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Acid-Base
Disturbance Cases
ZACHARY R. HEALY
• Includes 75 real-life
progressive cases to facilitate
knowledge application
• Includes interpretation of
triple-base disturbances
• Answers include rich rationales

that explain both correct and
incorrect answers
• Targets a vast array of topics in

internal medicine and critical care
ACCESS -..Medicine
•
CRITICAL CONCEPT
MASTERY SERIES
Acid-Base Disturbance Cases
NOTICE
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CRITICAL CONCEPT
MASTERY SERIES
Acid-Base Disturbance Cases
Zachary Healy, MD, PhD

Assistant Professor
Division of Pulmonary and Critical Care Medicine
Department ofMedicine
Duke University Hospital
Durham, North Carolina
New York Chicago San Francisco Athens London Madrid Mexico City
Milan New Delhi Singapore Sydney Toronto
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Preface..........................................................vii Case30 ...................................................... 301
Introduction ................................................. 1 Case31 ...................................................... 307
Case 1 ...........................................................35 Case32 ...................................................... 313
Casel ............................................................41 Case 33 ...................................................... 319
Case 3 ............................................................47 Case34 ...................................................... 327
Case4............................................................55 Case35 ...................................................... 337
Cases ............................................................65 Case36 ...................................................... 347
Case6............................................................73 Case37 ...................................................... 353
Case 7............................................................83 Case38 ...................................................... 359
Case8 ............................................................95 Case39 ...................................................... 367
Case9......................................................... 105 Case40 ...................................................... 373
Case 10 ...................................................... 113 Case41 ...................................................... 383
Case 11 ...................................................... 121 Case42 ...................................................... 393
Case 12 ...................................................... 133 Case43 ...................................................... 403
Case 13 ...................................................... 141 Case44 ...................................................... 411
Case 14 ...................................................... 149 Case45 ...................................................... 419
Case 15 ...................................................... 159 Case46 ...................................................... 431
Case 16 ...................................................... 169 Case47 ...................................................... 439
Case 17 ...................................................... 181 Case48 ...................................................... 445
Case 18 ...................................................... 193 Case49 ...................................................... 453
Case 19 ...................................................... 203 Case50 ...................................................... 459
Casel0 ...................................................... 213 Case 51 ...................................................... 469
Casell ...................................................... 221 Case52 ...................................................... 479
Case22 ...................................................... 229 Case53 ...................................................... 489
Case23 ...................................................... 241 Case54 ...................................................... 499
Case24 ...................................................... 251 Case55 ...................................................... 505
Case25 ...................................................... 259 Case56 ...................................................... 513
Case26 ...................................................... 269 Case57 ...................................................... 523
Case27 ...................................................... 279 Case58 ...................................................... 533
Case28 ...................................................... 287 Case 59 ...................................................... 541
Case29 ...................................................... 293 Case 60 ...................................................... 551
vi CONTENTS
Case 61 ...................................................... 559 Case 69 ...................................................... 643

case 62 ...................................................... 571 Case 70 ...................................................... 653
Case 63 ...................................................... 583 Case 71 ...................................................... 663
Case 64 ...................................................... 593 Case 72 ...................................................... 671
case 65 ...................................................... 603 Case 73 ....•........•.......•.......•.......•.......•.......• 679
Case 66 ...................................................... 615 Case 74 ...................................................... 685
Case 67 ...................................................... 625 Case 75 ...................................................... 695
case 68 ...................................................... 635 Index ............................................................703
This collection of clinical acid-base cases is meant to sharpen clinical skills in eval-
uating such disorders. We aim to do so by providing a structure for the evaluation
of acute and chronic, primary and secondary acid-base disturbances, as well as
approaches to identify the underlying etiologies. This series was conceived to provide
cases with a level of complexity that would appeal not only to medical students, but
also to residents and fellows, and it will intermittently include questions regarding
the most appropriate treatment of patients after identifying the aforementioned acid-
base disturbances. Although basic physiologic explanations are provided throughout,
this text is not intended to replace essential physiology texts. References to such texts
and supplemental peer-reviewed literature are provided throughout where appropri-
ate. Following are a few notes prior to diving into the approach.
While the approach to analysis provided herein may appear rather black-and-white,
real-world acid-base interpretation is often less clear, with plenty of gray area. This
may be due to a number of issues, including the timing of laboratory studies, the
growing use of point-of-care testing and venous blood gas data in the initial evalu-
ation of patients, and limitations of the linear equations describing respiratory and
metabolic compensation, among others. Importantly, we typically lack the necessary
quantitative information to define the chronicity of acid-base disorders, which then
makes interpretation of the acute disorders much more difficult. In such cases, we
are required to make assumptions that potentially introduce additional error. For
instance, in the first case in this series, you will see how a priori knowledge of a
chronic respiratory acidosis can significantly alter the interpretation of metabolic
acid-base disturbances (and underlying etiologies) in critically ill patients.
All of the cases presented here have been interpreted using the "bicarbonate" (or
"Boston") approach introduced by Relman and Schwartz, as opposed to utilizing
the base excess (BE) approach introduced by Siggard-Anderson, the standard base
excess (SBE) introduced by Van Slyk.e, or the more complex Stewart approach to acid-
base physiology. Each of these approaches will be briefly discussed. While there has
much debate regarding which of the bicarbonate and Stewart approaches to acid-
base physiology provides the greatest diagnostic and prognostic information, studies
comparing the two methods have been largely inconsistent or shown clinical equiv-
alence. As the bicarbonate approach remains the most popular approach taught in
medical education and does not require simultaneously solving multiple equations,
this approach will be utilized throughout the text. Additionally, we realize that there
are multiple variations and short-hand versions of the equations used to determine
the "delta-delta" as well as appropriate metabolic and respiratory compensation.
While many of these variations or shorthand rules will produce the same or similar
viii PREFACE
mathematical result, the physiologic principles underlying them are often lost or at
least less transparent. 1bis can often lead to transposition of terms or general confu-
sion in less-experienced clinicians, and such shorthand should be reserved for more
experienced practitioners. This text will utilize a consistent equation-based approach
for all calculations, and all necessary equations will be provided in the introduction
(as well as in the solutions to the case problems}.
Next, one of the most important aspects of acid-base interpretation is the application
of common sense, particularly with regard to taking the patient's medical and social
history into account. This cannot be overstated. For instance, an otherwise-healthy,
elderly patient presenting with an infiltrate on chest film, fever, productive cough,
hypotension, and an elevated anion gap acidosis is most likely to have a lactic acido-
sis secondary to sepsis rather than toluene toxicity from inhalation drug abuse. And
while it is always important to keep an open mind when formulating a differential
diagnosis, common diagnoses will remain common; you will encounter lactic acido-
sis and diabetic ketoacidosis (DKA) much more frequently than cyanide or carbon-
monoxide poisoning in practice. Finally, recall that most of the acid-base disorders
encountered throughout medicine (and this text) are in critically ill patients; it is
therefore not always possible to await confirmatory testing before instituting treat-
ment decisions, and such decisions about diagnosis and treatment will often be based
on imperfect information.
Zach Healy
PROCESS OF EVALUATION
The first step in the evaluation of the acid-base status is the clinical evaluation. This
should include a detailed history of the present illness, with particular attention to
the timing/duration of the patienfs symptom onset. In patients who are incapacitated
or encephalopathic, this should also include a detailed history of the environment in
which the patient was found (eg, prescription medications, over-the-counter [OTC]
medications, bottles of industrial cleaner, running vehicle, etc) as well as any collat-
eral history that is available. Additionally, it is important to include a detailed review
of systems with particular attention to those symptoms that could contribute directly
to an acid-base disorder (eg, emesis, diarrhea, pain, etc). A prior medical and surgical
history is also critical, with particular attention to conditions associated with chronic
acid-base disorders (eg, chronic renal insufficiency, chronic obstructive pulmonary
disease [COPD], history of abdominal or pelvic surgery), and a history of prior sui-
cidal ideation or suicide attempts. A complete medication list must also be obtained,
including OTC medications and herbal or dietary supplements. An appropriate social
and environmental history should include any history of substance abuse (alcohol,
opioids, benzodiazepines, etc) and hobbies. A complete physical examination should
also be included in the evaluation.
The next step in the evaluation process is to ensure that the appropriate or necessary
data are available. This should include an arterial blood gas (ABG) analysis (includ-
ing pH, Paco2, and Pao2 ), as well as a serum basic chemistry panel (sodium [Na],
potassium [K], chloride [Cl], carbon dioxide [C02 ], blood urea nitrogen [BUN],
creatinine [Cr]), and a serum albumin. These should be drawn at the same time
or in very close proximity, and if possible prior to intervention. While a peripheral
venous blood gas (VBG) or central venous blood gas analysis may also be used for
evaluation of acid-base status, note that this can introduce error into your calcu-
lation. Table 1-1 provides some general guidelines for correlating ABG and VBG
values.
If the laboratory data do not match the clinical situation, check for potential labo-
ratory errors in terms of the patient identification. Also, be alert to the potential for
venous blood samples to be contaminated or diluted with intravenous fluids, particu-
larly if a solution or medication is infusing distal to the site ofvenipuncture. The ABG
can often be helpful here as arterial samples should not be affected by infusions and
should therefore represent the clinical situation. Importantly, note that the reported
bicarbonate (HC03 ) in an arterial or venous blood gas is a calculated rather than a
measured value. Also note that the C02 from the serum chemistry panel represents
the total C02 in the serum sample; since the majority(> 95%) ofC02 is transported
2 CRITICAL CONCEPT MASTERY SERIES: ACID-BASE DISTURBANCE CASES
TABLE 1-1 • Differences between arterial, peripheral venous, and central venous blood
gas values.
Relative to ABG pH Pco2 mm Hg [HCO;l (mEq/L)
Peripheral VBG [0.03--0.04] lower [2-1 o mm Hg] higher [1-2 mEq/L] lower than
thanABG thanABG ABG
Mixed or [0.02--0.06] lower [3-6 mm Hg] hlghar [-1 to 1 m Eq/U
centralVBG thanABG thanABG different (no difference)
ABG, amrlal blood gas; HCO;, bkarbonate; Pco,. partial pressure ofcarbon dioxide; VBG, venous blood gas.
in the form ofHC03, we generally use the value reported for the C01 as the serum
HC03• In the case of suspected pseudohyponatremia, remember to use the measured
value rather than the corrected value in your studies. Finally, note that some sub-
stances can interfere with test results. Namely, hypertriglyceridemia or cell lysis can
significantly alter lab values. Similarly, some metabolites of ethylene glycol and meth-
anol can interfere with lactate determination, depending on the lab. Also, to check
for internal consistency, one can use the Henderson-Hasselbach equation to ensure
that the pH, partial pressure of carbon dioxide in arterial blood (Paco2 ), and HC03
values are consistent:
pH= 6.1 + log10 [ HCO, ]

[ 0.0307 *Paco2
l ; or pH= 7.61 + log10 [[HCOJ]
Paco 2
While the normal value for arterial pH can range from 7.35 to 7.45, patients with
appropriate compensation can have values within this range, and therefore acid-base
disorders can often be missed. Consequently, for the purpose ofthe text, we will con-
sider the normal range to be 7.38 to 7.42. Similarly, the normal values for HC03
range from 21 to 27 mEq/L, with a median value of 24 mEq/L; in order to prevent
missing a potential acid-base disorder, we will use a normal range of22 to 26 mEq/L.
The normal range for Paco2 is between 35 and 45 mm Hg with a median value of
40 mEq/L, although we will use a normal range of38 to 42 mm Hg.
The next step in the evaluation process is an attempt to identify the patient's "baseline"
acid-base status by defining any existing chronic acid-base disorders, if possible. This
generally requires evaluation of a patient's prior laboratory data and/or an available
blood gas when the patient was at baseline health. Tiris is particularly important for
patients with chronic respiratory acidosis, as, in addition to an elevated baseline Paco2,
the patient's "baseline" HC03 (and hence the chloride) can be significantly altered from
that of "healthy" or "normal" patients. For example, assume you have a patient with
advanced COPD who presents to the emergency department with blood gas values of
pH 7.25, Paco2 65 mm Hg, and HC03 27 mEq/L. The interpretation ofthis patient's
blood gas, if we assume the patient has a "normal" baseline (eg, Paco1 40 mm Hg,
HC03 24 mEq/L) would be an acute respiratory acidosis with an appropriate renal
INTRODUCTION 3
compensation; however, if you know that the patient has a chronic respiratory
acidosis with a baseline acid-base status of pH 7.30, Paco2 65 mm Hg, and HC03
36 mEq/L, you would be able to accurately diagnose that the patient has an acute
metabolic acidosis, with an acute-on-chronic respiratory acidosis. In the first case,
we were forced to assume a normal baseline, and this would have caused us to miss
that patient's metabolic acidosis initially, which could potentially be catastrophic.
This is particularly important in chronic respiratory acid-base disorders, where
both the Paco and the HC03 are altered. While some references suggest that the
ratio [HCO)]/tPaco2 ] can be used to determine if a respiratory process is acute or
chronic, this ratio does not provide a 1:1 mapping to a particular set of acid-base
disorders. For example, consider a patient presenting with a respiratory acidosis that
has a ratio of 0.2. Based on Figure I-1, this patient may have an acute-on-chronic
respiratory acidosis with or without a metabolic acidosis/alkalosis, an acute respira-
tory acidosis with a concomitant metabolic alkalosis, or a chronic respiratory acido-
sis with an acute metabolic alkalosis.
Unlike compensation in chronic respiratory acid-base disorders, the compensation in

chronic metabolic acid-base disorders is poorly characterized and inefficient; there-
fore, it is less important to identify these conditions initially.
The next step is to determine if the primary issue is an acidemia or alkalemia. This is
another instance where common sense must be utilized. While the normal value for the
arterial pH may be between 7.35 and 7.45, multiple acid-base disturbances may still be
present in a patient with a pH in this range. Therefore, it is important that one does not
AcutB n111plrmay acldoals

with appropriate
metabolic compensation
AculB rellpiratory acidosis

AculB r1111plratory acidosis with metabolic alkalosis
with rnatabollc acldoals 1---------------1---
: Acute-on-dlronlc n111plrmory
acidosis with metabolic
alkalosls
+--- 0.'1 --=- ~COafAPaca:z - -d.4 - - •
Acuta-on-dlronlc 1'88plratory
acldoals (with approprtata
compensation for each phase)
and no metabolic component
Aoot&-on-chronic l'llSpiratory 4 . - - + - - - - - - - - - - - - - - - 1
acidosis with metabolic acidosis
--+ Chronic r1111piratory acidoaia
Chronic rasplratory acidosis 4,--+---------------1 with metabolic alkalosia
with metabolic acidosis
Chronic n111plrmory acldoals

with approprtllls rnatabollc
compensation
Figure 1-1 • Potential combinations of acute and/or chronic metabolic and respiratory
disorders that may be seen at different ratios of the change in serum bicarbonate (HC03)
to the change in arterial co2.
Baseline Acid-Base Disorder?

