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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
Medicine is an ever-changing science. As new research and clinical experience broaden
our knowledge, changes in treatment and drug therapy are required. The authors and
the publisher of this work have checked with sources believed to be reliable in their
efforts to provide information that is complete and generally in accord with the stan-
dards accepted at the time of publication. However, in view of the possibility of human
error or changes in medical sciences, neither the authors nor the publisher nor any
other party who has been involved in the preparation or publication of this work war-
rants that the information contained herein is in every respect accurate or complete,
and they disclaim all responsibility for any errors or omissions or for the results obtained
from use of the information contained in this work. Readers are encouraged to confirm
the information contained herein with other sources. For example and in particular,
readers are advised to check the product information sheet included in the package of
each drug they plan to administer to be certain that the information contained in this
work is accurate and that changes have not been made in the recommended dose or in
the contraindications for administration. This recommendation is of particular impor-
tance in connection with new or infrequently used drugs.
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
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speak to Your Honour,’ replied he, ‘I own I am taken in an unhappy
affair, which neither malice nor inclination drew me into. But the
Head of the Country, notwithstanding I was the only child of my aged
parents, insisted, under great penalties, on my coming in to join him;
so that I beg you will pity me in my condition: but if it must be that I
die this night, pray! tell me what death you think it will be?’ Upon
which, not knowing what to think or what to say, I was somewhat at a
loss: his telling me of his aged parents, and his simplicity touched
me much: and how far I may be censured for my after-conduct, I
know not; but those who think I did amiss, I hope, will pardon me, as
being then but a young warrior. True, such a thing, I know, ought not
to have been publicly done; yet, when an opportunity presented itself
of doing an Act of Mercy without harm to the Cause, I am convinced
that this my behaviour will, with all generous minds, escape reproof.
The young boy continuing his lamentations, I told him to be of good
courage, for death was not so imminent as he expected; at which he
seemed to respire new vigor and life: And after some questions
asked, and promises made of his ever being grateful and upon his
telling me, that his home was not above fourteen miles from thence, I
asked him, if he could privately slip away thither. He replied, such a
favor would be too great for him to presume to request: So telling
him to do it if he could, I discharged him, ordering him to be a
support to his poor aged parents.
And now by this time we had almost conducted our prisoners to
Falkirk; and, after delivering them, we went thoroughly wet and cold,
to repose ourselves a little while on straw, and some in the open
fields or air, all places being by this time entirely filled, so that it was
then impossible to find any resource or ease for our excessive
hunger, wet and cold. So resting a few hours in that condition, they
soon after appeared; and when light, we went to see the field of the
slain; and number being made of them, we found near seven
hundred of the enemy slain, and about fifty of ours, which were
immediately interred. But this cheap-bought victory, you will say,
merited a better exit! The most distinguished among the slain were
Colonel Whitney and Sir Robert Monro, who was heard much to
blaspheme during the engagement, and as a punishment for which,
his tongue was miraculously cut asunder by a sword, that struck him
directly across the mouth. His brother, a physician, was likewise
killed at his side.[423] There were likewise found slain, some
Presbyterian Parsons,[424] who, fired with holy zeal, had quitted their
Bibles and took their swords. It was said, that one of these Parsons,
seeing the danger he was in of losing his life as a Soldier, had
recourse to his dignity, supposing that would be a cloak to save him.
‘Spare my life,’ said he to a Highlander, who was on the point of
taking it, ‘for I am a Minister of My Master Jesus Christ!’ To which the
other ingeniously replied: ‘If you are a good one, your Master has
need of you; if not, it’s fitting that you go and take your punishment
elsewhere!’—which dilemma was immediately solved by the
Highlander’s sword. Another Minister, seeing the case his Brother
was in, and being in a fair way to share the same fate, begged his
life of another Highlander for Prince Charles’s sake, by which means
he preserved what he would otherwise inevitably have lost.
We now took possession of the enemy’s baggage, camp, and
eight pieces of cannon; which they had not time to carry off—besides
a few prisoners, the chief of whom was Major Lockhart, who, after
having his life given him, and his liberty upon his parole of honour,
afterwards spurned against gratitude itself, by not only being
heinously perjured, but more than ordinarily thirsty of those
prisoners’ blood who just before had spared his life.[425]
We had now about one-hundred prisoners, one of whom seeing
his situation and ours, said with a grave countenance to his
companion: ‘By my soul, Dick, if Prince Charles goes on in this way,
Prince Frederick will never be King George!’ But of the five or six
thousand men that went with the Prince to the field of battle, scarce
three thousand returned back with him, for many of them, having
loaded themselves with booty, returned up to the hills. It was now a
great loss to us, that we had neither fort or other secure place to
keep our prisoners in, so that, if it were not merely out of mercy, it
was to no purpose to take prisoners, being without the means of
keeping them.
