Transcript Interpreting Blood Gases: The Respiratory Perspective

Blood Gases
David Creery, MD MSc FRCPC MHSc
Pediatric Critical Care, CHEO
Medical Director of Patient Safety, CHEO
Investigating Coroner, Ottawa
Associate Professor, Faculty of Medicine, Pediatrics
Objectives
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List the independently measured values in arterial blood
gases and outline the normal values of these variables.
Describe the measurement of oxygenation: saturation vs
partial pressure of the gases versus arterial oxygen
content.
Explain the inter‐relation between HCO3 and PCO2.
Explain how compensation occurs in blood gas disorders,
identify the importance of the normal compensation
values, and describe how this can be used to determine
whether relevant compensation has occurred.
Objectives
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Define respiratory acidosis and alkalosis, and metabolic
acidosis and alkalosis, and explain how respiratory and
metabolic compensation occur.
Define the following terms: acute respiratory acidosis,
acute respiratory alkalosis, chronic respiratory acidosis,
chronic respiratory alkalosis, metabolic acidosis and
metabolic alkalosis.
Develop an approach to identifying acute and chronic
metabolic acidosis and alkalosis, including mixed
disorders.
Arterial Blood Gas:
Normal Values
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pH = 7.35 - 7.45
PaCO2 = 35 - 45 mm Hg
PaO2 = 70 - 100 mm Hg
SaO2 = 93 – 98%
HCO3- = 22 - 26 mEq/L
Base Excess = – 2.0 to 2.0 mEq/L
Describe the measurement of
oxygenation: saturation vs
partial pressure of oxygen vs
arterial oxygen content.
PaO2 = Partial pressure of O2 in
the plasma phase of arterial blood
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Measured by an electrode that senses dissolved
oxygen molecules
Oxygen passes through the thin alveolarcapillary membrane and enters the plasma
phase as dissolved molecules…then most of
these molecules quickly enter the red blood cell
and bind with hemoglobin.
Once bound to Hb, the oxygen molecules no
longer exert any pressure.
PaO2 = Partial pressure of O2 in
the plasma phase of arterial blood
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The more dissolved molecules there are, the
more are available to bind to Hb.
Depending on the PaO2 and other factors, some
O2 molecules will be dissolved and some will be
bound.
SaO2 = Oxygen Saturation
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4 oxygen binding sites per Hemoglobin
Hemoglobin oxygen saturation = the percentage
of all the available heme binding sites saturated
with oxygen
Hemoglobin is like an smart sponge that
“chooses” when to soak up oxygen and when to
give it up.
PaO2 and SaO2: The
Relationship
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PaO2 is determined by alveolar PO2 and the
state of the alveolar-capillary interface.
PaO2, in turn, determines the oxygen saturation
of hemoglobin (along with other factors that
affect the position of the O2-dissociation curve).
Oxygen Content: Hb and its
relationship to SaO2 and PaO2
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The more hemoglobin available to bind the dissolved
oxygen molecules, the greater total number of
oxygen molecules the blood will contain.
PaO2 is not a function of hemoglobin level
PaO2 gives us valuable information about adequacy
of gas exchange within the lungs, when (and only
when) it is subtracted from the calculated alveolar
PO2 (big A).
We use the Alveolar Gas Equation to calculate PAO2.
Oxygen Content: How much
oxygen is in the blood?
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Tissues need a threshold amount of O2 molecules for
aerobic metabolism.
CaO2 = directly reflects the total number of oxygen
molecules in arterial blood, both bound and unbound to
hemoglobin
 = (1.39 x Hb x Sat) + (PaO2 x 0.003)
 Oxygen bound to Hb is much more important than
dissolved oxygen
CO = HR x SV
Oxygen Delivery = CO X CaO2
Oxygen Content: Hb and its
relationship to SaO2 and PaO2
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SaO2 is determined mainly by PaO2. The
relationship between the two variables is the
oxygen-dissociation curve.
PaO2 is the most important (but not the only)
determinant of SaO2.
The oxygen-Hb dissociation curve tells us about
Hb’s affinity for oxygen.
Some conditions shift the position of the oxygen
dissociation curve left or right.
Oxygen-Hb Dissociation Curve
Small
changes in
paO2 make
BIG change
in Sats
Shape and position of the curve
are the same irrespective of the
hemoglobin content.