Define new baseline ~ 1111W'or HC03
••Parficularly helpful lo identify chronio rNpifatary 11Cid03is
...
Ensure Quallty/Tlmlng ot Data
ABG and serum veno.. chemistry drawn at similar time
...
Serum pH
pH< 7.38 I pH> 7.42
+
Acldemla pH within 7.3&-7.42 Alkalemla
+
l /If+
Elcamine ~and H~
abnormal, oontinuewith algorithm~
~<22mEq/L _ ~<42mmHg Pa~<38mmHg
+
Metabolic Acidosis Respiratory Acidosis Respiratory Alkalosis Metabolic Alkalosis
Go to metabolic acidosis Go 1o respiratory acidosis Go to respiratory alkalosis Go 1o metabolic alkalosis
flowchart flowchart flowchart flowchart
Healthy Palietlt:
Baseline ~: 21-28 mEq/L, although we Bll8ume a median value of 24 mEq/L
Ballellne Pac:o2: 30-45 mm Hg, atthough we assume a median value of 40 mEqlL
Chronic Acid-Base DisotrJ9r:
Replace the values in red in the flow chart with the patient's baseline values
Figure 1-2 • Initial algorithm for the evaluation of acid-base disorders.
examine the pH, see that it is 7.39, and assume that no acid-base disorder is present. For
example, a patient recently presented to our emergency department with a pH of 7.39,
Paco2 of25 mm Hg, and serum HC03 of15 mEq/L and the diagnosis ofan acute pulmo-
nary embolus with cor pulmonale. Although the patient's pH was normal, this was due
to the presence of an anion gap acidosis due to lactic acidosis secondary to cardiogenic
shock and a concomitant respiratory alkalosis. Therefore, it is important to analyze the
pH, Paco2, and serum HC03 for every patient. Although we examine the pH first, this is
simply to provide some guidance as to what the primary acid-base disorders are in any
given patient If the pH is in the range of 7.39 to 7.41, it may not be possible to deter-
mine which is the primary process. The next step is to determine the primary processes
present, followed by examination for appropriate compensation and identification of any
secondary acid-base disorders present. Recall that even with "'complete" compensation,
the arterial pH does not reach 7.40; this is a common misconception, and therefore we
will use the term "appropriate" rather than "complete" compensation throughout the
text. Respiratory compensation is driven by pH changes in the cerebrospinal fluid,
leading to alterations in the respiratory centers. Metabolic compensation is driven
by pH-sensitive cells in the renal tubules. Once one has identified all existing primary
and secondary acid-base disorders present, one must go through each decision tree to
attempt to identify the etiologies responsible for each disorder, as this will guide treat-
ment decision making (see Figure 1-2). Again, it is also important to identify patterns of
disorders that are associated with particularly etiologies. For example, aspirin toxicity
can be associated with a respiratory alkalosis and an anion gap acidosis.
METABOLIC ACIDOSIS
Figure 1-3 represents the algorithm for a patient with a metabolic acidosis.
INTRODUCTION 5
Metabolic Acidosis
i
Is the respiratory
compensation appropriate?
Eitpectsd Paco2 = 1.5 • [actual HCOs] + 8 ± 2 (In mm Hg)
Concomitant AellplralDry Acldalllll

i
Approprlllle Compenallllon CoMomllllnt ReaplralDry Alkaloals
rwplmory acidosis flow chart rupRml)' .a.tosis flow chart
Cornicllon at axpac:llld anion a•P tar •rum albumin

Expected Anion Gap = 12 - (2.5) • [4.0 :L -Actual Serum Albumin]
i
Swum Anion Gap (SAG)
SS1Um Anion Gap (SAG) = [Na+] - [HC03] - [Gr]
Anion Gap =Sfl/1Jm Anion Gap - Eitpectsd Anion Gap
Non-Anion G•p Acidosis (NAGMA)

AChOmEqll. ...
Significant Anion Bap Acldm/a p,_f?
Urine pH < 11.5?
Urine [Na]+ < 20 mEq/l (pool" ,.,.., dlat.I Na drlllvwy)
I
v........
allhll-
i l NolDoll
ollhll-
......
Urln• Oamolal Gmp (UOG)
Calc:ulallon
Urlne Anion Gmp (UAG)
........
Calculation
--
-
· -(MAllllA) --
Figure 1-3 • Algorithm for evaluation of a metabolic acidosis.
The first step in a patient with a metabolic acidosis is to determine if the compensa-
tion is appropriate. For a metabolic acidosis, we do not differentiate between acute
and chronic when determining the compensation, as the respiratory compensation
for a chronic metabolic acidosis is poorly defined and generally inefficient. The equa-
tion we will use, called the Winter equation, is generally accurate for a serum HC03
between 5 and 22 mEq/L:
Expected Paco2 "' 1.5 * [Actual HC03] + 8 ± 2 (in mm Hg).
Respiratory compensation for a metabolic acidosis begins within minutes and is

"complete" within 12 to 24 hours. If the Paco1 falls within this range, this is termed
an "appropriate" or complete respiratory compensation, and no respiratory acid-base
disorder is present. If the Paco2 is lower than the expected range, there is a concom-
itant respiratory alkalosis, whereas if the Paco1 is higher than the expected range, a
concomitant respiratory acidosis is present. The limit of respiratory compensation is
between 8 and 10 mm Hg. Once this has been determined, the next step is to deter-
mine if an anion gap acidosis is present. The first step in determining if an anion gap
is present is to calculate the expected or "normal" anion gap. The serum anion gap
represents the unmeasured anions in the serum. In the most basic form the serum
anion gap is calculated as follows:
Serum Anion Gap= [Na+) - [HCO~] - [Cl-],
In which the units of measure are milliequivalents per liter (mEq/L). Recall that
the milliequivalent (mEq) is a measure of net charge (or valence), so 1 mmol of
potassium is equal to 1 mEq, whereas 1 mmol of calcium, which carries a net charge
of 2+, is equal to 2 mEq. Therefore, in this form, the unmeasured anions include
albumin, phosphorus, lactate, bromide, and negatively charged monoclonal pro-
teins. Phosphorus exists as an anion in the form of monohydrogen and dihydrogen
phosphate (HPO!- and Hl0;:). There are also unmeasured cations, which include
potassium, calcium, magnesium, and positively charged monoclonal proteins. Since
magnesium, phosphorus, calcium, and potassium are often measured, one could
write the equation as:
SerumAnionGap= [Na+]+ [K+) + [Ca2+) + [Mg2+]-[HC~] + [cl-J-[P"-1] (in m~ );

Alternatively, if the values are in mrnol,
If the values are in milligrams per liter (mg/L), this can be converted using the molec-
ular weights (mg/mrnol or g/mol): for calcium, 40.1; and for phosphorus, 31. Recall
that both phosphorus and calcium are typically expressed as mg!dL, so to convert
from mg/dL to millimoles per liter (mmol/L), multiply the calcium value by 0.401
and the phosphorus by 0.31 to covert to mmol/L. In an otherwise healthy patient,
these other unmeasured cations and anions generally cancel out; therefore, the major
anion responsible for the anion gap is albumin. For the most common form of the
serum anion gap equation (including only sodium, serum HC03, and chloride), we
must correct the expected anion gap for the patient's serum albumin, using the fol-
lowing equation:
Expected Anion Gap = 12 - (2.5) * [ 4.0 !- Actual Serum Albumin J.

While the expected anion gap is -12 mEq/L for an otherwise healthy patient with a
serum albumin of 4.0 gldL, this value will be lower in patients with hypoalbumine-
mia. There are conditions that can be associated with a low anion gap (< 3 mEq/L),
as well as those associated with a negative anion gap. Some of these conditions are
provided in Table I-2.
After determining the expected anion gap and calculating the serum anion gap, one
can determine the anion gap (AG):
Anion Gap = Serum Anion Gap (measured) - Expected Anion Gap (in m~q) .
INTRODUCTION 7
TABLE 1-2 • Unmeasured cations and anions, conditions associated with a low or negative
serum anion gap, and other potential anions that may be present in a patient with one of
these conditions.
Common Unmeasured Cations
• [K•]
• [Ca>+]
• [Mg>+]
• Monoclonal protein accumulation (some lgG forms)
Common Unmeasured Anions
• Phosphorus
• Lactate
• Bromide/iodide
•Albumin
• Monoclonal protein (lgM)
Causes of a Low Serum Anion Gap (~ 3 mEq/L)
• Laboratory error
• Hypoalbuminemia
• Severe NAGMA
• Lithium toxicity
• Monoclonal gammopathy, multiple myeloma
• Bromide/Iodine Ingestion (Interferes with serum [Cl-] measurement)
• Pseudohyponatremia
• HCO, infusion (chloride-deplete solution)
Causes of a Negative Serum Anion Gap
• Hyperlipidemia (falsely elevates serum [Cl-] measurement)
• Bromide Ingestion
• Pyridostigmine use
• Salicylate intoxication
NAGMA, non-<in/on gap metabolic acidosis.
If the anion gap is positive, this indicates that an anion gap acidosis is present,
whereas if the value is zero or less than zero, there is no anion gap acidosis, and only
a non-anion gap acidosis is present. At this point, it may be prudent to order some
additional laboratory studies pending the patient's presentation and other clinical
history (see Table 1-3).
TABLE 1-3 • Additional laboratory studies to consider for an anion gap and non-anion gap
acidosis.
Anion Gap Acidosis Non-Anion Gap Acidosis
• Complete blood count with dlfferentlal • Urine electrolytes (Na, K, Cl)
• Serum lactate (either arterial or venous) • Urlnalysls
• Urine drug screen • Urine osmolality
• Serum drug screen, which should include • Urine urea
ethanol, salicylates, and acetaminophen levels
• Liver function testing
• Serum osmolality
• Serum acetone or ketones (beta-hydroxybutyrate)
DELTA-DELTA CALCULATION
For a patient with an anion gap acidosis, the next step is to determine if the patient
has a pure anion gap acidosis, or there is also a concomitant non-anion gap acidosis
or a metabolic alkalosis. This is determined by using the delta-delta (.6..6.):
M = (Calculated Anion Gap) - (Expected Anion Gap).

(Expected Serum C0 2 )-(Actual Serum C0 2 )
The delta-delta equation compares the size of the anion gap to the magnitude of
change in the serum HC03• Recall that one should use the serum HC03 as a sur-
rogate for the serum C02 • Additionally, for the expected serum HC0 3, one should
use the patient's baseline serum HC03 ifit is known to be different than 24 mEq/L.
For patients with a pure anion gap, the ratio is generally between 1.0 and 2.0. Recall
that a strong acid dissolves in blood to an anion and a hydrogen molecule. The
hydrogen molecule reacts with an HC03 molecule to yield a water molecule and
a molecule of carbon dioxide. Therefore, for each molecule of acid, the change in
anion gap would be balanced by the loss of an HC03 molecule, yielding a 1:1 ratio.
However, this requires that renal function is maintained, and that the excretion of
anion and the acid component of strong acid are equal overall. Additionally, the
hydrogen ion released from the strong acid can also be buffered by bone or within
cells, and therefore the anion gap will be higher than the reduction in the serum
HC03• Obviously, as the serum HC03 level is further reduced, more of the acid
will be buffered by other means. Therefore, the delta-delta ratio can be elevated
up to a value of 2.0 and still represent a pure anion gap acidosis. A value of 1.6 is
commonly seen in patients with a pure type A lactic acidosis. It is important to note
here that the body does not produce lactic acid; rather, hydrogen ions are produced
as part ofthe anaerobic metabolism pathways that lead to lactate anion production.
Therefore, the ratio here is not 1:1. Additionally, many of the conditions leading to
a lactic acidosis (type A lactic acidosis) are also associated with reduced renal func-
tion (leading to an imbalance in anion and acid excretion) and more severe acidosis
(which pushes more H+ to be buffered in the bone and intracellularly).
Patients with a value less than 0.4, despite having an elevated anion gap are more
likely to have a pure non-anion gap acidosis without an actual anion gap acidosis.
This is simply due to the limits ofthe equations we use to describe much more com-
plex physiology. In this case, the reduction in the serum HCO3 significantly out-
weighs the increase in the anion gap. This scenario is usually seen in patients with a
very small but positive anion gap, but a significant reduction in serum HC0 3, such as
a type 1 renal tubular acidosis (RTA).
Patients with a value between 0.4 and 0.9 are diagnosed with a mixed anion gap and
non-anion gap acidosis. Patients with a value greater than 2.0 are diagnosed with an
anion gap acidosis and a metabolic alkalosis. For each additional acid-base disorder
present, one must pursue a diagnostic workup based on the provided algorithms.
terpretation ofdelta-delta values.
INTRODUCTION 9
TABLE 1-4 • Interpretation of the delta-delta equation valuesle.

Delta-Delta Value Condition Present
<0.4 Non-anion gap only
0.4-0.9 Anion gap and non-anion gap acidosis
1.0--2.0 Anion gap acldosls only
>2.0 Anion gap acldosls and metabolic alkalosls
SERUM OSMOLAL GAP

Once the delta-delta evaluation is completed, a serum osmolal gap should be calcu-
lated. While this is not necessary in patients with a clearly identifiable cause and con-
sistent clinical history, we generally include this as part of the algorithm to prevent
this step from being missed, as the timely identification of an anion gap acidosis with
a serum osmolal gap is critical to preventing significant morbidity. The serum osmo-
lal gap is important for determining whether toxic alcohol ingestions have occurred.
First, we calculate the serum osmolality (equivalent to the expected anion gap cal-
culation). Again, as with the serum anion gap calculations, there are a number of
ways this can be written, which can include additional variables. The most significant
solutes in plasma are sodium, HC03, chloride, glucose, urea, and ethanol. Therefore,
the most common form is written as follows:
+] [Glucose] [BUN] [Ethanol]

Calculated Serum 0 smolality=2* [Na + +--+ ,
18 2.8 3.8
where the units are as follows: serum osmolality, mOsm/kg (which is equivalent to
the serum osmolality when written mOsm/L of water, as 1 L of water weights 1 kg);
Na, mmol/L; glucose, mg/dL; BUN, mg/dL; ethanol, mg/dL. The conversion factors
for glucose, BUN, and ethanol shown in the preceding equation convert the units
from mg/dL to mOsm/kg. The sodium value is doubled to use as a surrogate for
the chloride and HC03 values. The following are additional terms (with conversion
factors) that may be used in the equation if the values are measured in milligrams
per deciliter (mg/dL) : methanol, 3.2; isopropyl alcohol, 6.0; ethylene glycol, 6.2; ace-
tone, 5.8. Finally, if the beta-hydroxybutyrate or lactate are measured, they may be
included directly (without conversion) in units of mmol/L.
Using the more common formulation for the calculated serum osmolality, we can
determine the serum osmolal gap by measuring the serum osmolality:
Serum Osmolal Gap = Measured Serum Osmolality - Calculated Serum Osmolality.
The serum osmolal gap, when normal, should fall in the range of -10 to + 10 mOsm/kg.
Anything greater than +10 mOsm/kg is considered a positive serum osmolal gap, and
a value greater than + 15 mOsm/kg is generally considered a critical value. Table 1-5
includes conditions that can lead to an increased serum osmolal gap with and without
a concomitant serum anion gap acidosis.
TABLE 1-5 • Conditions associated with an el11Yated serum osmolal gap with or without an
associated anion gap acidosis.
With an Elevated Serum Anion Gap
1. Ethanol ingestion with alcohol ketoacidosis (acetone is an unmeasured osmole, in addition to
ethanol)-the osmolallty Is usually elevated more so by the Increased ethanol concentration,
so the osmolal •gap" depends on whether the term for ethanol ls included in the osmolallty
calculation'
2. Organle alcohol Ingestions (methanol, ethylene glycol, dlethylene glycol, propylene glycol)
3. OKA-similar to ethanol ingestion, earlier, glucose and acetone contribute to the osmolality,
since the glucose term is always included in the calculation
4. Salicylate toxicity
5. Renal failure-the BUN Is nearly always included in the osmolallty
Without an Elevated Serum Anion Gap
1. Hyperosmolar therapy (mannitol, glycerol)
2. Other organic solvent Ingestion (eg, acetone)
3. lsopropyl alcohol ingestion (produces only acetone rather than an organic acid, so no anion
gap is seen)
4. Hypertriglyceridemia
5. Hyperprotelnemia
'A mildly elevated osmolol gap hos been reported in the literature in patients with lactic acidosis in critical illness,
particularly sl!\ll!re distributive shock. The pathology is not quite clear, although it likely is related to multiorgon
failure-particularly involving the liver and kidneys-and the release ofcellular components known to contribute
to the osmolol gap. This is typically around 10 mOsmll., although it may be as high as 20--25 mOsm!L
ANION GAP ACIDOSIS

Once all the calculations for the anion gap acidosis portion of the algorithm have
been performed, one can attempt to determine the underlying etiology. Common
and less common causes of an anion gap acidosis are provided in Tables I-6 and I-7.
Lactic acidosis, DKA, and chronic renal insufficiency/failure remain the most common
forms of anion gap acidosis seen clinically. Lactate, which is produced from anaero-
bic metabolism, can then be converted back to glucose in the liver via the Cori cycle,
excreted as an anion in kidney, or used in the Kreb cycle via conversion to pyruvate.
L-Lactic acidosis can be classified into type A and type B; a separate form of acidosis,
TABLE 1-6 • Causes of anion gap metabollc acidosis.

