Acid Base Workshop For OUWB Handout

a Precious Bodily Fluids production
Acid Base
Balance
Joel M. Topf, MD
Assistant Professor of Medicine

Oakland Beaumont Med School
Office 313.886.8787
@kidney_boy
http://pbfluids.com
Acid-Base Physiology! !
Joel M. Topf, MD
Introduction
At the beginning of every episode of ER, as the impossibly attractive patient is being rolled from the ambulance bay to the resuscitation room, the equally attractive doctor barks orders, I need a chem-20,
CBC, chest x-ray, and blood gas! The list may have a few other items but those four belong on the diagnosticians Mount Rushmore of tests.
Despite being common, learning to fully interpret any one of those tests means torturing the results to
extract the vary last byte of signal from the data. This handbook will guide you through all the steps to
pull as much data from the blood gas as possible.
Goals
Understand how pH is like an earthquake

The use and uselessness of the Henderson
Hasselbalch formula
Identify the 4 primary acid-base disorders
Calculate appropriate compensation for all
four primary acid-base disturbances
Understand and calculate the anion gap

Trash MUDPILES
Know: GOLDMARK
Non-anion gap metabolic acidosis
Delta-gap or gap-gap
Osmolar gap
2
Joel M. Topf, MD
Table of Contents
pH and the hydrogen ion concentration!..........................................................................4
Henderson-Hasselbalch equation!.....................................................................................5
There are four primary acid-base disturbances!..............................................................9
Compensation!......................................................................................................................9
Rapid interpretation of ABGs!............................................................................................12
Multiple primary acid-base disturbances!........................................................................13
Looking for second primary acid base disturbances the old timey way!....................14
Using the prediction equations!.........................................................................................15
The anion gap!......................................................................................................................18
Anion gap metabolic acidosis (AGMA)!...........................................................................19
Diabetic Ketoacidosis!..........................................................................................................20
Non-Anion Gap Metabolic Acidosis (NAGMA)!............................................................22
Osmolar Gap!........................................................................................................................24
Additional metabolic acid-base conditions!.....................................................................26
Answers!................................................................................................................................28
Joel M. Topf, MD
pH and the hydrogen ion concentration

Acid base physiology is the regulation of hydrogen ion concentration
Hydrogen ions are similar and different

from other physiologically important electrolytes. Like other electrolytes, hydrogen
ion concentrations need to be regulated. If
the concentration rises too high or falls too
low there are physiologic consequences and
illness. A normal hydrogen ion concentration
is 40 nmol/L and that leads to the principle
difference from other ions:
Hydrogen ions exist at such minute concentrations that inorganic chemists decided
to measure them on a negative log-rhythmic
scale so 0.00004 mmol/L converts to 7.4.
Every move of one point is a factor of ten.
a pH of 6.4 is 400 nmol/L and 8.4 is 4 nmol/
L. On this scale every change of 0.3 pH units
changes the hydrogen concentration by a
factor of two.
40 nmol/L
is
0.00004 mmol/L
pH
H+ concentration
(nmol/L)
6.8
160
7.1
80
7.4
40
7.7
20
Joel M. Topf, MD
Henderson-Hasselbalch equation
The primary buffer in the body is bicarbonate which is in equilibrium with carbon
dioxide and water. The relationship between
hydrogen ions, bicarbonate and carbon dioxide is governed by the law of mass action.
This mass action formula can be simplified

to a simple relationship called the
Henderson-Hasselbalch formula.
Joel M. Topf, MD
The Henderson Hasselbalch formula provides a critical relationship that governs all of acid
base physiology. It is the Mantra of Acid Base physiology.
Joel M. Topf, MD
Question
You have been told that one question on the boards will require you to use
the Henderson-Hasselbalch equation to determine if the ABG is possible.
Use the Henderson-Hasselbalch equation to determine if this ABG is possible.
pH = 6.8 / pCO2 = 50 / HCO3 = 15
Do the same for this ABG:

pH = 8.1 / pCO2 = 10 / HCO3 = 30
You will get one of these questions on the boards. There will be one acid-base question
where the right answer is some variance of:
E) There is a lab error.
or
B) This ABG is impossible.
One of the keys to the math on these problems is realizing that no one has a calculator and
it is rather difficult to do logs in your head so the test writers try to keep the numbers easy to
handle. The pCO2 x 0.03 will always be a tenth of the bicarbonate (so the log is 1 and the pH
should be 6.1+1 = 7.1) or a hundredth of the bicarbonate (so the log is 2 and the pH should be
6.1+2 = 8.1).
Use the Henderson Hasselbalch formula to calculate the normal pH from a normal bicarbonate of 24 and a normal pCO2 of 40 mmHg.
The pH is proportional to the serum bicarbonate over carbon dioxide. An increase

in the numerator, bicarbonate, increases pH.
A decrease in the denominator, carbon dioxide, also increases the pH. This relationship
of bicarbonate, CO2 and pH is critical and
you must have perfect knowledge of it to
understand even the basics of acid-base
physiology.
Joel M. Topf, MD
If the quantitative approach is not helpful

one can understand the relationship from a
simple qualitative approach. Bicarbonate is
alkaline so increases in its concentration occur with increases in pH. The carbon dioxide
is the acid so as its concentration rises the
pH falls.
Joel M. Topf, MD
There are four primary acid-base disturbances

