1) Ein 25-jhriger Diabetiker leidet seit einem Tag an Durchfllen und hat seit

dieser Zeit kein Insulin bekommen. Bei der Aufnahme ist der Blutdruck mit
100/60 mmHg stabil. Der Patient ist tachykard und er hyperventiliert (AF
28/min). Die Krpertemperatur ist normal. Laborchemisch finden sich folgende
Parameter:

Natrium: 135 mmol/l

Kalium: 3,5 mmol/l
Chlorid: 110 mmol/l
Harnstoff: 44 mg/dl
Kreatinin: 1,2 mg/dl
Glukose: 315 mg/dl
pH: 7,25
PaCO2: 20 mmHg
PaO2: 95 mmHg
Bikarbonat: 8 mmol/l
Ketonkrper i.S. nachweisbar

Welche Strung des Sure-Basen-Haushaltes liegt vor?

2) Ein Patient nach sophagusresektion hat einen primr unaufflligen

postoperativen Verlauf. Am 5. postoperativen Tag kommt es zum Auftreten
einer kollaren Anastomoseninsuffizienz, die durch die Anlage eines Drains
versorgt wird. Im Zuge dieses Geschehens entwickelt der Patient einen Ileus.
In den nchsten Tagen werden 1-2 Liter Darmsekret ber die kollare
Anastomosendrainage abgeleitet. Der Patient wird zunehmend verwirrt,
respiratorisch insuffizient und hyperventiliert. Nach Aufnahme auf die
Intensivstation zeigt die Blutgasanalyse folgende Werte:

Natrium: 142 mmol/l

Kalium: 3,4 mmol/l
Chlorid: 121 mmol/l
pH: 7,17
PaCO2: 27 mmHg
PaO2: 62 mmHg
Bikarbonat: 10 mmol/l
Laktat: 21 mg/dl
Natrium im Harn: 20 mmol/l
Kalium im Harn: 80 mmol/l
Chlorid im Harn: 70 mmol/l

Welche Strung des Sure-Basen-Haushaltes liegt vor?

3) Eine 32-jhrige Patientin erleidet ein schweres Polytrauma. Bei Aufnahme

im Schockraum findet sich im Abdomen massiv freie Flssigkeit. Bei der
sofortigen Laparotomie wird eine Leberruptur, sowie ein Mesenterial-einriss
operativ versorgt. Whrend der OP werden 15 Erythrozytenkonzentrate, 10
Fresh Frozen Plasmen und 1 Thrombozytenkonzentrat verabreicht. Die
Versorgung der schweren Extremittenverletzung wird auf die sekundre OP-
Phase verschoben. Bei Aufnahme auf die Intensivstation ist die Patientin
hmodynamisch stabil und bentigt nur eine geringe Kreislaufuntersttzung
mit Phenylephrine. Am Morgen des nchsten Tages zeigt die Blutgasanalyse
der zu diesem Zeitpunkt invasiv beatmeten Patientin folgende Werte:

Natrium: 145 mmol/l

Kalium: 4 mmol/l
Chlorid: 89 mmol/l
pH: 7,51
PaCO2: 37 mmHg
PaO2: 98 mmHg
Bikarbonat: 35 mmol/l
Laktat: 17 mg/dl
Natrium im Harn: 25 mmol/l
Kalium im Harn: 120 mmol/l
Chlorid im Harn: 40 mmol/l

Welche Strung des Sure-Basen-Haushaltes liegt vor?