Common Less Common
Lactic acidosis (lncludlng transient) Cyanlde poisoning
Renal failure [•uremia") Carbon monoxide poisoning
OKA Aminoglycosides
Alcohol ketoacidosis Phenformin use
Starvation ketoacldosls 0-Lactlc acidosis
Salicylate poisoning (ASA) Paraldehyde
Acetaminophen poisoning (paracetamol) Iron
Organic alcohol poisoning (ethylene glycol, methanol, lsoniazid
propylene glycol) Inborn errors of metabolism
Toluene poisoning ("glue-sniffing")
INTRODUCTION 11
TABLE 1-7 • Anions/metabolites associated with different causes of an anion gap acidosis.
Methanol -7 Formic acid
Ethylene glycol -7 Oxalic acid
Propylene glycol' -7 D-Lactic acid (potential metabolite)
Toluene -7 Hippuric acid
Ketoacldosls -7 Ketones (acetoacetone, beta-hydroxybutyrate)
Aspirin -7 Salrcylates
Acetaminophen -7 5-0xoproline (pyroglutamic acid)
Cyanide -7 2-Aminothiazoline-4-carboxylic acid (ATC)
•Pharmacologic Agents Potentially Utilizing Propylene Glycol
• Lorazepam
• Phenobarbital
• Bactrim
• Esmolol
• Nitroglycerin
termed D-lactic acidosis, occurs as a by-product of bacterial metabolism in patients

with specific risk factors. Type A lactic acidosis is seen more commonly, and is asso-
ciated with evidence of poor tissue perfusion or oxygenation, whereas type B lactic
acidosis is typically associated with delayed clearance or tissue utilization of lactate.
Causes of a type A lactic acidosis includes shock, limb ischemia, carbon monoxide, and
severe hypoxemia. Causes of a type B lactic acidosis include liver/renal failure, malig-
nancy, drug toxicity, and inborn errors of metabolism. Type D-lactic acidosis can result
from bacterial metabolism in patients with reduced small bowel absorption (short-gut
syndrome, gastric bypass with small bowel resection). It usually occurs after a large
carbohydrate load but may also be seen in patients with DKA (via metabolism of meth-
ylglyoxal) or patients receiving infusions of medications containing propylene glycol.
D-Lactate is filtered freely and is not well resorbed in the proximal tubule.
Patients with a ketoacidosis usually have preserved renal function. The anions are
excreted as salts with sodium or potassium rather than with ammonium. The admin-
istration of glucose (and insulin in DKA) reduces the production of ketone bodies,
while the administration of isotonic fluids leads to increased anion and acid excretion
(along with sodium, but not chloride). The anion gap is therefore usually "closed" or
resolved by a shift to a non-anion gap acidosis.
Chronic kidney disease (CKD) may be associated with a non-anion gap acidosis, a
pure anion gap acidosis, or a mixed anion and non-anion gap acidosis. Early in the
disease process, acid excretion is more significantly impacted than anion excretion,
leading to a non-anion gap acidosis. As the disease progresses, there is more impact
on anion excretion, leading to a mixed or pure anion gap acidosis.
NON-ANION GAP ACIDOSIS

The primary etiologies for a non-anion gap acidosis include acid ingestion/infusion,
RTA, and gastrointestinal (GI) losses of HC0 3• Aside from the history, the primary
tools for determining the etiology of a non-anion gap acidosis are urine studies,
including the urine pH, presence of kidney stones, the urine anion or osmolal gap,
and the serum potassium. Approximately 50 mEq of non-volatile acid is excreted

by the kidneys on a daily basis, although they are capable of handling up to 10-fold
increase in acid load. Renal acid excretion occurs predominantly via conjugation
of hydrogen ions to ammonia, forming ammonium (NH;). Therefore, the normal
response to a metabolic acidosis is to increase NH; excretion, thus reducing the urine
pH (typically< 5.5). This acid excretion primarily occurs in the distal tubules and
collecting duel In a type 1 (distal) RTA, type 4 RTA, and CKD, patients will have
reduced ammonium excretion in response to an acid load. It is important to differen-
tiate these conditions from those diagnoses associated with a loss ofHC03 via either
the GI tract or the kidney. In a proximal RTA, there is defective resorption of HC03
in the proximal tubule, which may be accompanied by other abnormalities in the
proximal tubule. In diarrhea, HC03 and potassium are lost via the GI tract.
In order to differentiate between GI losses ofHC03 and reduced renal acid excretion,
one may use a surrogate measure of serum ammonium excretion, in addition to the
urinary pH. Although some facilities can directly measure the urinary ammonium,
many cannot. Therefore, there are two primary options for estimating the urinary
NH; excretion: the urine anion gap and the urine osmolal gap.
The urine anion gap provides an indirect estimate ofthe urine ammonium excretion.
The urine anion gap is calculated as follows:
Urine Anion Gap =Na:ru,_ + K:ru,. - Cl•
The typical value ofthe urine anion gap is between + 10 and + 100 mEq/L in patients
consuming a Western diet Urinary chloride is most commonly excreted in com-
plex with sodium, potassium, or ammonium ions. Therefore, in a patient with intact
urinary acidification, as urinary ammonium excretion increases, more chloride is
excreted, and the urine anion gap will become more negative. In patients with a GI
source ofHC0 3 loss such as diarrhea, the urine anion gap will be considerably neg-
ative, typically between -20 mEq/L and -50 mEq/L. Alternatively, in patients with
dysfunctional urinary acidification, the urine ammonium excretion will not increase
significantly, and the urine anion gap will remain positive, usually within the normal
range (+10 to +100 mEq/L). A value between -20 and +10 is generally inconclusive.
There are several limitations to the use ofthe urine anion gap. First, the urine anion
gap can also be impacted by the excretion of other unmeasured anions not usually
present in the urine, so it should be used with significant caution in patients with a
concomitant anion gap acidosis. In these patients, the unmeasured anion (eg, lactate,
hippurate, 5-oxoproline, etc) will serve to falsely elevate the urine anion gap. Addi-
tionally, the presence of polyuria or a urine sodium level less than -10 to 20 mEq/L
can also make the urine anion gap less reliable.
An alternative to the urine anion gap is the urine osmolal gap. The urine osmolal gap
is calculated in a manner similar to the serum osmolal gap:
. 0 sm olality= 2 * ([Na+] + [K+]) +

Calculated Unne [U-re-
a]+[Gl
- uc
- os
-e]-
2.8 18
sured Urine Osmolality- Calculated Urine Osmolality
INTRODUCTION 13
The urine osmolal gap should be proportionate to the urinary ammonium, as this
is the only other major urinary solute not included in the above-calculated urine
osmolality (recall that vast majority of unmeasured anions will be complexed with
either sodium or potassium, which are included here). Therefore, the urine osmolal
gap is a more direct measure of the urine ammonium excretion. A normal value
in a patient with a normal acid-base balance falls between 10 and 100 mOsm/kg,
although in patients with an RTA these values are usually on the low end of this
spectrum ( < 20 mOsm/kg). When faced with an acid load, a patient with intact
urinary acidification (ie, diarrhea) will significantly increase the urine ammo-
nium excretion, and hence the urine osmolal gap will also increase significantly
(> 400 mOsm/kg). Since the ammonium must be also be complexed to an anion
for excretion, the urine ammonium concentration can be estimated as one-half
of the urine osmolal gap (ie, for a urine osmolal gap of 400 mOsm/L, the urine
ammonium concentration would be estimated as 200 mOsm/L). Generally, the
urine osmolal gap will not exceed -600 mOsm/L. Alternatively, in a patient with
dysfunctional urinary acidification (ie, type 1 or type 4 RTA), the serum osmolal
gap will not exceed 150 mOsm/kg.
Similar to the urine anion gap, there are limitations to the use of the urine osmolal
gap. First, the urine osmolal gap should not be used in a patient with increased uri-
nary excretion of non-ammonium solutes (eg, mannitol methanol), which would
yield a potentially inappropriate elevation in the urine osmolal gap. Additionally, a
urinary tract infection with a urease-producing bacteria can lead to inappropriate
elevation of the urine osmolal gap, as urea can react with water to produce ammo-
nium and HC03 , depending on the urine pH.
Once the urine anion gap or urine osmolal gap have been determined, the urine pH,
serum potassium, presence of renal stones, and other abnormalities of the urinalysis
can be used to determine the most likely diagnosis and underlying etiology. However,
it should also be noted that the urine pH is not helpful in differentiating the etiology
in chronic or prolonged metabolic acidosis that is also associated with hypokalemia
(eg, chronic diarrhea). in severe volume depletion, or in patients with urinary tract
infections secondary to urease-producing organisms.
A distal or type 1 RTA is classically associated with a more significant drop in the
serum HC03 (usually< 12 mEq/L), an elevated urine anion gap, a reduced urine
osmolal gap, an elevated urinary pH, the possible presence of renal stones, and
a low or normal serum potassium. Causes of a distal RTA are listed in Table 1-8.
The diagnosis of a proximal RTA requires a high degree of clinical suspicion, as it
cannot be diagnosed based on the urine anion gap or the urine osmolal gap (see
Table 1-9). In addition to abnormalities in urinary HC0 3 resorption, patients may
have abnormalities in the absorption of other solutes from the proximal tubule ( eg,
phosphate, uric acid, amino acids, glucose). This more generalized proximal tubule
dysfunction is termed Fanconi syndrome. The urine pH and urine anion/osmo-
lal gap calculations are not helpful unless the patient is receiving a HC03, or the
disease process is caught very early. Once the process becomes chronic, the patient
reaches a steady state in terms of the serum HC0 3 (12 to 18 mEq/L), and therefore
TABLE 1-8 • Evaluation of non-anion gap acidosis.

Evaluation Strategy
1. History (acute or chronic issues, medications. altered GI anatomy, genetic diseases. etc). Also, is
the patient receiving an acid load, such as TPN?
2. Does the patient have chronic renal insufficiency? If so, this alone may be responsible for the
non-anion gap acidosis.
3. Calculate urine anion gap and urine osmolal gap. The urine anion gap may be of limited value
in patients with severe serum anion gap acidosis, as it may be falsely elevated. Similarly, the
urine osmolal gap may be lnapproprlately elevated ln patients with a significant serum osmolal
gap (particularly due to mannitol).
4. Note the serum potassium as well as the urine pH.
s. If proximal RTA is suspected, look for evidence of other inappropriate compounds in the
urine (amino acids, elevated phosphate, glucosuria), and calculate the fractional resorption of
sodium bicarbonate (should be > 1 5%). Also check serum for evidence of dysfunction of the
PTH-vltamln D-calclum axis.
Cause of NAGMA
LowSerum Potaalum
GI: Diarrhea, pancreaticoduodenal fistula, urinary intestinal diversion
Renal: Type 1 RTA (distal), type 2 RTA (proximal)
Medications/exposures: Carbonic anhydrase inhibitors, toluene
Other: D-Lactlc acidosis
High (or Normal} Serum Potassium
GI: Elevated ileostomy output
Renal: Type 4 RTA or CKD
Medications: NSAIDs; antibiotics (trimethoprim, pentamldlne); heparin; ACE Inhibitors, ARBs,
aldosterone antagonists (spironolactone); acid administration (TPN)
Evaluation of RTA
Type1 RTA Type2RTA Type4RTA
Severity of metabolic Severe (< 10-12 mEq/L Intermediate Mild (15-20 mEq/L)
acidosis, [HC03 ] typically) (12-20 mEq/L)
Associated urine Urinary phosphate, Urine glucose, amino

abnormalities calcium increased; acids, phosphate,
bone disease often calcium may be
present elevated
Urine pH HIGH(>5.5) Low (acidic), until Low (acidic)
serum HC03 level
exceeds resorptive
abillty of proximal
tubule; then
becomes alkalotic once
reabsorptive threshold
ls crossed
Serum K+ Low to normal; should Classically low, although HIGH
correct with oral HCO, maybe
therapy normal or even high
with rare genetic defects;
worsens with oral HC03
therapy
Renal stones Often No No
(Continued)
INTRODUCTION 15
TABLE 1-8 • Evaluation of non-anion gap acidosis. (contlnuftll

Type1 RTA Type2RTA Type4RTA
Renal tubular defect Reduced NH4 secretion Reduced HC03 Reduced WIK+
in distal tubule resorption in proximal exchange in distal
tubule and collecting
tubules due to
decreased aldoster-
one or aldosterone
resistance
Urine anion gap > 10 Negative lnitlally; > 10
then positive when
receiving serum HCC,;
then negative after
therapy
Urine osmolal gap Reduced At baseline Reduced
(< 150 mOsm/L) during < 100 mEq/L; unreliable (< 150 mOsm/L)
acute acidosis during acidosis during acute acidosis
AC~ ang/otens/n-convertlng enzyme; ARB, anglotensln receptor blocker; Cl<D, chronic kidney disease; GI, gastrolntes-
tlnal; HCO,. bicarbonate; NSAJD, nonstero/dal anti-Inflammatory drug; PTH, parrithyrold hormon~ RTA. renaltubular
addosls; TPN, total parenteral nutrition.
the urine pH and anion gap will be inconclusive and appropriate for the patient's diet.
If the patient is placed on a HC03 infusion, and the serum HC03 levd surpasses the
patient's absorptive capabilities, the urine pH will increase rapidly. Altemativdy, one
can calculate the fractional excretion (FE) ofHC03• A value greater than 15% indi-
cates that a proximal RTA is likely.
FE =[Urine HCO;J•Serum Cr
Hco3 [Serum HCO;J•Urine Cr
A distal RTA is generally associated with a mild reduction in serum HC03 (-18 to
22 mEq/L), an elevated urine anion gap, a reduced urine osmolal gap, a normal urine
pH, and an devated serum potassium level.
Finally, for patients with any type of anion gap acidosis, the serum HC0 3 def-
icit can also be calculated. While HC03 therapy is administered only in severe
acidemia in patients with lactic acidosis, serum HC0 3 does have a role in the treat-
ment of certain toxicities and in the management of non-anion gap acidosis. First,
one must calculate the HC03 space, which can then be used to determine the total
HC0 3 deficit.
HCQ; space = [0.4 *( H~~; ) ] * Lean Body Weight (in kg)

HCQ; Deficit = HC03 space * HC03 Deficit/L
TABLE 1-9 • Causes of renal tubular addosls.