And now being come again to Stirling, the enemy being fled to
Edinburgh, and finding the siege of the Castle went on but slowly the
spirit of the army began much to change. Factions, grudges, and
private interest were now judged proper to be exercised, so that the
Prince was in a mortifying situation, seeing himself deserted by half
his army, and the others mightily turned. But as it is not for me to say
more than what relates to myself, I shall only mention the grudge I
have often dearly paid for—that exercised against my Colonel, who,
on the death of his brother had lately succeeded to the title of Lord
Balmerino. And here it may be proper to give some account of the
character of this brave man, which though sufficiently known, his
praises cannot enough be sung. He was a man of a noble
personage, of approved loyalty, and had the courage of a lion. He
possessed a mind and genius well ornamented with both natural and
acquired parts, being versed in most languages. He could recite
whole pages of Horace, Ovid, and Virgil at his age of fifty-eight, as
perfectly as a school-boy of sixteen, so that his memory for his years
was wonderful, the more so for its not being in the least impaired by
his hard drinking—his sole and predominant passion, which if he had
a little more restrained, he would have shone with the same lustre in
the army as he afterwards did on the scaffold. However, whilst with
the Prince, he was never failing with his duty; and proud he was of
having something, wherein he could shew his loyalty and obedience
to his Master.
But what was the cause of the quarrel betwixt him and Lord
George Murray, I know not; as Lord Balmerino did not ever directly
inform us why he was treated after that manner: only I remember,
His Lordship, when he saw himself so apparently ill-used, frequently
addressed his corps as follows. ‘Come let us do as we are ordered!
It is in vain to dispute; a time will come when I shall see all these
things righted, and that too at Lord George’s cost or mine. But at
present he is my superior, and we must obey as we tender the good
of the Prince.’ With such soothing expressions has he often accosted
us, when some were mutinying. And certainly he suffered a great
deal from Lord George, for, to my knowledge, we have been ordered
twenty or thirty miles, harassed and fatigued, and a courier sent after
us, ordering us immediately to return without halting—saying it was
my Lord George Murray’s orders.[426] And now a harder time than
ever came upon us, for I can safely say and prove, that from the time
of Falkirk Affair to the Battle of Culloden, notwithstanding the fatigue
of the day, I scarce slept three nights out of seven in bed.
And now having been some time before Stirling Castle, news
arrived from Edinburgh, that Cumberland was come thither with an
intention to rally General Hawley’s army and attack us again. As our
number had been so much diminished by the desertion of those who
after the battle of Falkirk had gone home loaded with plunder; it was
judged expedient for us to retire higher into the country, where we
were sure of being joined by some more forces. Accordingly we had
orders to proceed on our march; and on the morning on which we
began it, the Prince to St. Ringin,[427] distant about half a mile from
Stirling, to give the necessary directions for quitting the town and
raising the siege; which being done, we retired again, and when at a
short distance, we were surprized with a hideous noise just behind
us; and upon the Prince’s sending back to inquire what it was, it was
found to be a church blown up, just upon the place where a few
minutes before we had been standing. This church had been
converted into a magazine for our gun-powder, which by some
accident had been set on fire, and several of the town’s-people and
of our soldiers were killed by the explosion. However, continuing our
march, we arrived that night at Crieff a little town in the Highlands;
and the Prince lodged at Drummond Castle, the residence of the
illustrious Duke of Perth, which was only a short distance from the
said town. And now it was judged proper for the army to separate;
accordingly the Prince went the Highland way with the Highlanders
and prisoners for Inverness; and the Horse and Lowland Regiments
the Low-Country Road by the Sea-Coast, which was much longer, so
that it was three or four weeks before we again formed a junction.
And now we marched from Crieff to Perth, a large fine town; from
Perth to Cowpar-in-Angus; from Cowpar to Glams; from Glams to
Forfar; and so on to Montrose. The reason why I am so short in
mentioning these places, is, I have little to say; we passing them
quickly, and nothing extraordinary happening. But at Montrose we
halted a few days. It is a fine loyal seaport town and looked upon as I
was told there, to produce men of the greatest wisdom in Scotland.
Having staid three days there, we were a little surprised at the sight
of ships of war, that appeared a little distance off the Coast: and the
rumor being that Cumberland was pretty nigh us, we began to
apprehend lest they should land and intercept our passage; to
prevent which, we marched with all haste out of the town, the foot
going out the third day at night, and the rest following early the next
morning except the Hussars who remained some days longer to
watch the enemy’s motions.
Some of my readers may be curious to know what sort of men
these Hussars were. A set of braver fellows it would be very hard to
find; many of them having mounted themselves on horses which
they had taken from the enemy. Their Commander[428] also was a
wise, courageous virtuous man, and behaved himself in his station to
the admiration of all, regulating his corps with such order as to make
our enemies and the country, even fifty miles distant from us, have
more fear of them than almost the whole army. In fine, he was of
infinite service to the Prince, as also were his horse; for their conduct
was daring, and their courage was steeled, and few of them there
were, who would have scrupled to go, if possible to hell’s gates to
fetch away the keys.
