180
vB (venous blood), 29
Vd (dead space), 83–84, 181
Venous blood (vB), 29
Ventilation, 182
Ventilation support, 174, 182
Ventilation/perfusion ratio
(V/Q), 182
Ventilatory failure. See
Respiratory acidosis
Ventilatory state, 182
Vibration, 183
200  •   INDEX
Vitamin B12. See Cyanocobalamin;
Hydroxocobalamin
VO2 (oxygen consumption),
127, 183
Voice box. See Larynx
Volume–Time Graph, 176
vt (blood source), 29
vv (extracellular fluid source), 29
W
Water, electrolyte and, 20–21
Weisberg, Harry, 183
Whole blood, 51, 58, 61, 73, 96,
111, 143–147, 150, 168,
183–184
Windpipe. See Trachea
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