Causes of Type 1 (Distal) RTA
Primary
• Idiopathic or famlllal (may be recessive or dominant)
Secondary
• Medications: Lithium, amphotericin, ifosfamide, NSAIDs
• Rheumatologic disorders: Sj0gren syndrome, SLE. RA
• Hypercalciuria (idiopathic) or associated with vitamin D deficiency or hyperparathyroidism
• Sarcoldosls
• Obstructive uropathy
• Wilson disease
• Rejection of renal transplant allograft
• Toluene toxicity
Causes of Type 2 (Proximal) RTA
Primary
• Idiopathic
• Familial (primarily recessive disorders)
• Genetic Fanconi syndrome, cystinosis, glycogen storage disease (type 1), Wilson disease, galactosemia
Secondary
• Medications: Acetazolamlde, toplramate, amlnoglycoslde antlblotlcs, lfosfamlde, reverse
transcriptase inhibitors (tenofovir)
• Heavy metal poisoning: Lead, mercury, copper
• Multiple myeloma or amyloidosis (secondary to light chain toxicity)
• SJ(jgren syndrome
• Vltamln D detlclency
• Rejection of renal transplant allograft
Causes of Type 4 RTA (Hypoaldosteronism or Aldosterone Resistance)
Primary
• Primary adrenal insufficiency
• Inherited dlsorders assoclated with hypoaldosteronlsm
• Pseudohypoaldosteronism (types 1 and 2)
Secondary
• Causes of hyporeninemic hypoaldosteronism such as renal disease (diabetic nephropathy),
NSAID use, calcineurin inhibitors, volume expansion/volume overload
• Causes of distal tubule voltage defects such as sickle cell dlsease, obstructive uropathy, SLE
• Severe illness/septic shock
• Angiotensin II-associated medications: ACE inhibitors, ARBs, direct renin inhibitors
• Potassium-sparing diuretics: Spironolactone, amiloride, triarnterene
• Antibiotics: Trlmethoprlm, pentamldtne
ACl;. angiorensin-converting enzyme; ARB. angiotensin receptor blocker; NSAID, nonsteroidal anti-inflammatory drug;
RA. rheumatoid arthritis; RTA. renal tubular addosis; SLl;. systemic lupus erythematosus.
RESPIRATORY ACIDOSIS
The algorithm for the evaluation ofa respiratory acidosis is shown in Figure 1-4. It is
particularly helpful to determine whether a patient has a baseline respiratory acidosis
prior to evaluation as it will greatly aid in determining the acute acid-base disorders
present The first step in the evaluation is to determine if the metabolic compensation
is appropriate. This requires a decision as to whether the respiratory process is acute
INTRODUCTION 17
Respiratory Acidosis
•
18 metabollc compenaatory
response appropriate?
___
ACUTE: Expeol&d HC03 = Baseline HC"3 + (0.1 )[aawal PaCO:! - b&selirle PaCO:!]
CHRONIC: Exp9Ctfld HC03 ~ Bue/ine HC03 + (0.4)[acll/B/ PaCCJ:2 - b&selirle Pa~
• i •
acldoala pruent
.,,.,,
Cancomllllnt ~bollc Appraprlm metabollc
compenutlon
A-a gl'Hlant ( V Aa)

----
Concomitant melllbollc
alllllloal• p.-nt
99119/'B/: VAa = [F/0:2 • (PATM - P-)1- PaCJ:2- (1.25. Pa~

ar Sfla level: VAa = 150 mm Hg - Pao2 - (1.25 • Paco2)
VAac1&mmHg
•
Hypaventllallan wllhout chllnge In
parenchymal dllfUalng capacity
c... -.~,,_.,IBliliwt)
I
•
VAa>1&mmHg
Hypovenllladon with
reduced dllfllalng capacity
(... VQ~--)
Figure 1-4 • Algorithm for the evaluation of a respiratory acidosis.
Equation for the metabolic compensation for acute respiratory acidosis:

Expected HC03 =Baseline HC03 + (O.l)[Actual Paco2 - Baseline Paco2];
Equation for the metabolic compensation for chronic respiratory acidosis:

Expected HC03 =Baseline HC03 + (0.4)[Actual Paco2 - Baseline Paco1];
where the baseline HC03 and the baseline Paco2 should be determined from prior
laboratory studies, or if not known, values of 24 mEq/L and 40 mm Hg should be
used. If the actual value of the HC03 is less than the expected value, then a concom-
itant metabolic acidosis is present. If the actual HC03 is greater than expected, then
a metabolic alkalosis is present. If the actual value is as expected, then no metabolic
acid-base disorder is present, and the change in the HC03 is appropriate. Once this
has been determined, one may use the alveolar-arterial partial pressure of oxygen
gradient (A-a gradient) to help differentiate the underlying conditions. The A-a gra-
dient is elevated if it is greater than -15 mm Hg:
VA-a= [Fio2 * (PATM - pwater)] - Pao2 - (1.25) *Pacol

At sea level, the atmospheric pressure is 1 ATM or 760 mm Hg, the partial pressure
of water is 47 mm Hg, and the fraction of inspired oxygen (Fio1 ) is 0.21, so the A-a
oxygen gradient reduces the following:
VA-a,_leftl = 150 mm Hg- Pao2 - (1.25) * Paco1
However, many conditions may be associated with an A-a gradient, and the normal
A-a gradient can vary with a number of factors, including age. Additionally, patients
may have a baseline A-a gradient that is elevated and unknown (and does not cause
the patient to require supplemental oxygen), which may also complicate the picture.
Overall, the history and clinical presentation are generally adequate to narrow the
differential diagnoses (see Table I-10).
TABLE 1-1 O • Potential causes of respiratory addosls.

Central Nervous System and Neuromuscular Disease
• Stroke/cerebrovascu lar accident
• Head trauma, Increased lntracranlal pressure
• General or moderate anesthesia
• Opioid or other sedative toxicity
• Spinal cord injury (above the C6 level)
• Seizure
• Botulism
• Organophosphate or other anticholinergic toxicity
• Bulbar neuropathies
• Hypokalemic myopathy
• Myasthenia gravis
• Gulllaln-Bar~ syndrome (or variants}
• ALS (and other neuromuscular disorders, Including muscular dystrophles and mitochondrial
disorders)
• Multiple sclerosis
• Myxedema
Chest Wall
• Trauma (flall chest}
Pneumothorax. pleural effusion or other pleural space occupying lesions
• Kyphosis or other chest wall abnormality leading to abnormal respiratory mechanics
• Diaphragmatic dysfunction or paralysis
• Thymoma or other structure/tumor causing external airway compression
Pulmonary or Airway
• Upper or lower airway obstruction (Including tracheomalacla and obstructive sleep apnea}
• Tracheal stenosis
• Central sleep apnea
• Aspiration of foreign body with obstruction or massive aspiration event
• Angloedema
• Allergic reaction with airway involvement
Pulmonary or Airway (cont.)
• Laryngospasm
• Bronchospasm
• Vocal cord paralysis
• Status asthmatlcus
• COPD
• Bronchiolitis
• Interstitial lung disease with severe restriction
• Massive pulmonary edema
• ARDS (particularly ln the flbrotlc or flbroprollferatlve phase)
• Bronchiectasis, including end-stage cystic fibrosis
Vascular
• Pulmonaryembolism
• Fat embolism
• Cardiac arrest
Other
• Esophageal intubation (or other misplacement of airway device)
• Air-trapping during mechanical ventilation
• Snakebite with neurotoxin envenomation
AlS, amyotmphk/atMII sclerosis;ARDS, acutPrespimtotyd~syn~COPD, chronicobstrtJclMpu/monarydisease.
INTRODUCTION 19
METABOLIC ALKALOSIS
The algorithm for the evaluation of a metabolic alkalosis is shown in Figure 1-5.
The first step in evaluation is to determine whether the respiratory compensation is
appropriate. Similar to the case for metabolic acidosis, we have the following equation
to determine appropriate compensation:
Expected Paco1 =Baseline Paco1 - (0.7)[Actual HC03 - Baseline HC03 ]
Once it has been determined that the respiratory compensation is appropriate or

there is a concomitant respiratory acid-base disorder, the next step is to review
the history for any potential causes, including an alkali load, genetic conditions
such as a cystic fibrosis (CF), or the recent use of laxative (see Table 1-11). A
thorough review of the medications is also necessary at this point. The physical
examination is also critical as it may point to evidence of hypertension (HTN)
or a hyperaldosterone state. The next step in evaluation is to determine if the
condition is a chloride- or fluid-responsive condition (such as hyperemesis) or
a chloride-resistant process. This is accomplished by evaluating the urine chlo-
ride. Once this has been established, one may use a combination of the presence
or absence of HTN, the urine and serum potassium, and the plasma renin and
aldosterone levels.
Metabollc Alkalosla
i
Is the respiratory
compensation appropriate?
&peeled Paco2 = ba8eh Pac~ - (0.7) [Aclua/ HCIJa- &8eline HCOa]
+
Concomllllnt R•plr1111Dry Acldoalll
i +
Concomllllnt Rllllplratory Alkaloal8
Approprlm Companutlon
1Npbafmy acldaala lrow chart reapll"ll,.,,, 91hlml• lfow chatf
History (eg, allaall lngeallon, cyatlo tlbroal•)
Chlorldll-Rllllllltant Allcaloala
+ UCI > 20 mEq/L
I
•
Urine Chloride (Uci)
Chlo ride R11p Dnlllva Allmloala
Uc1 .: 20 mEq/L +
UK, blood pressure, l..oa8 of gastric acid (hyperemeaia, NGT),
Plasma renin and aldoaterone prior diuretic uae, post~ypercapnia, villoua adenoma
congenital chloridormea, CF, chronic laxative abuae
.~~~~~~.~~~~~~~~-Hype
~- rten
- s~
iw l
UK< 30 mEq/L UK> 30 mEq/L I

l
Law-normal BP
l
Low-normal BP Low plasma ranln
Elevated p~me renln Law plesmi aldostarone
Low plasma renln
High plas1 aldosterone
Laxallw abuse Current diuretic uae Renal artery atenoela Cushing syndrome Primary hypareldosteronlam
Hypokalemla Bertler syndrome Renln-aacratlng rumor Exogenous aterold use Adrenal edanoma
Hypomegnesemla Gitelman syndrome Renovaacular disease Genetic disorder Blllllaral adrenal hyperplasia
Liddle syndrome
Llco~ca toxicity
Figure 1-5 • Algorithm for the evaluation of a metabolic alkalosis.

TABLE 1-11 • Causes of metabolic alkalosls.

History
Rule Out the Following as causes
• Alkali load ("milk-alkali" or calcium-alkali syndrome, oral sodium bicarbonate, intravenous
sodium bicarbonate)
• Genetic causes (CF)
• Presence of hypercalcemia
• Intravenous (J-lactam antibiotics
• Laxative abuse (may also cause a metabolic acidosis depending on diarrneal HC01 losses)
If None of the Above, Then •••
Urine Chloride < 20 mEq/L (chlorldH'flsponsln cau.Ns)
• Loss of gastric acid (nyperemesis, NGT suctioning)
• Prior diuretic use (in nours to days following discontinuation)
• Post-nypercapnia
• Vlllous adenoma
• Congenital cnloridorrnea
• Cnronic laxative abuse (may also cause a metabolic acidosis depending on diarrheal HC01 losses)
•CF
OR: Urine Chloride > 20 mEq/L (chloride-resistant causes):
Urine Chloride > 20 mEq/L, Lack of HTN, Urine Potassium < 30 mEq/L
• Hypokalemia or hypomagnesemia
• Laxative abuse (If dominated by hypokalemla)
Urine Chloride > 20 mEq/L, Lack of HTN, Urine Potassium Variable
• Current diuretic use
• Bartter syndrome
• Gitelman syndrome
Urine Chloride > 20 mEq/L, Presence of HTN, Urine Potassium Variable but Usually> 30 mEq/L
Elwated plamia nnln lwel:
• Renal artery stenosls
• Renin-secreting tumor
• Renovascu lar disease
Lowplamia renin, low plasma aldosterone:
• Cusning syndrome
• Exogenous mlneralocortlcold use
• Genetic disorder (11-hydoxylase or 17-hydrolyase deficiency, 11 ~HSD deficiency)
• Liddle syndrome
• Licorice toxicity
Lowpltuma nnin, high plosmo aldoste«Jne:
• Primary hyperaldosteronism
• Adrenal adenoma
• Bilateral adrenal hyperplasia
11{J-HSD, 11beta-hydroxystero/d dehydrogenase; CF, cystic fibrosis; HTN, hypertension; NGT, nasogastrlc tube.
RESPIRATORY ALKALOSIS
The algorithm for the evaluation of a respiratory alkalosis is provided in Figure I-6.
Similar to respiratory acidosis, it is particularly helpful to determine if a patient has a
baseline respiratory alkalosis prior to evaluation as it will greatly aid in determining
INTRODUCTION 21
Respiratory Alkaloais
•
18 metabollc compenaatory
response appropriate?
+ i +
----
Concornllllnt mmlllbollc
..:ldosls prnent
Approprlllla matabollc
campanutlon
A-a gNdl•nt (VAm)

----
ConcomHant mBlllbollc
•llmlosls P - '
gtmel'lll: VAa = [F/CJ:! • (PATM - P-)] - PaCJ:!- [1.25. PaCO:!]

at sea /eve/: VAa = 150 mm Hg - Pao2 -[1.25 • Paco:i]
VAll<15mmHg I VAll>15mmHg
+
Hypmrvwntillltion without changm in
+
Hypal'Vllntilation with
pal'llncllymal diffusing capacity Nducmcl diffusing capacity
(•AMO-.pi--ie,-) c.. wi~-->
Figure l-6 • Algorithm for the evaluation of respiratory alkalosis.
the acute acid-base disorders present The first step in the evaluation is to determine
if the metabolic compensation is appropriate. This requires a decision as to whether
the respiratory process is acute or chronic in nature.
Equation for metabolic compensation for acute respiratory alkalosis:
Expected HC03 =Baseline HC03 - (0.2)[Actual Paco2 - Baseline PacoJ.
Equation for metabolic compensation for chronic respiratory alkalosis:
Expected HC03 =Baseline HC03 - (0.4)[Actual Paco2 - Baseline Paco2].
Once it has been determined if a concomitant metabolic add-base disorder is pres-

ent, the A-a gradient may be used to aid in determining the etiology of the respiratory
alkalosis (see Table 1-12).
This effectively rounds out the process for evaluation for acid-base disorders. Before
proceeding to the cases, we will briefly address the other methods for evaluation of
add-base disorders.
THE STEWART APPROACH TO ACID-BASE DISORDERS

The underlying physiochemical principles of the Stewart approach are as fol-
lows: (1) There is continual maintenance of electrical neutrality in the serum; (2)
weak acids are partially dissociated in water governed by dissociation equilib-
ria; and (3) mass must always be conserved in a closed system. In contrast to the
"bicarbonate" approach we employ in this text, the Stewart approach is founded
on the principle that the serum HC0 3 is a dependent rather than an indepen-
dent variable, and the primary independent determinants of the acid-base status
(and hence pH) are the Paco2 , the concentration of weak acids <Aro0 primarily
TABLE 1-1 :Z • Causes of respiratory alkalosls.