Looking at The Mantra it becomes apparent there are four disturbances which can
occur:
1. an increase in bicarbonate
2. a decrease in bicarbonate
4. a decrease in carbon dioxide
Any alteration of acid-base physiology requires at least one of these changes. The
acid-base disturbances are categorized by
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
1. An increase in bicarbonate is a metabolic

alkalosis
2. A decrease in bicarbonate is a metabolic
acidosis
3. an increase in carbon dioxide
Acid-Base disorder
the initial (i.e. primary) disturbance to The

Mantra:
3. An increase in carbon dioxide is a respiratory acidosis

4. A decrease in the carbon dioxide is a respiratory alkalosis
Primary disturbance
compensation
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
pH =
HCO3
CO2
Compensation
In order to remain in health, the body attempts to minimize changes in pH. Faced
with a change in one component of The
Mantra, the other factor changes in the same
direction so that the fraction remains nearly
constant. For example, the body responds to
a fall in bicarbonate by decreasing carbon
dioxide. This minimizes changes in the ratio

that determines the pH.
Joel M. Topf, MD
The important thing to recognize is that

carbon dioxide (respiratory alkalosis) will
the primary disturbance without any comincrease the pH.
pensation is a theoretical construct. In real
The quick method
patients,
Since bicarbonate is proportional to
compenpH, any ABG with pH and bicarsation ocIn metabolic disorders: pH, HCO3 and
bonate moving in concordant direccurs sipCO2 all move in the same directions
tions will be a primary metabolic
multanedisease. Then all you need to do is
ously with
determine if the pH is elevated,
the primary defect. This complicates trying
metabolic alkalosis, or decreased, metabolic
to sleuth out what is disease and what is
acidosis. Additionally, since the compensacompensation.
tory changes in carbon dioxide are in the
For example: a decrease in bicarbonate
same direction as the bicarbonate, all three
and carbon dioxide could be due to a priHenderson-Hasselbalch variables will move
mary decrease in bicarbonate with a comin the same direction in a metabolic acidpensatory decrease in carbon dioxide or a
base disturbance.
primary decrease in carbon dioxide with a
Conversely, since carbon dioxide is incompensatory decrease in bicarbonate.
versely related to pH, in a respiratory acidThe key to this mystery is the fact that
base disturbance the carbon dioxide and pH
compensation does not
move in discordant
completely erase the pridirections. Again
In respiratory disorders: pH, HCO3 and
mary change in pH. In
since compensation
pCO2 move in discordant directions
metabolic acidosis the pH
is always in the
falls, and the compensasame direction as
tory decrease in carbon
the primary disorder,
dioxide minimizes the change in pH but
in a respiratory acid-base disturbance the
does not erase it. So, a primary decrease in
three Henderson-Hasselbalch variables will
bicarbonate (metabolic acidosis) will demove in discordant directions.
crease the pH while a primary decrease in
10
Joel M. Topf, MD
Determine the primary acid-base disturbance:

1. pH = 7.27 / pCO2 = 34 / HCO3 = 15
normal values
pH=7.4
2. pH = 7.34 / pCO2 = 50 / HCO3 = 26
pCO2=40
HCO3=24
3. pH = 7.45 / pCO2 = 48 / HCO3 = 32
4. pH = 7.32 / pCO2 = 28 / HCO3 = 14
5. pH = 7.37 / pCO2 = 50 / HCO3 = 28
6. pH = 7.36 / pCO2 = 80 / HCO3 = 44
7. pH = 7.32 / pCO2 = 36 / HCO3 = 18
8. pH = 7.36 / pCO2 = 48 / HCO3 = 26
9. pH = 7.43 / pCO2 = 45 / HCO3 = 29
10. pH = 7.47 / pCO2 = 54 / HCO3 = 38
11. pH = 7.45 / pCO2 = 18 / HCO3 = 12
12. pH = 7.57 / pCO2 = 18 / HCO3 = 16
13. pH = 7.27 / pCO2 = 36 / HCO3 = 16
14. pH = 7.34 / pCO2 = 49 / HCO3 = 26
15. pH = 7.45 / pCO2 =50 / HCO3 = 33

11
Joel M. Topf, MD
Rapid interpretation of ABGs

A pH of 7.1 in methanol intoxication is an ominous sign.
A pH of 7.1 following a grand-mal seizure is routine and without significant morbidity.
A pH of 7.6 due to anxiety-hyperventilation syndrome is benign.
A pH of 7.6 in patients on digoxin and diuretics predisposes to serious arrhythmia.
From the above examples it should be
clear that it is the disease, not the pH that
determines morbidity. Because of this, it is
imperative to rapidly determine the etiology
of an acid-base disturbance. The ABG and
electrolyte panel allow one to easily narrow
the differential diagnosis. It also allows the
cagey physician to detect and categorize
multiple, simultaneous, primary acid-base
disorders.
1. Determine the primary acid-base disorder
To fully characterize an acid-base disorder there are as many as 5 steps:
5. If the patient has an AGMA, look for a

pre-existing non-anion gap metabolic
acidosis or metabolic alkalosis
2. Determine if there is a second primary

disorder affecting compensation
3. If the patient has a metabolic acidosis,
determine the anion gap
4. If the patient has an anion gap metabolic
acidosis (AGMA), determine if there is an
osmolar gap
12
Joel M. Topf, MD
Multiple primary acid-base disturbances

