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ABG’S™
THE ABC’S OF
ABG’S™
A Cyclopedic Dictionary
of the Testing Terms Used
in Critical Care
10 9 8 7 6 5 4 3 2 1
KEYWORDS
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.
In the Beginning . . .
1
There’s a great explanation of this entire process in Wikipedia under “Breathing.”
2 • THE ABC’S OF ABG’S™
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.
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
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™
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™
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
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
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
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™
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.
RESPIRATORY ALKALOSIS/HYPERVENTILATION
NON-RESPIRATORY/“METABOLIC” ACIDOSIS:
NORMAL ANION GAP
NON-RESPIRATORY/“METABOLIC” ALKALOSIS
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
a nalyzers (i.e., blood gas + CO-oximetry, etc.) have given rise to some
confusion in terminology.6
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
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
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™
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
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−]
A Acronym, 34
A-a gradient. See Alveolar–arterial Adenosine triphosphate (ATP),
oxygen gradient 34–35, 45
A-aDO2. See Alveolar–arterial Air sacs. See Alveolus
oxygen gradient Airway assessment, 1
a/A ratio (arterial/alveolar ratio), Airway-based diseases, 2
29, 43–44 Airway obstruction, 12, 155
aB (arterial blood), 28 Airway resistance (RAW), 35
Acid, 30–31 Albumin, low, correction of anion
Acid dissociation gap for, 41
constant (ka), 108 Alcohol abuse, DKA and, 41
Acid–base, 5–6 Alkalemia, 35–36. See also
balance, 31 Alkalosis; Acid–base
chart, 31–32 disorders; Acidosis;
disorders, 32 Acidemia
homeostasis, 7, 18–19 Alkalosis, 36. See also Alkalemia;
status interpretation, 15 Acid–base disorders;
Acid–base disorders, 32–33. See Acidosis; Acidemia; Base
also specific disorders excess of extracellular fluid
Acid–Base Status of the Blood, (B.E. (ecf))
The, 165 categories and measured
Acidemia, 33. See also Acidosis; values, 11
Acid–base disorders; non-respiratory. See
Alkalosis Nonrespiratory alkalosis
Acidosis, 33–34. See also respiratory, 10, 12–13, 33,
Acidemia; Base excess of 106, 156
extracellular fluid (B.E. (ecf)) Allen test, 36–37
categories and measured Alveolar air equation, 37
values, 11 Alveolar dead space, 83
nonrespiratory. See Alveolar gas (air) (A), 28. See also
Nonrespiratory acidosis End-tidal (end expiration)
respiratory, 10, 11–12, 32, air (et)
154–156, 182 exchange, 37–38
192 • INDEX
H Hypoxemia, 107
H-H equation decision criteria, 107
(Henderson–Hasselbalch defined, 16, 19
equation), 97, 99–101, 181 refractory, 108
H2CO3 (carbonic acid), 5–6, 67 Hypoxemic hypoxia, 108
Hasselbalch, Karl Albert, 97 Hypoxia, 12, 156
Hct. See Hematocrit hypoxemic, 108
Heart rate (HR), 96
Helium Dilution Method, 176 I
Hematocrit (Hct, PCV, ’crit), Ig/I (inspired air/inspired gas), 29
97–98 In vitro, 41
Hemiglobin (Hi), 98 In vivo, 41
Hemoximeter, 75–76 Initialism, 34, 108
Henderson, Lawrence Joseph, 99 Inspired air/inspired gas (Ig/I), 29
Henderson–Hasselbalch equation Intrapulmonary Shunt fraction
(H-H equation), 97, (Qsp/Qt). See Shunt fraction
99–101, 181 (Qsp/Qt)
Heparin, liquid, 42–43 Invasive ventilation, 182. See also
HHb (deoxyhemoglobin), Ventilation support
84, 159 Ionized calcium (iCa, Ca++), 57–58
Homeostasis, 7, 18–19 Isopleth, 108
Homeostatic systems, 4–5
J
Homeotherms, 101
Junction potentials, 28
HR (heart rate), 96
Hüfner, 101–102 K
Hüfner’s factor, 102 Ka (acid dissociation
Hydrogen carbonate (bicarbonate), constant), 108
5–6, 49–51, 103 Kalium (K), 108. See also
Hydrogen ion (pH). See pH Potassium
(hydrogen ion) Ketoacid, 6, 108–109
Hydrogen ion loss, 125 Ketoacidosis, 109
Hydronium ions, 103–104 KiloPascal (kPa), 109, 138
Hydroxocobalamin, 104–105 Kind of quantity, 109
Hypercapnia, 105 kPa (KiloPascal), 109, 138
Hyperkalemia, 24, 151 Kreb’s cycle, 71, 109
Hypermetabolism, 12, 156 Krebs, Hans, 109–110
Hypernatremia, 22, 169
Hyperoxia, 105–106 L
Hyperventilation. See Respiratory Lactate (lactic acid), 110–112
alkalosis Lactic acid (lactate), 110–112
Hypocapnia, 106 Large population study, 112
Hypokalemia, 24, 151 Larynx (Voice box), 112
Hyponatremia, 22, 169 Law of Mass Action, 8, 112–114
Hypoventilation. See Respiratory Li-heparin, 42–43
acidosis Liquid-(l), 113
196 • INDEX
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