MUNAR Acid-Base Cases TT

Acid-Base Cases
Myrna Y. Munar, Pharm.D.

Associate Professor
Blood Gases
pH PCO2 [HCO3]
mmHg mEq/L
Arterial 7.37 – 36 – 44 22 – 26
7.43
Venous 7.32 – 42 – 50 23 – 27
7.38
Metabolic or Respiratory
Acidosis or Alkalosis
Disorder pH H+ Primary Compensatory

Disturbance Response
Metabolic Dec Inc Dec [HCO3] Dec PaCO2
acidosis
Metabolic Inc Dec Inc [HCO3] Inc PaCO2

alkalosis
Respiratory Dec Inc Inc PaCO2 Inc [HCO3]
acidosis
Respiratory Inc Dec Dec PaCO2 Dec [HCO3]
alkalosis
Case 1
AB, a 35 year old, 94.3-kg woman, is
brought to the ER in a semi comatose
state. A neighbor found her on the
floor of her apartment. AB has a
history of drug and alcohol abuse.
The neighbor is unaware of any other
medical conditions and doesn’t know
if AB takes any medication.
PE
BP 125/60 (supine)
HR 110 bpm
RR 40 breaths/min
Pupils reactive to light

Labs
Na 140 mEq/L
K 5.8 mEq/L
Cl 103 mEq/L
BUN 25 mg/dL
SCr 1.4 mg/dL
Gluc 150 mg/dL
Serum osmolality 332 mOsm/kg (nl 280-295)

pH = 7.16
Is the patient acidemic or alkalemic?
A) acidemic
B) alkalemic
Determine the pt’s acid-base disorder

pH = 7.16; PaCO2 23 mmHg; HCO3 8 mEqL
What type of acid base disorder is occurring?
A) metabolic acidosis Bicarbonate is low so it is metabolic acidosis. If it

was high PaCO2, it would be respiratory acidosis.
B) metabolic alkalosis
C) respiratory acidosis
D) respiratory alkalosis
E) a mixed disorder
Compensation – Metabolic Acidosis
For every 1 mEq/L
decrease in [HCO3-] HCO3 :
below the average of 24 24(normal ) 8( pt ' s ) 16mEq / L
mEq/L, the PaCO2
decreases by Pa CO2 :
approximately 1.0-1.5 1.0 16mEq / L 16mEq / L
mmHg from the average
value of 40 mmHg 40 16 24mEq / L
HCO3 8 mEq/L (nl 22-26 1.5 16 24mEq / L
mEq/L)
PaCO2 23 mmHg (nl 36- 40 24 16mEq / L
44 mmHg)
PaCO2 is expected to be
16 – 24 mmHg
Compensation – Metabolic Acidosis
Respiratory compensation for HCO3 of 8 mEq/L
is expected to be a PaCO2 of 16 - 24 mmHg. The
measured PaCO2 is within this range at 23
mmHg.
Appropriate compensation for metabolic
acidosis
Metabolic Acidosis
Anion gap
Non anion gap

GI loss of HCO3--you can lose a lot of bicarbonate in the stool (ex: diarrhea)
Renal tubular acidosis (RTA)
Renal tubular dysfxn
Renal loss of HCO3
Anion Gap Derivation
AG = (serum Na + serum K) – (serum Cl +
serum HCO3)
Since K is relatively low, the formula can be
abbreviated to:
AG = serum Na – (serum Cl + serum HCO3)
= serum Na – serum Cl - serum HCO3
Calculate AG:Na 140, K 5.8, Cl 103, HCO3 8
What is the patient’s AG?
Need to know how to calculate this
on the exam. Equation will be given.
Calculate answer
The patient’s anion gap (AG) is XX?
34.8 with K
29 without K
Both is markedly elevated.
True or False
The patient has an AG metabolic acidosis
with appropriate respiratory
compensation.
True or False
Common causes of an AG are
M-U-D-P-I-L-E-S.
M-U-D-P-I-L-E-S Don't have to remember.
M: methanol; massive rhabdomyolysis

U: uremia
D: DKA: B-hydroxybutyrate
P: paraldehyde: organic acids;
phosphate
I: ingestions (many plus toluene:
hippurate; formaldehyde: formate); iron
L: lactic acidosis: lactate, D-lactate
E: ethylene glycol: glycolate, oxalate
S: salicylate: ketones, lactate, salicylate;
sulfate; starvation; strychnine
Osmolality
Equation will be given.
Need to know how to calculate on exam.
glucose(mg /dl) urea(mg/dl )