Big changes
in paO2
make
ALMOST NO
change in
Sats
But there’s more…the curve shifts
LEFT
SHIFT =
HARDER
TO
RELEASE,
EASIER TO
BIND
RIGHT SHIFT =
EASIER TO RELEASE,
HARD TO
BIND…..need higher
PaO2 to maintain
same Sat
Clinical Problem

A 28 yr old woman has just delivered a baby. She has
a PaO2 of 85 mm Hg, a SaO2 of 98%, and a
hemoglobin of 140. She then has a severe postpartum hemorrhage. The blood is replaced acutely
with normal saline, which leaves her with a
hemoglobin of 70. What will be her new PaO2, SaO2,
and CaO2?
Clinical Problem
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A 40 yr old woman has a PaO2 of 85 mm Hg, a SaO2
of 98%, and a hemoglobin of 140. She then has a
severe post-partum hemorrhage. The blood is
replaced acutely with normal saline, which leaves her
with a hemoglobin of 70. What will be her new PaO2,
SaO2, and CaO2?
* PaO2 unchanged, SaO2 unchanged, CaO2 reduced.
Hemoglobin content is suddenly reduced by half,
which will lower CaO2 by half. However, the PaO2 and
SaO2 will be unaffected, since their values are
independent of the content of hemoglobin present.
Define respiratory acidosis and alkalosis,
and metabolic acidosis and alkalosis, and
explain how respiratory and metabolic
compensation occur.
Interpreting Blood Gases
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Not complicated if you ask questions sequentially
Information about two distinct things: acid-base status
and oxygenation (key fact: how was the blood drawn?)
Acidosis is much more clinically important than alkalosis
CO2 “creates” acidosis (more CO2 is bad); bicarb
“creates” alkalosis (more bicarb is good)
Lungs compensate quickly, kidneys compensate slowly
Compensation starts immediately (key question: how
much compensation has occurred?)
We never overcompensate
A blood gas is a snapshot of a dynamic process
pH ≈ HCO3PaCO2
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pH is life and death
The system almost instantly reflects any
disturbances
The changes in degree and direction of bicarb
and CO2 are the keys to interpreting acid-base
disorders
Bicarb is good, CO2 is bad
Definitions:
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Acidemia: Blood pH < 7.35
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Acidosis: A primary physiologic process that,
occurring alone, tends to cause acidemia
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Can be acute or chronic
increased production of H+ by the body or the
inability of the body to form HCO3- in the kidney
e.g. metabolic acidosis from decreased perfusion (lactic
acidosis)
e.g. respiratory acidosis from hypoventilation
Definitions:

Alkalemia: Blood pH > 7.45
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Alkalosis: A primary physiologic process that,
occurring alone, tends to cause alkalemia.
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Can be acute or chronic
Decrease in H+ concentration
e.g. metabolic alkalosis from prolonged vomiting
e.g. respiratory alkalosis from acute hyperventilation
Definitions:

Primary acid-base disorder: One of the four
acid-base disturbances that is manifested by an
initial change in HCO3- or PaCO2.
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If HCO3- changes first, the disorder is either a
metabolic acidosis (reduced HCO3-) or metabolic
alkalosis (elevated HCO3-).
If PaCO2 changes first, the problem is either
respiratory alkalosis (reduced PaCO2) or respiratory
acidosis (elevated PaCO2).
Definitions:
Compensation: The change in HCO3- or PaCO2 that
occurs as a reaction to the primary event.
