Transcript Document

You Can’t Learn Blood
Gases from a Lecture!
Lawrence Martin, M.D.
Clinical Professor of Medicine
Case Western Reserve University School of Medicine, Cleveland
[email protected]
April 1, 2010
7/16/2015
1
Blood Gas Interpretation
means analyzing the data to determine patient’s state of:
Ventilation
Oxygenation
Acid-Base
You can’t learn this from a lecture!
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2
To interpret ABGs you need to look at all the
relevant data
To interpret ABGs you need to look at all the
relevant data
From the blood gas machine
PaCO2
PaO2
pH
HCO3
From the Co-oximeter
SaO2
CoHb
MetHb
To interpret ABGs you need to look at all the
relevant data
From the blood gas machine
PaCO2
PaO2
pH
HCO3
From the Co-oximeter
SaO2
CoHb
MetHb
From venous blood
Na+
K+
ClHCO3BUN
Creatinine
Hgb
To interpret ABGs you need to look at all the
relevant data
From the blood gas machine
PaCO2
PaO2
pH
HCO3
From the Co-oximeter
SaO2
CoHb
MetHb
From venous blood
From the environment
Na+
K+
ClHCO3BUN
Creatinine
FIO2
Barometric pressure
Hgb
To interpret ABGs you need to look at all the
relevant data
From the blood gas machine
PaCO2
PaO2
pH
HCO3
From the Co-oximeter
SaO2
CoHb
MetHb
And not least, the patient
Mental status
Resp. rate & effort
Ventilator settings (if intubated)
Pulmonary & ABG history
From venous blood
From the environment
Na+
K+
ClHCO3BUN
Creatinine
FIO2
Barometric pressure
Hgb
To interpret ABGs you need to look at all the
relevant data
From the blood gas machine
PaCO2
PaO2
pH
HCO3
From the Co-oximeter
SaO2
CoHb
MetHb
And not least, the patient
Mental status
Resp. rate & effort
Ventilator settings (if intubated)
Pulmonary & ABG history
From venous blood
From the environment
Na+
K+
ClHCO3BUN
Creatinine
FIO2
Barometric pressure
Hgb
7 arterial blood gas values
7 venous blood values
2 environmental values
Several patient variables
Lots of variables…how to figure it all out?
Give a man a fish and you
feed him for a day. Teach a
man to fish and you feed him
for a lifetime.
Chinese Proverb
What does this have to do with
blood gas interpretation?
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Just this. You need a framework, a
foundation to properly learn ABG
interpretation. If I tell you how to interpret
a given blood gas, you will understand that
blood gas only, and not the next one you
may encounter. Much better if I show you
an approach to interpreting all blood gases,
in all situations, so that you understand
them. But…
…like any other skill based on interpreting a large number of
variables (EKG, chest x-ray, physical exam), You Can’t Learn
Blood Gases from a Lecture.
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The best way to learn ABGs is to work on blood gas problems with some
knowledge of basic physiology, then check your work for instant
feedback. This ‘iterative process’ will teach you blood gas interpretation.
Books
Web sites
You Can’t Learn Arterial Blood Gases from a Lecture
You CAN learn ABGs from selected web sites.
See list at:
www.lakesidepress.com/ABGindex.htm
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The Key to Blood Gas Interpretation:
4 Equations, 3 Physiologic Processes
These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide
the basic foundation for understanding blood gas interpretation.
Equation
Physiologic Process
1)
Alveolar ventilation
PaCO2 equation
PaCO2 =
2)
VCO2 x 0.863
--------------VA
Alveolar gas equation
Oxygenation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
3)
Oxygen content equation
Oxygenation
CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma
CaO2 = (Hb x 1.34 x SaO2)
3)
+
Henderson-Hasselbalch equation
(.003 x PaO2)
Acid-base balance
HCO3pH ~ -------PaCO2
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Start with PaCO2. PaCO2 is the center of the blood gas
universe.
pH
PaO2
PaCO2
HCO3
SaO2
PaCO2 equation: PaCO2 reflects ratio of metabolic CO2
production (VCO2) to alveolar ventilation (VA) -- there is
nothing ‘clinical’ in the equation except respiratory rate (f)
PaCO2 =
VCO2 x 0.863
----------VA
VCO2 = CO2 production
VA = VE – VD
= f (tidal volume) – f (dead space volume)
0.863 converts units to mm Hg
PaCO2
35 - 45 mm Hg
Condition
in blood (PaCO2)
Eucapnia
State of
alveolar ventilation
Normal ventilation
200 ml/min x 0.863
40 mmHg = ------------------------4.3 L/min
>45 mm Hg
Hypercapnia
Hypoventilation
200 ml/min x 0.863
80 mmHg = ------------------------2.15 L/min
<35 mm Hg
Hypocapnia
Hyperventilation
200 ml/min x 0.863
20 mmHg = -------------------------8.6 L/min
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Hypercapnia
A serious respiratory problem
VCO2 x 0.863
PaCO2 =
-------------
VA
where VA = VE – VD
= f (tidal vol.) – f (dead space vol.)