Soon after our departure from Montrose, we arrived at Aberdeen,
where we staid two or three days; and notwithstanding our being in
the town the Presbyterian Ministers ceased not to preach and pray
publicly against us. And here it was that I happened to be bedfellow
to my Colonel, Lord Balmerino in the same bed where Cumberland
afterwards lay, it being in one of the Chief Provosts’ houses.
When we marched out of Aberdeen, it blew, snowed, hailed, and
froze to such a degree, that few Pictures ever represented Winter,
with all its icicles about it, better than many of us did that day; for
here men were covered with icicles hanging at their eyebrows and
beards; and an entire coldness seizing all their limbs, it may be
wondered at how so many could bear up against the storm, a severe
contrary wind driving snow and little cutting hail bitterly down upon
our faces, in such a manner that it was impossible to see ten yards
before us. And very easy it now was to lose our companions; the
road being bad and leading over large commons, and the paths
being immediately filled up with drifted snow. However, we continued
marching on till about three in the afternoon, when my horse
overcome by the inclemency of the weather, fairly gave it up and
would carry me no farther: and now by a little halt I quickly lost my
Company, and was obliged to alight and lead my horse leg-deep in
snow; being upon a wide common, as it appeared to me, not having
seen all that day’s march scarce a house, tree or barn. I now
expected every moment to perish, as I was quite benumbed and all
covered over with snow, and my horse refused to follow me. At last,
unable to proceed any farther, I sunk down, quite exhausted, upon
the snow. In this dreadful situation, I luckily recollected a little bottle
of spirits, which had been given me by the Provost’s Lady; and
accordingly tried to put my frozen hand into my riding-coat pocket to
take it out. On taking a draught of the liquor, I soon found that never
repose to the wearied traveller, never meat to a most ravenous
hunger, never drink to a most burning thirst, could be more
refreshing or agreeable than this was to me; and I should have
finished my bottle, if a reflection had not come into my head about
my poor horse, which seemed to be in as bad a situation as myself,
being one of a delicate and tender breed. Knowing that he could
drink beer, I resolved to make an experiment whether he would
partake of the contents of my bottle. So pouring the remainder of the
liquor into the crown of my hat, which I had pressed low down for the
purpose, and dissolving some snow in it, in order to mitigate the
spirits, I gave it my poor horse to drink: which to my great surprise
and pleasure, he did, his mouth, I believe, being so cold that he did
not know what he drank. However, now finding ourselves to respire
as it were new life and vigor, we endeavoured to proceed, and after
three quarters of an hour, being almost upon the relapse again, we
stumbled upon a house, and following the walls of it came to the
door, where entering together with my horse, I surprized the poor
people who were sitting at the fire. But they, seeing the condition I
was in, received me with a great deal of good-nature, and permitted
my horse to stand in the house till he was well rubbed, and then led
him to a little place for him to lie in, giving him hay and corn as he
wanted. After I had taken off my riding-coat and boots and well
warmed and refreshed myself, I heard of two more (who had been in
almost as bad a situation as myself except that their horses
continued to carry them), who were come to the next house
adjacent. So going out to see them, I found them to be two old
acquaintances, vizt., one Mr. Maxwell, and Mr. Ball, an English
Gentleman, who, after some chat, concluded, that two more
harassing marches, than that over the Esk and the present, could
scarcely be imagined. Accommodating ourselves as well as we
could for that night, being obliged to lie with our horses, we departed
early next morning for Old Meldrum, which place most of the army
had reached before us.
From Old Meldrum we marched the next day for Banff, a little
pretty agreeable town. About this time we heard, that the
Highlanders, who were with the Prince, had broke down the barracks
of Riven of Badenoch (which were a great eye-sore to them, having
been built to keep them in order), and having taken the Sergeant and
eleven more prisoners, were in full march for Inverness, distant
thence only twenty-four miles. And now, after a short stay at Banff,
we marched for Cullen; and by this time we heard that the Prince
had made himself master of the Lord President’s House, and after
some little resistance forced the soldiers in the town of Inverness to
retire into the Castle, which, after a regular siege, likewise soon
surrendered at discretion. About 200 men were taken prisoners here,
and several officers, the principal of whom were the Governor and
the Master of Ross. This rapid success of the Prince gave us great
courage. So, marching from Cullen, through Fochabers, over the
River Spey, Elgin, Forres and Nairn, towns only ten miles distant
from each other, we came to be greedy spectators of our dear Prince
again, and what he with his brave Highlanders had effected. And
now, to second our victorious arms, we were joined by several more
of the Clans and Chiefs, and the brave Amazon Lady McIntosh,[429]
Seaforth and others coming in, or causing their Clans to come in,
and many who had left us at Falkirk rejoining their colours, greatly
reinforced the army. When in this flourishing condition, it pleased the
Prince to make a visit to the Duke of Gordon’s, whither all the
Guards were ordered to attend him; and in going a curious fine
standard with this motto ‘Britons, strike home!’ that was taken at
Falkirk from Gardiner’s Dragoons, was honourably conferred upon
me by the Prince at the head of the whole Troop; and I had the
honor of carrying it ever after. Having passed Nairn, Forres, Elgin,
and the river Spey, just at the other side under Fochabers, we came
to the Duke’s seat.[430] What reception the Prince had, or what
passed there I know not: but after a short stay we attended our
Royal Master back again to Inverness. But as soon as we arrived
there, we had orders to conduct some of the chief officers, who had
lately been taken prisoners to Forres, and after leaving them there
(they being upon their parole of honor) to go to Cullen to inspect all
affairs there on that side of the country, and to observe the motions
of the enemy who lay at Aberdeen. While at Cullen, where we were
continually upon the watch by our patrolling parties, we heard that
Colonel Grant, a good French Officer, had with his Artillery taken
Fort Augustus, and made the garrison prisoners; that a part of Fitz-
James’ Horse had landed and joined the Prince;[431] and that Lord
George Murray had blocked up seven hundred men in the Castle of
Blair, when he behaved with a great deal of conduct and policy, for,
he appeared before the Castle with only a few men, having hid most
of the Highlanders with him in an adjacent wood. The garrison being
thus deceived made a sally upon him with about three hundred men;
but he immediately drew his party out of the wood and surrounded
them, upon seeing which, they immediately surrendered.[432] So,
sending them prisoners to Inverness he persevered in the siege of
the Castle: but the approach of the Hessians soon obliged him to
raise it and leave four hundred men remaining in the Castle.