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Two types: metabolic compensation or respiratory
compensation
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Snapshot of a dynamic process
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Lungs fast, kidneys slow; CO2 bad, bicarb good
The 4 Primary Acid-Base
Disorders
Primary Event
DISORDER
Compensatory
Event
↓HCO3PaCO2
Metabolic acidosis
↓pH
↓PaCO2
↑ HCO3PaCO2
Metabolic alkalosis
↑pH
↑ PaCO2
HCO3↑ PaCO2
Respiratory acidosis
↑pH
↑ HCO3-
HCO3↓ PaCO2
Respiratory alkalosis
↑ pH
↓HCO3-
But they’re not equal…
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Acidosis is +++ more important
Three types of acidosis:
Respiratory: too much CO2
Metabolic – Anion Gap: unmeasured anion
(CAT-MUDPILES)
Metabolic – Nonanion gap: loss of bicarb in
gut or kidneys
Alkalosis
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Metabolic alkalosis
Chloride-responsive (responds to NaCl/KCl)
- Diuretics, corticosteroids, gastric suctioning,
vomiting
Chloride-resistant
- Any hyperaldosterone state (e.g., Cushing’s
syndrome), severe K+ depletion

Respiratory alkalosis
Hyperventilation
Blood Gas Nomenclature
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Could be ABG, CBG or VBG (art, cap, venous)
Standard short form pH/pCO2/pO2/Bicarb in that order
Bicarb sometimes written HCO3
For CBG and VBG, pO2 usually omitted
So for ABG pH 7.35 pCO2 43 pO2 105 and Bicarb 23 it
would be written 7.35/43/105/23
For VBG and CBG it would be written 7.35/43/-/23
Steps to Acid-Base
Interpretation
1.
2.
3.
4.
Look at the pH. What is the acid/base
disturbance?
Look at the bicarb and the pCO2. Which
element is driving the pH? (Could be both)
Is there compensation occurring? How much?
pH-BicCO2-Comp
pH-BicCO2-Comp
An Example
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Patient with COPD
pH = 7.33, CO2 = 60, Bicarb = 31
pH is acidotic (barely)
CO2 is high (driving acidosis)
Bicarb is high (meaning compensation has
begun and working to restore normal pH
Which values are inside vs. outside the box?
Side with two (or three) X’s defines the condition
If third X is inside the box, compensation just starting
If outside opposite, compensation is underway
If pH is back within box, compensation has worked
If X’s outside same, it’s combined
©2011 by American Physiological Society
Blood gas data for a patient with COPD
pH = 7.33
CO2 = 60
Bicarb = 31
Dietz J R Advan in Physiol Edu 2011;35:454-455
©2011 by American Physiological Society
Side
with two (or three) X’s defines the condition
Side with two (or three) X’s defines the condition
If third
X is inside
the the
box,
compensation
just starting
If third
X is inside
box,
it’s uncompensated
If outside
opposite,
compensation
is
underway
If outside opposite, it’s compensated
If pH is backIf within
compensation
outsidebox,
same,
it’s combined has worked
If X’s outside same, it’s combined
pH-BicCO2-Comp
Another Example
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Patient with diabetic ketoacidosis
pH = 7.05, CO2 = 15, Bicarb = 6
pH is acidotic
Bicarb is low (driving the acidosis)
CO2 is low (i.e. NOT driving acidosis)
Compensation has begun, and is helping
(What would pH be if the CO2 was normal?)
but pH still very low
Same patient using the box
pH = 7.05
CO2 = 15
Bicarb = 6
Dietz J R Advan in Physiol Edu 2011;35:454-455
©2011 by American Physiological Society
Side with two (or three) X’s defines the condition
If third X is inside the box, compensation just starting
If outside opposite, compensation is underway
If pH is back within box, compensation has worked
If X’s outside same, it’s combined
pH-BicCO2-Comp
Another Example
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Patient post cardiac arrest
pH = 7.02, CO2 = 80, Bicarb = 6
pH is acidotic
Bicarb is low (driving the acidosis)
CO2 is high (i.e. ALSO driving acidosis)
Compensation has NOT begun, because the
acidosis is a COMBINED respiratory and
metabolic acidosis
Blood gas data for a patient in cardiopulmonary arrest.
pH = 7.02
CO2 = 80
Bicarb = 19
Dietz J R Advan in Physiol Edu 2011;35:454-455
©2011 by American Physiological Society
Side with two (or three) X’s defines the condition
Side with two (or three) X’s defines the condition
If third X is inside the box, compensation just starting
If third X is inside the box, it’s uncompensated
If outside
opposite,
compensation
is underway
If outside
opposite,
it’s compensated
If pH is back
within
box,
compensation
If outside same, it’s combined has worked
If X’s outside same, it’s combined
Answer:
Need more info.
You need 2 out of 3 variables to obtain the 3rd.
The pH could be acidemic or alkalotic.
Answer:
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HCO3-: usual value is 22 to 26, so this rose
50%
PCO2: usual value is 35 to 45, so this rose
50%
∆ Ratio = none
pH = 7.4
Case #1: Sarah Smith
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You are the on-call medical student for orthopedics. You
are called to see Sarah, a 16 yr. old who is post-op day
#2 following spinal instrumentation for scoliosis.