•
The PaCO2 equation shows that the only physiologic reason for elevated PaCO2 is inadequate alveolar ventilation
(VA) for the amount of CO2 production (VCO2). Since VA = VE – VD, hypercapnia can arise from insufficient VE (eg,
drug overdose), increased VD (eg, COPD), or a combination.
•
The PaCO2 equation also shows why PaCO2 cannot reliably be assessed clinically. Since you never know the patient's
VCO2 or VA, you cannot determine the VCO2/VA, which is what PaCO2 provides. (Even if tidal volume is measured,
you can’t determine the amount of air going to dead space.)
•
There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible respiratory
disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional change in PaCO2. A
patient in respiratory distress can have a high, normal, or low PaCO2. A patient without respiratory distress can have
a high, normal, or low PaCO2.
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PaCO2 and alveolar ventilation
A 60 yo man with severe chronic obstructive pulmonary disease is
seen in the ED, anxious and tachypneic with RR=30/minute.
The intern (who didn’t attend this lecture) says “he’s
hyperventilating” and wants to give him Xanax. You, being
wiser (since you attended), know better and demand a blood
gas. Blood gas shows:
PaCO2 = 85 mm Hg (severe hypo ventilation)
pH = 7.23
Explain tachypnea and hypoventilation in this patient.
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PaCO2 and alveolar ventilation
60 yo man
PaCO2 = 85 mm Hg
pH = 7.23
PaCO2 =
VCO2 x 0.863
------------VA
where VA = VE – VD
= f (tidal volume) – f (dead space volume)
Clinically all you know is this patient’s resp. rate, the “f” in the PaCO2 equation. You don’t know his
tidal volume, dead space volume or CO2 production, i.e., you don’t know the numerator or denominator
of the equation. Thus by exam alone, you cannot know even if he’s hypo- or hyper- ventilating. The
blood gas shows he’s hypoventilating. Though tachypneic, MOST OF EACH BREATH IS GOING TO
DEAD SPACE, NOT TO FUNCTIONING ALVEOLI!
There is no predictable correlation between PaCO2 and the clinical picture. In a patient with possible
respiratory disease, respiratory rate, depth, and effort cannot be reliably used to predict even a directional
change in PaCO2.
A patient in respiratory distress can have a high, normal, or low PaCO2.
A patient without respiratory distress can have a high, normal, or low
PaCO2.
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Hyperventilating? Hypoventilating? Normal ventilation?
PaCO2 =
VCO2 x 0.863
----------------VA
where VA = VE – VD
= f (tidal volume) – f (dead space volume)
PaCO2 is the center of the blood gas
universe. Understanding PaCO2 facilitates
understanding oxygenation & acid-base
balance.
PaCO2
Oxygenation
Acid-Base
PAO2 = FIO2 (BP-47) – 1.2 (PCO2)
HCO3-
pH ~
-----------PaCO2
PaO2
PaCO2 =
VCO2 x .863
-------------------VA
where VA = VE – VD
= f (tidal volume) – f (dead space volume)
Note:
PaCO2 is from ABGs. HCO3- is calculated from ABG measurement of pH and PaCO2 or
is measured in venous blood (serum) as part of electrolytes. When measured in
venous blood it is variously labeled ‘bicarbonate’, ‘HCO3- ’ or ‘CO2’ (the latter NOT to
be confused with PaCO2).
Arterial blood – blood gases
Venous blood - electrolytes
The Key to Blood Gas Interpretation:
4 Equations, 3 Physiologic Processes
These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide
the basic foundation for understanding blood gas interpretation.
Equation
Physiologic Process
1)
Alveolar ventilation
PaCO2 equation
PaCO2 =
2)
VCO2 x 0.863
--------------VA
Alveolar gas equation
Oxygenation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
3)
Oxygen content equation
Oxygenation
CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma
CaO2 = (Hb x 1.34 x SaO2)
3)
+
Henderson-Hasselbalch equation
(.003 x PaO2)
Acid-base balance
HCO3pH ~ -------PaCO2
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Alveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)
PAO2 is the average alveolar PO2
PIO2 is the partial
of) inspired oxygen in the trachea.