At this time President Forbes together with Lord Loudon, were
endeavouring to confederate and knit together what forces they
could: but to prevent their doing much mischief, a party of the brave
McDonalds, with some few others, were detached under the
Command of the Duke of Perth, who soon dispersed this rising
power, and obliged its heads, viz., Lord Loudon and the President to
save themselves in boats.
Some of my readers may be curious to know who this President
was, and what interest he had. He may truly be styled the Oracle of
his Country, for many resorted to him for advice; and had he been as
great a friend as he was an implacable enemy, James would in all
probability have swayed the English sceptre; for by his interest,
cunning and persuasion he brought over his own party, together with
Sir Alexander McDonald and several others, who before were just
sworn in to the Prince’s interest.[433] So, I say, had he been as firm a
friend as he was an implacable enemy, we should have seen,
instead of the four thousand men who marched into England, an
army of Eighteen or twenty thousand men.
About this time we heard, that the officers who were prisoners
upon their parole of honour had broken it, and escaped to the
enemy’s army, all of them except the Master of Ross and one or two
more.[434] But what will the world say, to see these officers, whom no
tie of religion, gratitude or honour could bind, protected and
cherished by their own party—nay sent against us, to endeavour to
destroy those who before had saved them!
And now we heard, that the Advanced Guard of the enemy was
approaching us, and were got up to Strathbogie. We who were also
of the advanced Guard, upon receiving this intelligence, quitted
Cullen, and retreated to Fochabers, where a considerable body of
our men were endeavouring to make a resistance at the River Spey,
and had for that purpose built barracks, and made all necessary
preparations, in case the passage of the river had been attempted.
But finding their army lay quiet at Aberdeen, and that their advanced
party in Strathbogie only made now and then some little excursions
towards us as far as Keith, we, though at first we were very diligent
and alert, we relaxed in our vigilance, nay fell asleep and at last into
a lethargy, in which we unhappily continued till awakened by the foul
affair of Culloden, which merits an epithet bitterer than I can give.
About this time an advanced party under the command of Major
Glascow went out at night, and hearing that some of the enemy were
at Keith,[435] surrounded that place, and having taken most of them
prisoners, with their arms and equipage, returned the next day with
great honour to Spey-side, where Lord John Drummond and Lord
Ogilvy commanded.
As we lay hereabouts a considerable time, assessments were
made upon the country for our support, and among others upon the
Earl of Findlater’s Estate, who on our arrival had taken wing and
joined Cumberland Will. The Earl’s Steward, being threatened with
military executions, if he refused to comply with our demands (which
were always seconded by such threats, though seldom put in
practice) begged leave to write to his Master for instructions how to
act. Upon this the Earl, having consulted with Cumberland, sent a
Letter addressed To the Man they call Lord John Drummond, telling
his Lordship, that if he or any other person should pretend to
exercise any military authority over any thing belonging to him, there
were Rebels’ houses enough, on which his Master Cumberland
promised him he should have his revenge. This Letter excited a
great deal of indignation among us; and was the cause of what
afterwards happened to his house;—for several of our party, without
any order being given, and indeed without the Prince’s being in the
then situation of his affairs, able to restrain their fury, ransacked it,
and carried away several articles of value, but without setting fire to
it, or wantonly destroying anything merely for destroying’s sake.[436]
At last news arrived that the enemy had left Aberdeen, and were
marching against us.[437] This intelligence gave great satisfaction to
many of us, who were in a manner tired out of our lives. Yet
notwithstanding the approach of the enemy, all the Prince’s
endeavours to collect his whole army, were ineffectual; for many
under pretence of cultivating their lands, or promising to come up
soon enough, went, staid, and came as they thought proper.
