ABG Interpretation
Normal Arterial Blood Gas Values
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PH 7.35-7.45
PaCo2 35-45 mm Hg
PaO2 70-100 mm Hg (depends on age)
SaO2 93-98%
HCo3- 22-26 mEq/L
%MetHg <2%
%COHb <2%
Base Excess -2.0-2.0 mEq/L
CaO2 16-22 ml O2/dl
The Keys to Understanding Arterial
Blood Gases
The determinants of PaCo2 (PaCo2
equation)
 The determinants of the PAo2 and Pao2
(Alveolar gas equation)
 Acid Base Balance (Henderson Hasselbalch
equation)

Determinants of Hypercapnia
PaCo2 is based on the production of Co2
(VCo2) and on alveolar Ventilation (VA)
 Alveolar Ventilation (VA) is defined as
minute ventilation (VE) minus dead space
ventilation (VD)
 PaCo2 = VCo2 x 0.86
or VCo2 x 0.86
VA
VE VD
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Determinants of Hypercapnia

PaCo2 increases with increased production
of Co2
 Hypermetabolism,
malignant hypothermia,
high carbohydrate diet

The decrease in (VA) may be due to a
decrease in minute ventilation (VE) or an
increase in dead space ventilation (VD)
since VA = VE-VD
Determinants of Hypercapnia

Clinical examples of an inadequate minute
ventilation VE leading to hypercapnia
include
 Sedative
Drug Overdose
 Respiratory muscle paralysis
 Central hypoventilation

Examples of increased dead space
ventilation (VD) leading to hypercapnia
include
 COPD
 Severe
restrictive lung disease with rapid shallow
breathing
Dangers of Hypercapnia
An elevated PaCo2 will lower the PaO2
 An elevated PaCo2 will lower the PH and
cause acidemia
 The Higher the baseline PaCo2 the greater
it will rise for a given decrease in Alveolar
Ventilation (VA)

Alveolar Gas Equation (Oxygenation)
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The partial pressure of oxygen in the alveolus
PAo2 is based on:
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Inspired Fio2
Pb ( barometric pressure ) (760 mm hg at sea level)
The water vapor pressure (47mm hg at normal body
temperature)
PACo2 ( equal to the PaCo2/RQ or PaCo2/0.8)
Thus the PAo2 = Fio2 * (Pb-47mmHg)-PaCo2 /
0.8
 In a pt breathing RA
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PAo2 = 150 – PaCo2/ 0.8
Alveolar Gas Equation (Oxygenation)
PAo2 = Fio2 * (Pb – 47) – PaCo2 / 0.8
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The PAo2 decreases with:
 Decreased
inspired Fi02
 Decreased Barometric Pressure (altitude)
 Increased PACo2 or PaCo2
P(A-a) O2
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The partial pressure difference between Alveolar and
arterial O2 is commonly referred to as the A-a gradient
A normal A-a gradient is between 5-25 mm Hg and it
increases with age. Part of this is due to normal
shunting via the thesbian circulation
(Age/4) + 4 estimates the normal A-a gradient for a
given age
An elevated A-a gradient indicates that oxygen is not
adequately transferred from the alveoli to the pulmonary
capillaries
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This usually signifies a lung problem or a cardiac shunt
Causes of a Low PaO2

