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Case 1

Mrs. Puffer is a 35-year-old single mother, just getting off the night
shift. She reports to the ED in the early morning with shortness of
breath. She has cyanosis of the lips. She has had a productive cough
for 2 weeks. Her temperature is 102.2, blood pressure 110/76, heart
rate 108, respirations 32, rapid and shallow. Breath sounds are
diminished in both bases, with coarse ronchi in the upper lobes.
Chest X-ray indicates bilateral pneumonia.

• ABG results are:

o pH= 7.44
o PaCO2= 28
o HCO3= 24
o PaO2= 54


• PaCO2 is low.
• pH is on the high side of normal, therefore compensated
respiratory alkalosis.
• Also, PaO2 is low, probably due to mucous displacing air in the
alveoli affected by the pneumonia.


• Mrs. Puffer most likely has ARDS along with her pneumonia.
• The alkalosis need not be treated directly. Mrs. Puffer is
hyperventilating to increase oxygenation, which is incidentally
blowing off CO2. Improve PaO2 and a normal respiratory rate
should normalize the pH.
• High FiO2 can help, but if she has interstitial lung fluid, she may
need intubation and PEEP, or a BiPAP to raise her PaO2.
• Expect orders for antibiotics, and possibly steroidal anti-
inflammatory agents.
• Chest physiotherapy and vigorous coughing or suctioning will
help the patient clear her airways of excess mucous and
increase the number of functioning alveoli.
Case 2

Mr. Worried is a 52-year-old widow. He is retired and living alone. He

enters the ED complaining of shortness of breath and tingling in
fingers. His breathing is shallow and rapid. He denies diabetes; blood
sugar is normal. There are no EKG changes. He has no significant
respiratory or cardiac history. He takes several antianxiety
medications. He says he has had anxiety attacks before. While being
worked up for chest pain an ABG is done:

• ABG results are:

o pH= 7.48
o PaCO2= 28
o HCO3= 22
o PaO2= 85


• pH is high,
• PaCO2 is low
• respiratory alkalosis.


• If he is hyperventilating from an anxiety attack, the simplest

solution is to have him breathe into a paper bag. He will
rebreathe some exhaled CO2.This will increase PaCO2 and
trigger his normal respiratory drive to take over breathing
• * Please note this will not work on a person with chronic CO2
retention, such as a COPD patient. These people develop a
hypoxic drive, and do not respond to CO2 changes.

Case 3

You are the critical care doctor about to receive Mr. Sweet, a 24-year-
old DKA (diabetic ketoacidosis) patient from the ED. The medical
diagnosis tells you to expect acidosis. In report you learn that his
blood glucose on arrival was 780. He has been started on an insulin
drip and has received one amp of bicarb. You will be doing finger
stick blood sugars every hour.

• ABG results are:

o pH= 7.33
o PaCO2= 25
o HCO3=12
o PaO2= 89


• The pH is acidotic,
• PaCO2 is 25 (low) which should create alkalosis.
• This is a respiratory compensation for the metabolic
• The underlying problem is, of course, a metabolic acidosis.


• Insulin, so the body can use the sugar in the blood and stop
making ketones, which are an acidic by-product of protein
• In the mean time, pH should be maintained near normal so that
oxygenation is not compromised

1. Mr. Frank is a 60 year-old with pneumonia. He is admitted with

dyspnea, fever, and chills. His blood gas is below:
pH 7.28
CO2 56
PO2 70
HCO3 25
SaO2 89%

What is your interpretation?

What interventions would be appropriate for Mr. Frank?

1. Mr. Frank has an uncompensated respiratory acidosis with hypoxemia

as a result of his pneumonia. This is due to inadequate ventilation and
perfusion. The treatment goals for Mr. Frank would be to improve both
ventilation and oxygenation. Ventilation may improve with the use of
bronchodilators and pulmonary hygiene. If not, Mr. Frank may require
CPAP, BiPAP, or intubation and mechanical ventilation. Oxygen therapy
should consist of only the minimal amount necessary to increase his oxygen
saturation to normal (95%).

2. Ms. Strauss is a 24 year-old college student. She has a history of

Crohn's disease and is complaining a of a four day history of bloody-
watery diarrhea. A blood gas is obtained to assess her acid/base
pH 7.28
CO2 43
pO2 88
HCO3 20
SaO2 96%

What is your interpretation?

What interventions would be appropriate for Ms. Strauss?