And now finding the enemy advanced pretty fast both by water
and land, the fleet bringing up their provisions and wearied soldiers;
frequent patrols were sent out by us in order to observe their
motions. Here I had the honour of commanding the last patrolling
party that ever crossed the Spey for the Prince’s cause. Lord John
Drummond (Commander at the Spey) having ordered me with ten
others to patrol all night towards the enemy, we began our work
about seven o’Clock and continued it till about five the next morning,
being then eight miles from Fochabers and two from the enemy;
when we took a man with a Letter from one of Cumberland’s
Secretaries to the Duchess of Gordon,[438] desiring her to employ all
her interest among her vassals in getting down provisions and
getting together what forces she could, as the Duke of Cumberland
intended to pass the river that day. Having secured the Messenger
and Letter, we continued our route, till we came up in a manner to
where they were encamped; for as they lay upon the declivity of a
hill, and had no guards on the top, we were able to approach very
near to them unperceived. But finding them drawn out in order of
battle, after seeing all we could see, and some bravadoes and
huzzas, we retired with all speed, leaving them to wonder what we
meant. We soon reached Fochabers (on the Spey) where I found
Lord John Drummond. Having given him the Letter taken from the
Duke of Cumberland’s Messenger and informed him of the situation I
had found the enemy in, I retired to repose myself a little while.
When fast asleep, a servant came in to tell me that the enemy was in
the town, and that it was too late to think of escaping, almost all of
our party having already passed the river. However, starting up in
great confusion, I resolved to risk all rather than fall into their hands,
and mounting my horse escaped by a back road. I had no sooner
crossed the river than I was ordered to join a party of about eighty
horse who were to remain behind on the banks of the Spey to
observe the motions of the enemy; whilst the foot, amounting to
about two thousand men, marched for Inverness, where the Prince
then lay with the greatest part of his army. Finding that the enemy
after a short halt at the Spey side, began to cross the river, we
likewise retired and followed our foot, to inform them of the enemy’s
being in full pursuit of us. This intelligence made our men pass
through Elgin, without halting, and straight on that night to Forres,
which was ten miles farther; and, after some stay there, to Nairn, out
of which we were next morning driven; the whole English Army
entering the town at one end, whilst we marched out at the other,
and continuing to pursue us sharply for three or four hours. And here
it was His Grace the Duke of Perth and Colonel O’Sullivan[439]
gained immortal honour by their bravery and conduct in bringing us
off in good order from under the very nose of the enemy; for
notwithstanding all their firing upon our rear, and though we were
much inferior in numbers, we lost not one man.
Soon after their desisting from pursuing us, we received orders to
halt, and encamp upon that very place, where the fatal battle of
Culloden was afterwards fought. Having accordingly encamped as
well as we could on the heath that grew upon the common, which
served us both for bedding and fuel, the cold being very severe, we
were soon after joined by the Prince and several of his Clans.
Finding that the enemy did not pursue us we rested ourselves all that
night upon the Common, and early next morning drew out in battle-
array. But that day being Cumberland’s birthday,[440] and the enemy
shewing no intention to attack us on it, we reposed ourselves again,
though still keeping ourselves in readiness, upon the place where we
had rested the preceding night; a biscuit being given to us for our
refreshment. In that situation we remained, till the brave Prince came
amongst us in the dusk of the evening, with the full resolution of
going to attack them that night in their camp, distant only seven
miles. Orders were accordingly given to that effect, which were
obeyed with the greatest pleasure and alacrity by the whole army.
We began our March about seven o’Clock leaving great fires burning
in our camp: but by some strange infatuation or misfortune the road
was not rightly taken, either through the ignorance or treachery of
Lord George Murray’s guide. This still remains doubtful, but this I can
say, that with the little knowledge I had of the country I could have
conducted them much better and sooner. After we had marched till
about three o’Clock in the morning, over double the ground that was
necessary, we at last came pretty nigh the enemy’s camp: and when
we were supposing to surround them, and for that purpose in some
measure drawing out; my Lord George Murray began to be missing;
notwithstanding the Prince’s Aides-de-Camp in riding from rank to
rank, and asking, for God’s sake! what has become of His Lordship,
and telling that the Prince was in the utmost perplexity for want of
him. In that situation did we remain a considerable time, till, day
breaking fast in upon us, we heard that Lord George Murray was
gone off with most of the Clans. Where he had been all that
considerable time, or what was his intention in it, I leave Time to
prove. Now, after we had stood some time on the brink of entering
their camp, the Prince, on receiving the unwelcome news of Lord
George Murray’s going off with the greatest part of the army, was
under the necessity of ordering us likewise, much to our
dissatisfaction, to march back again to our Camp. In this manner did
that noble and well-concerted scheme fall to ruin—and not only to
ruin, but in such a manner as to ruin us, who before had hopes of
ruining the enemy. But O! for Madness! what can one think, or what
can one say here![441]
The enemy at our departure, being fully awakened and seeing
the jeopardy they had been in, judged rightly, it was their time now to
pursue us in the unhappy situation we were then in, being harassed,
hungry and starved and fatigued, almost to the greatest extremity.