Non Respiratory Causes
Cardiac R to L Shunt ( increased A-a gradient, does
not respond to increased Fio2)
 Decreased inspired Fio2 or decreased barometric
pressure (normal A-a gradient)
 Low mixed venous O2 saturation ( due to increased
extraction of O2, not usually significant unless there is
also a VQ mismatch or diffusion barrier)
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Respiratory Causes
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Pulmonary R to L Shunt (Increased A-a gradient)
VQ mismatch (Increased A-a gradient)
Diffusion barrier (Increased A-a gradient)
Hypoventilation (Increased PaCo2 with a normal A-a
Acid Base Balance
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Henderson-Hasselbalch Equation
PH = pK + Log
[HCo3-]
.03 [PaCo2]
The 2 determinants of PH are the [HCo3-]
and the [PaCo2]
Acid Base Balance
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The first step in proper ABG interpretation
involves obtaining an accurate history and
physical exam. This will often provide clues to
the prevailing acid-base disorder and can aid in
narrowing the differential diagnosis
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A given set of acid base parameters is never in and of
itself diagnostic
This is especially true for pts with drug
ingestion, vomiting, diarrhea, and diabetes
mellitus.
Verifying the Accuracy of the Data
The components of the Hco3-Co2 system should
always be in equilibrium in the blood
 The PH, PaCo2 and serum HCo3 must be
consistent with the Henderson-Hasselbalch
equation. The HCo3 from the ABG is a
calculated HCo3
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ABG and chemistries should be drawn at the same
time
If the measurements do not fit reasonably well
into these equations an error in one or more of
the values has likely occurred and a repeat ABG
and serum Hco3 should be obtained
Henderson Equation
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The first step in ABG interpretation is
determining internal consistency
[H+] = 24 * PaCo2
[HCo3-]
A [H+] of 40 is equal to a PH of 7.40
For every 1 mmol/L change in the [H+]
the PH inversely changes by .01
Values for PH and corresponding
[H+]
PH
7.55
7.50
7.45
7.40
7.35
7.30
7.25
[H+] (mEq/L)
28
32
35
40
45
50
56
Determining the Serum Anion Gap
The anion gap is the difference between the
unmeasured anions (negatively charged molecules) and
the unmeasured cations (positively charged molecules)
in the serum
 The Concentration of all anions and cations in the serum
must balance
 Therefore: Na + UC = [Cl + HCo3] + UA
 Rearranged UA – UC = Na – [Cl + HCo3]
 Normal in most labs is 10 + or - 2
 Hypoalbuminemia, hyponatremia, and increased [k],
[mg],[ca] and [NH4] may all lower the anion gap.
 A decrease of the serum albumin by 50% can decrease
the anion gap by 5 meq/l.
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Determinants of the Anion Gap
Unmeasured Anions
Unmeasure Cations
Proteins (15 meq/L)
Organic Acids (5 meq/L)
meq/L)
Phosphates (2 meq/L)
Sulfates (1meq/L)
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UA = 23 meq/L
Calcium (5 meq/L)
Potassium (4.5
Anion gap = UA – UC = 12 meq/L
Mg (1.5 meq/L)
UC = 11 meq/L
Determining the Delta Gap
If a serum anion gap is present a Delta
gap should be calculated to evaluate for
an additional metabolic derangement
 The Delta gap can be calculated by the
following equation
 (calculated AG – normal AG) – (Normal
HCo3 – Measured HCo3) Or (Calculated
AG – 12) – (24 – measured HCo3)
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Interpreting the Delta Gap
A normal Delta gap is 0 indicating that the anion
gap metabolic acidosis is the only metabolic
derangement.
 A postive delta gap may indicate the presence of
an additional metabolic alkalosis or a respiratory
acidosis with metabolic compensation
 Conversely a negative delta gap may indicate an
additional metabolic acidosis or a respiratory
alkalosis with metabolic compensation
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Determining the Osmolar Gap
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The Osmolal gap is used to detect the presence of
ingested toxins such as ethylene glycol, methanol or
isopropyl alcohol
These Toxins often cause an increased AG acidosis. The
Osmolal gap is the difference between the measured
osmolality and the calculated osmolality
The calculated osmolality is determined by 2*[Na] +
Serum Glucose/18 + BUN/2.8 +Ethanol/4.5
An Osmolal gap >10mOsm suggests the presence of an
ingested toxin as a contributor to the anion gap acidosis
Simple Acid Base Abnormalities
The term simple acid-base disorder
denotes the presence of a single
abnormality associated with an expected
compensatory response
 The Four simple acid base disorders are
metabolic acidosis, metabolic alkalosis,
respiratory acidosis (both acute and
chronic) and respiratory alkalosis (acute
and chronic)
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Simple Acid Base Disorders
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Metabolic Acidosis – primary disturbance is a
decrease in HCo3 with compensatory
hyperventilation and a decreased PaCo2.
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The Predicted PaCo2 is determined using the Winter’s
equation
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PaCo2 = (1.5 x HCo3) + 8 + or – 2
Any significant deviation from the predicted PaCo2
signifies an additional respiratory disorder
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A PaCo2 higher than predicted signifies an additional
Respiratory Acidosis
A PaCo2 lower than predicted signifies an additional
Respiratory Alkalosis
Simple Acid Base Disorders