Her nurse called you because Sarah is difficult to rouse.
Sarah has been receiving morphine for pain control.
Her most recent vital signs are:
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HR 70
BP 110/50
RR 7
Sats 90% R/A
Temp 37.3 ax
Case #1: Sarah Smith
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On exam she has occasional upper airway sounds and
no accessory muscle use. You hear decreased air entry
at the bases with no crackles or wheeze. She is warm to
touch and is pink. She is unresponsive.
You perform an arterial blood gas, support her breathing
with a bag and mask and ask the nurse to draw up a
medication.
The results of the blood gas are:
 7.20/65/65/25
Your attending arrives on the ward and asks you what
you think is going on.
What you’re thinking…
7.20/65/65/25
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You have information about two distinct things: acid-base
and oxygenation
You remember pH-BicCO2-Comp
For acid-base, first look at pH (Acidosis!)
Then look at pCO2 and Bicarb (CO2 is high so it’s a
respiratory acidosis); bicarb is high so kidneys are trying
to compensate
For oxygenation, first question is how was blood drawn
(arterial, so pO2 is low)
What you’re thinking 2…
7.20/65/65/25
“What could cause a respiratory acidosis with partial
compensation and low arterial oxygen levels?”
“What could cause these findings in this patient?”
You mull over the following
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Could this be primary lung disease (pneumonia, pulmonary
embolus, fluid overload, pleural effusion, pneumothorax)
Could this be reduced respiratory drive (stroke, medications)
Could this be an airway obstruction?
You decide to put the results into the box…
Case #1: Sarah Smith
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7.20/65/65/25
Side with two (or three) X’s defines the condition
If third X is inside the box, it’s uncompensated
If outside opposite, it’s compensated
If outside same, it’s combined
You’re Ready to Speak…
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PaCO2 is elevated and pH is acidotic
This is an partially compensated respiratory acidosis (partially
because the bicarb is moving in the right direction but is not outside
the box yet and the pH is still low)
The bicarbonate is in the normal range because the kidneys have
not had adequate time to establish effective compensatory
mechanisms
Lungs are fast, kidneys are slow
The PaO2 is low, but in keeping with her oxygen saturation
She has received too much narcotic, and needs airway support +/naloxone
Primary Respiratory Problems:
Pathophysiology
PaCO2= CO2 Production / Alveolar ventilation
PaCO2 ~
CO2 production
Minute ventilation – Dead Space Ventilation
Primary Respiratory Problems:
Pathophysiology
PaCO2 ~
CO2 production
Minute ventilation – Dead Space Ventilation
CO2 EXCRETION
 Alveolar ventilation = MV (tidal volume x rate) – DS
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Alveolar ventilation regulated by:
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Dead space = all airways larger than alveoli
Does not contribute to gas exchange
More is bad (e.g. breathing through garden hose)
Central respiratory centers (pons, medulla)
Chemoreceptors for PaCO2, PaO2, and pH in the brainstem
Neural impulses from lung-stretch receptors
As long as the lungs excrete the volatile fraction (CO2)
through ventilation there is no acid accumulation
What can cause respiratory acidosis?
PaCO2 ~
CO2 production
Minute ventilation – Dead Space Ventilation
CO2 production
OR
CO2 excretion
 If Alveolar Ventilation does not match CO2 production 
PaCO2
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CNS impairment (head trauma, brainstem lesion, medications)
Airway obstruction
Mechanical impairment (chest trauma, pneumothorax, muscle
weakness, residual neuromuscular blockade)
Decreased perfusion (pulmonary embolus, cardiac arrest)
Parenchymal disease (pneumonia, edema)
Acute Respiratory Acidosis:
Important Points
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NOT a diagnosis - represents a failure of the respiratory
system in some aspect that requires investigation and
urgent treatment
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As PaCO2 increases, PAO2 (and hence PaO2) will fall
unless inspired oxygen is supplemented
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Alveolar Gas Law: “Limited space in the alveoli for gases;
CO2 crowds out oxygen”
Case #2: Nate Norman
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You are on-call for pediatrics and called to see Nate, an
8 month old ex-28 wk baby admitted 3 days ago with
respiratory distress and RSV bronchiolitis.