2. Ms. Strauss has an uncompensated metabolic acidosis. This is due to
excessive bicarbonate loss from her diarrhea. It is interesting to note that she
has no compensation. Normally, the respiratory center compensates quickly
for metabolic disorders. However, in Ms. Strauss' case she would have to
hyperventilate in order to compensate. This may not be possible in her
present condition, and should be evaluated further. Treatment would consist
of control of the diarrhea and bowel rest. It should not be necessary to
administer bicarbonate in her present condition.

3. Mr. Karl is a 80 year-old nursing home resident admitted with

urosepsis. Over the last two hours he has developed shortness of
breath and is becoming confused. His ABG shows the following
pH 7.02
CO2 55
pO2 77
HCO3 14
SaO2 89%

What is your interpretation?

What interventions would be appropriate for Mr. Karl?

3. Mr. Karl has a metabolic and respiratory acidosis with hypoxemia. The
metabolic acidosis is caused by his sepsis. The respiratory acidosis is
secondary to respiratory failure. This presentation of sepsis and associated
respiratory failure is consistent with ARDS. Treatment must be aggressive,
because his acidosis is severe. His respiratory status needs to be stabilized,
and would probably require mechanical ventilation. If hypotension exists,
aggressive fluid and vasopressor support would be warranted. This patient is
at high risk for further complications and should be managed in an ICU.
Bicarbonate should not be administered until the underlying sepsis and
respiratory failure is treated.
4. Mrs. Lauder is a thin, elderly-looking 61 year-old COPD patient.
She has an ABG done as part of her routine care in the pulmonary
clinic. The results are as follows:
pH 7.37
CO2 63
pO2 58
HCO3 35
SaO2 89%

What is your interpretation?

What interventions would be appropriate for Mrs. Lauder?

4. Mrs. Lauder has a fully-compensated respiratory acidosis with

hypoxemia. Full compensation is evidenced by the normal pH in spite of her
acid/base disorder. This is her baseline and doesn't require treatment.

5. Ms. Steele is a 17 year-old with intractable vomiting. She has some

electrolyte abnormalities, so a blood gas is obtained to assess her
acid/base balance.
pH 7.50
CO2 36
pO2 92
HCO3 27
SaO2 97%

What is your interpretation?

What interventions would be appropriate for Ms. Steele?

5. Ms. Steele has an uncompensated metabolic alkalosis. This is due to

vomiting that results in excessive loss of stomach acid. Treatment consists of
fluids, anti-emetics, and management of her electrolyte disorders
6. Mr. Longo is a 18 year-old comatose, quadriplegic patient who has
the following ABG done as part of a medical workup:
pH 7.48
CO2 22
pO2 96
HCO3 16
SaO2 98%

What is your interpretation?

What interventions would be appropriate for Mr. Longo?

6. As a result of his neurologic condition, Mr. Longo has chronic

hyperventilation syndrom. His blood gas shows a fully-compensated
respiratory alkalosis. This is a chronic and stable condition for him and
probably requires no treatment.

7. Mr. Casper is a 55 year-old with GERD. He takes about 15 TUMS

antacid tablets a day. An ABG is obtained to assess his acid/base
pH 7.46
CO2 42
pO2 86
HCO3 29
SaO2 97%

What is your interpretation?

What interventions would be appropriate for Mr. Casper?

7. Mr. Casper has overmedicated himself with TUMS, effectively absorbing

too much stomach acid. His ABG shows a partially-compensated metabolic
alkalosis. Treatment consists of better control of his GERD, possibly with
H2-blockers (Pepcid®) or proton-pump inhibitors (Prilosec®).
8. Mrs. Dobins is found pulseless and not breathing this morning.
After a couple minutes of CPR she responds with a pulse and starts
breathing on her own. A blood gas is obtained:
pH 6.89
CO2 70
pO2 42
HCO3 13
SaO2 50%

What is your interpretation?

What interventions would be appropriate for Mrs. Dobins?

8. Mrs. Dobins has a severe metabolic and respiratory acidosis with

hypoxemia. The metabolic component comes from her decreased perfusion,
and the respiratory component comes from inadequate ventilation.
Treatment would consist of intubation, mechanical ventilation, blood
pressure and circulatory support.