PAO pressure
= PIO - 1.2 (PaCO
2
2
2
PAO2 = PIO2 - 1.2 (PaCO2)
PIO2 = FIO2 (PB – 47 mm Hg) = 0.21 (760-47) =PIO
150
mm Hg
= FIO (P - 47).
where
2
2
B
Breathing room air at sea level,
PAO2 = 150 – 1.2 (40) = 150 - 48 = 102 mm Hg
Note: FIO2 is fraction of inspired oxygen and PB is the barometric pressure. 47 mm Hg is the water
vapor pressure at normal body temperature. This is the ‘abbreviated version’ of the AG equation,
suitable for clinical purposes.
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Alveolar Gas Equation
PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2)
In order to bring O2 into the blood, alveolar PO2 (PAO2) has to
always exceed arterial PO2 (PaO2). Whenever PAO2 decreases,
PaO2 decreases as well. Thus, from the AG equation:
• If FIO2 and PB are constant (i.e., constant PIO2), then as PaCO2 increases
both PAO2 and PaO2 will decrease: hypercapnia causes hypoxemia.
• If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will
decrease: suffocation causes hypoxemia.
• If PB decreases (e.g., with altitude), and PaCO2 and
FIO2 are constant, both PAO2 and PaO2 will
decrease: mountain climbing causes hypoxemia.
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See web site: “Blood Gases on Mt. Everest”
www.lakesidepress.com/pulmonary/MtEverest/bloodgases.htm.
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Alveolar Gas Equation
PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2)
What is the alveolar PO2 (PAO2) at sea level* in the following
circumstances?
a) FIO2 = .21, PaCO2 = 20 mm Hg
ANSWER: PAO2 = .21(713) - 1.2(20) = 126 mm Hg
b) FIO2 = .21, PaCO2 = 60 mm Hg
ANSWER: PAO2 = .21(713) - 1.2(60) = 72 mm Hg
c) FIO2 = .40, PaCO2 = 30 mm Hg
ANSWER: PAO2 = .40(713) – (1.2)30 = 249 mm Hg
*BP = 760 mm Hg
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P(A-a)O2
•
•
•
•
•
P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called
the “A-a gradient,” though it does not actually result from an O2 pressure gradient in the lungs.
Instead, it results normal ventilation-perfusion imbalance in the lungs (normal “venous
admixture,” about 3% of cardiac output).
PAO2 is always calculated, based on FIO2, PaCO2 and barometric pressure.
PAO2 = FIO2 (PB – 47 mm Hg) – 1.2(PaCO2)
PaO2 is always measured, on an arterial blood sample in the ‘blood gas machine’.
Normal P(A-a)O2 ranges from @ 5 to 25 mm Hg breathing room air (it increases with age and
with FIO2). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen
properly from alveoli into the pulmonary capillaries. Except for right to left cardiac shunts, an
elevated P(A-a)O2 signifies some sort of problem within the lungs that has caused ventilationperfusion imbalance (increase over the normal venous admixture).
Virtually all lung disease lowers PaO2
via the mechanism of increased V-Q
imbalance, e.g., COPD, pneumonia,
atelectasis, pulmonary edema.
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P(A-a)O2
Alveolar PO2 *
PaO2* *
P(A-a)O2*
a)
FIO2 = .21, PaCO2 = 20 mm Hg
PAO2 = .21(713) - 1.2(20) = 126 mm Hg
112 mm Hg
14 mm Hg (nl.)
b)
FIO2 = .21, PaCO2 = 60 mm Hg
PAO2 = .21(713) - 1.2(60) = 72 mm Hg
62 mm Hg
10 mm Hg (nl.)
c)
FIO2 = .40, PaCO2 = 30 mm Hg
PAO2 = .40(713) – (1.2)30 = 249 mm Hg
129 mm Hg
120 mm Hg
* Always a calculation
** Always a measurement
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P(A-a)O2: Test your
understanding
Calculate P(A-a)O2 using the alveolar gas equation (assume PB = 760 mm Hg).
a)
A 28 yo woman with PaCO2 30 mm Hg, PaO2 88 mm Hg, FIO2 0.21.
PAO2 = .21 (760 - 47) - 1.2(30) = 150 - 36 = 114 mm Hg; P(A-a)O2 = 114 - 88 = 26 mm Hg
The P(A-a)O is elevated. This means the PaO2 is lower than expected for this degree of hyperventilation,
indicating a gas-exchange problem. The patient was diagnosed with pulmonary embolism.
b)
A 22 yo anxious man with PaCO2 15 mm Hg, PaO2 120 mm Hg, FIO2 0.21.