4) Ein 28-jhriger Patient mit Diabetes Typ I entwickelt belkeit und leidet seit
2 Tagen an protrahiertem Erbrechen. Whrend dieser 2 Tage hatte der
Patient die chronische Insulintherapie pausiert. Die folgenden Laborwerte
wurden bei Aufnahme im Krankenhaus erhoben:

Natrium: 146 mmol/l

Kalium: 3,3 mmol/l
Chlorid: 92 mmol/l
Glukose: 525 mg/dl
Harnstoff: 62 mg/dl
pH: 7,41
PaCO2: 39 mmHg
PaO2: 82 mmHg
Bikarbonat: 24 mmol/l
Ketonkrper im Serum nachweisbar

Liegt eine Strung des Sure-Basen-Haushaltes vor und wenn ja, welche?
LSUNGEN

ad 1) Bei diesem Patienten liegt eine kombinierte metabolische Strung des

Sure-Basen-Haushaltes vor. Erniedrigtes Bikarbonat und erniedrigter pH
zeigen eine metabolische Azidose an. Der Anionengap ist mit 17 mval/l leicht
erhht. Das Bikarbonat ist jedoch um 16 mmol/l erniedrigt. Daraus ergibt sich
ein Delta-Gap von 11 mval/l (Delta-Gap = (17-12) - (24-8). Erwartetes PaCO2
bei reiner metabolischer Azidose = 1,5 x 8 + 8 = 20 mmHg. Die
respiratorische Kompensation ist adquat. Daraus kann geschlossen werden,
dass bei diesem Patienten eine kombinierte metabolische Azidose vorliegt.
Die AG-Azidose beruht auf Ketonkrpern. Zustzlich besteht eine Non-AG
Azidose, die wahrscheinlich durch die anhaltenden Durchflle verursacht
wurde.

ad 2) Bei diesem Patienten liegt eine metabolische Azidose vor. Dies ist
erkennbar an einem erniedrigten pH und einer erniedrigten
Bikarbonatkonzentration. Der Anionengap ist mit 11 mval/l normal. Es handelt
sich also um eine non-Anionengap Azidose. Zur Erhaltung der
Elektroneutralitt finden sich erhhte Serumchloridkonzentrationen
(hyperchlormische metabolische Azidose). Die Anionenlcke im Harn ist
erhht (20+80-70 = 30 mval/l). Dies schliet eine renal tubulre Azidose aus.
Da der Patient weder Kortison, Carboanhydrase-Hemmer noch
Ammoniumchlorid erhalten hat, muss die Azidose durch einen Verlust von
Bikarbonat verursacht sein. Der Bikarbonat-Verlust bei diesem Patienten ist
durch die hohen intestinalen Flssigkeitsverluste ber die sophageale
Anastomoseninsuffizienz erklrbar. Die respiratorische Kompensation ist
aufgrund der klinischen Auswirkungen der metabolischen Azidose nur
inadquat (erwarteter PaCO2: 1,5 x 10 + 8 = 23 mmHg).

ad 3) Bei dieser Patientin liegt eine metabolische Alkalose vor. Dies ist
erkennbar an einem erhhten pH und einer erhhten
Bikarbonatkonzentration. Die Serumchlorid-Konzentration ist kompensatorisch
erniedrigt (hypochlormische metabolische Alkalose). Die wahrscheinlichste
Erklrung fr diese metabolische Alkalose bei dieser Patientin ist die
Massivtransfusion mit hoher Zitratbelastung. Eine respiratorische
Kompensation ist aufgrund der maschinellen Beatmung nicht mglich. Da die
Harn-Chlorid-Konzentration bei 40 mmol/l liegt, handelt es sich sehr
wahrscheinlich um eine Chlorid-insensitive metabolische Alkalose und die
therapeutische Gabe von NaCl ist nicht sinnvoll. Obwohl nicht in groen
Studien belegt, wrden wir an unserer Abteilung bei dieser Patientin eine
Therapie mit Azetazolamid beginnen.
ad 4) Bei diesem Patienten liegt eine kombinierte metabolische Strung vor.
Auf den ersten Blick erscheint die Blutgasanalyse normal. Der Anionengap ist
jedoch mit 30 mval/l erhht und weist auf eine Anionengap-Azidose hin. Eine
solche ist durch die erhhte Ketonkrperkonzentration im Serum durch eine
Ketoazidose erklrbar (pausierte Insulintherapie). Da der Patient gleichzeitig
massiv erbrochen hatte, entwickelte er zustzlich eine metabolische Alkalose.
Aus diesem Grund zeigen sich in der vorliegenden Blutgasanalyse normale
Serumbikarbonatwerte (erniedrigte Konzentration bei Ketoazidose durch
erhhte bei metabolischer Alkalose ausgeglichen) und ein normaler pH. Da
die Bikarbonatkonzentration gesamt nicht verndert ist, kommt es zu keiner
kompensatorischen Vernderung der Serumchloridkonzentration.
Case 3