Patients are complex and often have multiple simultaneous primary acid-base disturbances. Think of the patient with gram negative sepsis causing metabolic acidosis and
fever causing respiratory alkalosis. Uncovering these complex cases can be done mathematically. My suggestion to you is to get a
computer. Patients are too important and

you are too bad at math to do the calculation
reliably.
On the iPhone and iPod Touch there are a
number of free and inexpensive applications
to accomplish this. I have tested ABG and
MedCalc and found both to be

reliable.
Alternatively one can use an
Acid-Base nomogram which
are accurate and easy to use.
Draw a line connecting the pH
and pCO2 or the pCO2 and
bicarbonate (the diagonal
lines).
Unfortunately neither computers nor nomograms are
available on the boards/shelf
exams. For this reason you
need to be able to fully interpret an ABG on your own.
13
Joel M. Topf, MD
Looking for second primary acid base disturbances

the old timey way
As discussed earlier, compensation occurs in every acid-base disturbance. In the
absence of a second primary-disorder the
degree of compensation can be determined
solely by the severity of the primary disturbance (and by the duration in the case of
metabolic compensation).
Disorder
We use the predictability of compensation to determine if additional primary disorders are present. If the degree of compensation falls in the predicted range then there
is no additional acid-base disturbance.
Each primary acid-base disturbance has
its own equation to calculate the predicted
degree of compensation. See the table below.
Primary disturbance /
Compensation
How to predict compensation
Metabolic
acidosis
decrease in bicarbonate
Metabolic
alkalosis
increase in bicarbonate
increase in carbon dioxide
CO2 increases 0.7 for every 1 mmol increase

in HCO3
Respiratory
acidosis
increase in carbon dioxide
Acute:
decrease in carbon dioxide
CO2 = 1.5 x HCO3 + 8 2

Winters formula
increase in bicarbonate
HCO3 increases 1 for every 10

mmHg of CO2
Chronic: HCO3 increases 3 for every 10

mmHg of CO2
Respiratory
alkalosis
decrease in carbon dioxide

decrease in bicarbonate
Acute:
HCO3 decreases 2 for every 10

mmHg of CO2
Chronic: HCO3 decreases 4 for every 10

mmHg of CO2
If the prediction equation explains the

compensation then you have a simple acidbase disorder. If the prediction equation does
not explain the compensation then a second
primary disorder exists.
In metabolic disorders, if the actual pCO2
is less than the predicted pCO2 there is an
additional respiratory alkalosis. If the actual
pCO2 is greater than the predicted pCO2

there is an additional respiratory acidosis.
In respiratory disorders, if the actual
HCO3 is greater than the predicted HCO3
there is an additional metabolic alkalosis. If
the actual HCO3 is less than the predicted
HCO3 there is an additional metabolic acidosis.
14
Joel M. Topf, MD
Using the prediction equations

Metabolic acidosis
Suppose a patient has a pH of 7.37, HCO3 of
10 and a pCO2 of 18.
All three variables are lower than normal
so the patient has a metabolic disturbance.
rises 0.7 for every 1 mmol/L increase in

HCO3.
An HCO3 of 36 is an increase of 12 from
normal. This should be compensated by
an increase in pCO2 of _______.
The pH is decreased so this is metabolic

acidosis.
The actual pCO2 is 48, so this patient has

an isolated metabolic alkalosis with
____________ respiratory compensation.
To look for a second primary condition the

first step is to use Winters formula to see if
the compensation is appropriate.
If the pCO2 was 58, the patient would

have an additional respiratory
____________.
With a bicarbonate of 10, Winters formula predicts a pCO2 of ______.
If the pCO2 was 42, the patient would

have an additional primary respiratory
____________.
The actual pCO2 is 18, below the predicted pCO2 so this patient has an additional primary respiratory __________.
If the actual pCO2 was 24, then the patient would have physiologically compensated metabolic acidosis without a
second primary ____________ disorder.
If the actual pCO2 was 28 then the patient
would have a pCO2 that was higher than
predicted or an additional primary respiratory _____________.
Metabolic alkalosis
36 and pCO2 of 48.
All three variables are higher than normal so the patient has a __________ disturbance.
The pH is ____________ so this is metabolic alkalosis.
To look for a second primary condition first
determine what the expected compensation
should be. In metabolic alkalosis the pCO2
The pH is decreased and both the HCO3
and pCO2 are elevated. Since the variables move in discordant direction it is a
_____________ disturbance.
The pH is decreased so this is respiratory
______________.
first step is to determine the expected bicarbonate.
The pCO2 is 16 above normal which corresponds to an expected increase in
HCO3 of 2 in ________ respiratory acidosis and 5 in _______ respiratory acidosis.
So the expected bicarbonate is 26 if the
respiratory acidosis is acute and 29 if it is
chronic. The actual HCO3 is 30 so there is
an additional _________ _______ if the
patient has acute disease and a pure res-
15
piratory acidosis if the condition is

_______.
Joel M. Topf, MD
The pH is increased so this is respiratory

alkalosis.
It is important to understand that the compensation equation can not tell you if the patient has acute or chronic disease. The physician must determine that.
Respiratory alkalosis
The pH is increased and the HCO3 and
pCO2 are both ________. Since the variables move in discordant direction it is a
__________ disturbance.