PAO2 = .21(760 – 47) - 1.2(15) = 150 - 18 = 132 mm Hg; P(A-a)O2 = 132 - 120 = 12 mm Hg
The patient had anxiety-hyperventilation syndrome. Hyperventilation can easily raise PaO2 > 100 mm Hg
when the lungs are normal, as in this case.
c)
A 54 yo woman with PaCO2 75 mm Hg, PaO2 95 mm Hg, FIO2 0.28.
PAO2 = .28(760 - 47) - 1.2(75) = 200 - 90 = 110 mm Hg; P(A-a)O2 = 110 - 95 = 15 mm Hg
Despite severe hypoventilation, there is no evidence here for lung disease. Hypercapnia
is most likely a result of disease elsewhere in the respiratory system, either the central nervous system or
chest bellows.
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The Key to Blood Gas Interpretation:
4 Equations, 3 Physiologic Processes
These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide
the basic foundation for understanding blood gas interpretation.
Equation
Physiologic Process
1)
Alveolar ventilation
PaCO2 equation
PaCO2 =
2)
VCO2 x 0.863
--------------VA
Alveolar gas equation
Oxygenation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
3)
Oxygen content equation
Oxygenation
CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma
CaO2 = (Hb x 1.34 x SaO2)
3)
+
Henderson-Hasselbalch equation
(.003 x PaO2)
Acid-base balance
HCO3pH ~ -------PaCO2
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SaO2 and oxygen content
•
Tissues need a requisite amount of oxygen molecules for metabolism. Neither the
PaO2 nor the SaO2 tells how much oxygen is in the blood. How much is provided by
the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as:
CaO2 = quantity O2 bound +
to hemoglobin
quantity O2 dissolved
in plasma
CaO2 = (Hb x 1.34 x SaO2) +
(.003 x PaO2)
CaO2 = 15 x 1.34 x .98
CaO2 =
19.7
(.003 x 100)
0.3
+
+
= 20 ml O2/dl blood
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of
hemoglobin with oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.
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Oxygen dissociation curve: SaO2 vs. PaO2
Also shown are CaO2 vs. PaO2 for two different hemoglobin contents: 15 gm% and 10 gm%.
CaO2 units are ml O2/dl. P50 is the PaO2 at which SaO2 = 50%.
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How much oxygen is in the blood?
PaO2 vs. SaO2 vs. CaO2
OXYGEN PRESSURE: PaO2
•
Since PaO2 reflects only free oxygen molecules dissolved in
plasma and not those bound to hemoglobin, PaO2 cannot tell us
“how much” oxygen is in the blood; for that you need to know
how much oxygen is also bound to hemoglobin, information
given by the SaO2 and hemoglobin content.
OXYGEN SATURATION: SaO2
•
The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen
saturation (in arterial blood, the SaO2). Note that SaO2 alone doesn’t reveal how much oxygen is in the
blood; for that we also need to know the hemoglobin content.
OXYGEN CONTENT: CaO2
•
Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide
information on the number of oxygen molecules, i.e., how much oxygen is in the blood. (Neither PaO2 nor
SaO2 have units that denote any quantity.) Only CaO2 (units ml O2/dl) tells how much oxygen is in the
blood; this is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content can
be measured directly or calculated by the oxygen content equation:
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
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See: “The Differences Between PaO2, SaO2 and Oxygen
Content”
www.lakesidepress.com/pulmonary/ABG/PO2.htm
31
SaO2 and CaO2
Which patient, (a) or (b), is more hypoxemic?
(a) Hb 15 gm%, PaO2 65 mm Hg, SaO2=88%
(b) Hb 10 gm %, PaO2 100 mm Hg, SaO2=98%
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SaO2 and CaO2
Which patient, (a) or (b), is more hypoxemic?
(a) Hb 15 gm%, PaO2 65 mm Hg, SaO2=88%
(b) Hb 10 gm %, PaO2 100 mm Hg, SaO2=98%
ANSWER: (b)
(a) CaO2 = .88 x 15 x 1.34 = 17.6 ml O2/dl + dissolved O2
(b) CaO2 = .98 x 10 x 1.34 = 13.1 ml O2/dl + dissolved O2
Oxygen content determines hypoxemia. Patient (b) has a much lower oxygen content and so is more
hypoxemic than (a). Note that PaO2 is not a significant factor in determining oxygen content
and (for this question) can be ignored. Note that the low PaO2 in patient (a) means there is an
oxygen transfer problem from air to blood, but in terms of what the body really needs –
OXYGEN CONTENT – patient (b) is definitely more hypoxemic.