A previously well 55 year old woman is admitted with a complaint of severe

vomiting for 5 days. Physical examination reveals postural hypotension,
tachycardia, and diminished skin turgor. The laboratory finding include the
following:

Electroyes: Na 140 , K 3.4, Cl 77 HCO3- 9, Cr 2.1

ABG: pH 7.23 , PCO2 22mmHg

Answer (using the step by step approach)

1. History: Based on the clinical scenario, likely acid base disorders in this
patient are:

Elevated anion gap acidosis secondary to lactic acidosis in the setting

of severe persistent vomiting which may lead to hypovolemia, and/or
Metabolic alkalosis in the setting of persistent vomiting

2. Look at the pH.

The pH is low, (less than 7.35) therefore by definition, patient is acidemic.

3. What is the process? Look at the PCO2, HCO3- .

PCO2 and HCO3- are abnormal in the same direction, therefore less
likely a mixed acid base disorder but not yet ruled out.

Again, need to distinguish the initial change from the compensatory response.
A low HCO3- represents acidosis and is consistent with the pH, therefore it
must be the initial change. The low PCO2 must be the compensatory
response. Since the primary change involves HCO3-, this is a metabolic
process, i.e. Metabolic Acidosis.

4. Calculate the anion gap

The anion gap is Na - (Cl + HCO3-) = 134 -(77 + 9) = 48
Since gap is greater than 16, it is therefore abnormal.

5. Is compensation adequate? Calculate the estimated PCO2.

Using Winter's formula; PCO2 = 1.5 [HCO3-]) + 8 2 = 1.5 9 + 8 2 =
19.5 - 23.5.

Since the actual PCO2 falls within the estimated range, we can deduce that
the compensation is adequate and there is no seperate respiratory disorder
present.

6. Since anion gap elevated, calculate the delta-ratio to rule out concurrent
metabolic alkalosis.

Delta ratio = Anion gap = (AG - 12) pppppp= (48- 12) pp= 36 = 2.6
Deppppppppp [HCO3-]pa(24 - [HCO3-])ppppp(24 - 9) pp 14
Since the delta ratio is greater than 2, we can deduce that there is a
concurrent metabolic alkalosis. This is likely due to vomiting.

Another possibility is a pre-existent high HCO3- level due to compensated

respiratory acidosis. But we have no reason to suspect respiratory acidosis
based on the history.

Assessment: Mixed elevated anion gap metabolic acidosis and metabolic

alkalosis likely due to lactic acidosis and vomiting

Case 7

A 50 year old insulin dependent diabetic woman was brought to the ED by

ambulance. She was semi-comatose and had been ill for several days.
Current medication was digoxin and a thiazide diuretic for CHF.
Lab results
Serum chemistry: Na 132, K 2.7, Cl 79, HCO3- 19 Glu 815,
Lactate 0.9 urine ketones 3+
ABG: pH 7.41 PCO2 32 HCO3- 19 pO2 82

What is the acid base disorder?

Answer (using the step by step approach)

1. History: Based on the clinical scenario, possible acid base disorders in this
patient are:

Elevated anion gap acidosis secondary to DKA

Metabolic alkalosis in the setting of thiazide diuretics use.