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Metabolic Alkalosis – Primary disturbance
is an increase in HCo3 with compensatory
hypoventilation and an increased PaCo2
 Predicted
PaCo2 = (0.7 x HCo3) + 21 + or –
1.5
 Any significant deviation from the predicted
PaCo2 signifies an additional Respiratory
disorder
Simple Acid Base Disorders
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Respiratory Acidosis – primary derangement is
an increased PaCo2 with a compensatory
increase in HCo3.
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In acute resp acidosis for every increase of 10 mm
Hg of PaCo2 the PH should drop by .08.
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In Chronic resp acidosis for every 10 mm Hg rise of
the PaCo2 the PH should drop by .03 as
compensation but not correction
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Increase in [HCo3] = change PaCo2/10 + or - 3
Increase in [HCo3] = 3.5 x change Paco2/10
Changes greater than those predicted signify an
additional metabolic disorder
Simple Acid Base Disorders
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Respiratory Alkalosis – primary derangement is a
decreased PaCo2 with a compensatory decrease
in the HCo3
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For every 10 mm Hg decrease in the PaCo2 the PH
should increase by .08 in an acute disorder
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For every 10 mm Hg decrease in the PaCo2 the PH
should increase by .03 in a chronic disorder
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Decrease in [HCo3] = 2x change in PaCo2/10
Decrese in [HCo3] = 5 x change in the PaCo2/10
Changes greater than those predicted signify an
additional metabolic disorder
Complex Acid Base Disorders
Framework for Metabolic Acidosis
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First as always take a thorough Hx and perform a physical
examination
Next determine the internal consistency of the ABG
Look at the PH. If it is less than 7.35 there is a primary acidosis. If
the HCo3 and PaCo2 are both low it is a primary metabolic acidosis
Calculate the predicted PaCo2 using the Winters equation [PaCo2=
(1.5 x Hco3) +8 + or – 2]. If the PaCo2 is lower than predicted
there is an additional respiratory alkalosis. If the PaCo2 is higher
than predicted there is an additional respiratory acidosis
Calculate the AG. If there is an AG present calculate the Delta gap.
If the Delta gap is 0 there is no additional metabolic derangement.
If there is a + delta gap there may be an additional metabolic
alkalosis. If it is negative there may be an additional non ag
metabolic acidosis
Lastly if there is an AG present with no obvious etiology calculate
the osmolal gap looking for toxic ingestion.
Classification of Metabolic Acidosis
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Increased Anion gap
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Lactic Acidosis
Ketoacidosis (Diabetes, Alcohol, Starvation)
Renal Failure
Toxic Ingestion
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Normal anion gap (Hyperchloremic metabolic Acidosis)
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Salicylates, Methanol, Ethylene Glycol, Paraldehyde, INH
GI loss of HCo3
Renal Loss of HCo3
Renal Tubular Disease
Pharmacological ( Ammonium Chloride, Dilutional, Hyperalimentation)
Urine Anion gap may be used to differentiate GI vs Renal causes of a non
ag metabolic Acidosis
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Urine AG = UA – UC = Na – [K + Cl]
A negative value usually indicates a GI loss of HCo3. A value of zero or a
positive value signifies a renal cause
Metabolic Acidosis
Clinical Signs and Symptoms
Kussmaul’s Respirations – deep and rapid
breathing
 Arrhythmias
 Suppressed myocardial contractility
 R shift of the oxyhemoglobin dissociation
curve
 Hyperkalemia
 Increased protein catabolism
 Insulin resistence
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Metabolic Alkalosis
The primary disturbance in metabolic alkalosis is
an increase in HCo3 or the loss of acid.
 The compensatory respiratory response is a rise
in PaCo2.
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Calculate the predicted PaCo2 using the following
equation: PaCo2= (0.7 x HCo3) +21 + or – 1.5.
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If the PaCo2 is less than predicted there is an additional
respiratory alkalosis. If the PaCo2 is higher than predicted
there is an additional respiratory acidosis.
Metabolic Alkalosis may be Hypovolemic Cldepleted or hypervolemic Cl- expanded
Metabolic Alkalosis
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The etiology of the hypovolemic Cl - depleted form includes:
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The etiology of the hypervolemic Cl-expanded form includes:
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GI loss of H+
Vomiting, Gastric suctioning, Cl- rich diarrhea
Renal loss of H+
Diuretics
Post hypercapnia
High dose carbenicillin
Primary hyperaldosteronism, hypercortisolism
ACTH excess, Hydrocortisone and mineralicorticoid excess
Renin secreting tumor
Hypokalemia, milk-alkali syndrome, Massive blood transfusion
History and Urine Chloride can be helpful in differentiating the two
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Urine Chloride is usually less than 20 in the chloride depleted form and greater
than 20 in the chloride expanded form
Metabolic Alkalosis
Clinical Signs and Symptoms
Tachycardia
 Arrhythmias
 Obtunted mental Status
 Increased risk of seizures
 Decreased cerebral blood flow
 Hypocalcemia
 hypokalemia
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Respiratory Acidosis