We had no sooner reached our camp again, than news came of the
enemy’s being in full march towards us, and of their intention to
attack us. This disagreeable intelligence vexed us much in our
present situation, the more so, as of the twelve thousand men, who
were actually in arms and in the pay of the Prince, not above Four
thousand were now with him many going every moment,
notwithstanding his orders to the contrary, to Inverness, and to
woods and houses adjacent, in order to repose and rest themselves
after their late excessive fatigue. Many of these were so far from
rejoining us, that they were taken asleep by the enemy after the
battle. Those, however, who staid, put the best face on the affair they
could, and all of us presently appeared surprizingly courageous, who
only seemed to survive and animated by the spirit of loyalty and love
for our dear Prince. But now why we resolved to fight, or why we did
not retire to Inverness, and keep that town till we were fully joined,
which might have been easily done, or even at last, if judged proper,
avoided fighting and make another expedition into England in spite
of them,—I may say it was Fortune’s will;—for, contrary to the
Prince’s inclination, Lord George Murray insisted on standing and
fighting them that day: and as for what he said of our wanting
provisions, it is most certain, though we did that day, we might have
retired to Inverness and found there a sufficiency of meat for two or
three days. However, the Prince, notwithstanding his great inclination
to avoid fighting, was at last obliged to give way to the importunity of
Lord George Murray, who even used terms very cutting in case of
refusal; and was also for fighting His Grace the Duke of Perth—but
this may be said for him, he doubted not but the same Hand that had
supported and miraculously conducted the Prince hitherto would
infallibly continue to support him, and make him a glorious
Conqueror.[442]
I shall now proceed to give account in what manner we were
ranged in battle-array. The brave McDonalds, who till then had led
the van, and behaved at all times with great courage and bravery,
were now displaced, and made to give way, at the pleasure of Lord
George Murray, to the Athol men, whom he commanded. The rest of
the front line was composed of Highlanders: the second, of
Lowlanders and French, with four pieces of cannon at each wing:
and in the rear was the Prince attended by all the horse, and some
foot. In this manner were we drawn up—four thousand men to fight
eleven thousand. The enemy being by this time in full view, we
began to huzza and bravado them in their march upon us, who were
extended from right to left in battle-array, it being upon a common.
But, notwithstanding all our repeated shouts, we could not induce
them to return one: on the contrary, they continued proceeding, like a
deep sullen river; while the Prince’s army might be compared to a
streamlet running among stones, whose noise sufficiently shewed its
shallowness. The Prince, the Duke of Perth, the Earl of Kilmarnock,
Lord Ogilvy, and several other Highland and Lowland Chiefs, rode
from rank to rank, animating and encouraging the soldiers by well-
adapted harangues.
The battle being now begun, the whole fury of the enemy’s
Artillery seemed to be directed against us in the rear; as if they had
noticed where the Prince was. By the first cannon shot, his servant,
scarcely thirty yards behind him, was killed; which made some about
the Prince desire, that he would be pleased to retire a little off: but
this he refused to do, till seeing the imminent danger from the
number of balls that fell about him, he was by the earnest entreaties
of his friends forced to retire a little, attended only by Lord
Balmerino’s corps. Frequent looks and turns the Prince made, to see
how his men behaved: but alas! our hopes were very slender, from
the continual fire of musketry that was kept up upon them from right
to left. We had not proceeded far, when I was ordered back, lest the
sight of my standard going off, might induce others to follow. In
returning, various thoughts passed my soul, and filled by turns my
breast with grief for quitting my dear Prince, now hopes of victory,
then fear of losing—the miserable situation the poor loyalists would
again be reduced to—and what we had to expect if we left the field
alive: these thoughts, I say, strangely wrought upon me, till, coming
to the place I was on before, and seeing it covered with the dead
bodies of many of the Hussars who at the time of our leaving had
occupied it, I pressed on, resolving to kill or be killed. Some few
accompanied my standard, but soon left it. At this time, many of ours
from right to left were giving way and soon the battle appeared to be
irretrievably lost. The enemy, after we had almost passed the two
ranks, flanking and galling us with their continual fire, forced us at
last back, broke our first line, and attacked the second, where the
French troops were stationed. I happened then to be there, and after
receiving a slight grazing ball on my left arm, met with Lord John
Drummond, who, seeing me, desired I would come off with him,
telling me all was over and shewing me his regiment, just by him,
surrounded. Being quickly joined by about forty more horse, we left
the field of battle in a body, though pursued and fired upon for some
time. When we arrived at the foot of the hills, some of us took one
way, and some another: I, however, with about six more, continued
with Lord John Drummond; and it was with some difficulty we passed
the rapid torrents and frozen roads, till one o’Clock that night, when
we came to a little village at the foot of a great mountain, which we
had just crossed. Here we alighted, and some went to one house
and some to another. None of these cottages having the
conveniences to take in our horses, who wanted refreshment as well
as we, many of them perished at the doors. I happened to be in one
of the most miserable huts I had ever met with during my whole life;
the people were starving to death with hunger. However, having laid
myself down on the floor to rest myself after having been almost
thirty hours on horse-back; the people came crying about me and
speaking a language I did not understand, which made my case still
more unpleasant. But by good luck, a soldier soon after came in,
who could speak both to them and me, and brought with him some
meal, which was very acceptable, as I was almost starving with
hunger. Of this meal we made at that time a very agreeable dish, by
mixing it very thick with cold water, for we could get no warm: and so
betwixt eating and drinking we refreshed ourselves, till four o’Clock
in the morning; when Lord John Drummond and the rest of us began
our march, we knew not whither, through places it would be in vain to
describe; for we saw neither house, barn, tree, or beast nor any
beaten road, being commonly mid-leg deep in snow, till five o’Clock
that afternoon; when we found ourselves near a village called
Privana a Badanich,[443] the barracks of which, as I mentioned
before, the Prince had destroyed. Being now, to our surprize, almost
upon it, we consulted amongst ourselves how we might best get
intelligence from it; for, as it lay on the road from Inverness twenty-
four miles we apprehended the enemy might be there. But
fortunately a soldier coming out told us, that the village was occupied
by the Prince’s men. This intelligence gave us great pleasure; and
having accordingly entered the place, we found a great many of the
Prince’s adherents, the chief of whom was Lord George Murray and
the Duke of Perth; but we heard no news where the poor Prince was.