Calculated Osm 2 Na
18 2.8
Serum Na = 140 mEq/L

Serum glucose = 150 mg/dl
BUN = 25 mg/dl
Calculate answer
What is the calculated osmolality?
297 mOsm/L
glucose(mg /dl) urea(mg/dl )

CalculatedOsm 2 Na
18 2.8
Measured Osm = 360 mOsm/L

What is the osmolar gap? 63 mOsm/L
Osmolar gap = Measured Osm –
Calculated Osm
Yes or No
Does this patient have a double gap i.e.
an anion gap and and osmolar gap?
Yes. Patient has an anion and an osmolar gap.
Need to know this table.
Relationship between AG & Osm Gap

AG Osm Gap Double
Gap
Ethylene + + Yes
Glycol
Methanol + + Yes
Renal + + Yes
Failure
Isopropyl - + No
Alcohol
Ethanol - + No
Methanol
Can be found in bootleg alcohol
Commonly used solvent
Found in:
antifreeze
paint remover
windshield washer fluid
photocopying fluid
Exposure can occur:

at home
at workplace
more commonly from intentional ingestion (suicide
attempt)
F
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Methanol Metabolism
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Methanol
Alcohol dehydrogenase
Formaldehdye
Aldehyde dehydrogenase
Formic Acid
Folate (co-factor)
CO2 + H2O
Toxicities are due to accumulation of:
A) Formaldehyde
B) Formic acid
C) CO2 + H2O
Accumulation of formic acid
Formic acid accumulates in the optic nerve;
classic visual sx
light flashes
blurring CNS symptoms often lead to coma.
dimness
can lead to blindness
Less specific s & sx:
N/V, abdominal pain, h/a, dizziness, seizures,
CNS sx often leading to coma
CV toxicity
Renal toxicity
What is fomepizole?
Fomepizole
Antizol (brand name)
Alcohol dehydrogenase inhibitor
By preventing the initial metabolism of
methanol, fomepizole arrests the initiation
of the metabolic toxicity cascade
arrests neurologic effects (altered mental status,
coma, seizures, visual disturbances), CV effects,
and renal toxicity
Also used for ethylene glycol (antifreeze)
poisoning
Fomepizole Dosing Don't have to memorize this.
LD: 15 mg/kg IV
MD: 10 mg/kg q 12 h x 4 doses, then 15
mg/kg q 12 h until methanol concentrations
are below 20 mg/dL
All doses should be given as a short IV
infusion over 30 minutes
It is dialyzable, therefore adjust doses
according to HD schedule (published HD
dosing guidelines are available)
F
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Methanol Metabolism
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Fomepizole Alcohol dehydrogenase
Aldehyde dehydrogenase
Folate (co-factor)
True or False
Believe it or not...
Methanol toxicity has been traditionally
treated with ethanol infusions to inhibit
the production of formic acid.
Competes with methanol for metabolism.
Ethanol infusions
Requires frequent monitoring and
titrations to maintain ethanol levels
greater than 0.10 g/dl so that it can compete with methanol metabolism.
Worsens CNS depression
Exacerbates methanol-induced
pancreatitis
Causes hypoglycemia
J Emerg Med 2003;24(4):433-6

How to Determine an Initial
Dose of Bicarb
Initial goal is to raise the pH to Don't need to know how to do.
approximately 7.2 -> level at which
arrhythmias are less likely
1st step: Determine [HCO3]desired
[HCO3]desired = 24/[H] x PaCO2
[HCO3]desired = 24/63 x PaCO2
note: pH = 7.2 -> [H] = 63
Pt’s PaCO2 23 mmHg
Calculate [HCO3]desired
Calculate [HCO3]desired
How to Determine an Initial
Dose of Bicarb
2nd step: calculate the HCO3 deficit:
HCO3 deficit = 0.7 x TBW x
([HCO3]desired - [HCO3]actual)
Need to know how to use this equation.
Pt’s TBW = 94.3 kg
Calculate HCO3 deficit
Calculate HCO3 deficit
Na Bicarb IV
Na Bicarb 50 mEq/L IV, repeat ABG in
30 minutes
Case 2
CD is a 67 yo man admitted for txmt of
pneumonia. His medical hx includes
a 10 yr h/o HTN controlled with BP
meds including chlorthalidone 100 mg
po QD. He also takes ASA 81 mg
daily.
pH = 7.64
A) acidemic
B) alkalemic