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The Key to Blood Gas Interpretation:
4 Equations, 3 Physiologic Processes
These 4 equations, crucial to understanding and interpreting arterial blood gas data, provide
the basic foundation for understanding blood gas interpretation.
Equation
Physiologic Process
1)
Alveolar ventilation
PaCO2 equation
PaCO2 =
2)
VCO2 x 0.863
--------------VA
Alveolar gas equation
Oxygenation
PAO2 = PIO2 - 1.2 (PaCO2)
where PIO2 = FIO2 (PB – 47 mm Hg)
3)
Oxygen content equation
Oxygenation
CaO2 = quantity O2 bound to Hb + quantity O2 dissolved in plasma
CaO2 = (Hb x 1.34 x SaO2)
3)
+
Henderson-Hasselbalch equation
(.003 x PaO2)
Acid-base balance
HCO3pH ~ -------PaCO2
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<>
ACID-BASE:
traditionally the most difficult
of the 3 physiologic
processes
•
•
•
•
•
•
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Acidemia: blood pH < 7.35
Acidosis: a primary physiologic process that,
occurring alone, tends to cause acidemia,
Alkalemia: blood pH > 7.45
Alkalosis: a primary physiologic process that,
occurring alone, tends to cause alkalemia.
Primary acid-base disorder: One of the four acidbase disturbances manifested by an initial change in
HCO3- or PaCO2. They are:
metabolic acidosis (MAc)
metabolic alkalosis (MAlk)
respiratory acidosis (RAc)
respiratory alkalosis (Ralk)
Compensation: The change in HCO3- or PaCO2 that
results from the primary event. Compensatory
changes are not classified by the terms used for the
four primary acid-base disturbances.
For example, a patient who hyperventilates (lowers
PaCO2) solely as compensation for MAc does
not have a RAlk, the latter being a primary
disorder that, alone, would lead to alkalemia.
In simple, uncomplicated MAc the patient will
never develop alkalemia.
35
Primary acid-base disorders: Respiratory alkalosis
• Respiratory alkalosis - A primary disorder where the first change is a
lowering of PaCO2, resulting in an elevated pH. Compensation
(bringing the pH back down toward normal) is a secondary lowering
of bicarbonate (HCO3) by the kidneys; this reduction in HCO3- is not
metabolic acidosis, since it is not a primary process.
Primary Event
HCO38pH ~ )))))
9PaCO2
Compensatory Event
9HCO3-
8
pH ~ )))))
9PaCO2
RESPIRATORY ALKALOSIS 9PaCO2 & 8 pH
Hypoxemia (includes altitude)
Anxiety
Sepsis
Any acute pulmonary insult, e.g., pneumonia, mild
asthma attack, early pulmonary edema, pulmonary
embolism
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Primary acid-base disorders: Respiratory acidosis
• Respiratory acidosis - A primary disorder where the first change is an
elevation of PaCO2, resulting in decreased pH. Compensation (bringing pH
back up toward normal) is a secondary retention of bicarbonate by the
kidneys; this elevation of HCO3- is not metabolic alkalosis, since it is not a
primary process.
Primary Event
HCO39pH ~ )))))
8PaCO2
Compensatory Event
HCO39pH ~ )))))
8PaCO2
8
RESPIRATORY ACIDOSIS
8PaCO2 & 9pH
Central nervous system depression (e.g., drug overdose)
Chest bellows dysfunction (e.g., Guillain-Barré syndrome,
myasthenia gravis) Disease of lungs and/or upper
airway (e.g., chronic obstructive lung disease, severe
asthma attack, severe pulmonary edema)
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Primary acid-base disorders: Metabolic acidosis
• Metabolic Acidosis - A primary acid-base disorder where the first
change is a lowering of HCO3-, resulting in decreased pH.
Compensation (bringing pH back up toward normal) is a secondary
hyperventilation; this lowering of PaCO2 is not respiratory alkalosis,
since it is not a primary process.