2. Look at the pH.

Note that the pH is normal which would suggest no acid base disorder. But
remember, pH may be normal in the presence of a mixed acid base disorder.

3. What is the process? Look at the PCO2, HCO3- .

PCO2 is low indicating a possible respiratory alkalosis. The HCO3- is also
low indicating a possible metabolic acidosis. Because the pH is normal, we
are unable to distinguish the initial, primary change from the compensatory
response.

We suspect however that the patient has DKA, and therefore should have a
metabolic acidosis with an anion gap that should be elevated. We can confirm
this by calculating the anion gap.
4. Calculate the anion gap
The anion gap is Na - (Cl + HCO3-) = 132 -(79 + 19) = 34
Since gap is greater than 16, it is therefore abnormal and confirms the
presence of metabolic acidosis.

Why is the pH normal? If the patient has metabolic acidosis, we suspect a low
ph unless there is another process acting to counteract the acidosis, i.e
alkalosis.

5. To rule out a metabolic alkalosis, let us check the delta ratio.

Delta ratio = Anion gap = (AG - 12) pppppp= (34 - 12) pp= 22 = 4.4
Deppppppppp [HCO3-]pa(24 - [HCO3-])ppppp(24 - 19) pp 5

Since the delta ratio is greater than 2, we can deduce that there is a
concurrent metabolic alkalosis. This is likely due to to the use of thiazide
diuretic. Note that DKA is often associated with vomiting, but in this
case;vomiting was not mentioned.

Another possibility is a pre-existent high HCO3- level due to compensated

chonic respiratory acidosis. But we have no reason to suspect chronic
respiratory acidosis based on the history.

Assessment: Mixed elevated anion gap metabolic acidosis and metabolic

alkalosis likely due to DKA and thiazide diuretics.
 Arterial Blood Gas Case Questions and Answers
In the space that follows you will find a series of cases that include arterial blood
gases. Each case is then followed by an explanation of the acid-base status, the
oxygenation status and a summary of the patients clinical picture.

The explanations of the acid-base status utilize the 5-step approach to

interpreting acid-base status that is laid out in the Arterial Blood Gas Primer,
which you can access by clicking here. In some of the cases below, information
is not available to calculate the anion gap or the delta delta. In such cases, you
should focus solely on identifying the primary and compensatory processes.

Case 1:
A 24 year-old woman is found down in Pioneer Square by some
bystanders. The medics are called and, upon arrival, find her with an
oxygen saturation of 88% on room air and pinpoint pupils on exam. She is
brought into the Harborview ER where a room air arterial blood gas is
performed and reveals: pH 7.25, PCO2 60, PO2 65, HCO3- 26, Base Excess 1.
On his chemistry panel, her sodium is 137, chloride 100, bicarbonate 27.

Acid-base status:

The patient has a low pH (acidemia)

The PCO2 is high (respiratory acidosis) and the bicarbonate is at the upper
end of normal. The low pH and high PCO2 imply that the respiratory acidosis
is the primary process
The anion gap is 10 and is, therefore, normal. The patient does not have an
elevated anion gap acidosis.
There is no compensatory process. Although the measured bicarbonate is
just above normal, the base excess of 1 tells us that there is no metabolic
alkalosis
The delta gap is 10 -12 = -2 and the delta-delta is -2 + 27 = 25. There is,
therefore, no metabolic process.
Summary: An acute, uncompensated respiratory acidosis leading to
acidemia.

Alveolar-arterial oxygen difference: The alveolar-arterial difference is 10

mmHg, a normal value, which tells us that her hypoxemia is entirely due to
hypoventilation.

Explanation for the clinical picture: The respiratory acidosis implies that the
patient is hypoventilating. This fact, in combination with the pinpoint pupils
suggests the patient is suffering from an acute narcotic overdose. In this case,
the narcotic is most likely heroin.
Case 2:
A 60 year-old man with amyotrophic lateral sclerosis is brought into clinic
by his family who are concerned that he is more somnolent than normal.
On further history, they report that he has been having problems with
morning headaches and does not feel very refreshed when he wakes up.
An arterial blood gas is performed and reveals: pH 7.37, PCO2 57, PO2 70,
HCO3- 32.