Check all that apply.
A) metabolic acidosis
E) a mixed disorder
Yes or No
pH = 7.64; PaCO2 = 32
Does the PaCO2 equal the last 2 digits of
the pH? No --> indicate this can be a mixed acid-base disorder.
Compensation – Metabolic Alkalosis
PaCO2 increases 6-7 mmHg for each 10
mEq/L increase in [HCO3], up to a PaCO2 of
about 50-60 mmHg
HCO3 34 mEq/L (22-26 mEq/L)
PaCO2 32 mmHg (36-44 mmHg)
HCO3 increases by approximately 10 mEq/L
PaCO2 should increase to PaCO2 of 36 + 7 = 43
to 44 + 7 = 51 mmHg
BUT measured PaCO2 = 32 mmHg
Respiratory compensation for HCO3 of 33 mEq/L
is expected to be a PaCO2 of 43 – 51 mmHg, but
measured PaCO2 is lower than expected at 32
mmHg.
Inappropriate compensation for metabolic
alkalosis
--> In this case, patient is not appropriate compensated.
Compensation –Respiratory Alkalosis
The [HCO3] is decreased by 4 mEq/L for
each 10 mmHg decrease in PaCO2.
Say PaCO2 decreases by about 10 mEq/L (42-32
= 10 mmHg)
[HCO3] should decrease to [HCO3] 22 – 4 = 18
to 26 – 4 = 22 mEq/L
BUT measured [HCO3] is 34 mEq/L
Metabolic compensation for PaCO2 of 32 mmHg
is expected to be [HCO3] of 18 – 22 mEq/L, but
measured [HCO3] is higher than expected at 34
mEq/L
Inappropriate compensation for respiratory
alkalosis
Don't have to know all of these for exams.

True or False
The patient has a mixed metabolic
alkalosis and respiratory alkalosis with
inappropriate compensation
What is/are the most likely cause(s) of the
metabolic alkalosis in this patient?
A) Pneumonia
B) HTN
C) Chlorthalidone
D) ASA
Thiazide (DCT) diuretics
Increased
aldosterone
Can cause hypovolemia --> increase

aldosterone --> hydrogen ion secretion
and loss in urine contributing to the
metabolic alkalosis.
Metabolic Alkalosis
Thiazide & Loop
Diuretics
Increased distal
Na delivery Volume
Increased contraction
aldosterone
Increased K
secretion Increased Decreased GFR
Increased H+
proximal NaHCO3 Decreased filtered
Hypokalemia secretion reabsorption load of HCO3
Ammoniagenesis
Maintenance of
Generation of Metabolic Alkalosis
Metabolic Alkalosis
Diuretic therapy can result in volume
contraction and also what acid-base
disorder?Metabolic alkalosis.
Should know this!

What is/are the most likely cause(s) of the
respiratory alkalosis in this patient?
A) Pneumonia
B) HTN
C) HCTZ
D) ASA
IV Fluids
What is an appropriate fluid to
administer to this patient?
a) NS
b) D5W
c) LR
d) 3% saline
Tubular
Cortical Collecting Tubule Lumen
H2O dissociates to
H+ & hydroxyl ions You have to give Cl so that it gets to the
kidneys so that bicarbonate is excreted. So
H+ secreted into you have to give a chloride containing solution.
peri-tubular H+
capillary by H-
ATPase pump H2O
Hydroxy combines
w/CO2 to from
HCO3 via CA OH + CO2 HCO3
HCO3 is secreted CL
via CL- HCO3
exchanger
Type B
Intercalated Cell
IV Fluids
What is an INappropriate fluid to
administer to this patient?
a) NS
b) LR --> because lactate is metabolized to bicarbonate.
Can worsen the alkalosis.
Case 3
EF is a 45 year old woman admitted to
the hospital with a h/o severe N/V x
past 3 days. The patient reports she
has had cyclic vomiting over the past
few years with no discernable cause.
She reports weakness, fatigue, and
dizziness. The patient has poor skin
turgor, orthostatic hypotension, and
tachycardia (HR 113 beats/min).
Decreased skin turgor
Labs
Na 138 mEq/L
K 2.5 mEq/L
Cl 90 mEq/L
SCr 0.9 mg/dl
BUN 28 mg/dl
pH = 7.49
A) acidemic
B) alkalemic

B) metabolic alkalosis pH and bicarbonate is high. It cannot be a
respiratory alkalosis because PCO2 is high.
E) a mixed disorder
Compensation – Metabolic Alkalosis
PaCO2 increases 6-7 mmHg for each 10 mEq/L

increase in [HCO3], up to a PaCO2 of about
50-60 mmHg
Say HCO3 increases by about 10 mEq/L (24 to 34)
PaCO2 should increase to PaCO2 of 36 + 7 = 43 to
44 + 7 = 51 mmHg
Measured PaCO2 = 46 mmHg
Respiratory compensation for HCO3 of 34 mEq/L is
expected to be a PaCO2 of 43 – 51 mmHg. The
measured PaCO2 is within this range at 46 mmHg.
Appropriate compensation for metabolic alkalosis
--> Patient has appropriate compensation.
Don't have to know how to do compensation for exam.