At first we had great hopes of rallying again: but they soon vanished,
orders coming for every one to make the best of his way he could.
So some went one way, some another: those who had French
Commissions surrendered; and their example was followed by my
Colonel, Lord Balmerino, tho’ he had none. Many went for the
mountains, all being uncertain what to do or whither to go.
In this perplexity I resolved to steer my course through the
mountainous country, notwithstanding the advice of many to the
contrary, who told me, it would be impossible for me to escape, and
begged I would go and surrender, assuring me, that if I attempted
the mountains, I should inevitably perish in them. But reflecting, how
nigh suffering my Father had been in the year 1715, taking Courage
and Patience for my guides, I resolved to enterprize a journey
through a Country that few of my Nation had ever passed before. So,
folding up my Standard, whose Motto was Britons! strike home! I put
it in my Riding-coat pocket, in hopes it might be of use another day,
and began my journey, in company with three others, for the
Highlands. Having discharged our horses, after a long day’s journey,
we came to a house situated on Garvie-more, twelve miles from any
other, where we met with many of our party, who had arrived there
before us. However, putting up in the best manner with what little we
could obtain, we set forward for Fort Augustus: but on the road, a
misfortune happened, that disconcerted all our plans; for a man who
carried our provisions of Oatmeal, fallen a little behind, by accident
met with some of the Brigade Picquets, who robbed him of our meal
and two riding-coats. This unexpected loss obliged us to separate
soon afterwards, being too many to subsist in this wild tract of
country, if we had kept together. However, having got betwixt Fort
Augustus and Fort William, we struck up into the country to the right,
and passed several large mountains in Lochiel’s Country, where we
staid three days, because we heard, that the brave Prince was nigh
us, and to take leave of one another, the necessaries of life being
exceedingly scarce, from the great number of people wandering over
the hills as well as we. I here went to wait upon the Duke of Perth,
who was at the house of Doctor Cameron, Lochiel’s Brother: but
being told by two sentinels at the door, that His Grace was
indisposed, I returned without seeing him. It was now reported, that
an English spy had been at Doctor Cameron’s house which obliged
me in all haste to quit that place; for certain it is, had I staid there any
longer, and the Highlanders supposed me to be the spy, they would
have made away with me. I therefore left my companions and set
forward to Lochaber, the wildest country I ever was in. And now it
was that I began to be truly miserable, and to endure hardships
which I had thought it impossible for human nature to support, for in
that most hideous place I was deprived of every thing that could give
me comfort: true it is, I found some few inhabitants; but in language
food and customs quite different from what I had ever seen before.
In this place I was forced to stay several days, on account of the
prodigious quantity of snow that fell upon the mountains, and
hindered me from discerning or making any road. During my stay, I
by good fortune got a pound of black bread to live upon. The snow
somewhat melting I set forward again from Lochaber towards the
sea-shore. On the road I was overtaken by about forty women, half-
starved to death who were wandering up and down for safety. Some
of them, who spoke English, told me, they had been driven out of
their houses by the soldiers who were sent out from Fort William to
ravage burn and plunder all before them and now it was that the
most heart-rending scenes of misery began to present themselves;
for many of these poor creatures with children in their arms, lay
extended in the clefts of the rocks half covered with snow, dead, and
a-dying in the most piteous manner. With these companions of
misery, and daily meeting with more I passed some days. I now
learned, that many of the unfortunate adherents of the Prince had
been famished to death on the hills and I expected it would soon be
my turn, for I began to be almost unable to proceed, my shoes being
worn out, and the sharp rocks wounding my feet. However, I
encouraged myself with the thought that my pursuers would have the
same difficulty to climb the rocks as I had; and on the twentieth
day[444] after our defeat at Culloden I came to the sea, in Clan-
Ronald’s Country; the view of which was most agreeable to me,
though even then I saw no prospect of escaping. Getting a little
refreshment from the people who dwelt on the sea-shore, I began as
it were to revive again, having been almost starved to death with
hunger and cold; for I had been obliged to lie down for whole nights
under the shelves of rocks, and was for two or three days together
without eating at all, as nothing could be obtained either for love or
money. Though I was fat and strong at the battle of Culloden, I was
now quite emaciated and reduced to so miserable a state, that, if I
had had another day to walk, I am sure I must have died; for I was
not only starved with hunger and cold, but frightfully covered with
vermin, which bit me all over my body so that there remained not
one whole place in my skin. This, joined with the pain in my torn feet,
made me often think that Job could not be in a more piteous
condition. Yet as he had God for his comforter, so had I; for the
justness of the cause I was suffering for, gave me great courage,
and supported me much: and though I saw daily enmities exercised
against me, it was a great satisfaction to me, to think, that, during the
time I had the honour of being a soldier under the banner of our dear
Prince, I could not accuse myself of one act that a Christian might
blush at.