Acid-base status:

The patient has a low pH (acidemia)

The PCO2 is high (respiratory acidosis) and the bicarbonate is high (metabolic
alkalosis). The low pH in combination with the high PCO2 tells us that the
respiratory acidosis is the primary process.
The metabolic alkalosis is the compensatory process.
Summary: A chronic respiratory acidosis with a compensatory metabolic
alkalosis.

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is 9

mmHg, a normal value, which tells us that the hypoxemia is entirely due to
hypoventilation.

Explanation for the clinical picture: The patient has a respiratory acidosis with
a compensatory metabolic alkalosis. The respiratory acidosis tells us that the
patient is hypoventilating while the compensatory metabolic alkalosis tells us that
this is a chronic process. The patient is likely hypoventilating due to progression
of his amyotrophic lateral sclerosis, a neurodegenerative disorder associated
with progressive muscle weakness that eventually involves the muscles of
respiration.

Case 3:
A 65 year-old man is brought into the VA hospital with complaints of severe
nausea and weakness. He has had problems with peptic ulcer disease in
the past and has been having similar pain for the past two weeks. Rather
than see a physician about this, he opted to deal with the problem on his
own and, over the past week, has been drinking significant quantities of
milk and consuming large quantities of TUMS (calcium carbonate). On his
initial laboratory studies, he is found to have a calcium level of 11.5 mg/dL,
a creatinine of 1.4 and bicarbonate of 35. The resident working in the ER
decides to draw a room air arterial blood gas, which reveals: pH 7.45, PCO2
49, PO2 68, HCO3- 34. On his chemistry panel, the sodium is 139, chloride
95, HCO3- 34.
Acid-base status:

The patient has a high pH (alkalemia)

The PCO2 is high (respiratory acidosis) and the bicarbonate is high (metabolic
alkalosis). The high pH and the high bicarbonate tell us that the metabolic
alkalosis is the primary process.
The anion gap is 10. This is a normal value
The respiratory acidosis is the compensatory process
The delta gap is 10 12 = -2. The delta delta is -2 + 34 = 32. This value is
above 26 and tells us that a metabolic alkalosis is present. This is the same
process that was identified in the second step above.
Summary: A primary metabolic alkalosis with respiratory compensation.

Alveolar-arterial oxygen difference: The alveolar-arterial difference is 14

mmHg. This value is mildly elevated but still within the normal range for someone
of this age. This suggests that his hypoxemia is likely due to hypoventilation.

Explanation for the clinical picture: The patient has hypercalcemia and a
metabolic alkalosis. In conjunction with a clinical history of heavy milk and
calcium carbonate consumption, these abnormalities suggest the patient is
suffering from milk-alkali syndrome. In response to metabolic alkaloses, patients
develop hypoventilation. This explains his elevated PCO2 and respiratory
acidosis that, in turn, explains his hypoxemia.

Case 4:
A 45 year-old woman with a history of inhalant abuse presents to the
emergency room complaining of dyspnea. She has an SpO2 of 99% on room
air and is obviously tachypneic on exam with what appears to be
Kussmauls respirations. A room air arterial blood gas is performed and
reveals: pH 6.95, PCO2 9, PO2 128, HCO3- 2. A chemistry panel revealed
sodium of 130, chloride 98, HCO3- 2.