True or False
The patient has a metabolic alkalosis with
appropriate respiratory compensation.
Compensation
The expected compensation would be
decreases in respiratory rate to increase
acid in the blood by increasing CO2. CO2
is not an acid, it combines with H2O
as it is added to the bloodstream to
form carbonic acid.
CO2 H 2O H 2CO3 H HCO3

Labs
Na 138 mEq/L
K 2.5 mEq/L
Cl 90 mEq/L
SCr 0.9 mg/dl
BUN 28 mg/dl
How would you characterize the acid-base disorder based on labs

and clinical data? (Hint: saline responsive or saline unresponsive?)
You lose Cl when you vomit. Pt Cl level is low. --> Saline responsive.
What type of metabolic alkalosis
does this patient have?
A) Saline responsive
B) Saline unresponsive
What are common causes of this type of acid-
base disorder? Choose all that apply...
A) Diuretic therapy
B) Extracellular volume contraction (gastric acid
loss egs vomiting, NG suction)
C) Exogenous alkali administration (egs
antacids, IV bicarb)
All of these can cause it.
For the patient, it is most likely caused by B.
What is the most likely cause in this
patient?
A) Diuretic therapy
B) Extracellular volume contraction (gastric acid
loss egs. vomiting
C) Exogenous alkali administration (egs.
antacids, IV bicarb)
Which therapeutic option(s) would you choose to
treat LW’s acid base disorder? All could be used for metabolic alkalosis.
A) Fluid replacement --since she has a lot of vomiting and fluid contraction.
B) Acetazolamide
C) Hydrochloric acid
D) Arginine HCl
E) Ammonium HCl
Tubular
Cortical Collecting Tubule Lumen
H2O dissociates to
H+ & hydroxyl ions
H+ secreted into
peri-tubular H+
capillary by H-
ATPase pump H2O
Hydroxy combines
w/CO2 to from
HCO3 via CA OH + CO2 HCO3
HCO3 is secreted CL
via CL- HCO3
exchanger
Type B
--> Give her NS! Intercalated Cell
Management Need to know this slide!
Saline-responsive: NS or 1/2 NS can

lower plasma [HCO3] in 3 ways:
reversing the volume contraction
component
removing the stimulus to renal Na
retention, thereby permitting NaHCO3
excretion in the urine
increasing distal Cl delivery -> promote
HCO3 secretion in the cortical collecting
tubule
Which fluids would you NOT use
in this pt?
A) Lactated Ringers aka Ringers Lactate
B) D5W
C) Normal saline
D) I would not use A and B
Treatment Plan
Pursue diagnosis and cause of N/V
Fluid replacement w/sodium chloride
Potassium chloride
Monitor electrolytes and ABG
Monitor volume status, urine output
Case 4
EF is a 22 yo student brought to the ED
by his classmates in an intoxicated
state. EF consumed 2 quarts of liquor
over the past few days following his last
final exam. He has severe N/V for 24
hours. EF wants to go home to sleep it
off, but the MD insists on an ABG,
Chem-7, and EtOH level.
Labs
Na 140 mEq/L
K 3.0 mEq/L
Cl 84 mEq/L
HCO3 24 mEq/L
BUN 28 mg/dL
SCr 1.3 mg/dL
Gluc 100 mg/dL
EtOH 56 mg/dL
E) a mixed disorder
F) ABG is normal
Should the patient be admitted or sent
home to sleep it off?
Calculate anion gap
serum HCO3)
∆AG / ∆HCO3 ratio Will NOT be on exam.
Aka “delta delta”