Central Nervous System
• Anxiety or panic
• Pain
•Volitional
• Psychosis
• Fever
• Stroke/cerebrovascular accident
- Trauma
•Tumor
Pulmonary and Airways
• High altitude
• Pneumonia/pneumonitis
• Aspiration of foreign body or other substance
• Severe hypoxemla due to atelectasls, ARDS, edema, carboxy/met-hemogloblnemla, etc
• Pulmonary embolism
•Asthma
- Chest wall trauma
• Pulmonary edema
Other Causes
• Drug toxicity (nicotine, progesterone, catecholamlnerglc vasoactlve drugs, sallcylates, xanthlnes,
doxapram)
• Pregnancy
• Liver failure/cirrhosis
• Excess mechanical ventilation
• Heatexposure/stroke
• Compensation and/or recovery from metabolic acidosis
ARDS. acutt respiratory distress 5Yndrorne.
albumin), and the concentration of strong ions (SIDAPP). The primary advantage of
this method is that is allows for consideration of a more complete number of vari-
ables impacting the acid-base status and provides a more physiologic explanation
for hyperchloremic metabolic acidosis. However, it is a far more complex method
of approaching acid-base evaluation, requires more laboratory studies, and has not
shown a consistent benefit in terms of diagnosing acid-base status or impacting
clinical outcomes compared with the more widely applied bicarbonate approach.
THE BASE EXCESS (BE) AND STANDARD BASE EXCESS (SBE)

APPROACHES
Proposed as an alternative to the use of an HC0 3 estimate of ABG measurements,
the base excess (BE) is a parameter derived by Siggard-Andersen in 1960. The BE
is the concentration of a strong acid or strong base (mmoL/L) required to return
the pH of a whole blood sample to pH 7.40, assuming a Pco2 of 40 mm Hg and
normal temperature, thus eliminating the respiratory component from the equation
lic component alone. Normal values range from -3 to
INTRODUCTION 23
+3 mmol/L (positive BE= alkalotic pH; negative BE= acidotic pH). The equation
used to calculate the BE is as follows:
BE= {[HCO;] -24.4} + {(2.3 * [Hb] + 7.7) *(pH - 7.4) * (1- 0.023 x [Hb]).
However, this equation is not truly invariant of changes in the Pco2 , as it only accounts
for buffering intravascularly, and does not take into account the entire extracellular
space. A modified version of the Van Slyke equation, called, the SBE, attempts to
account for this by assuming the buffering capacity ofhemoglobin (Hb) is distributed
throughout the extracellular fluid (ECF), so the Hb concentration is assumed to be
one-third the normal value (of 13 to 15 g/dL) rather than the patient's actual Hb to
ensure it is not dependent on the Paco2• The downside to each of these approaches
is that they ignore the respiratory components of acid-base status and provide no
means to differentiate between anion gap and non-anion gap causes of a metabolic
acidosis.
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INTRODUCTION 33
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A 68-year-old man presents to the emergency department (ED) with encephal-
opathy that has gradually been worsening over the past 2 days. He has advanced
COPD, GOID class D, with very severe expiratory airflow obstruction (FEV1 < 30%
predicted). He uses 3 to 4 Umin supplemental 0 2 via nasal cannula (NC). He
uses BiPAP intermittently at night as he feels it is "too claustrophobic" overall.
He uses a LAMA/LABA combination inhaler daily, in addition to albuterol PRN.
He is unable to provide significant history, but his wife notes that he developed
worsening shortness of breath and productive cough a week ago. A physician at his
local clinic ordered an anb'biotic and steroid taper, but the patient did not experi-
ence much of an improvement. He has been using albuterol nebulizers up to every
2 hours over the past 2 days. Over that time, he has appeared more groggy during
the day, eating and drinking less, and not performing his iADLs as he typically
does. His wife became very concerned about his breathing pattern and brought
him to the ED. The patient also has a history of gout and coronary artery disease,
for which he takes aspirin, carvedilol, and losartan. His vital signs on admis-
sion were 37.6°C, RR 33, HR 119, BP 166/69, and Sa02 88% on 6 Umin NC. His
examination is notable for the following findings: a very thin, elderly man in obvi-
ous distress, arousable only to sternal rub. He has diminished air movement in
all lung fields. Laboratory values are drawn before interventions are started. No
prior laboratory values are available for this patient in your computer system.
Laboratory results are as follows.
Laboratory data
ABGs Basic Metabolic Panel
pH 7.14 Na 142 mEq/L
Paco, 122mm Hg K 5.6mEq/L
Pao, 59mmHg Cl 89mEq/L
HC03 41 mEq/L co, 41 mEq/L
BUN 38 mg/dl
Cr 1.2 mg/dl
Lactate 23mmol/L
Albumin 4.0g/dl
QUESTIONS
Q1-1: What is/are the primary acid-base disturbance(s) occurring in this case?
A. Metabolic acidosis only
B. Respiratory acidosis only
C. Metabolic acidosis and a respiratory acidosis
D. Metabolic alkalosis and a respiratory alkalosis
E. Metabolic alkalosis
F. Respiratory alkalosis
Q1-2: This patient has a respiratory acidosis, but you are unsure if it is acute,
chronic, or acute on chronic. What would you expect the patient's pH and serum
HC03 to be if this entire respiratory process was acute!
A. pH 7.20, HC03 20 mEq/L
B. pH 7.11, HC03 30 mEq/L
C. pH 7.52, HC03 44 mEq/L
D. pH 6.91, HC03 33 mEq/L
Q1-3: For this question, let us assume the preceding information is true, and the
patient's respiratory acidosis is entirely an acute process. What other add-base
abnormality must be presentf
A. Anion gap metabolic acidosis
B. Non-anion gap metabolic acidosis
C. Respiratory alkalosis
D. Metabolic alkalosis
Q1 -4: What wouldyou expect the patient's pH and serum HC03 to be ifthe entire
respiratory process was chronic!
A. pH 7.25, HC03 53 mEq/L
B. pH 7.31, HC03 60 mEq/L
C. pH 7.07, HC03 40 mEq/L
D. pH 6.92, HC03 22 mEq/L
Q1-5: For this question, let us assume that the patient's respiratory acidosis is
entirely a chronic process. What other acid-base disorder must be present!
A. Metabolic alkalosis
B. Anion-gap metabolic acidosis
C. Non-anion gap metabolic acidosis
D. Respiratory alkalosis
Q1 -6: Now, let us assume this is a pure respiratory acidosis with no other ongoing
metabolic process (ie, no metabolic acidosis or alkalosis): How would you classify
the patient's respiratory acidosis!
A. Acute respiratory acidosis
B.C hronic respiratory acidosis atory acidosis
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gentilz hommez, pour famme, je ne sçay se elle fu vraie ou non, et
d’otel mort comme li dessus noummet, lesquelx on noummoit
messires Henris de Malatrait, messire Guillaumme Bacons, li sirez
de Roche Tisson et messires Richars de Perssi, tout rice homme et
gentil homme durement et de Normendie: dont vous devés savoir
que il despleut grandement à leurs prochains, car encore avoecq
tout che li roys de Franche saisi leurs terrez et maintint que il lez
avoient fourfaittez. De quoy li sirez de Clichon avoit ung jonne
escuier à fil, que on appelloit Olivier. Chilz se traist tantost en
Hainbon avoecq monseigneur Amauri de Clichon, son oncle, et le
jone dammoisiel de Montfort, liquel, quant il vinrent en eage, fissent
depuis très forte guerre en Bretaingne et en Franche, en
contrevengant les mors de leurs pèrez, car voirz fu que li comtez de
Montfort estoit mors ou castiel dou Louvre à Paris. Fº 79 vº.
—Ms. de Rome: Ensi se portèrent, en che temps dont je parole,
les querelles en Bretagne, et se desrompirent ces grans assamblées
sans bataille et sans riens faire. Et prist li rois d’Engleterre congiet à
la contesse de Montfort, et puis entra en sa navie et retourna en
Engleterre, et en remena toutes ses gens. Et esploita tant, par le
plaisir de Dieu et dou vent, que sa navie, sans peril et sans damage,
prissent terre à Pleumude en Engleterre. Et estoit conme prisonniers
en la compagnie dou roi messires Hervis de Lion, et fu amenés en
Engleterre; et qant il fu là venus, recreus courtoisement sus sa foi et
mis en la chité de Londres, et pooit partout aler et venir à sa
plaisance. Aultre constrainte de prison ne li fu faite.
Qant ces coses furent apaisies, et tout chil signeur retrais en lors
lieus, et se tenoient bien ces trieuves en Bretagne entre mesire
Carle de Blois et la contesse et lors gens, ne nuls ne les enfrandoit
ne brisoit, grandes nouvelletés et pités et grans rachines de tous
mauls avinrent ou roiaulme de France. Pluisseur hault baron et
chevalier de Bretagne et de Normendie, et qui loiaument s’estoient
acquité et porté ens ès gerres de Bretagne de la partie des François,
à l’avis et renonmée de tous ceuls qui ensonniiet s’en estoient, ne
qui parler en savoient, furent acuset de trahison, de laquelle
accusation on ot grant mervelle. Et ne s’en porent onques chil
escuser ne purger, qui accuset furent, et les en couvint morir
honteusement: dont tous li linages de ceuls furent grandement
courouchiet, et premiers, li sires de Cliçon, liquels fu en son temps
uns vaillans et loiaus chevaliers, et ne l’avoit on veu en nulle
defaute. Mais, pour le temps dont je parole, li cours de France estoit
si perilleuse à poursievir que li signeur ne s’i savoient conment avoir;
et se laisoient li rois Phelippes et son fil, li dus de Normendie, trop
legierement enfourmer. Et pour ce temps, il i avoit une roine en
France, mère dou roi Jehan, et qui fille avoit esté dou duch de
Bourgongne, trop crueuse fenme, car qui que elle encargoit en
haine, il estoit mors sans merchi. Et son fil, li dus Jehans de
Normendie, qui puis fu rois de France, tint assés de ses oppinions et
resgna hausterement, et fist faire moult de crueuses justices en son
temps. Par quoi li roiaulmes de France, par toutes ses parties, en fu
si grevés et si batus et si persequtés que, deus cens ans à venir, les
traces i parurent, ensi que vous orés recorder avant en l’istore.
Avoecques le signeur de Cliçon qui fu decolés à Paris, et voellent
bien li auqun maintenir que ce fu par envie, pour tant que li rois
d’Engleterre l’avoit delivré de prison, et il avoit retenu messire Hervi
de Lion, furent accuset de traison et mort et exequté à Paris li sires
de Malatrait et ses fils, li sires d’Avaugor et ses fils, mesires Tiebaus
de Montmorillon et jusques à diis chevaliers que barons de
Bretagne, et avoecques ceuls, quatre moult hauls gentils honmes de
Normendie, et liquel estoient aussi de grant linage en Bretagne, loist
à savoir mesire Henri de Malatrait, messires Guillaumes Bacons, li
sires de Roce Tison et li sires de Montboucier. Et n’i eut baron ne
chevalier en France, de leur linage, qui osast aler au devant ne dire:
«C’est mal fait,» tant estoient adonc les coses crueuses et
felenesces. Fº 94 vº.
P. 35, l. 20: li hayne.—Mss. A 1 à 33: l’envie. Fº 109.
P. 36, l. 12: d’Avaugor.—Mss. A 1 à 6, 23 à 33: de Vangour, de
Wangour. Fº 109.—Mss. A 7, 11 à 19: de Vaugour. Fº 104.—Mss. A
8, 20 à 22: d’Avaugor, d’Avaugoure. Fº 100.
P. 36, l. 13: Morillon.—Mss. A 1 à 6, 8 à 14: Montmorillon. Fº 108.
—Mss. A 20 à 22: Montarillon. Fº 161.
P. 36, l. 14: jusques à dix.—Ms. B 6: jusques à quatorse. Fº 235.
P. 36, l. 19: Roce Tison.—Mss. A 1 à 6, 8 à 19, 23 à 33: Roche
Tesson, la Roche Tesson. Fº 109.—Mss. A 7, 20 à 22: Roche
Tisson, Roche Tison. Fº 104.
§ 203. P. 37, l. 1: En ce temps.—Ms. d’Amiens: En ce tamps vint