first step is to determine the expected bicarbonate.
The pCO2 is 18 below normal which corresponds to an expected _________ in
HCO3 of 4 in acute respiratory alkalosis
and 8 in chronic respiratory alkalosis.
So the expected bicarbonate is 20 if the
respiratory alkalosis is acute and 16 if it is
chronic. The actual HCO3 is 23 so this is a
respiratory alkalosis with ________
___________ regardless if it is acute or
chronic.
Respiratory
acidosis
Respiratory
alkalosis
Acute
10:1
10:2
Chronic
10:3
10:4
For every rise of 10 in

the pCO2 the HCO3
will rise by 1 or 3
For every fall of 10 in

pCO2 the HCO3 will
fall by 2 or 4.
16
Joel M. Topf, MD
Brittany Spears has been out partying and wakes up vomiting. After six
hours she is still vomiting and calls her personal concierge physician
who gets the following ABG:
7.71 / 33 / 94 with a HCO3 of 40 on the electrolyte panel.
John Daley presents to the ED stuporous. His caddie says he has been
taking nips from a little bottle all day. His labs reveal the following:
7.22 / 17 / 112 !
147!
104!
38
4.2!
7!
1.8
Hunter Thompson is dragged in to your office by his attorney. Mr.

Thompson is incomprehensible but does not appear toxic. There is no
history of diarrhea. An ABG and lytes are drawn:
7.28 / 36 / 88!
136!
116!
16
2.8!
14!
0.8
John Wayne is admitted to a surgery center for a colonoscopy. During the

procedure the oxygen saturation monitor malfunctions so the gastroenterologist gets an ABG to confirm good oxygenation.
7.32 / 60 / 145 / 31
Aretha Franklin is undergoing chemotherapy for pancreatic cancer. She

develops nausea, vomiting and diarrhea. She is admitted for IV fluids. In
the ER a blood gas and chemistries are drawn:
7.54 / 43 / 104!
144!
91!
36
3.2!
36!
1.3
17
Joel M. Topf, MD
The anion gap

In respiratory acidosis the acid is known, its carbon dioxide. In metabolic acidosis the acid
(anion) can be anything and what it is can have profound implications for your patient.
Metabolic acidosis is categorized by the
In metabolic acidosis bicarbonate (an antype of acid which is consuming the bicarion) is decreased, so to keep the anions in
bonate. The acid has two components: a probalance with the unchanged cations another
ton, which reacts with bicarbonate and an
anion must fill the void. This is either chloride
anion which can accumulate in the body. The
as seen on the left or an other anion as seen
identity of the anion is how we name the difon the right.
ferent metabolic acidosis.
The anion gap is a way to quantify this
In all of clinical medicine there are only
two types of anions:
Its either chloride
or
Its not chloride
The anion-gap is a simple calculation
which allows you to determine if the excess
anion is chloride or not.
The total number of anions in the blood
must equal the total number of cations (otherwise touching blood would give you a
shock).
relationship:
Cl + HCO3 + Other anions = Na+ + Other cations
Then rearrange it to solve for the other ions:

Other anions Other cations = Na+ (Cl + HCO3 )
Define anion gap as the difference between

other anions and other cations:
Anion gap = Na+ (Cl + HCO3 )
On average the anion gap is 8-10 but varies

from hospital to hospital. Always use local
normal values. For this book the upper
limit of normal will be 12.
With metabolic acidosis, if the anion gap
is less than twelve then the increased hydrogen ions are associated with excess chloride
and if the anion gap is greater than twelve
the excess anion is something else.
Abnormally low anion gap
Though not related to an acid-base disturbance, a low
anion gap can also signal disease.
Increased chloride
Hypertriglyceridemia
Bromide
Iodide
Decreased Unmeasured anions

Albumin
Phosphorous
Increased Unmeasured cations

Hyperkalemia
Hypercalcemia
Hypermagnesemia
Lithium
IgG
18
Joel M. Topf, MD
Anion gap metabolic acidosis (AGMA)

Anion gap metabolic acidosis cause the
most serious acute metabolic acidosis. The
most important causes of AGMA are:
KETONES are produced as an alternative

energy supply when glucose is unavailable:
starvation ketosis
Lactic acidosis
alcohol induced hypoglycemia
Ketoacidosis
diabetic ketoacidosis
Toxic alcohols
Two types of lactic acidosis:
Insulin is a potent suppressor of ketogenesis

so treatment requires supplying insulin. In
starvation or alcohol ketosis administering
glucose allows the secretion of endogenous
insulin. In diabetic ketoacidosis, patients
cannot synthesize endogenous insulin and
need pharmaceutical insulin to reverse ketosis.
Type A: decreased perfusion causing

ischemia resulting in anaerobic metabolism and lactic acidosis. Shock.
THE TOXIC ALCOHOLS can cause AGMA

and will be discussed more in the section on
osmolar gap.
Type B: anaerobic metabolism due to

mitochondrial dysfunction. Aspirin
toxicity, NNRTI, metformin, malignancy
RENAL FAILURE variably causes AGMA.