AG metabolic acidosis
∆/∆ = 1 or ∆ minus ∆ = 0
Hyperchloremic metabolic acidosis or
respiratory alkalosis
∆/∆ < 1 or ∆ minus ∆ = negative
i.e. HCO3 is lower than normal
Metabolic alkalosis or respiratory acidosis
∆/∆ > 1 or ∆ minus ∆ = positive
i.e. HCO3 is higher than normal
Mixed disturbances if ratio <0.8 or >1.2
J Am Soc Nephrol 2007;18:2429-31
∆AG / ∆HCO3 ratio
∆/∆ = 1 or ∆ minus ∆ = 0
∆/∆ = 35 – 14 = 21 / 26 – 24 = 2; ∆/∆ = 10.5
∆ minus ∆ = 19…not 1 or 0 therefore…
Pt’s HCO3 should be close to 2, but the
measured HCO3 = 24 mEq/L
AG metabolic acidosis and a metabolic alkalosis
Case 5
A 43 yo woman overdosed on opiates
and is brought to the ED by her family.
She is breathing 6 times per minute and
is not arousable. As she is being
intubated, an ABG and Chem-7 are
obtained.
Labs
Na 140 mEq/L
K 7.7 mEq/L
Cl 99 mEq/L
HCO3 16 mEq/L
BUN 31 mg/dL
SCr 1.5 mg/dL
Gluc 135 mg/dL

pH = 6.87
A) acidemic
B) alkalemic

E) a mixed disorder
Compensation –Respiratory Acidosis
The [HCO3] will increase by 1 mEq/L above
24 mEq/L for each 10 mmHg increase in
PaCO2
Say PaCO2 increases by about 50 mEq/L (90-40
= 50 mmHg)
[HCO3] should increase to [HCO3] 22 + 5 = 27
to 26 + 5 = 31 mEq/L
BUT measured [HCO3] is 16 mEq/L
Metabolic compensation for PaCO2 of 90 mmHg
is expected to be [HCO3] of 27 – 31 mEq/L, but
measured [HCO3] is lower than expected at 16
mEq/L
Inappropriate compensation for respiratory
acidosis
Calculate anion gap
serum HCO3)
∆AG / ∆HCO3 ratio
∆/∆ = 1 or ∆ minus ∆ = 0
∆/∆ = 32.7 – 14 = 18.7 / 26 – 16 = 10; ∆/∆ = 1.87
or 2
∆ minus ∆ = 8.7 or 9
Discussion Questions
What is the most effective therapy for
acid-base disturbances? Treat the underlying cause!
What are the risks of administering
sodium bicarbonate?
Sodium --> increase --> can be hypernatremic
HCO3 --> increase --> can tip them to alkalosis
Potassium --> decreases --> can become hypokalemic
Calcium --> decreases (in alkalosis state, it is more
likely to bind to albumin)--> hypocalcemia
Do we automatically give
bicarbonate in lactic acidosis?
Yes Patient is in hypoxemic state which causes the lactic
No
acidosis.
Bicarbonate Risks Know this.
• Shifts oxygen-hemoglobin dissociation curve to the left

• Impairs oxygen release from Hb to the tissues
• Can worsen hypoxemia, therefore worsens lactic
acidosis
Know drug-induced causes of
the 3 different types of RTA’s.
Need to know this!
These equations will be given
on the exam:
Anion Gap
Calculated osmolality
HCO3 deficit
BRING YOUR CALCULATORS

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Acid-Base Cases

Myrna Y. Munar, Pharm.D.

Disorder pH H+ Primary Compensatory

Metabolic Inc Dec Inc [HCO3] Inc PaCO2

Pupils reactive to light

SCr 1.4 mg/dL

Gluc 150 mg/dL

Serum osmolality 332 mOsm/kg (nl 280-295)

Determine the pt’s acid-base disorder

A) metabolic acidosis Bicarbonate is low so it is metabolic acidosis. If it

Non anion gap

M: methanol; massive rhabdomyolysis

glucose(mg /dl) urea(mg/dl )

Serum Na = 140 mEq/L

glucose(mg /dl) urea(mg/dl )

Measured Osm = 360 mOsm/L

Relationship between AG & Osm Gap

Exposure can occur:

Fomepizole Alcohol dehydrogenase

J Emerg Med 2003;24(4):433-6

Determine the pt’s acid-base disorder

Don't have to know all of these for exams.

Can cause hypovolemia --> increase

Should know this!

SCr 0.9 mg/dl

Determine the pt’s acid-base disorder

PaCO2 increases 6-7 mmHg for each 10 mEq/L

Don't have to know how to do compensation for exam.

CO2 H 2O H 2CO3 H HCO3

SCr 0.9 mg/dl

How would you characterize the acid-base disorder based on labs

Saline-responsive: NS or 1/2 NS can

SCr 1.3 mg/dL

Gluc 100 mg/dL

Aka “delta delta”

SCr 1.5 mg/dL

Gluc 135 mg/dL

Determine the pt’s acid-base disorder

• Shifts oxygen-hemoglobin dissociation curve to the left

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