en pourpos et en vollenté au roy Edouwart d’Engleterre que il feroit
refaire et redefiier le grant castiel de Windesore, que li roys Artus fist
jadis faire et fonder là où premierement fu coumenchie et estorée la
noble Table Reonde, dont tant de bons chevaliers yssirent par le
monde, et feroit li roys une ordonnance de chevaliers de lui et de ses
enffans et des plus preus de sa terre, et seroient en somme jusques
à quarante, et lez nommeroit on les chevaliers du Bleu Gertier, et le
feste d’an en an le jour Saint Gorge. Et pour ceste feste
coummenchier, li roys englès asambla de tout son pays comtes,
barons, chevaliers, et leur dist sen entention et le grant desir que il
avoit de le feste emprendre; se li acordèrent liement. Et là furent
esleu quarante chevalier, par avis et par renommée lez plus preux
de tous lez autres; et saielèrent par foy et par sierment avoecq le roy
à tenir et à pourssuiwir le feste et lez ordonnanches telles que elles
en estoient accordées. Et fist li rois fonder et edefiier une cappelle
de saint Jorge ou castiel de Windesore, et estaubli et mist
chanonnes pour Dieu servir, et les arenta et aprouvenda bien. Et
pour ce que la feste fuist sceue et conneuwe par touttez marches, li
roys englès l’envoya publiier et denunchier par ses hiraux en
Franche, en Escoce, en Bourgoingne, en Flandres, en Braibant, en
Allemaingne et par tout jusqu’en Lombardie; et donnoit à tous
chevaliers et escuiers qui venir y volroient, quinze jours de sauf
conduit apriès le feste. Et devoit estre ceste feste une joustez de
quarante chevaliers dedens atendans [tous autres] et de quarante
escuiers, et seoir, le jour Saint Jorge prochain venant que on
compteroit l’an mil trois cens quarante quatre, ens ou castiel de
Windesore. Et devoit estre la roynne d’Engleterre acompaignie de
trois cens dammes et dammoiselles, tout pour son corps, touttes
noblez et gentilz dammez, et parées d’uns paremens sannables. Fos
79 vº et 80.
—Ms. de Rome: En ce temps vint en pourpos et en volenté au roi
d’Engleterre de faire redefiier le grant chastiel de Windesore, lequel
li rois Artus fist jadis faire et fonder, et là où premierement la Table
Reonde fu conmenchie, dont tant de bons et vaillans chevaliers
issirent et travillièrent en armes et en proèces par le monde; et feroit
li dis rois une ordenance de chevaliers de li et de ses enfans et des
plus preus et renonmés d’Engleterre et d’autres pais aussi, qui
estoient en son service, et seroient en sonme jusques à quarante, et
seroient nonmé li chevalier dou Bleu Gertier, et porteroient tous jours
continuelment en lor senestre jambe une ordenance dou Bleu
Gertier, et feroit faire et edefiier en l’onnour de Dieu et de saint
Gorge une capelle ou chastiel de Windesore, et le jour Saint Gorge
seroient tout li chevalier à la feste qui bonnement i poroient estre, et
là aueroit douse chanonnes bien aprouvendés qui feroient le service
de Dieu et priieroient pour les chevaliers de l’ordenance dou Bleu
Gertier. Qant la promotion de ceste feste faire vint en avis au roi
d’Engleterre, il manda une partie des nobles de son roiaulme, et
qant il furent venu, il leur dist son intension: «Il me vient en plaisance
et en devotion, de faire une ordenance en l’onnour de Dieu et de
saint Gorge par tèle et tèle manière;» et se leur compta tout au lonc
la matère et ordenance de l’emprise, ensi que ichi desus vous l’avés
oï. Li baron et li chevalier, qui là estoient à ce recort, s’i acordèrent et
dissent que che seroit bien fait. Ensi fu la feste de saint Gorge ens
ou chastiel de Windesore edefiie et conmenchie, et la capelle des
douse chanonnes tantos pourjettée. Et ausi fu li grans ouvrages dou
chastiel de Windesore conmenchiés et pourjettés à manière de un
grant palais de salles, de cambres et de toutes ordenances, si
plentiveusement que pour logier le roi et son estat, et la roine et son
estat, et les prelas, barons et chevaliers d’Engleterre, et tout à lor
aise. Et encores demoroient tout li viel ouvrage entier, qui
comprendoient grant fuisson, le dongnon de Windesore et les
cambres et le grande sale où li rois Artus faisoit au temps de son
resgne son tinel et tenoit son estat de chevaliers aventureus, de
dames et de damoiselles. Et pour avanchier les ouvrages de
Windesore, qui furent empris pour faire et conmenchiet l’an de grace
mille trois cens et quarante trois, ouvrier furent envoiiet querre parmi
tout le roiaulme d’Engleterre, et mis en oeuvre et paiiet et delivret au
samedi. Et eurent chil ouvrier un clerc qui entendoit sus euls et qui
les faisoit paiier, lequel on appella Willaume Wiqam. Et chils fu
depuis si grans mestres en Engleterre que evesques et canceliers,
et se passoient toutes coses par lui, et fu tellement en la grace dou
roi que par lui, son temps durant, fu tout fait en Engleterre, et sans li
n’estoit riens fait.
En celle edification de feste qui fu emprise sus la fourme que je
vous di, ot ou chastiel de Windesore joustes solempnèles de
chienqante chevaliers et de chienqante esquiers dedens. Et fu la
feste prononchie et criie et segnefiie par hiraus ens ou roiaulme
d’Escoce, en Alemagne, en Flandres, en Hainnau, en Braibant et
ens ès marces d’Aquitainnes. Et fu la roine Phelippe d’Engleterre,
acompagnie de deus cens dames nobles, parées et bien vesties, si
ricement conme elles pooient estre. Et avoit pour lors li fils dou roi
Edouwart d’Engleterre, Edouwars, li ainnés de tous ses enfans,
trèse ans d’eage ou environ, et fu là à celle feste creés et nonmés
prinches de Galles; et l’en fu baillie la signourie et aministration, et
en tint et entra lors en l’estat, et sera en avant nonmés prinches de
Galles. Li contes de Hainnau et son oncle, li sires de Biaumont,
furent mandé et priiet pour estre à celle feste et de l’ordenance dou
Bleu Gertier, mais point n’i furent, car il estoient ensonniiet aillours;
mais li sires d’Enghien, li sires de Haverec et li sires de
Gonmegnies, messires Oulfars de Ghistelles et pluisseur aultre i
furent. Et furent ces festes continuées en joies et en esbatemens, en
dons et en larguèches, car li rois Edouwars d’Engleterre et la roine
Phelippe sa fenme, en lors temps, furent moult large en dons et
courtois et plentiveus dou lour, et sceurent moult bien acquerir
l’amour et la grace de toutes gens. Fº 95.
§ 204. P. 38, l. 12: Entrues que.—Ms. d’Amiens: Entroes que li

roys englès faissoit son grant appareil pour recepvoir seigneurs,
dammes et dammoiselles qui à se feste venroient, li vinrent les
certainnes nouvellez de le mort monsigneur Olivier de Clichon et des
autres chevaliers desus nommés, encouppés de fauseté et de
traisson. De ces nouvellez fu li roys englès durement courouciés, et
li sambla que li roys de Franche l’ewist fait en son despit, et tint que,
parmy ce fait, les trieuwes acordées en Bretaingne estoient fallies et
brisies de par le dit roy Phelippe. Si eut en penssée de faire le
samblant fait del corps monseigneur Hervy de Lyon, que il tenoit
pour son prisonnier; et fait l’ewist en son irour et tantost, es ne fust
ses cousins li comtes Derbi qui li blamma durement et li moustra
devant son consseil tant de bellez raissons pour sen onneur garder
et son corage afrenner, et li pria souverainnement que il volsist
mettre le chevalier à raenchon soufissant et raisonnable, ensi que il
volroit que on fesist des siens en cas sannable. Il fu avis au roy que
ses cousins li comtez Derbi le conssilloit loyaument, et que tout ce
que il en disoit et prioit, il li venoit de grant gentilèce et noblèce de
coer; si refrenna son corrage et s’i acorda, et manda le dit
monseigneur Hervi par devant lui, liquel, sachiéz, y vint en grant
paour; car il cremmoit et supposoit que on le deuist mettre à mort
villainnement, ensi que on l’en avoit enfourmet. Quant li roys le vit
devant lui, il li dist: «Ha! messire Hervy, messire Hervy, li roys
Phelippes de Vallois a moustret se felonnie trop crueusement, quant
il a fait mettre à si villainne mort en mon despit et à grant tort si
nobles chevaliers, par famme et par fausses souppechons, comme
estoient li sirez de Clichon, li sires d’Avaugor, li sirez de Malatrait, li
sires de Roche Tisson et li autre de Bretaingne et de Normendie,
dont chacuns homs doit avoir pité. Et se je volloie regarder à se
fellonnie, je feroie de vous le sannable cas; car vous m’avés fait plus
de contraires en Bretaingne que nulx autres, mès je m’en soufferay
et li lairay faire ses vollentés, et garderay men honneur à mon pooir.
Et vous laisseray venir à raenchon legière et gracieuse seloncq
vostre estat, pour l’amour de mon cousin le comte Derbi qui chi est,
qui en a priiet, mès que vous voeilliés faire chou que je diray.»
Li chevaliers eut grant joie, quant il entendi qu’il n’aroit garde de
mort; si dist que il feroit vollentiers à son pooir tout ce que li
coummanderoit. Lors li dist li roys ensi: «Messire Hervy, je say bien
que vous estes ungs dez rices chevaliers de Bretaingne, et que je
aroie bien de vous une mout grant ranchon, se je vous volloie
presser, de trente mil escus et plus. Si diray que vous ferés: vous
yrés deviers le roy Phelippe de Vallois et li dirés de par moy que,
pour tant qu’il a mis à mort villainne si gentilz chevaliers comme chil
estoient et en men despit, je di et voeil porter oultre qu’il a enfraint et
brisiet les trieuwes, ce me samble, que nous avions enssamble; si y
renunche de mon costet et le deffie de ce jour en avant. Et
coumment que je sace veritablement que vous me paieriez bien
trente mil escus, je vous laisseray quitte pour dix mil escus, et les
vous creray sus vo foy à renvoiier à Londrez dedens quatre mois, ou
de revenir tenir prison.»—«Monseigneur, dist li chevaliers, Dieux
vous voeille merir le courtoisie que vous me faittez, et à
monseigneur le comte Derbi ossi. Et sachiés, monseigneur, que
vostre messaige feray je vollentiers, et le raenchon paieray dedens
le jour, et le vous meteray en sauf lieu à Bruges, et il vous
souffisse.» Dist li roys: «Il me plaist bien.»
Depuis ne demora mies plenté que li chevaliers tous joians
ordonna ses besoingnes pour partir. Et quant il fu prês, il vint
prendre congiet au roy, liquelx roys li dounna vollentiers, et li dist
encorrez enssi: «Monseigneur Hervi, nonobstant che que vos rois
m’ait courchiet et à son tort, et que par vous je li mande deffianchez,
vous dirés à tous chevalierz et escuiers de par delà que pour ce il ne
laissent mies à venir à nostre feste; car il y seront volentiers veus et
liement recheu, et n’y aront point de dammaige.»—«Sire, che
respondi messires Hervi, je feray tout ce que vous me
coummandés.» Lors se parti messires Hervi dou roy et s’en vint à
Douvrez, et là monta en mer pour venir à Bouloingne. Mès adonc
uns tempestes et fortunne le prist sour mer, si grande qu’il le couvint
sejourner sus l’aige et en grant peril tous les jours l’espasse de cinq
jours. Et fu si tourmentés et si demenés de la mer, que noient il
n’avoit apris, que une maladie le prist, de laquelle il morut à Paris
assés tost apriès ce qu’il eut fait son messaige, et parmy tant il fu
quittes de sa raenchon. Fº 80.
—Ms. de Rome: En ceste feste durant, vinrent au roi d’Engleterre
les certainnes nouvelles de la mort le signeur de Cliçon, et des
aultres chevaliers desus nonmés, accusés en France de fauseté et
de trahison. De ces nouvelles fu li rois d’Engleterre durement
courouchiés, et li sambla que li rois de France l’euist fait en son
despit, et tint que parmi ce fait les trieuwes acordées et données
devant Vennes en Bretagne estoient enfraintes et brisies. Si eut en
pensée et imagination de faire le parel fait dou corps mesire Hervi de
Lion, que il tenoit pour son prisonnier; et fait l’euist en sen irour et
tantos, se n’euist esté son cousin li contes Derbi, qui l’en reprist
durement et li remoustra devant son consel tant de belles raisons
pour son honnour garder et son corage affrener, que riens n’en fu
fait. Mais avint que tantos apriès la feste passée, et les signeurs et
les dames retrais et retournés en lors lieus, li rois d’Engleterre vint à
Wesmoustier, car là ot un grant parlement des nobles de son pais,
pour avoir consel sus l’estat de ses besongnes.
Ce parlement seant, li rois d’Engleterre, en la presence des
signeurs, fist venir mesire Hervi de Lion devant lui, et li dist ensi:
«Ha! messire Hervi! messire Hervi! mon adversaire Phelippe de
Valois a moustré sa felonnie trop crueusement, qant il a fait morir
vilainnement tels chevaliers que le signeur de Cliçon et tels et tels»
(et li nonma par noms, ensi conme il en estoit enfourmés), «laquelle
cose me desplaist grandement, et samble à auquns de ma partie, et
à moi aussi, que il l’a fait en mon despit. Et se je voloie regarder à sa
felonnie, je feroie de vous le samblable cas, et trueve bien qui le me
conselle; car vous m’avés fait plus de contraires en Bretagne, et à
mes gens, que nuls aultres chevaliers. Mais je m’en soufferai et li
laisserai faire ses volentés, et li osterai ce point inraisonnable et
garderai mon honnour, et vous laisserai passer parmi courtoise
raençon et legière, selonch vostre estat, pour l’amour de mon cousin
le conte Derbi, qui chi est, qui en a priiet bien acertes, mais que vous
voelliés faire ce que je vous dirai.» Li chevaliers fu tous resjois et se
reconforta en soi meismes, qant il entendi que il n’aueroit garde de
mort. Si respondi en li humeliant: «Très chiers sires, je ferai à mon
pooir loiaument tout ce que vous me conmanderés.» Lors dist li rois:
«Mesire Hervi, je sçai bien que vous estes uns des rices chevaliers
de Bretagne et que, se je vous voloie presser, vous paiieriés bien
trente mille ou quarante mille esqus. Je vous dirai que vous ferés.
Vous irés deviers mon adversaire Phelippe de Valois et li dirés de
par moi que, pour tant que il a mis à mort vilainne si vaillans
chevaliers et si gentils que chil estoient, de Bretagne et de
Normendie, en mon despit, je di et voel porter oultre que il a enfraint
et brisiet les trieuves que nous avions ensamble: si i renonche de
mon costé et le deffie de ce jour en avant. Et parmi tant que vous
ferés ce message, je vous laisserai passer sus diis mille esqus que
paierés ou envoierés en la ville de Bruges, cinq mois apriès ce que
vous auerés rapasset la mer.»
Li chevaliers remercia le roi de ceste parole et le tint à grant
courtoisie, et ordonna ses besongnes dou plus tos qu’il peut, et se
departi de Londres et vint à Douvres. Et là monta en mer et prist le
cemin pour venir à Boulongne; mais sus la mer li vens li fu si
contraires, et ot ils et sa compagnie tant de fortunes et de
tempestes, que il furent cinq jours sus la mer. Au sisime, il prissent
terre au Crotoi, et de là il vinrent à Abeville. Mesires Hervis de Lion
fu si grevés de la mer que il ne pot souffrir le cevauchier, et fu mis en
une litière et ensi amenés à Paris. Li là venu, il ala deviers le roi
Phelippe, et fist le message dont il estoit cargiés. Point n’i ot de
defaute, et s’aquita deviers le roi d’Engleterre de tous poins, et au
retour il s’alita à Angiers et là morut. Ensi avint de mesire Hervi de
Lion.
Li sires de Cliçon, qui fu decolés à Paris, avoit fil et fille. Le fil, on
l’envoia en Engleterre, et le retint li rois et le mist avoecques le jone
conte de Montfort. Et tout doi furent de la delivrance et ordenance
dou conte Derbi, car li rois de France, avoecques ce que il osta la
vie au signeur de Cliçon, il saisi tous ses hiretages de Bretagne et
de Poito, et les donna et departi aillours à sa plaisance. Fos 95 vº
et 96.
P. 39, l. 17: Malatrait.—Le ms. B 6 ajoute: le signeur de Quintin.
Fº 238.
P. 40, l. 5: escus.—Mss. A 15 à 17: frans. Fº 111 vº.
P. 40, l. 14: escus.—Mss. A 1 à 6, 15 à 17: frans. Fº 110.
P. 40, l. 30 et P. 41, l. 1: dix jours et plus.—Mss. A 1 à 6, 11 à 33:
plus de quinze jours. Fº 110 vº.—Mss. A 7 à 10: plus de cinq jours.
Fº 105.
P. 41, l. 6: Abbeville.—Mss. A 1 à 6: Aubeville. Fº 110 vº.
P. 41, l. 11: mès morut.—Le ms. B 6 ajoute: Dieu en ait l’ame! Ensi
fina messire Henry de Lion dont la contesse de Montfort fut moult lie,
car che lui estoit ung grant ennemy en Bretaigne. Fº 240.
P. 41, l. 12: d’Angiers.—Les mss. A 1 à 6, 11 à 14, 18, 19 ajoutent:
Dieu en ait l’ame par sa sainte pitié et misericorde! Fº 110 vº.—Ms. A
7: Diex en ait l’ame! Fº 105 vº.—Mss. A 20 à 22: Dieux en ait l’ame
par sa douce grace! Fº 163.—Mss. A 23 à 33: Dieu en ait l’ame par
sa grace. Amen. Fº 128 vº.
§ 205. P. 41, l. 13: Et approça.—Ms. d’Amiens: Or approcha li