Primary Event
9pH 
7/16/2015
Compensatory Event
9HCO3)))))
PaCO2
)))))
9HCO39pH

9PaCO2
AG = Na+ - (Cl- + HCO3); nl = 12 +/- 4
METABOLIC ACIDOSIS 9HCO3- & 9pH
Increased anion gap (>16 mEq/L)
lactic acidosis; ketoacidosis; drug
poisonings (e.g., aspirin, ethyelene
glycol, methanol)
Normal anion gap (<= 16 mEq/L)
diarrhea; some kidney problems, e.g.,
renal tubular acidosis, intersititial
nephritis
38
Primary acid-base disorders: Metabolic alkalosis
• Metabolic alkalosis - A primary acid-base disorder where the first change is
an elevation of HCO3-, resulting in increased pH. Compensation is a
secondary hypoventilation (increased PaCO2) which is not respiratory
acidosis, since it is not a primary process. Compensation for metabolic
alkalosis (attempting to bring pH back down toward normal) is less
predictable than for the other three acid-base disorders.
Primary Event
8pH 
Compensatory Event
8HCO3-
)))))
PaCO2
8HCO38pH
 )))))
8PaCO2
METABOLIC ALKALOSIS 8HCO3- & 8pH
• Chloride responsive (responds to NaCl or KCl therapy):
contraction alkalosis, diuretics; corticosteroids; gastric
suctioning; vomiting
• Chloride resistant: any hyperaldosterone state, e.g.,
Cushings’s syndrome; Bartter’s syndrome; severe K+ depletion
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Mixed Acid-base disorders are
common
• In chronically ill respiratory patients, mixed disorders
are probably more common than single disorders, e.g.,
RAc + MAlk, RAc + Mac, RAlk + MAlk.
• In renal failure (and other conditions) combined MAlk
+ MAc is also encountered. pH 7.40, PaCO2=40 mm
Hg, HCO3- = 24 mEq/L, AG=24 mEq/L
• In sepsis patients, MAc + Ralk is common. pH 7.40,
PCO2=20 mm Hg, HCO3- = 12 mEq/L
• Always be on lookout for mixed acid-base disorders.
They can be missed!
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Tips to diagnosing mixed
acid-base disorders
TIP 1. Don’t interpret any blood gas data
for acid-base diagnosis without closely
examining the venous electrolytes: Na+,
K+, Cl- and HCO3-.
•
•
•
•
A venous HCO3- out of the normal range always represents
some type of acid-base disorder (barring lab or transcription
error).
High venous HCO3- indicates metabolic alkalosis &/or
bicarbonate retention as compensation for respiratory acidosis
Low venous HCO3- indicates metabolic acidosis &/or
bicarbonate excretion as compensation for respiratory alkalosis
Note that venous HCO3- may be normal in the presence of
two or more acid-base disorders.
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Tips to diagnosing mixed acid-base disorders
(cont.)
TIP 2 . Single acid-base disorders do not lead
to normal blood pH. Although pH can end
up in the normal range (7.35 - 7.45) with a
mild single disorder, a truly normal pH with
distinctly abnormal HCO3- and PaCO2
invariably suggests two or more primary
disorders.
• Example: pH 7.40, PaCO2 20 mm Hg,
HCO3- 12 mEq/L, in a patient with sepsis.
Normal pH results from two co-existing and
unstable acid-base disorders: acute
respiratory alkalosis and metabolic acidosis.
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Tips to diagnosing mixed acid-base
disorders (cont.)
TIP 3. Simplified rules predict the pH and HCO3- for a given change in
PaCO2. If the pH or HCO3- is higher or lower than expected for the
change in PaCO2, the patient probably has a metabolic acid-base
disorder as well.
Below are expected changes in pH and HCO3- (in mEq/L) for a 10 mm
Hg change in PaCO2 resulting from either primary hypoventilation
(respiratory acidosis) or primary hyperventilation (respiratory
alkalosis).
ACUTE
CHRONIC
• Resp Acidosis
– pH 9 by 0.07 pH 9 by 0.03
– HCO3- 8 by 1*HCO3- 8 by 3-4
• Resp Alkalosis
– pH 8 by 0.08 pH 8 by 0.03
– HCO3- 9 by 2 HCO3- 9 by 5
*Units for HCO3- are mEq/L
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Predicted changes in HCO3- for a directional change in
PaCO2 can help uncover mixed acid-base disorders.
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a)
A normal or slightly low HCO3- in the presence of
hypercapnia suggests a concomitant metabolic acidosis,
e.g.,
pH 7.27, PaCO2 50 mm Hg, HCO3- 22 mEq/L.
Based on the rule for increase in HCO3- with
hypercapnia, it should be at least 25 mEq/L in this
example; that it is only 22 mEq/L suggests a concomitant
metabolic acidosis.
b)
A normal or slightly elevated HCO3- in the presence of
hypocapnia suggests a concomitant metabolic alkalosis,
e.g.,
pH 7.56, PaCO2 30 mm Hg, HCO3- 26 mEq/L.