Early in the course of CKD patients develop
NAGMA but in late CKD stage 4 and CKD
stage 5, sulfur based anions accumulate and
cause AGMA.
Renal failure
LACTIC ACID is produced during anaerobic metabolism. The production of lactic acid
restores NAD+ needed for glycolysis.
The classic mnemonic MUD PILES sucks. The new mnemonic is GOLD MARK. Know it.
G!
Glycols: ethylene glycol, diethylene

glycol, propylene glycol
O!
Oxoproline: Pyroglutamic Acid is a

rare cause of high anion gap (30s)
metabolic acidosis. It is seen with
acetaminophen, hypotension and infection.
L!
L-lactic acidosis.
D!
D-Lactic acidosis: Bacteria metabolize

carbohydrate to the isomer D-lactate.
LDH only recognizes L-lactate so Dlactate must be cleared by the kidney.
The anion gap is usually small and

transient because D-lactate is rapidly
cleared by the kidneys.
M!
Methanol
A!
Aspirin. The anion is actually lactate

in ASA toxicity.
R!
Renal failure
K!
Ketoacidosis: DKA, starvation, hypoglycemia

AN Mehta, JB Emmett , M Emmett, Lancet,
372, 9642, p 892, 2008
19
Joel M. Topf, MD
Diabetic Ketoacidosis
The most exciting diagnosis in internal medicine
In diabetic ketoacidosis, just about every
lab value that can go wrong has gone wrong.
DKA occurs when there is an absolute or
relative lack of insulin. In the absolute case,
the patient with DM1 forgets or fails to take
their insulin, in the relative case, patients on
a stable dose of insulin undergo a crisis that
requires additional insulin and if her insulin
prescription does not account for this, they
have a relative paucity of insulin and go into
ketoacidosis.
Sodium is decreased due to pseudohyponatremia. To estimate the corrected

Na+ add 1.6 mEq/L to the measured Na+
for every 100 mg/dL the glucose is
above 100 mg/dL.
Potassium is usually increased due to
solute drag. The lack of insulin prevents
a shift of K+ back into cells. Despite high
plasma levels, total body potassium is
decreased due to increased renal losses.
Triggers of DKA: a 7 Ied monster

initial (new diagnosis)
infection
illicit drug use
insulin (lack of, non-compliance)
infarction (myocardial)
incision (surgery)
infant (pregnancy)
Patients who present with DKA are typically quite toxic with hypovolemic shock,
altered mental status, abdominal pain, and
vomiting. Acetone can cause the breath to
smell fruity.
Diagnosis can be made from the combination of an anion gap metabolic acidosis,
hyperglycemia (500-800) and positive serum
ketones. The ketones can be acetoacetate, hydroxybutyrate or acetone. Only acetoacetate is detected by the routine serum ketone
assay.
The lab abnormalities are ubiquitous in
DKA:
Bicarbonate is decreased. Duh, metabolic

acidosis.
BUN and creatinine are elevated due to
pre-renal acute renal failure.
Glucose is elevated, usually above 300
mg/dL. Duh, diabetes.
Anion gap is increased due to the presence of ketone anions. The gap is often
greater than 20 mEq/L.
Phosphorous is decreased.
Amylase is increased because ketones
interfere with the laboratory assay. Lipase is usually normal.
pH is decreased.
20
PCO2 is decreased due to compensatory

hyperventilation (Kussmauls respiration).
The three core medicines used to treat

DKA are:
1. Insulin. Insulin will lower the glucose
but it is used to reverse the ketosis. The
insulin drip should be continued until
the anion gap has closed (indicating
complete reversal of the ketosis) even if
that requires starting a dextrose infusion
to prevent hypoglycemia.
2. 0.9 Normal Saline. Saline is used to
reverse the volume loss.
3. Potassium. Patients on initial presentation will usually be hyperkalemic despite total body potassium depletion.
When insulin is started, potassium will
shift into the cells and uncover hypokalemia. Potassium replacement should be
started when the potassium falls below 4
mmol/L. Potassium should be frequently
assessed during therapy.
Joel M. Topf, MD
A 14 year old actress has

been having increasing
fatigue for the past few
weeks. Her school performance has slipped and
her parents are worried
that she may have gotten
White blood cell count is increased due

to demargination.
The most profound abnormality is volume depletion. The osmotic diuresis vomiting ( a common symptom of DKA) can result in life-threatening hypovolemic shock.
into drugs.
She has been waking at night to go to the
bathroom 2-3 times a night. Today, her
mother found her unconscious on the floor
in a puddle of urine. In her purse the mom
found a bag of dried plant-matter and a bottle of unidentified pills.
Blood pressure is 80/P, HR 146, RR 32,
Wt 40 kg. Skin is cool, lungs are clear, heart
is tachycardic, abdomen is firm without rebound. She has no edema. She is nonresponsive.
Initial labs:
What is the primary
acid-base disorder?
ABG 7.20 / 16 / 96 / 6
128
94
44
6.4
1.8
764
Is compensation
appropriate?
What is her adjusted sodium?
What are first steps in resuscitation?
Initial diagnostic procedures?
Bicarbonate has been tested and should

not be used as it can prolong the ketosis and
promotes hypophosphatemia without improving patient outcomes.
21
Joel M. Topf, MD
Non-Anion Gap Metabolic Acidosis (NAGMA)

Non-anion gap metabolic acidosis occurs in
three clinical scenarios:
1. Excessive chloride intake, usually as
normal saline
2. Increased lower GI losses, usually as diarrhea
3. Failure of the kidney to excrete the daily
hydrogen load, renal tubular acidosis.
Chloride intake
Normal saline has a pH of 5.5. It also is a

massive source of chloride.
How would you compare the relative acidity
of saline versus plasma?
How much chloride is in all of the plasma?
How much chloride is found in a liter of
0.9% normal saline.
Almost all of the cases of excessive chloride
intake causing NAGMA are due to saline infusions, often erroneously called dilutional
acidosis. Hydrochloric acid intoxication or
chlorine gas poisoning can also cause
NAGMA via excessive chloride.
GI losses
GI secretions, distal to the highly acidic

stomach, have relatively high bicarbonate
concentrations:
Bile!.................................................30-40 mEq/L
Pancreatic secretions!.................80-100 mEq/L
Small intestine !..........................80-100 mEq/L
Large intestine !............................30-50 mEq/L
It should be apparent that diarrhea or a surgical drain could result in rapid and dra-
matic losses of bicarbonate. This causes a