Being somewhat recovered by the particular care of a worthy
Gentleman (whose kindness I had the satisfaction in a little time to
return by an agreeable meeting with him at Paris), I began to inquire,
if it were possible from island to island to make my escape out of the
country; for could I have sold myself at that time as a slave into
Turkey, I would have done it. My host told me, that it was impossible,
as all the boats had been destroyed by Cumberland’s order.
However, one morning, being in that perplexity of thought how to get
off, and fearing every moment the landing of soldiers to destroy the
country—news was brought us that two French ships had come into
the Lough just by—which mightily raised our hopes, that either a
restoration of the Prince’s affairs were at hand, or that we should
escape to France. So, running down to see and hear what we could
we found them to be ships destined for the Prince’s service, having
on board a great quantity of arms and ammunition, with five barrels
of gold, pretty large and nearly one-yard long—which before our late
fatal disasters might have been of great use.[445]
Notice being sent all about the Mountains, as far as time would
permit; several, who lay despairing, came down to the sea-shore,
and among the rest, my old patron the Duke of Perth, Lord John his
brother; Sir Thomas Sheridan, Secretary Murray, Mr. John Hay, and
Doctor Cameron. These being assembled together, judged it proper
though no one knew where the Prince was (many thinking he was
gone off for France) to have the money and arms brought on shore;
which was done on the evening after. Going securely to sleep that
night expecting to sail for France the next day, we were surprised by
the noise of cannon, which awakened us about three o’Clock in the
morning; and getting up to see what the matter was, we had for our
comfort the disagreeable news and sight of three English ships, that
were come from Fort William to attack the French, whose
appearance on the coast they had noticed, it seems. This sight
displeased us very much: however, fighting was the resolution of us
all. The two French Frigates (viz., the Mars and the Bellona), being
pretty strong, and having a sufficient quantity of men, cannon, and
ball, resolved to make head against the three English vessels, of
which one was the Baltimore,[446] that name being written upon her
rudder, which was carried off by a cannon-ball. The place they fought
in, was a creek of rocks, which held the French (the English coming
down upon them) as it were penn’d up, having the land on their back
and both sides. However it was easy for them to hold
communications with us on shore, who were four hundred armed
men or more; so that had they been obliged to abandon their Ships,
they might have saved themselves on shore. The Crews of the two
ships amounting to nearly eleven hundred men, might, with the
assistance of the Highlanders, have made an effectual resistance to
the English, if they had attempted to invade us. The battle furiously
beginning at three o’Clock in the morning, it remained doubtful till
four in the afternoon, who would be victors. Nor was it a small
pleasure to us to see those combatants engaged, and the skill of the
French, whose fire seldom missed the English; for many of us being
upon the rock as it were hung over these ships, in such a manner
that they could not hurt us with either cannon or musketry; we could
discern how matters went, and few balls were fired but we might see
whether they hit or missed, which latter the English frequently did.
During the engagement, the Highlanders were busied in carrying the
arms, money, and powder off from the sea-shore; which service they
performed with amazing resolution, many a cannon ball being fired,
in order to hinder them, by the largest of the English ships. Few
Highlanders there were but what had a cask of brandy hid privately
in the hills, with which some of them got merry before night. At last
we had the satisfaction to see the English hoist their sails, leave the
French, and sail to the main ocean. The French repaired their ships
as fast as possible, and endeavoured to make what haste out they
could, lest the English should return with a greater force.
All being over and hopes reviving again; one who had been in the
Guards with me, came and told me, he had found a barrel of money,
and that he would get me as much of it as I pleased. To this proposal
I replied, That I had no manner of use for it, for, if I should be so
fortunate as to escape into France, I had friends enough there, who
would take care of me; and that if I died or were taken, it would be of
no service to me. Moreover if the Prince should rally again, how
shocking it would be to have to reproach ourselves with being a
hindrance to our dear Prince’s designs. On hearing this reply, he,

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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:

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