Based on the rule for decrease in HCO3 with hypocapnia,
it should be at least 23 mEq/L in this example; that it is
26 mEq/L suggests a concomitant metabolic alkalosis.
44
Tips to diagnosing mixed acid-base
disorders (cont.)
TIP 4. In maximally-compensated metabolic
acidosis, the numerical value of PaCO2 should be
the same (or close to) the last two digits of arterial
pH. This observation reflects the formula for
expected respiratory compensation in metabolic
acidosis:
Expected PaCO2 = [1.5 x venous HCO3] + (8 ± 2)
• In contrast, compensation for metabolic alkalosis
(by increase in PaCO2) is highly variable, and in
some cases there may be no or minimal
compensation.
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Acid-base disorders: test your
understanding
A patient’s arterial blood gas shows pH of 7.14, PaCO2 of 70 mm Hg,
and HCO3- of 23 mEq/L. How would you describe the likely
acid-base disorder(s)?
Acute elevation of PaCO2 leads to reduced pH, i.e., an acute respiratory
acidosis. However, is the problem only acute respiratory acidosis or is
there some additional process? For every 10 mm Hg rise in PaCO2
(before any renal compensation), pH falls about 0.07 units. Because this
patient's pH is down 0.26, or 0.05 more than expected for a 30 mm Hg
increase in PaCO2, there must be an additional, metabolic problem. Also,
note that with acute CO2 retention of this degree, the HCO3- should be elevated 3
mEq/L. Thus a low-normal HCO3- with increased PaCO2 is another way to
uncover an additional, metabolic disorder. Decreased perfusion leading to mild
lactic acidosis would explain the metabolic component.
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Acid-base disorders: test your
understanding
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 compensated
respiratory acidosis. Without electrolyte data and more
history, you cannot diagnose an accompanying metabolic
disorder.
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Acid-base disorders: test your
understanding
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
bicarbonate.
f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of
two or more acid-base disorders.
g) A normal venous HCO3- value indicates there is no acid-base disorder.
h) Normal arterial blood gas values rule out the presence of an acid-base
disorder.
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Acid-base disorders: test your
understanding
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.
a) false
b) true
c) true
d) true
d) An abnormal serum CO2 value always indicates an acid-base disorder of
some type.
e) false
e) The compensation for chronic elevation of PaCO2 is renal excretion of
bicarbonate.
f) true
f) A normal pH with abnormal HCO3- or PaCO2 suggests the presence of
two or more acid-base disorders.
g) false
g) A normal venous HCO3- value indicates there is no acid-base disorder.
h) false
h) Normal arterial blood gas values rule out the presence of an acid-base
disorder.
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Summary ) Clinical and laboratory approach to
acid-base diagnosis
•
Determine existence of acid-base disorder from ABG and/or venous electrolytes.
•
Examine pH, PaCO2 and HCO3- for obvious primary acid-base disorder, and for deviations that indicate
mixed acid-base disorders (TIPS 2 through 4).
•
Use a full clinical assessment (hx, phys exam, other lab data, previous ABGs) to explain each acid-base
disorder. Co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when
there is an obvious acidosis, or low when there is an obvious alkalosis.
•
Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders.
Clinical judgment should always apply.
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Arterial Blood Gases – test your overall
understanding
Case 1. A 55-year-old man is evaluated in the pulmonary
lab for shortness of breath. His regular medications
include a diuretic for hypertension and one aspirin a
day. He smokes a pack of cigarettes a day.
FIO2
pH
PaCO2
PaO2
SaO2
.21
7.53
37 mm Hg
62 mm Hg
87%
HCO3%COHb
Hb
CaO2
30 mEq/L
7.8%
14 gm%
16.5 ml O2
How would you characterize his state of ventilation,
oxygenation and acid-base balance?
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Arterial Blood Gases – test your overall
understanding
Case 1 - Discussion
VENTILATION: Adequate for the patient's level of CO2 production; the patient is neither
hyper- nor hypo- ventilating.
OXYGENATION: The PaO2 and SaO2 are both reduced on room air. Since P(A-a)O2 is
elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q
imbalance, i.e., a pulmonary problem. SaO2 is reduced, in part from the low PaO2
but mainly from elevated carboxyhemoglobin, which in turn can be attributed to
cigarettes. The arterial oxygen content is adequate.