NAGMA.
In GI disturbances the pH follows the
food, with vomiting the food and pH
rises, with diarrhea the food and pH falls
Renal tubular acidosis
The kidneys role in regard to maintaining a

normal bicarbonate can be neatly divided
into three tasks:
Reabsorb all of the filtered bicarbonate. Like
other valuable small molecules and electrolytes that are freely filtered at the
glomerulus, the kidney avidly scavenges
these particles and reabsorbs them.
Synthesize new bicarbonate. The kidney
must also synthesize new bicarbonate to
replace bicarbonate consumed in daily
metabolism. Creating new bicarbonate
requires excretion of hydrogen ions from
the body.
Excrete hydrogen as ammonium (NH4+). In
order to synthesize de novo bicarbonate,
the kidney must excrete hydrogen ions in
the urine. These hydrogen ions make up
the daily acid load (approx. 1 mmol/Kg
body weight). The kidney cannot excrete
the daily acid load as free hydrogen and
must excrete the hydrogren as either titratable acids or ammonia.
Failure in the first bullet point results in type
2 or proximal RTA. Failure of the second bullet point results in RTA type 1. Failure of the
third bullet point results in hyperkalemic or
type 4 RTA.
22
Disorder
urine pH
Plasma K
Joel M. Topf, MD
urine anion gap
GI losses
< 6.0
Hypokalemia, variable
negative
Proximal RTA
at Tm < 6.0
above Tm, > 6.0
Hypokalemia during
treatment
at Tm negative
above Tm positive
Electrogenic
distal RTA
> 5.5
Hyperkalmia
positive
Classic distal
RTA
>5.5
Hypokalemia
positive
Hyperkalemic
RTA (type 4)
< 6.0
Hyperkalmia
positive
The ideal laboratory test to diagnose RTA would be a urinary ammonium assay. Outside of
specialized laboratories this does not exist. We can infer the presence of ammonium by looking
at the urinary anion gap.
We used the serum anion gap to look for non-specific
anions causing the metabolic acidosis. We will now use
the urinary anion gap to look for increased cations,
namely ammonium cations.
Urine Anion gap = (Na+ + K+) Cl
Normally, with urinary acidification, there is increased

ammonium in the urine which adds to the unmeasured cations. Unmeasured cations exceed unmeasured
anions so so the anion gap will be negative. A negative
urinary anion gap means good urinary ammonia levels.
In distal RTA, there is no urinary acidification. Without
acidic urine there is nothing to drive the formation of
NH4+ from NH3.
In type 4 RTA, the urine pH is low enough but the hyperkalemia blocks the release of NH3, so there is no
substrate to produce NH4+.
23
Joel M. Topf, MD
Osmolar Gap
In patients with metabolic acidosis and a large anion gap, consideration should be given to
ethylene glycol and methanol toxicity. Laboratory confirmation may take 24 hours. The osmolar gap allows one to infer the presence of these low molecular weight toxins.
If a patient has ingested ethylene glycol
or methanol, treatment must be initiated
rapidly. Usually therapy is begun prior to
confirming the diagnosis with a specific assay for the alcohol. One of the keys to building the clinical suspicion is demonstrating
an osmolar gap.
If the calculated osmolality is more than

10 mosm/Kg H2O less than the measured
osmolality you have an abnormal osmolar
gap. Elevated osmolar gaps are found with:
The osmolar gap demonstrates an increase in
the serum osmolality that can not be explained by the usual suspects: electrolytes,
glucose, urea and ethanol. Because the molecular weight of methanol and ethylene
glycol are low, a few grams equals many
osmoles and will increase the measured osmolality without affecting the calculated
osmolality. This provides the gap.
Calculated Osmolality:
Ethylene glycol
Methanol
Isopropyl alcohol
Ketoacidosis
Lactic acidosis
Mannitol infusion
Pseudohyponatremia
2 x Na + glucose/18 + BUN/2.8 + EtOH/3.7

The glucose, BUN and ethanol levels are divided by their
molecular weight (180, 28 and 46) to convert mg/dL to
mmol/dL and then multiplied by ten to get mmol/L.
Note: Ethanol does not behave as an ideal osmole. Empiric data indicates 3.7 is the correct divisor.
24
Joel M. Topf, MD
Problems: figure out the anion gap, calculated osmolality, and osmolar gap in the following
patients
1.!
!
!
148!
4.8!
!
111!
12!
!
10!
0.8!
!
!
!
!
Ethanol: 0! Glucose: 40! !

Osmolality: 337!
!
!
!
!
!
!
!
Anion gap: 25
Calculated Osm: 302
Osmolar gap: 35
2.!
!
!
146!
4.8!
!
105!
18!
!
14!
0.8!
!
!
!
!

Osmolality: 311!
!
!
!
!
!
!
!
Anion gap: 23
Calculated Osm: 301
Osmolar gap: 10
3.!
!
!
138!
4.8!
!
112!
14!
!
28!
1.8!
!
!
!
!