Acid-base status:

The patient has a very low pH (acidemia)

The patient has a low PCO2 (respiratory alkalosis) and a very low bicarbonate
(metabolic acidosis). The low pH in conjunction with the low bicarbonate tells
us that the metabolic acidosis is the primary process
The anion gap is elevated at 30. This tells us that the patient has a primary
elevated anion gap metabolic acidosis.
The respiratory alkalosis is the compensatory process, although in this case,
despite a huge compensatory increase in minute ventilation, the patient still
has a very low pH.
 The delta gap is 30-12 = 18 and the delta-delta is 18 + 2 = 20. Since the
delta-delta is below 22, we know that there is an additional non-gap metabolic
acidosis as well.
Summary: Combined elevated anion gap and non-gap metabolic acidoses
with compensatory respiratory alkalosis.

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is

11 mmHg. This tells us that the patient does not have any shunt or low V/Q areas
and, therefore, likely does not have any pulmonary parenchymal pathology as
the source of her dyspnea. Her PaO2 is actually well above 100 mmHg even
though she is breathing room air at sea-level. This is a result of her extreme
degree of hyperventilation, which leads to a rise in the alveolar PO2.

Explanation for the clinical picture: The patient has concurrent elevated anion
gap and non-gap acidoses with respiratory compensation. The acidoses are so
severe that, despite the high minute ventilation, the pH remains very low. This
patient has a history of inhalant abuse and one of the commonly abused
inhalants, toluene, can present with severe elevated anion gap acidosis with
respiratory compensation. The severe elevated anion gap acidosis is due to
accumulation of one of the main toluene metabolites, hippuric acid.

Case 5:
A 68 year-old man with a history of very severe COPD (FEV1 ~ 1.0L, < 25%
predicted) and chronic carbon dioxide retention (Baseline PCO2 58)
presents to the emergency room complaining of worsening dyspnea and
an increase in the frequency and purulence of his sputum production over
the past 2 days. His oxygen saturation is 78% on room air. Before he is
place on supplemental oxygen, a room air arterial blood gas is drawn and
reveals: pH 7.25, PCO2 68, PO2 48, HCO3- 31.

Acid-base status:

The patient has a low pH (acidemia)

The patient has a high PCO2 (respiratory acidosis) and a high bicarbonate
(metabolic alkalosis). The combination of the low pH and the high PCO2 tells
us that the respiratory acidosis is the primary process.
The metabolic alkalosis is the compensatory process. The pH is still low
despite this metabolic compensation
Summary: Primary respiratory acidosis with compensatory metabolic
alkalosis.

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is

17 mmHg. This value is elevated, suggesting that the hypoxemia is due to either
shunt or areas of low V/Q (the more likely explanation in a patient with COPD)
and cannot be explained by hypoventilation alone.

Explanation for the clinical picture: The patient has very severe COPD and
chronic carbon dioxide retention. As a result, you expect that at baseline, they
will have a chronic respiratory acidosis (his baseline PCO2 was 58) with a
compensatory metabolic alkalosis. In this case, the clinical history suggests the
patient is in an exacerbation. When the patient presents to the ER, his PCO2 is
elevated above his baseline. Because this is an acute change, the bicarbonate
has not had time to adjust and the pH falls. This case is, therefore, an example of
an acute on chronic respiratory acidosis.

Case 6:
A climber is coming down from the summit of Mt. Everest. At an altitude of
8,400 m (PB ~ 272 mmHg), he has a blood gas drawn while breathing
ambient air as part of a research project. The blood gas reveals pH 7.55,
PCO2 12, PO2 30 and HCO3- 10.5.

Acid-base status:

The patient has a high pH (alkalemia)

The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic
acidosis). The high pH in conjunction with the low PCO2 tells us that the
respiratory alkalosis is the primary process.
The metabolic acidosis is the compensatory process
Summary: Primary respiratory alkalosis with metabolic compensation.

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is

only 2.3! When you get to very low barometric pressures and low alveolar
oxygen tensions like the values seen in this case, the alveolar-arterial oxygen
difference can be very small. This is a normal value at this elevation. Hypoxemia
with a normal alveolar-arterial oxygen difference is due to either hypoventilation
or a low inspired PO2. In this particular case, it is the low inspired PO2 that is
responsible for the profound but well-tolerated hypoxemia.