9. After resuscitating Mrs. Dobins, you find Mr. Simmons to be in

respiratory distress. He has a history of Type-I diabetes mellitus and
is now febrile. (Wow, what a bad day). His ABG shows:
pH 7.00
CO2 59
pO2 86
HCO3 14
SaO2 91%

What is your interpretation?

What interventions would be appropriate for Mr. Simmons?

9. Wow, Mr. Simmons too! He, like Mrs. Dobbins, has a metabolic and
respiratory acidosis with hypoxemia. However, the cause is different. His
respiratory acidosis is probably the result of pneumonia (also causing the
fever). His pneumonia has altered his glucose metabolism, causing
hyperglycemia and diabetic ketoacidosis. Treatment should be three-
pronged: 1) increase his oxygenation with oxygen therapy; CPAP, BiPAP,
or mechanical ventilation, 2) treat his pneumonia with antibiotics,
antipyretics, and good pulmonary hygiene, and 3) administer insulin and IV
fluids to decrease his blood glucose and treat his DKA.

10. Ms. Berth was admitted for a drug overdose. She is being
mechanically ventilated and a blood gas is obtained to assess her for
weaning. The results are as follows:
pH 7.54
CO2 19
pO2 100
HCO3 16
SaO2 98%

What is your interpretation?

What interventions would be appropriate for Ms. Berth?

10. Mrs. Berth is being overventilated which caused a partially-compensated

respiratory alkalosis. Treatment would consist of decreasing ventilatory
support, or trying other modes of ventilation to decrease her minute volume.
She will be difficult to wean from the ventilator in this condition due to the
metabolic compensation. Therefore attempts should be made to allow her
CO2 to increase back to normal before weaning can proceed.
Explain the acid-base status of a 35-year-old man admitted to hospital
with pneumonia and the following lab values:


pH 7.52 Na + 145 mEq/L
PaCO2 30 mm Hg K+ 2.9 mEq/L
PaO2 62 mm Hg Cl- 98 mEq/L
CO2 21 mEq/L

His pH and PaCO2 fit into the band of acute respiratory alkalosis. He has
moderate hypoxemia and the blood gas data alone could be explained by
acute hyperventilation due to pneumonia. But the anion gap is elevated at 26
mEq/L, indicating a concomitant metabolic acidosis. The delta anion gap is
14 mEq/L, giving an expected serum CO2 of 13 mEq/L, and a bicarbonate
gap +8 mEq/L. Thus the patient manifests three separate acid-base
disorders: respiratory alkalosis (from pneumonia); metabolic acidosis (from
renal disease); and hypokalemic metabolic alkalosis (from excessive diuretic
therapy). The result of all this acid-base abnormality? Blood gas values that
are indistinguishable from those of simple acute respiratory alkalosis

Clinical Problem 8-3. A 45-year-old man comes to hospital complaining

of dyspnea for three days. Arterial blood gas reveals pH 7.35, PaCO2 60
mm Hg, PaO2 57 mm Hg, HCO3- 31 mEq/L. How would you characterize
his acid-base status?

PaCO2 and HCO3- are elevated, but HCO3- is elevated more than would be
expected from acute respiratory acidosis. Since the patient has been
dyspneic for several days it is fair to assume a chronic acid-base disorder.
Most likely this patient has a chronic or partially compensated respiratory
acidosis. Without electrolyte data and more history, you cannot diagnose
an accompanying metabolic disorder.
Clinical Problem 8-4. A 53-year-old man initially presents to the
emergency department with the following blood gas values:


FIO2 .21
PaO2 40 mm Hg
PaCO2 50 mm Hg
pH 7.51
HCO3- 39 mEq/L

At this point his acid-base disorder is best characterized as:

a) metabolic alkalosis alone

b) metabolic alkalosis plus respiratory acidosis

c) respiratory acidosis with metabolic compensation

d) can't be certain without more information

He is found to have congestive heart failure and is treated with

supplemental oxygen and diuretics. Three days later he is clinically
improved, with pH 7.38, PaCO2 60 mm Hg, HCO3- 34 mEq/L, and PaO2
73 mm Hg (on FIO2 24%). How would you characterize his acid-base
status now?