Osmolality: 302!
!
!
!
!
!
!
!
Anion gap: 12
Calculated Osm: 293
Osmolar gap: 9
4.!
!
!
146!
4.8!
!
106!
12!
!
196!
8.8!
!
!
!
!

Osmolality: 400!
!
!
!
!
!
!
!
Anion gap: 28
Calculated Osm: 381
Osmolar gap: 19
5.!
!
!
141!
4.8!
!
95!
8!
!
85!
2.4!
!
!
!
!

Osmolality: 338!
!
!
!
!
!
!
!
Anion gap: 38
Calculated Osm: 322
Osmolar gap: 16
6.!
!
!
135!
4.8!
!
105!
7!
!
45!
2.2!
!
!
!
!

Osmolality: 318!
!
!
!
!
!
!
!
Anion gap: 23
Calculated Osm: 309
Osmolar gap: 0
7.!
!
!
138!
4.8!
!
112!
10!
!
62!
2.2!
!
!
!
!

Osmolality: 333!
!
!
!
!
!
!
!
Anion gap: 16
Calculated Osm: 319
Osmolar gap: 14
8.!
!
!
146!
4.8!
!
114!
14!
!
127!
6.3!
!
!
!
!

Osmolality: 405!
!
!
!
!
!
!
!
Anion gap: 18
Calculated Osm: 364
Osmolar gap: 16
9.!
!
!
130!
4.8!
!
94!
6!
!
8!
0.6!
!
!
!
!

Osmolality: 313!
!
!
!
!
!
!
!
Anion gap: 30
Calculated Osm: 268
Osmolar gap: 45
10.!
!
!
148!
4.8!
!
120!
15!
!
18!
1.0!
!
!
!
!

Osmolality: 344!
!
!
!
!
!
!
!
Anion gap: 13
Calculated Osm: 339
Osmolar gap: 5
25
Joel M. Topf, MD
Additional metabolic acid-base conditions

There is a trick for patients with anion-gap metabolic acidosis that allows physicians to go
back in time prior to developing the anion gap and see what the bicarbonate was at that time.
From that you can deduce if the patient had either a pre-existing metabolic alkalosis or preexisting non-anion gap metabolic acidosis.
Earlier we looked at compensation to deQuestions
termine if a patient has a second primary
An over-rated NFL quarteracid-base disorder. Now we will look at the
back with a bad temper preanion gap to determine if the patient has an
sents to the ER appearing
additional primary acid-base disorder.
toxic and hypotensive. His
In order to use the anion gap to look for
additional acid-base disorders we assume
that for every increase in the anion gap over
12 the serum bicarbonate falls by one.
agent reports that he initially

developed diarrhea after eating some old chicken salad:
7.28 / 18 / 88!
128!
106!
16
glucose: ! 875!
5.6!
8!
1.8
1. What is the primary acid-base disturbance?

2. Is there a second primary acid-base disturbance, affecting compensation? What
is it?
We can establish a formula to represent
this:
HCO3 = Anion Gap
HCO3before HCO3now = AGcurrent AGnormal
3. What is the anion gap?

4. What is the diagnosis?
5. Calculate the bicarbonate before
6. Did he have a pre-existing acid-base disorder? What is it and why does he have
it?
HCO3 before = HCO3now + (AGcurrent 12)
By using the last formula we can actually

infer what the bicarbonate was prior to developing the anion gap. If this bicarbonate is
low we call this a pre-existing non-anion gap
metabolic acidosis. If the bicarbonate is elevated then the patient had pre-existing
metabolic alkalosis.
26
A manic patient with fever

and diarrhea presents to
the ER, hypotensive with
these initial labs:
Joel M. Topf, MD
Calculate the bicarb prior to the AGMA:

1.!
140!
110!
Anion Gap: 2
4.8!
18!
Bicarb before: 8
2.!
134!
104!
Anion Gap: 18
4.8!
12!
Bicarb before: 18
3.!
138!
114!
Anion Gap: 18
4.8!
6!
Bicarb before: 12
4.!
146!
114!
Anion Gap: 16
4.8!
16!
Bicarb before: 20
5.!
141!
105!
Anion Gap: 18
4.8!
18!
Bicarb before: 24
6.!
135!
94!
Anion Gap: 22
4.8!
19!
Bicarb before: 29
7.!
138!
101!
Anion Gap: 23
4.8!
14!
Bicarb before: 25
8.!
146!
114!
Anion Gap: 16
4.8!
16!
Bicarb before: 20
2. Is there a second primary acid-base disturbance affecting compensation? What

is it?
9.!
130!
96!
Anion Gap: 28
4.8!
6!
Bicarb before: 22
10.!
148!
106!
Anion Gap: 28
4.8!
14!
Bicarb before: 30
7.28 / 28 / 88!
142!
102!
16
glucose: ! 128!
3.2!
18!
1.8
1. What is the primary acid-base disturbance:

2. Is there a second primary acid-base disturbance affecting compensation? What
is it?
it?
A person of remarkable genetic luck returns from an
African safari with a cyclical
fever and profound vomiting. He appears toxic:
7.42 / 32 / 76!!
glucose: ! 56!
148!
98!
43
5.8!
28!
2.3
1. What is the primary acid-base disturbance:

it?
27
Answers
Determine the primary acid-base
disturbance:
1.
Metabolic Acidosis
2.
3.
Metabolic alkalosis
4.
Metabolic Acidosis
5.
Ms. Spears: both a primary metabolic

alkalosis and respiratory alkalosis
Mr. Daley: isolated metabolic acidosis
Mr. Thompson: metabolic acidosis
and respiratory acidosis
Mr. Wayne: isolated chronic respiratory acidosis or an acute respiratory
acidosis and metabolic alkalosis
Metabolic Acidosis
8.
1.
9.
Metabolic alkalosis
Anion gap: 25 Calc Osm: 302

gap: 35
2.