jours Saint Jorges que ceste grande feste se devoit tenir à
Windesore, et y fist li roys grant appareil; et y furent de son pays
comte, baron, chevalier, dammes, dammoiselles. Et là fu la feste
moult grans et mout noble, bien festiée et bien joustée, et dura par le
tierme de quinze jours. Et y vinrent pluisseurs chevaliers de dechà le
mer, de Flandrez, de Haynnau et de l’Empire; mès de Franche n’en
y eult nulx. La feste durant et seant, pluisseurs nouvellez vinrent au
roy de pluisseurs pays. Et par especial il y vinrent chevaliers de
Gascoingne, li sire de Lespare, li sirez de Chaumont et li sirez de
Mouchident, envoiiés de par le seigneur de Labreth, et le seigneur
de Pumiers et les seigneurs gascons qui pour englès se tenoient, et
en leur compaignie six bourgois especiaux de le cité de Bourdiaux,
liquel furent moult bien venu et conjoi dou roy et de son consseil. Et
remoustrèrent li dessus dit au roy coumment petitement et
foiblement ses bons pays de Gascoingne et si bon amit, ossi la
bonne cité de Bourdiaux, estoient conforté et secourut de lui; et se
briefment n’i envoioit si puissamment gens qu’il fuissent fort de
resister as Franchois, il metoit tout ce que il y tenoit en grant
aventure: si ques li roys en respondi moult liement, et leur dist que il
leur bailleroit un très bon cappittainne, fort et puissant, pour resister
contre ses ennemis de par delà, parmi les bonnes gens d’armes et
archiers, ossi que il li chargeroit des parolles le roy. Et de se
proummesse se contentèrent bien li baron de Gascoingne.
Et avint que, celle feste durant, li roys ordonna et noumma chiaux
qu’il volloit qui alaissent en Gascoingne et desquelz li comtez Derbi
seroit chiés, et y devisa le comte de Pennebrucq, le comte de
Kenfort, le baron de Stanfort, monseigneur Gautier de Mauni,
monseigneur Francke de Halle, monseigneur Jehan de Lille, messire
Jehan de Grea, messire Jehan de la Souche, messire Thomas Kok,
le seigneur de Ferrièrez, lez deux frères de Lindehalle, le Lieuvre de
Braibant, messire Ainmon dou Fort, messire Huon de Hastinges,
menseigneur Estievenon de Tomby, monseigneur Richart de
Hebedon, monseigneur Normant de Sinefroide, messire Robert
d’Eltem, monseigneur Jehan de Norvich, monseigneur Richart de
Roclève, monseigneur Robert de Qantonne et pluisseurs aultres. Et
furent bien trois cens chevaliers et escuiers, six cens hommez
d’armes et deux mil archiers. Et dist li roys à son cousin le comte
Derbi que il presist assés or et argent pour tenir son estat grant et
estoffet et pour bien paiier tous saudoiiers.
Encorres ordounna li roys, celle feste durant, monseigneur
Thummas d’Anghourne pour aller en Bretaingne deviers le comtesse
de Montfort, à lui aidier à garder et à deffendre son pays, quoyque
les trieuwes y fuissent, car il se doubtoit que li roys Phelippes n’y
fesist guerre sus lez parollez qu’il li avoit remandées par
monseigneur Hervy de Lyon. Pour tant y envoya il monseigneur
Thumas à cent hommes d’armes et cinq cens archiers.
Encorres ordonna li roys monseigneur Guillaumme de Montagut,
comte de Sallebrin, à aller sus lez marches d’Irlande et lui tenir en le
conté de Luuestre, car li Irois estoient durement revelé contre lui et
avoient ars en le dessus dite comté grant fuison de villes, pour che
que il se tenoient englèz. Si y envoya li rois le dessus dit comte à
deux cens hommes d’armes et cinq cens archiers. Fº 80 vº.
—Ms. de Rome: En celle grande feste, qui fu à Windesore le jour
Saint Gorge en l’an dessus dit, furent de Gascongne auquns barons,
tels que li sires de Labreth, li sires de Ponmiers, li sires de
Mouchident et li sires de Copane. Et les avoit conjois et honnourés li
rois d’Engleterre de tout son pooir, et aussi avoit fait la roine
d’Engleterre sa fenme, et li baron et dames d’Engleterre. Et avoient
requis chil signeur au roi que il vosist de là en Giane envoiier
auqunes gens d’armes et archiers de par li, pour tenir et faire
frontière à l’encontre d’auquns rebelles barons et chevaliers dou
pais, qui constraindoient ses honmes et ses obeissans ou pais de
Bourdelois, d’Auberoce, de Bregerac et de la Riole, par quoi on euist
vraie connissance en Giane que li rois d’Engleterre estoit lors sires.
Li rois d’Engleterre avoit respondu à ces barons de Gascongne et dit
ensi que volentiers il i envoieroit, car il i estoit tenus et voloit
conforter ses bonnes gens des lontainnes marces aussi bien que les
prochainnes. Or estoient chil signeur parti dou roi d’Engleterre tout
content et retourné en lor pais, et recordé as chevaliers et esquiers
des frontières de Bourdiaus ces nouvelles. Et assés tos apriès lor
departement, il ordonna, par la deliberation de son consel, gens
d’armes et archiers pour aller en Gascongne et viseter les
forterèces, et nonma son cousin, le conte Derbi, à chapitainne et
souverain de toutes ces gens d’armes, et avoecques li le conte de
Pennebruq, le conte de Kenfort, le baron de Stanfort, mesire Gautier
de Mauni, messire Franqe de Halle, messire Jehan de Lille, mesire
Jehan de Grea, mesire Jehan de la Souce, mesire Guillaume
Penniel, mesire Huge de Hastinges, mesire Thomas Kok, le signeur
de Ferrières, les deus frères de Lindehalle, mesire Richart de
Hebedon, mesire Normant de Senefroide, mesire Estievene de
Tombi, mesire Robert d’Eltem, mesire Jehan de Nordvich, mesire
Richart de Roclève, mesire Robert de Qantonne, mesire Ainmon dou
Fort et pluisseurs aultres. Et furent bien trois cens chevaliers et
esquiers, siis cens honmes d’armes et deus mille archiers. Fº 96.
P. 41, l. 15: Et y furent.—Ms. B 6: Et y eult plus de trois cens
chevaliers joustant et bien quatre cens dames et demoiselles, et fu
la feste bien ordonnée. Et fourjousta de cheulx de dedens messire
Franque de Halle, et de cheulx de dehors le conte de Mons en
Allemaigne et ung escuiier d’Escoche qui se nomoit Alixandre de
Ramesay, et de ceulx dedens le prinche de Galles. Fº 240.
P. 41, l. 28: Pumiers.—Mss. A 8, 9, 15 à 17, 23 à 29: Pommier,
Pommiers. Fº 101.
P. 41, l. 28 et 29: Monferant.—Mss. A 8, 9: Montferrat. Fº 101.
P. 41, l. 29: Landuras.—Ms. A 24: Duras.
P. 41, l. 29: Courton.—Mss. A 23 à 29: Curton. Fº 129.—Mss. A 15
à 17: Courron. Fº 112.
P. 42, l. 1: Longerem.—Mss. A 1 à 7, 11 à 14, 18 à 22: Longueren,
Longuerem. Fº 110 vº.—Ms. A 8: Longueran. Fº 101.—Mss. A 15 à
17: Langoran. Fº 112.—Mss. A 23 à 29: Langurant. Fº 128 vº.
P. 42, l. 16: ordonna.—Ms. B 6: Adonc ordonna le dit conte Derby
de aller en Gascongne à quatre cens hommes d’armes et mil archiés
pour garder les frontières. D’aultre part, le conte de Pennebruck eut
cherghe de deux cens hommes d’armes et quatre cens archiés, le
conte de Kenfort deux cens hommes d’armes et deux cens archiés,
et furent prins tous en Engleterre. Fº 241.
P. 42, l. 24: Grea.—Mss. A 20 à 22: Gea. Fº 163 vº.
P. 42, l. 24 et 25: Jehan de la Souce.—Ce nom manque dans les
mss. A.
P. 42, l. 25: Thumas Kok.—Mss. A 20 à 22: Thomas Rally.
Fº 163 vº.
P. 42, l. 26: Lindehalle.—Mss. A 20 à 22: Landehalle. Fº 163 vº.
P. 42, l. 27: Aymon dou Fort.—Ce nom manque dans les mss. A.
P. 42, l. 28: Tonrby.—Mss. A 15 à 19: Comby. Fº 112 vº.—Mss. A
20 à 22: Tomboy. Fº 163 vº.
P. 42, l. 29: Manne.—Mss. A 20 à 22: Name. Fº 163 vº.
P. 42, l. 29: Hebedon.—Ms. A 8: Hedebon. Fº 101 vº.
P. 42, l. 30: Finefroide.—Mss. A 8, 15 à 17: Sinefroide. Fº 101 vº.
—Mss. A 20 à 22: Sineroide. Fº 163 vº.
P. 42, l. 31: d’Eltem.—Mss. A 1 à 6, 11 à 14, 18, 19: d’Altem.
Fº 111.—Mss. A 20 à 22: d’Atam. Fº 163 vº.
P. 42, l. 31: Norvich.—Mss. A 20 à 22: Lorwich. Fº 163 vº.
P. 42, l. 32: Rocleve.—Ms. A 8: Noclene. Fº 101 vº.—Mss. A 15 à
17: Nocleve. Fº 112 vº.—Mss. A 1 à 6, 11 à 14, 18, 19: Rochene.
Fº 111.—Mss. A 20 à 22: Roclerie. Fº 163 vº.—Mss. A 23 à 29:
Rociens. Fº 129.
P. 43, l. 1: Quantonne.—Mss. A 1 à 6: Quatonne. Fº 111.
P. 43, l. 3: deux mille.—Mss. A 20 à 22: trois mille. Fº 163 vº.
P. 43, l. 3: arciers.—Ms. B 6: Adonc pria le conte Derby à messire
Gautier de Mauny que en che voyage il vaulsist estre son
compaignon, car le dit conte le tenoit pour tout le milleur chevalier
d’Engleterre... Car très donc en devant avoit messire Gautier à son
commandement grant foison de bons compaignons et d’archiés,
quant il volloit aller en une armée, car tout le servoient vollentiers
pour les hardies emprises de luy, sa proèche et son eur. Car
oncques ne fut le dit Gautier en plache qui ne fust pour luy et pour
ses gens. Celle fortune ot il tout son vivant: dont ly chevaliers et
escuiers et les compaignons de guerre l’en amoient de mieulz. Fos
241 et 242.
P. 43, l. 9: d’Augourne.—Mss. A 1 à 6, 8, 18 à 22, 30 à 33:
Angorne, Angourne. Fº 111.—Mss. A 15 à 17, 23 à 29: d’Agorne.
Fº 112 vº.
P. 43, l. 12: li rois Phelippes.—Mss. A 20 à 22: messire Charles de
Bloiz. Fº 163 vº.
P. 43, l. 19: de Dulnestre.—Mss. A 1 à 6, 8, 15 à 19, 23 à 33: de
Duluestre. Fº 111.—Ms. A 7: d’Uluestre. Fº 106.—Mss. A 11 à 14: de
Luestre. Fº 106.—Mss. A 20 à 22: Deulnestre. Fº 164.
P. 43, l. 19: li Irois.—Mss. A 1 à 7, 11 à 14, 18, 19, 30 à 33: les
Escos. Fº 111.—Mss. A 20 à 29: les Escoçois. Fº 164.
P. 43, l. 21 et 22: de Dulnestre.—Mss. A 1 à 19, 23 à 33: de
Duluestre. Fº 111.—Mss. A 20 à 22: d’Ulnestre. Fº 164.
§ 206. P. 43, l. 25: Ensi que.—Ms. d’Amiens: Ensi que vous me
povés oyr, departi li roys englès ses gens, chiaux qui yroient en
Gascoingne, chiaux qui yroient en Bretaingne, et chiaux qui yroient
en Yrlande. Et fist delivrer par sez tresoriers as chappittainnes assés
or et argent pour tenir leur estat et paiier les compaignons de leurs
gages: chil se partirent enssi que ordonné estoient.
Or parlerons premierement dou comte Derbi, car il eut le plus
grant carge et ossi lez plus bellez aventures d’armez. Quant touttes
sez besoingnes furent pourveues et ordonnées, et sez gens venus,
et si vaissiel freté, cargiet et abilliet, il prist congiet au roy et s’en vint
à Hantonne, et là monta en mer avoecq le kerke dessus ditte; et
singlèrent tant au vent et as estoilles qu’il arivèrent à Baione, une
bonne ville, forte et grosse, qui toudis s’est tenue au roy englès. Si y
prissent terre et descargièrent touttez leurs pourveanches le
cinquime jour de juing l’an mil trois cens quarante quatre. Et furent
liement recheu et requeilliés des bourgois de Baionne et des bonnes
gens de le ville, et trouvèrent là aucuns chevaliers et escuiers.
Quant li comtes Derbi eut sejourné en le bonne ville de Baionne
par six jours et touttes ses gens ossi, et il s’i furent bien rafreski, si
s’en parti et remerchia tous les bourgois de le bonne feste que fait li
avoient; et fist tant qu’il vint en le bonne chité de Bourdiaux, là où on
l’atendoit, et eurent grant joie de sa venue, car moult l’avoient
desiret. Si vinrent contre lui à grant pourcession, et l’amenèrent
dedens le cité à grant quantité de trompes et de pluisseurs
menestrandies. Si fu li corps dou comte logiés en l’abbeie de Saint
Andrieu, et li autre parmy le chité: il trouvèrent bien ù et coumment,
car elle est grande assés pour bien aisier une grant ost. Or vinrent
lez nouvellez au comte de Laille, qui se tenoit en Bregerach à quatre
lieuwez de là, que li comtez Derbi estoit venus à Bourdiaux et avoit
moult grant fuisson de gens d’armes et d’archiers, et estoit fors
assés pour tenir lez camps, et de assaillir, assegier et prendre
castiaux et bonnes villes. Ces nouvelles oyes dou dessus dit comte,
il manda tantost le comte de Commingnes, le comte de Pieregorth,
le visconte de Quarmaing, le viscomte de Villemur, monseigneur
Carle de Poitiers, comte de Valentinois, et tous lez barons et
chevaliers qui ens ou pays se tenoient de par le roy de France.
Quant il furent tout venu, il leur remoustra le venue dou comte Derbi
et se puissanche par oïr dire: si en demanda à avoir consseil. Et chil
seigneur respondirent que, pour yaux bien acquitter, il se tenroient
en le ville de Bregerach, car elle est clés et entrée de ce pays sus le
rivière de Geronde, et que il supposoient assés que li Englès se
trairoient celle part. Chilz consseil fu tenus. Il fissent leur amas et
leur assamblée de leurs aidans en Bregerach. Et se logièrent li
seigneur ens ès fourbours, qui sont grant et loncq et fort et enclos de
le rivière, et y atraissent le plus grant plenté de leurs pourveanches.
Fos 80 vº et 81.
—Ms. de Rome: Tout chil signeur fissent lors pourveances de ce
que il lor besongnoit, à Pleumude et à Dardemude, et là se traissent
petit à petit et trouvèrent navie toute preste que li rois lor delivroit. Si
entrèrent dedens, qant toutes lors pourveances furent prestes, et se
desancrèrent et tournèrent lors singles deviers Gascongne. Et
costiièrent Bretagne, Rocelle et Poito, et entrèrent ens ou havene de
la Geronde, et vinrent à Bourdiaus et là ancrèrent, et puis issirent
des vassiaus. Li seneschaus dou lieu pour le temps, mesires
Thomas Fouque, et li maires de la ville et tout li honme bourgois de
la chité de Bourdiaus les requellièrent doucement et liement, et lor
amenistrèrent ce que il lor besongnoit. Si missent hors des vassiaus
lors pourveances et tout ce que passet avoient. Et tout furent logiet
en la chité de Bourdiaus et s’i rafresqirent. Et se pourveirent de
chevaus ceuls qui nuls n’en avoient, et fissent remettre à point lors
selles et lors harnois et lors armeures. Fº 96.
P. 43, l. 28: Irlande.—Mss. A 1 à 6: Hillande. Fº 111.
P. 44, l. 12: ou havene de Bayonne.—Ms. B 6: au havre de
Bourdiauls. Fº 242.
P. 44, l. 23 et 24: Saint Andrieu.—Mss. A 1 à 6: Saint Andrey.
Fº 111 vº.
P. 44, l. 26: ou plus.—Les mss. A 11 à 14 ajoutent: mais par toute
l’isle. Fº 106.
P. 44, l. 28: en Bregerach.—Ces mots manquent dans les mss. A
1 à 7, 11 à 14, 18 à 33.
P. 45, l. 3: Lille.—Mss. A 20 à 22: Laigle. Fº 164.
P. 45, l. 4: Commignes.—Mss. A 7, 23 à 33: Commines. Fº 106.
P. 45, l. 5: Carmaing.—Mss. A 20 à 22: Carmaigne. Fº 164.
P. 45, l. 6: le visconte de Villemur.—Mss. A 1 à 6, 18, 19: le conte
de Villemur. Fº 111 vº.
P. 45, l. 7: Murendon.—Mss. A 1 à 6: Miradam. Fº 111 vº.—Mss. A
7, 11 à 14, 18 à 33: Muredam, Murdam, Muredain. Fº 106.—Mss. A
15 à 17: Murendon. Fº 113.—Ms. A 8: Ajurendon. Fº 102.
P. 45, l. 8: Taride.—Mss. A 1 à 6: Lestarde. Fº 111 vº.—Mss. A 11
à 14, 18, 19: Tarde. Fº 106 vº.
P. 45, l. 9: Chastielbon.—Mss. A 1 à 7, 11 à 14, 18 à 33:
Chastillon. Fº 111 vº.
P. 45, l. 10: Lescun.—Mss. A 1 à 33: Lescut. Fº 111 vº.—Les mss.
A 15 à 17 ajoutent: le seigneur de Tannay Boutonne. Fº 113.
P. 45, l. 16 et 17: Garone.—Mss. A 1 à 6: Gironde. Fº 111 vº.
§ 207. P. 45, l. 26: Quant li contes.—Ms. d’Amiens: Et quant li