Here the answer must be d, "can't be certain without more information." If

an acid-base disorder is found (from blood gas, electrolyte data), the next
logical step is to determine the clinical causes(s). Elevated PaCO2, pH and
HCO3- certainly suggest a metabolic alkalosis, but there are other
possibilities. Isolated blood gas values should be viewed as a single point
on a plot that can be arrived at from various pathways, and not as
diagnostic of any particular acid-base disorder. Making a diagnosis of
"metabolic alkalosis" solely on the basis of blood gas values has two
potential pitfalls.
PITFALL 1. It suggests a final diagnosis, which is not the case. There are
several causes of metabolic alkalosis and the clinical reason has to be
found and corrected. Acidosis and alkalosis, with their adjectives
metabolic and respiratory, are analogous to "anemia" or "fever." Acidosis
and alkalosis should always be viewed as manifestations of underlying
clinical problems and never as clinical diagnoses in themselves.

PITFALL 2. The patient may not have metabolic alkalosis or may have
metabolic alkalosis plus another serious acid-base disorder. In fact, this
patient"s initial blood gas values represent several clinical possibilities:
uncomplicated metabolic alkalosis, chronic respiratory acidosis followed
by acute hyperventilation (acute respiratory alkalosis), and respiratory
acidosis complicated by metabolic alkalosis. For example, suppose the
patient's pulmonary function tests and blood gas values were normal one
week earlier and in the interval he had taken diuretics; a primary
metabolic alkalosis would then be the most likely diagnosis. On the other
hand, he could be a patient with chronic CO2 retention, e.g., PaCO2 60
mm Hg and pH 7.41; he then develops pneumonia and hyperventilates,
lowering PaCO2 from 60 to 50 mm Hg and raising pH above normal. This
last situation would reflect a state of chronic respiratory acidosis plus an
acute increase in ventilation (respiratory alkalosis), not a primary
metabolic alkalosis. Thus the patient could have an isolated metabolic
problem, an isolated respiratory problem, or a combination. Only by a
detailed clinical and laboratory history, including previous blood gas data
if available, can the actual cause be determined.

After treatment for congestive heart failure, his baseline arterial blood gas
values reflect a state of chronic respiratory acidosis plus a mild metabolic
alkalosis. In retrospect, his blood gas values on admission were the result
of acute hyperventilation on top of chronic respiratory acidosis.

Clinical Problem 8-5. The following values are found in a 65-year-old

pH 7.51 Na + 155 mEq/L
PaCO2 50 mm Hg K+ 5.5 mEq/L
HCO3- 39 mEq/L Cl- 90 mEq/L
CO2 40 mEq/L
BUN 121 mg/dl
Glucose 77 mg/dl

Which of the following most closely describes this patient's acid-base


a) severe metabolic acidosis

b) severe respiratory acidosis

c) respiratory acidosis plus metabolic alkalosis

d) metabolic alkalosis plus metabolic acidosis

e) respiratory acidosis plus respiratory alkalosis

The answer is d: metabolic alkalosis plus metabolic acidosis. A patient

can have both vomiting (causing metabolic alkalosis) as well as uremia
(causing metabolic acidosis) at the same time. This patient has renal
failure (BUN 121 mg/dl) with the diagnosis of metabolic acidosis
confirmed by the elevated anion gap (25 mEq/L). Despite the AG
acidosis, serum CO2 is elevated at 40 mEq/L (bicarbonate gap is 26
mEq/L) indicating metabolic alkalosis. In this patient alkalosis is the
dominant condition, hence the blood is alkalemic (pH 7.51).

From the information provided one cannot rule out a primary respiratory
acidosis as an additional problem. (After this patient recovered he showed
no evidence of underlying lung disease. Sometimes it requires days or
weeks of follow up to fully characterize acid base disorders.)

Clinical Problem 8-6. A 52-year-old woman has been mechanically

ventilated for two days following a drug overdose. Her arterial blood gas
values and electrolytes, stable for the past 12 hours, show:


pH 7.45 Na + 142 mEq/L
PaCO2 25 mm Hg K+ 4.0 mEq/L
Cl- 100 mEq/L
CO2 18 mEq/L

Based on this information, how would you assess her acid-base status?

This patient's blood gas values suggest a state of chronic respiratory

alkalosis: very low PaCO2, slightly elevated pH. However this assessment
does not indicate a specific diagnosis but only suggests possibilities.
Accurate diagnosis must be made in conjunction with the clinical picture
plus other laboratory studies. Could this patient have a mixed problem
respiratory alkalosis plus metabolic acidosis? Her anion gap is

Na+ - (Cl- + CO2) = 142 - 118 = 24 mEq/L.