ACID-BASE: Elevated pH and HCO3- suggest a state of metabolic alkalosis, most likely
related to the patient's diuretic; his serum K+ should be checked for hypokalemia.
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Arterial Blood Gases – test your overall
understanding
Case 2. A 46-year-old man has been in the hospital two days, with
pneumonia. He was recovering but has just become diaphoretic,
dyspneic and hypotensive. He is breathing oxygen through a
nasal cannula at 3 l/min.
pH
PaCO2
%COHb
PaO2
SaO2
Hb
HCO3CaO2
7.40
20 mm Hg
1.0%
80 mm Hg
95%
13.3 gm%
12 mEq/L
17.2 ml O2
How would you characterize his state of ventilation,
oxygenation, and acid-base balance?
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Arterial Blood Gases – test your overall
understanding
Case 2 - Discussion
VENTILATION: PaCO2 is half normal and indicates marked hyperventilation.
OXYGENATION: The PaO2 is lower than expected for someone
hyperventilating to this degree and receiving supplemental oxygen, and
points to significant V-Q imbalance. The oxygen content is adequate.
ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates
combined respiratory alkalosis and metabolic acidosis. If these changes
are of sudden onset the diagnosis of sepsis should be strongly
considered, especially in someone with a documented infection.
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Arterial Blood Gases – test your overall
understanding
Case 3. A 58-year-old woman is being evaluated in the
emergency department for acute dyspnea.
FIO2
pH
PaCO2
%COHb
PaO2
SaO2
Hb
HCO3CaO2
.21
7.19
65 mm Hg
1.1%
45 mm Hg
90%
15.1 gm%
24 mEq/L
18.3 ml O2
How would you characterize her state of ventilation,
oxygenation and acid-base balance?
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Arterial Blood Gases – test your overall
understanding
Case 3 - Discussion
VENTILATION: The patient is hypoventilating.
OXYGENATION: The patient's PaO2 is reduced for two reasons: hypercapnia and V-Q
imbalance, the latter apparent from an elevated P(A-a)O2 (approximately 27 mm
Hg).
ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic
acidosis; the calculated HCO3- is lower than expected from acute respiratory
acidosis alone.
.
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Arterial Blood Gases – test your overall
understanding
Case 4. A 23-year-old man is being evaluated in the emergency
room for severe pneumonia. His respiratory rate is 38/min and he
is using accessory breathing muscles.
FIO2
pH
PaCO2
PaO2
SaO2
HCO3%COHb
Hb
CaO2
.90
7.29
55 mm Hg
47 mm Hg
86%
23 mEq/L
2.1%
13 gm%
15.8 ml O2
Na+
K+
ClHCO3-
154 mEq/L
4.1 mEq/L
100 mEq/L
24 mEq/L
How would you characterize his state of ventilation,
oxygenation and acid-base balance?
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Arterial Blood Gases – test your overall
understanding
Case 4 - Discussion
VENTILATION: The patient is hypoventilating despite the presence of tachypnea, indicating
significant dead space ventilation. This is a dangerous situation that suggests the need
for mechanical ventilation.
OXYGENATION: The PaO2 and SaO2 are both markedly reduced on 90% inspired oxygen,
indicating severe ventilation-perfusion imbalance.
ACID-BASE: The low pH (7.29), high PaCO2 (55) and normal HCO3- all point to combined acute
respiratory acidosis and metabolic acidosis. Anion gap is elevated to 30 mEq/L
indicating a clinically significant anion gap (AG) acidosis, possibly from lactic acidosis.
AG = Na - (Cl + HCO3-)
= 154 - (100 + 24) = 30 mEq/L
With an of AG of 30 mEq/L his venous HCO3- should be much
lower, to reflect buffering of the increased acid.
However, his venous HCO3- is normal, indicating a
primary process that is increasing it, i.e., a metabolic
alkalosis in addition to a metabolic acidosis. The cause
of the alkalosis is as yet undetermined. In summary
this patient has respiratory acidosis, metabolic
acidosis and metabolic alkalosis.
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Blood Gas Interpretation
means analyzing the data to determine patient’s state of:
Ventilation
Oxygenation
Acid-Base
Oh, did I mention you can’t learn this
from a lecture?
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The best way to learn ABGs is to work on blood gas problems with some knowledge
of basic physiology, then check your work for instant feedback. This ‘iterative
process’ will teach you blood gas interpretation.
Books
Web sites
You Can’t Learn Arterial Blood Gases from a Lecture
You CAN learn ABGs from selected web sites.
See list at:
www.lakesidepress.com/ABGindex.htm
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