His nurse called you because Nate seems to be working
harder to breathe.
He is receiving the usual supportive care and ventolin
q3-4hrs. His usual meds include flovent and lasix.
His most recent vital signs are:
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HR 150
RR 65
BP 80/55
Sats 88% R/A
Temp 37.6 ax
Case #2: Nate Norman
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You do an examination and find that he has a lot of
secretions, occasional nasal flaring but no grunting. He
has mild subcostal indrawing and decreased a/e in the
right upper lobe and ++wheezes on auscultation. You
don’t hear any murmurs and he is warm to touch with
capillary refill being less than 2 seconds. He is awake
and alert.
You ask the nurse to give him some ventolin and you
perform an arterial blood gas.
Your Attending arrives and asks you to interpret the
blood gas and the clinical situation.
The results of the blood gas are:
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7.36/70/55/34
You Consider the Key Points Again
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pH-BicCO2-Comp
Information about two distinct things: acid-base status
and oxygenation (How was the blood drawn?)
Acidosis much more clinically important than alkalosis
CO2 “creates” acidosis (more CO2 is bad); bicarb
“creates” alkalosis (more bicarb is good)
Lungs compensate quickly, kidneys compensate slowly
This is a static snapshot of a dynamic process
Inside Your Brain…
7.36/70/55/34
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You’re somewhat surprised to see that the pH is normal,
but the CO2 is high.
Them you realize that the CO2 is high, and the bicarb is
high, so there are two things going on
The pH is at the lower end of normal, so you decide that
this is a primary respiratory acidosis with metabolic
compensation
You think, if I had done a blood gas 12 hours ago, I might
have seen a partially compensated respiratory acidosis
Attending is tapping her fingers on the desk and looking
at her watch
You put the results in the box…
Case #2: Nate Norman (1)
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7.36/70/55/34
Side with two (or three) X’s defines the condition
If third X is inside the box, it’s uncompensated
If outside opposite, it’s compensated
If outside same, it’s combined
You’re Ready to Speak…
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PaCO2 is elevated and pH in acceptable range
Bicarbonate is elevated because the kidneys have had
adequate time to establish effective compensatory
mechanisms
Remember that we never overcompensate (unless there are
two distinct things going on)
The PaO2 is in keeping with his saturations
What could be causing these findings in this patient? You say
“Acute on chronic lung disease (RSV bronchiolitis on top of
lung changes of prematurity)”
Attending appears satisfied and moves on to grilling another
student
Case #2: Nate Norman
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You suggest to Nate’s nurse to give him oxygen,
increase the frequency of suctioning and ventolin and
start physiotherapy.
Four hours later you’re back to see him: he seems to be
getting tired and working harder.
His most recent vital signs are:
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HR 165
RR 80
BP 80/55
Sats 93% on 40% oxygen
Temp 38 ax
Case #2: Nate Norman
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On examination you find nasal flaring, grunting and
moderate to severe subcostal indrawing. He has
decreased a/e on the right side and ++wheezes on
auscultation. He appears tired and lethargic.
You ask the nurse to call for an x-ray and you perform
an arterial blood gas.
Your Attending arrives and asks you to interpret the
blood gas and the clinical situation.
The results of the blood gas are:

7.20/96/80/37
Inside Your Brain…
7.20/96/80/37
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You
You
You
The
You
You
consider the key points again
first look at the pH (acidotic!)
see that the CO2 is much higher than before
bicarb is higher (but is it “higher enough”?)