The anion gap is elevated and indicates a metabolic acidosis. However,

the acid-base disorder is not just metabolic acidosis since the blood is
alkalemic. There is good evidence she has both metabolic acidosis and
respiratory alkalosis, the latter disorder from excessive mechanical
ventilation. The cause of metabolic acidosis must be looked for since it is
not apparent from the information provided. Since the anion gap is
elevated, the possibilities include lactic acidosis from hypoperfusion and
drug-induced metabolic acidosis.
Clinical Problem 8-7. An 18-year-old college student is admitted to the
ICU for an acute asthma attack, after not responding to treatment received
in the emergency department. ABG values (on room air) show: pH 7.46,
PaCO2 25 mm Hg, HCO3- 17 mEq/L, PaO2 55 mm Hg, SaO2 87%. Her
peak expiratory flow rate is 95 L/min (25% of predicted value).

Asthma medication is continued. Two hours later she becomes more tired
and peak flow is < 60 L/minute. Blood gas values (on 40% oxygen) now
show: pH 7.20, PaCO2 52 mm Hg, HCO3- 20 mEq/L, PaO2 65 mm Hg. At
this point intubation and mechanical ventilation are considered. What is
her acid-base status?

The patient initially had chronic respiratory alkalosis, resulting from

several days of hyperventilation, during which time her kidneys had a
chance to excrete bicarbonate and return the pH toward normal. Now her
asthmatic condition has worsened; she has acutely hypoventilated. The
second set of blood gas values reflects acute respiratory acidosis on top of
a chronic respiratory alkalosis. Although her bicarbonate is low, there is
no primary metabolic process and treatment must be aimed at her
respiratory disorders.

Clinical Problem 8-8. A 72-year-old man is admitted in shock, with 70

mm Hg systolic blood pressure. He has a history of chronic obstructive
pulmonary disease, and his baseline ABG is 7.34, PaCO2 68 mm Hg,
PaO2 65 mm Hg (on supplemental oxygen), HCO3- 36 mEq/L. He takes
medication for a heart condition. Initial arterial blood gas results on
admission (FIO2 .40) show:
pH 7.10
PaO2 35 mm Hg
PaCO2 70 mm Hg
SaO2 58%
HCO3- 21 mEq/L

He is intubated. Repeat blood gases (on the same FIO2) show:


pH 7.30
PaO2 87 mm Hg
PaCO2 40 mm Hg
SaO2 98%
HCO3- 19 mEq/L

Assuming his anion gap is elevated at 23 mEq/L, how would you

described the acid-base changes?

This patient has more than respiratory acidosis because the initial
calculated bicarbonate is low (21 mEq/L). There is a concomitant
metabolic acidosis, confirmed by an elevated anion gap. He has two
causes of metabolic acidosis: shock and severe hypoxemia. After
intubation he is ventilated down to a "normal" PaCO2 of 40 mm Hg, a de
facto respiratory alkalosis, yet remains acidemic because his metabolic
process (lactic acidosis) has not been corrected. The last set of blood gas
values still shows metabolic acidosis and inadequate respiratory
compensation, or what some people would call respiratory acidosis.

NOTE: The terms "respiratory alkalosis" for his change in PaCO2 from 70
mm Hg to 40 mm Hg, and "respiratory acidosis" when his PaCO2 is 40
mm Hg with metabolic acidosis, are technically correct. However, as long
as you understand the changes, and how they came about, it is not
important how they are labeled; you could just as well use
"hyperventilation" instead of "respiratory alkalosis," and "inadequate
respiratory compensation" instead of "respiratory acidosis".
Clinical Problem 8-9. In review, state whether each of the following
statements is true or false.

a) Metabolic acidosis is always present when the measured serum CO2

changes acutely from 24 to 21 mEq/L.

b) In acute respiratory acidosis, bicarbonate initially rises because of the

reaction of CO2 with water and the resultant formation of H2CO3.

c) If pH and PaCO2 are both above normal, the calculated bicarbonate

must also be above normal.

d) An abnormal serum CO2 value always indicates an acid-base disorder

of some type.

e) The compensation for chronic elevation of PaCO2 is renal excretion of


f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of

two or more acid-base disorders.

g) A normal serum CO2 value indicates there is no acid-base disorder.

h) Normal arterial blood gas values rule out the presence of an acid-base

Clinical Problem 8-9.

a) false

b) true

c) true
d) true

e) false

f) true

g) false

h) false