comtes Derbi eut sejourné en le cité de Bourdiaux environ sept
jours, il s’en parti et entendi que li comtez de Laille se tenoit en
Bregerach; si fist tuit son charoy et son host arouter et traire de celle
part. Et vinrent celle première nuit gesir à ung castiel qui se tenoit
pour yaux, que on claimme Monkuk, à une lieuwe de Bregerach; et
s’y tinrent che soir tuit aise, car il avoient bien de quoy. L’endemain
bien matin, allèrent leur foureur sus le castelerie de Bregerach, et
trouvèrent assés à fourer et revinrent à leur host qui encorres se
tenoit à Monkuk, car li seigneur y volloient disner pour savoir
coumment il se maintenroient, et y disnèrent assés matin.
Endementroes que on seoit à table, messires Gautiers de Mauni
regarda deviers le comte Derbi et dist: «Monseigneur, se nous
estions bien appert et droite gens d’armes, nous buverions à ce
soupper des vins de ces seigneurs de Franche qui se tiennent en
garnison en Bregerach.» Et quant li comtez Derbi eut oy enssi parler
le dit monseigneur Gautier, il leva le chief et respondi: «Jà pour moy
ne demoura que nous n’en buvions.» Li compaignon qui oïrent le
comte ensi parler, missent leurs testez ensamble et dissent lis uns
as autrez: «Allons nous armer, nous chevaucherons tantost deviers
Bregerach.»
Il n’y eut plus dit ne plus fait: tout furent armet, et li chevaux
enssiellet en bien briefve espasse. Et quant li comtes Derbi les vit de
celle vollenté, si en fu tous joyans et dist: «Or chevauchons, ou nom
de Dieu et de saint Jorge, deviers Bregerach.» Dont s’aroutèrent
touttez mannières de gens, et chevauchièrent, bannierres
desploiiées, deviers le cité, en le plus grant calleur dou jour, et
fissent tant que il vinrent devant les bailles des faubours qui
n’estoient mies legier à prendre, car une partie de la rivierre de
Geronde les environne. Et si y avoit d’autre part bonnes gens
d’armes, qui estoient bien tailliéz dou garder et dou deffendre. Fº 81.
—Ms. de Rome: Quant li contes Derbi ot sejourné en la chité de
Bourdiaus environ quinze jours, il li prist volenté de cevauchier. Si le
fist segnefiier par ses hiraus à tout honme, et que casquns fust prês:
il le furent et se departirent un jour de Bourdiaus en grant arroi, et fist
marescal de son hoost mesire Gautier de Mauni. Et prissent le
cemin de Bregerach, et n’i a que quatre lieues de Bourdiaus, et
vinrent à un chastiel seans à une lieue priès, lequel on nonme
Montquq. Et se tenoit pour euls et en estoit chapitainne et gardiiens,
uns chevaliers de Gascongne qui se nonmoit mesires Rainmons de
Copane, qui rechut les Englois liement et lor amenistra tout ce que il
lor besongnoit. Si se reposèrent là les Englois une nuit. Et à
lendemain li contes Derbi envoia courir par mesire Gautier de Mauni
et mesire Franqe de Halle, à tout deus cens lances et trois cens
archiers, devant Bregerach et lever la proie. Et reboutèrent toutes
gens dedens; ne nuls de ceuls qui dedens estoient, ne s’osèrent
bougier ne issir, pour resqourre la proie. Qant mesires Gautiers de
Mauni et li Englois orent fait lor emprise, il retournèrent à Montquq,
et se traissent les chapitainnes deviers le conte Derbi. Là dist
mesires Gautiers de Mauni une chevalereuse parole: «Se nous
estions bien preu, et se nous faisions nostre devoir, ensi que gens
d’armes doient faire, qant il sont venu en un pais pour guerriier, nous
souperions encore à nuit en Bregerach dou vin de ces François.» Li
contes Derbi rechut ceste parole en grant joie et dist: «En moi ne
demorra pas que nous n’en faisoions, Gautier, Gautier, nostre
acquit.» Adonc fist li contes sonner les tronpettes et aparillier tout
honme, armer et monter à cheval. Et issirent de Montquq gens
d’armes et archiers, et ceminèrent viers Bregerach, et tantos i furent.
Si s’arestèrent devant la ville, qui est forte assés et doit estre par
raison, car la rivière de la Dourdonne, qui vient là d’amont de
Roergue, de Qersi et des frontières d’Agen et de Limosin, rentre là
en la Geronde. Fº 96 vº.
P. 46, l. 4: ordonna ses besongnes.—Ms. B 6: Et y vint le sire de
Monferant, le sire de Chaumont, messire Alixsandre son frère, le sire
de Courton, le sire de Chastre, le sire de Condon... Quant il furent
tous assamblet et qu’il se trouva le dit conte Derby acompaigniés de
douze cens hommes d’armes, quatre mille archiés et trois mille
brigans à lanches et à pavais, sy se party de Bourdieaulx. Fº 243.
P. 46, l. 7: trois liewes.—Mss. A 20 à 22: quatre lieues. Fº 164 vº.
P. 46, l. 9: Montkuk.—Mss. A 8, 15 à 17, 20 à 22: Moncuq,
Moncucq. Fº 102.—Mss. A 11 à 14: Monbruq. Fº 106 vº.—Ms. A 24:
Monkoulier.
P. 46, l. 9: à une petite liewe.—Mss. A 23 à 29: à huit petites
lieues. Fº 130.
§ 208. P. 47, l. 7: Ces gens d’armes.—Ms. d’Amiens: Si tost que li

Englès furent venus devant Bregerach, il coummenchièrent à
assaillir, et li archier à traire si espessement et si ouniement que nulx
ne s’osoit amoustrer pour deffendre, et gens d’armes apriès yaux à
aprochier. Là eut grant assaut et merveilleusement fort, car li Englès,
qui estoient fresch et nouvellement venus ou pays, se prendoient
priès de bien faire le besoingne, affin que il en ewissent le grace de
leur cappittainne. D’autre part, li Gascon franchois qui là estoient, se
deffendirent vassaumment et bien. Et dura chilz assaux, toudis
lanchant, traiant et assailant, jusquez à basses vesprez.
Finablement il fu si continués et si bien poursuivis des Englès, que
par force il gaegnièrent ces faubours où toutte ceste bonne gent
d’armes se tenoient, et les couvint de force retraire et rentrer ou
corps de le ville. Et sachiés que ou rentrer il y eut une moult villainne
et dure escarmuche, et moult de gentilz hommes en grant peril. Et
par especial il y fu mors ungs grans barons de Gascoingne et de
Pieregort, que on appelloit monseigneur Huge de Mirepois, et ne
peut oncquez venir à ranchon, car messires Gautiers de Mauni
l’avoit ainssi ordonné: le cause pourquoy, je le vous recorderai quant
nous venrons au conquèz de le Riolle.
Au rentrer dedens le ville de Bregerach, eult mout grant encauch
et moult dur, et pluisseurs hommes mors et blechiés. Touttesfois,
quant il furent ensi que tout retret et li gentil homme remis en le ville,
il cloirent leur portez et refremèrent les baillez. Et li Englèz se tinrent
ens ès faubours, qui bien se saisirent de ce qu’il trouvèrent, et
passèrent celle nuit en grant reviel. Fº 81.
—Ms. de Rome: Li gentilhonme, qui pour lors estoient en
Bregerach, orent consel de widier lor ville et de euls rengier et
ordonner devant les barrières et escarmuchier et asaiier la
poissance des Englois. Et avoient fait carpenter une bastide où il
pooient bien cinq cens honmes, et jà i estoient il entré pour
deffendre le cemin, et quidoient faire mervelles. Mais sitos que les
Englois furent venus, chil de Bregerach ne tinrent nuls conrois; car
les Englois vinrent, lances abaisies, et conmencièrent à asallir ces
François et ces Bidaus qui là estoient, et archier à traire d’autre part.
Tantos la bastide fu delivrée, et maint honme mort et blechiet et
reversé par terre. Fº 96 vº.
P. 48, l. 12: Lille.—Mss. A 7, 18, 19, 23 à 33: Laille. Fº 107.—Mss.
A 20 à 22: Laigle. Fº 165 vº.
P. 48, l. 13: contes.—Mss. A 1 à 6, 8, 15 à 19: viconte. Fº 112.

Critical Concept Mastery Series Acid Base Disturbance Cases 1St Edition Zachary Healy Full Chapter

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Critical Concept Mastery Series:

Acid-Base Disturbance Cases 1st

• Answers include rich rationales

• Targets a vast array of topics in

Zachary Healy, MD, PhD

eBook conversion by codeMantra

Case 61 ...................................................... 559 Case 69 ...................................................... 643

pH= 6.1 + log10 [ HCO, ]

Unlike compensation in chronic respiratory acid-base disorders, the compensation in

AcutB n111plrmay acldoals

AculB rellpiratory acidosis

Chronic n111plrmory acldoals

Baseline Acid-Base Disorder?

Figure 1-2 • Initial algorithm for the evaluation of acid-base disorders.

Concomitant AellplralDry Acldalllll

Cornicllon at axpac:llld anion a•P tar •rum albumin

Non-Anion G•p Acidosis (NAGMA)

Expected Paco2 "' 1.5 * [Actual HC03] + 8 ± 2 (in mm Hg).

Respiratory compensation for a metabolic acidosis begins within minutes and is

SerumAnionGap= [Na+]+ [K+) + [Ca2+) + [Mg2+]-[HC~] + [cl-J-[P"-1] (in m~ );

Expected Anion Gap = 12 - (2.5) * [ 4.0 !- Actual Serum Albumin J.

M = (Calculated Anion Gap) - (Expected Anion Gap).

TABLE 1-4 • Interpretation of the delta-delta equation valuesle.

SERUM OSMOLAL GAP

+] [Glucose] [BUN] [Ethanol]

Serum Osmolal Gap = Measured Serum Osmolality - Calculated Serum Osmolality.

ANION GAP ACIDOSIS

TABLE 1-6 • Causes of anion gap metabollc acidosis.

termed D-lactic acidosis, occurs as a by-product of bacterial metabolism in patients

NON-ANION GAP ACIDOSIS

and the serum potassium. Approximately 50 mEq of non-volatile acid is excreted

. 0 sm olality= 2 * ([Na+] + [K+]) +

TABLE 1-8 • Evaluation of non-anion gap acidosis.

Associated urine Urinary phosphate, Urine glucose, amino

Renal stones Often No No

TABLE 1-8 • Evaluation of non-anion gap acidosis. (contlnuftll

HCQ; space = [0.4 *( H~~; ) ] * Lean Body Weight (in kg)

TABLE 1-9 • Causes of renal tubular addosls.

A-a gl'Hlant ( V Aa)

99119/'B/: VAa = [F/0:2 • (PATM - P-)1- PaCJ:2- (1.25. Pa~

Figure 1-4 • Algorithm for the evaluation of a respiratory acidosis.

Equation for the metabolic compensation for acute respiratory acidosis:

Equation for the metabolic compensation for chronic respiratory acidosis:

VA-a= [Fio2 * (PATM - pwater)] - Pao2 - (1.25) *Pacol

TABLE 1-1 O • Potential causes of respiratory addosls.

Expected Paco1 =Baseline Paco1 - (0.7)[Actual HC03 - Baseline HC03 ]

Once it has been determined that the respiratory compensation is appropriate or

History (eg, allaall lngeallon, cyatlo tlbroal•)

UK< 30 mEq/L UK> 30 mEq/L I

Figure 1-5 • Algorithm for the evaluation of a metabolic alkalosis.

TABLE 1-11 • Causes of metabolic alkalosls.

A-a gNdl•nt (VAm)

gtmel'lll: VAa = [F/CJ:! • (PATM - P-)] - PaCJ:!- [1.25. PaCO:!]

Equation for metabolic compensation for acute respiratory alkalosis:

Expected HC03 =Baseline HC03 - (0.2)[Actual Paco2 - Baseline PacoJ.

Equation for metabolic compensation for chronic respiratory alkalosis:

Expected HC03 =Baseline HC03 - (0.4)[Actual Paco2 - Baseline Paco2].

Once it has been determined if a concomitant metabolic add-base disorder is pres-

THE STEWART APPROACH TO ACID-BASE DISORDERS

TABLE 1-1 :Z • Causes of respiratory alkalosls.

THE BASE EXCESS (BE) AND STANDARD BASE EXCESS (SBE)

Fddman M, Soni N, Dickson B. Influence ofhypoalbuminemia or hyperalbuminemia on the

Propofol Infudon Syndrome

HCQ; space = [0.4 ( H~~; ) ] Lean Body Weight (in kg)