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The major disturbance in respiratory acidosis is
ineffective ventilation and or increased production of
Co2.
In acute disorders for every increase of 10 mm Hg in the
PaCo2 the PH decreases by .08.
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If there is a further decrease in the PH there is an additional
metabolic acidosis. Likewise if the PH is higher than predicted
there is likely a metabolic alkalosis.
In chronic respiratory acidosis for every 10 mm Hg
increase of the PaCo2 the PH decreases by .03. Further
changes signify additional metabolic derangements
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The Maximum Renal compensation for chronic respiratory
acidosis is a HCo3 of 45. If the serum HCo3 is greater than 45
there must be an additional metabolic alkalosis
Respiratory Acidosis
Causes, Clinical Signs and Symptoms
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Causes
Airway obstruction, depression of the respiratory
center ( brain injury drugs )
 Increased Co2 production ( hyperthermia,
hypermetabolism, high carbohydrate diet )
 Neuromuscular diseases
 Pulmonary disorders ( obstructive, restrictive,
ARDS/ALI, OHS, Flail chest
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Clinical Signs and Symptoms
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Confusion, HA
Asterixis
Hypertension
Arrhythmias and peripheral vasodilitation
Respiratory Alkalosis
The primary derangement in respiratory alkalosis
is hyperventilation
 The compensatory responses are the same
numerically as they are in respiratory acidosis
although in the opposite directions for both
acute and chronic disorders
 Common causes of respiratory alkalosis are:
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Hypoxia, acute or chronic pulmonary disease
Overstimulation of the respiratory center (sepsis,
pregnancy, liver disease, progesterone, salicylates,
pain, and organic brain disease)
Respiratory Alkalosis
Clinical Signs and Symptoms
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Confusion
Seizures
Parasthesias
Arrhythmias
Muscle cramps
Hypokalemia
Hypophosphatemia
hypocalcemia
Examples # 1
A 28 y/o male presents with 1 day hx of
acute SOB and Diarrhea
 ABG 7.32/24/104/12/99%
 Serum HCo3 23
 What is the Acid base disorder?
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Example # 1
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First step in ABG interpretation is checking
the internal consistency using the
henderson equation
 [H]
= 24 x [PaCo2] / [HCo3]
 [H] = 24 x (24/23) = 25
 The expected PH for a [H] of 25 = 7.55
 The
ABG and serum HCo3 are not internally
consistent. An ABG and serum HCo3 need to
be repeated simultaneously
Example #2
A 72 y/o m with a Pmhx of COPD presents
with sob and AMS. He is intubated in the
ED on arrival and placed on mechanical
ventilation. ABG 1 hr after intubation
reveals PH 7.5 PCo2 50.
 What must The serum HCo3 be in order
for the PH to be internally consistent?
 What is the predominant acid base
disorder
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Example #2
PH 7.5 is equal to a [H] of 30
 30 = 24 x 50/x
 X = 40, so the serum HCo3 must be 40
 The predominant acid base disorder is a
post hypercapnic metabolic alkalosis due
to overventilation in a pt with chronic Co2
retention
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Example #3
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A physically fit 23 y/o f goes jogging.
After 20 minutes of running her RR has
doubled. If an ABG was performed at that
time what would you expect it to show
 A)
normal PCo2 and PH
 B)Low PCo2 and high PH
 C)High PCo2 and low PH
 D)Low PCo2 and low PH
Example # 3
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Answer. Normal PCo2 and normal PH.
During exercise Co2 production increases.
In a physically fit person alveolar
ventilation increases accordingly keeping
PaCo2 and PH in the normal range
 Remember
PaCo2 = VCO2/ VE - VD
Example # 4
A 26 y/o homeless male is admitted to the
ICU with AMS and persitent vomiting
 ABG 7.4 / 38 / 90 / 99%
 Na 149 K 3.8 Cl 100 HCo3 24 BuN 110
 Cr 8.7
 What is ( are ) the acid base disorder(s)
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Example #4
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Upon cursory review there appears to be no acid
base disorder
However there is an AG of 25 upon closer
inspection. 149 – [100 + 24] = 25
The Delta gap [25 – 12] – [24-24] is also + with
a value of 13.
Therefore there is an ag metabolic acidosis and
a metabolic alkalosis
This is likely secondary to uremia + vomiting
Given Ams and renal failure an osmolal gap
should also be calculated
Example #5
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A mountain climber ascends from sea level to 18
K feet over a 2 day period. Supplemental O2 is
not used. Which of the following will not change
A) Fio2
B) barometric pressure
C) PaO2
D) PaCo2
E) PH
Example # 6
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Since the early 1980’s mountain climbers have
climbed Mt Everest without supplemental O2.
How is this possible?
Barometric Pressure at the summit is 253 mm
Hg. Assume a PaCo2 of 40
PAo2 = Fi02 * ( 253 – 47 ) – 40/0.8
PA02 = .21 (206) – 50 = -6.7 ??
If we take into account a nml A-a gradient of 5
the PaO2 is –11.7??
Example # 6
In Fact these climbers profoundly
hyperventilate and have PaCo2 usually <
10 mm Hg. If we plug this into the
Alveolar gas equation we get a PAo2 of
about 35 mm Hg.
 Although this is profoudly low a physically
fit person can survive this, although they
develop dizziness, confusion and SOB
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The END