gap: 10
3.

gap: 9
4.

gap: 19
5.

gap: 16
Using the prediction equations
alkalosis
respiratory
6.

gap: 7
7.

gap: 9
8.

gap: 35
acidosis
! Metabolic alkalosis
metabolic
increased
8
9.

gap: 45
appropriate
acidosis
alkalosis
! Respiratory acidosis
10. Anion gap: 13 Calc Osm: 339

gap: 5
1. metabolic acidosis
acute
2. None
chronic
3. 14
metabolic alkalosis
4. DKA
chronic
4. 10
Calculate the bicarb before:

1.Anion Gap: 12 Bicarb before: 18
5. Yes. Pre-existing NAGMA due to

diarrhea
respiratory
Charlie Sheen. Winning!
decrease
1. metabolic acidosis
metabolic alkalosis
2. respiratory alkalosis
Multiple Acid-base disturbances.

Case vignettes
4. 38
Jay Cutler
acidosis
decreased
2. respiratory alkalosis
Gap-Gap case vignettes:
respiratory
! Respiratory alkalosis
Prince William
5. Patient had pre-existing metabolic

acidosis. The presence of an anion
gap in metabolic alkalosis or a
primary respiratory acid-base disorder indicates an additional
metabolic acidosis. This patient
also has a triple disorder. Lactic
acidosis of fulminant malaria,
7.
232
5. Patient had pre-existing metabolic

alkalosis. This patient has a triple
disorder: metabolic acidosis, respiratory alkalosis and metabolic
alkalosis. Alkalosis likely due to
crack cocain being cut with bicarbonate.
3. 22
! Metabolic Acidosis
Joel M. Topf, MD
1. metabolic alkalosis
6.
11. Respiratory alkalosis
Ms. Franklin: metabolic alkalosis and

respiratory acidosis
Problems: figure out the anion gap,
calculated osmolality, and osmolar
gap in the following patients
10. Metabolic alkalosis
3. 22
4. 28
28

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a Precious Bodily Fluids production

Assistant Professor of Medicine

Understand how pH is like an earthquake

Understand and calculate the anion gap

pH and the hydrogen ion concentration

Hydrogen ions are similar and different

This mass action formula can be simplified

Do the same for this ABG:

The pH is proportional to the serum bicarbonate over carbon dioxide. An increase

If the quantitative approach is not helpful

There are four primary acid-base disturbances

1. An increase in bicarbonate is a metabolic

3. an increase in carbon dioxide

the initial (i.e. primary) disturbance to The

3. An increase in carbon dioxide is a respiratory acidosis

dioxide. This minimizes changes in the ratio

The important thing to recognize is that

Determine the primary acid-base disturbance:

2. pH = 7.34 / pCO2 = 50 / HCO3 = 26

3. pH = 7.45 / pCO2 = 48 / HCO3 = 32

4. pH = 7.32 / pCO2 = 28 / HCO3 = 14

5. pH = 7.37 / pCO2 = 50 / HCO3 = 28

6. pH = 7.36 / pCO2 = 80 / HCO3 = 44

7. pH = 7.32 / pCO2 = 36 / HCO3 = 18

8. pH = 7.36 / pCO2 = 48 / HCO3 = 26

9. pH = 7.43 / pCO2 = 45 / HCO3 = 29

10. pH = 7.47 / pCO2 = 54 / HCO3 = 38

11. pH = 7.45 / pCO2 = 18 / HCO3 = 12

12. pH = 7.57 / pCO2 = 18 / HCO3 = 16

13. pH = 7.27 / pCO2 = 36 / HCO3 = 16

14. pH = 7.34 / pCO2 = 49 / HCO3 = 26

15. pH = 7.45 / pCO2 =50 / HCO3 = 33

Rapid interpretation of ABGs

1. Determine the primary acid-base disorder

To fully characterize an acid-base disorder there are as many as 5 steps:

5. If the patient has an AGMA, look for a

2. Determine if there is a second primary

Multiple primary acid-base disturbances

computer. Patients are too important and

MedCalc and found both to be

Looking for second primary acid base disturbances

How to predict compensation

CO2 increases 0.7 for every 1 mmol increase

increase in carbon dioxide

decrease in carbon dioxide

CO2 = 1.5 x HCO3 + 8 2

HCO3 increases 1 for every 10

Chronic: HCO3 increases 3 for every 10

decrease in carbon dioxide

HCO3 decreases 2 for every 10

Chronic: HCO3 decreases 4 for every 10

If the prediction equation explains the

pCO2 is greater than the predicted pCO2

Using the prediction equations

rises 0.7 for every 1 mmol/L increase in

The pH is decreased so this is metabolic

The actual pCO2 is 48, so this patient has

To look for a second primary condition the

If the pCO2 was 58, the patient would

With a bicarbonate of 10, Winters formula predicts a pCO2 of ______.

If the pCO2 was 42, the patient would

piratory acidosis if the condition is

The pH is increased so this is respiratory