see the PaO2 is higher (but Nate is now on O2)
put the values into the box…
Case #2: Nate Norman (2)

7.20/96/80/32
Side with two (or three) X’s defines the condition
If third X is inside the box, it’s uncompensated
If outside opposite, it’s compensated
If outside same, it’s combined
You’re Ready…
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The PaCO2 is elevated and pH is low, even though
bicarb is high (But not high enough)
Kidneys have not had adequate time to fully
compensate
You decide that Nate is getting quite a bit sicker and
needs some respiratory support
Nate is transferred to PICU and placed on BiPAP
An Example of Respiratory Failure
12 yo girl
pH
pCO2
Bicarb
10:00
10:25
11:25
13:35
13:55
18:10
7.06
69
20
7.17
58
21
7.23
48
20
7.35
36
20
7.33
37
20
7.37
34
20
Metabolic Acidosis
When you find a patient has a primary
metabolic acidosis, you must do more work:
The ANION GAP
Anion Gap: Na+ – (Cl- + HCO3-)
Normal Gap: 8-16
Can also calculate with the K. Normal range
about 4 higher
Causes of Anion-Gap Acidosis
Increased acid production:
 Ketones
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Lactic acid
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DKA, starvation
tissue hypoxia, sepsis, exercise,
EtOH/MeOH/ethylene glycol
ingestion, paraldehyde, Inborn
Error of Metabolism (IEM)
Everything else
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ASA, NSAID, Iron
Other Mnemonics
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DR. MAPLES
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SLUMPED
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D-DKA, R-Renal, M-Methanol, A-Alcoholic
Ketoacidosis, P-Paraldehyde, L-Lactate, E-Ethylene
Glycol, S-Salicylates
S-Salicylates, L-Lactate, U-Uremia, M-Methanol, PParaldehyde, E-Ethylene Glycol, D-Diabetes
GOLD MARK

G-Glycols, Oxoproline, L&D-L&D Lactate, M-Methanol,
A-Aspirin, R-Renal Failure, K-Ketoacidosis
Causes of NON-Anion Gap
Acidosis
Hyperchloremic metabolic acidosis

GI loss of HCO3
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Renal loss of HCO3
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Diarrhea, Necrotizing enterocolitis, small bowel
drainage/fistula
RTA, early renal failure, CA inhibitors
Administration of HCl or other chloridecontaining substances (i.e. NS)

hyperalimentation
Another Example:
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8 year old girl, Susie, presents to ER with
tachypnea, tachycardia, altered level of
consciousness
Calculate the anion gap
Vital signs:
HR 140
 RR 46
 BP 95/50
Gas:
 pH 7.05
 PCO2 20
 HCO3 7
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Na+ - (Cl- + HCO3)
Normal anion gap 12-16
More Labs:
Anion gap = 30
Na: 132
Cl: 95
HCO3: 7
Glucose: 44
Acute Metabolic Acidosis
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Primary metabolic acidosis, with increased
anion gap with respiratory compensation
CAT-MUDPILES
Lactate, Ketones, Everything else
DKA Example…
14 yo boy
pH
pCO2
Bicarb
8:20
9:45
11:40
13:15
17:10
21:00
7.05
33
9
7.03
26
7
6.94
33
7
7.05
33
9
7.26
35
16
7.28
36
17
Case #3: Diane Donaldson
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You are working in the ER and see Diane, a 27 yr. old
who is complaining of pleuritic chest pain of several
hours duration.
She also complains of upper respiratory tract symptoms
that started 2 days earlier.
She is otherwise healthy with no significant past medical
history.
She has no allergies and her only medication is the oral
contraceptive pill.
Last evening she returned from overseas by plane.
She is a half pack per day smoker.
Case #3: Diane Donaldson
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Her most recent vital signs are:
 HR 95
• Sats 94% in room air
 BP 110/70
• Temp 37.0 ax
 RR 28
On exam she is congested but in no distress. She is
tachypneic but has no accessory muscle use. You hear
equal air entry bilaterally and her chest is clear on
auscultation. She complains of discomfort when you ask
her to take big breaths.
You decide to order a chest x-ray and arterial blood gas.
Your Attending arrives and asks you to interpret the
blood gas and the clinical situation.
The results of the blood gas are:
 7.47/31/83/22
What you’re thinking…
7.47/31/83/22
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pH is high (alkalosis)
pCO2 is low, bicarb is low normal (primary
respiratory alkalosis) with partial compensation
It’s an arterial gas, so you can comment on
oxygenation
PaO2 in keeping with sats
But seems to be a primary oxygenation problem (!!!)
You put it in the box
Case #3: Diane Donaldson
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7.47/31/83/22
Side with two (or three) X’s defines the condition
If third X is inside the box, it’s uncompensated
If outside opposite, it’s compensated
If outside same, it’s combined
Respiratory Alkalosis
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PaCO2 is low and the pH is alkalotic
The increase in pH is caused by the decrease in paCO2
Bicarbonate is normal range because the kidneys have
just started to compensate (but do a gas in 2 hours and
compensation is likely to be more complete)
You mull over what could cause these findings (partially
compensated respiratory alkalosis and hypoxia) in this
clinical scenario
First, What Could Be Causing the
Respiratory Alkalosis?