Explanation for the clinical picture: The patient is climbing at extremely high
altitude where the low oxygen tensions in the arterial blood trigger the hypoxic
ventilatory response. This response is, in turn, responsible for the respiratory
alkalosis. As the patient spends increasing time at these high altitudes, metabolic
compensation occurs and allows the ventilatory response to increase even
further in magnitude. It is important to note that the person could not achieve this
degree of minute ventilation on acute exposure to this altitude and, as a result,
would not be able to maintain an adequate PaO2 to support life. It is only with
long periods spent acclimatizing to the environment that the person can achieve
sufficient levels of minute ventilation and maintain adequate levels or
oxygenation.

Case 7:
A 57 year-old woman presents with 2 days of fevers, dyspnea and a cough
productive of rust-colored sputum. Her room air oxygen saturation in the
emergency room is found to be 85% and the intern decides to obtain a
room air arterial blood gas while they are waiting for the chest x-ray to be
done. The blood gas reveals: pH 7.54, PCO2 25, PO2 65, HCO3- 22, Base
excess -1.

Acid-base status:

The patient has a high pH (alkalemia)

The PCO2 is low (respiratory alkalosis). The high pH in conjunction with the
low PCO2 tells us that the respiratory alkalosis is the primary process.
Although the bicarbonate is on the low side, the base excess of -1 tells us that
the patient does not have a metabolic acidosis. The patient, therefore, has not
mounted a compensatory response yet.
Summary: Acute, uncompensated respiratory alkalosis

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is

54 mmHg. This value is elevated and tells us that the patients hypoxemia is due
to either shunt or areas of low V/Q

Explanation for the clinical picture: The patient has a history suggestive of
pneumonia. The pneumonia has led to areas of shunt and/or low V/Q that have
led to her arterial hypoxemia. The arterial hypoxemia will, in turn, lead to the
hypoxic ventilatory response that is responsible for her hyperventilation and
respiratory alkalosis. Because the hypoxemia may have only been present for a
short time, there has not been adequate time for metabolic compensation to
occur.

Case 8:
A 47 year-old man with a history of heavy alcohol use presents with a two-
day history of severe abdominal pain, nausea and vomiting. On exam, his
blood pressure is 90/50 and he is markedly tender in his epigastrum. His
initial laboratory studies reveal a sodium of 132, chloride 92, HCO3- 16,
creatinine 1.5, amylase 400 and lipase 250. A room air arterial blood gas is
drawn and reveals pH 7.28, PCO2 34, PO2 88, HCO3- 16.

Acid-base status:
 The patient has a low pH (acidemia)
The PCO2 is low (respiratory alkalosis) and the bicarbonate is low (metabolic
acidosis). The combination of the low pH and the low bicarbonate tells us that
the metabolic acidosis is the primary process
The anion gap is elevated at 24. This tells us that the patient has a primary
elevated anion gap metabolic acidosis
The respiratory alkalosis is the compensatory process
The delta gap is 24-12 = 12. The delta delta is 12 + 17 = 29. Because the
delta-delta is greater than 26, we know that the patient has a concurrent
metabolic alkalosis.
Summary: Primary elevated anion gap metabolic acidosis with respiratory
compensation and a concurrent metabolic alkalosis.

Alveolar-arterial oxygen difference: The alveolar-arterial oxygen difference is

27. This suggests that the patients hypoxemia is due to either shunt or areas of
low V/Q.

Explanation for the clinical picture: A history of epigastric pain, nausea and
vomiting in conjunction with elevated lipase and amylase on laboratory studies is
consistent with the diagnosis of pancreatitis. As a result of the pancreatitis, the
patient has developed an elevated anion gap acidosis with respiratory
compensation. The concurrent metabolic alkalosis is likely due to vomiting, which
leads to hydrogen ion loss via the upper gastrointestinal tract.