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Central nervous system
 Pain, Anxiety, Psychosis
 Hyperventilation syndrome
 Fever
 Cerebrovascular accident
 Meningitis, Encephalitis
 Tumor
 Trauma
Hypoxia
 High altitude
 Severe anemia
 Right-to-left shunts
Drugs
eg. Salicylates
Endocrine
 Pregnancy
 Hyperthyroidism
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Pulmonary
 Pneumo/hemothorax
 Pneumonia
 Pulmonary edema
 Pulmonary embolism
 Aspiration
 Interstitial lung disease
 Asthma
 Emphysema
 Chronic Bronchitis
Miscellaneous
 Sepsis
 Hepatic failure
 Mechanical ventilation
 Heat exhaustion
 CHF
What you’re thinking 2…
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But most of these conditions don’t have an
impact on oxygenation (if anything, they tend
to increase PaO2)
So you go back to the list again…
What Could Be Causing Respiratory
Alkalosis AND Hypoxia?
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Central nervous system
 Trauma
Hypoxia
 High altitude
 Severe anemia
 Right-to-left intracardiac
shunt
Endocrine
 Late pregnancy
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Pulmonary
 Pneumonia
 Pulmonary edema
 Pulmonary embolism
 Aspiration
 Interstitial lung disease
 Asthma
Could this be a pulmonary embolism?
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Recent long travel, OCP, smoker
Respiratory alkalosis with hypoxia would fit
Others not c/w clinical exam
Steps to Oxygen Interpretation
1.
Ask “How was the blood drawn?”
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Can only comment on oxygenation for arterial
Consider the PaO2 relative to the patient’s
oxygen saturations
Calculate the alveolar-arterial (A-a) gradient
Think about the oxyhemoglobin dissociation
curve and where the values would fall
Oxygenation
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Are the lungs transferring oxygen properly from the
atmosphere to the pulmonary circulation?
Use the Alveolar Gas Equation to calculate PAO2
then find the A-a O2 difference
 If the A-a gradient is elevated, the answer is NO –
there is mismatch of ventilation and perfusion
 If the A-a gradient is normal the answer is YES
A-a O2 gradient = 28 (normal <10)
 Elevated  indicating a state of V-Q imbalance and
therefore some parenchymal lung disease or
abnormality.
 Hyperventilation should cause high PaO2, therefore
NO increased A-a O2 difference
You’re Ready…
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Diane’s PaCO2 is low and the pH is alkalotic
The increase in pH is caused by the decrease in paCO2
Bicarbonate is normal range because the kidneys have
just started to compensate (but do a gas in 2 hours and
compensation is likely to be more complete)
Her A-a oxygen gradient is elevated (meaning that there
is less oxygen in the arterial blood than there should be)
You order a spiral CT and diagnose a PE
Summary
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Information about two distinct things: acid-base status
and oxygenation
Acidosis is much more clinically important than alkalosis
CO2 “creates” acidosis (more CO2 is bad); bicarb
“creates” alkalosis (more bicarb is good)
Lungs compensate quickly, kidneys compensate slowly
Compensation starts immediately (key question: how
much compensation has occurred?)
We never overcompensate
A blood gas is a snapshot of a dynamic process
Summary: Steps in Acid-Base
Interpretation
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4.
5.
Look at the pH. What is the acid/base
disturbance?
Look at the bicarb and the pCO2. Which
element is driving the pH? (Could be both)
Is there compensation occurring? How much?
pH-BicCO2-Comp
Use the box if that helps you visualize
Summary: Steps in Oxygen
Interpretation
1.
Ask “How was the blood drawn?”
1.
2.
3.
4.
5.
Consider the PaO2 relative to the patient’s
oxygen saturations
Think about the oxyhemoglobin dissociation
curve and where the values would fall
Calculate the alveolar-arterial (A-a) gradient
Oxygen Content=(1.39 x Hb x Sat) + (paO2 x 0.003)
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6.
Only comment on oxygenation if it is arterial
Big contribution from Sat and Hb, v little from paO2
Oxygen Delivery = CO x CaO2
Thank you
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Questions and Discussion
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